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ED Primary Exam > Week 12 Pathology - Vascular, Coagulation and Haemodynamics > Flashcards

Week 12 Pathology - Vascular, Coagulation and Haemodynamics Flashcards

1
Q

What is oedema?

A

Increased fluid in interstitial tissue spaces

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2
Q

What are the different categories of oedema?

A

Increased hydrostatic pressure
Reduced plasma oncotic pressure (hypoproteinaemia)
Lymphatic obstruction
Sodium retention
Inflammation

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3
Q

What is the difference between transudate and exudate?

A

Transudate = increased hydrostatic pressure, leading to protein poor oedema (<30g/L protein)

Exudate = oedema occurring in inflammation due to increased vascular permeability (>30g/L protein)

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4
Q

What is an embolism?

A

Detached, intravascular mass (solid, liquid, gas) carried to a site distant from the point of origin

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5
Q

What factors increase risk of thrombosis?

A

Venous stasis/abnormal blood flow
Hypercoagulability
Endothelial damage

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6
Q

What are genetic causes of hypercoagulability?

A

Factor V Leiden (resistant to Protein C)
Protein C or S deficiency
Antithrombin III deficiency

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7
Q

What are secondary/acquired causes of hypercoagulability?

A

Nephrotic syndrome
Trauma/burns
Cancer
Prosthetic valves
Smoking

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8
Q

Describe the pathogenesis of atherosclerosis:

A
  1. Endothelial damage via turbulent flow, (as well as increased sheer forces, reduced NO production) causes endothelium damage and activation
  2. Endothelium when activated is more permeable to adhesion by leukocytes
  3. Accumulation of lipoproteins in vessel wall (LDL, oxidised)
  4. Monocytes attracted to the site, migrate and become macrophages –> foam cells –> cytokine release
  5. Proliferation of smooth muscle cells into the intimal layer, associated deposition of collagen and ECM
  6. Accumulation of lipids intracellular and in ECM
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9
Q

What is the morphology/structure of an atherosclerotic plaque?

A

Fibrous cap
Necrotic centre

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10
Q

What is the fibrous cap composed of?

What is the necrotic core composed of?

A

Macrophages, smooth muscle cells, elastin, collagen, lymphocytes

Cellular debris, cholesterol crystals, foam cells, calcium

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11
Q

How does plaque rupture cause thrombosis?

A

Subendothelial space exposed to blood, triggers coagulation process to cover wound, and platelets adhere to the sub endothelial collagen. Tissue factor of necrotic core contacts factor VII and initiates extrinsic pathway of coagulation —> generation of thrombus and potential to cause occlusive disease.

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12
Q

What are the different types of embolism?

A

Thrombus/thromboembolism
Fat embolus
Gas/N2 embolus
Amniotic fluid

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13
Q

What are the factors that influence the development of an infarct?

A
  1. Nature of blood supply, i.e. is it dual/multiple (liver, lungs) or single/end arterial (kidney, spleen)
  2. Rate of development, which influences whether time to develop collateral supply
  3. Vulnerability to hypoxia (neurons 3mins, myocytes 30 mins)
  4. Oxygen tension/content of blood (i.e. anaemia will lead to infarction sooner or if partial only in some circumstances)
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14
Q

What is the type of necrosis generally seen in infarction?

A

Ischaemic coagulative necrosis

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15
Q

What changes are seen/timeline of infarction on a histological level?

A

0-12 hours: cell death, no visible change
12-18 hrs: haemorrhage
24-48 hrs: inflammatory process at margins, phagocytosis of dead cells (macrophages, neutrophils)

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16
Q

What is shock?

A

Systemic hypoperfusion/failure to perfuse end organs adequately due to either decrease in cardiac output, or ineffective circulating blood volume

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17
Q

What are the 3 major categories of shock?

A
  1. Cardiogenic
  2. Hypovolaemic
  3. Distributive
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18
Q

What are causes of cardiogenic shock?

A

Myocardial damage (i.e. ischaemic)
Compression/tamponade
Arrhythmia
Obstruction to flow, i.e. PE

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19
Q

What are causes of hypovolaemic shock?

A

Trauma/haemorrhage
Burns
GIT losses

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20
Q

What are the different categories of distributive shock?

A

Septic shock
Anaphylaxis
Neurogenic shock (SCI, loss of vascular tone, venous pooling)

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21
Q

What is the pathogenesis of septic shock?

A

Bacterial endotoxins released into bloodstream when breakdown of bacteria cell wall –> LPS binds to plasma binding protein, which forms complex with CD14 molecules on leukocytes + endothelial cells –> initiation of inflammatory cascade

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22
Q

What are the 3 broad stages of shock?

A
  1. Initial non-progressive stage, with compensatory mechanisms that preserve perfusion (SNS, RAAS, baroreceptors, catecholamines)
  2. Progressive stage: widespread hypo perfusion and metabolic derangement –> lactic acidosis –> blunted vasomotor response –> arterial dilation and blood pooling –> decreased cardiac output and exacerbated cellular hypoxia and organ injury
  3. Irreversible stage: widespread cell injury, lysosomal leak, ischaemic bowel and perforation/translocation –> endotoxic shock, ATN and renal shutdown
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23
Q

Briefly, what is the cause of primary hypertension?

A

Changes in homeostatic mechanisms for blood pressure regulation due to overlapping syndrome of increased renal sodium retention and increased peripheral vascular resistance.

24
Q

What are the causes of secondary hypertension?

A
  1. Renal (RA stenosis, glomerulonephritis)
  2. Endocrine (Conn’s, Cushing’s, Phaeo, thyroid)
  3. Raised intracranial pressure
25
Q

Define aneurysm:

A

Localised abnormal dilation of structure, generally vascular structure (either in heart, vasculature)

26
Q

What’s the difference between true and false aneurysm?

A

True aneurysm contains all 3 layers of blood vessel wall (intimal, media, and adventitia)

False aneurysms generally a collection of blood between media and adventitia

27
Q

What is the pathophysiology of aneurysm formation?

A

Weakening of vessel wall due to endothelial damage (atherosclerotic plaque), HTN (increased pressure causing decreased perfusion to vessel walls of large arteries –> atrophy), or genetic structural disorders

28
Q

What is aortic dissection?

A

When blood enters the medial layer of the aortic wall through a tear or penetrating ulcer in the intima and tracks longitudinally along with the media, forming a second blood-filled channel (false lumen) within the vessel wall

29
Q

What is the Stanford Classification of aortic dissection?

A

Type A = involves any part of the aorta proximal to the origin of the left subclavian artery (A Affects Ascending Aorta)

Type B = type B arises distal to the left subclavian artery origin

30
Q

What is the DeBakey Classification of aortic dissection?

A

Type I = involves ascending and descending aorta
Type II = involves ascending aorta only
Type III = descending aorta only, commencing after origin of L) subclavian artery

31
Q

What is meant by the terms ‘primary’ and ‘secondary’ haemostasis?

A

Primary haemostasis = Platelet plug formation, ‘white thrombus’
Secondary haemostasis = stabilisation of platelet plug by fibrin linking, which is achieved via the coagulation cascade

32
Q

What is the lifespan of a platelet?

A

7 days

33
Q

Where is vWF synthesised, secreted, and how does it work?

A

Synthesised in endothelial cells, secreted into lumen, and attaches to sub endothelial collagen when exposed due to vascular injury

34
Q

What are the steps of primary haemostasis?

A
  1. Vascular smooth muscle contraction (caused by vascular injury, lasts 60 sec, caused by reflex mechanical response to injury, to reduce blood loss)
  2. Platelet aggregation/adhesion to site of injury via vWF receptors
  3. Platelet activation
  4. Platelet aggregation
35
Q

What is occurs in ‘platelet activation’?

A

Initiated by binding to vWF, activation includes:
- Conformational change
- Release of chemical messengers stored in platelets
- Change in shape of GPIIb/IIIa, to allow binding to other platelets

36
Q

What chemical messengers are released from platelets during activation, and their function?

A

ADP –> platelet activation
Thromboxane A2 –> vasoconstriction and platelet activation

37
Q

How does platelet aggregation occur?

A

Activated platelets bind fibrinogen, which allows platelets to cross-link between each other, forming a ‘somewhat unstable’ white thrombus

38
Q

What is the role of calcium in coagulation?

A

Binds to negatively charged activated platelets, allowing clotting factors to be able to adhere to cell membrane and perform enzymatic activity at site of injury

39
Q

What are the names of:
Factor I
Factor II
Factor III
Factor IV

A

I = Fibrin
II = Thrombin
III = Tissue factor
IV = Calcium

40
Q

How is the extrinsic pathway initiated?

A

III (tissue factor) forms a complex with factor VII (an example of ‘tens’) –> activates factor X in the common pathway

41
Q

What is the co-factor for factor X, and what does this complex do?

A

Factor V –> forms a complex with X to cleave prothrombin into thrombin (formation of factor II)

42
Q

What effect does thrombin (II) have?

A

Thrombin cleaves Factor 1 –> forms fibrin strands, and provides scaffolding for platelet plug

43
Q

What is the ‘tenase’ of the intrinsic pathway?

A

VIII + IX

44
Q

Once factor X is activated, what are the steps of the ‘common pathway’?

A

Factor Xa + Va causes formation of thrombin from prothrombin, which functions to cleave fibrinogen to fibrin

45
Q

What factor is responsible for clot stabilisation, and how is it activated?

A

Factor XIIIa, activated by thrombin

46
Q

What factors does Prothrombin time test?

A

2, 7, 9, 10 –> all the ‘carboxyl dependent’ factors which Vitamin K antagonists (warfarin) affect (Extrinsic pathway)

47
Q

What factors act to limit coagulation?

A

Anti-thrombin
Thrombomodulin
Protein C + S
Plasminogen

48
Q

How does antithrombin inhibit coagulation?`

A

Directly inhibits thrombin (along with other proteases 9, 10, 11, 12) and is activated by binding to heparin like molecules on endothelial cells

49
Q

How does thrombomodulin act to limit coagulation?

A
  1. Works in concert with Protein C + S to inactivate factors VIII and V (these are Vitamin K dependent as well)
  2. Thrombomodulin binds circulating thrombin to prevent its downstream effects
  3. Thrombomodulin + thrombin complex activates protein C, which complexes with Protein S
50
Q

How does plasminogen act to limit coagulation?

A

Activated by Factor XII, t-PA u-PA or streptokinase, lyses fibrin and fibrinogen, allows for breakdown of clot

51
Q

Complications of myocardial infarction?

A

Dressler syndrome (pericarditis)
Mitral valve chord tendinae rupture
Arrhythmia (AF, flutter, VT, heart block)
RE-infarction

52
Q

What is reperfusion injury?

A

Where oxygen supply is restored to previously hypoxic cells, which have undergone cellular injury.

These cells will have damaged membranes, cellular debris, which upon interactive with leukocytes will precipitate a mediator storms of cytokines –> can increase cycle of cellular damage and induce a distributive shock syndrome similar to septic shock

53
Q

What is Cor Pulmonale?

A

Right sided heart failure, causes by primary respiratory disease. Generally caused by RV having to pump against an elevated pulmonary arterial pressure.

54
Q

What are causes of Cor Pulmonale?

A

COPD
PE
Interstitial lung disease
CF
Primary pulmonary hypertension

55
Q

What are common causative organisms for IE?

A

Staph aureus
Staph epidermidis
Strep viridans
Enterococcus
HACEK Organisms

56
Q

What criteria is used for diagnosis of IE?

A

Dukes, either 2 major, or 1 major + 3 minor, or 5 minor:

Major:
1. Positive blood culture for typical organism x 2
2. Positive echo findings of echo
3. New valvular regurgitation

Minor:
1. Predisposition: predisposing heart condition or intravenous drug use
2. Fever: T> 38.0° C (100.4° F)
3. Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and Janeway lesions
4. Immunologic phenomena: glomerulonephritis, Osler nodes, Roth spots, and rheumatoid factor

ED Primary Exam (46 decks)

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