W7: Atherosclerosis II; SIHD; Angina; ACS; Stable CAD; Nutritional Aspects Flashcards

1
Q

Describe the pathophysiology of stable angina.

A

• chest pain associated MI but no necrosis and symptoms relieve on rest/ GTN Supply demand mismatch due to ↓flow to myocardium via coronary art.

* obstructive disease, abn flow, infarction

=> pallor, tachy, tremor, systolic murmur, plateau pulse, ++JVP, oedema

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2
Q

Stable angina diagnostic tests

A

lipids LFTs Thyroidfunct.

cxr: oedema
ecg: ST depr., t-inversion

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3
Q

Stable Angina Severity CCS

A

I - only exertional

II - slight limitation, +stressors walking and stairs

III - marked limitation walking and stairs -stressors

Iv - any activity!

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4
Q

Explain the importance of diagnosis and treatment of stable angina (Pharma)

A

PROPHYLAXIS > STATINS; >3.5mmol/L cholesterol ↓LDL

> ACE I: stabilise endothelium and ↓plaque rupture

> ASPIRIN/CLOPIDOGREL: ↓PT aggregation

SYMPTOM CONTROL

> BB: atenolol, bisoprolol fumarate

> CCB: amlodipine

> central CCB: diltiazem/verapamil (rate-limiting)

> alt: Ik Ch. Blocker: Ivabradine ↓Sinus node rate (long-acting nitrate) + Nitrate, GTN: altered release + Nicorandil (long-acting nitrate)

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5
Q

Explain the importance of diagnosis and treatment of stable angina (Surgical)

A
  1. PCI: ↑Blood Flow

* PTransluminal Coronary Angioplasty * Stenting

  1. CABG: multi-vessel - symptom alleviation only!
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6
Q

Beta Blocker Pharmacology

A

B1 & B2 Receptor Antagonists (never cardioselective for B1)

*block symp. ↓HR, contr, and systolic wall tension

=> ↑diastole time = ↑perfusion of subendothelium.

C-I: asthma (B2), HF (dependent on symp.); Bradycardia

=> alt: IVABRADINE

SFX = fatigue, brady, MI risk (therefore progressive reduction)

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7
Q

CCB Pharmacology

A

⇥L-CaCh. influx = -ve ionotropic

VASODILATOR TYPE = AMLODIPINE

CENTRAL HR LIMITING = VERAPAMIL

CI: post-MI and unstable ang.

SFX: ankle oedema, headache, flushing, palpitations

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8
Q

Nitrovasodilators Pharma. => effects

A

GTN, ISOSORBIDE MONONITRATE, ISOSORBIDE DINITRATE (sustained releases)

*nitrate tolerance = n-free period

➩ ↑cGMP = relaxation and ↓preload and O2 consumption and requirements

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9
Q

2nd Line Rx for Stable CAD

A

NICORANDIL: ATPsens-K+ channel activator INHIBITING Ca influx, similar to AMLODIPINE CCB, VASC SMC RELAXATION

IVABRADINE: ↓SINUS NODE = ↓HR (alt. to BB or combined w/ BB in poorly controlled)

RANOLAZINE: INHIBITS INa channels (persistent/late Na) = ↓Ca levels and ↓Heart wall tension and O2 requirements

(Abx. drug-drug)

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10
Q

Cholesterol-Lowering Agents

A

HMG CoA Reductase Inhibitors; Post-MI

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11
Q

Anti-PT

A

P2Y12R on platelets

Aspirin inhibits PT and Txane

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12
Q

Describe the pathophysiology of myocardial infarction.

A

• ↑Unstable coronary lesion; • ↑fat plaque = ↑thrombus => gives rise to new symptoms related to CORONARY ARTERIES

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13
Q

Know the clinical presentation of myocardial infarction.

A

Chest pain discomfort; weight; tightening +sweat, nausea, breathless grey clammy, general unwell, ↑venous pressure = STEMI

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14
Q

Describe the characteristic ECG changes and other diagnostic aids for myocardial infarction

A

ECG:

* STE, Q (3d) = complete occl.

* STE acute MI, LAD block = anterolateral STEMI

* ST depr., T inv., (no q) = partial* blocked RCA = inferior STEMI

* nil STE but opp effect on opp side (V1 -> V2) = posterior MI TROPONIN MYOGLOBINCK-MB

=> qualifying (1) +ve biomarkers

(2) ischaemia; ecg; coronary problems; new cardiac dmg.

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15
Q

MI ACS Classification

A

Type 1 = Primary coronary occl.

Type 2 = Non thrombotic ischaemia. Mismatch 2º to ischaemia.

Type 3 = sudden cardiac death,

STE Type 4 = reperfusion -related: a) PCI b) stent thomb.

Type 5 = CABG associated MI, Q waves

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16
Q

Significance of Q waves

A

Previous MI (3 Days) Deep & wide = previous MI Deep and narrow = ventr. hypertrophy (normal = <0.2s)

17
Q

Post MI Complications

A
  1. ARRYTHMIC

VF (common)

  1. MECHANICAL

tamponade, septal defect, papillary rupture

=> DEATH.

18
Q

STEMI Tx

A
  1. THROMBOLYSIS

*PCI (2hrs) w/ DOAC(hep; enoxapain; fonda.)

* BALLOON + STENT (cathlab)

  1. FIBRINOLYSIS

*ALTEPLASE (2-12hr): fibrin-spec; plasminogen convered to plasmin => enzymatic brkdwn

* STREPTOKINASE: systemic and non-fibrin-spec

+ DAPT (Clopidogrel + Aspirin)

!risk of bleeds and Hx!

19
Q

NSTEMI Tx

A

initial:
1. ASPIRIN: inhibit tx A2 prod; primary & secondary prevention (anti plt.)
+
FONDAPARINUX: inhibit Factor Xa (no need to monitor) s/cut injection (CI heparin) / HEPARIN: Xa and thombin inactivation; activated partial thromboplastin time (aPTT) monitoring!!
(antithrombin)

Use GRACE => low vs high
high: inclusion of angiography

  1. CLOPIDOGREL: P2YR antagonist inhibiting platelet aggr.

PRASUGREL
+ Aspirin
* CYP2C19 levels: genetic level efficacy. / TICAGRELOL, P2Y12 platelet inhibition / PRASUGREL

  1. ANGIOGRAPHY
  2. +BB if no C-I: indefinitine / VERAPAMIL | DILTIAZEM

(NICE 2024)

20
Q

Long-Term Considerations

A

* ACE I for MI/ACS

* BB for AMI, NSTEMI+ACS, STEMI, post-ACS

*STATINS post discharge

21
Q

Follow-Up & Non-Pharma in ACS

A

* ECG rpt.

* CARDIAC REHAB: lifestyle measures, exercise rehab.