Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CVS > IOD CVS Pathology I > Flashcards

IOD CVS Pathology I Flashcards

1
Q

Haemostasis?

A

Haemostasis occurs when there is damage to a blood vessel
it involves the formation of a solid plug from the constituents of blood
it stops loss of blood from the circulation at the site of injury
it is physiological (ie. it’s a good thing)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does haemostasis depend on?

A

close interactions between the vessel wall, platelets and the
coagulation cascade:
platelets stick to the wall
turbulent flow stimulates a chemical reaction in platelets to activate them
endothelial cells in the wall release cytokines and stimulate contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Process of haemostasis?

A

Endothelial injury leads to adhesion and aggregation of platelets
formation of a loose (primary) platelet plug
At the same time, exposure of tissue factor initiates the coagulation cascade  formation of insoluble fibrin
Fibrin stabilises the loose platelet plug to form a stable (secondary) platelet plug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

why is a cascade good?

A

exponential amplification of products

better control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

fibrinolysis?

A

The haemostatic plug is then broken down by activation of the fibrinolytic system

Fibrinolysis is activated by the same injury that initiates haemostasis

Plasminogen is converted to plasmin. Plasmin degrades insoluble fibrin to soluble products
more anti-clotting factors than pro-clotting factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

thrombosis?

A

Thrombosis occurs when there is inappropriate activation of haemostasis:
platelets and the coagulation system interact with the vessel wall to form a solid plug (=thrombus) in the blood vessel
the process overwhelms the capacity of the fibrinolytic system and coagulation inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

thrombus?

A

A thrombus is made up of the same components as a haemostatic plug ie. platelets, fibrin and red blood cells but is pathological

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

thrombus vs clot?

A

t-Composed of red blood cells, fibrin and platelets, flows in CVS in flowing blood
c-composed of rbcs a and fibrin no platelets-outside cvs in stationary blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Virchows triad?

A

Endothelial Injury Atherosclerosis Vasculitis
Direct trauma
Abnormal blood flow Turbulence
Stasis
Hypercoagulability Blood cells (too many)
Alterations in coagulation factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

most important risk factor in arterial thrombosis?

A

AS or endothelial injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

most important risk factor in venous thrombosis?

A

stasis and hypercoagulability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

causes of thrombi?

A 
smoking
malignancy-paraneoplastic eg small cell lung carcinoma
or SCC
protein c and s-vit K dep
Factor V leiden-mutation
OCP
Antiphospholipid syndrome
myeloproliferative
Haemoglobinuria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

complications of thrombi?

A

partial occlusion
complete occlusion
embolism distant site as undissolved material

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

which materials can occlude a vessel?

A 
TE
fat
DIC
air macro bolus/micro
amniotic fluid
tumour -LA myoxoma
infective endocarditis
cholesterol
foreign material
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

ischaemia?

A

tissue dysfunction due to interference with blood flow (supply or drainage) to a tissue. It is reversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

infarction?

A 
tissue death (necrosis) due to interference with blood flow (supply or drainage)
to a tissue. It is irreversible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

necrosis?

A

cell death due to a pathological process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

TE occlude where?

A

pulmonary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

TE in atrial/left side of feart occludes…?

A

systemic artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

AS?

A

chronic inflammatory process centred on the intima (endothelium) of large and medium sized arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

AS risk factors?

A

It is initiated by endothelial injury which is caused by well known risk factors including:
smoking
hypertension
diabetes
dyslipidaemia (abnormal lipoprotein levels ie. high ratio of LDL:HDL)/hypercholaemia LDL
FH
male

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

complications of AS?

A

Gradual enlargement of a stable plaque leading to luminal stenosis
Sudden disruption of a vulnerable plaque followed by thrombosis in the vessel lumen
Aneurysm formation
-rupture or TE
stable angina, ACS, TIA, CVA, Bowel ischaemia, renal artery stenosis and PVD

23
Q

what is plaque stability determined by?

A

smooth muscle cells (produce fibrous cap that stabilises the plaque)
inflammatory cells (digest the fibrous cap and kill smooth muscle cells
 destabilise the plaque)

24
Q

stable vs unstable plaques?

A

Stable plaques have a thick fibrous cap that is resistant to rupture. These stable lesions grow slowly in size over decades resulting in gradual stenosis
Unstable ‘vulnerable’ plaques contain more inflammatory cells and have a thinner fibrous cap that is prone to acute rupture

25
Q

definition stable angina?

A

An imbalance between O2 supply and O2 demand in the myocardium:
Exertion → ↑O2 demand by myocardium
→ mismatch O2 supply/demand
→ myocardial ischaemia
→ cardiac-type pain
Clinically:
– predictable cardiac-type pain (precipitated by exertion), relieved by rest
Cause: stenosis due to a stable plaque in a coronary artery

26
Q

ECG findings in stable angina?

A

ST elevation myocardial infarction (STEMI)
ST elevation in leads II, III and aVF
[there is also reciprocal ST depression in V1-3, I and aVL

27
Q

ACS definition?

A

Spectrum of clinical conditions when Sudden plaque disruption and thrombosis occurs
Partial or complete occlusion of the coronary artery at the site of disruption and marked spasm of the vessel

28
Q

Unstable angina and NSTEMI?

A

occur when there is partial occlusion of a coronary artery:
This results in ischaemia or infarction of the myocardium supplied by the affected coronary artery
Unstable angina and NSTEMI differ mainly in the severity of myocardial ischaemia:
– in NSTEMI the ischaemia is severe enough to result in release of cardiac troponins into blood

29
Q

How many ACS are each?

A

STEMI-40%

NSTEMI-60%

30
Q

STEMI?

A

occurs when there is complete occlusion of a coronary artery
ST elevation and raised troponin (greater than in NSTEMI)
There is transmural infarction of the myocardium supplied by the affected coronary artery

31
Q

Link to anatomy?

A 
RCA-RA, RV pacemaker inferior LV/MI 
ECG leads II, III, AVF
LCA-Lateral LV/MI 
ECG leads I, aVL, V5-6
LAD-anterior LV/MI
ECG leads V1-4
32
Q

body’s response to MI?

A

acute inflammation to myocyte necrosis

33
Q

timeline-0-12 hrs?

A

myocyte necrosis

34
Q

timeline-12-72 hrs

A

acute inflammatory response-neutrophils invade tissue

granulation tissue rim and solution of loose fibrous tissue and capillaries

35
Q

timeline 3-10 days?

A

hyperaemia, yellow to white fibrous scar as granulation tissue replaces cells

36
Q

timeline up to 6 wks?

A

scar formation due to collagen deposition-white scar

37
Q

Vfib?

A

It presents as cardiac arrest
It is probably related to K+ released from necrotic myocytes which induce arrhythmias in the hyper-excitable tissue around the infarct

Other arrhythmias may also occur as complications of MI (eg. bradycardia, ventricular tachycardia, supraventricular tachycardia)

Arrhythmias are more commonly seen in inferior MIs.

38
Q

inferior MI’s lead to arrhythmias as?

A

The right coronary artery supplies the inferior LV and the pacemaker
can lead to complete heart block

39
Q

what can rupture in an MI?

A

Rupture of the free wall of the ventricle → haemopericardium

→ cardiac tamponade

40
Q

what else can rupture in an MI?

A

IV septum-ventricular septal defect

41
Q

what muscle ruptures in an MI?

A

Rupture of the papillary muscle of the valve causing acute mitral regurgitation

42
Q

mural thrombus?

A 
thrombus inside ventricular wall
silent MI cause
endothelial injury
stasis
embolisation
43
Q

pericarditis?

A

A transmural infarct extends to involve the pericardium, inciting an inflammatory response
acute chest pain and STE and pleural rub

44
Q

ventricular aneurysms?

A

Complications include thromboembolism, arrhythmias and heart failure
NB. Ventricular aneurysms rarely rupture because they are composed of tough fibrous tissue

45
Q

Dressler’s syndrome?

A

Autoimmune pericarditis 2-10 months after full thickness MI

Risk of PE and pleural effusion

46
Q

shoulder hands syndrome?

A

left arm fatigue and atrophy due to lack of optimal loading

47
Q

spectrum of IHD?

A

see ppt

48
Q

How does chronic IHD lead to HF?

A 
low grade chronic ischaemia
progressive fine diffuse myocardial fibrosis
reduced contractile function
decompensation
CHF onset
49
Q

PE?

A

always due to transportation of thrombus in the bloodstream which then impacts in a pulmonary artery

The thrombus may originate in the:
leg (80%) – deep vein thrombosis
pelvis
arm
right ventricle
50
Q

Which system estimates a PE?

A

Two-level PE Wells score

see ppt

51
Q

signs of PE on ECG?

A

ECG sinus tachy, af, right bundle brunch block, s1 q3 t3

52
Q

ischaemic stroke pathophys?

A

Most commonly, an atherosclerotic plaque in an internal carotid artery ruptures and thrombus forms on the surface of the plaque
Part of the thrombus embolises and occludes one of the cerebral arteries resulting in a stroke

53
Q

AAA?

A

AS is single most important risk factor in developing an AAA

54
Q

Complications of AAA?

A

rupture
Thrombus formation
TE

CVS (30 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions