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Fiser Absite > Fiser Absite. Ch 01-02. Cell Biology. Hematology > Flashcards

Fiser Absite. Ch 01-02. Cell Biology. Hematology Flashcards

1
Q

What molecule increases membrane fluidity?

A

Cholesterol

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2
Q

What is responsible creating the charge of cells? What is does it move and what is the net charge (positive or negative)?

A

Na/K ATPase, 3 Na+ out and 2 K+ in, negative

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3
Q

What are the adhesion molecules that form cell-cell and cell-extracellular matrix adhesions?

A

desmosomes/hemidesmosomes

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4
Q

What forms cell-cell occluding junctions to form an impermeable barrier (ie epithelium)?

A

tight junctions

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5
Q

What type of junctions allow communication between cells and what are their subunits called?

A

gap junctions, connexin

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6
Q

What is the intramembrane protein that transduces a signal from receptor to response enzyme?

A

G proteins

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7
Q

What are the phases of the cell cycle?

A

G1, S, G2, M

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8
Q

Which phase of the cell cycle is the most variable and determines the cycle length?

A

G1

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9
Q

What is quiescent cell cycle phase called?

A

G0

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10
Q

What are the 4 phases of mitosis?

A

Prophase, Metaphase, Anaphase, Telophase

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11
Q

centromere attachment, spindle formation, nucleus disappears

A

Prophase

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12
Q

In which phase of mitosis does chromosome alignment occur?

A

Metaphase

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13
Q

In which phase of mitosis are the chromosomes pulled apart?

A

Anaphase

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14
Q

In which phase of mitosis does a separate nucleus form around each set of chromosomes?

A

Telophase

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15
Q

The outer membrane of the nucleus is continuous with what other structure?

A

rough endoplasmic reticulum

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16
Q

Where are ribosomes made?

A

Nucleolus

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17
Q

Steroid hormone - binds receptor in _____ then enters nucleus and acts as transcription factor.

A

nucleus

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18
Q

Thyroid hormone - binds receptor in ____, then acts as transcription factor.

A

cytoplasm

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19
Q

What are the purines?

A

adenine, guanine

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20
Q

What are the pyrimidines?

A

cytosine, thymidine, (uracil in RNA)

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21
Q

In glycolysis, 1 glucose molecule generates how many ATP and pyruvate molecules

A

2 each

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22
Q

Where does the Krebs cycle occur?

A

mitochondrial matrix

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23
Q

What is the overall ATPs produced from 1 molecule of glucose?

A

36

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24
Q

What is converted to glucose in gluconeogenesis?

A

lactic acid and amino acids

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25
Q

An elegant mechanism for the hepatic conversion of muscle lactate into new glucose. Pyruvate plays a key role in this process.

A

Cori Cycle

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26
Q

What organelle synthesizes proteins that are exported (increased in pancreatic acinar cells)?

A

Rough endoplasmic reticulum

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27
Q

In what organelle does lipid/steroid synthesis as well as drug detox (increased in liver and adrenal cortex)?

A

Smooth endoplasmic reticulum

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28
Q

What organelle modifies proteins with carbohydrates; proteins are then transported to the cell membrane, are secreted or are targeted to lysosomes?

A

Golgi apparatus

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29
Q

Activated by calcium and diacylglycerol (DAG). Phosphorylates other enzymes and proteins.

A

Protein kinase C

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30
Q

Activated by cAMP. Phosphorylates other enzymes and proteins.

A

Protein kinase A

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31
Q

Thick filaments. Uses ATP to cause muscle contractions.

A

Myosin

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32
Q

Thin filaments that interact with Myosin.

A

Actin

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33
Q

Form specialized cellular structures such as cilia, neuronal axons and mitotic spindles, also involved in the transport of organelles into the cell.

A

Microtubules

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34
Q

A specialized microtubule involved in cell division (forms spindle fibers, which pull chromosomes apart).

A

Centriole

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35
Q

What are the three initial responses to vascular injury?

A

vascular vasoconstriction, platelet adhesion, thrombin generation

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36
Q

Which pathway starts with: exposed collagen + prekallikrein + HMW kininogen + factor XII?

A

Intrinsic Pathway

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37
Q

Which pathway starts with tissue factor (injured cells) + factor VII?

A

Extrinsic pathway

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38
Q

What does thrombin do?

A

converts fibrinogen to fibrin

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39
Q

What comprises the prothrombin complex and where does it form?

A

X, V, Ca, platelet factor 3 and prothrombin

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40
Q

Which factor is the convergence for the intrinsic and extrinsic pathways?

A

Factor X

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41
Q

What does tissue factor pathway inhibitor inhibit?

A

Factor X

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42
Q

Combines with platelets to form platelet plug leading to hemostasis.

A

Fibrin

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43
Q

Which factor helps crosslink fibers?

A

XIII

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44
Q

What is the key to coagulation? Converts fibrinogen to fibrin, activates V, VIII and platelets.

A

Thrombin

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45
Q

What is the key to anticoagulation? Binds and inhibits thrombin. Inhibits IX, X, XI. And binds heparin.

A

Antithrombin III

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46
Q

Vitamin-K dependent. degrades factors V and VIII. degrades fibrin.

A

Protein C

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47
Q

Vitamin K dependent, protein C cofactor.

A

Protein S

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48
Q

Where is tissue plasminogen activator released from?

A

Endothelium

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49
Q

Degrades factors V and VIII, fibrinogen and fibrin

A

Plasmin

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50
Q

Natural inhibitor of plasmin, released from endothelium

A

Alpha 2 antiplasmin

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51
Q

Which coagulation factor has the shortest half-life?

A

VII

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52
Q

Which two coagulation factors are considered the labile factors, activity is lost in stored blood but activity not lost in FFP?

A

V and VIII

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53
Q

Which is the only coagulation factor not synthesized in the liver (synthesized in endothelium)?

A

Factor VIII

54
Q

Which are the vitamin k dependent coagulation factors?

A

II, VII, IX, and X, proteins C and S

55
Q

How long does it take for Vitamin K to take effect?

A

6 hours

56
Q

When does FFP take effect and how long does it last?

A

immediate and 6 hrs

57
Q

What is the normal half life of RBCs, platelets, and PMNs respectively?

A

120 days, 7 days, 1-2 days

58
Q

From the endothelium, decreases platelet aggregation and promotes vasodilation.

A

Prostacyclin (PGI2)

59
Q

Antagonistic to TXA2

A

Prostacyclin (PGI2)

60
Q

From platelets, increases platelet aggregation, and promotes vasoconstriction.

A

Thromboxane (TXA2)

61
Q

Triggers release of calcium in platelets, exposes GpIIb/IIIa receptor and causes platelet-to-platelet binding, platelet-to-collagen binding. Also activates the PIP system to further increase calcium

A

Thromboxane (TXA2)

62
Q

Contains highest concentration of vWF VIII; used in von Willebrand’s disease and hemophilia A (factor VIII deficiency), also contains fibrinogen

A

cyroprecipitate

63
Q

Has high levels of all factors (including labile factors V and VIII), protein C, protein S and AT-III

A

FFP

64
Q

What role does DDAVP and conjugated estrogens play in coagulation?

A

cause release of VIII and vWF from endothelium

65
Q

Measures II, V, VII, and X; fibrinogen; best for liver synthetic function

A

PT

66
Q

Measures most factors except VII and XIII (thus does not pick up factor VII deficiency); also measures fibrinogen

A

PTT

67
Q

INR > ____ is a relative contraindication to performing surgical procedures. INR > ___ relative contraindication to central line placement, percutaneous needle bx and eye surgery

A

1.5, 1.3

68
Q

Most common cause of surgical bleeding

A

Incomplete hemostasis

69
Q

Most common congenital bleeding disorder

A

von Willebrand’s disease

70
Q

Links Gp1b receptor on platelets to collagen?

A

vWF

71
Q

Which type of vW disease is most common? Which type causes the most severe bleeding?

A

Type I, Type III

72
Q

What is the difference in treatment between vW disease types I and III and II?

A

Type I and III - recombinant VIII:vWF, DDAVP, cryoprecipitate, conjugated estrogens

73
Q

Hemophilia A (VIII deficiency) levels need ___% preoperatively, keep ___% after surgery.

A

100%, 30%

74
Q

Will newborns with hemophilia A bleed at circumcision?

A

No factor VIII crosses the placenta.

75
Q

What is treatment for hemophiliac joint?

A

no aspiration

76
Q

Pt with Hemophilia A and epistaxis, intracerebral hemorrhage or hematuria. What is the tx?

A

recombinant VIII:vWF or cryoprecipitate, possibly DDAVP

77
Q

Christmas disease

A

hemophilia B

78
Q

Hemophilia B (IX deficiency) levels needed preoperatively

A

100%

79
Q

What is the PTT and PT in the hemophilias?

A

Prolonged PTT, normal PT

80
Q

What is the tx for hemophilia B?

A

recombinant factor IX concentrate or FFP

81
Q

What is the PT and PTT in Factor VII deficiency?

A

PT is prolonged, PTT is normal

82
Q

What is the tx for factor VII deficiency?

A

recombinant factor VII concentrate, FFP

83
Q

Name 2 medications that can cause acquired thrombocytopenia?

A

H2 blockers, heparin

84
Q

GpIIa/IIIa receptor deficiency on platelets. What is it called and what is the tx?

A

Glanzmann’s thrombocytopenia, platelets

85
Q

Gp1b receptor deficiency on platelets (cannot bind to collagen). What is it called and what is the tx?

A

Bernard Soulier, platelets

86
Q

What does uremia do to coagulation and what is the tx?

A

inhibits platelet function, tx hemodialysis (1st), DDAVP, platelets

87
Q

What does ticlopidine do and what is the tx?

A

decreases ADP in platelets, prevents exposure of GpIIb/IIIa. Tx is platelets

88
Q

Inhibits cAMP phosphodiesterase, increases cAMP, decreases ADP-induced platelet aggregation, Tx: platelets.

A

Dipyridamole

89
Q

What does pentoxifylline do? and what is tx?

A

inhibits platelet aggregation, platelets

90
Q

ADP receptor antagonist. Tx: platelets.

A

Clopidogrel

91
Q

What is the concern with PCN/cephalosporins and coagulation?

A

bind platelets, can increase bleeding time

92
Q

Thrombocytopenia due to antiplatelet antibodies. Can also cause platelet aggregation and thrombosis.

A

HITT (second T for thrombosis)

93
Q

What is the tx for HITT

A

stop heparin. Argatroban, hirudin, ancrod or dextran to anticoagulate

94
Q

Decreased platelets, prolonged PT, prolonged PTT, low fibrinogen, high fibrin split products, high D-dimer.

A

DIC

95
Q

Inhibits cyclooxygenase in platelets, decreased TXA2

A

ASA

96
Q

When to stop ASA before surgery?

A

7 days

97
Q

When to stop Coumadin before surgery?

A

7 days, consider starting heparin

98
Q

Keep platelets >____ before surgery and >____ after.

A

50K, 20K

99
Q

Prostate surgery can release ___ which activates plasminogen leading to thrombolysis. What is the treatment?

A

urokinase. e-Aminocaproic acid (Amicar)

100
Q

What is the best way to predict bleeding risk?

A

H and P

101
Q

What is the symptom common with vWF deficiency and platelet disorders?

A

Epistaxis

102
Q

What is the most common congenital hypercoagulability disorder?

A

Leiden factor

103
Q

What is the defect in Leiden factor and what is the tx?

A

defect on factor V that causes resistance to activated protein C; tx: heparin, warfarin

104
Q

What is the second most common hypercoagulability disorder and what is the treatment?

A

Hyperhomocysteinemia; Tx: folic acid and B12

105
Q

What is the treatment for Prothrombin gene defect G20210 A or Protein C or S deficiency?

A

heparin/warfarin

106
Q

What is the treatment for Antithrombin III deficiency?

A

(heparin does not work and this can develop after previous heparin exposure); tx: recombinant AT-III concentrate or FFP (highest concentration of AT-III) followed by heparin or hirudin or ancrod; warfarin

107
Q

Defect in platelet function; usually have thrombosis, can have bleeding.

A

Polycythemia vera

108
Q

What should the Hct and platelets be before surgery in a patient with polycythemia vera and was is the tx?

A

Hct < 48 and platelets < 400, ASA

109
Q

What is diagnosed with: prolonged PTT (not corrected with FFP), positive Russell viper venom time, false-positive-RPR test for syphilis?

A

Lupus anticoagulant (antiphospholipid antibodies)

110
Q

What is the treatment for Lupus anticoagulant?

A

heparin/warfarin

111
Q

What is the most common factor causing acquired hypercoagulability?

A

tobacco

112
Q

Pt >55 with venous thrombosis with no known cause. Best next step.

A

CT of chest, abdomen and pelvis to screen for CA.

113
Q

What can occur when a pt is placed on Coumadin without being heparinized first? and why?

A

Warfarin induced skin necrosis. The short half life of protein c and s results in a relative hyperthrombotic state

114
Q

Pts with what condition are the most susceptible to Warfarin induced skin necrosis.

A

Relative protein c deficiency

115
Q

What are the key elements in venous thrombosis? what about arterial?

A

virchow’s triad, endothelial injury

116
Q

Tx for 1st DVT? 2nd? 3rd?

A

1st - warfarin for 6 months; 2nd - warfarin for 1 year; 3rd or significant PE - warfarin for lifetime

117
Q

Most common source of DVT causing PE?

A

iliofemoral region

118
Q

What does dextran do?

A

inhibits platelets and coagulation factors

119
Q

Improve venous return but also induce fibrinolysis due to release of tPA from compression.

A

Sequential Compression Devices

120
Q

How does heparin work?

A

Activates antithrombin III

121
Q

What is the half-life of heparin and how is it cleared?

A

60-90 min; cleared by reticuloendothelial system

122
Q

Treatment for hypercoagulability in pregnancy?

A

Warfarin crosses the placenta, heparin doesn’t

123
Q

What are 2 sx of long term heparin?

A

osteoporosis, alopecia

124
Q

What percentage of pts treated with protamine develop protamine reaction and what are the sx?

A

4%-5%, hypotension, bradycardia and decreased heart function

125
Q

Leeches, irreversible direct thrombin inhibitor also the most potent; at increased for bleeding complications want PTT 60-90

A

Hirudin (Hirulog)

126
Q

Direct thrombin inhibitor, metabolized in the liver, half-life is 50 minutes, often used in pts with HITT.

A

Argatroban

127
Q

Reversable direct thrombin inhibitor, metabolized by proteinase enzymes in the blood; half-life is 25-30 minutes

A

Bivalirudin (angiomax)

128
Q

Malayan pit viper venom; stimulates tPA release

A

Ancrod

129
Q

Inhibits fibrinolysis by inhibiting plasmin. Used in DIC, persistant bleeding following cardiopulmonary bypass, thrombolytic overdoses.

A

e-Aminocaproic acid (Amicar)

130
Q

What do you follow after thrombolytics (streptokinase, urokinase, tPA)

A

fibrinogen <100 associated with increased risk and severity of bleeding

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