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DT1 > Hemodynamics and Clotting > Flashcards

Hemodynamics and Clotting Flashcards

1
Q

What does normal hemostasis rely on?

A

maintenance of blood in a fluid, clot free state

induction of rapid and localized hemostatic plug at site of vascular injury

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2
Q

What regulates hemostasis?

A

platelets
coagulation cascade
endothelium

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3
Q

What is the first event in primary hemostasis?

A

vasoconstriction as a result of endothelin and reflex

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4
Q

What steps occur in platelet adhesion?

A

bind to ECM via von Willebrand factor (produced by endothelium)

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5
Q

What occurs during platelet activation?

A

shape changes and release secretory granules which recruit more platelets

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6
Q

How is secondary hemostasis activated?

A

tissue factor-activates coagulation cascade
thrombin-converts fibrinogen to fibrin
cross-linked fibrin forms permanent plug

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7
Q

What are the primary sites for the coagulation cascade to occur?

A

phospholipids on activated platelets, bind Ca (cofactor for cascade)

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8
Q

What are the important mediators in platelet aggregation?

A

ADP and thromboxane A2-amplify aggregation forming primary hemostatic plug
thrombin binds to protease activated receptor on platelet membrane causing further aggregation
still reversible

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9
Q

What does fibrinogen bind to?

A

GP2b3a for aggregation

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10
Q

What moderates the size of clot?

A

fibrinolytic cascade

plasmin cleaves fibrin to fibrin split products

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11
Q

What are the anti-thrombotic properties of endothelial cells?

A

PGI2 and NO vasodilators

ADPase inhibits platelet aggregation by breaking down ADP

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12
Q

What is the mechanism of action for thrombomodulin?

A

binds thrombin
activates protein C
with protein S inactivates factors 5 and 8

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13
Q

What is the mechanism of action for anti-thrombin III?

A

inhibits the activity of thrombin, 10 and 9

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14
Q

What is the mechanism of action for tissue factor pathway inhibitor?

A

inhibits the activity of 7 and 10

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15
Q

What is the mechanism of action for tissue type plasminogen activator?

A

converts plasminogen to plasmin

plasmin cleaves fibrin, degrading thrombi

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16
Q

What are the pro-thrombotic properties of endothelial cells?

A

von Willebrand factor-cofactor in binding platelets to ECM
thrombomodulin-expression down regulated by activated endothelial cells
tissue factor-activates extrinsic coagulation cascade
plasminogen activator inhibitor-limits fibrinolysis

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17
Q

What stimulates the synthesis of tissue factor?

A

stimulated by TNF, IL-1, bacterial endotoxins

activates extrinsic coagulation cascade

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18
Q

What is Virchow triad?

A

endothelial injury
abnormal blood flow
hypercoagulability

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19
Q

What can cause injury to the endothelium?

A

HTN, turbulent flow, bacterial endotoxins

increased procoagulant factors, decreased anti-coagulant effectors

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20
Q

What is abnormal blood flow?

A

disruption of laminar flow
turbulence and stasis
turbulence from plaques
stasis from aneurysms, flaccid myocardium post MI, heart chamber dilation, a-fib

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21
Q

What are the causes of hypercoagulability?

A

primary-genetic-mutation in factor V, prothrombin, MTHFR (increases homocysteine), deficiencies in antithrombin III, protein C, protein S

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22
Q

What is factor 5 Leiden?

A

mutant factor 5 is resistant to cleavage by protein C
Arg to Glu at 506
heterozygotes 5x relative risk, homozygotes 50x relative risk

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23
Q

What happens due to a mutation in the prothrombin gene?

A

mutation causes elevated prothrombin levels

3x relative risk of venous thrombosis

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24
Q

What happens due to the MTHFR gene?

A

variant in 5,10 methylenetetrahydrofolate reductase

causes modest elevation of homocysteine (inhibits antithrombin III-promotes clotting)

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25
Q

What are the secondary hypercoagulability states?

A 
prolonged immobilization
MI, a fib, prosthetic cardiac valves
tissue damage
cancer
DIC
heparin-induced thrombocytopenia
antiphospholipid antibody syndrome
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26
Q

What is antiphospholipid antibody syndrome?

A

formerly called lupus anticoagulant syndrome
antibodies bind to protein epitopes exposed by phospholipids
clinical-recurrent thrombi and miscarriages, cardiac valve vegetations, thrombocytopenia, prolonged PTT
treatment-chronic anticoagulation, immunosuppression

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27
Q

What are other secondary risks (lower) for hypercoagulability?

A

cardiomyopathy, nephrotic syndrome, hyperestrogenic states, oral contraceptives, sickle cell anemia, advancing age (decrease PGI2), cigarette smoking, obesity

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28
Q

What are combined states of hypercoagulability?

A

homozygous mutations
concurrent inheritance of different mutations (combined heterozygosity)
mutations plus acquired risk factors
–patients under 50 with DVT should be checked for genetic risk factors even in setting of acquired risk factors

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29
Q

What are lines of Zahn?

A

pale layers are platelets
darker layers are fibrin and RBCs
more prominent in arterial thrombi

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30
Q

Where does a thrombus attach?

A

underlying heart or vessel wall

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31
Q

What are the characteristics of an arterial thrombus?

A

usually occlusive-coronary, cerebral, femoral
usually overlies atherosclerotic plaque
gray-white, friable mesh of platelets, fibrin, RBCs and WBCs
grows retrograde to blood flow (toward the heart)

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32
Q

What are the characteristics of a venous thrombus?

A

essentially always occlusive
lower extremities (90% of cases)
Red-more RBCs
grow in direction of blood flow (toward heart)
propagating tail-not well attached and prone to embolization

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33
Q

What are the characteristics of a post-mortem clot?

A

usually not attached
dependent portion is dark red
supernatant is yellow, gelatinous like chicken fat

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34
Q

What are the possible fates of a thrombus?

A

propagation
embolization
dissolution
organization and recanalization

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35
Q

What happens during organization and recanalization?

A

endothelial cells, fibroblasts, smooth muscle cells grow into clot
small channels develop through clot
clot may incorporate into vessel wall

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36
Q

What is the fate of a superficial venous thrombosis?

A

rarely embolize

cause edema distal to obstruction, predispose overlying skin to injury, infection, ulceration

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37
Q

What is a deep venous thrombosis?

A

at or above knee most likely to embolize
collateral circulation can relieve pain
diagnosis-ultrasound or angiogram
treat with anticoagulation

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38
Q

What does a coronary artery thrombosis cause?

A

MI

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39
Q

What does a cerebral artery thrombosis cause?

A

stroke, TIA

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40
Q

What does a femoral artery thrombosis cause?

A

gangrene

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41
Q

What does an atrial mural thrombus cause?

A

secondary to a-fib or mitral valve stenosis, can embolize

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42
Q

What does a ventricular mural thrombus cause?

A

secondary to MI, cardiomyopathy, can embolize

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43
Q

What is an embolism?

A

a detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin

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44
Q

What causes pulmonary thromboembolisms?

A

DVT in 90% of cases

often occurs as multiple emboli, sequentially or shower

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45
Q

What is the clinical presentation of massive occlusion of pulmonary circulation?

A

sudden death, right heart failure (cor pulmonale) or cardiovascular collapse

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46
Q

What is the clinical presentation of medium sized arterial occlusion?

A

hemorrhage but not infarction due to dual circulation

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47
Q

What is the clinical presentation of end arteriole occlusions?

A

infarction

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48
Q

What is a systemic thromboembolism?

A

80% come from heart (intracardiac mural thrombi)
others from aortic aneuysm, atherosclerosis, valvular vegetations
paradoxical (from R to L shunt) allows it to bypass lungs
go to lower extremities (most common) and cause ischemia or infarction-depends on extent of collateral or dual circulation

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49
Q

What is a fat embolus?

A

microscopic fat globules may be found in circulation after fracture of long bones

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50
Q

What is the clinical presentation of fat embolism syndrome?

A

1-3 days post injury
pulmonary insufficiency
neurologic effects
anemia and thrombocytopenia (see petechiae)
due to obstruction of pulmonary and cerebral microvasculature

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51
Q

What is an air embolus?

A

obstruction of circulation by large or coalesced gas bubbles
sources-neck and chest injuries, obstetric procedures, thoracentesis, hemodialysis

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52
Q

What is decompression sickness?

A

air breathed at high pressure increases amount of air that dissolves in the blood
gas bubbles out of the blood during rapid depressurization forming emboli
in muscle-the bends
treat with 100% O2, compression chamber

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53
Q

What is an amniotic fluid embolus?

A

infusion of amniotic fluid or fetal tissue into maternal circulation at delivery
initial sx-sudden severe dyspnea, cyanosis, hypotensive shock, then seizures and coma
late-pulmonary edema and DIC

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54
Q

anticoagulants

A

inhibit fibrin formation

heparin, LMW heparin, warfarin, fondaparinux, argatroban, dabigatran

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55
Q

antiplatelets

A

inhibit platelet aggregation

aspirin, dipyridamole, clopidogrel, ticlopidine, abciximab, eptifidatide

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56
Q

thrombolytics

A

dissolve formed fibrin clots

streptokinase, alteplase, anistreplase, tenecteplase

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57
Q

heparin

A

porcine unfractioned

cleaved by endo-D-glucuronidase into various fractions

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58
Q

MOA heparin

A

reversibly binds ATIII
active coagulation factors bind irreversibly to ATIII (Arg-Ser) to prevent fibrin generation
suicide substrate

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59
Q

heparin in pregnancy

A

approved because it does not cross the placenta

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60
Q

administration of heparin

A

injected sc or iv (im contraindicated induce hematoma)
monitor partial thromboplastin
increase lipoprotein lipase activity

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61
Q

adverse effects of heparin

A 
bleeding
HIT (type I non immune mediated, type II immune mediated based on heparin platelet factor 4 complex)
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62
Q

reversal of heparin induced bleeding

A

reverse with plasma, whole blood or protamine

do not give to NPH insulin or fish allergy for protamine

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63
Q

LMW heparin

A

too small to simultaneously bind ATIII and thrombin

specific for ATIII inactivation of X (low affinity for thrombin)

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64
Q

indications for LMW heparin

A

unstable angina or STEMI

monitor anti-X activity

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65
Q

advantages of LMW heparin

A

longer half life
outpatient
lower incidence of thrombocytopenia
predictable response

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66
Q

fondaparinux

A

administer iv or sc

inactivation of factor X

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67
Q

MOA warfarin

A

inhibits synthesis of biologically active vitamin K dependent clotting factors
clotting factors cant bind Ca (2,7,9,10,C,S)

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68
Q

time for action of warfarin

A

5-7 days for generation of coagulation factors incapable of binding Ca
oral administration

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69
Q

warfarin monitoring

A

monitor INR (prothrombin time)
measures extrinsic pathway
goal of 2-3 (2.5-3.5 for heart valve replacement)

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70
Q

polymorphisms for warfarin

A

CYP2C9*1 normal (2 and 3 decreased clearance)

VKORC1 G normal (A synthesizes less VKORC1 so less protein for warfarin to bind)

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71
Q

increase warfarin effect

A 
aspirin
ketoconazole and erythromycin
cimetidine
ibuprofen
cephalosporins
sulfa/trimeth
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72
Q

decrease warfarin effect

A

cholestyramine
rifampin
phenobarbital
cigarette smoking

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73
Q

contraindications for warfarin

A

not in pregnancy
causes nasal hypoplasia in first trimester
CNS, increased fetal death in second and third trimester

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74
Q

treatment of excessive bleeding on warfarin

A 
whole blood or plasma
viramin K (takes 24 hrs)
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75
Q

direct thrombin inhibitors

A

argatroban or dabigatran (oral)

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76
Q

argatroban

A

directly block active site on thrombin

use for patients with HIT

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77
Q

dabigatran

A

prodrug with affinity for free and fibrin bound thrombin

converted to active by plasma esterases

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78
Q

excretion of dabigatran

A

less drug interactions
substrate for p-glycoprotein
glucuronide metabolites
use with caution in diminished renal function

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79
Q

aspirin MOA

A

irrevesible inhibitor of Cox1/2

acetylates enzyme

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80
Q

adverse reactions aspirin

A

bleeding
GI irritation
GI ulcers

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81
Q

dipyridamole MOA

A

inhibits phosphodiesterase
increases platelet cAMP levels
used with warfarin

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82
Q

MOA clopidogrel and ticlopidine

A

prodrugs-metabolized to active thiol metabolite
irreversibly bind ADP P2Y12 R on platelets
inhibits ADP activation of 2b3a

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83
Q

ticlopidine and clopidogrel characteristics

A

irreversible inhibitors
Ticlo-forms dissulfide link between the drug and SH group on CYS of receptor
Ticlo longer lasting
clipidogrel less side effects

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84
Q

Ticlopidine and clopidogrel side effects

A

bleeding
agranulocytosis and thrombocytopenia
Thrombocytopenia purpura risk ticlopidine>clopidogrel

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85
Q

cangrelor

A 
reversible P2Y12 receptor inhibitor
administer IV (reversed in 1 hr)
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86
Q

abciximab

A

Ab binds to 2b3a receptor
more effective
longer half life

87
Q

eptifibatide

A

peptide derivative
less effective than abciximab
good for unstable angina or angioplasty

88
Q

contraindications for abciximab and eptifibatide

A

history of hemorrhagic stroke
surgery in past 6 weeks
thrombocytopenia
cannot use with warfarin

89
Q

tPA

A

more rapidly activates plasminogen bound better than in circulation
binds fibrin via lysine binding sites

90
Q

circulating plasmin inactivation

A

alpha 2 antiplasmin and PAI-1

91
Q

streptokinase MOA

A

binds to plasminogen to form complex

complex converts second molecule of plasminogen to plasmin

92
Q

adverse effects of streoptokinase

A

fever
bleeding
lytic state (plasmin exceeds capacity of alpha 2 antiplasmin)
highly antigenic

93
Q

contraindications of strepotkinase

A

surgery or trauma in past 10 days
pre-existing bleeing disorder
diastolic >110
intracranial trauma

94
Q

antistreplase

A

streptokinase and plasminogen with catalytic site acylated-removed by plasma enzymes
more specific binding to fibrin (less lytic state)

95
Q

tenecteplase

A

more specific binding to fibrin than alteplase
more resistant to PAI-1
longer half life

96
Q

adverse reactions for all thrombolytics

A

bleeding due to inducing hypocoagulable state

97
Q

aminocaproic acid

A

inhibitor of fibrinolysis

lysine analog binds to lysine binding sites on plasminogen and plasmin (inhibits interaction of plasmin and fibrin)

98
Q

causes of excessive bleeding

A

increased vessel fragility
platelet deficiency or dysfunction
derangement of coagulation

99
Q

platelet function analysis

A

stimulates in vivo conditions
utilizes platelet agonists
prolonged with ADP and Epi-vWD; normal with ADP from aspirin

100
Q

PTT partial thromboplaastin time

A

kaolin+cephalin+calcium

test intrinsic and common pathway

101
Q

PT prothrombin time

A

tissue thromboplastin+Ca

test extrinsic and common pathway

102
Q

mixing study

A

serum and pooled sera
if corrected PTT-factor deficiency
if still abnormal-inhibitor present

103
Q

clotting factors

A

specific factor poor plasma and patient plasma

104
Q

vessel abnormalities

A

see petechiae and purpura

drug complexes cana cause leukocytoclastic vaculitis

105
Q

impaired collagen support

A

scurvy-vitamin C def required for hydroxylation of procollagens
Ehler-Danlos
elderly
cushing-protein wasting

106
Q

Henoch-Schonlein Purpura

A

hypersensitivity disease complexes deposit in vessels

colicky abdominal pain, polyarthralgias, AGN

107
Q

hereditary hemorrhagic telangiectasia

A

AD

dilated tortuous vessels with thin walls

108
Q

amyloid infiltation

A

weakens vessel walls

109
Q

thrombocytopenia

A

spontaneous bleeding of small vessels <20k

skin, mucus membranes, GI, GU, intracranial

110
Q

etiologies of thrombocytopenia

A

decreased production (bone marrow)
increased peripheral destruction/decreased survival
sequestration
dilutional effect secondary to massive transfusions

111
Q

neoplastic thrombocytopenia

A

non-hematopoietic (prostate, breast, neuroblastoma)

hematopoietic-AML, ALL, MDS, lymphoma

112
Q

non neoplastic causes of thrombocytopenia

A

infections
drugs
EtOH, toxins
B12/folate deficiency

113
Q

immune thrombocytopenic purpura

A

primary-idiopathic autoimmune
secondary-identifiable etiology
chronic-SLE, HIV, viruses (peripheral blood with giant platelets increased MPV)
acute-abrupt onset after viral illness, self limited

114
Q

chronic ITP

A

IgG Ab against platelet antigens
removed by spleen but it is normal size
BM-increased megs with left shift

115
Q

treatment of ITP

A

immunosuppression with steroids
splenectormy
IVIG
Rituximab CD20 Ab

116
Q

HIT Type 1

A

most common
moderate thrombocytopenia
few days of heparin due to platelet aggregation

117
Q

HIT Type 2

A

5-14 days after heparin is started
moderate to severe drop in platelets
Ab directed against heparin-platelet factor 4 complex result in direct platelet activation
risk lower with LMW (but cannot give it again)

118
Q

HIV auto-immune thrombocytopenia

A

CD4 on surface of megs
results in dysregulation and hyperplasia of B cells
Auto Ab towards GP2b3a

119
Q

TTP pentad

A 
fever
thrombocytopenia
microangiopathic hemolytic anemia
neurologic sx
renal failure
120
Q

HUS symptoms

A

thrombocytopenia
microangiopathic hemolytic anemia
acute renal failure
mostly kids

121
Q

TTP pathogenesis

A

ADAMTS 13 deficiency

deficiency results in accumulation of HMW multimers can promote platelet microaggregation

122
Q

presentation of TTP

A 
hyaline thrombi (platelet aggregates) form
platelet consumption leads to thrombocytopenia
schistocytes and organ dysfunction
123
Q

treatment of TTP

A

total plasma exchange to remove auto-Ab

do not give platelet transfusions

124
Q

HUS presentation

A

bloody diarrhea and renal failure
associated with E. coli O157H7
treat with supportive care

125
Q

acquired platelet abnormalities

A

ASA, NSAID

uremia

126
Q

congenital platelet abnormaliteis

A

Bernard Soulier
Glanzmann
storage pool disorders

127
Q

Bernard Soulier

A

AR deficient Gp1b
everything works but ristocetin
giant platelets

128
Q

Glanzmann

A

AR Gp2b3a

only ristocetin works

129
Q

clinical findings of clotting abnormalities

A

prolonged bleeding after laceration, trauma or surgery
bleeding into GI/GU
bleeding into weight bearing joints

130
Q

von Willebrand Disease

A

prolonged bleeding from cuts, menorrhagia, mucous membrane bleeding
abnormal PFA and PTT
normal platelet count

131
Q

subtypes of von Willebrand Disease

A 
type 1-quantitaive AD
DDAVP before surgery 
type 2-qualitative AD
defective multimer assembly
type 3-quantitative decrease
low levels (give humate P)
132
Q

Hemophilia A

A

8 cofactor for 9

X linked recessive

133
Q

symptoms of hemophilia A

A

easy bruising, massive hemorrhage after surgery/trauma
hemarthrosis
no petechiae and no mucous membrane bleeding

134
Q

diagnosis of hemophilia A

A

prolonged PTT

treat with humate P or recombinant factor

135
Q

symptoms occur in hemophilia A

A

extrinsic is burst to get cascade moving but intrinsic pathway maintains it
inappropriate fibrinolysis not inhibited

136
Q

hemophilia B

A

x linked recessive

deficiency in IX

137
Q

acquired clotting factor abnormalities

A

vitamin K deficiency
liver disease
DIC

138
Q

DIC

A

pathologic activation of coagulation cascade in microvasculature

139
Q

DIC tests

A

prolonged PT, PTT
decreased platelets and decreasing fibrinogen
increased D-dimer

140
Q

etiologies of DIC

A

obstetric-placental abruption, retained products of conception, septic aborption
infections-gram negative sepsis and meningococcemia
neoplasms-APL and adenocarcinoma
massive tissue injury

141
Q

mechanism of DIC

A

tissue factor released leading to fibrin deposition in microvasculature
endothelial cell injury leads to hemorrhagic diathesis

142
Q

pathologic findings for DIC

A

thrombi in brain, heart, lungs, kidney, adrenals, spleen, and liver
micro-infarcts and hemorrhage

143
Q

Waterhouse-Friederichsen Syndrome

A

bilateral adrenal hemorrhage associated with meningococcus

144
Q

Sheehan syndrome

A

postpartum pituitary necrosis

145
Q

toxemia of pregnancy

A

microthrombi in placenta

146
Q

DIC presentation

A 
microangiopathic hemolytic anemia
petechiae and purpura
dyspnea
convulsions
oliguria, acute renal failure
circulatory shock
147
Q

DIC peripheral smear

A

schistocytes, increase reticulocytes
leukocytosis and neutrophilia, left shift
decrease in platelets

148
Q

shock

A

final common pathway for potentially lethal clinical events-massive hemorrhage, extensive trauma and burns, massive MI, massive PE, bacterial sepsis
hypoperfusion and cellular hypoxia result in injury-initially reversible but eventually irreversible

149
Q

categories of shock

A 
cardiogenic shock
hypovolemic shock
spetic shock
anaphylactic shock
neurogenic shock
150
Q

SIRS

A

exaggerated and generalized manifestation of a local inflammatory reaction, often fatal
massive inflammatory reaction due to cytokines (TNF, IL1, IL6, PAF)

151
Q

diagnosis of SIRS

A 
two or more signs of systemic inflammation
temp >100.4, <95
HR>90
RR>20
WBC>12k or <4k
>10% immature WBC
152
Q

Sepsis

A

SIRS with culture-proven infection or obvious infection

153
Q

Septic shock

A

clinical sepsis severe enough to lead to organ dysfunction and hypotension

154
Q

epidemiology of septic shock

A

mortality rate 20%

number one cause of deaths in ICUs

155
Q

triggers of septic shock

A

gram positive bacterial infections

gram negative and fungal infections

156
Q

pathophysiologic factors of septic shock

A 
inflammatory mediators
endothelial cell activation and injury
metabolic abnormalities
immune suppression
organ dysfunction
157
Q

inflammatory mediators for septic shock

A

TLR start sepsis
TNF, IL1, IFN gamma, IL12, IL18 creates pro-inflammatory state
prostaglandins and PAF activate endothelial cells, causing adhesion molecule synthesis and pro-coagulant state
complement cascade activated by microbial components

158
Q

endothelial activation in septic shock

A

results in thrombosis, increased vascular permeability, vasodilation

159
Q

thrombosis in septic shock

A

inflammatory mediators stimulate tissue factor and PAI-1 production
decreased production of tissue factor pathway inhibitor, thrombomodulin and protein C
decreased blood flow producing stasis
increased vascular permeability-third spacing and edema
vasodilation due to increased NO synthesis

160
Q

metabolic abnormalities in septic shock

A

hyperglycemia and insulin resistance
cytokines, stress hormones and catecholamines drive gluconeogenesis
pro-inflammatory creates insulin resistance
hyperglycemia decreases neutrophil function

161
Q

myocardial contractility

A

weakened by cytokines and secondary mediators decreasing cardiac output

162
Q

adult respiratory distress syndrome

A

decreased CO, increased vascular permeability and endothelial injury damage lungs

163
Q

nonprogressive phage of septic shock

A

reflex mechanisms compensate and tissue perfusion is maintained (SIRS)

164
Q

progressive stage

A

tissue hypoperfusion ensues with worsening circulatory and metabolic imbalances including acidosis

165
Q

irreversible state

A

extent of cellular and tissue injury is so great that death is inevitable even with infection control and hemodynamic correction

166
Q

treatment of septic shock

A 
control infection
fluid resuscitation and vasopressor drugs
insulin therapy for hyperglycemia
corticosteroids
anti-inflammatory (not successful)
activated protein C (controversial)
167
Q

ABO grouping

A 
difference is one sugar
B-galactose
A-N acetyl galactosamine
O-no sugar
most common is O
168
Q

universal donor

A

group O

169
Q

universal recipient

A

group AB

170
Q

Rh+

A

can give Rh negative to Rh positive
can give Rh positive to Rh negative if patient has no anti-D
15% Rh-

171
Q

Anti-D can cause

A

hemolytic disease of newborn

acute hemolytic transfusion reactions

172
Q

packed red blood cells

A 
increase blood oxygen carrying capacity
increase HCT 3%
give for symptomatic anemia
store 1-6C
can only give through IV with normal saline
173
Q

frozen RBC

A

frozen in glycerol for 10 yrs
thaw and use within 24 hrs
give for autologous units, rare blood types, IgA def

174
Q

washed RBC

A

washed in saline
shelf life 24 hrs
give for IgA def, allergic reactions to plasma proteins

175
Q

platelets

A

random or platelet apheresis from single donor
stored at room temp for 5 days
6 pack will raise 30k

176
Q

indications for platelets

A

thrombocytopenia (not actively bleeding)
bleeding without thrombocytopenia (aspirin, uremia)
massive transfusion

177
Q

platelet refractory

A

does not increase platelets after transfusion

causes-splenomegaly, accelerated consumption from DIC, sepsis, alloimmunization

178
Q

leukoreduced platelets and PRBC

A

reduces WBC content
decreases incidence of alloimmunization against WBC antigen, decreased risk of CMV transmission, decreased risk of febrile nonhemolytic transfusion

179
Q

fresh frozen plasma

A

within 8 hrs of drawing
1 IU of each coagulation factor per cc/plasma
18C until needed for 1 year
indications-significant bleeding with coagulation deficiency, correction of PTT and PT, TTP, massive transfusion

180
Q

inappropriate use of fresh frozen plasma

A

volume expansion

coagulation factor replacement

181
Q

cryoprecipitate

A

rich in fibrinogen, vWF, factor 8 and 13

used for fibrinogen replacement

182
Q

human derived products

A

factor 8, vWF (humateP), Rhogam, IVIG, 4 Prothrombin complex concentrate (2,7,9,10)

183
Q

type and screen

A

blood type and antibody screen

IAT-if positive blood is cross patched

184
Q

type and cross

A

type and screen
test donor cells against patient plasma
always protect transfused blood from antibodies in patient

185
Q

DAT

A

test patient RBC for attached IgG or compliment

186
Q

IAT

A

test patient serum for antibodies

done for TS and TC

187
Q

positive DAT

A

hemolytic transfusion reaction
patient antibody on transfused RBC
negative rules out majority of autoimmune anemias and acute hemolytic transfusion reactions

188
Q

positive IAT

A

alloantibody against foreign RBC antigens

autoantibody can also sometimes be detected

189
Q

febrile reactions

A 
acute hemolytic transfusion reaction
febrile non-hemolytic transfusion reaction
infection
TRALI
delayed hemolytic transfusion reaction
GVHD
infection
190
Q

nonfebrile reactions

A 
anaphylaxis
urticaria
TACO
hypotension
iron overload
infection
191
Q

distribution of water

A 
intra
extra
interstitial
intravascular 
(from high to low)
192
Q

forces governing movement of fluid in and out of blood vessel

A

hydrostatic pressure

osmotic or oncotic pressure

193
Q

increased intravascular oncotic pressure

A

venous side due to fluid loss due (from hydrostatic pressure)

194
Q

exudate

A

protein rich due to increased vascular permeability (inflammatory edema-allows large molecules to leak out of the vessels)

195
Q

transudate

A

non-inflammatory edema

protein poor

196
Q

causes of noninflammatory edema

A

increased hydrostatic pressure
reduced plasma oncotic/osmotic pressure (hypoproteinemia)
lymphatic obstruction
sodium and water retention

197
Q

DVT causing edema

A

increase hydrostatic pressure (localized)

198
Q

CHF causing edema

A

systemic edema due to generalized increase in hydrostatic pressure
treat with salt restriction, diuretics, aldo antagonists

199
Q

edema from reduced plasma oncotic pressure

A

albumin loss-nephrotic syndrome
reduced albumin syntehsis-liver cirrhosis, protein malnutirtion
loss of fluid from intravascualr space leads to decreased renal perfusion and activation of R/Angio/Aldo

200
Q

causes of lymphatic obstruction

A 
filariasis-inflammatory and obstructive
neoplastic obstruction (peau d'orange appearance of skin from lymphvascular invasion by breast cancer)
iatrogenic-axillary dissection
201
Q

sodium and water retention

A

increases hydrostatic pressure
decrease vascular osmotic pressure (dilutes proteins)
occurs in acute renal dysfunction

202
Q

diffuse edema

A

subq

affects all parts of body (seen in renal failure)

203
Q

dependent edema

A

subq

legs of mobile, sacrum of bed-ridden pt

204
Q

pulmonary edema

A

left sided heart failure, renal failure, lungs show frothy, blood-tinged fluid
from excess pre-load causing a backup
present with dyspnea, orthopnea, paroxysmal nocturnal dyspnea

205
Q

causes of cerebral edema

A

infection
neoplasm
hypertensive crisis (causes transudate)
venous obstruction

206
Q

effusions

A

accumulations of fluid in body cavities

207
Q

hyperemia

A

active process

increased blood inflow into tissues due to dilation of arterioles (inflammation, blushing, exercise), appears red

208
Q

congestion

A

passive process

stagnation of blood in capillaries due to impaired out flow, tissue appears dusky red or bluish

209
Q

heart failure cells

A

alveolar spaces contain hemosiderin-laden macrophages

210
Q

healing of ecchymoses

A

hemoglobin (red-blue) to bilirubin (blue-green) to hemosiderin (gold-brown)

211
Q

hypovolemic shock

A

> 20% loss of blood

212
Q

infarction color classification

A

red-hemorrhagic (venous occlusions, tissues with dual circulation)
white-end arterial circulation

213
Q

liquefactive necrosis

A

CNS

DT1 (4 decks)

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