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Clinical Pharmacology 2 > Cirrhosis, GERD, PUD > Flashcards

Cirrhosis, GERD, PUD Flashcards

1
Q

progressive fibrosis and distortion of the liver, commonly from alcohol, hepatitis, NAFLD, autoimmune hepatitis, leading to portal HTN and liver dysfunction, and with complications like ascites, varices, hepatic encephalopathy, SBP, and hepatorenal syndrome

A

cirrhosis

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2
Q

what are labs to assess cirrhosis

A

ALT/AST
albumin
PT
INR
GGT
ALP

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3
Q

hypoalbuminemia
decreased plasma oncotic pressure
excessive fluid leaks into peripheral tissues

A

ascites

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4
Q

volume expander, binds toxins/inflammatory mediators, renal perfusion support, if >5L is removed

A

albumin in cirrhosis

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5
Q

what are the three indications for albumin use?

A
  • large volume paracentesis
  • SBP w/ abx
  • hepatorenal syndrome
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6
Q

what’s dosing for albumin

A

6-8/L fluid removed
1.5g/kg on day 1, 1 g/kg on day 3

1g/kg/day for 2 days (max 100g/day)

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7
Q

use a combo of sprinolactone +/- furosemide with 100:40 ratio to avoid electrolyte imbalance in —

A

ascites

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8
Q

What are other treatments for ascites

A

salt restriction <2g/day
avoid NSAIDs

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9
Q

a common complication of cirrhosis is

A

esophageal varices

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10
Q

how do you treat variceal bleeding?

A
  • octreotide (reducing splanchic blood flow)
  • endoscopic band ligation (definitive)
  • antibiotics IV ceftriaxone x 8 days
  • non selective beta blockers for 2ndary prophylaxis (nadolol/propanolol)
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11
Q

if non selective BBs are contraindicated for variceal bleeding, use

A

imdur (isosorbide mononitrate)

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12
Q

mimics natural somatostatin and decreases splanchnic blood flow, decreasing pressure in varices, inhibiting vasodilation in splanchnic ciruclation
lower portal pressure = lower variceal bleeding = lower GI hormone release

A

octreotide

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13
Q

what are ADRs of octreotide?

A

glucose regulation, pancreatitis, diarrhea

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14
Q

NH3 –> urea –> increased ammonia –> confusion, reversal of day-night pattern, asterixis

A

hepatic encephalopathy

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15
Q

What’s first line for hepatic encephalopathy?

A

lactulose (acidifies the gut allowing conversion of ammonia –> ammonium), every 30 min to an hour until BM produced

Rifaximin (recurrent), avoid sedatives + opoids

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16
Q

non-absorbable antibiotic, inhibit bacterial RNA synthesis, altering glut flora –> less ammonia-producing bacteria, NOT USED AS MONOTHERAPY

A

rifaximin

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17
Q

rifaximin ADRs

A

peripheral edema/ascites, superinfection in gut

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18
Q

development of renal failure in patients with cirrhosis, renal vasoconstriction

A

hepatorenal syndrome

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19
Q

how do you treat hepatorenal syndrome

A

combo of albumin + octreotide + midodrine
to increase MAP

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20
Q

hepatorenal tx ADRs

A

supine HTN, paresthesia

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21
Q

medications for Type I hepatorenal syndrome

A

albumin + vasoconstrictors
midodrine + octreotide
norepinephrine in ICU
monitor MAP + UO
improve renal perfusion!

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22
Q

alpha 1 agonist, increasing systemic vascular resistance via vasoconstriction, increasing perfusion pressure to kidneys, used with octreotide and albumin

A

midodrine MOA

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23
Q

commonly caused by e.coli, klebsiella, strep
>/= 250 in ascitic flood
+ fever, leukocytosis, AMS

A

SBP

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24
Q

treating SBP –

A

empiric antibiotics = IV cefotaxime or ceftriaxone, FQs, priamry prophalyaxis/treatment for varices or ascites, secondary if had one episode previously (bactrim, ciprofloxacin)
+ albumin

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25
primary prophylaxis for SBP is for
high risk patients without prior but with ascitic fluid protein <1.5 AND impaired renal function or advanced liver disease
26
what is primary prophylaxis for SBP?
norfloxacin, ciprofloxacin, bactrim
27
secondary prophylaxis for SBP is for
any patient with prior SBP episode
28
What is secondary prophylaxis for SBP?
norfloxacin, ciprofloxacin, bactrim.. (Same?)
29
bile salt can cause itching for some patients -- how do you treat?
-antihistamines (1st gen) - bile acid sequestrants (separate from other meds!) - TCAs
30
non-pharm management of GERD
weight loss, elevating head of bed/staying upright after meals, avoid large meals and foods that wrsen, avoid eating 2-3 hours before bedtime, smoking cessation, avoid bending for prolonged periods, dietary modifications, smaller meals
31
what is the site of action?
parietal cells
32
what are other cells that help in acid secretion?
acetycholine (M3) histamine (H2) gastrin (CCK-B) H/K ATPase pump
33
What are general drug targets for GERD?
H2 blockers block H2 PPIs inhibit proton antacids neutralize acid misoprostol increase mucus and bicarb sucralfate form protective barrier
34
calcium carbonate, aluminum hydroxide, magnesium hydroxide
antacids
35
diarrhea is a common SE in what antacid?
magnesium hydroxide
36
other antacid SE?
constipation (aluminum) electorlyte imbalance
37
milk-alkali syndrome occurs with
calcium carbonate = hypercalcemia, metabolic acidosis, renal impairment
38
calcium antacids MOA
neutralize gastric acidity resulting in increased gastric and duodenal pH
39
what are DIs of calcium antacids?
decrease absorption of other meds, separate for at least 2 hours from other meds
40
what's the MOA of magnesium/aluminum antacids?
magnesium hydroxide reacts with HCl in stomach, aluminum hydroxide neturalizes hydrochloride to increase pH separate from other meds
41
magnesium/aluminum antacid CIs
avoid in renal failure, can accumulate leading to toxicity
42
inhibit histamine at H2 receptors, prevents histamine-induced H+ secretion, decreasing gastrin and pepsin
famotidine (H2 receptor blocker)
43
famotodine is for
symptoms <2x/week also for allergic reactions, 1-3 hours, antisecretory effect in 10-12 hours
44
What are SE of famotodine?
headache, diarrhea rare: gynecomastia, confusion, thrombocytopenia, QTc prolongation in renal impairment >/= 2 years = B12 deficiency DIs with CYP inhibition, cimetidine the worst
45
irreversibly inhibit proton pump in parietal cells, prodrugs, that must be taken on an empty stomach 1 hour before a meal (increased in elderly/asian patients) in those with symptoms >2x/week
PPIs
46
full acid inhibiton by PPIs occurs
3-4 days after 1st dose
47
PPIs are metabolized by
2C19, 3A4, inhibits 2C9, 2C19 (remember clopidogrel is converted by 2C19!
48
What are ADRs of PPIs?
headache, diarrhea, B12 deficiency, hypomagnesemia, increased risk of C. diff, fractures, pneumonia
49
long term PPI concern
refractory GERD, chronic anticoag, Barrett's, nutrinet malabsorption (Mg, Ca, B12), infection, bone health, renal disease, dementia
50
PGE1 analog, increasing mucus and bicarb secretion, preventing steroid and NSAID induced ulcers
misoprostol
51
What are ADRs of misoprostol?
diarrhea, cramping, uterine contractions (can lead to uterine rupture), pregnancy category X
52
forms viscious barrier at ulcer base by binding + charged proteins in exudate protecting from peptic acid, pepsin, bile salts, in use of duodenal ulcers, mucosal protection, taken QID, last line
sucralfate
53
can you use sucralfate with PPIs or H2 blockers?
NO, needs acid to be activated
54
What are ADRs of sucralfate?
constipation, affect absorption of other drugs
55
duodenal or gastric: burning, gnawing, aching, hunger-like, epigastric, empty stomach, nocturnal
duodenal
56
duodenal or gastric: early abdominal fullness, soon after eating, daytime
gastric
57
what helps h pylori survive in an acidic environment?
urease
58
what's the best dx test for h pylori?
stool antigen test
59
what's first line of H pylori?
PPI + bismuth + metronidazole + tetracycline / amox
60
What's second line non-bismuth?
PPI + clarithro + amox + metro PAC or PMC confirm eradication >/= 4 weeks later
61
What are tx for PUD?
antacids cytoprotective agents (sucralfate, misoprostol, bismuth)
62
dissociates to provide bicarb ion which neutralizes acid in GI tract, combined with other meds (NSAIDs or ASA, OTC with PPI)
sodium bicarbonate
63
What are ADRs of sodium bicarb?
GI: flatulence, bloating electorlyte disturbances absorption of other meds affected
64
PUD treatments for acid -
PPIs H2 receptor antagonists (not very popular)

Clinical Pharmacology 2 (13 decks)

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