Brainscape's Knowledge GenomeTM

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


See full index

Pathophysiology > GI: Biliary and Hepatic > Flashcards

GI: Biliary and Hepatic Flashcards

1
Q

cholelithiasis
-mc pt?

-name the type of stones– MC?

A

formation of gallstones from impaired metabolism of cholesterol, bilirubin and bile acids

Fat
Female
Forty 
Fertile 
Fair skinned

Three types: dep on chemical composition

  1. Cholesterol: yellow-grey
    - formed from bile that is superst with cholesterol produced by liver

2a. Pigmented (brown)
- formed from calcium bilirubinate and FA soaps that bind to calcium

2b. Pigmented (black)
- Calcium + billirubinate with mucin glycoproteins
- assoc with chronic liver dz and hemolytic dz

  1. Mixed stones MC–both choleserol and pigmented
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

5 F’s?

A 
Fair 
Fat
Female 
Fertile 
Forty 
****RF for cholelithiasis and then poss cholecystitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Cholecystitis

A

inflammation of GB or cystic duct (duct that goes from GB to common hepatic duct.. together form the common bile duct)

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

Choledocholithiasis

A

Gallstones in the common bile duct

  • now GB AND liver is getting back up of bile
  • ->start to see LFTs go up and jaundice bc billirubin being spilled into blood stream
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Cholangitis

A

biliary tract infection SECONDARY to obstruction of the common bile duct (choledocholithiasis)

*Fever, RUQ jaundice=Charcot triad

^traid + AMS + Hypotension

Obstruciton–infection–biliary stasis—bacterial overgrowth

LIFE THREATENING

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Jaundice

  • what is it caused by
  • types
  • characterized by?
A

caused by hyperbilirubinemia
TYPES
1. Obstructive–extrahepatic or intrahepatic obstructions
2. Hemolytic–prehaptic or excessive hemolysis of RBCs

characterized by

  1. dark urine
  2. yellow discoloration of scelra and skin
  3. light colored stools
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

whats the largest organ in the body

A

liver

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

what are the blood supplies to the liver

A 
hepatic artery (oxygen) 
portal vein (nutrients)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

majority of cells in liver are?

A

hepatocytes– they synthesize proteins, produce bile, regulate nutrients, conjugate bilirubin

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

causes of preheptatic jaundice

A

transfusion reactions
sickle cell anemia
autoimmune

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

causes of hepatic janduince

A 
hepatitis 
CA
cirrhosis 
congential 
drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

causes of post hepatic jaundice

A 
Gallstones 
inflammation 
scar tissue
CA 
***anything blocking the flow of bile into the intestine****
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

hepatobiliary mechanisms for jaundice— describe the steps

A
  1. intrahepatic obtructiev jaundice–>hepatocellular damange–>decr liver ability to excrete bilirubin–>conjugated and unconjugated hyperbilirubinemia–>biliruibin deposition in tissues aka jaundice
  2. extrahepatic obstructive jaundice–>bile duct obstruction (cholestasis)–>conjugated bilirubin accum. in liver and enters the bloodstream–>conjugated hyperbilirubinemia–>incr excretion of bili in urine + jaundice
  3. Heatolic mechanism–>hemolytic jaundice–>excessive lysis of RBCs–>hepatocytes cannot conjugate and excrete bili as rapidly as it forms–bili accumulates in BS–>UNconjugated hyperbilirubinemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

liver dz are generally categorized into?

A
  1. hepatocellular–>hepatitis, ETOH liver dz
  2. Cholestatic–>gallstones or malignant obstruction, primry biliary cholangitis
  3. mixed–drug induced liver dz
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Liver function tests:

  1. ALT/AST?
  2. ALK-P
A
  1. aminotransferases–ALT and AST
    - ALT is found in liver
    - AST found in many other tissues (skel, heart, kidney, brain)
  2. ALK-P: alkaline Phosphatase
    - found in the liver bone gut and placenta
    - elevated when there is obstruction to bile flow aka cholestasis
    - **if GGT levels are also elevarted.. points to hepatic in origin

3.

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

what dz does not show increase in BOTH AST and ALT

A

ETOH liver dz

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

AST and ALT levels for ETOH liver dz

A

ALT-AST ratio may be 1:2 or more

**the higher the ratio more likely etoh is contriuting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

albumin is decrease in whic dz states

A

chronic liver dz
nephrotic syndrome
malnutrition
inflammatory states–burns, sepsis, trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

80% of bilirubin is deribed from?

the rest comes from?

A

RBC b/d

-rest comes from myoglobin b/d and liver enzymes

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

what is converted into bilirubin in the spleen

A

hemoglobin

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

where is hemoglobin converted into bilirubin?

A

spleen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

define unconjugated bilirubin

A

waste product of hemoglobin breakdown into bilirubin in the spleen

  • indirect bilirubin
  • circulates in plasma, bound to albumin
  • not water sol
  • toxic– can cross BBB and cause neuro deficits

bilirubin/albumin complex NOT water solbule–so it cannnot be excreted in the urine—— it travels to the liver to be conjugated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

define conjugated bilirubin

A

albumin/bilirubin complex dissociated once inside the liver:
-bilirubin then is conjugated (direct) into a water soluble form— excreted into the intestines–bacteria act on it to produce urobilinogen and urobilin–>excreted in urine

  • loosely bound to albumin so it is water sol
  • when present in excess– it is excreted in urine– why we see dark urine ONLY in conjugated bilirubin
  • nontoxic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

when does unconjugated hyperbilirubinemia develop

A

defect BEFORE the liver uptake of the unconjugated albumin/bilirubin complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

when does conjugated hyperbilirubinemia develop

A

defect AFTER hepatic uptake of the albumin/bilirubin complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

clinical jaundice becomes evident at what levels

A

> 2mg/dl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

kernicterus

A

brain damage that can result from high levels of unconjugated bilirubin in a baby’s blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

dark urine results from?

A

CONJUGATED bilirubin build up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what drugs can cause jaundice

*is this unconjugated or conjugated

A 
UNCONJUGATED: 
sulfonamides
PCNs 
Rifampin 
Radiocontrast agent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

causes of jaundice (conjugated hyperbilirubinemia)

A

decr intrahepatic excretion of bili:

  • hepatocellualr dz: viral or ETOH hepatitis, cirrhosis
  • primary biliary cirrhosis
  • primary sclerosing cholangitis

Extrahepatic biliary obstruction:

  • gallstones
  • pancreatic (head) CA
  • cholangiocarcinoma
31
Q

causes of jaundice (unconjugated hyperbilirubinemia)

A

hemolytic anemias
red hepatic uptake of bili or impaired liver conjugation:
-drugs
-diffuse liver dz.. hepatitis or cirrhosis

32
Q

neonatal jaundice

-physiologic vs pathologic—-causes?

A

Physiologic: COMMON in healthy newborn
-lack of liver matuirty to billirubin uptake and conjugation
assoc with hemolytic dz, metabolic and endo dz, liver abnormalities and infections

Pathologic: associated with severe illness
-RF: fetal-maternal blood type incompatability, premmie, exclusive BF, maternal age over 25, male gender, delayed meconium passage, G6PD, excess truama during birth

33
Q

is neonatal jaundice MC unconjugated or conjugated

A

unconjugated

34
Q

serious cases of neonatal jaundice can lead to?

A

kernicteurs– cerebral dysfunction and encephalopathy

35
Q

when does physiologic jaundice present in newborn?

A

3-5 days of life

36
Q

causes of unconjuagted hyperbili physiologic jaundice in newborn

A
  1. Breastfeeding jaundice
  2. Breast milk jaundice
  3. Prematuirty
37
Q

BF jaundice

  • presents?
  • pathi
  • tx
A

presents very early on–w/in 1st week after birth
PATHO: insufficient milk intake leads to dehydration resulting in hemoconcetration of bilirubin— baby is not eating enough– not enough BMs— bilirubin builds up

fewer BM=incr in enterohepatic circulation of bilirubin

VERY YELLOW
*must intervene

tx:
- phototherapy– it make bilirubin water soluble
- continue breastfeeding**
- supplemental PO or IV fluids (PO preferred)

38
Q

Breast milk jaundice

  • presents?
  • patho ?
  • tx
A

presents AFTER 1st week of life

PATHO:
*infant liver is not developed enough to process lipids, –can interfere with the breakdown of bilirubin

Baby is not as yellow as breastfeeding jaundice
*not as serious as breastfeeding jaundice and intervention not always necessary

TX:
*phototherapy
*

39
Q

when does pathologic unconjugated causes of jaundice occur?

A

within first 24 hours of life

40
Q

list the pathologic unconjugatd hyperbilirubinemia causes

A

unconj made in the SPLEEN!! so its related to hemolytic (destruction RBC) and non-hemolytic aka metabolism issues

Hemolytic–G6PD def, drugs, sepsis

Non-hemolytic: 
-sepsis 
-hypothyroidism 
-Gilbert syndrome
-
41
Q

if you see conjugated hyperbilirubinemia– what is the immediate next step to take and why?

A

get abdominal US to rule out biliary atresia bc this is life threatening

42
Q

Gilbert Syndrome

  • define
  • -defect?
  • cm
A

genetic disorder of bilirubin metabolism
-defect is reduced activity of the enzyme UDP that b/d bili
-high levels of unconjugated bili
CM: very mild jaundice during times of physiologic stress…. illness, dehydration, etc)

43
Q

Viral hepatitis:

  • list the types–MC?
  • can cause?
  • phases
A

5 types: A B C D E
B AND C MC**

Can cause: acute, icteric illness

Phases:

  1. incubation:
  2. prodromal
  3. icteric
  4. recovery
44
Q

Hep B and C cirrhosis are imp RF for?

A

Hepatocellular carcinoma

45
Q

Hep A Virus

  • type of virual genome
  • transmission
  • incubation pd
  • diagnosis (acute vs past exposure)
  • possible chronic infection?
  • vaccine?
A
  • type of virual genome–RNA
  • transmission–fecal oral
  • incubation pd–14-28 days
  • diagnosis
    1. IgM Anti-HAV-specific antibodies–acute
    2. IgG HAV antibody with negative IgM
  • possible chronic infection?–no
  • vaccine?–yes
46
Q

Hep B Virus

  • type of virual genome
  • transmission
  • incubation pd
  • diagnosis (acute vs past exposure vs resolved)
  • possible chronic infection?
  • vaccine?
A
  • type of virual genome–DNA
  • transmission–blood and other body fluids
  • incubation pd–30-180 days
  • diagnosis (acute vs past exposure)
    1. ACUTE INF: +surface HBV antigen protein, positive core IgM antibody
    2. Chronic: +surface antigen, positive core IgG AB
    3. resolved infection: + surface antibody, positive core IgG antibody
  • possible chronic infection?–YES
  • vaccine?–yes
47
Q

Hep C:

  • type of virual genome
  • transmission
  • incubation pd
  • diagnosis (acute vs chronic)
  • possible chronic infection?
  • vaccine?
A
  • type of virual genome–RNA
  • transmission–blood
  • incubation pd–14days -6MO
  • diagnosis (acute vs past exposure)
    1. HCV RNA (more sensitive)
    2. Anti-HCV-AB
    3. chronic: both HCV RNA and Anti-HCV positive
  • possible chronic infection?–yes
  • vaccine?–no
48
Q

Hep D:

  • type of virual genome
  • transmission
  • incubation pd
  • diagnosis (acute vs past exposure)
  • possible chronic infection?
  • vaccine?
A

D for “defective” virus
*requires Hep B to cause co or superimposed infection

  • type of virual genome–RNA
  • transmission–Blood and other body fluids
  • incubation pd–requires Hep B for replication
  • diagnosis (acute vs past exposure)
    1. Anti-HDV Antibody
    2. HDV RNA
    3. also do HBV serologies
  • possible chronic infection?–yes
  • vaccine?–no
49
Q

Hep E:

  • type of virual genome
  • transmission
  • incubation pd
  • diagnosis (acute vs past exposure)
  • possible chronic infection?
  • vaccine?
A
  • type of virual genome–RNA
  • transmission–fecal-oral
  • incubation pd–14-70 days
  • diagnosis (acute vs past exposure)
    1. Anti-HEV AB
    2. HEV RNA
  • possible chronic infection?–Yes
  • vaccine?–No in US…. but yes in china
50
Q

how does a baby MC get Hep B?

A

infected by their mothers

51
Q

% of Hep A infections occur in kids?

A

30-50%

52
Q

which hepatitis can cause chronic infection in kids? MC?

A

HCV and HBV MC

53
Q

Fatty Liver Dz

  • also called?
  • list the two types
A

Steatohepatits

  1. Alcoholic liver Dz
  2. Nonalcoholic Fatty liver Dz (NAFLD)
54
Q

ETOH effect on liver

A

direct toxin to the hepatocytes
*messes with FA oxidation– causing fatty liver + oxidative stress–kills hepatocytes–inflammation and fibrosis of liver

when cells die– leaks out their content which causes inflammation

55
Q

Non alcoholic fatty liver dz

  • patho
  • etiologies
  • can progress to?
A

infiltration of hepatocytes with fat
occuring in the absence of ETOH intake
*fat accumulation– creates inflammation– incrs oxidative stress

Can progress to– NASH: non alcoholic steatohepatitis–>can progress to cirrhosis–>end stage liver dz
**very common

etiologies:
- obesity
- hyperlipidemia
- glucocorticoid use
- DM

56
Q

difference b/w NASH and NAFLD

A

NAFLD–relatively benign, not associated with fibrosis or malignant potential

NASH–assoc with inflammation and fibrosis, potential to progress to cirrhosis— can be premalignant

57
Q

whats a very common reson for incr LFTs?

A

nonalcoholic fatty liver dz

58
Q

Acute liver failure aka?

A

Fulminent hepatits

59
Q

timing for acute hepatitis

A

> 6 MO

60
Q

MCC of fulminant hepatitis (adults and kids)

A

Adults–acetominophen OD

kids– MCC is idiopathic, second MC is tylenol

61
Q

reye syndrome

A

kids are given ASA during or after a viral infection– can lead to fulminant hepatits

62
Q

cirrhosis

  • define
  • reversible?
  • two major physiologic events + their subsequent issues
  • how do we assess functional reserve?
A
  • chronic liver dz
  • fibrosis, disruption of liver architecture & widespread nodules in lover
  • fibrous tissue replaces damaged or dead hepatocytes
  • typically irreversible

**inflammation starts the process— very important to note
inflammation–>hepatocyte death–>scarring/fibrosis–>cirrhosis + portal HTN

  • **the distortion of liver anatomy causes:
    1. Decreased blood flow thru liver—biliary channels become blocked–> HTN in portal circulation—>ascites, periph edema, splenomegaly, varicosity of veins
  1. Hepatocellular failure–>impariment of biochemical functions such as: decr albumin synthesis and decr clotting factor synthesis

Assess hepatic functional reserve:

  • Child-Pugh Score*estimates the hepatic reserve in liver failure–measures dz severity and predictor of morbidity and mortality
  • Class C= more severe
  • Class A=milder
63
Q

what do we need to worry about with a cirrhotic patient going NPO

A

hypoglycemia**

because there is impaired gluconeogenesis

64
Q

complications from cirrhosis

A
  1. portal HTN–abnormally high pressure in the portal venous system caused by resistance to portal blood flow
    - ->intraheptic or posthepatic

Portal HTN can then further cause:
1. varices

  1. splenomegaly–>hepatopulmonary syndrome and portopulmonary syndrome
  2. Vomiting blood from bleeding esoph varices
65
Q

Portal HTN

  • develops when?
  • worsened by?
  • where is resistance
  • CM?
  • MCC in developed world ?
A
  • dev when resistance to portal blood flow
  • worsened by increased portal collateral blood flow
  • resistance MC in liver (cirrhosis)
  • can be prehepatic: portal vein thrombosis
  • can be posthepatic: Budd-Chiari syndrome

Often asymptto UNTIL complications develop—–splenomegaly, abdominal wall collateral vessels, thrombocytopenia (cannot clot properly)

MCC is cirrhosis–dev world
MCC is schistosomiasis (parasite) in underdev world

66
Q

how does liver dz lead to bleeding varices?

A
  1. cirrhosis of liver: causes incr in intrahepatic vascular resistance due to architectural distortion and deficiency of NO
  2. Portal HTN–>results from incr intrahepatic resistance (decr outflow) + splanchnic arteriolar vasodilation (increased inflow)
  3. Varcies form in esophagus and stomach by dilation of preexisting vessels and by active angiogenesis–>they increase in size w/ severity of portal HTN–can rupture and bleed when pressure reach maximal point
67
Q

varices develop seconary to?

  • result of?
  • % of cirrhotic PTs with varices
A

portal HTN

result of: collateral circulation

50% of cirrhosis pT have varices

68
Q

Ascites

  • define
  • MCC
  • development of it?
  • mortality rate? %
A

accumulation of fluid in the peritoneal cavity
MCC=cirrhosis

Development:
1. portal HTN–>decreased synthesis of albumin by liver–>decrs oncotic pressure–>splanchnic vasodilation–>renal sodium and water retention–>activates RAAS system

25% mortality rate in 1 yr if associated w/ cirrhosis

**decrease in the oncotic pressure moves fluid from the vascular space into the tissue

69
Q

hepatorenal syndrome

  • define
  • types
  • lab work to show this?
A

functional renal failure that develops as a complication of adv liver dz

Type 1: rapid: trigger–>sepsis or ETOH binge with a bad liver –HIGH mortality rate– weeks

Type 2: slow: diruetic resistance–still bad prognosis but takes months

CM:
Oliguria–small amt of urine
complications of adv liver dz

Lab work: rise in Creatinine in a cirrhotic patient—VERY SERIOUS*****

70
Q

Hepatic Encephalopathy

  • patho?
  • dev quickly with?
  • dev slowly with?
  • early s/s
  • later s/s
  • tx?
A

live failure–>inc ammonia levels–>increas in b/d of ammonia into glutamine in the brain–>acts like a neurotoxin

quickly with fulminant hepatitis
slowly with liver dz

early: subtle changes in personality, memory loss, irritability, disinhibition, lethargy and sleep disturbance
later: confusion, disorientation to time and space, flapping tremor (asterixis), slow speech, bardykinesia, stupor, convulsions, coma

TX:
-lactulose helps via inhibition of ammonia production in intenstines

71
Q

gluatmine has what kind of effects on braiN?

A

excitatory– can cause cerebral edema

72
Q

Wilson Dz

-what is it

A

autosomal recessive defect of COPPER metabolism
*causes toxic levels of copper to accum in liver, brain, kidneys, cornea

  • copper cannot metabolized
  • mutation of the ATP7B gene–>impairment Cu excretion into the bile–> (normally in the bile Cu is converted into ceruloplasmin and excreted out) but this does not happen and Cu accumulated to toxic levels
73
Q

Liver Cancer

  • etiology
  • types + CM
A

MC caused by mets spread from a primary site elsewhere

  1. hepatocellular carcinoma: associated with HBV/HCV and cirrhosis—- usuually asympto
  2. Cholangiocellular carcinoma (CA of biliary tree)–CM is insidious… pain, loss of apeptie, wt loss, gradual onset of jaundice
74
Q

Gallbladder CA

-causes?

A

usually caused by mets

  • chronic inflammation may trigger dysplasia and progress to met
  • early stages usally asympto
  • MC caught in later stages

Pathophysiology (13 decks)

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