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Cardiovascular > CV Pathology > Flashcards

CV Pathology Flashcards

1
Q

What is atherosclerosis ?

A

-Progressive chronic inflammation of arteries characterised by :

  • Inflammation(macrophages engulf LDL = Foam cells)
  • Fibrosis = connective tissue matrix formation
  • Lipid deposits (cholesterol in cells)
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2
Q

What are the atherosclerosis risk factor (who are at risk) (Aetiology) ?

A

Non modifiable
-Age 40-60, male, indigenous

Modifiable

  • Increase cholesterol
  • HTN
  • Smoking
  • Diabetes
  • Obesity
  • Metabolic syndrome
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3
Q

What is the Atherosclerosis pathogenesis (Mechanisms of disease) as a whole ?

A
  • Endothelial injury and activation (e.g. HTN or toxins)
  • Endothelial inflammation
  • Accumulation LDL due to endothelial damage = fatty streaks
  • LDL becomes oxidised, immune cells activated, macrophage engulfs and produces foam cells
  • Fibrosis occurs (Smooth muscle and calcium) = mature atheroma formation
  • Complicated plaque formation (rupture, thrombus then ACS)
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4
Q

Clinical complications of atherosclerosis?

A 
Heart - Angina and MI
Brain - Stroke
Kidneys - Renal failure
GIT - GI ischaemia or infarction
Lower extremities - Peripheral vascular disease
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5
Q

Investigations for atherosclerosis ?

A

Coronary angiogram

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6
Q

How do you manage the risk factors for atherosclerosis ?

A
  • Statins - Control cholesterol
  • ACE-I / B-Blockers
  • Diet and activity (obesity)
  • Decrease smoking and alcohol
  • Aspirin (control thrombosis)
  • Surgical interventions (Ballon angioplasty/stent bypass surgery)
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7
Q

What clinical manifestations of complicated plaques can occur in atherosclerosis ?

Hint: Think classic CHD

A
  • Plaque rupture (thrombosis) unstable
  • Narrowing/calcification - vessel fragility
  • Haemorrhage into plaque - narrowing of lumen
  • Fragmentation of plaque - distal emboli
  • Weakening of vessel wall - aneurysms

(Embolus, Thrombosis, Aneurysm, Haemorrhage)

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8
Q

Describe the Endothelium activation process in atherosclerosis ?

Hint: This causes the initial inflammation process

A
  • Increased cell permeability
  • Platelets adhere
  • Monocytes adhere and transform to macrophages
  • Blood LDLS enter and bind their apolipoprotein receptor which then causes oxidation
  • Oxidation of LDL causes inflammation
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9
Q

Describe the local inflammation process in atherosclerosis and fatty plaque formation?

Hint: Cycle feedback loop

A
  • Oxidised LDLS attract immune cells (cytokines, platelets, monocytes, smooth muscle etc.)
  • Macrophages engulf oxidised LDL which forms foam cells (lipid laden)
  • The building of plaque begins
  • Fatty streak gets more profound as foam cells unable to digest lipid content and then die
  • This causes cell debris and extracellular lipids
  • Oxidised LDL then starts positive feedback loop by attracting immune cells
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10
Q

Differences between atherosclerosis and arteriosclerosis ?

A

Arteriosclerosis is hardening of any medium or large arteries

Atherosclerosis is hardening of an artery due to an atheromatous plaque

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11
Q

What is a dilated cardiomyopathy ?

A

It is a progressive dilation & hypertrophy of the heart which causes systolic dysfunction

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12
Q

What are the proposed aetiologies of dilated cardiomyopathy ?

A
  • Commonly idiopathic
  • Chronic alcoholism
  • Post viral (myocarditis)
  • Genetic
  • Chemotherapy
  • Chronic anemia
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13
Q

What is the Pathogenesis / causes of dilated cardiomyopathy ?

A
  • Heart dilation and systolic dysfunction
  • Enlarged non elastic heart
  • AV Valve regurgitation (ejected blood re enters through valve)
  • Mural thrombi (can embolise)
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14
Q

What are the Clinical features of dilated cardiomyopathy ?

A

Nothing hugely standout

  • Any age
  • Presents congestive heart failure
  • Dyspnoea
  • Fatigue
  • Cough
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15
Q

What are Dilated cardiomyopathy complications ?

A
  • Mitral regurgitations
  • Arrhythmias
  • Possible thrombotic embolism
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16
Q

How would you investigate dilated cardiomyopathy ?

A
  • ECG
  • CXR
  • Echo (can see heart chambers and decreased ejection fraction)
17
Q

How does Hypertrophic Cardiomyopathy occur ?

A

A genetic variation in the muscle cell proteins that causes myofibril disarray an then subsequent muscle cell hypertrophy of ventricular walls / septum.

18
Q

Why is Hypertrophic Cardiomyopathy a diastolic dysfunction ?

A
  • Hypertrophied septum and ventricular walls causes smaller chamber sites
  • This decreases the filling capacity available
  • Which is diastolic potion of heart cycle
19
Q

Clinical features / complications of Hypertrophic Cardiomyopathy ?

A
  • Dyspnoea, orthopnoea
  • Syncope caused by ventricular outflow obstruction
  • Angina
  • Arrhythmias
  • Mural thrombus (Stroke)
  • Sudden death
20
Q

Investigations of Hypertrophic Cardiomyopathy ?

A

ECG
Echo (main one to see diastolic filling)
CXR

21
Q

Why would Beta-B help in Hypertrophic Cardiomyopathy treatment ?

A
  • Decreases contractility and HR
  • High HR + contractility reduces diastolic filling and therefore the ventricular chambers are smaller
  • There is now an increased intermittent ventricular outflow obstruction
22
Q

What are the aetiologies of Restrictive Cardiomyopathy ?

A
  • Amyloidosis (build of / deposit of amyloid protein in the myocardium
  • Sarcoidosis (development of granulomas inherit tissue)
  • Scleroderma (An AI condition that can result in changes to the skin, blood vessels, muscles, and internal organs)
  • Haemochromatosis (Increased iron deposits within the heart)
23
Q

What is the pathogenesis (follow on from initial cause) of Restrictive Cardiomyopathy and what may you seen upon an echocardiogram ?

A
  • Stiffness of the myocardium reduces the ventricular filling (diastolic dysfunction)
  • Consistent ejection fraction due to normal sized and volume ventricles
  • However, there is a reduced volume of blood being ejected as a whole
24
Q

Clinical features (S&S) of Restrictive Cardiomyopathy ?

A

Symptoms:

  • Cough, Dyspnoea
  • Fatigue (greatly with exercise)
  • Chest pain, palpitations

Signs:

  • Elevated Jugular venous pressure
  • Peripheral oedema due to blood being backed up
  • Arrhythmias
  • Lung crepitations
25
Q

Why would there be bi-atrial enlargement on Restrictive Cardiomyopathy ?

A
  • Heart chambers can’t expand and fill with blood

- Blood gets backed up and atrial enlarge to cope with backed up blood

26
Q

Investigations for Restrictive Cardiomyopathy ?

A
  • ECG
  • CXR
  • Echo (will show normal ejection fraction)
  • Myocardial biopsy - determines aetiology
27
Q

Why do your arteries harden during atherosclerosis ?

A
  • Smooth muscle cells migrate into plaque and cause a fibrous cap to contain the plaque
  • Smooth muscle also deposits calcium into plaque upon death signals from foam cells which causes the hardening of the mature plaque

Cardiovascular (3 decks)

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