Download NURS 5315 UTA Exam 2 Questions with Solution and more Exams Nursing in PDF only on Docsity!
NURS 5315 UTA Exam 2 Questions with Solution
1. HIV EIA (3rd generation immunoassay): can use urine, saliva, or serum (most accurate), need to wait until 12
weeks post exposure to see antibodies, >99% accurate 4th generation immunoassay- "gold standard" measures P24 antigen can test 10 days post exposure
2. Mast cell: Cellular bags of granules located in loose connective tisssue close to blood vessels. Activation initiates
inflammatory process.
3. Histamine: Causes vasodilation, increases vascular permeability, increases blood flow to the site of injury-
causes erythema and swelling.
4. Cytokines: Soluble factors that contribute to the regulation of innate or adaptive resistance by affecting other
neighboring cells. Can be pro-inflammatory or anti-in- flammatory. Can react quickly or be more delayed.
5. Leukotrienes: Released when mast cells degranulate, prolong the inflammatory process. Cause vasodilation, attract
neutrophils, monocytes, and eosinophils. Target of inhibition for singular.
6. Prostaglandins: Released when mast cells degranulate, are produced by the arachidonic pathway. Cause
vasodilation, platelet aggregation at site of injury, pain, and fever.
7. Chemotactic factors: Biochemical substance that attracts leukocyte to the site of inflammation
8. Neutrophils: Predominant leukocyte at work during the early stages of acute inflammation
9. Monocytes: Become macrophages when entering the tissue, responsible for pre- senting antigens to the CD4 cell
which triggers T-cell immunity and B-cell immunity. Releases additional cytokines IL1, IL6, TNF.
10. Cytokine IL1 function: Causes fever, activates phagocytes & lymphocytes and also increases the release of IL6a
11. Cytokine IL6 function: Stimulates production of acute phase reactants and promotes growth and stimulation
of RBCs
12. Cytokine TNF function: Causes fever, increases synthesis of proinflammatory proteins by liver, causes muscle
wasting, induces thrombosis
13. Cytokine growth factor function: Promotes production and maturation of neu- trophils
14. Complement: Functions include bacterial lysis, vasodilation and increased vas- cular permeability, triggers mast
cell degranulation, chemotaxis, and opsonization.
15. Kinin: Converted to bradykinin which is responsible for pain and chemotaxis, and it increases vascular
permeability and vasodilation.
16. Coagulation cascade: Factor XII activates kinin. Function is to form fibrin mesh to stop bleeding and trap micro
organisms.
17. COX1: Prostaglandin of arachidonic pathway. Provides gastroprotection, platelet aggregation, fluid/electrolyte
balance
18. COX2: Prostaglandin of arachidonic pathway. Responsible for pain, fever, renal protection, tissue repair,
reproduction development.
19. COX2 inhibitors- clinical implications: Protect gastric mucosa- prevent ulcers and bleeding. Removed from
market r/t cardiac events except for Celebrex. Can impair renal function , monitor labs.
20. Arachidonic pathway purpose: Synthesis of prostaglandins
21. Non-selective NSAIDS: Inhibit COX1 and COX2, risk for gastric ulceration, GI bleeds, edema, renal impairment
receptors and inhibit synaptic transmission of acetylcholine. Leads to muscle weak- ness and paralysis (mind to ground) Guillain-Barre' syndrome- antibodies bind with myelin sheath of the peripheral nervous system, triggering the immune response. Causes demyelination of the peripheral nerves and a rapidly progressive, ascending paralysis (ground to brain)
31. Type III hypersensitivity: Widespread immune and inflammatory response not specified for any cell or tissue.
SLE, RA
Antibodies are formed against and bind to circulating antigens, antigen-antibody complex deposits in vessel walls or tissue. Causes cellular and tissue damage. IgG and IgM response, spread via circulation- not specific to a cell or tissue- widespread damage.
32. Type IV hypersensitivity: T-cell lymphocyte mediated reaction that does not require antibody activation.
Delayed response- 24-72 hours. Contact dermatitis- poison ivy, topical drugs, chemicals such as nickel or formalde- hyde. Antigens too small to cause a reaction bind to proteins, response includes rash, red bumps, itching, and blisters. Reactive tuberculin test- PPD cause and induration in 24-72 if person was previously exposed to tuberculin antigen Solid organ transplant rejection- 11-14 days after 1st exposure, 5-6 days after 2nd exposure, results in mononuclear infiltration, decreased circulation, and tissue necrosis.
33. Systemic Lupus Erythematosus: E. Primarily women aged 20-40, Type III hypersensitivity. Antibodies are
formed against DNA Genetic, leads to tissue damage. Exacerbated by infections, UV light, estrogen, meds, stress Diagnosed by serum ANA C.M. Butterfly rash (cheeks), photosensitivity, nonerosive arthritis of at least 2 periph- eral joints, inflammation of serous sacs, proteinuria, seizures, anemia, leukopenia, thrombocytopenia
34. Rheumatoid Arthritis: E. Primarily women 30-50, systemic autoimmune dis- ease
Progressive, irreversible leads to deformity and disability Tx includes PT, NSAIDS,
corticosteroids C.M. Joint inflammation, pain, destruction of synovial membrane, widespread sym- metrical joint swelling, erythema joints warm to touch, loss of function, morning stiffness- improves with movement, weight loss, weakness, anorexia
35. -Osis or -philia: Elevated count of blood cells
36. -penia: Low count of blood cells
37. Leukocytosis: Increase in number of total WBC
38. Leukopenia: Decrease in number of total WBC
39. Neutrophilia- definition and causes: Elevated neutrophil count From bacterial infections,
inflammation, and necrotic tissue
40. Neutropenia- definition and causes: Decreased # of neutrophils From liver disease, viral
infections, drugs
41. Eosinophilia- definition and causes: Increased # of eosinophils From allergic reactions and
parasitic infections
42. Eosinopenia- definition and causes: Decreased # of eosinophils From pancytopenia and steroid
use
43. Basophilia- definition and causes: Increased # of basophils From allergic reactions
44. Monocytosis- definition and causes: Increased # of monocytes From TB infection or during
recovery from an infection
45. Monocytopenia- definition and causes: Decreased # of monocytes From steroid use of HIV
52. Discuss some clinical implications of solid organ transplant rejection: - rejection is an immune response,
mostly T-cell mediated. Slow process, Type 4 hypersensitivity Patients are highly susceptible to infections r/t use of immunosuppressants
53. Describe the role of HLA in solid organ rejections: HLA is typed and matched on donor and recipient to decrease
risk of rejection HLA is targeted response for rejection
54. clinical manifestations of influenza: fever, sore throat, myalgias, headache, nasal discharge, weakness and severe
fatigue, cough and other respiratory symp- toms, tachycardia, red, watery eyes, pharyngitis
55. clinical implications of influenza: prevention is key- vaccinate at 6+ months, annual
diagnosed by rapid swab treat with antivirals- Tamiflu
56. clinical manifestations of measles: fever >104, lasts 4-7 days, malaise, anorexia, 3c's- conjunctivitis, cough,
coryza (inflammation of mucous membrane of nose), photophobia, periorbital edema, myalgias, Koplik spots (bluish- gray specks on red base, on buccal mucosa), rash- begins at hairline, spreads in 48 hours
57. Clinical implications of measeles: One of most contagious infectious dis- eases, lasts 7-10 days
Educate parents on importance of vaccination Immune globulin can be administered within 6 days of exposure Can be fatal for HIV patients Immunocompromised may have no rash Need serologic testing per CDC Tx is supportive- rehydration, Vit A
58. Antiretroviral medications: Used to impede viral replication of HIV virus, come in 6 classes
1. Nucleoside reverse transcriptase inhibitors
2. Non-nucleoside reverse transcriptase inhibitors
3. Protease inhibitors
4. CCR5 inhibitors- inhibits binding to CCR
5. Fusion inhibitor- inhibits fusion between HIV and cell membrane
6. Integrate inhibitor- inhibits viral integrate enzyme
59. Effects of genetic mutation of CCR5 cell receptor: Some people of European descent carry the CCR5 delta
mutation. The mutation makes a person functionally resistant to the HIV virus, and might be a cure for those individuals
60. Describe the difference between HIV and AIDS, and clinical implications-
: CD4 count >200 is HIV, If the CD4 count drops below 200 and an AIDS defining illness occurs then the patient is said to have AIDS. Once they have progressed, they will always have AIDS, even if CD4 count goes up. AIDS defining illnesses: PCP, toxoplasmosis, progressive multi focal leukoen- cephalopathy, disseminated MAC, Kaposki's sarcoma, lymphoma, TB, esophageal or tracheal candida infection, invasive cervical cancer, CMV infection, and histoplas- mosis
61. What are CM that indicate a compromised immune system in a person with HIV: Thrush, cervical dysphasia,
cervical carcinoma in situ, fever of 38.5 (101.3) or greater X 1 month, oral hairy leukoplakia, herpes zoster, immune thrombocytopenia purpura (ITP), PID, peripheral neuropathy, vaginal yeast infections, Kaposi sarcoma, presence of any opportunistic infections. Should be treated with prophylactic antibiotics
62. HIV EIA: 3rd generation immunoassay, can use urine, saliva, or serum (best),
99% accuracy
DIC
71. give CM and example of thrombocytopenia hemorrhage: CM- mucosal bleeding, epistaxis, GI or GU
bleed, oral bleeding, hemoptysis, heavy menses, immediate bleeding after trauma, possible petechiae ITP
72. what are causes of thrombocytopenia: post-op hemodilution (nadir 2-4 days), splenomegaly, HIV, bone marrow
failure, hemolysis, multiple medications
73. Primary Immune Thrombocytopenic Purpura- patho and CM: immune me- diated destruction of platelets-
primary or secondary (caused by another etiology) CM- petechiae, purpura, easy bruising, epistaxis, gingival bleeding, menorrhagia CM vary with age- worse in elderly
74. Heparin Induced Thrombocytopenia- patho and CM: immune system de- struction of platelets initiated by
heparin Type 1- mild, 2 days post heparin admin, return to normal with continued adminis- tration Type 2- severe, drug reaction which destroys platelets risks- female, heparin use > 1 week, post-op thromboprophylaxis CM0 unexplained drop in platelets 5-10 days post admin (can be up to 2 weeks post), some will have rapid onset
75. discuss hemophilia A: affects 1 in 5-10K males sex linked recessive
disease, deficient in factor VIII normal platelets and PT, prolonged PTT, decreased factor VIII CM: knee, elbow, and ankle bleeds, GI bleeds
76. discuss hemophilia B: affects 1 in 20-30K males Christmas disease-
deficient in factor IX normal platelets and PT, prolonged PTT, decreased factor IX CM: knee, elbow, and ankle bleeds, GI bleeds
77. discuss DIC: activation of the coagulation system causes widespread intravas- cular fibrin deposition, fibrinolytic
products attempt to break down fibrin- adhere to platelets to prevent adhesion. coagulation products are eventually consumed and bleeding occurs. may cause organ failure r/t micro-thrombi triggers: malignancy, sepsis, infection, ob complications, trauma, Sx, ARDS, rhabdo, venomous snake bites CM: oozing, bleeding from all puncture sites, bleeds from all body cavities, prolonged PT/PTT, elevated d-dimer, platelet count <100,
78. discuss Vitamin K deficiency: CM: easy bruising, oozing from nose or gums, excessive wound bleeding,
menorrhagia
79. discuss liver disease: all factors of clotting can be affected
80. Hageman deficiency: deficiency of factor XII- rare genetic disorder asymptomatic, causes prolonged clotting test
with no clinical bleeding or risk present
81. causes of thrombus: Triad of Virchow- injury to blood vessels, abnormality in blood flow, hypercoagulability
some medications increase risks
82. discuss macrocytic, microcytic, and normocytic anemias: classified by size of RBC
macrolytic- MCV >100, includes pernicious and folic acid anemias, can be caused by ETOH microlytic- MCV <80, folic acid anemia normolytic- MCV 80-100 (normal range), sickle cell is an example
83. Pathophysiology and clinical implications of pernicious anemia: A Vitamin B12 deficient leads to fewer RBCs-
intrinsic factor is lacking- RBCs get big, but not mature Macrocytic Typical at age 60 as 10 years of B12 is stored in body
84. Risk factors and CM of pernicious anemia: Risk: vegan, gastrectomy, atrophy of gastric mucosa r/t autoimmune
disease
92. Define acute leukemia: Rapid onset- aggressive accumulation of immature cells, causes overproduction of
leukocytes by the bone marrow, causes overcrowd- ing, prevents formation of normal blood cells
93. Chronic leukemia: Gradual onset, cells appear normal but do not function appropriately and accumulate
94. Lymphocytic leukemia: Excessive production of lymphocytes
95. Myelogenous leukemia: Excessive production of granulocytes
96. Multiple myeloma pathophysiology and CM: Chromosomal abnormality that leads to production of malignant
plasma cells, cells secrete antibodies which are deposited in organs (mostly bones) and grow malignant tumors, 3 yr life span Vertebrae, skull, ribs and pelvis most frequently affected CM: hypercalcemia, recurrent infections, renal failure
97. Risk factors for multiple myeloma: African descent Males more common
Around 6th decade of life
98. Etiology and pathophysiology of Hodgkin's Lymphoma: Malignant neo- plasms of cells called
99. CM of Hodgkin's Lymphoma: Large painless lump/mass- usually on neck, eosinophilia, fever, weight loss, night
sweats, pruritus, adenopathy, thrombocytosis, leukocytosis, mediastinal or abdominal mass
100. Epidemiology of Hodgkin's Lymphoma: Possibly Epstein Barr, unknown
101. Etiology and Epidemiology of Non-Hodgkin's Lymphoma: Malignant trans- formation of lymphocytes, no
Reed-Sternberg cells Caused by immunosuppression, AIDS, Hep C, EBV, post transplantation
102. CM of Non-Hodgkin's Lymphoma: Generalized lymphadenopathy Late stages bring fever, night
sweats, weight loss
103. Acute Lymphocytic Leukemia (ALL): Marked by >30% lymphoblasts in blood or marrow
Most common in children Survival rate decreases with age CM: fever, pallor, bleeding, fatigue, lymphadenopathy, infection, joint pain, splenomegaly, hepatomegaly, night sweats, weight loss, anemia, thrombocytopenia, petechiae, ecchymosis
104. Acute Myelogenous Leukemia (AML): Marked by proliferation of immature myeloid cells, decreased
apoptosis, and lack of cellular differentiation Most common in adults Remission is inversely related to age CM: fever, pallor, bleeding, fatigue, lymphadenopathy, infection, joint pain, splenomegaly, hepatomegaly, night sweats, weight loss, anemia, thrombocytopenia, petechiae, ecchymosis
105. Chronic Lymphocytic Leukemia (CLL): Malignant transformation of B-lym- phocytes
Increased occurrence over 40 Survival 10yrs or longer CM: suppression of humoral immunity, increased infections
106. Chronic Myelogenous Leukemia (CML): Presence of Philadelphia chromo- some
Increased occurrence over 40 Bone marrow transplant may be curative CM: splenomegal (most common), hepatomegaly, hyperuricemia, infection, fever, weight loss
