Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology > cardio and renal > Flashcards

cardio and renal Flashcards

1
Q

staging and treatment of heart failure

A
  • used to aid drug choice
  • stage A: no evidence of CAD, no symptoms, no limitations to ADLs-ACE inhibitors or ARBS
  • stage B: minimal CAD, mild symptoms, slight limitations to ADLs, comfortable at rest-ACE, beta blockers
  • stage C: moderate/severe CAD, marked limitation on ADLs, comfortable only at rest-ACE, beta blockers, diuretic, digoxin
  • stage D: severe CAD, severe limitations, symptoms even at rest-dubutamine, LVAD, transplant list, hospice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

pharmacodynamics of ACE inhibitors

A
  • decrease angiotensin II and aldosterone by decreasing angiotensinogen
  • lowers vascular resistance without decreasing CO or GFR-no reflexive tachycardia
  • increases o2 to heart muscle and reduces remodeling after MI
  • improves insulin sensitivity or affect glucose metabolism
  • doesn’t raise lipid levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

ACE on special pt groups

A
  • Use with young Caucasians with angina, DM pts, or HF pts
  • Not as effective on African Americans but if in combo with diuretic ethnicity doesn’t matter
  • African and Asian Americans greater risk of angioedema
  • category D-not to be used if pregnant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ADRs for ACE

A
  • dry cough (more likely in older pt)
  • angioedema
  • decreased K+
  • pancreatitis, renal failure
  • rash
  • orthostasis (within 1 hr of first dose)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

pharmocodynamics of ARBs

A
  • inhibits RAAS system by blocking angiotensin II receptors (on kidneys, brain, heart, and arterial wall)
  • use in kidney dz-not renal protective unless late stage of renal failure
  • an alternative to ACE inhibitors
  • many combined with HCTZ
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

pharmacokinetics of ARBs

A

-extensive 1st pass-only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

ADRs of ARBs

A

decreased BP, angioedema, increased K+, renal failure

  • food doesn’t effect it
  • cat D-don’t use in pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

direct renin inhibitors-Alsikiren (Tekturna)

A
  • works on RAAS system-blocks conversion of antiotensinogen to angiotensin I
  • not same renal protective qualities
  • cat D-don’t take during pregnancy
  • high fat diet decreases absorption
  • effect takes 2 weeks to be seen
  • ADR: increased K+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

pharmacodynamics of calcium channel blockers

A

-act as vasodilators by lowering Ca++ into smooth muscles
-2 classes: type 1 NDHP: diltiazem, verapamil-strong inotropic effect avoid using with HF pts
type 2 DHP: amlodipine, nicardipine
-DHP has no chronotropic effect
-NDHP: effects conduction through AV node and therefore decreases chronotropic effect and decreases HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

pharmacokinetics of calcium channel blockers

A
  • metabolized by liver CYP450 3A4
  • ADRs: contipation, dizziness, headache, edema, rash, gingival hyperplasia-encourage oral care
    • using CCB with ACE decreases peripheral edema by 50% rather than increasing dose of CCB alone
  • if pt has GERD-symptoms may be worse due to decrease of esophageal tone
  • pt avoid NSAIDS, ETOH, alone in jacuzzi
  • pregnancy cat C
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Digoxin

A
  • highly selective ATP inhibitor-leads to increased contractility (increased inotropy) and decreased chromotropy
  • seruim concentrations> 1 mg/mL increase mortality (higher risk in women general)–initiate treatment at lowest dose
  • best used for severe HF, enlarged hrt, 3rd heart tone, pt who have tried ACE and beta blockers
  • steady state achieved in about 1 wk.
  • not heavily metabolized–excreted unchanged by kidneys
  • half-life 36-48 hrs
  • drug interactions with amiodorone, diltiazem, verapamil
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

ADRs of digoxin

A

-GI: n/v/d, anorexia
CNS: fatigue, DPN
toxicity: yellow vision, green halos, hallucinations
cardiac: bradycardia d/t blocking AV junction
-needs to be monitored clinically and with labs (toxicity serum>2 mg/ml-consider giving K+)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

arrhythmias

A

-caused by physiological/and or anatomical consequences to prevent normal cardiac action potential

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

normal HR

A

-depends on intrinsic electrical impulses initiated at SA node and conducted to AV node and over ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

absolute refractory period

A

-cell not depolarizing no matter how strong the stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

relative refractory period

A

-stronger than normal stimuli can induce depolariztion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

refractoriness

A
  • state of cell that determines polarization

- damaged cell could keep constant of refractions or none at all

18
Q

spontaneous depolarizing cells

A
  • AV and SA node

- purkinje fibers

19
Q

automaticity

A

-ability of heart cell to depolarize and action potential

20
Q

re-entry phenomena

A
  • paroxysmal tachycardia d/t altered, enhanced,damaged cell, biochemical disturbances
  • 2 types: anatomical and physiological impulses
  • alternate pathways lead to firing upon itself possibly leading to vtach and SVT
21
Q

class I antiarrhythmic drugs

A

sodium channel blockers (membrane stabilizing agents)
IA: lengthens duration of action potential; reduce rate of rapid firing, reduce speed of conduction by increasing effective refractory period; increase conduction rate at AV node; (i.e.procainamide, quinidine)
IB: shortens duration of action potential-eliminating unindirectional blocks but may trigger reentry arrhythmias; rapidly acts with Na+ channels-blocks active and inactive channels, does not affect automaticity of AV or SA node; reserved for severe vtach pts whom other drugs have not worked (i.e. lidocaine, phenytoin)
IC: no effect on action potential (or minimally); slowly acts with sodium channels (i.e. encainide, iorcanide)

22
Q

class II antiarrhythmic drugs

A

beta blockers

  • reduce andrenergic activity in hrt
  • increase threshold and prolong effective refractory period–decrease hr and conduction velocity
  • produce negative inotropic effect
  • i.e. sotalol, metoprolol, propanolol
23
Q

class III antiarrhythmic drugs

A

potassium channel blockers

  • prolong effective refractory period by blocking potassium channels–decreases rate of automaticity of ventricular ectopic beats
  • little effect on depolarization
  • i.e. amiodarone, bretylium
24
Q

class IV antiarrhythmic drugs

A

calcium channel blockers

  • vasodilator lowering calcium influx into smooth muscle
    i. e. verapamil, diltiazem, beptidil
25
Q

beta adrenergic blockers

A
  • more effective in African American and elderly
  • decreased HR and decreased CO
  • no longer first line for HTN
  • can not stop suddenly will have rebound HTN because beta receptors are more sensitive
26
Q

Amiodarone

A
  • onset of action 3 days-3 weeks (PO)
  • excreted via feces
  • ADRs: bradycardia, neurological symptoms, blue skin/discoloration
  • many drug interactions
  • effected by grapefruit juice
  • ventric arrhythmia: 800mg-1600 mg BID for 3 weeks; decrease to 300-400 mg BID; maintenance 400 mg daily
27
Q

Nitrates

A
  • dilation of venous capacitance vessels and all parts of vascular system response
  • in higher doses atrial dilation–decreases afterload and leads to decrease myocardial demand and increase o2 supply
  • has little effect on atherosclerotic coronary arteries
  • ADRs: headache, hypotension, contact dermititis
  • contra-indicated with vasodilators or erectile dysfunction
  • monitor: hypotension
28
Q

nitroglycerine

A
  • used for acute attack use NTG-sublingual 0.4-0.6 every 5 minutes with maximum of 3 doses
  • predictable angina use isosorbide: isosorbide dinitrate 10-40 mg BID/TID or SR 40-80 mg daily; isosorbide mononitrate 20 mg BID
29
Q

peripheral vasodilators

A
  • i.e. hydralizine and minoxidil (more potent)
  • direct relaxation of arterial muscle and preventing vascular resistance
  • 25 mg QID for HTN (max dose 200 mg/daily)
  • increases contractility, increases CO
  • not first line for HTN
  • ADRs: K+/Na+ retention, headache
  • NSAIDS may decrease effects
  • give vitamin B6 to decrease peripheral nephritis
30
Q

hyperlipidimia

A
  • atherosclerosis major cause of CAD
  • all lipoproteins contain triglycerides, phospholipids, and cholesterol
  • can occur through 2 pathways: exogenous: absorption on lipids in GI intestines or endogenous pathway: through liver
31
Q

drug therapy for dyslipidemia

A

HMG CoA reductase inhibitors (statins)

  • fibrates
  • bile acid sequestrants
  • niacin
  • ezetimibe (zetia)
  • vitamins/antioxidants/herbs/natural products: vit. A, E, folic acid, fish oil, flax seed, coconut oil
  • active liver disease-contraindicated except bile acid sequestrants
32
Q

statins

A
  • blk synthesis of cholesterol
  • decrease level LDL
  • pregnancy category X
  • decreases LDL 25-60%; triglycerides 10-40%, increases HDL 5-7%
33
Q

pharmocokinetics of statins

A
  • ALL statins are metabolized at least part by CYP3A
  • CYP3A inhibitors may increase statin concentrations with verapamil, azoles, erythmomycin, diltiazem
  • CYP3A inducers may decrease statin concentration with rifampin, phenytoin, phenobarbital
  • may also interact with other CYP3A substrates-i.e. cyclosporins
34
Q

statin ADRs

A
  • most common: n/d, pain, GI symptoms
  • myopathy-only 0.04%
  • if LFTs increases should d/c statin
  • don’t combine statins with fibrates
35
Q

statin dosing and monitoring

A
  • start lower dose and increase needed according to LDL response (start 10mg at first 2-4 weeks before changing dose)
  • rosuvastatin most potent
  • monitoring: lipid levels 4-6 weeks until achieved level (for 3-4 months)
36
Q

fibrates

A

-inhibit cholesterol synthesis
-decreases triglyceride synthesis and lipid synthesis in adipose tissue
-decrease VLDL
-increased clearance of triglyceride
-DM 2 are good pt. for drug
-dosing: gemfibrozil: 600 mg BID
micronized fenofibrate: 67mg
clofibrate: 2g
-ADRs: n/v, cholythiasis, phtosensitivity, phototoxic
-drug interactions: if used with statin or niacin-increased hepatotoxicity or myopathy
-effects protein binding drugs-i.e. warfarin

37
Q

pharmacodynamics of fibrates

A
  • monitor LDL, triglycerides, HDL, and LFTs-especially if on statin
  • ADRs: constipation and flatulence
38
Q

bile acid sequestrants

A
  • changes cholesterol to bile acid in liver
  • bind with cholesterol in intestines and excreted in bound form
  • good for pt. with liver disease and mildly elevated cholesterol
  • can be used with statins
  • reduced folate levels over long period of time-give supplement
  • ADRs: n/v, constipation
  • can interfere with drug absorption
  • possible stool softeners may be needed
39
Q

niacin

A
  • inhibits free fatty acid release from fatty tissue
  • decreases TLC, VLDL, triglycerides, and increases HDL
  • decreases ischemic hrt. dz. mortality and decreases risk for recurrent non-fatal MI
  • dosing: initial 250 mg at hs and increase in 4-7 day intervals to 1.5-2 g/daily
  • put on ASA
40
Q

pharmacokinetics of niacin

A
  • ADRs: flushing, puritis, fatigue, gastritis, impaired glucose control, increased acid (leading to gout)
  • ASA taken at least 30 minutes prior
  • ETOH abusers-higher risk of hepatotoxicity
41
Q

Ezetimibe (Zetia)

A
  • selectively inhibits intestinal absorption of cholesterol/phytosterols
  • decreases TCL, LDL, triglycerides, increase HDL
  • most effective in combo with statin
  • pregnancy cat. C–don’t give children
42
Q

diuretics

A
  • ADRs: decreased K+ and electrolyte imbalance
  • K+ sparing selective aldosterone blocks CYP340-if taken with azoles, grapefruit juice, and calcium channel blocker–it can increase effect of K+ supplement

Pharmacology (37 decks)

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