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Year 5 - Pathology > HISTO: Cardiovascular > Flashcards

HISTO: Cardiovascular Flashcards

1
Q

True or false

“In the Western world atheroma causes half of all deaths and more morbidity and mortality that any other disorder”

A

True

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2
Q

What is shown?

A

Atherosclerosis

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3
Q

Define atheroscelrosis.

A

an arteriosclerosis characterized by atheromatous deposits in and fibrosis of the inner layer of the arteries

Atheroscelrosis is characterized by intimal lesions - atheroma (atheromatous plaques) - that protrude into vessel lumen

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4
Q
A
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5
Q
A
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6
Q

What are the characteristics of an atheromatous plaque?

A
  • Raised lesion
  • Soft lipid core
  • White fibrous cap
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7
Q

What are the risk factors for atherosclerosis?

A
  • Age
  • Gender
  • Genetics
  • Hyperlipidaemia
  • Hypertension
  • Smoking
  • Diabetes Mellitus
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8
Q

What kind of effect does having multiple RFs have on risk of atherosclerosis?

A

Risk factors have a MULTIPLICATIVE EFFECT e.g.

  • 2 risk factors increase the risk fourfold
  • 3 risk factors increase the risk sevenfold
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9
Q

Hwo does age affect atherosclerosis risk?

A

Atherosclerosis progressive between 40->60 years

incidence myocardial infarction (MI) X 5

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10
Q

How does gender affect atherosclerosis?

A

Premenopausal women protected (HRT no protection)

Postmenopausal risk increases (older ages greater than men)

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11
Q

How do genetics affect risk of atherosclerosis?

A

Family history most significant independent risk factor

Some mendelian disorders (eg Familial Hypercholesterolaemia)

Most multifactorial (genetic polymorphisms -> clustered risk factors HT, DM)

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12
Q

What is a modifiable risk factor for atherosclerosis? How is this risk modified?

A
  1. Hyperlipidaemia (Hypercholesterolaemia)
  • LDL – bad HDL – good
  • Diet rich in cholesterol/saturated fat – bad
  • Statins inhibit HMG-CoA reductase rate limiting enzyme in liver cholesterol synthesis - good
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13
Q

How does HTN affect risk of atherosclerosis?

A

Modifiable RF 2: HTN

  • Systolic & Diastolic important
  • Ht alone increases risk of IHD by 60%
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14
Q

How does smoking affect risk of athrosclerosis?

A
  1. Smoking
  • Definite risk in men, probable in women
  • Prolonged smoking doubles death rate from IHD
  • Stopping reduces risk considerably
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15
Q

Why is DM a RF for atherosclerosis?

A
  1. DM
  • Induces hypercholestrolaemia
  • Increases risk of atherosclerosis
  • 2 x risk IHD in DM if all other factors equal
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16
Q

Which of these is not a major RF for ischaemic heart disease?

  • Age
  • Male sex
  • High alcohol
  • Smoking
  • HTN
A

High alcohol consumption is not a major RF

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17
Q

What are some other RFs for atherosclerosis?

A
  • Inflammation
  • Hyperhomocyteinaemia
  • Metabolic syndrome
  • Lipoprotein (a)
  • Haemostasis (procoagulation)
  • Lack of exercise
  • Stress
  • Obesity (Ht, Dm, low HDL)
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18
Q

What is the pathogenesis of atherosclerosis? (Response to Injury Hypothesis)

A

Response to Injury Hypothesis

  1. Chronic inflammatory and healing response of arterial wall to endothelial injury
  2. Endothelial injury
    • Lipoprotien accumulation (LDL)
    • Monocyte adhesion to endothelium
  3. Monocyte migration into intima -> macrophages & foam cells
  4. Platelet adhesion
  5. Factor release
  6. Smooth muscle cell recruitment
  7. Lipid accumulation -> extra & intracellular, macrophages & smooth muscle cells
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19
Q

How does endothelial damage occur?

A

Early atheroma arises in intact endothelium

Endothelial dysfunction important – increase permeability, gene expression & adhesion

  • Haemodynamic disturbance -> dysfunction
  • Hypercholesterolaemia -> dysfunction
  • Inflammation -> vicious circle
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20
Q

What are the characteristics of smooth muscle proliferation in atherosclerosis pathogenesis?

A
  • Intimal smooth muscle proliferation
  • Some from circulating precursors – (have synthetic & proliferative phenotype)
  • ECM matrix deposition
  • Fatty streak -> mature atheroma & growth
  • PDGF, FGF, TGF-alpha implicated
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21
Q

What are the layers seen here in an artery?

A
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22
Q

What is the earliest lesion in atherosclerosis?

A

Fatty streak

  • Earliest lesion
  • Lipid filled foamy macrophages
  • No flow disturbance
  • In virtually all children >10yrs
  • Relationship to plaques uncertain
  • Same sites as plaques
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23
Q

What is seen here?

A

Fatty streak

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24
Q

What are the characteristics of an atherosclerotic plaque?

A
  • Patchy – local flow disturbances
  • Only involve portion of wall
  • Rarely circumferential
  • Appear eccentric
  • Composed of – cells, lipid, matrix
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25
What sites of an arterial tree does atherosclerosis usually occur in?
bifurfations and curvatures
26
What are the complications of an atheromatous plaque?
Can obstruct or rupture
27
At what % occlusion does stenosis usually occur in atheroma? What is the result?
\>70% occlusion demand\>supply OR diameter \<1mm ## Footnote **--\> Stable angina**
28
What type of plaque disruption is this?
Type II - eccentric ragged edges stenosis
29
What are 3 ways in whch atherosclerotic plaques can change?
* Rupture – exposes prothrombogenic plaque contents * Erosion - exposes prothrombogenic subendothelial basement membrane * Haemorrhage into plaque – increase size
30
Which plaques are most at risk of complications?
* Lots foam cells or extracellular lipid * Thin fibrous cap * Few smooth muscle cells * Clusters inflammatory cells * Stress - * Adrenaline increases blood pressure & causes vasoconstriction * Increases physical stress on plaque * Hence emotional stress increases risk of sudden death * Circadian periodicity to sudden death (6am-noon) * Vasoconstriction - reduces luminal size e.g. sue to adrenergic factors, platelet factors, reduced endothelial relaxing factors, mediators from perivascular cells
31
What characteristics of atherosclerosis are seen here?
Human coronary atherosclerotic plaque with a yellow core of lipid separated from the lumen by a fibrous cap. Opposite the plaque is an arc of normal vessel wall.
32
What is the leading cause of death for men and women worldwide?
IHD 7million/year
33
What does IHD refer to ?
Group of conditions resulting from myocardial ischaemia
34
What % of blood flow obstruction occurs fo MI to occur?
90% long silent progression prior to symptoms
35
What 4 conditions can IHD present as?
1. Angina pectoris 2. Myocardial infarction 3. Chronic IHD with heart failure 4. Sudden cardiac death.
36
What is the pathogenesis of IHD?
Insufficient coronary perfusion relative to myocardial demand Due to chronic progressive atherosclerotic narrowing of epicardial coronary arteries and variable degrees of superimposed plaque change, thrombosis and vasospasm
37
What % stenosis is require to cause chest pain during exercise vs at rest?
75% for pain precipitated by exercise 90% for pain at rest
38
After which level of stenosis can vasodilation no longer compensate for?
\>75%
39
Where do atherosclerosis usually occur in IHD?
* Plaques mainly in first few cm of LAD or LCX * Entire length RCA
40
What is acute coronary syndrome caused by?
Stable plaque becomes unstable Due to rupture, erosion, haemorrhage etc Generally leads to superimposed thrombus which increases occlusion
41
What is the difference between Prinzmental vs Stable vs Unstable angina?
Stable = comes on with exertion, relieved by rest, no plaque disruption Unstable = more frequent, longer, onset with less exertion or at rest Prinzmetal = uncommon, due to artery spasm
42
What is angina pectoris? Is there ischaemia?
Yes - transient ischaemia but **not producing myocyte necrosis**
43
What is MI? How common is it in the UK?
Death of cardiac muscle due to prolonged ischaemia Incidence 5/1000 per year UK (ST elevation)
44
What is the most common cause of death in postmenopausal women?
MI
45
What is the myocardial response to MI?
Myocardial blood supply compromised leading to ischaemia --\> * Loss of contractility within 60 seconds * Therefore heart failure can precede myocyte death * Potentially reversible * Irreversible after 20-30 minutes
46
Which artery is most commonly affected in MI?
LAD – 50%, ant wall LV, ant septum, apex RCA - 40%, post wall LV, post septum, post RV LCx - 20%, lat LV not apex
47
Which part of the myocardium does LAD supply?
* Ant wall LV * Ant septum * Apex
48
Which part of the myocardium does the RCA supply?
* Post wall LV, * Post septum * Post RV
49
What part of the myocardium does LCx supply?
* Lat LV * NOT apex
50
What is the gross pathology of the myocardium post-MI (1hr to 6 weeks)?
1. **Under 6 hours** – normal by histology (CK-MB also normal) 2. **6–24 hrs** loss of nuclei, homogenous cytoplasm necrotic cell death 3. **1-4 days** – infiltration of polymorphs then macrophages (clear up debris) 4. **5-10 days** removal of debris 5. **1-2 weeks** granulation tissue, new blood vessels, myofibroblasts, collagen synthesis 6. **Weeks-months** strengthening, decellularising scar
51
When does loss of nuclei, homogenous cytoplasm necrotic cell death occur post MI?
6–24 hrs
52
1
53
Which days post MI is this and what is seen?
MI 10-14 days granulation tissue, macrophages
54
How long after MI would this appearance occur?
\>2 months
55
What % of MI is asymptomatic?
10 – 15% asymptomatic Common in elderly & diabetes mellitus
56
Which type of MI will not cause usual ST changes?
Subendocardial infarct
57
What time frame do most MI deaths occur in?
50% of deaths within the first hour (most do not reach hospital)
58
Who has worse prognosis with MI?
Age Female DM Previous MI history
59
What is the cause or reperfusion injury post angioplasty? What are the clinical features?
Due to oxidative stress, Ca overload, inflammation * Arrhythmias common * Biochemical abnormalities last days -\> weeks * Thought to cause “stunned myocardium” – reversible cardiac failure lasting several days
60
What is a hibernating myocardium? Is it reversible?
Chronic sub lethal ischaemia -\> lowered metabolism in myocytes “hibernating myocardium” Reversed with revascularisation
61
What are the complications of MI? When do they usually occur?
* **Contractile dysfunction** – 40% infarct-\> cardiogenic shock with 70% mortality rate * **Arrhythmia** due to myocardial irritability & conduction disturbance * **Myocardial rupture** - free wall most common, septum less common, papillary muscle least common. (At mean 4-5days, range 1-10 days) * **Pericarditis** (Dressler syndrome) 2nd or 3rd day * **RV infarction** * **Infarct extension** – new necrosis adjacent to old * **Infarct expansion** – necrotic muscle stretches -\>mural thrombus * **Mural thrombus** * **Ventricular aneurysm,** late -\> thrombus, heart failure, arrhythmia, do not rupture * **Papillary muscle rupture** * **Chronic IHD** = progressive late heart failure
62
What is Dressler syndrome and when does it occur?
Pericarditis post-MI = Dressler syndrome 2nd or 3rd day post MI
63
Complication time frames:
64
What is the mortality with a year of MI?
* Total mortality = 30% in one year * 3-4% mortality per year after first
65
What is chronic IHD?
Progressive heart failure due to ischaemic myocardial damage. There may be no prior infarction.
66
What are the gross histopathological features of chronic IHD?
* Enlarged heavy heart, hypertrophied, dilated LV * Atherosclerosis * Maybe mural thrombi * Fibrosis (microscopic)
67
Define sudden cardiac death. What is the usual cause?
Unexpected death from cardiac causes in individuals without symptomatic heart disease or early (1hr) after onset of symptoms Usually due to lethal arrhythmia on background of IHD in most (90%). In most cases triggered by myocardial ischaemia.
68
What % of sudden cardiac death is caused by atherosclerosis?
90% due to marked atherosclerosis (of \>75% stenosis) 10% due to non atherosclerotic cause (long QT etc, some cases heritable)
69
What symptoms are usually caused by left vs right sided heart failure?
**Left sided** -\> SOB, pulmonary oedema **Right sided** -\> peripheral oedema
70
What side of the heart does congestive heart failure affect?
Left and right
71
What are the causes of cardiac failure?
* Ischaemic heart disease * Valve disease * Hypertension * Myocarditis * Cardiomyopathy * Left sided heart failure (Right)
72
What are the complications of cardiac failure?
* Sudden Death * Arrhythmias * Systemic emboli * Pulmonary oedema with superimposed infection
73
What are the histopathological features of cardiac failure including gross and microscopic?
**Gross**: Dilated heart, scarring & thinning of the walls **Microscopy**: fibrosis and replacement of ventricular myocardium
74
Name these types of cardiomyopathy.
Left to right 1. Normal 2. Dilated 3. Hypertrophic 4. Restrictive
75
What is the pathophysiology of dilated cardiomyopathy?
Progressive loss of myocytes --\> dilated heart
76
What are the causes of dilated cardiomyopathy?
1. **Idiopathic** 2. **Infective** – viral myocarditis 3. **Toxic**: alcohol, chemotherapy (adriamycin, daunorubicin), cobalt, iron 4. **Endocrine**– hyper-, hypo- thyroid, diabetes, peri-partum (?) 5. **Genetic** – haemochromatosis, Fabry’s, McArdle’s 6. **Immunological** – myocarditis incl. Viral (hypersensitivity component
77
What type of cardiomyopathy is shown?
Dilated
78
What is the most common cause of hypertrophic cardiomyopathy?
Familial in 50% - autosomal dominant inheritance with variable penetrance Mutation to the beta-myosin heavy chain
79
What is the gross histopathology of hypertrophic cardiomyopathy (HCM)?
Left ventricular hypertrophy Thickening of septum narrows left ventricular outflow tract
80
What is shown?
Hypertroophic cardiomyopathy (left ventricular)
81
What are the gross histopathological features of restrictive cardiomyopathy? What is it caused by ?
* Impaired ventricular compliance * Normal size heart – big atria Idiopathic or secondary to myocardial disease eg amyloid, sarcoidosis
82
What are the features of chronic rheumatic valvular disease? Which valve is most commonly affected?
Predominantly left-sided valves (almost always mitral) * Mitral \> Aortic \> Tricuspid \> Pulmonary * Mitral alone 48%, Mitral + aortic 42% Thickening of valve leaflet, especially along lines of closure Fusion of commissures Thickening, shortening and fusion of chordae tendineae
83
What is the cause of chronic rheumatic valvular disease?
Sequelae of earlier rheumatic fever predominantly affecting left-sided vlaves (mitral)
84
What is the most common cause of aortic stenosis?
Calcification of the aortic valve Affects patients aged 70-80yrs
85
What are the complications of calcified aortic stenosis?
* Impairs opening * Orifice is compromised * Outflow tract obstruction
86
What are the causes of aortic regurgitation?
* **Rigidity** - rheumatic, degenerative * **Destruction** - microbial endocarditis * **Disease of aortic valve ring** --\> dilatation --\>valve insufficient to cover increased area * Marfan's Syndrome * Dissecting aneurysm * Syphilitic aortitis * Ankylosing spondylitis
87
What is a true vs false aneurysm?
**True** - all layers wall **False** – extravascular haematoma
88
What are the causes of aneurysms?
**Causes: Weak wall** * **Congenital** eg Marfans * **Atherosclerosis** * **HTN**
89
What is shown?
**Aneurysm** * Atherosclerosis may weaken the wall of the aorta such that it bulges out to form an aneurysm. * This typically occurs in the abdominal portion below the renal arteries, as shown here. * Aortic aneurysms that get bigger than 6 or 7 cm are likely to rupture.

Year 5 - Pathology (89 decks)

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