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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
multiple episodes of acute pancreatitis
can lead to chronic pancreatitis loss of digestive ability Increased scarring tissue of the pancreas
26
chronic pancreatitis is marked by
loss of exocrine and endocrine function of pancreas chronic LUQ pain calcification of pancreas on imaging
27
liver function
metabolism manufactures storage detoxification and excretion
28
metabolism in liver
of carbohydrates, proteins, fat from the portal system
29
manufacturing in liver
plasma proteins and coagulation factors are produced here inc. albumin
30
storage in liver
liver stores vital chemicals such as vitamin 12, D, A, etc
31
detoxification and excretion in liver
chemicals, drugs are detoxified bc of cytochrome P-450 and glucuronidation
32
basic anatomy of liver
located in RUQ, under diaphragm liver weighs 3lbs
33
dual circulation of liver
partially deoxygenated blood from the gut via portal system fully oxygenated blood from hepatic artery
34
where do the two liver circulatory systems mix in liver
**hepatic sinusoid** and drained by hepatic v. to IVC
35
lobule
**hepatocytes** organized in plate like structures **around central large capillary** where blood is mixed (sinusoid)
36
blood percolation in lobule
**percolates from outside of lobule inward** during this time *toxins are neutralized* and *nutrients are absorbed* before the blood is shunted into sinusoid
37
blood flow in liver
flows from periphery of liver lobules (portal tracts) to the center (central veins)
38
bile flow
bile flows from center of liberal lobules (central veins) to the periphery (portal tired)
39
cells near portal tracts
rich in nutrients and high in oxygen less susceptible to damage by toxin or shock
40
cells near central veins
low in nutrients and oxygen more susceptible to damage by toxin and shock
41
inflammation of liver
hepatitis
42
best way to measure liver function?
PT/INR Bc coagulation factors are made in liver
43
LFT
best way to measure liver inflammation elevation of transaminases ALT/AST/ALKP/bilirubin
44
types of viral hepatitis
Hepatitis A Hepatits B Hepatits C
45
hepatits A
food and waterborne outbreaks only kind to cause spiking fevers only acute hepatitis, no chronic carrier state
46
hepatitis B
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
hepatitis C
spread by needles and medical equipment difficult to get but can cause chronic hepatitis curable now
48
acute viral hepatitis lab
transaminase elevation (ALT/AST) in thousands
49
chronic viral hepatic lab
transaminase LFTs in hundreds
50
HAC treatment
supportive care alone
51
HCV and HBV treatment
if chronic, treatment with antivirus
52
fatty liver disease
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
alcohol on liver
directly hepatotoxic damage is done with long term daily drinking more common in women then men
54
alcoholic liver disease
**daily drinking with concomitant nutritional deficiencies** from poor PO intake --\> worsens liver disease transaminase elevations in hundreds **AST 2x ALT**
55
portal HTN
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
portal HTN in the vessels effect
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
cirrhosis
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
hepatic encephalopathy
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
hepatic encephalopathy can be precipitated by
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
diffuse scarring of liver parenchyma leads to...
**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
collateral circulation forms in which places
1. esophageal varices 2. internal hemorrhoids 3. capat medusae easily ruptured, non compressible vessels
62
why are cirrhotic patients likely to have severe bleeding when collateral vessels rupture?
Liver is responsible for coagulation production If liver isn't working we won't get as much/any coagulation factor production
63
why do liver patients get ascites and anasarca?
unable to produce adequate plasma proteins Decreased onchoitc pressure (and increased hydrostatic pressure for ascities)
64
when RBCs die....
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
what does heme become after RBC breakdown
unconjucated bilirubin must be processed by liver
66
bilirubin
transports heme in body removed from blood by liver conjugated with another substance to render it soluble/less toxic = excreted by kidney
67
conjugated bilirubin is known as
direct bilirubin reacts directly to testing reagent
68
unconjugated bilirubin
indirect less soluble not excreted by kidneys, more toxic
69
jaundice
yellow discoloration of skin and sclera due to elevation of bilirubin
70
etiologies of jaundice
**hepatocellular disease** (hepatitis, cirrhosis, hepatocellular carcinoma) **obstructive disease** (gallstone, cancer of head of pancreas) **hemolytic disease** (lg hematoma, ABO/Rh incompatibility, hemolytic anemia)
71
composition of bile
conjugated biliruben (bile salt) lecithin cholesterol bile is stored in the gallbladder
72
bile salt
hydrophilic and hydrophobic detergent like, emulsifies fat to facilitate digestion by lipase
73
lecithin
phospholipid functions like bile salts
74
cholesterol
vitamin D hormones part of cell membrane structure
75
gallstones
occurs when cholesterol, lectin or bilirubin is at a higher quantity than the other two typically the cholesterol in US
76
five 5s of gall balder disease
1. Fat (more cholesterol) 2. 40 (takes time to accumulate) 3. Fertile (many children =progesterone, improper emptying) 4. Female (estrogen) 5. Family history
77
chronic cholecystitis
if gallstones move into GB neck and tries to go thru cystic duct then roll back into GB AKA gallbladder colic
78
s/s of gallbladder colic
pain in the RUQ radiates to shoulder and lasts several hours before subsiding
79
acute cholecystitis
gallstone moves into GB neck and becomes lodged at entrance of cystic duct
80
symptoms of acute cholecystitis
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
treatment of acute cholecystitis
urgent surgical removal of GB
82
What type of bilirubin in Jaundice caused by hepatocellular disease
Mixed Some conjugated, some unconjugated
83
What type of bilirubin in Jaundice caused by obstructive disease
Conjugated
84
What type of bilirubin in Jaundice caused by hemolytic disease
Unconjugated
85
Cirrhosis or end stage liver disease leads to which problems
**Cardiac** (tachycardia, LVH, volume overload, b-blocker) **Sodium balance** (hyponatremia due to fluid loss)
86
Solution for cirrhosis?
Educate patients on what is disruptive Frequent monitoring Frequent hospitalization
87
How can we tell difference between chronic or acute cholecystitis
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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