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Pathophysiology > Hemolytic Disorders (Exam 1) > Flashcards

Hemolytic Disorders (Exam 1) Flashcards

1
Q

Ischemic stroke

A

arteries to the brain become narrowed or blocked

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2
Q

two types of ischemic strokes

A

thrombotic stroke and embolic stroke

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3
Q

thrombotic stroke

A

clot forms in the arteries that supply blood to the brain

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4
Q

embolic stroke

A

clot forms elsewhere and travels to the arteries in the blood stream

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5
Q

von willebrand disease

A

most common inherited bleeding disorder
ability to form a platelet plug

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6
Q

type 1 von willebrand disease

A

most common, usually mild to moderate

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7
Q

type 2 VWF

A

moderate to severe

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8
Q

type 3 VWF

A

rare and severe

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9
Q

factor XI deficiency

A

typically genetic, over 200 distinct pathogenic variants are known

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10
Q

Hemophilia

A

bleeding disorder caused by deficiency in specific clotting factor
X linked recessive

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11
Q

Hemophilia A

A

deficiency in clotting factor VIII

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12
Q

Hemophilia B

A

deficiency of clotting factor IX

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13
Q

Pathogenic bleeding

A

due to a genetic or use of a drug
can effect primary or secondary hemostasis

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14
Q

drugs for pathogenic bleeding

A

antiplatelets and anticoagulants

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15
Q

Stoke symptoms (5)

A

trouble with speaking/understanding
paralysis/numbness of the face, arm and leg
trouble with sight in one/both eyes
headache
trouble with walking

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16
Q

stroke

A

blood supply to part of the brain is interrupted or reduced

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17
Q

hemorrhagic stroke

A

a blood vessel in the brain leaks and breaks

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18
Q

two types of hemorrhagic stroke

A

intracerebral hemorrhage
subarachnoid hemorrhage

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19
Q

intracerebral hemorrhage

A

bleeding occurs in the brain

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20
Q

subarachnoid hemorrhage

A

bleeding occurs in the space between the surface of the brain and the skull

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21
Q

Hematopoiesis

A

Development of blood elements from bone marrow stem cells

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22
Q

Transient ischemic attack (TIA)

A

temporary block of blood flow to your brain

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23
Q

Myocardial Infarction

A

heart attack
clot occurs in coronary artery

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24
Q

Cytokines

A

Small signaling proteins

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25
Q

Deep Vein thrombosis

A

only half people show signs and symptoms
swelling of the leg alone in the vein
pain/tenderness while standing or walking

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26
Q

Production of RBCs

A

Hypoxia –> Kidneys produce EPO
EPO –> Erythropoiesis in bone marrow

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27
Q

Pulmonary embolism

A

clot that travels to the lung
started as DVT
shown on an angiogram

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28
Q

treatment for pulmonary embolism

A

heparin or coumadin

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29
Q

Reticulocytes

A

Immature RBCs

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30
Q

heparin

A

inactivates thrombin

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31
Q

coumadin

A

interferes with vitamin K
prevents new clots from forming

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32
Q

Erythrocytes

A

Mature RBCs

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33
Q

arterial thrombi

A

formed under high pressure
more platelet rich

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34
Q

venous thrombi

A

formed under low pressure
more fibrin rich

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35
Q

Virchow’s triad

A

three factors that increase risk of pathogenic thrombus:
endothelial injury
abnormal blood flow
hypercoahulability

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36
Q

primary erythrocytosis

A

disorder of the bone marrow
Polycythemia vera

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37
Q

endothelial injury

A

main influence on thrombus formation in the heart and the arterial circulation

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38
Q

endothelial injury is caused by

A

hypertension, hyperlipidemia, high glucose in diabetes mellitus, traumatic vascular injury

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39
Q

abnormal blood flow

A

the state of turbulence and stasis rather than laminar flow

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40
Q

abnormal blood flow is caused by

A

hyperlipidemia, aneurysm, MI, cardiac arrhythmia, immobility and paralysis

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41
Q

hypercoagulability

A

increased tendency to develop blood clots due to an acquired or inherited factor

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42
Q

two types of hypercoagulability

A

inherited (primary)
acquired (secondary)

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43
Q

types of acquired hypercoagulability

A

cancer
smoking
pregnancy
medications such as heparin, estrogen

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44
Q

types of inherited hypercoagulability

A

Factor V Lieden
Protein C or S deficiency

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45
Q

Factor V lieden

A

point mutation in the gene for Factor V
causes resistance to the anticoagulant effects of activated protein C

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46
Q

examples of endogenous anticoagulants

A

antithrombin
Protein S
Protein C
Tissue factor pathway inhibitor

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47
Q

antithrombin

A

inactivates factor IIa (thrombin) and Xa

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48
Q

Protein S

A

cofactor for protein C

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49
Q

Protein C

A

inactivates factors Va and VIIIa

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50
Q

Tissue factor pathway inhibitor

A

inhibits the tissue factor VIIa and Xa

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51
Q

coagulation

A

process of forming a blood clot in response to injury

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52
Q

Hemostasis process (3 steps)

A
  1. vasoconstriction
  2. formation of a platelet plug
  3. formation of a clot (thrombus)
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53
Q

primary hemostasis

A

formation of a weak platelet plug

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54
Q

secondary hemostasis

A

formation of a thrombus which helps stable the platelet plug

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55
Q

embolism

A

obstruction of blood vessel by a foreign substance

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56
Q

thromboembolism

A

clot breaks off, travels through circulation and gets stuck in a small blood vessel

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57
Q

fibrinolysis

A

breakdown of a clot

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58
Q

what does damages tissue release and what does it do?

A

releases plasminogen activator (tPA)
converts plasminogen to plasmin

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59
Q

what does plasmin do?

A

breaks down fibrin and dissolves the clot

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60
Q

coagulation cascade two pathways

A
  1. extrinsic
  2. intrinsic
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61
Q

extrinsic pathways

A

external trauma that causes blood to leave the circulatory system (bleeding)

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62
Q

intrinsic pathways

A

activated by trauma inside the vascular system

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63
Q

extrinsic players

A

factor 7 and 10

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64
Q

intrinsic players

A

factors 8-12

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65
Q

where do the extrinsic and intrinsic pathways converge?

A

at factor x
“common pathway”

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66
Q

what does factor X do?

A

converts prothrombin to thrombin

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67
Q

under normal physiological conditions, there is a balance between? what does the balance prevent?

A

procoagulant system and anticoagulant system
prevents excessive blood loss

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68
Q

normal platelets

A

150,000-450,000 per uL

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69
Q

thrombocytopenia

A

low platelets ( less than 150,000)

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70
Q

when there is less than 50,000 per uL of platelets,

A

bleeding occurs easily

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71
Q

when there is less than 20,000 per uL

A

spontaneous bleeding can occur in the absence of injury

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72
Q

examples of decreased platelet production

A

bone marrow disorders
liver disease

73
Q

examples of increased platelet destruction

A

drug associated immune thrombocytopenia

74
Q

example of platelet trapped in the spleen

A

splenomegaly (enlarged spleen)

75
Q

thrombocytosis

A

high platelets (over 450,000 per uL)

76
Q

what could thrombocytosis be due to?

A

cancer, removal of the spleen or genetic mutations

77
Q

formation of the platelet plug (3 steps)

A
  1. platelet adhesion
  2. platelet activation
  3. platelet aggregation
78
Q

platelet adhesion

A

exposes collagen and VWF

79
Q

platelet activation

A

platelets undergo an irreversible change in shape to increase surface area and secrete granules

80
Q

platelet aggregation

A

circulating fibrinogen binds to GP receptors on platelets and cross links them forming the platelet plug

81
Q

after the vessel wall is broken, what is the blood exposed to?

A

collagen and VWF

82
Q

what responds to the injury and what does it release?

A

neutrophils and macrophages
Platelet Activating factor

83
Q

Platelet activating factor

A

activates platelets and causes them to stick to the vessel wall at the site of injury

84
Q

what do activated platelets release?

A

ADP, serotonin and thrombaxone A2

85
Q

what is the end result of blood clotting?

A

vasoconstriction

86
Q

when there is no injury, how does the intact epithelium prevent platelet activation?

A

separating the blood from collagen
secreting NO and prostaglandin I2
CD39

87
Q

what does NO and PGI2 do?

A

inhibit platelet aggrergation

88
Q

what does CD39 do?

A

breaks down ADP in the blood which would normally promote platelet aggregation

89
Q

Hemostasis

A

forming clots in the walls of damaged blood vessels and preventing blood loss while maintaining blood in a fluid state

90
Q

How does hemostasis stop bleeding?

A

constrict blood vessels and insoles platelets

91
Q

platelets

A

anucleate cells found in blood

92
Q

How does a break in the skin close again?

A
  1. hemostasis
  2. inflammation
  3. proliferation
  4. remodeling
93
Q

splenomegaly

A

enlarged spleen
higher risk of rupturing, can lead to life threatening bleeding

94
Q

hyperslenism

A

spleen is overreactive, removing too many blood cells too quickly
leads to cytopenia

95
Q

cytopenia

A

shortage of blood cells

96
Q

congestive splenomegaly

A

spleen becomes enlarged and engorged with blood due to impaired blood flow through the splenic vein

97
Q

infiltrative splenomegaly

A

enlarged spleen caused by foreign cells invading the spleen

98
Q

Lymphoblastic Lymphoma

A

clone of immature T cells that become malignant in the thymus

99
Q

Multiple Myeloma (MM)

A

malignant proliferation of plasma cells that infiltrate bone marrow
aggregate into tumor masses in skeletal system

100
Q

Non-hodgkin Lymphoma

A

diverse group of lymphomas linked to chromosome translocations

101
Q

Risk factors of non-hodgkins lymphoma

A

older, male, white, having immune disorders, etc.

102
Q

Burkitt Lymphoma

A

most common NH lymphoma in children
very fast growing tumor on jaws and facial bones

103
Q

Hodgkin Lymphoma

A

presence of Reed-Sternberg cells in the lymph nodes

104
Q

Prescence of Reed-Sternberg cells in the lymph nodes are necessary for

A

diagnosis but not specific to Hodkins lymphoma

105
Q

Symptoms of Hodgkin Lymphoma

A

fever, weight loss, night sweats, pruritus

106
Q

can adult Hodgkin lymphoma be cured?

A

yes with early diagnosis and treatment

107
Q

Malignant Lymphomas

A

diverse group of neoplasms that develop from the proliferation of malignant lymphocytes in the lymphoid system

108
Q

how are malignant lymphomas classified?

A

REAL classification

109
Q

the two major categories of malignant lymphomas

A

Hodgkins Lymphoma
Non-Hodgkin Lymphoma

110
Q

Lymphadenopathy

A

enlarged lymph nodes that become palpable and tender

111
Q

Two types of Lymphadenopathy

A

local and general

112
Q

local lymphadenopathy

A

drainage of an inflammatory lesion located near the enlarged node

113
Q

general lymphadenopathy

A

occurs in the presence of malignant or nonmalignant disease

114
Q

most common way to detect a lymph node

A

ultrasonography

115
Q

chronic leukemias examples

A

chronic myelogenous leukemia
chromic lymphocytic leukemia

116
Q

chronic myelogenous leukemia

A

too many blood cells made in the bone marrow

117
Q

chronic lymphocytic leukemia

A

too many immature lymphocytes
slow progression

118
Q

most common adult leukemia in the western world

A

chronic lymphocytic leukemia

119
Q

most common adult leukemia

A

acute myelogenous leukemia

120
Q

acute leukemias examples

A

acute myelogenous leukemia
acute lymphocytic leukemia

121
Q

acute myelogenous leukemia

A

too many myeloblasts

122
Q

acute lymphocytic leukemia

A

too many lymphoblasts
mostly in children

123
Q

treatment for acute leukemia

A

chemotherapy

124
Q

acute leukemias are manifested by

A

bone marrow depression, fever, anorexia, neurologic symptoms

125
Q

Leukemias

A

malignant disorder of the blood and blood forming organs
excessive accumulation of leukemic cells

126
Q

Pancytopenia

A

cells crowd bone marrow

127
Q

acute leukemia

A

presence of undifferentiated/immature cells
usually blast cells

128
Q

chronic leukemia

A

predominant cell is mature but does not function properly

129
Q

Lymphocytosis

A

increase in the number of proportion of lymphocytes in the blood
includes acute viral infections: epstein barr virus

130
Q

Lymphocytopenia

A

decrease in the number of circulating lymphocytes in the blood

131
Q

quantitative disorders

A

increases or decreases in cell numbers
bone marrow disorders/ response to infectious organisms

132
Q

leukocytosis

A

normal protective physiologic response to stressors

133
Q

leukopenia

A

not normal/beneficial
a low white count predisposes a patient to infections

134
Q

polycythemia vera

A

rare cancer of the blood producing cells of bone marrow
mutation in the JAK2 gene

135
Q

secondary erythrocytosis

A

due to increased EPO production

136
Q

what can lead to overproduction of EPO?

A

chronic low oxygen levels can cause a compensatory increase in hemoglobin production
renal tumor
drugs (testosterone, Epotein)

137
Q

erythrocytosis

A

increase in the production of RBCs leading to elevated hemoglobin

138
Q

signs/symptoms of erythrocytosis

A

hypertension, frequent nosebleeds/bruising, pruritus

139
Q

Sickle Cell Disease

A

2 alpha globin chains and 2 mutated beta global chains due to a non-conservative missence mutation

140
Q

sickle cell carrier

A

has one copy of the gene and one normal gene
no health problems
reduced risk of malaria

141
Q

autosomal recessive disease

A

two copies of the altered hemoglobin gene
SCD

142
Q

Sickle cells can get stuck in small capillaries and lead to

A

vase-occlusion, ischemia and pain crisis

143
Q

sickling of cells in SCD is due to

A

deoxygenated hemoglobin becoming aggregated –> loss of normal shape

144
Q

how much folate can be stored in the liver?

A

1 month

145
Q

how much B12 can be stored in the liver?

A

large quantities
3000-5000mcg

146
Q

Sideroblastic anemias

A

rare disorder in which bone marrow produces abnormal RBCs called ringed sideroblasts
microcytic anemia
plasma iron levels are normal to high

147
Q

pathophysiology of sideroblastic anemias

A

abnormal heme synthesis and inability to incorporate iron into heme
genetic/aquired dysfunction of one of the many enzymes in heme biosynthesis pathway (Shaman pathway)

148
Q

Thalassemias

A

genetic, microcytic anemia
abnormal or absent production of alpha or beta globin

149
Q

Alpha thalassemia

A

alpha globin gene deletion resulting in reduced or absent production

150
Q

beta thalassemia

A

point mutations in beta globin gene

151
Q

beta thalassemia minor

A

mild, asymptomatic

152
Q

beta thalassemia intermedia

A

mild to moderate symptoms

153
Q

beta thalassemia major

A

severe, complete absence of beta chains
lifelong blood transfusions

154
Q

Hemochromatosis

A

iron overload occurs in the body, causing iron toxicity
storage of iron in the heart, liver, pancreas and causing organ failure

155
Q

gene involved in hemochromatosis

A

HFE gene
affects pattern of iron absorption

156
Q

ferritin

A

protein that stores iron

157
Q

transferrin

A

protein that transfers iron in the blood

158
Q

about how much dietary iron per day is required

A

10-20 mg

159
Q

Porphyrias

A

heme proteins are constantly synthesized and degraded
cells do not convert porphyrins to heme in a normal manner

160
Q

rate limiting step in porphyrias

A

succinyl CoA and glycine –> delta aminolevulinic acid
ALA synthase is the enzyme

161
Q

symptoms of porphyria

A

formation of superoxide radicals leads to
skin damage from exposure to light

162
Q

two erythrocyte disorders

A

anemia (low Hb)
erythrocytosis (high Hb)

163
Q

two leukocyte disorders

A

leukopenia (low WBC)
leukocytosis (high WBC)

164
Q

two thrombocyte disorders

A

thrombocytopenia (low platelets)
thrombocytosis (high platelets)

165
Q

two disorders of coagulation

A

hemorrhage (excessive bleeding)
thrombosis (blood clot)

166
Q

hematopoiesis

A

development of the formed elements of blood from bone marrow stem cells

167
Q

hematopoietic cells are found in the

A

peripheral blood and in bone marrow

168
Q

reticulocytes

A

immature RBCs
make up 1-2% of circulating RBCs

169
Q

erythrocytes

A

mature RBCs
circulate for 120 days and destroyed by macrophages

170
Q

what has a higher affinity for heme than oxygen?

A

CO

171
Q

at higher elevations, what has a higher affinity to heme?

A

myoglobin because there is less oxygen so more is trying to go to the tissues

172
Q

myoglobin has a higher binding affinity in the _____ while hemoglobin has a higher binding affinity in the ______

A

tissues
lungs

173
Q

hemoglobin has a ______ binding affinity for oxygen at high pressure

A

even lower

174
Q

what regulates the binding and release of oxygen in Hb

A

allosteric interactions

175
Q

does the mother or baby have a higher affinity for oxygen?

A

the baby

176
Q

fetal hemoglobin

A

2 alpha and 2 gamma chains

177
Q

difference between hemoglobin and fetal hemoglobin

A

fetal hemoglobin has a serine residue instead of histidine
reduction of 2 positive charges
reduced affinity for 2,3 BFG and increased affinity for oxygen

178
Q

the lower the P50,

A

the higher the binding affinity

Pathophysiology (16 decks)

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