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Disease Processes > Cardiac Pathology > Flashcards

Cardiac Pathology Flashcards

1
Q

What is the difference between angina & a myocardial infarction (MI).

A

Angina —> caused by Transient ischaemia (temporary). Causes pain due to heart muscles anaerobically metabolising and producing lactic acid. Blood flow is restored hence, no necrosis or scarring

Myocardial infarction —> caused by acute ischaemia, leads to chronic heart failure. Necrosis and scarring in the myocardium

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2
Q

Describe the inflammation & repair that occurs following an MI.

A

Cause acute inflammation

Heals through organisation (in growth of granulation tissue and maturation into collagen
scar)

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3
Q

Briefly describe what complications can occur following an MI

A
  • Chronic heart failure

Due to organisation, loss of function

Cannot conduct electric impulses in the same way (causes arrhythmia)

Does not produce anti-coagulants, prone to thrombus

Not as strong, prone to aneurysm

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4
Q

Describe the causes of left- versus right-sided heart failure (HF).

A

Left sided heart failure causes:

  • Ischaemic heart disease.
    - Systemic hypertension.
    • Aortic/mitral valve disease.

Right sided heart failure causes:

  - Left sided heart failure 
  - Elevated resistance within pulmonary circulation
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5
Q

Backward effects and symptoms of Left sided failure

A
  • Reduced venous return from pulmonary circuit.
  • Pulmonary congestion- increase in hydrostatic pressure
  • Pulmonary oedema
  • Dyspnea/cough
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6
Q

What are the ‘forward’ effects of HF i.e. what compensatory mechanisms are triggered from a reduction in cardiac output?

A 
Same for both RHF and LHF
Renal response to reduced CO:
   Reduced renal perfusion.
   Activation of RAAS.
   Salt/water retention.
   Increased blood volume.
   Increased vascular resistance.
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7
Q

Describe some of the common causes & possible consequences of endocarditis.

A

Causes - Issue with the valves and innerlinings. Autoimmune, ageing, accumulation of calcium, infective endocarditis

Consequences - Leads to stenosis and incompetence. Therefore, congestive heart failure

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8
Q

Describe some of the common causes & possible consequences of pericarditis.

A 
Causes: Intrinsic HD
Disease in lungs, pleura, mediastinum, Generalised disorders
Extension of inflammation
Secondary deposits of cancer
radiation therapy
Autoimmune disorder
Myocardial infarction

Effects -
Pain
Restricts heart’s ability to move freely
Heart failure

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9
Q

What impact does ageing have on the cardiovascular system?

A
  • Fewer myocytes in older heart
  • Hypertrophy occurs
  • Stiff connective tissue
  • Regression of capillary beds
  • Atherosclerosis
  • Calcification of soft tissue
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10
Q

Stenosis

A

Valve does not open properly, increased resistance of flow. Disrupts preload

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11
Q

Incompetence

A

Valve does not close properly

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12
Q

Aneurysm

A

an abnormal, localised, dilatation of an artery or ventricle

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13
Q

Types of Hypertension

A

Systemic
Pulmonary
Portal

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14
Q

Systemic hypertension

A

Blood pressure throughout the systemic arterial circuit
Blood coursing under high pressure
Dialating artery leads to decreased blood pressure

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15
Q

Pulmonary hypertension

A

Right sided and in the pulmonary artery system

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16
Q

Portal Hypertension

A

In the two blood supplies of the liver

17
Q

Layers of the heart

A

Endocardium - inner lining of heart, produces anti-coagulants

Myocardium - muscle of the heart

Pericardium - outer part

18
Q

Systole

A

contraction of heart

19
Q

Diastole

A

relaxation of heart

20
Q

Cardiac Output

A

• CO = amount of blood ejected from the ventricles every minute
• CO = indicates cardiac performance
CO = HR x SV (stroke volume)

21
Q

Heart rate

A

beats per min

22
Q

Pre load

A

volume/ loading conditions after diastole

related to blood volume and venous return

23
Q

Afterload

A

force required to eject blood out of the ventricles

related to resistance (constriction of blood vessels)

24
Q

Eject fraction

A

% of blood pumped out the ventricles with every contraction (normal = 65%)

25
Q

Risk factors of Cardiovascular disease

A
  1. Smoking
    1. Male gender
    2. Increasing age
    3. Systemic hypertension
    4. Hyperglycaemia
  2. Genetics
26
Q

Atherosclerosis leads to

A
  • Reduced vascular elasticity
  • Increased vascular resistance
  • Swelling/bleeding in plaque
27
Q

Atherosclerosis —> vascular pathology

A
  1. Thrombus
    1. Embolus
  2. Aneurysm - due to weakening
28
Q

Angina

A

ischemia with blood flow restored. Heart muscles anaerobically metabolism, produces lactic acid (causes pain). No necrosis and no scarring

29
Q

Ischaemic Infarction

A
  • Sub-endocardial region most susceptible. inner 1/3 to 1/2.
  • Non-Stemi (depressed ST wave in ECG, partial blockage of coronary artery), smaller area than transmural. Some scar and muscle
  • Transmural - most common, full thickness of muscle wall has been lost to necrosis. Mostly scarring
30
Q

Most common artery involved in heart attacks

A

Right coronary artery - 30% of cases
Left anterior descending artery obstruction - 50%, artery of sudden death
Circumflex artery - 20%

31
Q

Complications of Myocardial infarction

A
  1. Anterior myocardial rupture in an acute infarct, through the muscular wall
    1. Rupture in the ventricular septum
    2. Complete rupture of a necrotic papillary muscle
    3. Exudate fluid build up in pericardial sac, impacts relaxation stage, causes pain
    4. Greater risk of thrombus formation
    5. Aneurysm due to differing pressures caused by scar tissues
32
Q

Congestive Heart Failure

A

Heart increases in size to meet demands of maintaining blood pressure and cardiac output

  • In response to pressure overload; hypertrophy of L.V. (increased wall thickness)
  • In response to volume overload: volume of chamber increased. Heart failure
33
Q

Impact of dysfunction on ejection fraction

A

• Systolic dysfunction – impaired contractility –>Decreased ejection fraction and CO

Diastolic dysfunction–> Normal ejection fraction but impaired filling – Decreased preload, SV and CO

34
Q

Backward effects and symptoms of right sided failure

A

Congestion of blood within venous system leads to:

  • Liver/spleen/kidney disease (pressure necrosis).
  • Oedema of bowel with production of ascites (fluid collects in spaces within the abdomen).
  • Peripheral oedema: swelling of ankles & legs a hallmark feature.

Passive Congestion —> increased hydrostatic pressure —> oedema
Venous system congestion

35
Q

Infective endocarditis

A
  • made up of connective tissue (avascular), does not have a good acute response
  • Bacteria sticks to valve and acute response does not occur
  • Antibiotics blocked by platelets and fibrins
  • Usually occurs due to age and drug use
  • Bacteria can embolise
36
Q

Valve disease: Rheumatic HD

A

Autoimmune disease

Straight to chronic

From Strep- A bacteria

Anti body cross reacts and attacks parts of the heart

Can lead to pericarditis, myocarditis, endocarditis

Predispose to Heart failure

37
Q

Cirrhosis

A

scarring in the liver

functional units are not functioning and creates resistance and congested

Disease Processes (13 decks)

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