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
What is Right Ventricular Failure?
Systemic capillary pressure increases and fluid will accumulate in the body, especially the tissues of the legs and abdominal organs.