More clin path Flashcards

(49 cards)

1
Q

requirements for hemostasis

A
  1. intact and healthy vessels
  2. normal platelet numbers
  3. normal platelet function
  4. normal amount and function of clotting factors
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2
Q

petechiae and echymoses

A

pin point red spots on skin/mucus membranes
indicating problem with platelets

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3
Q

megakaryocytes

A

in bone marrow
pinched off parts of cytoplasm containing granules turns into platelets

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4
Q

thromboxane A2 and ADP

A

activates platelets

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5
Q

vonWillebrands factor

A

platlets bind to receptor on vWF when exposed

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6
Q

platelets

A

from cytoplasm of metakaryocytes
binds to vWF and fibrinogen (cross linking)
+ charge to bind to - charge

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7
Q

automated platelet count

A

hematology analyzer
pro: quick and easy
cons: clumping = false decrease

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8
Q

estimated platelet count

A

stained blood smear
pro: cheap, small sample volume, subjective if clumping
cons: clumping, time and technical skill

look at monolayer under 100x objective
multiply number in field by 15,000

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9
Q

thrombopathy

A

platelets are not working properly
can be extrinsic or intrinsic

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10
Q

extrinsic platelet thrombopathy

A

something from outside the platelet is not working
most common: vonWillebrands disease
diagnosis:
* normal platelet count, PT, PTT
* prolonged buccal mucosal bleeding time (BMBT)
* measure vWF

problem with PRIMARY hemostasis

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11
Q

intrinisc hereditary thrombopathy

A
  • uncommon
  • various mechanisms
  • specialized testing

diagnosis
* bleeding, poor clot formation, normal platelets, normal PT/PTT, normal vWF

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12
Q

intrinsic acquired thrombopathy

A

drugs: COX inhibitors (NSAIDs, steroids), b-lactam antbiotics, calcium channel blockers
uremia (renal failure, toxins in circulation impairs platelets)
DIC: fibrin and fibrinogen in excess interfere with platelts
liver dz
infections

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13
Q

thrombocytopenia main causes

A

Sequestration
Decreased Production
Utilization/consumption
Destruction

SPUD

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14
Q

sequestration thrombocytopenia

A

platelets trapped in spleen
splenomegaly

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15
Q

decreased production thrombocytopenia

A

selective and generalized marrow injury
severy thrombocytopenia

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16
Q

utilization/consumption thrombocytopenia

A

DIC (hypercoagulation forms microclots, then runs out and hemorrhage)
moderate thrombocytopenia
schistocytes/fragmenatation RBCs

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17
Q

destruction thrombocytopenia

A

severe
immune mediated usually
infection, drugs

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18
Q

Thrombocytosis causes

A

Not Neoplasia (Common)
* Physiologic/Excitement (splenic contraction)
* Inflammation (reactive, most common)
* Hemorrhage (regeneration)
* Iron deficiency
* Vincristine
* Glucocorticoids

Neoplasia (rare)
* Essential Thrombocythemia (Chronic megakaryocytic leukemia)
* >1,000,000/uL

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19
Q

Where are clotting factors produced?

A

liver

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20
Q

coagulation factor I

21
Q

coagulation factor II

22
Q

coagulation factor III

A

tissue factor (TF)

23
Q

Coagulation factor VIII 8

24
Q

coagulation factor IX 9

25
Intrinsic coagulation pathway
inside the blood vessel initiated by contact with - charged substances (exposed collagen, platelet, endotoxins)
26
extrinsic coag cascade
things outside of the blood vessel (ex tissue factor III)
27
Intrinsic cascade coagulation factors
12 > 11> 9 > 8 | Its not $12, its $11.9
28
common coagulation cascade factors
10 > 5 > 2 > 1
29
common coagulation cascade factors
10 > 5 > 2 > 1
30
extrinsic coag pathway factors
3 > 7
31
vitamin K dependent factors
2, 7, 9, 10
32
which vit k dependent coag factor has the shortest half life?
7 will shoe deficiency first
33
blue top tube
contains citrate, stops clotting
34
coagulation test for intrinsic and common cascades?
Activated clotting time (ACT): not as sensitive, can do at clinic Partial thromboplastin time (PTT): must go to lab
35
coagulation test for extrinsic and common cascades?
Prothrombin time (PT)
36
coagulation test for fibrinogen concentration?
Thrombin time (TT)
37
prolonged PTT/ACT, normal PT
Problems with intrinsic pathway usually hemophilia A (8) or B (9)
38
prolonged PT, normal PTT/ACT
problem with extrinsic pathway factor 7 or 3 (TF) deficiency early vit K deficiency (7 has shortest half life)
39
prolonged TT
**Fibrinogen deficiency**/dysfunction Thrombin inactivation **liver failure, DIC** NOT vit k deficiency
40
Increased PTT/ACT and PT
vit K deficiency (if normal TT) DIC (schistocytes, thrombocytopenia, increased TT, increased D dimers) liver failure (low other liver products- glucose, BUN, albumin, cholesterol)
41
Causes of intravascular coagulation
**Thrombosis:** Initially **unbalanced hemostasis** Virchow’s triad * Stasis of blood flow * Endothelial injury * Hypercoagulability Inciting processes * Congestive heart failure * Heartworm * Protein-losing nephropathy **DIC** Initially **balanced hemostasis** Massive coagulation initiation * **Massive TF exposure or release** Inciting processes * Trauma * Cancer * Shock * Sepsis
42
DIC causes
Initially balanced hemostasis Massive coagulation initiation * Massive **TF exposure or release** Inciting processes * Trauma * Cancer * Shock * Sepsis | **TISSUE FACTOR**
43
Thrombosis causes
Initially **unbalanced hemostasis** Virchow’s triad * **Stasis of blood flow** * **Endothelial injury** * **Hypercoagulability** Inciting processes * Congestive heart failure * Heartworm * Protein-losing nephropathy
44
plasminogen activator
in endothelial cells converts plasminogen into plasmin plasmin chops up fibrin and makes d dimers
45
fibrinogenolysis/fibrinolysis
1. **plasma activator** released from endothelial cells 2. PA cleaves **plasminogen into plasmin** 3. plasmin **breaks down fibrin and fibrinogen** into **D dimers and fibrin degredation factors (FDP)**
46
increased fibrin degredation products
fibrin and fibrinogen degredation products increased when there is plasmin mediated cleavage of fibrinogen/fibrin increase = clot formation and breakdown **suggest DIC**
47
increased D dimers
specific type of fibrin degredation product suggest clot formation and breakdown **suggest DIC**
48
heparin
anticoagulant
49
antithrombin III
**MOST POTENT antihemostasis** protein in body **destroys thrombin** anticoagulant amplified by heparin **lose by: Protein-losing disorders** * Protein-losing nephropathy (PLN) * Protein-losing enteropathy (PLE)