Test #4 Bloodcells

Front 1

Why are MCV, MCH and MCHC important?

Back 1

determine shape and size of RBC and determine type of anemia

Front 2

Plt count have to do with _______

Back 2

clotting

Front 3

If you have someone who has been ill and taking asprin daily, when will the asprin stop affecting plts?

Back 3

7-10 days

Front 4

hgb avg norm count

Back 4

11-12

Front 5

RBC count normal is?

Back 5

4.2-4.8

Front 6

wbc count norm?

Back 6

4.5-11

Front 7

Iron Deficiency

Back 7

type of anemia indicated by tiny and pale cells
tx: medical and nursing

Press "h" for slide 3

Hint 7

Porth 289-290

dietary deficiency, loss of iron through bleeding, or increased demands. Decreased iron leads to decreased hemoglobin synthesis and consequent impairment of 02 delivery.

Iron is recycled, but a little is lost in the feces and need to be replaced.

The usual reason for iron def. in adults in the Western world is chronic blood loss b/c iron cannot be recycled to the pool (e.g. GI bleeds, peptic ulcers, hemorroids or cancer, excessive aspirin intake. The need for iron increases during pregnancy and infant/child growth.

Tx: prevention is also important for those at risk (infants, children, pp with blood loss) . TX includes stopping blood loss, increasing dietary intake of iron and admin supplemental iron. Ferrous sulfate is the usual oral replacement therapy and Parenteral iron is used if oral is not tolerated.

Front 8

Anemias of Renal
Disease and
Chronic Disease

Back 8

type of anemia

Front 9

Megaloblastic
–B-12 or Folate
deficiencies

Back 9

type of anemia due to b-12, or folate def OR heriditary hemochromatosis

Tx for B-12=add b12
tx for folate def=add folate
Tx for hemochromatosis: drain blood (to get ride of excess iron)

Hint 9

Porth 290

Caused by impaired DNA synthesis that results in enlarged red cells (MCV>100 fL) due to impaired maturation and division.

Vit b12 and Folic acid def are the most common conditions associated with megaloblastic anemias.

Vit B12 def--B12 is important for DNA synthesis and nuclear maturation, which in turn leads to normal red cell maturation and division. Also breakdown of myelin may occur which causes neurologic manifestations. b12 def is usually found in vegetarians (foods of animal orgins are good sources of b12)

Pernicious anemia is a specific type of megalobastic anemia caused by atrophic gastritis which leads to failure to absorb vit b12.

TX: IM B12 or high doses or oral b12

Folic Acid Def. Folic acid is req for DNA sythesis and red cell maturation.

Front 10

Aplastic

Back 10

type of anemia

Front 11

Myelodysplastic
Syndromes

Back 11

type of anemia

Front 12

Sickle Cell

Back 12

type of anemia identified by sickle shaped RBCs (sludge like blood)
treated w/ RBC replcment & pain mgmt

Front 13

Thalassemia

Back 13

type of anemia

hit H to know more (slide 3)

Hint 13

Porth pg 288:
Thalassemias are a group of inherited disorders of hemoglobin synthesis leading to decreased synth of either the alpha or beta globin chains of HbA.
two factors contribute to anemia that occurs in thalassemia: low intracellular hemoglobin (hypochromia) due to the decreased synthesis of the affected chain, coupled with cntinued production and accumulation of the unaffected globin chain. The reduced hemoglobin synthesis results in a hypochromic, microcytic anemia, whereas the accumulation of the unaffected chain interferes with normal red cell maturation and contributes to membrane changes that lead to hemolysis and anemia.

Front 14

Hereditary
Spherocytosis

Back 14

type of anemia

Front 15

Immune
Hemolytic

Back 15

type of anemia

Front 16

What are reticulocytes?

Back 16

immature RBC

Front 17

Why is an increase of reticulocytes an important indicative factor?

Back 17

indicative of anemia because severe shortage of RBC.

Front 18

Increase in SED rate means?

Back 18

inflammatory processes have begun (good at measuring if there is an autoimmune dz present--e.g. loopis, RA)

Front 19

Why would we look at a bone marrow?

Back 19

Assess the quantity and
quality of each type of cell
produced in the bone marrow

Front 20

What is a polycythemia?

Back 20

too many/increase in cells

Front 21

Polycythemia happens alot in _____pts due to their chronic conditions of lack of O2.

Back 21

COPD

Front 22

Pulmonary fibrosis has ______numbers of RBCs

Back 22

high numbers of RBCs

Front 23

What kind of blood and components can we give?

Back 23

Whole Blood
Packed RBCs (PRBC)
Platelets
Fresh Frozen Plasma (FFP)
Special preparations: Factor VIII, Factor IX,
albumin, immune globulin

Front 24

fresher blood the more _____ ______ capacity

Back 24

Oxygen carrying

Front 25

when do you transfuse a patient (at what hgb count)?

Back 25

hgb=below 8

Front 26

best o2 carrying capacity, you want the hgb to be a which count?

Back 26

hgb=10

Front 27

what is cryoprecipitate?

Back 27

FACTOR 8 (VIII) (clotting factor)

Front 28

If a pt has hemophilia/von willebrands or fibrinogen < 100, what would be given?

Back 28

cryoprecipitate

Front 29

What are some transfusion complications?

Back 29

1. Febrile, non-hemolytic reaction
2. Acute hemolytic reaction
3. Allergic reaction
4. Transfusion-related acute lung injury
–―TRALI‖
5. Blood transmitted diseases

Front 30

what would a non-hemolytic reaction to a transfusion be?

Back 30

fever, flank pain, SOB (not related to the blood)

Front 31

Describe a hemolytic reaction (tranfusion complication).

Back 31

anaphylaxis--can happen even if the blood types match (are correct)

Cells LYSE---very bad for pt=death

Front 32

What is TRALI? related to tranfusion complication

Back 32

transfusion related acute lung injury.

lungs get stiffer so 02 and C02 can't transfuse to lungs

Front 33

What is circulatory overload? (related to tranfusion complication

Back 33

pulm. edema pts are given extra volume and are overloaded. to avoid, get one unit at a time and give LASIX. Take away plasma for the RBC carrying capacity so that heart is not over-working

Front 34

monocyte think===

Back 34

phagoctye (eat)

Front 35

what is hemostasis?

Back 35

stop of bleeding

Front 36

What is thrombosis?

Back 36

abnormal clotting--keep clotting even when we don't need it (could cause an obstruction)

Front 37

emboli vs thrombosis?

Back 37

emboli travels

Front 38

what are the normal values for platelets?

Back 38

150,000-450,000

Front 39

What is the lifespan of a plt?

Back 39

10 days approx

Front 40

Thrombocytosis is?

Back 40

increase in plts

Front 41

Plt are attracted to _______ areas.which is why they attach to plaque in arteries.

Back 41

uneven

Front 42

Von willebrans factor is important for ______ to v_______ w_______

Back 42

Von willebrans factor is important for adherence to vessel wall

Front 43

TXA2 is?

Back 43

? look it up

Front 44

Waht are factors impacting plts?

Back 44

1. Medication (antibiotics, aspirin, anticoag)
2. Bone marrow disorders
3. Stress response

Front 45

Zosin (antibiotic) eats p_____.

Back 45

Platelets

Front 46

What is ITP? (Immune Thrombocytopenic Purpura ) Name 1. causes, 2. lab values for plts, PTT and FSP, and 3. TX

Back 46

1. causes: meds (sulfa, thiazides, quinidines) & HIV

2. Labs: plts <50, PTT and Fibrin slit products normal

3. Tx: steroids, IVIG (immunoglobulin), chemotherapy

Front 47

What is Heparin Induced Thrombocytopenia
(HIT) ? 1. Define 2. Labs 3. Tx

Back 47

1. Allergic response to heparin
Intense production of emboli due to
coag. Pathway

2. Labs: 50% drop plt. over 5 days, plt <50

3. TX: Stop heparin & give blood produccts

Front 48

What is Thrombotic Thrombocytopenic
Purpura (TTP) ? 1. define 2. Labs (rbcs, reticulocyte, bili, LDH) 3. Tx 4. complications

Back 48

1. Exaggerated immune response to
vessel injury due to clots. develop little bruises all over.

2. Labs: decrease in RBCs, increase in
reticulocyte count, increase bili & LDH

3. TX: thrombolytics, blood products, pain mgmt.

4. Complications: limb loss, septicemia

Front 49

What is the max dose for the antidose, protamine sulfate?

Back 49

50 mg dose in adults and 1mg of PS for q 100 mg heparin

Front 50

Who do you have to give extra caution to when giving the heparin antidote (Protamine sulfate), and which drugs might you give along with the PS?

Back 50

Fish allergies. Give benadryl and perhaps steroid

Front 51

What would you give to someone with HIT that needs herparin?

Back 51

Fondaparinux (Arixtra)

Front 52

Fondaparinux (Arixtra) inhibits or binds to which factor in cascade?

Back 52

Factor Xa

Front 53

How long does it take for coumadin to become affective?

Back 53

a week or so, but depends on the pt's metabolism (could take a month)

Front 54

What is the normal value for INR?

Back 54

<2.0

Front 55

What would the INR therapeutic value for cardiac therapy?

Back 55

2-3'

Front 56

What is the name of the warfarin antidote?

Back 56

Aqua­Mephyton (phytonadione)

Front 57

Name antiplatelet drugs.

Back 57

Ex. Aspirin (ASA), Ticlopidine (Ticlid), Tirofiban (Aggrastat)Aggrastat interferes w/ Von willebrans factor, Aspirin (Ecotrin), Dipyridamole (persantine), Copidrogel (Plavix) DECREASES PLT ABILITY TO STICK

Front 58

intrinsic cascade pathway

Back 58

injury from inside out (clots, stents)

Front 59

petechiae

Back 59

pinpoint hemorrahges

Front 60

purpura

Back 60

irregular bruises under the skin. Larger than a pinpoint

Front 61

ecchymoses

Back 61

bruise

Front 62

hematoma

Back 62

poolof blood trapped under the skin

Front 63

extrinsic cascade

Back 63

turned on by injury from outside to in (GSW, car crash lesion)

Front 64

what is an appropriate abbreviationforDisseminated intravascular coagulation

Back 64

DIC

Front 65

What drug is given to someone with DIC?

Back 65

Heparin

Front 66

Describe DIC. 1. Define,2. Causes, 3. labs (PTT, Hgb, FSP, fibrinogen, D-dimer), 4. complications?

Back 66

"1. Hyperclotting state until depleted
2. Causes: shock, sepsis, childbirth,
trauma, tumors
3. Labs: PTT>40, Hgb. <10, FSP increase,
fibrinogen decrease, increase D­Dimer
4. Complications: MOSF (mult. Organ failure)"

Front 67

What are s/s of poor clotting?

Back 67

nosebleeds, bruises, black stool, blood in urine, sensitive tissue (IV site, brushing teeth)

Front 68

Which medications would you monitor for pp with clotting disorders?

Back 68

aspirin, steriods (due to gastric bleeding SE)

Front 69

"What is the mechanism of action for Anticoagulants?

"

Back 69

": prevent clot formation
and extension (coumadin & heparin) "

Front 70

"What is the mechanism of action for Antiplatelet drugs?
"

Back 70

": interfere with platelet
activity (Plavix) "

Front 71

What is the mechanism of action for Thrombolytic agents?

Back 71

dissolve existing thrombi (Streptokinase)

Front 72

Heparin (Onset? Duration? Half life?)

Back 72

"
Pharmacokinetics
–onset:
•20 ­60” sq
–Duration:
•IV: 2 ­6 h
•sq: 8 ­12 h
–Half life: 90” "

Front 73

How is heparin given (i.e. IV, Oral, IM, Subq?)

Back 73

injectable ONLY: IV or Subq NeVER IM

Front 74

Name the factors in the intrinsic pathway that herparin binds to?

Back 74

Intrinsic Path: works on 9a, 11a, 12a

Front 75

Name the factors in the extrinsic pathway that herparin binds to?

Back 75

Extinsic Path: works on 10a, thrombin

Front 76

Before you lower the dose/concentration of the heparin, youmust do what?

Back 76

have a second nurse double check the dose and sign off

Front 77

What is the heparin antidote?

Back 77

Protamine sulfate!

Front 78

ANTICOAG FUNTION

Back 78

PREVENT CLOTS

Front 79

ANTI PLT FUNCTION

Back 79

INTERFERE WITH PLT FUNCTION

Front 80

THROMBOLYTIC FUNCTION

Back 80

RESOLVE EXISTING THROMBI

Front 81

WHY IS LDL MORE DANGEROUS THAN HDL AT HIGH LEVELS?

Back 81

MACROPHAGES AND FOAM CELLS

Front 82

WHAT ARE FOAM CELLS?

Back 82

OXIDIZED LDL THAT CAUSES PLAQUE ON VESSELS

Front 83

Normal Values:
Total Cholesterol < ____

Back 83

Total Cholesterol < 200

Front 84

Normal Values:
LDL < ____; [<____ if CAD or DM]

Back 84

LDL < 130; [<100 if CAD or DM]

Front 85

Normal Values:
HDL > ___

Back 85

HDL > 45

Front 86

Normal Values:
Triglycerides < ____

Back 86

Triglycerides < 150