Brainscape's Knowledge GenomeTM

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


See full index

Fall 2013 > Top 200 Drug Grids > Flashcards

Top 200 Drug Grids Flashcards

1
Q

ACE Inhibitor: Mechanism of Action

A

Normally, Angiotensin II causes an increase in blood pressure or hypertension. Angiotensin II is formed from angiotensin in the blood by ACE. ACEI inhibits the activity of ACE which decreases levels of Angiotensin II. Results in dilation of blood vessels and reduced blood pressure.

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

ACE Inhibitor: Side Effects

A
  • Dizziness (5 to 12%)
  • Cough (4 to 9%)
  • Syncope (5.1 to 7%)
  • Headache (4 to 6%)
  • Hypotension (1% to 4%)
  • Hyperkalemia (2 to 5%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

ACE Inhibitor: Interactions

A
  • Food: Salt substitutes containing K+ or foods high in K+ will increase retention of K+ in the body.
  • Drugs: NSAIDS reduce renal secretion of ACEI, so this increases ACEI concentration in the body.
  • General: Food or antacids that slow gastric emptying and/or raise gastric pH reduce ACEI bioavailability.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Benzodiazepines: Mechanism of Action

A

binding to GABA receptors, which increases GABA activity by opening chloride channels, which then blocks cortical and limbic arousal.

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

Benzodiazepines: Side Effects

A
  • anterograde amnesia
  • tachycardia
  • Problems with coordination
  • Decrease in appetite
  • Drowsiness
  • Difficulty breathing
  • Body Aches
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Benzodiazepines: Interactions

A
  • Alcohol: further excites GABA(A) receptors in addition to benzodiazepines and results in a fatal decrease of neuronal activity.
  • Barbiturates: acts as a CNS depressant, same as barbiturates, but more potent and addictive. Overrides benzodiazepines.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

H2-Antagonist: Mechanism of Action

A

Competitively inhibits histamine binding to H2 receptors in the stomach which reduces the amount of stomach acid secreted. Decreases the total volume of gastric juice, pepsin secretion, and the amount of stomach acid released in response to stimuli such as food, caffeine, insulin, etc.

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

H2-Antagonist: Side Effects

A
  • Headache
  • Dizziness
  • Constipation
  • Itching
  • Dryness of mouth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

H2-Antagonist: Interactions

A
  • Triazolam: Absorption of Triazolam in increased when taking either H2 antagonist. The elevation in gastrointestinal pH allows for greater absorption of triazolam.
  • Atazanavir: Solubility of Atazanavir decreases as gastrointestinal pH increases. To manage the interaction, change the dosage of the H2 antagonist and take Atazanavir with food after a set number of hours after taking the H2 antagonist.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Proton Pump Inhibitor: Mechanism of Action

A

covalently bind to the H+/K+-ATPase enzyme system at the secretory surface of the gastric parietal cell. This action of inhibition of H+/K+-ATPase blocks the final step of gastric acid production, leading to inhibition of both basal and stimulated acid secretion.

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

Proton Pump Inhibitor: Side Effects

A
  • Headache
  • Diarrhea
  • Nausea
  • Stomach pain
  • Vomiting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Proton Pump Inhibitor: Interactions

A
  • Warfarin: increased International Normalized Ratio (INR) and prothrombin time
  • Ketaconazole: loss of ketoconazole efficacy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

SSRI: Mechanism of Action

A

It is a selective inhibitor of neuronal serotonin uptake in the CNS. Therefore the level of serotonin in the synaptic cleft increases. These serotonin can bind to the receptor on post synaptic neurons. Some can weakly inhibit norepinephrine and dopamine.

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

SSRI: Side Effects

A
  • Dizziness
  • Headache
  • Insomnia
  • Diarrhea
  • Nausea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

SSRI: Interactions

A
  • MAOIs: Both drugs increase levels of serotonin in the brain. Drugs should not be taken together because serotonin levels would become too high. Treatment with MAOIs should not begin until after 5 weeks of stopping treatment with SSRIs.
  • Interaction with drugs that interfere with hemostasis such as NSAIDs, aspirin, or warfarin. Drugs should not be used together because there will be an increased risk of gastrointestinal bleeding.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Statins: Mechanism of Action

A

Reduce the cholesterol production and lowers plasma cholesterol level via three mechanisms:

1) inhibition of cholesterol biosynthesis
2) enhancement of receptor mediated LDL uptake
3) reduction of very low density lipoprotein

Competitive Inhibitor: Statins are molecularly similar to HMG-CoA and they compete with this substrate for the binding site on HMG-CoA reductase, inhibiting the enzyme and reducing rate of production of mevalonate in the cholesterol-producing cascade pathway.

17
Q

Statins: Side Effects

A
  • GIT [gastrointestinal tract] disturbance (most common)
  • Elevation of hepatic [liver] transaminase level shortly after initiating therapy.
  • Myalgia [muscle pain] and Myopathy [muscle weakness due to non-function muscle fibers]
  • Muscle cramp
  • Rhabdomyolysis [muscle damage]
18
Q

Statins: Interactions

A
  • Azole Antifungal & Amiodarone: increase the risk of severe myopathy (rhabdomyolysis)
  • Protease Inhibitors (eg, darunavir, nelfinar, ritonavir): may result in elevated statin plasma levels, increasing the risk toxicity
  • Grapefruit Juice: increases absorption of the statin into the bloodstream causes too much of the drug to stay in the body, increasing risk of muscle breakdown and kidney failure
19
Q

Sulfonylurea: Mechanism of Action

A

Sulfonylurea binds to ATP dependent K+ channel. K+ builds up inside cell, causing depolarization. Depolarization causes voltage-gated Ca2+ channels to open. Ca2+ influx facilitates exocytosis of insulin filled vesicles. Insulin reduces plasma glucose levels.

20
Q

Sulfonylurea: Side Effects

A
  • Hypoglycemia
  • Weight gain
  • Abdominal upset
  • Headache
  • Hypersensitivities
21
Q

Sulfonylurea: Interactions

A
  • Insulin and other antidiabetic drugs
  • Drugs that induce or inhibit cytochrome P450 2C9 and P-glycoprotein
  • Highly protein bound drugs
  • Ethanol
22
Q

Fluoroquinolones: Mechanism of Action

A

synthetic, antibacterial agents that inhibit DNA gyrase and topoisomerase IV. DNA gyrase is essential enzyme that is involved in the replication, transcription, and repair of bacterial DNA. Topoisomerase IV is an enzyme that partitions the chromosomal DNA during bacterial cell division. Fluoroquinoloes inhibit these topoisomerase enzymes by stabilizing either the DNA—DNA gyrase complex or the DNA—topoismerase IV complex; these stabilized complexes block movement of the DNA replication fork and thereby inhibit DNA replication resulting in cell death.

23
Q

Fluoroquinolones: Side Effects

A
  • Nausea
  • Diarrhea
  • CNS disturbance, headache, restlessness
  • Abnormal liver function tests
  • Eosinophilia, rash
24
Q

Fluoroquinolones: Interactions

A
  • Theophylline Derivatives: decrease the metabolism of theophylline derivatives. Theophylline/quinolone therapy might augment the seizure-producing potential of each of the individual agents. Theophyllines may potentiate quinolone-induced inhibition of γ-aminobutyric acid (GABA), thus possibly potentiating CNS stimulation.
  • Anticoagulant: may enhance the anticoagulant effect of vitamin K antagonists. This may be done by ciprofloxacin displacing the anticoagulants from serum albumin binding sites.
25
Q

Beta-blockers: Mechanism of Action

A

bind to beta-adrenoceptors and thereby block the binding of NE and epinephrine to these receptors

26
Q

Beta-blockers: Side Effects

A
  • Hypotension
  • Depression
  • Bradyarrhythmia
  • Dizziness
  • Fatigue
  • impotence
  • trouble sleeping
27
Q

Beta-blockers: Interactions

A
  • alpha-1 antagonists may result in an exaggerated hypotensive response to the first dose of the alpha antagonist
  • Calcium channel blockers (digoxin, amiodarone, quinidine) may have additive cardiovascular effects
28
Q

ARB: Mechanism of Action

A

selectively block/antagonize the angiotensin II (the principal agent of the renin-angiotensin system, with effects that include vasoconstriction, stimulation of synthesis and release of aldosterone, cardiac stimulation, and renal reabsorption of sodium) at the AT1 receptor which prevents vasoconstriction of vascular smooth muscles. This leads to less blood pressure and treating hypertension.

29
Q

ARB: Side Effects

A
  • Hyperkalemia
  • Hypotension
  • Acute Renal Failure
  • Diarrhea
  • Abdominal Pain
30
Q

ARB: Interactions

A
  • ACE Inhibitors: Cause renal dysfunction and hyperkalemia. If coadministration of an ACE inhibitor and an ARB is required, closely monitor renal function.
  • aliskiren (Tekturna): contraindicated in patients with diabetes due to increased risk of hyperkalemia, hypotension, and renal impairment. The combination should also be avoided in patients with renal impairment.
31
Q

NSAID: Mechanism of Action

A

inhibition of prostaglandin synthesis. NSAIDs inhibit cyclooxygenase (COX), which is an enzyme that catalyzes the synthesis of cyclic endoperoxides from arachidonic acid, which will eventually form prostaglandins. NSAIDs inhibit COX enzymes, lowering prostaglandin levels, reducing inflammation and pain in tissue, relieving symptoms of arthritis, fever, headaches, migraines, and pain in the joints. Inhibition of COX-2 leads to anti-inflammatory effects, inhibition of COX-1 may lead to stomach ulcers and GI tract bleeding.

32
Q

NSAID: Side Effects

A
  • Indigestion and stomach ulcer.
  • Headaches- drowsy or dizzy
  • Several skin reaction
  • Diarrhea
  • Nausea
33
Q

NSAID: Interactions

A
  • Celecoxib/ Warfarin: NSAIDs can cause GI bleeding, inhibit platelet aggregation, and prolong bleeding time.
  • Indomethacin/ Atenolol: antihypertensive effect. Their interaction leads to the production of vasodilation and renal prostaglandins, resulting in high blood pressure.

Fall 2013 (11 decks)

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