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Heme/Onc > Test 3 > Flashcards

Test 3 Flashcards

1
Q 
What are the effects of the following on vasculature? Where do they come from?
TXA2
ADP
Thromboplastin (TF3)
Plasmin
PGI2
Nitric Oxide
Endothelin-1
Thrombomodulin
tPA
A

TXA2: released by platelets, facilitates platelet aggregation
ADP: released by platelets, facilitates platelet aggregation by binding to P2y receptors
Thromboplastin (TF): released by activated platelets and injured endothelial cells,
Plasmin: released by activated platelets?

PGI2: released by uninjured endothelial cells as vasodilator, working against platelet aggregation
Nitric Oxide: released by uninjured endothelial cells as vasodilator, working against platelet aggregation

Endothelin-1: released from injured endothelial cells, causes vasoconstriction
Thrombomodulin: expressed on injured endothelial cells, activates Protein C by helping Thrombin

tPA: released from endothelial cells, converts plasminogen to plasmin

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2
Q 
Where are the following drugs site of action?
Aspirin
ClopidoGREL, TicaGRELor
Abciximab, Eptifibatide, Tirofiban
Vorapaxar
A

Aspirin: blocks COX1
ClopidoGREL, TicGRELor: blocks ADP receptor
Abciximab, Eptifibatide, Tirofiban: blocks IIb-IIIa receptor
Vorapaxar: blocks thrombin receptor

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3
Q

What must happen to Vit K before it can be integrated into the coagulation cycle? Then what does it do?

A

Vit K must be reduced by Vit K reductase

then it helps Vit K dependent clotting factors undergo carboxylation to get activated

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4
Q

What CFs are Vit K dependent? anything else?

A

CF II, VII, IX, X

Protein C and S

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5
Q

What does Thrombin activate?

A 
Thrombin (II) activates:
5, 8 ((normally circulating in blood bound to vWF, thrombin cleaves it), 11, 13
Fibrinogen → Fibrin
Protein C → activated PC
platelets by binding to PAR-1
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6
Q

What are the 5 elements in the prothrombinase complex

A 
Prothrombinase Complex
1 Ca
2 Activated phospholipid membrane
3 Factor Xa
4 Factor Va
5 Prothrombin
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7
Q

Walk through steps of fibrinolysis

A

Fibronilysis:
Endothelial cells replease tPA
tPA converts Plasminogen to Plasmin (after plasminogen’s bound to fibrin)
Plasmin cleaves Fibrin

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8
Q 
What are the drugs that act on the following sites?
blocks COX1
blocks ADP receptor
blocks IIb-IIIa receptor
blocks thrombin receptor
A

Aspirin: blocks COX1
ClopidoGREL: blocks ADP receptor
Abciximab, Eptifibatide, Tirofiban: blocks IIb-IIIa receptor
Vorapaxar: blocks thrombin receptor

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9
Q

What are 7 ways blood clotting is controlled?

A

1: factor activation restricted to activated platelets or damaged endothelium
2: Antithrombin III circulates and inhibits Thombin and Factors 9-12
3: Endothelial thrombomodulin binds and inactivates Thrombin
4: Protein C+S inactivated Factors 5 and 8
5: Endothelial secretion of Tissue Factor Pathway Inhibitor (TFPI) inactivates Factor 10/5 and 9/8 complexes
6: Endothelial secretion of NO and PGI2 inhibit platelet aggregation
7: Endothelial secretion of tPA

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10
Q

What’s genetic etiology (and mutation), pathophysiology, and clinical presentation for Antithrombin deficiency?
How does it present if Complete AT Deficiency?

A

genetics: AD for serine protease mutation in Antithrombin that reduces AT activity
Pathophys: Serine protease normally inhibits Factors 9, 10, 11, 12, and 2 (Thrombin)
clinical: DVT, mesenteric vein thrombosis, and recurrent thrombotic episodes by 40yo
Complete AT Deficiency = fatal

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11
Q

What’s genetic etiology (and mutation), pathophysiology, and clinical presentation for Factor V Leiden?
Which populations see a prevalence?

A

Genetics: AD, G→A Arg506Gln point mutation in Factor 5’s aProteinC cleavage site
Pathophys: Factor V can’t be cleaved
Clinical: risk DVT and pregnancy loss, decreased susceptibility to spesis and bleeding and PEs
Caucasian/Greek prevalence

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12
Q

What’s genetic etiology (and mutation), pathophysiology, and clinical presentation for Prothrombin gene mutation?

A

Genetics: AD, mRNA accumulation of G20210A mutation leads to increased translation and prothrombin (Factor 2) levels)
Pathophys: Increased levels of Prothrombin aka Factor 2
Clinical: risk venous thrombosis

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13
Q

Differentiate MOA of Heparin, LMWH, and Fondaparinux

A

Heparin: binds w/ATIII to inactivate Thrombin and Factors 9-12
LMWH: binds w/ATIII to inactivate Factor 10
Fondaparinux: indirect Factor 10 inhibitor

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14
Q

How do you reverse Heparin, LMWH, Fondaparinux?
Direct Factor 10 inhibitors Rivaroxaban/Apixaban, Warfarin, Direct Thrombin inhibitors Dabigatran/Argatroban/Bivalirudin?

A

Heparin: Protamine
LMWH: Protamine, but RecombFactor 7a is more effective
Fondaparinux: RecombFactor7
Rivaroxaban/Apixaban: can’t
Warfarin: Vit K
Dabigatron/Argatroban/Bivalirudin: Idarucizumab

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15
Q

Rivaroxaban/Apixaban, and Dabigatran/Argatroban/Bivalirudin MOA?

A

Rivaroxaban, Apixaban = Direct Factor 10 block

Dabigatran, Argatroban, Bivalirudin = Direct Thrombin (Factor 2) and Factor 10 block

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16
Q

What are the 2 Factor 10a inhibitors drugs?

What’s the 3 Direct Thrombin inhibitor drugs?

A

Factor 10a inhibitor: Rivaroxaban, Apixaban

Direct Thrombin inhibitors: Dabigatran, Argatroban, Bivalirudin

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17
Q

What’s the most common inherited hypercoaguable disease?
most common aquired hypercoaguable?
most common inherited hemophilia disease?
most common drug-induced thrombocytopenia in adults?

A

Inherited Hypercoaguable: Factor V Leiden
Acquired Hypercoaguable: Antiphospholipid Ab syndrome
Inherited Hemophilia: vWD
Drug induced thrombocytopenia: HIT (heparin induced thrombocytopenia)

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18
Q

Differentiate ITP and HIT

A

Immune Thrombocytopenic Purpura: Abs target GP IIb/IIIa (usually, rarely Ib/9), bind to Fc receptors on macrophages
HIT: body makes Ab to Heparin+Factor4, Abs bind to platelets, splenic macrophages remove platelets

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19
Q

Differentiate vWD and Glanzmann’s thrombasthenia

A

vWD: vWF defect, doesn’t allow platelets to clot appropriately
Glanzmann’s thrombasthenia: GPIIb/IIIa defect

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20
Q

How can you treat ITP?

A 
ITP tx:
steroids 
IV IgG to compete w/macrophage activity against  
IGs
splenectomy
immunosuppression
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21
Q

50% of CLL pts have thrombo_________, d/t ________

A

50% of CLL pts w/CLL have thrombocytopenia, d/t lack of normal differentiation of megakaryocytes and bone marrow repalcement

22
Q

What’s the genetic etiology, pathophys, and clinical presentation for von Willebrand Disease?

A

Genetic etiology: AD
pathophys: vWF mutations affect primary hemostasis (platelet adhesion to endothelium defect) and secondary hemostasis (Factor8 not stabilized and gets degraded)
Clinical: mucocutaneous bleeding, high variability of penetrance to create quantitative and qualitative mutations

23
Q

What gene is mutated, pathophys, and clinical presentation for Bernard Soulier syndrome?

A

Genetic etiology: GP1b alpha
pathophys: mutations in GP1b don’t allow vWF to bind
Clinical: assoc w/intermarriage, easy bruising, excessive bleeding, petechiae, epistaxis, heavy menstrual flow

24
Q

What’s the normal synthesis, processing, release, and storage of von Willebrand Factor?

A

synthesis: continually secreted from endothelial cells in small amounts
Processing: CK region on C terminal allows for dimerization, D region on N terminal allows for multimerization
release: when endothelium stimulated by Histamine, Thrombin, Fibrin, and beta-adrenergic agonists
storage: vWF normally in serum stabilizing Factor8, and in Weibel-Palade bodies in endothelial cells

25
Q

Why use Desmopressin to treat vWD, and why’s there subsequent fluid intake concerns?

A

Desmopressin causes vWF release from endothelial cells

Desmopressin stimulates renal V2 receptors, increasing H2o resorption and can have hyponatremia CNS ADEs

26
Q

What’s the genetic etiology (and mutation), pathophys, and clinical presentation for Hemophilia A?
why’s it more common in men?

A

Genetic etiology: X-liked recessive, X inversion makes 2 Factor 8 copies
Pathophys: Factor8 deficiency
Clinical: excessive bleeding, esp in joints, soft tissue, mucocutaenous, intracranial, muscle… severity correlates w/level of deficit

27
Q

What’s the genetic etiology (and mutation), pathophys, and clinical presentation for Hemophilia C?
why’s it more common in Ashkenazi Jews?

A

Genetic etiology: AR, 2 point mutations
Pathophys: Factor 11 deficiency
Clinical: oral cavity and urinary tract bleeding after injury, but spontaneous bleeding is uncommon

28
Q

How does Aminocaproic acid help clotting factor deficiencies?
How does Tranexamic acid?

A

Aminocarpoic acid and Tranexamic acid inhibit fibrinolysis by blocking Plasminogen activation

29
Q

What’s genetic etiology, pathophysiology, and clinical presentation for Protein C/S deficiency?
What happens w/a complete deficiency?

A

Genetics: AD
Pathophys: deficiency in Protein C
Clinical: NOT assoc w/mesenteric vein thrombosis, at risk for warfarin-induce skin necrosis, venous thrombosis by 40yo
Complete deficiency lethal w/o tx, w/tx will have purpura fulminas, DIC, thrombosis, and blindness can occur d/t intrauterine retinal thrombosis

30
Q

How does Protamine reverse Heparin/LMWH?

A

Protamine binds Heparin or LMWH better than they bind to their substrates, inactivating them

31
Q

What’s the genetic etiology (and mutation), pathophys, and clinical presentation for Hemophilia B?
why’s it more common in men?

A

Genetic Etiology: X-linked recessive, missense substitution
Pathophys: Deficiency in Factor 9
Clinical: severity correlates w/severity of mutation, but in general B is less bad than A

32
Q

What are the natural controls of fibrinolysis?

A

Natural controls of fibrinolysis:
PAI = Plasminogen activator inhibitors, inactivates tPA
Alpha 1 antiplasmin, inactivates plasmin that escapes the area

33
Q

What’s the most common organ affected by amyloidosis, and how do you diagnose, and most common cause of death?

A

Amyloidosis
most commonly affects kidneys
Dx: Congo red stain, then birefringence apple green
most common cause of death is progressive renal failure

34
Q

What types of renal involvement is seen in amyloidosis?

A

Amyloidosis

1) non-selective proteinuria
2) Nephrotic syndrome
3) Chronic renal failure

35
Q

What are 3 types of Langerhans Histiocytosis, and differentiate?
Common feature?

A

Langerhans Histiocytosis (APCs of skin)
1) Eosinophilic Granuloma-localized, no skin involvement, pathologic fxs
2) Hand-Schluller-Christian-disseminated skin rash, scalp rash, diabetes insipidus, exophthalmos, kids >3yo
3) Letterer-Siwe-fulminant and fatal, malignant, skeletal defects in kids <2yo
ALL have Birkbek granules like tennis rackets on EM

36
Q

how to differentiate Hand-Schuller-Christian from Multiple Myeloma? (focus on HSC)

A

HSC: radiolucent skull lesions BUT diabetes insipidus and exopthalmos in kids >3yo, 30% have liver and spleen involved
MM: black men >65yo w/lytic skull lesions BUT hypercalcemia, renal failure d/t Bence Jones proteins (light chains), pathologic vertebral fxs, and hypercalcemia

37
Q

What cells does EBV infect? what is subsequently affected?

A

EBV infects Bcells, but Tcells react against infected Bcells and become large/activated/Atypical

38
Q

Clinical presentation of Mono?

A

Common: Fatigue, sore throat, muscle aches, cervical lymph node and facial and eyelid swelling
Less common: Rash, tonsilar pseudomembrane, splenomegaly

39
Q

Pathophys behind Antiphospholipid Antibody Syndrome?
How does coagulation cascade get messed up?
Who gets this?

A

Antiphospholipid Antibody Syndrome:
Autoantibodies against phospholipids, esp Cardiolipin, Apolipoprotein H, and Lupus anticoagulant
Abs against Apo-H bind Protein C and S, blocking them, creating thromi
Preggos, assoc w/pregnancy complications like miscarriage, stillbirth, placental infarctions, preterm delivery, severe pre-eclampsia

40
Q

What are 2 viral infections assoc w/AIDS?
What’re the 2 fungal infections?
What’s the Protozoal infection? assoc w/?

A

HSV and CMV
Cryptococcus (most common cause of meningitis) and Histoplasma
Toxoplasmosis, assoc w/Periventricular CAlcifications

41
Q

What blood disorder’s common in cancer, and why?
What happens clinically?
What types of cancer?

A

Acquired Thrombophilia’s assoc w/malignancy bc cancer cells activate clotting system by releasing procoagulants and inflammatory cytokines
Will see DVT w/PE
Pancreas, lungs, AML, MM and BrCa

42
Q

What are Orthochromatic Normoblasts? What else are they called?

A

Orthrochromatic Normoblasts aka nucleated RBCs are immature RBCs w/Hg and Pyknotic (condensed) nucleus

43
Q

What’s the cause of iron deficiency anemia in adult men and postmenopausal women until proven otherwise?

A

GI loss d/t malignancy or lesion!

44
Q

What is Mycosis fungoides? what cells are affected and what’s it look like?
Differentiate from Sezary Syndrome

A

Mycosis fungoides:
T-helper cell tumor that hones to skin, Neoplastic Tcells have cerebriform appearance

Sezary Syndrome:
T-helper cell tumor w/generalized, exfoliative erythoderma

45
Q

What makes up the Intrinsic Tenase?

What makes up the Extrinsic Tenase?

A 
Extrinsic = 3a, 7a, Ca, PL, 10
Intrinsic = 9a, 8a, Ca, PL,  10
46
Q

What are the 2 LMWH drugs, and their MOA?

A

Enoxaparin and Dalteparin bind to ATIII to potentiate the inactivation of Factor 10

47
Q

What 3 drugs can you use in Hemophilia tx, and why?

A

Hemophilia tx:
Desmopressin increases vWF and F8 release from Weibel-Palade bodies
Aminocaproic acid and Tranexamic acid inhibit fibrinolysis by blocking Plasminogen

48
Q

What are N gonorrhoeae’s methods of evading Abx?

A

N. Gonorrhoeae: Alters proteins of ribosomes, topoisomerase, and PBPs, beta-lactases, efflux pumps

49
Q

What are Enterococcus’s methods of evading Abx?

A

Enterococcus: Makes D-ala-D-lactate wall, so Vancomycin resistant

50
Q 
What are the MOA of the following Abx?
Glycopeptides(Vancomycin): 
Beta-lactam: 
Tetracyclines: 
Chloramphenicol: 
Macrolides: 
Sulfonamide: 
Trimethaprim: 
Fluoroquinoloes:
A

Glycopeptides(Vancomycin): binds directly to D-ala-D-ala wall
Beta-lactam: binds to PBP
Tetracyclines: block 30s ribosome
Chloramphenicol: block 50s ribosome
Macrolides: block 50s ribosome
Sulfonamide: PABA analog
Trimethaprim: block dihydrofolate reductase
Fluoroquinoloes: block RNA topoisomerase (like DNA gyrase)

Heme/Onc (3 decks)

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