Repro/gi Wk2 Liver

Front 1

204

Back 1

204

Front 2

How is the liver broken up

Back 2

8 complete segments (instead of old lobes)

Front 3

What is the ligament in the center of the liver

Back 3

Falciform (w/ umbilical/paraumbilical channels)

Front 4

What is the name of the liver capsule & what is it made out of?

Back 4

Glisson's capsule – type 1 & 3 collagen

Front 5

What is the blood supply to the liver?

Back 5

Portal vein (from intestines) & hepatic artery

Front 6

What comes out of the liver

Back 6

Bile ducts & hepatic vein (R & L)

Front 7

Components of portal triad

Back 7

Hepatic artery, bile duct, portal Vein

Front 8

Lobular vs Acinar arrangement of liver

Back 8

Lobular – central vein in center. Acinar – portal triad in center (zone 1) vein in outside (zone 3)

Front 9

Where is most detox in liver?

Back 9

Near central vein (centrilobular)

Front 10

Zonal necrosis

Back 10

Ex = tylenol. Production of toxic by product results in necrosis of zone 3 cells.

Front 11

Protein malnutrition – hepatic signs

Back 11

Periportal fatty change in liver.

Front 12

Nutmeg liver

Back 12

CHF results in nutmeg appearance of liver.

Front 13

Typical pattern of regeneration in liver:
Of neoplasm:

Back 13

Regen: Two cell thick sinusoids
Neoplasm >2 cells (i.e. 3-6)

Front 14

One cause of hepatization of pancreas

Back 14

Deficinet copper diet.

Front 15

NonPerenchymal liver cells & function (3)

Back 15

Kupffer – macrophages. Endothelial.
Stellate (ito) – Store Vit A and pathologically act as myofibroblasts.

Front 16

Where do kupffer cells live?

Back 16

In the sinusoids of the liver.

Front 17

Causes of NASH

Back 17

(nonalcoholic steatohepatitis) –
Obesity
Diabetes Mellitis
Metabolic disturbances (Fatty acids)
“Syndrome X”

Front 18

Direct vs indirect bilirubin testing

Back 18

Direct: Water soluble(unconjugated).
Indirect: Fat soluble (conjugated)

Front 19

Prehepatic jaundice

Back 19

When more bilirubin is produced (from hemolysis) than the liver can conjugate.

Front 20

Bilirubin pathway

Back 20

Unconjugated Biliribin --> liver – conjugated --> portal blood --> systemmic circ --> kidney –conjugated out urine

Front 21

205

Back 21

205

Front 22

Micro vs Macro nodular cirrhosis

Back 22

Micro is < 3mm

Front 23

Causes of macronodular cirrhosis

Back 23

HCV, HBV, Toxic chemicals.

Front 24

4 common complications of cirrhosis

Back 24

(PILE)
Portal hypertension,
infection
liver cell carcinoma,
Endocrine changes

Front 25

Budd Chiari syndrome

Back 25

Hepatic vein thrombosis from any cause. Common causes – hypercoagulability, neoplasm, parasites. Clinical signs – Hepatomegaly, abdominal pain, ascites.

Front 26

Portal hypertension – anastamoses

Back 26

Gastroesophogeal (varices), Anorectal (hemorrhoids), periumbilical (spider angiomas)

Front 27

Endocrine problems w/ cirrhosis

Back 27

Peripheral conversion of testosterone and androstenedione into estrone and estradiol results in feminization. (Also, estrogen escapes the liver via anastomoses)

Front 28

What happens to male repro system in cirrhosis?

Back 28

Infertility due to loss of spermatogenic cells (don't know why)

Front 29

206/207

Back 29

206/207

Front 30

Which hepatitises can be chronic?

Back 30

B,C,D (also spread parenterally)

Front 31

Hep B is in which body fluids?

Back 31

Blood, semen, vaginal, saliva.

Front 32

Dane Particle

Back 32

Particle of HepB

Front 33

Three hep B antigens

Back 33

HBsAg - envelope of virus, cytoplasm of hep.
HBcAg - Nucleocapsid of virus, nucleus
HBeAg - nucleocapsid of virus, nucleus.

Front 34

Ground Glass Cell

Back 34

Hepatocyte with large glassy cytoplams. Indicative of HepB

Front 35

Which of the Hep B antigens does NOT confer long term immunity?

Back 35

HBeAg

Front 36

Def of chronic Hep B

Back 36

Persistance of HBsAg for more than 6 mos

Front 37

HDV dependent on?

Back 37

HBsAg from HepB

Front 38

Two types of HDV infections

Back 38

Coinfection (both at same time), Superinfection (serial infections)

Front 39

HBsAg antigen/antibody significance

Back 39

(as expected) Ag+Ab- = acute carrier, Ag-Ab+ = recovered

Front 40

HBcAg antigen/antibody significance

Back 40

Ag-Ab+ is EITHER carrier OR complete recovery

Front 41

What indicates active, infectious HBV

Back 41

HBeAg, or Dane particles.

Front 42

What makes HCV so likely to be chronic?

Back 42

Genome mutations (error prone viral polymerase)

Front 43

How are hepatitises removed from the body?

Back 43

Via destruction of affected hepatocytes (hence chronic causes liver damage)

Front 44

Councilman bodies

Back 44

Apoptic cells in the liver.

Front 45

Histo features of CAH

Back 45

1. Piecemeal necrosis,
2. Fibrous bridges,
3. Liver cell rosettes,
4. Groundglass cells

Front 46

HBV vs HCV

Back 46

See slide 73

Front 47

210

Back 47

210

Front 48

Abnorm. Alkaline phosphatase is indicative of:

Back 48

Bile duct damage

Front 49

Murphy's sign

Back 49

Sensitivity to pressure on gall bladder area.

Front 50

Ampulla of Vater

Back 50

Sphincter in the common bile duct

Front 51

Sphincter of Oddi

Back 51

Spincteer b/t common bile duct and duodenum

Front 52

Primary Biliary Cirrhosis

Back 52

(unknown etiology). Slow progressing cholestatic liver disease. More common in women. Elevated Alk Phosph, GGT. Often AMA pos. Lymphocytes around bile duct.

Front 53

Functions (2) of bile salts

Back 53

1. Detergent for fat dig/abs (and prevent bile stones).
2. Stim phosphatidylcholine change to bile.

Front 54

Clin uses of Bile Salt therapy (ursodeoxycholic acid)

Back 54

1. Treat cholestatic liver disease,
2. Treat pruritis ass. W/ cholestasis
3. Gallstone dissolution therapy

Front 55

What enzyme conjugates bilirubin?

Back 55

Bilirubin UDP-Glucoronysyltransferase (bUDP-GT)

Front 56

Ntcp

Back 56

Transporter for bilirubin – Involved in Estrogen induced cholestasis, Jaundice of sepsis

Front 57

MRP2

Back 57

Transporter for bilirubin – Involvied in Dubin -Johnson and Jaundice of sepsis

Front 58

spgp/BSEP

Back 58

Trasporter for bilirubin. Involve in Estrogen & Sepsis induced jaundice, gall stones, PFIC2

Front 59

MDR3

Back 59

Bilirubin transporter. Involved in PFIC-3

Front 60

Fic1

Back 60

Ibilirubin transporter in the Ileum. Involved in BRIC, PFIC1

Front 61

Gilbert's disease

Back 61

Failure of bUDP-GT (extra TA in TATA box) results in jaundice when sick/stressed.

Front 62

Jaundice in newborns – cause, timeline

Back 62

Caused by hemolysis, hematoma. (inc RBC breakdown). UDP-GT is activated at birth, so jaundice peaks at ~day 4-5, regardless of expecting date.

Front 63

4 causes of hyperbilirubinemia

Back 63

1. Inc production (via RBC breakdown)(unconj)
2. Decrease uptake or transport (unconj)
3. Defect in conjugation (unconj)
4. Defect in excretion (conjugated)

Front 64

Kernicterus

Back 64

Brain damage secondary to hyperbilirubinemia in newborn (unconj)

Front 65

211

Back 65

211

Front 66

Sup Mesenteric Vein drains:

Back 66

Righ colon, small int.

Front 67

Inferior Mesenteric vein drains:

Back 67

Left colon

Front 68

Most common cause of portal hypertension

Back 68

Schistosomiasis

Front 69

Space of disse

Back 69

Area under endothilial cells in liver capillaries. (Home of ito cells)

Front 70

4 collateral circulations in portal hypertension

Back 70

1. Azygous. 2. Umbilical. 3. Retroperitoneal 4. Rectal

Front 71

Formula for surface tension

Back 71

T = press*rad/width

Front 72

Drugs to lower Portal inflow -

Back 72

1. Beta Blockers 2. Vasopressin 3. Somatostatin

Front 73

Drugs to lower portal resistance

Back 73

Nitrates.

Front 74

3 factors in ascites (cirrhotic)

Back 74

1. Low albumin.
2. Hepatic outflow block
3. Portal hypertension

Front 75

Hepatorenal syndrome

Back 75

Progressive renal failure w/ advance cirrhosis/ascites

Front 76

Hepatic encephalopathy

Back 76

Asterixis, Abnormal EEG, impaired cerebral function in advanced liver disease

Front 77

Asterixis

Back 77

Loss of of postural control of hands.

Front 78

4 stages of Hep Encephalopathy

Back 78

1. Confusion
2. Drowsiness
3. Somnolence
4. Coma.

Front 79

Lactulose

Back 79

Initial treatment for hepatic encephalopathy (a non digestable disaccharide)

Front 80

Three theories of hepatic encephalopathy

Back 80

1. Ammonia (block glutamine rec) 2. Tryptophan (block monoamine trans) 3. GABA benzodiazepine (Inc GABA)

Front 81

Underfill hypothesis of ascites

Back 81

Transudation of fluid in ascites causes increased sodium reabs

Front 82

Overfill hypothesis of ascites

Back 82

Retention of Na --> vol expansion --> ascites

Front 83

ALT

Back 83

Aminotransferase in liver. Increased in nonalcoholic disease, decreased in alcoholic

Front 84

AST

Back 84

Aminotransferase found in most tissues. Relatively constant concentration in blood.

Front 85

Normal ALT:AST

Back 85

1

Front 86

Alkaline phosphatase

Back 86

Liver enzyme from plasma membrane. Marker of biliary tract disease

Front 87

GGT

Back 87

Liver enzyme, also sensitive for biliary tract.

Front 88

What 2 things favor zone 1 necrosis?

Back 88

Yellow phosphorous, and toxemia of pregnancy

Front 89

Liver growth enzymes

Back 89

HGF, TGF-a, EGF (require TNF, IL-6)

Front 90

TGF-B

Back 90

Negative regulator of hepatocyte growth.

Front 91

2 death receptors on hepatocytes

Back 91

Fas and TNF-R1

Front 92

PPARa

Back 92

Combustion - oxidizes fatty acids

Front 93

PPARy

Back 93

Conservation - stores fatty acids

Front 94

Causes of micronodular cirrhosis

Back 94

Alcohol, nutritional.