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CRS > Lecture 9+10 > Flashcards

Lecture 9+10 Flashcards

1
Q

ARB examples

A

Losartan / Valsartan

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2
Q

ARB drug MOA

A

first-line agents
alternative for those that cant have ACEI’s

Block angiotensin-2 type 1 receptors:

decrease BP by causing arteriolar & venous dilation

Block aldosterone secretion → decrease Na+ & H20
retention

decrease diabetic nephropathy

DOES NOT increase bradykinin

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3
Q

AE’a of the ARB’s

A

Similar to those of ACE inhibitors

Dry cough does not occur

Angioedema risk is significantly lower than with
ACEI’s

Losartan reduces plasma uric acid levels by inhibiting
URAT1 transporter

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4
Q

ARB contraindication

A

Pregnancy

Patients with bilateral renal artery stenosis

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5
Q

renin inhibitor example

A

Aliskiren

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6
Q

MOA of renin inhibtors

A

Inhibits enzyme activity of renin and prevents conversion of angiotensinogen into angiotensin I

Inhibits production of both angiotensin II and
aldosterone

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7
Q

AE of renin inhibitors

A

• Similar to those of ACE inhibitors
• Dry cough does not occur (due to no effect on
bradykinin levels)
• Angioedema risk is significantly lower than with
ACEI’s

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8
Q

examples of Ca channel blockers

A

first line for black/elderly patients

non-dihydropyridines:
Verapamil / Diltiazem

Dihydropyridines:
Nifedipine / Amlodipine

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9
Q

verapamil

A

non-dihydropyridine

Significant effects in cardiac & vascular smooth muscle

Used to treat angina, supraventricular tachyarrhythmias, hypertension, migraine & cerebral vasospasm

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10
Q

Diltiazem

A

non-dihydropyridine

Effects in both cardiac & vascular smooth muscle

Used to treat angina, hypertension, supraventricular
tachyarrhythmias & cerebral vasospasm

good side-effect profile

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11
Q

Amlodipine and nifedipine

A

dihydropyridines

Greater affinity for vascular Ca2+-channels than for cardiac Ca2+-channels

Reduce Ca2+ entry into smooth muscles to cause
coronary & peripheral vasodilatation & lower BP

Primarily used in treating hypertension

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12
Q

MOA of Ca blockers

A

If you block the Ca channel… there is less movement of Ca, and thus decreased force of muscle contraction

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13
Q

clinical apps. of Ca blockers

A

• Hypertension (1st line, particularly for black and/or
elderly patients)
• Have intrinsic natriuretic effect (no need for diuretic)

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14
Q

risk of taking Ca channel blockers

A

increased risk of MI ((excessive vasodilation & reflex cardiac stimulation)

High-doses of short-acting dihydropyridine

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15
Q

AE of verapamil

A

Constipation (~7%), negative inotropic effects, gingival

hyperplasia

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16
Q

AE of Diltiazem

A

Negative inotropic effects

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17
Q

AE of the dihydropyridine’s

A

Hypotension, peripheral edema (esp. feet & ankles),
dizziness, headache, fatigue, gingival hyperplasia,
flushing, reflex tachycardia can occur (especially in
short-acting preparations)

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18
Q

contraindications of the dihydropyridine’s

A

in patients taking b-blockers, or who have 2nd or 3rd degree AV block, or severe left ventricular systolic dysfunction

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19
Q

use thiazides 1st line for?

A

first line treatment for most, especially AA and elderly.

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20
Q

when to use loop diuretics

A

Used primarily in patients who do not respond to

thiazide therapy adequately

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21
Q

beta blockers

A

Propranolol / Metoprolol / Atenolol / Pindolol

Used only as add-on therapy to first line agents in
primary prevention patients

First-line therapy only for patients with coronary
artery disease, heart failure or post-MI

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22
Q

MOA of the Beta blockers

A

Reduce BP by cardiac output, contractility & heart rate

Inhibit both release of norepinephrine and renin (b1 R) (→ decrease in angiotensin II & aldosterone secretion)

takes weeks to develop full effects

23
Q

AE of beta blockers

A 
hypoglycemia 
bradycardia 
hypotension 
decreased libido 
disrupted lipid metabolism

no one can take if they have pulmonary issue

24
Q

alpha blocker examples

A

Prazosin / Doxazosin

25
Q

MOA of alpha blockers

A

Competitively block a1 -adrenoceptors

decreased peripheral vascular resistance & arterial BP by relaxing both arterial & venous smooth muscle

no long term tachy

can have H20 and Na retention

can lower BP.. but have more AE

26
Q

clinical app of alpha blockers

A

hypertension
benign prostatic hyperplasia
Have been used in heart failure

27
Q

AE of alpha blockers

A

orthostatic hypotension
Dizziness, drowsiness, headache, lack of energy, nausea, and palpitations,

Doxazosin shown to increase rate of congestive HF

28
Q

mixed alpha and beta blocker

used? adverse?

A

labetalol

Used in hypertension management (safe in pregnancy)

IV labetalol = rapid reduction in BP

no reflex increase in HR or cardiac output

AE: orthostatic hypotension

29
Q

central alpha2 agonist

A

clonidine

reduces sympathetic outflow
decrease in PVR and CO = lower BP

does not decrease renal blood flow

used in HTN management or crisis

30
Q

clonidine AE

A

Drowsiness, dry mouth, dizziness, headache & sexual
dysfunction occur commonly

Rebound hypertension may occur following abrupt
withdrawal

31
Q

methyldopa

A

central alpha2 agonist

decrease peripheral resistance and BP

does not decrease renal blood flow or CO

used for pregnancy induced HTN or HTN management

32
Q

AE of methyldopa

A

Sedation, drowsiness, dizziness, nausea, headache,
weakness, fatigue, sexual dysfunction, hypoprolactinemia

Nightmares, mental depression, vertigo (infrequent)

can develop of + coomb’s test (long term)

33
Q

direct vasodilators

A

Hydralazine / Minoxidil

not first line for HTN

direct acting on SM

Produce reflex tachycardia, increase plasma renin → Na+ & H20 retention

Major side effects can be blocked if combined with diuretic & b-blocker

34
Q

hydralazine

A

direct vasodilator

acts mainly on the arterioles

Used to treat pregnancy induced hypertension / preeclampsia

Used in management of hypertension as last-line therapy

35
Q

AE of hydralazine

A

Fluid retention & reflex tachycardia are common
Reversible lupus-like syndrome
Headache, nausea, sweating, flushing

Usually administered with b-blocker & thiazide

36
Q

minoxidil

A

direct acting vasodilator

Causes direct peripheral vasodilatation of arterioles

Oral treatment for severe-malignant hypertension
(refractory to other treatments)

37
Q

AE of minoxidil

A

Reflex tachycardia & fluid retention may be severe
(combine with loop diuretic & b-blocker)

Causes hypertrichosis (also used topically to treat
male pattern baldness)
38
Q

pulmonary HTN

A

An increase in blood pressure in the pulmonary
artery, pulmonary vein or pulmonary capillaries

Treatments
• Prostaglandins (epoprostenol)
• Inhibitors of endothelin synthesis and action
(bosentan)
• Vasodilators (sildenafil)
39
Q

Epoprostenol

A

synthetic PGI

Lowers peripheral, pulmonary, and coronary resistance

Adverse effects include flushing, headache, jaw pain,
diarrhea and arthralgias

40
Q

Bosentan

A

Nonselective endothelin receptor blocker

Blocks both the initial transient depressor (ETA) and the prolonged pressor (ETB) responses to endothelin

Pregnancy category X

41
Q

Sildenafil (vasodilator)

A

Inhibitor of phosphodiesterase 5 (PDE5)

Increased cGMP → smooth muscle relaxation

Adverse Effects: headache, flushing, dyspepsia,
cyanopsia

Contraindications: Nitrates

42
Q

Angina Pectoris

A

paroxysmal and usually recurrent attacks of substernal
or precordial chest discomfort caused by transient (15 seconds to 15 minutes) myocardial ischemia that is insufficient to induce myocyte necrosis

eitopatho:
consequence of the ischemia induced release of adenosine, bradykinin, and other molecules that stimulate sympathetic and vagal afferent nerves

43
Q

stable or typical angina

A

most common form - has transient recurrent attacks

associated with increased demand (PA)

Due to reduction of coronary perfusion because of fixed stenosis

Crushing or squeezing substernal pain, may radiate down the left arm

Relieved by rest and vasodilators

44
Q

prinzmetal or variant angina

A

Occurs at rest, awakens the patient from sleep

Associated with ST segment elevation on ECG, of
transmural ischemia

occurs due to coronary artery spasm producing transient squeezing chest pain

Responds to vasodilators

45
Q

unstable (crescendo) angina

A

Pain that occurs with progressively increasing
frequency and is precipitated with progressively less effort, often occurs at rest, and tends to be of more prolonged duration

Induced by disruption of plaque with superimposed thrombosis and possibly vasospasm

responds to vasodilators

46
Q

transmural infarctions

A

Involve the full thickness of ventricular wall in the distribution of a single coronary artery (STEMI)

Usually associated with acute plaque changes and
superimposed, completely occlusive thrombosis

Can also occur with Cocaine abuse

47
Q

Subendocardial infarctions

A

Limited to the inner one third or at most one half of the ventricular wall also called NSTEMI

Associated with diffuse stenosing coronary atherosclerosis or with prolonged hypotension
(Global/Circumferential infarctions)

May occur due to transient/partial arterial obstruction (Regional)

Less serious than transmural infarction

48
Q

histology of MI

gross?

A 
0-12 hours = wavy fibers and early coagulative necrosis 
not much (gross) change

12-24 = early neutrophil filtrate
dark mottling

1-3 days = heavy neutrophil filtrate
mottling (yellow/tan center)

3-7 days = macrophages appear
center softening / hyperemic border

7-10 = granulation tissue
max softening

10-14 days = collagen deposition
grayish discoloration

2 months+ = dense scar
scarring complete

49
Q

clinical features of MI

A 
1. chest pain 
retrosternal, crushing in nature 
may radiate 
the pain is persistent for >30 min (unlike angina) 
Not relieved by vasodilators or rest
  1. dyspnea
  2. rapid weak pulse
  3. diaphoresis, nausea and vomiting
  4. silent MI (common in elderly)
50
Q

Troponins (I and T) after MI

A

Most sensitive and specific marker

Normally not detectable in circulation

Rises in 3-12 hrs
peaks at 24 - 48 hrs. and persists for 7-10 days

51
Q

Creatine Kinase isoenzymes (CK-MB) after MI

A

A dimer composed of M & B subunits: MM, MB, BB

CK-MB: most specific for the heart among the CKs

Rises in 3-12 hrs
Peaks at 18 - 24 hrs. and disappears by 48 - 72 hrs.

Useful for detection of reinfarction

52
Q

complications of MI

A
  1. ischemic (Extension of the infarction, Reinfarction,
    Angina)
  2. Arrhythmic: most common cause of SCD
    (Myocardial irritability and conduction disturbances,
    Electrolyte imbalance, Hypoxia)
  3. Embolic:
    mural thrombi (common in LV).. can lead to systemic emboli
    stroke
4. mechanical 
contractile dysfunction
papillary muscle dysfunction 
myocardial rupture
ventricular aneurysm
  1. inflammatory
    pericarditis
    Dresslers’ syndrome (autoimmune)
53
Q

chronic ischemic heart disease

A

insidious onset of CHF in patients who have past episodes of MI or anginal attacks

patho:
cardiac decompensation owing to exhaustion of the
compensatory hypertrophy of non- infarcted viable myocardium or severe coronary obstructive disease → diffuse myocardial dysfunction

Arrhythmia, intercurrent MI are common and fatal

gross:
o Enlarged and heavy heart due to hypertrophy and dilation
o Discrete gray white scars of healed previous infarcts
o Patchy fibrous thickening of mural endocardium

histo:
o Myocardial hypertrophy
o Diffuse subendocardial vacuolization - Myocytolysis
o Scars of previously healed infarcts

CRS (16 decks)

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