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Year 1: Patho/Pharm > Angina PHARM > Flashcards

Angina PHARM Flashcards

1
Q

Angina
Goal of Treatment

A
  1. Increase oxygen delivery to heart
  2. Decrease oxygen demand of heart
    - decrease afterload, preload
    - decrease workload: HR, conduction, contractility

Supply = Demand of heart

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1
Q

Angina
Example Treatments

A
  1. Nitrates
    - Nitroglycerine
    - Isorbide mononitrate
    - isorbide dinitrate
  2. Calcium channel blockers
    - dihydropyridines
  3. Beta blockers
    - OLOLs
  4. Ranazoline
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2
Q

Types of Angina

A
  1. Stable angina
    - angina of exertion
    - CAD and ischemia due to atheroscelerosis, complicated lesion
  2. Prinzmetal angina
    - vasospastic angina
    - due to vasospasm of the coronary arteries
    - decrease oxygen delivery of heart
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3
Q

Treatment
Vasospastic angina

A

Patho: vasospasm of the coronary artery

Treatment: vasodilation of the coronary artery

  1. CCB
  2. long acting nitrates

*Beta blockers will not work (it is not increased demand)

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4
Q

Nitrates
Examples

A

Nitroglycerine
- rapid onset, shorter acting: SL, spray
- slow onset, long acting: transdermal, ointment

Isorbide mononitrate/dinitrate
- slow onset, intermediate/long acting: oral tablets

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5
Q

Types of Nitrates
Onset, duration

A
  1. rapid acting, short duration
    Ex. Nitroglycerin
    - SL, spray
    - onset 1-3 minutes
    - duration: 30-60 minutes
    - repeat every 5 minutes 3x
    - seek medical attention
  2. slow acting, longer duration
    Ex. nitroglycerin
    - onset: 30-60 minutes
    - transdermal (24 hours), ointment (12 hours)
    Ex. isorbide mono/dinitrate
    - oral
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6
Q

MOA
Nitrates

A
  • prodrug
  • uptake vascular smooth muscle
  • conversion nitrate –> nitric oxide (bioactive)
  • *conversion requires sulfylhydryl groups
  1. Vasodilation smooth muscle
    - coronary arteries
    - veins
  • activaiton guanylyl cyclase -> cGMP -> dephosporylation myosin
  • breaks the cross bridge
  • relaxes muscle
  1. increase blood flow to heart (coronary artery vasodilation)
  2. decrease preload (vasodilation veins)
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7
Q

Nitrates
Pharmacokinetics

A

100 metabolized by first pass effect
do not crush, chew tablets
will be inactivated

1/2 life 5-7 minutes

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8
Q

SE/AE
Nitrates

A
  1. Orthostatic hypotension
    - vasodilation
    - blood pools in veins
  2. HA, dizziness, flushing
  3. Rebound tachycardia
    - can worsen angina
    - drop in BP, activation baroreceptor reflex, rebound tachycardia
    - heart works harder = worsen ischemia = MI
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9
Q

Drug interactions
Nitrates

A

Any hypotensive drug

Can worsen angina by causing rebound tachycardia and worsen ischemia to the heart
- beta blockers
- CCB
- Phosphodiesterase 5 inhibitors (erectile dysfunction medication)

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10
Q

Nitrates
Tolerance

A
  • Sulfylhydryl groups. used
  • cannot convert Nitrate to NO
  • Tolerance develops rapidly (cross tolerance)
  • nitrate free period minimum 8 hours
  • lower dosage
  • withhold for period
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11
Q

Monitoring
Nitrates

A

BP, HR
severity, frequency of angina
triggers of angina
rebound tachycardia, worsening angina after administration

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12
Q

Contraindications
Nitrates

A

phosphodiesterase 5 inhibitors
Erectile dysfunction medication
within 24 hours
severe hypotension
Ex. Sildenafil

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13
Q

Routes
Nitrates

A

sublingual
spray
transdermal
oral
IV

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14
Q

Prescriber considerations

A
  • start low
  • titrate up
  • nitrate free period (tolerance develops, saturation sulfhydryl groups)
  • withdrawal slowly - vasospastic rebound
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15
Q

Indications
Long acting nitrates

A

Heart failure

vasospastic angina

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16
Q

Beta blockers
Indications

A
  1. Angina exertion (stable angina)

*not for vasospastic angina

  1. Post MI
  2. HF , LVEF </= 40%
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17
Q

Beta blockers
MOA

A
  1. reduce HR, conduction, contractility
    - decrease demand for oxygen
    - used to treat CAD angina

block g-protein activation
prevention cAMP signal
blocks opening calcium channel
prevents depolarization
slow and fast action potentials in the heart

phase 0 and 4 , slow action potential AV and SA node
phase 2, fast action potential, contractility

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18
Q

Beta blockers
SE/AE

A
  • heart blocks
  • heart failure precipitated NY class Iii
  • bradycardia
  • impaired awareness hypoglycemia (IAH)
  • hypoglycemia
  • depression, insomnia, nightmares
  • bronchoconstriction
  • sexual dysfunction
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19
Q

Beta blockers
contraindications

A
  • heart blocks (2/3 degree)
  • heart failure class iv
  • asthma
  • caution: diabetes, anaphylaxis
  • right sided heart failure
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20
Q

Which class beta blocker is used?

A

Beta 1 selective
Generation 2

21
Q

Calcium channel blockers
Type and indication

A
  1. dihydropyridines
    - example: amloDIPINE
    - indication: stable angina, HTN, vasospastic angina, HF
  2. non-dihydropyridines
    - example: verapamil, diltiazem
    - indication: dysrhythmias
22
Q

CCB dihyropyridine
MOA

A
  1. Vasodilation peripheral arteries and coronary arteries
    - increase blood flow to heart
    - block calcium channels in VSM
    - results in vasodilation and increased blood delivery
  2. Decrease afterload
    - vasodilaiton peripheral arteries
    - decrease workload heart pumps against

Dihydropyridines do not act on calcium channels in the heart

23
Q

CCB dihyropyridine
SE/AE

A
  1. flushed, dizziness, orthostatic hypotension
  2. rebound tachycardia (treat with beta blocker) and worsening angina
  3. eczema
  4. edema
24
Q

Ranolazine
MOA

A

Reduce accumulation of sodium and calcium in the myocardiocytes

Use energy more efficiently

25
Q

Ranolazine
Indications

A

Adjunct to
- nitrates
- beta blockers
- CCB

stable angina

26
Q

Ranolazine
SE

A

HTN

QT interval, torsade de pointes

27
Q

Ranolazine
Contraindications

A

QT prolongation drugs

CYP3A4 inhibitors

28
Q

Treatment Pathway
Acute Coronary Syndrome

A
  1. Hospital admission

MONA
- morphine
- oxygen
- nitrates
- anti-platelet therapy

29
Q

MOA
MONA Therapy

A

Morphine
- bradycardia
- hypotension
- decrease oxygen demand of heart
- treatment pain prevents activation SNS

Oxygen
- supply to meet demand

Nitrates
- converted by VSM into NO by sulfhydryl groups
- guanylyl cyclase dephosphorylation myosin, breaking cross bridge, relaxation smooth muscles
- vasodilation
- coronary arteries - increase oxygen supply to heart
- veins - decrease preload and work of heart

Anti-platelet therapy
- dissolve the clot which is causing ischemia
- prevent clots

30
Q

Treatment Pathway
Stable angina

A
  1. Nitrate (PRN)
  2. Beta blocker and/or CCB dihydropyridine
  3. ACEi/ARB

HTN:
CAD with stable angina
- first line beta blocker / CCB
- decrease oxygen demand of heart to decrease angina precipitation

HTN:
Post MI
- beta blocker + ACEi

HTN:
HF
- Beta blocker + ACEi = MRA

31
Q

GPIIb/IIIa Platelet receptor

A

GPIIb/IIIa platelet receptor
activated conformation
binds to fibrinogen
forms the cross linking for the fibrin clot

Activated by:
1. TXA 2 converstion to AA by COX
2. Thrombin, Collagen, PAF
3. P2Y12 receptor signaling binds ADP

32
Q

Anti-platelet therapy
Examples

A
  1. ASA
    - aspirin
    - Blocks COX
    - prevents conversion AA to TXA2 which activates the GPIIb/IIIa receptor
    - prevents platelet aggregation
  2. P2Y12 receptor blockers
    - Clopidogrel
    - Prasugrel
    - Ticlopidine
    - Ticagrelor
33
Q

ASA
Indication

A
  1. Stable angina
  2. post-ACS
  3. secondary prevention CVE
    - angina
    - MI
    - TIA, stroke
    - CAD, PAD, etc.

*not usually recommended for primary prevention (unless large number of risk factors)

34
Q

ASA
MOA

A

1.anti-platelet
IRREVERSIBLE INHIBITION platelet aggregation

  • block COX
  • prevent arachadonic acid -> thromboxane A2
  • prevents activation GPiib/iiia receptor platelet
  • prevents binding and cross linking fibrinogen
  • prevent formation platelet plug
  1. Vasodilation
    - prevents TXA2 which causes vasoconstriction
  2. Decrease MI risk and sudden cardiac death
    CARDIOPROTECTIVE
35
Q

ASA
SE/AE

A
  • GI ulceration and bleeding, melena stools
  • decrease blood flow, mucous, bicarb,
  • Kidney damage
  • decrease blood flow to kidney
  • Reye’s sydnrome (fatty liver, cerebral edema) children < 18 years
  • salicylism (elderly)
  • thrombocytopenia
  • asthma (increase AA to lipooxygenase pathway production leukotrienes increases)
36
Q

ASA
Contraindications

A
  • pregnancy
  • children < 18 years
  • BP > 150mmHg (hemorrhage)
  • GI ulceration and bleeds
  • alcohol
  • smoking
  • thrombocytopenia
  • asthma
37
Q

SAPT vs. DAPT

A

Dual anti-platelet therapy

ASA + Ticagrelor

Single anti-platelet therapy

ASA or P2Y12 inhibitor

38
Q

P2Y12 Inhibitor
Examples

A

Clopidogrel

Ticagrelor

Prasugrel (most potent)

39
Q

P2Y12 inhibitor
MOA

A
  1. reversible inhibition platelet aggregation

inhibits ADP binding to P2Y12
prevents activation of GPiib/iiia receptor
prevenets platelet aggregation
cannot bind fibrinogen cross link

40
Q

SE/AE
P2Y12 inhibitors

A
  • GI upset
  • Thrombotic thrombocytopenic purpura (TTP)
  • hemolytic anemia
  • kidney damage
  • bleeding risk (hematuria, epitstaxis)

*high risk TTP in first 2 weeks

41
Q

Monitoring
P2Y12 inhibitors

42
Q

Pharmacokinetics
P2Y12 inhibitors

A

Prodrug
converted by CYP2C19

Drugs decrease activity
- PPI
- H2 blockers
- Azoles

*take for GI upset

43
Q

Indication
P2Y12 inhibitors

A
  1. ACS
  2. secondary prevention MI, stroke, PCI
44
Q

Contraindications
P2Y12

A

TTP
hemolytic anemia
low platelets
liver disease
pregnancy
GI ulcerations
gout

45
Q

Indication for DAPT

A

DAPT
= ASA + P2Y12 inhibitor

*high risk for bleeding

  1. ACS (STEMI/NSTEMI) + PCI
    - 1 year DAPT
    - assess bleeding risk
    - no risk
    - continue for 3 years DAPT

High bleeding risk
- frail < 60kg
- low hemoglobin <110
- NSAID or prednisone therapy
- CKD
- prior bleed
- age > 75

46
Q

Stable Angina or
ACS
Pharmacotherapy at discharge from hospital

A
  1. nitrates PRN
  2. Beta blocker + ACEi
    - reduce post MI mortality, CVE
    - monotherapy with beta blocker or CCB if stable angina with CAD
  3. DAPT
    - for up to 4 years post NSTEMI/STEMI with PCI
    or
  4. SAPT
    - ASA or P2Y12 inhibitor
47
Q

ACE Inhibitors
Indication

A
  1. monotherapy sustained HTN
    - not for African americans (unless kidney)
  2. Post MI
    - beta blocker + ACEi
  3. HF LVEF < 40%
    - beta blocker + ACEi
  4. HTN DM kidney disease
    - ACEi +/- CCB dihydropyridine
48
Q

ACEi
MOA

A

Decrease blood pressure
cause vasodilation
decrease fluid/sodium retention
decrease cardiac and vascular remodelling
decrease activation SNS

  1. block angiotensin converting enzyme from making angiotensin II
  • vasodilation
  • decrease activation SNS
  • prevent remodelling VSM and heart
  1. Block downstream effect of aldosterone
  • prevent uptake fluid, sodium (decrease BP)
  • prevent cardiac remodelling
  • NE reuptake not inhibited
  • baroreceptor setpoint can re-set to normal
  1. Prevent breakdown of bradykinin
    - vasodilator
49
Q

ACEi
SE/AE

A
  1. cough (8% cross reactivity with ARB)
  2. angioedema
  3. first dose hypotension (severe if angiotensin II is high)
  4. neutropenia (infection risk)
  5. Kidney failure (contraindicated bilateral renal stenosis)
  6. hyperkalemia
  7. teratogenic
50
Q

ACEi
Contraindications

A

TERATOGENIC

Potassium supplements/sparing diuretics
D/C 2-3 days before start

Toxicity
digoxin, lithium

Angioedema Hx.

Bilateral renal stenosis

51
Q

Which ACEi do you use post MI?

A

RAMIPRIL
- reduce MI
- reduce CVA
- reduce CV all cause mortality

Year 1: Patho/Pharm (45 decks)

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