Hematology

Question 1

Thrombus

Answer 1

Blood clot

Question 2

Embolus

Answer 2

Blood clot on the move

Question 3

Embolism

Answer 3

Embolism that gets stuck in a blood vessel

Question 4

Arterial thrombosis

Answer 4

Often caused by atherosclerotic lesions on arterial endothelium and usually consists of a platelet-rich clot (white clot).

Question 5

Venous thrombosis

Answer 5

Often triggered by blood stasis or inappropriate activation of the coagulation cascade and usually consists of a fibrin clot (red clot).

Question 6

Platelet aggregation inhibitors

Answer 6

(antiplatelet drugs) prevent platelet clots.

Question 7

Two types of PCIs

Answer 7

Balloon angioplasty & stenting

Question 8

PCI

Answer 8

Percutanteus coronary intervention

Question 9

Thrombin inhibitors and vitamin K antagonist

Answer 9

(anticoagulants) prevent fibrin clots.

Question 10

Indications for Anticoagulants

Answer 10

deep vein thrombosis (DVT) prophylaxis and treatment and pulmonary embolism (PE) prophylaxis and treatment.

Question 11

Primary Adverse Reactions: Antiplatelet and anticoagulant medications

Answer 11

Bleeding, such as hemorrhagic stroke or GI hemorrhage.

Question 12

COX-1 inhibitor

Answer 12

Inhibits thromboxane A2 production to decrease platelet aggregation. Ex. aspirin.

Question 13

ADP Inhibitors

Answer 13

Inhibit adenosine diphosphate’s involvement in stimulating platelet aggregation. Examples - Clopidogrel, prasugrel; ticagrelor, ticlopidine

Question 14

GP IIb/IIIa Blocker - tirofiban based on the venom of an Asian viper

Answer 14

Physically block glycoprotein IIb/IIIa receptors to prevent fibrinogen, etc. from cross-linking platelets during platelet aggregation. Examples - abciximab, eptifibatide, and tirofiban

Question 15

Antiplatelet / vasodilators

Answer 15

dipyridamole – coronary vasodilator - Used in combination with aspirin or warfarin to prevent thrombo- embolism in patients with a prosthetic heart valve. Cilostazol – peripheral vasodilator - Used for intermittent claudication.

Question 16

Direct Thrombin Inhibitors

Answer 16

Unfractionated heparin, bivalirudin and lepirudin. Directly bind to and inhibit thombin to prevent it from converting fibrinogen to fibrin.

Question 17

Indirect Thrombin Inhibitors

Answer 17

low-molecular-weight heparins (dalteparin, enoxaparin and tinzaparin), apixaban, fondaparinux and rivaroxaban. Directly bind to and inhibit Factor Xa to prevent it from converting prothrombin to thrombin.

Question 18

Vitamin K antagonist drug

Answer 18

warfarin

Question 19

Vitamin K antagonist action

Answer 19

Directly interferes with the function of vitamin K and inhibits the synthesis of clotting factors II (prothrombin), VII, IX and X in the liver.

Question 20

Endogenous fribrinolytic system

Answer 20

tissue plasminogen activator (tPA) and urokinase convert plasminogen to plasmin.

Question 21

Plasmin

Answer 21

degrades fibrin and dissolves fibrin clots, thus allowing blood flow to resume

Question 22

Thrombolytics

Answer 22

recombinant versions of tPA and urokinase which are used to treat acute myocardial infarction, acute ischemic stroke and pulmonary embolism.

Question 23

Clot busters

Answer 23

Thrombolytics; breaks up bad clots AND good clots that are preventing bleeding

Question 24

Aminocaproic acid

Answer 24

inhibits plasminogen’s activation to plasmin to control hemorrhage in fibrinolytic disorders

Question 25

Tranexamic acid

Answer 25

Tranexamic acid has the same mechanism as aminocaproic acid and is used for bleeding prophylaxis in some hemophilias.

Question 26

Protamine

Answer 26

binds to and neutralizes unfractionated heparin and LMWH to treat heparin/LMWH overdose

Question 27

Vitamin K

Answer 27

reverses warfarin’s inhibition of clotting factor synthesis to treat warfarin overdose

Question 28

Anemia definition

Answer 28

A below-normal plasma hemoglobin concentration. Typically due to a decreased number of circulating red blood cells or an abnormally low total hemoglobin content per unit of blood volume.

Question 29

Causes of anemia

Answer 29

Causes include chronic blood loss, bone marrow abnormalities, increased hemolysis, toxic effects of some medications and dietary deficiencies.

Question 30

Dietary requirements for normal RBC production

Answer 30

Iron, folic acid and vitamin B-12 (cyanocobalamin)

Question 31

Iron deficiency

Answer 31

results from a negative iron balance due to depletion of iron stores as occurs with acute or chronic blood loss and/or inadequate intake or absorption of iron in food or supplements.

Question 32

Hypochromic anemia

Answer 32

RBCs are pale

Question 33

Microcytic anemia

Answer 33

RBCs are smaller than normal

Question 34

Tx for hypochromic/microcytic anemia

Answer 34

Iron supplementation

Question 35

Folate deficiency

Answer 35

associated with an increased demand in pregnancy and lactation, poor absorption due to some small intestine conditions, alcoholism and exposure to drugs such as methotrexate and trimethoprim

Question 36

Megaloblastic anemia

Answer 36

RBCs are larger than normal due to folate deficiency or B-12 deficiency

Question 37

Megaloblastic anemia tx

Answer 37

Vitamin B-12 and folic acid are both required for other megaloblastic anemias.

Question 38

Cyanocobalamin (vitamin B-12) deficiency

Answer 38

typically associated with decreased absorption due to inadequate intrinsic factor production by gastric parietal cells, bariatric surgery and nonspecific malabsorption syndromes.

Question 39

pernicious anemia

Answer 39

Type of megaloblastic anemia due to inadequate intrinsic factor

Question 40

Pernicious anemia tx

Answer 40

Vitamin B-12 supplementation

Question 41

Erythropoietin

Answer 41

glycoprotein hormone that is produced in the kidneys. It regulates red blood cell proliferation and differentiation in the bone marrow

Question 42

Erythropoietin Uses

Answer 42

Recombinant versions are used to treat anemia caused by end-stage renal disease, HIV infection and cancer

Question 43

Sickle cell disease

Answer 43

inherited red blood cell disorder in which RBC’s contain abnormal hemoglobin S that causes them to dehydrate and become hard and sticky and to take on the shape of a farmers’ sickle.

Question 44

Sickle cell pain crisis

Answer 44

Sickle cell disease can cause “sickle cell pain crisis” and can damage blood vessels and eventually major organs.

Question 45

Hydroxyurea

Answer 45

increases the amount of hemoglobin F in RBC’s and protects them from the harmful effects of hemoglobin S.

Question 46

Pentoxifylline

Answer 46

acts by increasing RBC flexibility and reducing the viscosity of the blood thereby improving blood flow and tissue oxygenation.