Coronary Heart Disease Flashcards

(32 cards)

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
Hypertension often remodels the heart such that...
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
treatment for HF( mainly HFrEF)
* Lifetsyle changes * sodium, weight, diet, exercise * we want to decrease cardiac workload * ACE inhibits, beta blockers, diuretic * increase cardiac contractility
27
ACE inhibitors mechanism of action and examples
* prevent ang II formation and inhib bradykinin breakdown * decreases peripheral resistance * increases sodium and water excretion captopril, enalapril, perindopril
28
ACE inhibitors used to treat...
Hypertension, heart failure as a first-line treatment and finally to preserve renal function in diabetes
29
adverse effects of ACEi
* 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
ARBs mechanism of action and examples
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
ARBs used to treat...
Hypertension, HF, Diabetic nephropathy and FOR PATIENTS INTOLERANT TO ACEi(who get the cough)
32
ARBs adverse events
same as ACEi ( hypotension, hyperkalemia, angioedmea)