Gastrointestinal System Flashcards

1
Q

Define peptic ulcer

A

Defined as breach or break in the mucosa of stomach or duodenum
Imbalance between:
Aggressive factors:
gastric acid, pepsin,h.pylori
Defensive factors :
HCO3, mucus, prostaglandin

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2
Q

What are the major receptors of the stomach ?

A

3 main secretagogues:
H2 receptor : secrete Histamine
M3 receptor: secrete Ach
CCK receptor: Gastrin

1 defensive: PG receptor-secrete PG via EP3

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3
Q

How is acid released into the stomach ?

A

Food in the stomach activates gastrin and Ach from ganglion cells that act on CCK+M2 receptors on ECL. Release histamine from ECL.
Act on H2 receptors of parietal cells—> generation of CAMP—>activates H+K+ATPase—->acid release into lumen.

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4
Q

Cytoprotective roles of PG (5)

A
  1. Inhibit gastric acid secretion
  2. Stimulate gastric mucosa secretion
  3. Inhibit gastrin release
  4. Promote mucus and HCO3 secretion
  5. Ability to reinforce the mucus layer covering gastric and duodenal mucosa which is buffered by HCO3 secreted into this layer.
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5
Q

How does H pylori break defence mechanism of stomach?

A

Inhibits somatostatin which removes the inhibitory action on gastrin —> stimulating acid release.

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6
Q

4 approaches to treat peptic ulcer

A
  1. Drugs inhibiting / decreasing acid secretion in stomach
  2. Neutralize acids
  3. Ulcer protectives
  4. Anti H pylori drugs
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7
Q

What are the gastric acid secreting inhibitors ?

A
  1. Acting on H2 receptors
  2. PPI
  3. Anticholinergics
  4. Prostaglandin analogue-misoprostol
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8
Q

MOA of H2 blockers

A

Competitive blockers of H2 receptors on parietal cells.

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9
Q

Uses of H2 blockers (5)

A
  1. PUD
  2. Stress and gastric ulcers
  3. ZES
  4. GERD
  5. Prophylaxis of aspiration pneumonia
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10
Q

Long term s/e of cimetidine

A

Inhibit binding of DHT to androgen receptors—> loss of libido, gynecomastia, galactorrhoea, impotence .

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11
Q

Problem with bolus of iv injection of H2 blockers

A

Rapid release of histamine —> arrhythmias and cardiac arrest

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12
Q

H2 blockers cause transient elevation of ….
CNS effects of H2 blockers (7)

A

Plasma aminotransferases
1. Confusion-delirium
2. Headache
3. Dizziness
4. Hallucinations
5. Restlessness
6. Coma
7. Convulsions

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13
Q

What are the egs of Enzyme inhibitors?

A

Vit K cannot cause enzyme inhibition
Valproate
Ketoconazole
Cimetidine
Carbamazepine
Erythromycin
INH

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14
Q

Least potent and most potent H2 blocker

A

Least: cimetidine
Most: famotidine

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15
Q

All H2 blockers are competitive blockers except ….

A

Famotidine : competitive-non competitive
Loxatidine : competitive

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16
Q

Famotidine has …….action on receptors

A

Inverse agonist

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17
Q

Nizatidine importance

A
  1. Has anticholinergic activity —>cause bradycardia and increase gastric emptying
  2. 100% bioavailability
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18
Q

All H2 blockers except famotidine …..
Absorption of ……not affected by food.

A

Inhibit gastric first pass metabolism of ethanol

Cimetidine

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19
Q

Omeprazole is inactive at …..ph
MOA of omeprazole

A

Neutral ph

Omeprazole is enteric coated tablet, goes into the intestine , diffuses into the blood, gets into the parietal cell- at ph <5; it breaks into sulfonamide compound , which inhibit H+/K+ ATPase irreversibily and decrease acid secretion.

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20
Q

All PPI are enteric coated .why?
PPI that can be given iv (3)

A

To protect them from acidic gastric juice.
Thus they should not be crushed or broken before swallowing.

Esomeprazole
Lansoprazole
Pantoprazole

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21
Q

All PPIs are prodrugs, they get converted to active moeity ……in intestine

t1/2 of PPI…..
Duration of action of PPI….

A

Sulfenamide

1.5 hours
24 to 48 hours

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22
Q

PPI must be taken half an hour before food. Why?
On prolonged Rx, PPI cause ……

A

Coz food decreases bioavailability.
Atrophic gastritis

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23
Q

Most potent PPI and longest acting PPI

A

Most potent : lansoprazole
Longest acting: rabiprazole

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24
Q

Safest PPI in pregnancy
…… and …… are enzyme inhibitors that decrease metabolism of ……

A

Lansoprazole

Omeprazole and esomeprazole
Diazepam

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25
Q

Lansoprazole enhances metabolism of ……..

……..have only oral formulation

A

Theophylline

Omeprazole

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26
Q

Anticholinergic drugs egs (4)

A

Pirenzepine
Telenzepine
Propantheline
Oxyphenonium

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27
Q

MOA of anticholinergics

A

Inhibit M3 receptors on gastric mucosa—> decrease gastric secretion.

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28
Q

Anticholinergics are not preferred. Why? (4)

A
  1. They exhibit weak antisecretory effect compared to H2 blockers
  2. They decrease basal acid secretion by 40-45%
  3. Also in doses needed to decrease gastric secretion, there is dryness of mouth, urinary retention, tachycardia, glaucoma.
  4. Decrease volume of gastric juice without raising its PH.
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29
Q

What are PGE1 and PGE2 analogues of prostaglandin ?

A

PGE1: misoprostol
PGE2: enprostil, rioprostil

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30
Q

What are the types of antacids?

A

Systemic antacids: sodium compounds
Non systemic antacids: calcium, Mg, Al,mix

Magaldrate: Mg-Al mix

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31
Q

S/e of antacids

A
  1. Cause hypokalemia
  2. Do not decrease gastric acid, just raise the gastric Ph, —>more gastrin release—»thus leading to acid rebound.
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32
Q

Pharmacokinetics of antacids

A

Antacids taken on empty stomach acts only for 30-60 mins as it takes soo much time for gastric acid to pass into duodenum.

But if given with meals, they act for about 2-3 hours.

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33
Q

Which are the weak and strong antacids?

A

Weak: aluminum compound
Strong: mg compound.

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34
Q

S/e of aluminum compound (2)

A
  1. Inhibit motility, delays emptying causes constipation
  2. Inhibit PO4 reabsorption
    Increase calcium reabsorption from bones

—>hypercalcemia,hypercalciuria, osteomalacia

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35
Q

S/e of Mg compounds
C/I of mg compounds

A

Strong, longer duration of action.
Increase GI motility, cause diarrhoea

Renal insufficiency
5-10% get reabsorbed, rest eliminated into kidney.

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36
Q

Advantages of Magaldrate (3)

A
  1. Fast (Mg) and slow (aluminium)
  2. Mg salts-laxative, Al salts- constipation
  3. Gastric emptying least affected as
    Aluminium salts tend to delay it
    And Mg salts hasten it.
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37
Q

Uses of antacids (2)

A
  1. Self prescribed by patients
  2. Relieve intermittent pain relief and acidity.
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38
Q

Eg of MagAldrate

Which anti ulcer drug act neither by secretion nor reducing secretion of gastric acid ?

A

gelusil

Sucralfate - at Ph<4; it’s gastroprotective

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39
Q

DOC for prevention of NSAID induced peptic ulcers
Most specific drug for NSAID induced PUD

A

PPI

Misoprostol

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40
Q

Which PPI cause least CYP2C 19 inhibition?
What is CYP2C19 do?
Which PPI causes max CYP2C19 inhibition?

A

Pantoprazole > Rabeprazole

Responsible for activation of clopidogrel

Omeprazole
Esomeprazole

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41
Q

Ranitidine + sucralfate is bad idea. Why?

A

Sucralfate at ph<4, it polymerises and stick to the base of the ulcer, ranitidine can’t act.
( Ranitidine increases gastric Ph )

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42
Q

Long term side effect of PPI (3)

A
  1. Decrease absorption
    a). Fe- fe deficiency anemia
    b). Ca- osteoporosis-increase fracture
    c). B12- megaloblastic anemia
    d). Mg- hypomagnesemia
  2. Increase infection
    C. Difficile pneumonia
  3. Dementia, CKD
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43
Q

Adverse effects of cimetidine (3)

A
  1. Antiandrogen effect
  2. Increase prolactin - galactorrhoea
  3. Increase lipid soluble- cross BBB
    Confusion, headache, dry mouth
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44
Q

Anti H pylori drugs

A

Triple therapy:
C-clarithromycin
A-amoxicillin / M-Metronidazole
P- PPI

Quadruple therapy:
T- Tetracycline
O-omeprazole
M-Metronidazole
B-Bismuth

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45
Q

Ulcer healing drug taken away from market .why?

A

Carbenoxolone
Due to its mineralocorticoid action-HTN, hypokalemia

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46
Q

Pathology of vomiting

A

Due to vomiting center in medulla oblongata.
Near the vomiting center are centres for respiratory,salivation, vascular control.

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47
Q

Vomiting center impulses are from :..(4)

A

CTZ: receptors: M, CB1, NK1,5HT3,D2
NTS receptors: M,H1,NK1,5HT3,D2
Cerebellum : M , H1
Cortex: smell, sight, pain, psychological

48
Q

Impulse of vomiting from GIT

A

Cytotoxic drugs,radiation, other Git irritants
Release 5HT from enterochromaffin cells
Act on 5HT receptors on extrinsic pathway of enteric NS
Send impulse that acts on 5HT3 receptors of CTZ,NTS -to vomiting centre-vomit.

49
Q

Impulse of vomiting from blood.

A

Huge release of 5HT / release of 5HT from platelets ; spill into circulation, reach CTZ via blood vessels, act on 5HT3 receptors on CTZ —> signals to VC—>vomiting.

50
Q

Impulse of vomiting from vestibular appendix

A

If body is rotated/equilibrium lost/ Ototoxic drug given —> vestibular apparatus in inner ear is activated —> send impulse to cerebellum, act on H1 and M1 receptors —> impulse to VC—>vomiting.

51
Q

Egs of anticholinergic antiemetics . Use

A

Hyosine
Dicyclomine

Use for motion sickness

52
Q

Disadvantages of hyosine (4)

A
  1. Brief duration
  2. Produces sedation
  3. Dry mouth
  4. Poor efficacy for vomiting of other etiologies
53
Q

Use of dicyclomine (2)

A

Motion sickness
Morning sickness

54
Q

Egs of H 1 antihistamines (6)

A
  1. Diphenhydramine
  2. Dimenhydrinate
  3. Doxylamine
  4. Meclizine
  5. Promethazine
  6. Cinnarazine
55
Q

MOA of H1 antihistamines (2)

A

Block H1 receptors in CTZ and NTS
Minor M blocking action

56
Q

Use of H1 antihistamines (2)

A
  1. Motion sickness for 4-6 hours
  2. Chemotherapy induced NV (CINV)
57
Q

Drawbacks of antihistaminics (2)

A

Dry mouth, sedation

58
Q

H1 antihistaminic with prominent anticholinergic action

Importance of meclizine . Use

A

Doxylamine

Meclizine:
Less sedating, long acting

Use: sea sickness for 24 hours

59
Q

Egs of neuroleptics (4)

A
  1. Chlorpromazine
  2. Triflupromazine
  3. Prochlorperazine
  4. Haloperidol
60
Q

MOA of antiemetics with neuroleptics (3)

A
  1. Block D2 in CTZ,NTS
  2. Block M and H1 receptors
61
Q

5 uses of antiemetics (5)

A
  1. Post op N&V
  2. Disease induced vomiting: gastroenteritis,uremia, liver disease, vomiting etc.
  3. Malignancy associated and chemotherapy induced vomiting
  4. Radiation sickness
  5. Morning sickness- only for hyperemesis gravidarum
62
Q

Egs of NK1 receptor antagonist (2)
MOA

A

Aprepitant
Fosaprepitant

Highly selective NK1 receptor antagonist for NK1 receptors of CTZ,NTS

63
Q

Uses of Aprepitant (2)

A
  1. Cisplatin induced vomiting
    Multiple cycles of chemo
  2. Post operative nausea and vomiting
64
Q

MOA of ondansetron

A
  1. Block 5HT3 receptor in gut and CTZ,NTS
    ie, block both central and peripheral relay
65
Q

Rx for cisplatin induced vomiting (2)

A

Acute vomiting : ondansetron
Delayed vomiting :
ondansetron+ Aprepitant

66
Q

Iv injection of ondansetron can cause what s/e (4)

A

Hypotension
Bradycardia
Chest pain
Allergic reaction

67
Q

Importance of ganisetron (2)

A

10-15 times more potent than ondansetron.
More effective in repeat cycle of chemotherapy

68
Q

Max affinity for 5HT3 receptor

5HT3 antagonist removed from market. Why?

A

Palonasetron

Alosetron- constipation, ischemic colitis

69
Q

Newer 5HT3 antagonists (3)

A

Dolasetron
Palonasetron
Tropisetron

70
Q

Longest acting and most potent 5HT3 blocker
Shortest acting 5HT3 blocker

S/e of dolanosetron

A

Palonasetron

Ondansetron

QT prolongation

71
Q

Egs of prokinetics (5)

A

Metoclopramide
Domperidone
Cisapride
Mosapride
Ito pride

72
Q

MOA of prokinetics

A

Neurotransmitters that act on GIT
1. Excitatory: 5HT4 agonist
Ach release - prokinesis
2. Inhibitory: DA,5HT3 receptors
NO release- relaxation
Therefore:
Prokinetics act by increasing 5HT4 agonist , and D2,5HT3 blockers

73
Q

Site of action of different prokinetics (4)

A

Metoclopramide: 5HT4+, 5HT3-,D2-
Cross BBB- cause EPS

Domperidone : D2 - does not cross BBB,no EPS

Cisapride: 5HT4 agonist , 5HT3 antagonist

Tegaserod: 5HT4 agonist

74
Q

Newer congeners of cisapride (3) . Importance

A

Mosapride
Renzapride
Zacopride

They don’t cause QT prolongation like cisapride

75
Q

Metoclopramide has prokinesis of Gastric but not ….

Antiemetic given for levodopa induced vomiting

A

Colonic

Domperidone- as it doesn’t cross BBB

76
Q

Use of metoclopramide beyond ……weeks causes tardive dyskinesia

A

12 weeks
C/I for <20 yr old

77
Q

Most potent antiemetic in preoperative period is …..

A

Ondansetron > palonasetron

78
Q

Which antiemetic rx for diarrhoea dominant IBS and not for N/V?

Antiemetic that can also decrease acid secretion by acting on H1 receptors

A

Alosetron

Promethazine

79
Q

MOA of stool softeners

A

Decrease stool surface tension by increasing water penetration into stool

80
Q

What are the 2 kinds of stool softeners and s/e

A
  1. Liquid paraffin:
    S/e:
    a. unpleasant- swallowing wax
    b. Decrease fat soluble absorption
    c. Granulomas in intestinal wall
    d. leakage of paraffin wax from anus is embarrassing
  2. Docussate -better, as they don’t interfere with fat reabsorption
81
Q

Eg of stimulant purgatives . MOA
C/I

A

Prune juice
Senna
Bisacodyl

They act on colon -to stimulate/irritate the mucosa -to increase secretion and motility.

Subacute intestinal obstruction
Pregnancy- can contract the uterus.

82
Q

Which drug causes melanosis coli? (2)
Define melanosis coli

S/I of bisacodyl

A

Senna , Carcara
Lipofusin deposit in the colonic wall -harmless

Increase NO release

83
Q

Rx for IBS types

A

Constipation predominant:
Rx:
1. Dietary fiber
2. Antidepressant:SSRI
3. Increase Cl- into colon:
Lubiprostone-PG activate CFTR
Linaclotide- guanyl cyclase activator

  1. Tegaserod-increase colon secretion by 5HT4 agonist .

Diarrhea:
Rx: 1. antimotility-loperamide
2. TCA

84
Q

S/e of tegaserod
Newer 5HT4 agonist . Importance.

A

MI/Stroke -drug banned

Prucalopride- not cause MI/stroke can be used to rx constipation

85
Q

Egs of osmotic laxatives (2)
MOA

A

Lactulose
Magnesium

They attract and retain water in GIT.

86
Q

Egs of suppositories (2)

A

Bisacodyl
Sodium phosphate enema

87
Q

Chronic laxative use can cause …..

A

Hypokalemia

88
Q

Drugs for rx opioid induced constipation (5)

A

PAMORA
Peripherally acting M opioid Receptor Antagonist
1. Methylnaltrexone
2. Naldemedine
3. Naloxegol
4. Alvimopan
5. Lubiprostone

89
Q

Loxiglumide is ……..

A

CCK receptor antagonist -gastric prokinetic agents

90
Q

MOA of plecanatide
Use

A

Guanylate cyclase stimulator which acts by increasing CGMP- which stimulates CFTR-increasing Cl-ion into gut.

Use for idiopathic constipation

91
Q

Abusing with anthranoid laxatives/senna causes…..

A

Ammonium urate kidney stones

92
Q

Laxative that decreases blood ammonia in hepatic encephalopathy

A

Lactulose

93
Q

Drugs to decrease ammonia in hepatic encephalopathy?

A
  1. Neomycin-
    Kill Gi bacteria- decreases NH3
    S/e: intestinal villi atrophy
  2. Lactulose-preferred.
    Nh3–>NH4
    Nh4 is not reabsorbed-excreted.
94
Q

Non diarrhoeal uses of ORS (4)

A
  1. Burns
  2. Heat stroke
  3. Post trauma
  4. TPN—> enteral nutrition
95
Q

MOA of racecadotril

A

Inhibit enkephalinase
Enkephalin—> broken down by enkephalinase. Racecadotril inhibits that.

It’s an oral drug

96
Q

DOC for secretary diarrhoea (3)

A

Octreotide
Atropine
Racecadotril

97
Q

Anti diarrheal drug chemically related to opioid analgesic-meperidine

What are the peripherally acting opioid M agonist ?

A

Loperamide

Act on GIT—> decrease motility
Diphenoxylate: cross BBB- euphoria,abuse
Prevent this by adding atropine.

Loperamide- does not cross BBB.

98
Q

Preferred drug for acute exacerbation of UC
Drug for worsening of UC/long term control.

A

Prednisolone / budesonide(oral)

5ASA - mesalamine

99
Q

Which biological rx used in IBD is associated with risk of PML?

A

Natalizumab.

100
Q

Name 2 alpha integrin therapy. Importance

A

Natalizumab - cause PML
Vedolizumab - don’t cause PML.

101
Q

Opioid agonist act on GIT for diarrhoea by …..(2)

A
  1. Decrease intestinal motility- stimulate m receptors
  2. Decrease secretions- delta receptors

-on small and large intestines

102
Q

Anticholinergics used for diarrhoea. Moa

A

Dicyclomine
Hyoscyamine
Decrease intestinal motility and cramps

103
Q

MOA of clonidine in diarrhoea (3)

A
  1. Facilitates absorption
  2. Increase intestinal transit time
  3. Inhibits secretion of fluid and electrolytes.
104
Q

Use of clonidine (2)

A

Diabetic diarrhoea
Diarrhoea caused by opiate withdrawal

105
Q

Synthetic somatostatin agonist for anti diarrhoea

Moa (3)

A

Octreotide

  1. Decrease GI motility
  2. Decrease intestinal secretion
  3. Inhibit 5HT,gastrin,CCK,motilin,pancreatic polypeptide
106
Q

Use of Octreotide (2)
S/e

A
  1. Rx secretary diarrhoea due to carcinoid Tumor
  2. VIPoma

Increased risk of gall stones due to CCK inhibition.

107
Q

Indication of antiobesity drugs

A

Long term rx
BMI >30kg/sqm or
BMI >27kg/sqm with significant comorbidity

108
Q

MOA of orlistat
S/e (5)

A

Gastric and pancreatic lipase inhibitor
S/e:
1. Steatorrhoea
2. Oily spotting
3. Fecal urgency
4. Abdominal pain
5. Headache

109
Q

Risk of ……with orlistat (4)

A

Cholilithiasis
Oxalate Nephrolithiasis
Add Vit ADEK
Increases warfarin effect

110
Q

Lorcaserin is ……
S/e (4)

A

5HT2C agonist
1. Dry eyes
2. Dry mouth
3. Constipation
4. Hyperprolactinemia

111
Q

Risk of ……with lorcaserin (5)

A

Serotonin syndrome
NMS
Cardiac valve defects
Mood disorder
Priapism

112
Q

MOA of liraglutide
S/e (3)

A

GLP-1 agonist
S/e:
1. GI upset
2. Pancreatitis
3. Acute cholelithiasis/ cholecystitis

113
Q

Risk of …….with liraglutide

A

Thyroid cell hyperplasia
Injectable drug -use sc OD

114
Q

Worsening of depression is seen with ….antiobesity drug

A

Phentermine+ topiramate ER
Ne+ GABA agonist

115
Q

S/e of phentermine+topiramate (6)

A

Headache
Dry mouth
Cognitive impairment
Acute myopia
Glaucoma
Tachycardia

116
Q

Worsening of migraines seen with …..
MOA

A

Naltrexone + bupropion ER
Opiate antagonist + DA/NE reuptake inhibitor

117
Q

S/e of naltrexone+ bupropion (3)

A

Tachycardia
Suicidal thoughts
HTN