CARDIOLOGY
effects Orthostasis
CHEST PAIN pain changes with body position or breathing? chest wall tenderness? pain on exertion? Get an EKG: compare with an old EKG ST depression give LMW heparin ST elevation angioplasty or thrombolytics Quality of pain Pleuritic, changes with respiration Pleuritic Pleuritic Radiates to back Tenderness Epigastric pain
Non-Cardiac Chest Pain Features Likely Dx Fever, cough, Pneumonia sputum, dyspnea Sudden onset, Pneumothorax or sharp pain, dyspnea PE Positional, relief Pericarditis with sitting up wide mediastinum Aortic dissection on CXR Tender on palpation Costochondritis Burning quality GERD
Anaphylaxi s PE
Tests X-ray, ABG, oximeter X-ray, ABG, oximeter CT angiogram for PE EKG CT angiogram, MRA, TEE None Improves with antacids
HYPOTENSION systolic BP ≤ 90 mmHg treat first, diagnose later! 1. repeat BP manually 2. position patient feet up, head down 3. give fluid bolus 250 - 500 mL normal saline over 15 to 30 minutes Etiology Dehydratio n
Initial clues BUN:creatinine ratio > 15 - 20:1
Sepsis
Fever leukocytosis Rales S3 JVD on exam
MI
Arrhythmia Drug side
Palpitations, syncope β-blocker or Ca++
Confirm with… Low urine Na+ ˂ 20 mEq/L High urine osmolarity ˃ 500 mOsm/L Blood cultures
CXR echo high BUN troponin EKG Drugs in history
channel blocker BP normalizes lying flat Foods, insect bites, drug reaction Sudden dyspnea; recent surgery
Tilt table test
History of drug allergies elevated eosinophils CT angiography
How NOT to Kill Your Patient (Contraindications to Therapy) Treatment What to ask about Antiplatelets: ASA, clopidogrel Bleeding Enoxaparin, heparin Bleeding ASA Allergy β-blockers Low BP, severe asthma, COPD Nitrates Low BP Statins Liver dysfunction, myositis ACE inhibitors Hyperkalemia, Hx of cough from ACE-I ARB, spironolactone, eplerenone Hyperkalemia Spironolactone Gynecomastia heme-postive stool alone is not a contraindication to using ASA, clopidogrel, prasugrel, ticagrelor, or heparin ACUTE CORONARY SYNDROME (ACS) HISTORY consistent with ischemia is more important than EKG or enzymes treat for ACS even if the EKG is normal Troponin & CK-MB do not rise until 3 - 4 hours after the onset of pain pain is ischemic if it is described as: dull, squeezing, or pressure on exertion substernal lasts 15 - 30 min/episode does not change with position, respiration, or on palpation pain is NOT ischemic if it is described as: o left/right sided o worsen or improves with positon or breathing o sharp, stabbing, or point-like o few seconds in duration o continuous for hour or 1-2 days
Stress Testing: used when uncertain if patient has an acute ischemic event Angiography STEMI ST depression with persistent chest pain despite ASA, clopidogrel, heparin, metoprolol, & nitrates
ST depression with recurrent chest pain recurrent episodes of ischemic-type chest pain with normal EKG reversible ischemia on stress test
Troponin
CK-MB
Cardiac Enzymes Rises at 3 – 4 hours Max sensitivity at 12 - 18 hours positive for 1 – 2 weeks
Rises at 3 – 4 hours Max sensitivity at 12 – 18 hrs positive for 1 – 2 days
Myoglobin
Rises at 1 – 4 hours
Catheterization
clear history & abnormal EKG need evaluation for angiography
Brain Natriuretic Peptide (BNP)
when etiology of dyspnea unclear
Stress test
when history & EKG are not clear
Echocardiogra m
Telemetry
continuous EKG monitoring
looks at wall & valve motion ejection fraction
negative first test excludes nothing positive test suggests MI false positive with CHF & renal failure cannot detect reinfarction from last week negative first test excludes nothing positive test suggests MI best for detecting reinfarction lacks specificity negative test at 4 hours excludes MI positive test is USELESS continued pain with max medical therapy requires angiography normal BNP excludes CHF abnormal test is nonspecific looks for reversible ischemia catheterize abnormals normal wall motion excludes MI high troponin with normal wall motion = false-positive troponin required for ALL ACS patients
ENDOCRINE
ICU consult underlying cause of DKA
DIABETES MELLITUS Stress hormones: cortisol, catecholamines (Epi/NE), glucagon, growth hormone raises glucose & FFA levels IMPORTANT Diagnostic Tests ICU: labs every 2-4 hr for the first 24 hr serum HCO3-, anion gap (acidosis elevates K+) serum HCO3-, glucose, & K+ glucose & K+ levels ABG or VBG pH in DKA: ABG = VBG ABG (or VBG) ICU: treat to resolve acidosis Treatment 1-2L NS/hour for 2-3 hr ICU admission based on acidosis (low serum HCO3- & pH <7.3), NOT glucose level IV insulin: 0.05-0.1 units/kg/hr Severe acidosis needs IV insulin (may also add IV HCO3-) IV HCO3- if pH <7.0-7.1 Death is likely when HCO3- <8-10, pH <7.0, K+ >7.0 DKA usually resolves over 12-24 hr o serum HCO3- >18-22 mEq/L DKA o pH >7.3 MC in Type I, but occurs in both Type I & II diabetes o K+ <4.5-5 mEq/L insufficiency or resistance to insulin, no glucose into cells o glucose < 250 mg/dL metabolized fat creates acid ketones, HCO3- gets used up to buffer them once DKA resolves… H+ is absorbed into cells to buffer the acid, K+ is released in exchange, o start SC insulin resulting in hyperkalemia o add K+ to IV fluids when <4.5 mEq/L kidneys excrete K+ to prevent arrhythmia, total body K+ is depleted o add glucose or dextrose to IV fluids when acidosis resolves, hypokalemia occurs unless replaced o transfer to floor Presentation… hyperventilation (respiratory compensation of metabolic acidosis) Nonketotic Hyperosmolar Syndrome confusion (hyperosmolar state) elevated glucose levels generalized weakness (severe volume depletion) BUT normal serum HCO3-, K+, anion gap & no ketones polyuria, polydipsia, polyphagia same treatment as for DKA: high volume IV NS & insulin Presenting Lab Findings _____________________________________________________________________ metabolic acidosis (pH < 7.2-7.3) low serum HCO3Inpatient Management of DM respiratory alkalosis (pCO2 <35-40 mmHg) as compensation if serum HCO3- is normal, manage on regular floor anion gap elevated (>12 mEq/L) DO NOT stop outpatient meds on admission hyperglycemia (700Anion gap = Na+ - (Cl- + HCO3-) DO NOT stop oral diabetic meds 800 mg/dL) cut insulin dose in half; monitor with finger-sticks & sliding scale insulin ketones in blood & urine KNOW starting & max doses of pt’s diabetic meds glucose in urine glucose levels will differ in hospital vs. home pseudohyponatremia (low Na+ from hyperglycemia) if NPO: glucose will be lower in hospital leukocytosis if on IVF: glucose will be higher in hospital elevated HbA1c Lab values you should know… Treatment… last 48 hr finger sticks at least 1-2L IV last serum glucose Causes of DKA saline last outpatient HbA1c medications (lack of, or inability to take) next set of labs have meds been given? (not just ordered) infection (stress hormones inhibit insulin) ordered major illness (MI, pancreatitis, stroke) new onset disease
contact pt’s PCP; oral hypoglycemic take 2 wks to adjust psychiatric bone menstruation
Hypothyroid depression, dementia none menorrhagia
Hyperthyroid anxiety, nervousness osteoporosis oligomenorrhea
Hypothyroidism MCC from primary gland failure (“burn out” Hashimoto’s) presents with fatigue test: low free T4 & elevated TSH
Ambulatory Management of DM screening: HTN, obese, age <45, family Hx diagnostic criteria… HbA1c >6.5% Hyperthyroidism FBG >125 mg/dL on 2 occasions test: elevated T4 in any type single glucose > 200 mg/dL with symptoms Graves’ Silent Subacute Pituitary Synthyroid OGTT 2 hr postprandial >200 mg/dL “Painless” Thyroiditis Adenoma (TH) abuse Thyroiditi treatment: diet, exercise, & weight loss s medications TSH low low low HIGH low start with metformin 500 mg bid Radioactive HIGH low low high low (renal insufficiency may lead to metabolic or lactic acidosis) I- uptake can add sulfonylurea, TZDs, or DPP-4 features eye/skin non-tender TENDER involuted, if 3-4 oral meds not effective HbA1c Common Oral Hypoglycemics Contraindications findings, non-palpable <7%, switch to or add insulin Metformin Renal proptosi insufficiency gland o alternative is GLP incretins Sulfonylurea: glyburide, glimepiride, glipizide hypoglycemia mimetics: exenatide or Ab’s CHF TSI TZDs: rosiglitazone, pioglitazone liraglutide DPP-4 INH: sitagliptin, saxagliptin, linagliptin pancreatitis o GIP & GLP insulin from Hypothyroidism Treatment pancreas, glucagon, & gastric motility hormone replacement: levothyroxine/Synthroid o DPP-4 inhibitors decrease incretin metabolism allow 6-8 wks between dosing changes follow up with TSH & free T4 for response Long-term Management of DM go slow with coronary disease, may provoke ischemia BP control: ACE-I or ARB; goal is < 130/80 mmHg LDL control: statin; goal is <100 mg/dL chronic treatment urine: microalbumin screening annually (use ACE-I or ARB if present) Graves’: radioactive iodine ablates thyroid eye exam: screen annually for proliferative retinopathy subacute thyroiditis: ASA for pain o neovascularization or vitreous hemorrhages silent thyroiditis: resolves spontaneously o Tx with laser photocoagulation pituitary adenoma: trans-sphenoidal surgery foot exam: microfilament to detect neuropathy Thyroid Storm Treatment _____________________________________________________________________ beta-blockers: propranolol, or metoprolol (stops action at target organ) FAST! THYROID DISORDERS PTU or methimazole (stops production & conversion of T4 to T3) steroids (stops peripheral conversion) tests: TSH & free T4 iodinated contrast agents (stops iodine uptake into gland) thyroid Ab’s are minimally altered surgery only with pregnancy or airway compression DO NOT treat empirically, Dx first
Thyroid Nodules check TSH & free T4 if TSH & free T4 are normal, FNA biopsy (Nodules need needles!!) sonogram used to guide biopsy excisional biopsy for “follicular adenoma” nuclear thyroid scans & sonograms are not useful (can’t exclude cancer)
ADRENAL DISORDERS Hypercortisolism Presentation fat redistribution: truncal & facial obesity (“moon face”); thin arms & legs easy bruising & osteoporosis menstrual abnormalities acne (excess adrenal androgens) HTN (cortisol increases Na+ reabsorption & potentiates catecholamine effects on vasculature) asymptomatic leukocytosis*** hyperglycemia & hyperlipidemia metabolic alkalosis (aldosterone excretes acid) hypokalemia (aldosterone excretes K+) Hx of corticosteroid use (prednisone, dexamethasone, methylprednisolone) *hyptercortisolism is a/w hyperaldosterone effects Diagnostic Tests (NEVER start with a scan) 24-hr urine cortisol (elevated results confirms the Dx) 1 mg overnight dexamethasone suppression test (a normal result excludes hypercortisolsm; false positives are common) if 24-hr urine cortisol is elevated, do ACTH test: o decreased ACTH = adrenal adenoma o elevated ACTH = pituitary adenoma, ectopic source, or cancer if ACTH is elevated, do high-dose dexamethasone test o if ACTH is suppressed = pituitary adenoma o if ACTH remains high = ectopic source or cancer Treatment adrenal adenoma: laparoscopic adrenalectomy
pituitary adenoma: trans-sphenoidal pituitary removal (hypophysectomy) ectopic source in lung or cancer: remove __________________________________________ Hyperaldosteronism (Conn’s Syndrome) Presentation HTN hypokalemia metabolic alkalosis (H+ excretion) “I feel weak” & decreased muscle strength (hypokalemia impairs muscle contraction) **serum Na+ level is normal due to “sodium escape” Diagnostic Tests confirm with low renin & high aldosterone adrenal gland CT: MCC is solitary adrenal adenoma Treatment laparoscopy (adenoma & cancer) lifelong spironolactone or eplerenone to inhibit (B/L hyperplasia) Hypoadrenalism (Addison’s Disease) MCC is autoimmune adrenal destruction Presentation weakness, fatigue skin hyperpigmentation (due to increased ACTH) hypotension hyperkalemia & metabolic acidosis Diagnostic Tests cosyntropin stimulation (or ACTH): measure cortisol before & after normal: rise in cortisol; abnormal: no change in cortisol level Treatment hydrocortisone, prednisone or fludrocortisone (highest mineralocorticoid or aldosterone-like effect) ______________________________________ Pheochromocytoma Presentation (non-specific findings) episodic HTN flushing, headache, sweating, tachycardia failure of HTN control with 3+ medications Diagnostic Tests 24-hr urine catecholamines & metanephrines (98% sensitive & specific) plasma metanephrines abdominal CT: confirm location (or MIBG scan for occult detection) Treatment o phenoxybenzamine & propranolol prior to surgical removal
_______________________________________
kidney stones blood in urine Enzyme Deficiency HTN Virilization Adrenal Incidentaloma flank pain or abdo pain 21-hydroxylase No Yes CT or MRI done for bowel movement difficulty or frequency 11-hydroxylase Yes Yes reasons confusion, sleepiness, disorientation Malignant lesion 17-hydroxylase Yes No Benign lesion other Hx of bone fracture w/o trauma (vertebral) small <4 cm large >4 cm than adrenal lesion symptoms nephrogenic DI (nocturia): causes volume depletion round & smooth irregular muscle weakness low density high density Other causes of hypercalcemia… renal tubular acidosis (low serum HCO3- with normal anion gap) elevated chloride level ulcers: Ca++ stimulates gastrin release pancreatitis possible malignancy should undergo CT-guided needle biopsy Diagnostic Tests benign-appearing lesions should exclude subclinical endocrine functionality BUN & creatinine: hypercalcemia causes renal toxicity (90% are nonfunctional) EKG: short QT (hypocalcemia causes long QT) Diagnostic Tests Na+ levels: nephogenic DI 1 mg overnight dexamethasone suppression test U/A (or 24-hr urine Ca++ to r/o familial hypocalciuric hyercalcemia) 24-hr urine catecholamine & metanephrine phosphate levels: LOW plasma aldosterone:renin ratio for hypertensive patients PTH level: exclude primary hyperPTH (high Ca++ & PTH) Treatment remove malignant or endocrinologically functional lesions hypercalcemia of malignancy is rare, usually from metastatic disease Congenital Adrenal Hyperplasia MCC is enzymatic deficiencies in adrenal gland, may not present until adulthood DHEA or androsteinedione is overproduced… o clitoromegaly, deep voice, hirsutism, & masculinization in women o not noticeable in men 95% due to 21-OH deficiency Diagnostic Tests all 3 forms have high ACTH, low aldosterone, & low cortisol 21-OH deficiency has increased 17-hydroxyprogesterone Treatment glucocorticoids has negative feedback on ACTH ___________________________________ Hypercalcemia MCC is hyperparathyroidism (outpatients) & malignancy (inpatients) also Vit. D intoxication, sarcoidosis & granulomatous disease, thiazids, lithium, Vit. A toxicity, hyperthyroidism Presentation asymptomatic if symptomatic, DO NOT wait for Dx
Treatment For symptomatic, acute hypercalcemia… high volume fluids: IV NS 200-500 mL/hr bisphosphonates (takes 1-2 days): Zoledronic acid & Pamidronate calcitonin if still high after hydration, while waiting for bisphosphonates glucocorticoids (for sarcoidosis & granulomatous disease) loop diuretics (only if CHF, fluid overload, or renal insufficiency) For hyperparathyroidism… surgical removal ONLY (solitary adenoma in 80% of cases) o all symptomatic patients o nephrogenic DI o renal stones or decreased renal function o osteoporosis & bone lesions o young pt (age <50) w/ Ca++ > 1 point above normal 4-gland hyperplasia: remove all glands & lifelong Ca++ & Vit D _______________________________________ Hypocalcemia check albumin level first
low albumin lowers total Ca++ free Ca++ will be normal Presentation commonly asymptomatic low free Ca++ causes neuromuscular hyperexcitability seizures arrhythmia from prolonged QT Chvosteck’s sign (facial nerve tetany, tapping on face/cheek) perioral numbness & tingling Etiology renal failure: 1,25-dihydroxy Vit D deficiency Vit D deficiency hypo-Mg++ causes failure of PTH release hypo-PTH due to surgery, neck radiation, autoimmune destruction drug-induced: phenytoin (Vit D damage), foscarnet, cinacalcet (inhibits PTH) Treatment acute symptomatic: IV Ca++ gluconate or Ca++ chloride chronic: oral Ca++ with Vit D
PITUITARY DISORDERS microadenomas are more common macroadenomas causing bitemporal hemianopsia is rare Hyperprolactinemia Presentation amenorrhea or menstrual irregularities glactorrhea erectile dysFx infertility (due to GnRH inhibition) Diagnostic Tests NEVER START WITH A SCAN! exclude pregnancy measure prolactin level look for causes other than a pituitary lesion o hypothyroidism stimulates TRH o phenothiazine, SSRIs, metoclopramide, opiates, verapamil, cimetidine
o chest wall injury or excess stimulation (zoster of the chest) o estrogen stimulates prolactin during pregnancy o renal failure once other causes excluded pituitary MRI Treatment dopamine-agonists: cabergoline, bromocriptine trans-sphenoidal surgery to remove lesion radiation (last resort) _____________________________________ Acromegaly GH increases IGF; IFG grows proteins in the body Presentation cardiomyopathy diaphoresis (enlarged sweat glands) colonic polyps (colon cancer risk) carpal tunnel (nerve entrapment) joint pain obstructive sleep apnea hyperglycemia & hyperlipidemia (GH has anti-insulin effects) Diagnostic Tests IGF level (best initial test due to long half-life); GH level (short half-life) glucose suppression (best confirmatory test): failure to suppress GH NEVER start with an MRI (10% have nonfunctional lesions) Treatment trans-sphenoidal surgery: remove pituitary Pegvisomant (GH Rc-antagonist), octreotide (somatostatin), or cabergoline (DA agonist) Panhypopituitarism MCC: infarction, infection, or mass effect from tumor presents with adrenal insufficiency or hypothyroidism Diagnostic Tests ACTH, cortisol, TSH, T4, IGF (normal levels exclude pituitary insufficiency) Arginine stimulation test (normal: increase in GH release) Metyrapone (inhibits 11-hydroxylase & reduces cortisol; normal response is increased ACTH level) Treatment replace glucocorticoids & thyroxine (T4) DDx Empty Sella Syndrome: obese women with headache; no treatment needed Kallmann Syndrome: hypogonadotropin, low FSH/LH, anosmia; Rx: sex hormone Diabetes Insipidus
o o
Ccentral DI: insufficient ADH production from CNS damage (trauma, tumor, hypoxia, infection) Nephrogenic DI: kidneys do not respond to ADH; due to kidney damage, chronic pyelonephritis, sickle cell, hypercalcemia, hypokalemia, lithium
orthostasis: drop in BP or rise in pulse upon standing or sitting SBP decreases >20 mmHg or pulse increases > 10/min used to evaluate severity of bleeding if no orthostasis on initial assessment, bleeding is NOT severe (CBC f/u takes 6-12 hr to determine if Hct drop is consistent w/ severe bleeding) for severe bleeding, give: fluids, PLTs, blood, plasma
Esophageal Varices add Octreotide immediately banding via endoscopy (alternative is: sclerotherapy) EKG: assess for MI due to severe anemia & GI bleeding beta-blockesr (propranolol & nadolol) DO NOT help acute bleeding know pt’s…CBC, PT/INR, BP, & response to fluids if asked CBC CANNOT determine severity of bleeding! Hct only drops 2-3 points with hydration. Symptomatic anemia requires a transfusion. symptoms: lightheadedness, dyspnea, fatigue, chest pain Evaluating GI Bleed #1 is to establish SEVERITY! CHECK for ORTHOSTASIS! WHEN did bleeding start? STOOL is red or black? VOMITING bright red or dark “coffee grounds”? NUMBER of bowel movements or vomiting w/ bloody or black stools? SYMPTOMS: lightheadedness, SOB, chest pain? HEART DISEASE Hx? SCOPE via mouth or rectum previously? ANTACID use? GASTROENTEROLOGY GI BLEEDING severity is more important than etiology if bleeding is severe…resuscitate with fluids & blood! SBP <90 mmHg = extremely severe bleeding (~30% volume loss) Rx:IV NS 500 mL immediately CBC sent, checked, & repeated untill CBC stops changing if PLT <30-50,000 w/ severe bleeding PLT transfusion if PT or INR is increases FFP start PPI’s for upper GI bleeds start type & cross for packed RBC’s Orthostatic Hypotension
Lower GI Bleed Etiology *causes bright red blood on bowel movement (upper GI bleed in 10% of cases) diverticulosis angiodysplasia or AVM polyps cancer
Hemorrhoid Bleed features *can mistaken for serious GI bleed; blood in toilet may exaggerate severity no change in Hct w/ repeat testing hemorrhoids found on rectal exam normal BP & pulse absence of orthostatic change in BP or pulse *guaiac-positive, brown stool is not severe Upper GI Bleed Etiology MCC: ulcers (gastric & duodenal) gastritis esophagitis duodenitis varices: esophageal & gastric due to portal HTN (most dangerous) cancer Diagnostic Tests endoscopy! Treatment IV fluids, frequent CBC checks, & correct coagulopathies PPI’s for ALL upper GI bleeds epinephrine injection or electrocautery for actively bleeding ulcers NG-tube does not aid in management variceal bleeds: start octreotide, which decreases portal pressure, no major A/E do not wait for endoscopy to confirm “band” varices that bleed propranolol or nadolol ONLY prevent the next bleed transjugular intrahepatic portosystemic shunt (TIPS) for persistent bleeds despite banding & octreotide; creates a shunt btwn portal & hepatic veins Blakemore tube: balloon in esophagus & stomach to “compress” vessels, temporarily slow the bleeding until TIPS can be done Minor GI Bleed usually a/w microcytic anemia & guaiac (heme) positive stool findings: normal BP/pulse, no orthostasis, no recent Hct changes if no localizing symptoms present, perform tests: colonoscopy, upper endoscopy, pill endoscopy (rarely) Epigastric Pain mostly benign, causes “dyspepsia”. all forms of pain do not have tenderness on exam (except pancreatitis) MCC: “non-ulcer dyspepsia” = pain w/o pathology others: ulcer disease, pancreatitis, GERD, esophagitis/duodenitis/gastritis, cancer
ask about…duration, intensity, time of onset, aggravating/relieving factors also ask about… weight loss dysphagia odynophagia bleeding (stool or vomit) nausea/vomiting relieved with antacids? Diagnostic Tests EGD (esophagogastroduodenoscopy) = upper endoscopy for “alarm symptoms” or if age >45-55 or symptoms persist/worsen despite PPIs EGD… only way to exclude cancer! (stomach biopsy of gastric ulcers) most accurate test of stomach (more accurate than barium studies) allows banding of varices & cautery of visible ulcer vessels distinguishes gastric vs. duodenal ulcer H. pylori testing is best done on biopsy Rx: PPI, clarithromycin, amoxicillin stool Ag or breath test are not as good, but can differentiate btwn old vs. current infection serology is useless only treat those with ulcers or gastritis (ulcers will recur if H. pylori is not eradicated) Stress Ulcer Prophylaxis *reserved ONLY for… mechanical ventilation/intubation head trauma burns coagulopathy **NSAIDS & steroid use are NOT indications PPIs are benign, BUT risks include…. C. difficile colitis osteoporosis from decreased Ca++ absorption pneumonia (gastric acid protects from gastric colonization)
Zollinger-Ellison Syndrome (ZES) caused by elevated gastric acid & serum gastrin Presentation
larger ulcer > 1 cm or multiple ulcers recurrence after H. pylori eradication distal location near ligament of Treitz diarrhea (due to acid inactivation of lipase) Diagnostic Tests serum gastrin (pt must be off PPIs & antacids) confirm with secretin testing (normal: decrease in gastrin; abnormal: gastrin stays high) confirm ZES is local & resectable by excluding metastasis via endoscopic U/S & nuclear somatostatin receptor scan Treatment surgical removal of local disease lifelong PPIs for metastatic or unresectable disease Diabetic Gastroparesis chronic DM causes nerve damage Presentation bloating nausea constipation abdominal discomfort Diagnostic Tests nuclear gastric emptying study with barium-soaked bread Treatment metaclopramide erythromycin GERD MCC: abnormally relaxed LES; causes 25% of chronic cough ask about… radiating pain/discomfort? heartburn? chest pain? bad taste in mouth? tastes like metal? sore throat? hoarseness? night cough? Diagnostic Tests assess response to Rx with PPIs; 95% resolve within 1 day specific tests only if symptoms persist perform EGD or 24-hr pH surgical resection (Nissen fundoplication) if uncontrolled with PPIs *H. pylori DOES NOT cause GERD
Barrett’s Esophagus
a/w long-standing GERD >5 yrs Dx by EGD (confirm with biopsy) 0.5%/yr develop adenocarcinoma Rx: PPIs & repeat EGD every 2-3 yrs Esophageal Dysplasia from Barrett’s Esophagus Low-grade dysplasia: PPI & reassess every 6 months High-grade dysplasia: PPI & endomucosal resection w/ endoscope, OR distal esophagectomy Pancreatitis Presentation severe epigastric pain & tenderness on palpation! radiating to the back nausea & vomiting Hx of alcohol use Hx of gallstone disease (increasing due to obesity) Diagnostic Tests elevated amylase & lipase (lipase is more specific) Ranson’s Criteria (obsolete): elevated WBC, low Ca++, age >55, high AST & LDH determines the need for surgical debridement (before CT scans were in use) CT scan is most sensitive to confirm Dx (but usually unnecessary) CT & U/S show causes of pancreatitis (stones, obstruction, etc) used to determine if stone removal is needed MRCP (magnetic resonance cholangiopancreatography) can diagnostically visualize ductal structures of pancreas & biliary system ERCP therapeutically removes stones & dilates strictures *MRCP finds the obstruction, ERCP fixes it! Treatment provide “rest” of the pancreas & IV fluids (150-250 ml/hr) MCC of death in acute pancreatitis is inadequate fluid replacement
pancreatic inflammation releases mediators that cause capillary “leaks” NPO analgesics PPIs may help CT with >30% necrosis needs imipenem or meropenem & CT-guided biopsy
infected necrotic pancreatitis (rare) need surgical debridement
Infectious Diarrhea
SEVERE = volume-depleted & febrile know about…. duration of symptoms fever? frequency of bowel movements lightheadedness? blood in stool? others with diarrhea? Diagnostic Tests blood is only present with invasive pathogens: Campylobacter, Salmonella, Shigella, Yersinia, or Vibrio. fecal leukocytes (WBCs) = invasive pathogens present stool culture helps distinguish between pathogens if blood is NOT visible…. occult blood (guaiac) fecal leukocytes (methylene blue stain) culture ova & parasite exam History Organism AIDS <100 CD4 cells Cryptosporidium camper/hiker Giardia ABX use C. difficile hemolysis, low PLTs, elevated E. coli 0157:H7 BUN & creatinine
Test modified acid fast stain ELISA stool Ag, ova & parasite stool toxin assay sorbitol MacConkey agar (does not grow on routine media)
flushing, wheezing after eating fish
Scombroid
stool culture
Treatment initial treatment is based on SEVERITY, not etiology most cases are self-limiting & benign; ABX not required anti-motility agents: diphenoxylate (Lomotil) or loperamide (Imodium) used only if no blood or fever ABX for “severe” diarrhea
Pathogen-Specific Treatments
Giardia
Metronidazole (also for recurrence; Vanco is 2nd-line) severe cases get both drugs Metronidazole, tinidazole
Cryptosporidia
Nitazoxanide
Campylobacter
Azithromycin or erythromycin if confirmed
E. coli O157:H7
AVOID ABXs
Scombroid
Diphenhydramine
Viral, Staph, Bacillus cereus
supportive therapy with fluids ABXs do not help
C. difficile
Malabsorptive Diseases
“Severe” diarrhea fever blood in stool hypotension/tachycardia abdo pain or tenderness
