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Pharmacology I > Unit 2- concepts > Flashcards

Unit 2- concepts Flashcards

1
Q

aldosterone

A
  • released from adrenal cortex in response to high K+ and H+ levels or low Na+ levels
  • acts on distal tubules of kidney to cause retention of Na+ and excretion of K+/H+
  • Na+ retention leads to water retention -> BP rise
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2
Q

aldosterone and Na+/K+ exchange

A
  • stimulates reabsorption of Na+ from DCT

* causes K+ to be secreted

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3
Q

fxns angiotensin (5)

A
  1. constricts vessels, increasing vascular resistance
  2. stimulates aldosterone release from adrenal cortex
  3. stimulates release of vasopressin (ADH) from pituitary
  4. facilitates NE release and inhibits re-uptake from nerve endings (-> SNS)
  5. stimulates cardiac/vascular hypertrophy
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4
Q

decrease of angiotensin II results in…

A 
•vasodilation
•decreased blood volume
•decreased cardiac/vascular remodeling
•K+ retention
•fetal injury
*accomplished by ACE inhibs
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5
Q

first dose hypertension

A
  • orthostatic hypotension after the first dose of BP medication
  • often results in syncope
  • common with ACE inhibs
  • can be avoided by taking the first dose at night
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6
Q

reflex tachycardia

A
  • in response to decreased blood volume the heart beats faster in attempts to raise it
  • causes include orthostatic hypotension, meds, and FVD
  • avoided by combining anti-HTN w/ beta blocker
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7
Q

myocardial infarction (MI)

A

•occurs when artery is completely occluded

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8
Q

angina pectoris

A
  • chest pain due to CAD and myocardial ischemia
  • result of imbalance b/t myocardial O2 supply and demand
  • tx to prevent MI, pain, etc
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9
Q

exertional angina

A

•angina (pain) occurs durning physical exertion/stress

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10
Q

vasospastic angina

A
  • may occur at any time

* due to coronary artery vasospasm

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11
Q

untreated CAD and angina may lead to…

A
  • MI

* death

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12
Q

nitric oxide

A

•potent vasodilator of blood

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13
Q

heart failure

A
  • weakening of contractile fxn of heart
  • blood/fld accum. in heart, lungs, abdomen, and lower extremities
  • dec. CO and BP unable to meet body’s O2 needs
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14
Q

cardiovascular reflexes for CHF

A
  • vasoconstriction
  • tachycardia
  • Na+/H2O retention
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15
Q

s/s CHF

A
  • dec. tissue perfusion- weak/activity intolerance
  • L side- pulmonary congestion
  • R side- systemic congestion
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16
Q

dromotropic effects on heart

A
    • inc. SPEED of ctx

* - dec. SPEED of ctx

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17
Q

inotropic effects on heart

A
    • inc. FORCE of ctx

* - dec FORCE of ctx

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18
Q

chronotropic effects on heart

A
    • inc. SA HR

* - dec. SA HR

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19
Q

angioedema

A

•swelling affecting deeper layers of skin
•most common around eyes and lips
*hives under skin

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20
Q

goal of dysrhythmia tx

A

•keep HR b/t 60 and 100 bpm

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21
Q

what does HR have to be to admin dig

A

•60 bpm

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22
Q

important before admin/taking cardiac drugs

A

•take BP and HR

23
Q

CCB for angina pectoris

A

•decreases myocardial contractility

24
Q

CCB for HTN

A

•relaxes smooth muscle

25
Q

CCB for dysrhythmia

A

•slows HR and AV conduction

26
Q

CCB interaction w/ Quinidine, carbamazepine, cyclosporine

A
  • inhibits their metabolism

* leads to toxicity

27
Q

best HDL raising drug

A
  • Nicotinic acid (Niacor)

* Niacin (Niaspan)

28
Q

very low density lipoproteins (VLDLs)

A

•triglycerides

29
Q

low density lipoproteins (LDLs)

A
  • bad
  • contribute to atherosclerosis
  • levels should be less than 100 mg/dL
30
Q

high density lipoproteins (HDLs)

A
  • good
  • prevent atherosclerosis
  • levels should be greater than 40 mg/dL
31
Q

important about fibrates

A

•reduce levels of TGs, not LDLs

32
Q

class I medications

A
  • sodium-channel blockers

* slow conduction

33
Q

class II medications

A
  • beta blockers

* prevent SNS stimulation of heart

34
Q

class III medications

A
  • K+ channel blockers

* prolong refractory period

35
Q

class IV medications

A
  • CCBs
  • decrease force of ctxn
  • relax smooth muscle
  • decrease HR and AV conduction
36
Q

A client with hypertension is receiving furosemide (Lasix). Which data indicates the medication is effective?

A

8-hour intake is 1800 ml and output is 2300ml

37
Q

A client with essential hypertension is prescribed hydrochlorothiazide (Diuril). The nurse should provide this information to the client

A

drink adequate amounts of fluid

38
Q

contraindications for Lasix or HCTZ

A
  • pregnancy
  • lactation
  • diabetes
  • hypokalemia
39
Q

digoxin (Lanoxin) and furosemide (Lasix) interaction

A

•ventricular dysrhythmias in presence of hypokalemia
•Dig is very dependent on K+, so will get dig toxicity
*K+ sparing agents often admin to prevent
*monitor heart and K+ levels

40
Q

primary reason to stop ACEI therapy

A

•cough

41
Q

digoxin effect time

A
  • t1/2: 1.5 days
  • plateauL 6 days
  • oral effects: 30 min- 2 hr
  • peak: 4-6 hrs
42
Q

halo effect with digoxin use

A

•visual disturbance indicating overdose

43
Q

digoxin toxicity tx

A
  • stop drug
  • treat cause
  • treat dysrhythmia
  • admin Digoxin Immune FAB (digibind)
44
Q

positive inotropic effect of digoxin

A

•increase contractile force of myocardial ctx

-results in improved SC and CO

45
Q

negative chronotropic effect of digoxin

A

•decreased HR-

  • results in more time for ventricular filling
  • results in increased SV and CO
46
Q

hyperkalemia and cardiac glycoside interaction

A

•decreases actions of cardiac glycoside

47
Q

hypercalcemia and cardiac glycoside interactions

A

•increases actions and toxicity of cardiac glycosides

48
Q

digoxin dosing

A
  • initial digitalization doses to rapidly attain effective therapeutic concentration
  • lower daily doses given to maintain therapeutic concentrations
49
Q

digitalization

A
  • using loading dose to achieve therapeutic levels quickly
  • usually 4 divided dose of 0.25 mg
  • admin PO or slow IV push (5 min)
50
Q

digoxin maintenance

A

•adults 0.125-0.5 mg/day
•typical is 0.25 mg/day
*HR MUST be above 60 and stable BP before admin

51
Q

digoxin therapeutic plasma levels

A

•0.5-2.0 ng/mL

52
Q

diuretic therapy for CHF

A
  • eliminates excess Na/fld
  • results in more effective heart fxn
  • can be used in combo w/ cardiac glycosides and other drugs, but monitor K+
53
Q

vasodilator therapy for CHF

A

•relax/dilate blood vessels
•decreases peripheral resistance, allowing more efficient blood flow
*most common are ACEIs and ARBs

54
Q

Phosphodiesterase inhibitors

A
  • amrinone; milrinone
  • short term IV therapy for CHF
  • positive inotropic agents w/ vasodilator properties
  • increase myocardial contractility

Pharmacology I (9 decks)

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