Blood and Circulatory System Disorders Flashcards
Chapter 10
1
Q
Arteries
A
branch off into arterioles,
They transport oxygenated blood away from the heart
2
Q
Veins
A
Return blood to the heart, this has a higher concentration of carbon dioxide and this is going to be exchanged in the lungs for new oxygen
3
Q
Capillaries
A
Microcirculation within tissues goes around cells. They are one layer thick and very permeable. They allow oxygen out via tissues, and also they allow carbon dioxide back in to be carried away.
4
Q
Venules
A
are the smallest veins, and blood flows from venules into larger veins that eventually return blood to the heart
5
Q
Pulmonary circulation
A
Gas exchange in the lungs
5
Q
Systemic Circulation
A
Exchange of gases, nutrients, and waste in tissues
6
Q
Tunica intima
A
Inside lining. It is made of endothelium( simple squamous epithelium)
7
Q
Tunica media
A
Middle layer , smooth muscle layer (Layer that contracts)
8
Q
Tunica adventitia(Externa)
A
Connective tissue with fibrocytes , collagen (type I) and elastic fibers
9
Q
Blood Function
A
Transport oxygen and nutrients to all tissues
Remove waste products of cellular metabolism
Play a critical role in the body’s defenses/immune system, and
Serve in maintaining body homeostasis
10
Q
Composition of Blood
A
Plasma(liquid part)
Plasma proteins( Helps keep it’s concentration of solid & liquid)
Cellular component
Erythrocytes
Leukocytes(immune cells)
Thrombocytes (platelets)
11
Q
Hematopoiesis
A
he process of creating blood cells and bone marrow cells, such as red blood cells, white blood cells, platelets, and more
12
Q
Erythrocytes (Red Blood Cells)
A
Biconcave flexible discs(Sickle cell anemia loses the disk)
No nucleus in mature state because erythrocytes has to carry a maximum amount of oxygen per cell , so the nucleus isn’t needed anymore. The cell is mature has it’s job and knows what it needs to do. That space is taken up by hemoglobin & oxygen. Also carby hemoglobin to carry carbon dioxide back.
Contains hemoglobin
Globin portion
Heme group
Life span—≈120 days(Then they self destruct)
Erythropoietin produced in the kidney stimulates erythrocyte production.
13
Q
Blood Clotting—Hemostasis
A
Three steps:
Vasoconstriction or vascular spasm after injury
Platelet clot
Coagulation mechanism
Plasmin will eventually break down the blood clot.
14
Q
Clot Formation
A
Production of prothrombin factor due to tissue damage
Prothrombin or factor II is converted into thrombin
Thrombin converts Fibrinogen (factor I) into fibrin threads
A fibrin mesh forms to trap cells
The clot gradually shrinks or retracts, pulling the edges of damaged tissue closer together and sealing the site
15
Q
Blood Typing
A
Blood typing is based on antigens in the plasma membrane of the erythrocytes.
ABO system
Based on the presence or absence of specific antigens
Antibodies in the blood plasma
Rh system
Antigen D in plasma membrane: Rh+
Absence of antigen D: Rh−
16
Q
Type O
A
Has no antigens. Has antibodies that will attack the antigen A or the antigen B if it comes into the bloodstream. Type O can only receive their own blood.
17
Q
Type A
A
Has the A antigen. Contains Anti-B antibodies in plasma. It can only receive donor blood group O or A.
17
Q
Type B
A
Has antigen B. Contains Anti-A antibodies in plasma. Can receive donor blood group B or O.
18
Q
Type AB
A
Has both antigen A&B. Has no antibodies in plasma. They can receive donor blood group O , A , B or AB.
19
Q
Diagnostic Tests (1 of 3)
A
Complete blood count (CBC)
Includes total red blood cells (RBCs), white blood cells (WBCs), and platelets
Leukocytosis (increased WBCs)
Associated with inflammation or infection
Leukopenia (decreased WBCs)
Associated with some viral infections, radiation, chemotherapy
Increased eosinophils
Common in allergic responses
Differential count for WBCs
20
Q
Leukocytosis
A
(increased WBCs)
Associated with inflammation or infection
21
Q
Leukopenia
A
(decreased WBCs)
Associated with some viral infections, radiation, chemotherapy
22
Q
Increased eosinophils
A
Common in allergic responses
23
Diagnostic Tests (2 of 3)
Morphology
Observed with blood smears
Shows size, shape, uniformity, maturity of cells
Different types of anemia can be distinguished.
Hematocrit
Percent by volume of cellular elements in blood plasma(How much solid vs liquid)
Hemoglobin
Amount of hemoglobin per unit volume of blood
Mean corpuscular volume (MCV)
Indicates the oxygen-carrying capacity of blood
24
Diagnostic Tests (3 of 3)
Reticulocyte count
Assessment of bone marrow function
Chemical analysis
Determines serum levels of components, such as iron, vitamin B12, folic acid, cholesterol, urea, glucose
Bleeding time
Measures platelet function
Prothrombin time (PT) and partial thromboplastin time (PTT)
Measure function of various factors in coagulation process
International normalized ratio (INR) is a standardized version.
25
Blood Therapies (1 of 2)
Whole blood(500ml or less that has all the components), packed red blood cells(Removed a good portion of plasma , mostly cells) , packed platelets(Given to those bleeding , problem clotting)
For severe anemia or thrombocytopenia
Plasma or colloid volume-expanding solutions
To maintain blood volume
Artificial blood products
Compatible with all blood types
None of them can perform all the complex functions of normal whole blood.
26
Blood Therapies (2 of 2)
(Epoetin alpha)(Stimulate production of red blood cells)
Artificial form of erythropoietin
Before certain surgical procedures
Anemia related to cancer
Chronic renal failure
(Bone marrow or stem cell transplantation)
Close tissue match necessary
Treatment of some cancers
Severe immunodeficiency
Severe blood cell diseases
(Drug treatment)
Aids in the clotting process
27
The Anemias (1 of 2)
Anemia causes a reduction in oxygen transport.
The basic problem is hemoglobin deficit
Oxygen deficit leads to:
Less energy production in all cells
Cell metabolism and reproduction diminished
Compensation mechanisms
Tachycardia and peripheral vasoconstriction
General signs of anemia
Fatigue, pallor (pale face), dyspnea, tachycardia
28
The Anemias (2 of 2)
Oxygen deficit leads to:
Decreased regeneration of epithelial cells
The digestive tract becomes inflamed and ulcerated, leading to stomatitis
Inflamed and cracked lips
Dysphasia
Hair and skin may show degenerative changes.
Severe anemia may lead to angina or congestive heart failure (CHF).
29
Iron Deficiency Anemia
Insufficient iron impairs hemoglobin synthesis.
Microcytic, hypochromic RBCs(They don't have hemoglobin & are tiny)
Result of low hemoglobin concentration in cells
Very common
Ranges from mild to severe
Occurs in all age groups, but is more common in women of childbearing age
Estimated that one in five women is affected
The proportion increases for pregnant women
Frequently signs of an underlying problem
30
Causes Of Iron Deficiency Anemia
Dietary intake of iron below minimum requirement
Chronic blood loss
As from bleeding, ulcers, hemorrhoids, cancer
Impaired duodenal absorption of iron
In many disorders, malabsorption syndromes
Severe liver disease
May affect iron absorption as well as storage
31
Signs and Symptoms Of Iron Deficiency Anemia
The pallor of skin and mucous membranes
Fatigue, lethargy, cold intolerance
Irritability
Degenerative changes
Stomatitis and glossitis
Menstrual irregularities
Delayed healing
Tachycardia, heart palpitations, dyspnea, syncope
32
Pernicious Anemia: Vitamin B12 Deficiency (1 of 2)
Basic problem is lack of absorption of vitamin B12 because of lack of intrinsic factor
Intrinsic factor secreted by gastric mucosa
Required for intestinal absorption of vitamin B12
Characterized by very large, immature, nucleated erythrocytes
Carry less hemoglobin
Shorter life span
33
Pernicious Anemia: Vitamin B12 Deficiency (2 of 2)
Dietary insufficiency is very rarely a cause.
Genetic factors have been implicated.
More common in light-skinned women of northern European ancestry
Often accompanies chronic gastritis
May also be an outcome of gastric surgery
34
Vitamin B12 is needed for the function and maintenance of
neurons.
35
A significant deficit of vitamin B12 will cause symptoms in the
peripheral nerves.
These may be reversible.
36
Pernicious Anemia Manifestations
The tongue is typically enlarged, red, sore, and shiny
Digestive discomfort, often with nausea and diarrhea
The feeling of pins and needles, tingling in limbs
Treatment(B12 via injection IM)
37
Diagnostic Test For Pernicious Anemia
Microscopic examination (erythrocytes)
Bone marrow examination (hyperactive)
Vitamin B12 serum levels below normal
Presence of hypochlorhydria or achlorhydria
Presence of gastric atrophy
38
Aplastic Anemia (1 of 2)
Impairment or failure of bone marrow to produce RBC or WBC
May be temporary or permanent
Often idiopathic but possible causes include:
Myelotoxins
Radiation, industrial chemicals, drugs
Viruses
Particularly hepatitis C
Genetic abnormalities
Myelodysplastic syndrome
Fanconi’s anemia
39
Aplastic Anemia (2 of 2)
Blood counts indicate pancytopenia.
Anemia, leukopenia, thrombocytopenia
Bone marrow biopsy may be required.
Erythrocytes often appear normal.
Identification of cause and prompt treatment needed for bone marrow recovery
Removal of any bone marrow suppressants
Failure to identify cause and treat effectively is life-threatening!
40
Hemolytic Anemia
Results from excessive destruction of RBCs
Causes
Genetic defects
Immune reactions
Changes in blood chemistry
Infections such as malaria
Toxins in the blood
Antigen-antibody reactions
Incompatible blood transfusion
Erythroblastosis fetalis
41
Sickle Cell Anemia (1 of 6)
Genetic condition
Autosomal
Incomplete dominance
Anemia occurs in homozygous recessive.
Diagnostic testing is available.
More common in individuals of African ancestry
Heterozygous condition is somewhat protective against malaria.
One in ten African Americans is heterozygous for the trait.
42
Sickle Cell Anemia (3 of 6)
Abnormal hemoglobin (HbS)
Sickle cell crisis occurs whenever oxygen levels are lowered.
Altered hemoglobin is unstable and changes shape in hypoxemia.
Sickle-shaped cells are too large to pass through the microcirculation.
Obstruction leads to multiple infarctions and areas of necrosis.
43
Sickle Cell Anemia (6 of 6)
Multiple infarctions affect the brain, bones, organs
In addition to basic anemia:
Hyperbilirubinemia, jaundice, gallstones
Caused by high rate of hemolysis
Clinical signs
Do not usually appear until the child is about 12 months old
44
Signs and Symptoms(Sickle Cell Anemia)
Severe pain because of ischemia of tissues and infarction
Pallor, weakness, tachycardia, dyspnea
Hyperbilirubinemia—jaundice
Splenomegaly
Vascular occlusions and infarctions
In lungs
Acute chest syndrome
Smaller blood vessels
Hand-foot syndrome( Hands and feet cramp up)
Delay of growth and development
Congestive heart failure
45
Diagnostic Tests(Sickle Cell Anemia)
Blood test- determine abnormal RBC morphology
Hemoglobin electrophoresis
Prenatal DNA analysis
46
Treatment(Sickle Cell Anemia)
Hydroxyurea has reduced the frequency of this crisis
Dietary supplementation with folic acid
Bone marrow transplantation
Immunization in children
Against pneumonia, influenza, meningitis
47
Hydroxyurea
Hydroxyurea is in a class of medications called antimetabolites. Hydroxyurea treats cancer by slowing or stopping the growth of cancer cells in your body. Hydroxyurea treats sickle cell anemia by helping to prevent the formation of sickle-shaped red blood cells.
48
Polycythemia
Primary polycythemia—polycythemia vera
Increased production of erythrocytes and other cells in the bone marrow
Neoplastic disorder(Abnormal growth of tissues)
Serum erythropoietin levels are low.
Secondary polycythemia—erythrocytosis
Increase in RBCs in response to prolonged hypoxia
Increased erythropoietin secretion
Compensation mechanism to provide increased oxygen transport
49
Signs and Symptoms(Polycythemia)
Distended blood vessels, sluggish blood flow
Increased blood pressure
Hypertrophied heart
Hepatomegaly
Splenomegaly
Dyspnea
Headaches
Visual disturbances
Thromboses and infarctions
49
Diagnostic Tests(Polycythemia)
Tests to determine:
Increased cell counts
Increased hemoglobin and hematocrit values
Hypercellular bone marrow
Hyperuricemia
50
Treatment(Polycythemia)
Identify specific cause
Drugs or radiation
Suppression of bone marrow activity
Periodic phlebotomy
51
Indications of Blood-Clotting Disorders
Persistent bleeding from gums
Repeated epistaxis(nose bleed)
Petechiae
Pinpoint, flat, red spots on skin and mucous membrane
Frequent purpura and ecchymosis
More than normal bleeding in trauma
Bleeding into joint—hemarthroses
Swollen, red, painful
Hemoptysis(coughing up blood)
52
Hematemesis
Coarse brown particles (coffee ground emesis)in vomit
53
Blood-Clotting Disorders
Hematemesis
Coarse brown particles (coffee ground emesis)in vomit
Blood in feces
Black or occult
Anemia
Feeling faint and anxious
Low blood pressure
Rapid pulse
54
Hemophilia A (1 of 2)
Classic hemophilia
Deficit or abnormality of factor VIII
The most common inherited clotting disorder
X-linked recessive trait
Manifested in men, carried by women
Varying degrees of severity
Prolonged bleeding after minor tissue trauma
Spontaneous bleeding into joints
Possible hematuria or blood in feces
55
Hemophilia A (2 of 2)
Diagnostic tests
Bleeding time and PT normal
PTT, activated PTT (aPTT), coagulation time prolonged
Serum levels of factor VIII are low.
Treatment
Desmopressin (DDAVP)
Replacement therapy for Factor VIII
56
Von Willebrand’s Disease
Most common hereditary clotting disorder
Three major types
Signs and symptoms include:
Skin rashes
Frequent nosebleeds
Easy bruising
Bleeding of gums
Abnormal menstrual bleeding
Treatment based on type and severity
57
Disseminated Intravascular Coagulation (DIC) (1 of 2)
Involves both excessive bleeding and clotting
Excessive clotting in circulation
Thrombi and infarcts occur.
Clotting factors are reduced to a dangerous level.
Widespread, uncontrollable hemorrhage results.
Very poor prognosis, with high fatality rate
Complication of many primary problems
Obstetrical complications, such as abruptio placentae
Infections
Carcinomas
Major trauma
58
Thrombophilia
Group of inherited or acquired disorders
Risk of abnormal clots in veins or arteries
Blood testing for clotting factor levels and abnormal antibody levels
Causative condition should be treated.
(They make too many clots)
59
Myelodysplastic Syndromes
Diseases that involve inadequate production of cells by the bone marrow
Signs and symptoms include anemia; dependent on type of deficiencies that occur
May be idiopathic or occur after chemotherapy or radiation treatment
Treatment depends on deficiency type.(Which blood cells are deficiency)
Transfusion replacement
Chelation therapy to reduce iron overload
Bone marrow transplantation
60
The Leukemias (1 of 3)
Group of neoplastic disorders involving white blood cells
Uncontrolled WBC production in bone or lymph nodes(Unfunctioning cells)(Immature)
Other hemopoietic tissues are reduced.
One or more types of leukocytes are undifferentiated, immature, and nonfunctional.
Large numbers released into general circulation
Infiltrate lymph nodes, spleen, liver, brain, other organs
61
Acute leukemias (ALL and AML)
High proportion of immature nonfunctional cells in bone marrow and peripheral circulation
Onset usually abrupt , marked signs of complications
Occurs primarily in children and younger adults
62
Chronic leukemias (CLL and CML)
Higher proportion of mature cells but with reduced function
Insidious onset
Mild signs and better prognosis
Common in older adults
63
Signs and Symptoms of
Acute Leukemia
Usual signs at onset
Frequent or uncontrolled infections
Petechiae and purpura
Signs of anemia
Severe and steady bone pain
Weight loss, fatigue, possible fever
Enlarged lymph nodes, spleen, liver
Headache, visual disturbances, drowsiness, vomiting
64
The Leukemias (3 of 3)
Diagnostic tests
Peripheral blood smears
Immature leukocytes and altered numbers of WBCs
Number of RBCs and platelets decreased
Bone marrow biopsy for confirmation
Treatment
Chemotherapy
ALL young children respond well to drugs
Biological therapy (interferon)
May be used to stimulate the immune system
65
Complications of Leukemia(immunosuppresents)
Opportunistic infections, including pneumonia
Sepsis
Congestive heart failure
Hemorrhage
Liver failure
Renal failure
CNS depression and coma due to immunosuppressants and toxins
66
Arteriosclerosis
General term for all types of arterial changes
Degenerative changes in small arteries and arterioles
Loss of elasticity
Lumen gradually narrows and may become obstructed
Cause of increased BP
67
Atherosclerosis
Presence of atheromas in large arteries
Plaques consisting of lipids, calcium, and possible clots
Related to diet, exercise, and stress
68
Lipid Transport
Lipids are transported in combination with proteins.
Low-density lipoprotein (LDL)
Transports cholesterol from liver to cells
Major factor contributing to atheroma formation
High-density lipoprotein (HDL)
Transports cholesterol away from the peripheral cells to liver—“good” lipoprotein
Catabolism in liver and excretion
69
Risk Factors for Atherosclerosis
Nonmodifiable
Age
Gender
Genetic or familial factors
Modifiable
Obesity
Sedentary lifestyle
Cigarette smoking
Diabetes mellitus
Poorly controlled hypertension
Combination of oral contraceptives and smoking
Serum lipid levels
LDL, HDL
Exercise stress testing
Screening for arterial obstruction
Nuclear medicine studies
Determine the degree of tissue perfusion
Treatment
Weight loss
Increase exercise
Dietary modification
Reduction of sodium intake
Control hypertension
Control of primary disorder
Cessation of smoking
Antilipidemic drugs(used to treat hyperlipidemia, or an excess of lipids in the blood)
Surgical intervention
coronary artery bypass grafting
70
Peripheral Vascular Disease: Atherosclerosis
Disease in arteries outside the heart
Increased incidence with diabetes
Most common sites
Abdominal aorta
Carotid arteries
Femoral and iliac arteries
Diagnostic tests
Blood flow assessed by Doppler studies and arteriography
Plethysmography measures the size of limbs and blood volume in organs or tissues.
71
Most common sites(Peripheral Vascular Disease: Atherosclerosis)
Abdominal aorta
Carotid arteries
Femoral and iliac arteries
72
Signs and Symptoms(Peripheral Vascular Disease: Atherosclerosis)
Increasing fatigue and weakness in the legs
Intermittent claudication (leg pain)
Associated with exercise caused by muscle ischemia
Sensory impairment
Tingling, burning, numbness
Peripheral pulses distal to occlusion become weak
Appearance of the skin
Marked pallor or cyanosis
Skin dry and hairless
Toenails thick and hard
73
Treatment(Peripheral Vascular Disease: Atherosclerosis)
Maintain control of blood glucose level
Reduce body mass index
Reduce serum cholesterol level
Platelet inhibitors or anticoagulant medication
Cessation of smoking
Increase activity and exercise
Maintain the dependent position for legs
Peripheral vasodilators
Observe skin for breakdown and treat promptly.
If gangrene develops, amputation is required
74
Aortic Aneurysm
Localized dilation and weakening of arterial wall
Develops from a defect in the medial layer
Different shapes
Saccular
Bulging wall on the side
Fusiform
Circumferential dilation along a section of artery
Dissecting aneurysm
Develops when there is a tear in the intima of the wall and blood continues to dissect or separate tissues
75
Etiology(Aortic Aneurysm)
Atherosclerosis
Trauma
Syphilis and other infections
Congenital defects
76
Signs and Symptoms(Aortic Aneurysm)
Bruit may be heard on auscultation
Pulse may be felt on palpation of the abdomen
Frequently asymptomatic until they become large or rupture
Rupture may lead to moderate bleeding but usually causes severe hemorrhage and death
77
Diagnostic Tests
Radiography
Ultrasound
CT scanning
MRI
78
Abdominal Aortogram
An abdominal aortogram is a procedure that allows doctors to see the aorta, the body's main artery, in the abdomen.
79
Treatment(Aortic Aneurysm)
Maintain blood pressure at normal level
Prevent sudden elevations caused by exertion
Prevent stress, coughing, constipation
Surgical repair
80
Varicose Veins
Irregular, dilated, tortuous areas of superficial veins
Familial tendency
Increased body mass index, parity, and weight lifting are risks.
In the legs
May develop from defect or weakness in vein walls or valves
Appear as irregular, purplish, bulging structures
Treatment
Keep legs elevated, support stockings
Restricted clothing, crossing legs to be avoided
81
Thrombophlebitis
Thrombus development in an inflamed vein (e.g., IV site)
82
Phlebothrombosis
Thrombus forms spontaneously without prior inflammation; attached loosely
83
Factors for thrombus development
Stasis of blood or sluggish blood flow
Endothelial injury
Increased blood coagulability
