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Patho Exam 4 > Patho exam 4- hemo and chemo > Flashcards

Patho exam 4- hemo and chemo Flashcards

1
Q

What does it mean when someone has a clotting issue?

A

There is an issue with platelets or coagulation factors. They can either be hypo or hypercoaguable

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2
Q

Platelets are also known as

A

thrombocytes

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3
Q

Platelets live for how long and are stored where

A

Live for 8-9 days in circulation in an inactive form and are stored in the spleen, released when needed.

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4
Q

How many platelets are usually in the blood

A

150,00-400,000

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5
Q

Where are megakaryocytes formed

A

in the bone marrow and are immature and released when needed. They break apart to form platelets

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6
Q

Thrombopoietin

A

controls the platelet production.

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7
Q

Where is thrombopoietin made

A

the liver, kidney, smooth muscle, bone marrow

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8
Q

low levels of thrombopoietin..

A

very rare

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9
Q

Stages of normal clotting:

A
  1. ) vessel spasm
  2. )Formation of platelet plug
  3. ) Blood coagulation
  4. ) clot retraction/contraction
  5. ) clot dissolution
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10
Q

Stage 1:Vessel Spasm

A

transient occuring in less than a minute
allows less blood to be lost
due to hormonal thromboxane A2

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11
Q

Thromboxane A2

A

stimulates the activation of new platelets and increases aggragation

NSAIDS and Aspirin block this

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12
Q

Stage 2: Formation of platelet plug

A

Occurs within seconds

Damaged vessel leaves collagen exposed

Von Willebran factor is released and attracts and activated platelets

Activated platelets change shape and release chemical mediators causing platelet aggragation

Forms a loose platelet plus and activates clotting cascade

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13
Q

Stage 3: Blood coagulation

A

process by which fibrinogen is converted to fibrin which forms meshwork that holds the blood cells together in clot form

Coagulation factors become activated on platelet surface and initiate clotting cascade (intrinsic and extrinsic pathway

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14
Q

intrinsic pathway

A

occurs in vascular system and is slow..

Stage 3

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15
Q

extrinsic pathway

A

occurs in tissues and is fast

Stage 3

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16
Q

Both intrinsic and extrinsic end with..

A

activation of factor X leading to conversion of prothrombin to thrombin which converts fibrinogen to fibrin

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17
Q

Procoagulation factors

A

circulate in blood, activated and converted to coagulation factors in specific series of steps

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18
Q

procoagulation factors initiate

A

clotting

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19
Q

Calciums importance on coagulation

A

Factor IV and is needed in almost all steps of coagulation. Hypocalcemic patients will have clotting issues

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20
Q

Anticoagulation factors

A

inhibit clotting such as antithrombin 3, protein C, protein S, heparin

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21
Q

Antithrombin 3

A

anticoagulation factor that neutralizes thrombin

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22
Q

Protein C

A

anticoagulation factor that inhibits thrombin

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23
Q

Protein S

A

enhances the action of protein C

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24
Q

Heparin is contained in granules in..

A

basophils (wbcs)

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25
Q

Deficiency state of antithrombin, protein C, protein S and heparin causes

A

hypercoaguability

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26
Q

Stage 4:clot retraction

A

platelets contract and squeeze out serum of clot and pull vessel edges together

clot dries us and shrinks

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27
Q

Stage 5: fibrinolysis: clot dissolution

A

Clot starts to dissolve shortly after clot formation

sequence of steps with activators and inhibitors leading to formation of plasmin which lyses clots

Plasminogen circulates in the blood and is activated by tPA and urokinase plasminogenn activators

Activators are rapidly inactivated by inhibitors (PAI-1)

Activators and inhibitors are usually in state of balance and both are synthesized by the liver

Breakdown of fibrin leads to production of fibrin degradation products and can be measured in serum

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28
Q

tPA

A

clot buster in medication form that activates or starts the clot dissolution process occuring in stage 5

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29
Q

FDP will be measured in the blood if..

A

they have been clotting a lot and there will be an increase in this number. Stage 5

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30
Q

hypercoagulable conditions occur due to

A

increased platelet function

increased activity of coagulation system

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31
Q

increased platelet function: hypercoaguable condition: occurs due to..

A

a disturbance in blood flow, endothelial damage, increased sensitivity of platelets to clotting factors

Seen in diseases such as: atheroscerlosis, hypertension, diabetes, smoking, HF, cancer which all cause increases in platelet function

Thrombocytosis: >1 million platelets

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32
Q

Increased activity of coagulation system: hypercoaguable conditions: occurs due to

A

hereditary conditions- inherited defects of factor V or prothrombin gene- increased incidence of recurrent DVTs

Stasis of blood flow- risk factors for DVT, causes accumulation of platelets , seem with immobility and heart failure

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33
Q

Hypercoaguability can cause

A

MI, CVA, DVT, PVD, PE

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34
Q

Who is at risk for developing hypercoaguable conditions

A

post op patients, neuromuscular diseases, high levels of estrogen, cancer

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35
Q

DVT: risk factors

A

Virchows traid:

Stasis: bedrest, immobility, CHF, shock

Vessel wall injury: catheters, surgery or trauma

Hypercoaguability: genetic factors, trauma, pregnancy, BCP, cancer

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36
Q

DVT manifestations

A

asymptomatic or positive homan signs, pain, swelling, redness, fever

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37
Q

DVT treatment

A

anticoagulants to prevent additional thrombi and minimize venous valve damage

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38
Q

anticoagulants to not dissolve a clot but..

A

prevent further complications

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39
Q

Bleeding disorders are caused by defects of

A

platelets, coagulatiom pathways, blood vessels

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40
Q

Thrombocytopenia

A

decrease in the number of circulating platelets due to:

decreased production of platelets (antineoplastics, quinine, sulfa, antibiotics, heparin)

Increase sequestration of platelets in spleen: splenomegaly, cirrhosis, lymphomas (meaning the spleen holds on to more platelets)

Decreased platelet survival: immune process breakdown of platelets or increased consumption DIC or TTP

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41
Q

S/S of thrombocytopenia

A

petichiae, purpura

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42
Q

ITP: idiopathic or immune thrombocytopenic purpura

causes, children, adults, etc

A

Autoimmune disease: platelet antibodies formed and platelets are destroyed in spleen

causes severe thrombocytopenia (

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43
Q

Removal of spleen might be helpful when a patient has

A

Bleeding disorder such as ITp (idiopathic thrombocytopenic purpura)

the spleen recognizes foreign antibodies of platelets and destroys platelets

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44
Q

S/S of ITP

A

increased bruising, bleeding, INCREASED SPLEEN SIZE, petechia, purpura

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45
Q

diagnosis of idiopathic thrombocytopenic purpura

A

platelets are

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46
Q

Treatment for ITPL (idiopathic thrombocytopenic purpura)

A

corticosteroids, immune globulin, splenectomy, thrombopoietin, receptor agonists (meds that stimulate thrombopoeitin receptors)

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47
Q

TTP: thrombotic thrombocytopenic purpura

A

combination of thrombocytopenia, hemolytic anemia and widespread vascular occlusion due to platelet thrombi

abrupt onset and may be fatal

RBC are fragmented as the move through partially occluded vessels

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48
Q

TTP is similar to DIC but it

A

does not involve the clotting cascade

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49
Q

S/S of TTP:

A

fever, neurological changes such as headache, seizures (grand mal), decreased LOC, petechiae, pupura

50
Q

Treatment for TTP

A

plasma exchange, steroids

51
Q

Bleeding disorders: coagulation disorders result from

A

decrease in 1 or more clotting factors

may be due to decreased production or increased consumption (common after trauma)

52
Q

hereditary disease for bleeding/coagulation disorders involve which factor

A

VII, IX or von willebrands factor

hemophilia A, hemophilia B, von willebrands disease

53
Q

Vitamin K is needed for synthesis of

A

factors VII, IX, X and prothrombin

remember “1972” missing

warfarin can decrease this

PTT HIGH

54
Q

conditions that decrease the GI flora and decrease absorption of vitamin K also lead to

A

decreased production of clotting factors

55
Q

decreased production for coagulation disorders involves impaired synthesis of

A

clotting factors with liver disease: factors V, VII, IX, X, XII, prothrombin and fibrinogen

56
Q

Hemophilia A

A

Bleeding disorder: coagulation disorder

X-linked recessive inheritance that is passed on through the mom

57
Q

hemophilia A primarily affects

A

males

58
Q

S/s of hemophilia A

A

bruising, bleeding, GI bleeds, joint stiffness, contraction of joints, inflammation, nose bleeds

59
Q

treatment for Hemophilia A

A

Factor VIII therapy given IV as prophylactic or for bleeding episodes

Gene therapy: carrier detection and prenatal diagnosis

60
Q

Teaching a patient with hemophilia A..

A

avoid trauma, diagnosed mainly in kids, should avoid NSAIDS and aspirin, prophylactic treatments

61
Q

Hemophilia B

A

Factor IX deficiency (christmas disease)

62
Q

factor IX is needed for activation of

A

factor X in coagulation cascade, common pathway activation–>fibrin clot

63
Q

signs and symptoms of hemophilia B

A

similar to hemophilia A but A is more common than B

64
Q

Treatment for hemophilia B

A

administer recominant factor IX prophylactically and with acute bleeding episodes

65
Q

Von Willebrand’s disease

A

diagnosed as an adult
hereditary
defect in von willebrands factor-carried factor VII and results in decreased platelet aggregation and adhesion

66
Q

Von willebrand’s disease S/s

A

bleeding following OR, dental procedures, PG/delivery, heavier menstraul bleeding, epistaxis

67
Q

Treatment for von willebrands disease

A

avoid aspirin
DDAVP (desmopressin acetate)- synthetic ADH wich controls spontangeous trauma induced and operative related bleeding when given IV 30 minutes before OR procedure.

Factor VII and cryoprecipitate infusions

68
Q

DIC (disseminated intravascular coagulation)

A

always a secondary problem- viral, bacerial, trauma, blood stasis, OB disorders

have 3 processes occurring at the same time: blood clot, clot dissolution and bleeding

due to massive activation of clotting cascade and fibrinolytic cascade

excess clotting and microthrombi which cause vessel occlusion and ischemia–>multiple organ failure

after clotting factors are used up it causes massive bleeding

69
Q

release of endotoxins seems to be a common mediating factor for

A

DIC

70
Q

S/S of DIC

A

due to bleeding: petechiae, purpura to oozing from puncture sites, CV shock

Due to microemboli: ischemia which may lead to renal, respiratory and circulatory failure or convulsions, coma, hemolytic anemia and RBCs are damaged through partially occluded vessels

71
Q

Treatment for DIC

A

manage underlying disease

replace clotting components- plasma, platelets, cryoprecipitate

prevent further activation of clotting mechanisms- HEPARIN is used to decrease clotting but may cause more hemorrage, IV volus

72
Q

vascular disorders occur due to

A

bleeding from small blood vessels due to naturally weak vessel walls or due to inflammation or immune process

73
Q

hemorrhagic telangiectasia

A

rare hereditary disorder with thing, dilated capillaries

vascular disorder

74
Q

vitamin C deficiency (Scurvy)

A

decreased collagen synthesis and fragile vessel walls

vascular disorder

75
Q

cushing disease

A

loss of vessel tissue and protein wasting- too much steroids such as predinisone

vascular disorder

76
Q

s/s of vascular disorders

A

easy burising with normal platelets and coag factors

77
Q

anticoagulants are used to

A

prevent thrombus formation, not dissolve formed clots but to prevent or manage the thromboebolic disorders such as MI, DVT, or PE

78
Q

Heparin

A

HIGH ALERT DRUG- change for serious error is high

synthetic preparation of natural anticoagulant produced by mast cells/basophils

give IV and SQ not orally

binds to antithrombin 3 and inactivated clotting factors IX,XI, XII (intrinsic pathway) and X (common pathway)

inhibits prothrombin to thrombin

79
Q

for heparin, assessed PTT by

A

measuring intrinsic pathway function at factors IX and VIII

80
Q

What do we want PTT to be at

A

1.5 or 2.5 baseline
control–(30 seconds normal) to be therapeutic

range differs depending on anticoagulation desired

81
Q

the longer the time of PTT the..

A

more anticoagulation or hemorraging

82
Q

PTT might be prolonged with

A

heparin use, clotting factor deficiencies warfarin

83
Q

does heparin cross the placental barrier

A

no

84
Q

what do we reverse heparin with

A

protamine sulfate

85
Q

AE of heparin

A

bleeding, HIT, HITT

s/s would occur 4-10 days after heparin exposure

86
Q

low molecular weight heparin example

A

enoxaparin (lovenox) and fondaparainus (atrixa)

87
Q

low molecular weigth heparin has similar actions and usese as..

A

heparin

88
Q

administer low molecular weight heparin in

A

the abdomen ALWAYS and further away from umbillicus, do not expel the air bubble

**it does not require close monitoring of blood coags

less thrombocytopenia than heparin

89
Q

Warfarin (coumadin)

A

most common oral anticoagulant,

acts in the liver and prevents sythesis of vitamin K dependent clotting factors such as:
* factor VII EXTRINSIC and factors II and X-common pathway*

HIGHLY protein bound and depends on how much protein the person has in their bodies

90
Q

similar to vitamin K in structure and acts as a competitive agonist to hepatic use of vitamin K

A

Warfarin (coumadin)

91
Q

How long does warfarin take to become therapeutic

A

3-5 days. HAS NO EFFECT ON PLATELET FUNCTION

92
Q

warfarin uses

A

long term prevention or management for venous thromboemolic disorders and prevents clots with A fib and prosthetic heart valves to decrease reinfarction

93
Q

warfarin is contraindicated in

A

GI bleeds or history of bleeding, severe kidney or liver disease, pregnancy

94
Q

antidote for warfarin

A

Vitamin K.

95
Q

Warfarin is assessed and dosed by

A

PT/INR

96
Q

drug interactions: herbal and dietary supplements to avoid when taking warfarin

A

avoid dietary supplements containing MVI’s

avoid: garlic, ginger, ginko, ginseng since it can increase the effects of the med

97
Q

When warfarin is initiated it should be overlapped with what

A

heparin for 4-6 days until the INR is >2.0 on two consecutive days

98
Q

INR measures

A

warfarin

99
Q

PT/INR measures

A

extrinsic and common pathway clotting cascased.

assessed daily until maintenance dose is reached then every 2-4 weeks

100
Q

control for PT/INR

A

10 seconds; therapeutic is 2X the control

101
Q

INR value ranges

A

2.0-3.5

102
Q

direct thrombin inhibitors uses

A

used to prevent stroke with atrial fib

incstead of coumadin in patients where coumadin is contraindicated or have difficulty regulating INR

103
Q

AE of direct thrombin inhibitor

A

bleeding,

less food interactions, take twice daily, no INR monitoring, no antidote!!!

104
Q

direct thrombin inhibitor example

A

dabigatran (Pradaxa)
anticoagulant

Direct factor Xa inhibitor, binds thrombin and prevents conversion of fibrinogen to fibrin

105
Q

what medication prevents the conversion of fibrinogen to fibrin

A

dabigatran- direct thrombin inhibitor

106
Q

antiplatelet agents prevent

A

platelet aggragation and decrease platelet plug.

107
Q

what is an example of an antiplatelet agent

A

thromboxaine A2

108
Q

ASA (aspirin) prevents

A

formation of thromboxaine A2 and effects last for the life of the plaetelet 7-10 days

109
Q

NSAIDS inhibit

A

COX

110
Q

adenosine diphoshate receptor agonist example

A

Ticlopidine (Ticlid), Cilostazol (Pletal) and Chlopidogrel (plavix)

they ihhibit aggregation by preventing ADP induced binding b/n platelets and fibrinogen

111
Q

Glycoprotein IIb/IIIa Receptor Antagonists examples

A

abicimab
tirofiban

prevents binding of clotting factors or by preventing the action of IIb/IIIa and inhibits platelet aggregation

USE POST MI WITH STENT PLACEMENTS

112
Q

Dipyridamole (persantine)

A

mechanism is unknown, inhibits platelet adhesion,

prevents thromboembolic events

may be used in conjunction with warfarin or aspirin

113
Q

Thombolytic agents:

A

streptokinase, urokinasem tPA

converts plasminogen to plasmin, lyses fibrin and dissolves clots

114
Q

thombolytic agents are used for

A

treatment of MI, ischemic stroke and arterial clots

115
Q

most common adverse effect for thrombolytics

A

intracranial bleeding)

116
Q

contraindications for thrombolytics

A

history of intracranial hemorrage or aneurysm, suspected aortic dissection, active bleeding, significant closed head or facial trauma within 3 months, history of poorly controlled hypertension, ischemic stroke greater 3 months, active PUD

117
Q

if fibrinogen levels are low…

A

DIC (clotting factors)

118
Q

if fibrinogen levels are high…

A

CV disease or inflammation

119
Q

Alkylating agents are used for the treatment for which types of cancers

A

blood cancers, breast, ovarian, lung

120
Q

alkylating agents break down

A

DNA helix strands, interfering iwth replication- CCNS

121
Q

cyclophophamid (cytoxan) is what type

A

alk agent- nitroous mustard

122
Q

ALKYLATING AGENTS AE?

A

Hemorrhagic cystitis- sudden onset of hematuria, bladder pain, inflammation. Sepsis

Patho Exam 4 (2 decks)

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