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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
ventricles supposedly filled with cerebrospinal fluid are | filled with blood
intraventricular hemorrhage
26
``` hemorrhagic stroke (differentiate from ischemic stroke), neural deficits depend on area of hemorrhage ```
Intraparenchymal hemorrhage
27
usually hemorrhage of a meningeal artery (usually the middlemeningeal), manifests rapidly, unlike subdural hematoma
Epidural hematoma
28
usually due to venous rupture; there is a delay in the manifestation of symptoms; may happen in the very young or the very old
Subdural hematoma
29
What is a thrombosis?
abnormal clotting
30
Participants in normal hemostasis include
endothelium platelets coagulation factors
31
Steps in vasoconstriction in normal hemostatic process
Vascular injury ->neurogenic reflex + endothelin -> transient vasoconstriction of the arteriole -> Exposure of subendothelial tissue
32
Steps in primary hemostasis
Platelet adhesion Platelet aggregation Platelet secretion
33
Steps in secondary hemostasis
 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)
34
Un-injured state of endothelium a. anti-thrombic plug predominates b. pro-thrombic plug predominates
A
35
Counter-regulatory mechanisms to stop plug | formation and necessary to stop clotting and prevent blocking of blood vessels
tissue plasminogen activator
36
[Pro-thrombotic Function of the Endothelium] | exposure attracts platelets
Sub-endothelial collagen
37
allows plateletcollagen binding, allows platelet-ECM binding
Von Willebrand factor (VIII)
38
what activates the extrinsic pathway
Factor III (tissue factor)
39
[Function ] | Prostacyclin (PGI2) and Nitric oxide (NO)
stops endothelial injury
40
give (2) anticoagulants that are involved in anti-thrombic function of the endothelium
Heparin-like molecules | Thrombomodulin
41
binds to thrombin, stops pro-thrombotic properties, potent anticoagulant
Thrombomodulin
42
FibronectinFactor V, Factor VII,Platelet factor 4, TGF-beta are degraded by
tPA
43
What is the only known way to stabilize initial platelet adhesion against high shear forces of flowing blood ?
Von Willebrand Factor – glycoprotein-Ib interaction
44
describe Bernard-Soulier syndrome
no Glycoprotein 1b receptor
45
describe von Willebrand disease
no vWF
46
What is the function of TXA2 and ADP
platelet aggregation
47
Participation of thrombin and fibrin a. Primary hemostatic plug b. Secondary hemostatic plug
B
48
[Disease] | Deficient/Inactive GpIIB, II-a
Glanzmann thrombasthenia
49
Extrinsic pathway proteins
VII,X,V,II.I
50
Intrinsic pathway proteins
XII,XI,IX,VIII,X,V,II,I
51
What does Prothrombin Time test?
Protein function of extrinsic pathway
52
How is PT assesed?
add TISSUE FACTOR and PHOSPHOLIPIDS to citrated plasma and initiate coagulation by adding exogenous CALCIUM
53
What is Partial Thromboplastin Time for?
assess protein function of intrinsic pathway
54
Enumerate Virchow's Triad
Endothelial Injury Blood Flow Blood hypercoagulability
55
What are the causes of endothelial injury
``` Atherosclerosis Hemodynamic stress (e.g. HPN) Inflammation Endotoxins Hypercholesterolemia Homocysteinuria Trauma ```
56
What is the end result of endothlial injury?
Exposure of subendothelial collagen matrix
57
Give clinical settings where normal blood flow is altered
``` Atherosclerotic plaques Aneurysms Infarcted myocardium Polycythemia vera Sickle cell anemia ``` Note: all leads to stasis except atherosclerotic plaques
58
Mutant factor V making it resistant to cleavage by protein C is a.k.a
Leiden Mutation
59
[Function] | Protein C and S
inactivate Va and VIIIa
60
[Function] | Plasmin system
breaks down fibrin
61
[Function] | Anti-thrombin III
inactivates thrombin, IXa, Xa, XIa, XIIa (9,10,11,12)a
62
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
G
63
Easily detached a. Thrombus b. Postmortem clot
B
64
Adherent to wall a. Thrombus b. Postmortem clot
A
65
lines of ZAHN a. Thrombus b. Postmortem clot
A
66
Firm consistency a. Thrombus b. Postmortem clot
A
67
Takes the shape of the vessel a. Thrombus b. Postmortem clot
B
68
Gelatinous a. Thrombus b. Postmortem clot
A
69
Common sites of arterial thrombi
coronaries, cerebral, femoral arteries
70
thrombi in heart chambers are called
mural thrombi
71
embolus at the bifurcation of vessels, causing sudden death
saddle embolus
72
T/F Venous thromboses, especially in superficial leg veins, commonly embolize
F; venous thrombosis usually embolize but not in superficial leg veins. usually involves deep veins
73
What is Trosseau syndrome
inflammation of vein with formation and migration of thrombus (Migratory thrombophlebitis)
74
What are the fates of a thrombus?
``` Lysis Propagation organization Canalization Embolization ```
75
[Identify] Not a disease, complication/endpoint of many | conditions Characterized by widespread thromboses – forms thrombus which disseminates throughout the body
Disseminated Intravascular Coagulation
76
T/F DIC begins as a thrombotic disorder but ends up with serious bleeding
T
77
How does consumptive coagulopathy in DIC lead to thrombocytopenia?
In disseminated intravascular coagulation, disseminated thrombi attract more and more platelets causing decrease in platelets in the blood.
78
The ff can embolize a. detached thrombi b. fat c. gas d. tumor e. AOTA
E
79
What is the most important cause of sudden death in immobilized post-operative patient with Congestive Heart failure?
Pulmonary embolism due to DVT
80
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
None of the above
81
Give complications of Pulmonary embolism
Sudden death due to dyspnea Right heart failure Pulmonary infarction Pulmonary hypertension
82
Systemic embolism usually arise from a. DVT b. SVT c. Mural thrombus
C
83
Left atrium mural thrombi associated with a. mitral stenosis b. atrial fibrillation c. myocardial infarction d. a and b e. b and c
D
84
If emoboli lodge at branches of the carotid artery esp. middle cerebral artery, the result will be
cerebral infarction
85
If emoboli lodge at branches of the mesenteric artery esp. middle cerebral artery, the result will be
hemorrhagic infarction of the intestine
86
If emboli lodge at branches of the renal artery the result will be
Infarction of the renal cortex
87
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
Paradoxical emboli
88
[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
Fat embolism
89
How much air is required for a gas embolism to have a clinical effect?
1cc
90
Formation of gas bubbles in skeletal muscles | and joints
Bends
91
chronic form of decompression | sickness, may lead to ischemic necrosis
Caisson disease
92
What complications can arise from amniotic fluid embolism?
activation of coagulation leading to Disseminated Intravascular Coagulation and sudden death
93
Causes of infarction
``` arterial thromboembolism (99%) vasospasm external compression (tumor) torsion (volvolus) septic infarct ```
94
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
95
White infarcts can most likely happen to (give more than one answer) a. lungs b. small intestine c. spleen d. kidneys e. heart
c-e
96
________ happens when infected heart valve vegetations embolize or when microbes seed the area of necrosis and infarct becomes an abscess
septic infarct
97
Factors affecting development of infarcts
Nature of vascular supply Rate of development of occlusion Tissue vulnerability to hypoxia Oxygen content of blood
98
What are the causes of cardiogenic shock?
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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