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Pathophysiology Final Exam (Exam 4) > Liver, Gallbladder, Pancreas > Flashcards

Liver, Gallbladder, Pancreas Flashcards

1
Q

elevated AST, ALT, or LDH suggest disease of what part of the liver

A

parenchyma

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2
Q

caval obstruction of the liver can lead to what

A

pedal edema

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3
Q

esophageal varices and splenomegaly can be seen due to liver dz due to what

A

portal HTN

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4
Q

why do liver patient’s not clot well

A

prothrombin is made by the liver and the liver is damaged

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5
Q

INR above 1 means what in terms of clottin

A

slow clot and bleeding too much

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6
Q

INR less than 1 means what

A

blood is too thick and clot too much

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7
Q

why is circulating plasma protein decr in liver patients

A

liver makes the plasma proteins

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8
Q

what happens when plasma protein is decreased in liver patients?

A

lots of edema in tissue space (anasarca)

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9
Q

what is anasarca and who is it commonly seen in

A

generalized edema. seen in liver patients

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10
Q

what is ascites and who is it seen in

A

hepatic enlargement due to accumulation of fluid in the peritoneal cavity

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11
Q

what is acites due to (4 reasons)

A
  1. Abdominal organs weeping plasma
  2. Compression of hepatic lymphatic vessels weeping fluid
  3. Hypoalbuminemia (albumin helps hold fluid into the vessels and this is gone in liver pateints)
  4. Sodium/H20 retention due to decreased renal circulation
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12
Q

jaudice/icterus in liver patient’s is caused by what

A

elevated plasma bilirubin (bilirubin cannot become conjugated so it cannot be made water soluble bc the liver is where it is conjugaged with glucoronic acid)

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13
Q

why is breast enlargement seen in liver dz

A

liver is not able to metabolize estrogen

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14
Q

high MELD score = highest chance for mortiality than a low MELD

A

yes

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15
Q

causes of liver disease

A
  1. Autoimmune (hepatitis)
  2. Infections
  3. Toxic damage (drug or alcohol use)
  4. Neoplasia
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16
Q

route of transmission for Hep A

A

oral-fecal

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17
Q

serological blood marker for Hep A

A

IgM antibodies

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18
Q

is there a vaccine for hep a

A

yes

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19
Q

does hep a often cause long term damage to liver

A

no

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20
Q

route of transmission for hep b

A

needles, oral-fecal, STD, dental or medical procedure, childbirth

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21
Q

is hep b a rna or dna virus

A

dna

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22
Q

HAA is associated with what type of hepatitis

A

hep b

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23
Q

Austrialian antigen is associatedd with what hepatitis

A

hep b

24
Q

do most people with hep b recover

A

yes
90% completely recover
10% have chronic, progressive hepatitis and cirrhosis

25
Q

is there a hep b vaccine

A

yes

26
Q

route of transmission for hep c

A

STD, tattoos, childbrith, blood transfusion

27
Q

is there a vaccine for hep c

A

NO

28
Q

does hep c cause long term damage

A

yes.
50% develop chronic hepatitis
20% develop cirrhosis and/or hepatocellular carcinoma

29
Q

what is the route of transmission for hep d

A

STD, needles, oral-fecal, dental and medical procedure (like hep b)

30
Q

which heptatis only occurs as a simulatenous infection with HBV

A

HDV

31
Q

true or false: hep b with hep d has the highest overall mortality rate of all acute viral infections

A

true

32
Q

route of transmission for hep E

A

oral fecal transmission

33
Q

does hep e have a vaccine

A

yes

34
Q

hep e is not very deadly and not seen much in the US but is dangerous for who

A

those who are pregnant

35
Q

causes of Non-alcohiolic fatty liver disasee

A
  • DM
  • Obesity
  • Elevated Cholesterol and Trigs
36
Q

Sclerosing Cholangitis is what

A

autoimmune causing the ducts to scar and things to back up into the liver

37
Q

Cirrhosis of the liver is marked with what

A

Ascites

38
Q

does Prothrombin time and the INR incr or decr with ESLD

A

increases, so someone does not clot as easily and bleeds easily

39
Q

why are low levels of platelets seen with ESLD

A

bc there are low levels of Cytokine Thrombopoientin which is prodcued by the liver and stimulates the production of plateletes

40
Q

why does the pH drop and metabolic acidosis occur during ESLD

A

failure to detoxify NH3 into urea in the liver, so NH3 is converted to NH4+ which throws and extra H+ ion into the bloostream which can lead to acidosis

41
Q

is arterial or venous blood usually more acidic

A

venous blood (venous blood has a lower pH)

42
Q

pH below what level is metabolic acidosis

A

7.35

43
Q

two compensatory mechanisms for metabolic acidosis

A
  1. incr resp rate

2. renal compensation

44
Q

stages of hepatoceullular encephaloapthy

A 
1 = personality changes
2 = muscle involvement
3 = violence
4 = hepatic coma
45
Q

The Glasgow Come scale is on a scale of 3-15 based on 3 things

A
  1. Best eye response
  2. Best verbal response
  3. Best motor response
46
Q

Acute pancreatitis refers pain where usually

A

the back

47
Q

main cause of acute pancreatitis

A

overuse of alcohol

48
Q

prolonged cases of acute pancreatits can result in what

A

auto-digestion of pancreas

49
Q

chronic pancreatitis can come from what

A
  1. acute pancreatitis

2. chronic alcohol abuse

50
Q

what can cause chronic pancreatitis in kids

A

cystic fibrosis (gradual replacement of functional tissue occurs

51
Q

pancreatic neoplasia most often occurs in what type of people

A

those who are black males

52
Q

Cholesithiasis (Gall Stones) most often occurs in who

A

females 40-50 years old

53
Q

6 F’s for Gall Stones

A
  1. Fair
  2. Fat
  3. Female
  4. Fertile
  5. Flatulent
  6. Forty
54
Q

what causes gall stones

A

precipitation of cholesterol and bile pigments. stasis of bile occurs

55
Q

sign and sx of gall stones

A

pain in the upper right quadrant. May radiate in the mid upper back and shoulder

56
Q

Does pain get worse or better when you eat with Gall Stones

A

worse (feel better before you eat)

Pathophysiology Final Exam (Exam 4) (7 decks)

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