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Pathology Term 1 > Week 2 - CVS > Flashcards

Week 2 - CVS Flashcards

MI/IHD, Atherosclerosis, Aneurysms

1
Q

What is the best way to salvage ischaemic myocardium and how?

A

Rapid reperfusion:

  • thrombolysis
  • PTCA +/- stenting
  • CABGs

*Keep in mind re-perfusion injury!

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2
Q

What is atherosclerotic plaque separation caused by?

A

Proteolytic enzymes

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3
Q

What are the 3 types of aortic dissection classifications?

A
  • Debakey I –> whole aorta
  • Debakey II –> ascending only
  • Debakey III –> descending only
  • Type A Stanford = Debakey I and II
  • Type B Stanford = Debakey III
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4
Q

What is the most important cause of aneurysms?

A

Atherosclerosis

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5
Q

Where are berry aneurysms common?

A

Cerebral arteries

  • haemorrhage (rupture)
  • stroke (thromboembolism)
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6
Q

What are complications of aneurysms?

A
  • mural thrombosis/embolism –> COMMONEST
  • fatal hemorrhage (if rupture)
  • surrounding organ compression
  • ischaemic organ damage!
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7
Q

What is the pathogenesis of aneurysms?

A

Cystic medial degeneration

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8
Q

What are vasa vasorum?

A

small blood vessels that supply wall of blood vessels

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9
Q

What is an aneurysm and its types?

A

Abnormal dilatation of an artery

  • True (all layers involved) –> saccular/berry; fusiform
  • False (not truly enlarged - escaped blood causes bulge) –> hematoma; dissecting
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10
Q

Which cardiac marker is best for lab evaluation of an MI?

A

Troponins I + T

  • increased within 2-4hrs
  • peak @48hrs
  • remain elevated for 7-10 days
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11
Q

What are the MI markers?

A
  • myoglobin
  • troponin I + T
  • CK + CK-MB
  • lactate dehydrogenase
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12
Q

What are chronic complications of MI?

A
  • chronic IHD - CHF
  • arrhythmias
  • ventricular aneurysm
  • mural thrombosis
  • papillary muscle contraction –> Mitral regurgitation
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13
Q

What are acute complications of MI?

A
  • heart failure
  • arrhythmias
  • CHF
  • cardiogenic shock
  • pericarditis
  • mural thrombosis
  • myocardial wall rupture –> tamponade (3-10days)
  • papillary muscle rupture –> mitral regurgitation
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14
Q

Which coronary arteries are commonly affected by infarction?

A
  • LAD (ant/septum) –> 50% (most commonly affected)
  • RCA (posterior) –> 30%
  • Left marginal (L circumflex) (lateral) –> 20%
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15
Q

What are the 3 types of myocardial infarcts?

A
  1. Sub-endocardial
    - partial obstruction
    - NSTEMI
  2. Transmural
    - complete obstruction
    - STEMI
  3. Multiple Small (Microscopic)
    - small vessels affected
    - normal ECG
    - gives rise to chronic IHD
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16
Q

Where in the artery is an atheroma located within?

A

Tunica Intima

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17
Q

Compare the 3 types of aneurysms

A
  1. Berry
    - from one side of artery producing a ‘fruit-like bulge’
    - common in cerebral arteries
  2. Fusiform
    - whole circumference of artery dilates due to AS plaque with inflammation weakening the arterial wall
  3. Dissecting
    - plaque ruptures in middle, blood rushes inside splitting wall into 2 layers (blood between tunica intima and media)
    - common in aorta; blood enters ruptured plaque
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18
Q

What are the complications of atherosclerosis?

A
  • ischaemia/infarction of organ supplied
  • progressive block
  • thrombosis/thromboembolism
  • aneurysm
  • rupture –> haemorrhage
  • MACROANGIOPATHY
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19
Q

What is the pathogenesis of atherosclerosis?

A
  1. Endothelial injury
  2. LDL entry and oxidation in intima
  3. Oxidised LDL causes adhesion and entry of monocytes/T-cells across endothelium via pro-inflammatory mediators
  4. Monocytes –> macrophages which consume large amounts of LDL –> Foam cells
  5. Foam cells release cytokines which cause inflammation and smooth muscle cell/fibroblast proliferation –> fibrous cap formation
20
Q

Compare the 2 types of plaques

A

Unstable Plaque (10%):

  • large lipid core
  • severe inflammation (IFN-gamma) –> M1
  • thin fibrous cap
  • low SMC
  • rapid change
  • pain at rest (unstable angina)

Stable Angina (90%):

  • small lipid core
  • low inflammation (IL-4/IL-13) –> M2
  • thick fibrous cap
  • high SMC
  • slow progressive
  • pain on exertion (stable angina)
21
Q

True or False?

Unstable plaque cannot regress back to stable plaque

A

False

  • atheroma plaque = balance between inflammation and healing
  • increased inflamm. = unstable
  • increased healing = stable
  • with modifications of risk factors, unstable plaque can –> stable (and vice versa)
22
Q

What are the 2 pathways of macrophage activation?

A
  1. Classic Path
    - Th1 –> IFN-gamma –> M1
  2. Alternate Path
    - Th2 –> IL-4/IL-13 –> M2
23
Q

Where does plaque accumulation start in BVs and why?

A

At the bifurcation of arteries

- due to increased trauma here from blood hitting this area with increased force

24
Q

What are the risk factors for atherosclerosis?

A
  1. Non-modifiable
    - age, male, family history, genetics
  2. Modifiable
    - hyperlipidemia, HTN, smoking, DM, lifestyle
  3. Additional
    - CRP, hyperhomocysteinemia, metabolic syndrome, pro-coagulants
25
Q

What are the clinical manifestations associated with unstable plaque?

A
  • unstable angina
  • acute MI
  • sudden cardiac death
26
Q

What is the earliest microscopic feature in atheroma formation?

A

Foam cells

27
Q

Outline gross and microscopic changes to heart post-MI

A 
Gross:
<4hrs - none
4-12hrs - occasional dark mottling
12-24hrs - dark mottling
1-3days - mottling + yellow tan centre
3-7days - pale/yellow centre with hemorrhagic border
7-10days - max. yellow tan + red margins
1-3wks - red-grey depressed borders, thin (loss of tissue mass)
>3wks - small silvery white scar

Micro:
<4hrs - none (loss of LDH/glycogen - special stain*)
4-12hrs - oedema, hemorrhage, beginning of necrosis
12-24hrs - coagulative necrosis, contraction bands, oedema, hemorrhage, neutrophils, pyknosis of nuclei
1-3days - necrosis, loss of nuclei, interstitial neutrophils
3-7days - dead myocytes, dying neutrophils, phagocytosis by macrophages
7-10days - macrophages, granulation tissue
1-3wks - no muscle, new BVs, granulation, fibroblasts (collagen), macrophages
>3wks - dense fibrosis (collagen scar), NO inflammation

28
Q

What is granulation tissue?

A

Collective term for structure composed of new BVs and collagen fibres formed in the healing process approximately 7-10 days post-MI

29
Q

When is the most dangerous time during healing post-MI for rupture of ventricular walls to occur and why?

A

Between 3-7days
-macrophages are present and begin phagocytosing dead debris (neutrophils and dying myocytes) –> thus potentially thinning the wall to the point of rupture –> CARDIAC TAMPONADE

30
Q

What is Metabolic Syndrome X?

A

Collection of disorders that occur together and increase the risk of developing T2DM and CVD. Dx. is made when a person has >/= 3 of:

  • central obesity
  • HTN
  • increased triglycerides
  • increased LDLs/decreased HDLs
  • increased BSLs
31
Q

Where do coronary arteries arise from and when do they receive blood supply?

A
  • from behind the the cusps of aortic valve

- receive blood during DIASTOLE, from L+R coronary sinuses

32
Q

What are gross and microscopic features of chronic IHD?

A

Gross:

  • LV dilatation and hypertrophy
  • myocardium will show multiple grey-white scars (old MIs)
  • evidence of atherosclerosis
  • patchy white scars in endothelium –> mural thrombi

Micro:

  • myocyte hypertrophy and vacuolisation
  • fibrosis
33
Q

What is the commonest cause of clinical angina?

A

Decreased coronary blood flow (90%)

-90% of this is atherosclerosis

34
Q

What are contraction bands and when do they occur?

A
  • bright, eosinophilic bands of condensed contractile proteins that run at right angles to the long axis of the cardiac myocyte
  • occur after acute MI (12-24hrs)
35
Q

What are the stages of AS plaques?

A

Foam cells –> fatty streak –> intermediate lesion –> atheroma –> fibrous plaque –> complicated lesion/rupture

36
Q

What is cystic medial degeneration?

A
  • elastic fibre degeneration
  • small cyst-like spaces of necrosis in media
  • commonest pathogenesis of aortic aneurysms
  • caused by atherosclerosis
  • separation of media tissue by elastic fragmentation forming cleft-like spaces in media
37
Q

What is IHD?

A

Primarily a consequence of inadequate coronary perfusion relative to myocardial demand –> angina pectoris

38
Q

What % of the coronary artery is required to be occluded to cause symptoms?

A
  • <70% = asymptomatic
  • > 70% = critical stenosis (symptomatic on exertion - stable angina)
  • > 90% = symptomatic at rest - unstable angina
39
Q

What is collateral perfusion?

A

Remodelling of coronary vessels over time to provide compensatory blood flow for at-risk areas

40
Q

After how long does loss of function and necrosis occur with lack of O2?

A

loss of function –> 1-2mins

necrosis –> 20-40mins

41
Q

What is the pathogenesis of ischaemic pain in cell injury/inflammation?

A

-decreased oxidative phosphorylation = decreased ATP = increased anaerobic glycolysis = increased lactic acid = decreased pH –> PAIN

42
Q

What are the CXR findings of cardiac failure?

A 
A - alveolar bat wings
B - kerley B lines
C - cardiothoracic ratio > 50%
D - dilated upper lobe vessels
E - pleural effusion
43
Q

What is Nutmeg liver?

A

Passive venous congestion of liver, characteristic of RHF

44
Q

Give examples of ischaemic vs. non-ischaemic causes of cardiac pain.

A

Ischaemic:

  • stable angina
  • unstable angina
  • MI

Non-ischaemic:

  • myocarditis
  • pericarditis
  • aortic dissection
45
Q

Outline management process for ACS pts.

A

M - morphine/fentanyl (analgesia)
O - oxygen if hypoxic
N - nitrates if pain not controlled by opioids
A - aspirin ASAP
L - leads (ECG)
I - IV access + blood tests taken (cardiac markers)
S - streptokinase (+ other thrombolytics)
A - anti-platelet therapy as required

*Re-perfusion Tx. if pts. present within 12hrs of symptom onset

Pathology Term 1 (6 decks)

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