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PPP Fall Midterm > Midterm Stuff > Flashcards

Midterm Stuff Flashcards

1
Q

Atropine Indic.

A

Bradycardia (blockade of M2 on SA node)
AV block
AntiChE toxicity

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2
Q

Antimuscarinic Side effects

A 
Xerostomia
Inc. Temp
Urinary retention
Constipation
Blurred vision
Tachycardia
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3
Q

Cholinesterase Inhibitor AE

A

DUMMBBELLSS

Muscle weakness, paralysis

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4
Q

Muscaranic Agonist AE

A

N/V/D
Cramps
Urinary urgency
Vision problems

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5
Q

Immediate Release Nifedipine

A

Not used - Severe reflex tachy.C. and precipitates angina pectoris & MI

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6
Q

MVO2 determinants (3 of them)

A

HR
Contractility
Intramyocardial wall tension during systole (PL, AL)

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7
Q

Pharm Agents that Dec O2 demand

A

Beta blocker
Organic nitrate
CCB
Ranolazine

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8
Q

Pharm Agents that Inc O2 Supply

A

Vasodilators (CCB)
Statins
Antithrombotics

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9
Q

AL and Resistance Vessel Pressure

A

Dec P –> Dec AL

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10
Q

Nitrate Effects

A 
Inc MVO2
Dec AL
Dec O2 Demand
(3x) Dec PL
Dec BP
Dec CO
Inc HR (BRR Tachy C)
Inc IS
Inc CBF
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11
Q

Nitrate Effects

A 
Inc MVO2
Dec AL
Dec O2 Demand
(3x) Dec PL
Dec BP
Dec CO
Inc HR (BRR Tachy C)
Inc IS
Inc CBF
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12
Q

Nitrate AE

A 
Fatigue
Dizziness
Orthostasis
Organ Injury (Low Perfusion)
HA
Flushing
Edema 
Reflex TachyC --> Inc HR
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13
Q

Non DHP Effects

A

Negative Inotropy

DEC:
SA-N rate
AV-N Cond
Cond. Velocity
Myoc. Contr.

INC:
Refractory Period
PR interval

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14
Q

Non DHP Effects

A 
DEC:
SA-N rate
AV-N Cond
Cond. Velocity
Myoc. Contr.

INC:
Refractory Period
PR interval

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15
Q

CCB DHP AE

A

HOTN
HA
Peripheral edema
Reflex Tachy C

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16
Q

Loop Diuretics

A

Meh for HTN alone
Relieve actue edmatous stress
More effective than Thiazides if CrCl < 30 mL/min

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17
Q

Loop Diuretics

A

Meh for HTN alone
Relieve actue edmatous stress
More effective than Thiazides if CrCl < 30 mL/min

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18
Q

Most effective thiazide

A

Chlorthalidone > HCTZ

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19
Q

Alpha Blockers and HTN

A

Only if the pt already has BPH. Not a monotherapy.
Alpha 1 blockage dec SM cont.
ALpha 2 blockage dec SM contr but has a (-) feedback for NE on nerve

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20
Q 
Ischemic Heart CCB Effect
HR
AL
PL
Contractility
Collateral Flow
Vasodil
O2 Supply
Demand
A 
\+/- or Dec HR
2 or 3x Dec AL
\+/- PL
\+/- or 2x Dec Contractility
Inc
Collateral flow
Inc 3x vasodil
Inc 2x O2 Supply
\+/- O2 Demand (Inc as a reflex)
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21
Q 
BB Effect on Ischemic O2 Balance
HR
AL
Heart Size
Contractility
O2 wastage
O2 demand
Diastolic Perfusion
Exercise &amp; Vasoconst
Spasm
Supply
Defecit &amp; anaerobic metab.
A 
2x dec HR
Dec AL
Inc Heart Size
Dec Contractility
Dec O2 Wastage
3x Dec O2 demand
Inc Diastolic Perfusion
Inc Less exercise vasoconst.
? Dec Spasm
2x Dec O2 deficit &amp; Anaerobic Metab
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22
Q

Ranolazine DDI

A

CYP3A4 and 2D6 Inhib

Diltiazem and Verapamil

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23
Q

Ranolazine DDI

A

CYP3A4 and 2D6 Inhib

Diltiazem and Verapamil

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24
Q

Causes of Inc CO

A 
Hypervolemia
Hyperaldosteronism
Pregnancy
Phaeochromocytoma
Renal dz
Hypersecretion of ADH
Stress
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25
Q

Centrally Acting Alpha 2 Agonist

A

Potent antiHTN reserved for resistant patients

Binding of alpha2 on nerve –> (-) feedback –> Dec NE released from synaptic vesicle

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26
Q

Hydralazine AE

A
  • *Lupus like symptoms**
  • fever, rash, myalgia, arthritis, hematologic abnormalities

Vasodil
Peripheral Edema
BRR Reflex TachyC

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27
Q

Nitrate MOA

A

Activate GTP –> Inc cGMP -> Inc cGMP dep KP
Causes 2 things:
- Dec Ca in cytosol
- Dephosphorylation of MLC -> VSM relaxation

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28
Q

Nitrate MOA

A

Activate GTP –> Inc cGMP -> Inc cGMP dep KP
Causes 2 things:
- Dec Ca in cytosol
- Dephosphorylation of MLC -> VSM relaxation

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29
Q

Minoxidil MOA

A

Open K+ Channels in SKM –> VSM hyperpolarization –> volt gated Ca2+ channel closure –> Dec [Ca2+]i

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30
Q

Minoxidil AE

A

Hypertrichosis

Edema
BRR TachyC –> Angina (T wave)
Headache
Flushin

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31
Q

Nitroprusside Effects

A

Inc MVO2 supply
3x dec PL
Dec MVO2 deman
Dec AL

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32
Q

Nitroprusside AE

A

HOTN –> Dizziness, syncope
BRR TachyC –> Inc HR

Cyanide
Hypoxemia, tachC, ANS instability, AMS, metab. acidosis, seizures, almond breath

Thyocyanate
AMS, tinnitus, hyperrelexia, tremor, hypothyroidism

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33
Q

Nitroprusside AE

A

HOTN –> Dizziness, syncope
BRR TachyC –> Inc HR

Cyanide
Hypoxemia, tachC, ANS instability, AMS, metab. acidosis, seizures, almond breath

Thyocyanate
AMS, tinnitus, hyperrelexia, tremor, hypothyroidism

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34
Q

What drugs Inc. Phase 0 threshold?

A

BB and CCB

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35
Q

What drugs dec Phase 4 slope?

A

Na Blockers and BB

36
Q

What happens in the Cardiac Cycle with the P wave?

A

Depolarization of atrial myocardium

37
Q

What happens in the Cardiac Cycle with the QRS complex?

A

Depolarization of ven. myocardium

38
Q

What happens in the Cardiac Cycle with the T wave?

A

Repolarization of vent. myocardium

39
Q

How can a Na channel blocker affect the ECG?

A

Inc. QRS interval

40
Q

Where does the AV-N relate to the ECG?

A

PR interval

41
Q

Where does the SA-N affect the ECG?

A

Affects the firing rate so the RR interval

42
Q

What interval does Cipro affect?

A

Inc. QTc interval

43
Q

Which interval does a K Channel Blocker affect?

A

No change to HR
Inc. QT
Inc. QTC

44
Q 
NE effects as a sympathetic regulator
HCN channels
Phase 4 slope
firing rate
LTCC
Phase 0 slope
Conduction velocity
HR
APD
Refractory period
A 
INC:
HCN channels
Phase 4 slope
firing rate
LTCC
Phase 0 slope
Conduction velocity
HR

Dec:
APD
Refractory period

45
Q

NE effects as a sympathetic regulator

A 
INC:
HCN channels
Phase 4 slope
firing rate
LTCC
Phase 0 slope
Conduction velocity
HR

Dec:
APD
Refractory period

46
Q

Supraventricular BradyAr

A

Sinus Brady.C

AV block

47
Q

Supraventricular TachyAr

A

Sinus Tachy.C
AF/AFl
PSVT

48
Q

Ventricular BradyAr

A

Bundle branch block

49
Q

Ventricular TachyAr

A

VT
TdP
VF

50
Q

Bradyarrhythmia caused by:

A

Dec Firing rade

Dec. Conduc. Velocity

51
Q

TachyAr caused by

A 
Inc automaticity
(dec. firing rate and inc refractoriness)

Reentry
(Dec. cond. vel. and inc refractoriness)

Triggered activity
(EAD’s dec refractoriness and DAD’s dec Ca overload)

52
Q

DAD

A 
ischemia
CHF
digoxin
Inc HR
Stress
53
Q

DAD

A 
ischemia
CHF
digoxin
Inc HR
Stress
54
Q

Tx of Inc automaticity in TachyAr

A

Dec firing rate with Na or B blockers (dec Phase 4 slope) or with CCB (inc Phase 0 threshold)

Inc Refractoriness by inc APD, affect Phase 3 with K blockade

Dec conduction velocity by dec phase 4 slope (Na, Ca, B blockers)

55
Q

EAD tx

A

unblock K, stim B

56
Q

DAD tx

A

Remove cause of Ca overload

57
Q

Narrow therapeutic index

A

Any drug that tx Ar can also cause it

58
Q

Rhythm Control

A

Na & K blockers
Stop the Ar
Little effect on HR or AV-N conduction
Treats both SVT and VT

59
Q

Rate Control

A

CCB and BB
May not be intended to stop the Ar
Slow vent rate to allow adequate filling & output
Treats SVT (not VT)

60
Q

When in a state dependent block is K binding the highest?

A

In the resting state (slow HR)

Greater effect/toxicity with slow HR

61
Q

When in a state dependent block is Na binding the highest?

A

In the active and inactive states (fast HR)

Greater effect with fast HR and during ischemia (during which more channels are inactivated)

62
Q

Sinus tachycardia

A

Inc firing rate of SA-N
Will see short RR intervals

Tx: BB

63
Q

Sinus tachycardia

A

Inc firing rate of SA-N
Will see short RR intervals

Tx: BB

64
Q

BB AE

A

bronchospasm
hypoglycemic unawareness
rebound tachyc & htn?

65
Q

AF and AFi

A

rapid extopic foci w/in/near atria
reentry circuits w atria
ventr. rate varies w AV-N conduction velocity and refractoriness

Can use rhythm control drugs

66
Q

AF and AFi

A

rapid extopic foci w/in/near atria
reentry circuits w atria
ventr. rate varies w AV-N conduction velocity and refractoriness

67
Q

Class IA Na Blockers effects

A

Inc QRS int
Inc APD via K+ blocking
Block ACh for antiACh effects

68
Q

Class IB Na Blocker effects

A

No change in QRS interval

Dec APD

69
Q

Class IC Na Blocker effects

A

3x Inc in QRS int
No change APD
May inc PR int
May dec contractility

70
Q

K Channel Blocker Effects

A

Inc APD
Inc refractoriness
Inc QTc –> Inc risk of Torsades de Pointes

71
Q

K Channel Blocker Effects

A

Inc APD
Inc refractoriness
Inc QTc –> Inc risk of Torsades de Pointes

72
Q

Rate Control + BP is stable use:

A

BB

CCB

73
Q

Rate Control + BP is unstable use:

A

Amiodarone

Digoxin

74
Q

Digoxin MOA

A

Inhibit Na/K ATPase –> Inc [Ca]i –> Contraction
BRR –> Inc PANS tone
–SA-N –> dec firing rate
–AV-N –> dec conduction velocity

75
Q

Adenosine effects

A

Binds to adenosine receptors
SA-N: Dec firing rate
AV-N: 3xDec conduction velocity

Gi binding: Inc K, Dec Ca
Inc vasodil via Gs
Rapid PK

Halts all AV conduction for a few seconds

76
Q

Isoproterenol MOA

A

B stim:
Inc HR
Dec APD
Dec QT int

Dec risk of EAD’s and TdP

77
Q

Isoproterenol MOA

A

B stim:
Inc HR
Dec APD
Dec QT int

Dec risk of EAD’s and TdP

78
Q

IA Na Block AE

A

Disopyramide - highly antiACh

Quinide - cinchonism, NVD, thrombocytopenia, hepatitis, autoimmune

Procainamide - autoimmune; metabolite is a K blocker

79
Q

IC Na Block AE

A

GI
CNS

Propafenone: Beta blockade –> CI in asthma and COPD

Metallic taste

80
Q

IC Na Block AE

A

GI
CNS

Propafenone: Beta blockade –> CI in asthma and COPD

Metallic taste

81
Q

Na+ affects which phases?

A 
Phase 0 (fast fibers)
Phase 4 (slow fibers)
82
Q

Ca2+ affects which phases?

A 
Phase 2 (Fast fibers)
Phase 0 (Slow fibers)
83
Q

K+ affects which phases?

A 
Phase 3 (Fast fibers)
Phase 3 (Slow fibers)
84
Q

Which phases affect firing rate?

A

Phase 4 slope, Phase 0 threshold

85
Q

Which phase affects refractory period?

A

Phase 3 slope

86
Q

Which phase affects refractory period?

A

Phase 3 slope

87
Q

Notable Procainamide Symptom

A

Lupus

PPP Fall Midterm (3 decks)

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