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Pathophysiology > Ch. 12 > Flashcards

Ch. 12 Flashcards

1
Q

What does hemostasis mean?

A

Stopping blood flow.

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2
Q

What does the process of hemostasis require?

A

platelets
coagulation system
endothelial lining

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3
Q

What is considered normal hemostasis?

A

When a broken vessel wall is sealed.

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4
Q

What is considered abnormal hemostasis?

A

inappropriate clotting

insufficient clotting

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5
Q

describe platelets.

A

AKA thrombocytes

formed in the bone marrow from pieces of magakaryocytes

Stored in the spleen and released when needed

8-9 day life in circulation

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6
Q

What do platelets do?

A

help in the clotting process by
produce chemical mediators of hemostasis:

react with proteins to start clotting

help platelets stick together

Stimulate wound healing

help platelets stick to vessel wall

constrict blood vessels

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7
Q

What is our normal number of platelets?

A

150,000 - 400,000

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8
Q

What controls the production of platelets?

A

Thrombopoetin

Made in the liver, kidney, smooth muscle, and bone marrow

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9
Q

What makes the activate platelet stick to fibrinogen and other platelets?

A

The GPIIb or GPIIIa glycoprotein which has binding sites for calcium.

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10
Q

What are the two different categories of coagulation factors

A

Plasma proteins

Calcium

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11
Q

Describe plasma proteins.

A

Most are synthesized by the liver

Von willebrand factor is made by the endothelium

These circulate as INACTIVE procoagulation factors

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12
Q

What are the 5 steps of hemostasis?

A
  1. vessel spasm
  2. formation of platelet plug
  3. blood coagulation
  4. clot retraction
  5. clot dissolution
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13
Q

describe the vessel spasm

A

When the vessel wall in injured platelets release thrombaxin a2 which causes vasoconstriction.

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14
Q

describe the formation of the platelet plug.

A

The endothelial lining of the vessel releases von willebrand factor ( carries VIII) which bind to receptors of platelets and tells them to start sticking to the exposed collagen fibers at the vessel wall. The platelets are still releasing thrombaxin a2 and ADP at this point in the process, which attracts more platelets and aggregates and activates them.

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15
Q

Describe the blood coagulation (clot formation).

A

This is when a clot forms over the platelet plug by either the intrinsic or extrinsic pathways.

Intrinsinc - VII activates intrinsic

Extrinsic - Tissue factor released from endothelial cells activate extrinsic.

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16
Q

Where does coumadin or warfrin work in the clotting process?

A

Decreases the amount of prothrombin and vitamin k dependent coagulation factors.

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17
Q

where does heparin work in the clotting process?

A

inactivates thrombin which stops fibrinogen from turning to fibrin, also inhibits factor Xa and other clotting factors that suppress formation of fibrin. NATURALLY MADE BY MAST CELLS

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18
Q

Where are most of our clotting factors made?

A

THE LIVER

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19
Q

Describe the clot retraction.

A

This is when the actin and myosin in the platelets start contracting and pulling together, pulling the fibrin strands nice and tight. This squeezes out the extra serum our, shrinking the clot.

This also causes the muscle of the vessel walls to come back together which helps the healing process.

20
Q

describe clot dissolution?

A

This is when plasminogen is turned into plasmin by t-PA (tissue plasminogen activator) and starts to break up the clot by digesting fibrin strands of the clot.

21
Q

What is van willebrand disease?

A

This is were there is a deficiency in the formation and release of van willebrand factor (VIII), which causes poor platelet adhesion and in turn very poor clotting.

22
Q

What does plavix do?

A

prevents platelet aggregation

23
Q

What does aspirin do?

A

This impairs the synthesis TXA2, affects vessel spasm and platelet plug formation.

24
Q

What are the cyclooxygenase enzymes?

A

These are enzymes that produce the chemical mediators of hemostasis.

25
Q

What does celebrex do?

A

COX-2 inhibitor, increases TXA2 levels which leads to widespread vasoconstriction and morethan likely a higher blood pressure.

it also inhibits the formation of prostacyclin and in turn prostanglandins, this also makes it a great anti-inflammatory and anagleisic drug for people with arthritis.

26
Q

What are the 2 main forms of hypercoagulability?

A

Increase in platelets function

    • increase platelet number
  • -disturbance in blood flow
  • -endothelial damage

accelerated activity of the coagulation system (increased clotting activity)

    • Primary (genetic or inherited: example: Factor V mutation or the leiden mutation puts at risk for DVT)
    • secondary (acquired)
27
Q

What do both forms of hypercoagulability increase the risk of?

A

clot or thrombus formation.

28
Q

What causes arterial thrombus?

A

turbulent blood flow leading to platelet adherence - plaque formation because of high cholesterol (atherosclerosis)

diabetes

smoking

elevated cholesterol

increased platelet levels

29
Q

What can cause a venous thrombus?

A

Conditions that cause the stasis of blood flow with increased concentration of coagulation factors

pregnancy

oral contraceptives

post-surgical state

immobility

CHF

malignant diseases

30
Q

What is the term for decreased platelet levels?

A

Thrombocytopenia

31
Q

What can cause thrombocytopenia?

A

decreased production - bone marrow suppression

increased destruction - auto-immune, physical destruction by implanted heart valve being rough on them

platelets used up in forming lots of clots

There are even problems where the spleen doesnt release platelets right, and they start pooling in the spleen.

impaired platelet function

32
Q

What are the signs of throbocytopenia?

A

Bleeding of the small blood vessels of the skin and mucous membranes (petechiae or purpura

33
Q

At what platelet count is someone considered to be thrombocytopenic?

A
34
Q

At what count of platelets will someone have spontaneous bleeding?

A
35
Q

What are the two types of thrombocytopenia that she talks about?

A

idopathic thrombocytopenic purpura (ITP)

thrombotic thrombocytopenic purpura (TTP)

36
Q

What is ITP (idiopathic throbocytopenic purpura)?

A

This is an auto-immune disorder that results in platelet antibody formation that causes excessive destruction of platelets.

More common in children, and usually follows a viral infection

37
Q

What is TTP (throbotic thrombocytopenic purpura)?

A

This is a combination of thrombocytopenia, hemolytic anemia, widespread microvascular occlusion (lot of clots in vessels), fever, and neurological abnormalities.

abrupt onset and can be fatal

usually caused by endothelial damage and activation of inravascular thrombosis

38
Q

What is thrombocytopathia?

A

impaired platelet function (lasts the life of the platelet 8-10 days)

39
Q

What are the etiologies of throbocytopathia

A

Most common - use of aspirin and other NSAIDs (the effects of aspirin last for the lifetime of the platelet)

—- other NSAIDs effects last only for the duration of the drug action

It can be genetic (von willebrand; hemophilia A which is a factor VIII deficiency)

can also be acquired through drugs, diseases, extracorporeal circulation (circulation that goes outside the body)

40
Q

Describe von willebrands disease and its symptoms.

A

most common hereditary bleeding disorder

deficiency in vWF which makes forming the platelet plug very hard

because vWF also carries factor VIII, there may also be a deformity in the formation of clots.

bruising, excessive menstrual flow, spontaneous bleeding from nose, mouth, and GI tract.

41
Q

Describe hemophilia and its symptoms.

A

only in males, CAN BE PASSED DOWN FROM MOTHER

faulty factor VIII (90% produce too little factor VIII, 10% produce enough but it is a defective form)

severity of bleeding depends on how much normal factor VIII is produced

manifestations: bleeding in soft tissues, GI tract and joints. Also joint pain and swelling

treated by recieving factor VIII

42
Q

What is DIC (disseminated intravascular coagulation) and its symptoms?

A

This is widespread intravascular coagulation and bleeding.

This is caused usually by a trauma, which activates a massive sequence of the coagulation sequence because of unregulated production of thrombin. LEADS TO SYSTEMIC FORMATION OF FIBRIN

Oozing from the wound site

43
Q

Why is DIC so fatal?

A

It uses up all of our major coagulants, results in major hemorrhage.

generates many microthrombi which occludes vessels and causes ischemia, LEADS TO ORGAN FAILURE

It uses up all of your clotting factors, later on leads to thrombocytopenia

44
Q

Does liver disease lead to impaired synthesis of clotting factors?

A

YES

V, VII, IX, X, XI, XII

also prothrombin and finbrinogen are synthesized here

45
Q

Can a vitamin K deficiency lead to impaired synthesis of clotting factors?

A

YES

VII, IX, X

prothrombin

all of these require vitamin K for normal activity

46
Q

What else can cause issues with clotting?

A

Vitamin C deficiency - needs to be pretty significant

calcium - usually have very adequate stores though (ELDERLY DONT THOUGH)

Pathophysiology (13 decks)

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