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Pathology > Chapter 4- Hemodynamic Disorders > Flashcards

Chapter 4- Hemodynamic Disorders Flashcards

1
Q

What is the most important cause of morbidity and mortality in western society?

A

Cardiovascular disease

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2
Q

What two pressures counteract each other within the vascular system?

A

Hydrostatic (BP)

Plasma colloid osmotic

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3
Q

What protein primarily drives colloid osmotic pressure?

A

Albumin

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4
Q

Under normal circumstances what direction is the net movement of fluid within the vasculature?

A

Small movement of fluid to interstitium (lymphatics drain)

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5
Q

What is edema?

A

Fluid in tissues

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6
Q

What are effusions?

A

Fluid build up within cavities

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7
Q

What is the difference between transudate and exudate?

A

Transudate- protein poor

Exudate- protein rich

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8
Q

What is anasarca?

A

Severe, systemic edema

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9
Q

What conditions can increase hydrostatic pressure?

A

DVT
CHF
Liver cirrhosis
Lymphatic obstruction

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10
Q

What conditions can reduce plasma osmotic pressure?

A

Nephrotic syndrome (albumin loss)

Reduced renal perfusion (reduced plasma volume)

Sodium retention (increased water retention)

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11
Q

What is subcutaneous edema dependent upon?

A

Gravity

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12
Q

What tissues does periorbital edema affect?

A

Loose connective tissue

Eg) eyelids

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13
Q

What is pulmonary edema characterized by?

A

Heavy lungs

Frothy, blood-tinged fluid

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14
Q

What are the risks associated with brain edema?

A

Cerebral blood flow impediment

Herniation

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15
Q

What is the morphology of generalized edema in the brain?

A

Narrow sulci, distended gyri

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16
Q

What does left sided heart failure cause?

A

Forces fluid back into lungs

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17
Q

What is the difference between hyperemia and congestion?

A

Hyperemia- active augmentation of blood flow due to arteriolar dilation, erythema

Congestion- passive fluid build up due to impaired tissue outflow, cyanosis

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18
Q

What are the two kinds of congestion?

A
  1. Systemic (CHF)

2. Local (isolated venous obstruction)

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19
Q

What is the difference between acute and chronic congestion?

A

Acute- distended vessels, grossly hyperemic organs

Chronic- focal hemorrhage, hemosiderin laden macrophages

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20
Q

What are heart failure cells?

A

Hemosiderin laden macrophages in the lungs

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21
Q

What does congestion in the lungs cause?

A

Interstitial edema and airspace transudates

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22
Q

How does congestion manifest in the liver?

A

Central vein and sinusoidal distension

Nutmeg liver

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23
Q

What is the function of hemostasis?

A

Maintenance of blood flow in a fluid state while inducing a rapid and localized hemostatic plug at the site of vascular injury

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24
Q

What are the phases of the hemostatic response?

A
  1. Vasoconstriction
  2. Primary hemostasis (plt plug formation)
  3. Secondary hemostasis (fibrin deposition)
  4. Clot stabilization and resorption (fibrin and plt contraction)
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25
Q

What is exposed upon vascular injury?

A

vWF

BM/ECM

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26
Q

What is the difference between adhesion and aggregation?

A

Adhesion- plts bind endothelium via vWF (GpIb)

Aggregation- plts bind each other via fibrinogen (GpIIb)

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27
Q

What starts the coagulation cascade?

A

TF exposure activates factor VII

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28
Q

What does the coagulation cascade result in?

A

Thrombin formation and the conversion of fibrinogen to fibrin

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29
Q

How do activated plts contribute to secondary hemostasis?

A

Thromboxane production- induces aggregation

Calcium binding- nucleation sites for coagulation factor complexes

30
Q

What counter regulatory mechanisms prevent the clot from over growing?

A

vWF and TF aren’t exposed at intact endothelium

tPA

Anticoagulant factors

31
Q

What is extravasation?

A

Leakage beyond the container

32
Q

What is hemorrhagic diathesis?

A

Unusual susceptibility to bleed due to coagulopathy

33
Q

What are the sizes of various hematomas?

A

Petechiae- 1-2mm

Purpura- <1cm

Ecchymoses- >1cm

34
Q

What deficiencies are associated with aggregation and adhesion?

A

Aggregation- Glanzmann thrombasthenia (GpIIb)

Adhesion- Bernard-Soulier syndrome (GpIb) and von Willebrand disease (vWF)

35
Q

PT is associated with which pathway of the coagulation cascade?

A

Extrinsic

36
Q

What are the functions of thrombin?

A
  1. Fibrinogen to fibrin conversion
  2. Induction of plt activation and aggregation
  3. Pro-inflammatory effects (protease activated receptors)

4! Anticoagulant when normal endothelium present

37
Q

What does intact endothelium produce to exert anticoagulant effects?

A

NO
Prostaglandin
tPA

38
Q

What is the function of plasmin?

A

Breaks down fibrin, interferes with polymerization

39
Q

Where does plasmin come from?

A

tPA cleaves plasminogen

40
Q

What is the function of alpha-2-antiplasmin?

A

Binds and inhibits free plasmin

41
Q

How does the endothelium prevent a hemostatic response when it is not required?

A

Plt inhibitory effects- plts are shielded from vWF and collagen (aggregation inhibited)

Anticoagulant effects- plts are shielded from TF (coagulation inhibited)

Fibrinolytic effects- tPA secretion

42
Q

What is the difference between primary and secondary hemorrhagic disorders?

A

Primary- involves plts or vWD

Secondary- coagulation factor disorders

43
Q

What are the components of Virchow’s triad that lead to thrombosis?

A
  1. Endothelial injury
  2. Abnormal blood flow
  3. Hypercoaguability
44
Q

How do you distinguish between an arterial and venous thrombi?

A

Arterial- retrograde growth, occlusive

Venous- grow in the direction of blood flow

45
Q

Where do mural thrombi occur?

A

Heart chambers or aorta

46
Q

How are post-mortem clots different from thrombi?

A

Lack lines of Zahn

Gelatinous (dark red portions and yellow chicken fat portions)

47
Q

What are vegetations?

A

Thrombi on heart valves

48
Q

What are the different types of vegetations?

A

Infective endocarditis- blood borne infection

Nonbacterial- sterile, hypercoaguable states

Sterile verrucous endocarditis/Libman Sacks (SLE)

49
Q

What are the possible fates of a thrombus?

A
  1. Propagation
  2. Embolization
  3. Dissolution
  4. Organization and recanalization
50
Q

What is phlebothrombosis?

A

Superficial thrombi in varicose saphenous veins

Rarely embolize

51
Q

What is Trosseau syndrome?

A

Tumour associated procoagulant disease

Cancer cells form migratory microvenous thrombi

52
Q

What veins are usually associated with DVT?

A

Popliteal
Femoral
Iliac

53
Q

What are two major causes of arterial thrombi?

A
  1. Atherosclerosis

2. MI

54
Q

What is DIC?

A

Widespread fibrin microthrombi due to diffuse thrombin activation

Can cause circulatory insufficiency

55
Q

What is an embolism?

A

Any mass carried by blood flow to a distant site

56
Q

What are some complications of emboli?

A

Vascular occlusion

Ischemic necrosis

57
Q

What is the most common form of embolism?

A

Pulmonary

58
Q

What are the different types of emboli?

A
  1. Pulmonary
  2. Systemic (left/arterial)- intracardiac mural thrombi
  3. Fat and marrow- bone fractures
  4. Air- decompression sickness
  5. Amniotic fluid
59
Q

What is Caisson disease?

A

Chronic form of decompression sickness, has emboli persist

60
Q

What is a paradoxical embolism?

A

Venous embolus passes through a defect in the heart and enters systemic circulation

61
Q

What can multiple pulmonary emboli lead to?

A

Hypertension and right ventricular failure

62
Q

What is an infarction?

A

Area of ischemic necrosis caused by occlusion of supply or drainage

63
Q

What is the most common cause of an infraction?

A

Arterial thrombosis/embolism

64
Q

What does venous thrombosis commonly cause?

A

Congestion

65
Q

How are infarcts classified?

A

Colour- red (venous) vs white (arterial)

Infection- septic (vegetation’s embolize)

66
Q

What factors influence the development of infarcts?

A

Anatomic pattern of vascular supply (dual circulation, anastomosing, end arterial)

Rate of occlusion

Vulnerability to hypoxia

Oxygen content of the blood

67
Q

What is shock?

A

Systemic hypoperfusion

68
Q

What are the three kinds of shock and their causes?

A
  1. Cardiogenic- low cardiac output
  2. Hypovolemic- low blood volume
  3. Associated with systemic inflammation- outpouring of inflammatory mediators
69
Q

What is the cause of septic shock?

A

Microbial injury leads to inflammatory response causing systemic vasodilation, hypercoaguable state and DIC

Multi-organ dysfunction

70
Q

What are the phases of shock?

A
  1. Non-progressive- reflex compensatory mechanisms
  2. Progressive- hypoperfusion, electrolyte disturbances
  3. Irreversible- damage too severe

Pathology (25 decks)

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