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High Acuity Final Exam > Hematology chap 27-29 ppt > Flashcards

Hematology chap 27-29 ppt Flashcards

1
Q

What are the components of blood?

A

Plasma, RBCs, WBCs, Platelets

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2
Q

What is the function of erythrocytes? Where do they mature? What stimulates RBC production?

A
  • Transport 02 to cells
  • Mature in blood or spleen
  • Production is stimulated by erythropoietin (produced by the kidneys) in response to decreased tissue oxygenation
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3
Q

What is a platelet? Life span? Function, stored where? What stimulates production?

A
  • Cell fragments
  • 10 day life span
  • Circulate blood; stored in spleen
  • Production is stimulated by thrombopoietin
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4
Q

What is hemostasis? What occurs during this process?

A
  • Injury to vessel

* Forms a platelet plug, fibrin clot, aids in clot retraction and dissolution

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5
Q

What is DIC? How do we tx it? What is it associated with?

A
  • Inappropriate clotting and bleeding
  • Treat the underlying condition (SEPSIS, trauma, brain injury, heat stroke, transfusion reaction, liver disease, leukemia, pregnancy complications)
  • Associated with HIGH mortality
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6
Q

What are the clinical findings of DIC? Lab findings? Tx?

A

• Clinical findings include BLEEDING, altered mental status, abnormal kidney function, and respiratory changes
• Lab evaluation:
high bleeding time, low platelets, high PT/PTT, low fibrinogen
• Treatment: underlying disease, cryo/FFP, Heparin?

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7
Q

d

A

d

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8
Q

What is the function of the immune system? What are the primary and secondary lymphoid organs?

A
  • Immune system is a surveillance system that destroys foreign cells (immune system is able to distinguish self from non-self), has memory, and reacts as needed.
  • Primary Lymphoid Organs: Bone marrow and thymus gland
  • Secondary Lymphoid Organs: Tonsils, adenoids, lymph nodes, spleen
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9
Q

What is the difference between innate (natural) and adaptive (acquired) immunity?

A
  • Innate immunity is non-specific (meaning that innate immunity will react to any pathogen), first responders are WBCs, nonadaptive (meaning the immune response will start from the beginning every time even if its seen the pathogen)
  • Adaptive immunity is specific (meaning that it will react to the specific pathogen), second responder system (other immune cells will act such as helper T, etc other than WBC), targets specific pathogens based on previous exposures/antigen recognition, adaptive (immune response is quick b/c body knows what to do)
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10
Q

What is our first, second, and third line of defenses against pathogens? How do the defenses work?

A
  • First line defenses: skin, mucous membranes, flora (stop pathogens from getting in)
  • Second line defenses: phagocytes, macrophages, natural killer cells (innate immunity: kills pathogens)
  • Third line defenses: lymphocytes, t-cells (t-helper 1 & 2), b-cells (adaptive immunity: Th1 - direct attack, Th2 - antibodies)
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11
Q

Describe innate (natural) immunity.

A
  • Natural, born with specific immunities
  • Species specific
  • Includes natural resistance/physical and chemical barriers
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12
Q

What are the major cells/components of innate immunity?

A

Neutrophils, monocytes, macrophages, natural killer (NK) cells, cytokines, compliment system

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13
Q

Define phagocytosis.

A

Eating cells

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14
Q

What are major cytokines of the immune response?

A

Interleukins (IL), interferons (IF), tumor necrosis factor (TNF), granulocyte monocyte colony-stimulating factors (GM-CSF)

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15
Q

What is the function of the various major cytokines?

A

IL - inflammatory mediator, activates lymphocytes and helps them grow and differentiate, attracts neutrophils
IF - inflammatory mediator, activates macrophages, inhibits virus from replicating
TNF - inflammatory mediator, programs cell death (apoptosis) of tumor cells, aids in endothelial activities
GM-CSF - STIMULATE MY COLONY OF WBCs, inflammatory mediator that acts in bone marrow, differentiates neutrophils and monocytes

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16
Q

Describe the compliment cascade.

A

Group of >20 proteins that when activated damage pathogen membrane by initiating vasodilation, chemotaxis, and opsonization

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17
Q

Describe adaptive (acquired) immunity.

A
  • Antigen specific/responds to antigen exposure
  • B and T lymphocytes respond (humoral/cell mediated immunity)
  • Different types: Passive and Active Acquired Immunity
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18
Q

Describe humoral immunity, a type of adaptive (acquired) immunity.

A

Consists of B lymphocytes. These attack bacterial infections by producing antibodies (immunoglobulins) and memory B cells

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19
Q

What are the different types of antibodies (immunoglobulins) and what is the role of each?

A

IgG - released w/ bacterial and viral infections, crosses placenta
IgA - protects mucous membranes from pathogens, found in body secretions (tears, saliva, breast-milk, vaginal, bronchial, and intestinal secretions)
IgM - produced with immune response to antigens/actiates complement, found in body secretions, forms ABO antibodies
IgD - wdk, may influence B cell maturation, primary found in blood
IgE - allergies, circulates through body in small amounts but is powerful af

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20
Q

Describe cell mediated immunity, a type of adaptive (acquired) immunity.

A

Consists of T lymphocytes. These mature in the thymus and protect the body from pathogens that get inside the cells by marking the infected cells for destruction by phagocytes

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21
Q

What are major differences between B and T lymphocytes?

A
  • Matures in: B-lymph bone marrow vs t-lymph thymus
  • Type of immunity: B-lymph humoral vs t-lymph cell mediated
  • Secretes: B-lymph antibodies vs t-lymph cytokines
  • Receptor cell acts on: B-lymph surface Ig vs t-cell receptor
  • Where found: B-lymph spleen vs t-lymph blood/lymph nodes
  • Targets: B-lymph bacteria/parasites vs t-lymph viruses/infected cells/tumor cells
  • Is there memory: B & T T lymph have memory
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22
Q

What type of immunity is passive and active immunity? What’s the difference?

A
  • Acquired immunity.
  • Passive immunity is immunity that is temporary such as the transfer of antibodies. This type of immunity is rapid but short lived. It’s a gift from one person to another.
  • Active immunity is immunity that you work for thus it is not temporary. In time the body will be able to recognize certain antigens and initiates a response based on that antigen. The first time the body is exposed to an antigen it takes awhile to build immunity vs the second time around the response is fast since the body knows what to do.
23
Q

What immunoglobulin is responsible for a type I hypersensitivity reaction? What triggers this reaction?

A

IgE - allergies, anaphylaxis, immediate response to allergic rhinitis, allergic asthma, and latex allergies

24
Q

What immunoglobulin is responsible for a type II hypersensitivity reaction? What triggers this reaction?

A

IgG/IgM - cytotoxic, hemolytic responses such as a transfusion reaction, Rh incompatibility of newborns (hemolytic disease of the newborn), hemolytic anemia

25
Q

What immunoglobulin is responsible for a type III hypersensitivity reaction? What triggers this reaction?

A

IgG & complement - immune complex diseases such as arthritis reaction, serum sickness, SLE

26
Q

What cell is responsible for a type IV hypersensitivity reaction? What triggers this reaction?

A

T-cell - delayed responses to: GVHD, positive TB test, contact dermatitis from poison ivy

27
Q

Describe a type I hypersensitivity reaction.

A

An allergic or anaphylactic response that can either be mild or severe. This reaction is mediated by IgE and mast cells (large granule containing tissue cells that are located in connective tissues). There are local reactions such as allergic asthma or allergic rhinitis and systemic reactions such as anaphylaxis.

28
Q

What type of hypersensitivity reaction is allergic rhinitis (hay fever)? What causes it? What are the s/s? Tx?

A

A type I hypersensitivity reaction (allergic reaction) caused by pollens: ragweed, timothy, birch, and dust mites. Signs and symptoms include sneezing, nasal congestion, nasal itching, itching in throat and soft palate, dry cough, hoarseness, and HA. Treat this reaction with antihistamines and steroids (inhaled, oral, or topical)

29
Q

What are the primary and secondary mediators of a type I hypersensitivity reaction?

A

Primary: Histamine, chemotaxis factors (ECF-A/NCF)
Secondary: Leukotrienes, prostaglandins, platelet activating factor (PAC)

30
Q

What type of hypersensitivity reaction is systemic anaphylaxis? What causes it? What are the s/s? Tx?

A

A type I hypersensitivity reaction (allergic reaction) caused by drugs, serum, venoms, and peanuts. Signs and symptoms include RAPID loss of plasma into interstitial space, profound HYPOtension, myocardial ischemia, organ death, edema, bronchoconstriction (to the point of asphyxia). Treat this reaction with epi, tracheostomy, o2, steroids, antihistamines, cromolyn, theophylline

31
Q

Describe a type II hypersensitivity reaction. Examples?

A

A cytotoxic/hemolytic reaction in which IgG or IgM react with the surface of the antigen causing an activation of complement which destroys cells. Examples include: hemolytic transfusion reaction (ABO incompatibility), Rh incompatibility in newborns (do coomb’s test), drug induced reaction (recephin, piperacillin, quinine), myasthenia gravis, autoimmune hemolytic anemia

32
Q

What are two types of transfusion reactions? Complication & s/s of second type of reaction?

A

Febrile: recipient antibodies act against donor WBC
Hypersensitivity reaction: recipient antibodies attach to donor blood proteins. Type II cytotoxic response is a complication in which antibodies attach to donors RBC → compliment → phagocytes destroy donor RBC → fragments of RBC travel to kidneys → mess up dah kidneys. s/s include: heat and redness, HA, back pain, chills, fever, chest heaviness and dyspnea, tachycardia, hypotension, hematuria, and death.

33
Q

Describe the nursing care of a transfusion reaction.

A

Stop the transfusion and notify the MD, start or open an IV, check VS Q5mins, place pt in fowler’s position, give o2, anticipate emergency drugs: antihistamines, vasopressors, fluids. Obtain urine specimen to send to lab (checking for Hg), send blood bag, tubing, label, transfusion record to lab. Document.

34
Q

Describe type III hypersensitivity reaction. Examples?

A

Involves IgG & IgM antibodies which can bind to form antigen-antibody complexes. These complexes travel through the circulation and can get lodge into the kidneys, joints, and skin causing an inflammatory response. It’s not the immune complex but altered blood flow and increased capillary permeability that cause tissue damage. This type of reaction can be localized or systemic. Examples: chronic graft rejection, autoimmune disorders (cause lung, joint, and skin damage), glomerulonephritis (leads to kidney damage).

35
Q

Name some examples of type III hypersensitivity reactions. What are complications of each?

A
  • SLE → nephritis, skin lesions, arthritis
  • Immune complex glomerulonephritis → nephritis
  • Polyarteritis nodosa → systemic vasculitis
  • Reactive arthritis → acute arthritis
  • Serum sickness (circulation) → arthritis, vasculitis, nephritis
  • Arthus reaction (localized) → cutaneous vasculitis
36
Q

Describe type IV hypersensitivity reactions. Examples? Tx?

A

Involves NO antibodies. This is a delayed response involving T lymphocytes. Examples: positive TB test, contact dermatitis (poison ivy), GVHD, hashimoto thyroiditis, RA, type I DM. Tx: steroids or immunosuppressants

37
Q

Describe the nursing care of contact dermatitis (poison ivy), a type IV hypersensitivity reaction.

A

Avoid exposure, wash area with lots of water to remove irritant, cold compress over site, and apply topical meds: calamine lotion, topical antihistamines, topical corticosteroids, short term oral corticosteroids

38
Q

Free Card: Summary of hypersensitivity reactions

A
  • Type I (Allergic, anaphylactic): an immediate reaction allergy that occurs in 15-30 minutes. Examples hives, hay fever, asthma, eczema, gastric disturbances, and anaphylactic shock
  • Type II (Cytotoxic, hemolytic response): an antibody dependent cytotoxic reaction that occurs in 1-3 hours. Examples: transfusion reaction
  • Type III (Antigen/antibody immune complex mediated): an immune complex reaction that occurs in 1-3 hours. Antibody complexes cannot be cleared from the body. Examples: damage of body tissues
  • Type IV (Delayed responses): a delayed reaction that occurs in less than 48 hours. Results from repeated exposure to allergen.
39
Q

Describe autoimmune disorders.

A

The immune system incorrectly sees self as foreign and initiates a destructive response against targeted tissue. Abnormal activation of T & B cells or the complement system. Can involve any of the four hypersensitivity reactions although type II and III are most common. A patient can have a genetic predisposition to an autoimmune disorder that may be trigger involved. Autoimmune disorders increase w/ age and females are more affected.

40
Q

Name examples of autoimmune disorders. What tissues/systems do these disorders target?

A
  • MS, myasthenia gravis, rheumatic fever → neuromuscular tissue
  • SLE, scleroderma, RA, ankylosing apondylitis → connective tissue
  • Autoimmune hemolytic anemia, autoimmune thrombocytopenic purpura → hematologic tissue
  • Goodpasture disease → pulmonary
  • Cardiomyopathy → CV
  • Ulcerative colitis, crohn’s disease, pernicious anemia → GI
  • Grave’s disease, type I DM, addison’s disease, partial pituitary deficiency → endocrine
  • Immune complex glomerulonephritis → renal
41
Q

Describe SLE. Triggers?

A

An inflammatory condition characterized by autoantibodies that develop against nuclear antigens affecting multiple body systems and organs (type III hypersensitivity reaction). SLE can be mild to life threatening and has periods where it goes away or stays active for a while. Young non-white woman of childbearing age can acquire this disorder. Triggers: UV light, meds. May be caused by Epstein-bar virus or genetic predisposition.

42
Q

What are the s/s of SLE?

A

s/s: malaise, fatigue, fever, weight loss, joint pain, skin changes

43
Q

How do you diagnose SLE?

A

Dx: R/O drug induced etiologies, antinuclear antibody/erythrocyte sedimentation rate, complement lvls, 4 or more of 11 criteria: arthritis, hematologic disorder such as hemolytic anemia/leukopenia/thrombocytopenia, immunologic disorder such as positive LE cell prep/anti-DNA antibodies/anti-Sm antibodies/false positive serologic test to syphilis, neurologic disorder such as seizure/psychosis, renal disorder such as persistent proteinuria/cellular casts, serositis (pleuritic or pericarditis), antinuclear antibody aeb elevated titer, discoid rash, malar rash (butterfly), oral ulcers in the mouth or nasopharynx, photosensitivity such as rash on skin exposed to sunlight.

44
Q

How do you treat SLE?

A

Tx: combination of NSAIDs, Hydroxychloroquine (Plaquenil), steroids. Immunosuppressive agents such as imuran, cytoxan, mycophenolic acid (MMF), rituxan, methotrexate

45
Q

What is the prognosis of SLE?

A

Px: 90% of pts live up to 10 yrs following dx, death is caused by injury to organs or infection, SLE leads to accelerated atherosclerosis which causes heart attacks, stroke, and kidney disease

46
Q

Describe the patient teaching of SLE.

A

Be sure the pt is knowledgeable about the disease: how it is caused, what it is, how its diagnosed, how to manage it. Be sure the pt knows the triggers such as UV light, sunlight, meds, smoking, Echinacea (a type of flower) and how to avoid them: wear heat, long sleeve shirt/pants, umbrella, stop smoking, read cold remedy labels and avoid use. Be sure the pt exercises regularly, gets their immunizations (flu yearly/pneumo q5yrs), has a healthy diet (low-fat). Be sure the pt knows all the info around the meds they take to control the disease, how to maintain bone health if on long term steroid therapy (use calcium/vit D), knows how to get a cancer screening (this may happen w/ SLE).

47
Q

Name some tumor related oncologic crises.

A

Spinal cord compression, superior vena cava syndrome, leukostasis

48
Q

Name some therapy related oncologic crises.

A

Heart, lung, liver, GI/GU, sepsis, tumor lysis syndrome, hypercalcemia

49
Q

What happens when there is a tumor in the vertebral column of the spinal cord?

A

Tumor causes edema and ischemia to the spinal cord from build of up pressure in vertebral column

50
Q

Define superior vena cava syndrome.

A

An obstruction of blood flow through SVC that results in impaired venous drainage and venous engorgement

51
Q

Define leukostasis.

A

An obstruction of blood flow in microvasculature caused by leukocyte microthrombi. WBC are at least 50,000 if they’re >100 this is bad.

52
Q

Define tumor lysis syndrome. Tx?

A

A syndrome of abnormal accumulation of electrolytes (hyperuricemia, hyperphosphatemia, hyperkalemia, hypocalcemia) due to destruction of tumor cells which go into the circulation at a rate that exceeds that kidney’s ability to excrete them. Tx: hydration and loop diuretics, allopurinol and rasburicase (both antigout meds to protect kidney), dialysis

53
Q

What are some system specific complications of tumors?

A

Full body toxicities: heart, lungs, liver, intestines, bladder

High Acuity Final Exam (2 decks)

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