Gi Block Two Day 3

Front 1

Most commun acute form of hepatitis in US

Back 1

Hep B

Front 2

Time course for Hep A

Back 2

IgM disappears after 5 months; ALT is elevated for 3 months; Need to take vaccine two weeks before exposure

Front 3

What type of hepatitis is found in Mexico?

Back 3

Hep E; No chronicity; 40 day incubation period

Front 4

What type of hepatitis is the leading cause of hepatocellular carcinoma worldwide

Back 4

Hep B; greater risk for chronicity in younger patients; blood and serum are the main transfer methods

Front 5

Hep B surface antigen indicates?

Back 5

CURRENT Hep B

Front 6

Core Hep B antibody indicates?

Back 6

Natural exposure (no vaccine)

Front 7

Acute infection of Hep B is indicated by what?

Back 7

Surface antibody and envelope antibody present; IgM goes away in both acute and chronic

Front 8

Chronic infection of Hep B is indicated by what?

Back 8

Envelope and surface ANTIGEN remain; No envelope or surface antibody

Front 9

What type of Hep D infection will IgG diappear (not a protective antibody)

Back 9

Coinfection (worse initial infection)

A superinfection is more likely chronic

Front 10

What infection is the number one indication for transplant?

Back 10

Hep C

Front 11

Most likely cause of Hep B

Back 11

Sexually transmitted

Front 12

Most likely cause of Hep C

Back 12

IV drug use; alcohol or obesity quicken the progression of fibrosis

Front 13

What determines infection in Hep C?

Back 13

Viral RNA being present; antibody is present in all exposures

Front 14

What is the tx for chronic Hep B?

Back 14

Eliminate or suppress HBV replication; want to try and seroconvert; prevent HCC; Interferon-->cytokines, Activate immune system (PEG-INTERFERON alfa-2a-->used in a Low viral load with HIGH ALT/AST) Can cause neuropsychiatric symptoms/depression; Nucleotide/nucleoside analoguesBlock reverse transcriptase which is necessary for HBV replication (ENTECAVIR, TENOFOVIR); Both first line therapy with low resistance!)

Front 15

What is the tx for Hep C?

Back 15

Interferon Based therapy

Front 16

Fulminant Liver Failure

Back 16

Hepatocyte Necrosis; Coagulopathy, Encephalopathy, Cerebral Edema (Number one cause of death; glutamine in the brainastrocyte sweeling and brain herniates) the Cerebral edema is NOT a consequence of Cirrhosis!!

Front 17

What is the leading cause of acute liver failure?

Back 17

Acetamenophen

Front 18

What are the classic manifestations of cirrhosis?

Back 18

Muscle wasting (temporal muscles first)
Scleral icterus
Spider Angioma (accentuated with estrogensalso pregnancy)
Palmar Erythema (too much vasodilators, Low blood pressure)
Dupuytren’s Contractures (can’t extend digits)
Caput Medussae (Extend from the periunbilical veins to the stomach; bypassing normal circulation)
Gynecomastia (excess estrogen)
Varicies
Ascites
Spontaneous Bacterial Peritonitis
Hepatopulmonary syndrome
Hepatic Encephalopathy

Front 19

What is the tx for Varicies?

Back 19

Non selective B-blockers (propranolol, nadolol) decreases CO and splanchnic vasoconstriction

If already bleeding you can give Somatostatin/Octreotide

Front 20

What is the tx for Ascites?

Back 20

Sodium restricted diet, Diuretics (spironolactone and furosemide)

Front 21

Pathophys of Ascites

Back 21

Fluid has leaked out into BV; Low amounts of Albumin

The renin-Ag, aldosterone vasopressin are activated-->More water retention-->HYPOnatremia

Front 22

Spontaneous Bacteria Peritonitis

Back 22

Abdominal Pain and Fever; Most are gram negative; E. coli and strep!

Front 23

Hepatorenal Syndrome

Back 23

Progressive renal failure; No other cause of renal failure; decr. Urine output and increase serum creatinine

Kidneys sense they arent being perfused; cant overcome vasodilation

Front 24

Acute tubular necrosis

Back 24

Urine sodium is high (>20)

Front 25

Prerenal acute renal

Back 25

Urine sodium is low

Front 26

Hepatopulmonary syndrome

Back 26

Cant saturated all your RBC d/t abnormal capillaries; can correct with 100% O2 (not the case with emphysema)

Front 27

Hepatic Encephalopathy with grades

Back 27

Gut derived neurotoxinshepatic insufficiencycross BBBCNS changes (Encephalopathy, make you confused, cant stop traffic-Asterixis) Grade 1: short attention; 2: inappropriate behavior (hospitalized); 3: somnolence; 4: coma; Treat with IV fluids; better to be wet and wise

Front 28

Pre-hepatic portal HTN

Back 28

Portal vein thrombosis; doesnt have decreaed perfusion

Front 29

Intrahepatic portal HTN

Back 29

Cirrhosis

Front 30

Post Hepatic Portal HTN

Back 30

Hepatic vein thrombosis; R heart failure, valvular heart disease, Nut meg liver, Budd-chiari syndrome

Front 31

Lactulose

Back 31

Disaccharide; conversion to ammonium so it can be excreted; Rifaximin (works better but expensive) and lactulose both decrease Asterixis

Front 32

Oral contraceptives

Back 32

Hepatic Adenoma

Front 33

Extrahepatic Malignancy buzz word

Back 33

Metastatic Disease

Front 34

Underlying liver diseaese buzz word for liver lesions

Back 34

Hepatocellular Carcinoma

Front 35

History of Primary sclerosing cholangitis buzz word

Back 35

Cholangiocarcinoma (CCA)

Front 36

most common benign lesion; NON-CIRRHOTIC LIVER; congenital vascular malformations (blood filled cavities); 30-50 year olds; 1-20 cm large; NO MALIGNANT Potential

Back 36

Hemangioma

Front 37

Central Stellate Scar; hyperperfusion; Benign

Back 37

Focal Nodular Hyperplasia

Front 38

Benign proliferation of hepatocytes; in women of childbearing age; RISK of HEMMORRHAGE and Malignant Transformation

Back 38

Hepatic Adenoma

Front 39

HCC most common cause

Back 39

Hep C (esp, non Asians)

Front 40

Blood flow characteristics

Back 40

HCC has a greater increase in arterial flow and a decrease in portal vein flow

Front 41

Alpha fertoprotein

Back 41

produced by fetal liver and placenta and is elevated in 60-70% of patients with HCC; can be elevated in cirrhosis in the absence of HCC; Values greater than 200 ng/ml in conjunction with liver lesion on imaging=HCC (YOU DON’T need to biopsy)

Front 42

Metastatic Carcinoma

Back 42

GI, Lung, Melanoma; Multiple lesions in non cirrhosis liver is likely metastatic carcinoma with the AFP being normal

Front 43

Causes of Acute Pancreatitis

Back 43

Gallstones (most common), Alcohol (activates stellate cells); Smoking, Hypertriglyceridemia, Pancreas Divisum (ducts dont fuse); Post ERCP; Genetic (Serine protease 1 (PRSS1): childhood/adolescence)

Front 44

Pathogenesis of Acute Pancreatitis

Back 44

Inflammation of pancreas

Early-->intraacinar activation of proteolytic enzymes (generation of large amount of trypsin); vacuoles containing active trypsin rupture, Overwhelming of normal defense mechanism, Pancreatic autodigestion d/t release of enzymes;
Microcirculatory injury: Damage of vascular endothelium, vasoconstriction, stasis, ischemia, increased permeability and pancreatic gland swelling
Leukocyte
chemoattraction: complement activation; Release of cytokines
Systemic response-->SIRS, renal failure, bacterial translocation from gut

Front 45

Presentation of Acute Pancreatitis

Back 45

Severe Epigastric Abdominal pain, radiates to the back

Front 46

Labs for Acute Pancreatitis

Back 46

Amylase: Elevated within 6-12 hours; short half life; Lipase: elevated 4-8 hours, peaks at 24 hours, normal in 8-14 days

Front 47

Treatment of Acute Pancreatitis

Back 47

Pain control with IV fluids (Lactated Ringer's solution), ENTERAL nutrition; Prevetion of ERCP pancreatits-->Indometacin

Front 48

Chronic Pancreatitis causes

Back 48

Alcohol abuse and Cigarette Smoking
Genetic: SPINK1 and CFTR; PRSS1 mutation autosomal dominant; increased risk for pancreatic cancer
Tropical Pancreatitis-->South India, children
Congential-Pancreas divisum, biliary cysts

Front 49

Pathogenesis of Chronic Pancreatitis

Back 49

Progressive fibroinflammatory process resulting in permanent structural damage; Proteinaceous ductal plugs-->protein in ducts-->calcification-->stones-->duct scarring and obstruction; Ischemia perpetuates but doesn’t initiate; Decreased antioxidants

Front 50

Is Acute or Chronic pancreatitis typically asymptomatic?

Back 50

Chronic

Front 51

Serum amylase and lipase in CP

Back 51

usually normal

Front 52

Clinical manifestations in CP

Back 52

Abdominal pain after eating (progressive throughout meal); Fat malabsorption (means 90% of function lost; pancreatic lipase; greasy stinky stools); Diabetes later in the disease

Front 53

Indirect Tests for chronic pancreatitis

Back 53

"Indirect:
- Fecal elastase and chymotrypsin
- Serum trypsinogen
- Fecal fat
- Secretin MRI
- Pancreolauryl test
- 13 C breath test"

Front 54

Pseudocyst in 10% of CP

Back 54

ductal disruption, expand and infect; watchful waiting, drainage; Increases risk of pancreatic cancer

Front 55

Bile duct/duodenal obstruction in CP

Back 55

extrinsic compression from inflammation and fibrosis; tx) ERCP, surgery, surgical endoscopic pseudocyst drainage; increased risk of pancreatic cancer

Front 56

Splenic Vein Thrombosis in CP

Back 56

Inflammation along the poster pancreas; Gastric varices from portal HTN; tx-Splenectomy

Front 57

Pseudoaneurysim in CP

Back 57

Blood leakage from an artery into the surrounding tissue; tx) angiography with embolization

Front 58

Presents with a pancreatic Mass that can mimic cancer; diffusely enlarged pancreas with featureless borders

Back 58

Autoimmune Pancreatitis-Responds to glucorticoid therapy

Front 59

Autoimmune Pancreatitis what type of cells in the tissue?

Back 59

IgG4 Plasma Cells

Front 60

Higher the viral load the worse the disease in

Back 60

Hep B

Front 61

SIRS

Back 61

two of more abnormalities in temp, HR, resp, or WBC
NOT related to infection