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Pharma Flashcards

1
Q

What is the mechanism of action Cimetidine (ranitidine, famotidine, nizatidine)?

A

Reversible H2 blockade

- decreased secretion of H+ by parietal cells

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2
Q

Which H2 blocker is a CYP inhibitor?

A

Cimetidine

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3
Q

Which H2 blocker has anti-androgenic effects?

A

Cimetidine

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4
Q

What are the anti-androgenic effects seen with Cimetidine?

A

Prolactin release
Gynecomastia
Impotence

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5
Q

Which H2 blockers decrease renal excretion of creatinine?

A

Cimetidine and ranitidone

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6
Q

What class of drug is Omeprazole (lanzoprazole, esomeprazole, pantoprazole, dexlansoprozole)?

A

PPI, used in peptic ulcer, gastritis, GERD, and Z-E syndrome

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7
Q

What is the mechanism of action of Omeprazole?

A

Irreversibly inhibits Na/K ATPase in Parietal Cells of stomach

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8
Q

What class of drug is Cimetidine?

A

Inhibits acid secretion in peptic ulcer disease, gastritis, GERD

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9
Q

What drug is used in Zollinger-Ellison Syndrome?

A

Omeprazole

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10
Q

What GI drug/class of acid inhibitors increased risk of C. diff?

A

PPIs

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11
Q

What GI drug/class of acid inhibitors causes increased risk of hip fractures?

A

PPIs

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12
Q

What is the mechanism of action of bismuth and sucralfate?

A

Bind to the base of the ulcer

Provide physical protection so HCO3- can re-establish mucosa pH

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13
Q

What is the mechanism of action of Misprostol (GI) ?

A

PGE1 analog

Increased production, secretion of gastric mucosal barrier
Less acid production

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14
Q

What is the mechanism of action of Octreotide?

A

SST analog

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15
Q

What are the indications for Octreotide?

A

Acute variceal bleeds
VIPoma
Carcinoid tumors

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16
Q

What is a common side effect of all antacids?

A

Hypokalemia

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17
Q

What antacid causes constipation?

A

Aluminum hydroxide

Aluminimum amount of feces

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18
Q

What antacid causes hypophosphatemia?

A

Aluminum hydroxide

Aluminimum amount of phosphate

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19
Q

What antacid causes hypercalcemia?

A

Calcium carbonate

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20
Q

How does calcium carbonate decrease the effectiveness of other drugs?

A

Calcium carbonate chelates

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21
Q

What antacid causes diarrhea?

A

Magnesium hydroxide

Mg = Must go…to the bathroom

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22
Q

What antacid can cause seizure?

A

Aluminum hydroxide

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23
Q

What antacid can cause cardiac arrest?

A

Magnesium hydroxide

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24
Q

What are the osmotic laxatives (3)?

A

Magnesium hydroxide
Magnesium citrate
Polyethylene glycol
Lactulose

Ma(y) Po(op) a Lact

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25
Q

What osmotic laxative is also used to treat hepatic encephalopathy?

A

Lactulose

  • Gut flora degrade into metabolites (lactic acid and acetic acid) that promote nitrogen excretion as NH4+
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26
Q

What does Infliximab target?

A

TNF-a

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27
Q

What does Infliximab treat?

A

Crohn’s, UC, RA, Ankylosing spondylitis, psoriasis

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28
Q

What two functions does sulfasalazine bring together?

A

Anti-bacterial and anti-inflammatory

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29
Q

What does sulfasalazine treat?

A

UC and Crohn’s (mild-moderate)

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30
Q

What is a 5HT3 antag used for anti-emesis?

A

Ondansetron

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31
Q

What is a D2 receptor antag used to create GI motility?

A

Metoclopramide

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32
Q

In what diseases in Metoclopramide contraindicated?

A

Parkinson’s

Obstructed small bowel

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33
Q

What are some purine synthesis inhibitors used to treat IBD?

A

Azathioprine and Mercaptopurine

- Cause immunosuppression

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34
Q

What is a dihydrofolate reductase inhibitor used to treat IBD?

A

MTX

  • Blocks THF synthesis from folic acid
  • Causes immunosuppression
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35
Q

What is the function of LTB4, produced in the LOX pathway?

A

Neutrophil chemotactic agent

Neutrophils arrive B4 others

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36
Q

What are the functions of LTC4, D4, E4, produced in the LOX pathway?

A

Bronchoconstriction (mainly)
Vasoconstriction
Contraction of smooth muscle
Increased vascular permeability

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37
Q

What is the function of PGI1, produced on the COX pathway?

A

Platelet-Gathering-Inhibitor

Inhibits platelet aggregation
Promotes vasodilation (decreased vascular tone)

(Also decreased bronchial tone, uterine tone)

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38
Q

What is the action of corticosteroids in the arachidonic acid pathway?

A

Phospholipase A2 inhibition

Also inhibitors of protein synth in the COX pathway

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39
Q

What drug is a LOX pathway inhibitor?

A

Zileuton is a lipoxygenase inhibitor

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40
Q

What drugs are the COX pathway inhibitors?

A

NSAIDs, aspirin, and acetaminophen are COX-2 inhibitors

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41
Q

What drugs are Leukotriene inhibitors (and which ones are inhibited)?

A

Zafirlukast, Montelukast

Inhibit LTC4, D4, E4

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42
Q

What is the mechanism of Aspirin?

A

Irreversible inhibitor of COX-1 and COX-2 by covalent acetylation

This decreases synthesis of TXA2 and prostaglandins

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43
Q

How does aspirin affect bleeding time, PT, PTT?

A

Increased bleeding time until new platelets are produced (7 days)

No change in PT, PTT

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44
Q

What are the different functions of aspiring at low, medium, and high doses?

A

Low: decreased platelet aggregation

Medium: antipyretic and analgesic

High: anti-inflammatory

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45
Q

What is the effect of aspirin in treating children with viral illness?

A

Reye’s Syndrome! Contraindication!

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46
Q

How does aspirin affect the respiratory centers?

A

Hyperventilation > Respiratory Alkalsosis

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47
Q

What are GI side effects of aspirin?

A

Gastric ulceration
Acute renal failure
Interstitial nephritis
Upper GI bleed

(with chronic use)

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48
Q

What is a neuro side effect of aspirin?

A

Tinnitus (CN VIII)

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49
Q

What is the function of PGE2 and PGF2, produced in the COX pathay?

A

Increase uterine tone

Decrease bronchial tone

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50
Q

What is the function of TXA2, produced int he COX pathway?

A

Increased platelet aggregation
Increased vascular tone
Increased bronchial tone

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51
Q

What products of the arachidonic acid pathway increase bronchial tone?

A

LTC4, LTD4, LTE4 & TXA2

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52
Q

What products of the arachidonic acid pathway decrease bronchial tone?

A

PGI2, PGE2, PGF2

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53
Q

What drugs (besides aspirin) are classified as NSAIDs?

A

Be KIIND to your body with NSAIDs

Ketorolac, Indomethacin, Ibuprofen, Naprozen, Diclofenac

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54
Q

What is the mechanism of action of NSAIDs?

A

REVERSIBLY inhibit COX-1 and COX-2, block PG synth

contrast Aspirin, IRREVERSIBLE

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55
Q

… is an NSAID used to close a PDA.

A

Indomethacin

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56
Q

What is the effect of prostaglandins on the renal arterioles?

A

PGs vasodilate afferent arteriole

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57
Q

What drug is a selective COX-2 inhibitor?

A

Celecoxib

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58
Q

What is the action of a COX-2 inhibitor as compared to COX-1 and 2?

A

COX-2 works against inflammation and pain

Spares COX-1

  • Maintains gastric mucosa–no corrosive effects
  • Spares platelet function, as TXA2 depends on COX-1
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59
Q

What are the clinical indications of Celecoxib?

A

RA, osteoarthritis; patients with gastritis or ulcers

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60
Q

What are the adverse effects of Celecoxib?

A

Increased risk of thrombosis

Sulfa allergy

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61
Q

What is the difference between the use cases of Acetaminophen and Aspirin/NSAIDs?

A

Acetaminophen is not anti-inflammatory

Is still antipyretic and analgesic

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62
Q

What is the mechanism of aciton of Acetaminophen?

A

Reversible COX inhibitor, mostly in the CNS

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63
Q

What is the main toxicity of Acetaminophen?

A

Hepatic necrosis

NAPQI depletes glutathione and forms toxic tissue adducts in liver

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64
Q

What is the antidote to Acetaminophen hepatotox?

A

N-acetylcysteine

Regenerates glutathione

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65
Q

Name a bisphosphonate.

A

Alendronate (all are -dronates)

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66
Q

What is the mechanism of action of a bisphosphonate?

A

Pyrophosphate analog that binds hydroxyapatite in bone

Inhibits osteoclasts

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67
Q

What are the clinical indications for bisphosphonates?

A

Osteoporosis
Hypercalcemia
Paget disease of bone

68
Q

Why are patients advised to take bisphosphonates with water and remain upright for 30 mins?

A

Corrosive esophagitis & osteonecrosis of jaw are potential adverse effects

69
Q

What is the MOA of Allopurinol?

A

Inhibits Xanthine Oxidase, which ends up making less uric acid

70
Q

How does Allopurinol affect concentrations of Azathioprine and 6-MP?

A

Increases concentrations, because both are metabolized by XO

71
Q

What are the indications of Allopurinol?

A

Preventative for Gout

Also used in lymphoma and leukemia to prevent tumor lysis associated urate nephropathy

72
Q

What is the MOA of Febuxostat?

A

Inhibits XO

73
Q

What are the indications of Febuxostat?

A

Preventative for Gout

74
Q

What is the MOA of Probenecid?

A

Uricosuric

Inhibits reabsorption of uric acid in the PCT
Also inhibits secretion of penicilin

75
Q

What are the indications of Probenecid?

A

Preventative for Gout

76
Q

What types of drugs work during acute gout?

A

NSAIDs
Glucocorticoids
Colchicine
TNF-a inhibitors

77
Q

What NSAIDs are used in acute gout?

A

Naproxen, Indomethacin

78
Q

How does Indomethacin affect T and B cells?

A

Actually increases T and B cells!

79
Q

What is the MOA of Colchicine?

A

Binds and stabilizes tubulin
This inhibits microtubule polymerization
Impairs leukocyte chemotaxis and degranulation

80
Q

What are the indications of Colchicine?

A

Acute and Preventative for gout

81
Q

What are the side effects of Colchicine?

A

GI side effects

82
Q

What must be tested for before administering a TNF-a inhibitor?

A

TB, because TNF blockage prevents activation of macrophages

83
Q

Name 3 TNF-a inhibitors.

A

Etanercept
Infliximab
Adalimumab

84
Q

What is a fusion protein receptor for TNF-a, IgG, and Fc?

A

Etanercept

EtanerCEPT is a TNF decoy reCEPTor
Basically mops up these substances

85
Q

What are the indications of Etanercept

A

RA, Psoriasis, Ankylosing Spondylitis

86
Q

What is the MOA of Infliximab (and adalimumab)?

A

anti-TNF-a monoclonal antibody

87
Q

What are the indications for infliximab (and adalimumab)?

A

IBD, RA, Psoriasis, Ankylosing Spondylitis

88
Q

What is a recombinant uricase used in refractory gout?

A

Pegloticase

89
Q

What is the MOA of insulin on the liver?

A

Increases uptake of glucose to be stored as glycogen

90
Q

What is the MOA of insulin on muscle?

A

Increases glycogen and protein synthesis

Also K+ uptake

91
Q

What is the MOA of insulin on fat?

A

Increases TG storage

92
Q

What type of receptor does insulin bind/use to mediate its effects?

A

TK

93
Q

What are the rapid acting insulins?

A

Lispro
Aspart
Glulisine

no LAG

94
Q

What are the indications for rapid acting insulin?

A

Postprandial glucose control in

  • DM 1
  • DM 2
  • GDM
95
Q

What is a short acting insulin?

A

Regular insulin

96
Q

What are the indications for regular insulin?

A
  • DM 1
  • DM2
  • GDM
  • DKA (IV)
  • Hyperkalemia (+ glucose)
  • Stress hyperglycemia
97
Q

What is intermediate acting insulin?

A

NPH

98
Q

What are the indications for NPH insulin?

A
  • DM 1
  • DM2
  • GDM
99
Q

What are the long acting insulins?

A

Glargine
Detemir

GlaDe: long-lasting scent

100
Q

What are the indications for long acting insulin?

A

Basal glucose control

  • DM1
  • DM2
  • GDM
101
Q

What is the main adverse reaction of all the exogenous insulins?

A

Hypoglycemia

102
Q

… is a Biguanide that is the 1st line therapy in DM 2.

A

Metformin

103
Q

What is the MOA of Metformin?

A

Mainly decreases gluconeogenesis

Increases glycolysis
Increases peripheral glucose uptake (insulin sensitivity)
- No risk of hypoglycemia b/c it’s only using the insulin that is there endogenously

104
Q

What are the indications for Metformin?

A

First line therapy in DM 2

Also used in:

  • Patients without islet function
  • PCOS
105
Q

What is the most serious side effect of Metformin?

A

Lactic acidosis (thus contraindicated in renal failure)

106
Q

What is the MOA of sulfonylureas?

A

Close K+ channel in beta-cell membrane, so cell depolarizes > Ca influx > release of endogenous insulin

107
Q

What are the indications for sulfyonylureas?

A

DM 2

Require some islet fx, so useless in DM 1

108
Q

What are the first generation sulfonylureas?

A

Tolbutamine
Chlorpropamide

(DM 2)

109
Q

What are the second generation sulfonylureas?

A

Glyburide
Glimepiride
Glipizide

(DM 2)

110
Q

What are the adverse effects of first generation sulfonylureas, used in diabetes treatment?

A

Disulfiram-like effects

111
Q

What are the adverse effects of second generation sulfonylureas, used in diabetes treatment?

A

Hypoglycemia

112
Q

What is an adverse effect of all sulfonylureas, used in diabetes treatment?

A

Risk of hypoglycemia increases with renal failure

113
Q

What is the mechanism of action of Thiazolidinediones in treating diabetes?

A

Increase insulin sensitivity in peripheral tissue

Bind PPAR-g nuclear transcription regulator

114
Q

What is the role of PPAR-g in glucose control?

A

Genes activated by PPAR-g regulate fatty acid storage and glucose metabolism.

Activation of PPAR-g increases insulin sensitivity and levels of adiponectin

115
Q

What are the two main Thiazolidinediones?

A

Pioglitazone
Rosiglitazone

“Zone P(par) is where you want to be”

116
Q

What are the indications for Pioglitazone and Rosiglitazone in treating diabetes?

A

Monotherapy in DM 2 or combined with other agents

117
Q

What are the adverse effects for Pioglitazone and Rosiglitazone in treating diabetes?

A

Weight gain, edema, hepatotox, heart failure

118
Q

What is the MOA of a-glucosidase inhibitors in treating diabetes?

A

Inhibit intestinal brush border a-glucosidases

  • Delayed sugar hydrolysis and glucose absorption
  • Decreased postprandial hyperglycemia
119
Q

What are the two main a-glucosidase inhibitors?

A

Acarbose
Miglitol

bAM! inhibitors
(brush border, Acarbose, Miglitol)

120
Q

What are the indications for Miglitol and Acarbose in treating diabetes?

A

Monotherapy in DM 2 or combined with other agents

121
Q

What are the side effects of the a-glucosidase inhibitors in treating diabetes?

A

GI: flatulence!

Cannot treat hypoglycemia with disaccharides, must use dextrose

122
Q

…is an amylin analog that decreases gastric emptying and decreases glucagon.

A

Pramlintide

123
Q

What are the indications for Pramlintide in treating diabetes?

A

DM 1

DM 2

124
Q

What are the adverse effects of Pramlintide in treating diabetes?

A

Hypoglycemia
Nausea
Diarrhea

125
Q

GLP-1 analogs like… and…prime insulin release, so you can respond immediately to food.

A

Exenatide

Liraglutide

126
Q

What is the MOA of Exenatide and Liraglutide in diabetes treatment?

A

Increase insulin, decrease glucagon release

Cause weight loss and appetite suppression

127
Q

What are the indications of Exenatide and Liraglutide in treating diabetes?

A

DM 2

128
Q

What are the side effects of Exenatide and Liraglutide in treating diabetes?

A

N/V, pancreatitis

129
Q

What are the DPP-4 inhibitors of diabetes management?

A

Linagliptin
Saxagliptin
Sitagliptin

130
Q

What is the MOA of the DPP-4 inhibitors (-gliptins) in diabetes management?

A

Increased insulin, decreased glucagon release through increasing GLP, GIP

131
Q

What are the indications for DPP-4 inhibitors (-gliptins) in diabetes management?

A

DM 2

132
Q

What are the side effects of the DPP-4 inhibitors (-gliptins) in diabetes management?

A

Mild UTI or RTI

133
Q

What are the SGLT 2 inhibitors used in diabetes management?

A

Canagliflozin

Dapagliflozin

134
Q

What is the MOA of the -gliflozins used in diabetes management?

A

Block SGLT 2 so glucose cannot be reabsorbed from the kidney > glucosuria

135
Q

What are the indications for the -gliflozins used in diabetes management?

A

DM 2

136
Q

What are the side effects of -gliflozins used in diabetes management?

A

UTI
Mycotic infections
Increased urination
Increased creatinine

137
Q

… and … are two drugs that block the oxidation and organification of iodine to inhibit thyroid hormone synthesis.

A

Propylthiouracil (PTU) and Methimazole

138
Q

What specific hormone do both PTU and Methimazole block to inhibit iodine oxidation and organification?

A

Thyroid peroxidase

139
Q

What additional action toes PTU have in inhibiting the action of thyroid hormone?

A

Also blocks 5’ deiodinase, which decreases peripheral conversion of T4 to T3

140
Q

What are the indications of PTU and Methimazole?

A

Hyperthyroidism

141
Q

Which drug used to treat hyperthyroidism can be used in pregnancy?

A

PTU

PTU: Peripheral and Pregnancy

142
Q

What drug used in hyperthyroidism blocks T4 release from the thyroid?

A

Potassium iodide

143
Q

What drug used in hyperthyroidism blocks iodide uptake into the thyroid?

A

Perchlorate

144
Q

What are two drug replacements for thyroxine?

A

Levothyroxine

Triiodothyronine

145
Q

What are the adverse effects of both PTU and Methimazole in treating hyperthyroidism?

A

Agranulocytosis (rare)
Aplastic Anemia
Skin Rash

146
Q

What is an adverse effect of PTU in treating hyperthyroidism?

A

Hepatotox

147
Q

What is an adverse effect of Methimazole in treating hyperthyroidism?

A

Teratogen, can cause aplasia cutis

148
Q

What are the indications for Levothyroxine and T3?

A

Hypothyroidism

Myxedema

149
Q

What are the adverse effects of Levothyroxine and T3?

A

Tachycardia
Heat intolerance
Tremors
Arrhythmia

(basically effects of overactive hormone)

150
Q

What are the clinical indications for Growth Hormone?

A

GH deficiency
Turner’s Syndrome
wasting in HIV/AIDs
Short bowel syndrome

151
Q

What is the MOA of Octreotide?

A

SST analog

152
Q

What are the indications for Octreotide?

A 
Acromegaly
Carcinoid
Gastrinoma
Glucagonoma
Esophageal varices
153
Q

What are the indications for Oxytocin?

A

Stimulate labor, uterine contractions
Milk let-down
Control uterine hemorrhage

154
Q

What are the indications for ADH (DDAVP, Desmopressin)?

A

Central DI (not nephrogenic)

155
Q

What is the MOA of Demeclocycline?

A

ADH antagonist

156
Q

What are the indications for Demeclocycline?

A

SIADH

157
Q

What are the adverse effects of Demecloclycine?

A

Nephrogenic DI
Photosensitivity
Abnormalities of bone and teeth

158
Q

What are two dopamine agonists used to treat prolactinomas?

A

Bromocriptine

Cabergaline

159
Q

What are the adverse effects of DA agonists use to treat prolactinomas?

A

N/V, headache, orthostatic hypotension, psych sx

Valvular heart disease (Cabergaline only)

160
Q

What is the mechanism of action of glucocorticoids?

A

Metabolic, catabolic, anti-inflammatory, and immunosuppressive effects mediated by interactions with glucocorticoid response elements and inhibition of transcription factors like NF-kB

161
Q

What are the indications for glucocorticoids?

A

Many, but mainly:

  • Addison’s disease (chronic primary adrenal insufficiency)
  • Inflammation
  • Immune suppression
  • Asthma
162
Q

What are some signs of glucocorticoid toxicity?

A

Cushing’s Syndrome: buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy brusing, osteoporosis, adrenocortical atrophy, peptic ulcer, diabetes

163
Q

What can occur if glutocorticoids are stopped abruptly after chronic use?

A

Adrenal insufficiency

164
Q

… is a steroid that works 1:1 at glucocorticoid and mineralocorticoid receptors.

A

Hydrocortisone

165
Q

… is a steroid that works at glucocorticoid > mineralocorticoid receptors.

A

Prednisone

- Stronger at gluco receptors than hydrocortisone

166
Q

… is a steroid that works at glucocorticoid&raquo_space;> mineralocorticoid receptors, a pure glucocorticoid agonist.

A

Dexamethasone

UWorld (15 decks)

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