Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathophysiology - Gastrointestinal > GI Pharmacology 1 and 2 > Flashcards

GI Pharmacology 1 and 2 Flashcards

1
Q

Who tends to get gastric vs duodenal ulcers?

A

Gastric - older females

Duodenal - younger males

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are considered the high risk vs low risk NSAIDs for causing ulcers?

A

High risk - indomethacin, ketoroLAC (mainly used as analgesic per sketchy), aspirin, piroxicam (think of the sox cam in sketchy)

Low risk: Ibuprofen, diclofenac, naproxen, meloxicam (more COX-2 per sketchy, thus less side effects), especially celecoxib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the risk factors for chronic ulcers?

A

Age > 60 years
Concurrent use of corticosteroids / anticoagulants
Use of several or high dose NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the adverse drug reactions by all H2 receptor antagonists?

A

Headache, drowsiness, fatigue, can cross BBB and cause confusion and dizziness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What adverse drug effects are more specific to cimetidine?

A

Cimetidine - potent inhibitor of CYP450, so rarely used for this release

Also decreases renal excretion of creatinine - remember from renal

Can cause gynecomastia and hyperprolactinemia - think of boobs in sketchy and milk shooting from nose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

When do proton pump inhibitors become active? What does it inhibit?

A

They are absorbed as an inactive prodrug and must be absorbed first and enter parietal cells through basolateral surface -> takes around a day to be come effective, and is dose-dependent

Inhibit only ACTIVE H+/K+ ATPase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the two recommended triple therapy regimens for H. pylori? How long should therapy last?

A

MOC: Metronidazole, omeprazole, and clarithromycin

or

COA: Clarithromycin, omeprazole, amoxicillin

Therapy should last 14 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the quadruple therapy and when must it be used?

A

PPI + bismuth + tetracycline + metronidazole

Must be used if patient has a penicillin allergy or there has been past macrolide use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the mechanism of action of sucralfate and the adverse effect of concern?

A

Undergoes extensive crosslinking in ulcer base if the environment is acidic

Concern - contains aluminum hydroxide -> special care for patients who may have aluminum overload, i.e. renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is gastroparesis?

A

Delayed gastric emptying in absence of gastric outlet obstruction or ulceration

-> occurs when vagus nerve is damage or stomach/intestinal muscles are not functioning properly

Causes vomiting and other nonspecific symptoms cause food has nowhere to go

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What conditions are especially associated with gastroparesis?

A

Diabetes mellitus

Surgery on stomach or vagus nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What two medications are used for gastroparesis and which is used most commonly? What are there mechanisms of action?

A
  1. Metoclopramide - used most commonly - D2 receptor antagonist, and 5HT4 agonist - me tickle guy hanging from the D2 ropes
  2. Domperidone - D2 receptor antagonist

The D2 receptor inhibits Ach release and thus motility if not blocked.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is one thing that is better about domperidone than metoclopramide but why is it never used?

A

Domperidone doesn’t cross the BBB

It is never used due to QT prolongation -> another side effect of metoclopramide (think of the torsades tapes by the judge’s table)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the adverse effects of metoclopramide? What are the contraindications?

A

Increased parkinsonian effects, tardive dyskinesia. (think of the tardive dyskinesia and NMS judge’s table)

Contraindicated in small bowel obstruction (think of the sign in front) or Parkinson’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the mechanism of action of erythromycin in the treatment of gastroparesis?

A

Stimulates motilin receptors in smooth muscle cells

-> intestinal peristalsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What medications lower LES tone?

A

NSAIDs, estrogens, anticholinergics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the first-line treatment for GERD if it is intermittent or mild/moderate?

A

Intermittent - antacids, i.e. calcium carbonate

Mild-moderate - OTC H2RA i.e. ranitidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the treatment for severe GERD?

A

max daily dosing of a PPI

Antacids can be used for adjunctive relief as well

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the acute management of upper GI bleed?

A

Fluid resuscitation with normal saline or lactated ringers

Blood replacement with packed RBCs or fresh frozen plasma, up to 7 mg/dL of Hgb

Endoscopy within first 24 hours to see extent of damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the treatment for esophageal varices vs non-variceal bleeding?

A

Varices - sclerotherapy and variceal ligation

Non-variceal bleeding - electrocautery and epinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What medical therapy must be given following non-variceal upper GI bleed?

A

PPI for at least 72 hours, may be IV drip or taken orally

-> prevents rebleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the target pH needed for healing of peptic ulcers?

A

Probably around pH 5, must use a PPI to achieve this

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What medical therapy must be given for variceal upper GI bleed?

A

PPI infusion, and octreotide

Mechanism - octreotide reduces portal pressures by inhibiting glucagon-mediated splanchnic vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the adverse effects of octreotide?

A

Flushing, edema, abdominal pain, NVD (lack of absorpton due to decreased CCK and digestion)
-> these symptoms may cause further mucosal damage and upper GI bleed, risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the potential adverse effects of PPI’s?

A

Increased risk of C. difficile infection - acid needed to prevent, think of chocolate fountain in sketchy

Increased risk of pneumonia - think of girl with exposed lungs coughing - due to acid needed to clear bacteria

Hypomagnesemia with prolonged use - think of magnets. Can also be associated with hypocalcemia and low iron (H+ needed to absorb these)

26
Q

How is mild vs moderate vs severe ulcerative colitis determined?

A

Mild: <4 stools per day
Moderate: >4 stools per day
Severe: >4 stools per day with evidence of systemic toxicity (fever, leukocytosis, toxic megacolon, etc)

27
Q

What antinflammatory medication class is the first line treatment for ulcerative colitis, especially during acute episodes? What is its mechanism of action?

A

Oral aminosalicylates / 5-ASA preparations, especially mesalamine

Mechanism of action: anti-inflammatory effects via inhibition of prostaglandin and leukotriene synthesis in inflammation

28
Q

What is the major drawbacks of aminosalicylates?

A

Drawback is mostly the high pill burden -> need to ingest 4 grams per day

Many intolerable GI upset effects due to high amount taken (N/V/D)

29
Q

Which aminosalicylate should be avoided in sulfa allergy? Which are considered first line? What guides your choice of a specific one?

A

Sulfasalazine - sulfa allergy

Balsalazide and mesalamine are non-sulfa drugs considered first line

Choice is guided mostly by location of absorption in GI tract -> match it to where you want the drug most, each is different

30
Q

What are the treatment guidelines for acute disease and maintenance therapy in ulcerative proctitis?

A

Acute: 5-ASA enema targeting rectum

Maintenance: same treatment

31
Q

What are the treatment paradigms for acute vs maintenance of ulcerative colitis when it is mostly on the left side vs when it has spread to right?

A

Acute - Oral 5-ASA is preferred in right-sided involvement. Left-sided still 5-ASA enema/suppository

Maintenance: Enema or oral 5-ASA for left-sided. Immunomodulator can be added to oral 5-ASA for right-sided.

32
Q

What is the treatment for severe active ulcerative colitis and then maintenance afterwards?

A

Severe acute - Oral prednisone with 5-ASA + IV steroids if extremely severe

Maintenance - immunomodulator therapy

33
Q

How long may it take to see an improvement in UC symptoms with oral 5-ASA?

A

As long as 4-8 weeks

Can generally be faster with rectal suppository

34
Q

What is the mechanism of action of corticosteroids and how can they cause leukocytosis?

A

Decrease inflammation by upregulating inhibitors of PLA2, inducing apoptosis of lymphocytes, suppress lymphocyte function via inhibiting NF-kB, and inhibiting margination of PMNs

Can cause artificial leukocytosis by causing demargination of PMNs into bloodstream - pg 116

35
Q

What are the side effects of corticosteroids?

A

Cushing syndrome
Adrenal insufficiency - negative feedback causes atrophy
Hyperglycemia / diabetes - insulin resistance and increased gluconeogenesis
Psychosis - insomnia first
Cataracts
Hypokalemia - via mineralocorticoid effects
Osteoporosis with avascular necrosis of femoral head - broken chairleg
Skin thinning / bruising with streaks from capillary atrophy

36
Q

What corticosteroids are typically used in the treatment of ulcerative colitis and when?

A

Typically used in acute episodes only, try to avoid maintenance treatment with it, although about 1/3 of patients are steroid-dependent

Moderate disease -> oral budesonide which is not absorbed, stays in GI tract

Severe disease - IV steroids i.e. methylprednisolone / hydrocortisone

37
Q

What are the non-biologic immunomodulators commonly used in the treatment of both types of IBD? What are the adverse effects of concern?

A

Azathioprine (must be activated by HGPRT) or 6-mercaptopurine

Adverse effects:
Thrombocytopenia
Drug-induced pancreatitis

38
Q

What are two important warnings that need to be shared with those undergoing immunomodulator therapy for inflammatory bowel disease?

A
  1. TNF-alpha inhibitors - can cause reactivation TB, hepatitis B, or predispose to PJP pneumonia
  2. All immunomodulators (including 6-MP) Increased risk for T-cell lymphoma
39
Q

What are the anti-TNF-alpha antibodies which are used as immunomodulators in IBD?

A
  1. Adalimumab
  2. Infliximab
  3. Certolizumab pegol - long-acting
  4. Golimumab

SEE PG 118

40
Q

What other biologic immunomodulator class is being used in IBD? Which is the drug of choice in this and why?

A

Anti-alpha4-integrins - used for WBC adhesion

Vedolizumab - treatment of choice because it doesn’t cross BBB like Natalizumab which is used in the treatment of multiple sclerosis (increased risk of PML)

41
Q

What is the treatment for perianal fistulas in Crohn’s disease?

A

High dose metronidazole, ciprofloxacin, as well as immunomodulators (TNF, integrin, immunosuppressive)

42
Q

Which IBD might nicotine be useful in the treatment of?

A

Ulcerative colitis, since it is associated with non-smokers

43
Q

What is the main underlying difference in the acute treatment of Crohn disease vs ulcerative colitis?

A

Much more heavy reliance on steroids in Crohn disease because the inflammation can be anywhere -> difficult to get immunotherapy to an exact spot

44
Q

What is the overall takehome message of the treatment plan for Crohn’s disease?

A

Oral 5-ASA for acute episodes and maintenance, with steroids if it doesn’t work (prednisone / budesonide)

Oral mesalamine and immunomodulators of all types for maintenance therapy / remission

45
Q

What are the typical dietary triggers of IBS?

A 
Large meals
Foods: wheat, rye, barley, chocolate, milk, alcohol
Longterm Abx use
Drinks with caffeine
Stress, conflict, or emotional distress
46
Q

What is the best way to manage IBS?

A

Nonmedical management, i.e.:

  1. Diet modification
  2. Stress management
47
Q

What drugs are the mainstay for antispasmodic treatment for IBS-D? Side effects?

A

Hyoscyamine, dicyclomine

  • > antimuscarinic medications which predominately block Ach release in smooth muscle GI tract
  • > side effects include dry mouth, dry skin, and urinary retention
48
Q

What drug is active on cGMP and is used as a first-line agent for treatment of IBS-C? How does it work?

A

Linaclotide - agonizes cGMP in lumen of intestine resulting in increased bicarbonate and chloride secretion into the GI tract

49
Q

What is Alosetron used for? Mechanism of action?

A

Used for treatment of IBS-D, it is a 5HT3 antagonist (similar to zofran) which is specific to causing constipation in the gut by slowing movement

50
Q

Where is the vomiting center in the brain and what receptors are there?

A

Vomiting center = nucleus tractus solitarius, in the medulla

Receptors: M1, H1, and 5-HT3

51
Q

What are the afferents to the vomiting center?

A

Chemoreceptor trigger zone -
area postrema, at base of fourth ventricular, outside BBB

CN8 - vestibular system

Vagus nerve

Vagal and spinal afferents from GI tract

52
Q

What makes you more likely to vomit during chemotherapy or post-surgery?

A

Chemotherapy - young females who don’t drink alcohol

Surgery - usage of intraoperative and post-operative opioids

53
Q

What is the first-line treatment for nausea in chemotherapy? Mechanism of action and side effects?

A

-setrons i.e. ondansetron dancer

Antagonizes 5-HT-3 receptors in the gut AND the CNS

-side effects: constipation (gut with rope around it), headache (ball hitting head), QTc prolongation (streamer around dancer)

54
Q

What corticosteroid is used in the treatment of nausea / vomiting in chemotherapy? Major adverse effect?

A

high dose dexamethasone
-> causes severe insomnia

Mechanism of action unknown (?prostaglandin inhibition in cortex)

55
Q

What psych drugs are good at stopping nausea and how do they work? Adverse effects

A

Metoclopramide, prochlorperazine

D2 receptor antagonism at area postrema (chemoreceptor trigger zone)

Adverse effects: Drowsiness, akathisia, dystonia, EPS

56
Q

What H1 receptor antagonists are used in the treatment of nausea? What types of nausea are they good at preventing?

A

Diphenhydramine, Meclizine

Good at treating motion sickness and post-operative emesis since they tend to work on inner ear

Cause drowsiness obviously

57
Q

What is the expensive but highly effective drug used as a last line for vomiting during chemotherapy? Adverse effects?

A

Aprepitant - think participant in sketchy

NK1 / Substance P(ee) receptor antagonist in area postrema

Can cause CYP interactions and increase the INR

58
Q

What are the two stimulant laxatives and what is their relative strength?

A

Senna - slow-acting, weak - think of the senna suntan lotion stimulating that man’s belly in sketchy

Bisacodyl - very strong

These both stimulate the enteric nervous system directly and produce strong but brief peristaltic movements

59
Q

What are bulk-forming laxatives and give a few examples?

A

Drugs which increase fecal mass, resulting in stimulation of peristalsis

  • > Psyllium - seaweed
  • > methylcellulose
  • > polyethylene glycol
60
Q

What are two opiate drugs used in the treatment of non-infectious diarrhea?

A
  1. Loperamide - lop-eared bunnies, stimulate GI peristalsis back and forth so there is no net movement
  2. Diphenyoxylate - dolphins, given in combination with atropine to slow bowel movements and also to reduce dependence as diphenoxylate also binds mu and delta receptors in the brain

Pathophysiology - Gastrointestinal (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions