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40 Cards in this Set

  • Front
  • Back
Abdominal Pain
1. epigastric
2. RUQ
3. periumbilical
4. RLQ
5. LLQ
6. suprapubic
7. diffuse
1. gastritis, ulcer, esophangeal
2. liver, gallbladder, small bowel, lower lungs
3. pancreas, referred
4. appendix, ovarian, tubal
5. colitis, diverticulitis, ovary, tubal
6. bladder, uterine
7. perforation/peritonitis
Abdominal Exam Pearls
1. writhing pain
2. worse pain on movement
3. high pitched bowel sounds
4. no sounds
5. gaurding
6. fluid shift/wave
1. obstruction (GB, bowel, ureter)
2. peritonitis
3. obstruction
4. ileus
5. peritoneal irritation
6. ascites
Abdominal Pain: Lab and Radiology
1. elevated WBC
2. low Hb
3. low bicarbs
4. LFTs: elevated alk phosp
5. elevated amylase, lipase
6. KUB, upright XR: distal loops of bowel vs. free air on upright
1. infection
2. chronic bleeding (cancer, ulcer)
3. ischemic bowel, acute abdomen
4. gall bladder/biliary
5. pancreatitis or infarcted bowel (amylase)
6. obstruction vs. perforated viscus
GI Bleed
1. hematemesis
2. melena
3. hematochezia
4. normal Hgb
5. orthostatic hypotension
6. vascular access
7. replace...
8. tests
1. above ligament of treiz (attach duod to diaphragm)
2. upper GI
3. lower GI or rapid bleed
4. indicates nothing
5. indicates at least 15% volume loss
6. large bore venous catheter X2
7. FFP, platelets
8. endoscopy, colonoscopy, tagged RBC scan
Treatment plan for:
1. hematemesis
2. melena
3. hematochezia
1. EGD..treat as appropriate
2. EGD...if negative do colonoscopy...if negative do small bowel studies
3. pass nasogastric tube...if negative for blood/bile do colonoscopy...any findings do EGD first and then if that's negative do colonoscopy
Barrett's Esophagus
change to epithlium due to reflux of stomach acid; precursor of espohageal cancer
Esophageal dysphagia
1. presentation
2. solid food only ddx (mechanical obstruction)
3. solid and liquid ddx (neuromuscular disorder)
1. food stops or sticks after swallowing
2. intermittent = lower esophageal ring...progressive w/ chronic heart burn = peptic stricture...progressive w/ weight loss and age >50 = carcinoma
3. intermittent w/ CP = esophageal spasm. . . progressive with chronic heart burn = scleroderma . . .progressive w/ regurg and weight loss = achalasia
Stimulation of parietal cells = release of HCl (3 types)
1. vagal nerve: acetylcholine to M3 (muscarinic receptor)
2. paracrine: entercrhomaffin and mase cells release histamine
3. endocrine: antral G cells produce gastrin which stimulates parietal cells and enterchromaffin-like cells
Prostaglandin mediate...
-they are inhibited by...
1. mucous production
2. rapid cell turnover
3. excellent perfusion (enhanced healing)
-COX-1 and COX-2 inhibitors (selective COX2 more involved with inflammation, slightly less incidence of GI bleeding- celebrex)
Stress Ulceration
1. occurs w/...
2. treatment
1. critical illness, hypotension, sepsis
2. prevention by decreasing gastric acid production- IV H2 blocker (ranitidine), IV PPI (pantaprazole, Protonix)
H. Pylori
1. pathogenes
2. tests
3. treatment
1. produces urease that cleaves urea into ammonia in MALT mucosa causing inflammation and injury
2. urease or "clo" test (slightly acidic urea agar turns to pink with pH >6), antibody tests, fecal antigen tests
3. always changing
Dyspepsia Tx
1. H2 blockers
2. PPI
3. Antacids
4. Prostaglandin analogs
5. mucosal protectants
6. surgery
1. block histamine, reducing but not preventing HCl production by parietal cells
2. effective, put expensive
3. raise pH, but stomach will respond by inc acid production; limited use for ulcers mostly for intermittent dyspepsia
4. misoprostol; poorly tolerated
5. sucralfate; thick mucus barrier, has to be given often
6. done before H2 blockers; vagotomy (less acetylcholine stimulating M3), antrectomy (gastrin producing G cells mostly in antrum
Zollinger Ellison Syndrome
1. what is it?
2. presentation
3. diagnosis
4. treatment
1. gastrin producing tumor of the pancreas or duodenum
2. multiple or recurrent ulcers without other cause (NSAIDs, H. pylori)
3. elevated gastrin (can also be due to H. pylori or PPI), do confirmatory test
4. surgical removal, if can't be found use PPI for acid reduction
Gastric Emptying Problems (gastroparesis)
1. causes
2. treatment
1. long standing DM (most common non-iatrogenic cause), medications (opiates, TCAs, dopamine agonists, anticholinergics)
2. metoclopramide, erythromycin (works, but side effects usually intolerable
Dumping Syndrome
1. cause
2. symptoms
1. pylorus allows food to reach duodenum too quickly, cascade of nutrients overwhelms small bowel and liver, causes release of vasoactive peptides
2. flushing, nausea, fullness, hyperglycemia and pain followed by hypoglycemia (pancreas overshoots insulin)
Gastric Volvulus
1. what happens?
2. primary vs. secondary
3. result
1. stomach twists on itself
2. primary (above diaphragm, laxity of ligaments) vs. secondary (below diaphragm, assoc with paraesophageal hernias)
3. obstruction, ischemia, necrosis
Malabsorption phases
1. Luminal
2. Mucosal
3. Transport
3. vasculitis, lymphangiectasia, irradiation
Malabsorption
1. signs
2. diagnosis
1. wt loss, fatigue, vitamin/iron def, oily stools that float (steathorrhea), bloating, diarrhea
2. fecal fat analysis, 24hr fecal fat collection, small bowel bx (looks for mucosal damage), D-zylose (absorbed and secreted into urine; slower than 20% in 5 hrs = malabsorption)
B12 Deficiency: Schilling Test
1. pernicious anemia due to loss of parietal cells (achlorydia)
2. bacterial overgrowth
3. pancreatic insufficiency
4. all 3 fail
1. B12* found when Pt loaded w/ IM B12, then given radiolabeled B12* + IF
2. resorption of B12 + IF + antibiotics
3. resorption of B12 + pancreatic enzymes
4. disease of transport at terminal ileum (chrons, transcobalamin deficiency)
Celiac Disease
1. cause
2. symptoms/signs
3. diagnosis
1. allergy to wheat gluten (non tropical sprue)
2. chronic diarrhea and malabsorption; dermatitis herpetiformis, may present as iron/single vit def, weakness, arthralgia, osteoporosis
3. anti-endomysial or anti-gliadin antibodies, small bowel bx, trial of gluten free diet shows improvement
Stool Osmolality
1. compared to serum
2. calculation
3. stool osmolar gap
4. causes of osmotic diarhhea
1. same; non-osmoles contribute to consistency (fiber, mucous)
2. Na + K X 2
3. serum osmolality-stool osmolality (usually low)
4. lactose intolerance, laxative abuse, carb malabsorption
Secretory Diarrhea
1. stool osmolar gap
2. cause
3. effect of fasting
1. low
2. toxin (cholera) damages epithelium causing active secretion of solute (Cl-) into gut
3. does NOT stop diarrhea
Inflammatory Diarrhea
1. causes
2. blood and pus
3. effect of fasting
1. infections, autoimmune (crohn's, UC), processes that damage epithelium > impaired resorption of solute
2. cathartics (irritants) that cause perceived diarrhea- inc frequency and tenesmus, less than 200ml volume
3. stops or reduces diarrhea
Malabsorptive Diarrhea
1. causes
2. effect of fasting
1. transit too fast for absorption or resorptive area too small (bowel resection, fistula, hyperthyroid, scleroderma)
2. resolution
Lactose Intolerance
lactase present at birth is lost; bacteria cleave lactose in large bowel to osmotically active acids; may result in osmolar gap
Unconjugated Bilirubin Disorders
1. too much bilirubin
2. underdeveloped liver
3. impaired uptake
4. impaired conjugation
1. hemolysis
2. neonatal jaundice
3. Gilbert, most common, benign
4. Crigler-Najar (rare), hepatocellular, drug inhibition
Conjugated/Direct Bilirubin Disorders
1. inherited
2. hepatocellular
3. intrahepatic
4. extrahepatic
1. Rotor, Dubin-Johnson
2. not enough cellular energy to pump bili out of hepatocyte
3. ducts in liver damaged (PBC)
4. ducts outside liver damaged (GB, tumor, stricture, clonorsis sinensis)
Alkaline Phosphatase
1. 4 isoenzymes
2. found on...
3. elevated by...
4. confirming liver source
1. liver, bone, intestine, and placenta
2. surface of hepatocytes
3. cholestasis (AST/ALT may be normal), liver infiltration (cancer, granuloma); conjestion (RVHF)
4. if AST/ALT normal check GGT, can do isoenzyme assay
GGT and 5' nucleosidase
1. specificity
2. elevated by...
3. main use
1. non-specific
2. estrogens (OCP) anabolic steroids, many meds, etoh
3. confirming liver source if AST/ALT or alk phosph elevated
Hepatocellular Patterns: AST:ALT
1. AST vs. ALT
2. over 1000
3. 40-200
4. AST > ALT (2:1, 3:1)
1. AST in metabolic organs (muscle, liver), ALT more specific to liver
2. necrosis (tylenol, mushroom), fulminant viral infection
3. NASH, chronic hepatitis
4. alcohol, hep C
Prothrombin Time
1. INR checks...
2. livers synthetic ability
3. what else affects INR?
1. factor VII; has shortest half life
2. can produce albumin and normal INR until 80-90% of liver gone
3. vit K def; can't assume end stage liver disease
1. elevated bilirubin
2. elevated alk phos and bili
3. elevated alk phos
1. hemolysis
2. biliary tree(GB)
3. biliary tree or intrahepatic (cancer, RVHF)
Autoimmune Hepatitis
1. demographic
2. indistinguishable from...
3. testing
4. cause
1. women
2. NASH
3. anti-smooth mm. antibody anti-microsomal antibody
4. always suspect drugs
Primary Biliary Cirrhosis vs. Primary Sclerosing Cholangitis
women vs. young men
Role of biopsy
1. shows...
2. dx of...
3. limited role...
4. limited role
1. amount of inflammation and scarring around portal triad
2. AI, PBC, PSC
3. NASH; tx is weight loss and DM management regardless
Hepatitis A
1. transmission
2. recovery
3. prevention
4. virion release
1. fecal oral
2. look very sick, but almost always recover
3. vaccination for travelers or IS
4. virion excreted during prodromal phase
Hepatitis B
1. structure
2. transmission
3. prevention,
4. post-exposure
5. serologic markers: HBcAg, HBsAg, HBeAg
6. tx
1. DNA
2. vertical: mostly blood, also sex and maternal-fetal
3. vaccine exists
4. give concurrent HepB Ig + vaccine
5. first marker, sign of immunity, carrier state
6. interferon + lamivudine for Pts with evidence of cirrhosis (bad side effects)
Hepatitis C
1. prevalence
2. transmission
3. long term risk
3. Dx
4. complications
5. Tx
1. more popular in USA than Hep B, but not worldwide
2. blood borne (IV drug users, tattoos, transfusions)
3. hepatocellular carcinoma, cirrhosis
3. HCV-Ab (doesn't confer immunity nor tell if pt is infectious; HCV Viral load and serotyping
4. cryoglobulinemia, polyarteritis nodosa
5. interferon + ribavarin (doesn't work as well on genotype I), limited by side effects so only 50% can get tx
Hepatitis D
1. structure
2. concurrent infection
3. superinfection
1. RNA, no capsule
2. requires concurrent infection with Hep B
3. superinfection on Hep B chronic Pt results in worsening disease
Hepatitis E
1. transmission
2. recovery
3. geography
1. fecal oral
2. usually full recovery
3. some latin and asian countries; not USA