week 5- upper GI

Question 1

• What are the types of esophageal CA?

Answer 1

o Benign tumors: many types, may cause dysdphagia, ulcer, leiomyoma most common, good px
o CA: Primary: SCC, adenocarcinoma, other malignant tumors (sarcoma, melanoma, etc)
o Secondary: often from melanaom, breast CA, seed loose CT stroma around E

Question 2

• What is prevalence and risk factors of E SCC?

Answer 2

o In proximal 2/3 of E
o ~8000/yr. in US
o 4-5x more in African-Americans than whites
o M>F (2-3x)
o Worldwide more in Asia and South Africa
o Risks: alcohol, tobacco, achalasia, HPV, lye ingestion, sclerotherapy, Plummer-Vinson, irradiation, esophageal webs

Question 3

• What is prevalence of E adenocarcinoma? Risks? Ddx?

Answer 3

o 50% of E carcinoma in whites (4x more common)
o Risks: smoking but NOT alcohol, most arise in Barrett’s E
o Ddx: adenocarcinoma of gastric cardia invading distal E

Question 4

• What are ssx of esophageal CA?

Answer 4

o early is asx!!! (often sxs don’t occur until lumen <14mm)
o Progressive dysphagia (solid → semisolid →liquid →saliva)
o Weight loss
o Hoarseness (compressed recurrent laryngeal n → vocal cord paralysis)
o Horner’s syndrome (compressed sympathetic n)
o Nerve compression: spinal pain, hiccups, diaphragm paralysis
o Dyspnea (dt pleural effusion, mets)
o (intraluminal): odynophagia, vomiting, hematemesis, melena, IDA, aspiration, cough

Question 5

• What is work-up for E cancer? Px?

Answer 5

o Endoscopy w bx, then CT and endoscopic US

o Px: metastasis to lung, liver. overall poor (5-yr. survival <5%)

Question 6

• What are E varices? Ssx?

Answer 6

o Dilated veins in distal E/stomach dt hi P in portal veins, usu dt cirrhosis
o Ssx: sudden, painless, upper GI bleeding, often massive; mb ssx of shock

Question 7

• What is work-up for E varices? Px?

Answer 7

o Eval for coagulopathy, CBC w platelets, PT, PTT, LFT
o Endoscopy
o Px: bleeding resolves spontaneously in 80%, >50% mortality (assoc w liver dz); common recurrence

Question 8

• What causes foreign bodies in E? ssx? Tx?

Answer 8

o usu in narrow space (cricopharyngeus, aortic arch, above GEJ)
o Intentional: kids, mentally ill, smugglers
o Unintentional: swallowing poorly chewed food, dentures elderly, inebriated
o Ssx: Complete obstruction: vomiting; Drooling if can’t swallow saliva
o Tx: removal w endoscopy

Question 9

• What are the conditions of the stomach?

Answer 9

o	H. pylori
o	Gastritis
o	PUD
o	Gastric CA
o	Bezoars
o	Foreign bodies

Question 10

• What is H. pylori infection? Etio? Prevalence?

Answer 10

o In stomach → gastritis, PUD, gastric adenocarcinoma, low grade gastric lymphoma.
o Etio: Oral-fecal route
o In US: 50% by 60; more in blacks, Hispanics, Asians; Nurses and gastroenterologists at high risk
o 3-6x more likely to develop stomach CA

Question 11

• What is the pathophysiology of H. pylori infection?

Answer 11

o Depends on location in stomach
o Antral: ↑ gastrin dt local impairment of somatostain → acid hypersecretion → mb prepyloric, duodenal ulcers
o Body: ↑ IL-1→ gastric atrophy, ↓acid → mb gastric ulcer, adenocarcinoma
o Mixed: combo

Question 12

• What are ssx of H. pylori? Work-up?

Answer 12

o Mb asx, mb gastritis, PUD
o Work-up: only in sx pts
o Non-Invasive tests: Serologic (Sn, not Sp), Urea breath test, stool Ag assay
o Invasive: Endoscopy (only if more ddx requires), mucosal bx rapid urease test (RUT), histology

Question 13

• What causes gastritis? Ssx? Work-up?

Answer 13

o inflammed gastric mucosa
o etio: Infection (H. Pylori), Drugs (NSAIDs, Alcohol), Stress, AI (atrophic gastritis)
o many asx, Dyspepsia, GI bleeding
o Work-up : endoscopy

Question 14

• What are the types of gastritis?

Answer 14

o Erosive, non-erosive, post-gastrectomy, uncommon gastritis syndromes, AI Metaplastic Atrophic Gastritis (AMAG)

Question 15

• What is erosive gastritis? Causes?

Answer 15

o gastric mucosal erosion dt damaged mucosal defenses
o usu acute, w bleeding (or subacute, chronic)
o Cause: NSAIDS, alcohol, stress, Radiation, viral infx (eg CMV), vascular infx, direct trauma

Question 16

• What are ssx of erosive gastritis? Dx?

Answer 16

o Often asx. Dyspepsia, N/V. Often 1st sign is hematemesis, melena, blood in nasogastric → aspirate in 2-5 days. bleeding mild-mod, or massive if deep ulcer
o Dx: endoscopy

Question 17

• What is non-erosive gastritis? Ssx? Dx?

Answer 17

o mainly dt H. Pylori
o ssx: usu asx, or mild dyspepsia
o Dx: Endoscopy (st incidental)

Question 18

• What is postgastrectomy gastritis?

Answer 18

o gastric atrophy after partial or subtotal gastrectomy

Question 19

• what are the uncommon gastritis syndromes?

Answer 19

o	Ménétrier’s dz
o	Eosinophilic gastritis
o	Mucosa-associated lymphoid tissue (MALT) lymphoma
o	dt systemic dos
o	dt physical agents
o	Infectious (septic)

Question 20

• What is Autoimmune Metaplastic Atrophic Gastritis (AMAG)? Work-up?

Answer 20

o Genetic, attacks parietal cells →hypochlorhydria ↓IF
o Consequences: Atrophic gastritis, B12 malabsorption, Pernicious anemia, 3x risk gastric adenocarcinoma
o Work-up: labs mb macrocytic anemia; endoscopic bx

Question 21

• What is PUD? Prevalence? Etio?

Answer 21

o erosion in GI mucosa, usu stomach (GASTRIC ULCER) or proximal duodenum (DUODENAL ULCER), penetrates muscularis mucosae
o any age, usu middle age
o Etio: H. Pylori (50-70% of duodenal ulcers, 30-50% of gastric ulcers)
o NSAIDs, smoking, FHx (50-60% duodenal ulcers)
o Zollinger-Ellison Syndrome (gastrin tumor, ↑HCl)

Question 22

• What are general ssx of PUD? Gastric and duodenal ulcers?

Answer 22

o Ssx: mb asx, pain common (epigastrium, burning, gnawing), relieved by food, antacids; course often chronic, recurrent
o Gastric: no consistent pattern (eating st exacerbates, not relieve pain)
o Duodenal: More consistent pain, none after wake in am, starts mid-am, relieved by food, recurs 2-3 hrs. after meal. Awakens at night

Question 23

• What is work-up for PUD?

Answer 23

o dx by endoscopy (must r/o stomach CA); st serum gastrin levels

Question 24

• what are some complication of PUD?

Answer 24

o Hemorrhage (most common) hematenesis (fresh or “coffee ground”), Hematochezia, melena, weakness, orthostasis, syncope, thirst
o Penetration (confined perforation): pain persistent, intense, referred (usu back). CT or MRI to dx
o Free perforation: sudden, intense, continuous epigastric pn, spreads rapidly thru abdomen, RLQ, may refer to shoulders, deep breathing worsens (lie still), diminished or absent bowel sounds, painful abdominal palpation, rigidity, rebound tenderness. Dx: w CT or x-ray (lateral) w air under diaphragm, in peritoneal cavity
o Gastric Outlet Obstruction: mb dt scarring, spasm, infiltration of ulcer. Recurrent, large-volume vomiting, more at end of the day, mb 6 hr after meal. Loss appetite, bloat, full, after eating
o Recurrence: mb dt refractory H. Pylori (>50% recurrence when not eradicated), NSAIDs, smoking, gastrinoma (less common)
o Gastric Cancer: only pts w H. pylori-assoc ulcers at inc risk gastric cancer later in life (3-6x)

Question 25

• What are the types of gastric cancer? Incidence? Risk factors?

Answer 25

o Gastric adenocarcinoma most common (95%) o Less: gastric lymphomas and leiomyosarcoma o Incidence: varies by country; ↑ w age o Risk: H. Pylori, AI atrophic gastritis, Gastric polyps, o Dietary, risky foods: smoked, salted meat, pickled veg (nitrates, nitrites → bacteria convert to carcinogen)

Question 26

• What are ssx of gastric CA?

Answer 26

o Initial: non-specific, eg dyspepsia o Later: early satiety if CA obstructs pyloric region o Weight loss, weakness o Dysphagia if obstructs GEJ o Uncommon: massive hematemesis or melena o Occasionally 1st sx dt metastasis

Question 27

• What is found on PE for gastric CA? work-up? Px? Ddx?

Answer 27

o PE: May be unremarkable o Late: Epigastric mass; umbilical, L supraclavicular (Virchow’s) or L axillary LN; HM; Pulmonary, CNS, bone lesions; (+) hemoccult o Work-up: Endoscopy, bx, CT and endoscopic US o Px: overall poor (5 yr survival <5-15%), usu present w advanced dz. o Ddx: Peptic ulcer and its complications

Question 28

• What are bezoars? Ssx? Imaging?

Answer 28

o tightly packed, partially/un-digested material, can’t exit stomach. In pts w abn gastric emptying: Diabetic gastroparesis, post-gastric surgery o Ssx: usu asx, mb post-prandial fullness, N/V, pain, GI bleeding o Imag: Endoscopy; detectable as mass lesion on most tests (x-ray, US, CT)

Question 29

• What are the 3 types of bezoars?

Answer 29

o Phyto: vegetable matter; mb dt Hypochlorhydria, ↓antral motility, incomplete mastication (all more common in elderly) o Tricho: hair, usu w psychiatric dos o Pharmaco: medications

Question 30

• What are the complications of foreign bodies in the stomach?

Answer 30

o Usu asx, unless obstruction or perforation o 80-90% pass spontaneously o 10-20% require non-operative intervention o ≤ 1% require surgery

Question 31

• What are the dos of the pancreas?

Answer 31

o Acute/chronic pancreatitis o Pancreatic CA o Pancreatic endocrine tumors

Question 32

• What is acute pancreatitis? Etio? Pathophysiology?

Answer 32

``` o Inflammation (mild-severe) of pancreas (st adjacent tissue) dt release of activated pancreatic enzymes o Etio: 80% biliary tract dz or alcoholism; drugs, infx, heredity, mechanical, toxins o Path: enzymes activated in pancreas → damage tissue, activate complement, cytokines→ inflammation, edema, necrosis ```

Question 33

• What are ssx of acute pancreatitis?

Answer 33

o Steady, boring, upper abdominal pain, often radiates to back (50%), hrs-days. o Pain moderately relieved by sitting forward, lying on side w knees flexed o N/V, lo fever

Question 34

• What is found on PE for actute pancreatitis? Px? Ddx?

Answer 34

o Abdomen: TTP, ↓ BS, palpable mass 2+ weeks after onset (inflammatory mass, infected necrosis, early pseudocyst) o Chest: mb pleural effusion o Px: 5-10% mortality o Ddx: Cholecystitis, PUD, splenic infarction, intestinal infarction, ectopic pregnancy

Question 35

• What is work-up for acute pancreatitis?

Answer 35

o Labs: ↑serum amylase, lipase (3x +); ↑WBC (12-20,000) o Imaging: xray abdomen: calcifications in pancreatic ducts o CXR: atelectasis or pleural effusion o US if suspect gallstone pancreatitis o Once pancreatitis is Dx, usu CT

Question 36

• What is chronic pancratitis? Etio? Pathophysiology?

Answer 36

o persistent inflammation of pancreas → permanent structural damage, fibrosis, ductal strictures → decline in exocrine/endocrine function o etio: 70-80% alcoholism in US; idiopathic 15-25%; hereditary, hyperparathyroidism, obstructed pancreatic duct by stenosis, stones, CA o path: mb ductal obstruction by protein plugs; Diabetes develops in 20-30% within 10-15 yrs of onset

Question 37

• what are ssx of chronic pancreatitis?

Answer 37

o Post-prandial pain: 85% o Severe episodic abdominal pain, hrs-days (↓spontaneously after 6-10 yrs. as acinar cells that secrete pancreatic digestive enzymes are progressively destroyed) o sit up, lean forward (“pancreatic position”), on side w knees to chest o lipase, protease secretions <10% → steatorrhea (passing greasy stools, oil droplets), and creatorrhea (undigested muscle fibers in feces) → mb sxs of glucose intolerance

Question 38

• what is work-up for chonic pancreatitis? Dx?

Answer 38

o Labs: amylase, lipase often normal (dt sig loss of pancreatic fxn) o Image: xray abdomen, chest (pancreatic calculi) o Abdominal CT (r/o pancreatic CA) o St MRCP, endoscopic US, ERCP o Dx: hx abdominal pain, long hx of alcoholism (few pts have classic triad: pancreatic calculi, DM, steatorrhea)

Question 39

• What is the primary type of pancreatic cancer? When are they diagnosed?

Answer 39

o primary ductal adenocarcinoma (90%) o Most often in head of pancreas: Dx early (early onset obstructive jaundice_ o Body, tail: multifocal, infiltrate thru gland; Dx at more advanced stages, poorer px

Question 40

• What are ssx of pancreatic CA?

Answer 40

o At Dx, 90% w advanced tumors, retroperitoneal structures, regional LN, met to liver, lung o Severe upper abdominal pain, radiates to the back, relieved by bending forward, fetal position o Weight loss o In head: Jaundice and pruritus (80-90%) o Body, tail: splenic vein obstruction → SM, gastric and esophageal varices, GI hemorrhage o → diabetes in 25-50% → sxs of glucose intolerance (polyuria, polydipsia)

Question 41

• What is work-up for pancreatic CA? px?

Answer 41

o Labs: ↑alk phos and bilirubin indicate bile duct obstruction or liver mets; normal amylase and lipase o CA 19-9 Ag (to monitor pts w Dx) o Image: CT or MR cholangiopanreatography (MRCP) o Px: overall poor (5-yr survival <2%)

Question 42

• What are the other types of pancreatic CA?

Answer 42

o Cystadenocarcinoma, intraductal papillary-mucinous tumor, | o Acinar cell carcinoma, giant cell carcinoma, adenosquamous carcinoma, leiomyosarcoma, lymphoma

Question 43

• What is pancreatic cystadenocarcinoma? Ssx? Imaging? Px?

Answer 43

o rare adenomatous, dt malignant degeneration of mucous cystadenoma o ssx: upper abdominal pain, palpable abdominal mass o image: Abdominal CT, MRI (cystic mass w debris, mb misinterpreted as necrotic adenocarcinoma or pancreatic pseudocyst) o px: relatively good

Question 44

• what is pancreatic intraductal papillary-mucinous tumor? Ssx? Imaging?

Answer 44

o Rare, mucus hypersecretion, ductal obstruction; 80% F, tail of pancreas o Ssx: abdominal pain, recurrent bouts of pancreatitis o Imaging: dx w CT, st endoscopic US, MRCP, ERCP

Question 45

• What are pancreatic endocrine tumors? 2 manifestations?

Answer 45

o from islet and gastrin producing cells; often produce many hormones o Non-functioning tumors: obstruct biliary tract or duodenum, GI bleeding, abdominal masses o Functioning tumors: Hypersecrete a particular hormone, causing various syndromes

Question 46

What are the types of pancreatic endocrine tumors?

Answer 46

o Insulinoma o Zollinger-ellison syndrome o Vipoma o Glucagonoma

Question 47

What is insulinoma? Ssx? Work-up?

Answer 47

o Rare, -cell tumor hypersecretes insulin o Ssx: hypoglycemia during fasting o Work-up: 48-72 hr fast, measure glucose and insulin; mb C-peptide or proinsulin o Endoscopic US

Question 48

• What is zollinger-ellison syndrome?

Answer 48

o Dt gastrin-producing tumor usu in pancreas or duodenal wall → gastric acid hypersecretion, peptic ulceration o usu small, grow slowly; 50% are malignant o 40-60% pts w gastrinoma have MEN o Suspect when sxs are refractory to standard acid suppressive therapy!

Question 49

• What are ssx of zollinger-ellison syndrome? Work-up? Px?

Answer 49

o Ssx: usu aggressive PUD, ulcers in atypical locations; Diarrhea: initial sx in 25-40% o Work-up: ↑serum gastrin (>150pg/mL); CT, scintigraphy, PET to localize o Px: Isolated tumor removed surgically (5-10yr survival >90%); incomplete removal (5-yr 43%, 10-yr: 25%)

Question 50

• Wat is vipoma? Ssx? Work-up? Dx?

Answer 50

o non--islet cell tumor secretes vasoactive intestinal peptide (VIP); 50-75% malignant, mb large (7cm) at Dx o ssx: Prolonged massive watery diarrhea, crampy abdominal pain, vomit, dehydration, lethargy, muscle weakness o work-up: hypokalemia, acidosis, ↑serum VIP; Endoscopic US, PET o Dx: Confirmation of secretory diarrhea (diarrhea close to plasma osmolality)

Question 51

• What is glucagonoma? Epidemiology?

Answer 51

o -cell tumor secretes glucagon→hyperglycemia, characteristic skin rash o Very rare, similar to other islet cell tumors (primary and metastaic lesions slow-growing: 15-yr. survival is common_ o 80% are malignant o avg age sx onset 50; 80% F

Question 52

• what are ssx of glucagonoma? PE? Work-up?

Answer 52

o Ssx: same as diabetes, weight loss o PE: Skin: necrolytic migratory erythema (chronic eruption on extremities, brownish red, erythematous lesion wi superficial necrolysis); Mouth: smooth, shiny, vermilion tongue, cheilitis o Work-up: Serum glucagon (>1000 pg/mL), normochromic anemia; CT, endoscopic US to localize

Question 53

• How is general hx taken for liver dz?

Answer 53

o HPI, FHx | o SHx: Exposed to toxins? Alcohol, Rx, non-Rx drugs, hepatotoxic herbs, supplements. Occupational, chemical exposure

Question 54

• What ROS Qs are asked for liver dz?

Answer 54

o General: fatigue, anorexia, fever o Skin: color change (jaundice), pruritis o GI: Nausea or vomiting? Bowel Movements? Color change?Loose fatty stools (steatorrhea,w cholestasis). def fat-soluble vitamins (A, D, E, K → bleeding, osteoporosis). RUQ pain (OPQRST)? o GU: Erectile dysfunction? o Neuro: confusion? Disorientation? Tremors?

Question 55

• What labs are done for liver dz? Imaging?

Answer 55

o UA: color (dark), bilirubin, urobilinogen o Viral serology, Igs, α-fetoprotein o Serum: albumin, total protein, bilirubin, LDH o Liver: ALT (rr ≤ 40 IU/L), AST (high, >500 IU/L dt HepV, toxin/drug-induced, ischemic hepatitis, hepatic infarction. ALP, GGT, serum bilirubin, albumin, PT o Imaging: US, CT, MRCP, liver bx

Question 56

• What is ddx for abn labs with liver dz?

Answer 56

o >40 → screened for hemochromatosis o <30 → screened for Wilson’s dz o AI disorders o Malaria and schistosomiasis (if travel Hx) o screening for 1-antitrypsin def (lung, COPD, liver dz)

Question 57

• what is hepatitis? Causes? Types?

Answer 57

o Liver inflammation w diffuse, patchy necrosis o Major causes: viruses, alcohol, drugs o Acute viral, fulminant, chronic

Question 58

• What is actute viral hepatitis? Ssx? Px?

Answer 58

o Diffuse liver inflammation dt specific hepatotropic viruses o Prodromal or pre-icteric phase: Anorexia, malaise, N/V, fever, RUQ pain, mb urticaria, arthralgias o Icteric Phase: dark urine, jaundice, systemic sxs regress; HM, TTP, but soft, smooth o Px: usu resolve spontaneously, may → chronic hepatitis

Question 59

• What are the 5 hepatitis viruses?

Answer 59

o HAV: most common, fecal→oral; does NOT → chronic O HBV: 2nd most common; blood.CAN → chronic, cirrhosis, hepatocellular carcinoma (w/o cirrhosis) O HCV: blood. 75% → chronic; 20-30% → cirrhosis → hepatocellulr carcinoma o HDV: w HBV; IV drug users o HEV: enteric, fecal-oral, does NOT → chronic

Question 60

• What is work-up for acute hepatitis?

Answer 60

o LFTs: hi AST and ALT (>400IU/L); ALT>AST o Viral serologic: IgM a-HAV, HBsAg, IgM a-HBc (HepB core), a-HCV o Imaging, bx usu unnecessary unless dx is unclear

Question 61

• What is fulminant hepatitis? Px?

Answer 61

o Rare, massive necrosis of liver parenchyma, ↓liver size (acute yellow atrophy), post-infection w hepV, toxins, drug injury o 50% involve HBV and HDV coinfection o Px: Poor survival rate w/o transplantation

Question 62

• What is chronic hepatitis? Causes? Sxs? PE?

Answer 62

o >6months) o Common causes: HBV, HCV, AI, drugs o Ssx: usu asx, malaise, anorexia, fatigue, lo fever, upper abdominal discomfort, usu no jaundice o PE: SM, palmar erythema, spider nevi

Question 63

• What is the work-up for chronic hepatitis? Px?

Answer 63

``` o ALT>AST, but mb ormal if dz is quiescent o Viral serologic testing o Possibly Abs, Igs, 1-antitrypsin o Serum albumin and P o liver bx o px: variable and depends on type ```

Question 64

• what is fatty liver? 2 non-alcoholic types?

Answer 64

o Aka hepatic steatosis: lipid accumulation in hepatocytes (most common liver response to injury) o Non-alcoholic Fatty Liver Disease (NAFLD): benign o Nonalcoholic Steatohepatitis (NASH)

Question 65

• What is NASH? Risks? Ssx? PE?

Answer 65

o histologically indistinguishable from alcoholic hepatitis; 40-60, or any age o risks: obesity, dyslipidemia, Glucose intolerance o ssx: usu asx, Fatigue, malaise, RUQ discomfort o PE: HM 75%

Question 66

• What is work-up for NASH? Dx?

Answer 66

o hi AST, ALT; st hi ALP, GGT o Liver bx o Dx: Presence of risk factors; Absence of HBV/HCV, excess alcohol

Question 67

• What are risks factors for alcoholic liver dz?

Answer 67

o Quantity and duration of alcohol consumption (usu >8yr) o M:F = 2:1 o Genetic and metabolic traits o Poor nutritional status

Question 68

What is pathophysiology of alcoholic liver dz dt alcohol absorption and metabolism?

Answer 68

o Alcohol catabolized in liver by alcohol dehydrogenase (ADH), cytochrome p-450 2E1 (CYP2E1), microsomal enzyme oxidation system (MEOS) o ↑ redox potential in liver inhibits fatty acid ox and gluconeogenesis, → fat accumulation in liver

Question 69

What is pathophysiology of alcoholic liver dz dt hepatic fat accumulation?

Answer 69

o TGLs accumulate in hepatocytes dt ↓fat export from liver, ↑fat Input

Question 70

• What is pathophysiology of alcoholic liver dz dt endotoxins in gut?

Answer 70

o Alcohol changes gut permeability, ↑ absorption of endotoxins of gut bacteria o →damage liver, and can no longer detoxify) o liver M0s release free radicals → ↑ox damage

Question 71

• What is pathophysiology of alcoholic liver dz dt oxidative stress/damage?

Answer 71

o ↑ by: o liver hypermetabolism dt alcohol o free-radical induced lipid peroxidative damage o ↓ protective antioxidants (glutathione, vits A, E) dt alcohol related undernutrition o alcohol ox products bind liver cell proteins→ inflammation, ↑ WBCs, cytokines

Question 72

• What is pathophysiology of alcoholic liver dz w inflammation, cell death, fibrosis?

Answer 72

o → Cell necrosis, apoptosis | o →hepatocyte loss → fibrosis

Question 73

• What are the sequential consequences of alcoholic liver dz?

Answer 73

o Fatty liver (>90%)→ alcoholic hepatitis (10-35%) →cirrhosis (10-20%)

Question 74

• What is alcoholic fatty liver?

Answer 74

o most common consequence of excessive EtOH. Potentially reversible o Pathology: TGL droplets accumulate, replace hepatocyte nucleus o Often asx o PE: HM, NTTP

Question 75

• What is alcoholic hepatitis? Ssx? PE? Course?

Answer 75

o Combo of fatty liver, diffuse liver inflammation, necrosis. Damaged hepatocytes swell, severe damage →necrotic o Ssx: Moderate dz: undernourished, fatigue, fever, jaundice, RUQ pain o PE: HM, st hepatic bruit o Course: mild to life-threatening; Severe: ascites, portal-systemic encephalopathy, variceal bleeding, liver failure

Question 76

• What is cirrhosis? Ssx? PE?

Answer 76

o extensive fibrosisdisrupts normal liver architecture o ssx: mb asx; mild-severe o PE: Small liver, mb nail clubbing

Question 77

• What are ssx of chronic alcoholism (>80g ingested/day)?

Answer 77

o Vascular spiders o Peripheral neuropathy o Dupuytren’s contractures of palmar fascia o In men: hypogonadism, feminization (infertility, gynecomastia) o Under-nutrition: folate and thiamin deficiencies

Question 78

What is work-up for chronic alcoholism?

Answer 78

o Hi GGT (first to rise); hi AST, ALT (AST:ALT >2:1) o CMP: ↓albumin (under-nutriton) o CBC: Macrocytosis, MCV>100 early. GI blood loss may ↓ MCV o Severity: ↑serum Bilirubin (secretory function); ↑ PT, INR (↓ production of clotting factors) o Usu no imaging. US/CT: fatty liver, SM, ascites. o Liver bx: confirms dz, stage of injury

Question 79

• What is the effect of liver dz on drug metabolism?

Answer 79

o alter intestinal absorption, plasma protein binding, hepatic extraction ratio, liver blood flow, portal-systemic shunting, biliary excretion, extrahepatic circulation, renal clearance o → ↑ level of bioavailable drug →toxic effects

Question 80

• What is DILI? Risks? 2 types?

Answer 80

o Drug-induced liver injury; Some drugs, medicinal herbs, plants, supplements o Risk: >18, obesity, pregnancy, Concomitant alcohol consumption, genetic polymorphisms o Hepatocellular (serious): ex: acetaminophen; malaise, RUQ pain; ↑AST,ALT → hyperbilirubinemia (mortality rates as high as 50%) o Cholestatic (less serious): ex: amoxicillin/clavulanate; pruritus, jaundice; ↑ALP