14. When the Cardiovascular System Goes Wrong! Flashcards

1
Q

What is Primary Hypertension?

A

Essential/ Idiopathic
“Of unknown medical cause”

Linked to: genetic predisposition, alcohol intake, obesity, lack of exercise, diabetes, intrauterine environment, etc

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2
Q

What is Secondary Hypertension?

A

“Of known medical cause”

  1. kidney disease - increase angiotensin II (vasoconstriction, expansion of extra cellular fluid).
  2. general endocrine disorders e.g. diabetes, Cushing’s, etc.
  3. adrenal medulla disease
    (phaeochromocytoma) - excessive adrenaline secretion
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3
Q

What are the treatments for hypertension?

A
  • Angiotensin II receptor blocker
  • Thiazide diuretics
  • Calcium-channel blocker
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4
Q

What do Angiotensin II receptor blockers do?

A

Inhibit the actions of angiotensin ll on aldosterone production
= preventing renal Na+/H2O absorption and blood volume increase, and prevents vasoconstrictor actions of angiotensin II.

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5
Q

What do Thiazide diuretics do?

A

They increase loss of Na+ and water in the kidneys

= decrease fluid volume = ↓ venous return, ↓cardiac output (CO)

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6
Q

What does an α-Andrenoceptor Antagonist (α-blockers) do?

A

Reduce TPR by inhibiting the action of noradrenaline.

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7
Q

What does an β-Andrenoceptor Antagonist (β-blockers) do?

A
  • decreases CO
  • decreases SNS activity centrally
  • decrease renin release = favourable secondary actions
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8
Q

Hypertension increases the risk of:

A
  • Atherosclerosis
  • Stroke/ Cerebrovascular Accident
  • Heart Failure
  • Renal Failure
  • Aneurysms
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9
Q

What is Atherosclerosis?

A
  • Major cause of death in developed countries
  • Can be treated by statins, fibrates and bile acid- binding resins
  • Caused by damage to endothelium
  • Fatty plaques are present on the blood vessel wall
  • Fibrous cap of a dense extracellular matrix narrows lumen of vessels & restricts blood flow
  • Lipid accumulation, macrophages, proinflammatory mediators, white cells, endothelial cells, smooth-muscle cells. Etc
  • Fragments of plaques can detach and become lodged in small vessels causing thrombosis.
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10
Q

What is Arteriosclerosis?

A
  • Hardening and thickening of artery walls
  • Loss of tissue elasticity as part of the natural ageing process
  • Narrowing of the vessel lumen in the absence of fatty plaques
  • Build up of calcium deposits in the vessel wall
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11
Q

Define Angioplasty

A

Procedure that involves the insertion of a balloon catheter to enlarge the opening in the artery.

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12
Q

What is a DVT?

A

Most commonly found in the leg vein; deep vein thrombosis (DVT).

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13
Q

What is pulmonary embolism?

A

A blood clot in the lungs: pulmonary embolism (PE).

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14
Q

Define Regurgitation.

A

Valve Defect

Inadequate closure leading to backflow & turbulence; followed by a decrease in cardiac output.

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15
Q

Define Stenosis.

A

Valve Defects.
Inadequate opening; obstructs flow.

Caused by: thickening of the valve, papillary muscle or cordae tendinae following disease. Rheumatic fever can cause mitral valve stenosis up to 20 years after infection.

Severe occlusion: → hypertrophy to maintain CO, but will lead to increased blood pressure → oedema and dilatation of heart chambers → heart failure

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16
Q

What is an Arrhythmia?

A

“Deviation of the heart’s normal sinus (SAN) rhythm”

May be asymptomatic or cause palpitations, dizziness, syncope, heart failure, or sudden death.

17
Q

What is Bradycardia?

Causes & Treatment

A

A slow rhythm <60bpm
Causes:
- slowed signal from the SAN = sinus bradycardia
- ‘‘pause” in the normal activity of the SAN - sinus arrest
- block of the electrical impulse due to SAN, AV or conducting tissue damage

Treatment
Artificial pacemaker

18
Q

What is Tachycardia?

A

A fast rhythm >100bpm

19
Q

What is Sinus Tachycardia?

A

Sinus Tachycardia

Inappropriate Sinus Tachycardia (1ST) can involve caffeine, amphetamines, or overactive thyroid gland on the SNS.

20
Q

What is Non-Sinus Tachycardia?

A

Results from the addition of abnormal impulses to the normal
cycle. Detected by an ECG. Caused by:-
○ Automaticity - enhanced pacemaker
○ Triggered Beats - early or delayed depolarization
○ Re-Entry Activity / Circus Activity - conduction profile defect

Uncontrolled twitching or quivering of muscle fibers (fibrils)
During ventricular fibrillation, blood is not removed from the heart
Sudden cardiac death results

21
Q

What is the Pathogenesis of Non-Sinus Tachycardia?

A

Congenital heart disease; electrocution accidents or injury to the heart; cardiomyopathies; heart surgery; ischaemia.

22
Q

What is LQT Syndrome?

A
  • Relatively rare - prevalence is about 1 in 5,000-10,000 persons, but potentially lethal.
  • A disease of the young; generally <25 years old
  • Many cases arise from defects in the ion channels that regulate ventricular action potentials
  • Cause spontaneous multiple depolarizations leading to ventricular arrhythmias
  • Produce a sustained abnormal rhythm.
23
Q

What is Chronic Heart Failure?

A
  • Cardiac output is inadequate, despite normal venous return - Congestive Heart Failure
  • Due to a decline in contractility and an inability to develop forceful contracture
  • Caused by damage to cardiac muscle e.g. CAD; additional work of the heart e.g. hypertension, or valve defects.
  • Causes breathlessness & fatigue
  • May affect the left, right, or both sides of the heart.
24
Q

What is Left Ventricular Failure?

A

Fluid will build up in the lungs due to congestion of the veins of the lungs

25
Q

What is Right Ventricular Failure?

A

Systemic capillary pressure increases and fluid will accumulate in the body, especially the tissues of the legs and abdominal organs.