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KCSU17 Patho/Pharm Submodule 2 > GI 6/12/17 > Flashcards

GI 6/12/17 Flashcards

1
Q

disordered intestinal and colonic motility

A

irritable bowel syndrome also have hyperalgesia

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2
Q

symptoms of IBS

A

alternation of constipation and diarrhea abdominal cramps bloating perceived distention

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3
Q

what can trigger IBS>

A

stress

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4
Q

treatment for IBS

A

supportive, once other causes are ruled out

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5
Q

Abx associated colitis AKA

A

C. diff colitis pseudomembranous colitis increasingly common

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6
Q

Abx associated colitis

A

prolonged abx use causes other enteric flora to die off and C. difficile grows

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7
Q

symptoms of C. difficile infection

A

enterotoxin causing diarrhea and colonic inflammation

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8
Q

when might you expect c diff colitis?

A

suspected in patients with any Abx exposure who develop diarrhea if immunosuppressant, can occur without Abx use

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9
Q

lab and diagnosis of C. diff colitis

A

labs: very high WBC (>18k) diagnosis: test for toxin or organism DNA in stool samples

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10
Q

treatment of C. diff colitis

A

metronidazole (Flagyl) or oral vancomycin

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11
Q

two main bariatric surgical procedures

A

Lap band Gastric bypass

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12
Q

lap band

A

reversible banding of stomach to make it smaller and increase satiety not as effective

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13
Q

gastric bypass

A

greatly reduces the stomach size and bypass duodenum to reduce absorption permanently esophagus carries food to a stomach pouch pancreatic and gall bladder secretions rejoin digestive system after duodenum

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14
Q

SE of gastric bypass

A

vitamin deficiencies surgical complications (leak, infection)

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15
Q

why do patients lose weight on gastric bypass surgery?

A

Decreasing stomach size and malabsorption

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16
Q

anatomy: movement of bile

A

cystic duct

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17
Q

anatomy: common bile duct

A

site where the cystic duct and extrahepatic bile duct join

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18
Q

zymogens

A

secreted by the pancreas pre-enzyme secreted used for digestion of fat, carbs, and proteins activated only at brush boarder of small intestine

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19
Q

acute pancreatitis

A

activation of zymogens prematurely so enzymes begin to digest the surrounding pancreatic tissue

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20
Q

main causes of acute pancreatitis

A

alcohol gallstones

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21
Q

s/s of acute pancreatitis

A

develop severe boring pain in epigastrium or LUQ with N/V

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22
Q

severe acute pancreatitis

A

2nd degree burn inside peritoneum massive amounts of fluid leave vascular space due to leaky capillaries -patient can easily develop multiple electrolyte abnormalities

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23
Q

acute pancreatitis labs

A

amylase and lipase elevation

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24
Q

treatment of acute pancreatitis

A

supportive trie to put pancreas at rest = NPO control pain and hydrate

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25
Q

multiple episodes of acute pancreatitis

A

can lead to chronic pancreatitis loss of digestive ability Increased scarring tissue of the pancreas

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26
Q

chronic pancreatitis is marked by

A

loss of exocrine and endocrine function of pancreas chronic LUQ pain calcification of pancreas on imaging

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27
Q

liver function

A

metabolism manufactures storage detoxification and excretion

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28
Q

metabolism in liver

A

of carbohydrates, proteins, fat from the portal system

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29
Q

manufacturing in liver

A

plasma proteins and coagulation factors are produced here inc. albumin

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30
Q

storage in liver

A

liver stores vital chemicals such as vitamin 12, D, A, etc

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31
Q

detoxification and excretion in liver

A

chemicals, drugs are detoxified bc of cytochrome P-450 and glucuronidation

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32
Q

basic anatomy of liver

A

located in RUQ, under diaphragm liver weighs 3lbs

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33
Q

dual circulation of liver

A

partially deoxygenated blood from the gut via portal system fully oxygenated blood from hepatic artery

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34
Q

where do the two liver circulatory systems mix in liver

A

hepatic sinusoid and drained by hepatic v. to IVC

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35
Q

lobule

A

hepatocytes organized in plate like structures around central large capillary where blood is mixed (sinusoid)

36
Q

blood percolation in lobule

A

percolates from outside of lobule inward during this time toxins are neutralized and nutrients are absorbed before the blood is shunted into sinusoid

37
Q

blood flow in liver

A

flows from periphery of liver lobules (portal tracts) to the center (central veins)

38
Q

bile flow

A

bile flows from center of liberal lobules (central veins) to the periphery (portal tired)

39
Q

cells near portal tracts

A

rich in nutrients and high in oxygen less susceptible to damage by toxin or shock

40
Q

cells near central veins

A

low in nutrients and oxygen more susceptible to damage by toxin and shock

41
Q

inflammation of liver

A

hepatitis

42
Q

best way to measure liver function?

A

PT/INR Bc coagulation factors are made in liver

43
Q

LFT

A

best way to measure liver inflammation elevation of transaminases ALT/AST/ALKP/bilirubin

44
Q

types of viral hepatitis

A

Hepatitis A Hepatits B Hepatits C

45
Q

hepatits A

A

food and waterborne outbreaks only kind to cause spiking fevers only acute hepatitis, no chronic carrier state

46
Q

hepatitis B

A

spread by infection bodily fluids and sex hardy outside the body so easily causes acute but not chronic hepatitis Via needle sharing, vertical transmission, needle sticks, tattoos

47
Q

hepatitis C

A

spread by needles and medical equipment difficult to get but can cause chronic hepatitis curable now

48
Q

acute viral hepatitis lab

A

transaminase elevation (ALT/AST) in thousands

49
Q

chronic viral hepatic lab

A

transaminase LFTs in hundreds

50
Q

HAC treatment

A

supportive care alone

51
Q

HCV and HBV treatment

A

if chronic, treatment with antivirus

52
Q

fatty liver disease

A

increasingly common extra fat is deposited in liver with release of free radicals, causes damage to hepatocytes asymptomatic but can cause cirrhosis causes liver enzyme elevation and hundreds ALT>AST

53
Q

alcohol on liver

A

directly hepatotoxic damage is done with long term daily drinking more common in women then men

54
Q

alcoholic liver disease

A

daily drinking with concomitant nutritional deficiencies from poor PO intake –> worsens liver disease transaminase elevations in hundreds AST 2x ALT

55
Q

portal HTN

A

diseased liver parenchyma

blood has difficult time getting thru hepatic sinusoids

causes less effective detoxification as well as back up of portal flow

body response is to increase portal pressure = HTN in portal vessels

56
Q

portal HTN in the vessels effect

A

backed up blood causes esophageal varicies and rectal varicies/hemerrhoids

tortured veins, close to surface, easily ruptured

systemic hypotension (blood stuck in liver)

leaky fluid/Ascities

Jaundice

Encephalopathy

hypersplenism

arteriovenous shunting/mechanical obstruction

57
Q

cirrhosis

A

end stage liver disease caused by chronic hepatitis, fatty liver disease or alcoholic liver disease

liver loses capacity to produce plasma proteins and detoxify substances normally

cognitive dysfunction –> hepatic encephalopathy

fibrotic, scarred down liver

58
Q

hepatic encephalopathy

A

cognitive dysfunction due to decreased ability to detoxify and secrete substances from protein metabolism and colonic bacteria activity results in ammonia and other toxin accumulation

59
Q

hepatic encephalopathy can be precipitated by

A
  1. alcohol binge 2. GI bleed (increase in digested protein) 3. reduced liver blood flow (2/2 shock, dehydration infection or protosystemic shunt procedures)
60
Q

diffuse scarring of liver parenchyma leads to…

A

portal venous obstruction and increased portal blood pressures

this causes weak veins to engorge and collateral to form to accommodate back up backed up pressure = leaky capillaries and decreased onchotic pressures =ascites

61
Q

collateral circulation forms in which places

A
  1. esophageal varices 2. internal hemorrhoids 3. capat medusae easily ruptured, non compressible vessels
62
Q

why are cirrhotic patients likely to have severe bleeding when collateral vessels rupture?

A

Liver is responsible for coagulation production If liver isn’t working we won’t get as much/any coagulation factor production

63
Q

why do liver patients get ascites and anasarca?

A

unable to produce adequate plasma proteins Decreased onchoitc pressure (and increased hydrostatic pressure for ascities)

64
Q

when RBCs die….

A

Hgb is broken down to HgB and iron by reticuloendothelial cells (spleen, liver sinusoids, bone marrow lymph)

iron is recycled for new HgbB and transported to marrow

65
Q

what does heme become after RBC breakdown

A

unconjucated bilirubin

must be processed by liver

66
Q

bilirubin

A

transports heme in body

removed from blood by liver

conjugated with another substance to render it soluble/less toxic = excreted by kidney

67
Q

conjugated bilirubin is known as

A

direct bilirubin reacts directly to testing reagent

68
Q

unconjugated bilirubin

A

indirect less soluble not excreted by kidneys, more toxic

69
Q

jaundice

A

yellow discoloration of skin and sclera due to elevation of bilirubin

70
Q

etiologies of jaundice

A

hepatocellular disease (hepatitis, cirrhosis, hepatocellular carcinoma)

obstructive disease (gallstone, cancer of head of pancreas)

hemolytic disease (lg hematoma, ABO/Rh incompatibility, hemolytic anemia)

71
Q

composition of bile

A

conjugated biliruben (bile salt) lecithin cholesterol bile is stored in the gallbladder

72
Q

bile salt

A

hydrophilic and hydrophobic detergent like, emulsifies fat to facilitate digestion by lipase

73
Q

lecithin

A

phospholipid functions like bile salts

74
Q

cholesterol

A

vitamin D hormones part of cell membrane structure

75
Q

gallstones

A

occurs when cholesterol, lectin or bilirubin is at a higher quantity than the other two typically the cholesterol in US

76
Q

five 5s of gall balder disease

A
  1. Fat (more cholesterol) 2. 40 (takes time to accumulate) 3. Fertile (many children =progesterone, improper emptying) 4. Female (estrogen) 5. Family history
77
Q

chronic cholecystitis

A

if gallstones move into GB neck and tries to go thru cystic duct then roll back into GB AKA gallbladder colic

78
Q

s/s of gallbladder colic

A

pain in the RUQ radiates to shoulder and lasts several hours before subsiding

79
Q

acute cholecystitis

A

gallstone moves into GB neck and becomes lodged at entrance of cystic duct

80
Q

symptoms of acute cholecystitis

A

pain on RUQ that radiates to shoulder and lasts several hours but doesn’t go away become more ill and develop fever and systemic toxicities

81
Q

treatment of acute cholecystitis

A

urgent surgical removal of GB

82
Q

What type of bilirubin in Jaundice caused by hepatocellular disease

A

Mixed Some conjugated, some unconjugated

83
Q

What type of bilirubin in Jaundice caused by obstructive disease

A

Conjugated

84
Q

What type of bilirubin in Jaundice caused by hemolytic disease

A

Unconjugated

85
Q

Cirrhosis or end stage liver disease leads to which problems

A

Cardiac (tachycardia, LVH, volume overload, b-blocker)

Sodium balance (hyponatremia due to fluid loss)

86
Q

Solution for cirrhosis?

A

Educate patients on what is disruptive Frequent monitoring Frequent hospitalization

87
Q

How can we tell difference between chronic or acute cholecystitis

A

Symptoms

Chronic: pain will subside

Acute:pain will never stop, monitor for fever

Do ultrasound

Chronic: thick wall, stones

Acute: hypertrophy and inflammation =fluid accumulation)

KCSU17 Patho/Pharm Submodule 2 (14 decks)

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