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Nurs 323 > Final exam meds > Flashcards

Final exam meds Flashcards

1
Q

Anti-ulcer antibiotics

A

primarily for H.Pylori (amoxicillin, tetracycline, clarithromycin, metronidazole, tinidazole)

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2
Q

H2 receptor antagonist
Prototype
MOA
Adverse effects

A

Antisecretary agent for ulcers
-H2 Receptor antagonist: 1st choice drug for gastric and duodenal ulcers. Used in conjuction with antibiotics to treat hpylori

Prototype: Cimetidine (Tagamet) [anything ending in -tidine]

MOA: Selectively blocks H2 receptors in parietal cells of the stomach, inhibiting gastric acid secretion (it reduces basal, food-stimulated, and nighttime amounts).

Adverse effects: Decreases libido (Antiandrogenic effect), can produce CNS effects (lethargy, confusion, depression) in the elderly with renal and hepatic problems, headache, and GI disturbances such as diarrhea and constipation.

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3
Q

Proton pump inhibitors
Prototype
MOA
Adverse effects

A

antisecretary/ulcer treatment

Prototype: Omeprazole (Prilosec)[endings with –azole]

MOA: Binds irreversibly to H+, K+-ATPase in parietal cells to decrease basal and stimulated acid secretion. The effect lasts for 3-5 days after the drug intake has stopped, and is the most effective antisecretory agent.

Adverse effects: Insignificant with short term use, but can have mild headache, diarrhea, and N/V in low incidences.

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4
Q

Antacids
Prototype
MOA
Adverse effects

A

ulcer treatment

Prototype: Aluminum hydroxide gel (Amphojel)

MOA: Neutralized stomach acid, inactivates pepsin, and (may) stimulate prostaglandins.

Adverse effects: Constipation because of the calcium and aluminum components, diarrhea because of the magnesium compounds, and fluid retention with antacids that contain sodium.

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5
Q

Mucosal protectant
Prototype
MOA
Adverse effects

A

Ulcer treatment

Prototype: Sucralfate (Carafate)

MOA: The acidity of the stomach converts sucralfate into a substance that coats the ulcer and acts as a protective barrier. NO EFFECT ON ACID SECRETION.

Adverse effects: No systemic effects; may cause constipation

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6
Q

Antisecretary/increases mucosal defenses
Prototype
MOA
Adverse effects

A

Ulcer treatment

Prototype: Misoprostol (Cytotec)

MOA: Works as an endogenous prostaglandin, and increases bicarbonate and mucus secretion while suppressing gastric acid secretion. Will also cause vasodilation and increase mucosal blood flow.

Adverse effects: Diarrhea, abdominal pain, uterine contractions, and dysmenorrhea/spotting.

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7
Q

Phenytoin (Dilantin)
MOA
Indication
Side effects

A

MOA: suppress sodium influx

  • effective against all except absence and myoclonic seizures
  • Drug of choice for tonic-clonic seizures
  • Side effects: CNS effects including nystagmus, ataxia, diplopia, sedation and cognitive impairment, Gingival hyperplasia, Hirsutism, metabolic bone disease, Phenytoin is a teratogen (e.g. causes cleft palate, hydrocephalus), Can cause cardiac dysrhythmias and hypotension when administered IV.
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8
Q

Carbamazepine (Tegretol)
MOA
Indication
Side effects

A

MOA: suppress sodium influx

  • Used for partial (simple and complex) seizures, tonic-clonic seizures, and bipolar disorders
  • Side effects: Minimal effect on cognitive function, CNS effects include nystagmus, diplopia, blurred vision, dizziness, drowziness, lethargy, vertigo, staggering gait and headache, Anemia, granulocytopenia, thrombocytopenia
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9
Q

Valproic acid (Depakene)
MOA
Indication
Side effects

A

MOA: suppress sodium influx
and suppress calcium influx

  • Used for partial, generalized & absence seizures
  • Used for bipolar disorders and migraine headache
  • Side effects: GI upset: N & V, indigestion, Sedation, Unsteadiness, Tremor, Thrombocytopenia , Acute hepatic failure, Acute pancreatitis, Alopecia, Weight gain
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10
Q

Lamotrigine (Lamictal)
MOA
Indication
Side effects

A

MOA: suppress sodium influx

  • Used for partial and tonic clonic seizures
  • Used for bipolar disorders
  • Side effects: Diplopia, Headache, Dizziness, Unsteadiness
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11
Q

Ethosuxamide (Zarontin)
MOA
Indication
Side effects

A

MOA: Suppress calcium influx

  • Only indicated in absence seizures
  • Adverse effects include: CNS effects (ataxia, drowsiness, sleepiness, lightheadedness, fatigue), GI effects (N & V), Skin rashes
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12
Q

Ezogabine

general info

A

Promote potassium efflux: during an action potential, influx of sodium causes neurons to depolarize (fire), and then efflux of potassium causes neurons to repolarize (relax). Ezogabine acts on voltage gated potassium channels to facilitate potassium efflux. This action is believed to underlie the drugs ability to slow repetitive neuronal firing and thereby provide seizure control.

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13
Q 
Benzodiazepines
MOA
Uses
Side effects
Drugs in class
A

MOA: Potentiate GABA

Used in status epilepticus

Side effect: Respiratory depression

Drugs:
Diazepam (Valium)
Clonazepam (Rivotril, Klonopin)
Lorazepam (Ativan)

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14
Q 
Barbiturates
MOA
Uses
Side effects
Drugs in class
A

MOA: Potentiate GABA

Used for partial and generalized tonic-clonic seizures. Not effective against absence seizures.

Adverse effects include: Drowsiness, sedation, Confusion, Anxiety, Ataxia, Hyperactivity, Headaches

Drugs:
Phenobarbital (Luminal)

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15
Q

Gabapentin (Neurontin)
MOA
Uses
Side effects

A

MOA: Potentiate GABA

Used for partial seizures, Also used for neuropathic pain and prevention of migraine headaches

Adverse effects include: Dizziness, Fatigue, Somnolence, Pedal edema, Weight gain

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16
Q

Tiagabine
MOA
Uses

A

MOA: Potentiate GABA

only used in partial seizures, children over 12

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17
Q

Vigabatrin
MOA
Uses

A

MOA: Potentiate GABA

add on therapy or infantile therapy

18
Q

Felbamate

MOA

A

Antagaonize glutamate: Glutamic acid (glutamate) is the prmary excitatory transmitter in the CNS working through two receptors NMDA and AMPA. Felbamate and topiramate block the actions of glutamate at NMDA and AMPA thereby suppressing neuronal excitation.

19
Q

Topiramate

MOA

A

Antagaonize glutamate: Glutamic acid (glutamate) is the prmary excitatory transmitter in the CNS working through two receptors NMDA and AMPA. Felbamate and topiramate block the actions of glutamate at NMDA and AMPA thereby suppressing neuronal excitation.

20
Q

Insulin

Short duration: rapid acting

A 
Insulin lispro (Humalog)
Insulin aspart (NovoLog)
Insulin glulisine (Apidra)
Works within 30-90 miuntes	
Lasts 3-5 hours
21
Q

Insulin

Short during: slower acting

A

Regular insulin (Humulin R, Novolin R)
Works within 30-60 minutes
Lasts 6-8 hours

22
Q

Insulin

Intermediate duration

A

Neutral protamine Hagedorn (NPH) insulin
Insulin detemir (Levemir)
Works within 1-2 hours
Lasts 16-24 hours

23
Q

Insulin

Long duration

A

Insulin glargine (Lantus)
Works within 1 hour
Lasts 24 hours

24
Q

Sulfonylureas

A

MOA:
Increase endogenous insulin secretion
Decrease A1C by 1.5-2%
No specific effect on plasma lipids or blood pressure

Drugs in this class

  • First generation: chlorpropamide (Diabinese), tolazamide, acetohexamide (Dymelor), tolbutamide (Orinase)
  • Second generation: glyburide (Micronase, Glynase, and DiaBeta), glimepiride (Amaryl), glipizide (Glucotrol, Glucotrol XL)
  • First generation drugs have lower potency relative to second generation drugs
25
Q

Bigaunides

A

Bigaunides
MOA:
↓ hepatic glucose production
↑ insulin-mediated peripheral glucose uptake (potentiating insulin action).

Drugs in this class
metformin (Glucophage), metformin hydrochloride extended release (Glucophage XR)
26
Q

Thiazolidinediones

A

Thiazolidinediones (TZDs, Glitazones)
MOA:
↓ insulin resistance & ↓ hepatic glucose production
6 weeks for maximum effect

Drugs in this class:
pioglitazone (Actos), rosiglitazone (Avandia), [troglitazone (Rezulin) - taken off market due to liver toxicity]

27
Q

Meglitinides

A

Meglitinides

MOA:
Stimulate insulin secretion (rapidly and for a short duration) in the presence of glucose.

Drugs in this class:
repaglinide (Prandin), nateglinide (Starlix)

28
Q

Alpha-glucosidase Inhibitors

A

Alpha-glucosidase Inhibitors

MOA:
Block the enzymes that digest starches in the small intestine

Drugs in this class:
acarbose (Precose), miglitol (Glyset)

29
Q

ASA

MOA

A

•ASA (Aspirin)

Inhibits COX1 which decreases thromboxane A2 formation → decreased platelet activation (pg 491)

30
Q

ADP

MOA

A

•Adenosine Diphosphate Receptor Blockers (ADP Blockers)
Irreversibly blocks ADP receptors on platelets
→ decreased platelet aggregation

31
Q

Glycoprotein IIb/IIIa Platelet Receptor Antagonist

MOA

A

•Glycoprotein IIb/IIIa Platelet Receptor Antagonist
Called super aspirin
Irreversibly blocks glycoprotein IIb/IIIa platelet receptors
Stops fibrinogen from aggregating platelets together
Stop the final step in aggregation therefore, these drugs can prevent aggregation stimulated by all factors including collagen, thomboxane A2, ADP. Thrombin, and platelet activation factor.
Most EFFECTIVE antiplatelet drug

32
Q

Beta Blockers
Cardio selective
Nonselective

A 
Cardioselective: Metoprolol (lopressor)
-Block only b1  receptors resulting in:
-↓ CO
-↓ Contractility
-↓ rate of conduction through the AV node
-↓ renin secretion
Nonselective: Propanolol (Inderal)
-Blockade of B1 and B2 (can cause bronchoconstriction and hypoglycemia)
33
Q

Calcium Channel Blockers

A

Nifedipine: act primarily on arterioles
-Block calcium channels in blood vessels resulting in vasodilation primarily of peripheral arterioles and coronary arteries and arterioles→ ↓ BP

Verapamil and Diltiazem

  • Act on arterioles AND the heart
  • Block calcium channels in blood vessels and heart resulting in vasodilation of arterioles → ↓ BP and ↑ coronary artery blood flow
  • ↓ cardiac contractility
  • Blockade at SA node → ↓ HR
  • Blockade at AV node →↓ AV node conduction
  • Veins not significantly affected
34
Q

Cardiac Glycosides

A

Digoxin
Positive inotropic effect-↑ contractility
-Inotropic effect is due to inhibition of Na+/K+ ATPase in plasma membrane
-Relationship of potassium to inotropic action
-Potassium competes with Digoxin to combine with Na+/K+ ATPase
-Potassium levels must be kept within normal physiologic range when giving Digoxin

Negative chronotropic effect-↓ HR

  • Low to normal dose →↓automaticity (SA conduction)→↓ HR
  • High dose →↑ automaticity → abnormal firing→ arrhythmias

Negative dromotropic effect-↓ Conduction

  • Decrease conduction at AV node → prolonged refractory period of AV node
  • Low to normal dose →↓ automaticity (SA conduction)→↓ HR
  • High dose →↑ automaticity → abnormal firing→ arrhythmia
35
Q

Nitrates

A

NTG ↓ myocardial O2 demand by dilating veins and decreasing preload

Prevents coronary artery spasm →↑ O2

Main purpose of nitrates is the venous dilation

36
Q

Side effects of loop and thiazide diuretics

A

•Loop: furosemide (latex)
Hypochloremia, hyponatremia and dehydration
Hypokalemia
Hypotension and postural hypotension (volume loss and venodilation)
Ototoxicity with high dose (use with certain antibiotics can increase this risk)
Hyperuricemia, hyperglycemia, increase LDL and triglycerides, decrease HDL, increase ca+ excretion

•Thiazide: hydrochlorothizide (HydroDIURIL)
Same as loop except for ototoxicity

37
Q

Indications for loop diuretics

A

•Loop: Furosemide (Lasix)
Hypertension (not routinely used)
Pulmonary edema caused by CHF
Reserved for conditions not responsive to other diuretics such as edema caused by liver, cardiac or renal disease
Effective in patients with impaired renal blood flow and decreased GFR

38
Q

Indications for thiazide

A

•Thiazides: hydrochlorothiazide (HydroDIURIL)
First choice for hypertension
Only works in NORMAL renal flow and GFR
Moderate diuresis

39
Q

Indication for Potassium sparing diuretics

A

•Potassium sparing: spironolactone (aldosterone antagonists)
Used with other diuretics for the potassium sparing effects
Used with hypertension, HF, edema

40
Q

potassium levels and cardiac glycosides (digoxin)

A

•Potassium ions compete with digoxin for binding to Na, K, ATPase. Because potassium competes with digoxin, when potassium levels are low, binding of digoxin to Na, K, ATPase increases. This increase can result in toxicity. Conversely, in potassium levels are high it can impair the therapeutic responses of digoxin. Potassium level should be kept between 3.5-5

41
Q

Chronotropic and Inotropic drugs

A 
•Chronotropic drugs effect HR
Negative chronotropic drugs decrease HR
-Beta blockers (i.e. metoprolol)
-Acetycholine
-Digoxin
-Verapamil

Positive chronotropic drugs increase HR
-Theophylline

•Inotropic drugs effect Contractility
Negative inotropic drugs decrease contractility
-Beta Blockers
-Calcium channel blockers

Positive inotropic drugs increase contractility
-Digoxin

Nurs 323 (2 decks)

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