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
What is exposed upon vascular injury?
vWF BM/ECM
26
What is the difference between adhesion and aggregation?
Adhesion- plts bind endothelium via vWF (GpIb) Aggregation- plts bind each other via fibrinogen (GpIIb)
27
What starts the coagulation cascade?
TF exposure activates factor VII
28
What does the coagulation cascade result in?
Thrombin formation and the conversion of fibrinogen to fibrin
29
How do activated plts contribute to secondary hemostasis?
Thromboxane production- induces aggregation Calcium binding- nucleation sites for coagulation factor complexes
30
What counter regulatory mechanisms prevent the clot from over growing?
vWF and TF aren’t exposed at intact endothelium tPA Anticoagulant factors
31
What is extravasation?
Leakage beyond the container
32
What is hemorrhagic diathesis?
Unusual susceptibility to bleed due to coagulopathy
33
What are the sizes of various hematomas?
Petechiae- 1-2mm Purpura- <1cm Ecchymoses- >1cm
34
What deficiencies are associated with aggregation and adhesion?
Aggregation- Glanzmann thrombasthenia (GpIIb) Adhesion- Bernard-Soulier syndrome (GpIb) and von Willebrand disease (vWF)
35
PT is associated with which pathway of the coagulation cascade?
Extrinsic
36
What are the functions of thrombin?
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
What does intact endothelium produce to exert anticoagulant effects?
NO Prostaglandin tPA
38
What is the function of plasmin?
Breaks down fibrin, interferes with polymerization
39
Where does plasmin come from?
tPA cleaves plasminogen
40
What is the function of alpha-2-antiplasmin?
Binds and inhibits free plasmin
41
How does the endothelium prevent a hemostatic response when it is not required?
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
What is the difference between primary and secondary hemorrhagic disorders?
Primary- involves plts or vWD Secondary- coagulation factor disorders
43
What are the components of Virchow’s triad that lead to thrombosis?
1. Endothelial injury 2. Abnormal blood flow 3. Hypercoaguability
44
How do you distinguish between an arterial and venous thrombi?
Arterial- retrograde growth, occlusive Venous- grow in the direction of blood flow
45
Where do mural thrombi occur?
Heart chambers or aorta
46
How are post-mortem clots different from thrombi?
Lack lines of Zahn Gelatinous (dark red portions and yellow chicken fat portions)
47
What are vegetations?
Thrombi on heart valves
48
What are the different types of vegetations?
Infective endocarditis- blood borne infection Nonbacterial- sterile, hypercoaguable states Sterile verrucous endocarditis/Libman Sacks (SLE)
49
What are the possible fates of a thrombus?
1. Propagation 2. Embolization 3. Dissolution 4. Organization and recanalization
50
What is phlebothrombosis?
Superficial thrombi in varicose saphenous veins Rarely embolize
51
What is Trosseau syndrome?
Tumour associated procoagulant disease Cancer cells form migratory microvenous thrombi
52
What veins are usually associated with DVT?
Popliteal Femoral Iliac
53
What are two major causes of arterial thrombi?
1. Atherosclerosis | 2. MI
54
What is DIC?
Widespread fibrin microthrombi due to diffuse thrombin activation Can cause circulatory insufficiency
55
What is an embolism?
Any mass carried by blood flow to a distant site
56
What are some complications of emboli?
Vascular occlusion Ischemic necrosis
57
What is the most common form of embolism?
Pulmonary
58
What are the different types of emboli?
1. Pulmonary 2. Systemic (left/arterial)- intracardiac mural thrombi 3. Fat and marrow- bone fractures 4. Air- decompression sickness 5. Amniotic fluid
59
What is Caisson disease?
Chronic form of decompression sickness, has emboli persist
60
What is a paradoxical embolism?
Venous embolus passes through a defect in the heart and enters systemic circulation
61
What can multiple pulmonary emboli lead to?
Hypertension and right ventricular failure
62
What is an infarction?
Area of ischemic necrosis caused by occlusion of supply or drainage
63
What is the most common cause of an infraction?
Arterial thrombosis/embolism
64
What does venous thrombosis commonly cause?
Congestion
65
How are infarcts classified?
Colour- red (venous) vs white (arterial) Infection- septic (vegetation’s embolize)
66
What factors influence the development of infarcts?
Anatomic pattern of vascular supply (dual circulation, anastomosing, end arterial) Rate of occlusion Vulnerability to hypoxia Oxygen content of the blood
67
What is shock?
Systemic hypoperfusion
68
What are the three kinds of shock and their causes?
1. Cardiogenic- low cardiac output 2. Hypovolemic- low blood volume 3. Associated with systemic inflammation- outpouring of inflammatory mediators
69
What is the cause of septic shock?
Microbial injury leads to inflammatory response causing systemic vasodilation, hypercoaguable state and DIC Multi-organ dysfunction
70
What are the phases of shock?
1. Non-progressive- reflex compensatory mechanisms 2. Progressive- hypoperfusion, electrolyte disturbances 3. Irreversible- damage too severe