Coronary Heart Disease Flashcards

1
Q

Acute presentation of CHD

A

encompassed by ACS and includes angina, AMI

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2
Q

Chronic aspect of CHD

A

Stable angina and heart failure

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3
Q

T/F

coronary arteries fill in systole

A

False, they fill in diastole

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4
Q

which zone of the heart is vulnerable to ischaemia

A

sub-endocardial zone

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5
Q

Acute Coronary Syndrome

A

any condition that causes sudden, reduced BF to the heart. Its leading symptom os chestpain

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6
Q

cardiac biomarkers of AMI

A

Creatine Kinase and Cardiac Troponin

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7
Q

Creatine Kinase

A

in both heart and skeletal muscle

exists as a dimer in 3 isoforms- BB, MM and MB which is heart specific

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8
Q

Cardiac Troponin

A

supersedes CK-MB as a biomarker

2 isoforms

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9
Q

Cardiac troponin release after AMI

A

4-10hrs after AMI troponin is detected, peaks at 12-48hrs and then normal for the next 4-10 days

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10
Q

Risk factors for angina

A

Hypertension, cholesterol, smoking

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11
Q

angina can be precipitated by

A

exertion, cold, stress, large meals

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12
Q

Treatment of angina

A
  1. modif of risk factors
    • smoking, obesity, hypertension, hyperlipidemia, diabetes mellitus
  2. surgical
    • angioplasty, stent
  3. pharmacological
    • for acute
      • tPA
    • for relatively stable forms of angina
      • B1- antagonist
      • Ca2+ antagonist
      • vasodilators
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13
Q

mechanisms of treatment of angina

A

increase coronary perfusion to increase O2 supply or decrease metabolic demand. btoh can be used too

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14
Q

Nitrovasodilators cellular mechanism of action for angina treatment ( chronic and acute)

A

Nitrate donates NO from its structure –> increase in Guanyl cyclase (an enzyme that converts GTP to cGMP–> increased cGMP–> increased relaxation

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15
Q

Nitrovasodilators systemic mechanism of action for angina treatment ( chronic and acute)

A

Venous dilation–> reduced venous pressure and preload and therefore a fall in cardiac O2 consumption

Arterial dilation–> reduced peripheral resistance and afterload and thus fall in cardiac O2 consumption

no effect of NO on cardiac and skeletal muscle

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16
Q

when are Nitrates used for treatment

A
  • acute attack of angina
  • immediate prophylaxis (. if someone knows that they’re going to be exerting themselves)( can take a short acting from of ntiric vasodilators)
  • chronically for stable angina
17
Q

limitations of NOs

A
  • decreased BP associated with reflex tachycardia
  • tendenacy to increase cardiac O2 consumption
  • tolerance can develop thus we have a nitrate free period for 8hrs every 24hrs
18
Q

Adverse events of Nitrates

A
  • Hypotension (fainting)(should not be combined with Viagra or similar drugs)
  • Tachycardia
  • Headache
  • Flushing
19
Q

Define

Heart Failure

A

CO unable to meet metabolic demands

20
Q

Cardiac remodelling in HF can be caused by

A
  • Acute heart failure
    • caused by events like trauma and AMI
  • chronic heart failure
    • increasing incidence due to better treatments at prolonging life
21
Q

Systolic dysfunction in HF( cardiac remodelling)

A

when there impaired contraction thus HF with reduced ejection fraction (HFrEF)

22
Q

Diastolic dysfunction in HF( cardiac remodeling)

A

contraction is ok but impaired filling so that HF has preserved ejection fraction (HFpEF)

23
Q

Prevalence of HFpEF assocated with

A
  • fibrosis
  • older populations
  • females
  • hypertensives
  • diabetes
24
Q

Infarct often remodels the heart such that…

A

there is thinning of the ventricular wall leading to a dilated ventricular space or systolic heart failure( HFrEF)

25
Q

Hypertension often remodels the heart such that…

A

there is hypertrophy in the heart and thus diastolic heart failure(HFpEF). Thus relaxation is impaired and there would be lower CO with exercise

26
Q

treatment for HF( mainly HFrEF)

A
  • Lifetsyle changes
    • sodium, weight, diet, exercise
  • we want to decrease cardiac workload
    • ACE inhibits, beta blockers, diuretic
  • increase cardiac contractility
27
Q

ACE inhibitors mechanism of action and examples

A
  • prevent ang II formation and inhib bradykinin breakdown
    • decreases peripheral resistance
    • increases sodium and water excretion

captopril, enalapril, perindopril

28
Q

ACE inhibitors used to treat…

A

Hypertension, heart failure as a first-line treatment and finally to preserve renal function in diabetes

29
Q

adverse effects of ACEi

A
  • common
    • cough because of increased bradykinin
    • headache
    • marked hypotension because of a dosing problem
    • hyperkalemia
      • if too high can lead to cardiac arthymia
  • infrequent
    • rash/itch, angioedema
  • contraindications
    • pregnancy
30
Q

ARBs mechanism of action and examples

A

Inhibits the AT1 receptor which stoped ang induced vasoconstriction and aldosterone output.

it results in decrease in TPR and increase in Na and water excretion

31
Q

ARBs used to treat…

A

Hypertension, HF, Diabetic nephropathy and FOR PATIENTS INTOLERANT TO ACEi(who get the cough)

32
Q

ARBs adverse events

A

same as ACEi ( hypotension, hyperkalemia, angioedmea)