CVS Flashcards

1
Q

causes of primary vs secondary hypertension

A
  • Primary (essential) hypertension (90-95% of cases)
    • Multitude of genetic and environmental factors
    • Modifiable risk factors
      • Stress, obesity, smoking, physical activity, heavy salt consumption
  • Secondary Hypertension (5-10% of cases)
    • Renal: Renal Artery Stenosis
    • Endocrine: Cushing’s syndrome, pheochromocytoma
    • Neurological: Increased intracranial pressure
    • Aortic: Aortic coarctation, atherosclerotic rigidity of
      aorta
    • Labile: psychogenic, stress-related
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2
Q

modifiable and non-modifiable risk factors of atherosclerosis

A
  • Constitutional (Non-modifiable) Risk Factors
    • Age
    • Gender (Male)
    • Family history
    • Genetics
  • Modifiable Risk Factors
    • Hyperlipidaemia
    • Hypertension
    • Diabetes
    • Smoking
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3
Q

consequences of atherosclerosis

A
  1. Ischaemia: Vessel thickening → Narrowed lumen → Poor tissue perfusion → Ischaemia
  2. Aneurysm formation: Loss of elasticity → Predisposition to aneurysm formation, rupture** and haemorrhage
  3. Endothelial changes → Predisposition to thrombosis
  4. Acute plaque change
    • Rupture/fissuring
    • Erosion/ulceration
    • Haemorrhage
    • Can lead to
      • MI
      • Cerebral Infarction
      • Aortic aneurysm
      • Peripheral vascular disease
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4
Q

causes of ischaemic heart disease

A
  • Atherosclerosis of coronary vessels (90-95%)
  • Embolism
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5
Q

differences between stable angina, prinzmetal (variant) angina, unstable angina

A
  • Stable Angina
    • Most common and typical form
    • Relieved by rest or vasodilators (e.g Glyceryl trinitrate)

Prinzmetal (Variant) Angina
- Uncommon form of episodial myocardial ischaemia
- Due to coronary arterial spasm; underlying mechanism unknown
- Responds to vasodilators

  • Unstable Angina
    • Increasingly frequent pain, prolonged duration (>20 minutes)
    • Occurs at lower levels of activity or at rest
    • Increased risk of MI
      • Also serves as a warning that an acute MI is imminent
    • Leads to severe but transient reductions in coronary blood flow
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6
Q

most common locations of myocardial infarction

A
  • Left anterior descending coronary artery: 40-50%
  • Right coronary artery: 30-40%
  • Left circumflex coronary artery: 15-20%
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7
Q

myocardial infarction symptoms and diagnosis

A
  • Symptoms
    • Severe, crushing central chest pain
    • Rapid weak pulse, profuse sweating (diaphoresis)

Diagnosis:
- ECG Changes
- Transmural infarcts:
-ST elevation MI (STEMI)
- Subendocardial infarcts:
- non-ST elevation MI (non-STEMI)
- Elevated cardiac enzyme levels
- Troponin I & T
- Creatine Kinase (CK-MB)

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8
Q

morphology and histology of myocardial infarction

A

Morphology:
12-24 hours:Pale with botchy discolouration
3-10 days: Hyperaemic border around yellow area
6-8 weeks: Fibrous scar - white

Histology:
12-24 hours: Infarcted muscle brightly eosinophilic, loss of nucleus, intercellular oedema
24-72 hours: Neutrophil infiltration
3-10 days: Granulation tissue appears
6-8 weeks: Dense collagenous scar (fibrous)

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9
Q

complications of myocardial infarction

A
  • Ventricles
    • Left Ventricular Failure → Congestive Heart Failure
    • Ruptured myocardium
      • Usually 2 to 4 days post MI
  • Conduction system
    • Arrythimas → Sudden cardiac death
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10
Q

cause of aortic stenosis

A

Aortic Valve Calcification
- age associated degeneration of aortic valve
- Most common of all valvular abnormalities

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11
Q

mitral regurgitation cause

A

Mitral Valve Prolapse
- Young women (7:1 F:M ratio)
- Cause is usually unknown

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12
Q

two types of infective endocarditis and the organisms that cause them

A
  • Subacute endocarditis
    • Streptococcus viridans – 75% of cases (normal flora of oral cavity)
    • Insidious infection of abnormal heart valves (includes congenital defects)
  • Acute endocarditis
    • S. aureus (IV drug abusers)
    • Highly virulent pathogenic organisms directly invade normal heart valves valve and cause rapid destruction
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13
Q

5 types of pericarditis and their causes

A
  • Serous Pericarditis
    • Causes: Non-infectious inflammatory diseases (immune-mediated, uremic, tumours)
  • Fibrinous Pericarditis (can overlap with serous)
    • Causes: post-myocardial infarction, rheumatic heart disease
  • Suppurative (purulent) Pericarditis
    • Causes: infections
  • Haemorrhagic Pericarditis
    • Causes: Direct spread or malignant metastases
  • Caseous Pericarditis
    • Causes: tuberculosis
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14
Q

clinical features of pericarditis

A
  • Sharp, more left-sided pain
    • Reduced when leaning toward, worsens when lying down
  • Radiation to shoulder tip, neck or jaw
  • Worse on lying down
  • Pericardial rub in 50% of patients
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15
Q

ecg signs of atrial fibrillation

A

No P waves, Fibrillatory baselines (f waves), Irregularly irregular R-R intervals

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16
Q

associations of atrial fibrillation

A

Associated with thyrotoxicosis, mitral valve disease, cardiac failure, ischaemic heart disease, hypertension, chronic lung disease, aging

17
Q

definition of heart failure

A

Heart failure is a clinical syndrome with current or prior
- Symptoms and or signs caused by a structural and/or functional cardiac abnormality (EF < 50%, moderate to severe ventricular hypertrophy etc)
- and corroborated by at least one of the following
- Elevated natriuretic peptide levels
- Objective evidence of cardiogenic pulmonary or systemic congestion by diagnostic modalities such as imaging

18
Q

heart failure diagnostic results

A
  • Chest X-Ray
    • Peri-hilar reticulo-nodular shadowing
    • Upper lobe diversion
    • Effusion
  • ECG
    • Different ECG patterns
  • Lab tests & Biomarkers
    • BNP or NT-proBNP
19
Q

what is the framingham criteria for heart failure diagnosis

A

Simultaneous presence of at least 2 major criteria or 1 major criteria in conjunction with 2 minor criteria

Major Criteria:
Paroxysmal nocturnal dyspnea
Neck vein distention
S3 gallop
Hepatojugular reflex

Minor Criteria:
Bilateral ankle edema
Nocturnal cough
Dyspnea on ordinary exertion
Tachycardia

20
Q

compensatory mechanisms of heart failure

A

-Compensatory measures in response to increased cardiac workload or impaired cardiac function
- Hypertrophy
- Increased sympathetic stimulation
- Frank-Starling mechanism: increased EDV dilates heart and causes increased cardiac myofiber stretching leading to increased CO
- Increased stimulation of RAAS

21
Q

causes of left sided heart failure

A
  • Volume overload
    • Valvular disease (aortic & mitral insufficiency)
  • Pressure overload
    • Systemic hypertension
    • Valvular disease (aortic stenosis)
  • Myocardial defect
    • Ischaemic heart disease (myocardial infarction)
  • Restricted filling
    • Pericardial effusion
22
Q

complications of left sided heart failure

A
  • Backward failure
    • Pulmonary venous hypertension
    • Pulmonary oedema (with associated symptoms of dyspnea, orthopnea, paroxysmal nocturnal dyspnea)
  • Forward failure
    • Decreased cardiac output & hypotension
23
Q

causes of right sided heart failure

A

Left-sided heart failure
- Most common cause of right-sided heart failure
- Due to resultant pulmonary hypertension which eventually places a burden on the right heart

24
Q

complications of right sided heart failure

A
  • Congestive hepatosplenomegaly
  • Effusions (ascites, pleural effusion)
  • Peripheral subcutaneous oedema
  • Venous congestion & hypoxia of organs (e.g. chronic passive congestion of liver)
    • hepatomegaly and splenomegaly
25
Q

complications of congenital heart disease

A
  • L / R Ventricular hypertrophy & subsequent HF
  • Pulmonary hypertension
  • Shunt reversal
    • In left to right shunt, problem of Eisenmenger Syndrome arises when there is shunt reversal
25
Q

4 cardinal features of tetralogy of fallot

A
  • Pulmonary stenosis
  • Right ventricular hypertrophy
  • Ventricular septal defect (VSD)
  • Overriding aorta