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Pathophysiology > chapters 13,14,11 > Flashcards

chapters 13,14,11 Flashcards

1
Q

Whole blood consists of: %’s

A

55% plasma

45% formed elements

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2
Q

55% of whole blood is plasma, which consists of

A 
water 91.5%
solutes 1.5%
proteins 7%
- albumin
- fibrinogen 
- globulins
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3
Q

45% of whole blood consists of formed elements which consists of

A

erythrocytes: 4.2-6.2 million
Platelets: 140,000-340,000
Leukocytes: 5,000-10,000

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4
Q

Leukocytes breaks down into

A 
neutrophils: 57-67%
eosinophils
basophils
lymphocytes: 25-33%
monocytes
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5
Q

alpha globulin transports

A

bilirubin
lipids
steroids

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6
Q

beta globulin transports

A

iron

copper

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7
Q

gamma globulin

A

contains anitbody molecules

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8
Q

fibrinogen

A

inactive precursor of fibrin, which forms framework of bloodclots.

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9
Q

1/3 of platelets reserved in

A

spleen

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10
Q

erythrocytes functions

A

transport O2
Remove CO2
buffer blood pH
no cytoplasmic organelles, nucleus, mitochondria, or ribosomes
live 80-120 days
reversible deformity: biconcave and torpedo-like

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11
Q

platelets are fragments..

A

cytoplasmic fragments of megakaryocytes.

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12
Q

hematopoiesis

A

developmental process of pluripotential stem cells.
RBC. neutrophils
eosinophils. basophils
monocytes. platelets

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13
Q

hematopoises occurs

A

in bone marrow

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14
Q

hematopoiesis can be accelerated by

A

increase in differentiation of daughter cells
increase number of stem cells
conversion of yellow bone marrow to red marrow.

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15
Q

erythropoietin

A

hormone secreted by kidney to stimulate erythrocyte production

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16
Q

erythrocyte development stages

A

erythroblast
reticulocyte
erythrocyte

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17
Q

reticulocyte

A

small disk with no nucleus

leaves bone marrow and enters blood stream to where it matures to an erythrocyte.

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18
Q

hemoglobin synthesis

A

2 pairs of polypeptide chains; globins

- each with an attached heme molecule composed of iron

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19
Q

where is iron found in body

A

67% total body iron bound to heme
30% stored bound to ferritin
3%: lost daily

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20
Q

nutrition requirements for erythropoiesis

A

iron: hemoglobin
vitamins: b12, folate, b6

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21
Q

how is b12 absorbed

A

required intrinsic factor in stomach

- secreted by parietal cells

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22
Q

stimulant of erythopoiesis

A

low oxygen saturation

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23
Q

red cell destructions

A

80%-90% in spleen and liver
broken down into amino acids and iron is recycled
byproduct is bilirubin
-conjugated in liver and excreted in bile
- increased RBC destruction = increased bilirubin = jaundiice

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24
Q

anemia clinical manifestations

A 
decreased O2 carrying capacity
tissue hypoxia
compensatory mechanisms
- inc. pulmonary and cardiac function 
-inc. O2 extraction 
selective tissue perfusion (short-term)
increased RBC production long-term
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25
Q

anemia s/s

A

fatigue
weak
tachycardia
exertional dyspnea

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26
Q

moderate to severe anemia s/s

A

hypotension. tachycardia
vasoconstriction. murmur
pallor. angina
tachypnea. heart failure
dyspnea muscle cramps
headache. dizzy

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27
Q

aplastic anemia

A

normocytic-normochromic anemia
stem cell disorder
dec. in hematopoietic tissue in bone marrow
pancytopenia

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28
Q

acquired aplastic anemia comes from

A

ebstein-Barr
HIV
Dengue

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29
Q

Familial aplastic anemia

A

fanconi constitutional pancytopenia
pancreatic deficiency in children
putative hereditary defect in cellular uptake of folate.

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30
Q

pancytopenia (aplastic anemia) s/s

A 
RBC:
weakness
fatigue
pallor
dyspnea
palpitations, murmurs 
WBC: 
fever, chills
bacterial infections
PLATELETS:
petechiae
bruising
bleeding
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31
Q

aplastic anemia treatment

A

bone marrow transplant
maintenance of essential hemoglobin and platelets
prevention and management of infection
no transplant: immunosuppression, stimulation of hematopoiesis, bone marrow regeneration.

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32
Q

anemia of chronic renal failure

A

impaired erythropoietin production
impaired excretory function
- hemolysis, bone marrow depression, blood loss

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33
Q

anemia of chronic renal failure treatment

A

dialysis
administer erythropoietin
monitor hct and hgb
replacement of b12, iron, and folate (restricted diet)

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34
Q

where are clotting factors synthesized

A

liver

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35
Q

granulocytes

A

phagocytes:

  • neutrophils
  • eosinophils
  • basophils
  • mast cells

All granular

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36
Q

agranulocytes

A

phagocytes:
- monocytes
-macrophages
Immunocytes:
- lymphocytes (B & T)
- natural killer cells (granular)

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37
Q

granulocytes

A 
digestive enzymes: 
- kill microorganisms
- catabolize debris 
Biochemical mediators
- inflammatory
- immune functions
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38
Q

Eosinophils

A

allergic reactions

parasites

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39
Q

basophils

A

vasoactive amines:

  • histamin
  • serotinin
  • heparin
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40
Q

mast cells

A

histamine, chemotactic factors and cytokines

acute/chronic inflammation, fibrotic disorders, wound healing

41
Q

monocyte/macrophage

A

ingest and destroy microorganisms and foreign material, debris, and defective/ dead cells.

42
Q

lymphopoiesis

A

B cells
T cells
fully mature in blood stream

43
Q

stimulation of platelets

A

thrombopoiten

44
Q

pediatric blood cell counts

A

higher than adult levels at birth
lymphocytes count higher at birth
platelets normal

45
Q

3 main components of hemostasis

A

vasculature: endothelial cells
platelets
clotting factor

46
Q

primary hemostasis

A

vascular damage
vasoconstriction
platelet plug

47
Q

secondary hemostasis

A

coagulation cascade

blood clot

48
Q

tertiary hemostasis

A

clot dissolution

fibrinolysis

49
Q

extrinsic system

A

tissue factors
vitamin K
VII

50
Q

intrinsic system

A 
platelets
XII
Xi
Vitamin K
IX
VIII
51
Q

where extrinsic and intrinsic meet

A

Factor X

52
Q

prothrombin

A

inactive precursor to thrombin

53
Q

thrombin

A

acts upon fibrinogen to make active form fibrin.

54
Q

Prostaglandin derivatives: positive hemostasis regulation

A

thromboxane

  • platelets
  • inc. fibrinogen receptors, cause degranulation, vasoconstriction
  • aggregation
55
Q

Negative hemostasis regulation

A 
prostacyclin
- endothelial cells
- inhibit degranulation
- vasodilation
Nitric oxide
- endothelial cells
- vasodilation , inhibits adhesion/ aggregation
56
Q

lysis of blood clots

A

t–PA
plasminogen-> plasmin
- degrading enzyme
fibrin degradation

57
Q

megaloglastic anemia

A

large stem cells
defective DNA synthesis
- dec. vitamin b12 or folate

58
Q

pernicious anemia

A 
Macrocytic- normochromic
Lack of IF from gastric parietal cells 
- no vitamin b12 absorption 
slow onset
- nerve demyelination
59
Q

sickle cell anemia

A

hypochromic anemia
genetic defect of hemoglobin synthesis
sickled cells cause vascular occlusion
severe anemia, RBC of different shapes, sizes, and recurrent painful episodes

60
Q

iron deficiency anemia

A 
microcytic hypochromic anemia
most common world wide
inadequate dietary intake/ blood loss 
insufficient iron delivery/use
brittle, thin, coarsely ridged, and spoon-shaped nails
red, sore and painful tongue
61
Q

sideroblastic anemia

A

microcytic-hypochromoic
anemia due to mitochondiral metabolism of Fe, unable to use iron.
splenomegaly and hepatomegaly
ringed sideroblasts within the bone marrow
- RBC contain Fe granules that have not been synthesized into Hb

62
Q

thalassemia

A

microcytic-hypochromic
increased RBC destruction
alpha or beta globin synthesis impaired
polypeptide chain with deficient synthesis of alpha or beta globins

63
Q

faconi anemia

A

normocytic-normochromic anemia
genetic alteraion
defects in DNA repair

64
Q

hemolytic anemia

A 
normocytic-normochromic anemia
accelerated destruction of RBC
- inherited
- autoimmune
- drug- induced
-- penicillin, cephalosporins
-- Quinidine 
- a-methyldopa
65
Q

Anemia of chronic disease

A 
reduced response to EPO
AIDS
rheumatoid arthritis
lupus
hepatitis
renal failure
- dec. RBC life span
- ineffective bone marrow response
- altered iron metabolism
66
Q

polycythemia

A

overproduction of RBC

67
Q

relative polycythemia

A

dehydration

fluid loss

68
Q

absolute polycythemia

A

1st: abnormality of bone marrow stem cells (vera)
2nd: increased EPO in response to chronic hypoxia

69
Q

Polycythemia vera stages

A

1: prediagnostic by symptomatic
2: initial remission with treatment
3: myeloid-metaplasia (myelofibrosis)
4: acute leukemia
hypervolemic: reactive to increased RBC

70
Q

qualitative leukocyte disorders

A

disruption of cellular function in cellular defense

- phagocytes, respond to antigen

71
Q

hematologic leukocyte disorders

A

infectious mononucleosis
leukemia
lymphoma

72
Q

infectious monomucleosis

A

acute: self-limiting infection of B lymphocytes.
- eventually develop an immune response.
caused by Epstein-Barr virus

73
Q

leukemia

A

malignant disorder of blood/blood forming organs (bone marrow)
increased proliferation
genetic: translocation between 9 and 22

74
Q

acute leukemia

A

presence of undifferentiated usually blast cells

75
Q

chronic leukemia

A

predominant cell is mature but does not function normally

76
Q

acute lymphocytic leukemia (ALL)

A

> 30% lymphoblasts in bone marrow/ blood

most common in children

77
Q

acute myelogenous leukemia (AML)

A

abnormal proliferation of myeloid precursors

- immature blast replacement of normal cells

78
Q

Chronic myelogenous leukemia (CML)

A

myeloproliferative disorder

- polycythemia vera

79
Q

Chronic lymphocytic leukemia (CLL)

A

accumulation of B lymphocytes

failure to develop into plasma cells

80
Q

hodgkin lymphoma

A

localized to single axial group
reed-sternberg cells in the lymph nodes
mesenteric nodes rarely involved
orderly spread

81
Q

non-hodgkin lymphoma

A 
chromosome translocations
viral and bacterial infections
environmental agents
immunodeficiencies 
autoimmune disorders
Clonal expansion of B, T, and NK cells
multiple periphery nodes
mensenteric nodes commonly involved
sporatic spread
82
Q

thrombocytopenia

A

platelet count less than 100,000

83
Q

immune thrombocytopenic purpura (ITP)

A

autoimmune

increased platelet destruction

84
Q

thrombotic thrombocytopenic purpura (TTP)

A

platelets aggregate and occlude arterioles and capillaries
all platelets are being used up
- less circulating

85
Q

Disseminated intravascular coagulation (DIC)

A 
widespread activation of thrombin
- activates fibrin
- clot formation 
multiple thrombi
release of TF or thromboplastic agents 
injury to endothelial cells 
acute bleeding vs chronic thrombotic complications
86
Q

geriatric blood cell findings

A 
RBC life span normal
RBC replaced less quickly
- less iron
Lymphocyte function decreased with age
Platelets more sticky
87
Q

protein C and S are pro-thrombotic

A

false

anti-thrombotic

88
Q

synthesis of coagulation factors occurs

A

liver

89
Q

with the exception of factor III, all coagulation factors are plasma proteins that circulate in the blood stream in an inactive state T/F

A

True

90
Q

heparin inactivates

A

thrombin

  • inhibition of clotting factor function
  • useful in DIC
91
Q

fibrinolysis occurs in response to

A

plasmin

92
Q

philadelphia chromosome is diagnostic for

A

CML

93
Q

benign growth of cells is characterized by?

A

hyperplasia

94
Q

protooncogene

A

portion of gene controlling protein synthesis

-off position

95
Q

oncogene

A

activated protooncogene

- one mutation: continuous cell growth and division in cancer

96
Q

P53

A

initiates DNA repair

97
Q

tumor suppressor genes

A

produce proteins that inhibit cellular division

-mutation: requires 2 gene mutations to trigger a role in cancer

98
Q

challenges to treating cancer

A

traditional cancer therapies target all proliferating cells in the body
cancer is very heterogeneous disease
genetic instability
- adapt to new conditions, drug resistance.

Pathophysiology (80 decks)

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