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LU4 HS 202 E1 > Hemodynamic Disorders > Flashcards

Hemodynamic Disorders Flashcards

1
Q

___% lean body weight is due to water
___intracellular; ___ extracellular
___ %intravascular (in plasma)
The rest is in the interstitial space

A

60% lean body weight is due to water
2/3 intracellular; 1/3 extracellular
5% intravascular (in plasma)
The rest is in the interstitial space

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2
Q

Enumerate Starling forces

A
  1. Intravascular Hydrostatic Pressure

2. Plasma colloid oncotic pressure / Intravascular oncotic pressure

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3
Q

If imbalance is not corrected, there will be too much

for the lymphatics to clear, leading to

A

EDEMA

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4
Q

[Type of edema: Transudate/exudate : Protein Rich/Poor:Specific gravity]

Inflammatory: _________ : ________ : ________

A

Inflammatory: Exudate:ProteinRich:>1.020

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5
Q

[Type of edema: Transudate/exudate : Protein Rich/Poor:Specific gravity]

NonInflammatory: _________ : ________ : ________

A

NonInflammatory:Transudate:ProteinPoor:<1.012

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6
Q

Mechanisms of Edema

A
  1. Increased intravascular hydrostatic pressure
  2. Decreased plasma oncotic pressure
  3. Lymphatic drainage obstruction
  4. Increased Sodium and Water Retention
  5. Increased capillary permeability
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7
Q

In the ff conditions, decrease plasma oncotic pressure will be observed EXCEPT in

a. Congestive Heart Failure
b. Severe Liver Disease
c. Nephrotic Syndrome
d. Protein Malnutrition

A

A

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8
Q

In the ff. conditions, there is systemic increase in intravascular hydrostatic pressure except

a. Congestive Heart failure
b. Leg vein thrombosis

A

A; Leg vein thrombosis cause local increase

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9
Q

Lymphedema may be secondary to (3)

A

radiation, scarring post-surgery, filariasis

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10
Q

What does periorbital edema indicate

A

severe renal disease

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11
Q

accumulation of clear fluids in

the tunica vaginalis

A

Testicular hydrocoele

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12
Q

Local increase in the volume of blood within a

particular tissue

A

Hyperemia or congestion

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13
Q

Manifests with bluish discoloration from deoxygenated
blood; Morphology: Cyanosis;Brought about by obstruction along venous end; Prolonged congestion leads to tissue hypoxia and cell death

A

Congestion

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14
Q

Manifests with redness from oxygenated blood
Morphology: Erythema
Brought about by arteriolar dilatation (exercise)
Physiologic response to increased functional demand

A

Hyperemia

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15
Q

Hemosiderin-laden macrophages are a.k.a

A

heart failure cells

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16
Q

Characterized by scarring and fibrosis and heart failure cells

a. Acute congestion
b. Chronic congestion

A

B

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17
Q

______________
o Thickened; fibrotic alveolar septa
o Contain heart failure cells (hemosiderin-laden
macrophages; appear brown)

A

Chronic Passive Congestion of the Lung

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18
Q

morphology of CPC liver

A

Nutmeg liver with centrilobular necorsis

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19
Q

[size]

petechiae

A

1-2mmq

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20
Q

[size]

purpura

A

> 3mm

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21
Q

[size]

Ecchymoses

A

> 1cm

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22
Q

Occurs due to
o Trauma
o Vasculitides

A

Purpura

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23
Q

Occurs due to
o Chronic congestion
o Platelet disorders
o Clotting factor defects
o These are not only seen in the skin, it can also be
seen on organ surfaces like those of the heart.

A

Petechiae

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24
Q

Hypovolemic shock happens when how much of blood is lost?

A

20% of blood volume

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25
Q

ventricles supposedly filled with cerebrospinal fluid are

filled with blood

A

intraventricular hemorrhage

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26
Q 
hemorrhagic stroke (differentiate from ischemic 
stroke), neural deficits depend on area of 
hemorrhage
A

Intraparenchymal hemorrhage

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27
Q

usually hemorrhage of a meningeal artery (usually the middlemeningeal), manifests rapidly, unlike subdural
hematoma

A

Epidural hematoma

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28
Q

usually due to venous
rupture; there is a delay in the manifestation of
symptoms; may happen in the very young or
the very old

A

Subdural hematoma

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29
Q

What is a thrombosis?

A

abnormal clotting

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30
Q

Participants in normal hemostasis include

A

endothelium
platelets
coagulation factors

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31
Q

Steps in vasoconstriction in normal hemostatic process

A

Vascular injury ->neurogenic reflex + endothelin ->
transient vasoconstriction of the arteriole -> Exposure of
subendothelial tissue

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32
Q

Steps in primary hemostasis

A

Platelet adhesion
Platelet aggregation
Platelet secretion

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33
Q

Steps in secondary hemostasis

A

 Release of tissue factor (Factor III/Thromboplastin)
 Release of phospholipid complex
 Coagulation cascade – results in formation of
thrombin that converts fibrinogen to fibrin (forms secondary hemostatic plug)

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34
Q

Un-injured state of endothelium

a. anti-thrombic plug predominates
b. pro-thrombic plug predominates

A

A

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35
Q

Counter-regulatory mechanisms to stop plug

formation and necessary to stop clotting and prevent blocking of blood vessels

A

tissue plasminogen activator

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36
Q

[Pro-thrombotic Function of the Endothelium]

exposure attracts platelets

A

Sub-endothelial collagen

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37
Q

allows plateletcollagen binding, allows platelet-ECM binding

A

Von Willebrand factor (VIII)

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38
Q

what activates the extrinsic pathway

A

Factor III (tissue factor)

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39
Q

[Function ]

Prostacyclin (PGI2) and Nitric oxide (NO)

A

stops endothelial injury

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40
Q

give (2) anticoagulants that are involved in anti-thrombic function of the endothelium

A

Heparin-like molecules

Thrombomodulin

41
Q

binds to thrombin, stops pro-thrombotic properties, potent anticoagulant

A

Thrombomodulin

42
Q

FibronectinFactor V, Factor VII,Platelet factor 4, TGF-beta are degraded by

A

tPA

43
Q

What is the only known way to stabilize initial
platelet adhesion against high shear forces of
flowing blood ?

A

Von Willebrand Factor – glycoprotein-Ib interaction

44
Q

describe Bernard-Soulier syndrome

A

no Glycoprotein 1b receptor

45
Q

describe von Willebrand disease

A

no vWF

46
Q

What is the function of TXA2 and ADP

A

platelet aggregation

47
Q

Participation of thrombin and fibrin

a. Primary hemostatic plug
b. Secondary hemostatic plug

A

B

48
Q

[Disease]

Deficient/Inactive GpIIB, II-a

A

Glanzmann thrombasthenia

49
Q

Extrinsic pathway proteins

A

VII,X,V,II.I

50
Q

Intrinsic pathway proteins

A

XII,XI,IX,VIII,X,V,II,I

51
Q

What does Prothrombin Time test?

A

Protein function of extrinsic pathway

52
Q

How is PT assesed?

A

add TISSUE FACTOR and PHOSPHOLIPIDS to citrated plasma and initiate coagulation by adding exogenous CALCIUM

53
Q

What is Partial Thromboplastin Time for?

A

assess protein function of intrinsic pathway

54
Q

Enumerate Virchow’s Triad

A

Endothelial Injury
Blood Flow
Blood hypercoagulability

55
Q

What are the causes of endothelial injury

A 
Atherosclerosis
Hemodynamic stress (e.g. HPN)
Inflammation
Endotoxins
Hypercholesterolemia
Homocysteinuria
Trauma
56
Q

What is the end result of endothlial injury?

A

Exposure of subendothelial collagen matrix

57
Q

Give clinical settings where normal blood flow is altered

A 
Atherosclerotic plaques
Aneurysms
Infarcted myocardium
Polycythemia vera
Sickle cell anemia

Note: all leads to stasis except atherosclerotic plaques

58
Q

Mutant factor V making it resistant to cleavage by protein C is a.k.a

A

Leiden Mutation

59
Q

[Function]

Protein C and S

A

inactivate Va and VIIIa

60
Q

[Function]

Plasmin system

A

breaks down fibrin

61
Q

[Function]

Anti-thrombin III

A

inactivates thrombin, IXa, Xa, XIa, XIIa (9,10,11,12)a

62
Q

The ff can cause secondary hypercolaguability EXCEPT

a. Prolonged bed rest/immobilization
b. MI, atrial fibrillation
c. Disseminated malignancy
d. Smoking and obesity
e. Anti-phospholipid antibody syndrome (APAS)
f. AOTA
g. NOTA

A

G

63
Q

Easily detached

a. Thrombus
b. Postmortem clot

A

B

64
Q

Adherent to wall

a. Thrombus
b. Postmortem clot

A

A

65
Q

lines of ZAHN

a. Thrombus
b. Postmortem clot

A

A

66
Q

Firm consistency

a. Thrombus
b. Postmortem clot

A

A

67
Q

Takes the shape of the vessel

a. Thrombus
b. Postmortem clot

A

B

68
Q

Gelatinous

a. Thrombus
b. Postmortem clot

A

A

69
Q

Common sites of arterial thrombi

A

coronaries, cerebral, femoral arteries

70
Q

thrombi in heart chambers are called

A

mural thrombi

71
Q

embolus at the bifurcation of vessels, causing sudden death

A

saddle embolus

72
Q

T/F Venous thromboses, especially in superficial leg veins, commonly embolize

A

F; venous thrombosis usually embolize but not in superficial leg veins. usually involves deep veins

73
Q

What is Trosseau syndrome

A

inflammation of vein with formation and migration of thrombus (Migratory thrombophlebitis)

74
Q

What are the fates of a thrombus?

A 
Lysis
Propagation
organization
Canalization
Embolization
75
Q

[Identify] Not a disease, complication/endpoint of many

conditions Characterized by widespread thromboses – forms thrombus which disseminates throughout the body

A

Disseminated Intravascular Coagulation

76
Q

T/F DIC begins as a thrombotic disorder but ends up with serious bleeding

A

T

77
Q

How does consumptive coagulopathy in DIC lead to thrombocytopenia?

A

In disseminated intravascular coagulation, disseminated thrombi attract more and more platelets causing decrease in platelets in the blood.

78
Q

The ff can embolize

a. detached thrombi
b. fat
c. gas
d. tumor
e. AOTA

A

E

79
Q

What is the most important cause of sudden death in immobilized post-operative patient with Congestive Heart failure?

A

Pulmonary embolism due to DVT

80
Q

The ff increases risk of DVT and pulmonary embolism EXCEPT

a. Inactivity
b. Trauma
c. Surgery
d. Burns
e. Injury to vessels
f. Procoagulant substance from tissue

A

None of the above

81
Q

Give complications of Pulmonary embolism

A

Sudden death due to dyspnea
Right heart failure
Pulmonary infarction
Pulmonary hypertension

82
Q

Systemic embolism usually arise from

a. DVT
b. SVT
c. Mural thrombus

A

C

83
Q

Left atrium mural thrombi associated with

a. mitral stenosis
b. atrial fibrillation
c. myocardial infarction
d. a and b
e. b and c

A

D

84
Q

If emoboli lodge at branches of the carotid artery esp. middle cerebral artery, the result will be

A

cerebral infarction

85
Q

If emoboli lodge at branches of the mesenteric artery esp. middle cerebral artery, the result will be

A

hemorrhagic infarction of the intestine

86
Q

If emboli lodge at branches of the renal artery the result will be

A

Infarction of the renal cortex

87
Q

left-sided emboli that originate in the venous
circulation that gain access to the arterial circulation
through a right to left shunt, most often through a
patent foramen ovale or atrial septal defect

A

Paradoxical emboli

88
Q

[Identify]
 Fracture of long bones
 Particles of bone marrow and other fatty intraosseous
tissue that enter the circulation as a result of severe
fractures
 Lodge in lungs, brain, kidneys, and other organs

A

Fat embolism

89
Q

How much air is required for a gas embolism to have a clinical effect?

A

1cc

90
Q

Formation of gas bubbles in skeletal muscles

and joints

A

Bends

91
Q

chronic form of decompression

sickness, may lead to ischemic necrosis

A

Caisson disease

92
Q

What complications can arise from amniotic fluid embolism?

A

activation of coagulation leading to Disseminated Intravascular Coagulation and sudden death

93
Q

Causes of infarction

A 
arterial thromboembolism (99%)
vasospasm
external compression (tumor)
torsion (volvolus)
septic infarct
94
Q

True of red or hemorrhagic infarcts EXCEPT

a. arterial occlusions
b. happens in organs with loose tissue support - lungs
c. organs with dual circulation - small intestines, lungs
d. AOTA
e. NOTA

A

A

95
Q

White infarcts can most likely happen to (give more than one answer)

a. lungs
b. small intestine
c. spleen
d. kidneys
e. heart

A

c-e

96
Q

________ happens when infected heart valve vegetations embolize or when microbes seed the area of necrosis and infarct becomes an abscess

A

septic infarct

97
Q

Factors affecting development of infarcts

A

Nature of vascular supply
Rate of development of occlusion
Tissue vulnerability to hypoxia
Oxygen content of blood

98
Q

What are the causes of cardiogenic shock?

A

o Myocardial infarction
o Ventricular arrhythmias
o Extrinsic compression
o Outflow obstruction (e.g. saddle embolus)

LU4 HS 202 E1 (6 decks)

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