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Selective GI and Renal Conditions. Gastrointestinal Disorders GERD Gastritis Peptic Ulcer Disease Irritable Bowel Syndrome.

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Presentation on theme: "Selective GI and Renal Conditions. Gastrointestinal Disorders GERD Gastritis Peptic Ulcer Disease Irritable Bowel Syndrome."— Presentation transcript:

1 Selective GI and Renal Conditions

2 Gastrointestinal Disorders GERD Gastritis Peptic Ulcer Disease Irritable Bowel Syndrome

3 GERD Gastroesophageal Reflux Disease Commonly known as ‘Heartburn’

4 Esophagus (1 of 3) Muscular tube that extends from pharynx to stomach with sphincters at both upper and lower ends – Upper sphincter relaxes to allow passage of swallowed food – Lower (gastroesophageal or cardiac) sphincter relaxes to allow passage of food to the stomach Diseases – Failure of cardiac sphincter to function properly – Tears in lining of esophagus from retching and vomiting – At gastroesophageal junction from repetitive, intermittent, vigorous contractions that increase intraabdominal pressure – Esophageal obstruction from carcinoma, food impaction, or stricture

5 Esophagus (2 of 3) Symptoms – Difficulty swallowing (dysphagia) – Substernal discomfort or pain – Inability to swallow (complete obstruction) – Regurgitation of food into trachea – Choking and coughing Two major disturbances of cardiac sphincter – 1. Cardiospasm: sphincter fails to open properly due to malfunction of nerve plexus; esophagus becomes dilated proximal to constricted sphincter from food retention Treatment: periodic stretching of sphincter; surgery – 2. Incompetent cardiac sphincter: sphincter remains open; gastric juices leak back into esophagus

6 Esophagus (3 of 3) Complications of incompetent cardiac sphincter – Reflux esophagitis: inflammation – Ulceration and scarring of squamous mucosal lining – Barrett’s esophagus: glandular metaplasia; change from squamous to columnar epithelium; ↑risk for cancer -a disorder in which the lining of the esophagus is damaged by stomach acid. Esophageal obstruction – Carcinoma: can arise anywhere in esophagus – Tumor narrows lumen of esophagus, infiltrates surrounding tissue, invades trachea (tracheoesophageal fistula) – Food impaction: distal part – Stricture: from scar tissue due to necrosis and inflammation from corrosive chemicals such as lye

7 Figure 23.13 Tongue Trachea Pharynx Epiglottis Glottis Bolus of food Epiglottis Esophagus Uvula Bolus Relaxed muscles Circular muscles contract Bolus of food Longitudinal muscles contract Stomach Relaxed muscles Gastroesophageal sphincter opens Gastroesophageal sphincter closed Upper esophageal sphincter is contracted. During the buccal phase, the tongue presses against the hard palate, forcing the food bolus into the oropharynx where the involuntary phase begins. Food is moved through the esophagus to the stomach by peristalsis. The gastroesophageal sphincter opens, and food enters the stomach. The uvula and larynx rise to prevent food from entering respiratory passageways. The tongue blocks off the mouth. The upper esophageal sphincter relaxes, allowing food to enter the esophagus. The constrictor muscles of the pharynx contract, forcing food into the esophagus inferiorly. The upper esophageal sphincter contracts (closes) after entry. 12 4 3 5

8 Figure 23.13, step 4 Relaxed muscles Bolus of food Stomach Circular muscles contract Longitudinal muscles contract Gastroesophageal sphincter closed Food is moved through the esophagus to the stomach by peristalsis. 4



11 Gastric mucosal tear caused by retching and vomiting Mallory–Weiss syndrome or gastro-esophageal laceration syndrome refers to bleeding from tears (a Mallory-Weiss tear) in the mucosa at the junction of the stomach and esophagus, usually caused by severe retching, coughing, or vomiting.

12 Gastritis

13 Acute Gastritis Inflammation of the gastric lining Self-limited inflammation of short duration May be associated with mucosal ulceration or bleeding From nonsteroidal anti-inflammatory drugs (NSAID) that inhibit cyclooxygenase (COX) enzyme: aspirin, ibuprofen, naproxen – COX-1: promotes synthesis of prostaglandin that protects gastric mucosa – COX-2: promotes synthesis of prostaglandin that mediate inflammation Drugs that selectively inhibit COX-2 increase risk for heart attack and stroke Alcohol: a gastric irritant; stimulates gastric acid secretion

14 Figure 23.15a Mucosa Surface epithelium Lamina propria Muscularis mucosae Oblique layer Circular layer Longitudinal layer Serosa (a) Layers of the stomach wall (l.s.) Stomach wall Muscularis externa (contains myenteric plexus) Submucosa (contains submucosal plexus)

15 Figure 23.15c (c) Location of the HCl-producing parietal cells and pepsin-secreting chief cells in a gastric gland Pepsinogen Mitochondria Pepsin HCl Chief cell Enteroendocrine cell Parietal cell

16 Figure 23.18 Stomach lumenChief cell Parietal cell Inter- stitial fluid Carbonic anhydrase Alkaline tide HCO 3 – Blood capillary CO 2 Cl – CO 2 + H 2 O H 2 CO 3 HCO 3 – - Cl – antiporter HCO 3 – H+H+ Cl – l K+K+ K+K+ H+H+ H + -K + ATPase HCI

17 H. Pylori Gastritis (1 of 2) Small, curved, gram-negative organisms that colonize surface of gastric mucosa Grow within layer of mucus covering epithelial cells Produce urease that decomposes urea, a product of protein metabolism, into ammonia Ammonia neutralizes gastric acid allowing organisms to flourish; organisms also produce enzymes that break down mucus layer

18 H. Pylori Gastritis (2 of 2) Common infection that increases with age (50% by age 50) Spreads via person-to-person through close contact and fecal-oral route Increased risk of gastric carcinoma: intestinal metaplasia Increased risk of malignant lymphoma (mucosa- associated lymphoid tissue, MALT)

19 Figure 23.16 Bacteria Mucosa layer of stomach (a) A gastric ulcer lesion (b) H. pylori bacteria

20 Peptic Ulcer

21 Pathogenesis – Digestion of mucosa due to increased acid secretions and digestive enzymes (gastric acid and pepsin) – Helicobacter pylori injures mucosa directly or through increased acid secretion by gastric mucosa – Common sites: distal stomach or proximal duodenum Complications: hemorrhage, perforation, peritonitis, obstruction from scarring Treatment – Antacids: block acid secretion by gastric epithelial cells – Antibiotic therapy: against H. pylori – Surgery if medical therapy fails

22 Figure 23.16 Bacteria Mucosa layer of stomach (a) A gastric ulcer lesion (b) H. pylori bacteria

23 Gastric ulcer, eroded a blood vessel at base of ulcer causing profuse bleeding Large, chronic duodenal ulcer

24 Irritable Bowel Syndrome Also known as spastic colitis or mucous colitis Episodes of crampy abdominal discomfort, loud gurgling bowel sounds, and disturbed bowel function without structural or biochemical abnormalities Alternating diarrhea and constipation Excessive mucus secreted by colonic mucosal glands Diagnosis: by exclusion – Rule out pathogenic infections, food intolerance, and inflammatory conditions Treatment – Reduce emotional tension – Improve intestinal motility

25 Renal Disorders Glomerulonephritis Nephrotic vs. Nephritic Syndrome Urinary Tract Infection Vesicourethral Reflux Renal Stones Stress Urinary Incontinence

26 Glomerulonephritis Inflammation of the glomeruli caused by antigen- antibody reaction within the glomeruli Immune-complex glomerulonephritis – Usually follows a beta-streptococcal infection – Circulating antigen and antibody complexes are filtered by glomeruli and incite inflammation – Leukocytes release lysosomal enzymes that cause injury to the glomeruli – Occurs in SLE; immune complexes trapped in glomeruli – Occurs in IgA nephropathy Anti-glomerular basement membrane (anti-GBM) glomerulonephritis: autoantibodies attack glomerular basement membrane

27 Nephrotic versus Nephritic Syndrome Nephritic syndrome is a collection of signs (syndrome) associated with disorders affecting the kidneys, more specifically glomerular disorders. It's characterized by having small pores in the podocytes of the glomerulus, large enough to permit proteins (proteinuria) and red blood cells (hematuria) to pass into the urine. By contrast, nephrotic syndrome is characterized by only proteins (proteinuria) moving into the urine. Both nephritic syndrome and nephrotic syndrome result in hypoalbuminemia due to protein albumin moving from the blood to the urine.

28 Diabetic Nephropathy Kimmelstiel-Wilson syndrome Complication of long-standing diabetes Nodular and diffuse thickening of glomerular basement membranes (glomerulosclerosis), usually with coexisting nephrosclerosis Manifestations – Progressive impairment of renal function – Protein loss may lead to nephrotic syndrome – No specific treatment can arrest progression of disease – Progressive impairment of renal function may lead to renal failure

29 Urinary Tract Infections (1 of 2) Very common; maybe acute or chronic Most infections are caused by gram-negative bacteria Organisms contaminate perianal and genital areas and ascend urethra Conditions protective against infection – Free urine flow – Large urine volume – Complete bladder emptying – Acid urine: most bacteria grow poorly in an acidic environment

30 Urinary Tract Infections (2 of 2) Predisposing factors – Any condition that impairs free drainage of urine – Stagnation of urine favors bacterial growth – Injury to mucosa by kidney stone disrupts protective epithelium allowing bacteria to invade deeper tissue – Introduction of catheter or instruments into bladder may carry bacteria

31 Cystitis Affects only the bladder – More common in women than men; shorter female urethra, and, in young sexually active women, sexual intercourse promotes transfer of bacteria from urethra to bladder – Common in older men, because enlarged prostate interferes with complete bladder emptying Clinical manifestations – Burning pain on urination – Desire to urinate frequently – Urine contains many bacteria and leukocytes – Responds well to antibiotics – May spread upward into renal pelvis and kidneys

32 Urethra Figure 25.18a, b

33 Pyelonephritis Involvement of upper urinary tract from – Ascending infection from the bladder (ascending pyelonephritis) – Carried to the kidneys from the bloodstream (hematogenous pyelonephritis) Clinical manifestations: similar with an acute infection – Localized pain and tenderness over affected kidney – Responds well to antibiotics – Cystitis and pyelonephritis are frequently associated – Some cases become chronic and lead to kidney failure

34 Vesicoureteral Reflux Urine normally prevented from flowing back into the ureters during urination Failure of mechanisms allows bladder urine to reflux into ureter during voiding – Predisposes to urinary tract infection – Predisposes to pyelonephritis


36 Vesicoureteral reflux

37 Urinary Calculi (1 of 3) Stones may form anywhere in the urinary tract Predisposing factors – High concentration of salts in urine saturates urine causing salts to precipitate and form calculi Uric acid in gout Calcium salts in hyperparathyroidism – Urinary tract infections reduce solubility of salts in urine; clusters of bacteria are sites where urinary salts may crystallize to form stone – Urinary tract obstruction causes urine stagnation, promotes stasis and infection, further increasing stone formation

38 Urinary Calculi (2 of 3) Staghorn calculus: urinary stones that increase in size to form large branching structures that adopt to the contour of the pelvis and calyces Small stones may pass through ureters causing renal colic Some become impacted in the ureter and need to be removed Manifestations – Renal colic associated with passage of stone – Obstruction of urinary tract causes hydronephrosis- hydroureter proximal to obstruction

39 Urinary Calculi (3 of 3) Treatment – Cystoscopy: snares and removes stones lodged in distal ureter – Shock wave lithotripsy: stones lodged in proximal ureter are broken into fragments that are readily excreted




43 Stress Urinary Incontinence Involuntary loss of urine due to increases in intra-abdominal pressure

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