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Disease Mechanisms > Ch. 4: Hemodynamic Disorders, Thromboemboylic Disease, and Shock > Flashcards

Ch. 4: Hemodynamic Disorders, Thromboemboylic Disease, and Shock Flashcards

1
Q

define effusion

A

accumulation of fluid in cavities

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2
Q

define transudate

A

fluid deficient in proteins

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3
Q

define exudate

A

fluid rich in proteins

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4
Q

define pitting edema

A

accumulating of low protein fluid in the interstitial space
*tissue pits when pressure is applied

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5
Q

define dependent (nonpitting) edema

A

accumulation of high protein fluid in the interstitial fluid
*tissue does not pit when pressed on because the proteins prevent the fluid from moving

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6
Q

disorders of what three systems can cause edema and effusions

A

cardivascular, renal, and hepatic

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7
Q

what causes impaired venous return

A

DVT
widespread heart failure
can cause increased hydrostatic pressure

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8
Q

what causes increased hydrostatic pressure

A

impaired venous return
arteriolar dilation

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9
Q

define hypoproteinemia

A

reduced plasma albumin due to either increase loss for decrease in synthesis

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10
Q

what causes reduced plasma osmotic pressure

A

reduced plasma albumin

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11
Q

how does the reduction of plasma osmotic pressure lead to edema and effusions

A

number of plasma proteins goes down
intravascular volume goes down
renal hypoperfusion (less blood flow to kidney)
secondary hyperaldosteronism (too much aldosterone)
salt and water retention
edema

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12
Q

what is filariasis

A

a type of parasite that blocks lymphatic drainage and leads to extreme edema, espeically in the lower limbs

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13
Q

what is hyperemia

A

ateriole dilation leading to an increase in blood flow
affected areas turn red (erythema)

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14
Q

what is congestion

A

reduced venous blood outflow leads to accumulation of deoxygenated hemoglobin
affected tissues turn a blue-red color (cyanosis)

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15
Q

define hemostasis

A

blood clotting at sites of vascular injury

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16
Q

what are platelets made of

A

granules which contain clotting factors, enzymes, mitochondria, and glycogen

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17
Q

what does the cytoskeleton of a platelet contain

A

microtubules that have actin and myosin filaments

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18
Q

what is the important surface receptor on platelets

A

GpIb (glycoprotein 1B)

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19
Q

explain how platelets are formed

A

hematopoietic stem cell
myloid cell
megakaryoblast
megakaryocyte
fragmentation

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20
Q

what is thrombopoietin

A

hormone made in the liver that stimulates megakaryoctes to make cytoplasmic extensions to go through clefts in the basement membrane
extensions break off to create platelets

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21
Q

what is the lifespan of a platelet and which 2 organs remove them

A

7-10 days
liver and spleen

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22
Q

what is the name for excessive clotting disorders

A

thrombotic disorders

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23
Q

explain how vascular spasm works

A

injured, bleeding vessel spasms and vasoconstricts
less blood flow allows less blood loss

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24
Q

explain primary hemostasis (platelet plug formation)

A

endothelial cells produce von Willebrand factor (vWF) in response to exposed collagen fibers of the injured vessel
vWF binds to platelets which activates them and causes them to stick to the exposed collagen
activated platelets releases granules
granules attract more platelets which aggregate to form the patch

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25
what are the 3 main platelet granules released during primary hemostasis (platelet plug formation)
TXA2, calcium, and clotting factors
26
what is the main purpose of the coagulation cascade
getting fibrinogen activated to fibrin
27
which clotting factors require Vitamin K to be synthesized
clotting factors 2, 7, 9, and 10 and proteins C and S
28
what happens during the intrinsic pathway of secondary hemostasis (coagulation)
slower exposed collagen fibers activate factor 12 factor 12a activated factors 9 and 11 factor 9a and 8a combine with calcium to activate factor X
29
what happens during the extrinsic pathway of secondary hemostasis (coagulation)
subendothelial cells display tissue factor tissue factor activates factor 7 factor 7a combines with calcium to activate factor 10
30
what happens during the common pathway of secondary hemostasis (coagulation)
clotting factors 10a and 5a combine with calcium to change prothrombin into thrombin thrombin turns fibrinogen into fibrin fibrin glues plug together
31
where are factors 5a and 8a coming from during the coagulation cascade
there is some thrombin already activated floating around that activates factors 5 and 8
32
explain clot retraction
actin and myosin fibers in the platelet cytoskeleton contract, bringing the edges of the wounded vessels closer together serum is squeezed out of the clot
33
what is serum
fluid consisting of plasma without clotting proteins
34
what is thrombolysis
process that begins after injury has healed and blood clotting is no longer necessary process of fibrinolysis
35
what is fibrinolysis
process that breaks down fibrin glue
36
what happens during fibrinolysis
endothelial cells release tissue plasminogen activator (tPA) tPA activates plasminogen plasmin degrades fibrin and clot dissolves
37
what is urokinase and what does it do
enzyme produced in the kidney that can initiate thrombolysis (fibrinolysis)
38
what three chemicals do endothelial cells produce and secrete
nitric oxide prostacyclin anticoagulants
39
what is nitric oxide and what does it do
chemical released by endothelial cells turns off hemostasis, specifically it counteracts the first and second events, vascular spasm and platelet plug formation causes vasodilation and inhibits platelet adhesion and aggregation
40
what is prostacyclin and what does it do
prostaglandin released by endothelial cells counter act the second event, platelet plug formation inhibits platelet aggregation
41
what produces anticoagulants and what do they do
produced by the endothelial cells and liver inhibit third event, coagulation
42
what are the four types of anticoagulants produced by the liver and endothelial cells
antithrombin 3 tissue factor pathway inhibitor heparin sulfate protein C
43
what does antithrombin 3 (AT-111) do
protein that binds and inhibits activity of clotting factors 9 and 10 and thrombin also prevents making of new thrombin
44
what does tissue factor pathway inhibitor do
blocks the events of the tissue factor in the extrinsic pathway
45
what does heparin sulfate do
polysaccharide that enhances antithrombin activity
46
what does protein C do
type of anticoagulant is activated by protein S and thrombomodulin complex catalyzes reactions that degrade clotting factors 5 and 8
47
what are three types of procoagulants
clotting factors fresh frozen plasma cryoprecipitate
48
what are three types of anticoagulants
heparin warfarin asprin
49
what are three types of fibrinolytic drugs
tPA streptokinase urokinase
50
what is the name of bleeding disorders
hemorrhagic diathesis
51
what are petechiae
1-2mm hemorrhages on skin caused by an increase in intravascular pressure or decrease in platelet count or function
52
what are purpura
3 mm hemorrhages on skin caused by increase in intravascular pressure or a decrease in platelet count or function can also be seen in vascular trauma, inflammation, or increased vascular fragility
53
what is eccymoses
1-2cm hemorrhages on the skin subcutaenous hematomas (bruises)
54
how do infections affect vessel walls
microbes cause damage to blood vessels (vasculitis)
55
how do drug reactions affect vessel walls
deposition of drug induced immune complexes causes damage to blood vessels (vasculitis)
56
how does Ehlers-Danlos syndrome affect vessel walls
collagen defects weaken vessel walls causing microvascular bleeding
57
how does Henoch-Schonlein purpura affect vessel walls
this is a systemic immune disorder in which there is a deposition of immune complexes within a vessel
58
how does Hereditary Hemorrhagic Telangiectasia (webe osler-rendu syndrome) affect vessel walls
mutation which leads to dilated, tortuous vessels with thin walls cause upper GI bleeds (nose, mouth, etc)
59
what is thrombocytopenia and what are its four main causes
low blood platelet counts caused by: decreased platelet production decreased platelet survival sequestration (spleen removing too many) dilution
60
what causes decreased production of platelets
nutritional deficiencies: B12 and folate aplastic anemia (bone marrow can't make enough)
61
what causes decreased platelet survival
certain drugs: quinidine, heparin, and sulfa compounds disseminated intravascular coagulation (abnormal clotting)
62
what is thrombotic thrombocytopenic purpura (TTP)
a thrombotic microangiopathy caused by dysfunction of the plasma metalloprotease ADAMTS13 excessive platelet activation and aggregation causes occlusion in small vessels can be chronic (genetic) or aquired idiopathic (unsure of cause)
63
what is the purpose of the plasma metalloprotease ADAMTS 13
breaks down large vWF proteins into smaller molecules
64
what is a tell-tale symptom of thrombotic thrombocytopenia purport (TTP)
microangiopathic hemolytic anemia
65
what is heparin-induced thrombocytopenia (HIT)
issue caused by treating a patient with unfractionated heparin immune reaction directed against the complex of heparin and PF4 leads to platelet consumption treated with LMW heparin (anticoagulant)
66
explain the mechanism of heparin induced thrombocytopenia (HIT)
platelet factor 4 is released, binds to a platelet, and is activated factor 4a binds to heparin to create a factor 4a+heparin complex complex binds to IgG which causes complex to become anti-heparin complex binds to Fc receptor on platelet platelets become activated and is removed by splenic macrophages
67
what is a hereditary deficiency in regards to clotting factors
deficiency that affects a single clotting factor such as 8 (hemophilia A) or vWF
68
what is an acquired deficiency in regards to clotting factors
deficiency that involves multiple coagulation factors ex. vitamin K deficiency, liver disease, and disseminated intravascular coagulation
69
what is disseminated intravascular coagulation (DIC)
issue where multiple coagulation factors are consumed leading to their deficiency usually occurs secondary to something else leads to fibrinolysis, bleeding, occlusions from thrombi, and tissue hypoxemia
70
what is von willebrand disease
most common inherited bleeding disorder mutation of vWF leads to unnoticed bleeding tendencies no platelet adhesion or stabilization of factor 8 diagnosed with ristocetin agglutination test treated with desmopression or vWF
71
what products are common in DIC
fibrin split products
72
define shock
state of systemic circulatory failure which leads to impaired tissue perfusion and cellular hypoxia
73
what are the three major types of shock
cardiogenic hypovolemic distributive
74
explain cardiogenic shock
shock that is due to heart failure which leads to decreased cardiac output shock specifically can be caused by things like MIs, arrhythmias, valve insufficiencies, and obstructions
75
what is hypovolemic shock
shock due to reduced intravascular volume, reduced preload, and reduced cardiac output can be caused by bleeding (hemorrhagic) or reduced intravasular volume due to things like vomit (non-hemorrhagic)
76
what is distributive (vasodilatory) shock
shock due to severe peripheral vasodilation and pooling of blood tissue ends up being under perfused different types of distributive shock: septic shock, neurogenic shock, anaphylactic shock, drug and toxin shock, or endocrine shock

Disease Mechanisms (19 decks)

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