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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
Q

Niacin indication

A

modifies all lipoproteins and lipids favorably

26
Q

Niacin interactions

A

careful w/ cadmic of statins & fibrates b/c of overlapping toxicities

27
Q

Niacin ADR

A
  • prostaglandin related = flushing (Niaspan extended release causes least flushing and hepatotoxicity)
  • aggravate glucose intolerance
  • aggravate gout
28
Q

Antiarrhythmic drug class ADR

A
  • All anti-arrhythmic drugs can CAUSE arrhythmias which may be fatal
  • QT prolongation
  • careful in pts w/ bradycardia/heart blocks
29
Q

Torsades is more common with

A

hypokalemia, hypomagnesemia, and bradycardia

30
Q

Antiarrhythmic class interactions

A
  • 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
Q

Class I antiarrhythmics : list and MOA

A

Modulate or block Na channels

  • Ia = Quinidine, procainamide, disopyramide
  • Ib = lidocaine, mexiletine
  • Ic = flecainide, propafenone
32
Q

Class II antiarrhythmics: list and MOA

A

inhibit sympathetic activity

-beta blockers

33
Q

Class III antiarrhythmics: list and MOA

A

block K channels

-sotolol, defotilide, ibutilide, AMIODARONE, dronedarone

34
Q

Class IV antiarrhytmics: list and MOA

A

block Ca2+ channels

-verapamil and diltiazem

35
Q

Amiodarone Interactions

A
  • likely inhibits p-glycoprotein so digoxin excretion may be effected
  • avoid other QT prolongers
  • multiple CYP concerns
36
Q

Amiodarone ADR

A

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
Q

NONdihydropyridine CCB list and usages

A

Diltiazem is used more than verapamil

-dysrthmias (SVT, afib) > HTN (rate drug not HTN drug)

38
Q

NONdihyrdopyridine CCB ADRs

A
  • hypotension, bradycardia, - ionotrope, peripheral edema
  • headache
  • *w/ verapamil constipation is common
39
Q

Digoxin indications

A
  • rate control in afib
  • Heart failure is most likely
  • *doesnt alter mortality
40
Q

Digoxin Interactions

A

Oral steroids and diuretics decrease K or Mg and increase digoxin distribution to the heart and muscles = increased toxicity

41
Q

Digoxin ADR-Acute toxicity

A

Rhythm disturbance is most concerning = PVC

42
Q

Digoxin ADR-Chronic toxicity

A

Rhythm disturbance - PVC

Yellow/green or blurred vision

43
Q

Loop diuretic MOA

A

-interferes w/ Na/K exchange in ASCENDING segment of loop of henle by inhibiting Na/K ATPase

44
Q

Thiazide diuretic MOA

A

-interferes w/ K/Na exchange in early DISTAL CONVOLUTED tubule by inhibiting Na/K ATPase

45
Q

Loop diuretic indications

A
  • edematous states (HF)

- acute hypercalcemia

46
Q

Thiazide diuretic indications

A

-essential HTN

47
Q

Loop and thiazide diuretic interactions

A

hypotension w/ other antiHTN

digoxin and lithium toxicity via electrolyte alterations

48
Q

Diuretic ADRs

A
  • Electrolyte disturbances (loops > thiazides)
  • HYPOKALEMIA > hyponatremia
  • orthostatic hypotension
  • glucose intolerance
  • hyperuricemia
49
Q

ACEI MOA

A

vasodialtes efferent arteriole (decreasing glomerular pressure)

50
Q

ACEI ADRs

A

Cough
HYPERKALEMIA
Angioedema (more common in blacks, #1 drug to cause)
Birth defects contraindication = pregnancy

51
Q

alpha adrengergic blocker ADR

A

**postural hypotension common = titrate drug
sedation/fatigue
nasal congestion

52
Q

Non Selective B blockers

A

Propranolol (more bronchospasm)

53
Q

B1 selective B blockers

A

Metoprolol > atenolol

54
Q

B blockers w/ alpha blocking activity

A

Carvedilol

more for heart failure than HTN

55
Q

Betablocker ADRs

A

bradycardia, bronchospasm, erectile dysfunction, exercise intolerance

56
Q

CCB - Dihydropyridines

A

1st gen = nifedipine (fast acting)

2nd gen = amlodipine

57
Q

Clinical use of dihydropyridine CCB

A

HTN, Angina, Reyndaud phenomenon

58
Q

ADRs of dihydropyridine CCB

A

HEADACHE, dizziness/lightheadedness
-peripheral edema, reflex tachycardia
GINGIVAL HYPERPLASIA (nifedipine > amlodipine)

59
Q

Other meds that cause gingival hyperplasia

A

Phenytoin and Cyclosporine A (immunosuppressant)

PANCE (18 decks)

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