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Pharm PTFE Flashcards

1
Q

Angiotensin-converting enzyme (ACE) inhibitor mode of action

A

produce vasodilation
decrease peripheral vascular resistance
increase venous capacitance

decreases afterload

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2
Q

Beta blocker mode of action

A

decrease HR
decrease cardiac contractility

(also lowers BP)

  • Decreased myocardial oxygen demand by decreasing HR and contractility
  • Block the action of beta receptors of sympathetic nervous system (fight or flight) located in lungs, heart, skeletal muscles
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3
Q

Statin-induced Side effects

A

myalgia/myopathy - skeletal breakdown
liver impairments (asterixis, CTS, ascites, etc)
rhabdomyolysis
fever
nausea
vomiting
aching muscles in legs, trunk, or arms
Burning
Tenderness
Stiffness
Cramping

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4
Q

Beta blockers

A

atenolol, metoprolol, propranolol (lol meds)
Used for cardiac arrhythmias
Blocks Beta receptors - attenuates sympathetic stimulation
decrease cardiac stress
decreases HR

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5
Q

Atenolol

A

Beta blocker

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6
Q

Metoprolol

A

Beta blocker

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7
Q

Propranolol

A

Beta blocker

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8
Q

ACE (Angiotensin-Converting Enzyme) inhibitors

A

captorpril, enalapril, lisinopril, ramipril (pril meds)
Blocks production of ACE
Reduces BP
Decreases load of heart

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9
Q

Captorpril

A

ACE inhibitor

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10
Q

Enalapril

A

ACE inhibitor

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11
Q

Lisinopril

A

ACE inhibitor

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12
Q

Ramipril

A

ACE inhibitor

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13
Q

Calcium Channel Blockers (CCB)

A

Amlodipine, Nifedipine, Verapamil, Diltiazem)
Used for HTN and CHF
Blocks calcium entry into cardiac muscle tissue
This causes Vasodilation
Decrease vascular resistance (decrease BP)
Decreases HR

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14
Q

Potential side effects of Calcium Channel Blockers

A
  • Could cause excessive bradycardia
  • could cause peripheral vasodilation and lead to dizziness and HA>
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15
Q

Amlodipine

A

CCB

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16
Q

Nifedipine

A

CCB

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17
Q

Verapamil

A

CCB

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18
Q

Diltiazem

A

CCB

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19
Q

Nitrates (Nitroglycerin)

A

Used for Angina Pectoris
Vascular smooth muscle dilation
Decrease preload (blood returning to heart) and after afterload (vascular resistance)
Results in: decreased stress on hearts and decreased myocardial oxygen demand

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20
Q

Nitrates adverse effects

A

OH
Headache
Dizziness

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21
Q

Nitroglycerin

A

Nitrate

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22
Q

Cardiac glycosides

A

Digoxin, digitoxin, digitalis
Increase myocardial contraction force
Inhibits sympathetic nervous system
Slows sodium-potassium pump

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23
Q

Cardiac glycosides Toxicity

A

GI distress
nausea
vomiting
diarrhea
Arrhythmias (PAC, PVC, A-tach, AV Blocks)

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24
Q

Digoxin

A

Cardiac glycosides

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25
Q

Digitoxin

A

Cardiac glycosides

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26
Q

Digitalis

A

Cardiac glycosides

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27
Q

Statin treats?

A

Hyperlipidemia

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28
Q

Atorvastatin (Lipitor)

A

Statin

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29
Q

Simvastatin (Zocor)

A

Statin

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30
Q

Beta Agonist treats?

A

Asthma
COPD

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31
Q

Beta Agonist (beta-2 agonist) mode of action

A

A bronchodilator medicine that opens the airways by relaxing the muscles around the airways that may tighten.
Activate the Beta-2 receptor on muscles surrounding airways.
Have a short duration of action

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32
Q

Beta Agonist Administration

A

Inhaler

33
Q

Beta Agonist side effects

A

Anxiety
Tremor
Palpations of fast HR
low blood potassium

34
Q

Albuterol (Ventolin, Proventil)

A

Beta-2 agonist

35
Q

Metaproterenol (Alupent)

A

Beta-2 agonist

36
Q

Medication for Heart Failure

A

Digoxin/Digitalis
Increases myocardial contractility, increases cardiac output and blocks AV node conduction
Helps with 1st, 2nd, and 3rd degree block, paroxysmal tachycardia.
Digitalis toxicity: DIG FAST
D - Distractability
I - Indiscretion
G - Grandiosity
F - Flight of ideas
A - Activity intolerance
S - Sleep deficit
T - Talkativeness

37
Q

Medication for HTN that is normally tried first

A

Diuretics

38
Q

Types of Diuretics

A

Thiazide Diuretics
Loop Diuretics
Potassium Diuretics
Potassium sparing Diuretics

39
Q

Hydrochlorothiazides

A

Thiazide Diuretics

40
Q

Adverse effects of Thiazide Diuretics

A

Can cause lithium toxicity, Digoxin toxicity
Hyperglycemia
Hyperurecemia
Hypercalcemia
Increased LDL levels
Hypokalemia (because of the inhibiting of reabsorption of Na+ and Cl-

41
Q

Furosemide, bumex, edecrin

A

Loop Diuretics

42
Q

Adverse Effects of Loop Diuretics

A

Hyperglycemia
Hyperurecemia
Increased LDL levels
Hypokalemia

43
Q

Aldactone, dyrenium, and midamo

A

Potassium Diuretics

44
Q

What does Potassium sparing diuretics do differently than other diuretics?

A

Weaken diuretic that prevents hypokalemia (low potassium)

45
Q

Adverse effects of Potassium sparing diuretics

A

Hyperkalemia (especially if they are on ACI inhibitor and K+ supplements)

46
Q

Most common side effects of Diuretics

A

Spasms

47
Q

Disease Modifying Anti Rheumatic Drugs (DMARDS)

A

Used with active continuing inflammatory disease (RA).
The goal is to stop inflammation and joint destruction. Best if used early and aggressively.

48
Q

Methotrexate, Anticytokines, Cyclosporine

A

DMARDS

49
Q

Methotrexate Adverse Effects

A

Side effects: loss of appetite, N/V, GI hemorrhage
Adverse effects: anemia, leukopenia, GI ulcerations, rashes, photosensitivity, HA, drowsiness, fatigue, hepatotoxicity, pulmonary toxicity.
PT considerations: HA, N, joint pain/swelling.
Folic acid may decrease its adverse effects

50
Q

Anti osteoporotic agents

A

Alendronate

51
Q

Alendronate (Fosamax) Adverse Effects

A

Major side effects include myalgias and esophageal lesions (they should take 30 min prior to breakfast and they should be standing or sitting for 30 min after drug admin.

52
Q

Aspirin

A

Inhibits the cox enzyme that inhibits prostoglandins
Anti-inflammatory, anti-platlet, anti-pyretic, anti-pain

53
Q

Aspirin Adverse Effects

A

Side effects: GI upset, N/V, bleeding, ulcers
Adverse effects: prolonged bleeding time can be an issue with hemophilia, Vit K deficiency, liver disease
Methotrexate toxicity: decreases methotrexate excretion!!! This increases the amount in the body. —- Used for RA!!
Aspirin Overdose (Salicylate posioning)
Tinnitus, N/V, Lethargy/Excitiability, hyperventilation, severe, fever
Works directly on platelets so if going to have sx stop 8-10 days prior to sx (the life of a platelet)

54
Q

NSAIDs (ibuprofen, advil, motrin)

A

Cox 1 : responsible for “good prostoglandins”
Cox 2: involved with inflammation
Acute inflammation: supposed to take in the first 72 hours and then stop to allow the bodies natural enzymes to heal

55
Q

Adverse effects of NSAIDS

A

Taking these in excess can set up to rhabdomyolysis (because they are masking the damage to their body).
Side effects: fluid retention, edema, GI irritation (less than aspirin)
Adverse effects: Lithium toxicity (diarrhea, vomiting, m weakness, lack of coordination)

56
Q

Cox-2 NSAID

A

Selective inhibitor NSAIDS (celexicob)
Only one that selectivity inhibits the COX! So it only targets the bad prostoglandins
Causes less side effects

57
Q

Muscle Relaxants

A

Diazepam (Valium)
Tizanidine (Zanaflex)
Flexeril (cyclobenzaprin)
Robaxin (methocarbamol)
Baclofen (lioresal)
Dantrolene (Dantrium)

58
Q

Diazepam (Valium) Adverse effects

A

serious drowsiness
abuse can lead to withdrawal

59
Q

Diazepam (Valium) indication:

A

to treat muscle spasms

60
Q

Tizanidine (Zanaflex) Adverse effects

A

Hypotension

61
Q

Tizanidine (Zanaflex) Indication

A

Spasticity

62
Q

Flexeril (cyclobenzaprin) and Robaxin (methocarbamol) indications

A

Temporary relief of local, acute muscle spasm

63
Q

Flexeril (cyclobenzaprin) adverse effects

A

Can interact with MAOI to cause HTN crisis. Also can cause tachycardia, blurry vision and dry mouth

64
Q

Baclofen (lioresal) Adverse effects

A

Treat spasticity and painful flexion or extensor spasm

65
Q

Baclofen (lioresal) adverse effects

A

Drowsiness
increased seizures if pt has epilepsy

66
Q

Dantrolene (dantrium) indications

A

chronic spasticity

67
Q

Dantrolene (dantrium) adverse effects

A

3 D’s: drowsiness, diarrhea, and dizziness.
Also photosensitivity

68
Q

Pt on lebodopa/carbidopa therapy with Parkinson’s disease will experience all of the following except?
1. Off phase
2. Dizziness
3. Involuntary movements
4. Marked bradycardia

A
  1. Marked bradycardia - will actually cause tachycardia
69
Q

Pt in on antiviral drug therapy (for treatment of AIDS). Which of the following adverse reactions during the treatment might be encountered MOST frequently during therapy?
1. Elevated BP
2. Aggressive and inappropriate behavior
3. Neuralgia and myopathies
4. Sedation and incoordination

A
  1. Neuralgia and myopathies
70
Q

In what way is flexeril somewhat unique among m relaxants that effect the CNS?
1. Flexeril has more peripheral effects
2. Flexeril shares pharmacological characteristics with the tricyclic anti depressants agents
3. Flexeril is a GABA agonist similar to barbiturates
4. Flexeril acts at the acetylcholine receptors, producing NM blockade.

A
  1. Flexeril shares pharmacological characteristics with the tricyclic anti depressants agents
71
Q

Aspirin in an acetylsalicylic acid, that inhibits platelet aggregation like all NSAIDs but is the drug of choice for thromboprophylaxis because:
1. It has predictable irreversible mechanism of action
2. It has predictable reversible mechanism of action
3. It has longer half life compared to other NSAIDs
4. It has no COX II effects

A
  1. It has predictable irreversible mechanism of action
72
Q

Pt in on long term NSAID therapy. The drugs reduce inflammatory process by:

A

Reducing the formation of the prostaglandins

73
Q

A pt on long term corticosteroids during therapy might show all of the following except:
1. Depressed mood
2. Orthostatic hypertension
3. Anemia
4. Muscle loss

A
  1. Anemia - doesn’t affect the RBC
74
Q

If a pt abruptly stop a 3y course of treatment with prednisone, which of the following would you expect to observe?
1. Hypernatremia and hyperglycemia
2. Hypotension
3. Increased responsiveness to injections of ACTH
4. Decreased production of IL 1 and IL 2 (interleukins)

A
  1. Decreased production of IL 1 and IL 2 (interleukins)
    The answer would be the opposite of what the action/side effect of the drug would be. It does have hyperglycemia, hypernatremia, hypertension, and decreased production of interleukins when taking the drug.
75
Q

If a pt s/p TKA that has been taking oxycodone comes to clinic 2 days after sx and begins complaining of chest burn. What questions should be asked?

A

GI distress
Oxycodone can cause severe constipation. So ask the pt when the pt has a last bowel movement. Can continue with therapy with this question.

76
Q

What are the most serious side effects of thiazide diuretics?

A
  • Hypovolemia - decreased extracellular volume
  • Hyponatremia - sodium depletion
  • Hypokalemia - potassium depletion
77
Q

What is a side effect of long term use of Lithobid (lithium)

A
  • Osteoporosis is a big sifde effect - due to this care must be taken to improve bone mass and avoid traumatic forces to the bones.
  • taken for the treatment of a bipolar disorder
78
Q

Big side effect of opioids?

A

Impaired cognitive functioning

Opioids cause a general slow-down of function, both cognitively and physiologically.

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