Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

DERS (GIT) > L12- GIT Pathology VI (liver) > Flashcards

L12- GIT Pathology VI (liver) Flashcards

You may prefer our related Brainscape-certified flashcards:
Git Commands flashcards
1
Q

describe structure of liver lobule and acinus

A

(acinus is half a lobule)

  • central vein
  • surrounded by 6 portal triads
  • triads: hepatic artery, portal vein, bile duct
  • Zone 1 near periphery, Zone 3 surrounds central vein
  • Zone 3 most susceptible to hypoxia

Note- blood flow is outside in; bile flow is inside out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

list the cells of the liver

A

-Hepatocytes: thin plates/cords 1-2 cells thick

  • endothelial cells (blood)
  • Kupffer cells (liver macrophages)
  • stellate cells (perisinusoidal / ito cells): stores fat / vitE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

track the movement of bile (from production until it reaches intrahepatic ductules)

A

1) excreted by hepatocytes
2) into bile canaliculi
3) canals of Hering
4) bile ducts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

list the general clinical features of liver disease

A
  • RUQ pain
  • jaundice
  • anorexia
  • pruritus
  • fever
  • mental confusion
  • easy bruising
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

list the lab investigations for the liver

A
  • Serum Bilirubin: conjugated, unconjugated
  • Transaminases: ALT, AST, ALP/ALK, GGT
  • Serum Albumin
  • AFP
  • serum ammonia
  • ceruloplasmin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

LFT result indicating alcoholic liver disease….

A

AST:ALT >2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

LFT result indicating viral hepatitis….

A

AST:ALT <1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

LFT result indicating cholelithiasis (biliary obstruction)….

A

elevated ALP, GGT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

LFT result indicating HCC….

A

(hepatocellular cancer)

α-fetoprotein (AFP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

LFT result indicating hepatic failure….

A

elevated ammonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

LFT result indicating Wilson’s disease….

A

dec Ceruloplasmin (Cu carrier)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Indicate the *liver disease with the following LFT results:

  • (1) elevated GGT, ALP
  • (2) elevated ALP alone
  • (3) elevated GGT alone
  • (4) AST:ALT > 2
  • (5) AST:ALT < 1
A 
1- cholestasis / biliary obstruction
2- infiltrative diseases / metastasis, congestive diseases via RHF
3- alcohol use
4- alcoholic liver disese
5- viral hepatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Indicate the *liver disease with the following LFT results:

  • (1) inc AFP
  • (2) dec serum albumin
  • (3) dec ceruloplasmin
  • (4) inc PT
  • (5) inc NH3+
A 
1- HCC
2- chronic liver disease
3- Wilson's disease
4- acute or chronic liver disease
5- hepatic failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

list the radiographic techniques used to investigate liver disease

A

Visualization of biliary tree:

  • ERCP (endoscopic retrograde cholangiopancreatogram): diagnostic, therapeutic
  • MRCP (magnetic resonance cholangiopancreatogram): diagnostic

Other:

  • MRI, CT, US
  • liver biopsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

chronic liver disease is defined as lasting longer than…..

A

6 mos

= chronic hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

describe how severity of liver disease is determined

A

*Morphological pattern of hepatocyte

  • reversible / self-limiting injury: normal function returns after removing offending agent
    e. g. fatty degen. via EtOH, cholestasis

-irreversible damage / fibrosis + progressive = cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

describe the 2 types of hepatocellular injury

A
  • Ballooning: large hepatocytes w/ regularly clumped cytoplasm
  • Feathery: fine, foamy cytoplasm due to detergent action of bile salts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

describe the morphological features of hepatic injury

A
  • Hepatocellular injury (ballooning, feathery)
  • Necrosis: focal, bridging, massive
  • Apoptosis: councilman bodies / acidophil bodies
  • Regeneration: hepatocyte cord thickening, mitosis, acinar change (rosettes)
  • Fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

list the types of steatosis and their causes

A

Macrovesciular steatosis: alcohol, NASH, malnutrition

Microvesicular steatosis: acute fatty liver of pregnancy, Reye syndrome, drugs, obesity, DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

describe Macrovesicular Steatosis (+ causes)

A

Large Droplet: single fat vacuole, displaces nucleus to periphery

Small droplet: multiple fat vacuoles (not as fine as microvesicular)

Causes: alcohol, NASH / NAFLD (non-alcoholic steatohepatitis / non-alcoholic fatty liver disease), malnutrition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

describe Microvesicular Steatosis (+ causes)

A

-multiple fine vacuoles, nucleus is central

Causes: acute fatty liver in pregnancy, Reye syndrome, drugs, obesity, DM

22
Q

Signs of Liver Disease seen in acute and chronic conditions

A
  • icterus / jaundice
  • hepatomegaly
  • RUQ pain / tenderness
  • peripheral edema
23
Q

Signs of Liver Disease seen in only chronic conditions

A
  • splenomegaly (portal HTN)
  • palmar erythema
  • spider angiomas
  • gynecomastia + testicular atrophy (men)
  • Dupuytren contracture (hand fibrosis contracts ulnar nerve digits)
  • parotic enlargement
  • clubbing
  • white nails (leukonychia)
  • muscle wasting
24
Q

Jaundice:

  • defined as (1)
  • presence in the eye is (2), and will be seen clinically with (3) lab values
  • accumulation of (3) also leads to (4) in newborns
  • (5) / (6) describe the results of retaining two other substances
A 
1- skin yellowing
2- scleral icterus
3- bilirubin >2.0 mg/dL
4- kernicterus (neonatal jaundice => brain damage) 
5- cholesterol --> skin xanthomas
6- bile salts --> pruritus
25
Q

list the classifications of jaundice

A
  • pre-hepatic
  • hepatic
  • post-hepatic
26
Q

list the causes of pre-hepatic jaundice

A

excess production of bilirubin:

  • hemolytic anemia
  • inc blood resorption from hemorrhage
  • ineffective erythropoiesis
27
Q

list the causes of post-hepatic jaundice

A

impaired bile flow:

  • gallstones, head of pancreas cancer, extra hepatic bile ducts
  • biliary atresia (neonates)
28
Q

list the causes of hepatic jaundice

A
  • reduced uptake: drugs, diffuse liver disease
  • impaired conjugation (neonates)
  • dec excretions: drugs, transporter deficiency (related to impaired conjugation)
  • impaired bile flow –> bile duct obstruction
29
Q

Cirrhosis defining characteristics

A
  • bridging fibrous septa
  • parenchymal nodules created by regeneration
  • diffuse liver involvement

NOTE- end stage result of many liver diseases are irrespective of primary etiology

30
Q

define Cirrhosis classification

A

based on nodule size:

  • Micronodular, <3mm nodules
  • Macronodular, >3mm nodules
31
Q

list the disease types that can cause Cirrohosis

A

Hepatic diseases: viral / autoimmune hepatitis, steatohepatitis (alcoholic/NASH)

Biliary diseases: primary biliary cholangitis, primary sclerosing cholangitis (UC)

Metabolic diseases: hereditary hemochromatosis, Wilson’s disease, AAT deficiency

Cyptogenic / Idiopathic

32
Q

describe the clinical features of cirrhosis

A

(possibly silent / asymptomatic)

  • portal HTN –> ascites, splenomegaly, varices
  • liver failure

-inc risk of HCC

33
Q

what are the consequences of portal HTN (often seen in liver disease, e.g. cirrhosis)

A
  • ascites
  • hepatic encephalopathy
  • congestive splenomegaly –> thrombocytopenia
  • portosystemic shunts: esophageal / gastric varices, hemorrhoids in rectum, retroperitoneum affected, caput medusae of abdominal wall
34
Q

(1) is the most common infectious disease of the liver, caused mostly by (2), although (3) infections can involve the liver

A

1- viral hepatitis
2- Hepatitis A, B, C, D, E
3- EBV (infectious mononucleosis), CMV, yellow fever

35
Q

HepA:

  • (1) genome
  • causes (acute/chronic) hepatitis
  • commonly affects (3), spreading via (4) route
  • (5) incubation period
A 
1- non-enveloped (+)ssRNA (picornavirus family)
2- acute (no chronic disease)
3- children (unvaccinated)
4- fecal-oral
5- 2-6 wks
36
Q

HepA:

  • diagnosis either requires (1) or (2)
  • (3) does not occur with hepA virus
A

1- IgM anti-HepA at onset
2- IgG after few months
3- carriers

37
Q

HepB:

  • (1) genome
  • aka (2), explain
  • (3) transmission
  • (4) incubation period
A

1- enveloped dsDNA
2- serum hepatitis b/c present in all body fluids
3- blood transfusion, sex, IV drug use, needle stick injuries
4- 4-26 wks

38
Q

discuss the distribution of HepB complications post-acute infections

A

healty carriers, 5-10%

subclinical disease, 60-65% (–> recovery)

acute hepatitis, 20-25% (–> recovery, rarely fulminant/death)

perisistent infection, 4% (–> most recover, some advance to chronic HepB –> cirrosis / —> HCC / death)

39
Q

HepB Histology:

  • (1) general hepatocyte appearance
  • (2) intracellular characteristic
  • immunostaining for (3) is necessary to confirm its abundant presence in cells, include color
  • (4) is a key trait of chronic hepatitis
A

1- ground-glass

2- large pale, finely granular pink cytoplasmic inclusions (H&E)

3- HepB surface Ag, brown

4- portal tract expansion via lymphoid follicle

40
Q

HepC:

  • (1) genome
  • causes mostly (acute/chronic) hepatitis
A

1- enveloped (+)ssDNA (flavivirius)

2- both, high propensity for chronic infections

41
Q

discuss the distribution of HepC complications post-acute infections

A
  • resolution, 15%
  • chronic hepatitis, 85% (–> either stable disease or cirrohosis with its complications)
  • fulminant, rare
42
Q

explain HepD infection

-what needs to occur for infection, which method is more dangerous

A

-its a defective RNA virus

-becomes infective when encapsulated by HBsAg (hepatitis B surface Ag)
OR
-co-infection with HepB (more dangerous = superinfection)

43
Q

HepE:

  • (1) genome
  • causes mostly (acute/chronic)
  • (3) transmission, mostly affecting (4) people
  • possibly fatal in (5) population
  • (6) is a popular complication
A 
1- non-envelope
2- mostly acute
3- enteric (endemics)
4- immunosuppressed (post-liver transplant Pts)
5- pregnant
6- cholestasis
44
Q

what are the clinical results of viral hepatitis

A

1- asymptomatic infection
2- carrier state

3- acute hepatitis
4- chronic hepatitis
5- fulminant hepatitis

45
Q

Autoimmune hepatitis:

  • more in (males/females)
  • involves Ig(2) against (3) in adults or (4) in children
  • responds to (5)
A

1- females
2- IgG
3- anti-nuclear / anti-smooth muscle Abs (type I)
4- anti-LKM (liver kidney microsomal) Abs (type II)
5- immuno-suppressive therapy

46
Q

Autoimmune hepatitis histological description (hepatitis type and defining cells)

A

focal lobular hepatitis w/ prominent plasma cells

47
Q

list the patterns of alcoholic liver disease

A
  • hepatic stenosis
  • alcoholic hepatitis (steatohepatitis)
  • variable amounts of fibrosis –> can progress to cirrhosis

(micronodular cirrhosis –> progresses to macronodular)

48
Q

NAFLD = (1):

  • (2) Sxs
  • (3) risk factors
A

1- nonalcoholic fatty liver disease

2- asymptomatic OR mild elevation of serum transferases, may lead to cirrhosis

3- obesity, insulin resistance, DM, hyperlipidemia

49
Q

NAFLD = (1):

-similar presentation to (2- include features)

A

1- nonalcoholic fatty liver disease

2- alcoholic liver disease:

  • steatosis
  • steatohepatitis = ballooning, Mallory hyaline
  • fibrosis around central vein
  • may progress to cirrhosis
50
Q

fulminant hepatitis definition

A
  • acute liver disease, rapid progression
  • encephalopathy develops w/in 8 wks

-pathology: massive necrosis, submassive necrosis

51
Q

liver necrosis:

  • (1) general appearance
  • confluent necrosis in (2) region
A

1- small, bile-stained, soft, congested

2- periventricular region

DERS (GIT) (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions