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IHO Final- Krafts > Krafts- General Principles of Homeostasis > Flashcards

Krafts- General Principles of Homeostasis Flashcards

1
Q

What is the balancing act in homeostasis?

A

Pro-clotting (plugs up holes in blood vessels)

Anti-clotting (keeps clotting under control)

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2
Q

What are the three steps to clotting?

A

Constrict the blood vessel in the region of the hole
form a platelet plug
seal the plug w/ fibrin

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3
Q

Why do blood vessels constrict?

A

Decrease blood loss

Helps platelets and factors to stick together when they bump into eachtoher

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4
Q

What happens when the platelets form a plug?

A 
proteins are exposed
platelets adhere
granules release contents
platelets aggregate
phospholipids are exposed

**this is primary hemostasis!

It would fall apart if fibrin didn’t come next

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5
Q

How does fibrin seal up the plug?

A

TF is exposed
cascade begins
cascade makes fibrin
fibrin solidifies the plug

**this is SECONDARY hemostasis

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6
Q

How is clotting stopped?

A

Inhibit coagulation cascade

Lyse portions of clot to keep it down to a reasonable size

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7
Q

What factors inhibit the coagulation cascade?

A

ANTI-CLOTTING TEAM

TFPI
ATIII
Proteins C,S

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8
Q

What does TFPI do?

A

shuts off tissue factor (extrinsic) pathway by inhibiting VIIa

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9
Q

What does ATIII do?

A

Inhibits the serine proteases (IIa, VIIa, IXa, Xa, XIa, XIIa) shuting off all THREE pathways

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10
Q

What potentiates ATIII?

A

Heparin

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11
Q

What does protein C do?

A

It is a serine protease which destroys VA and VIIa thereby shutting down coagulation.

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12
Q

What does protein S do?

A

It is a co factor that helps protein C?

**C is batman, S is robin

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13
Q

What factors are responsible for clot lysis?

A

tPA

plasmin

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14
Q

What does tPA do?

A

it binds to fibrin (which is great b/c it keeps it’s action localized to the clot) and converts plasminogin to plasmin

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15
Q

What does plasmin do?

A

breakes down fibrin into FDPs (split products) which inhibit thrombin and fibrin formation

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16
Q

Are platelets cells?

A

Not really—they don’t have a nucleus.

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17
Q

What are platelets?

A

fragements of cytoplasm shed by gigantic precursor megakaryocytes that live in bone marrow

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18
Q

Where are most platelets found?

A

Most are in the blood (and BM)

but 1/3 are sequestered in teh spleen

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19
Q

What are the two major components of a platelet?

A

Granules (found in purplish region of granulomere, peripheral region is graunule free= hyalomere)
Membrane

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20
Q

What are the components of a platelet membrane?

A

phospholipids (coag factors need to bind to be activated)
GP Ia (binds collagen)
GP Ib (binds vWF)
GP IIb-IIIa (binds fibrinogen)

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21
Q

What is found in the granules of platelets?

A

alpha granules (specific)–fibrinogen, vWF

gamma granules (dense)- serotonin, ADP, Ca2

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22
Q

How do platelets form a plug?

A

Endothelial damage exposes subendothelial proteins (like collagen)>
attracts platelets>
Platelets stick to subendothelilum via vWF (adhesion)>
platelets change shape and release granule contents>
attracts more platelets>
form temporary plug (aggregation)>
platelets contract and seal vessel wall

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23
Q

Where does TF come from?

A

“hidden” cells exposed during injury (not normally in contact w/ blood)
microparticles floating in blood
endothelial cells and monocytes (during inflammation)

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24
Q

What should you tattoo on your leg?

A

THE WHOLE POINT OF THE COAGULATION CASCADE IS TO TURN FIBRINOGEN INTO FIBRIN

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25
What are all the coagulation factors?
enzymes or cofactors
26
What is the major activator of the extrinsic pathway?
Tissue factor
27
What happens in the extrinsic pathway?
TF binds to VII> actiates it> TF-VIIA complex kicks off coagulation cascade> Xa> TFPI turns off TF> Extrinsic pathway shut down preventing over clotting and thrombosis
28
What is the main activator of the intrinsic pathway?
Thrombin
29
The final common pathway consists of what cofactors?
X, V, II (thrombin) and I (fibrinogen)
30
How do the pathways interact in real life?
1. vascular injury exposes TF to blood stream 2. coagulation started along extrinsic pathway (make Xa and thrombin along the way) 3. Xa turns off extrinsic pathway (through TFPI) 4. Thrombin activates the intrinsic pathway 5. mush platelet plug is transformed into solid mass by fibrin
31
What turns on protein C?
Thrombin Thrombin binds thrombomodulin> complex activates protein C
32
What are two types of platelet tests?
Count- done by particle counter, 150-450 x 10^9 L Morphology-size/granulation
33
What are irregular morphologies seen in platelets?
Normal--have hyalomere and granulomere (w/ granules!) Hypogranular/agranular platelets LARGE platelet
34
Why is bleeding time measured?
to evaluate platelet response to vascular injury * some platelet disorders have a long bleeding time
35
How is bleeding time measured?
Inflate blood pressure cuff make incision time how long it takes to stop bleeding (2-9 mins usually, longer in children)
36
What is closure time?
an alternative to bleeding time Platelet funciton analyzer 100 measures how quickly platelets occlude small holes in a membrane
37
Closure time is better at detecting what two things?
* better at detecting aspirin related bleeding and vW disease
38
Why is platelet aggregation measured?
To find platelet function abonormalities
39
How is platelet function measured?
Add aggregating agents to pt's sample see if platelets aggregate measure DECREASE ins ample turbidity
40
How do you make your diagnosis by looking at platelet aggregation?
Pattern of response helps you to narrow down diagnosis NORMAL platelets respond to every aggregating agent. In platelet disorders, platelets do not respond the same to every aggregating agent.
41
How do you do a coagulation lab test?
draw blood into citrate tube spin tube, decant plasma add reagents to plasma watch for formation of fibrin
42
What is prothrombin time?
Plasma+ thromboplastin | Measures extrinsic pathway
43
``` VII: what makes it? What does it need? Coumadin effects? Half life? ```
Made by liver needs K decreased by coumadin SHORT half life
44
``` Decreased: VII, X, V, II, I coumadin heparin DIC ``` leads to increased...
PT (prolonged)
45
What increases PT?
Coumadin Heparin DIC
46
When should you order a PT?
prothrombin time---NEVER! order an INR instead
47
What is an INR?
a corrected PT | internationalized normalized ratio
48
When should you order an INR?
To assess liver function monitor coumadin therapy diagnose DIC* Assess pre-op status
49
What is partial thromboplastin time and what does it measure?
Pasma + phospholipid measures the INTRINSIC pathway APTT = same thing
50
What increases PTT?
``` hemo A hemo B DIC heparin inhibitors ```
51
When should you order a PTT?
``` To investigate hx of abnormal bleeding monitor heparin therapy diagnose DIC diagnose atiphospholipid Ab assess pre-op status ```
52
What is thrombin time?
plasma+ thrombin measures conversion of fibrinogen to fibrin bypasses intrinsic and extrinsic pathways
53
What increases TT?
decreased fibrinogen | increased FDPs
54
When should you order a TT?
When the PTT is prolonged and when you want to rule out fibrinogen problems (rare)
55
What are the ingredients for a PTT mixing study?
Pooled plasma + pt plasma+ phospholipid
56
What happens if the PTT corrects?
something is missing-- usually a coagulation factor
57
What happens if PTT doesn't correct?
Inhibitor present even though you added a bunch of normal plasma to the mix, the pts plasma still couldn't clot normally so there must be a problem w/ the pt's plasma
58
When should you order a mixing study?
When PTT is prolonged but TT is normal
59
What is a fibrin degradation protein assay?
Measures FDPs which are the result of breakdown of fibrin by plasmin VERY sensitive
60
What causes FDPs to go up?
thrombi | minor clotting
61
When should you order an FDP assay?
Not to rule in a clot | but to RULE OUT a clot
62
What does a fibrinogen assay do?
Measures fibrinogen...duh.
63
What causes fibrinogen to go down?
DIC | Massive bleed
64
When shouldl you use a fibrinogen level?
To diagnose DIC | to follow pts w/ a massive bleed

IHO Final- Krafts (11 decks)

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