Week 3 (ch. 10 blood and circulatory system) Flashcards
(130 cards)
1
Q
Functions of the blood
A
Transport O2 and nutrients
Removes waste
Helps maintain homeostasis
Critical role in immune system
2
Q
Arteries / arterioles function
A
Transfer blood away from heart
3
Q
Veins / Venules function
A
Return blood back to the heart
4
Q
Capillaries function
A
Microcirculation within tissues
5
Q
Systemic circulation
A
Exchanges of gas, nutrients and wastes in tissues
6
Q
Pulmonary circulation
A
Gas exchange in lungs
7
Q
Hematocrit
A
Proportion of cells in blood; indicated viscosity
Cells = erythrocytes, leukocytes and thrombocytes
8
Q
Plasma
A
Clear, yellowish fluid remaining if cells removed, plasma proteins
9
Q
Serum
A
Fluid and solutes left after cell and fibrinogen removed
10
Q
Where are all cells made
A
Bone marrow
11
Q
What do blood cells develop from
A
Single stem cell
12
Q
What is hemotopoesis
A
production of blood cells and platelets which occurs in bone marrow
13
Q
Dyscrasia
A
Disorder involving irregular components of blood
14
Q
Erythrocytes structure
A
Biconcave flexile disc, similar to a donut with thin center instead of the hole
15
Q
Erythrocyte life span
A
~ 120 days
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
17
Q
Where is hemoglobin found?
A
In erythrocytes
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
19
Q
Where does hemoglobin become fully oxygenated
A
Lungs
20
Q
What is the small portion of CO2 carried in hemoglobin transported in the blood as?
A
Bicarbonate ion
21
Q
Describe the hemoglobin aging process
A
- Phagocytosis in spleen in liver
- 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 - Heme converted to bilirubin and sent to the liver
— in the liver, combines with glucuronide
— excreted in bile
22
Q
Hemolysis
A
Destruction of RBC
23
Q
What does excessive hemolysis lead to?
A
Elevated serum bilirubin - results in jaundice
24
Q
Lymphocytes
A
T and B lymphocytes - immune response
25
Neutrophils
1st to respond to tissue damage, beings phagocytosis
26
Basophils
Become mast cells, release histamine and heparin
27
Eosinophils
Combat histamine effects, increase in allergic reaction and parasitic infections
28
Monocytes
Become macrophages
29
Thrombocytes are
Platelets
30
Explain the function of thrombocytes
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
31
Hemostasis
The blood clotting process
32
Hemostasis - process of stopping bleeding: 3 steps
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
33
Describe step 3 (Blood clotting = coagulation) of the hemostasis process
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
34
Factor I
Fibrinogen
35
Factor II
Prothrombin
36
What is required for the synthesis of most clotting factors
Vitamin K
37
What are two examples of coagulation inhibitors
Prostaglandin
| Heparin
38
Where are coagulation inhibitors in the body
Circulating in the blood
39
Prostaglandin
Prevents platelets from sticking to undamaged tissue nearby
40
Heparin
Released from basophils, blocks thrombin
| - does not dissolve it by prevents it
41
What are blood types determined by
The presence of specific antigens on cell membrane of RBC
| - inherited
42
What is the ABO system determined by?
The presence/absence of antigens
O = no antigens
AB = A and B antigen presence
Etc,
43
Rh system
Antigen D in plasma membrane = Rh+
| Absence of antigen D in plasma membrane = Rh-
44
Complete blood count (CBC)
Total RBC, WBC, platelet counts, cell morphology, differential for WBCa, counts for H&H (hematocrit and hemoglobin)
45
Blood smear
Size, shape, maturity, uniformity and about of hemoglobin, anemia’s
46
Diagnostic tests: H&H
Hematocrit = percent of blood composed of RBC and fluid and cell content
MCH = mean cellular hemoglobin - O2-carrying capacity of blood
47
What are diagnostic tests in regard to blood?
```
CBC
Blood smear
Hematocrit and hemoglobin
Bone marrow function
Chemical analysis
```
48
Diagnostic tests for blood clotting disorders
Bleeding time test
| Prothrombin time
49
Diagnosistic tests: Bone marrow function
Reticulocytes, immature non-uncleared RBC and aspiration w/ biopsy
50
Diagnostic test: chemical analysis
Serum levels of iron, vitamins B12, folic acid, cholesterol, glucose, bilirubin
51
Blood clotting disorder diagnostic test: bleeding time test
Tests platelet function
52
Blood clotting disorder diagnostic test: Prothrombin time test
Measures the function of various factors in coagulation process
Partial prothrombin time = intrinsic pathway, international normalized ratio = extrinsic pathway
53
What is differential count
Counts for each of the individual WBC
54
What are blood therapies used to treat anemia or thrombocytopenia
While blood, packed RBCs, pack platelets
| - have to match donor to recipient
55
Blood therapies: plasma or colloid volume expanding solutions
Free of antigens/antibodies, no risk for reaction, aid in osmotic and hydrostatic pressure
56
Blood therapies: artificial blood products
None perform all functions of whole blood
57
Blood therapies: Epoetin Alfa
Artificial form of erythropoietin
| — stimulates production of RBC
58
Blood therapies: bone marrow or stem cell transplants
Close match, takes several weeks for normal cells to appear
59
Blood therapies: aid in clotting ability drugs
Closely monitored
60
Describe anemia’s and how they are classified
Reduced O2 transport d/t decrease in hemoglobin content
Classified by cell characteristics or etiology
61
Describe the sequence of events that O2 deficit leads to
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
General s/s anemia
Fatigue, pallor (pale face), dyspnea, tachycardia
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o2 deficit leads to decreased regeneration of epithelial cells —> what are the outcomes of this
Digestive tract becomes inflamed and ulcerated, leading to stomatitis
Inflamed and cracked lips, dysphasia, hair and skin may show degenerative changes
64
Severe anemia can lead to what
Angina or CHF
65
Iron Deficiency Anemia
Insufficient iron impairs hemoglobin synthesis
— small (microcytic), lack color (hypochromic) RBCs - low hemoglobin
Very common
66
What are risk factors to iron deficiency anemia?
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
iron deficiency anemia: s/s
```
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
What might you see in a diagnostic test with someone who has iron deficiency anemia
Low H&H, MCV, MCH, serum ferritin and iron
69
iron deficiency anemia: treatment
Treat underlying cause
70
Pernicious Anemia (Vitamin B12 Deficiency) what is it and what does it result from?
Megoblastic anemia - large immature uncleared erythrocytes
| — results from deficit of folic acid (vitamin B9) or Vitamin B12
71
Why is lack of vitamins B12 not good?
Lack of this impairs maturation of RBCs and they get destroyed prematurely
72
Pernicious Anemia (Vitamin B12 Deficiency) : etiology
```
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
What is malabsorption of Vitamin B12 due to?
Lack of intrinsic factor
| - intrinsic factor secreted by gastric mucosa, required for absorption
74
Pernicious Anemia (Vitamin B12 Deficiency): s/s
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
Pernicious Anemia (Vitamin B12 Deficiency): Diagnostics
```
Microscopic examination (erythrocytes)
Bone marrow examination (hyperactive)
Vitamin B12 serum levels below normal
Presence of hypochlorhdria
Presence of gastric atrophy
```
76
Pernicious Anemia (Vitamin B12 Deficiency): treatment
Oral supplements of B12
| Replacement B12 injection
77
Aplastic Anemia
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
Aplastic Anemia: causes
Often idiopathic, but possible causes could be...
- Myelotoxins (radiation, industrial chemical, drugs)
- viruses (particularly Hepatitis C)
- genetic abnormalities
79
Aplastic Anemia: s/s
```
Gradua
Anemia
Leukopenia
Thrombocytopenia
Uncontrollable infection and hemorrhage
```
80
Aplastic Anemia: diagnostic test
Bone marrow biopsy
| Tests may show Pancytopenia
81
Aplastic Anemia: treatments
Prompt ID of cause!
- removal of any bone marrow suppressants
- blood transfusions
- bone marrow transplant
82
Hemolytic Anemia’s (Sickle cell and Thalassemia): what?
Results from excessive destruction of RBCs
83
Hemolytic Anemia’s (Sickle cell and Thalassemia): causes
```
Genetic
Immune reactions
Changes in blood chemistry
Infections (i.e., malaria)
Toxins in the blood
Antigen-antibody reactions (incompatible blood transfusion, erythroblastosis fetalis)
```
84
Sick Cell Anemia: what is it
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
Sickle cell anemia —> obstruction due to RBC being too large to pass thru micro-circulation —> ______
Leads to multiple infarctions and areas of necrosis
| - affects brain, organs and bones
86
Sick Cell Anemia: s/s
```
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
Sick Cell Anemia: describe the impacts that the symptoms of “vascular occlusion and infarction” has
Lung (acute chest syndrome)
Smaller blood vessels
Hand-foot syndrome
88
Sick Cell Anemia: Diagnostics
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
Sick Cell Anemia: treatment
Hydroxyurea has reduced the frequency
Dietary supplementation with folic acid
Bone marrow transplantation
Preventative measures for infection, dehydration, exposure to cold
90
Thalassemia
Genetic defect where hemoglobin are missing or variant
- most common genetic defect in the world
Alpha and Beta types
91
Thalassemia: alpha
Reduction in or lack of alpha chains
- Indian, Chinese, southwest Asian descent
Accumulation of available chain damages the RBC
92
Thalassemia: Beta
Decrease or lack of beta chains
- Mediterranean countries (Greece, Italy)
Accumulation of available chain damages the RBC
93
Thalassemia: s/s
Growth and development implaired
Impaired normal skeletal development
Heart failure
94
Thalassemia: diagnostics
RBCs microcytic, low hemoglobin, increase in erythropoietin levels
95
Thalassemia: treatment
Blood transfusions = only treatment
Folate
Bone marrow transplant
96
What are indicators of blood clotting disorders
```
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
Hemophilia A: what is it
Most common inherited clotting disorder; deficit or abnormality of factor VIII
- varying degrees of severity
98
Hemophilia A: s/s
Prolonged bleeding after minor tissue trauma
Spontaneous bleeding into joints
Possible hematuria or blood in feces
99
Hemophilia A: diagnostic tests and results
Bleeding time and PT normal
PTT, activated PTT (aPTT), coagulation time prolonged
Serum levels of factor VIII are low
100
Hemophilia A: treatment
Desmopressin (DDAVP)
| Replacement therapy for factor VIII
101
Von Willebrand Disease
Most common hereditary clotting disorder
| Three major types
102
Von Willebrand Disease: s/s
```
Skin rashes
Frequent nosebleeds
Easy bruising
Bleeding of gums
Abnormal menstrual bleeding
```
103
Von Willebrand Disease treatment
Based on type and severity
104
Disseminated intravascular coagulation (DIC): what is it / what happens
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
Disseminated intravascular coagulation (DIC) prognosis
Very poor prognosis, with high fatality rate
106
Disseminated intravascular coagulation (DIC) is a complication of what problems?
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
Thrombophilia: what is it? What does it affect?
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
Thrombophilia: diagnostic
Blood testing for clotting factor levels and abnormal antibody levels
109
Thrombophilia: treatment
Causative condition should be treated
| Anticoagulants
110
Myelodysplastic syndromes: what is it?
Inadequate production of cells by the bone marrow
111
Myelodysplastic syndromes: s/s
Anemia; dependent on type of deficiencies that occur
112
Myelodysplastic syndromes: cause
May be idiopathic or occur after chemotherapy or radiation treatment
113
Myelodysplastic syndromes: treatment
Treatment depends on deficiency type
- transfusion replacement
- chelation therapy to reduce iron overload
- bone marrow transplantation
114
Primary Polycythemia: what is it?
Polycythemia Vera
º increased production of erythrocytes and other cells in the bone marrow
º neoplastic disorder
º serum erythropoietin levels are low
115
Secondary Polycythemia: what is it?
Erythrocytosis
º increase in RBCs in response to prolonged hypoxia
º increased erythropoietin secretion
º compensation mechanism to provide increased O2 support
116
Polycythemia: s/s
```
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
Polycythemia: diagnostic tests to determine
Increased cell counts
Increased hemoglobin and hematocrit values
Hypercellular bone marrow
Hyperericemia
118
Polycythemia: treatment
ID specific cause
Drugs and radiation
Suppression of bone marrow activity
Periodic phlebotomy
119
Leukemias: what are they?
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
Acute Leukemia: what is it?
High proportion of immature nonfunctional cells in bone marrow and peripheral circulation
121
Acute Leukemia: onset
Usually abrupt, marked signs of complications
122
Acute Leukemia: who?
Primarily children and younger adults
123
Chronic Leukemia: what is it
Higher proportion of MATURE cells, but with reduced function
| - mild signs, better prognosis than acute leukemia
124
Chronic leukemia: onset
Insidious, gradual onset
125
Chronic leukemia: who?
Common in older adults
126
Acute Leukemia: s/s
```
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
Chronic leukemia: s/s
Gradual onset - milder signs, typically found in routine blood check
- fatigue, weakness, frequent infections
128
Leukemia’s: diagnostic tests
Peripheral blood smears
- immature leukocytes and altered numbers or WBC
- number of RBCs and platelets decreased
Bone marrow biopsy for confirmation
129
Leukemia’s: treatment
Chemo
ALL in young children responds well to drugs
Biologic therapy (interferon)
- may be used to stimulate the immune system
130
Leukemia: complications
```
Opportunistic infections (including pneumonia)
Sepsis
CHF
Hemorrhage
Liver failure
Renal failure
CNS depression and coma
```
