Gastroenterology Flashcards
Gastroesophageal Reflux Disease (GERD)
S+S
- Chest pain, but lasts min-hrs, and resolves spontaneously or with antacids, often positional (worse when lying down + after meals), can awaken pt from sleep
- Heartburn, regurgitation, chronic cough, sore throat, hoarseness
- Wheezing, halitosis, dental erosions, pharyngeal erythema
Tx
- Can give empirically when high suspicion: PPI for 4-6 wks (dx + tx)
Liver Enzymes
Hepatocellular
- Preformed, ↑ fast with inflamm
- ALT: in liver
- AST: in liver, and also cardiac muscle > skeletal muscle > kidneys > brain
Cholestatic
- Produced, gradually ↑ with inflamm
- ALP: in liver, bone, intestine, kidney, placenta
- GGT: in many organs, only use if ALP also high. Sensitive but not specific
Approach to Abnormal Liver Enzymes
1) Which enzymes are elevated, and by how much
2) R/o non-liver causes of inc LEs
3) Hepatocellular dominates if >2x cholestatic
4) If both hepatocellular + cholestatic are elevated, cholestatic dominates bc it is harder to raise of the 2.
Cholestatic (ALP + GGT) –> U/S to assess if dilated bile ducts
- Yes: extra-hepatic cholestasis (gall bladder, cystic duct, common hepatic duct, common bile duct).
- -> Common bile duct gallstones, bile duct compression (pancreas, cancers) → ERC/ MRCP to look for obstruction
- No: intra-hepatic cholestasis (bile canalculi).
- -> Intrinsic: PBC (AMA), PSC (ERCP/ MRCP).
- -> Systemic: sepsis, TPN, drugs.
- -> Infiltrative: TB, amyloid, leukemia/ lymphoma, sarcoid.
- -> Space-occupying: blood (hemiangioma), pus (abscess), water (cysts), solid (tumours).
Hepatocellular (ALT/ AST) –> tests
- Acquired: viral hepatitis (screen), alcohol (AST: ALT > 2:1), drugs (hx), fatty liver/ NASH (wt change, U/S)
- 1°: autoimmune hepatitis (ANA, SMA, IgG), Wilson’s (abnormal Cu), hemochromatosis (Fe/ TIBC, ferritin), A1AT def (A1AT level)
- Other (rare): hepatic vascular thrombus, shock liver, acute cholelithiasis
Ulcerative Colitis
- Mucosal/ submucosal inflamm only in the colon, commonly involving rectum.
S+S
- Bloody frequent diarrhea, colicky abdo pain, urgency, tenesmus, incontinence.
- May have systemic signs (fever, fatigue, wt loss, anemia)
- If you see a stricture, be worried about colon cancer.
- Hyperchromasia on biopsy with pre-malig + malig states
Dx Criteria
- Chronic diarrhea >4 wks
- Active inflamm on endoscopy
- Chronic changes on biopsy
- Other causes of colitis excluded
Labs/ Investigations
- ↓ Ferritin, ↑ ESR, abnormal lytes, +pANCA (not commonly ordered)
- Stool culture, C.diff, E.coli, O+P, Giardia stool Ag test
- Specific STI serology (including Neisseria gonorrhea, HSV, Treponema pallidum)
- Endoscopy: superficial ulcers, continuous lesions
Ddx
- Crohn’s, other colitis (infectious, radiation, diversion, diverticular, drug-induced)
Tx/ Prognosis:
- “Step-up approach”: oral or rectal 5-ASA + rectal corticosteroids +/- oral prednisone depending on severity. Purine analogs as well.
- Only “cure” is colectomy.
- If only have proctitis (inflame of the lining of the rectum), then there is no ↑ risk of malignancy
- Fecal transplant for resistant (twice treated) c. Diff
- Note: have an ↑ risk of arthritis, #, DVT
Huge hepatocellular liver enzyme increase (>500 and increasing)
1) Tylenol overdose -> Acetylcysteine as fast as you can, ideally within 8 hrs but can give after. Also salicylate.
2) Viral hepatitis: A, B, D, E, varicella zoster, HSV, CMV, EBV -> often supportive care
3) Shock liver
4) Autoimmune hepatitis -> prednisone, steroids
5) Budd-chiari syndrome
Charcot’s Triad & Reynold’s Pentad
- Charcot’s Triad: fever, jaundice, abdo pain (usually RUQ)
- Reynold’s Pentad: altered mental status, shock
- Ddx: obstructive ascending cholangitis, cholecystitis
Appendicitis
- Most common cause of acute abdo pain in s point, abdo rigidity, +psoas sign
Labs/ Investigations
- Leukocytosis + fever (sensitive, non-specific)
- Abdo CT + contrast is gold std, US + XR is not good
Crohn’s Disease
- Transmural (deeper) inflamm anywhere in the GI tract. (40% in SI, esp ileum, 30% ileum + colon, 30% colon. 1/3 of all of them have peri-anal disease, but usually spares rectum)
S+S
- Can have for many yrs pre-dx.
- Hallmarks: fatigue, prolonged diarrhea + abdo pain (usually crampy), wt loss, fever, usually no gross blood (is microscopic), mouth ulcers.
Dx
- Clinical hx + endoscopy.
- Diarrhea → colonoscopy, abdo pain → imaging.
- String sign, esp in terminal ileum.
- Granulomas on histology.
Labs/ Investigations
- CBC, lytes, ↓ albumin, renal fncn, liver tests, blood glc, ESR, CRP, serum Fe, serum B12, stool sample if diarrhea (culture, O+P, C.diff), +ASCA (but not commonly ordered)
- Endoscopy: usually deep ulcers, and lesions can skip
Ddx
- IBS, lactose intolerance, UC, infectious colitis
Tx
- Meds (5-ASA, abx, glucocorts, immunomodulators, biologics – via enema, foam, oral, or IV)
- Surgery (fistula, abscess, perforation, fibrotic stricture, hemorrhage, cancer, doesn’t respond to meds)
Prognosis
- Intermittent exacerbation of sx → periods of remission.
- More severe if: <40 yrs old, has perianal or rectal disease, smoking, ↓ education, need glucocorts initially.
- Many ultimately need intestinal resection bc of intractability of sx, obstruction, or perforation.
- Some tend to follow a pattern of either recurrent obstructions or perforations – latter tend to have more aggressive disease + earlier post-op recurrence + needing more surgeries.
- Note: have an ↑ risk of arthritis, #, DVT
Pancreatitis - Acute
Etiology
- Top 3: gallstones + chronic alcohol abuse + idiopathic
- Also hypertriglyceride, post-ERCP hyperamylasemia, hyperCa, genetics, drugs (class I + II)
- Trypsinogen -> trypsin too soon -> destroys pancreas
Dx
- Sx: usually RUQ or epigastric abdo pain, N/V, well localized (stones) vs poor (alcohol), rapid onset (stone) vs gradual (alcohol), 50% have radiation to back
- Hx: previous sx or hx of gallstones, alcohol, hypertriglyceride, hyperCa, family hx, drugs, trauma, autoimmune
- > 3x inc pancreatic enzymes (amylase + lipase), but degree of elevation beyond that doesn’t correlate with severity.
- Mild acute: no organ failure or complications
- Moderately severe acute: transient organ failure (=1 organ
Labs/ Investigations
- Serum amylase or lipase, triglycerides, Ca, liver tests
- ANA, serum IgG4 - if suspect autoimmune
- Abdo US (check for cholelithiasis or choledocholithiasis
- Further options: CT, MRI, MRCP, ERCP
Tx
- Supportive (IV fluid* + electrolyte replacement, closely monitor vitals + urine output)
- Other (O2, analgesia, anti-emetic, naso-gastric suction, nutrition, abx if infection)
Pancreatitis - Chronic
- 1 of the 3 main causes of malabsorption
Etiology
- Alcohol, smoking, genetics (CF, hereditary pancreatitis), ductal obstruction (trauma, pseudocysts, stones, tumours, possibly pancreas divisum), tropical pancreatitis, systemic disease (SLE, hypertriglyceridemia), autoimmune (systemic, 2 types), idiopathic
Dx
- Sx: abdo pain* (epigastric, radiates to back, occasionally N+V, may help to sit up, may be worse after eating, intermittent or continuous) + pancreatic insufficiency (malabsorption: protein, carbs, but esp fat → steatorrhea, pancreatic DM). Can be asx.
- Histology: calcification, fibrosis, inflammation, acinar cell loss, dilation of pancreatic ducts → progressive, irreversible
- Imaging: MRCP* (can show calcifications + pancreatic duct obstruction), MRI/ CT/ endoscopy US, pancreatic calculi on CT*
- Labs: pancreatic fncn tests (direct for early via CCK or secretin stimulation + indirect for more advanced via serum trypsinogen, fecal fat). Pancreatic enzymes may often be normal bc fibrosis dec enzymes.
Tx
- Stop alcohol/ smoking, analgesia (TCAs, opioids, pregabalin), anti-oxidants, duct decompression, stone removal, pseudocyst drainage
Acute GI Bleed
- VBG = fastest Hgb. Then stat CBC
- Note the volume of blood, presence of clots
- Vitals every 5 mins. Watch for dec BP + inc HR (but be careful if pt is on rate control, ie metoprolol)
- Group + match (few hrs though)
- Transfusion consent
- Consult GI bleed
- Stop any anticoagulants
- Boundary bw upper + lower GI = Ligament of Treitz (bw duodenum + jejunum of SI)
Abdo Compartment Syndrome
Etiology
- Massive ascites, edematous bowe -> inc intra-abdo pressure -> abdo compartment syndrome
S+S
- Pre-renal AKI (dec renal arterial perfusion + renal venous outflow)
Abdo Pain Ddx by region
- Most common cause of acute abdo pain:
- > > 50 yro = biliary pain
- > <50 yro = appendicitis
RUQ
- Acute cholangitis (bili, AST, ALT), pneumonia, acute viral or alcoholic hep (AST, ALT), Fitz-hugh-curtis (gonococci, leukocytosis, pelvic adnexal tenderness), cholecystitis (radiates to R shoulder, bili, AST, ALT, US)
Epigastric/ Umbilical
- Acute pancreatitis (radiates to back, N/V, amylase/ lipase), acute appendicitis (radiates to RLQ, McBurney pt, psoas sign, CT), inferior MI, perforating peptic ulcer (post-prandial pain, wt loss, pain out of proportion to tenderness on palpation), mesenteric ischemia (thumbprint sign on XR), small bowel obstruction (colicky pain, XR/ CT), aortic dissection/ rupture (old, vascular disease, sudden, severe, radiates to back/ lower extremity), DKA
R or L LQ
- Ectopic pregnancy (nausea, fever, leukocytosis), ovarian cyst/ torsion, pelvic inflamm disease, nephrolithiasis (flank pain, may radiate to groin, hematuria), pyelonephritis (fever, dysuria, flank pain, leukocyte casts)
RLQ
- Acute appendicitis
LLQ
- Acute diverticulitis, toxic megacolon
Irritable Bowel Syndrome (IBS)
Dx
- Rome criteria: >=3 mos of continuous/ recurrent abdo pain. And relieved with defectation, and/or change in stool frequency and/or consistency. (And >=2/5 supplementary sx details)
- -> Sens 50%, spec 100%
- Manning criteria: abdo pain + >=2/6 supplementary sx (relief with defectation, looser or more frequent stools at onset of pain, abdo distention, mucous, feeling of incomplete evacuation)
- -> Sens 60%, spec 80%. Inc accuracy in F or young.
- Should last for >12wks total in the last 12 mos.
- May also have other GI/extra-GI sx.
- V unlikely if rectal bleeding, nocturnal or progressive pain, wt loss, anorexia, or signs of malnutrition
- R/o other causes including parasitic infection, UC, Crohn’s, celiac, lactose intolerance
- Labs/ investigations should all be N
3 Sub-types
- Diarrhea dominant vs constipation vs pain
Pathophys
- Mutlifactorial, not well known. Possibly from altered GI motility, visceral hypersensitivity, inflamm/ infection, altered fecal flora, inc bacteria, genetics, psych association, food sensitivities
- PET of pre-frontal cortex shows altered ability to dampen pain
Tx
- No cure, focus on dec sx of the pts sub-type: constipation (fibre, laxative), diarrhea (anti-diarrheal, bile acid sequestrant, anti-depressant), pain (anti-spasmodics, anti-depressant)
- Also CBT, avoid food triggers, dec stress
- Educate pt: no organic abnormality, how best to live with it
