Q2 - Cardiac Flashcards

1
Q

If a patient has stage 1 hypertension but is young and has a very low ASCVD risk, what is the 1st line of tx?
65yo patient with stage 1HTN and mod-high ASCVD risk?

A

No drug therapy needed- diet and lifestyle modifications first

Lifestyle mods AND drug therapy.

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2
Q

If an individual has albuminuria, what does that mean in relation to their BP?

A

Threshold for starting anti-hypertensive meds is lower and need ACEi and ARBs.

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3
Q

Which antihypertensive classes work on the vascular smooth muscle? MOA?

A

A1 blockers, CCBs and AT receptor blockers.
Vasodilation.

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4
Q

What 2 classes of antihypertensives influence renin and therefore lower BP?

A

Beta blockers and thiazide diuretics.

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5
Q

Study pharm free form image 1

A
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6
Q

What are 1st and 2nd line therapies for the tx of hypertension?

A

1st line = ACD (Ace/ARB, CCB and diuretics)
2nd = AA (aldosterone agonists), BB, vasodilators and alpha blockers (peripheral and central)

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7
Q

Clinical considerations with the use of ACE inhibitors.

A

-Check SCr 7-10 days post therapy initiation.
-No K supplements or salt substitutes
-Do not combine ACE with ARBs or direct renin inhibitor.
-avoid in pregnancy
-can cause angioedema.

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8
Q

Do not combine ACE inhibitors with ______

A

ARBs or direct renin inhibitors.

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9
Q

Examples of ACE inhibitors.
Which ones give on an empty stomach?

A

“-April or -opril”
Catopril /Moexipril

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10
Q

Acronym for ACEi SEs?

A

C cough
A angioedema
P pressure (low)
T taste (metallic)
O omit in pregnancy
P potassium elevation
R renal impairment/rash
I impotence
L leukocytosi

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11
Q

Examples of ARBs.
Clinical considerations?

A

“-sartan”
-Do not combine with ACE or direct renin inhibitors
- increases risk of hyperK in CKD
-do not use if hx of angioedema with ARBs/ACEi
-avoid in pregnancy

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12
Q

What is special about losartan?

A

ARB
Prodrug so not all patients have hormones necessary to convert to active drug form.
Can lower Uric acid and prevent gout attacks.

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13
Q

ARB/Sartan SE acronym

A

S systolic BP lowering
A angioedema
R renal impairment (NOT use in bilateral renal artery stenosis)
T too much K
A abdominal px, diarrhea, vomiting
N not in pregnancy

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14
Q

What are the 2 sub groups of CCBs and their MOAs?
Which ones preferentially affect the heart?

A

non-dihydropyridine (non-DHP)
Dihydropyridine (DHP)
MOA: block cellular entry of Ca through L-type ca channels.

non-DHP CCB preferentially affect the heart
DHP preferentially affect the smooth muscle (acting peripherally)

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15
Q

What class of medications can be used in variant angina?

A

Or prinzmental’s angina
CCBs.

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16
Q

Why can LE swelling be an SE of CCBs?

A

CCBs act to dilate the arteries but not much action on the veins (like a 3lane highway merging into a 2 lane highway) so blood gets backed up in the venous system.

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17
Q

How can you differentiate LE swelling as an SE of CCBs or LE swelling from heart failure?

A

CCB related LE swelling does not respond to diuretics.

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18
Q

Clinical considerations for CCBs?

A

DHP
-Do not use in HFrEF (except for amLodipine or felodipine)
non-DHP
-avoid combo with BB -> bradycardia and heart block
-substrate and CYP3A4 inhibitor so lots of DIs.

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19
Q

Examples of CCBs

A

“-dipine” (DHPs) and
Diltiazem and Verapamil (non-DHP)

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20
Q

Do DHPs have central or peripheral effects?

A

Peripheral.
Non-DHP preferentially affect the heart centrally.

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21
Q

Good medication for females with benign tachycardia and HTN?

A

Diltiazem (non-DHP CCB)

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22
Q

What CCB should be taken on an empty stomach?

A

Nifedipine.
Sometimes this is the issue with patients who do not have an expected response to this medication - all they have to do is start taking it on an empty stomach and they will start to see >10mmHg decrease in SBP.

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23
Q

DHP CCB (peripheral) and non-DHP (central) SEs acronym

A

DHP
C constipation
H headache
A ankles (edema)
P palpitation
P pulmonary E edema
D dizziness (orthostatis)

non-DHP
L limit grapefruit juice (CYP3A4)
I insomnia
P potent CI
S skin rash

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24
Q

Clinical consideration for diuretics

A

Electrolyte imbalances (hypO Na and K, HypER glycemia and uricemia)

K sparing diuretics (Amiloride/triamtaren) are usually used in combo

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25
Q

Chlorthalidone is preferred over ________ based on_______

A

Hydrochlorothyazide
Prolonged half life and reduction in CVD.

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26
Q

Examples of Loop diuretics
Clinical considerations?

A

Ethacrynic Acid
Bumetanide
Furosemide
Torsemide

Preferred in patients with HF
Preferred in patients with CKD.

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27
Q

Which diuretics are preferred in patients with HF and CKD?
Patients with primary aldosteronism and resistant HTN?

A

Loop diuretics

Aldosterone antagonists.

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28
Q

SE of spironolactone?

A

gynecomastia

(Lactone sounds like lactose in milk from boobs)

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29
Q

Spironolactone is the ____ line aldosterone agonist diuretic.

A

1st

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30
Q

Where do loop diuretics work?
Thiazides?
K sparing diuretics?

A

Distal end of loop of Henle
DCT
Collecting duct

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31
Q

Diuretic SEs acronym

A

D decrease in Na uptake
I increase in K excretion (xcept for K sparing)
U uricemia (gout)
R renal fxn (not effective if eGFR is <30)
E electrolyte disturbances
T take in the AM (xcept HCTZ)
I increased orthostasis
C calcemia

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32
Q

What antihypertensives may be favorable in elderly females?

A

Diuretics . Increased Ca reuptake which helps slow Osteoporisis development.

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33
Q

Which beta-adrenoceptor agonists (or BBs) are okay for use in COPD and asthma?

A

Beta1 selective agonists

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34
Q

Examples of BBs
And clinical considerations

A

“-lol”
-BB not recommended as 1st line
-Carvedilol no longer preferred in pts with HFrEF
-avoid abrupt cessation

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35
Q

A patient who has been taking carvedilol has lost 20lbs and been on the Mediterranean diet for 3 months. She wants to stop her BP meds to see if her BP has returned to baseline with her lifestyle modifications. You advise her to:

A

Do not stop abruptly and titration to avoid adverse effects.
BBs should not be stopped abruptly.

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36
Q

BB SE acronym?

A

B bradycardia/B bronchoconstricton (B2)
L lipidemia increased/L libido decreased
O ocular SEs
C conduction abnormalities
K konstriction peripherally (cold fingers/nose)
E exhaustion (sleep disturbances/lethergy)
R reduces recognition of hypoglycemia.

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37
Q

A diabetic patient shares with you that she knows when her sugars are low because she starts to get “the shakes”. How should you council her before starting a new BB medication?

A

BBs can mask the effects of hypoglycemia (such as tremors or shakes) so she should use other methods to check if her sugars are low.

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38
Q

What is Aliskiren

A

A direct renin-inhibitor
2ndary agent.
Do not combine with ACE/ARB

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39
Q

Examples of Alpha 1 blockers, indications for use and MOA

A

Doxazosin (urinary BPH symptoms), Prazosin (PTSD nightmares), Terazosin (urinary BPH symp)

Take at bedtime. May increase risk for stroke
Reduce artery resistance by relaxing the muscle tone.

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40
Q

Alpha 1 blockers are ______ acting while alpha 2 blockers are _____ acting

A

1 = peripheral
2 = central.

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41
Q

What line of tx are alpha 2 agonists? Why?
Example?
Clinical considerations?

A

Last line - too many CNS SEs since they are centrally acting.
Clonidine.
Taper. Avoid abrupt discontinuation = rebound HTN

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42
Q

Which type of HF is associated with pulmonary HTN? What are the two types of Lsided HF?

A

R sides
L HFpEF = diastolic dysfxn
L HFrEF = systolic dysfxn.

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43
Q

Pre-HF (stage____) have an LVEF of ______. Appropriated Meds for this stage?

A

B
< or equal to 40%
ACEi/ARB or BB.

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44
Q

Stage A, B, C and D for HF

A

A = increased risk
B = LVEF> or = to 40%
C = LVEF < or = to 40%
D = refractory HF.

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45
Q

CDMMT (comprehensive Disease-Modifying Medical Therpy) decreases what outcomes if implemented early?

A

CV death or HF hospitalization
Or emergency urgent visits for worsening HF.

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46
Q

Which beta blocker is used for patients with HFrEF

A

Metoprolol succinate.

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47
Q

What might be the DI if a patient with HF is not getting an adequate response from taking a direct vasodilator medication?

A

Since vasodilation activates the baroreceptor reflex resulting in an increased SNS outflow = Tachy, increased CO and renin release.

If the patient is also taking a sympathetic inhibitor or a diuretic, this response will be blunted.

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48
Q

Direct vasodilators approved for HF + MOA

A

Hydralazine - reduces afterload through arterial smooth muscle relaxation
Isosorbide - reduces preload by causing venous vasodilation.

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49
Q

What medication could work the same as nitrates in treating HF and eliminate the need for a nitrate free interval?

A

Hydralazine Isosorbide

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50
Q

What is ivrabadine?
MOA:

A

A medication approved to treat HF for patients in NSR (CI in AFIB) who are still having symptoms after max BB dose and HR still >70.

DC if HR<50bpm.

MOA:selectively inhibit cardiac pacemaker current If in the SA node which slows and decreases HR.

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51
Q

What is Digoxin’s MOA? What is it used to treat? Considerations?

A

Inhibits the Na/K pump in myocardial cells which increases intracellular Na which increases Ca influx which increases cardiac contractility.
HF in patients with AFIB and NSR.
N/V/D, electrolyte disturbances and s/s of toxicity (anorexia, blurred/yelllow vision, confusion)

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52
Q

As a PCP, when should I refer my HF patients to a specialist? Acronym

A

I intravenous inotropes
N NYHA class IIB/IV or persistently elevated BNP
E end-organ dysfunction
E EF <35%
D defibrillator shocks
H hospitalization >1
E Edema despite escalating diuretic
L low SBP<90 and high HR
P progressive intolerance or downtitration of GDMT

53
Q

If someone has a “recovered LVEF” what does that mean?

A

HFrEF with a > or = 10% improvement.

54
Q

What are the 4 medication classes for HFrEF GDMT (Guideline Directed Medical Therapy)

A

RAAS Inhibitors (ACEi, ARB, ARNi), BB, MRA (spironolactone-Mineralocorticoid) and SGLT2i

55
Q

What is HFmrEF>

A

LVEF of 41-49%

56
Q

Improved LVEF patients should ________ taking their HF medications

A

Continue

57
Q

H2FPEF score of 3-5 would mean?

<2?
>6?

A

Additional testing needed to confirm dx of HF - ie exercise TTE or cardiac cath.

HF unlikely

HF very likely

58
Q

In HF, we want to control:

A

Weight, diet, BP, lipids and glucose

59
Q

If a HF patient is Class II “warm and wet” what does that mean?
Class III “Cold and dry”?

What are the other 2 classes?

A

Perfusion/congestion
Warm and wet means they are perfuming but they have lung congestion(pulmonary edema)
Cold and dry means they are not perfusing and they do not have any pulmonary edema.
Class I = warm and dry
Class IV = cold and wet.

60
Q

What are the treatment guidelines for the classes of HF?

A

Class I (warm + dry) = optimize oral meds (target PCWP 15-18 and CI 2.2L/min)
Class II (warm + wet) = IV diuretics+- IV venous dilators (target PCWP >18 and CI >2.2L/min)
Class III (cold + dry) = IVF if PCWP<15mmHg, IV dopamine if PCWP >15 but MAP <50, if PCWP is >15 and Map >50, then Inotrope, or arterial vasodilator
Class IV (cold + wet) = IV diuretics + IV dopamine, Inotrope or vasodilator depending on MAP.

61
Q

What class are Dobutamine and milrinone?

A

Inotropes used to treat class IV Cold/wet or cold/dry classIII

62
Q

What IV vasodilators can be used for HF exacerbation?

A

Warm and wet class II
Sodium Nitroprusside
Nesiritide
IV Nitroglycerin.

63
Q

What is a frequent cause of arrhythmia?

A

Coronary artery disease.

64
Q

Which classes of medications are used to treat arrhythmias?
Which phases of the cardiac cycle are each used in?

A

Na Channel blockers
CCBs
Potassium channel blockers.
“Block those arrhythmias!”
“Summit, Plummit, Continue, Plummet”
Summit = Sodium = phase 0 Influx of Na
Plummit = Potassium = phase 1 slight K efflux.
Continue = Calcium = phase 2 calcium influx and k efflux
Plummit = Potassium = phase 3 major potassium efflux
Resting phase phase 4

65
Q

What class of antiarrythmics are Sodium channel blockers? Where do they work? Example?

A

Class I
Phase 0 to block Na influx.
ProcaNAmide

66
Q

What class of antiarrythmics are calcium channel blockers? Where do they work? Example?

A

Class IV
Phase 2 (blocking calcium influx)
Verapamil

67
Q

What class of med is Propanolol? What is it used to treat and where in the cardiac cycle?

A

Class II beta-adrenergic blocker
Phase 2

68
Q

What class is amiodarone and where in the cardiac cycle does it work?

A

Class III
Potassium channel blocker
Phase 3 blockings K efflux.

69
Q

Acronym for antiarrhythmic drugs.

A

Class I all Na channel blockers)
IA: Police Department Questions (Procainimide, disopyramide, quinidine)
IB: Liquored Man (Lidocaine, Mixiletine)
IC: For Peeing (Flecainide, Propafenone)
Class II BBs (not included in neumonic)
Class III Ca channel blockers
III: After Drinking Scotch In Dark (Amiodarone, Dronedarone, Sotalol, Ibutilide, Dofetilide)
Class IV K channel blockers
IV: Dirty Vehicle (Diltiazem, verapamil)

70
Q

What medication can be used as a “pill in pocket” therapy for palpitations?

A

Propanolol 30-60mg/day in 2-3 doses.

71
Q

What is the issue with Vaughan William’s Classifications for antiarrythmics?

A

It is incomplete and not pure (many agents have properties of more than one class)

72
Q

What is a common SE of Ca Channel blockers such as Diltiazem or Verapamil?

A

Constipation.

73
Q

MOA for adenosine?
What is IV Mg infusion used for in arrhythmia?

A

Interrupts the re-entry pathways through the AV node to restore NSR.

Torsades.

74
Q

What is Virchow’s Triad?

A

Injury to vessel wall, altered blood flow and abnormal coagulability all contribute to development of thrombosis.

75
Q

Difference between “white” and “red” thromboses?

A

White = arterial mainly platelets in a fibrin mesh, associated with atherosclerosis (lipids and platelets are white
Red = thrombus broken away and forming an embolus.

76
Q

DOC for non cancer associated VTE?

A

DOACs.

77
Q

T/F: after an unprovoked VTE, you can stop anticoagulant therapy after 3 months.

A

False. For unprovoked, you may stop after 3 months only in patients with high risk of bleeding (continue indefinitely for those who are mod-low bleeding risk.
You can stop anticoagulant therapy after 3 months for a PROVOKED VTE

78
Q

How do we measure heparin response?

A

APTT = 1/5-2.5x the control range.

79
Q

Heparin has a very _____ onset and a very ____ half life.

A

Rapid
Short

80
Q

What medication can be used in HIT/HITT?

A

Fondaparinux (synthetic pentasaccharide)

81
Q

Which is preferred - LMWH or unfractionated heparin?

A

LMWH (enoxaparin and dalteparin) heparin fragments
Due to a more predictable monitoring and response.

82
Q

HIT vs HITT

A

HIT = NONimmunie induced low platelets but >100,000. Few complications
HITT = IMMUNE induced low platelets >20,000. high risk of thrombosis and mortality.

83
Q

Warfarin decreases production of which clotting factors?

A

II, VII, IX and X and protein C+S.

84
Q

Goal INR for warfarin therapy depends on _______

A

Indication for therapy (VTE, AVR, MVR, etc)

85
Q

Dabigatran, Argatroband and hirundin analogs (bivaliruding/desirudin) work to inhibit

A

Thrombin (IIa) directly

86
Q

Factor Xa inhibitors? Preferred?

A

Rivaroxaban(Xarelto)
Apixaban (Eliquis)
Eliquis is preferred - Xarelto has a higher bleeding risk.

87
Q

what are the 2 major criteria of diagnosing infective endocarditis?

A

Positive blood cultures
Endocardia’s involvement (seen on echo or new valvular regurgitation)

88
Q

What are the different categories of infective endocarditis and how is this clinically relevant?

A

NVE - native Valve endocarditis
PVE - prosthetic valve endocarditis
IVDA - intravenous drug abuse endocarditis

Different abx therapies are selected based on which category the infection falls under.

89
Q

70% of NVE infections are caused by ______ and the other 24% by ______.
Therefore treat with:
Average Length of therapy?

A

Streptococcus species
PenicillinG and Gentamicin for streptococcus coverage.
Can also use Ceftriaxone or Vanc. Usually in combination.
2-4 weeks

Staphylococcus species = more aggressive
Nafcillin/Oxacillin, Cefazolin, Vanc, Daptomycin.
6weeks

Enterococcus = ampicillin, PCN G, gentamicin, ampicillin + Ceftriaxone.
4-6weeks.

90
Q

Early PVE (w/in _______days) is more likely caused by ____ while LATE PVE is more likely by _______
Therefore treat with:
Therapy length?

A

60 days
S. Epidermis it’s
Streptococci and enterococci.

Strep tx w/ Vancomycin and gentamycin
Can also use Ceftriaxone and/or PCN G.
6weeks

Enterococcus (same as NVE)
ampicillin, PCN G, gentamicin, ampicillin + Ceftriaxone.
4-6weeks.

91
Q

IVDA most common pathogen?
Therefore treat with:

A

S. Aureus - mainly MRSA.

Nafcillin and gentamicin. If MRSA is suspected replace Nafcillin with vancomycin.

92
Q

Why is IE so difficult to treat?

A

High concentration of organisms present on the vegetation
Position of organisms deep within the thrombus is hard to reach
Fibrin and white cells interfere with abx action.

93
Q

What additional medication can be helpful in the tx of IE to target biofilm penetration.

A

Rifampin. Since this med AND Vanc can be nephrotoxic, replace Vanc with Linezolid in patients with unstable renal fxn also receiving rifampin.

94
Q

Gent and Vang peak?

A

Gent peak = 3mcg/ml
Vanc peak = 30-45mcg/ml

95
Q

What do antianginal drugs do?

A

Reduce oxygen demand of cardiac tissue by decreasing HR, contractility, afterload and preload.

96
Q

The ABCDE treatment for angina

A

A - aspirin, antianginal therapies
B - BBs
C - cigarette-smoking cessation, cholesterol management, CCBs
D - diet
E - education and exercise

97
Q

Stable angina has pain with ______, unstable has pain with _______

A

Activity, rest

98
Q

1st line tx for angina
MOA?

A

BBs
Slow HR by preventing intracellular Ca release.
Heart switch to using oxygen-conserving glucose vs oxygen-wasting fatty acids for energy.

99
Q

What are the BEAM drugs?

A

Beta 1 selective antagonists.

Bisoprolol
Esmolol
Atenolol
Metoprolol

100
Q

Metoprolol Succinate given ______ which tartrate is ordered ______

A

Single daily dose
Twice/day

101
Q

What are the PLaNS-C drugs?

A

Non-selective B antagonists
Propanalol
Labetolol
Nadelolol
Sotalol
Carvedilol.

102
Q

Non-selective B-antagonists should be titrated based on _____

A

Resting HR 55-60bpm

103
Q

Which non-selective B antagonists (PLaNS-C) are NOT used in angina?

A

Labetolol + Sotalol.

104
Q

Do not abruptly stop BBs.

A
105
Q

What should we tell diabetic (esp insulin dependent diabetic patients) who are on BBs?

A

May mask the symptoms of HYPOglycemia and/or cause HYPERglycemia.

106
Q

Patients on BBs should be educated to

A

Change positions slowly since HR is slowed, they may have orthostatic hypotension when changing positions too quickly.

107
Q

What dietary consideration is important with verapamil and Diltiazem in treatment of cardiac issues?

A

Verapamil and dilt are strong CYP3A4 inhibitors so don’t drink grapefruit juice as this could potentiate effects of the medication.

108
Q

Why are nitrates so effective in tx of anginal pain? (MOA)

A

Relaxes vascular smooth muscle to reduce preload and afterload. It dilates the COLLATERAL blood vessels that circumnavigate the clot or narrowing. Other vasodilators may not dilate the collateral vessel.

109
Q

What is an off-label use with organic nitrate medications?

A

Relaxation of esophageal and biliary smooth muscle so can be used to treat spasms with eating

110
Q

SEs and DIs of Nitrates

A

CI in SBP < 90mmHg or HR <50bpm
CI if viagra-like drug (PDE4 inhibitor) taken w/in past 24hrs
Nitrate-free interval (6-8hours)
HA and postural HypOtention.

111
Q

Although vasodilators are important medications with angina it is important to ________

A

Treat the underlying cause - HTN and dyslipidemia.
Statins

112
Q

Most statins should be taken _______ except for _______

A

At night (lipid is made at night)
Simvastatin and pravastatin can be taken any time.

113
Q

Most statins are _________philic but _____ and ________ are the only _____philic ones.

A

Lipophilic
Pravastatin and rosuvastatin
Hydrophilic.

114
Q

Statins are selected and dosed based on _________

A

How much the patients LDL needs to be lowered. If lowered by <30%, then patient can be prescribed a low intensity statin (simvastatin, pravastatin, lovastatin and fluvastatin low dose).
LDL needs lowered by >50%? Then high intensity statin is needed - Astor a statin and rosuvastatin high dose.

115
Q

Your patient on statins is having s/s of myopathy (muscle pain, weakness and fatigue). He is also having elevated LFTs. What should you do?

A

Switch to a hydrophilic statin.

116
Q

myalgia with statins is linked to?

A

Low vit D levels. Can supplement and/or switch to a hydrophilic statin.

117
Q

What additional tx measures are added on with tx of unstable angina?

A

Revascularization PCI procedure
Aspirin or other anti platelet drugs.

118
Q

Types of antiplatlet drugs (APD) and examples

A

Cox inhibitors (aspirin)
P2Y12 receptor blockers
- reversible (ticagrelor, cangrelor)
- irreversible (clopidogrel, prasugrel)
GP IIbIIa inhibitors (abciximab, eptifibatide/tirofiban)
^ IV administration

119
Q

Prasugrel (an irreversible P2Y12 inhibitor) works at this stage in the cascade to inhibit clotting:
A. Cox inhibition
B. Platelet adhesion and secretion
C. Platelet aggregation
D. ADP used for platelet recruitment and activation

A

D.
A - aspirin is a COX inhibitor
B - no APDs work at this level high up in the cascade
C - GP IIbIIIa inhibitors like abiciximab work here

120
Q

When is aspirin therapy CI?
What is the normal antiplatelet therapy dose for ASA?
DI with aspirin?

A

Pt’s with bronchospasm
75-325mg/day although 162mg/day is enough for aspirin naive patients

NSAIDS and ASA need to be separated - ASA 1hr before or 2hrs post NSAID

121
Q

Prasugrel (irreversible ADP antagonist) should not be used in ______
Clopidogrel is a prodrug which means_______

A

Hx of TIA or wt < 60kg - increased risk for bleeding.

Not all people possess the enzyme needed to activate it - and it could be innefective (esp people of East Asian descent)

122
Q

As part of his antiplatelet therapy, your patient is prescribed (abiciximab) a GP IIB/IIIa inhibitor.
T/F: this is an appropriate therapy.

A

False. GP IIb/IIIa are IV medication used in the cath lab.

123
Q

Pharmacological therapy for variant angina

A

Calcium antagonists and organic nitrates AND statin AND aspirin.

124
Q

What is a unique feature of Ranolazine? What is it NOT used to treat?

A

It can be used for tx of angina WITHOUT lowering the BP.

Acute anginal episodes. Prevention only.

125
Q

Fibrinolytic therapy should not be used for more than_______

A

12hrs

126
Q

Your patient is having an MI. He is high risk and his symptoms started 14hours ago.
T/F: he is a candidate for fibrinolytic therapy.

A

FALSE. Fibrinolytics are for low-med risk patients whos symptoms started <12hrs ago. This patient would need an OR or a PCI.

127
Q

Post MI, pharmacotherapy focuses on:

A

Reducing stress on/squeeze of the heart - BB and/or ARBs/ACEis
Prevention of angina- organic nitrates
Treatment of underlying atherosclerosis - statins
Prevention of thrombosis - aspirin and P2Y12 inhibitor for 12 months after stenting

128
Q

Which ACEis should you give on an empty stomach?

A

Catopril + Moexipril