Internal Medicine 1

INTERNAL MEDICINE EOR EXAM REVIEW CRITICAL CARE Acute adrenal MC cause of primary adrenal insufficiency is Addison dz insufficiency Adrenal crisis occurs in the following situations: 1) stress 2) sudden withdrawal of adrenocortical hormone in pt with chronic insufficiency or chronic use of corticosteroids = MC cause of secondary insufficiency 3) following bilateral adrenalectomy or removal of a functioning adrenal tumor that had suppressed the other adrenal 4) following sudden destruction of the pituitary gland (necrosis) 5) when thyroid hormone is given to pt with hypoadrenalism 6) following injury to both adrenals by trauma, hemorrhage, anticoag therapy, thrombosis, infection following admin of etomidate – used for IV anesthesia induction or intubation s/s: h/a, lassitude, n/v, abd pain, diarrhea, confusion, coma, fever >40.6, low BP sometimes: cyanosis, dehydration, skin hyperpigmentation, sparse axillary hair hypoglycemia with lessening required need for insulin in Type I DM pts Lab: eosinophil count high, Low Na and high K, Hypoglycemia, >’d Ca Dx made by: cosyntropin stimulation test (normal cortisol level is >20 mcg/dL) and plasma ACTH (>200 pg/mL) Tr: 2 phases 1) acute phase: draw blood to determine cortisol level and treat with hydrocortisone 100-300 mg IV and saline immediately without waiting for the results. Following, give hydrocortisone phosphate or hydrocortisone sodium succinate 100 mg IV immediately and continue IV infusions 50-100 mg q 6 st nd hrs for 1 day. Give the same amt every 8 hrs on the 2 day, then adjust dose based on clinical picture. 2) Convalescent phase: hydrocortisone PO 10-20 mg q6hrs, and reduce to maintenance level as needed (typically given q12hrs 10-20 mg am and 5-10mg pm + fludrocortisone acetate .05-.2mg PO daily. After rapid treatment and crisis has passed, assess for possible cause and permanent treatment options Thyroid storm Extreme thyrotoxicosis triggered by: 1) stressful illness 2) thyroid sx 3) RAI administration s/s: marked delirium, severe tachycardia, vomiting, diarrhea, dehydration, very high fever mortality high tr: thiourea drug (eg methimazole 15-25 mg PO qhrs) or propylthiouracil 150-250mg PO q6hrs) + Ipodate sodium 500 mg/day PO 1 hr after thiourea + iodine (Lugol solution 10 drops 3x’s/day PO or sodium iodine ig IV slowly) given 1 hr later + propranolol 0.5-2mgIV q4hrs or 20-120 mg PO q6rs + hydrocortisone is usually given in doses of 50 mg orally q6hr (reduce rapidly as pt improves) Diabetic Can be initial manifestation of type I DM, or d/t >’d insulin requirement in type 1DM during infection, Ketoacidosis/acute trauma, MI, or sx; may occur in Type 2DM with severe stress (sepsis, trauma) hypoglycemia Mortality greater in elderly than mental stupor -> coma PE: stuporous pt w/ rapid deep breathing and a “fruity” breath odor of acetone = strong suggestion of dx Labs: moderately severe: Glucose 350-900 mg/dL Serum ketones at a dilution of 1:8 or greater Hyperkalemia 5-8 mEq/L – occurs despite total body K depletion b/c shift of K from intra to extracellular spaces d/t systemic acidosis

Acute glaucoma

Pulmonary embolism

Slight hyponatremia 130 mEq/L – d/t vomiting and polyuria Hyperphosphatemia 6-7 mg/dL Elevated blood urea nitrogen and serum creatinine Acidosis severe ranging from 6.9-7.2 Serum bicarb 5-15 mEq/L PCO2 is low related to hyperventilation Fluid depletion Hyperosmolar coma – occurs when osmolality exceeds 320-330 Mild = pH 7.25-7.3 – alert – treat in ER Mod = pH 7.0-7.24 – either alert or a little drowsy – admission to ICU Severe = 220/110 -Tx is to lower BP in clinic slowly over several hours (≤160/100) with labetalol, clonidine, captopril -Close follow-up

Pharm for HTN

Acute Gastrointestinal bleed

Hypertensive emergency = rapidly progressing end organ damage -Papilledema if malignant -Chest pain, AMS, weakness, MI, acute CHF, renal failure, ICH, eclampsia, aortic dissection -Don’t lower BP by more than 25% original value Monitoring HTN: -Annual urine microalbumin -Annual BMP -Annual lipids -Baseline EKG, look for LVH single agents only lower by 10-20 mm Hg, may need a 2nd agents Thiazides: HCTZ, chlorthalidone -DOC for HTN but can’t use once CrCl < 30 -Ca sparing = good for osteoporosis pts -Need to check BMP before and after starting -Chlorthalidone has the most evidence but my preceptor thinks it causes a lot of hypokalemia Loops: furosemide K-sparing: spironolactone, Not very potent eplerenone ACEi’s: benazepril, enalapril, -Cough lisinopril -Can cause renal failure = need to monitor BMP 1 week and 1 month after starting and periodically after that, STOP if serum Cr ↑ by 30% -Ok to use in patients with no renal function left -Pregnancy D ARBs: irbesartan, losartan, -Same AEs as ACEIs and also pregnancy D olmesartan, valsartan CCB’s: dihydropyridine (nifedipine, -Useful in the elderly amlodipine) -FDA warning about amlodipine, verapamil, and diltiazem and non-dihydropyridine (verapamil use with simvastatin and diltiazem) -Contraindicated in heart failure Other direct vasodilators: hydralazine, minoxidil -Clonidine: only for refractory HTN due to risk of falls α-blockers -Methyldopa: DOC for HTN in pregnancy -Questionable role in the treatment of essential HTN unless patient β-Blockers also has CHF or MI -Need strict β-1 blockers for asthma/COPD patients so that bronchial relaxation is not blocked (atenolol or metoprolol) -Propranolol and labetalol block at multiple sites -Can mask signs of hypoglycemia -Contraindications: heart block Upper GI bleed causes: coffee ground or red hematemesis -> bleeding proximal to the ligament of Treitz. Frank blood -> mod to severe bleeding that may be ongoing; coffee ground -> limited bleeding Lower GI bleed: melena (black tarry) proximal to the ligament of Treitz; Hematochezia (red or maroon blood in stool) -> lower GI bleed or massive upper GI bleed that’s associated with orthostatic hypotension Potential sources of GI bleed: varices or portal hypertensive gastropathy w/ liver dz or alcohol abuse Aorto-enteric fistula Angiodysplasia PUD w/ H pyolori Medication hx – aspirin or NSAID use, antiplatelet agents, iron, bismuth Esophageal ulcer Mallory-weiss tear Variceal hemorrhage Malignancy PE: mild to mod hypovolemia (resting tachy), stool color, abd pain, rebound tenderness and involuntary guarding can indicate perforation

History & Physical

Lab: CBC (hemoglobin loss with normocytic/chromic RBC’s), CMP, ALT/AST, Alk Phos, PTT/PT, INR, EKG, cardiac enzymes with MI risk pts with chest pain/dyspnea; elevated BUN/CR ratio (higher ratio = upper GI) Dx studies: upper endoscopy, angiography for upper GI, colonscopy for Lower GI bleed Triage: all pts w/ hemodynamic instability -> admit to ICU for resuscitation and close monitoring Oxygen, fluid resuscitation (500mL normal saline or lactate Ringer over 30 minutes), type and crossed, and transfused for pts