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PANCE > Pharmacology 1: Blood, Heart, HTN > Flashcards

Pharmacology 1: Blood, Heart, HTN Flashcards

1
Q

Aspirin MOA

A

Decreases platelet aggregation; Irreversible platelet effect

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2
Q

Aspirin ADRs

A

Dyspepsia->GI bleeding
Kids w/ viral infection = Reyes Syndrome
Associated w/ SNHL (ringing) = salicylism
Bronchospasm in asthma patients
ASA triad = asthma, nasal polyps, ASA intolerance

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3
Q

Clopidogrel MOA

A

irreversible platelet binding

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4
Q

Warfarin MOA

A

antagonizes vit V epoxide reductase complex 1 (VKORC1)

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5
Q

What proteins does warfarin inhibit?

A

II, VII, IX, X
and
Protein C& S

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6
Q

How to reverse warfarin?

A
  • Non life threatening hemorrhage = vitamin K PO

- life threatening hemorrhage = IV vit K + prothrombin complex concentrates (PCC > FFP)

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7
Q

Warfarin Interactions

A

Substrate CYP2C9

ABX often cause issues w/ warfarin (don’t let warfarin leave the body)

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8
Q

Warfarin ADRs

A
  • bleeding, hemorrhage
  • purple (blue) toe syndrome
  • warfarin induced skin necrosis (rare)
  • TERATOGENIC
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9
Q

UFH MOA

A 
indirect thrombin inhibitor
inactivates IIa (thrombin)> Xa LL XIIa, Xia & IXa
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10
Q

how to monitor UFH

A

monitor platelets

check aPTT

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11
Q

How to reverse UFH

A

Turn down/stop heparin
if urgent = protamine (only when desperate b/c if ever need this again there is a 1% risk of anaphylaxis)
FFP/PCC does not reverse heparin products

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12
Q

ADRs of UFH

A

Bleeding/hemorrhage
HIT (transient decrease in platelets; insignificant)
HITTS aka HIT type 2 (more serious)

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13
Q

LMWH drug names & MOA

A

Enoxaparin (other -parin drugs)

Inactivated factor Xa&raquo_space; IIa

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14
Q

How to monitor LMWH

A

Don’t measure PT/PTT can measure anti-Xa levels to check anticoagulation
*monitoring is most helpful during treatment not prophylaxis

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15
Q

ADRs of LMWH

A

Injection site pain/hematoma
Hemorrhage < than w/ heparin
thrombocytopenia < than w/ heparin
**category B in pregnancy

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16
Q

-aban drug MOA & indications

A

Rivaroxaban, Apixaban
direct Xa inhibitors
approved for nonvalvular a fib and VTE prophylaxis and treatment

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17
Q

Dabigatran MOA & indications

A

direct thrombi inhibitor

approved for non-valvular atrial fib

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18
Q

Statin MOA

A

inhibition of HMG CoA reductase causes up regulation of LDL receptor gene and causes decrease of LDL

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19
Q

Clinical monitoring in patients on statins

A

LFTs: at baseline and recheck if indicated
CPK (if myalgia symptoms)
FLP (3-4 wks after initiation, then yearly once at goal)

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20
Q

Statin interactions

A

Simvastatin and atorvastain are CYP3A4 & P glycoprotine substrates
**additive myopathy/hepatotoxicity w/ niacin/fibrates

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21
Q

Statin ADRs

A
  • mylagia/myopathy
  • reversible hepatotoxicity
  • increased blood glucose
  • category X in pregnancy
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22
Q

Fibrates names and indication

A

Gemfibrozil and fenofibrate

-use for hyertriglyceridemia when pancreatitis is a risk

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23
Q

Fibrate interactions

A

careful w/ stains b/c of overlapping toxicity profiles

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24
Q

Fibrates ADRS

A

reversible hepatotoxicity and myopathy

25
Niacin indication
modifies all lipoproteins and lipids favorably
26
Niacin interactions
careful w/ cadmic of statins & fibrates b/c of overlapping toxicities
27
Niacin ADR
- prostaglandin related = flushing (Niaspan extended release causes least flushing and hepatotoxicity) - aggravate glucose intolerance - aggravate gout
28
Antiarrhythmic drug class ADR
- All anti-arrhythmic drugs can CAUSE arrhythmias which may be fatal - QT prolongation - careful in pts w/ bradycardia/heart blocks
29
Torsades is more common with
hypokalemia, hypomagnesemia, and bradycardia
30
Antiarrhythmic class interactions
- avoid other QT prolongers (IE: macrolides) - most are metab by CYP3A4 or 2D6 - drugs that cause hypokalemia/hypomag (IE loop diuretics) increase toxicity risk
31
Class I antiarrhythmics : list and MOA
Modulate or block Na channels - Ia = Quinidine, procainamide, disopyramide - Ib = lidocaine, mexiletine - Ic = flecainide, propafenone
32
Class II antiarrhythmics: list and MOA
inhibit sympathetic activity | -beta blockers
33
Class III antiarrhythmics: list and MOA
block K channels | -sotolol, defotilide, ibutilide, AMIODARONE, dronedarone
34
Class IV antiarrhytmics: list and MOA
block Ca2+ channels | -verapamil and diltiazem
35
Amiodarone Interactions
- likely inhibits p-glycoprotein so digoxin excretion may be effected - avoid other QT prolongers - multiple CYP concerns
36
Amiodarone ADR
1) cardiac toxicity = Bradycardia and AV nodal block 2) Pulmonary toxicity (subacute cough and progressive dyspnea associated w/ patchy interstitial infiltrates on CXR: tx = d/c amiodarone + supportive measures +/- steroids) 3) Thyroid Toxicity (hypothyroidism from excess iodine) 4) Dermatologic Toxicity (photosensitivity, recommend sunscreen if repeated sun exposure = bluish skin discoloration)
37
NONdihydropyridine CCB list and usages
Diltiazem is used more than verapamil | -dysrthmias (SVT, afib) > HTN (rate drug not HTN drug)
38
NONdihyrdopyridine CCB ADRs
- hypotension, bradycardia, - ionotrope, peripheral edema - headache * *w/ verapamil constipation is common
39
Digoxin indications
- rate control in afib - Heart failure is most likely * *doesnt alter mortality
40
Digoxin Interactions
Oral steroids and diuretics decrease K or Mg and increase digoxin distribution to the heart and muscles = increased toxicity
41
Digoxin ADR-Acute toxicity
Rhythm disturbance is most concerning = PVC
42
Digoxin ADR-Chronic toxicity
Rhythm disturbance - PVC | Yellow/green or blurred vision
43
Loop diuretic MOA
-interferes w/ Na/K exchange in ASCENDING segment of loop of henle by inhibiting Na/K ATPase
44
Thiazide diuretic MOA
-interferes w/ K/Na exchange in early DISTAL CONVOLUTED tubule by inhibiting Na/K ATPase
45
Loop diuretic indications
- edematous states (HF) | - acute hypercalcemia
46
Thiazide diuretic indications
-essential HTN
47
Loop and thiazide diuretic interactions
hypotension w/ other antiHTN | digoxin and lithium toxicity via electrolyte alterations
48
Diuretic ADRs
- Electrolyte disturbances (loops > thiazides) - HYPOKALEMIA > hyponatremia - orthostatic hypotension - glucose intolerance - hyperuricemia
49
ACEI MOA
vasodialtes efferent arteriole (decreasing glomerular pressure)
50
ACEI ADRs
Cough HYPERKALEMIA Angioedema (more common in blacks, #1 drug to cause) Birth defects ****contraindication = pregnancy****
51
alpha adrengergic blocker ADR
**postural hypotension common = titrate drug sedation/fatigue nasal congestion
52
Non Selective B blockers
Propranolol (more bronchospasm)
53
B1 selective B blockers
Metoprolol > atenolol
54
B blockers w/ alpha blocking activity
Carvedilol | more for heart failure than HTN
55
Betablocker ADRs
bradycardia, bronchospasm, erectile dysfunction, exercise intolerance
56
CCB - Dihydropyridines
1st gen = nifedipine (fast acting) | 2nd gen = amlodipine
57
Clinical use of dihydropyridine CCB
HTN, Angina, Reyndaud phenomenon
58
ADRs of dihydropyridine CCB
HEADACHE, dizziness/lightheadedness -peripheral edema, reflex tachycardia GINGIVAL HYPERPLASIA (nifedipine > amlodipine)
59
Other meds that cause gingival hyperplasia
Phenytoin and Cyclosporine A (immunosuppressant)

PANCE (18 decks)

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