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336 Pharmacology > Exam 3- Cardiac, diuretics, anticoagulants, thrombolytics > Flashcards

Exam 3- Cardiac, diuretics, anticoagulants, thrombolytics Flashcards

1
Q

Flow of blood through the heart and

systemic v pulmonary circuit

A 
inferior/sup vena cava
R atria
tricuspid valve
R ventricle
pulm semilunar valve
pulm trunk
pulm arteries
lungs
reoxygenated blood into heart via pulm veins
L atria
mitral valve
L ventricle
aortic semi-lunar valve
aorta
ascending aorta
body

pulmonary circuit- pulmonary arteries to veins (lungs)
systemic circuit- aorta-vena cava (body)

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2
Q

electrical stim pathway of heart

A

top to bottom

SA node, AV, apex, Purkinje fibers, ventricles (contraction starts at bottom)

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3
Q

primary pacemaker of heart- signal from atria to ventricles

A 
stimulated by bradycardia (sympathetic ns)
function- depolarize
sinoatrial node (in uppr prt right atrium)

transfer signal via AV

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4
Q

beta 2 v beta 1 receptors

A

beta 1- stimulate AV node= inc heart contractility
can contribute to vent remodeling w/ pt that have heart failure

beta 2- stimulate sympth nervous system= bronchodilation

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5
Q

L v R sided heart failure

A

L- blood backs into pulm system, hypertrophy/ overstretched L ventricle= dec SV= dec CO
“congestive heart faliure” s/s hypoxia and trouble breathing

R- blood backs into venous system= inc p pulm arteries= pulm edema, jugular venous distention, ascites

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6
Q

alpha 1 receptors

A

cause vasoconstriction and sm musc contraction

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7
Q

s/s heart failure

A

dec cardiac output= fatigue, exercise intol
FVO- crackles (L HR), pulm edema, inc rr, SOB, distress dec o2
(R HR)- distended jugular veins, periph edema

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8
Q

systolic v diastolic HF (b/ left sided)

A

systolic- dec contractility- hF w/ reduced ejection fraction

diastolic- shortened filling/relaxation time- HF w/ preserved ejection fraction

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9
Q

classification of HF- AHA stage v NYHA functional

A

aha- structural- A-D *need to know ejection fraction to test structural changes
A= high fisk but no structural changes of s/s
B-=structural changes, no s/s
C= structural changes w/ prior or current s/s
D= changes and s/s at rest- need specialized interventions

functional- s/s I-IV (based on pt ability to function, and complete ADL)
I-asympt
II-symptom w/ mod exertion
III- sympt w/ minimal exertion
IV- symtom at rest
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10
Q

heart failure def + causes

A

dec tissue perfusion
abnormal heart function
cause- CAD, HTN

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11
Q

cardiac output

A 
hr x stroke vol
min/mL
amnt blood pumped/min
normal 3-7 L/min
dec heart rate or sv= dec co
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12
Q

stroke vol

A

mL/contraction x # beats/min

dec sv=dec co

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13
Q

contractility

A

(inotropy) strength of muscular contraction of the heart
dec contractility = dec co
inc contractility= inc sv=inc co *till a certain point (if too stretch myosin fibers have no leverage)

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14
Q

preload- def and causes of inc/dec

A

amnt stretching of ventricular cardiac musc before a contraction begins
dependant on vol fluid in ven

heart failure= inc preload
inc vol= inc preload= inc contractility (until certain point)
dec vol= dec preload= dec stroke vol= dec contractility= dec co
ideal is btw 8-12

causes dec= hemorr shock, dehydration= dec contact btw actin and myosin fibers (too srunched)
inc= fluid overload= dec contact of fibers

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15
Q

ejection fraction

A

percent of blood in LV leaving w/ e/ contraction

dec contractility= dec EJ

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16
Q

afterload

A

resistance against which LV has to work to push blood into arteries
factors- SVR (p in arteries) can inc w/ vasoconstriction
inc svr= inc afterload (P)

inc svr + additional V fluid from heart failure (preload) w small valve opening = inc p/workload= L ventricular remodeling

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17
Q

purpose of measuring bp

A

tells us lvl resistance
diastolic- resting state
systolic= CO
MAP= afterload

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18
Q

pathway of hf

A

dec EF- dec contractility- dec CO- inc sympathetic activation- stimulation of beta 1 recep. (vasoconstriction, fluid retention)- inc hr and contractility- alpha 1 recep activation (inc pvr and inc afterload P)- inc myocardial workload- dec co- dec renal perfusion- inc renin secretion- inc angiotensin 1- angiotensin 2 (vasoconstriction, fluid retention and inc bp) *also cardiotoxic at high lvls can cause v remodeling
fluid retention bc- inc aldosterone (na and h2o retention- further inc preload- L HF-pulm edema and R HF- peripheral edema)

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19
Q

natrietic peptides

A

stimulated by hypertrophy LV

anp/bnp- natural diuretic/vasodil

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20
Q

goals of pharmacologic therapy in hf

A

improve QOL and dec mortality/morbidity

by inc contractility
dec afterload, elevations in preload, ventricular remodeling, peripheral (R) and pulm edema (L)

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21
Q

classes meds to trt hf

A 
ace inhib
angiotensin recep neprilisyn inhib (ARNI)
cardiac glycosides
diuretics
beta blockers
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22
Q

ace inhib- types, action and indications

A

lisinopril, enalapril, captopril, benazepril
action- dec conversion from ang 1 to ang2= dec preload and afterload
indications- hf, htn, dec mortality and morbidity after MI, prevn diab nephropathy (dec p and therefore damage of glomerular basement mem)
need to take if EF < 50% or s/s HF bc can dec prel, afterload and vent remodeling while improving EF

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23
Q

ace inhib- containdications, pharmacokin

A

coindiated- preg/lactation, hypersen (angioedema), renal impairment
pharmacokin- Po, duration 24h, 100% renal elimination

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24
Q

ace inhib- ae

A

hypotension (dec ang2= dec ability vasoconstrict)
watch after 1st dose! and espec if FVD (dehydration)
persistant dry cough- if block converting enzyme= inc bradykinin= inc dry cough
angioedema- inc risk as inc bradykinin (swelling of throat, feeling fullness, something stuck in throat)
hyperkalemia- flip btw na and K, dec ang 2= dec aldosterone= dec fluid retention= inc K 3.5-5 can result in vent tachy- cardiac dysrhyth

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25
Q

angiotensin II receptor blockers (ARBs)- types-action and indication

A

Valsartan, Losartan, Candesartan
block effects ang 2
so same effect as ace just different chemical process (not acutally inhibit converting enzyme so no inc bradykinin)
therefore no inc problems w/ dry cough and angioedema

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26
Q

angiotensin II receptor blockers (ARBs)- pharmacokin v ace i

A

valsartan- liver metab, majority excreted via feces
losartan- extensive liver metab, excreted by kid as active metab
candesartan- prodrug- excreted in urine and majority in feces

** more liver metab, less kidney excretion worry

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27
Q

relationship btw vasodil and afterload

and aldosterone and preload

A

inc vasodil= dec SVR= dec constriction= dec afterload (P)

dec aldosterone= dec fluid retention= dec preload

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28
Q

Angiotensin recept- Neprylisin inhib (ANRI)- type, action, indication

A

ARB (valsartan) combo w/ neprylisin inhib (sacubitril) Entresto
neprylisin enzyme inactivates natrietic peptides (respon diuretic/vasodil)
inhibiting enzyme will inc anp/bnp= inc diuresis= dec preload and vasodil= dec afterload

preferred med if not taking anything to control HF
if switching to this frm acei need to stop taking acei or arb for 36h or high risk for angioedema

trial- improved HR s/s, dec hospitalizations and reduced mortality

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29
Q

nursing considerations for acei, ARB and ANRI

A

monitor bp (hypotension), incl orthostatic changes
monitor angioedema (esp w/ acei or switching)
monitor bun, cr, K+
renal bc acei fully excreted via kidneys, risk for hyperkal in acei
pt education- change position slowly, avoid salt sub w/ acei (already high ris k for inc K due to dec aldosterone)

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30
Q

cardiac glycosides (Digoxin)- action, indication

A

trt a-fib and control hr
action- inc contractility by inc Ca into musc cells= stronger contraction and enhance parasympath ns (vagal influences)= dec onduction via AV node frm artrial to ven= dec hr aka “rate ventricular contracting”

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31
Q

cardiac glycosides (Digoxin)- containd, route, pharmacokin

A

contraind- av heart block (rhythm abnormality delays conduction thru AV) so adding digoxin can exacerbate block
WPW- abnorm conduction pathway otherthan AV, so if shut off main pathway can overstim alt pathways
hypokalemia
renal impairment, acute MI (inc contractility= inc o2 demand= ae of MI)
trt MI before admin
route- Po or IV
pharmacokin- unchanged by kid

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32
Q

cardiac glycosides (Digoxin)-ae and inc risk

A

ae- bradycardia**
n/v, anorexia, abdom discomfort earliest s/s
blurred vision, green/yellow aura (halo arnd lights)

inc risk w/-
hypokalemia (K and med compete for same cardiac cell recep so if K is depelted med has more room to be activated and therefore cause toxicity)
extremes in age (inc sensitivity)
use loading doses
give inc dose so drug reaches theraputic range faster but can overshoot this and cause toxicity)
hypoxia (inc contract= inc o2 demand)
impaired renal function

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33
Q

cardiac glycosides (Digoxin)- nursing considerations

A

monitor apical pulse 1 min- hold if <60
continuous EKG for IV admin
assess therapeutic effect (should hold hr and stop afib)
geriatric consdier (ink risk falls if bradycardia bc dec sv=dec co= dec perfusion= syncope)
monitor labs (cr, bun, gfr, K+)
pt ed- how assess own pulse
hold med if <60
s/s dig toxicity (GI, visual changes, bradycardia)

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34
Q

test for pt w/ possible digoxin toxicity

A

K, bun, cr, gfr labs
akg
continuous heart monitor

if comes back positive- dig lab lvl
hold med
k supplement
temporary pacemaker (external transcut or transvenous)

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35
Q

types diuretics

A

loop
thiazide
aldosterone antagonists

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36
Q

loop diuretics- types, moa, indication

A

bumetanide (Bumex) po oriv
furosemide (lasix) po/iv *can dev resistance
torsemide (Demadex) iv only
moa- act on ascending loop to dec na and h20 resorption= inc excretion

indications- edema, s/s HF (dec vol= dec P on vessles= dec afterload), renal dis, hepatic cirrhosis, HTN

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37
Q

loop diuretics- pharmacokin, ae

A

absorbed in GI tract
onset po- 1h, IV 5-10 min
ae- electrolyte depletion (K)
s/s- weakness, dizziness, leg crmps, vomiting, confusion, dysrthmias
need K replacement -always check!
Gi disturb- diarrh, anorexia, stomach pain/cramping
hypotension- hold if <100
ototoxicity w/ IV admin if push too fast!
impaired glucose tol (might need inc insulin)
FVD or s/s overdiuresis- dry muc mem, dec urine output
reflected in labs- dec blood vol= dec LV supply= dec preload= dec sv= dec co= dec kidney function
=inc Cr, BUN, gfr (rapid)

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38
Q

loop diuretics- interactions

A

digoxin- toxicity/ hypokalcemia

corticosteroids- hyperglycemia and hypokalemia

warfarin- inc anticoag effect

inc hypotension w/ o/ antihtn meds

aminoglycoside antib “gentamicin”- ototoxicity

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39
Q

thiazide diuretic- type, moa, indication

A

hydrochlorthiazide (HCTZ)
moa- block na and cl reabsorption in distal tubule
indications- htn,
edema-HF, renal dis, cirrhosis, corticosteroids, estrogen therapy

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40
Q

thiazide diuretic- pharmacokin and contraindications

A

pharm- po, excreted unchanged by kidneys

contraind- allergy to sulfonamides. impaired renal function, lactation, pregnancy (jaundice/thrombocytopenia)

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41
Q

thiazide diuretic- ae and interactions

A

ae- hypokalemia, hypotension, inc uric acid (gout), hyperglycemia, gi (n/v, constipation), hepatitis (liver inflamm), pancreatitis

interactions- inc hypotension w/ o/ anti htn
corticosteroids- hyperglycemia, inc excretion k (hypokalemia)
digoxin- toxicity and hypokalemia
*similar to loop diuretics

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42
Q

aldosterone antagonist- type, action, indication

A

K+ sparing (dec aldosterone = inc K)
“Spironolactone” (Aldactone)
action- inhib aldosterone dec h2o and na resorption, inc K
indication- excess fluid assoc w/ HF and hepatic cirrohsis
can inc survival in pt w/ mod-severe HF

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43
Q

aldosterone antagonist- ae and interactions/ contraindicated

A

ae- hyperkalemia, skin rash, gi disturb, dizziness, sex hormone abnormalities (menstrual and gynecomastia)
interactions- caution w/ acei (inc risk hyperkalemia)
anticoag inc risk bleeding
digoxin- med can inc dig accum= inc risk toxicity

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44
Q

general diuretic considerations and pt ed

A 
admin in am and early evening- prevent falls
admin iV slowly 20mg/mL
po diur w/ food dec gi
monitor bp, hold if <100
weigh daily, I&Os
labs- cr, bun, gfr, K
bg's
fluid imbalance (excess or deficiet)
pt ed- older women don't take cause can cause incontin
K+ supplements and s/s hypokalemia 
low sodium diet (no salt sub w/aci bc risk hyperkalemia)
postural hyptension
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45
Q

structural effects hf meds- all types

A 
acei / ARBs- dec afterl and prel, dec vent remodeling
ANRI (neprilisyn inhib)- dec afterl and prel, dec vent remodeling
cardiac glycosides (digoxin)- inc contactility
diuretics- dec prel, afterl, and edema (pulm and peripheral)
beta blockers- dec afterl, dec SNS stim of heart, dec vent remodeling
46
Q

Virchow’s triad- purpose

A

factors involved in increased clotting risk

47
Q

Virchow’s triad- genetic/ aquired

A

genetic- prothrombin deficiency, alteration in clotting cascade

aquired- inflamm response (inc platelet or rbc) 
Chronic hypoxemia (COPD), stimulation of erythropoietin (Polycythemia) 
Can vary w/ geographic areas (elevation changes)
48
Q

Virchow’s triad- 3 causes

A

Damage to endothelium
IVs, fractures, dislocations, CVD (atherosclerotic changes)
Blood stasis
Surgery, decreased mobility, atrial fibrillation
Venous (DVT/PE)
Hypercoagulability
Dehydration (inc viscosity), hematological disorders
Drugs- ex. Oral contraceptive

49
Q

anticoag action

A

prevent clot formation and extension

Taken after surgery

50
Q

antiplatlet action- venous v arterial

A 
interfere with platelet activity
Venous v arterial clots
V- DVT d/t venostasis
Composed of clumped RBC 
A- caused by platelet aggregation (atherosclerotic changes) CAD
Dec ratio of RBC
51
Q

thrombolytic agent action

A

dissolve existing thrombi

clot lysis

52
Q

anticaog- types

A

heparin (UFH)
low molecular weight heparin
enoxaparin (lovenox)- parental

oral- zarelto and warfarin (coumadin)

53
Q

intrinsic pathway

A

contact activation
monitors heparin
labs- PTT
thrombin

54
Q

extrinsic pathway

A

act. w/ tissue damage
warfarin
monitor PT/INR
prothrombin

55
Q

role thrombin

A

converts fibrinogen to fibrin (end stage clot dev)

heparin inhib thrombin
warfarin inhib prothrombin (step before)

56
Q

PTT lab

A

intrinsic (heparin)

range- 1.5-2.5 times baseline

57
Q

heparin assay

A

same as PTT but more expensive

range- 0.3-0.7

58
Q

PT/INR

A

extrinsic (warfarin)
range- 2-3 sec commonly
2.5-3.5 for mitral mechanical valves

59
Q

PT/INR, heparin assay/ PTT needed in?

A

anticoag

not applicable if admin anti-thrombotics!!

60
Q

short-acting parenteral anticoag- types

A

heparin and LMWH (Lovenox/ enoxaparin)

61
Q

heparin- action and indications

A 
Actions
Potentiates the action of antithrombin
Inhibits factor Xa
Prevents formation of thrombin
Blocks thrombin activity (converting fibrinogen to fibrin)
Inhib intrinsic or common pathway

Indications
Prevention and management of thromboembolic disorders
Ex: DVT, PE, Atrial fibrillation, MI, CVA
Maintain patency of IV catheters

62
Q

heparin- route

A

IV drip- for therapeutic trtment (PE)
SubQ- prophylactic (given q8/ 12 depending on risk)
Not Po (cannot cross GI mem., lrg molecular size)

63
Q

heparin- pharmacokin

A

metab- liver,
elim- some renal, most endothelial cells
* no predictable action after subq

subq peak- 2h, duration8-12h
IV peak- 5-10 min, duration 2-6h

64
Q

heparin– IV admin

A

used as therapeutic trtmnt

dosed as bolus w/ continuous IV (weight based)

65
Q

heparin IV considerations

A

Monitor PTT (partial thromboplastin time)
Therapeutic range 1.5-2.5 Xs baseline or level determined by specific lab (varies w/ facility)
Normal PTT 25-35
Ex. Normal therapeutic range- 1.525 and 2.535= (37.5- 87.5)
Alternative: Monitor heparin assay (Anti-Factor Xa Level)—goal 0.3-0.7
Benefit- less variable btw individ.

66
Q

heparin subq admin and considerations

A

abdomen only, dec risk bleeding, less mvmnt):
SubQ route effective for prophylaxis only
Dosed 5000 units SubQ every 8-12 hours
Never given IM (inc risk bleeding bc high vascularity)

67
Q

most severe bleeding site v most common

A

common- GI

severe-cranial

68
Q

protamine- def, indication

A

heparin antagonist

indication- GI, cranial bleed or neuro compromise

69
Q

protamine- route, goal, considerations

A

loading dose + infusion (drip)
(roughly 1mg of Protamine neutralizes 100 units of heparin activity)
goal- return clotting factor levels to baseline
keep in mind heparin activity w/in last hr
800u/hr- give 8mg/ hr of protamine

PTT should be used to monitor the effect of protamine in neutralizing heparin

70
Q

protamine- ae

A

flushing, nausea, vomiting, dyspnea

71
Q

lovenox (LMWH)- action, indication, and route

A

Action: inhibits factor Xa
Indications:
Prevention and treatment of VTE (DVT, PE)
MI
Unlabelled use: systemic anticoagulation for other diagnoses
Route: SubQ (abdomen only)

72
Q

Lovenox- pharmacokin

A

metab- liver
elim- kidneys (clearance dec by 30% w/ renal impairment) ei- do not give w/ severe renal fun
no need for IV drip
duration 12h

73
Q

lovenox- dosing- prophylaxis v therapeutic

A

prophylaxis- for VTE (30-40mg every 12h)

therapeutic- MI, Afib, VTE (1 mg/kg every 12h)

74
Q

heparin v enoxaparin- contraindications

A 
Hypersensitivity
Active, major bleeding
GI ulcerations
Intracranial bleeding
Dissecting aortic aneurysm
Recent eye/brain/spinal cord surgery
Severe thrombocytopenia (low platelet count)
Hemorrhagic CVA
75
Q

heparin v enoxaparin- caution in

A

Uncontrolled HTN (inc p cerebral arteries, risk hemorr)
Severe liver or kidney dysfunction (drug accum wl LMWH)
Last trimester of pregnancy or immediate post-partum period (inc risk bleeding)
Spinal/epidural anesthesia or lumbar puncture (have bleeding at site= blood accum in epidural space, inc p on spinal c= permeant paralysis)
Hold anticoag 24h after dc anticoag

76
Q

heparin v enoxaparin- ae

A

BLEEDING
Hematoma, bruising
Differentiate by palpation
Hematoma= hard
Bruise= soft
Thrombocytopenia
Heparin induced (HIT) – allergic rxn
Heparin causes inapprop act platelets (too much clotting)
Inc clotting- dec platelets (use platelets faster than can produce)
Presents w/ drop 50% platelets after admin heparin
Mre common in heparin (UFH)

77
Q

enoxaparin- nursing considerations

A

Double check doses
Assess for bleeding
Petechiae, excessive bruises, drop in bp, inc hr, pale, cool skin color, dec urine output (dec renal perfusion), weak pulses, I+O’s, LOC, severe headache (hemorr stroke)
Assess for hypersensitivity (fever, chills, urticaria, hives)
Monitor H/H, platelets
SubQ route: rotate sites, assess for hematomas

78
Q

IV heparin- considerations

A

Monitor aPTT or heparin assay to regulate therapy, double check compatibility with other IV solutions
For significant bleeding:
Hold heparin—short half-life when given IV
Consider Protamine or FFP (fresh, frozen plasma- replacing clotting factors) administration, if necessary

79
Q

heparin v enoxaparin- disadvantages

A

hep- Short duration of action
Need for continuous IV gtt for full anticoagulation
Frequent lab draws (PTT, HA)
Inc risk HIT

enox- Longer duration of action
More accumulation with renal dysfunction

80
Q

heparin v enox- advantages

A

hep- Effective anti-coagulation with IV gtt
Short duration of action- better for pre-procedure
Stop 1-2h before

enox- Does not require monitoring of blood ***coagulation tests
SubQ route can be used for full-dose therapy
Can be used for outpatient anticoagulant therapy
Less thrombocytopenia
Longer duration of action (12h)

81
Q

direct acting oral anticoagulants- pros v cons

A

pros- predictable response (not need regular lab testing)
low incidence brain bleeds

cons- more expensive, inc risk bleeding GI tract

82
Q

DOAC’s- zarelto or eliquis-action and indication

A

oral version enoxaparin
inhib factor Xa
indication- preve/trtmnt VTE, prev. embolic CVA in afib

83
Q

DOAC’s- Pradaxa- action and indication

A

action- inhib thrombin (converting factor for prothrom to fibrin)

use- Prevention of embolic CVA in nonvalvular afib
Prevention/treatment of DVT/PE

84
Q

long acting anticoag

A

warfarin (coumadin)

85
Q

warfarin- action and indication

A

Action: Acts in the liver to prevent synthesis of vitamin K-dependent clotting factors (II, VII, IX, and X)
**Not inhib existing factors- instead inhibits synthesis of factors in the liver
Vitamin K antagonist
Indications
Prophylaxis and treatment of:
Oral meds for full anticoag therapeutic trtment (not a prophylaxis)
VTE (DVT/PE)
Afib with embolization
Management of MI
Prevention of thrombus formation and embolization after prosthetic valve

86
Q

warfarin- route, pharmacokin

A 
Route:  Oral
Pharmacokinetics:
Well-absorbed from GI tract
Metabolized by liver, excreted by kidneys
Half-life 42 hrs
DD and food interactions
87
Q

warfarin- dosing

A

start w/ 5mg
*overlap w/ heparin (or LMWH) by 4-5 days till drug kicks in

monitor w/ INR (PT) daily
until therap goal achieved, then 1-4 weeks

88
Q

warfarin- therap INR goal

A

VTE, afib, MI, aortic mech valve- 2.0-3.0

mitral mech valve- 2.5-3.5

89
Q

INR therap window- low v high

A

low- thromboemoblic = progression of clot

high- INR of 4, hemorrh complications (brain bleed, GI, hemorr shock)

90
Q

warfarin- ae and considerations

A

ae- bleeding

Monitor for/prevent bleeding
Monitor INR
Patient education
Consistent dietary intake of vitamin K
No alcohol
Bleeding precautions
Follow-up lab work
Drug/food interactions
Foods high K- leafy green veg, in moderation, consistent w/ intake certain foods 
Drugs- high risk interactions, notify provider if add new vitamin or OTC
91
Q

relationship btw vitamin K and INR in warfarin

A

Inc vitamin K= dec INR= inc risk overclotting

Dec K= inc INR= inc risk bleeding

92
Q

Warfarin drug/food interactions

A

Drugs- inhibit (dec effect) anti-infectives (nafcillin), cardiovasc (cholestyramine), CNS (barbiturates)
Drugs- potentiation (inc effect, cause excess anticoag)
Anti-infectives (ciprofloxacin, erythromyacin) cardiovasc (fenofibrate, propranolol), CNS (alcohol, sertraline)
*no indivi vitamin supplements
supplements- ginseng, ginko, garlic suppl
Liquids- cranberry juice, alcohol
Foods- green leafy vegetables
Kale, spinach, greens, collards, parsley, broccoli (all can be bad if cooked too)

93
Q

warfarin- antagonist- vitamin K and FFP

A 
Vitamin K 
Used in less severe bleeding
Takes around 24 hours to reverse INR
Subq or IM
Clotting factors have v different half lifes- prolonged time to see change

Fresh frozen plasma (FFP)
Immediately replaces clotting factors (warfarin not inactive. Existing Clotting factors, only synthesis in liver)

94
Q

platelet lifecycle

A

sub endoth. Exposure, act. Platelet adhesion and later aggregation- forms platelet plug

95
Q

risk for endothelial damage- atherosclerosis and PCI

A

HTN, Diabetes, Hyperlipidemia, smoking
CAD-MI
Cerebrovascular dis, carotid artery plaque- cva (ischemic)

S/P PCI (percutaneous coronary intervention) cath goes into artery and balloon expands w/ metal splice

96
Q

antiplatelet- aspirin patho

A

inhib cyclooxygenase, dec production A2- dec expression GP receptor

97
Q

antiplatelet- plavix patho

A

Plavix- blocks ADP recep, prevent stimuli of GP receptor

98
Q

role of GP receptor

A

causes platelet aggregation

inhib by aspirin and plavix

99
Q

aspirin- action, indication and dosing

A 
Action	MI prophylaxis 
Prevents thrombus formation by preventing the production of thromboxane A (TXA2), a prostaglandin that causes platelets to aggregate.  Aspirin irreversibly inhibits cyclooxygenase, which synthesizes TXA2, in the platelet. 
Indications
MI prophylaxis
Ischemia CVA/TIA prophylaxis
Dosing
81-325 mg po daily
100
Q

aspirin- ae and interactions

A 
ae-Nausea, vomiting
GI upset 
Heartburn (take with food)
Bleeding (easy bruising, gum bleeding)
Tinnitus
Thrombocytopenia

interactions- Oral anticoagulants, heparins
Steroids, alcohol, NSAIDS

101
Q

clopidogrel (plavix)- action and indication

A

Mechanism of Action:
Irreversibly inhibits platelet aggregation by blocking ADP receptors on platelets, preventing platelet aggregation

Indications:
Prophylaxis against thrombotic events in patients with recent MI, recent stroke
Prophylaxis against thrombotic events s/p stent
(super aspirin, stronger action)
Use w/ coronary stents (PCI)

102
Q

clopidogrel- dosing, ae, interactions

A

Dosing
Recent MI or stroke: 75mg daily
Acute coronary syndrome/stent: 600mg po x 1 then 75mg daily with aspirin

Adverse effects
Minor bleeding, headache, dizziness
Rash, abdominal pain, hypertension, edema
Thrombocytopenia Dec platelets= exacerbate clotting factors

Interactions
Increased risk of bleeding with NSAID, warfarin
PPIs may decrease effectiveness

103
Q

thrombolytics- first gen

A

streptokinase, urokinase

104
Q

thrombolytics- second gen

A

tPA

105
Q

thrombolytics- third gen

A

reteplase, TNKase

106
Q

thrombolytics- action, dosing and indications

A 
Action—breaks down fibrin clot lysis
Dosing
IV
Based on patient’s weight or fixed dosing (depending on drug and indication); not to exceed maximum doses for particular agents
Immediate onset
Indications
Myocardial infarction
CVA (ischemic ONLY)
Pulmonary embolism (not systemic, only at specific site)
Deep vein thrombosis
Arterial thrombosis
Occluded intravenous catheter	temporary treatment
107
Q

thrombolytics- ae

A

Cardiac arrhythmias (good sign, indicates perfusion) with coronary reperfusion; hypotension
BLEEDING, especially watch for: INTRACRANIAL HEMORRHAGE, GI/GU BLEEDING. Most common sites of bleeding—venipunctures
Urticaria, nausea, vomiting, fever
Anaphylaxis, especially with Streptokinase (first gen)

108
Q

thrombolytics- absolute contraindications

A

Intracranial hemorrhage (ICH) on CT or history of ICH
Suspected subarachnoid hemorrhage
Uncontrolled HTN (SBP> 185, DBP>110) (inc risk intracranial hemorrhage)
Neurologic surgery, serious head trauma or previous stroke in previous 3 months. (area brain damaged frm prev stoke has inc risk for bleeding)
Seizure at stroke onset
Arteriovenous malformation (AVM), neoplasm, or aneurysm
Suspected/confirmed endocarditis (risk bleeding brain)
Known bleeding risk (thrombocytopenia, receiving anticoagulants, prolonged bleeding times)
BG <50 or >400 (need to be able to determine what change in mentation is from)

109
Q

thrombolytics- considerations (labs)

A

Only administered in critical care settings: ED, ICU, cath lab
Assess bleeding times prior to administration (PTT, INR, platelet count, fibrinogen). Fibrinogen is assessed 2-3 hrs after start of therapy to check for fibrinolysis.

110
Q

thrombolytics- considerations (time constraints)

A

Begin therapy ASAP after onset of symptoms
Time windows (time after which the risk outweighs benefit):
STEMI—within 12 hours (MI w/ ST elevation)
Permanent damage heart occurs after 12 h
Ischemic CVA—within 4.5 hours (previously 3)

111
Q

thrombolytics- considerations (assessment)

A

Assessment:
VS—continuously
Assess pt carefully for bleeding every 15 min during 1st hr of therapy
Neuro changes (H/A, decreased LOC)
GI bleeding- Abdominal pain with coffee-ground emesis or black, tarry stools
GU bleeding- Hematuria
Avoid invasive procedures (IM injections, arterial punctures). If punctures necessary, hold pressure for at least 30 min after.
Start 2 IVs prior to initiating infusion

336 Pharmacology (5 decks)

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