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
Centrally Acting Alpha 2 Agonist
Potent antiHTN reserved for *resistant* patients Binding of alpha2 on nerve --> (-) feedback --> Dec NE released from synaptic vesicle
26
Hydralazine AE
* *Lupus like symptoms** - fever, rash, myalgia, arthritis, hematologic abnormalities Vasodil Peripheral Edema BRR Reflex TachyC
27
Nitrate MOA
Activate GTP --> Inc cGMP -> Inc cGMP dep KP Causes 2 things: - Dec Ca in cytosol - Dephosphorylation of MLC -> VSM relaxation
28
Nitrate MOA
Activate GTP --> Inc cGMP -> Inc cGMP dep KP Causes 2 things: - Dec Ca in cytosol - Dephosphorylation of MLC -> VSM relaxation
29
Minoxidil MOA
Open K+ Channels in SKM --> VSM hyperpolarization --> volt gated Ca2+ channel closure --> Dec [Ca2+]i
30
Minoxidil AE
**Hypertrichosis** Edema BRR TachyC --> Angina (T wave) Headache Flushin
31
Nitroprusside Effects
Inc MVO2 supply 3x dec PL Dec MVO2 deman Dec AL
32
Nitroprusside AE
HOTN --> Dizziness, syncope BRR TachyC --> Inc HR **Cyanide** Hypoxemia, tachC, ANS instability, AMS, metab. acidosis, seizures, almond breath **Thyocyanate** AMS, **tinnitus**, hyperrelexia, tremor, hypothyroidism
33
Nitroprusside AE
HOTN --> Dizziness, syncope BRR TachyC --> Inc HR **Cyanide** Hypoxemia, tachC, ANS instability, AMS, metab. acidosis, seizures, almond breath **Thyocyanate** AMS, **tinnitus**, hyperrelexia, tremor, hypothyroidism
34
What drugs Inc. Phase 0 threshold?
BB and CCB
35
What drugs dec Phase 4 slope?
Na Blockers and BB
36
What happens in the Cardiac Cycle with the P wave?
Depolarization of atrial myocardium
37
What happens in the Cardiac Cycle with the QRS complex?
Depolarization of ven. myocardium
38
What happens in the Cardiac Cycle with the T wave?
Repolarization of vent. myocardium
39
How can a Na channel blocker affect the ECG?
Inc. QRS interval
40
Where does the AV-N relate to the ECG?
PR interval
41
Where does the SA-N affect the ECG?
Affects the firing rate so the RR interval
42
What interval does Cipro affect?
Inc. QTc interval
43
Which interval does a K Channel Blocker affect?
No change to HR Inc. QT Inc. QTC
44
``` NE effects as a sympathetic regulator HCN channels Phase 4 slope firing rate LTCC Phase 0 slope Conduction velocity HR APD Refractory period ```
``` INC: HCN channels Phase 4 slope firing rate LTCC Phase 0 slope Conduction velocity HR ``` Dec: APD Refractory period
45
NE effects as a sympathetic regulator
``` INC: HCN channels Phase 4 slope firing rate LTCC Phase 0 slope Conduction velocity HR ``` Dec: APD Refractory period
46
Supraventricular BradyAr
Sinus Brady.C | AV block
47
Supraventricular TachyAr
Sinus Tachy.C AF/AFl PSVT
48
Ventricular BradyAr
Bundle branch block
49
Ventricular TachyAr
VT TdP VF
50
Bradyarrhythmia caused by:
Dec Firing rade | Dec. Conduc. Velocity
51
TachyAr caused by
``` 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
DAD
``` ischemia CHF digoxin Inc HR Stress ```
53
DAD
``` ischemia CHF digoxin Inc HR Stress ```
54
Tx of Inc automaticity in TachyAr
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
EAD tx
unblock K, stim B
56
DAD tx
Remove cause of Ca overload
57
Narrow therapeutic index
Any drug that tx Ar can also cause it
58
Rhythm Control
Na & K blockers Stop the Ar Little effect on HR or AV-N conduction Treats both SVT and VT
59
Rate Control
CCB and BB May not be intended to stop the Ar Slow vent rate to allow adequate filling & output Treats SVT (not VT)
60
When in a state dependent block is K binding the highest?
In the resting state (slow HR) | Greater effect/toxicity with slow HR
61
When in a state dependent block is Na binding the highest?
In the active and inactive states (fast HR) | Greater effect with fast HR and during ischemia (during which more channels are inactivated)
62
Sinus tachycardia
Inc firing rate of SA-N Will see short RR intervals Tx: BB
63
Sinus tachycardia
Inc firing rate of SA-N Will see short RR intervals Tx: BB
64
BB AE
bronchospasm hypoglycemic unawareness rebound tachyc & htn?
65
AF and AFi
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
AF and AFi
rapid extopic foci w/in/near atria reentry circuits w atria ventr. rate varies w AV-N conduction velocity and refractoriness
67
Class IA Na Blockers effects
Inc QRS int Inc APD via K+ blocking Block ACh for antiACh effects
68
Class IB Na Blocker effects
No change in QRS interval | Dec APD
69
Class IC Na Blocker effects
3x Inc in QRS int No change APD May inc PR int May dec contractility
70
K Channel Blocker Effects
Inc APD Inc refractoriness Inc QTc --> Inc risk of Torsades de Pointes
71
K Channel Blocker Effects
Inc APD Inc refractoriness Inc QTc --> Inc risk of Torsades de Pointes
72
Rate Control + BP is stable use:
BB | CCB
73
Rate Control + BP is unstable use:
Amiodarone | Digoxin
74
Digoxin MOA
Inhibit Na/K ATPase --> Inc [Ca]i --> Contraction BRR --> Inc PANS tone --SA-N --> dec firing rate --AV-N --> dec conduction velocity
75
Adenosine effects
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
Isoproterenol MOA
B stim: Inc HR Dec APD Dec QT int Dec risk of EAD's and TdP
77
Isoproterenol MOA
B stim: Inc HR Dec APD Dec QT int Dec risk of EAD's and TdP
78
IA Na Block AE
Disopyramide - highly antiACh Quinide - cinchonism, NVD, thrombocytopenia, hepatitis, autoimmune Procainamide - autoimmune; metabolite is a K blocker
79
IC Na Block AE
GI CNS Propafenone: Beta blockade --> CI in asthma and COPD **Metallic taste**
80
IC Na Block AE
GI CNS Propafenone: Beta blockade --> CI in asthma and COPD **Metallic taste**
81
Na+ affects which phases?
``` Phase 0 (fast fibers) Phase 4 (slow fibers) ```
82
Ca2+ affects which phases?
``` Phase 2 (Fast fibers) Phase 0 (Slow fibers) ```
83
K+ affects which phases?
``` Phase 3 (Fast fibers) Phase 3 (Slow fibers) ```
84
Which phases affect firing rate?
Phase 4 slope, Phase 0 threshold
85
Which phase affects refractory period?
Phase 3 slope
86
Which phase affects refractory period?
Phase 3 slope
87
Notable Procainamide Symptom
Lupus