GI Diseases Flashcards
fatigue, nausea, anorexia, fever, arthralgia, mylagia, h/a, RUQ pain
All Hepatitis: Symptoms
jaundice, scleral icterus, coca-cola urine, hepatomegaly
All Hepatitis: Signs
very high ALT/AST, high TP+AP, bilirubin in urine, increase IgM
All Hepatits: Labs
diffuse periportal lymphocytic inflammation, hepatocellular ballooning
All Hepatitis: Biopsy
Oral-fecal, asympotomatic in children
Hepatitis A: MOI
ALT and symptoms peak in 1 month, IgM peaks 3 months post-infxn
Hep A
Nonenveloped ssRNA virus; @2wks - excreted in stool; @4wks - increased ALT, Sx begin; @8wks - resolution
Hepatitis A: Pathophysiology
Never chronic, no tx but gamma-globulin vaccine available (passive)
Hepatitis A: Treatment/Notes
Horizontal (IVDU, sex) in US
Hepatitis B: Epi/MOI
The only enveloped, partially double-stranded DNA virus; 6-8wk incubation, 20% serum sickness prodrome
Hepatitis B: Pathophysiology
Progresses to chronic in 4%, Tx and vaccine (passive + active)
Hepatitis B: Treatment/Notes
Epi: HepB coinfection/hx
Hepatitis D: Epi/MOI
Delta agent, uses HBsAg protein coat, HepB must be present
Hepatitis D: Pathophysiology
Pigs
Hepatitis E: Epi/MOI
~HepA, waterborne, endemic in Asia, N. Africa, Mexico
Hepatitis E: Pathophysiology
350M; 1M in US
Chronic Hepatitis B: Epi/MOI
Labs: increased ALT+AST >6mo, (+)HBsAg, (+)HBcAb IgG; Biopsy: Ground glass
Chronic Hepatitis B: Signs/Symptoms/Findings
Vertical transmission predominant in most parts of the world; can lead to HCC; see charts on Chronic Hepatitis B
Chronic Hepatitis B: Pathophysiology
PEG-interferon, tenofovir / entecavir to decrease HBV DNA levels; not curative
Chronic Hepatitis B: Treatment/Notes
170M; 3M in US;
Chronic Hepatitis C: Epi/MOI
Labs: increased ALT+AST >6mo, (+)anti-HCV, (+)HCV RNA; Biopsy: Portal lymphoid aggregates, interface hepatitis
Chronic Hepatitis C: Signs/Symptoms/Findings
Unlike chronic HepB, anti-HCV doesn’t kill virus; but also unlike HBV, HepC can be cured (in ~75%), since no virus in nucleus
Chronic Hepatitis C: Pathophysiology
PEG-interferon, ribavirin, (+boceprevir/telaprevir in genotype 1); SNP encoding interferon(IFN lamba 3) = 2x change in response
Chronic Hepatitis C: Treatment/Notes
Decades of alcohol use
Alcoholic Hepatitis / ASH (Alcoholic Steatohepatitis : Epi/MOI
Acute jaundice, liver failure, hepatomegaly, ascites, encephalopathy; increased AST+ALT, AST:ALT >2:1; PMNs, ballooned hepatocytes, Mallory bodies, centrilobular macrosteatosis, chicken-wire fibrosis
Alcoholic Hepatitis / ASH (Alcoholic Steatohepatitis : Signs/Symptoms/Findings
Acetaldehyde (toxic metabolite of alcohol) damages central hepatocytes, leads to production of TGs; some degree of fibrosis but generally not cirrhotic; can see portal HTN from hepatic swelling
Alcoholic Hepatitis / ASH (Alcoholic Steatohepatitis : Pathophysiology
Tx: Abstinence, banana bag, steroids (esp. if discriminant fxn >32, which = poor prognosis), pentoxifylline (anti-TNF), need 6 mo abstinence for xplant
Alcoholic Hepatitis / ASH (Alcoholic Steatohepatitis : Treatment/Notes
Metabolic syndrome, M>F, 40-60 yo
NAFL (Non-Alcoholic Fatty Liver)& NASH: Epi/MOI
Same as ASH except mixed PMNs + lymphos, AST:ALT <1; also see perivenular and sinusoidal fibrosis
NAFL (Non-Alcoholic Fatty Liver) & NASH: Signs/Symptoms/Findings
1st hit: increased TG’s, FFA; 2nd hit: oxidative stress leads to lipid peroxidation, cytokine release, damage to cell membranes + mitos
NAFL (Non-Alcoholic Fatty Liver) & NASH: Pathophysiology
Less cirrhosis risk than ASH; Tx: wt loss, exercise, glycemic/lipid control, pioglitazone, vitamin E
NAFL (Non-Alcoholic Fatty Liver)& NASH: Treatment/Notes
Rare Steatosis
Small Droplet Steatosis: Epi/MOI
Small fat vacuoles, nucleus at center
Small Droplet Steatosis: Signs/Symptoms/Findings
Severe mitochondrial injury leads to decrease beta-FA oxidation
Small Droplet Steatosis: Pathophysiology AND Treatment/Notes
Normal blood bilirubin
<17microM, 1 mg/dL
In real life, unconjugated serum bilirubin percent
96%
Lab overestimates conjugated bili by up to
30%
bilirubin level leading to jaudince
> 35 microM
conjugated hyperbilirubinemia always caused by
impaired secretion of BDG from hepatocytes OR biliary obstruction
heptocellular causes of conjugated hyperbilirubinemia
cirrhosis, acute hepatitis (drugs, viral, alcohol)
biliary obstruction causes of cinjugated hyperbilirubinemia
gallstones, tumors, primary biliary cirrhosis
Dubin-Johnson syndrome (ABCC2) & Rotor syndrome (SLCO1B1/IB3)
genetic conjugated hyperbilirubinemia
unconjugated hyperbilirubinemia: overproduction causes
hemolysis, bad erythropoesis
unconjugated hyperbilirubinemia: impaired uptake causes
fast, sepsis, drugs (probenicid)
unconjugated hyperbilirubinemia: impaired conjugation causes
inherited mutations/polymorphisms
Crigler-Najjar (UGT1 mut) & Gilbert sydrome (polymorphism)
cause impaired conjugation unconjugated hyperbilirubinemia
less H bonding in E diastereoisomers, makes unconj. Bili more water soluble
phototherapy in neonates with jaudice
metabolism produces a hepten that binds to cells, triggers T-cells and eosinophils
drug-induced hepatitis
M>F (due to .’s), N. Euros. Variable penetrance
Hemachromatosis: Epi/MOI
Bronzing diabetes, HCC, cirrhosis, cardiomyopathy; transferrin saturation (TIBC) >50% in F, >60% in M
Hemachromatosis: Signs/Symptoms/Findings
HFE mutation (C282Y +/+ or H63D/C282Y) results in decrease hepcidin, which is usually inhibitor of iron absorption, recycling, storage
Hemachromatosis: Pathophysiology
Tx: phlebotomy; liver xplant if bad; can also see iron overload due to causes other than HFE mutation. Can halt symptoms, but cannot reverse damage
Hemachromatosis: Treatment/Notes
AR, 1/30K, 2-40 yo
Wilson’s Disease: Epi/MOI
Kayser-Fleischer rings, decrease ceruloplasmin, urinary Cu high, stool low (25% direct, 50% as metallothionin),low AlkP, AST+ALT > 2.2, renal dz
Wilson’s Disease: Signs/Symptoms/Findings
ATP7B on chr17 encodes metal-transporting ATPase, mutation results in excessive copper in liver and brain
Wilson’s Disease: Pathophysiology
Chelation (penicillamine), zinc (prevents absorbtion), transplant if bad (always fatal without tx)
Wilson’s Disease: Treatment/Notes
Biopsy: (+)PAS granules; Labs: decrease alpha 1AT;Chronic hepatitis, cirrhosis
Alpha-1-Antitrypsin Deficiency: Signs/Symptoms/Findings
SERPINA ZZ, some ZS, rarely SS leads to alpha 1AT getting trapped within ER of hepatocytes, leads to fibrosis, cirrhosis, HCC
Alpha-1-Antitrypsin Deficiency: Pathophysiology
Serpina Pi null-null
no a1t, severe lung disease, no liver dz
Tx: smoking cessation, abstinence, pneumovax, alpha 1AT, manage chronic liver dz, augementum for lungs, only xplant cures liver
Alpha-1-Antitrypsin Deficiency: Treatment/Notes
F>M 4:1, dx by exclusion, biopsy
Autoimmune Hepatitis (AIH), overlap syndromes: Epi/MOI
Acute hepatitis (30%), occ fulminant, 34% asympt; increased ALT + AST, IgG, gamma-globulin ; plasma cell infiltrate + interface hepatitis
Autoimmune Hepatitis (AIH), overlap syndromes: Signs/Symptoms/Findings
97% are Type 1: anti-smooth muscle Ab (SMA) and/or ANA, age 16-30; Type 2: anti-ILKM1, affects kids 2-14yo; type III looks like one, adults 30-50
Autoimmune Hepatitis (AIH): Pathophysiology
Tx: Prednisone + azathioprine, 10yr survival 90% but 3yr relapse 90%; long-term Tx usually necessary; xplant
Autoimmune Hepatitis (AIH), overlap syndromes: Treatment/Notes
AIH + (PBC or PSC)
Overlap Syndromes: Pathophysiology
F>M, other AI diseases
Primary Biliary Cirrhosis (PBC): Epi/MOI
(+)AMA, increased AlkP and gamma-globulin, fatigue, pruritus, cirrhotic Sx, chronic cholangitis
Primary Biliary Cirrhosis (PBC): Signs/Symptoms/Findings
AMA (anti-mitochondrial Ab) vs. small intrahepatic bile ducts
Primary Biliary Cirrhosis (PBC): Pathophysiology
Tx: Ursodeoxycholic acid; cholestyramine for pruritus
Primary Biliary Cirrhosis (PBC): Treatment/Notes
M>F 3:1, 20s-30s, 80% IBD (mostly UC)
Primary Sclerosing Cholangitis (PSC): Epi/MOI
increased increased AlkPhos+TB, increased ALT+AST, gamma-globulin, (+)pANCA, ANA, SMA, (-)AMA; Onion-skin fibrosis on biopsy, Beads-on-a-string on ERCP
Primary Sclerosing Cholangitis (PSC): Signs/Symptoms/Findings
ANCA>ANA>SMA vs. both intrahepatic and extrahepatic bile ducts
Primary Sclerosing Cholangitis (PSC): Pathophysiology
Median survival 12 yrs; transplant is only way to improve; watch for colon cancer, cholangiocarcinoma, gallbladder dz, IBD, metabolic bone disorder
Primary Sclerosing Cholangitis (PSC): Treatment/Notes
Cholestasis: increased direct bili, pruritus, jaundice, xanthomas, fibrosis, ADEK deficiency, fat malabsorption, hepatocellular injury, acholic stool (grey/white)
Infectious Hepatitis, TPN-associated cholestasis, galactosemia, tyrosemia, idiopathic neonate hepatitis: Signs/Symptoms/Findings
ToRCHeS - Toxo, Rubella, CMV, HSV, Syphilis; Coxsackie; Echovirus
Infectious Hepatitis: Pathophysiology AND Treatment/Notes
Premies
TPN-Associated Cholestasis: Epi/MOI
Lipids in TPN worsens underlying dz
TPN-Associated Cholestasis: Pathophysiology
Tx: feed, cycle or stop TPN
TPN-Associated Cholestasis: Treatment/Notes
AR pediatric liver diseases
Galactosemia, Tyrosemia, PFIC, Congential Hepatic fibrosis: Epi/MOI
Galactose-1-phosphate-uridyl transferase mutation leads to fatty liver
Galactosemia: Pathophysiology
Tx: galactose/lactose-free formula
Galactosemia: Treatment/Notes
Fumaryl acetoacetate hydrolase deficiencylead to increased succinyl acetone
Tyrosinemia: Pathophysiology
Dx: urinary succinyl acetone; Tx: transplant curative
Tyrosinemia: Treatment/Notes
Jaundice in 1st week of life, fulminant in 30% (giant cell hepatitis, necrosis)
Idiopathic Neonatal Hepatitis: Pathophysiology
Also increased indirect bili; 30-40% of neonatal cholestasis;
Idiopathic Neonatal Hepatitis: Treatment/Notes
1/10K, 1wk old, acholic stools,
Biliary Atresia : Epi/MOI
Biopsy: swirly, neuron-like ductule cells with bile plugs
Dx: abd USG to r/o other causes, HIDA w/ phenobarb, increased direct bili
Biliary Atresia : Signs/Symptoms/Findings
Idiopathic proliferation of bile ductules with bile plugs leading to blockage of bile ducts; cause of 50-60% of liver transplants in kids
Biliary Atresia : Pathophysiology
Kasai hepatic porto-enterostomy to delay progression to biliary cirrhosis and transplant
Biliary Atresia : Treatment/Notes
Abdominal ultrasound shows cysts, dilation (in children)
Choledochal Cyst: Signs/Symptoms/Findings
Congenital weakness in wall of common bile ductlead to dilation, cyst
Choledochal Cyst: Pathophysiology
Resection due to malignancy potential
Choledochal Cyst: Treatment/Notes
AD, variable penet. Pediatric liver dz
Alagille Syndrome: Epi/MOI
Triangular facies, ocular / CV / vertebral anomalies, decrease growth, pruritus, xanthomas
Alagille Syndrome: Signs/Symptoms/Findings
JAG1 mutation results in dysfunctional Notch signaling, malformation and paucity of intrahepatic bile ducts, arteriohepatic dysplasia
Alagille Syndrome: Pathophysiology
Prolonged survival good but defective spermatogenesis
Alagille Syndrome: Treatment/Notes
increased AlkPhos, pruritus, normal GGT; biliary paucity, giant cells
Progressive Familial Intrahepatic Cholestasis (PFIC): Signs/Symptoms/Findings
Defect in ATP8B1 (type 1: ATPase) or BSEP (2: salt pump) leads to bile transport problems
Progressive Familial Intrahepatic Cholestasis (PFIC): Pathophysiology
External biliary diversion, esp. in type 1; transplant
Progressive Familial Intrahepatic Cholestasis (PFIC): Treatment/Notes
Abd pain, cholangitis, varices; ductular cells, no cirrhosis (in children)
Congenital Hepatic Fibrosis: Signs/Symptoms/Findings
Malformation of embryonic ductal plate leads to fibrosis, ARPKD
Congenital Hepatic Fibrosis: Pathophysiology
Comorbid with Caroli’s
Congenital Hepatic Fibrosis: Treatment/Notes
75% M
Caroli’s Disease: Epi/MOI
Abd pain, hepatomegaly, Gm- sepsis, CBD normal
Caroli’s Disease: Signs/Symptoms/Findings
Multiple saccular dilatations of intrahepatic ducts (~choledochal cyst)
Caroli’s Disease: Pathophysiology
Stenting, Abx, pain meds, transplant curative
Caroli’s Disease: Treatment/Notes
CT: lumpy-bumpy, enlarged liver; Biopsy: collagen; increased TB (Tx: see PBC), increased PT/INR
Cirrhosis: Epi/MOI AND Signs/Symptoms/Findings
Chronic inflammationlead to fibrosis from stellate cells, regenerative nodules, distortion of liver parenchyma; etiologies = HepB/C, EtOH, autoimmune, congenital, toxins
Cirrhosis: Pathophysiology
Pro-oncogenic environment (1-5% / yr progress to cancer); prognosis: compensated 8.9 yrs, decompensated 1.6 yrs
Cirrhosis: Treatment/Notes
Other sequelae include hepatic hydrothorax (Tx: ~ascites), hyponatremia (Tx: decrease fluids, vaptans), hepatoencephalopathy, varices, portopulmonary syndrome
Portal Hypertension: Epi/MOI AND Signs/Symptoms/Findings
Portal pressure increased >7mm Hg (>10 is “significant”) from increased outflow resistance (fibrosis or vasoconstriction) + increased inflow; Tx: beta blockers, octreotide
Portal Hypertension: Pathophysiology AND Treatment/Notes
SAAG >1.1, nl glucose, low LDH, low protein+amylase
Ascites: Signs/Symptoms/Findings
> 10mmHglead to fluid in peritoneal cavity from lymphatic backflow
Ascites: Pathophysiology
Tx: Low Na+ diet, diuretics, LVP, TIPS
Ascites: Treatment/Notes
increased WBC (>500, or >250 with more than half polys), (+)culture (klebsiella, e.coli, entercoccus, pneumococcus)
Spontaneous Bacterial Peritonitis (SBP): Signs/Symptoms/Findings
Ascites fluid infected by bacteria or fungi w/o gut perforation
Spontaneous Bacterial Peritonitis (SBP): Pathophysiology
Tx: 3G cephalosporin x 5d
Spontaneous Bacterial Peritonitis (SBP): Treatment/Notes
Serum Cr >1.5, despite volume expansion, d/c diuretics
Hepatorenal Syndrome: Signs/Symptoms/Findings
Renal insufficiency with cirrhosis and ascites; Type 1 worse than Type 2
Hepatorenal Syndrome: Pathophysiology
Tx: Albumin, midodrine, octreotide, TIPS, liver xplant
Hepatorenal Syndrome: Treatment/Notes
Platypnea-orthodeoxia, clubbing, cyanosis
Hepatopulmonary Syndrome: Signs/Symptoms/Findings
V-Q mismatch from vasodilation in lung due to NO from portal HTN
Hepatopulmonary Syndrome: Pathophysiology
Tx: O2, liver transplant
Hepatopulmonary Syndrome: Treatment/Notes
Gross: “Nutmeg liver” Biopsy: congestion near central vein
Centrilobular Congestion: Signs/Symptoms/Findings
Right-sided heart failure (or biventricular heart failure)
Centrilobular Congestion: Pathophysiology AND Treatment/Notes
Biopsy: necrosis near central vein
Centrilobular Necrosis: Signs/Symptoms/Findings
Left-sided heart failure
Centrilobular Necrosis: Pathophysiology
Ascites & increased coag state
Budd-Chiari Syndrome: Signs/Symptoms/Findings
Liver (cont’d)
Budd-Chiari Syndrome: Cat
Thrombi/tumor invade hepatic vein/IVC; liver blocked, congested
Budd-Chiari Syndrome: Pathophysiology
50% due to Tylenol
Acute Liver Failure (ALF): Epi/MOI
Acute, change MS, coagulopathy (increased INR), no cirrhosis; coagulative necrosis
Acute Liver Failure (ALF): Signs/Symptoms/Findings
Drugs, viruses, toxins, metabolic dz, ischemia, etc. leads to liver damage; can lead to encephalopathy, infection, cerebral edema, renal failure, SIRS
Acute Liver Failure (ALF): Pathophysiology
ICU, IV N-acetylcysteine if acetaminophen, early liver transplantation (other organs usually recover)
Acute Liver Failure (ALF): Treatment/Notes
28% Tylenol, 52% indeterminate (probably viral)
Pediatric Acute Liver Failure: Epi/MOI AND Signs/Symptoms/Findings
Acetaminophen better prognosis than viral/indeterminant
Pediatric Acute Liver Failure: Pathophysiology
OLT (King’s college criteria)
Pediatric Acute Liver Failure: Treatment/Notes
Asterixis, stupor, coma, change LOC
Hepatic Encephalopathy: Signs/Symptoms/Findings
Gut neurotoxin (e.g. NH3) bypass liver due to portal-systemic shunt
Hepatic Encephalopathy: Pathophysiology AND Treatment/Notes
1M die / yr
Hepatocellular Carcinoma: Epi/MOI
Screen with liver USG q6mo in at-risk pts, vaccinate for HBV
Hepatocellular Carcinoma: Signs/Symptoms/Findings
Screen ALF pts every 6 mos
for Hepatocellular Carcinoma
Chemo, RF ablation
Hepatocellular Carcinoma: Treatment/Notes
hepatic failure + iron deposition
gestational alloimmune liver disease
complement cascade activates, intrauterine onset. Anti-human C5B9 complex
gestational alloimmune liver disease
IVIg, exchange transfusion, OLT
gestational alloimmune liver disease
PT prolongs within
one day of liver dysfunction
marked ALT/AST elevation
hepatocellular
marked AlkP, TB elevation
cholestatic
marked AlkP only
infiltrative
normal albumin
3.5-5.3
normal AST
six-40
normal Alk-P
30-120
normal TB
0.1-1
normal direct B
0.1-0.4
normal GGT
0-42
normal INR (PT ratio)
1
dx biliary obstruction
MRCP (costly)
test to access cirrhosis
liver-spleen scan (medium)
will not evaluate liver function, can’t detect fibrosis, rarely reveals etiology
CT, MRI/MRCP
mild elevation
<5x normal
severe elevation
> 15x normal
decreases UGT1 activity, increased bili production, bad erthropoesis and decreased RBC survival
why babies be jaundiced
female, advanced age, DM, obese, chronic viral disease, alcohol, decreased renal fxn, nutritional deprivation
factors associated with drug-related liver damage
acetominophen, after P450, produced
toxic NAPQ1
tylenol and beer both
deplete glutathione, leading to mercapturic acid conjugates and mitochondrial dysfunction
picornaviridal hepatovirus
hep A
hepandaviridae
hepB
flaviveridal hepacivirus
hep C
unclassified viroid, delta virus
hep D
unclassified, toga- and alphavirus-like
hep E
mono, lymphadenopathy, splenomegaly and hepatitis
EBV
immunocompromised with hepatitis
CMV?
HBsAg
acute or chronic hep B
Anti-HBc IgM
acute hep B
HBeAg
increased infectivity hep B
Anti-HBe
decreased infectivity hep B
Anti-HBs
hep B immunity
Anti-HBc IgG + HBsAg
hep B chronic infxn
Anti-HBc IgG + Anti-HBs
hep B resolved infxn
Hep C incubates for
6-8 weeks
Hep C becomes chronic for
80%
Hep C becomes cirrhotic for
20%
HCV RNA positive at
2 weeks post-infxn
Anti-HCV appears
12-24 weeks post infxn
AST:ALT in alcoholic hep
> 2:1
three effects of alcohol ingestion
aldehyde adducts, increased ROS, increase NADH:NAD+ ratio
required abstinence for xplant
six months
predict progression in NAFLD
DM, high initial fibrosis, obesity
portal hepatic pressure gradient PV-HV
7 is normal, 10 is significant, balloon is in the HV
NO increases in PHTN because
shear stress activates eNOS in splanchnic beds, increased TNF and VEGF
spontaneous bacterial peritonitis, refractory ascites, dilutional hyponatremia, hepatorenal syndrome
prognosis in PHTN, worst to best
GI bleed/hypotension, advanced liver disease, prior Hx
risk factors for spontaneous bacterial perotinitis
All tx for end-stage liver dz, except OLT
supportive not curative
INR in ALF
> 1.5
barbituates, mannitol, hyperventilation, head elevation
may prevent encephalopathy in fulminant liver failure
discrimination function equation
4.6*(patient’s PT-control PT) + total bili
DF>32
alcoholic hepatitis, treat with steroids
pH100 and creatinine>3.5, in III/IV coma
King’s College OLT criteria in acetominophen poisoning
PT>100, or three of these:PT>50, younger than 10 or older than 40, jaundice 7 days prior to encephalopathy, bili>17, not hep A or B
Kings College OLT criteria (not ACM)
associated with polysplenia, heterotaxia, intraabdominal vascular abnormalities
biliary atresis
alaguille’s prognosis is good except defective sperms and
CNS aneurysms
percent of HCC due to HBV
80%!
HBV, HCV, alcoholic cirrhosis, NAFLD, metabolic syndrome, aflatoxin (from corn, soy, nuts), dirty water
HCC risk factors
Lymphocytes in islets lead to
Type I Diabetes Mellitus: Signs/Symptoms/Findings
Autoimmune vs. beta cells
Type I Diabetes Mellitus: Pathophysiology
Amyloid buildup in pancreas
Type II Diabetes Mellitus: Signs/Symptoms/Findings
Insulin resistance in beta cells
Type II Diabetes Mellitus: Pathophysiology
Hypoglycemia
Islet Cell Adenoma (Insulinoma): Signs/Symptoms/Findings
Benign but functional encapsulated tumor of islet cell origin
Islet Cell Adenoma (Insulinoma): Pathophysiology
Complete (IPF1 single nucleotide deletion) or partial lack of pancreas
Pancreatic Agenesis: Pathophysiology
Partial still has full function
Pancreatic Agenesis: Treatment/Notes
Obstructed pancreatic fluid flow, canlead to chronic pancreatitis
Pancreas Divisum: Signs/Symptoms/Findings
10% of the people
Pancreas Divisum: Epi/MOI
dx w/Ultrasound, ECRP. Think of in patients with recurrent pancreatitis
Pancreas Divisum
Pancreas separated, not fused together
Pancreas Divisum: Pathophysiology
Completely separated pancreas strangulates duodenum
Annular Pancreas: Pathophysiology
Surgical resection
Annular Pancreas: Treatment/Notes
35% alcohol use, 45% gallstones
Acute Pancreatitis: Epi/MOI
Epigastric abd pain rad to back, rapid onset, N/V, may have Cullen’s/Grey-Turner’s signs; increased Serum lipase + amylase (3x nl), liquefactive necrosis, elastase destruction of blood vesselslead to
Acute Pancreatitis: Signs/Symptoms/Findings
No initial abx if severe. ERCP for stones
Acute Pancreatitis
Dx requires 2 of: imaging, characteristic pain, amylase/lipase 3x normal
Acute Pancreatitis
Intracellular enzymes released, digest pancreatic fat, lobules, blood vessels; most common cause is gallstones, followed by alcohol, post-ERCP, drugs (E2, valproate, thiazide diuretics, PIs)
Acute Pancreatitis: Pathophysiology
Tx: IV fluids, NPO; can lead to fat necrosis, hemorrhage, ARDS, hypovolemia, hypocalcemia, coagulopathy, hyperglycemia,
Acute Pancreatitis: Treatment/Notes
Alcohol #1 cause
Chronic Pancreatitis: Epi/MOI
Calcified pancreas on XR/CT; exocrine insufficiency; large duct disease (more common in males, alcohol) vs. small duct (females, idiopathic); pain
Chronic Pancreatitis: Signs/Symptoms/Findings
Episodes of repeated acute pancreatitis and resultant fibrosis; EtOH increased mRNA production of degradation enzymes, blocks apical migration of lysosomes
Chronic Pancreatitis: Pathophysiology
Tx: abstinence, analgesics, octreotide, enzyme replacement, ERCP/neurolysis for pain, Puestow procedure. Can cause DM by destroying islets
Chronic Pancreatitis: Treatment/Notes
AD, 80% with mutation develop inflammation
Hereditary Pancreatitis: Epi/MOI
PRSS1 mutation results in increased intracellular enzymes
Hereditary Pancreatitis: Pathophysiology
High risk for pancreatic cancer (>40%)
Hereditary Pancreatitis: Treatment/Notes
Other AI disorders, plus pancreatitis
Autoimmune Pancreatitis: Epi/MOI
IgG deposits, especially IgG4
Autoimmune Pancreatitis: Signs/Symptoms/Findings
Autoantibodies results in narrowing of main pancreatic duct
Autoimmune Pancreatitis: Pathophysiology
Tx: steroids
Autoimmune Pancreatitis: Treatment/Notes
Fat, Forty, Fertile Female; 10-15% of adults, hispanic>white>black
Gallstones (Cholelithiasis): Epi/MOI
USG: hyperechoic with shadow
Gallstones (Cholelithiasis): Signs/Symptoms/Findings
Cholesterol stones (85%, radiolucent), black pigment stones (radiodense, from hemolysis), or brown pigment stones (infectious)
Gallstones (Cholelithiasis): Pathophysiology
Cholecystectomy
Gallstones (Cholelithiasis): Treatment/Notes
Steady epigastric/RUQ pain, rad to back/R shoulder
Biliary Colic: Signs/Symptoms/Findings
Most common complication; = pain from GB stones or CBD stones
Biliary Colic: Pathophysiology
Onset of pain >1hr after meals and at night
Biliary Colic: Treatment/Notes
Fever, leukocytosis, mild LFTs in 25%, N/V, RUQ pain rad to back, worse with movement or cough, HIDA scan, Murphy’s sign, stones + thick wall on USG
Acute Cholecystitis: Signs/Symptoms/Findings
Inflammation of gallbladder itself; can be calculous (impaction of stone at GB necklead to inflammation, bacteria) or acalculous (immunocompromised)
Acute Cholecystitis: Pathophysiology
Tx: NPO, supportive care, antibiotics, surgery, cholecystectomy, endo-scopic cystic duct stenting, meperedine for pain
Acute Cholecystitis: Treatment/Notes
Biliary colic, obstructive jaundice, cholangitis, pancreatitis; Dx: intraductal or radial endoscopic USG
Choledocholithiasis: Signs/Symptoms/Findings
CBD blocked by stones (any type)
Choledocholithiasis: Pathophysiology
Tx: ERCP w/ cannulation, sphincterotomy, or stone retrieval; surgical biliary bypass, cholecystectomy
Choledocholithiasis: Treatment/Notes
Charcot’s triad in 60-70% (fever, jaundice, RUQ pain); infected bile, frank pus, increased LFTs, less severe tenderness
Acute Cholangitis: Signs/Symptoms/Findings
stents, tumors, congenital cysts, pancreatitis, ascaris lumbroides, HIV
Acute Cholangitis: Associated Conditions
BD stone results in bacterial (usually Gm-, multiple agents) infection of bile ducts, usually with partial or complete cholestasis
Acute Cholangitis: Pathophysiology
Tx: broad spectrum antibiotics (cypro, zocin), NPO, hydration, ERCP if emergent(better than surgery)
Acute Cholangitis: Treatment/Notes
acini cells (84%), then ducts (5) then islets (1)
by mass, pancreas is mostly
cues acinar enzyme secretion
CCK via IP3
cues ducts to secrete water, Na and bicarb
secretin via cAMP
Cough, aspiration; more problems with liquids
Oropharyngeal Dysphagia: Signs/Symptoms/Findings
Difficulty transferring bolus out of mouth
Oropharyngeal Dysphagia: Pathophysiology
Caused by Zenker’s diverticulum, stroke, ACS, parkinson’s MS, muscular dystrophy
Oropharyngeal Dysphagia
Sense of bolus “sticking”
Esophageal Dysphagia: Signs/Symptoms/Findings
Bolus trapped in esophagus
Esophageal Dysphagia: Pathophysiology
Only solid food impaction (with forced regurgitation), often progressive (especially malig.)
Mechanical, Schatzki Ring, Esophageal Stricture, Esophageal Carcinoma: Signs/Symptoms/Findings
Can also be caused by Barrett’s
Mechanical: Pathophysiology
Ring at squamo-columnar junction, dysphagia with large boluses of food
Schatzki Ring: Pathophysiology
Steakhouse syndrome
Schatzki Ring: Treatment/Notes
Can be asymptomatic, usually caused by acid reflux
Esophageal Stricture: Pathophysiology
Tx: with esophageal dilators
Esophageal Stricture: Treatment/Notes
Irregular stricture with lots of ulcers
Esophageal Carcinoma: Pathophysiology
Tx: chemotherapy, resection, radiation, stents
Esophageal Carcinoma: Treatment/Notes
Liquid impaction, nocturnal
Motor: Signs/Symptoms/Findings
Aperistalsis, LES HTN and incomplete relaxationlead to distal narrowing
Achalasia: Signs/Symptoms/Findings
Idiopathic or Chagas results in esophageal denervation/dilation, failure of smooth muscle relaxation
Achalasia: Pathophysiology
Tx: laparoscopic myotomy, Botox, pneumatic dilation
Achalasia: Treatment/Notes
Esophageal dysmotility, weak LES, weak contraction, LES hypotension, GERD
Scleroderma: Signs/Symptoms/Findings
Aka CREST syndrome, where smooth muscle becomes fibrotic
Scleroderma: Pathophysiology
Tx: immunosuppression
Scleroderma: Treatment/Notes
Heartburn, atypical sx: chest pain, ENT problems, vocal changes, asthma, cough; Biopsy: basal cell hyperplasia, mixed inflammatory cells, erosions
Gastroesophageal Reflux Disease (GERD): Signs/Symptoms/Findings
LES transiently relaxes, leading to esophagitis due to acid, can lead to strictures
Gastroesophageal Reflux Disease (GERD): Pathophysiology
Dx: 24hr pH monitoring, Bravo capsule study, etc. Tx: avoid precipitants, wt loss, PPI > H2RA
Gastroesophageal Reflux Disease (GERD): Treatment/Notes
most common GI referral, late complication: Barretts
GERD
no fatty food, alcohol, caffeine, small meals, raise bed, antacids
Mild GERD tx
histimine 2 receptor antagonist: Cimetidine
severe GERD tx
Junctional: mucinous glands; Gastric fundic: parietal cells; normal cells, just abnormal location
Barrett’s Esophagus (Columnar Metaplasia): Signs/Symptoms/Findings
Intestinal metaplasia (i.e. esophagus looks like small intestine) due to injury to squamous mucosa and subsequent stem cell repair
Barrett’s Esophagus (Columnar Metaplasia): Pathophysiology
Cancer risk (adenocarcinoma)
Barrett’s Esophagus (Columnar Metaplasia): Treatment/Notes
Vomiting, reflux symptoms; >20 eos per HPF, rings, strictures, white papules, linear furrows
Eosinophilic Esophagitis (Allergic): Signs/Symptoms/Findings
Children/YA, M>F
Eosinophilic Esophagitis (Allergic): Epi
Hypersensitivity to dietary or airborne allergens
Eosinophilic Esophagitis (Allergic): Pathophysiology
Tx: corticosteroids, diet, avoid allergens, AA formulas. Anti-reflux drugs ineffective
Eosinophilic Esophagitis (Allergic): Treatment/Notes
Red inclusion bodies, multiple nuclei per cell, molded cells, ground glass nuclei, affects squamous cells
HSV Esophagitis: Signs/Symptoms/Findings
Fairly common, self-limited, peripheral ulcers secondary to infxn. Relapse frequent
HSV Esophagitis: Pathophysiology
Cytomegaly, intranuclear inclusions, granules and pale zone, epithelium spared
CMV Esophagitis: Signs/Symptoms/Findings
In immunocompromised patients, enlarged stromal cells (endos, histiocytes, nerve, muscle). Dx w/ulcer base biopsy
CMV Esophagitis: Pathophysiology
AIDS/DM
Candida Esophagitis: Epi/MOI
White pseudomembranes grossly, pseudohyphae and yeasts on silver stain
Candida Esophagitis: Signs/Symptoms/Findings
Indicator of AIDS, must see tissue invasion
Candida Esophagitis: Pathophysiology
NSAIDs, tetracycline, bisphosphonates, potassium, vitamin C, iron
Pill Esophagitis
dx: clinic pathology, or biopsy (iron)
pill Esophagitis
2-3 weeks post, self-limiting, esophageal ulcers
radiation esophagitis: acute
3-6 months post, fibrosis, treat with stents and dilation
radiation esophagitis: chronic
10% lifetime prevalence, 50% have H. pylori
Peptic Ulcer Disease: Epi/MOI
Dyspepsia, relieved (DU) or worsened (GU) by food; majority asymptomatic; can result in upper GI bleeding; DU (right), GU (left)
Peptic Ulcer Disease: Signs/Symptoms/Findings
Recurrent ulcers in upper GI tract, especially near mucosal junctions; due to increased acid+pepsin and decrease PGE-related protective factors (HCO3, mucus, etc.)
Peptic Ulcer Disease: Pathophysiology
H. pylori classical cause, NSAIDs becoming more common (decrease PGE2 from decrease COX-1);dx: upper endoscope and biopsy; Tx: PPI + amox
Peptic Ulcer Disease: Treatment/Notes
Parietal cell/IF antibodies, loss of parietal and chief cells, intestinal metaplasia
Autoimmune (Type A) Chronic Atrophic Gastritis: Signs/Symptoms/Findings
Rarest form, associated with pernicious anemia (B12 malabsorption)
Autoimmune (Type A) Chronic Atrophic Gastritis: Pathophysiology
Can result in gastrin cell tumors; mostly affect body / fundus
Autoimmune (Type A) Chronic Atrophic Gastritis: Treatment/Notes
H. pylori seen outside cells; Dx: urea breath test / stool test
H. Pylori (Type B) Chronic Atrophic Gastritis: Signs/Symptoms/Findings
children with multifocal gastritis, gastric ulcer, gastric cancer
H. Pylori (Type B) Chronic Atrophic Gastritis: Signs/Symptoms/Findings
adults with chronic gastritis, duodenal ulceers
H. Pylori (Type B) Chronic Atrophic Gastritis: Signs/Symptoms/Findings
H. pylori produces urease, leading to increased ammonia; can lead to gastric adenocarcinoma
H. Pylori (Type B) Chronic Atrophic Gastritis: Pathophysiology
Usually affects antrum / pylorus, but can be corpus (elderly) or pangastric
H. Pylori (Type B) Chronic Atrophic Gastritis: Treatment/Notes
Foveolar hyperplasia, mucosal edema and fibrosis, mild chronic inflammation
Reactive Gastritis (Type C): Epi/MOI AND Signs/Symptoms/Findings
aka Chemical; NSAIDs (decrease COX, decrease prostaglandins, low protection and platelet inhibition), reflux, EtOH
Reactive Gastritis (Type C): Pathophysiology
Rare, 25% hereditary
Zollinger Ellison Epi
Very thick mucosa, increased gastrin, acid, PUD
Zollinger-Ellison (Gastrinoma) Syndrome : Signs/Symptoms/Findings
Parietal and chief cells hyperplastic, hypersecreting, due to MEN1 (25%) or islet cell tumor
Zollinger-Ellison (Gastrinoma) Syndrome : Pathophysiology
Surgical resection, high dose PPIs. Only cure is surgery
Zollinger-Ellison (Gastrinoma) Syndrome : Treatment/Notes
Large hyperplastic folds, antrum-sparing
Menetrier’s Disease : Signs/Symptoms/Findings
Mucus cells hyperplastic
Menetrier’s Disease : Pathophysiology
Watermelon stomach in GAVE (gastric antral vascular ectasia)
Vascular Lesions: Signs/Symptoms/Findings
Gastric varices, gastric hypertensive gastropathy, or GAVE
Vascular Lesions: Pathophysiology
Usually a complication of portal HTN
Vascular Lesions: Treatment/Notes
Fundic most common
Gastric Polyps: Epi/MOI
Hyperplastic = oddly shaped, fundic = cystically dilated
Gastric Polyps: Signs/Symptoms/Findings
Hyperplastic, fundic gland, adenomatous, or fibroid polyps
Gastric Polyps: Pathophysiology
Adenomatous has malignancy potential
Gastric Polyps: Treatment/Notes
C-section, early or late gluten exposure
Celiac Disease (Gluten-Sensitive Enteropathy): Epi/MOI
Steatorrhea, malabsorption, weight loss; Biopsy: CD3+ IELs, Inflammation, villous atrophy (<4:1 V:C ratio) Labs: anti-tTG, EMA, and gliadin
Celiac Disease (Gluten-Sensitive Enteropathy): Signs/Symptoms/Findings
Gliadin gets activated by tTG, presented to APCs because of HLA DQ2/8, cross-reaction with small bowel tissue; can be comorbid with lymphocytic gastritis/colitis
Celiac Disease (Gluten-Sensitive Enteropathy): Pathophysiology
Response to gluten-free diet is both diagnostic and primary treatment; rule out other causes of villous atrophy
Celiac Disease (Gluten-Sensitive Enteropathy): Treatment/Notes
common (1% prevalence) only 17% dx in US, twins is 70%
Celiac
H. pylori protects, best tests are tTG IgA and DGP
Celiac
Diarrhea in <2 yo, growth issues at all ages
Pediatric Celiac Disease: Epi/MOI AND Signs/Symptoms/Findings
No diarrhea, IBS, incidental, decrease Fe anemia, dermatitis herpetiformis
Silent Celiac Disease: Signs/Symptoms/Findings
Non-diarrheal presentations of celiac disease; oral lesions is from interaction with tTG in skin
Silent Celiac Disease: Pathophysiology
Can also get enamel abnormalities (dental applications!)
Silent Celiac Disease: Treatment/Notes
Type I: CD8+, responds to immunosuppression; Type II: refractory to immunosuppression, malignancy risk (T-cell lymphoma)
Refractory Sprue: Epi/MOI AND Signs/Symptoms/Findings
Celiac that doesn’t respond to gluten-free diet; can be from noncompliance, wrong diagnosis
Refractory Sprue: Pathophysiology AND Treatment/Notes
Increased collagen in subepithelial area
Collagenous Sprue: Signs/Symptoms/Findings
Travel
Tropical Sprue: Epi/MOI
Vs. celiac: distal bowel affected more than proximal, macrocytic anemia from B12 malabsorption
Tropical Sprue: Signs/Symptoms/Findings
Post-infectious (e. coli, heterophilus) sprue that doesn’t respond to gluten-free diet
Tropical Sprue: Pathophysiology
Tx: doxycycline, B vitamins
Tropical Sprue: Treatment/Notes
Vs. celiac: other Crohn’s Sx AND No hematochezia, RLQ pain, aphthous ulcers Gross: skip areas, crypt malformation, giant cells, granulomas, pyloric metaplasia
Crohn’s Disease: Signs/Symptoms/Findings
Vs. celiac: gastric heterotopia (duodenum looks like stomach)
Peptic Duodenitis: Signs/Symptoms/Findings
H. pylori infection in duodenum, gastric metaplasia
Peptic Duodenitis: Pathophysiology
Vs. celiac: much more eosinophils
Eosinophilic Gastroenteritis: Signs/Symptoms/Findings
Mucosal dominant: most common, see diarrhea, bleeding; mural: abd pain, obstruction, N/V; serosal: eosinophilic ascites
Eosinophilic Gastroenteritis: Pathophysiology AND Treatment/Notes
Vs. celiac: anti-enterocyte/anti-goblet cell Abs
Autoimmune Enteritis: Signs/Symptoms/Findings
Can affect entire gut, see virtually no goblet or Paneth cells on biopsy
Autoimmune Enteritis: Pathophysiology
Vs. celiac: reduced plasma cells, chronic giardiasis
Common Variable Immunodeficiency: Signs/Symptoms/Findings
Hypogammaglobulinemia, B lymphocytes fail to mature
Common Variable Immunodeficiency: Pathophysiology
Responds to steroids (not curative)
Common Variable Immunodeficiency: Treatment/Notes
Vs. celiac: metaphase mitoses (colchicine), increased apoptosis (mycophenolate)
Drug-Related Enteritis: Signs/Symptoms/Findings
NSAIDs, mycophenolate, colchicine, chemo, radiation
Drug-Related Enteritis: Pathophysiology
Vs. celiac: histiocytes (Whipple’s), (+)acid fast (MAI), (+)silver (Histo), worms+cysts (strongy)
Infectious Enteritis: Epi/MOI AND Signs/Symptoms/Findings
Can be from adenovirus, CMV, calicivirus, Whipple’s disease, MAI, histoplasmosis, strongyloides, AIDS
Infectious Enteritis: Pathophysiology AND Treatment/Notes
Rule of 2s: 2% of people, 2ft from ileocecal valve, 2cm, 1/2 heterotopic mucosa (gastric or pancreatic)
Meckel’s Diverticulum: Epi/MOI AND Signs/Symptoms/Findings
True diverticulum from persistence of vitelline duct leads to an appendix-like lesion in terminal ileum
Meckel’s Diverticulum: Pathophysiology
Complications: inflammation, bleeding ulcer, obstruction
Meckel’s Diverticulum: Treatment/Notes
Intussusception (2nd to masses in adults), volvulus, herniation, adhesions
Intestinal Obstruction: Pathophysiology AND Treatment/Notes
reduced risk in smokers
Ulcerative Colitis
increased risk in smokers
Crohns
15-25, 50-65; M=F, Jews, FMHx, White>Black
Ulcerative Colitis: Epi/MOI
Bloody diarrhea, 6+ BMs/day, LLQ pain, anemia Gross: red friable mucosa, pseudopolyps Biopsy: flat ulcers, overhanging mucosa, crypt abscesses, Paneth metaplasia, crypt irregularity
Ulcerative Colitis: Signs/Symptoms/Findings
Environmental triggers (smoking, diet, NSAIDs, stress, etc.) + genetic predisposition + increased immune response (TNF- alpha , alpha 4beta7); complications include toxic megacolon, low-grade or high-grade dysplasia, carcinoma
Ulcerative Colitis: Pathophysiology
Tx: 5-ASA (mesalamine) formulation depending on location (e.g. Asacol or Lialda for ileocolitis), oral/IV steroids, infliximab (anti-TNF), 6-mercaptopurine / azathiprine, cyclosporins / tacrolimus, biologics
Ulcerative Colitis: Treatment/Notes
no blood in stool, RLQ pain, apthous ulcers, skip areas, cobblestoning Biopsy: fissures, transmural dz, pyloric metaplasia, non-caseating granulomas
Crohn’s
Smoldering disease with chronic inflammation of terminal ileum, ileum+colon, colon, or upper GI tract; complications: strictures, perianal fistulae, dysplasia, colon cancer (4-20x greater risk)
Crohn’s Disease: Pathophysiology
Tx: 5-ASA (mesalamine) formulation depending on location (e.g. Asacol or Lialda for ileocolitis), oral/IV steroids, infliximab (anti-TNF), 6-mercaptopurine / azathiprine, cyclosporins / tacrolimus, biologics
Crohn’s Disease: Treatment/Notes
Travel, c.diff
Infectious Colitis: Epi/MOI
(-) stool culture in 70%, PMNs in lamina propria, crypts intact
Infectious Colitis: Signs/Symptoms/Findings
Acute, self-limited
Infectious Colitis: Pathophysiology
Resolved by Abx
Infectious Colitis: Treatment/Notes
Volcano lesions, membranous white plaques, PMNs in lamina propria
Pseudomembranous Colitis: Epi/MOI AND Signs/Symptoms/Findings
C. diff overgrowth destroys epithelium
Pseudomembranous Colitis: Pathophysiology AND Treatment/Notes
> 70 yo, increased coag state
Ischemic Colitis: Epi/MOI
LLQ pain, hematochezia, urgency; crypt atrophy, fibrotic lamina propria
Ischemic Colitis: Signs/Symptoms/Findings
Slowly progressing, affects crypts (most O2 demand); can result in hemorrhage, ulcer, stricture, infarct
Ischemic Colitis: Pathophysiology
Middle age
Microscopic Colitis: Epi/MOI
Watery (secretory) diarrhea, grossly normal on colono/endoscopy
Microscopic Colitis: Signs/Symptoms/Findings
Lymphocytic or collagenous colitis, only microscopically inflamed
Microscopic Colitis: Pathophysiology
Not improved with fasting, osmotic gap 1L, maybe blood, happens in the night
Secretory Diarrhea: Signs/Symptoms/Findings
Iso-osmotic fluid secreted; caused by toxins, function hormone tumors, etc. (E.coli, cholera, inflammation)
Secretory Diarrhea: Pathophysiology
Tx: ORS, ribosylates Gsalpha
Cholera: Signs/Symptoms/Findings
Vibrio cholerae toxin increased Na+ export
Cholera: Pathophysiology
Resolves with fasting, watery, osmotic gap >50 mOsm/kg, <1L
Osmotic Diarrhea: Signs/Symptoms/Findings
sorbitol, fructose intolerance, sprue, celiac
Osmotic Diarrhea causes
Osmotically active substance in lumen; often lactase deficiency
Osmotic Diarrhea: Pathophysiology
Foul-smelling, floaters, multiple flushes, increased w/ fat ingestion
Fatty Diarrhea: Signs/Symptoms/Findings
Fat malabsorption
Fatty Diarrhea: Pathophysiology
make illness 1-2 days shorter, increase salmonella populations, make c. dif and ecoli worse
Abx in Diarrhea
Can result in nephrolithiasis (FAs out-compete oxalate for Ca+)
Short Bowel Syndrome: Signs/Symptoms/Findings
After resection, <200cm SB
Short Bowel Syndrome: Pathophysiology
Bloody, mucus, tenesmus
Inflammatory Diarrhea: Signs/Symptoms/Findings
Invasive infectious result in bloody, proteinaceous, exudative diarrhea with decrease serum protein + albumin
Inflammatory Diarrhea: Pathophysiology
AIDS
Cryptosporidiosis: Epi/MOI
Blue dots on Giemsa stain
Cryptosporidiosis: Signs/Symptoms/Findings
Invasive infectious result in bloody, proteinaceous, exudative diarrhea with decrease serum protein + albumin
Cryptosporidiosis: Pathophysiology
AIDS
CMV Colitis: Epi/MOI
Owl’s eye epithelial nucleus
CMV Colitis: Signs/Symptoms/Findings
Invasive infectious result in bloody, proteinaceous, exudative diarrhea with decrease serum protein + albumin
CMV Colitis: Pathophysiology
22%, F>M (3:1), >40yo
Irritable Bowel Syndrome: Epi/MOI
Abdominal pain (3d/mo for 3+ mos) relieved by defecation, change stool freq/form
Irritable Bowel Syndrome: Signs/Symptoms/Findings
increased Permeability leads to inflammation, activation of mast cells leads to ENS hyper-sensitivitylead to symptoms
Irritable Bowel Syndrome: Pathophysiology
IBS-D = diarrhea, IBS-C = constipation; 5HT and IL-10 both implicated; Tx: chart
Irritable Bowel Syndrome: Treatment/Notes
50% of >60, 2/3 of >80, more men than women only if 20-30
Diverticular Bleeding (Diverticulosis): Epi/MOI
Diverticulae common in L colon but bleeding often from R; bleeding sudden, often painless
Diverticular Bleeding (Diverticulosis): Signs/Symptoms/Findings
Low fiber dietlead to decrease stool volumelead to herniations of colonic mucosa through muscularis (pseudodiverticulae)
Diverticular Bleeding (Diverticulosis): Pathophysiology
NSAIDs or aspirin worsens risk; Tx: resuscitation, vasopressin, embolization
Diverticular Bleeding (Diverticulosis): Treatment/Notes
> 50%
Hemorrhoidal Bleeding: Epi/MOI
Scant hematochezia; most common cause of LGIB
Hemorrhoidal Bleeding: Signs/Symptoms/Findings
Tx:increased fiber, topical anti-inflammatory, ligation, etc.
Hemorrhoidal Bleeding: Pathophysiology AND Treatment/Notes
Lifetime 7%, usually young adults
Appendicitis: Epi/MOI
Periumbilicallead to RLQ pain, nausea, Rovsing’s sign, fever, increased WBC; abd CT most diagnostic
Appendicitis: Signs/Symptoms/Findings
Obstruction of appendiceal lumenlead to polymicrobial (e. coli, b. fragilis, etc.) bacterial overgrowth, inflammation
Appendicitis: Pathophysiology
Tx: appendectomy, earlier surgery = better prognosis, Abx prophylaxis
Appendicitis: Treatment/Notes
Self-limited and mild in some cases
Clostridium Difficile: Epi/MOI
Fever, diarrhea, toxicity, increased WBC, pain; Dx: tissue culture assay for cytotoxin
Clostridium Difficile: Signs/Symptoms/Findings
Antibiotics, esp. clindamycin; complications include toxic megacolon, colonic perforation
Clostridium Difficile: Pathophysiology
Tx: d/c antibiotic if possible, oral ABx or IV metronidazole (+rifampin if relapse)
Clostridium Difficile: Treatment/Notes
10% of diverticuli pts
Diverticulitis Epi
LLQ pain, change in bowel habits, fever, increased WBC, bladder fistula, peritonitis, CT with IV contrast
Diverticulitis: Signs/Symptoms/Findings
Gm- infect diverticulum (sigmoid) after fecalith impacts;lead to perforations; occurs in 10-25% of diverticulosis, mostly sigmoid
Diverticulitis: Pathophysiology
Tx: metronidazole + other Abx, colonoscopy 4-6wk later, surg after 3rd episode
Diverticulitis: Treatment/Notes
Abx that cover enterobacter, bacteroids, (less: pseudomonas and enterococci), 4-6 weeks, follow up with colonoscopy
Diverticulitis
relapse rate 10-30%
diverticulitis
M>F 3:1
Sigmoid Volvulus: Epi/MOI
Distended abd, plain films
Sigmoid Volvulus: Signs/Symptoms/Findings
Lengthened sigmoid gets twisted
Sigmoid Volvulus: Pathophysiology
Tx: Non-op decompression + surgery, resection if relapse
Sigmoid Volvulus: Treatment/Notes
bird’s peak deformity
Sigmoid Volvulus
3rd world, high plant fiber diet
Sigmoid Volvulus
Obstipation, abd pain, distention
Large Bowel Obstruction: Signs/Symptoms/Findings
Any mechanic obstruction
Large Bowel Obstruction: Pathophysiology
Tx: surgery, enteral stents
Large Bowel Obstruction: Treatment/Notes
decrease BS or high-pitched; abd pain; Dx: barium enema
Ileus: Signs/Symptoms/Findings
Failure of peristalsis
Ileus: Pathophysiology
Tx: neostigmine, supportive
Ileus: Treatment/Notes