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368 Cards in this Set

  • Front
  • Back
define odynophagia
painful swallowing
causes of esophageal chest pain
GER, dysmotility, increased visceral sensitivity
define dysphagia
difficulty swallowing, food sticking
what causes oropharyngeal dysphagia?
inability to protect nasopharynx or larynx during swallowing
what are symptoms of OP?
nasal regurgitation, coughing, aspiration
liquids or solids cuasing more problems in OP?
OP most commonly associated with which types of conditions?
cerebral or brainstem conditions (swallowing center), probs with striated muscle, imparment of UES opening
dysphagia for liquids alone suggests:
dysphagia for solids alone suggests:
structural abnormality
dysphagia for solids and liquids suggests:
motility disorder
long history of intermittent dysphagia for solids suggests:
structural abnormality
worsening of solid food dysphagia suggests:
progressive narrowing due to stricture
significant weight loss in dysphagic patients over 50 suggests:
esophageal adenocarcinoma
significant weight loss in dysphagic childred suggests:
combination of chest pain and dysphagia suggests:
diffuse esophageal spasm
raynaud's phenomenon and dysphagia suggests:
confirm esophageal motility disorder with
define reflux esophagitis
macroscopic damage to the esophagus visible at endoscopy as erosions or ulcerations
causes of GERD
abnormal LES (hypotonic LES, transient LES relaxations), hiatal hernia, defect in esophageal clearance mechanisms
atypical reflux symptoms
asthma, laryngitis, chronic cough, chest pain
Diagnostic tests for GERD
upper endoscopy, ambulatory pH monitoring
complications from GERD
stricture, Barrett's, ulcer
where do strictures tend to occur?
distal esophagus (greatest acid concentration)
what is barrett's esophagus?
when metaplastic columnar epithelium replaces normal squamous epithelium in distal esophagus
what does barrett's look like?
orange-red epithelium (vs. white/yellow for nl)
How do you confirm a dx of Barrett's?
mucus biopsies
What type of monitoring should you do for patients with Barrett's?
endoscopy/biopsy every 3 years
What to do if patient is unresponsive to GERD medical treatment?
laproscopic gastric fundoplication
List structural lesions of the esophagus
esophageal cancer, strictures, webs/rings, zenker's diverticulum
difference between a web and a ring?
ring is circumferential ring at squamocolumnar junction, web is semilunar and in mid to upper esophagus
what is a Zenker's diverticulum?
protrusion of the pharyngeal mucosa at pharyngoesophageal jxn through UES
how do you treat Zenkers Diverticulum?
surgical resection
Causes of esophagitis not due to GER (3)
pill induced, caustic injury, infectious esophagitis (in immcomp: candida, HSV, CMV)
List esophageal motility disorders (3)
Achalasia, Diffuse Esophageal Spasm, scleroderma esophagus
Pathophysio of Achalasia
denervation of esophagus from loss of ganglion cells in Auerbach's plexus, lose peristalsis in smooth muscle and impaired LES relaxation
Clinical findings in achalasia?
gradual onset of dysphagia for solid and liquid, regurgitation and vomiting
typical radiographic hallmark of Achalasia?
bird's beak
what is pseudo-achalasia?
a cancer that might resemble achalasia
clinical findings in Diffuse Esophageal Spasm?
intermittent, non-progressive dysphagia for solids and liquids, chest pain
pathophysio of scleroderma esophagus
atrophy and fibrosis of esophageal smooth muscle, hypotonic LES, severe reflux
Esophageal location of esophageal squamous cell carcinoma
throughout esophagus
esophageal location of esophageal adenocarcinoma
lower 1/3 of esophagus
symptoms of esophageal carcinoma
progressive solid food dysphagia, hoarseness, weight loss
list 5 causes of Dyspepsia
PUD, GERD, gastric cancer, non-ulcer dyspepsia, meds
what types of meds cause dyspepsia?
alcohol, caffeine, iron, NSAIDS, antibiotics
which symptoms suggest peptic ulcers?
pain between meals or at night and releived by food or antacids
four sources of afferent input into vomiting center
Vagal/splanchnic from GI (visceral distention, peritonitis), vestibular system, higher CNS, CTZ
where is the CTZ?
fourth ventricle
what stimulates the CTZ?
drugs, chemotherapeutics, toxins
some CNS related causes of vomiting
Increased ICP, Vestibular disorders, infections (encephalitis, meningitis)
Define gastroparesis
decreased gastric motility
define Ileus
decreased intestinal motility
causes of peritoneal irritation (4)
cholecystitis, acute pancreatitis, appendicitis, perforations
what is the common cause of acute vomiting without abdominal pain?
food poisoning, infectious gastroenteritis, drugs
acute onset of vomiting with severe pain suggests:
intestinal obstruction or peritonitis
chronic or recurrent vomiting suggests
obstruction of pylorus or small intestine, gastroparesis, or CNS and systemic disorders
define hematemesis
bright red emesis
define melena
jet black tarry fould smelling stool
define hematochezia
bright red bloody bowel movements
list 4 causes of UGI bleeding
PUD, portal hypertension, gastric neoplasms, and erosive gastritis, Mallory Weiss tears
Is initial hematocrit a good indicator of acute blood loss?
not really, takes 24-72 hrs for equilibration
how much does one unit of blood raise hct?
define erosions
single or multiple, small (<3mm) white linear breaks that don’t extend through the muscularis mucosa
define ulcers
mucosal breaks with obvous depth, white base, larger in size
most common sites of ulcers
duodenal bulb and gastric antrum
Causes of PUD
Hp, NSAIDs, Gastrinoma
How does Hp protect itself?
burrows into mucus layer by epithelial cells (pH 7) and uses urease to generate ammonia
how does Hp cause disease?
suppression of somatostatin
Mechanisms of NSAID induced injury
topical damage, PG inhibition thus loss of mucosal defense mechanisms, platelet inhibition so easier to bleed
clinical findings in peptic ulcer disease
complications from PUD
penetration or perforation, extensive bleeding, edema/scarring leading to obstruction
Who gets stress gastritis?
ICU patients: severe burns/trauma/sepsis etc
Causes of gastroparesis (3)
neuropathic (enteric or extrinsic nerves), myopathic process (involving gastric smooth muscle), post-surgical probs (vagotomy, gastric resection)
symptoms of gastroparesis
nausea, vomiting, early satiety, bloating
when does vomiting occur with gastroparesis?
after a meal
definition of constipation
two or less bowel movements per week or excessive difficulty or straining on defacation
which pelvic floor muscles are responsible for continence?
pubococcygeus and puborectalis
common causes of constipation
poor dietary (to little fiber/fluids) or toilet habits, structural abnormalities (malignancy), systemic disease (myopathy, neuropathy, endocrine disorder, lyte imbalance, medication use)
first line treatment for constipation?
dietary fiber supplement
constipation lab tests available?
colonic transit study, defecography, anal manemtry
Major causes of lower GI bleeding (6)
diverticulosis, vascular ectasias, neoplasms, IBD, ischemic colitis, anorectal disease
describe lesions from Vascular Ectasias
small, multiple, painless, red flat submucosal blotch of vessels, looks like a fern
first thing to do w/ patient with acute GI bleed?
assess volume status and rescucitate if necessary
which acute GI bleed patients get colonoscopy?
anyone who is hospitalized due to bleeding
evaluation tests for acute GI bleed?
anoscopy, sigmoidoscopy, colonoscopy, angiography, nuclear bleeding scan (99Tc RBC scan)
what is damaged in Celiac Sprue?
diffuse damage to proximal small intestinal mucosa = malabsorption
which genes are associated with celiac sprue?
describe celiac sprue pathogenesis:
gluten sensitive T cells respond, Th1 reaction leading to inflammation and damage of intestinal mucosa
what 3 nutrients are absorbed in the proximal small intestine?
calcium, iron, folate
impaired calcium absorption leads to:
impaired iron absorption leads to:
iron deficiency anemia
impaired folate absorption leads to:
megaloblastic anemia
Sprue in jejunum and ileum leads to:
carb malabsorption: flatulence, steatorrhea, weight loss, cramps
clinical features of sprue in infancy:
failure to thrive, anorexia, irritability, abd pain, hypotnia, muscle wasting, abd distension, soft malodorous stool
clinical presentation of sprue in older children:
growth retardation, amenorrhea, rickets, osteoporosis, anemia
how to confirm diagnosis of sprue?
IgG and IgA against gliadin, foolow up + test with anti-tTG (tissue transglutaminase), if +, then sprue, confirm with bx
what disorder is associated with sprue?
dermatitis herpetiformis (pruritic papulovesicles over extremities and trunk), some px develop t-cell small bowel lymphoma (fatal)
treatment of sprue?
gluten free diet, celiac support group
3 main small bowel disorders
sprue, bacterial overgrowth, short bowel syndrome
causes of bacterial overgrowth (5)
gastric achlorydia, anatomic abnormalities leading to stasis, motility disorder that slows transit, fistula b/w colon and sm intestine, misc (elderly, AIDS)
how does bacterial overgrowth lead dz?
bacteria deconjugate bile acids --> less micelle formation, direct damage to brush border, take up B12
resection of terminal ileum results in:
malabsorption of bile salts and B12
how much small bowel resection do you need to cause steatorrhea?
>100cm of ileum resected --> bile salts arent taken up, steatorrhea, malabsorption of fat soluble vitamins
four major bowel disorders
diverticulosis, polyps, neoplasms, appendicitis
what are colonic diverticula?
mucosal protrusions that go through the muscular wall
what causes diverticula?
low fiber diet, high bowel intraluminal pressure lead to muscular hypertrophy, vasa recta penetrate to nourish, weaken wall, and pseudo-diverticula form
which region of colon most involved in diverticula?
sigmoid: muscular contractions increase distally
does rectum get diverticula?
no, no tenia coli
complications of diverticula?
pain 2ndary to muscle spasm, perforation (diverticulosis), diverticular bleeding
describe diverticular bleeding?
abrupt onset, brisk output, red color, causes hemodynamic instability, 80% need transfusion
two types of colon polyps
adenomatous and non-adenomatous (hyperplastic, juvenile, hamartomas, inflammatory)
describe hyperplastic polyps
common, small (usu <5mm), in rectosigmoid region, elongated crypts w/ papillary fronds w/ lots of epithelial cells, not malignant
three types of adenomatous polyps
tubular adenomas (lowest risk), tubluvillous adenomas, villous adenomas (highest risk)
underlying pathophys of appendicitis?
obstruction of tiny appendiceal lumen (fecalith, inflammation, tumor, muscle hypertrophy)
presentation of appendicitis?
abd pain, cramps, vomiting, nausea, sense of constipation, RLQ pain, mild fever, leukocytosis
4 bowel motility disorders
acute intestinal obstruction, acute small bowel ileus, acute colonic pseudo obstruction ("colonic ileus"), IBS
who gets ileus?
commonly seen in hospitalized patients
when does IBS present?
early in life (first 2 decades)
IBS clinical presentation:
chronic lower abd pain, crampy, intermittent, not at night, worse 1-2h after meals, relieved by defacation
two causes of acute bowel ischemia
thrombotic SMA occlusion in px w/ atherosclerosis, embolic event in px w/ afib or LV thrombus
pathophys of ischemic colitis?
transient episodes of low blood flow, esp in watershed areas fed by both SMA/IMA
SMA-IMA watershed areas?
splenic flexure and distal sigmoid colon
clinical presentation of acute bowel ischemia?
bowel infarction, fever, tachy, hypoT, abd tenderness w/ guarding, leukocytosis, metabolic acidosis
clinical presentation of ischemic colitis?
usu elderly, mild LLQ cramps, tenesmus, blood in stool
diff b/w internal and external hemorrhoids?
internal: painless bleeding; external: no bleeding, but can get thromboses w/ pain/tenderness
define diarrhea
>2 loose stools/day or increased liquidity
define non-inflammatory diarrhea
leads to increased fecal fluid but does not disrupt the intestinal epithelium, characterized by watery, non-bloody and absence of fecal leukocytes
define inflammatory diarrhea
caused by infections, agents, or events which disrupt intestinal mucosa, most infectious causes usu affect colon so volume is less, frequent smaller volume bowel movements and lower abd cramps, dysentery, + fecal leukocytes
causes of acute diarrhea
infectious agents, bacterial toxins, medications, ingestion of non-absorbable osmotically active substances
how to distinguish inflammatory from non-inflammatory diarrhea?
presence of fecal leukocytes
signs of dehydration:
dry mouth, decreased urination, weakness, lethargy, dry mucus membranes
signs of severe inflammatory diarrhea
fever >38.5, dysentery >8x/day, severe abd pain/tenderness, elderly, imunocompromised
Oral rehydration solution:
3.5g NaCl, 2.5g NaHCO3, 1.5g KCl, 20g Glucose in 1L of water
homemade oral rehydration solution
1/2 tsp salt, 1 tsp baking soda, 8 tsp sugar, 8 oz OJ, in 1L water
six physological categories of diarrheas:
osmotic, secretory, inflammatory, motility, chronic infection, malabsorption
how big of an osmotic gap for osmotic diarrhea?
>50 mosm/Kg
when does osmotic diarrhea resolve?
when patients are fasting, because no longer ingesting osmotically active substance
common causes of osmotic diarrhea?
carb malabsorption (lactose, sorbitol), inorganic ion digestion (laxatives)
cause of fictitious diarrhea?
laxative abuse: consider in young women w/ eating disorder, px with psychiatric problems
pathophys of secretory diarrhea
increased intestinal secretion of lytes and water or decreased absorption, has normal osmotic gap
does secretory diarrhea resolve with fasting?
no, not due to an osmotically active substance
causes of secretory diarrhea
certain laxatives, endocrine tumors (VIPoma, calcitonin tumor), malabsorption of bile acids
causes of inflammatory diarrheas:
UC, Crohn's, infections
motility disorders causing diarrhea
rapid intestinal transit (irritable bowel syndrome), stasis leading to bacterial overgrowth (vagotomy, anatomic abnormalities)
causes of diarrhea due to malabsorption
impaired intraluminal digestion (pancreatic insufficiency, bile salt deficiency, gastrectomy), inadequate epithelial absorption (reduced surface area, small intestinal mucosal disorders), defective absorption via lymphatics
causes of pancreatic insufficiency
chronic pancreatitis, cystic fibrosis, surgical removal
causes of bile salt depletion:
bacterial overgrowth (bile salt deconjugation), disease or removal of terminal ileum, chronic liver disease, bile duct obstruction
causes of poor intestinal epithelial absorption
reduced surface area (resection), mucosal disorders (celiac sprue, tropical sprue, whipple's disease, crohn's disease)
malabsorbed nutrient in: megaloblastic anemia
malabsorbed nutrient in: tetany, paresthesias
calcium, vitamin D
malabsorbed nutrient in: night blindness
vitamin A
uncomplicated diarrhea resolves with fasting suggests:
osmotic process
profuse water diarrhea with dehydration suggests:
secretory diarrhea
dysentery suggests:
inflammatory diarrhea
voluminous gas suggests:
carb malabsorption
useful stool analysis tests (6)
fecal fat, fecal weight, stool osm and lytes, fecal leukocytes, lax screen, screen for ova/parasites
What does fecal fat quantity tell you?
>10g is significant, >20g suggest pancreatic insufficiency
describe d-xylose test
d-xylose is pentose sugar, passively absorbed across from lumen if normal intestinal mucosa and thus abnormality from pancreatic insufficiency
how to test for bacterial overgrowth in small bowel
aspirate small bowel fluid for culture, breath hydrogen analysis after oral carb administration
What does schilling test do?
tests if B12 deficiency due to pernicious anemia, terminal ileum disease, or bacterial overgrowth
Two types of gallstones
cholesterol stones and pigmented stones (calcium salts of bilirubin, carbonate, phosphate, palmitate)
three stages of cholesterol stone formation
formation of saturated bile, nucleation, growth of stone
two types of nucleation
homogenous and heterogenous
what is homogenous stone nucleation?
coalescence of cholesterol moolecules to precipitate
what is heterogenous stone nucleation?
some particle other than that of pure cholesterol acts as the nidus of nucleation
conditions associated with stone formation?
obesity, diet (high calorie, fasting), increased serum triglyceride, decreased serum HDL, clofibrate, cholestyramine, malabsorptive disorders, estrogen, pregnancy, Pima Indian
how does clofibrate predispose to stones?
raises cholesterol saturation of bile
how does cholestyramine predispose to gallstones?
prevents reabsorption of bile acids
list gallstone related diseases (5)
asymptomatic gallstones, symptomatic cholelithiasis and chronic cholecystitis, acute calculous cholecystitis, choledocholithiasis, bacterial cholangitis
most common presentation of gallstone disease?
biliary colic, caused by transient gallstone obstruction of biliary tract
describe biliary colic pain
abrupt onset, gradually subsides, minutes to hours, RUQ and epigastrium, w/ nausea/vomiting
cause of cholecystitis
repeated minor episodes of cystic duct obstruction, leads to chronic inflammation and scarring
chronic cholecystitis predisposes to:
gallbladder adenocarcinoma
most sensitive test for gallstones?
treatment of cholelithiasis and cholecystitis?
what is acute calculous cholecystitis?
gallstone impacts and obstructs cystic duct
causes of gallbladder inflammation on acute calculous cholecystitis
release of phospholipase from gallbladder mucosal cells and its conversion to toxic substances
signs and symptoms of acute calculous cholecystitis?
RUQ pain, tender, fever, leukocytosis, murphy's sign
what is murphy's sign?
instruct patient to breath deeply during palpation in right subcostal area, sudden increase in pain and sudden termination of inspiration
complications of acute cholecystitis?
gallbladder empyema, sepsis, perforation
diagnosis of acute cholecystitis
US shows thickened wall, fluid surrounding wall
treatment of cholecystitis
IV hydration, IV abx, cholecystectomy
what is choledocholithiasis?
stones IN the bile duct
signs and symptoms of choledocholithiasis?
same as acute calculous cholecystitis
diagnosis of choledocholithiasis?
US shows dilated bile ducts, endoscopic ultrasound, cholangiography
treatment of choledocholithasis?
must be removed, even if asymptomatic
what is charcot's triad?
biliary colic, juandice, fever
symptoms of bacterial cholangitis
charcot's triad
treatment of bacterial cholangitis?
IV abx
who gets acalculous cholecystits?
patients hospitalized with serious illness
what is Primary sclerosing cholangitis?
idiopathic inflammaotry and fibrosing dz of biliary tree, immune mediated, progressive, cirrhosis and death
symptoms of PSC
often asyx, eventual elevation of alkaline phosphatase, pruritus, juandice, RUQ pain
Dx of PSC?
Sphincter of Oddi Dysfunction and Papillary Stenosis causes?
biliary type pain
causes of acute pancreatitis
alcohol and gallstones most common, then drug induced and idiopathic
presentation of pancreatitis
begins abruptly, often after meal, severe epigastric pain, nausea, vomiting, more severe when supine, tachy, dehydration, leukocytosis, hemoconcentration
diagnosis of acute pancreatitis
elevated serum amylase, elevated serum pancreatic lipase, US and CT
serum amylase and gallstone or alcohol causes of acute pancreatitis?
in EtOH related, elevation persists for days and slowly drops, in gallstone related, amylase falls abruptly w/in 24-48 hrs
systemic complications of acute pancreatitis?
vascular instability, shock, DIC, renal insufficiency
local complications of acute pancreatitis?
pancreatic hemorrhage, hemosuccus pancreaticus, acute pancreatic fluid collections, pancreatic pseudocyst, necrosis
risk assessment of acute pancreatitis?
use Ranson's Criteria, the more criteria fulfilled, the worst outcome
treatment of acute pancreatitis?
supportive, limit systemic complications, prevent necrosis, prevent infection, lots of fluid resuscitation
leading cause of chronic pancreatitis?
alcohol, NOT gallstones
how does chronic pancreatitis manifest?
abd pain, impaired pancreatic excretions, chronic inflammation, fibrosis, atrophy, calicifications
complications of chronic pancreatitis
pancreatic pseudocyst, ascites, splenic vein thrombosis, biliary stricture
how to treat pancreatis pseudocyst?
surgical drainage
how to diagnose chronic pancreatitis?
fecal fat, CT, ERCP
treatment of chronic pancreatitis?
sx management
predisposing factors to pancreatic cancer?
cigs, EtOH, gallstones, animal rich diet, DM, chronic pancreatitis
sx of pancreatic cancer?
compression and invasion of adjacent structures, pruritus, enlarged liver
List 4 inflammatory bowel diseases
UC, Crohn's, microscopic colitis, collagenous colitis
central pathophys in IBD?
immune dysregulation, too much Th1, not enough Th2/3
CD genetic predisposition gene?
what does NOD2 do?
activated NFkB in response to bacterial LPS, key in innate response to gut bacteria
typical initial lesion in Crohn's?
Apthous ulcer of mucosa (small shallow ulceration, white base)
Pathology of Crohn's
extending through all layers of intestinal wall, skip lesions, ulcers enlarge and deepen to form linear ulcerations, cobblestone appearance, perfs and abscesses, stricture and granulomas
List the three patterns of Crohn's
Inflammatory, Perforating, Fibrostenotic
highlight of inflammatory crohn's?
mucosal inflammation with erosion and ulceration predominating
highlight of perforating CD?
transmural inflammation, perf of bowel, formation of fistula and contained abscesses
sx of CD?
constitutional (fever, fatigue, weight loss), Diarrhea (multifactorial origin), abd pain, malnutrition, mild leukocytosis, anemia, fistula
rectal exam in CD reveals?
often, fistual-in-ano and anal fissures
Imaging studies for CD?
barium enema, CT, Colonoscopy
DDx of CD?
acute appendicitis, intestinal TB, fungal infxn, malignancy, vasculitis of intestinal vessels, UC
what is UC?
chronic inflammatory dz of colonic mucosa
do you get transmural inflammation in UC?
No, only in CD
UC progression?
from mild edema to ulcerations, fibrosis of colon, pseudopolyps (regenerating mucosa), crypts get messed up
Crypt damage in UC
crypt abscesses, distortion of crypts with shortening and branching
UC distribution
continuous, begins in columnar mucosa of anorecal junction, works proximally, no rectal sparing
what do you call UC if limited to rectum?
ulcerative proctitis
what do you call UC if limited to sigmoid?
limited UC
what do you call UC if extends throughout colon?
clinical presentation of UC
bloody diarrhea, tenesmus, cramps, fever, weight loss
dx of UC?
DDx of UC?
infectious colitis, acute (shig, salm, campy, ecoli), radiation induced colitis, ischemic colitis
treatment of UC
surgical resection, but use Crohn's drugs too
extra-intestinal manifestations of IBD
joints, skin, eyes, liver
joint manifestations of IBD
peripheral arthritis, ankylosing spondylitis, sacroileitis
skin manifestations of IBD
erythema nodosum, pyoderma gangrenosum
ocular manifestations of IBD
conjuctivitis, scleritis, uveitis
liver manifestations of IBD
patients younger than 30 likely to have (liver dz)?
parenchymal disease
patients older than 65 likely to have (liver dz)
gallstones and malignancies
patients between 30-50 likely to have (liver dz)
chronic liver disease
children and young adults likely to have (liver dz)
viral hepatitis
at what bilirubin level is juandice apparent?
> 3 mg/mL
stigmata of chronic liver disease
cachexia, muscle wasting, spider nevi, palmer erythema, dupuytren's contracture, leuconychia, parotid enlargement, skin pigmentation, gynecomastia, loss of secondary sexual hair
small nodular liver suggests:
large nodular liver suggests:
ascites in presence of juandice suggests:
aspartate aminotransferase, from cytosol and mito and found in liver and lots of other cells
define ALT/SGPT
alanine aminotransferase, from cytosol only and only in liver
what to AST/ALT signify?
liver cell injury, ALT more specific than AST
define AP
widely distributed enzyme, usu from liver/bone
what does elevated liver AP signify?
increased synthesis due to obstruction of bile flow
AST/ALT levels above 1000 signifiy?
severe acute hepatitis, drug associated injury, or prolonged hypoT
define cholestasis
physiological and clinical manifestations result from impaired bile flow
What is the most sensitive marker of cholestasis?
elevated AP
predominant hepatocellular injury signified by which lab results?
elevated AST/ALT relative to AP and elevated bilirubin relative to AST/ALT
what type of bilirubin is elevated in cholestasis?
causes of unconjugated bilirubinemia
overproduction of BR due to hemolysis or ineffective erythropoiesis, inheretied (UGT-1A1)
what is Gilbert's Syndrome?
UGT activity reduced to 25%, unconjugated Bremia
what is UGT?
uridine diphosphate glucuronosyltransferase
how to diagnose Gilbert's Syndrome?
elevated unconjugated BR in absence of overt hemolysis in an otherwise healthy person
treatment of Gilbert's Syndrome?
what is Crigler Najjar Syndrome?
rare, severe UGT deficiency, results in brain injury from high unconjugated BR levels
Causes of conjugated bilirubinemia?
Rotor Syndrome, Dubin-Johnson Syndrome
total bilirubin levels in Rotor syndrome
2 to 5
pathophys of dubin-johnson syndrome
impaired ATP mediated transport of bilirubin diglucuronide
liver histology of dubin-johnson?
black liver!
how to determine between clotting factor sythesis disorder or vit K deficiency?
give Vitamin K to see if they improve
which hepatitis viruses can cause acute hepatits?
which hepatitis viruses cause chronic hepatitis?
non hepatitis viruses that can cause hepatits?
CMV, EBV, HSV, leptospirosis
whats the most common cause of end stage liver disease?
Alcoholic Liver Disease
list the various types of ALD
Alcoholic Steatosis, Alcoholic Hepatitis, Alcoholic Cirrhosis
histological manifestation of alcoholic steatosis?
hepatocytes containing large vesicles filled with triglyceride
is alcoholic steatosis reversible?
histological manifestation of alcoholic hepatitis?
lobular predominant polys, Mallory Bodies, steatosis, bile duct proliferationpericellular fibrosis
clinical features of alcoholic hepatitis?
fever, RUQ pain, juandice, high WBC, increased PT, AST > ALT (2:1), increased uric acid, increased lactase
how to determine prognosis in alcoholic hepatitis?
MDF: maddrey determinant function
how much alcohol intake for alcoholic cirrhosis to develop?
30-60g/d for 15-20 years
mechanisms of alcohol injury?
EtOH induces CYP2E1: increases ROS, stims lipogenesis so increased serum free fatty acids, decreased VLDL, steatosis, lipid peroxidation, inflammation, cytokines
histological characterization of NAFL
soley hepatocytes containing large fat vesicles
histological characterization of NASH
macrovesicular steatosis with added liver cell necrosis and inflammation
when is NAFLD suspected?
elevated liver enzymes (ALT>AST)
how to confirm diagnosis of NAFLD?
what hints at likelihood of disease progression in NAFLD?
hepatocyte necrosis and fibrosis
metabolic hallmark of NAFLD?
hepatic insulin resistance
what mediates hepatic insulin resistance in NAFLD?
altered hepatocyte insulin signaling
what are the "Two Hits" in NAFLD?
shift in fatty acid metabolism to net lipogenesis from lipolysis and oxidant stress and cytokine injury leading to fibrosis
how to treat NASH?
List the AutoImmune Hepatitises
autoimmune hepatitis, PBB, PSC
describe Autoimmune Hepatitis?
chronic inflammatory dz, gradual progression to cirrhosis
which gender gets AIH more often?
what are the charateristics of AIH?
serum autoantibodies, hyperglobulinemia, periportan hepatitis
clinical findings in AIH?
from nothing to fatigue, anorexia, nausea, abd pain, cirrhosis, acute liver failure, acne, amenorrhea
extrahepatic manifestations of AIH?
arthralgias, hemolytic anemia, TPP, DM, thyroiditis, UC
Type 1 AIH characterized by?
ANA and ASMA (anti smooth muscle antibodies), responds to corticosteroids
Type 2 AIH characterized by?
antibodies to liver/kidney microsomes (LKM)
Type 3 AIH characterized by?
antibodies to soluble liver antigen (SLA)
histopathological features of AIH?
portal mononuclear and plasma cell infiltrate into hepatic parenchyma, normal bile ducts
age peaks when AIH occurs?
under 30 and 50-60
how to treat AIH?
what is PBC?
chronic, non-suppurative cholangitis characterized by injury to duct
histo features of PBC?
lymphoid aggregates, epithelial injury
which gene predisposes to PBC?
Which gender gets PBC more?
95% women
lab results with PBC?
increased AP, + anti-mitochondial antibody, increased IgM, hypercholesterolemia
treatment of PBC?
symptomatic and supportive and ursodeoxycholic acid, finally transplant
histo features of PSC?
progressive fibrosing inflammation, disappearance of intra and extrahepatic bile ducts
chilnical picture of PSC?
intermittent cholangitis, labs reflect cholestasis
how to diagnose PSC?
visualize biliary tree w/ cholangiography
treatment of PSC?
endoscopic therapy to maintain patency, early liver transplant preferred
mechanisms of drug related liver toxicity
metabolized to more toxic product, ROS generation, Cyt450 induction
how much acetominophen ingested for toxicity?
over 10g
mechs of NAPQI toxicity?
conjugated to GSH decreasing GSH availability, react with protein sulfhydryls, interfere with cellular Ca2+ transport/balance, Redox cylcing generating ROS
chronology of acetominophen toxicity
24-48 hrs: nausea/vomiting, liver disease after 72h
how to treat acetominophen tox?
N-acetylcysteine given immediately, eventual liver transplant
whats Hereditay Hemochromatosis?
defect/dysregulation in Divalent Metal Transporter, too much Fe uptake from intestine
mutations in which gene lead to HH?
pathophys of HH?
HFE mutation = inability of intestinal crypt cells to sense systemic iron stores through interaction with transferrin, overexpresses DMT
manifestations of HH?
chronic liver disease, endocrine dysfunction, heart failure, arthritis
treatment of HH?
Fe depletion through repeated phlebotomy
what is wilson's dz?
hereditary disorder of cellular copper export, leading to marked decrease in billiary copper excretion
clinical presentation of Wilson's
AST/ALT elevation, chronic hepatitis, hepatic steatosis, cirrhosis, acute liver failure
where does copper accumulate in wilsons?
liver, kidney, basal ganglia, corneas
what are kayser-fleisher rings?
green rings at periphery of cornea in px with Wilson's Dz
how to diagnose Wilson's Disease?
low serum ceruloplasmin, increased renal excretion during 24h collection, elevated liver tissue [Cu]
how to treat Wilson's?
low copper diet, chelators, transplant
what is Alpha-1-Antitrypsin deficiency?
inherited deficiency, disease in lungs and liver
whats A1AT?
protease inhibitor synthesized in hepatocytes, acts in lungs to protect from proteases released from neutrophils
how does A1AT cause disease in liver?
accumulated unsecreted abnormal protein, manifest as intracellular globules
main causes of acute liver failure?
acetominophen, drug rxns, Hep A/B
List 5 liver diseases common in pregnancy
Hyperemesis Gravidarum, intrahepatic cholestasis of pregnancy, AFLP, Pre-eclampsia, HELLP
what is hyperemesis gravidarum?
intractable nausea/vomiting in first trimester
whats ICP?
intrahepatic cholestasis of pregrancy
hallmark of ICP?
intense pruritus, usually in third trimester
what suggests ICP?
increased total serum bile acids (up to 100x) w/ pruritus
what is pre-eclampsia?
multisystem disorder associated with proteinuria, HTN, peripheral edema, hyperreflexia, massive aminostransferase increase
what is HELLP?
hemolysis, elevated liver enzymes, low platelet count
cirrhosis results from what pathophys change?
fibrous associated structural changes in intrahepatic sinusoidal channels ana altered vasomotor tone
results of portal hypertension?
variceal hemorrhage, ascites, hepatic encephalopathy, prominent abd cuteaneous veins, splenomegaly
lab manifestation of splenomegaly?
how to measure portal blood pressure
directly during surgery, percutaneously, or with balloon wedge pressure
what is portal hypertensive gastropathy?
pressure related increase in gastric mucosal blood flow and vessel caliber, causes bleeding
how high of a portal blood pressure is required for esophagela vericeal rupture?
> 12mm Hg
endoscopic signs of varices
red wale sign and cherry red spot
management of variceal bleeding
hospital, large bore IV, fluid rescucistion, ocreotide to lower pressure, band ligation, variceal ligation, TIPS
define ascites
presence of free fluid in the periotneal cavity
mechanism of ascites?
change in hepatic structure, sequestration of larger than normal fraction of blood, decreased peripheral arterial resistance, increased renal retention of Na/H2O
what is hepatic hydrothorax?
when ascited fluid gains access to thoracic cavity
how to evaluate ascites?
paracentesis, Serum-Ascites Albumin Gradien (SAAG), send for culture/white count
management of cirrhotic ascites?
restrict dietary sodium, use diuretic, large volume paracentesis, TIPS
pathophys of Spontaneous Bacterial Peritonitis
SBP: infection of ascitic fluid in absence of intra-abdominal cause, most often in px with ALD
two factors to predispose to SBP
portal HTN increases translocation of bacteria from GI, low ascites protein concentration leads to lower opsonization
clinical presentation of SBP
fever, abd pain/tenderness, altered mental status
dx of SBP?
complete analytic paracentesis, high poly count
typical bacterial causes of SBP?
E. Coli, s pneumo, klebsiella, usually monobacterial
management of SPB?
systemic antibiotics
pathphys of hepatic encephalopathy?
decreased clearance of toxins in portal blood that alter brain metabolism and function
precipitating factors for hepatic encephalopathy?
increased nitrogen load, deteriorating liver fxn, hypovolemia, acid/base or lyte imbalance, incrase portal/systemic shunting
management of HE?
correct precipitating factors, laculose, acidify luminal contents
complications of cholestasis
pruritus, hepatic osteodystrophy, fat soluble vitamin deficiency
treatment of pruritus?
topical moisturizing soap, anion exchange resin, vile salets, doxepin, opioid antagonists (naloxone)
what is hepatic osteodystrophy?
bone disease in px with chronic liver disease, osteoporosis and osteomalacia
how to detect osteodystrophy?
dual energy xray absorptiometry (DEXA)
end stage liver disease presentaiton?
GI hemorrhage, juandice, HE, coagulopathy, thrombocytopenia, ascites, renal failure, liver dysfunction
how to determine liver disease prognosis?
MELD: model fo end stage liver disease; predicts 3 month mortality