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Pathophysiology > Week 3 (ch. 10 blood and circulatory system) > Flashcards

Week 3 (ch. 10 blood and circulatory system) Flashcards

1
Q

Functions of the blood

A

Transport O2 and nutrients
Removes waste
Helps maintain homeostasis
Critical role in immune system

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2
Q

Arteries / arterioles function

A

Transfer blood away from heart

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3
Q

Veins / Venules function

A

Return blood back to the heart

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4
Q

Capillaries function

A

Microcirculation within tissues

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5
Q

Systemic circulation

A

Exchanges of gas, nutrients and wastes in tissues

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6
Q

Pulmonary circulation

A

Gas exchange in lungs

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7
Q

Hematocrit

A

Proportion of cells in blood; indicated viscosity

Cells = erythrocytes, leukocytes and thrombocytes

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8
Q

Plasma

A

Clear, yellowish fluid remaining if cells removed, plasma proteins

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9
Q

Serum

A

Fluid and solutes left after cell and fibrinogen removed

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10
Q

Where are all cells made

A

Bone marrow

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11
Q

What do blood cells develop from

A

Single stem cell

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12
Q

What is hemotopoesis

A

production of blood cells and platelets which occurs in bone marrow

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13
Q

Dyscrasia

A

Disorder involving irregular components of blood

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14
Q

Erythrocytes structure

A

Biconcave flexile disc, similar to a donut with thin center instead of the hole

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15
Q

Erythrocyte life span

A

~ 120 days

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16
Q

Erythropoietin

A

Hormone

  • originates in the kidney
  • stimulates erythrocyte production in red bone marrow in response to hypoxia

It is important to recognize that the erythropoietin stimulates the production of RBC in response to hypoxia - not that bone marrow is stimulated

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17
Q

Where is hemoglobin found?

A

In erythrocytes

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18
Q

What does hemoglobin consist of?

A

Globin, amino acid chains, heme groups which contain ferrous iron atom
— O2 molecule attaches to the ferrous iron atom

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19
Q

Where does hemoglobin become fully oxygenated

A

Lungs

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20
Q

What is the small portion of CO2 carried in hemoglobin transported in the blood as?

A

Bicarbonate ion

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21
Q

Describe the hemoglobin aging process

A
  1. Phagocytosis in spleen in liver
  2. Broken into globin and heme
    — globin becomes amino acids, iron ruptured to bone marrow for reuse
    — excess iron stored as ferritin in liver, blood and tissues
  3. Heme converted to bilirubin and sent to the liver
    — in the liver, combines with glucuronide
    — excreted in bile
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22
Q

Hemolysis

A

Destruction of RBC

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23
Q

What does excessive hemolysis lead to?

A

Elevated serum bilirubin - results in jaundice

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24
Q

Lymphocytes

A

T and B lymphocytes - immune response

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25
Q

Neutrophils

A

1st to respond to tissue damage, beings phagocytosis

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26
Q

Basophils

A

Become mast cells, release histamine and heparin

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27
Q

Eosinophils

A

Combat histamine effects, increase in allergic reaction and parasitic infections

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28
Q

Monocytes

A

Become macrophages

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29
Q

Thrombocytes are

A

Platelets

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30
Q

Explain the function of thrombocytes

A

Essential in blood clotting process (hemostasis)
— stick to damages tissue or each other, form platelet plus/seal
— may adhere to rough surfaces or foreign material
— may initiate coagulation process

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31
Q

Hemostasis

A

The blood clotting process

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32
Q

Hemostasis - process of stopping bleeding: 3 steps

A
  1. Immediate response (vasoconstriction or vascular spasm = decreased blood flow)
  2. Thrombocytes adhere to tissue at the site of injury and form platelet plug is small vessel
  3. Blood clotting = coagulation (required for larger vessels)

Plasmin eventually breaks down the blood clot

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33
Q

Describe step 3 (Blood clotting = coagulation) of the hemostasis process

A

Production of prothrombin activator due to tissue damage
— prothrombin (factor II) is converted into thrombin

Thrombin converted Fibrinogen (factor I) into fibrin threads

A fibrin mesh forms to trap cells, creates solid clot (thrombus)

The clot gradually shrinks or retracts, pulling the edges of damaged tissue closer together and sealing the site

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34
Q

Factor I

A

Fibrinogen

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35
Q

Factor II

A

Prothrombin

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36
Q

What is required for the synthesis of most clotting factors

A

Vitamin K

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37
Q

What are two examples of coagulation inhibitors

A

Prostaglandin

Heparin

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38
Q

Where are coagulation inhibitors in the body

A

Circulating in the blood

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39
Q

Prostaglandin

A

Prevents platelets from sticking to undamaged tissue nearby

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40
Q

Heparin

A

Released from basophils, blocks thrombin

- does not dissolve it by prevents it

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41
Q

What are blood types determined by

A

The presence of specific antigens on cell membrane of RBC

- inherited

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42
Q

What is the ABO system determined by?

A

The presence/absence of antigens
O = no antigens
AB = A and B antigen presence
Etc,

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43
Q

Rh system

A

Antigen D in plasma membrane = Rh+

Absence of antigen D in plasma membrane = Rh-

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44
Q

Complete blood count (CBC)

A

Total RBC, WBC, platelet counts, cell morphology, differential for WBCa, counts for H&H (hematocrit and hemoglobin)

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45
Q

Blood smear

A

Size, shape, maturity, uniformity and about of hemoglobin, anemia’s

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46
Q

Diagnostic tests: H&H

A

Hematocrit = percent of blood composed of RBC and fluid and cell content

MCH = mean cellular hemoglobin - O2-carrying capacity of blood

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47
Q

What are diagnostic tests in regard to blood?

A 
CBC
Blood smear
Hematocrit and hemoglobin
Bone marrow function
Chemical analysis
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48
Q

Diagnostic tests for blood clotting disorders

A

Bleeding time test

Prothrombin time

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49
Q

Diagnosistic tests: Bone marrow function

A

Reticulocytes, immature non-uncleared RBC and aspiration w/ biopsy

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50
Q

Diagnostic test: chemical analysis

A

Serum levels of iron, vitamins B12, folic acid, cholesterol, glucose, bilirubin

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51
Q

Blood clotting disorder diagnostic test: bleeding time test

A

Tests platelet function

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52
Q

Blood clotting disorder diagnostic test: Prothrombin time test

A

Measures the function of various factors in coagulation process

Partial prothrombin time = intrinsic pathway, international normalized ratio = extrinsic pathway

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53
Q

What is differential count

A

Counts for each of the individual WBC

54
Q

What are blood therapies used to treat anemia or thrombocytopenia

A

While blood, packed RBCs, pack platelets

- have to match donor to recipient

55
Q

Blood therapies: plasma or colloid volume expanding solutions

A

Free of antigens/antibodies, no risk for reaction, aid in osmotic and hydrostatic pressure

56
Q

Blood therapies: artificial blood products

A

None perform all functions of whole blood

57
Q

Blood therapies: Epoetin Alfa

A

Artificial form of erythropoietin

— stimulates production of RBC

58
Q

Blood therapies: bone marrow or stem cell transplants

A

Close match, takes several weeks for normal cells to appear

59
Q

Blood therapies: aid in clotting ability drugs

A

Closely monitored

60
Q

Describe anemia’s and how they are classified

A

Reduced O2 transport d/t decrease in hemoglobin content

Classified by cell characteristics or etiology

61
Q

Describe the sequence of events that O2 deficit leads to

A
  1. Less energy production in all cells
    - cell metabolism and reproduction diminished
  2. Compensation mechanisms
    - tachycardia and peripheral vasoconstriction
  3. Manifestation of s/s
  4. Decreased regeneration of epithelial cells
62
Q

General s/s anemia

A

Fatigue, pallor (pale face), dyspnea, tachycardia

63
Q

o2 deficit leads to decreased regeneration of epithelial cells —> what are the outcomes of this

A

Digestive tract becomes inflamed and ulcerated, leading to stomatitis

Inflamed and cracked lips, dysphasia, hair and skin may show degenerative changes

64
Q

Severe anemia can lead to what

A

Angina or CHF

65
Q

Iron Deficiency Anemia

A

Insufficient iron impairs hemoglobin synthesis
— small (microcytic), lack color (hypochromic) RBCs - low hemoglobin

Very common

66
Q

What are risk factors to iron deficiency anemia?

A
  1. Dietary intake of iron below minimum requirement
  2. Chronic blood loss (bleeding, ulcers, hemorrhoids, cancer)
  3. Impaired duodenal absorption of iron
  4. Severe liver disease (may affects iron absorption / storage)
67
Q

iron deficiency anemia: s/s

A 
A. Pale skin and mucous membranes
B. Fatigue, lethargy, cold intolerance
C. Irritability
D. Degenerative changes
E. Stomatitis, glossitis
F. Delayed healing
G. Tachycardia, palpitations, dypsnea, syncope
68
Q

What might you see in a diagnostic test with someone who has iron deficiency anemia

A

Low H&H, MCV, MCH, serum ferritin and iron

69
Q

iron deficiency anemia: treatment

A

Treat underlying cause

70
Q

Pernicious Anemia (Vitamin B12 Deficiency) what is it and what does it result from?

A

Megoblastic anemia - large immature uncleared erythrocytes

— results from deficit of folic acid (vitamin B9) or Vitamin B12

71
Q

Why is lack of vitamins B12 not good?

A

Lack of this impairs maturation of RBCs and they get destroyed prematurely

72
Q

Pernicious Anemia (Vitamin B12 Deficiency) : etiology

A 
Dietary insufficiency (rare because B12 is found in protein, fats, dairy)
- vegetarians and vegans are prone to it because they do not eat these foods

Malabsorption

  • genetic factor
  • gastric surgery
  • alcoholics
73
Q

What is malabsorption of Vitamin B12 due to?

A

Lack of intrinsic factor

- intrinsic factor secreted by gastric mucosa, required for absorption

74
Q

Pernicious Anemia (Vitamin B12 Deficiency): s/s

A

Tongue = enlarged, red, shiny and sore
Nausea / diarrhea

Neurological FX = tingling/burning of extremities, loss of muscle control
— due to B12 needed for function and maintenance of neurons

75
Q

Pernicious Anemia (Vitamin B12 Deficiency): Diagnostics

A 
Microscopic examination (erythrocytes) 
Bone marrow examination (hyperactive)
Vitamin B12 serum levels below normal 
Presence of hypochlorhdria 
Presence of gastric atrophy
76
Q

Pernicious Anemia (Vitamin B12 Deficiency): treatment

A

Oral supplements of B12

Replacement B12 injection

77
Q

Aplastic Anemia

A

Impairment of bone marrow
- loss of stem cells and pancytopenia (decreased number of RBCs, WBCs, and platelets)

May be temporary or permanent
Can be life threatening

78
Q

Aplastic Anemia: causes

A

Often idiopathic, but possible causes could be…

  • Myelotoxins (radiation, industrial chemical, drugs)
  • viruses (particularly Hepatitis C)
  • genetic abnormalities
79
Q

Aplastic Anemia: s/s

A 
Gradua
Anemia
Leukopenia 
Thrombocytopenia 
Uncontrollable infection and hemorrhage
80
Q

Aplastic Anemia: diagnostic test

A

Bone marrow biopsy

Tests may show Pancytopenia

81
Q

Aplastic Anemia: treatments

A

Prompt ID of cause!

  • removal of any bone marrow suppressants
  • blood transfusions
  • bone marrow transplant
82
Q

Hemolytic Anemia’s (Sickle cell and Thalassemia): what?

A

Results from excessive destruction of RBCs

83
Q

Hemolytic Anemia’s (Sickle cell and Thalassemia): causes

A 
Genetic
Immune reactions 
Changes in blood chemistry
Infections (i.e., malaria)
Toxins in the blood 
Antigen-antibody reactions (incompatible blood transfusion, erythroblastosis fetalis)
84
Q

Sick Cell Anemia: what is it

A

Genetic condition - autosomal
- abnormal hemoglobin (HbS)

  • Altered hemoglobin is unstable and changes shape (crescent) in hypoxemia
  • Sickle-shaped cells are too large to pass through microcirulation
  • Obstruction leads to multiple infarctions and areas of necrosis
  • Hemolysis
85
Q

Sickle cell anemia —> obstruction due to RBC being too large to pass thru micro-circulation —> ______

A

Leads to multiple infarctions and areas of necrosis

- affects brain, organs and bones

86
Q

Sick Cell Anemia: s/s

A 
A. don’t appear until about 1 y/o
B. Severe pain d/t ischemia of tissues and infarction
C. Pallor, weakness, tachycardia, dypsnea
D. Hyperbilirubinemia - jaundice
E. Splenomegaly 
F. Vascular occlusions and infarctions 
G. Delayed growth and development 
H. CHF
87
Q

Sick Cell Anemia: describe the impacts that the symptoms of “vascular occlusion and infarction” has

A

Lung (acute chest syndrome)
Smaller blood vessels
Hand-foot syndrome

88
Q

Sick Cell Anemia: Diagnostics

A

Blood tests
- determine abnormal RBC morphology

Hemoglobin electrophoresis

  • aka “sick cell screen”
  • measures the different types of hemoglobin in your RBC

Prenatal DNA analysis s\

89
Q

Sick Cell Anemia: treatment

A

Hydroxyurea has reduced the frequency

Dietary supplementation with folic acid

Bone marrow transplantation

Preventative measures for infection, dehydration, exposure to cold

90
Q

Thalassemia

A

Genetic defect where hemoglobin are missing or variant
- most common genetic defect in the world

Alpha and Beta types

91
Q

Thalassemia: alpha

A

Reduction in or lack of alpha chains
- Indian, Chinese, southwest Asian descent

Accumulation of available chain damages the RBC

92
Q

Thalassemia: Beta

A

Decrease or lack of beta chains
- Mediterranean countries (Greece, Italy)

Accumulation of available chain damages the RBC

93
Q

Thalassemia: s/s

A

Growth and development implaired
Impaired normal skeletal development
Heart failure

94
Q

Thalassemia: diagnostics

A

RBCs microcytic, low hemoglobin, increase in erythropoietin levels

95
Q

Thalassemia: treatment

A

Blood transfusions = only treatment

Folate

Bone marrow transplant

96
Q

What are indicators of blood clotting disorders

A 
º persistent bleeding from gums
º repeated epistaxis
º Petechiae (pinpoint, flat, red spots
º frequent purpura and ecchymosis 
º more than normal bleeding in trauma
º bleeding into joint (hemarthroses; swollen, red, painful)
º coughing up blood (hemoptysis) 
º vomiting blood (hematemesis)
º blood in feces (black or occult - hidden)
º anemia
º feeling faint and anxious 
º hypotension 
º rapid pulse
97
Q

Hemophilia A: what is it

A

Most common inherited clotting disorder; deficit or abnormality of factor VIII
- varying degrees of severity

98
Q

Hemophilia A: s/s

A

Prolonged bleeding after minor tissue trauma
Spontaneous bleeding into joints
Possible hematuria or blood in feces

99
Q

Hemophilia A: diagnostic tests and results

A

Bleeding time and PT normal

PTT, activated PTT (aPTT), coagulation time prolonged

Serum levels of factor VIII are low

100
Q

Hemophilia A: treatment

A

Desmopressin (DDAVP)

Replacement therapy for factor VIII

101
Q

Von Willebrand Disease

A

Most common hereditary clotting disorder

Three major types

102
Q

Von Willebrand Disease: s/s

A 
Skin rashes
Frequent nosebleeds
Easy bruising
Bleeding of gums
Abnormal menstrual bleeding
103
Q

Von Willebrand Disease treatment

A

Based on type and severity

104
Q

Disseminated intravascular coagulation (DIC): what is it / what happens

A

Involved excessive blood AND clotting
- excessive clotting in circulation —> thrombi and infants occur

  • Clotting factors are reduced to a dangerous level —> wide spread, uncontrollable hemorrhage results
105
Q

Disseminated intravascular coagulation (DIC) prognosis

A

Very poor prognosis, with high fatality rate

106
Q

Disseminated intravascular coagulation (DIC) is a complication of what problems?

A

Complication of many primary problems

  • obstetrical complications, such as abruptio placentae
  • infections
  • carcinomas
  • major trauma

This makes is a secondary infection/problem (not sure if its an infection, but since it happens secondary to primary problems)

107
Q

Thrombophilia: what is it? What does it affect?

A

Group of inherited or acquired disorders

- risk of abnormal clots in veins or arteries; can affect any system or organ where the clot is formed

108
Q

Thrombophilia: diagnostic

A

Blood testing for clotting factor levels and abnormal antibody levels

109
Q

Thrombophilia: treatment

A

Causative condition should be treated

Anticoagulants

110
Q

Myelodysplastic syndromes: what is it?

A

Inadequate production of cells by the bone marrow

111
Q

Myelodysplastic syndromes: s/s

A

Anemia; dependent on type of deficiencies that occur

112
Q

Myelodysplastic syndromes: cause

A

May be idiopathic or occur after chemotherapy or radiation treatment

113
Q

Myelodysplastic syndromes: treatment

A

Treatment depends on deficiency type

  • transfusion replacement
  • chelation therapy to reduce iron overload
  • bone marrow transplantation
114
Q

Primary Polycythemia: what is it?

A

Polycythemia Vera
º increased production of erythrocytes and other cells in the bone marrow
º neoplastic disorder
º serum erythropoietin levels are low

115
Q

Secondary Polycythemia: what is it?

A

Erythrocytosis
º increase in RBCs in response to prolonged hypoxia
º increased erythropoietin secretion
º compensation mechanism to provide increased O2 support

116
Q

Polycythemia: s/s

A 
º distended blood vessels, sluggish blood flow 
º increased BP
º hypertrophied heart 
º hepatomegaly
º splenomegaly 
º dyspnea
º HA
º visual disturbances 
º thromboses and infarctions
117
Q

Polycythemia: diagnostic tests to determine

A

Increased cell counts
Increased hemoglobin and hematocrit values
Hypercellular bone marrow
Hyperericemia

118
Q

Polycythemia: treatment

A

ID specific cause
Drugs and radiation
Suppression of bone marrow activity
Periodic phlebotomy

119
Q

Leukemias: what are they?

A

Group of neoplastic disorders involving WBC

  • uncontrolled WBC production in bone or lymph nodes; large numbers released into general circulation and infiltrate lymph nodes, spleen, liver, brain, and other organs
  • one or more type of leukocytes are undifferentiated, immature, and nonfunctional
  • other hematopoietic tissues are reduced
120
Q

Acute Leukemia: what is it?

A

High proportion of immature nonfunctional cells in bone marrow and peripheral circulation

121
Q

Acute Leukemia: onset

A

Usually abrupt, marked signs of complications

122
Q

Acute Leukemia: who?

A

Primarily children and younger adults

123
Q

Chronic Leukemia: what is it

A

Higher proportion of MATURE cells, but with reduced function

- mild signs, better prognosis than acute leukemia

124
Q

Chronic leukemia: onset

A

Insidious, gradual onset

125
Q

Chronic leukemia: who?

A

Common in older adults

126
Q

Acute Leukemia: s/s

A 
Frequent or uncontrolled infections 
Petechiae and purpura 
Signs of anemia 
Severe and steady bone pain
Weight loss, fatigue, fever
Enlarged lymph nodes, spleen, liver 
Headache, visual disturbances, drowsiness, vomiting
127
Q

Chronic leukemia: s/s

A

Gradual onset - milder signs, typically found in routine blood check
- fatigue, weakness, frequent infections

128
Q

Leukemia’s: diagnostic tests

A

Peripheral blood smears

  • immature leukocytes and altered numbers or WBC
  • number of RBCs and platelets decreased

Bone marrow biopsy for confirmation

129
Q

Leukemia’s: treatment

A

Chemo
ALL in young children responds well to drugs
Biologic therapy (interferon)
- may be used to stimulate the immune system

130
Q

Leukemia: complications

A 
Opportunistic infections (including pneumonia)
Sepsis
CHF
Hemorrhage
Liver failure
Renal failure
CNS depression and coma

Pathophysiology (11 decks)

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