Information.

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Golden topics

Lambert-Eaton myasthenic syndrome is a rare form of paraneoplastic syndrome. Proximal muscles tend to be involved first. Similar to many paraneoplastic syndromes, it is most often associated with small cell carcinoma of the lung. The autoantibodies are directed against calcium channels at motor nerve terminal membranes. Patients with chronic viral hepatitis may have generalized malaise and weakness that is not related to specific muscle disease. Diabetes mellitus also may produce peripheral neuropathy, but more often involving distal, not proximal, regions first. Duchenne muscular dystrophy is an X-linked disease that manifests early in childhood. Lead poisoning leads to peripheral neuropathy, often with central nervous system findings.

Von Hippel–Lindau disease is rare and results from acquired or inherited mutation in a tumor suppressor gene. The neoplasms in this case include, in order, retinal angiomas, adrenal pheochromocytoma, cerebellar hemangioblastomas, and renal cell carcinomas producing erythropoietin. Gardner syndrome has the same mutation in the adenomatous polyposis coli (APC) gene as familial polyposis, but also has osteomas, epidermal cysts, and fibromatoses. The MET oncogene is mutated in papillary renal carcinomas (not associated with other tumors elsewhere) and in Denys-Drash syndrome, which also includes Wilms tumor plus gonadal dysgenesis and nephropathy. Neurofibromatosis type 2 includes schwannomas, meningiomas, gliomas, and ependymomas. Tuberous sclerosis is one of the phakomatoses with cortical hamartomas called tubers, renal angiomyolipomas, cardiac rhabdomyomas, and subungual fibromas. Beckwith- Wiedemann syndrome includes Wilms tumor, hemihypertrophy, and adrenal cytomegaly.

which muscle was not strengthened by a particular exercise (very odd, wtf-type question at first), but the correct answer was the only one that was sympathetically innervated, whereas the others were somatic, so of course it couldn't be strengthened by exercise.

Though Staphylococcus aureus infection is responsible for 80% to 90% of all cases of osteomyelitis in which an organism can be cultured. Salmonella osteomyelitis is especially common, however, in patients with sickle cell anemia. Group B streptococcal infections causing osteomyelitis are most common in neonates. Klebsiella pneumoniae osteomyelitis may rarely be seen in adults with urinary tract infections caused by this organism. Tuberculosis is a rare cause of osteomyelitis in adults who have had active pulmonary disease with dissemination, most likely because of a poor immune response.

Avascular necrosis of bone (osteonecrosis) represents a localized area of bone infarction, most often in a metaphyseal medullary cavity or subchondral epiphyseal location. The femoral head is most often affected. Underlying conditions associated with osteonecrosis include hemoglobinopathies (sickle cell disease in particular), fracture, barotrauma, hypercoagulable states, and hyperlipidemia. Glucocorticoid therapy decreases osteoblastogenesis to promote avascular necrosis, as in this patient with systemic lupus erythematosus and glomerulonephritis. An enchondroma is a benign tumor of hyaline cartilage that arises in the medullary space of young adults. Osteoarthritis may produce some cartilaginous erosion, but not collapse or bone infarction. Osteomyelitis typically is not so localized, and there is irregular new bone formation (involucrum). The patient’s course is quite short for renal osteodystrophy, which is mediated through chronic renal failure and produces lesions such as osteitis fibrosa cystica

Acute mesenteric ischaemia will result in severe abdominal pain that is out of proportion to an otherwise relatively normal physical exam. It occurs most often at the splenic flexure (same as with chronic), and the colon grossly demonstrates "patchy areas of necrosis and haemorrhage."Collateral circulation is not well-developed between the middle (SMA) and left (IMA) colic arteries.

For chronic mesenteric ischaemia, I've seen this asked in some tricky ways. They'll tell you the patient has a Hx of cardiovascular disease, but then they'll also tell you that he or she has pain that worsens after meals and weight loss due to food aversion, making you think that it could be a gastric ulcer. In this case, the CVD info is not a distractor, and the answer is actually chronic mesenteric ischaema, not gastric ulcer. Whereas acutely, ischaemia can be due to thrombus/embolus, chronic mesenteric ischaemia is almost always due to atherosclerosis. The USMLE wants you to know that this condition (and its pain)is very similar to angina pectoris. Whereas acutely you have the patchy areas of necrosis, in the chronic state, you have mucosal atrophy and loss of villi in hypoperfused areas. The other thing: the middle and left colic arteries anastamose via the marginal artery. This anastamosis is better developed in the chronic state. Also, the distal sigmoid is a watershed between the IMA and hypogastric arteries.

Somewhat drug-unique mechanisms: Aminoglycosides: phosphorylation, acetylation, adenylation (perhaps PAPA) Macrolides: decreased influx Tetracyclines: increased efflux Chloramphenicol: plasmid-encoded acetyltransferase that inhibits drug Shared mechanisms: Modified ribosomal binding site (23S rRNA): macrolides, chloramphenicol I'm actually over-simplifying it (going off the top of my head here). There are a few more, if someone else wants to fill in the gaps. However I also remember that all antibiotic resistance is plasmid-encoded, except for fluoroquinolones (mutated gyrase), which is chromosome-encoded.

Another question: How exactly does the spleen clear encapsulated bacteria? I haven't found anywhere that is explicit. Since the capsule is supposed to help escape phagocytosis, are we left assuming that immunoglobulins clear the SHiN+salmonella bugs? As far as encapsulated bacteria are concerned, it has been my understanding that they require opsonization for eradication, which necessitates IgM/G binding to the capsule using the Fab fragment; complement then binds to the Fc regions of these same Igs, enabling macrophages to phagocytose. Because the cords of Billroth of the spleen house ~50% of the body's reservoir of cells of monocytic lineage and the spleen itself is such a prominent secondary lymphoid organ, hypo- or asplenia results in decreased phagocytosis of opsonized pathogens. I'm fairly sure Klebisella also falls into this category. Someone please add to that if I'm missing something.

A 61-year-old woman with a long history of poorly controlled hypertension suddenly has excruciating anterior upper sternal pain radiating to the neck and back. On admission to the emergency department, her blood pressure is 210/110 mm Hg. Fifteen minutes later, while lying down, it is 110/64 mm Hg. Transesophageal echocardiography shows aortic insufficiency, a suggestion of a double lumen of the ascending aorta, and a pericardial effusion. She dies suddenly while awaiting an operation. Which of the following is the most likely cause of death? A. Acute hemopericardium B. Acute myocardial infarct C. Cerebral infarct D. Congestive heart failure E. Massive retroperitoneal hemorrhage I had encountered this in probably GT QBank that, as you said, the most common cause of death in aortic dissection is cardiac tamponade, not choice E. Acute aortic insufficiency means that the dissection has stretched proximally to the aortic valve, so a haemopericardium is likely.

For instance, they want you to realize that increased coiling vs tubular shape = secretory/luteal vs proliferative/follicular. If they show you a picture, know what you're looking at. They also want you to know early-secretory vs late-secretory phase histo. You've got coiled glands in both, but in the early-phase, you've got superficial vacuoles, whereas in the late-phase, the contents have been released. Another thing: menstruation is apoptosis, not atrophy. Menopause is atrophy. But then it increases again as your "secondary peak" roughly midway through the luteal phase. The rationale is that the increased progesterone can be converted to estrogen via the same pathway that's outlined in FA at the beginning of the endocrine chapter.

Recent test takers, have you by any chance been asked questions on the Pi3K/Akt/mTOR pathway? I know Pi3K is seen with the insulin pathway to cause GLUT-4 protein synthesis, but what about when used with Akt/mTOR? Glut 4 translocation: Insulin/IGF binds to its receptor. Receptor transphosphorylates itself and then phosphorylates IRS which causes PI3K to convert PIP2 to PIP3 on cell membrane. PIP3 causes Pdk to activate Akt (protein kinase B), which phosphorylates AS160 to allow Glut 4 translocation to the cell membrane and glucose to enter skeletal muscle cell/adipocyte. In its unphosphorylated state, AS160 inhibits Glut 4 translocation. Exercise can also cause AMP Kinase to phosphorylate AS160, resulting in same event as mentioned above. For muscle hypertrophy/protein synthesis: Same ligand-receptor event as above, except IGF-1 is ligand. Same PI3K pathway to eventually activate Akt, which then stimulates mTOR to stimulate P7056K. In addition, Akt inhibits the FOXO pathway, which is involved in protein catabolism. Therefore, protein synthesis is the favored pathway. There is muscle buildup. Glut 4 is only a glucose transporter for this pathway. Doesn't play a role in protein synthesis here.

the black widow spider causes hypocalcaemia and tetany, whereas the brown recluse spider causes abdominal pain. I didn't think vesicles themselves could be depleted. Maybe the black widow upregulates calcium consumption presynaptically (which is why the ACh release and tetany occur), leading to calcium depletion (hypocalcaemia and failure of vesicular fusion) that cannot be compensated for acutely merely with calcium. Calcium gluconate is the treatment, so we're clearly trying to restore presynaptic calcium. Vesicles wouldn't bind to the membrane without calcium (same process as in phototransduction)

* toll like receptor is which CD?

TLR 1 - triacyl lipoproteins TLR 2 - lipoproteins and peptidoglycans TLR 3 - dsRNA TLR 4 - LPS TLR 5 - flagellin TLR 6 - diacyl lipoprotein TLR 7 - ssRNA TLR 9 - CpG DNA

Mesolimbic: tegmentum of midbrain --> limbic system Mesocortical: tegmentum of midbrain --> cortex Nigrostriatal: substantia nigra pars compacta --> striatum Tuberoinfundibular: arcuate nucleus --> median eminence of hypothalamus Here's one for you: be very careful when you read these types of questions. Sometimes they'll mention a simple vignette (e.g. a guy with Parkinson's), then they'll ask you where the receptors are located in a non-obvious way (in this case would be tempting to click substantia nigra, but putamen would be correct; on the real USMLE, they might have you identify the location on a gross specimen or MRI as opposed to just clicking the name - this is very high-yield).

The mechanism of absence of neutrophil in C. perfringens
1. Alpha toxin activate the platelet adhesion molecule gpIIb/IIIa leading to platelet aggregation causing occlusion of blood vessels. 2. Alpha toxin induced upregulation of leukocyte CD11b/CD18 integrins. 3. Alpha toxin–induced upregulation of platelet P-selectin and its binding to leukocyte P-selectin glycoprotein ligand The platelets interaction with neutrophils (step 3 above) , produce intermediates in lipoxin synthesis. 5. The lipoxins inhibit leukocyte recruitment, chemotaxis and adhesion to endothelium. 6. Alpha toxin also stimulated production of endothelial cell derived IL-8. High concentrations of IL-8 causes reduced diapedesis & transmigration of leukocytes through endothelium.

Lichen sclerosus will normally be described in a question as a whitish lesion with thinning of the skin. Chronic irritation/scratching is also implicated.

Rb is phosphorylated by CyclinD-CDK4/6, which enables Rb's dissociation from E2F, thereby enabling E2F-induced transcription and progression of the cell cycle. Rb is not phosphorylated by p53 (as far as I'm aware). p53 (protein) is produced from the TP53 gene. p53 binds to DNA and induces transcription of several cell cycle regulatory proteins, including p21. So for p53, I would literally just remember: TP53 gene; induces transcription of inhibitory regulators, including p21; Li-Fraumeni syndrome; tumour-suppressor. Given that there are thousands (literally) of intra- and inter-cellular proteins regulating the cell cycle, Rb and p53 likely do influence one another via up-/down-stream substrate interactions, but I'm fairly sure the p53-Rb proteins don't directly interact on a level that we need to know for the USMLE. In mantle cell lymphoma, upregulated CyclinD means increased phosphorylation of Rb.

Von Hippel–Lindau Disease An autosomal dominant disorder, von Hippel– Lindau disease is caused by heterozygous germline inactivation of the VHL tumor-suppressor gene, which resides on chromosome 3p25.21 It is characterized by the development of multiple hemangioblastomas in the central nervous system and retina, clear-cell carcinoma of the kidney, and pheochromocytoma

Robbin's says 2% chance of progression for complete mole and "rarely" for partial mole (p. 735, 8th ed.). It then goes on to say "Overall, 80% to 90% of moles do not recur after thorough curettage; 10% of complete moles are invasive, but not more than 2% to 3% give rise to choriocarcinoma. Partial moles rarely give rise to choriocarcinomas...Approximately 50% of choriocarcinomas arise in complete hyaditidiform moles; about 25% arise after an abortion, and most of the remainder occur during what had been a normal pregnancy" (736-7). Also know that haematogenous spread to the lungs is the high-yield point regarding mets of choriocarcinoma

On the USMLE, they'll assess this by telling you that a med student elicited the sign in a patient who just had thyroid surgery, and then they'll want to know which vessel was damaged (superior/inferior thyroid arteries, because they also supply the parathyroids). Or someone will elicit the sign, then they'll ask you about the embryology, and you'd have to know the parathyroids are the dorsal wings of the third pouch (inferior) or the dorsal wings of the fourth pouch (superior).

By the way, I've read on some forums/threads that Mg2+ is a cofactor for cAMP, which is blatantly wrong. Mg2+ is a cofactor for the production of cAMP, not for the actual molecule itself. Firstly, Mg2+ and Ca2+ act on the same negative feedback receptor on parathyroid chief cells. The receptor is called CaR. Magnesium is considered a partial agonist because it has 2-3x lesser affinity for CaR than calcium (both Ca and Mg are group2 alkali metals, so it's reasonable that they'd both bind given their 2s electrons). The activation of CaR induces G-protein activity via both G-alpha-i and G-alpha-q cascades (if you don't know what that means, the chart on the bottom of p.263 in FA runs you through the different G-protein pathways), thereby causing transient cytoplasmic calcium influx, activation of phospholipase-A2, decreased cAMP activity and subsequent inhibited release of PTH. It is the combination of both G-alpha-i and G-alpha-q proteins, as stimulated by CaR, that is required for inhibition of PTH release. As serum [Mg2+] decreases, CaR activation decreases and PTH secretion increases. This mechanism represents the inverse relationship that we'd expect for both the calcium-PTH relationship as well as the Mg-PTH one. So far so good. However, when serum [Mg2+] falls below 0.5mM, the inverse relationship no longer holds and PTH release decreases. This is known as the "paradoxical block of PTH secretion." As long as [Mg2+] is > 0.5mM, there will always be some degree of Mg2+ binding to CaR, because even though Mg2+ is only a partial agonist of the receptor (decreased Vmax), the receptor's affinity for Mg2+ is still high (low Km). Now, even though Mg2+ binding to CaR induces inhibitory effects on PTH secretion, its binding at baseline quantities maintains functionality of the PTH-inhibitory cascade, so in the "absence" of Mg2+ (<0.5mM), CaR loses functionality, but in such a fashion that it is constitutively activated, rather than non-signalling. Therefore, with hypomagnesaemia reaching serum [Mg2+] < 0.5mM, constitutive CaR activity inhibits PTH secretion. This explains why some patients with hypocalcaemia are refractory to Tx with Ca2+ and vitamin D; only restoration of serum Mg2+ will restore serum [Ca2+] when the patient is dual hypocalcaemic and magnesaemic.

Magnesium and the parathyroid ;
The serum levels of parathyroid hormone and magnesium depend on each other in a complex manner. The secretion of parathyroid hormone by the parathyroid is physiologically controlled by the serum calcium level, but magnesium can exert similar effects. While low levels of magnesium stimulate parathyroid hormone secretion, very low serum concentrations induce a paradoxical block. This block leads to clinically relevant hypocalcemia in severely hypomagnesiemic patients. The mechanism of this effect has recently been traced to an activation of the alpha-subunits of heterotrimeric G-proteins. This activation mimicks activation of the calcium sensing receptor and thus causes inhibition of parathyroid hormone secretion. In addition to the effects of magnesium on parathyroid hormone secretion, parathyroid hormone in turn regulates magnesium homeostasis by modulating renal magnesium reabsorption. The distal convoluted tubule is of crucial importance for parathyroid hormone-regulated magnesium homeostasis.

Abs specific for oncogene product e. g
Abs specific for oncogene product e.g. Abs against HER2/neu (Herceptin or trastuzumab)

First Aid 2012 (page 451) said hyperreflexia but the newest errata says hyporeflexia. At least from my google search, it seems that hyporeflexia is true,,, but in the diagram for B12 deficiecny, corticospinal tract is damaged with gray matter of anterior horn spared... which makes me think that it's an UMN lesion...which should result in hyperreflexia. Does anyone know the mechanism by which B12 deficiency results in hyporeflexia? Or is first aid errata wrong to say that B12 deficiency causes? It would have to be hyper-reflexia bc if it were hypo-, then we'd also expect fasciculations, atrophy, etc., and those aren't classic SCD signs (as far as whether there's actually a Babinski's or hypertonia to support my argument though, I actually haven't heard of those as being associated with SCD either).

Lead poisoning directly inhibits ALA dehydratase and ferrochelatase
Lead poisoning directly inhibits ALA dehydratase and ferrochelatase. Lead poisoning can cause sideroblastic anemia which inhibits ALAsynthase. So in short, lead poisoning inhibits ALA dehydratase directly and ALA synthase indirectly. vit B6 deficiency effects on ALA synthase.

Mitral Stenosis - High Yeild Topics For USMLE, 10 Points You Should Know Rheumatic heart disease (most common), congenital (rare)(MCQ) Most cases occur in women.(MCQ) Signs and symptoms Dyspnea on exertion (DOE)(MCQ) Rales Cough Hemoptysis Systemic embolism (due to stagnation of blood in enlarged left atrium) Accentuated right ventricle precordial thrust Signs of right ventricular failure(MCQ) Hoarse voice(MCQ) due to enlarged left atrium impinging on recurrent laryngeal nerve Diagnosis Murmur (MCQ) mid-diastolic with opening snap low-pitched rumble.

Jejunum  folic acid absorption
Ileum  vit b12 absorption

Parkinson's disease is one of the major neurodegenerative disorders
Parkinson's disease is one of the major neurodegenerative disorders. This disease is mainly characterized by tremor, bradykinesia, rigidity and postural instability that results primarily from a loss of dopaminergic neurons of nigrostriatal pathway. MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) is well known to damage the nigrostriatal dopaminergic pathway as seen in Parkinson's disease. Recent evidence shows that glial-related response plays a key role in the MPTP neurotoxic process and the blockade of glial activation may be a new therapeutic approach, which has applicability for Parkinson's disease. On the other hand, dopamine transporters (DAT) are important to the appearance of MPTP neurotoxicity because to be neurotoxin, an MPTP metabolite must first gain access to the dopaminergic neurons via DAT. Several studies suggest that DAT is a mandatory factor for expression of MPTP neurotoxicity and may explain the selective neuronal damage in the substantia nigra in MPTP toxicity. Therefore, DAT is thought to play an important role in the MPTP neurotoxic process and specific blockade of DAT with high-affinity inhibitors in neurodegenerative diseases such as Parkinson's disease, where the effective levels of dopamine are markedly reduced, may have beneficial consequences. In view of these new insights, this article suggests that the overexpression of S100beta protein secreted by glial cells may be an exacerbating factor in the neurodegeneration of dopaminergic cells. In this review, we also demonstrate the possible role of DAT in the brain cells in MPTP neurotoxicity. Thus this review provides valuable information for progressive neurodegeneration of the nigrostriatal dopaminergic neuronal pathway.

VHL disease with pheochromocytoma, hemangioblastomas of the medulla and spinal cord, and renal and hepatic cysts, retinal angiomas, and renal cell carcinomas producing erythropoietin. Tuberous sclerosis, with lymphangioleiomyomatosis of lungs, angiomyolipomas and cystic disease in kidneys, cerebral cortical tubers, retroperitoneal lymphangiomyoma, and cardiac RHABDOMYOMA ,Epiloia , mulberry tumor (retinal astrocytoma), Subependymal nodule, Poliosis, subungual nodule in fingers, hamartomatous polyps. Tuberous sclerosis is an autosomal dominant disease arising from a genetically programmed hyperplasia of ectodermal and mesodermal cells and manifested by a variety of lesions in the skin, CNS (hamartomas), heart, kidney, and other organs. The principal early manifestations are the triad of seizures, mental retardation, and congenital white spots. Facial angiofibromata are pathognomonic but do not appear until the third or fourth year.

1) I'd say the highest yield ECG tidbit is recognizing the absence of P-waves. Know atrial fib for sure. Sometimes they'll just show you the ECG then want you to know mural thrombus --> stroke, etc. So that's very high-yield. 2) Know what the WPW delta-wave looks like. 3) Be able to identify the peaked T-wave vs U-wave for hyper-/hypokalaemia. In terms of what I've seen, when they want you to identify the peaked T-wave, it's absurdly peaked, so don't flip out about it. 4) Know the spiking pattern for atrial flutter. The HR is almost always 150/min as well.

5) Simple MI (usually ST-elevation in 3 leads)
5) Simple MI (usually ST-elevation in 3 leads). It would be rare to see a posterior infarct, but be vigilant for a potential ST-depression in the anterior leads. 6) Diffuse ST-elevations +/- PR-depressions = pericarditis. 7) Sinusoidal pattern = TdP 8) Wide-complex tachy = SVT with BBB, or VT. In this case, if it's one or the other, the answer is VT. 9) Mobitz I (gradually increasing PR-segments and then finally a QRS drop) + Mobitz II (random QRS drop). 10) Complete (third-degree) heart block = QRS complexes show a HR of and the P-waves don't have any consistent pattern relative to the QRSs. 11) And as retarded as this sounds, know how to identify a normal ECG too. I had seen a question with a vignette of a guy with chest pain who had personal Hx of atherosclerosis and a family Hx of heart disease, but the answer was actually GERD because apparently the ECG in the question was normal. So rule of thumb: don't get tricked. I got tricked on that one needless to say. I think that may have been GT QBank.

Aspirin toxicity has two main physiologic effects: 1
Aspirin toxicity has two main physiologic effects: 1. The respiratory effects of salicylism are due to stimulation of the respiratory center in the medulla mediated by aspirin's effects on prostaglandins. This respiratory stimulation induces hyperventilation and respiratory alkalosis. 2. ASA's uncoupling effects on the ETC induce hyperthermia and metabolic acidosis. Initial presentation is respiratory alkalosis followed by fever and metabolic acidosis develops later. Incidentally, can you see why aspirin toxicity is such an easy diagnosis to miss? Hyperthermia, metabolic acidosis, and tachypnea in an older patient looks identical to sepsis.

Psittacosis caused by Chlamydophila ( or Chlamydia) psittaci, a gram-negative bacterium.
Clinical Features In humans, fever, chills, headache, muscle aches, and a dry cough. Pneumonia is often evident on chest x-ray. Endocarditis, hepatitis, and neurologic complications may occasionally occur. Severe pneumonia requiring intensive-care support may also occur. Fatal cases have been reported.

HYPERSENSITIVITY PNEUMONITIS :
A. Granulomatous reaction to inhaled organic antigens (e.g., pigeon breeder's lung) B. Presents with fever, cough, and dyspnea hours after exposure; resolves with removal of the exposure C. Chronic exposure leads to interstitial fibrosis.

Nitrous oxide abuse (repeated use) depletes you vitamin B12 stores and causes brain damage by causing Lhermitte's sign (electrical sensation that runs down the back and into the limbs Multiple sclerosis also cause Lhermitte's sign. The shock-like sensation on neck flexion that they described is called Lhermitte's sign and is caused by damage to the posterior columns. You can have muscle weakness as well but it isn't a requirement. I would think a pure sensory stroke would cause problems on one half of the body, not bilateral lower extremities. Also remember if you give someone folic acid who is deficient in B12 their neuro symptoms will get worse. Chronic alcoholism -> among other manifestations, liver disease (fatty -> hepatitis -> cirrhosis) + chronic pancreatitis. 1. Any degree of alcoholic liver disease (or any liver disease) would decrease the stores of B Chronic pancreatitis -> pancreatic insufficiency -> malabsorption -> depleted fat-soluble vitamins & B12.

AFP is down in Edward's. Omphalocoele can be associated with Edward's, but it's not a given.
Omphaloceles are associated with increased AFP.

## What nutritional deficiencies can cause myelopathy and neuropathy?
1. Vitamin B12 deficiency 2. Copper deficiency 3. Vitamin E deficiency 4. Folate deficiency All of above are right . ## What are the clinical features of copper deficiency? The main neurologic symptom of copper deficiency is gait difficulty. Examination shows predominantly large fiber sensory loss in the distal legs, spasticity in the lower extremities, hyperreflexia, and extensor plantar response. Nerve conduction studies and needle EMG show an axonal sensorimotor neuropathy. Somatosensory evoked potential study shows impairment of central conduction. Anemia is a known associated laboratory finding, but the neurologic symptoms can be present in the absence of hematologic abnormalities. like subacute combined degeneration.

15. What are the risk factors for copper deficiency?
1. Zinc overdose 2. Gastric bypass surgery 3. Malabsorption syndrome 4. Total parenteral nutrition without adequate copper supplementation 5. Gastrectomy and small bowel resection 6. Nephrotic syndrome

ASD is when there's a hole between the right and left atrium
ASD is when there's a hole between the right and left atrium. This is physiologic in the newborn who needs it to shunt oxygenated blood from the inferior vena cava into the left atrium and to the aorta so that the brain and upper extremities can get the oxygen they need. This hole is made by the septum primum because the cells can't quite reach the rest of the endocardial cushion and leaves a hole called the ostium primum. Then they realize their mistake and some of the cells move down to cover the hole but leave open a hole called the ostium secundum. Then another group of cells come down and form the septum segundum, closer to the right atrium. They have the same problem as the first septum but don't move down so that there's a hole between the ostium secundum and the foramen ovale. Normally, when a newborn is born, the force of the first breath clears out the fluid from the alveoli into the interstitium and the increased oxygen tension leads to a closing of the pda. Opening the alveoli means more oxygen gets into the pulmonary vasculature which increases the oxygen tension and decreases resistance. Remember that lower oxygen tension decreases vascular resistance in most other systems because if they have low oxygen, then the cells need more blood flow to get enough oxygen to survive. But in the lungs, if you close off the blood supply to where there is low oxygen tension, and sends the blood to areas of high oxygen tension so that they can be more efficient at picking up oxygen. So when the pulmonary vascular resistance goes down, more blood goes through the pulmonary system and the pressure differential between the right and the left atrium increases which normally "closes" the foramen ovale by pressing it up against the septum primum. The hole is still there which is visible as the fossa ovale. Sometimes the membranes don't fuse and that's called a patent foramen ovale which can lead to a paradoxical embolus. Ostium primum defect is when the septum primum doesn't close because there's no fusion of the superior and inferior endocardial cushions in the anterior, inferior aspect of the atrial septum. So where there is supposed to be a bunch of tissue that fills in the space where the foramen ovale should be in the septum secundum, there's a hole so this is a ostium primum ASD. This is associated with down syndrome. Ostium secundum is an asd in the upper portion of the atrial septum because the tissue underestimated how much there needs tobe to cover the hole of the foramen ovale. This problem can be due to an enlarged foramen ovale (so that it is not completely covered by the septum primum), inadequate growth of the septum secundum (so there's a part of the hole that's not covered) or excessive absorption of the septum primum.

A 7-year-old boy arrived to the emergency department by his parents because is not developing appropriately. The parents say that: the patient has cold intolerance, easy fatigability, and polyuria. A physical examination is notable for short stature and bilateral papilledema. Thyroid function tests are notable for low levels of T3, T4, and TSH. An MRI shows an enhancing multilobulated suprasellar mass with ring calcification in the region of the sella turcica. If the lesion represent a primary intracranial neoplasm, which of the following may be a complication(s) in this boy? A) Hypercalcemia, hypercalciuria, hypophostemia: Hyperparathyroidism B) Puffy-faced child with protruding umbilicus due to lack of Iodine: Cretinism C) Diabetes insupidus & obesity due to pituitary stalk dysfunction: Complications of craniopharyngioma include: Diabetes insupidus, obesity, endocrine dysfunction, GH(75%), GnRH(40%), ACTH or TSH in 25% deficiencies, and prolactinemia in 20% D) Temporal hemianopsia & cardiovascular due to diminution(for my friend that means Lessen in size or decreased) of GnRH:Pituittary adenoma(most common prolactinoma) and cardiovascular can occur in patient with prolactinoma due to adrenocortical deficiency E) Increased of cortisol due to a variety of cause: Cushing's syndrome F) Increased of TBG during pregnancy: In pregnancy due to estrogen

CIMETIDINE is a P450 inhibitor, and P450s metabolize most of the statins, except PRAVASTATIN which is transformed enzymatically in the liver cytosol

Myalgia, fever plus edema = Trichinella spiralis
Myalgia, fever plus edema = Trichinella spiralis. But that's pork or bear meat. Myalgia can also be cysticercosis (Taenia solium), but that's pork.

Intractable chronic asthma : ACTH and cortisol both low because these patients are on long-term prednisone. Exogenous steroids = most common cause of Cushing syndrome.

Patient with rheumatoid arthritis diagnosed 5 years ago in whom NSAIDs are not effective: NSAIDs and steroids are used strictly for pain relief. This patient would also be on one or more DMARDs.

High blood pressure in man of 6-months duration, cataract in left eye, impotence; Most common endogenous cause of Cushing syndrome is Cushing disease. So ACTH high and cortisol high. The diagnosis would need to be confirmed, but these values should be the initial suspicion. Impotence is likely secondary to uncontrolled diabetes, as is the cataract.

Non-smoker, woman, 3-cm central coin lesion on CXR, 4-month history of ataxia; ACTH high, cortisol high. This is a small cell bronchogenic carcinoma. USMLE textbooks stress paraneoplastic secretion of ACTH and/or ADH, but anti-Hu and anti-Yo antibodies associated with cerebellar dysfunction are actually really really HY. That is on the Step 1. And of course don't forget small cell causing Lambert-Eaton as well.

5) Patient with fasting glucose of 110, potassium of 3
5) Patient with fasting glucose of 110, potassium of 3.7, sodium of 142, MRI of pituitary reveals no abnormality, no Hx of chronic disease, purple striae on upper-medial thighs bilaterally; ACTH low, corisol high. Likely cortisol-secreting tumor of zona fasciculata. Corisol has subtle mineralocorticoid effects if present at high levels. Baseline sugars are up and electrolytes may or may not be perturbed. Lack of chronic disease suggests against exogenous steroids.

till upper rectum-----------> Inferior mesenteric L
till upper rectum > Inferior mesenteric L.N ( is there a point of demarcation? if they say adenocarcinoma of rectum what are we to assume?) lower Rectum > Internal Iliac L N anal canal above pectinate line---> internal iliac LN below pectinate Line------> Superficial Inguinal LN

Mnemonic to remember kluver bucy syndrome (bilateral lesions of Hippocampus & Amygdala)= "HIP HIP" H = Hypermetamorphosis (old visual stimuli approached as if they are new) I = Increased oral exploratory behavior (putting everything in mouth like monkeys) P = Placidity (no aggression) H = Hypersexuality + Hyperphagia I = Impaired memory (Anterograde Amnesia) P = Psychic Blindness (objects in visual field treated inappropriately)

Latrotoxin Latrotoxin (α-Latrotoxin) found in venom of widow spiders also affects the neuromuscular junction by causing the release of acetylcholine from the presynaptic cell. Mechanisms of action include binding to receptors on the presynaptic cell activating the IP3/DAG pathway and release of calcium from intracellular stores and pore formation resulting in influx of calcium ions directly. Either mechanism causes increased calcium in presynaptic cell, which then leads to release of synaptic vesicles of acetylcholine. Latrotoxin causes pain, muscle contraction and if untreated potentially paralysis and death.

pseudobalbar palsy refers to UMNL while bulbar palsy refers to lower motor neuron disease

Pseudobulbar palsy is bilateral impairment of the function of the lower cranial nerves 9, 10, 11 and 12 due to upper motor neuron lesion of the bulbar muscles from lesions of the corticobulbar pathways in the pyramidal tract. Causes * Vascular causes: Bilateral hemisphere infarction * Degenerative disorders: motor neuron disease * Inflammatory disorders: Multiple sclerosis * Malignancy: High brain stem tumors Symptoms * Dysphagia (difficulty in swallowing) * Labile affect * Dysarthria Signs * Speech is slow, thick and indistinct * Gag reflex is normal or exaggerated * Tongue is small, stiff and spastic * Jaw jerk is brisk * There may be upper motor neurone lesion of the limbs. Bulbar palsy is a similar disorder but is caused by lower motor neurone lesions

FA is being more specific since the term hemorrhoids means normal structures in anal canal. When these normal structures (hemorrhoids) in anal canal becomes diseased (bleeding/thrombosis) by unknown cause they are called hemorrhoidal disease (loosely described as Internal/External hemorrhoids). When there is dilation of the submucosal veins associated with a known cause like cirrhosis it is called varices, no matter the site. Remember, hemorrhoids are specialized structures in anal canal as compared to submucosal collateral vessels in rectum which dilate due to cirrhosis.

A 2 month old boy is broughbt to the emergency department with respiratory insufuicency and failure to thrive after an uneventful pregnancy and perinatal course. Generalized hypotonia and weakness are noted. The patient's hospital stay is remarkable for the development of tracheobronchomalacia and respiratory insufficency that requires mechanical complications. Muscle biopsy shows denervation and panfasciular atrophy. What condition is the infant suffering from? A Becker's muscular dystrophy B. Duchenne's C. Kugelberg Welander Disease D. Spinal Muscular atrophy type II E/ Werdnig-Hoffmann Disease

The lateral spinothalamic tract transmits pain and temperature The anterior spinothalamic tract (or ventral spinothalamic tract) transmits crude touch. Dorsal column tract transmits fine touch , tactile discrimination , vibration sensation , joint and muscle sensation(conscious proprioception)

Which one of the following is a characteristic feature of Charcot Marie Tooth disease? A. Muscular hypertrophy. B. Normal sensation. C. Talipes cavus. D. Thickening of the peroneal nerve The correct answer is C. Choices A, B, and D are incorrect. Charcotâ“Marieâ“Tooth disease is both genetically and phenotypically heterogeneous. Characteristic physical features include the presence of talipes cavus and hammer toes, presumably reflecting long-term muscular weakness and imbalance between the flexor and extensor muscles of the feet and toes. This disease is characterized by slowly progressive weakness, muscular wasting, and sensory impairment predominantly involving the distal legs. Thickening of the peroneal nerve is not a characteristic feature.

epiconus syndrome urethral sphincter problems, saddle anesthesia, fecal incontinence, impotence+ lower limb abnormalities. conus medullaris syndrome------urethral sphincter problems, saddle anesthesia, fecal incontinence, impotence with no lower limb involvement cauda equina syndrome------motor and sensory weakness in lower limbs and fecal incontinence without urethral sphincter problems and impotence(rarely seen)

Synringomyelia associated with Chiari I malformation
Synringomyelia associated with Chiari I malformation. Other sources are saying it's Chiari II malformation. Which one is correct? They both are associated with syringomyelia. Only type-II has the myelomeningocoele, but they both have syringomyelia. Utting to the chase though, the way the USMLE will test this: If it's type-II, they'll practically always tell/show you there's the myelomeningocoele, and the patient will likely be an infant. With type-I, they'll likely give you a teenager / young adult with the typical bilateral loss of temperature/pain sensation in a cape-like distribution. That indicates the syringomyelia at the anterior white commissure.

High altitudes physiology
At high altitudes there's less oxygen in air so the first effect is hypoxia and decreased dissolved oxygen in the blood. The immediate response will be stimulation of peripheral chemoreceptors which in turn in send signals to respiratory drives to breath more. So hyperventilation develops which in turn leads to Respiratory Alkalosis. Respiratory alkalosis will shift the hemoglobin dissociation curve to the left so that Hb can pick up O2 easier. The kidney will respond to alkalosis by generating hydrogen ions and this will correct the PH back to normal. After 2-3 days the 2,3 Diphosphoglycerate level in RBC will increase and this will shift the Hb curve (this time) to the right making O2 delivery easier to tissues. (Athletes go to mountains before the olympics, so that when they return to sea level, they have a right shifted Hb curve and so easier O2 delivery to their muscles during their competitions). Another change that start right away is the increase of eryrthopoietin secretion but this takes a week or so before we can see polycythemia and increased hematocrit level. These changes in turn will correct the dropped down oxygen content of the blood. Note that no matter how long you stay in high altitudes the PAO2, PACO2, and Hemoglobin saturation will remain decreased as we breath less FIO2 and we continue to hyperventilate.

Q Patient notes that food tastes funny and has irregular breathing
Q Patient notes that food tastes funny and has irregular breathing. What nucleus is affected? A) Nucleus ambiguus B) Solitary nucleus C) Inferior salivatory nucleus D) Superior salivatory nucleus E) Dorsal motor nucleus of X Taste fibers, from the taste buds, are predominantly (from the front 2/3 of the tongue, anyway) carried by the facial nerve. (Keep in mind that touch and pain sensation from the tongue is V, and motor to the tongue is XII.) Taste from the back of the tongue and palate is carried by the glossopharyngeal nerve. Regardless of their origin, the taste fibers enter the solitary tract of the medulla, and synapse in the surrounding solitary nucleus.

Facial nerve for the anterior 2/3 of the tongue and soft palate.
Glossopharyngeal nerve for the posterior 1/3 of the tongue as well as portions of the upper pharynx.

1) Patient notes that food tastes funny and has irregular breathing
1) Patient notes that food tastes funny and has irregular breathing. What nucleus is affected? A) Nucleus ambiguus B) Solitary nucleus C) Inferior salivatory nucleus D) Superior salivatory nucleus E) Dorsal motor nucleus of X 2) A 50 year old woman comes in complaining of hoarseness and difficulty with swallowing. She also has nasal regurgitation of liquids. What nucleus is affected? A) Nucleus ambiguus B) Solitary nucleus C) Inferior salivatory nucleus D) Superior salivatory nucleus E) Dorsal motor nucleus of X

The facial nerve is destroyed as it comes from the brain stem
The facial nerve is destroyed as it comes from the brain stem. What nuclei is affected? A) Nucleus ambiguus B) Solitary nucleus C) Inferior salivatory nucleus D) Superior salivatory nucleus E) Ventral cochlear nucleus b) In response to previous part (a), where is this nuclei located? A) rostral medulla B) caudal pons C) rostral pons D) caudal medulla E) midbrain

Patient experiences decreased parotid secretions
Patient experiences decreased parotid secretions. What nuclei is affected? A) Nucleus ambiguus B) Solitary nucleus C) Inferior salivatory nucleus D) Superior salivatory nucleus E) Ventral cochlear nucleus b) In response to previous part (a), where is this nuclei located? A) rostral medulla B) caudal pons C) rostral pons D) caudal medulla E) midbrain

Patient experiences analgesia and thermal anesthesia on tooth pulp
Patient experiences analgesia and thermal anesthesia on tooth pulp. What nuclei is affected? A) Oral part of spinal nucleus of V B) Interpolar part of spinal nucleus of V C) Caudal part of spinal nucleus of V D) trigeminal ganglion E) trigeminal nerve Patient experiences analgesia and thermal anesthesia on her right side of her face and her scalp. What nuclei is affected? A) Oral part of spinal nucleus of V B) Interpolar part of spinal nucleus of V C) Caudal part of spinal nucleus of V D) trigeminal ganglion E) trigeminal nerve

COMT An enzyme that catalyzes the degradation of catecholamines, including the neurotransmitters dopamine, epinephrine, and norepinephrine. COMT is also important in the metabolism of catechol drugs used in the treatment of hypertension, asthma, and Parkinson disease. A genetic polymorphism (a common normal variant) in COMT contributes to the responses to pain and stress.

Waardenburg syndrome associated with white forelock and hearing loss (sensorineural hearing loss) , premature graying of the hair (before age 30), Poliosis, Vitiligo Pendred syndrome or Pendred disease is a genetic disorder leading to congenital bilateral (both sides) sensorineural hearing loss and goitre with occasional hypothyroidism (decreased thyroid gland function)

In both the lateral meduallary syndrome (Wallenburg syndrome) and in the lateral pontine syndrome we have these lesions: Ipsilateral horner because of lesioned descending hypothalamics Contralateral loss of pain and temperature due to the spinothalamic tract cut Ipsilateral cerebellar ataxia because of a lesion in the cerebellar peduncles (inferior in the case of the medulla and middle in the case of pons) Vertigo, vomiting, and nystagmus due to vestibular nuclei involvement Ipsilateral loss of pain and temperature in the half of the face due to spinal V nucleus lesion Ipsilateral hearing loss due to cochlear nucleus involvement So how to tell the difference between the two? Nucleus ambiguous and nucleus solitarius with resultant loss of gag, taste, dysphagia, swallowing, etc is seen only in Wallenburg Motor involvement of the Trigeminal is seen only in lateral pontine (specially if it is a rostral lesion) with ipsilateral loss of touch and mastication on the side of the face Facial involvement is sometimes seen in lateral pontine but not in lateral medullary syndrome with it's loss of anterior 2/3 taste, lacrimation, facial expression, corneal reflex, and hyperacusis

Not only is the olive-shaped mass hypertrophic pyloric stenosis, but if they ask about possible Sx, jaundice secondary to conjugated hyperbilirubinaemia can occur due to compression of the common bile duct running through the hepatoduodenal ligament. I had encountered that in a practice question somewhere. They'll try to throw epigastric pain at you, but if jaundice is there, that's the answer. And I also recall Kaplan QBook, which loves its minutiae, having mentioned that Smith-Lemli-Opitz is a notable genetic disease that presents with pyloric stenosis (as well as high forehead, syndactylyl of the second and third toes and MR). Pyloric stenosis is always 2-3 weeks post-birth (non-bilious vomiting). Duodenal atresia is always 2-3 days post-birth (bilious vomiting). If the patient has constipation and bilious vomiting, even if they don't mention distended abdomen or failure to pass meconium, it's Hirschsprung's, not duodenal atresia.

Leigh syndrome is a severe neurological disorder that typically arises in the first year of life. This condition is characterized by progressive loss of mental and movement abilities (psychomotor regression) and typically results in death within a couple of years, usually due to respiratory failure. A small number of individuals develop symptoms in adulthood or have symptoms that worsen more slowly. The first signs of Leigh syndrome seen in infancy are usually vomiting, diarrhea, and difficulty swallowing (dysphagia) that leads to eating problems. These problems often result in an inability to grow and gain weight at the expected rate (failure to thrive). Severe muscle and movement problems are common in Leigh syndrome. Affected individuals may develop weak muscle tone (hypotonia), involuntary muscle contractions (dystonia), and problems with movement and balance (ataxia). Loss of sensation and weakness in the limbs (peripheral neuropathy), common in people with Leigh syndrome, may also make movement difficult. Several other features may occur in people with Leigh syndrome. Many affected individuals develop weakness or paralysis of the muscles that move the eyes (ophthalmoparesis); rapid, involuntary eye movements (nystagmus); or degeneration of the nerves that carry information from the eyes to the brain (optic atrophy). Severe breathing problems are common in people with Leigh syndrome, and these problems can worsen until they cause acute respiratory failure. Some affected individuals develop hypertrophic cardiomyopathy, which is a thickening of the heart muscle that forces the heart to work harder to pump blood. In addition, a substance called lactate can build up in the body, and excessive amounts are often found in the blood, cerebrospinal fluid, or urine of people with Leigh syndrome. The signs and symptoms of Leigh syndrome are caused in part by patches of damaged tissue (lesions) that develop in the brains of people with this condition. A procedure called magnetic resonance imaging (MRI) reveals characteristic lesions in certain regions of the brain and the brainstem (the part of the brain that is connected to the spinal cord). These regions include the basal ganglia, which help control movement; the cerebellum, which controls the ability to balance and coordinates movement; and the brainstem, which controls functions such as swallowing, breathing, hearing, and seeing. The brain lesions are often accompanied by loss of the myelin coating around nerves (demyelination), which reduces the ability of the nerves to activate muscles used for movement or relay sensory information back to the brain.

In Ca Breast: Dimpling of the skin is due to infiltration of the suspensory ligaments. Nipple retraction is due to infiltration of the lactiferous ducts. Edema or peau d’orange is due to lymphatic obstruction/infiltration of dermal lymphatics.

Increased ICP causes compensatory intracranial vasoconstriction, which secondarily triggers a peripheral SNS response (to attempt to override the vasoconstriction), thereby causing peripheral hypertension; the latter leads to reflex bradycardia, and respiratory depression occurs late with brainstem dysfunction In terms of your question regarding FA vs BRS, the increased ICP is the basis of the problem, so central chemoreceptors must act if the SNS response is to be induced. More simply: cerebral vasoconstriction --> increased cerebral pCO2 --> central chemoreceptor activation --> increased peripheral SNS response mounted to raise perfusion pressure in an attempt to augment cerebral CO2 clearance. Notice that the central chemoreceptor response is the bridge in the mechanism, so BRS is right here. However FA is also right in the sense that peripheral baroreceptors are responsible for the characteristic reflex bradycardia that occurs secondary to the peripheral SNS response. As far as I'm aware, baroreceptors don't measure intracranial pressure directly.

Breath Smells : Acetone: Diabetic Ketoacidosis Garlic: Arsenic poisoning Bitter Almond: Cyanide poisoning Foul smell: Halitosis Fetor hepaticus: breath smells musty in Cirrhosis Urea breath test: H. Pylori (yeah this wouldn't be using your nose!) Metallic taste: lead poisoning sweet grape-like scent: Pseudomonas aeruginosa

bulls eye rash = lyme disease
ring lesions in brain - toxoplasma gondi. swiss cheese appearance of brain-tenia solium soap bubble lesion in brain-crptococcus neoformans spongiform cortex-prions disease. temporal lobe encepahlitis- herpes simplex 1 lens- shaped = epidural hematoma crescent-shaped = subdural hematoma periventricular calcification in newborn = CMV encephalitis frontotemporal atrophy= Pick's disease bulls eye rash = lyme disease

staccato cough: C. trachomatis barking cough: RSV seal-like barking cough: parainfluenza whooping cough: B. pertusis dry harsh cough in a young adult: mycoplasma

Drugs\diseases that cause Gingival hyperplasia are:
1- Calcium channel blockers; specifically Nifedipine and Verapamil 2- Anticonvulsants; sepcifically Phenytoin but also others 3- Cyclosporine M5 AML may also cause gingival enlargement. I-cell disease which caused by deficiency of phosphotransferase.

enamel hypoplasia as a side-effect in neonates of maternal-use of tetracyclines during pregnancy. Tooth discoloration + enamel hypoplasia are characteristic!

Gynecomastia and hCG , What is the mechanism?
hCG has the same alpha unit as LH, FSH, TSH. Increase in hCG -> increase in LH -> more testosterone (via Leydig cells) -> more estrogen (via aromatase in adipose tissue and testis) -> gynecomastia.

A 64-year-old woman suddenly experienced difficulty in getting the words out and was not able to answer questions. On neurologic examination, she was able to identify body parts by indicating with her finger. She had difficulty following lengthy, complex commands. She was able to repeat words and sentences (much better than spontaneous speech). She was not able to name objects and shapes. What kind of aphasia was present in this patient? A. Broca aphasia B. Conduction aphasia C. Transcortical motor aphasia D. Transcortical sensory aphasia E. Wernicke aphasia This language disorder is almost identical to Broca’s aphasia, in which a person ..."cannot produce spontaneous speech" In essence, people with transcortical motor aphasia cannot say what they want to say. They simply can’t form the words. However, if you asked them to repeat something, they can do it without difficulty. For instance, a person with this disorder who wants to express that she is thirsty cannot say “I am thirsty." She could, however, repeat the sentence “I am thirsty” if she were asked to do so. -Capacity to "Repeat"(words, phrases and statements)----- *Preserved while in Broca's they have "Trouble Repeating".

Broca's area is the most basic unit for speech production
Broca's area is the most basic unit for speech production. Not language, just speech. Wernicke's area is the most basic area for comprehension of speech/the written word. Again, not language, just speech. The arcuate fasciculus is the connection between these two areas. When I say just speech, what I mean is words. Broca's area contains the neural pathways to create words, phrases and sentences in a functional way (articulation) using your mouth. Wernicke's area contains neurons that associate auditory and written patterns with their respective words. Without Broca's area, creating and stringing together words (and articulation) is difficult. Without Wernicke's area, speech is just sound, and writing is just art. Without the arcuate fasciculus, the link between audition and speech output (i.e. repetition) is lost. Conduction aphasia is fluent because the Broca's area is intact, it is entirely possible to create new speech. It has good comprehension because the Wernicke's area is intact, it is entirely possible to understand speech and writing. The most basic aspect of comprehension is to be able to hear and see. The most basic aspect of motor speech is to be able to move your muscles. Along with this, the complexity of language means that there must be some higher centers to control nuances of language, and this is where the surrounding areas come into play. Now you can understand the entity of transcortical aphasia, where the Wernicke-arcuate-Broca complex is intact but isolated from the rest of the brain. Transcortical sensory aphasia: Sound cannot be understood as speech. Written words cannot be processed. Reading and writing are no longer possible. The nuances of language, basically lexical semantics are affected, i.e. there is no understanding of speech as a component of language, and so the very purpose of speech, i.e. to communicate is lost. Since the Wernicke-Broca complex is intact, speech can be generated de novo, although it has no propositional meaning. Repetition is, of course, intact, even for very complex and long sentences. Echolalia is often seen. It is still possible to recite from memory. Transocortical motor aphasia: The frontal lobe may be affected, the link between Broca's area and the premotor cortex, basal ganglia and thalamus may be damaged and so initiation and organisation of speech is poor, but well articulated (since Broca's area itself is intact). In dialogue, the patient cannot construct complex answers to questions but can answer with one word responses. Speech and higher language processing is generally intact. Repetition is also intact. alicealicealice's post gives a great overview of aphasias. Remember that in reality, lesions are rarely so clean and so absolute, so don't be surprised by the intact nature of some faculties in any lesion.

Broca’s (motor) aphasia: nonfluent, good comprehension, poor repetition Transcortical motor aphasia: nonfluent, good comprehension, good repetition Wernicke’s (sensory) aphasia: fluent, poor comprehension, poor repetition Transcortical sensory aphasia: fluent, poor comprehension, good repetition Conduction aphasia: fluent, good comprehension, poor repetition Global aphasia: nonfluent, poor comprehension, poor repetition

an acuteextensive bilateral lesion in reticular formation in the tegmentum of midbrain is most likely to result in a.insomnia b.intractable pain c.loss of consciousness d.narcolepsy e.REM

Gastroparesis is a condition in which the spontaneous movement of the muscles (motility) in your stomach does not function normally. in many cases, gastroparesis is believed to be caused by damage to a nerve that controls the stomach muscles (vagus nerve). signs and symptoms of gastroparesis include: Vomiting Nausea A feeling of fullness after eating just a few bites Abdominal bloating Abdominal pain Changes in blood sugar levels Lack of appetite Weight loss and malnutrition

A 40-year-old woman, 5 feet, 1 inch (155 cm) tall and weighing 188 pounds (85.5 kg), seeks your advice on how to lose weight. Her waist measured 41 inches and her hip 39 inches. A physical examination and blood laboratory data were all within the normal range. Her only child, who is 14 years old, her sister, and both of her parents are overweight. The patient recalls being obese throughout her childhood and adolescence. Over the past 15 years she had been on seven different diets for periods of 2 weeks to 3 months, losing from 5–25 pounds. On discontinuation of each diet, she regained weight, returning to 185–190 pounds. Which one of the following best describes this patient? A. She is classified as overweight. B. She shows an “apple” pattern of fat distribution. C. She has approximately the same number of fat cells as a normal-weight individual, but each adipocyte is larger. D. She would be expected to show lower than normal levels of circulating leptin. E. She would be expected to show lower than normal levels of circulating triacylglycerols

Apple shape is defined as a waist to hip ratio of more than 0
Apple shape is defined as a waist to hip ratio of more than 0.8 for women, and more than 1.0 for men. She has, therefore, an apple pattern of fat distribution, more commonly seen in males. Compared with other women of the same body weight who have a gynecoid fat pattern, the presence of increased visceral or intra-abdominal adipose tissue places her at greater risk for diabetes, hypertension, dyslipidemia, and coronary heart disease. For this patient BMI = weight (kg)/height (m2) = 85.5/(1.55)2 = 35.6 kg/m2. The result indicates that the patient is classified as obese. Individuals with marked obesity and a history dating to early childhood have an adipose depot made up of too many adipocytes, each fully loaded with triacylglycerols. Plasma leptin in obese humans is usually normal for their fat mass, suggesting that resistance to leptin, rather than its deficiency, occurs in human obesity. The elevated circulating fatty acids characteristic of obesity are carried to the liver and converted to triacylglycerol and cholesterol. Excess triacylglycerol and cholesterol are released as VLDL, resulting in elevated serum triacylglycerols. Thanks to odin. I did not know adipocytes are such long lived cells. From now on I will tell my wife not to make me dieting :) As the Leptin thing come... I will put some of my notes about Leptin... [thanks to gdl21 she helped me to prepare this] Leptin acts on receptors in the hypothalamus of the brain where it inhibits appetite by 1. Counteracting the effects of neuropeptide Y (a potent feeding stimulant secreted by cells in the gut and in the hypothalamus); 2. Counteracting the effects of anandamide (another potent feeding stimulant that binds to the same receptors as THC, the active ingredient of marijuana); and 3. Promoting the synthesis of α-MSH, an appetite suppressant.

Leptin binds to neuropeptide Y (NPY) neurons in the arcuate nucleus, in such a way that decreases the activity of these neurons. Leptin signals to the brain that the body has had enough to eat, or satiety [This is the most important part to remember]. A very small group of humans possess homozygous mutations for the leptin gene that leads to a constant desire for food, resulting in severe obesity. This condition can be treated somewhat successfully by the administration of recombinant human leptin. Ghrelin is a hormone produced mainly by P/D1 cells lining the fundus of the human stomach and epsilon cells of the pancreas that stimulates hunger. Ghrelin levels increase before meals and decrease after meals. It is considered the counterpart of the hormone leptin, produced by adipose tissue, which induces satiation when present at higher levels. Ghrelin is also produced in the hypothalamic arcuate nucleus, where it stimulates the secretion of growth hormone from the anterior pituitary gland. Receptors for ghrelin are expressed by neurons in the arcuate nucleus and the lateral hypothalamus. The ghrelin receptor is a G protein-coupled receptor, formerly known as the GHS receptor (growth hormone secretagogue receptor). Ghrelin plays a significant role in neurotrophy, particularly in the hippocampus, and is essential for cognitive adaptation to changing environments and the process of learning. Recently, ghrelin has been shown to activate the endothelial isoform of nitric oxide synthase in a pathway that depends on various kinases including Akt (serine/threonine protein kinase). Ghrelin levels in the plasma of obese individuals are lower than those in leaner individuals except in the case of Prader-Willi syndrome-induced obesity. Those suffering from the eating disorder anorexia nervosa have high plasma levels of ghrelin compared to both the constitutionally thin and normal-weight controls. These findings suggest that ghrelin is inversely related to calorie intake. Lack of sleep produces ghrelin, which stimulates appetite and creates less leptin, which, among its many other effects, suppresses appetite. Ghrelin levels are also high in patients that have cancer-induced cachexia. Anti-TNF alpha Pro-apoptotic.

One serious side-effect of a vagotomy is a vitamin B12 deficiency later in life - i.e., 10 years - that is similar to pernicious anemia. The vagus normally stimulates the stomach's parietal cells to secrete acid and intrinsic factor. Intrinsic factor is needed to absorb vitamin B12 from food. The vagotomy reduces this secretion and ultimately leads to the deficiency, which, if left untreated, causes nerve damage, tiredness, dementia, paranoia, and ultimately death.

A 20-year-old, mentally retarded woman saw the physician because she had flank pain for 1 week. Physical examination showed right costovertebral angle tenderness. Patches of leathery-appearing (shagreen patches) and hypopigmented (ash-leaf patches) skin were scattered over her body. There was a subungual nodule on her right index finger. Abdominal CT scan showed bilateral renal cysts and tumor masses. MRI of the brain showed subependymal nodules and 1- to 4-cm cortical foci with loss of the gray-white distinction. CT scan of the chest showed a 3-cm mass involving the interventricular septum. Two years later, she has sudden, severe headache. MRI now shows a nodule obstructing the cerebral aqueduct. Neurosurgery is performed, and a subependymal giant-cell astrocytoma is removed. What is the most likely diagnosis? (A) Down syndrome (B) Krabbe disease (C) Neurofibromatosis type 1 (D) Neurofibromatosis type 2 (E) Tuberous sclerosis (F) Von Hippel–Lindau disease Tuberous sclerosis is one of the phakomatoses—rare inherited disorders in which hamartomas and neoplasms develop throughout the body, along with cutaneous abnormalities. Patients with tuberous sclerosis have cortical tubers, which are hamartomas of neuronal and glial tissue; other characteristic findings include renal angiomyolipomas, renal cysts, subungual fibromas, and cardiac rhabdomyomas. In Down syndrome (trisomy 21), patients may develop acute leukemia, but not brain neoplasms, and individuals who survive to middle age develop Alzheimer disease. Krabbe disease is a leukodystrophy that results in deficiency of galactocerebroside β-galactosidase and an onset of neurologic deterioration in infancy. Neurofibromatosis type 1 is characterized by deforming cutaneous and visceral neurofibromas, cutaneous café-au-lait spots, and neurofibrosarcomas. In neurofibromatosis type 2, acoustic schwannomas, meningiomas, gliomas, and ependymomas are present. Von Hippel–Lindau disease is characterized by hemangioblastomas in the cerebellum, retina, and spinal cord, and by pheochromocytomas.

treat essential tremor with beta-blockers(which is in FA on p. 439)
treat essential tremor with beta-blockers(which is in FA on p. 439). I've never delved into the mechanism, but my assumption would be, for essential tremors, that treatment with beta-blockers causes decreased intracellular cAMP --> decreased PKA --> increased tone of peri-fascicular vascular smooth muscle via phosphorylation of MLCK --> decreased muscle blood flow --> decreased muscle tone --> relief of tremor. therefore, beta-agonists probably do the opposite: increased cAMP --> increased PKA --> increased rate of dephosphorylation of MLCK (likely due to PKA-mediated phosphate transfer to other moieties) --> decreased tone of peri-fascicular vascular smooth muscle --> increased muscle blood flow --> increased muscle tone --> tremor (possibly due to temporal heterogeneity of beta-agonist uptake).

Could someone provide with details how exactly thiamine deficiency affects dorsomedial nucleus of thalamus and mammillary bodies in hypothalamus? Simply because it affects PDH and ATP synthesis? the four B1-dependent enzymes: PDA, alpha-KGD, transketolase, branched-chain amino acid dehydrogenase. Since alpha-KG normally goes to succinyl-CoA in the TCA cycle, if you don't have alpha-KG dehydrogenase, you've got increased alpha-KG. Pyruvate + glutamate <--> alpha-KG + alanine. If you are B1-deficient, you increase alpha-KG and shift the equilibrium to the left, causing increased glutamate (i.e. neuroexcitotoxicity), which leads to structural damage. Although pyruvate would also increase because PDA is also B1-dependent, pyruvate can shunt to lactic acid (i.e. lactic acidosis) as a secondary pathway, whereas alpha-KG must shunt through here. The decreased pyruvate (despite the increased glutamate) leads to fasting hypoglycaemia and a reduction in ATP production.

A 3-year-old girl ruptured her eardrum when she inserted a pencil into her ear. Her mother took her to the emergency department after noticing that the child was crying and complaining of pain in her ear with a few drops of blood in the external auditory meatus. The attending doctor examined the child for possible injury to a nerve that runs across the eardrum. The most likely nerve to be injured is the: 1.Auricular branch of the vagus 2.Chorda tympani 3.Glossopharyngeal (CN IX) 4.Lesser petrosal 5.Trigeminal (CN V) The correct answer is: 2.chorda tympani When this girl ruptured her eardrum, she damaged the tympanic membrane. So, you need to think about the nerve and structures that are associated with the tympanic membrane (ie, on the lateral wall of the middle ear). Chorda tympani lies across the tympanic membrane, so it's possible that this nerve was injured by the pencil. The auricular branch of the vagus nerve is a small branch of the vagus that supplies afferent sensory innervation to the external acoustic meatus. This nerve is not close to the tympanic membrane The glossopharyngeal nerve and lesser petrosal nerve are associated with the promontory of the ear, which is on the medial wall of the middle ear. The trigeminal nerve is not close to the ear and would not be damaged by the injury. What might happen if chorda tympani was injured? No taste sensation to the anterior 2/3 of the tongue and no secretomotor innervation to the sublingual and submandibular glands!

pyloric stenosis is due to hypertrophy of the muscularis propria More specifically it's the circular layer of the muscularis propria.

Cyclosporine acts by inhibting interleukin-2 and several cytokines ,mainly T-helper lymphocytes Most common side effects of cyclosporine are: 1.Nephrotoxicity: This is the most common side effect.May manifest as reversible azotemia or irreversible progressive renal disease.Hyperuricemia with accelerated gout,hyperkalemia etc HUS may also occur. 2.Hypertension: This is due to renal vasoconstriction and sodium retention. 3.Neutrotoxicity: reversible. 4.Glucose intolerance 5.Infection 6.Malignancy:There is increased risk of squamous cell CA of the skin and lymphoproliferative disease 7.Gingival hypertrophy and hirsutism 8.GI manifestations.anorexia nausea vomiting but mild 9- hemorrhagic cysyiitis A.Tarcolimus same mechanism as cyclosporine.also similar toxic profile but tacrolimus does not cause hirsutism or gum hypertrophy C.Azathioprine does related diarrhea ,leukopenia and hepatotoxicity. D.Mycophenolate bone marrow supression

drugs can cause Parkinson like syndrome :
D2 antagonist. metoclopramide; antiemitic (It blocks D2 receptors within CTZ) , prokinetic drug

Weight loss:Topirimate, and any drug that increases insulin release, Thyroid hormones increases the activity of the Na+/K+ ATPase pump and burn up all dat ATP (hyperthyroidsm) , metformin, type 1 diabetes, hyperthyroidism, achlasia, peptic ulcer, Malabsorption syndromes( such as celiac and crohn) , adenocarcinoma of colon , hepatitis Weight gain: Valproic acid, Fluoxetine, Corticosteroids, Clozapine, olanzapine, Risperidone, hypothyroidism, cushings.

PT/aPTT are normal in strict platelet disorders
PT/aPTT are normal in strict platelet disorders. Such examples would be Glanzmann thrombasthenia and Bernard-Soulier syndrome. Uremic platelet dysfunction is also HY (platelet count normal but bleeding time increased). vWD has increased aPTT sometimes in addition to bleeding time. The coagulation cascade has nothing to do with platelets, so ITP wouldn't relate to that.

Pathophysiology of Uremic platelet dysfunction There are lot of factors contributing to the platelet dysfunction, and really it's WAY beyond the scope of STEP1. I have a funny way of remembering that there is platelet dysfunction in renal failure, maybe this'll help: 1) Ca2+ is needed for platelet adhesion, I kind of think of Ca2+ as a sticky positively charged "double-sided tape" for all the negatively charged molecules so that they can bind. e.g. GPIIb/IIIa, vWF, cadherins, etc etc etc. 2) In renal failure, one of the complications is renal osteodystrophy - you can't dump phosphate or synthesize calcitriol, so you get DECREASED serum Ca2+ with increased serum phosphate and blah blah blah. Point is, serum Ca2+ is decreased. 3) Without Ca2+, you don't have the double sided tape anymore, now all those negatively charged molecules are going to repel each other rather than stick to each other - i.e. you no longer have platelet aggregation/adhesion/things sticking to the negatively charged vWF, glycoproteins, phospholipids and collagen. 4) Dialysis would correct for the electrolyte imbalance and "fix" the problem. Again, it's actually way more complicated than that (since you can have platelet dysfunction without electrolyte imbalance), and I can't even begin to understand the whole picture, but for the purposes of STEP1 this is enough to help me remember that there are going to be problems with platelet functions in renal failure.

تابع لسلايد 100 EDIT: Did some digging and it does seem like there is a GIANT laundry list of reasons for platelets to not work in renal failure, but I really wouldn't worry about remembering all of these: Factors related to the vessel wall Decreased production of the largest multimers of von Willebrand’s factor Enhanced nitric oxide production Enhanced prostacyclin production Factors related to platelets Abnormal mobilization of calcium ions in platelets Defective activation of glycoprotein IIb -IIIa receptors Defective cyclooxygenase activity (reduced ability to generate thromboxane A2) High levels of cyclic adenosine monophosphate Low levels of serotonin and adenosine diphosphate Factors related to the blood Anemia Altered blood rheology (ie, deranged radial transport of platelets) Altered transfer of adenosine diphosphate from erythrocytes to platelets Uremic toxins (eg, guanidinosuccinic acid, phenol, phenolic acid, urea)

Kallman syndrome is X-linked
Kallman syndrome is X-linked. For Step1, all you need to know: X-linked, anosmia, tertiary hypogonadism (decreased GnRH); failure of cell migration. For Step2CK: X-linked, anosmia, tertiary hypogonadism, renal insufficiency in 50% of patients (i.e., what other investigations would you carry out in this patient? --> renal function).

Ototoxic drugs ; cause hearing loss
Aminoglycosides, vancomycin, erythromycin, loop diuretics, antimalarials, cisplatin, sildenafil, cocaine

A 50-year-old man has hearing loss due to cerumen impaction in his right ear. Which of the following abnormalities are most likely on Weber and Rinne testing? Weber Testing Rinne Testing of Right Ear A) Lateralizes to the left air conduction > bone conduction B) Lateralizes to the left bone conduction â€˜ air conduction C) Lateralizes to the right air conduction> bone conduction D) Lateralizes to the right bone conduction > air conduction E) Nonlateralizing air conduction > bone conduction F) Nonlateralizing bone conduction > air conduction

Rinne: Hit fork. Place bottom of fork on mastoid
Rinne: Hit fork. Place bottom of fork on mastoid. Count till person says they can't hear. That bone conduction time (BC). Then quickly put the tines of the fork next to their ear and count till person says they can't hear. Thats air conduction time (AC). If BC>AC, or if they can't hear the fork at all after your remove it from the mastoid, its conductive loss. Rinne is not really useful for sensorineural loss as both would be diminished equally (so the times would be shorter compared to a normal person, but AC is still > than BC). Weber: Hit fork, place on midline on top of head. Sound lateralizes to bad ear in conductive hearing loss (stick your finger in your ear and hum to prove it to yourself) and to good ear in sensorineural hearing loss. Malignant otitis externa: diabetics, pseudomonas, tx PO ciprofloxacin (topicals dont work) BPPV (Benign Position Paroxysmal Vertigo): Dx with Dix Hall Pike, TX with Epley maneuver. NO hearing loss, NO tinnitus, NO ataxia, NO CN palsy. Menineres Disease: Tinnitus, Hearing loss, profound vertigo lasting 30 mins with nasuea/vomiting. Some doctor dude records himself on youtube while hes having an attack and describes it as it occurs, watch that and youll never forget the presentation. HY Pathogenesis: Due to Increased Endolymphatic Fluid (endolymph hydrops). LOW frequency hearing is lost first. Unlike neuritis and labyrinthitis, it is relapsing and remitting. The first line treatment is diuretics and salt restriction. Vestibular Neuritis: Viral prodrome followed by vertigo. Affects vestibular nerve only therefore NO hearing loss or tinnitus . Tx symptoms with meclizine (antihistamine). Labyrinthitis: Viral prodrome. Affects the whole labyrinth, therefore BOTH hearing loss/tinnitus and vertigo (distinguished from vestibular neuritis). Presbyacusis: Age related bilateral senorineural hearing loss that comes from atrophy of the apparatus at the base of the cochlear membrane therefore you lose HIGH frequency first. This results in difficulty hearing in crowded areas with background noise. Noise Induce hearing Loss: Either due to one time acoustic trauma (explosion) or continued exposure (rock band), sensorineural (affects the cochlea, specifially the cilia). Note that not all acoustic trauma = a ruptured eardrum. Otosclerosis: Usually unilateral conductive hearing loss in a young (20-30 year old) patient. Differentiated from menieres by being bilateral and/or having conductive instead of sensorineural hearing loss. Also no tinnitus. Supported by (+) Family History of hearing loss.

تابع للسلايد اللي قبله Cholesteatoma: keratin accumulation in middle ear that presents with ear discharge, conductive hearing loss, facial twitching and weakness. Ear Discharge + Hearing Loss = Cholesteatoma until proven otherwise. (look up some pics) Petrosal Bone Fracture: Sensorineural hearing loss after major head trauma with hemotympanum, due to laceration of CN8 Acoustic Neuroma = Vestibular Schwannoma: insidious ipsilateral sensorineural hearing loss + tinnitus + ataxia in a yo or a pt with NF Pagets Disease of Bone: Sensorineural hearing loss in old man with increasing hat size and headaches. Isolated elevated alk phos. Nerve impingement due to ostetitis deformans Bacterial Meningitis (especially basilar) Hypothyroid: Can cause Sensorineural hearing loss Drugs: Quinine (cinchonism), Aminoglycosides, Furosemide + cepahlosporin combo, cisplatinum, Aspirin overdose in questions presents with tinnitus, hyperthermia (oxidative phosphorylation decoupling), and mixed metabolic acidosis and respiratory alkalosis (hyperventilation due to direct action on respiratory center) Also, hearing loss or tinnitus + nystagmus = peripheral nystagmus (CN8). Vertical or bidirectional nystagmus = central nystagmus (cerebellar). PCP intoxication classically presents with vertical nystagmus and violent behavior.

Vitamin A/all-trans retinoic acid somehow interacts with the arachnoid granulations and inhibits reabsorbtion of the CSF and therefore increasing the ICP.

old patient has a lot of risk factors/diseases associated with atheroscerosis. Therefore you have to assume that the celiac/mesenteric (esp. SMA) arteries also are involved --> decreased intenstinal perfusion normally asymptomatic, symptomatic when O2 demand inreases (i.e. food intake) --> Chronic mesenteric ischemia ("intestinal angina"). If the patient was younger/without the aforementioned risk factors - the vignette then would describe Peptic ulcer disease, more specifically Gastric ulcer(weight loss, epigastric pain shortly after meals).

external ear and inner ear are ectodermal derivatives , and the Middle ear along with the Eustachian tube are endodermal origin .

Mnemonic; hisTAMine release where TAM stands for tubocurarine,amphotericin,morphine.

In HYPOthyroidism, the mechanism for amenorrhea is decreased free T3/T4 causing upregulation of TRH, thereby increasing prolactin secretion, which decreases LH/FSH secretion. In HYPERthyroidism, amenorrhea occurs because free T3/T4 increases sex-hormone binding globulin (SHBG) secretion from the liver, thereby decreasing the ratio of free-/bound-estradiol (and in a male, testosterone and DHT). Since higher free-estradiol concentrations are ultimately responsible for the ovulation-inducing LH-spike, decreased free-estradiol would decrease the probability of the LH-spike occurring.

Eye physiology Light -> phosphoisomerization of rhodopsin (later regeneration of rhodopsin due to Vit A) -> formed metarhodopsin II activates Gt -> stimulation of cGMP PDE -> decrease cGMP -> Na channels close -> hyperpolarization -> closure of voltage-gated Ca2+ channels --> glutamate-containing vesicles cannot fuse with plasma membrane (bc they require calcium to do so) --> decrease glutamate (excitory) release -> inhibition of optic nerve bipolar cells relieved -> initiation of signal transduction to cortex

E. coli sepsis is seen in classic galactosemia.
Galactosemia in newborns and infants is associated with the following symptoms: jaundice, hepatomegaly, failure to thrive, feeding difficulties, hypoglycemia, convulsions, lethargy, amino- aciduria, cataracts, hepatic cirrhosis, ascites, and mental retardation. If the preliminary evaluation indicates galactosemia, there is high risk for E. coli sepsis and death. Strong consideration should therefore be given for early antibiotic therapy in infants with suspected galactosemia in spite of the absence of clinical signs or symptoms of sepsis.

Clozaril (clozapine) can cause a life threatening drop in white blood cell count called aggranulocytosis.

Hypokalemic Periodic Paralysis: channelopathy, a paralysis after severe exersice or large high carb meals due to low potassium levels

The hypokalaemia in renal tubular acidosis occurs for two reasons: 1) there's a defective apical intercalated cell K+/H+ antiporter, leading to K+-wasting (and reduced proton secretion). Stressedmedstud, I notice you've mentioned the intercalated cell H+ uniporter, but there's also a K+/H+ antiporter present. 2) This results in increased HCO3- reabsorption at the PCT (via aldosterone). However, because K+ is deficient, there is a compensatory increase in the KHCO3/NaHCO3 PCT-reabsorption ratio, resulting in Na+-wasting (normally Na+ is the predominant cation reabsorbed with HCO3-). This loss of K+ at the PCT is secondary to the loss of it at the intercalated cell, not primary. The principal cells of the collecting duct are not affected, so some Na+ is recaptured there (following PCT loss), but additional K+ is secreted still. When the hypokalaemia gets severe, the basolateral principal cell Na+/K+-ATPase exchanges H+ for Na+ instead of K+. This limits the severity of the hypokalaemia (although it is already substantial) as well as chastens the increase in pH of the urine (because it's increased in RTA-I). The big thing to remember about RTA-I is that it's associated with Sjogren's syndrome and the patient will have bilateral nephrolithiasis in thesubstance of the kidney, not in the tubules. The vignette you'll get on the exam might sound straight forward, but it's easy to miss it. Watch out for severe flank/groin pain or opacities on a renal ultrasound in an acidotic patient with low K+ (or they might just tell you he or she has dental caries!). Side info: RTA-II, not I, is associated with Fanconi syndrome, leading to rickets/osteomalacia. The most common causes of RTA-IV are diabetic nephropathy and chronic tubulointerstitial nephritis.

RTA 1 -> decreased functioning of alpha intercalated cells that normally create and excrete H+ and resorb the bicarb they make via carbonic anhydrase -> decreased H+ in tubular lumen -> K+ is drawn more strongly into the lumen to fix the electronegative difference -> hypokalemia and metabolic acidosis RTA 2 -> PCT cells decrease function (Wilson's disease causing Fanconi Syndrome, or acetazolamide) -> tons more Na/K/bicarb etc in tubular lumen than would normally be -> Na is preferentially saved in the collecting tubules at the expense of K+ -> hypokalemia and metabolic acidosis RTA 4 -> decreased aldosterone or aldosterone insensitivity (adrenal failure, Legionaire's disease) -> hyperkalemia and metabolic acidosis

TCAs, anti-psychotics and first gen H1 antagonists all have anti-muscarinic effects. The mechanism is that they bind directly to the receptors. As thehundredthone has put it, this is due to non-selectivity.

If the case indicates an infant who shortly after birth develops jaundice, hepatomegaly, intractable seizures, facial abnormalities, hypotonia, developmental delay and later mental retardation, vision and hearing abnormalities, and deterioration of renal function then we have to think of Zellweger syndrome. Zellweger syndrome is an autosomal recessive disorder in which there's abnormal development of peroxisomes which are the cellular organelles responsible for beta oxidation of very long chain fatty acids.

pseudotumor cerebri is just increased ICP due to generally idiopathic causes. However, I've seen a couple practice USMLE practice questions already where they like danazol as causing it. I think ~13% got that right on USMLE Rx when I had gone through that QBank. Danazol is also associated with peliosis hepatis.

pseudotumor cerebri is a consequence of chronic Vit A toxicity, Obesity, tetracyclin, Danazol, and growth hormone .

Symptoms of pseudotumor cerebri — In one case series and in the Idiopathic Intracranial Hypertension Treatment Trial, the most common symptoms of idiopathic intracranial hypertension (IIH) were : ●Headache (84 to 92 percent) ●Transient visual obscurations (68 to 72 percent) ●Intracranial noises (pulsatile tinnitus) (52 to 60 percent) ●Photopsia (48 to 54 percent) ●Back pain (53 percent) ●Retrobulbar pain (44 percent) ●Diplopia (18 to 38 percent) ●Sustained visual loss (26 to 32 percent) These symptoms, even as a cluster, are not specific for IIH. In one case-control study, these symptoms were also common in age and gender-matched controls who were recruited from hospital waiting areas; although the prevalence, severity, and frequency were lower in this group . Pulsatile tinnitus was the most useful distinguishing feature.

Lichen Simplex Chronicus from Chronic Scratching
Lichen sclerosus will normally be described in a question as a whitish lesion with thinning of the skin. Chronic irritation/scratching is also implicated.

glutamate activates NMDA receptors, it increases morphine tolerance.
ketamine blocks NMDA receptors, it decreases morphine tolerance In schizophrenia and Alzheimer disease, there is increase in glutamate , so to decrease that we can block NMDA receptor by drug called Memantine.

Well there's a drug called teriparatide, which is a PTH analogue used in osteoporosis. The idea is that, given appropriate dosing/frequency/etc., the osteoblastic mechanism is upregulated and then the drug is removed before the osteoclastic activity can predominate.

Vancomycin is known for causing red man syndrome when infused too quickly.

the Bruton's child will present with recurrent bacterial infections
the Bruton's child will present with recurrent bacterial infections. Whereas the child with scid has a much more severe immune deficiency, so they can get everything from viruses, fungi, bacteria and protozoa. You'll see organisms that you'd expect to see only in AIDS patients in scid. Bruton's agammaglobulinemia thymic shadow is intact because it is just a B cell disorder. With SCID thymic shadow is absent because there is no T cells. In FA 2012 page 237 you can find that with Bruton's Agammaglobulinemia there is an absence of the thymic shadow but this is a mistake they corrected in the errata, so don't get confused.

Orlistat is a drug designed to treat obesity
Orlistat is a drug designed to treat obesity. Its primary function is to prevent the absorption of dietary fats, thereby reducing caloric intake. It is intended for use in conjunction with a physician-supervised reduced calorie diet. Orlistat works by inhibiting pancreatic lipase, an enzyme that breaks down triglycerides in the intestine. Without this enzyme, triglycerides from the diet are prevented from being hydrolyzed into absorbable free fatty acids and are excreted undigested. Only trace amounts of orlistat are absorbed systemically, the primary effect is local lipase inhibition within the GI tract after an oral dose. The primary route of elimination is through the feces. At the standard prescription dose of 120 mg three times daily before meals, orlistat prevents approximately 30% of dietary fat from being absorbed. The primary side effects of the drug are GI-related. Side effects were most severe within the first year of therapy. Because its main effect is to prevent dietary fat from being absorbed, the fat is excreted unchanged in the feces and so the stool may become oily or loose. Increased flatulence is also common. Bowel movements may become frequent or urgent. Rare occurrence of fecal incontinence have been seen in clinical trials. To minimize these effects, foods with high fat content should be avoided. The absorption of fat-soluble vitamins are inhibited by the use of orlistat. A multivitamin tablet containing these vitamins (D, E, A and beta-carotene) should be taken once a day, at least 2 hours before or after taking the drug. Contraindications Malabsorption Reduced gall bladder functionpregnancy/breast feeding renal disease

Orlistat is one of the "obesity drugs"
Orlistat is one of the "obesity drugs". Orlistat interferes with pancreatic enzymes (lipases) and causes steatorrhea. Also important side effect is: Crystalline Nephropathy (SOMATIC mnemonic for drugs cause Crystalline Nephropathy : Sulfadiazine Orlistat Methotrexate Acyclovir Triamterene Indinavir Ciprofloxacin)

Side effects of antiepileptic drugs
Carbamazepine: Hyponatremia, ataxia, agranulocytosis, aplastic anemia Phenytoin: Coarse facial features, ataxia, gingival hyperplasia, lymphadenopathy, hypertrichosis, neuropathy, serum sickness Valproate: tremor, weight gain, hair loss, pancreatitis, thrombocytopenia Topiramate: kidney stones, acute myopia and glaucoma, weight loss, CNS symptoms (fatigue, dizziness,...) Tiagabine: Abdominal pain Gabapentin: somnolence, ataxia Oxcarbazepine: hyponatremia, SJS Lamotrigine: rash, aseptic meningitis Vigabatrine: vision loss, psychosis, MRI abnormalities Zonisamide: renal stones, anorexia, in children hyperhydrosis and fever Phenobarbital /primidone: alteration of sleep wake cycle, hyperactivity, sedation, behavioral change, tolerance, dependence, dupuytren's contracture Ethosuximide: Nausea and vomiting, hyperactivity, somnolence. Phenytoin, phenobarbital, primidone, valproate, carbamazepine, lamotrigine all can cause SJS and TEN Felbamate: Aplastic anemia Levetiracetam: infection

Teratogens drugs : Valproate, Carbamazepine, Lithium, Lamotrigine, Antipsychotics, Antidepressants, Sulphonamides, Aminoglycoside , Fluoroquinilone, Erythromycin, Metronidazole, Tetracycline, Ribavarin, Griseofulvin, Chloramphenicol, Clarithromycin, Also Isotretinoin

leukocyte alkaline phosphatase(lap) reduced in CML, AML and PNH.

99% of mitral stenoses are due to old rheumatic fever (sore throat + other RF signs as a kid = MR initially, followed by MS later in life). The answer is almost never MS unless you have a reason to believe the person had RF early in life. Or if the USMLE does tell you someone has MS, they'll want you to pick the answer that somehow relates to RF. 60% of SLE patients with antiphospholipid syndrome develop Libman-Sacks endocarditis (small, verrucous vegetations). This can sometimes lead to MS too. But on Step 1, MS essentially/invariably = RF early in life. Endocarditis (large, friable vegetations) is always MR if affecting the mitral valve MR is holo-/pan-systolic. Pan- = holo- . In contrast, mid-/crescendo-decrescendo systolic = AS. MS = opening snap in diastole MR you get after papillary muscle rupture secondary to MI (sudden dyspnea within a few days after MI = increased LAP = increased PCWP = pulmonary edema). MS can present with dyspnea in pregnancy (increased preload in pregnancy makes a previously asymptomatic MS symptomatic).

Two enzymes affected in Ehlers-Danlos you need to know: 1) procollagen peptidase 2) lysyl oxidase For Ehlers-Danlos, for all intents and purposes, it is PROCOLLAGEN PEPTIDASE DEFICIENCY. You've gotta know that when the collagen is extruded from the cell, it still has its non-helical N- and C-terminal regions (heavy in S-S bonds) attached. When procollagen peptidase cleaves off these regions, the collagen becomes MUCH LESS water soluble. Without procollagen peptidase, the collagen is weaker. For Menkes syndrome (Ehlers-Danlos type-IX), you've gotta know that there's defective COPPER UPTAKE from the intestines. Copper is a co-factor for lysyl oxidase, so in Menkes, active lysyl oxidase is deficient I had encountered two questions on Menkes syndrome during my prep year. I wish it had showed up on my exam bc I was ready for it. It presents similar to vitamin C deficiency bc you get "kinky" or "wiry" hair + bruising.

hepatitis C associated with cryoglobulinemia.
Signs and symptoms of cryoglobulinemia; 1- palpable purpuric lesions 2- Gangrene/acrocyanosis 3- Athralgias >> arthritis

From all my studying, all I have learned is that a PSYCHIATRIST can NEVER date a patient, and other PHYSICIANS cannot date a CURRENT patient. This point was made even in MTB2 for step 2. So I think that's the right answer.

Most common causes of polyneuropathy are diabetes mellitus, alcohol abuse and HIV. But of course you have to watch out for drug induced neuropathy. Other etiologies of peripheral neuropathy can be broken down in nutritional (B6, B12), hereditary (Friedreich's ataxia, Charcot-Marie-Tooth), Infections (HIV, Lyme disease), and others. I will focus here on some classical examples of drug induced peripheral neuropathy. HIV Drugs Nucleoside analogues (esp. Didanosine, Stavudine) A challenge would be here to differentiate between HIV neuropathy and drug-induced neuropathy. Watch out for the classic NRTIs that cause neuropathy or a patient, that is not on triple therapy. Chemotherapy-induced peripheral neuropathy (CIPN) Vincristine Cisplatin Taxanes (Paclitaxel) Classic Example: A patient, that is on chemotherapy for weeks and develops now "stocking glove neuropathy". They will ask you is this because of the drug or because of cord compression of a metastasis? A Cord compression would give you also back pain, upper motor symptoms, prominent motor deficits. Antimicrobial Drugs Isoniazid (prevent with B6) Linezolid Immunosuppressive Drugs / Inflammatory drugs Colchicine Cyclosporine Toxins Arsenic poisoning (chronic) Classic Example: Wood preservatives, weed killers, pesticides. As an interesting side note: Watch out for a patient with Diabetes, who is taking Metformin and develops polyneuropathy after years of treatment. Metformin interferes with the absorption of folate and B12, and the question is now: Is the neuropathy due to diabetes or B12-deficiency? (Get CBC with MCV and look for your macrocytic anemia with hypersegmented neutrophils. Measure B12 levels. Metronidazole, diphtheria, and Pyridoxine (vit B6) toxicity can cause peripheral neuropathy

pompes disease restrictive cardiomyopathy (Initially is Restrictive, but eventually it can become dilated cardiomyopathy. But keep in mind Restrictive.) ,other causes systemic sclerosis ,sarcoidosis, amyloidosis hypertrophic cardiomyopathy in athletes outflow obstruction dilated cardiomyopathy (SYSTOLIC DYSFUNCTION) doxorubucin , daunorubucin,lymes disease,c.diphtheria,wet beri beri, and any cause of myocarditis can progress to DCM. Pompe Disease : "The glycogen that enters into the lysosomes is not broken down, but continuously builds up and disrupts the normal functions of the lysosome. This means that in Pompe disease (Type II GSD disease), where there is no enzyme to break down the glycogen in the lysosomes, that the lysosomes in the heart (also known as cardiac muscle) and other muscles quickly accumulate large deposits of glycogen. Over time these large deposits of glycogen cause the lysosomes to grow larger and larger and eventually breakdown, thus disrupting the function of the cell and organs that the cells make up, in this case the heart and muscles. Infants usually present during early infancy (4-8 months of age) with weakness and floppiness, are unable to hold up their heads and cannot do other motor tasks common for their age, such as rolling over. The muscles in the arms and legs look typical, but are very weak. Breathing muscles are also weak. The heart muscle thickens (cardiomyopathy) and progressively fails in its blood pumping function. Without treatment, infants with Type II GSD usually die before 12 months of age due to heart failure and respiratory weakness." Remember it develops restrictive cardiomyopathy.

Conditions mimic schizophrenia:
Huntington's disease (tremors, gait abnormality). Multiple sclerosis. Temporal lobe epilepsy. Cushing syndrome. Acute intermittent porphyria. Niemann–Pick disease type C

Pregnancy may be associated with transient diabetes mellitus (hyperglycemia).
When mother has hyperglycemia, her infant may be born with hyperplasia of pancreatic islets and hypoglycemia.

Asbestosis affects the lower lobe
Asbestosis affects the lower lobe. The other conditions (even Berylliosis) will affect the upper lobe. Pt has dyspnea, confusion & petechiae 72 hours after femur fracture. What is the likely diagnosis? Fat air emboli. Treatment is supportive

Jaundice usually occurs within 3 weeks with hepatitis A and within 3 months with hepatitis B.

The most common type is Duchenne muscular dystrophy, an X-linked recessive disorder of dystrophin.
Duchenne muscular dystrophy Look for muscle weakness, markedly elevated levels of creatine phosphokinase, pseudohypertrophy of the calves.

the left colon has a smaller diameter than the right
the left colon has a smaller diameter than the right. So, when the cancer develops in the left colon and wants to form a polyp, it goes around – annular (napkin ring), and produces constriction. Open bowel in left colon, see one edge of the cancer on each side of the bowel and bowel is constricted – have signs of obstruction (left side obstructs, right side bleeds). In the right colon, b/c of there is a bigger diameter; it has a bigger chance of going out and forming a polyp. Therefore, it is sitting in the stool, leading to a bleed (therefore left side obstructs, right side bleeds). So, which is side is more likely to have Fe deficiency? Right sided lesion because there is bleeding Which is more likely to have alteration in bowel habits (constipation/diarrhea)? Left sided. Left (descending colon) has stenotic lesion (apple core on Barium enema) so it presents as obstruction since the stool is formed by the time it reaches descending colon. Right (ascending) colon has cauliflower like lesion which is more prone to bleeding and as the stool is soft it does not present as obstruction. Rectum (not left colon) presents as Hematochezia.

Just read that bottle feeding and Macrolide use ( mother and child) are risk factors for Congenital Pyloric stenosis.

Not only is the olive-shaped mass hypertrophic pyloric stenosis, but if they ask about possible Sx, jaundice secondary to conjugated hyperbilirubinaemia can occur due to compression of the common bile duct running through the hepatoduodenal ligament. I had encountered that in a practice question somewhere. They'll try to throw epigastric pain at you, but if jaundice is there, that's the answer. And I also recall Kaplan QBook, which loves its minutiae, having mentioned that Smith-Lemli-Opitz is a notable genetic disease that presents with pyloric stenosis (as well as high forehead, syndactylyl of the second and third toes and MR). Pyloric stenosis is always 2-3 weeks post-birth (non-bilious vomiting). Duodenal atresia is always 2-3 days post-birth (bilious vomiting). If the patient has constipation and bilious vomiting, even if they don't mention distended abdomen or failure to pass meconium, it's Hirschsprung's, not duodenal atresia.

Petechiae are more of a sign of a bleeding time, not PT or aPTT, issue
Petechiae are more of a sign of a bleeding time, not PT or aPTT, issue. However that doesn't mean that they couldn't occur with vitamin K deficiency, but they are definitely not reflective of it, as you've mentioned. I'm also not 100% sure how far along you are with your studies at this point, but here are a few things to be aware of: Vitamin K2 is inactive. Vitamin K1 is active. Warfarin inhibits the K2 --> K1 conversion by inhibiting vitamin K epoxide reductase. You already know that. However, don't confuse that enzyme with the one that vitamin K is a cofactor for, which is gamma glutamyl carboxylase. That enzyme name isn't written in FA, although it's more just implied, but I've seen it come up in practice questions, and they'll throw the epoxide reductase in there as a distractor. With regard to what I've encountered in practice questions, if there's bleeding in a newborn, immediately think vitamin K deficiency or factor XIII deficiency. Neonates have sterile intestines, so they require vitamin K immediately after birth, so that deficiency is the most common, particularly if there is "bleeding from the umbilical stump." I had encountered factor XIII deficiency in a Kaplan QBook question. Apparently that's fairly common too, and it presents like vitamin K deficiency in a neonate. In contrast, factor XII, not XIII, deficiency results in pro-coagulation because Hageman factor (factor XII) converts prokallikrein to kallikrein, and kallikrein converts plasminogen to plasmin. So without factor XII, there's pro-coagulation (or anti-anti-coagulation). I've also seen vitamin K as an answer choice to an easy question, but it was listed as phytonadione, so be aware that that's the medical name for vitamin K1. It's also called phylloquinone, but I've only seen the former show up so far, not this latter one. And the other thing to know is that factor VII has the shortest half-life of any of the factors, so that's why vitamin K deficiency prolongs PT, not aPTT, first. Last thing, I had remembered from MS1 that parsley is the best known source of vitamin K, in addition to the cruciferous vegetables (which you can remember by saying "BBCC"), which include broccoli, Brussell sprouts, cauliflower and cabbage, however, in terms of practice questions, green leafy vegetables almost always points to folate, not vitamin K. The USMLE is overly obsessed with intestinal flora as being the vitamin K association.

Marantic endocarditis, also known as Non-Bacterial Thrombotic Endocarditis (NBTE), is the deposition of small sterile vegetations on valve leaflets. Marantic vegetations are often associated with previous rheumatic fever. The previous term for nonbacterial thrombotic endocarditis (NBTE) was marantic endocarditis, from the Greek marantikos, meaning â€œwasting away.â€ [1] Other risk factors include: hypercoagulable states, mucin-producing adenocarcinomas, lupus and trauma (e.g., catheters). The disease affects the valves with the following predilection: mitral valve > aortic valve > tricuspid valve > pulmonary valve. Grossly, vegetations form along lines of valve closure and are generally symmetric with a smooth or verrucoid (warty) texture. Histologically, lesions are composed of fibrin (eosinophilic) and platelets but, unlike bacterial etiologies, contain little evidence of PMNs, microorganisms or inflammation. Due to the non-invasive nature of NBTE, clinical examination may or may not reveal a new murmur. It is imperative to take the blood pressure in both arms. Marantic endocarditis ➔ thrombus deposition + fibrinous material on valves ➔ hypercoagulable states, adenocarcinomas + Lupus

What is the MOA of benzodiazepines?
Can benzos act on the Cl- channel without GABA? Which benzodiazepine binding sites do you know? Which ones mediate anxiolysis, anti-seizure activity, sedation, amnesia? Where does ethanol bind at? Which two benzos have no active metabolites? With which drugs do benzodiazepines generally interact? What are the adverse effects of benzodiazepines? Is flumazenil a selective or non-selective benzodiazepine site antagonist? Why can't flumazenil antagonize the depressant defect of barbiturates or alcohol? The administration of flumazenil can precipitate which serious condition in patients who have developed a tolerance to benzodiazepines? Name a short acting, an intermediate acting, and a long-acting anxiolytic benzodiazepine? Name a short acting, an intermediate acting, and a long-acting sedative benzodiazepine? Under which FDA pregnancy categories are benzodiazepines grouped? What are the "z drugs"? Where do they bind at? What are the classic side-effects of "z-drugs"?

Benzodiazepines bind to GABA A receptor at a site distinct from the GABA agonist site and enhance the actions of GABA. They act as positive allosteric modulators. Increase frequency of chloride ion channel openings produced by GABA. Contrast this with barbiturates, which increase the duration. No. Benzodiazepines alone cannot open the chloride ion channel without GABA. α1 and α5: Sedation, amnesia (Z-drugs work here) α2 and α3: Anxiolysis and anti-seizure activity. α4 and α6: Benzos have no activity on these receptors. Ethanol binds here. Mnemonic: Sleep at age 15, Seize at age 23, Drink at age 46. Oxazepam, Lorazepam Both are directly conjugated and have no active metabolite Drug Interaction with: CYP450 inhibitors; other CNS depressants Adverse effects: Drowsiness and sedation (long-acting); Rebound insomnia (short-acting); Motor incoordination (don't drive with benzos); Anterograde amnesia; Coma + resp depression when used with other CNS depressants (ethanol) Flumazenil: non-selective benzodiazepine site antagonist Because of the binding sites Administration of flumazenil can precipitate withdrawal seizures in patients who have developed a tolerance to benzos. Anxiolytic Short: Midazolam Intermediate: Alprazolam, Lorazepam Long: Diazepam (MAD) Sedative Short: Triazolam Intermediate: Temazepam Long: Quazepam Anxiolytic benzos --> All Class D Sedative all class X (ex Quazepam, class D) Zolpidem, Zaleplon,.... Work on α1,5. Strong affinity. Class C in pregnancy. Can be reversed by flumazenil,.... α1,5 Parasomnia. Crazy night stories with Z-Drugs.

seizure disorders (long acting anxiolytic benzos)
alcohol withdrawal Chlordiazepoxide Older drug, still used! Used in Alcohol-withdrawal situations Clorazepate Diazepam Long acting Oxazepam seizure disorders (long acting anxiolytic benzos) Clonazepam status epilepticus (IV) Long acting, IV Many active metabolites Lorazepam Long acting, IV pre-op sedation and anxiety relief Midazolam Very short acting Used to trigger anterograde amnesia Inducer of anesthesia FDA black box warning for respiratory depression/ respiratory arrest panic disorder Alprazolam Only benzodiazepine used for anxiety associated with depression

chlordiazepoxide, diazepam and lorazepam are longer acting and used for delirium tremens, alcoholic hallucinosis, and alcohol withdrawal in general. diazepam and lorazepam are also good for status epilepticus first-line before phenytoin, phenobarbital and propofol. Midazolam is the short-acting one used for anxiolysis / pre-surgery.

Boot-shaped heart is commonly seen on xray in which condition
Boot-shaped heart is commonly seen on xray in which condition? Tetralogy of Fallot

Succimer (DMSA) is a water-soluble analog of dimercaprol (BAL)
Succimer (DMSA) is a water-soluble analog of dimercaprol (BAL). Like dimercaprol and edetate disodium calcium (EDTA), succimer increases the urine excretion of lead. The main advantage is the route of administration: it can be given orally. In addition to that, it has less toxicity (and less urinary loss of essential minerals), than BAL. Succimer may cause elevated LFT's and cause hemolysis in individuals with G6PD deficiency. You have to adjust the dose to weight or body surface: Give 10 mg/kg two times per day. So dosages can be quite high for adults, that's why it is not prefered in adult. How do you screen for lead poisoning? Capillary blood levels. If elevated, get venous lead levels. Treat according to the venous lead level. 5-14 ug/dL Evaluate source, provide education, measure again in 3m 15-19 ug/dL Evaluate source, provide education, measure again in 2m, refer to health department 20-44 ug/dL Evaluate source, provide education, measure again in 1m, refer to health department 45-70 ug/dL Evaluate source, provide education, measure again in 1m, refer to health department Treat: Dimercaprol (BAL) (single dose) or succimer (DMSA) oral (preferred in kids) >70 ug/dL Treat: Hospitalization + two-drug IV treatment: EDTA + BAL

Mirtazapine is alpha-2 antagonist and that it's good in anorexic patients because it causes hunger.

St. john's wort used in depression.
side effects of st.john’s wort 1- Serotonin syndrome (Confusion, agitation, mydriasis, hyperthermia, hypertension, tachycardia, Tremor, myoclonus, hyperreflexia, clonus, diaphoresis, flushing, trismus, rigidity, diarrhea, coma). 2- induces p450( Due to the induction of CYP 3A4, concurrent use of St.john's wort may reduce the effectiveness of oral contraceptives) 3- Transient photosensitivity is generally the most common side effect of St. John’s wort at higher dosages.

PCOS = high androgens (hence the symptoms)
PCOS = high androgens (hence the symptoms). High circulating androgens are converted to estrone in the periphery which causes endometrial hyperplasia over time. Also PCOS = anovulatory bleeding. If you are not ovulating, you never have progesterone to balance out your estrogen = prolonged states of estrogen stimulation without counterbalance.

serum antibacterial antibodies are present in patients with ulcerative colitis, they are much more common and are found in higher titers in patients with Crohn's disease. Furthermore, the range of antibodies against bacterial antigens (anti-I2, anti-OmpC, and anti-CBir1 antibodies) and fungal antigens (anti–Saccharomyces cerevisiae antibodies [ASCA] is broader in Crohn's disease, whereas the only ulcerative colitis–associated antibody is perinuclear antineutrophil cytoplasmic antibody (pANCA), which recognizes nuclear antigens that may cross-react with bacterial antigens.

Knowledge of the influence of anesthetics on cerebral blood flow and metabolism is the key to both safe neuroanesthesia practice and understanding the possible neuroprotection offered by these agents. In this paper the authors summarize recent data from the literature. All volatile anesthetics (except for nitrous oxide) produce a dose dependent decrease in cerebral metabolism. The changes in cerebral blood flow depend on the changes in cerebral metabolism and on direct vasodilatory effects; frequently volatile anesthetics increase cerebral blood flow. Cerebral autoregulation is dose-dependently altered. While CO2-response is preserved in the normal brain, this is not necessarily the case in injured brain or in presence of brain edema or tumor. Therefore, the volatile anesthetics are probably not the best choice when brain perfusion is impaired. Intravenous anesthetics (except ketamine) cause a dose-dependent decrease in cerebral metabolism and blood flow. Propofol has identical effects as the other intravenous agents. Autoregulation is preserved during the administration of propofol. The effects of narcotic agents depend largely on the background anesthetic. Pathological conditions induced physiologic changes, and coadministration of other drugs can greatly alter the effects of anesthetics on the brain.

Rose Gardener Syndrome caused by what bug
Rose Gardener Syndrome caused by what bug? fungus known as Sporothrix schenckii causes Rose Gardeners Syndrome

they are talking here about the "leucovorin rescue" effect, which is commonly used to counteract the side effects seen in high-dose methotrexatetherapy (when used as an anticancer, antimetabolite). Make sure, not to confuse folinic acid (FH4) and folic acid (the vitamin prior to the metabolic reduction to FH4 through DHF reductase). Leucovorin = "active" folinic acid (= reduced folate = FH4). Leucovorin "bypasses" the metabolic block caused by methotrexate on DHF reductase. Interestingly, leucovorin predominantly rescues "normal" cells and not cancer cells (the mechanism here is not completely understood). Leucovorin must be given within h after administration of methotrexate. If you want to go more in detail, read about "polyglutamation effect of methotrexate". In chronic, low-dose methotrexate therapy ( in the context of rheumatoid arthritis f.e.), folic acid is used on a daily basis. Folinic acid, in low-dose methotrexate therapy, is only be used in patients who have not had a satisfactory response to folic acid (folinic acid is also much more expensive).

PCOS have higher baseline insulin levels, triggering a greater GnRH pulsation frequency, leading to an increased baseline LH/FSH ratio. The increased production of LH relative to FSH leads to androgen production occurring greater than the rate of aromatization, leading to hirsutism. Keep in mind that oestrogens negatively feedback on LH + FSH production prior to ovulation (particularly FSH). This means that the greater basline oestrogen levels will result in lower than normal FSH prior to ovulation. Then, when oestrogen levels get high enough to trigger the LH surge, because FSH had had a lower pre-ovulatory baseline, the follicles hadn't matured enough such that a Graafian one could be released --> anovulatory cycles. The bottom line is that, in PCOS, a hyperinsulinaemic state leads to increased pre-ovulatory oestrogen levels, thereby suppressing FSH and follicular maturation.

Chlamydia C. psittaci: Causes psittacosis, an interstitial pneumonia contracted from birds C. pneumoniae: Causes pneumonia, bronchitis , and pharyngitis in school aged children C. trachomatis: Spectrum of diseases related to the serotype Ocular trachoma in developing countries. This is a common cause of blindness. Lymphogranuloma venereum is caused by invasive lymphatic disease Genital infections including urethritis, epididymitis, cervicitis, and salpingitis are sexually transmitted. Transmission to newborns from infected mothers occurs at delivery and can cause infant conjunctivitis and pneumonia .

Mumps The mumps virus is a member of the paramyxovirus group and only one serotype is known. Before the introduction of the vaccine, mumps parotitis was a common pediatric illness. Children presented with a low grade temperature and parotid swelling, often bilaterally. The submaxillary and sublingual glands may also be infected in 10-15% of the cases. Epidemiology Although the vaccine was introduced in 1968, it was not universally recommended until 1977. Cases are related to lack of immunization rather than a failure of the vaccine. Spread is by respiratory droplets Transmission may be occur about 24 hours prior to parotid swelling and 3 days after swelling is gone. There is transplacental antibody protection that lasts 6-8 months Incubation period is days with a peak at 17 days. Clinical Manifestations There is a prodrome of fever, headache, sore neck, and malaise followed by parotid swelling that may be rapid at first and peaks at 3 days. The swelling is preauricular and extends downward to obscure the angle of the jaw and reaches the mastoid. The ear is pushed upwards and out. The temperature elevation is moderate and rarely >40 C. The swelling lasts about 3-7 days The gland is tender and eating spicy or sour foods will increase the pain There may be swelling around Stenson's duct on the buccal mucosa. Complications Aseptic meningitis. May be seen clinically in 10% of cases and monos can be found in the CSF in 65% of individuals with mumps. May be associated with low CSF glucose and may think that you are dealling with a bacterial meningitis. Orchitis- usually in adolescent boys with the acute onset of testicular swelling associated with high temperature and pain. Treatment is local support and analgesics. Atrophy of the teste in 30% and 13% infertility rate. Pancreatitis, myocarditis, nephritis, thyroiditis, unilateral hearing loss, eye involvement Mumps in pregnant women has been associated with an increased rate of spontaneous abortion but not with an increase in congenital malformations. Complications may occur without parotitis.

Hirsutism:Excessive male-pattern hair growth in the female.
Pathogenesis A result of the relationship bewteen androgen levels and hair follicle response to androgen. Hirsutism can be caused by either increased levels of androgens or by increased sensitivity to the androgens Increased androgen activity causes increased hair growth in androgen sensitive areas and increased hair follicle size, hair fiber diameter, and the proportion of time terminal hairs spend in the anagen phase Cosmetically, this results in increase in coarse, dark hair in a typically male distribution Hormones that can be in excess include: Testosterone: generally of ovarian origin Dehydroepiandrosterone sulfate (DHEA-S): generally of adrenal origin Androstenedione: can be either of adrenal or ovarian origin SHBG (sex hormone binding globulin) levels can also dictate the level of active androgen SHBG can be suppressed in the setting of hyperinsulinemia or hypothyroidism Virilization occurs when androgen levels cause hirsutism plus additional symptoms such as voice changes, increased musculature, clitoromegaly, etc. Note: though often of non-serious etiology, hirsutism can cause mental anguish and emotional trauma for patients and can be a serious cosmetic problem Differential Diagnosis Hypertrichosis: hair would be distributed in a generalized, non-sexual pattern Often due to the use of medications such as phenytoin, glucocorticoids, minoxidil, or cyclosporine. Idiopathic (familial trait, more common in some ethnic groups) Various causes of hyperandrogenism PCOS (most common cause of hirsutism) Insulin resistance leads to increased insulin levels; insulin stimulates ovarian theca cells to produce more androgens Congenital adrenal hyperplasia (Non-Classical) Androgen-secreting tumors Would see a rapid rate of hair growth a, evidence of virilzation (clitoromegaly, increased muscularity) Cushing's syndrome Hyperthecosis Increased production of testosterone from theca cells of the ovaries Hyperprolactinemia Acromegaly Thyroid Dysfunction Obesity or insulin resistance Idiopathic Hyperandrogenism Idiopathic production of androgen precursors leads to increased androgen levels

A deficiency of Ornithine Transcarbamyolase enzyme would result in elevation of the serum level of which of the following? A- Ammonia B- Urea C- Arginine D- Citrulline E- Putrescine Ornithine Transcarbamoylase (OTC) deficiency is a disruption of the urea cycle. The urea cycle is the means through which the body gets rid of the surplus ammonium produced as a byproduct of amino acid metabolism. As indicated by its name, OTC introduces a carbamoyl subgroup into ornithine, and thus a new compound is synthesized, which is citrulline, the first molecule in the cycle of urea. The carbamoyl subgroup results from the combination of ammonium with carbondioxide. As a result, when OTC is deficient, ammonium piles up (constitutional laboratory finding in OTC deficiency -- choice A is correct), as well as other intermediate products of urea cycle (such as ornithine and arginine), but this finding is not invariably evident (choice C is not correct). OTC deficiency provokes an apparent malfunction of the urea cycle, consequently urea is UNDERproduced (choice B is incorrect). As already mentioned, OTC produces citrulline from carbamoyl phosphate & ornithine, thus OTC deficiency causes low levels of citrulline (choice D is incorrect). Putrescin is a molecule also deriving from the catabolism of amino acids in decaying tissues and is notorious for the odors produced in bacterial vaginosis, bad breath and decomposing corps. In this case, the surplus ammonium, instead of combining with carbon dioxide, it attaches to an aliphatic carbon chain. If I am correct, OTC does not take part in this process (choice E is incorrect). this is from FA: answer is A because: OTC is a most common urea cycle disorder (worth memorizing). its x-linked recessive. interferes with body's ability to eliminate ammonia. often evident in the first few days of life, but may present with late onset. excess carbomyl phosphate is converted to orotic acid (part of the pyrimidine synthesis pathway) findings in OTC deficiency: orotic acid in blood and urine, decreased BUN, and hyperammonemia symptoms.

3 types of rigidities : 1- Lead pipe- seen in Parkinson's, but it is also typically seen in NMS. 2- ClaspKnife - UMN Lesion 3- CogWheel – Parkinson

The disorders contributing to high-output heart failure include:
Systemic arteriovenous fistulas Hyperthyroidism Anemia, including the anemia of chronic kidney disease Beriberi (vitamin B1 or thiamine deficiency) Dermatologic disorders (eg, psoriasis) Renal disease Hepatic disease Skeletal disorders (eg, Paget disease, multiple myeloma) Sepsis

In Paget's disease, the extensive bone turnover underlies an increase in blood flow. The increased vascularity in pagetic bone can lead to the development of an AV shunt and this is what leads to the high ouput cardiac failure. If you think about Paget's it's defined by excessive and disorganized bone remodeling, so as a consequence you can end up with small arteriovenous fistulas in the vascularity of the involved bone that eventually amount to an AV shunt. this is another question. A high-put HF is basically your heart is fine but it's not pumping well enough to oxygenate the blood such is in AV shunt? Is that the def of high-put HF? In what other pathology would you see high-put HF? It's like your heart is working on overdrive to meet the increased demand for blood flow and eventually it burns out. You see it classically in hyperthyroidism, beriberi, anemia, or an AV fistula caused by trauma, like a healed knife wound, or dialysis shunt.

Metformin, a biguanide and insulin-sensitizing agent, has been used to restore menstrual cyclicity and induce ovulation in PCOS without the use of additional fertility drugs. Use of this agent is associated with reductions in serum levels of bioavailable androgen, LH, and atherogenic lipids. Metformin is presently classified as a category “B” risk in pregnancy, which indicates that there are no apparent fetal defects associated with its use in the late trimester of pregnancy, on the basis of animal studies. Because the human effects of first-trimester use are unknown, discontinuation of therapy at the onset of pregnancy confirmation has been standard. However, a recent prospective study of women with PCOS who continued metformin therapy through the first trimester of pregnancy showed no evidence of fetal harm, calling into question this recommendation. Metformin therapy is associated with a slight risk of lactic acidosis and is not used in patients with impaired liver or renal function.

Situations in which it would be advisable to hold or not to use metformin include:
iodinated radio contrast dye, hypoxia, acidosis from any reason, major surgery, and serious kidney or liver disease and in anyone who is seriously ill or not taking anything by mouth

Medications that commonly cause ejaculatory dysfunction in men include beta-blockers, alpha-blockers, antipsychotics and selective serotonin reuptake inhibitors. Hydrochlorozide can cause erectile dysfunction and decreased libido. Omeprazole and bupropion often do not negatively impact sexual functioning Tricyclics and selective serotonin reuptake inhibitors frequently cause sexual dysfunction. Bupropion actually decreases the orgasm threshold and is least likely to cause sexual dysfunction.

Bupropion is contraindicated for patients with seizure disorder , cuz it may precipitate the attack of seizure.

For acute gout: first answer is always indomethacin (or an NSAID, e. g
For acute gout: first answer is always indomethacin (or an NSAID, e.g., naproxen). If that doesn't work, the next answer is steroids. If that doesn't work --> colchicine. And Worldbeater has raised a great point that if the patient is a renal transplant recipient or has renal insufficiency of any kind, intra-articular steroid injection is correct over NSAIDs or colchicine. If the gout is polyarticular in this case, answer is PO/SC/IM/IV steroids (answer would be oral or IV). And if the patient is on aspirin as a regular med and gets acute gout, answer is still indomethacin over steroids. For chronic gout: allopurinol or febuxostat is the first answer. Avoid probenecid or sulfinpyrazone if the patient is an over-excreter (cuz these further increase risk of urate stones). Rasburicase or pegloticase are often never the answer unless they specifically ask for which drug is a urate oxidase analogue. Never give allopurinol or febuxostat if giving 6-MP or azathioprine (since these latter two drugs require xanthine oxidase for breakdown).

The DIC is thought to be from myeloperoxidase entering the blood
The DIC is thought to be from myeloperoxidase entering the blood. Auer rods contain myeloperoxidase (a blue-green heme-containing pigment, hence the blue/auer color of the rods). AML M3 is the best answer for DIC. I would think any AML could do it, but M3 is the USMLE classic.

Hypothermia and acidosis compromise thrombin-generation kinetics via different mechanisms. Hypothermia primarily inhibits the initiation phase, whereas acidosis severely inhibits the propagation phase of thrombin generation. Similarly, hypothermia and acidosis affect fibrinogen metabolism differently. Hypothermia inhibits fibrinogen synthesis, whereas acidosis accelerates fibrinogen degradation, leading to a potential deficit in fibrinogen availability. In addition, coagulation complications caused by acidosis cannot be immediately corrected by pH neutralization alone.

the left colon has a smaller diameter than the right
the left colon has a smaller diameter than the right. So, when the cancer develops in the left colon and wants to form a polyp, it goes around – annular (napkin ring), and produces constriction. Open bowel in left colon, see one edge of the cancer on each side of the bowel and bowel is constricted – have signs of obstruction (left side obstructs, right side bleeds). In the right colon, b/c of there is a bigger diameter; it has a bigger chance of going out and forming a polyp. Therefore, it is sitting in the stool, leading to a bleed (therefore left side obstructs, right side bleeds). So, which is side is more likely to have Fe def? Right sided lesion because there is bleeding Which is more likely to have alteration in bowel habits (constipation/diarrhea)? Left sided.

Left(descending colon) has stenotic lesion (apple core on Barium enema) so it presents as obstruction since the stool is formed by the time it reaches descending colon. Right (ascending) colon has cauliflower like lesion which is more prone to bleeding and as the stool is soft it does not present as obstruction. Rectum (not left colon) presents as Hematochezia.

neuroleptic malignant syndrome vs. malignant hyperthermia
The mechanism for both is the same, which is over-activation of the ryanodine channel on the sarcoplasmic reticulum, so there is excessive muscle rigidity + autonomic instability + fever. I say that because I know you can use dantrolene to treat both, and dantrolene shuts down the ryanodine channel. The only "difference" I can think of is that a dopamine-agonist (e.g. bromocriptine) can be used instead of dantrolene to treat minor or nascent cases of neuroleptic malignant syndrome, whereas malignant hyperthermia due to succinylcholine + halothane (or one of the other -fluranes) needs to be treated with strictly dantrolene.

The clotting factors that are produced by the liver are I, II, V, VII, IX and X. The order in which the levels of these are reduced in liver disease is: VII - the earliest to be reduced II, X - next to be reduced I, V - these persist despite severe liver disease

Patient presents 3 hours after aspirin OD: respiratory alkalosis
Patient presents 3 hours after aspirin OD: respiratory alkalosis. Patient presents 12 hours after aspirin OD: mixed respiratory alkalosis - metabolic acidosis. The common point of confusion is that it's a mixed acid-base status because the metabolic acidosis is NOT a compensation for the respiratory alkalosis; the aspirin itself causes both. Salicylate stimulates the medullary respiratory center and increases the sensitivity of the respiratory center to pH and carbon dioxide partial pressure (PCO2 ), causing increased alveolar ventilation. Prolonged high serum concentrations depress the respiratory center. Respiratory alkalosis is initially limited by compensatory mechanisms, including buffering by the hemoglobin-oxyhemoglobin system, the exchange of intracellular hydrogen ions for extracellular cations, and the urinary excretion of bicarbonate. Loss of bicarbonate decreases buffering capacity and intensifies the metabolic acidosis. Salicylates inhibit Krebs cycle dehydrogenases, which increases production of lactic and pyruvic acids. Acidosis is further intensified by increased lipid metabolism and production of ketone bodies. Salicylates uncouple oxidative phosphorylation, increasing the bodyâ€™s metabolic rate and temperature. Production of tissue carbon dioxide increases, as does oxygen consumption. Uncoupling increases tissue glycolysis, which predisposes patients to hypoglycemia. Hepatic gluconeogenesis and release of adrenaline cause the less common hyperglycemia.

4-year-old boy accidentally ingested an unknown quantity of aspirin
4-year-old boy accidentally ingested an unknown quantity of aspirin. By the time he was brought to the ER, he was semi-unconscious. the diagnosis of salicylic acid poisoning was made and appropriate treatment started. Which of the following describe the patient's condition A. Resp alkalosis Metabolic acidosis ph normal B. Resp Acidosis Metabolic alkalosis ph normal C. Resp Alkalosis Metabolic alkalosis ph increase D. Resp Acidosis Metabolic acidosis ph decrease E. Metabolic acidosis ph decrease Correct answer is "D" :) Aspirin causes stimulation of the respiratory center and hyperventilation in adults and in older children/adolescents. But in infants and younger children, the response is rather more a respiratory center depression, and they respond with hypoventilation and metabolic acidosis instead. Respiratory alkalosis in younger children is usually absent or transient.

Agranulocytosis is sometimes used interchangeably with neutropenia
Agranulocytosis is sometimes used interchangeably with neutropenia. If someone told me a patient was experiencing agranulocytosis, I'd assume mandatory neutropenia, then +/- eosinopenia/basopenia, even though it could technically be any or all of the three.

drugs that cause agranulocytosis:
Carbamazepine Clozapine Colchicine Propylthiouracil Methimazole Dapsone Ticlopidine Mnemonic: Can Certainly Cause Pretty Major Damage Too; Causes Pretty Major Collapse ToDefense Cells; Gangs CCCrush Myeloblasts and Promyelocytes DMARDS.

The paradoxical effect of thiazide in the treatment of nephrogenic diabetes insipidus is not fully understood and has been puzzling scientists. One proposed theory is that when you give thiazide (it works on the distal tubule) you'll initially increase sodium excretion which then leads to contraction of the ECF which then leads to increased proximal convoluted tubules reabsorption of Sodium and water and thereby ameliorating the diuresis. Therefore, any diuretic that is going to work in NDI must be working at the distal parts of the nephron such as thiazides or amiloride (and furosemide may not be a good choice). The only example of drug induced NDI that is ever going to be seen in your clinical practice (hence your USMLE exam) is the Lithium induced. Lithium is a cation just like Sodium and giving it for prolonged periods will be just like giving Sodium to the patient and therefore you end up with polyuria and diuresis. How that is resistant to the action of ADH is yet to be determined but the message is that, use the most distal diuretic (e.g amiloride) to treat the specific Lithium induced DI.

in hemochromatosis: S. Fe is increased TIBC is decreased S ferritin is increased why is transferrin synthesis decreased in haemachromatosis? Cellular iron uptake and storage are coordinately regulated through a feedback control mechanism mediated at the post-transcriptional level by cytoplasmic factors know as iron-regulatory proteins 1 and 2. These proteins "sense" levels of iron in the transit pool and, when iron in this pool is scarce, they bind to stem-loop structures known as iron-responsive elements on the 5' untranslated region of the ferritin mRNA and 3' untranslated region of the transferrin mRNA. Such a binding inhibits translation of ferritin mRNA and stabilizes the mRNA for transferrin . The opposite scenario develops when iron in the transit pool is plentiful. This remarkable regulatory mechanism prevents the expansion of a catalytically active intracellular iron pool, while maintaining sufficient concentrations of the metal for metabolic needs.

in DIC Proteins C & S are consumed rapidly (as well as fibrinogen [when it goes to fibrin]); that explains why factors V and VIII would be low, given that they're specifically regenerated by proteins C/S.

Urease Positive bugs I've encountered S. saprophyticus in practice questions as being urease-positive. Via all of the practice questions I've done so far, I've come up with "BacK PPUNCHeS" Bacteroides Klebsiella Proteus Providencia Ureaplasma Nocardia Cryptococcus H. pylori S. saprophyticus The clinical relevance of S. saprophyticus being urease-positive is that, like Proteus, it can also cause staghorn calculi. I also cannot recall 100% which source I had encountered Providencia, but it's known to grow on catheters / IV lines, with greater prevalence in nursing homes. So if S. epidermidis isn't an answer and Providencia is, go with it. Edit: I just remembered: Zaslau's Board Buster is where I had seen Providencia (but I wouldn't recommend the text as a whole).

UWorld specifically said that the hepatic encephalopathy (in the particular patient in the vignette) was likely precipitated by his haematemesis. They also said there was increased NH3 absorption Moreover, important points I've grabbed regardless: Serum BUN is decreased in liver disease because arginase synthesis is decreased, so the urea cycle is impaired. This is what causes inability to process excess NH3, although it is not the reason for the increased NH3; increased gut absorption of NH3 causes the hyperammonaemia. Increased NH3 shunts alpha-KG to produce H2O + glutamate. This shuts down the TCA cycle, thereby causing the Sx of hepatic encephalopathy due to neurotoxicity. Increased GABA synthesis occurs, since glutamate is the precursor of GABA and glutamate is increased.

How does increased ammonia deplete alpha-keto glutarate
How does increased ammonia deplete alpha-keto glutarate? Is it because free ammonia combines with alpha keto glutarate? (an internet search vaguely suggests this is the reason) Or does it have something to do with glutamate / ammonium transport? I guess what I am asking is, does ammonemia by itself deplete alpha KG or is it depleted during the body's attempt to clear it off as urea in the liver? Answer ; Alpha-KG + alanine <--> glutamate + pyruvate This is the same as: alpha-KG + NH3 <--> glutamate + H2O To answer your question: increased ammonia on its own can deplete alpha-KG. In liver disease, decreased hepatic arginase synthesis leads to decreased BUN (increased BUN is kidney disease) and hyperammonaemia. This depletes your alpha-KG, shutting down your TCA cycle, leading to encephalopathy, etc. You'd also get increased glutamate synthesis, leading to neuroexcitotoxicity.

How does increased glutamate cause neuroexcitation
How does increased glutamate cause neuroexcitation? Doesn't it form GABA which is a (-) NT? So, you are saying ammonia combines with alpha-KG to form glutamate regardless of the intention of the body to convert that glutamate to urea right? And as long as we are on the subject of biochemistry, could you clarify my other very basic doubt? I understand as far as the fact that neutral particles cross membranes easier than charged ones. This is the basis for acidifying urine to eliminate basic products and alkalanizing urine to eliminate acidic products, trapping them in urine. And similarly, lactulose is used to acidify GIT to trap ammonium which is basic in GIT, preventing absorption. My question is how does this translate to amino acids? In cystinuria, lysine and arginine are not absorbed. They are both basic amino acids. So what is the logic behind using acetazolamide for treatment which alkalanizes urine? And how does lactic acidosis cause increased urine pH? (von Gierke -> gout) What is the basic chemistry concept here? Answer ; Glutamate, via glutamate decarboxylase and vitamin B6, can form GABA, but the glutamate is still formed in excess, hence the neuroexcitotoxicity. Ammonium is acidic, not basic. NH4+ doesn't transcytose the enterocytes and therefore remains in the lumen. Cystinuria is associated with COLA malabsorption (cysteine, ornithine, lysine, arginine), which are the basic amino acids. If you alkalinize the urine by using acetazolamide, then I'd assume you'd make it easier to reabsorb the basic amino acids because there'd be a decreased proclivity for them to protonate. If you have metabolic acidosis via lactic acidosis, you should have decreased urine pH.

Involvement of dermal lymphatics causes blockage of lymph flow, causing lymphoedema of sorts. The breast tissue swells up (however marginally) uniformly, except for where the suspensory ligaments are attached. This is why you get peau d'orange, it's not really inward pulling at the attachment site, rather it is outward swelling of the surrounding area. Since it is generalised, it looks like an orange peel. With direct suspensory ligament involvement, there is actual inward pulling of discrete attachment site(s) causing dimpling. Nipple retraction in case of malignancy works similarly.

In Cancer of Breast: Dimpling of the skin is due to infiltration of the suspensory ligaments. Nipple retraction is due to infiltration of the lactiferous ducts. Edema or peau d’orange is due to lymphatic obstruction/infiltration of dermal lymphatics.

1) one of the questions is about a neonate born with PDA but the description of PDA is " continuous machine like murmur along left sternal border , increased precordial activity and bounding peripheral pulses " Answer was simple just asking about indomethacin . Is it typical for PDA to have that location and description of murmur .Why are there AR signs here Phloston said ; 1) Lesson from clinical practice is murmurs can be heard anywhere. You could hear an aortic stenosis by all means in the axilla if it's a loud one. But on boards it's second intercostal on the right sternal border with radiation to the carotids. To answer your question though, that's fair game for PDA, as is above the clavicle. Could also be described as "to-and-fro" or "pan-systolic-pan-diastolic"; both = continuous, machinery-like. "Machine like murmur" is a classic clue for PDA 2) question is about iron deficiency anemia .Hb is 8.2g/dl , hematocrit is 25% and MCV is 69%.The reticulocyte count is 0.8% .Isn't this a normal reticulocytes count ?( % N) while it shouldnt be . Which anemias has low reticulocyte count ? Phloston said; 2) Reticulocyte count can be variable. If it's high you think acute blood loss in conjunction with healthy bone marrow. If it's low you think the BM isn't producing adequately (e.g., aplastic anaemias, chemotherapy, B9/B12 deficiencies). Iron deficiency can definitely lead to decreased reticulocyte count. But it doesn't have to be low if anaemia is not chronic or severe. Your MCV is less than 70, so it is microcytic anemia. If they didn't give you iron deficiency, your options are: Fe deficiency, anemia of chronic disease, sideroblastic, thalassemia, lead poisoning, sickle cell "FAST LeadS" If your reticulocyte is high, in addition to acute blood loss you can think of something that is "chewing up" the RBCs, like a metal valve or something lysing the RBCs. Schistocytes would be present in this case.

67 year old comes for routine examination
67 year old comes for routine examination.Her brother and mother had colon cancer.She only allows FOBT .The physician explains that FOBT is not appropriate in her case because of a) low sensitivity ( correct answer) b) low specificity c) uncertain PPV d) uncertain NPV isnt FOBT a high sensitivity test and that is why it is a screening test .All screening tests should be sensitive Phloston said ; 3) FOBC isn't sensitive because you'll get many false-negatives. (TP/TP+FN). Not all cancer bleeds, so you know you'll have false-negatives with FOBC. Colonoscopy would be most sensitive. On that note, FOBC isn't specific either cuz lots of things can cause bleeding (e.g., diverticular disease, angiodysplasia, polyps, etc.). Ah, it's the FN that's screwing up the sensitivity, thanks for putting in the equation, makes more sense now. I was thinking about sensitivity being "SPIN in"/ruling in, that wasn't helping with this particular question.

Ankle jerk: S1 Knee jerk: L2-L4 Biceps: C5-C6 Triceps: C7-C8 Jaw jerk: CN 5 Abdominal reflexes: Upper - T7, Lower - T10 Cremasteric: L1 Gag reflex : CN 9 , CN10

If they say a patient had a small polyp per colonoscopy --> APC
If they say a patient had a small polyp per colonoscopy --> APC. If they say a pt had a small polyp that wasn't excised but then went back a year later and had a larger polyp --> RAS. If they show you a histological image without BM penetration --> APC or RAS. If they mention/show any form of invasion --> p53. I've never actually seen DCC show up in a practice question (even though it's in FA), but it theoretically goes hand in hand with p53. If they mentioned a DCC mutation, I'd go with basement membrane penetration.

Methanol ingestion --> Formic acid --> optic nerve --> flashes of light, blurring of visual fields; may progress to complete loss of vision

The sweat glands are innervated by the sympathetic nervous system and are part of the fight or flight response system. Their innervation consists of two parts, a preganglionic and postganglionic neuron. The preganglionic neuron is short, originates from the thoracolumbar region of the spinal cord, uses acetylcholine as its neurotransmitter, and synapses with the postganglionic neuron via a nicotinic acetylcholine. The postganglionic neuron for sweat gland innervation differs from other sympathetic postganglionic neurons in that it releases acetylcholine to act on muscarinic receptors; all other sympathetic postganglionic neurons, with the exception of the adrenal medulla, use norepinephrine.

Infections associated with cancer :
1) Streptococcus bovis (group D) -- Colon cancer 2) H. pylori -- Gastric adenocarcinoma 3) EBV -- Nasopharyngeal carcinoma 4) Schistosoma haemotobium -- Squamous cell carcinoma of the bladder 5) Clonorchis sinensis -- Cholangiocarcinoma 6) EBV also causes endemic Burkitt lymphoma, is associated with Hodgkin lymphoma, nasopharyngeal ca, lymphoma in cns in HIV patient. 7)HHV8: kaposi sarcoma in HIV/AIDS and transplanted pts. 8) HVB/HCV: hepatocellular carcinoma. 9)HPV: cervical carcinoma (also penile, anal, throat, neck) mostly the serotypes 16 and ) HTLV-1: adult T-cell lymphoma/leukemia. 11) HBV : HCC

Scurvy: myalgia, arthralgia, wkness, wt loss, irritability, ecchymosis, brittle corkscrew hair, poor healing, swelling, hypotonia, anemia.

Characteristic findings in visceral leishmaniasis (kala azar) include: pancyopenia.
Fever, diarrhea and eosinophilia : Ascaris

the pathophysiology of gynecomastia in Choriocarcinoma?
Sex hormone profiles were studied in serum and tumor extracts of a man with pulmonary choriocarcinoma and gynecomastia. Although levels of serum estrogens were elevated as expected, serum androgen levels were uncharacteristically quite high. Tumor extract contained increased quantities of both androgens and estrogens when compared with surrounding normal lung tissue, but lacked the enzymes necessary for androgen biosynthesis while retaining aromatase activity. It is concluded that unlike the usual male patient with choriocarcinoma, the tumor-derived beta-human chorionic gonadotropin stimulated testicular androgen production. These androgens were in turn concentrated by the tumor and converted in part to estrogens. Furthermore, gynecomastia can occur even in the face of high serum androgen concentrations provided total estrogen levels are also disproportionately elevated."

LIVER ENZYME INDUCERS (PCBRAS) Phenytoin Carbamazepine Barbiturates Rifampicin Alcohol Sulphonylureas LIVER ENZYME INHIBITORS (OAAK DEVICCES) Omeprazole Amiodarone Allopurinol Ketoconazole Disulfram Erythromycin Valproate Isoniazid Ciprofloxacin Cimetidine Ethanol Sulphonamides

Positive Silver Methanamine stain of bronchoalveolar lavage is suggestive of which dx? Pneumocystic jiroveci.

Pulsus paradoxus is a exaggerated drop in systolic BP, whereas Kussmaul's sign is a rise in JVP. During inspiration, intrathoracic pressure drops, which causes venous blood to return to the right atrium, and then to the right ventricle. Also, lungs become inflated, pooling the blood inside the lung. Both of these result in decreased venous return to the left ventricle. According to the Frank-Starling mechanism, decreased venous return (=decreased end-diastolic LV volume) would decrease stroke volume, which would be manifested as a decreased systolic BP. If there is another mechanism which further decreases blood return to the left ventricle (such as cardiac tamponade), this physiological response will become exaggerated, using the same flow of events. As for Kussmaul's sign: Like I've said above, during inspiration, blood will return to the right atrium, meaning JVP would drop. If there is a mechanism through which blood can no longer enter the right heart, it will instead pool backing up, resulting in an increase JVP. Now this part often get mixed up: If there is just cardiac tamponade, there won't be Kussmaul's sign, but there will be elevated JVP. In constrictive pericarditis, elevated JVP and Kussmaul's sign will both be present.Elevated JVP itself does not equal to Kussmaul's sign; Kussmaul's is the rise in JVP with inspiration. In summary: cardiac tamponade = pulsus paradoxus; constrictive pericarditis = Kussmaul's sign. Both will have elevated JVP.

Cardiac tamponade: 1. Pulsus paradoxus 2
Cardiac tamponade: 1. Pulsus paradoxus 2. JVD with no collapse during diastole (i.e. attenuated y descent) 3. Hypotension with muffled heart sounds. Constrictive pericarditis; 1. Kussmaul's sign (lack of normal decrease and /or increase in Jugular Venous Pressure during inspiration) 2. JVD with rapid collapse during diastole (i.e. exaggerated y descent)

N-acetylcysteine can be used instead of Mesna to prevent haemorrhagic cystitis associated with cyclophosphamide/ifosfamide

in the spironolactone-treated group
in the spironolactone-treated group. Thus, spironolactone does alter the peripheral metabolism of testosterone resulting in changes in the ratio of testosterone to estradiol, which could contribute to the production of gynecomastia.

Basically any mass in the mediastinum can cause Horner's/SVC syndrome/TOS depending on which structure it is compressing. Pancoast tumor can lead to compression of SVC and/or can cause TOS. TOS is usually described as having a benign cause & can be B/L since the classic cause is cervical rib/subclavius muscle. SVC syndrome is usually described as having a malignant cause.

Compensatory mechanisms that maintain normal ICP in the face of an increasing intracranial mass lesion in adults include reduction in venous blood volume and reduction in CSF volume. This is the doctrine of Monro–Kellie. It states that the head is a closed box that cannot expand. It contains brain, blood and CSF. An expanding mass lesion will initially cause reduction in venous blood volume and CSF volume and therefore pressure will remain constant. As the mass lesion increases, it may compress the brain. Arterial volume is maintained until the late stages. At a certain point the mass lesion will overcome the compensatory mechanisms and ICP will start to rise. At this point, small increases in volume will cause large increases in pressure. This can be shown as a pressure–volume curve. This is why neurosurgical patients can rapidly deteriorate having been apparently stable and why it is so important to take seriously small deteriorations in function or level of consciousness

Gitelman - essentially the same effect as a thiazide diuretic
Gitelman - essentially the same effect as a thiazide diuretic. Leads to increased activity of aldosterone in the collecting duct (increased reabsorption of Na and loss of K and H). Liddle - hyperactivity of ENaC channel. Essentially like hyperaldosteronism except there will actually be low aldosterone in this patient. Bartter Syndrome= Loop diuretics Gitelman syndrome=Thiazide diurectics

loom Syndrome is a mutation in the HELICASE enzyme

Based on the STAR Trial: Tamoxifen is approved for the prevention and treatment of breast cancer. Raloxifene is approved for the prevention and treatment of osteoporosis as well as the prevention of breast cancer.

there is a deficiency in the enzyme methylmalonyl coA mutase or the cofactor vitamin B12 and you can't produce succinyl CoA from methylmalonyl CoA which means no succinylcoA and that means the TCA cycle can't go forward. Without the TCA cycle you won't generate enough Oxaloacetate which gets converted to aspartate to enter the urea cycle. basically a long explanation meaning without the first enzyme --> no succinyl coA --> no TCA--> no urea cycle = build up ammonia in the blood

Vit A deficiency "increases vulnerability to infection (especially measles).“
Measles may increase the body's utilization of vitamin A, possibly because of the rapid destruction of epithelial surfaces.

Monoclonal antibodies ( Alirocumab and Evolocumab) against PCSK9 (proprotein convertase subtilisin kexin 9). LDL-R on hepatocytes bind to LDL particles and remove them from the circulation. Normally PCSK9 binds LDL-receptor on the liver that clears cholesterol. This leads to LDL-receptor being destroyed and recycled. Now PCSK9 inhibitors binds PCSK9. Therefore, LDL- receptor stays on the liver longer and clears more cholesterol from the body. Bottomline: PCSK9 inhibitors leads to decreased LDL-receptor degradation > increased recirculation of the receptor to the surface of hepatocytes > lowering of LDL cholesterol in blood.

Acetyl CoA is an an obligate enzyme activator for Pyruvate Carboxylase, which is one of the key enzymes in Gluconeogenesis. Decreased Acetyl CoA = no activation of Pyruv Carboxylase = decrease Gluconeogenesis.

Vitamin A as an immunomodulating agent
Vitamin A as an immunomodulating agent. Abstract Findings on the benefits and mechanism of action of vitamin A in measles and other infectious diseases and immunocompromised states are discussed. Vitamin A deficiency is one of the world's major malnutrition problems and is most commonly found in children under the age of five years. An association between vitamin A status and immune function has been suggested by community studies and animal experiments. Mortality and susceptibility to infection and diarrhea are higher in children with vitamin A deficiency. The association between increased mortality and morbidity and vitamin A deficiency is strongest in children with measles. Vitamin A supplementation reduces mortality and complications resulting from measles. Measles may increase the body's utilization of vitamin A, possibly because of the rapid destruction of epithelial surfaces. Vitamin A may boost immune responses in the elderly, persons with high exposure to ultraviolet light, patients who have undergone surgery, and persons with parasitic infection, but more studies are needed. The immune defect caused by vitamin A deficiency may be due to alterations in the glycoproteins of the lymphocyte membrane, an adverse effect on helper T-cell function, the effect on epithelial tissue, or some other mechanism. Vitamin A therapy is relatively safe, and its effectiveness in children with measles and possibly other groups appears to justify public health campaigns to eliminate vitamin A deficiency. Vitamin A apparently has important immunomodulating properties, notably in patients with measles.

Femoral triangle NAVEL Going from lateral to medial we have N = femoral nerve A = femoral artery V = femoral vein E = Empty space (which is the inguinal ring) L = Lacunar ligament According to my copy of First Aid 2008, there's a mistake in this book, in which they mention L as lymphatics! Please don't rely on First Aid in this particular point. Here's a nice diagram that shows what goes beneath the inguinal ligament Copyright notice: this image is in the public domain in USA and is copied from wikimedia commons Note in the image that the femoral sheath does not include the femoral nerve. Also pay attention to the location of the Iliacus, Psoas major, and Pecitneus in the image (as they also serve as landmarks and can be asked about in the exam). So Femoral hernias goes through the femoral ring (see image above) and therefore, unlike inguinal hernias which slide above the inguinal ligament, femoral hernias (more common in females) slide below the inguinal ligament. Most surgeons are aware that trying to reduce a femoral hernia will risk crushing the intestines against the lateral sharp edge of the lacunar ligament and thereby risking incarceration. Note that the boundaries of the femoral triangle are different which are: The inguinal ligament superiorly The sartorius laterally The adductor longus medially (not gracilis) Floored by the muscles iliopsoas, pectineus, and adductor longus Roofed by the fascia lata

umbilical hernia is midline muscle defect. Skin is ok
umbilical hernia is midline muscle defect. Skin is ok. like other types of hernias. gastchochisis is midline muscle and also skin defect, intestines are out on air, irritated matted, can easily perforate. and defect is always away from midline. O is muscle, skin defect but covered with amniotic sac and umbilical cord protrudes thru it. you clearly see bowels in it, and portion of liver usually. if you dont rupture it kids may do totally fine. skin will grow over it by time with some betadine around skin daily. called "paint and wait" method. than it will turn in ventral hernia and you will treat it like usual muscle defect.

how you get the spider angioma, small testicles and gynecomastia in chronic alcoholism, cirrhosis and HCC ? Decrease steroid binding globulins leads to increase free estrogen, this hyperestrogenism --> increased SHBG (remember estrogen increases SHBG and TBG) --> decreased free testosterone --> leading to sexual dysfunction

Loss of hypotonic fluid: sweating, hypotonic urine (diabetes insipidus, alcohol). Loss of isotonic fluid: diarrhea (except infant<-hypotonic loss), vomiting, hemorrhage. Loss of hypertonic fluid: SIADH (inappropriate ↑ in urine osmolarity). Gain of hypotonic fluid: tap water, hypotonic saline. Loss of NaCI: e.g. loss of 1 L sweat, drink 1 L of tap water.

two drinks of alcohol per day is healthy.

barbiturates contraindicated in porphyria patients?
barbiturate induces p450 enzyme system and increases the formation of heme? and as in porphyrias there is enzyme deficiency such as urobillinogen decarboxylase and porphobillinogen decarboxylase etc .. so more heme formation provokes porphyrias .. can anyone explain more plz .... Answer; sure it's cuz the p450 enzymes contain heme in their structure.. So if u have a deficiency in one of the enzymes of the heme pathway, and u take a barbiturate it will increase synthesis of p450 which will result in accumulation of the substrates that come before the enzymes deficient in the heme pathway..

a) In acute intermittent porphyria, why is there an increase in urinary uroporphyrin, considering uroporphyrins come below the enzyme block (PBG deaminase)? b) how does low calorie diet, alcohol and enzyme inducing drugs lead to low heme in the liver? (which then lead to porphyria)? a) Are you sure you are reading it right? It's Porphyria cutanea tarda which causes an increase in urinary Uroporphyrin. Acute intermittent porphyria causes an increase in urinary porphobilinogen. b) The classic inducers of porphyria are chemicals or situations that boost heme synthesis. This includes fasting and drugs. In general, drugs that lead to increased activity of the hepatic P450 system, such as phenobarbital, sulfonamides, estrogens, and alcohol, are associated with porphyria. Cytochromes P450 (CYPs) belong to the superfamily of proteins containing a heme cofactor. In response to these drugs, the synthesis of CYP proteins increases (need more enzymes to metabolize these drugs), leading to an increased consumption of heme (since heme is a co-factor for cytochromes P450) causing a decrease in heme concentration in liver. The decrease in heme concentration also activates ALA synthase making things worse.

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