Patho & Pathophis Cardiovascular Flashcards

1
Q

What is CAD

A

Coronary Artery Disease (CAD)
This is where the arteries loose their elasticity and the lumen becomes narrowed due to atherosclerosis (where fatty deposits occlude arteries)

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2
Q

What is the difference between unstable and stable plaque

A

Fixed/stable - is a fixed obstruction meaning that it will not break off (mostly commonly associated with angina)

Unstable/vulnerable plaque - this can rupture causing platelet adhesion & thrombus formation (this is the cause of MI, stroke & SCD)

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3
Q

What can cause CAD to be asymptomatic

A

This is because of collateral circulation (smaller vessels enlarging over time to compensate for the reduction in blood flow of the larger vessels)

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4
Q

What is the time limit that the heart muscle can survive without proper perfusion.

A

10 secs you can have reversible changes.
Several mins - anerobic respiration occurs
Prolonged - tissue injury/death

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5
Q

What is the difference between IHD & ACS

A

IHD - Ischemic heart disease is the transient event of reoccurring episodes of ischemia due to stable atherosclerosis or vasospasm

ACS - Acute coronary syndrome is where the plaque is no longer stable

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6
Q

What are the different types of IHD

A
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7
Q

What are the differences of stable and unstable angina

A
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8
Q

What is a silent MI?

A

This is where the patient is experiencing ischemia of the heart but it is painless. This is unclear but could be as a result of less tissue being affected or episodes of ischemia being shorter. Patients may not experience pain because of autonomic neuropathy

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9
Q

What is Variant (Vasospastic/Prinxmetal) angina

A

This is caused by spasm of coronary arteries. The causes are not completely understood.
It usually occurs during rest/minimal exercise, mainly at night, and mainly with arrhythmias may occur with severe pain

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10
Q

What is unstable angina

A

This is where a thrombus breaches and causes ischemia in the coronary artery but it is not formed a complete blockage. it usually comes on with a rapid onset, lasts longer than 20mins, little to no effect with GTN.

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11
Q

What is a MI

A

This indicated heart tissue death because of hypoxia and ischemia.

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12
Q

What is the difference between NSTEMI & STEMI

A

A NSTEMI is where there is no ST elevation on the ECG and a STEMI is where there is obvious ST elevation on the ECG. Doctors determine if you have had a heart attack with doing a blood test looking for elevated troponin levels this is usually done by two blood tests with 1 at the time of the incident and another 1-4 hours later.

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13
Q

What is different with STEMI & NSTEMI

A
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14
Q

What is systoclic and diastolic heart faliure

A

Systolic heart failure - inability for the heart to contract (Impaired contractility causing decrease ejection fraction and CO)

Diastolic heart failure - inability for the heart to relax (Normal ejection fraction but impaired ventricular relaxation causing decreased ventricular filling decreased preload, SV & CO) This can because by hypertension leading to hypertrophy.

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15
Q

What is ejection fraction

A

Percentage of blood pumped out of ventricles each contraction, normal 55-70%

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16
Q

What categorizes right sided heart failure

A

This is where blood backlogs into right atrium and the peripheral circulation. This leads to peripheral oedema and JVD

17
Q

What are some symptoms of right sided heart failure

A

Peripheral oedema
JVD (jugular vein distortion)
Congestion of peripheral tissues
Liver pain (Blood backing up into the hepatic vein)
Aseities (Oedema in the abdomen)

18
Q

What can left sided failure cause

A

Pulmonary oedema (CPO)

19
Q

What compensatory mechanisms are triggered

A

Sympathetic nervous system

Because of poor perfusion to kidney Renin angiotensin - Aldosterone system

20
Q

Why does CPO occur

A

The failure of the left ventricle means that there is a bag log of blood in the pulmonary circuit. This increases the hydrostatic pressure in the alveoli. This pressure then exceeds the osmotic pressure in the alveoli which is keeping fluid out. With the increased hydrostatic pressure fluid gets pushed into the alveoli and therefore gas exchange can not take place as effectively

21
Q

What are the layers of the pericardium

A

Visceral - thin inner most layer adhering to the epicardium
Parietal - outer fibrous layer attached to great vessels

22
Q

What is pericarditis

A

This is inflammation of the pericardium most commonly from a bacterial infection.

This causes friction when the pericardial layers rub together.
This can be categorized with the fluid associated with the inflammation.
(Fibrinous - dry course deposits, Effusive - purulent, serous or hemorrhagic exudate)

23
Q

What is the patho of percarditis

A
24
Q

What happens in Chronic constrictive pericarditis

A

This results in a thick/stiff pericardium. The fibrous calcified develops between the visceral & parietal. Since the heart is now contained in a thick shell it can no longer properly fill leading to decreased SV & CO

25
Q

What is cardiac tamponade

A

This is where there is fluid, pus, or blood in the pericardial sack. The pressure then put more pressure on the heart. With each contraction more fluid goes in and therefore puts more pressure on the heart leading to reduced CO

26
Q

What is becks triad

A

This is a group of symptoms that indicate a cardiac tamponade
Muffled heart sounds
JVD
Hypotention

This is usually accompanied by a history of trauma.

And this results in cardiogenic shock

27
Q

What is an AA

A

An AA (Aortic Aneurysm)
Aneurysm: Abnormal localised dilation of blood vessel

Dissecting aneurysm: Tear in intimal layer, allowing blood to enter vessel wall

28
Q

What are some common causes of AA’s

A

Some common causes are atherosclerosis or vessel degeneration.
Hypertension can put more pressure on the walls of the arteries and weaken them