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GI/GU > GI/GU > Flashcards

GI/GU Flashcards

1
Q

medication classes that can cause GERD (7)

A 
Anticholonergics
ASA / NSAID
Barbiturates
BZDs
Bisphosphonates
CCBs
Electrolytes (Fe, K+)
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2
Q

How do anticholinergics cause GERD?

A

anti-cholingergics = anti- SLUD, so causes constipation, slowing gastric emptying = reflux

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3
Q

How do ASA / NSAIDs cause GERD?

A

inhibit prostaglandin secretion. prostaglandin helps form protective layer in stomach. Without it, ulcers and bleeding may occur.

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4
Q

How do barbiturates cause GERD?

A

slow gastric emptying

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5
Q

How do BZDs cause GERD?

A

causes less LES functioning

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6
Q

How do bisphosphonates cause GERD?

A

they can cause problem directly on the esophagus

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7
Q

How do CCBs cause GERD?

A

Ca causes constipation, slowing system down, delaying gastric emptying

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8
Q

How do electrolytes cause GERD?

A

a lot of N/V and GI upset with these medications

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9
Q

TYPICAL symptoms of GERD (and what does “typical” mean?) [4]

A

Typical symptoms are those that are subjective and patient-reported, so a clinician may not observe them themselves.

Typical symptoms of GERD: heartburn/pyrosis
regurgitation
hypersalivation
belching

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10
Q

OTHER symptoms of GERD [4]

A

WHEN: water brash, hiccups, early satiety, N/V

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11
Q

ALARM SIGNS of GERD (and what does “alarm signs” mean?) [6]

A

Alarming signs: severe, hospitalize

Alarming signs of GERD:
continual pain
dysphagia/odynophagia
coffee-ground emesis
melena stool
unexplained weight loss
anemia
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12
Q

ATYPICAL symptoms of GERD (and what does “atypical” mean?) [6]

A

atypical symptoms- are signs/symptoms that are a little more alarming, but not quite an alarm sign

Atypical symptoms of GERD:
non-cardiac chest pain
chronic cough
vocal cord irritation
hoarseness
pharyngitis
dental erosions
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13
Q

signs vs symptoms

A

signs- measurable (lab values, tests), objective; something a healthcare provider can measure, observe and/or document

symptoms- subjective to the patient (ex: pain) willing to or remembering their experience

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14
Q

Modifications for GERD

A

avoid trigger foods or take TUMS or Pepcid after eating
avoid having large meals; causes irritation/preventing closing of the LES
don’t eat before you sleep
sometimes pill gets lodged in back of throat; drink with water
stop smoking
limit alcohol intake
lose weight
elevate head of bed by 6-8 inches so food goes down via gravity
tight-fitting clothes restrict and push contents back up

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15
Q

PUD

A

PUD = peptic ulcer disease; ulcerative disorder

the ulcers can be duodenal or in the upper GI tract.
Once an ulcer forms, it’s kind of like a pothole; these erosions keep getting bigger as bile acids settle there- can spread to muscularis mucosa

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16
Q

clinical presentation: duodenal ulcer vs gastric ulcer

A

duodenal ulcers typically present with epigastric pain, food will RELIEVE pain of the ulcer, H. pylori known to cause

gastric ulcers; you may see epigastric pain, but more commonly see N/V, food will WORSEN the pain because it stimulates even more bile acid formation, NSAID like aspirin cause (inhibit protective production of prostaglandins, sit on stomach)

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17
Q

PUD vs GERD

A 
PUD = ulcers
GERD = disfunction of LES, reflux of food into esophagus

PUD can present similar to GERD but are different

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18
Q

Contributory factors: GERD

A 
aspirin
worry/stress
caffeine
spicy foods
all tobacco use (especially smoking)
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19
Q

Top 200 GERD / PUD agents

A

PPIs and H2RAs

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20
Q

PPIs vs H2RAs in treatment of GERD or PUD

A
  • both highly effective
  • both gastric anti-secretory
  • PPIs work better to prevent acid production, but in general
  • H2RAs work after acid is produced and block histamine 2 receptors
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21
Q

PPIs (Top 200 name brand and generic)

A
  • omeprazole (Prilosec)
  • pantoprazole (Protonix)
  • lansoprazole (Prevacid)
  • esomeprazole (Nexium)
  • dexlansoprazole (Dexilant)
22
Q

H2RA (Top 200 name brand and generic)

A

ranitidine (Zantac)

famotidine (Pepcid)

23
Q

H2RA use

A
  • PUD, mild-moderate GERD
  • MOA: inhibit gastric parietal cell H2 receptors, thus suppressing basal and post-prandial acid secretions.
  • Absorbed in the intestine; don’t directly act directly in stomach- go though intestines and body and then have their effect.
  • Generally safe and well-tolerated (HA, somnolence, dizziness; may take without regard to meals
  • IV and PO
  • Tachphylaxis may occur
24
Q

PPI

A

PUD, mild-moderate GERD

MOA: inhibiting proton pump (H/K ATPase), preventing acid from even being produced, so that’s why it’s effect is a little better than the H2RAs

This drug is not going to be active locally initially, must be absorbed, go to liver, and do its work there. prodrugs= not activated until absorbed, goes to liver, converted to active form, circulated back to stomach and inhibits those proton pumps

CYP 2C19 is the enzyme that converts it to active form

Well tolerated (HA, diarrhea, abdominal pain)

Consequences:

  • Lower Ca and B12 absorption
  • increased risk of community acquired pneumonia and CDAD
25
Q

FDA warning for PPIs

A

PPIs + Plavix
both require CYP2C19 to be activated to convert prodrug to active form
-increased risk of CV events
-if you really need to take a PPI with Plavix, use the PPI with the least CYP2C19:
= pantoprazole and rabeprazole (Aciphex)

26
Q

sucralfate

A

Carafate

Use for relief of pain associated with PUD; coats ulcers

27
Q

What electrolytes cause constipation? diarrhea?

A

Constipation: Ca, Al, Fe
Diarrhea: Mg

28
Q

contsipation

A

less than 3 poops a week

29
Q

Modifications: constipation

A
  • increase fiber with fruits and vegetables,
  • drink more fluids,
  • exercise more as it can promote peristalsis, -poor bowel habits = basically holding it on, making your body slow itself down
30
Q

Drug-induced constipation [7]

A
  • Analgesics
  • Narcotics
  • Antacids (Al, Ca)
  • Anticholinergics
  • Ca supplements
  • CCBs
  • Iron tablets
31
Q

Laxative

A

drugs that help treat constipation

Miralax, Glycolax = PEG 3350
MOA: hyperosmotic agent
pulls fluid from the body into the digestive tract. This pulling also causes distention which this pulling/pressure tells brain to promote peristalsis

32
Q

Diarrhea: Etiologies

A
  • infections
  • IBD (Crohn’s, ulcerative colitis)
  • malabsorption (lactose intolerance)
  • secretory hormonal tumor
  • drug-induced
  • motility disturbance (diabetic gastroparesis, IBS, hyperthryoidism)
33
Q

Drug-induced Diarrhea

A 
Laxatives
Antacids (Mg)
Chemotherapy
Antibiotics
metformin
quinidine
digitalis/digoxin
antiretrovirals
NSAIDs
colchicine
34
Q

Non-pharmacological treatment: Diarrhea

A

Explore possible causes and fix that first
Water, electrolyte, and acid-base (HCO3) disturbances may occur
Diarrhea is a host-defense mechanism; our body’s natural way to get rid of stuff

35
Q

Pharmacological treatment: Diarrhea

A

anti-motility agent = Lomotil (diphenoxylate w/ atropine) spelling
MOA:
diphenoxylate is the opioid, small dose. Causes constipation.
atropine = anti-cholinergic/anti-muscarinic, used to prevent/discourage abuse of opioid

36
Q

Treatment: IBS

A

Anti-spasmodic agents are generally for short term relief
usually anti-cholinergic; act on smooth muscles to block over-peristalsis

dicyclomine (Bentyl)
blocking acetyl choline at the parasympathetic sites (anti-SLUD side effects)
anti-SLUD side effects

37
Q

Nausea: drugs

A

anti-emetics

prochlorperazine (Compazine), promethazine (Phenergan), Zofran, Reglan

all anti-nauseas are antagonists of some sort; multiple ways to prevent nausea

38
Q

prochlorperazine (Compazine) vs promethazine (Phenergan)

A

prochlorperazine (Compazine):

  • anti-dopaminergic effect (blocks dopamine receptors in CNS, blocks vagus nerve GI)
  • Side effects: orthostasis, EPS, blurry vision, CNS depression, tardive dyskinesia

promethazine (Phenergan):
anti-histaminic effect (h1 blocker) and anti-dopaminergic effect
-Side effects: sedation, confusion, disorientation, EPS, orthostasis

39
Q

Zofran

A

MOA: selective 5-HT3 antagonist (SI)
1st line for chemotherapy induced N/V
Pregnancy
Side effects: HA, fatigue, constipation

40
Q

Reglan

A

metaclopramide

MOA: dopamine 2 receptor antagonist, increase peristaltic activity in gut, causes some CNS side effects, EPS. safe to use in pregnancy

41
Q

Urinary Bladder Modifiers

A

oxybutyinin (Ditropan)
tolterodine (Detrol)
solifenacin (Vesicare)

anti-muscarinics
anti SLUD side effects

for women

42
Q

alpha 1 blockers for hypertension also helped with urinary control, dribbling, and force

A

terazosin (Hytrin)
doxazosin (Cardura)
peripheral vasodilation^

tamsulosin (Flomax)
more localized vasodilation on neck of bladder and prostate. does not cause as much peripheral side effects

Side effects: abnormal ejaculation, infection, pharyngitis, sinusitis, HA, dizziness, asthenia

43
Q

prostate anti-inflammatory

A

finasteride (Proscar)
dutaseride (Avodart)
suppress conversion of testosterone to 5-alpha-DHT which is responsible to increase size of prostate

these drugs are very effective, but very difficult to be on: causes depression, decreased libido, growth of breast tissue

Side effects:

  • breast tissue overgrowth/gynacomastia
  • depression
  • male infertility
  • decreased libido

Avodart does not have as much side effects (mainly depression)

44
Q

PDE-5 inhibitors

A

sildenafil (VIagra)
tadalafil (Cialis)

Side effects: HA, flushing, priapism(overshoot)

45
Q

If someone of Imdur (a nitrate), and come in with sildenafil (Viagra) or tadalafil (Cialis)- it is contraindicated (do not dispense)

A

Contraindication: nitrates with alpha-1 adrenergic blockers (2 vasodilators, cause over expression) and alpha-1 blockers

also don’t want to use with alpha 1 blockers because they block alpha 1 in periphery and also cause peripheral vasodilation (lead to over-expression of vasodilation- hypotension, blood drawing away from the heart), but you COULD use tamsulosin (because it is a SELECTIVE alpha 1 blocker on the neck of the bladder and prostate)

46
Q

Many NT receptors are located in the ______, ______, ______. What types of receptors?

A

vomitting center, CTZ, GI tract

cholinergic, dopaminergic, histaminic, and serotonergic receptors

47
Q

All anti-emetics ______ receptors

A

antagonize

48
Q

How long does may it take to produce a bowel movement when using PEG 3350?

A

2-4 days

49
Q

dicyclomine blocks ___ at ________ sites, decreasing smooth muscle contraction

A

Ach; parasympathetic

50
Q

Urinary bladder modifiers are anti_____ agents with _______ side effects

A

anti-muscarinic agents; predictable

51
Q

_____ are preferred for BPH treatment over ________ because of the male sexual side effects associated with them, leading to non-adherence.

A

alpha-1 blockers preferred

over 5-alpha reductase inhibitors

52
Q

PDE5-inhibitors are effective but have major DDI interactions with _____ and ______ used to treat hypertension

A

nitrates and alpha-1 blockers (exception = Flomax)

-can cause hypotension

GI/GU (1 decks)

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