Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CMOD Week 5 > Pathos Chapter 4 > Flashcards

Pathos Chapter 4 Flashcards

1
Q

Hemostasis occurs in what two stages?

A

primary and secondary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does primary hemostasis involve?

A

forms a weak platelet plug and is mediated by interaction between platelets and the vessel wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What does secondary hemostasis involve?

A

stabilizes the platelet plug and is mediated by the coagulation cascade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the first step of primary hemostasis?

A

Transient vasoconstriction of the damaged vessel that is mediated by reflex neural stimulation and endothelin release from endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the second step of primary hemostasis?

A

Platelet adhesion to the surface of disrupted vessel via vMF binding to exposed sub endothelial collagen and GPIb on platelet surface.

vMF comes from Weibel-Palade bodies of endothelial cells and a-granules of platelets when activated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the third step of primary hemostasis?

A

Platelet degranulation caused by adhesion that induces shape change in the platelets and release of the contents of alpha and dense granules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the contents of dense granules of platelets?

A

ADP which promotes exposure of GPIIb/IIIA receptor on platelets and calcium which is needed for the coagulation cascade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the fourth step of primary hemostasis?

A

Platelet aggregation at the site of the injury via GPIIb/IIIa using fibrinogen (from plasma) as a linking molecules; results in formation of a weak platelet plug that is stabilized in secondary hemostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the normal platelet count in blood?

A

150-400 K/ul; less than 50 K/ul leads to symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a normal bleeding time for cutaneous cuts?

A

2-7 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is Bernard-Soulier syndrome?

A

genetic deficiency of GPIb on platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is Glanzmann thrombasthenia?

A

genetic deficiency of GPIIn/IIIa impairing platelet aggregation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the main purpose of secondary hemostasis?

A

Stabilizing the weak platelet plug formed during primary hemostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does secondary hemostasis make a clot stronger?

A

The coagulation cascade generates thrombin, which converts fibrinogen in the platelet plug to fibrin. The fibrin is then cross-linked to form a stable thrombus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Coagulation cascade factors are made where?

A

the liver in inactive states

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What things are needed to activate the coagulation cascade?

A

intrinsic- subendothelial collagen activates factor XII
extrinsic- tissue thromboplastin activates factor VII

phospholipid surface of platelets

calcium from dense granules of platelets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is PT?

A

prothrombin time- measures extrinsic (factor VII) and common (factors II, V, X, and fibrinogen) pathways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is PPT?

A

partial thromboplastin time- measures intrinsic (factors XII, XI, IX, and VIII) and common (factors II, V, X, and fibrinogen) pathways

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is hemophilia A caused by?

A

genetic factor VIII deficiency

20
Q

What is the MOI of hemophilia A?

A

X-linked; more common in men

can arise simplex

21
Q

When should hemophilia a be suspected?

A

Pt experiences deep tissue, joint, and post surgical bleeding

22
Q

How does Hemophilia A affect PT and PTT? Other lab findings?

A

PT- normal
PTT- elevated
VIII- low
normal platelet count and bleeding time

23
Q

What is hemophilia B caused by?

A

aka Christmas disease

genetic factor IX deficiency

24
Q

Clinical finding of Hemophilia B?

A

same as hemophilia A (PT normal, PTT elevated, normal platelet and bleeding time), but IX is low instead of VIII

25
Q

What is Von Willebrand disease caused by?

A

genetic vMF deficiency- most common inherited genetic disorder

26
Q

MOI of Von Willebrand disease?

A

AD

27
Q

Clinical finding of Von Willebrand disease?

A

mild mucosal and skin bleeding

low vMF

increased bleeding time and elevated PTT

decreased VIII half-life (vMF stabilizes it usually) however, no deep tissue, joint, and post surgical bleeding seen n hemophilia A

Abnormal ristocetin test- ristocetin induces platelet agglutination by causing vMF to bind to GPIb; lack of vMF= impaired agglutination= abnormal test

28
Q

How do you treat Von Willebrand disease?

A

desmopressin (ADH analog) which increases vMF release from Weibel-Palade bodies on endothelial cells

29
Q

How does vitamin K deficiency impair coagulation?

A

Vitamin K is needed for gram carboxylation of factor II, VII, IX

30
Q

What might cause vitamin K deficiency?

A

Newborns can be deficient of the normal flora of the GI that synthesize vitamin K (vitamin K is given prophylactically to all newborns at birth to prevent hemorrhagic disease)

Long-term antibiotic therapy disrupts vitamin-K producing bacteria in the GI tract

Malabsorption leads to deficiency of fat-soluble vitamins, including vitamin K

31
Q

What does tissue plasminogen activator do?

A

tPA converts plasminogen to plasmin, which is responsible for cleaving fibrin and serum fibrinogen, destroying coagulation factors and blocking platelet aggregation

32
Q

What inactivates plasmin?

A

a2-antiplasmin

33
Q

What could decrease the levels of a2-antiplasmin in the body?

A

cirrhosis of the liver

34
Q

What prevents the activation of plasminogen (e.g. for treatment in cirrhosis)?

A

aminocaproic acid

35
Q

What are the three major risk factors for thrombosis?

A

disruption in blood flow
endothelial cell damage
hyper coagulable state (Virchow triad)

36
Q

Why does disruption in blood flow increase the risk of thrombosis?

A

blood flow is normally continuous and laminar, keeping platelets and factors dispersed and inactivated. Turbulent flow and stasis disrupts this

37
Q

Why does endothelial cell damage increase the risk of thrombosis?

A

exposes the sub endothelial collagen and underlying tissue factor and prevents the formation of PGI2 and NO from healthy endothelial cells that cause vasodilation and prevent platelet aggregation

prevents healthy endothelial cells from producing heparin-like molecules (augment antithrombin III which inactivates thrombin and other factors)

prevents healthy endothelial cells from producing tPA from converting plasminogen to plasmin

prevents healthy endothelial cells from producing thrombomodulin which redirects thrombin to activate protein C, which inactivates factors V and VIII

38
Q

What are some common causes of endothelial cell damage?

A

atherosclerosis, vasculitis, and high levels of homocysteine

39
Q

What would cause an increase in levels of homocysteine?

A

vitamin B12 and folate deficiency

Mechanism:

i. folic acid circulates as methyl-THF in the serum
ii. Methyl is transferred to cobalamin (vitamin B12), allowing THF to participate in the synthesis of DNA precursors
iii. Cobalamin transfers methyl to homocysteine resulting in methionine
iv. Lack of vitamin B12 or folate lead to decreased conversion of homocysteine to methionine resulting in buildup of homocysteine

or Cystathionine beta synthase (CBS) deficiency- with homocysteinuria

i. CBS converts homocystine to cystathionine
ii. characterized by vessel thrombosis, mental retardation, lens dislocation, and long slender fingers

40
Q

What causes hypercoagulable state?

A

i. due to excessive procoagulant proteins or defective anticoagulant proteins; may be inherited or acquired

classic presentation is recurrent DVTs or DVT at a young age

ii. Protein C or S deficiency (AD)
iii. Factor V Leiden
iv. Prothrombin 20210A
vi. ATIII deficiency
vii. Oral contraceptives

41
Q

How does protein C or S deficiency cause a hypercoagulable state?

A

protein C and S normally inactivate factors V and VIII

this causes increased risk for warfarin skin necrosis
-the initial stage of warfarin therapy results in a temporary deficiency of proteins C and S (due to shorter half life) relative to factors II, VII, IX, and X

42
Q

How does Factor V Leiden cause a hypercoagulable state?

A

mutated form of factor V that lacks the cleavage site for deactivation by proteins C and S

43
Q

How does Prothrombin 20210A cause a hypercoagulable state?

A

an inherited point mutation in prothrombin that results in increased gene expression, increasing risk of thrombus formation

44
Q

How does ATIII deficiency cause a hypercoagulable state?

A

decreases the protective effect of heparin-like molecules produced by the endothelium, increasing the risk for thrombosis

heparin-like molecules normally activate ATIII, which inactivates thrombin and coagulation factors

45
Q

How do oral contraceptives cause a hypercoagulable state?

A

estrogen indues increased production of coagulation factors

CMOD Week 5 (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions