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pathophysiology > Blood and Coagulation > Flashcards

Blood and Coagulation Flashcards

1
Q

hypoalbuminemia

A

drugs bound to serum proteins to a various drug and only a free drug is pharmacologically active. can lead to a significant increase in free drug concentration - not enough albumin

consequence- drug toxicity - recommend lowering the dose - based on where the albumin is synthesized and what the organ is affected (liver)

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2
Q

what explains feeling tired all the time and walking up the stairs is hard

A

low hemoglobin levels, o2 capacity is reduced - anemia from a ulcer

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3
Q

RDW high. what does that mean?

A

the higher the red blood cell distribution width the more variable the size of the RBC - means the body is trying to make more blood cells trying to compensate for RBC - RBC has no mitochondria which reflects the release of large immature RBC

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4
Q

MCV

A

mean corpuscular volume - determines the average red blood cell size

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5
Q

MCH

A

mean corpuscular hemoglobin - hemoglobin value x 10 divided by the RBC

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6
Q

MCHC

A

Mean corpuscular hemoglobin content: hemoglobin x 100 divided by the HCT

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7
Q

Normochromic

A

normal MCH or MCHC

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8
Q

hypochromic

A

low MCH/MCHC

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9
Q

microcytic

A

low HCT and low MCV or small red cell anemia

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10
Q

macrocytic

A

low HCT and high MCV or large RBC anemia

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11
Q

normocytic

A

low HCT (hemocrit, volume of RBC in blood) and normal MCV – or normal RBC anemia

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12
Q

anemias

A

group of diseases characterized by a decrease in HB or RBC resulting in reduced oxygen-carrying capacity of the blood
results from inadequate RBC production, increased RBC destruction or hemolysis or blood loss

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13
Q

hyproliferative

A 
anemia class
marrow damage
iron deficiency
decreased deficiency
decreased stimulation 
inflammation
metabolic disease
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14
Q

maturation disorders

A

anemia class

cytoplasmic defects - thalassemia (less O2 carrying, heme messed up), iron deficiency, sideroblastic (ucleated erythroblasts (precursors to mature red blood cells) with granules of iron accumulated in the mitochondria surrounding the nucleus)

nuclear maturation defect- folate deficiency, vitamin b12 deficiency, refractory anemia

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15
Q

hemorrhage/hemolysis

A

anemia class

blood loss, intravascular hemolysis, autoimmune disease, hemoglobuinopathy, metabolic/membrane defect,

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16
Q

normocytic normochromic anemia

A

destruction or sudden loss of red cells: hemolytic anemia/acute blood loss

disorders of erythropoietin (produced in kidneys) production/efficacy

chronic diseases: chronic infections (HIV, hepatitis B/C, bacterial endocarditis, or osteomyelitis) autoimmune disease (RA, Crohns, systemic lupus erythematoses), lymphomas, chronic liver or renal disease

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17
Q

erythropoieten (EPO

A

differentiation into erythrocytes is dependent on EPO as it speeds of the stages of pro erythroblasts
EPO is synthesized by the kidney and released into the blood stream as a response to hypoxia (lack of o2) upon reaching the bone marrow, EPO stimulates RBC progenitors via transmembrane receptors - glycoprotein made of 166 amino acids

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18
Q

microcytic hypochromic anemia

A

deficiency in Hb synthesis - iron deficiency or poor iron utilization, or chronic blood loss

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19
Q

Macrocytic Normochromic Anemia

A

megoblasts are distinct cells that express a biochemical abnormality of retarded DNA synthesis resulting in unbalanced cell growth. may affect all hematopoietic cell lines.

caused by B12 or folate deficiencies and hemolytic anemias (RBC destroyed faster than they can be made)

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20
Q

why are hemolytic anemias macrocytic

A

early appearance of large quantity of reticulocytes (immature RBC larger than normal cells bc normal cells shrink after time ) in peripheral circulation (reticulocytosis) indication of increased RBC production. DNA synthesis is impaired. the larger red cells are always associated with insufficient numbers of cells and often also insufficient hemoglobin content per cell.

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21
Q

mild anemia

A

no clinical symptoms and may be found on accident. healthy patients may acclimate to very low Hb conc if anemia is developed slowly

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22
Q

anemia symptoms

A

fatigue, dizziness, irritability, weakness, vertigo, shortness of breath, chest pain, decreased exercise tolerance, neurologic symptoms in vitamin B12 deficiency

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23
Q

anemia rapid onset symptoms: … why?

A

palpitations, tachycardia, angina, breathlessness. body can’t compensate for all of the changes because it is a rapid onset

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24
Q

onset more chronic:

A

fatigue, weakness, headache, dyspnea on exertion, vertigo, faintness, sensitivity to cold, loss of skin tone. allows for compensating mechanisms because onset is not acute. not associated with any CV symptoms

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25
Q

anemia signs

A

tachycardia, pale, dec mental acuity, inc intensity of cardiac valve murmurs, diminished vibratory sense or gait abnormal

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26
Q

chronic hemolytic anemia

A

sickle cell - inherited recessive hemoglobinopathy resulting in abnormal hemoglobin hemolobin S

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27
Q

sickle cell trait (SCT)

A

sickle cell syndrome - heterozygous inheritance of one normal b-globin gene producing HbA and one sickle gene producing HbS gene - asymptomatic

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28
Q

Sickle cell disease (SCD)

A

homozygous or compounded heterozygous.

29
Q

sickle cell treatment

A

decitabine induces HbF inhibits DNA methylation - DNA methylation silences genes

chronic transfusions therapy primarily for stroke prevention and amelioration of organ damage - not actually treating the disease

hydroxyurea increases production of fetal Hb and not he adult form. HbF interferes with the crystallization of Hb, so RBCs no longer sickle

30
Q

pathophys sickle cell

A

stresses of ciruclation and repetitive sickle-unsickle cycles lead to RBC fragmentation - severe alteration in membrane structure and function - typical sickled cell survives for about 16 to120 days, whereas the life span of a normal RBC is 120 days
reticulocytes
Hb S has reduced oxygen affinity which increases its polymerization - when it gives up oxygen : polymerization pulls RBC into a sickle shape - sickled RBC becomes tangled with others that block blood flow resulting in tissue damage and pain from hypoxia - abnormal b-polypeptide chain

31
Q

blood group

A

classification of blood based on the presence or absence of inherited antigens = carbs present on surface of RBC

32
Q

alloantibodies

A

all individuals produce antibodies to the carbohydrate antigen that they lack

33
Q

inheritance of ABO blood group

A

genes determining the A and B phenotypes expressed in mendelian co-dominant manner each coding for glycosyltransferase to a attach a specific carbohydrate

34
Q

issoagglutinins

A

naturally occuring anti-A and anti-B antibodies - type A produces anti-B and type B produces anti-A isoagglutinin
no isoagglutinin found in AB - universal recipient
type O produce both anti-A and anti-B - universal donors (cells not recognized by any ABO isoagglutinins)

35
Q

if your blood cells do not stick together in the presence of anti-A or Anti-B

A

you have O type blood because O type blood produces both antibodies

36
Q

if your blood cells stick in anti-B

A

you have B type blood because B blood produces anti-A not anti-B

37
Q

Rh system

A

antigen found on a 30-32 kDa RBC membrane protien with no defined function -

  • D antigen is Rh positivity
  • lack D antigen Rh negative
  • Rh-negative exposed to Rh-positive can allow them to create the anti-D alloantibody
38
Q

Rh negative blood transfusion

A

should be given Rh-negative so that the patient doesn’t have alloimmunization to the D antigen. Rh-positive blood can only be used once in the case of an emergency because after that they will develop the antibody already

39
Q

Rh negative women pregnant with Rh positive baby

A

Rh antibodies after second pregnancy cross the placenta and attack the blood of Rh-positive fetus = hemolytic anemia in the fetus

prevented with Rh immunoglobulin - prevents production of Rh antibodies but it doesn’t help if the patient sis already sensitized

40
Q

anti- A serum (agglutination), anti-B serum (agglutination), anti Rh serum (no agglutination)

A

AB-

41
Q

Rh positive people can donate to _______ and Rh negative people can donate to _______

A

Rh + donate to RH +

Rh - donate to anyone

42
Q

too little hemostasis

A

allows excessive bleeding

43
Q

hemostasis (3 steps)

A

ability to stop blood loss from a damaged vessel

  1. vasoconstriction
  2. platelet plug formation
  3. coagulation
44
Q

too much hemostasis

A

too much creates a thrombus, blood clot that adheres to the undamaged wall of a blood vessel and stops blood flow

45
Q

platelet plug formation

A

begins with platelet adhesion to exposed collagen, followed by platelet activation with the local release of cytokines. release of these factors reinforce local vasoconstriction and platelet activation. platelet aggregate to one another to form a loose plug.

exposed collagen binds and activates platelets
release of platelet factors
factors attract more platelets
platelets aggregate into platelet plug

46
Q

what prevents the platelet plug from continuing to spread and form

A
  1. intact endothelium prevents platelet adhesion

2. intact endothelium releases prostacyclin and nitric oxide which prevents platelet adhesion

47
Q

platelet disorders

A
  1. low numbers - platelet count of 5,000-10,000 is required to maintain vascular integrity in the microcirculation
    • decreased production
    • sequestration (enlarged spleen)
    • increased distruction
  2. high number
  3. dysfunction
48
Q

decreased in production of low platelet numbers targets which tissue? why does this come about?

A

targets bone marrow

usually because of an infection compromising the low platelet numbers or drug-induced chemo can depress bone marrow

49
Q

why does an enlarged spleen have low platelet numbers?

A

spleen is usually a good filter : sequestered means the platelets will get stuck!

50
Q

how does an increased destruction of platelets happen?

A

immune mediated: antibodies that react with specific platelet surface antigens and result in thrombocytopenia (deficiency in platelets and causes bleeding)

51
Q

petechiae

A

pinpoint, non-blanching hemorrhage (put pressure on it and it doesn’t go away), thrombocytopenia

52
Q

purpura

A

larger, non-blanching flat patch, thrombocytopenia

53
Q

thrombocytopenia

A

deficiency in platelets and causes bleeding

54
Q

ecchymosis

A

larger than purpura, non-blanching hemorrhage

55
Q

heparin

A

anticoagulant action by accelerating the activity of antithrombin III to inactivate factor 4, 5, 6, 7

56
Q

intrinsic- contact activation

A

collagen or other factors activates factor 12

57
Q

extrinsic- cell injury

A

damage exposes tissue factor 3 which activates factor 7

58
Q

if you have a patients with existing clots can heparin lyse those closts

A

no because it inhibits thrombin preventing activation of plasminogin to plasmin to break down the fibrin polymer

59
Q

conversion of fibrinogen into fibrin and subsequent fibrinolysis

A
  1. fibrinogen converted to fibrin polymer which forms a clot - activated by thrombin
  2. fibrin polymer is activated by thrombin, plasminogen, and tpa to activate plasmin which is needed to destroy the fibrin polymer called fibrinolysis
60
Q

heparin induced thrmobocytopenia

A
  • heparin reacts with PF-4 which is normally present on the surface of endothelial cells or released in small quants from the circulating platelets
  • specific antibodies react with these conjugates to form immune complexes and the complex binds to fragment receptors on the circulating platelets
  • this releases PF-4 from alpha-granules in platelets
  • newly released PF-4 binds to additional heparin and the antibody forms more immune complexes, establishing a cycle of platelet activation
  • as activated platelet are destroyed the number of platelets will decrease and will estaablish thrombocytopenia
    excess pf-4 binds to heparin-like molecules on endothelial cells which leads to immune-mediated EC injury and increaes thrombosis and disseminated intravascular coagulation
61
Q

heparin induced thrombocytopenia differs from other drug-induced tcp

A
  1. thrmobocytopenia not usually as severe
  2. not associated with bleeding by increaes the risk of thrmobosis 50%
    treamtment: prompt discontinuation of heparin and use of alternative anticoagulats if bleeding risk does not outweigh thrmobotic risk
62
Q

high platelet number

A

iron deficiency, secondary to inflammation or infection: reactive thrombocytosis, myeloproliferative process (cancer-like)

63
Q

platelet dysfunction (2)

A

inherited mutations: secretion defects (cant do hemostasis and platelet plug or vasoconstriction - can’t have platelet activation - platelet gets activated ad they secrete platelet factors - cant release factors when they do this - function is displaced)
acquired: drugs

64
Q

drug induced platelet dysfunction: clopidogrel (plavix

A

adp induces platelet activation by binding platelet receptor P2Y12
clopidogrel prevents binding ofadenosine diphosphate to platelet P2Y receptor
impaired activation of the GPIIb/IIIa complex inhibits platelet aggregation

65
Q

coagulation factors (3)

A
  1. vitamin k-dependent factors: 2,6,9,10
  2. contact activation factors: 11 and 12, prekallikrein, high molecular weight kininogen
  3. thrombin sensitive factors: 5, 7, 13, fibrinogen
66
Q

coagulation definition

A

exposed collagen and tissue factor initiates the formation of a fibrin protein mesh to stabilize platelet plug into a clot. fibrin is the end product of a series of enzymatic reactions = coagulation cascade

67
Q

warfarin

A

inhibits the synthesis of vitamin k dpendent coagulation factors
warfarin exerts anticoagulant effect by inhibiting vitamin k epoxide reductase and inhibiting vitamin k quinone reductase
limits the gamma-carboxylation of the vitamin-k dependent coagulant proteins

68
Q

coagulation cascade - common pathway

A

unite pathways to create thrombin that converts fibrinogen into fibrin polymer - active factor 13 will convert fibrin into a cross linked polymer that stabilizes the clot

69
Q

fibrinolysis

A

as the wall vessel slowly repairs itself the clot disintegrates: thrombin works with a second factor called plasminogen activator tPA to convert inactive plasminogen into plasmin
plasmin breaks down fibrin polymers which is a process known as fibrinolysis

pathophysiology (11 decks)

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