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ABBEY MSII Unit 2 > Lange 6. > Flashcards

Lange 6. Flashcards

1
Q

Hematopoisesis

A

developmental process of all mature formed elements of blood

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2
Q

How many cells are produced by the bone marrow each day?

A

> 100 billion

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3
Q

What cells are produced at a ratio of 3:1?

A

3 WBC for every 1 RBC (because shorter half life)

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4
Q

What is the major hormone that stimulates production of erythrocytes? Where is it produced?

A

erythropoietin: kidneys

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5
Q

What is the feedback system for erythropoietin?

A

blood hemoglobin levels fall - oxygen delivery to kidneys falls, produce more erythropoietin

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6
Q

What are the most common WBCs?

A

granulocytes (cytoplasm filled with granules)

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7
Q

Neutrophils

A

most prevalent granulocyte - most important cell in producing inflammation

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8
Q

Myelopoisesis

A

granulocyte production

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9
Q

What cytokines are important for granulocyte production? (myelopoisesis)

A

IL-3, G-CSF, GM-CSF

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10
Q

What is the difference between G-CSF and GM-CSF?

A

GM-CSF stimulates the maturation of a different WBC lin - monocyte-macrophage line

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11
Q

How are platelets produced?

A

fragments of megakaryocytic (larger multinucleate cells in the marrow)

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12
Q

What cytokines stimulate platelet production?

A

IL-3, IL-6, IL-11, thrombopoietin (TPO)

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13
Q

Where is thrombopoietin produced? What does it do?

A

produced by liver, kidney, skeletal muscle, marrow stroma - stimulates platelet production

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14
Q

How long do erythrocytes function before removed by the spleen?

A

120 dayss

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15
Q

How do reticulocytes appear on blood smear stained with Wright Stain?

A

bluer (basophilic) - contain some ribosomes and mitochondria for a few days after nuclei are extruded

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16
Q

Hemoglobin structure

A

tetramer made of two alpha protein and two beta protein subunits

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17
Q

Hemoglobin A

A

two alpha and two beta subunits

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18
Q

How do granulocytes appear on blood smear?

A

nuclei are convoluted and multi lobed with granules in cytoplasm, which contain variety of enzymes, prostaglandins, mediators of inflammation

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19
Q

How do basophils appear on blood smear?

A

very dark blue granules that obscure the nucleus

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20
Q

When do basophils function?

A

hypersensitivity reactions - also increased in chronic myelogenous leukemia (CML)

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21
Q

How do eosinophils appear on blood smear?

A

stain red - bilobed nucleus

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22
Q

When do eosinophils function?

A

part of the inflammatory response to parasites too large to be engulfed by individual immune cells - also involved in allergic reactions

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23
Q

What is the major function of neutrophils?

A

major function in tissues - granules contain myeloperoxidase which along with free radical oxygen ions produced by NADPH oxidase kill bacteria

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24
Q

What is the half-life of neutrophils?

A

8 hours (why so many are made)

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25
Q

How do less mature neutrophils appear?

A

characteristic horseshoe-shaped nucleus that is not fully lobulated (called bands)

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26
Q

Monocytes lifespan

A

only ~3 days in circulation before residing in tissues where they phagocytose bacteria

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27
Q

How do monocytes appear on smear?

A

largest cells - irregular but not multi lobed nuclei and pale blue cytoplasm

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28
Q

How do lymphocytes appear on smear? What is special about their maturation?

A

appear small but slightly larger than erythrocyte, dark nuclei essentially filled the cell - thin rim of light blue cytoplasm - little to no granules. mature outside the marrow

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29
Q

What is the half-life of platelets?

A

10 dayss

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30
Q

What happens to platelet count in thrombocytopenia? Why?

A

half life of platelet decreases because they are consumed in the routine maintenance of vascular integrity

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31
Q

How do platelets contribute to coagulation?

A

important source of phospholipids and contain important receptors that allow attachment to endothelial cells in order to form platelet plug

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32
Q

What is contained in the cytoplasm of platelets?

A

dense granules and alpha granules

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33
Q

What is degranulation of platelets?

A

platelet activation

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34
Q

What initiates platelet activiation?

A

exposure of platelets to activated blood coagulation factor thrombin, ADP, or collagen

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35
Q

What is released from granules during platelet activation?

A

ADP and platelet factor four

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36
Q

What happens to platelets after activation?

A

change shape from discoid to spherical with filopodial extensions and finally to a flat shape that allows coverage of vessel injury

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37
Q

How do immature platelets appear?

A

Larger than normal platelets

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38
Q

What is the end result of the activated coagulation system

A

complex of cross-linked fibrin molecules and platelets that terminate hemorrhage

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39
Q

How do most coagulation factors circulate?

A

enzymes (serine proteases) that remain dormant until needed

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40
Q

How are inactive forms of coagulation factors written?

A

without annotation (factor II)

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41
Q

How are active forms of coagulation factors write?

A

signified by the letter “a” (fator IIa)

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42
Q

Where are most coagulation factors made? Exceptions?

A

liver: exceptions = factor XIII (platelets) and factor VIII (endothelial cells)

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43
Q

What are factors II, VII, IX, X dependent on?

A

liver enzyme gamma carboxylase which is dependent on vit K (as are protein S and C)

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44
Q

What is the mechanism of warfarin?

A

anticoagulant that interferes with vit K activity

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45
Q

Primary hemostasis

A

vasoconstriction and platelet adhesion and activation at sites of endothelial injury - collagen and thrombin activate platelets

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46
Q

Secondary hemostasis

A

process where fibrin is formed - includes initiation, amplification, and propagation

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47
Q

Initiation of hemostasis

A

release of TF (thromboplastin) by injured cells acting factor VII (to make TF-VIIa) which activates both factor IX and X. Factor Xa and Va catalyze conversion of prothrombin to thrombin (IIa) which cleaves fibrinogen into fibrin

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48
Q

Amplification of hemostasis

A

occurs at surface of platelets - thrombin activates platelets and coagulation factors V, VII, and XI found on platelet surface. IX activates IX to IXa which provides supplemental factor IXa at platelet surface

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49
Q

What is factor VIII normally complexed to?

A

vWF

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50
Q

Propagation of hemostasis

A

activate platelets recruit other circulating platelets and formation of two major complexes: tenase and prothrombinase

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51
Q

What do the tenase and prothrombinase do?

A

activate factor X which then forms the prothrombinase complex with factor Va on the platelet surface which forms another complex that catalyzes the cleavage of prothrombin II to thrombin IIa

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52
Q

Factor XIIIa

A

activated by thrombin - incorporates alpha2-antiplasmin into the clot to protect it from fibrinolytic proteases (further solidifies the fibrin polymer)

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53
Q

Fibrinolysis

A

the process of breaking down fibrin

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54
Q

Major catalytic enzyme in fibrinolysis

A

plasmin - serum protease that cleaves fibrin

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55
Q

What catalyzes the formation of plasmin from precursor plasminogen?

A

thrombin (negative feedback) or tissue plasminogen activator (t-PA)

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56
Q

What are inhibitors of fibrinolysis?

A

plasminogen activator inhibitor and alpha-2-antiplasmin

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57
Q

TFPI: tissue factor pathway inhibitor

A

inhibits further activity of factor Xa itself but also prevents Xa from binding to the platelet surface - a check on the coagulation system

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58
Q

antithrombin (AT)

A

protease inhibitor - physically blocks the action of the serine proteases in the coagulation system (activity enhanced by heparin)

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59
Q

Protein C

A

activated by thrombin - cleaves factor Va into an inactive form sot hat the prothrombinase complex cannot cleave prothrombin II into thrombin

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60
Q

Protein S

A

cofactor for protein C - complex also inactivates factor VIIIa

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61
Q

PT

A

assess the extrinsic TF-dependent (factor VII) and common pathways of the classical coagulation cascade - monitor effects of warfarin

62
Q

PTT

A

assess the intrinsic non-TF dependent and common pathways - sensitive to presence of heparin bound to AT

63
Q

What happens in the blast crisis of CML?

A

the majority of myeloid and lymphoid cells in the blood express bcr-abl Philly chromosome

64
Q

Anemia

A

abnormally low hemoglobin concentration in the blood

65
Q

What is a normal MCV?

A

around 90

66
Q

Pokilocytosis

A

relative nonuniformity of cell shapes

67
Q

Anisocytosis

A

relative nonuniformity of cel sizes

68
Q

What are microcytic anemias due to?

A

hemoglobin production abnormalities

69
Q

What are microcytic anemias due to?

A

either abnormal nuclear maturation or a higher fraction of young, large, red cells (reticulocytes)

70
Q

Megaloblastic

A

when the nuclei of maturing red cells appear too young and large for the amount of hemoglobin in the cytoplasm

71
Q

What are normocytic anemias due to?

A

decreased numbers of red cell precursors in the marrow (aplastic anemia, replacement of marrow elements with cancer, certain viral infections, autoimmune inhibition), low levels of erythropoitein (kidney disease), chronic inflammatory diseases that affect availability of iron

72
Q

What can normocytic anemias be secondary to?

A

decreased life span of cells produced (acute blood loss, autoimmune hemolytic anemias, sickle cell, hereditary spherocytosis)

73
Q

When does erythrocytosis occur? (elevated hemoglobin concentration)

A

smokers and people who live at high altitudes - also renal tumors (making more erythropoietin)

74
Q

Persistent elevation of lymphocyte numbers suggests what?

A

malignancies, esp CLL

75
Q

What are common causes of lymphopenia?

A

complication of corticosteroid therapy and immunodeficient states (HIV)

76
Q

When is thrombocytopenia due to decreased production occur? Increased degradation?

A

decreased production: when marrow is affect by disease or when TPO production by liver is impaired (cirrhosis). increased degradation: hypersplenism or immune-mediated consumption by drugs or autoantibodies

77
Q

What are autoantibodies against platelets usually directed against?

A

platelet membrane antigen gpIIb/IIa

78
Q

von Willebrand disease results in what?

A

either quantitative or qualitative defects of vWF - carrier protein of factor VIII and bridge between platelets and endothelium

79
Q

When does functional platelet disorders occur?

A

uremia or aspirin

80
Q

What are the quantitative disorders that commonly cause bleeding?

A

hemophilia A and B (X-linked)

81
Q

What is DIC (disseminated intravascular coagulation) generally due to?

A

overwhelming infection, specific leukemias or lymphomase, massive hemorrhage - coagulation factors become depleted

82
Q

What is the main cause of loss of iron in the developing world?

A

blood loss form GI or genitourinary tracts (GI malabsorption if no source of bleeding is uncovered)

83
Q

What regulates the export of iron to plasma?

A

hepcidin (produced by liver)

84
Q

What happens when iron stores are low?

A

hepcidin production is reduced and ferroportin molecules are expressed on the basolateral membrane of enterocytes where they transfer iron from the cytoplasm of enterocytes to plasma transferrin

85
Q

What happens to iron transport in inflammatory states?

A

Hepcidin production is increased, leading to the internalization of ferroportin on macrophages and trapping of recycled iron within macrophage stores

86
Q

Where is iron predominately found?

A

hemoglobin, also in myoglobin (oxygen-storing protein of skeletal muscle)

87
Q

What is the final step of heme synthesis?

A

ferrous iron is inserted into protoporphrin IX by ferrochelatase

88
Q

What happens in early iron deficiency?

A

hemoglobin level of the blood falls but individual erythrocytes appear normal - erythropoietin levels rise but hemoglobin level cannot because of iron deficiency. Eventually, hemoglobin concentration falls leading to microcytic, hypo chromic erythrocytes

89
Q

What is seen on blood smear of iron deficient anemia?

A

abnormally low MCV, substantial anisocytosis and poikilocytosis, target cells

90
Q

What is diagnostic of iron deficiency?

A

low serum ferritin or high ratio of serum soluble transferrin receptor (sTfR) to ferritin

91
Q

How do macrophages stain if there is an iron deficiency?

A

NOT AT ALL because there is no hemosiderin (which is easily visualized with Prussian blue)

92
Q

What are clinical manifestations of iron deficiency anemia?

A

fatigue, pale, tachycardia, glossitis, gastric atrophy with achlorhydria (absence of stomach acid), pica (craving for nonnutritive substances)

93
Q

Pernicious anemia

A

abnormal erythrocyte nuclear maturation - megaloblastic anemia - hemoglobin synthesis normal - autoimmune in origin

94
Q

What is the ultimate effect of pernicious anemia?

A

loss of adequate stores of vitamin b12 cobalamin (cofactor in DNA synthesis)

95
Q

What can cobalamin deficiency be a result of?

A

pernicious anemia, bacterial overgrowth, intestinal malabsorption of vit B12, surgical removal of antrum, dietary deficiency (rare)

96
Q

What is the pathogenesis of pernicious anemia?

A

gastric parietal cells affected by autoimmune shit that leads to loss of gastric acid and intrinsic factor - cobalamin can not be released from foodstuffs (no acid) and can’t be absorbed in terminal ileum

97
Q

What can be used to reverse pathologic effects of pernicious anemia?

A

corticosteroid therapy

98
Q

Why does vit B12 deficiency develop slowly?

A

liver stores are adequate for several years

99
Q

What is dependent upon vit B12?

A

production of Succinyl CoA and production of purines

100
Q

Chronic atrophic gastritis

A

pernicious anemia: normally tall columnar epithelium replaced by thin mucosa - increased risk for gastric adenocarcinoma

101
Q

What is seen in the blood smear in early stages of pernicious anemia? full blown megaloblastic anemia?

A

early: mild macrocytic anemia and large ovoid erythrocytes. full blown: sig anisocytosis and poikilocytosis in RC and hyperhsegmented neutrophils = nuclear dysgenesis from abnormal DNA —> can be mistaken for acute leukemia because cells look so fucked

102
Q

What are other consequences of pernicious anemia?

A

spinal cord abnormalities (demyelination of the posterolateral spinal columns) because no B12

103
Q

What do lab findings for pernicious anemia show?

A

elevated lactate dehydrogenase (LDH) - directly released from lysed red cells; low serum vi B12, antibodies to intrinsic factor, serum elevations of methylmalonic acid (MMA) and/or homocysteine

104
Q

Clinical findings in pernicious anemia?

A

fatigue, dspnea, dizziness, anemia, tachycardia, left ventricular failure, GI symptoms - esp glossitis, neurologic symptoms including loss of balance and coordination, impaired proprioception (position sense) and vibration sense

105
Q

Absolute neutropenia

A

neutrophil counts less than 1500-2000

106
Q

Cyclic neutropenia

A

lifetime history of neutrophil counts that decrease to zero or near zero for 2-5 days at a time every 3 weeks and then rebound (monocytes counts oscillate in opposite phases)

107
Q

What is cyclic neutropenia due to?

A

germline mutations in the gene ELANE (elastase neutrophil expressed)

108
Q

What is the average life span of a mature neutrophil IN THE BLOOD?

A

12h

109
Q

How long does it take a neutrophil to fully develop?

A

2w

110
Q

Neutrophil elastase

A

inhibits the differentiation of myeloblasts in a negative feedback loop - oscillatory wave

111
Q

When the number of neutrophils drops, the production of neutrophil elastase……..

A

delcines - allowing the number of neutrophils ot climb

112
Q

What can the myeloid progenitor for neutrophil also produce?

A

monocytes

113
Q

What is the difference between normal individuals and those with cyclic neutropenia?

A

cyclic neutropenia does not have large storage pool of granulocytes

114
Q

Which marrow elements cycle?

A

neutrophils, monocytes, platelets, reticulocytes

115
Q

neutrophil elastase mutations cause what?

A

acceleration of apoptosis in early progenitor cells

116
Q

G-CSF

A

saves patients from neutrophil elastase mutations and cyclic neutropenia

117
Q

Clinical manifestations of cyclic neutropenia?

A

recurrent infections and deaths from infections with intestinal organisms - skin most common and respond to antibiotic therapy (also gums and chronic gingivitis)

118
Q

Pathologic features of cyclic neutropenia?

A

mostly seen in lab - individual neutrophils normal, bone marrow has striking differences depending on the day of the cycle

119
Q

How long after exposure does drug induced thrombocytopenia occur?

A

5-7 days

120
Q

Which drug is the most importnat cause of thrombocytopenia?

A

heparin

121
Q

What is the mechanism of quinine or NSAID induced thrombocytopenia?

A

tight binding of antibody to normal platelets only in the presence of the sensitizing drug - usually goes for glycoprotein IIb/IIIa or Ib/IX complexes (major platelet receptors for fibrinogen and vWF

122
Q

What is the mechanism for penicillin and cephalosporin antibiotics?

A

hapten-dependent antibodies - drug acts as a happen

123
Q

Which drugs can induce autoantibodies even in the absence of the sensitizing drug?

A

gold salts, procainamide, sulfonamides

124
Q

What is the mechanism of thrombocytopenia in antithrombotic agents that block the binding of fibrinogen to gpIIb/IIIa receptors (abciximab, tirofiban, eptifibatide)

A

natually occurring antibodies recognize the murine component of abciximab or structural changes to the gpIIb/IIIa receptor caused by binding to tirofiban or eptifibatide

125
Q

Heparin mechanism of thrombocytopenia

A

binding to a platelet protein (platelet factor 4 PF4) from alpha granules - causes mild thrombocytopenia via promotion of platelet binding to fibrinogen and subsequent aggregation

126
Q

Heparin-induced thrombocytopenia type I (HIT type I)

A

non-immune based adhesion of heparin to PF4 leads to mild thrombocytopenia via promotion of platelet binding to fibrinogen and subsequent aggregation

127
Q

Heparin-induced thrombocytopenia type II (HIT type II)

A

combination of of heparin with PF4 can also act as an antigenic stimulus provoking production of IgG directed against the combination - then destroyed by spleen

128
Q

How can HIT type II lead to a prothrombotic state?

A

via the additional binding of the heparin-PF4 portion to the PF4 receptor on platelets - promoting cross linking, activation and aggregation - clinically decreasing the numbers of circulating platelets but leading to creation of thrombus at site of activation

129
Q

What are the clinical manifestation of drug induced thrombocytopenia?

A

severe bleeding unusual despite extremely low platelet count - see easy bruising with minimal trauma and petechiae with platelet counts less than 5000, bleeding time prolonged under 90,000

130
Q

primary abnormal clotting states

A

genetic predisposition

131
Q

secondary abnormal clotting states

A

changes in coagulation factors, blood vessels, or blood flow

132
Q

What is Virchow’s triad?

A

decreased blood flow, vessel injury or inflammation, changes in the intrinsic properties of the blood

133
Q

What is the major inhibitor of factor Va?

A

protein C - cleaves into an inactive form

134
Q

What does protein C inhibit?

A

factor Va and VIIIa

135
Q

What inhibits factors II, IX, X, XI?

A

AT

136
Q

What characterizes most hyper coagulable states?

A

lack of adequate anticoagulant activity rather than overproduction of procoagulant activity

137
Q

Activated Protein C Resistance

A

most common inherited hyper coagulable state - single DNA base pair mutation in the factor V gene (G replaced by A) - leads to loss of a cleavage product that is normally formed when factor V is inactivated by APC

138
Q

Protein C deficiency

A

thrombosis uncommon - need additional genetic factors - simply less inhibition of the prothrombinase complex = unrestricted clot formation

139
Q

What is protein C dependent on?

A

presence of platelet PL and calcium

140
Q

Type I protein C deficiency vs Type II

A

type I: individuals with decreased level of protein C. Type II: normal protein C level but love activity

141
Q

Protein S deficiency: type I, type II, type III

A

type I: low free and total protein S level. type II: abnormal functioning protein. type III: only low levels of free protein S

142
Q

Function of protein S

A

exposes site on Va so that protein C can cleave (cofactor)

143
Q

Antithrombin deficiency

A

uncommon - AT binds to each factor (IX, X, XI

144
Q

What accelerates the action of antithrombin?

A

heparin

145
Q

Hyperprothrombinemia

A

mutation in the untranslated region of the prothrombin gene - associated with elevated palm prothrombin levels and increased risk of thrombosis —> excess thrombin generation

146
Q

What is the only hereditary thrombophilia associated with overproduction of procoagulant factors?

A

hyperprothrombinemia

147
Q

Pathology of inherited hyper coagulable states

A

indistinguishable from genetically normal except greater likelihood of clot in unusual site - most are lab findings

148
Q

Most thromboembolic events encountered in clinical practice are what?

A

secondary not primary (sluggish blood flow and trauma to blood vessels in extremities)

149
Q

How do DVTs present?

A

pain, swelling, redness below the level of the thrombus, normal arterial pulses, distal extremity perfusion

150
Q

What is the major source of morbidity with DVTs?

A

pulmonary emboli - SOB, hypoxemia, initial DVT

151
Q

How do heterozygotes who develop thrombosis usually present?

A

setting of a typical risk factor: injury, immobilization, surgery, pregnant

ABBEY MSII Unit 2 (19 decks)

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