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MDTI > Hematology - Sheet1 > Flashcards

Hematology - Sheet1 Flashcards

2
Q

What activates platelets

A

adhesion with vWF, binding thrombin, ADP, TxA2

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3
Q

Molecule stored in platelet granules

A

ADP, fibrinogen, VWF, calcium

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4
Q

Glanzmann’s thrombasthenia

A

platelets fail to expres 2 proteins for firbinogen receptor Integrin a2bb3

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8
Q

Thrombi

A

Thrombi

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9
Q

common location venus thrombi

A

around the valve in the vein

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10
Q

2 identifying features of thrombus

A

lines of zahn and site of attachment to vessel wall

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11
Q

postmortem clot layers

A

very red layer - current jelly and gelatinous yellow layer - chicken fat

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13
Q

Inherited Bleeding Disorders

A

Inherited Bleeding Disorders

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14
Q

factor for hemophilia A

A

8a

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15
Q

Factor for hemophilia B

A

9a

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16
Q

Glanzmann thrombasthenia clinical symptoms

A

easy brusing, epistaxis, Menorrhagia

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17
Q

Dual function Von Willebrand factor

A

platelet adhesion to endothelium. binds and carries coagulation factor 8 in plasma

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18
Q

Weibel-Palade bodies

A

storage granules in endothelial cells that store VWF and P-selecten

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19
Q

VWF central role in which disease

A

microcirculatory occlusions in thrombotic thrombocytopenic purpura

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20
Q

What proteolyzes VWF

A

ADAMTS13

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21
Q

VWF disorder inheritance pattern

A

autosomal dominant

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22
Q

VWF disorder typical bleeding

A

brusiing, bleeding after surgery, dental procedures

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23
Q

VWF disorder locations without bleeding

A

No muscle or joint bleeding

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24
Q

VWF disoder type 1

A

decreased amounts of normal

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25
Q

VWF disorder type 2

A

decreased amounts abnormal

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26
Q

VWF disorder type 3

A

severely decreased concentration and activity

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27
Q

VWF disorder functional measure

A

Use Ristocetin co-factor activity

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28
Q

VWF disorder multimer analysis

A

Type 1 has normal gel with less of everything. Type 2 has abnormal gel bc actual protein is messed up

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29
Q

PT and aPTT in VWF disorder

A

PT normal. aPTT can be abnormal if factor 8 levels are affected

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30
Q

VWF disorder treatment DDAVP

A

this causes release of vWF from endothelial storage sites.

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31
Q

VWF disorder treatment plasma

A

Plasma from factor 8 concentrates with vWF activity

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32
Q

VWF disorder treatment alternatives

A

provide anti-fibrolytic agents and simple pressure, ice etc.

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33
Q

hemophilia delayed bleeding

A

happens because platelets are functioning normally but can’t produce fibrin well so clot dissolves

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34
Q

Hemophilia common bleed sites

A

Joints, knees, elbows, shoulders, ankles, hips

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35
Q

Hemophilia PT aPTT

A

Prolonged aPTT

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36
Q

Why can’t you measure factor 9 at birth

A

Factor 9 always low at birth so cannot diagnose neonatal Hemophilia B

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37
Q

Primary vs Secondary Prophylaxis Hemophilia

A

Provide factor infusion before or after first joint bleeds

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38
Q

3 Treatment options Hemophilia

A

Plasma from factor concentrates, recombinant factor, Factor 7 recombinant to bypass the problems

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40
Q

Acquired Disorders

A

Acquired disorders

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41
Q

Which factor used to compare liver vs vitamin K problems

A

Factor 5 bc it is not vitamin K dependent. Helps diagnose long PT

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42
Q

Factor 8 response in liver disease

A

not affected the same. Often elevated bc not made by hepatocytes

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43
Q

thrombophlebitis

A

thrombosis and inflammation in veins near the skin. Can happen w thrombosis from adenocarcinomas

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44
Q

DIC initiation hypothesis

A

exposure of blood to tissue factor

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45
Q

lupus anticoagulant effect

A

causes artificial elongation of aPTT in vitro bc binding to phospholipids.

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46
Q

DIC bleeding vs thrombosis

A

Bleeding normally in acutely ill patients. Thrombosis classic with cancer

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47
Q

DIC PT aPTT

A

both elongated. aPTT less sensitive than PT

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48
Q

DIC significant lab

A

platelet counts are low. prsenece of fibrin degredation (D-dimers).

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49
Q

DIC cell pathology

A

RBC fragments (schistocytes) and thrombocytopenia bc mciroangiopathic hemolytic anemia.

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50
Q

Schistocytes

A

RBC fragments

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51
Q

Factor 13 function

A

cross-links fibrin. Need this before you get D dimers

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53
Q

DIC w cancer treatment

A

heparin to inhibit coagulation

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54
Q

DIC bleeding treatment

A

provide FFP, fibrinogen cryoprecipitate and platelet transfusion

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55
Q

antiphospholipid antibodies

A

includes lupus. some bind to phospholipids, others bind to phospholipid assocated proteins

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56
Q

Antiphospholipid antibody syndrome requirements

A

presence of antibodies at least 2 occasions w Thrombosis, pregnancy morbidity, or thrombocytopenia

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57
Q

5 Hereditary Thrombophilias

A

Factor 5 leiden, prothrombin mutation, protein c deficiency, protein s deficiency, antithrombin deficiency

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58
Q

Most important risk of hereditary thrombophilias

A

increased risk of venous thromboembolism or VTE

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59
Q

heparin mechanism

A

imrpoves anticoagulant activity of AT

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60
Q

Antithrombin deficiency genetics

A

autosomal dominant

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61
Q

antithrombin deficiency Type 2 groups

A

Thrombin binding site defects, heparin binding site defects, defects affecting thrombin and heparain binding

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62
Q

AT deficiency assays

A

antigen assay measure AT levels. Functional assays measure ability to neutralize thrombin and FXa

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63
Q

AT function

A

forms complexes and inhibits thrombin and FXa

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64
Q

Protein C activation

A

Pro form activated by thrombin that is bound to thrombomodulin on endothelial surface

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65
Q

Protein S function

A

Protein S improves function of activated protein C

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66
Q

Protein C function

A

lyses coagulation factors Va and VIIIa

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67
Q

Protein C type 1 and type 2 deficiency

A

Again has to do with total amount and then total function

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68
Q

Protein S, 3 Types

A

Type 1 = amount, type 2 = functional abnormal, type 3 = normal total levels but reduced functional

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69
Q

Protein S carrier

A

half unbound and half bount to C4-binding protein

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70
Q

Neonatal Purpura fulminans

A

severe homozygous protein C deficiency. Purpura and necrosis

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71
Q

Neonatal purpura fulminans treatment

A

anticoagulation and protein C

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72
Q

Warfarin induced skin necrosis

A

Half life of different factors causes initial increased clotting

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73
Q

Vitamin K protiens

A

2,7,9,10 and Protein C adn Protein S

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74
Q

Vitamin K protein degredation rate

A

Protein C,S and factor 7 decline slower than the 2,9,10

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75
Q

Warfarin induced skin necrosis mechanism

A

thrombotic imbalance leads to cutaneous vessel thrombosis = purpuric and necrtoic skin lesions

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76
Q

Factor V leiden mechanism

A

point mutation making factor 5 unaffected by Activated protein C

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77
Q

Factor 5 leidin genetics

A

autosomal dominant

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78
Q

Prothrombin mutation mechanism

A

change in a non-coding region making mRNA more stable and higher levels of prothrombin

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79
Q

prothrombin mutation effect

A

increased levels of prothrombin and significant increase risk of clot

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80
Q

post VTE treatment length

A

3-6 months of anticoagulation

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81
Q

best indicator of risk for VTE

A

having a previous VTE. tips balance away from testing for Hereditary thromphilias

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83
Q

Anticoagulant and Antiplatelet agents

A

anticoagulant and antiplatelet agents

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84
Q

Anticoagulants

A

inhibit thrombin or 10a or decrease levels of prothrombin and other zymogens

85
Q

fibrinolytic agents

A

degrade existing clots

86
Q

antiplatelet agents

A

inhibit platelet plug formation

87
Q

Anticoagulant list

A

unfractionated heparin, lmw heparin, direct inhibitors of thrombin/factor10a, coumadin

88
Q

proteins inactivated by unfractionated heparin

A

2a, 10a, 9a, 11a, 12a

89
Q

Large heparain useful because

A

have the long pentasaccharide sequence to help inhibit thrombin and factor 10a

90
Q

Unfractionated heparin usage issues

A

short half-life that is variable. Have peaks and troughs in administration. Only IV leads to steady state levels

91
Q

Unfractionated Heparin uses

A

acute thromboembolism, prevent thromboembolism, maintain a coronary artery bypass graft

92
Q

unfractionated heparin significant toxicity

A

osteoporosis, and HIT

93
Q

Heparin induced thrombocytopenia with thrombosis

A

heparin/PF4 complex binds to platelet Fc. Causes platelet aggregation and destruction. So get thrombocytopenia with thrombosis of platelets being aggregated

94
Q

Test used to monitor unfractionated heparin

A

use aPTT - want 1.5-2x baseline

95
Q

LMW heparin target

A

affects 10a more than 2a. Does not affect aPTT as much

96
Q

LMW heparin benefits

A

half-life longer. less beleding and thrombocytopenia

97
Q

Direct thrombin inhibitors

A

Lepirudin and Argatroban

98
Q

Lepirudin

A

recombinant hirudin. for HIT and thrombi prevention after surgery. Renal excretion. comes from active ingredient used by leeches. IV USE

99
Q

Argatroban

A

active site inhibitor, hepatic excretion IV USE

100
Q

Factor 10a inhibitors

A

Rivaroxiban, Apixaban, Fondaparinux (indirect)

101
Q

Thrombin 2a inhibitors

A

Dabigatran (direct) renal excretion

102
Q

Rivaroxiban

A

Factor 10a inhibitor

103
Q

Apixaban

A

Factor 10a inhibitor

104
Q

Fondaparinux

A

Indirect factor 10a inhibitor

105
Q

Dabigatran

A

Direct 2a inhibitor

106
Q

Warfarin mechanism

A

inhibits re-use of vitamin K

107
Q

Vitamin K purpose

A

Vitamin K carboxylation of glutamate

108
Q

Warfarin in the body

A

bound to albumin

109
Q

Warfarin degraded by

A

P450

111
Q

International normalized ratio

A

(Patient PT/average control PT)^ISI

112
Q

Coumadin in first trimester

A

causes an embryopathy

113
Q

Limitation of oral factor 10 and 2 inhibitors

A

no quick reversing mechanism currently

114
Q

Fibrinolytic agents

A

Fibrinolytic Agents

115
Q

Plasmin function

A

cleaves fibrinogen and fibrin

116
Q

Plasminogen activators

A

Streptokinase, urokinase, recombinant t-PA

117
Q

Plasminogen activator contradiction

A

some trauma or surgery that puts you at risk of bleeding or massive hemorrhage

118
Q

Antiplatelet agents

A

ADP, thrombin receptor antagonists, aspirin, dipyridamole, integrin blockers

119
Q

Platelet receptor blockers

A

Clopidogrel (plavex) nad Vorapaxar (SCH530348)

120
Q

Platelet receptor blocked

A

AD P2y12

121
Q

ADP p2y12 receptor antagonists requiring metabolism

A

Ticlopidine, clopidogrel, prasugrel

122
Q

ADP p2y12 receptor antagonist direct

A

Cangrelor

123
Q

Platelet signal blockers

A

Aspirin and dipyridamole

124
Q

Platelet integrin blockers

A

ReoPro (abiciximab), Integrilin (Epifibatide), Tirofiban (Aggrastat)

125
Q

dipyridamole

A

increase cAMP and block signal in platelet aggregation

127
Q

hemodynamic disorders

A

hemodynamic disorders

128
Q

Hyperemia vs congestion

A

Hyperemia is an active process

129
Q

Hyperemia causes

A

erythema

130
Q

Congestion causes

A

cyanosis

131
Q

Liver congestion where does blood back up

A

in regions such as sinusoids around the central vein. spares periportal regions

132
Q

nutmeg liver

A

chronic passive congestion of liver.

133
Q

nutmeg liver discoloration

A

dark red is centriolbular congestion. Periportal fatty change is yellow

134
Q

Direction of clot formation

A

always towards the heart.

135
Q

Virchow’s triad

A

endothelial injury, hypercoagulability, abnormal blood flow

136
Q

white thrombi

A

arterial thrombi. more platelets and fibrin w less RBC. Prominent lines of Zahn

137
Q

mural thrombi

A

a thrombi that is stuck to the wall of the vessel and not really occlusive

138
Q

small/medium artery w arterial thrombi

A

generally occlusive

139
Q

red thrombi

A

venous thrombi, lines of zahn not as prominent. more red blood cells bc more about stasis and sitting blood

140
Q

paradoxical embolus

A

venous thrombus passes to systemic circulation through patent foramen ovale or vsd or patent ductus arteriosus

141
Q

thrombus organization

A

ingrowth of granulation tissue and smooth muscle cells into thrombus. convert to fibrous tissue

142
Q

pulmonary web

A

indicates that a prior thrombus had existed

143
Q

white infarct

A

arterial infarct when solid organ has one blood supply

144
Q

red infarct

A

hemorrhagic infarct or venous infarct, organ with 2 blood supplies. Or white infarct w/ reperfusion

145
Q

dual blood supply w infarct

A

if one is blocked and second compromised than you can get tissue with ischemia and blood supply that is not enough to prevent the ischemia

147
Q

Anemia

A

Anemia

148
Q

Microcytic anemia differential

A

iron deficiency, anemia of chronic inflammation/chronic disease, thalassemia, sideroblastic anemia

149
Q

iron deficiency anemia presentation

A

low hemoglobincMicrocytic, hypochromic anemia

150
Q

iron deficiency anemia pathology

A

pencil cells, , low MCV, high RDW

151
Q

Prussian blue stain

A

stain when assessing iron. Wil stain iron blue

152
Q

Thalassemia trait unique

A

have microcytosis without anemia

153
Q

thalassemia presentation

A

microcytic, hypochromic anemia. Very low MCV

154
Q

Thalassemia pathology

A

target cells

155
Q

Normocytic anemia differential

A

hemolytic anemia, hemorrhage/blood loss, sicke cell disease, anemia of chronic inflammation/disease, aplastic anemia

156
Q

hemolytic anemia cause

A

hereditary spherocytosis

157
Q

hereditary spherocytosis

A

defect in proteins making RBC cytoskeleton. shortened lifespan RBC

158
Q

Hemolytic anemia presentation

A

normocytic, normochromic anemia with high reticulocyte count

159
Q

spherocyte

A

cells that have lost membrane and take spherical shape. Lack central pallor

160
Q

Macrocytic differential

A

megablastic anemia (B12 deficiency, folate deficiency), liver disease, alcohol, yelodysplastic syndrome

161
Q

B12/folate deficiency effect

A

disrupt pathway for DNA synthesis. ineffective erythropoiesis

162
Q

megaloblastic anemia pathology

A

large RBCs. hypersegmented neutrophils

163
Q

Retic count correction in anemia

A

corrected retic count = reticulocyte x actual Hct/ideal Hct

164
Q

Hemolytic anemia: intravascular hemolysis minfestation

A

anemia, hemoglobinemia, hemoglobinuria, hemosiderinuria, jaundice

165
Q

Intravascular hemolysis cause

A

mechanical injury, complement fixation ,intracellular parasites

166
Q

Extravascular hemolysis cause

A

premature destruction of cells in phagocytes bc alteration akes RBC less deformable

167
Q

megaloblastic anemia cause

A

impaired synchrony of nuclear and cytoplasmic maturation

168
Q

3 B12 proteins

A

intrinsic factor, transcobalamin II, R protein

169
Q

Pernicious anemia

A

intestines cannot properly absorb B12, get an anemia because of failure for DNA production.

170
Q

Megaloblastic anemia signs

A

tiredness, pallor, jaundice, epithelial esions on gums, gastric mucosa, cervical lesions

171
Q

B12 neurologic problems

A

demyleination and subacute combine systems disease, paresthesias of hand and feet, spastic ataxia, etc

172
Q

B12 lab assessment

A

B12 down. Methylmalonic acid and homocystein increase

173
Q

Folate deficiency assessment

A

Homocystein down more in isolation than in B12

175
Q

Folate deficiency poor nutrition

A

goat milk anemia, poverty, early birth etc.

176
Q

folate deficiency absorption

A

nontropical or tropical spruce. disease of small intestine

177
Q

folate deficiency increased requireent

A

pregnancy, increased cell turnover from chronic hemolytic anemia, exfoliative dermatitis

178
Q

Nitrous oxide exposure

A

Acute megaloblastic anemia,

179
Q

inborn cobalamin deficiency

A

Imerslund-grasbeck disease, congenital deficiency of IF, transcobalamin II deficiency

180
Q

inborn error folate metabolism

A

congenital malabsorption, dyhydrofolate reductase deficiency, N …. transferase deficiency

181
Q

increased LDH

A

marker of hemolysis. Leaking out of destroyed RBC’s. enzyme for converting pyruvate to lactate

182
Q

hyperbilirubinemia

A

marker for hemolysis from broken down heme

183
Q

increased plasma hemoglobin

A

marker of intravascular hemolysis as hee leaks into circulation

184
Q

low plasma haptoglobin

A

marker for intravascular hemolysis bc haptaglobin is depleated to bind hemoglobin and take to spleen

185
Q

hemoglobinuria

A

sign of intravascular hemolysis bc extra hemoglobin is not picked up and instead comes out in urine

186
Q

extravascular hemolysis causes

A

intrinsic RBC efects, extracorpuscular defects

187
Q

Intravascular hemolysis causes

A

problems w hemoglobin, problems with RBC membrane, deficiencies of enzymes

188
Q

hereditary spherocytosis osotic fragility test

A

red cells placed in hypotonic saline, %lysis measured HS RBC’s lyse at greater concentration of hypotonic salinethan normal RBCs

189
Q

G6PD deficiency mechanism

A

withotu G6PD, hemoglobin more succeptible to oxidative damage.

190
Q

heinz bodies

A

damaged hemoglobin aggregate to make heinz bodies

191
Q

bite cells

A

macrophages rmeove heinz bodies from RBC’s causes bite cells and inducing hemolysis

192
Q

G6PD deficiency genetics

A

X chromosome. more males affected

193
Q

G6PD deficiency at risk populations

A

A variant = african americans. B variant = mediterranean and asian ancestry

194
Q

Warm autoimmune hemolytic anemia

A

IgG bind to RBC surface at warm temp leading to microspherocytes

195
Q

Warm AIHA test

A

DIrect Coombs test to see if RBC’s coated with IgG

196
Q

causes of warm AIHA

A

idiopathic autoimmune disorders lupus,lymphoproliferative disorders

197
Q

Cold AIHA

A

IgM binding below 37 degrees. activate complement that remains and causes lysis of RBCs

198
Q

Kuppfer cells

A

complement receptor expressing cells in liver that take out RBC’s in Cold AIHA

199
Q

Cold AIHA diagnosis

A

blood reachign room temp will agglutinate.

200
Q

3 mechanisms of drug induced hemolytic anemia

A

hapten mediated - drug binds RBC and serves as IgG target. neoantigen - drug binds membrane gets new conformation for IgG. Drug alters membrane causing new antigen

MDTI (10 decks)

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