Exam #3, Quiz 1 Flashcards
1
Q
What does cells primarily reply on?
A
Oxygen
2
Q
What is the normal body pH?
A
7.35-7.45
3
Q
What are the four primary functions of blood? x4
A
- Transport oxygen and nutrients to all tissues
- Remove wastage products of cellular metabolism?
- Active in the bod’s defenses/ immune system
- Help maintain body homeostasis
4
Q
What are the two separate circulatory systems and what does each do?
A
- Pulmonary circulation: allows the exchange of oxygen and carbon dioxide in the lungs
- Systemic circulation provides for the exchange of nutrients and waste between the blood ad the cells throughout the body
5
Q
What do arteries do?
A
Transport blood back to the heart.
6
Q
Blood flows
A
Arteries -> Arterioles -> Capillaries -> Venules -> Veins _> back to the heart -> lungs
7
Q
What is in the larger veins that help push blood towards the heart
A
Valves
8
Q
Why does blood flow in the wrings depend on?
A
Skeletal muscle action, respiratory movements, and gravity
9
Q
What are the three layers of walls of arteries and veins made of?
A
- Inner layer: tunica intima, an endothelial layer
- Middle layer: Tunica media, a layer of smooth muscle that controls the diameter of lumen size (diameter) of the blood vessels
- Outer layer: tunica adventitious, or external, connective tissue later that contains elastic and collagen fibers
Capillary walls have a single endothelial later allows for easier transport into tissues
10
Q
What is hematocrit levels and what do they do?
A
Number of cells in the blood
Proportion of cells in blood
Viscosity, thickness, of blood
Males average 42-52%
Females averages 37-48%
Elevated HCT- Dehydration of excess cells
Decrease HCT- blood loss or anemia
11
Q
What is plasma?
A
Yellowish fluid remaining after cells are removed
12
Q
What is plasma protein?
A
Albumin- maintains osmotic pressure. (Keeps fluid where its suppose to be)
Globulins and antibodies- immune response
Fibrinogen- clotting
13
Q
Where do blood cells originate?
A
Red bone marrow
14
Q
What are myeloid stem cells?
A
Precursors for RBCs, platelets, and granulocytes (Eosinophils, Basophils, and Neutrophils)
15
Q
What are Lymphoid stem cells?
A
Precursors for B lymphocytes, T lymphocytes, and natural killer cells
16
Q
What is erythropoietin?
A
From the kidneys stimulates erythrocytes, rbc production. (Hematopoisesis) in response to tissue hypoxia
17
Q
What does adequate RBC production and maturation depend on?
A
Amino acids, iron, Vitamin B12 and B6, Folic acid
18
Q
When does hemoglobin become fully saturated?
A
With oxygen in the lungs
19
Q
What color is oxyhemoglobin?
A
Bright red
Also is a good indicator for distinguishing the difference from arterial blood from venous blood
20
Q
What happens as blood circulates through the body?
A
Oxygen dissociates from hemoglobin to enter tissues
Deoxygenated blood is dark blush’s red in color
Found in venous blood
21
Q
What can oxygen easily be displaced from hemoglobin by?
A
Carbon monoxide, which binds tightly to the iron in place of oxygen, causing a fatal hypoxia, takes all four oxygen receptor sites
CO2 Poisoning can be recognized by the bright cherry red color in the lips and face
22
Q
What is hemolysis of erythrocytes?
A
Excessive hemolysis or deconstruction of RBCs, as with hemolytic anemias, may cause elevated serum bilirubin levels»_space;> jaundice
23
Q
What is leukopoiesis?
A
The production of WBCs, it is stimulated by colony stimulating CSFs produced by cells such as macrophages and T lymphocytes
24
Q
What are lymphocytes? (B and T cells)
A
Immune response
25
What are neutrophils?
First responders to tissue damage
26
What are immature neutrophils called?
Band, immature
27
What does bands do? Also what is the phrase we use when we indicate this?
Often increase in number in response to bacterial infection
Shift to the left (shift as in bands)
28
What are basophils?
Become mast cells that release histamine
29
What are eosinophils?
Active in allergic reactions and parasitic infections: asthmatics
30
What are monocytes?
Become macrophages active in phagocytosis
Also known as pac man cells
31
What are the three steps in hemostasis?
(Thrombocytes, platelets, essential part of the blood clotting process)
1. Immediate response of a blood vessel to injury is vasoconstriction or vascular spasm
2. Thrombocytes, platelets, adhere to the underlying tissue at the site of injury and can form a platelet plug in the vessel if its small
3. It its a larger vessel, platelets can trigger the clotting, coagulation cascade.
32
Where are clotting factors produced primarily?
Liver
33
What is Vitamin K required for?
Synthesis of most clotting factors, especially prothrombin
34
Calcium
Also essential in the clotting factor
35
What helps with the clotting cascade?
Applying pressure, cold application, or thrombin solution can help speed up clotting
36
What happens if you have liver issues with the clotting cascade?
No clotting, increase bruising
37
Human Blood Clotting: Chart
Starts:
Damage blood vessel: injury to vessel lining triggers the release of clotting factors
->
Clotting Factors
->
Prothrombin ->Thrombin. -> Fibrinogen (soluble). -> Fibrin. (Insoluble) ->
1. Activated platelet: Formation of platelet plug, vasoconstriction limits blood flow and platelets form a sticky blue
2. Fibrin Strand - Blood Clot: Development of Clot: Fibrin strands adhere to the lug to form an insoluble clot
38
What are blood types determined by potencies of?
Specific antigens on surface of RBCs
39
What blood type is the universal donor?
Type O-
40
What blood type is the universal recipient?
AB
41
What is important about an RH factor?
May cause blood incompatibility in the mother if RH negative and the fetus us RH positive
42
Why can plasma be administered without risk of a reaction?
Because it does not have antigens or antibodies?
43
What are transfusion reactions, clinical manifestations?
Base line vitals, always needed
Feeling of warmth in that involved vein, flushed face, headache, fever and chills, pain in the chest and abdomen, decrease blood pressure, rapid pulse
44
What is a CBC?
Overall cell count
45
What is a CBC with differential?
Closed look at percentages f the different EBCs; can help identify diagnosis— separate all cells out
46
What is a blood smear?
Looks at cell structures (anemias), cell shape, size, and color
47
What is hemoglobin and hematocrit anemias?
Low hemoglobin enemia
48
What is reticulocyte?
Immature RBC Production, sickle cell
49
What is bone marrow aspiration and biopsy?
Bone marrow function, cancer test
50
What are serum levels?
Iron, Vitamin B12, folic acid, glucose
51
What is a PTT, INR?
Coagulation indicators, coagulation - warfarin/cumiden
52
What are the four treatments for low cell count?
1. Whole blood, Packed RBCS, Platelets- replace cells or platelets
2. Plasma products or colloid infusions-expand volume and balance osmotic pressure
3. Epoetin (made in kidneys) - simulates production of red bloodcells: sympathetic eurothropostein
4. Bone marrow or stem cell transplants treatment of some cancers and immunodeficiencies specialties
53
What is reduced oxygen supple due to decreased hemoglobin?
ANEMIAS
54
General caused of anemia X4
Blood loss
Decreased Erythrocyte RBC production
Increased erythrocyte destruction
Deficiency of necessary components
55
What are some etiologies and risk factors of anemia? X6
Blood Loss: Trauma, heavy periods, gi bleeds, surgical
Rapid Metabolic Activity: pregnancy, adolescence, infection
Increased hemolysis: Sickle cell, autoimmune disorders
Inadequate dietary intake or metabolism: iron, vitamin B12, folic acid, crohns, vegans, vegetarians
Bone Marrow Suppression: radiation, chemo
Age: hugger occurrence nutrient deficits, misdiagnosis, GI bleed
56
What are signs and symptoms/ clinical manifestations of anemia?
Decreased ph, pallor, fatigue, somnolence, headache, irritability, dyspnea on excretion, cold intolerance, dizziness, syncope fainting, tachycardia, palpitations, nail bed deformities, smooth, sore, bright red tongues, numbness/ tingling in extremities, Vitamin B 12 deficiency, Pain and hypoxia
57
What are the four anemia specific labs, and what does each do?
1. Mean Corpuscular Volume (MCV): Size of RBCs normcytic, micro cystic, Micocytic
2. Mean Corpuscular Hemoglobin MCH: Amount of Hbg in RBCs: Normochromic RBC vs. Hypochromic RBS Pale
3. Mean Corpuscular Hbg Concentration MCHC: Hbg amount relative to size of cell
4. Iron Studies: Total iron binding TIBC- Indirect measurement of transferrin- binds with iron and transports it for storage. Ferritin- total iron stores in body
58
4 different type of non specific anemia labs
1. Hemoglobin electrophoresis: separates normal Hbg from abnormal, used in diagnosis in of sickle cell thalassemia
2. Sickle cell test: Evaluates suckling of RBCs when decreased oxygen present
3. Schilling Test: Measures vitamin B12 absorption with and without intrinsic factor (used to differentiate between malabsorption and pernicious anemia)
4. Bone marrow aspiration: Diagnosis of aplastic anemia
59
What is iron deficiency anemia?
Not enough iron in to make Hbg >> less O2 transported in blood
Usually an underlying problem accompanies
Microlytic, hypochromic RBCs = pregnancy/. Breast feeding
60
Etiology of iron deficiency anemia
Low dietary intake: especially during growth spurts and pregnancy
Chronic blood lose (ulcer hemorrhoids, cancer, excessive menses)
Malabsorption EAT Lagoons, meats, leafy greens
Liver disease, storage of iron
61
Labs off Iron Deficiency Anemia
Low H/H
Serum ferritin, serum iron
62
Signs and Symptoms or Iron deficiency Anemia
Pallor, fatigue, lethargy, cold intolerance, irritability, brittle hair, spoon shaped/ ridged nails, stomatitis/ glossitis, tachycardia, dyspnea, syncope
63
Management of iron deficiency anemia
Treat cause, supplement oral or iV
EDUCATION: Oral stains teeth, Constipation and darker stools are commonly seen, take the food, take with vitamin C, helps absorption juice
64
What is pernicious anemia?
Vitamin B12 Deficiency
Megaloblastic anemia- very large, immature, nucleated RBCs
65
What is the etiology of pernicious anemia?
Deficit of folic acid, B9, OR vitamin B12
- Poor dietary intake, vegans and vegetarians
- Malabsorption disorders
- Folic acid deficiency increases risk for spina bifocals and other neural tube problems
**** B12 Injecetions for life
**** B9 think Crohns, lack of absorption, folic acid
66
Patho of pernicious anemia
Lack of INTRINSIC FACTOR, IF, produced in gastric mucosa which is necessary for absorption
Achlorhydria: atrophy gastric mucosa - less acid production - decrease protein and iron absorption
67
Diagnosis of Pernicious Anemia
Schilling test
68
Signs and Symptoms of pernicious Anemia
Large, red, sore, or burning tongue BEEFY
GI Upset, nausea and diarrhea
Neurological effects from demyelination of peripheral nerves and spinal cord
Parasthesia: Burning, tingling, numbness
Ataxia: Abnormal gait
69
Management of pernicious anemia
Oral supplements to prevent, preg females and vegetarians
Vitamin B12 injections for LIFE to treat
If problem is not absorption, oral, but can stain teeth
70
What is Aplastic Anemia?
Impairment of bone marrow >> loss of stem cells >> pancutopenia ,, Not making stem cells
Unknown cause: idiopathic
TOXINS: radiation, chemicals, chemo
VIRUSES: Hep c
AUTOIMMUNE DISORDERS: lupus
Everything is low: PANCYTOPENTA
RBC >> anemia
WBC>> recurrent or multiple infections
Platelets>> pet hair, bleeding tendencies, hemorrhage
71
What is diagnosis and management of Aplastic Anemia?
Diagnosis: CBC, Bone Marrow Biopsy
Management: Treat cause, blood transfusion, bone marrow transplant
72
What is sickle cell anemia?
GENETIC
Autosomal Recessive: genetic mutation results in abnormal hemoglobin, Hbg S formation
HOMOZYGOUS: mom and dad both have. Sickle cell disease , HBG is replaced by HBG S
HETEROZYGOUS: sickle cell trait, only occurs with severe hypoxia, got from mom OR dad
HEMOLYTIC Anemia
73
What individuals usually inherit sickle cell?
African and middle eastern individuals
74
PATHO OF SICKLE CELL ANEMIA
HBG is deprived from O2 >> Cell Crystallizes ad changes to sickle shape >> Damages cell membrane >> Hemolysis >> short life span
Sickle cell >> Occlude blood vessels >> increase thrombus formation and infractions in tissue throughout thee body deprived from O2 >> blood clots, strokes
Increase breakdown of RBC >> Jaundice, hyperbilirubinemia, gallstones
Seen in teens and young adults 20s
75
Triggers of sickle cell
Dehydration, strenuous activity, high altitudes, illness, infection, exposure to cold
Crisis: Pain, SOB
Keep volume up, ampule space
76
Symptoms of sickle cell and onset in 1 yr old, fetal Hbg fully replaced by HbG
ANEMIA - pallor, weakness, tachycardia, SOB
JAUNDICE- gallstones from high bile levels
SPLENOMEGALY- then infarction, resivior infection response
PAINFUL CRISES, ACUTE CHEST SYNDROME
DELATED GROWTH AND DEVELOPMENT
Heart failure
Frequent infections
STROKES AND HEART ATTACKS POSSIBLE
77
Sickle cell diagnosis: trait or disease
Hemoglobin electrophoresis, determines trait
78
Management of sickle cell
HYDRATION, HIGH VOLUMES KEEP PASSAGES OPEN
HYPOXYUREA
PAIN MANAGEMENT
BLOOD TRANSFUSIONS
BONE MARROW TRANSPLANT
IMMUNIZATIONS UP TO DATE
AVOID TRIGGERS
PCA pumps
79
What is thalassemia?
Genetic disorder one or more genders for Hbg are missing or abnormal
Homozygous: mom and dad, thalassemia Major, severe life threatening anemia
Heterozygous: mom OR dad, thalassemia minor, milds of anemia
Less normal hemoglobin made , alpha or beta chains affected
Cell membranes are damaged and easily destroyed
Microcytic hypochromic ( kidney signals) RBCs, increased erythropoietin levels
80
Signs and Symptoms, AND Manifestations of Thalassemia
S/S
Delayed Growth and development, hypoxia, decreased activity and released to fatigue
Altered skeletal development: hyperactivity n bone marrow
Heart failure: increased workload
Management:
Blood transfusions
Chelation therapy for excess iron, binds and get out of body
81
Clotting Disorders
Bleeding of the guns, nosebleeds
Petechaie, purpura- frequent bruising
Hemarthroses: Blood/ bleeding in the joints
Hemolysis: coughing up blood and Hematemesis: Vomitting up blood
Tarry Stools: gi bleed
Anemia
Feeling faint, anxious, low BP, rapid pulse
82
Potential causes of clotting disorders
Low platelet counts — think infection, HIV, large liver/spleen
Chemo, Radiation
Aspirin, NSIAD, Coagulants,,, Peptic ulcers
Liver disease, Vitamin K Deficiency: clotting factors
Genetic Disorders
83
What is Hemophilia A and the S/S?
GENETIC: X linked recessive, disorder manifested in males, carried by females
Deficit in Blood factor VIII (8)
S/S
Prolonged bleeding, severe hemorrhaging
Hemarthrosis: bleeding in joint
Blood in all fluids that come out
MALES SHOW S/S
FEMALES: CARRIERS
84
Management of Hemophilia A
Management:
Desmopressin: stimulates release of stored factor 8
Replacement factor 8 infusions: periodic before procedures that could cause bleeding
85
Von Willenbrand Disease Cause, S/S, Management
Hereditary deficiency of von willer and factor: clotting factors >> help platelets clump, not aggregating platelets
S/S similar to hemophilia A but MILDER
Easy bruising
Management:
Desmopressin, Replacement Therapy
Not sex linking
86
What is Disseminated intravascular Coagulation DIC and the Etiologu
Both excessive bleeding and excessive clotting: uses up clotting factors and platelets which stimulates fibrinolytic process thereby causing bleeding and severe hemorrhage
Etiology: OB Complications, Infection, sepsis, Carcinomas, Major trauma
CAN BE LIFE THREATENING
87
S/s and Management of Disseminated Intravascular Coagulation DIC
S/S: Clotting or hemorrhage flip flop
Petechiae, bruising, purpura
Mucosal bleeding, hematocrit, low BP, Shock, Infarcts.
Management: Acute
1. Focus on the most pressing concer at the time be it bleeding or blood clots antiiicoagulants vs blood products
2. Ultimately must treat causes to resolve
88
What is Thrombophilia: S/S and management
Not genetic
Group of inherited or acquired (sedentary, immobility, smoking, postop, estrogen products) disorders
Increase the risk of developing abnormal clots in the veins/ arteries
Increase risk for dvt, pe, pvd, mi, stroke
S/S: Depends on clot area
Management:
Treat cause for acquired thrombophilia
Anticoagulants, Coumadin
89
What is Polycythemia? Primary and Secondary
Increased production of erythrocytes in bone marrow
Primary: Polycythemia Vera- no idea why, cancer, neoplastic disorder involving overproduction of RBCs
Secondary Polycythemia: Compensation mechanism. > increase O2 transport Chronic lung Disease or Heart disease or from living in high altitudes
Prolonged hypoxia: COPD or Heart Disease
Increased erythropoietin secretion, renal carcinoma
90
Polycythemia: Increased blood viscosity and volume
Blood vessels are distended and blood flow is sluggish leading to frequent thromboses and infarctions
HTN, Cardiomegaly
Spleen and liver are congested and enlarged: resivors
Bone marrow is hyper cellular
Increase hemo, thick sludgey. blood viscosity
Overload of RBC, JDV.
91
What is leukemia?
Cells made in bone marrow lack of platelets suppress any other type of cell production, enmity, lack of RBC, Thrombocytopenia, lack of platelets, poor response to infection
NO TUMOR, cancer is in WBC and RBC, Increase in WBC = non functional, increase bruising and bleeding
92
How do kids respond to Leukemia
WELL in Treatment
93
Leukemia overview more in detailed
Neoplastic disorders involving WBCs; no solid tumor, crowd out bone marrow = bone pain
One or more of the leukocytes types are present as undifferentiated, immatured bonfunction cells that multiply uncontrollably in bone marrow
Pain
Suppress production of other normal cells leading to anemia, thrombocytopenia and a lack of normal functional leukocytes
94
Acute Vs. Chronic Leukemia classification
Acute: high proportions of very immature nonfimcytional cells, blast cells, in the bone marrow and peripheral circulation
Onset is usually abrupt
Marked signs and complications
Chronic: higher proportions of mature cells, although they have reduced function
Insidious onset and mild signs
Better prognosis
95
Cell Type and Age onset for Acute lymphocytic leukemia, ALL
Cell type: B lymphocytes
Age onset: young children
96
Acute Myelogenous Leukemia AML Cell Type and Age onset for
Cell type: Granulocytic stem cells
Age onset: Adults
97
Chronic lymphocytic leukemia CLL Cell Type and Age onset for
Cell Type: B lymphocytes
Age onset: Adults >50
98
Chronic Myelogenous leukemia CML Cell Type and Age onset for
Cell Type: Granulocytic stem cells…. Specialized WBC
Age Onset: Adults 30-50
99
Signs and Symptoms of leukemia
Multiple infections
Severe hemorrhage - thrombocytopenia
Anemia - fatigue
Bone Pain
Weight loss, fatigueHypermetabolism
Lymph nodes, spleen and liver are often enlarged and cause discomfort
100
Diagnosis and Management of Leukemia
Diagnosis: Peripheral blood smears and Bone marrow Biopsy
Management: Chemo and Bone marrow transplants
Acute: more abrupt onset, kids
Chronic: gradual symptom onset
101
Four main functions of the lymphatic system
1. Return excess interstitial fluid and protein to the blood
2. Filter and destroy unwanted material from the body fluids
3. Initiate an immune response
4. Interact with all other body systems
102
Lymphatic structures X5
Lymphatic vessels : movement of fluids
Lymphatic Tissue: Protects, line of defense
Lymph Nodes: Immune response of B and T lymphocytes, disappears during infection
Spleen, left side: Defense, Reservoir for bloo
Thymus gland: secretes hormones
103
What is lymph?
Clear watery isotonic fluid circulated through the lymphatic vessel
104
What is lymphadenopathy?
Inflammation or infection of lymph nodes
Common sign of another disease, viral/ malignancies
105
What is the manifestation as a swollen lymph node?
An increase in size and extent over time usually indicates cancer
106
Diagnosis of lymphadenopathy
Exam, Ultrasound, Fine Needle Biopsy, PET CT:
We can not usually see or feel metabolic
107
How to treat lymphadenopathy
Treat the cause!
108
What are lymphomas?
Malignant neoplasms involving lymphocytes proliferation in the lymph nodes.
Cause: higher incidence in adults who received radiation treatments during childhood
109
Hodgkin lymphoma pathology
Initially a SINGLE lymph node (often in neck) > spreads to adjacent nodes then organs via lymphatic vessels
Works its way down, orderly
Orderly contagious spread
T lymphocytes defective and the lymphocyte count is decrease - increased R/F recurrent infections
T Cells: Killer vs. helper cells
110
Diagnosis of Hodgkin lymphoma?
DX Marker - Reedsternberg cells
Ann Arabor staging system
111
Signs and Symptoms of Hodgkin lymphoma
1ST Sign: enlarged lymph NODE often cervical, that is painless and no tender
Spleenomegaly
Other enlarged lymph nodes
General cancer signs
Fatigue
Weight loss
Anorexia
112
Treatment for Hodgkin lymphoma
Radiation, Chem, Surgery
113
What is non Hodgkin lymphoma
Tends to be more widespread that Hodgkin lymphoma
More lymph nodes involved
Unorganized widespread metastasis
Extranodal involvement common : growth outside the lymph nodes
No Reee Sternberg cells
Most cases involve B Lymphocytes
114
Age affected with non Hodgkin lymphoma
Over 60
115
What are the signs and symptoms of Hodgkin lymphoma
Same as Hodgkin lymphoma
Usually seen more frequently in patients with HIIV
1ST symptom enlarged painless lymph node
116
Treatment of non Hodgkin lymphoma
Difficult to treat due to widepresad metastates and extranodal involvement
Less responsive to treatment
Radiation, Chemo, Surgery
117
What is multiple myeloma
Malignancy involving plasma cells (mature B lymphocytes involved in production of antibodies
Increased number if malignant plasma cells replace the bone marrow and erode the bone
Blood cell and antibody production is impaired
118
What does multiple myeloma do?
Multiple tumors with bone destruction develop in vertebrae, pelvis, and sill
Pathological or spontaneous fractures
HYPERCALCEMIA cur as bone is destroyed
119
What type of onset is multiple myeloma ?
INSIDIOUS onset, usually well advanced by the time of discovery
120
Manifestations of multiple myeloma
Frequent infections
Pain related to bone involvement, present at rest and with activity
Pathological fractures
Anemia and bleeding tendencies because bone marrow is impaired not making platelets, wbcs, RBcs
Protenuria and kidney failures
121
Management of multiple myeloma
CHemo
Supportive care
Analgesics for bone pain
122
What is lymphedema?
Tissue in the extremities sell due to obstruction of lymphatic vessel and accumulation of lymph
123
Etiology of lymphedema
Primary lymphedema’s congenital
Secondary- due to cancer, tumor, radiation therapy, damage during surgery, remove of lymph nodes
124
Manifestations of lymphedema
Swelling, initially soft but progresses to firm, painful, and unresponsive to treatment
Increase risk for frequent infections
125
Management of lymphedema
Bed rest, massage, elevation
126
What is elephantiasis?
Form of lymphedema resulting from infestation and blockage of lymph vessels by a parasitic worm (filaria)
127
Why is extreme swelling so significant
Causes extremity to look like an elephants leg
128
S/S. Of elephantiasis
Thickening of subcutaneous tissue, frequent infections, skin ulceration ,fever
129
Management of elephantiasis
Skin care and elevation
Antiparasitic drugs
Surgeries for shunt
130
What is castleman disease?
Lymphoproliferation disorder, not cancer — overgrowth of lymphoid tissue
Associated with higher risk for cancers, such as lymphoma
Unicentric — affects. ONE LYMPH NODE
S/S: Depnds on location - large lump, difficulty breathing or eating, weight losss poor appetite cough
T/x: REMOVE STHE NOSE OF POSSIBLE/ IF NOT STEROIDS OR RADIATION TO SHRINK OR DESTROY THE NODE
Multicentric. — affects multiple lymph nodes decreases immune response
S/S: more systemic, fever night sweats N/X weight loss weakness spleomegaly heaptomeaglay
T/X: more difficult, too many odes to remove meds steroids anti cancer immuomadulating
