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
2
Q
Platelets are also known as
A
thrombocytes
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.
4
Q
How many platelets are usually in the blood
A
150,00-400,000
5
Q
Where are megakaryocytes formed
A
in the bone marrow and are immature and released when needed. They break apart to form platelets
6
Q
Thrombopoietin
A
controls the platelet production.
7
Q
Where is thrombopoietin made
A
the liver, kidney, smooth muscle, bone marrow
8
Q
low levels of thrombopoietin..
A
very rare
9
Q
Stages of normal clotting:
A
- ) vessel spasm
- )Formation of platelet plug
- ) Blood coagulation
- ) clot retraction/contraction
- ) clot dissolution
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
11
Q
Thromboxane A2
A
stimulates the activation of new platelets and increases aggragation
NSAIDS and Aspirin block this
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
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
14
Q
intrinsic pathway
A
occurs in vascular system and is slow..
Stage 3
15
Q
extrinsic pathway
A
occurs in tissues and is fast
Stage 3
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
17
Q
Procoagulation factors
A
circulate in blood, activated and converted to coagulation factors in specific series of steps
18
Q
procoagulation factors initiate
A
clotting
19
Q
Calciums importance on coagulation
A
Factor IV and is needed in almost all steps of coagulation. Hypocalcemic patients will have clotting issues
20
Q
Anticoagulation factors
A
inhibit clotting such as antithrombin 3, protein C, protein S, heparin
21
Q
Antithrombin 3
A
anticoagulation factor that neutralizes thrombin
22
Q
Protein C
A
anticoagulation factor that inhibits thrombin
23
Q
Protein S
A
enhances the action of protein C
24
Q
Heparin is contained in granules in..
A
basophils (wbcs)
25
Deficiency state of antithrombin, protein C, protein S and heparin causes
hypercoaguability
26
Stage 4:clot retraction
platelets contract and squeeze out serum of clot and pull vessel edges together
clot dries us and shrinks
27
Stage 5: fibrinolysis: clot dissolution
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
28
tPA
clot buster in medication form that activates or starts the clot dissolution process occuring in stage 5
29
FDP will be measured in the blood if..
they have been clotting a lot and there will be an increase in this number. Stage 5
30
hypercoagulable conditions occur due to
increased platelet function
increased activity of coagulation system
31
increased platelet function: hypercoaguable condition: occurs due to..
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
32
Increased activity of coagulation system: hypercoaguable conditions: occurs due to
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
33
Hypercoaguability can cause
MI, CVA, DVT, PVD, PE
34
Who is at risk for developing hypercoaguable conditions
post op patients, neuromuscular diseases, high levels of estrogen, cancer
35
DVT: risk factors
Virchows traid:
Stasis: bedrest, immobility, CHF, shock
Vessel wall injury: catheters, surgery or trauma
Hypercoaguability: genetic factors, trauma, pregnancy, BCP, cancer
36
DVT manifestations
asymptomatic or positive homan signs, pain, swelling, redness, fever
37
DVT treatment
anticoagulants to prevent additional thrombi and minimize venous valve damage
38
anticoagulants to not dissolve a clot but..
prevent further complications
39
Bleeding disorders are caused by defects of
platelets, coagulatiom pathways, blood vessels
40
Thrombocytopenia
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
41
S/S of thrombocytopenia
petichiae, purpura
42
ITP: idiopathic or immune thrombocytopenic purpura
causes, children, adults, etc
Autoimmune disease: platelet antibodies formed and platelets are destroyed in spleen
causes severe thrombocytopenia (
43
Removal of spleen might be helpful when a patient has
Bleeding disorder such as ITp (idiopathic thrombocytopenic purpura)
the spleen recognizes foreign antibodies of platelets and destroys platelets
44
S/S of ITP
increased bruising, bleeding, INCREASED SPLEEN SIZE, petechia, purpura
45
diagnosis of idiopathic thrombocytopenic purpura
platelets are
46
Treatment for ITPL (idiopathic thrombocytopenic purpura)
corticosteroids, immune globulin, splenectomy, thrombopoietin, receptor agonists (meds that stimulate thrombopoeitin receptors)
47
TTP: thrombotic thrombocytopenic purpura
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
48
TTP is similar to DIC but it
does not involve the clotting cascade
49
S/S of TTP:
fever, neurological changes such as headache, seizures (grand mal), decreased LOC, petechiae, pupura
50
Treatment for TTP
plasma exchange, steroids
51
Bleeding disorders: coagulation disorders result from
decrease in 1 or more clotting factors
may be due to decreased production or increased consumption (common after trauma)
52
hereditary disease for bleeding/coagulation disorders involve which factor
VII, IX or von willebrands factor
hemophilia A, hemophilia B, von willebrands disease
53
Vitamin K is needed for synthesis of
factors VII, IX, X and prothrombin
remember "1972" missing
warfarin can decrease this
PTT HIGH
54
conditions that decrease the GI flora and decrease absorption of vitamin K also lead to
decreased production of clotting factors
55
decreased production for coagulation disorders involves impaired synthesis of
clotting factors with liver disease: factors V, VII, IX, X, XII, prothrombin and fibrinogen
56
Hemophilia A
Bleeding disorder: coagulation disorder
| X-linked recessive inheritance that is passed on through the mom
57
hemophilia A primarily affects
males
58
S/s of hemophilia A
bruising, bleeding, GI bleeds, joint stiffness, contraction of joints, inflammation, nose bleeds
59
treatment for Hemophilia A
Factor VIII therapy given IV as prophylactic or for bleeding episodes
Gene therapy: carrier detection and prenatal diagnosis
60
Teaching a patient with hemophilia A..
avoid trauma, diagnosed mainly in kids, should avoid NSAIDS and aspirin, prophylactic treatments
61
Hemophilia B
Factor IX deficiency (christmas disease)
62
factor IX is needed for activation of
factor X in coagulation cascade, common pathway activation-->fibrin clot
63
signs and symptoms of hemophilia B
similar to hemophilia A but A is more common than B
64
Treatment for hemophilia B
administer recominant factor IX prophylactically and with acute bleeding episodes
65
Von Willebrand's disease
diagnosed as an adult
hereditary
defect in von willebrands factor-carried factor VII and results in decreased platelet aggregation and adhesion
66
Von willebrand's disease S/s
bleeding following OR, dental procedures, PG/delivery, heavier menstraul bleeding, epistaxis
67
Treatment for von willebrands disease
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
DIC (disseminated intravascular coagulation)
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
release of endotoxins seems to be a common mediating factor for
DIC
70
S/S of DIC
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
Treatment for DIC
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
vascular disorders occur due to
bleeding from small blood vessels due to naturally weak vessel walls or due to inflammation or immune process
73
hemorrhagic telangiectasia
rare hereditary disorder with thing, dilated capillaries
vascular disorder
74
vitamin C deficiency (Scurvy)
decreased collagen synthesis and fragile vessel walls
vascular disorder
75
cushing disease
loss of vessel tissue and protein wasting- too much steroids such as predinisone
vascular disorder
76
s/s of vascular disorders
easy burising with normal platelets and coag factors
77
anticoagulants are used to
prevent thrombus formation, not dissolve formed clots but to prevent or manage the thromboebolic disorders such as MI, DVT, or PE
78
Heparin
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
for heparin, assessed PTT by
measuring intrinsic pathway function at factors IX and VIII
80
What do we want PTT to be at
1.5 or 2.5 baseline
control--(30 seconds normal) to be therapeutic
range differs depending on anticoagulation desired
81
the longer the time of PTT the..
more anticoagulation or hemorraging
82
PTT might be prolonged with
heparin use, clotting factor deficiencies warfarin
83
does heparin cross the placental barrier
no
84
what do we reverse heparin with
protamine sulfate
85
AE of heparin
bleeding, HIT, HITT
s/s would occur 4-10 days after heparin exposure
86
low molecular weight heparin example
enoxaparin (lovenox) and fondaparainus (atrixa)
87
low molecular weigth heparin has similar actions and usese as..
heparin
88
administer low molecular weight heparin in
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
Warfarin (coumadin)
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
similar to vitamin K in structure and acts as a competitive agonist to hepatic use of vitamin K
Warfarin (coumadin)
91
How long does warfarin take to become therapeutic
3-5 days. HAS NO EFFECT ON PLATELET FUNCTION
92
warfarin uses
long term prevention or management for venous thromboemolic disorders and prevents clots with A fib and prosthetic heart valves to decrease reinfarction
93
warfarin is contraindicated in
GI bleeds or history of bleeding, severe kidney or liver disease, pregnancy
94
antidote for warfarin
Vitamin K.
95
Warfarin is assessed and dosed by
PT/INR
96
drug interactions: herbal and dietary supplements to avoid when taking warfarin
avoid dietary supplements containing MVI's
avoid: garlic, ginger, ginko, ginseng since it can increase the effects of the med
97
When warfarin is initiated it should be overlapped with what
heparin for 4-6 days until the INR is >2.0 on two consecutive days
98
INR measures
warfarin
99
PT/INR measures
extrinsic and common pathway clotting cascased.
assessed daily until maintenance dose is reached then every 2-4 weeks
100
control for PT/INR
10 seconds; therapeutic is 2X the control
101
INR value ranges
2.0-3.5
102
direct thrombin inhibitors uses
used to prevent stroke with atrial fib
incstead of coumadin in patients where coumadin is contraindicated or have difficulty regulating INR
103
AE of direct thrombin inhibitor
bleeding,
less food interactions, take twice daily, no INR monitoring, no antidote!!!
104
direct thrombin inhibitor example
dabigatran (Pradaxa)
anticoagulant
Direct factor Xa inhibitor, binds thrombin and prevents conversion of fibrinogen to fibrin
105
what medication prevents the conversion of fibrinogen to fibrin
dabigatran- direct thrombin inhibitor
106
antiplatelet agents prevent
platelet aggragation and decrease platelet plug.
107
what is an example of an antiplatelet agent
thromboxaine A2
108
ASA (aspirin) prevents
formation of thromboxaine A2 and effects last for the life of the plaetelet 7-10 days
109
NSAIDS inhibit
COX
110
adenosine diphoshate receptor agonist example
Ticlopidine (Ticlid), Cilostazol (Pletal) and Chlopidogrel (plavix)
they ihhibit aggregation by preventing ADP induced binding b/n platelets and fibrinogen
111
Glycoprotein IIb/IIIa Receptor Antagonists examples
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
Dipyridamole (persantine)
mechanism is unknown, inhibits platelet adhesion,
prevents thromboembolic events
may be used in conjunction with warfarin or aspirin
113
Thombolytic agents:
streptokinase, urokinasem tPA
converts plasminogen to plasmin, lyses fibrin and dissolves clots
114
thombolytic agents are used for
treatment of MI, ischemic stroke and arterial clots
115
most common adverse effect for thrombolytics
intracranial bleeding)
116
contraindications for thrombolytics
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
if fibrinogen levels are low...
DIC (clotting factors)
118
if fibrinogen levels are high...
CV disease or inflammation
119
Alkylating agents are used for the treatment for which types of cancers
blood cancers, breast, ovarian, lung
120
alkylating agents break down
DNA helix strands, interfering iwth replication- CCNS
121
cyclophophamid (cytoxan) is what type
alk agent- nitroous mustard
122
ALKYLATING AGENTS AE?
Hemorrhagic cystitis- sudden onset of hematuria, bladder pain, inflammation. Sepsis
