GI Medicine
Terms
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- 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?
- liquids
- 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:
- OP
- 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:
- achalasia
- combination of chest pain and dysphagia suggests:
- diffuse esophageal spasm
- raynaud's phenomenon and dysphagia suggests:
- scleroderma
- confirm esophageal motility disorder with
- manometry
- 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?
- 3-4%
- 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
- dyspepsia
- 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?
- HLA-DQ2 and HLA-DQ8
- 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:
- osteoporosis
- 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
- B12
- 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?
- US
- treatment of cholelithiasis and cholecystitis?
- cholecystectomy
- 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?
- cholangiogram
- 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?
- NOD2
- 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?
- pancolitis
- clinical presentation of UC
- bloody diarrhea, tenesmus, cramps, fever, weight loss
- dx of UC?
- biopsy
- 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
- PSC
- 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:
- cirrhosis
- large nodular liver suggests:
- malignancy
- ascites in presence of juandice suggests:
- cirrhosis
- Define AST/SGOT
- aspartate aminotransferase, from cytosol and mito and found in liver and lots of other cells