Presentation on theme: "Senior Case Presentation by Octavio Ruiz MD 10/20/05."— Presentation transcript:
Senior Case Presentation by Octavio Ruiz MD 10/20/05
Case presentation History: a) Chief complaint: Naucea/ vomiting for 4 days. b) HPI: Patient c/o n/v intermittently for last 9 months, almost all day for the last 4 days, along with progressive weakness, fatigue, poor appetite, and myalgias. Denies fever, diarrhea, abd. pain, dysuria. Pt. went to MD 2 wks ago gave him Tigan and Prilosec witch made no change.
Case presentation c) Past Medical Hx: None d) Past Surgical Hx: Pin Rt. Leg 20 y. ago e) Medications: Tigan, prilosec. f) Allergies: NKDA g) Family Hx: Mother breast Ca. and thyroid problem??, Father DM. h) Social Hx: Tobacco ½ ppd/30 y., Cannabis daily, ETHO none, IVDA none.
Case presentation i) Review of systems: + weight loss 4 lbs/2 wks., dizziness, SOB, cough and sputum. - diarrhea, polyuria, polydipsia, seizures, hallucinations, depression.
Case Presentation j) PE: T 96.8, HR 85, RR 16, B/P 94/66, Wt 155 lbs. General: A+O X 4, NAD. Skin: decreased skin turgor with some increased pigmentation on elbows. HEENT: NC/AT, PERLA, dry oral mucosa, pt. crying with tears. Neck: No JVD Chest: Symmetric, lungs CTA. Heart: RRR, PMI 5 th IC space L MC line.
Case Presentation Cont… PE Vascular: Good pedal and radial pulses B. Abdomen: Flat, Nl BS, soft, NT/ ND, no organomegalies. Genitalia: No masses, no skin changes. Structural: No CVA tenderness. Extremities: No edema, no cyanosis. Neuro: DTR’s 1+ B., no focal deficits, CN II-XII intact Lymph. Nodes: None palpable.
Case Presentation Labs: What labs would you like to order? Why? CBC: WBC 10.1, HBG 15, HCT 43, Pl. 408 CMP: Na 112, K 7.0, Cl 82, CO2 14, BUN 40, Cr. 1.4, Ca 10.8, Gap 16 Serum Osml. 249 UA: SG 1.005, Osm 286, Na 64, K 13.6 Screen: Baseline cortisol, ACTH and aldosterone levels, then give ACTH measure cortisol and aldos. At 30 and 60 min.
Case Presentation With info provide what is your Dx? Hyponatremia (see copy provided) a) Adrenal insufficiency: -Primary (Addison’s disease) -Secondary (low ACTH production)
Case Presentation Addison disease: Etiology: Most common cause world-wide Tb., in developed West countries is autoimmune destruction “adrenalitis” usually as part of the polyglandular deficiency sx., all fungi except Monilia cause adrenal destruction, hemorrhage, mets., AIDS, amyloidosis, adrenoleukodysytrophy, congenital adrenal hypoplasia.
Case Presentation Pathogenesis: Primary adrenal insufficiency is due to destruction of the adrenal cortex 2ry to: autoimmune destruction, infection, neoplastic, iatrogenic, traumatic, vascular and metabolic. When 90% of cortex destroyed signs and symptoms appear, feedback inhibition of the hypothalamus and pituitary gland is interrupted and ACTH is released continuously. ACTH and MSH (melanocyte stimulating hormone) are components of same progenitor hormone.
Case Presentation Epidemiology and Risk factors: Incidence: 5 – 6 cases/ 1,000,000 population per year. Prevalence: 60 – 110 cases per 1,000,000 population. Sex: Male to female ratio 1: 1.5 – 3.5 Age: Most common in people aged Risk factors: Expression of adrenal cortex antibodies (ACAs).
Case Presentation Diagnosis: Symptoms/ PE: Weakness and weight loss of 1-15 Kg are universal features of Addison's dz. In adults. N/V, abd. pain present in about 90% of pts. Depression, irritability and decreased concentration. Physical exam: Skin hyperpigmentation, Nl skin or vitiligo, women loss of hair in androgen stimul. Areas, S/D BP low. Labs/x-rays: Absent aldosterone = Low Na, High K, AM 6-8AM cortisol levels > 19 mg/dl normal no further workup, < 3 Dx., 3-19 indeterminate.
Case Presentation Dx. Contin… Indeterminate: Then do ACTH (Cortrosyn) stimulation test 350 mg IV then blood cortisol at 30 and 60 min. Level > 18 mg/dl exclude Dx., indeterminate, < 13 Dx. Adrenal antibodies and TB. Should be R/O. MRI/ CT equally good. Diff. Dx: Acanthosis Nigracans, Lentigo, malignant melanoma, vitiligo, hypoth. Depression, Anorexia nervosa.
Case Presentation Treatment: Cortison 25/300 mg qd. PO/IM divided q 8 hrs., hydrocortison 100 mg IV then contin. Infusion 100 mg q 8 hrs for 24/48 hrs.once stable 50 mg po q 8hrs. New studies: Best Pract Res Clin Endocrinol Metab Mar;19(1): (The populations with the highest risk of Autoimmune AD are first relatives of patients with AAD and patients with autoimmune diseases, particularly those with chronic hypoparathyroidism or with premature ovarian failure. Acta Paediatr Dec;93(12): (Thyroxine replacement unmasked Addison's disease and precipitated an acute adrenal crisis. On physiological steroid replacement therapy, her "hypothyroidism" resolved. Intensive Care Med Mar;31(3): Epub 2005 Feb 10 (A single bolus infusion of etomidate could be a major risk factor for the development of relative adrenocortical deficiency in ICU patients for at least 24 h after administration. Female gender is an independent protective factor. Information gather from PubMed.and the NLM.