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Physio 2 > 1-hematology > Flashcards

1-hematology Flashcards

1
Q

what system is blood part of?

A

cardiovascular system (heart + blood vessels + blood)

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2
Q

is blood a connective tissue?

A

YES

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3
Q

3 functions of blood?

A
  1. trans
  2. regulation
  3. protection
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4
Q

components of blood?

A

fluid and cellular elements:

plasma, buffy coat, red blood cells (platelets, leukocytes, and erythrocytes)

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5
Q

Buffy Coat components?

A

white blood cells and platelets 1%

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6
Q

Hematocrit (PVC)

A

% of total blood vol red blood cells 40%

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7
Q

Plasma

A

proteins (7g/dl) (albumins 50%, globulins 45%, fibrogen 4%, and others 1%), water 91.5%, other solutes (electrolytes, nutrients, gases, regulators, vitamins, waste prod)

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8
Q

Plasma proteins do what?

A

maintain plasma oncotic pressure (water balance b/w intra and extracellular fluid compartments)

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9
Q

where are plasma proteins derived?

A

liver

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10
Q

what are plasma proteins involved in?

A

trans, defense, and blood pressure

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11
Q

plasma protein can increase inflammations called? haemo-concentrations?

A

acute phase proteins (greater in lg animals) ABSOLUTE increase or increase haemo-concentration/dehydration RELATIVE increase

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12
Q

what do plasma proteins do in end stage liver disease?

A

can decrease (lack of production)

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13
Q

where do all formed blood elements originate from?

A

the same pluri-potent stem cell pool

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14
Q

pluri-potent differentiates into?

A

myeloid and lymphoid

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15
Q

myeloid stem cells create?

A

rbc, platelets, monocytes, and granulocytes

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16
Q

lymphoid stem cells create?

A

B and T lymphocytes

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17
Q

Hemopoiesis occurs?

A

in the rd bone marrow and lymphoid tissues (before birth in the spleen, liver thymus, yolk sac, and lymph nodes)

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18
Q

major site for erythropoiseis in adults?

A

flat bones-sternum, ribs, pelvis (liver and spleen contribute when challenged)

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19
Q

what conrols hemopoiesis?

A

colony stimulating factors (interlukins, cytokines, thrombopoietin, and erythropoietin)

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20
Q

total blood vol in adults?

A

6-8% of body weight or 60-80 ml/Kg BW (cats are lower than dogs adn warm blooded horses and birds are higher)

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21
Q

how much blood can be safely withdrawn from a patient?

A

1% of BW or 10 ml/Kg, MAX 2% or 20ml?kg in a healthy donor animal

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22
Q

fluid into a severely dehydrated patient?

A

can give up tot he equivalent of their total blood vol within 1hr using crystalloids. 7% of BW after and 1h 75% of the fluid will have moved to tissues rehydrating ECF and ICF.

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23
Q

mx fluids?

A

same vol over 24 hrs

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24
Q

RBC/Erythrocytes

A

contain ox carrying hemoglobin, main function is the exchange of gases (oxygen and carbon dioxide) and regulate pH

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25
Q

erythroid

A

precursors and RBCs

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26
Q

RBC shape

A

biconcave round or oval (camelids) discs-lg surface area for gas exchange

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27
Q

RBC size

A

7um in man 4-8um in animals

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28
Q

RBC concentration

A

5 million/ul in man 5-10 million in animals

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29
Q

RBC content

A

33% hemoglobin NO mitochondria, NO golgi, NO ER

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30
Q

RBC metabolism

A

energy depends on anaerobic glycolysis (no mitochondria no krebs no beta oxidation no ETC) glucose dependent

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31
Q

RBCs in Reptiles/Amphibians/Birds

A

nucleated (non functional), larger, oval, almond shape

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32
Q

Largest known RBC

A

salamander 3-x65um

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33
Q

RBCs in Fish

A

nucleated, produced in spleen and liver (bony fish), within circulation in cartilaginous fish (shark)

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34
Q

RBC functions

A
  1. oxygen transport (influences by temp, pH, metabolism, and carbonmonoxide)
  2. carbon dioxide trans (23% of total CO2 binds to flobulin portions)
  3. Carbon dioxide trans as bicarbonate to buffer (tissues-co2 into RBC HCO3 back into plasma and H to globin, Lung-HCO3 back into RC H binds and CO2 expired)
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35
Q

RBC travel and life span?

A

2.5km or 1.5 mi, 4-5 month life (cat and pig are 2 months and 5 weeks in birds)…..1% die everyday RBC production = RBC death/removal

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36
Q

removal of aged RBCs?

A
  1. rupture during spleen passage and absorbed by macrophages

2. selectively removed by phagocytic system, spleen, liver, and bone marrow

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37
Q

globulin recycled?

A

reused for protein synth

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38
Q

protoporphyrin recycled?

A

hem after Fe removal–> bilirubin —> liver bile

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39
Q

Fe recycle?

A

binds to plasma –> Transferin released when needed .. when fll Fe stores in liver, pancreas, and heart, can leade to toxic cell damage.

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40
Q

tissue oxygenation controls?

A

erythropoiesis-hypoxia–>renal (90-95%) Liver (5-10%)–>EPO—>bone marrow–>stimulation–> new RBCs

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41
Q

extrusion of nucleus

A

reticulocyte

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42
Q

stem cell to reticulocyte?

A

4-5 days

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43
Q

reticulocytes

A

immature RBC, marrow into circulation and mature in 1-2 days, 1-2% in normal blood (horses and ruminants no reticulocytes)

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44
Q

peak RBC production after challenge? replacement?

A

7 days, 14 days

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45
Q

3 ways to eval erythron?

A
  1. hematocrut
  2. RBC count
  3. hemoblobin content
46
Q

MCV, mean corpuscular volume in femtoliter

A

MCV = Hct x 10/RBC

47
Q

MCV, nomocytic

A

normal

48
Q

MCV, microcytic

A

smaller, iron deficiency

49
Q

MCV, macrocytic

A

larger than normal, immature RBC (cells haven’t expelled all organells)

50
Q

MCHC, mean corpuscular hemoglobin concentration

A

MCHC = Hb x 100/Hct

51
Q

MCHC, normochromic

A

normal concentration of Hb within RBC 33%

52
Q

MCHC, hypochromic

A

low concentration, iron deficiency, immature RBCs

53
Q

MCHC, hyperchromic

A

beyond saturation point, artifact due to hemolytic sample

54
Q

MHC, mean corpuscular hemoglobin

A

Hb content of 1 RBC …. inaccurate and not used anymore

55
Q

anemia

A

deficiency in oxygen carrying capacity

56
Q

anemia causes could be?

A
  1. low RBC count
  2. low Hb content
  3. malfunctional RBCs
57
Q

Types of anemia causes?

A
  1. haemorrahagia
  2. haemolytic
  3. dyshemopoietic (reduced or defective eruthropoisis)
58
Q

types of anemia according to bone marrow?

A
  1. regenerative

2. degenerative

59
Q

types of anemia according to RBC parameters?

A
  1. RBC size: normo, micro, macrocytic

2. Hb content: normo, hypochromic

60
Q

hemorrhagic anemia

A

due to acute blood loss-plasma replaces in 1-3 days RBCs 2 weeks, but signs of regeneration are seen in 3-5 days

61
Q

hemolytic disorders

A

blood parasites, toxins, immune mediated (IMHA), inherent defects (sickle cell anemia)

62
Q

dyshemopoietic anemias

A
  1. non-regenerative, nutritional def, lack of iron… initially regenerative but quickly turn into non regen.
  2. ACD, AID - Anemia of chronic disorders - cancer, necrosis, sepsis-shorten RBC life
  3. chronic renal diseases - lackc of EPO
  4. Drug related suppression - estrogene
63
Q

hemorrhagic and hemolytic anemias

A

become chronic (GI ulcers) –> exhuastion of iron stores–> become non regen.

64
Q

polycythemia types?

A

increased RBC numbers

  1. primary (rare) - lack of feedback control
  2. secondary (common) - physio responce to oxygen deficiency due to high altitudes, caardiac failure, lung diseases
  3. transient - spleenic contraction due to excitement, exercise..horses, cats, sight hounds
  4. relative (very common) - dehydration, fluid loss
65
Q

two types of antigens are known?

A

natural and those withou natural antibodies

66
Q

o-a-b

A

humans

67
Q

a-b

A

cats

68
Q

a-c-q-r-s

A

horses

69
Q

1.1,1.2,3,4,5,6,7,8,

A

dogs

70
Q

b-j-a-f

A

cattle

71
Q

natural antibodies are present in?

A

cat and man

72
Q

mismatched blood transfusions can lead to …?

A

fatal reactions

  1. rupture of capillaries –> shock
  2. phagocytosis –> attack RBCs
  3. precipitation of excess Hb–> renal blockage and acute renal failure
73
Q

before you do a blood transfusion you?

A

blood type or cross match recipients plasma with donors RBCs to avoid rxns

74
Q

dog should be neg for?

A

DEA 1.1, 1.2, and 7

75
Q

major rxns in cross matching vs minor?

A

major - donors RBCs to Recipients plasma
minor - recipients RBCs to Donors plasma

observe for agglutination in both.

76
Q

Hemostasis definition?

A

sequence of responses that stop bleeding

77
Q

hemostasis is?

A

fast, localized, and carefully controlled

78
Q

5 steps of hemostasis?

A
  1. vascular spasm
  2. platelet plug formation = primary
  3. blood clot formation = coagulation = secondary
  4. healing
  5. clot removal = fibrinolysis
79
Q

platelets

A

thrombocytes

80
Q

platelet shape

A

round to oval, enucleated discs

81
Q

platelet size

A

2-4um, birds and reptiles 4-8um nucleated

82
Q

platelet concentration

A

150-300/ul

83
Q

platelet half life

A

10 days

84
Q

platelet origin

A

bone marrow - megacaryocytes (myeloid) - controlled by hepatic thrombopoietin

85
Q

platelet contents

A
  1. contractile proteins (actin, myosin, thrombosthenin)
  2. ADP, ATP
  3. prostaglandins, serotonin, clotting factors, endothelial growth factors
  4. calcium
86
Q

platelet functions

A
  1. release chemicals to promote vasospasm
  2. formation of plug
  3. release coagulation factors
  4. heal
87
Q

Vasospasm (step 1)

A
  1. occurs immediately upon injury (reduced blood flow, blood loss)
  2. caused by release of endothelin form damaged cells then from thromboxane A2 and serotonin from platelets
  3. can last min to hrs
88
Q

Platelet plug (step 2)

A

damaged endothelial cells release von Willbrand Factor (vWF) - they bind with collagen fibers and receptor sites for platelets. then adhesion begins.

89
Q

Binding in step 2 activated platelets to?

A
  1. send out pseudopodia (degranulation)
  2. release serotonin and thromboxane A2 –> promote vasospasm
  3. release ADP and thromboxane A2 –> attract more platelets (aggregation)
  4. release ADP and Fibronectin –>promote adhesion
  5. release several platelet factors (V and VII) and calcium –> clotting
  6. expose receptor sites for fibrinogen and prothrombin –> later clotting
    * *** plug is formed in 1-2 min
90
Q

deficiency in platelet plug formation

A

Petechial bleeding

91
Q

Clot formation (step 3)

A

secondary hemostasis - cascades of chem rxns. 3-6 min,

  1. extrinsic and/or intrinsic path –> prothrombin activator complex
  2. Common path –> activation of prothrombin to thrombin
  3. convert soluble fibrinogen to insouble fibrin
92
Q

> …..clotting factors

A

50, lack of any can lead to a bleeding disorder

93
Q

extrinsic-tissues bases

A

tissue factor thromboplastin 15-30 sec —>prothrombin activator complex

94
Q

intrinsic-plasma based

A

endothelial bind and activate plasma factor XII 1-6 min –> CTIVATED ENZYMATIC XASCADE (XI, IX, VIII< X, V, CA) —> PROTHROMBIN ACTIVATOR COMPLEX

95
Q

extrinsic vs intrinsic

A

extrinsic is faster and more powerful intrinsic is an amplifier

96
Q

prothrombin

A

a hepatic alpha globulin, liver synth Vit K dependent, attaches to activated platelets

97
Q

Healing (step 4)

A

fibrin meshwork serves as a scaffolding for invading fibroblasts, endothelial growth factor and scar formation begins.

98
Q

fibrinolyis (step 5)

A

clot is removed after healing sets in. plasminogen to plasmin= proteolytic enzyme –> FDP fibrin degrading products, removes clot and opens blood vessels

99
Q

intact WBC and endothelial cells …??

A

secrete prostacyclin and nitric oxid –> inhibit platelet adhesion

100
Q

Prevention of excessive clot formation

A
  1. fibrin binds to thrombin –> limits formation and pos feedback
  2. anti-thrombin III –> deactivated thrombing and other factors
  3. heparin from mast cells/basophils with andti thrombin III augment effectiveness
  4. in vitro - Ca binding agents
  5. in vivo - heparin, vit K antagonists
101
Q

platelet count

A

via blood smears … inaccurate

102
Q

mucosal bleeding time

A

incision into skin or mucosa (expected clot 1-5 min)

103
Q

OSPT - one stage prothrombin time

A

measures clot formation –> extrinsic common pathway (< 10 sec)

104
Q

APTT - activated Partial thromboplastin time

A

measures clot formation after clean veinpuncture plasma and contact activator, measures intinsic path (60 - 120 sec)

105
Q

thrombocytopenia (bleeding disorder)

A

decreased production or increased destruction (immune mediated) or consumption

106
Q

bleeding disorders

A
  1. thrombocytopenia
  2. vWF disease
  3. Vit K dificiency
  4. hemophilias
107
Q

vWF disease

A

most commono- genetic lack —> platelets fail to adhere to injury sites –> spont. bleeding –> petechial
*** highest prevalence in dobermans

108
Q

Vit K def/rodenticide

A

impairs liver synth and clotting factors

109
Q

hemophilias

A

very rare - genetic def in clotting factor

110
Q

Thrombosis

A

clotting in an unbroken blood vessel-due to stasis, atherosclerosis, trauma, parasites or tumors. If it dislodges –> embolisms –> ischemia ex. saddle thrombus in cats

Physio 2 (2 decks)

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