1.3a Immune Flashcards
1
Q
External Factors:
A
External Factors:
nutritional status, chemical exposure, UV radiation, and environmental Pollution
2
Q
Internal Factors:
A
Internal Factors:
Genetics, functioning of neurological and endocrine systems, chronic illnesses, variations on our anatomy and physiology
Increased morbidity and mortality related to infections
Increase in cancer and autoimmune disorders
3
Q
The Patient with H I V Infection
what is it
A
Human immunodeficiency virus (H I V)
Progresses to acquired immunodeficiency syndrome (AIDS)
Final, fatal stage of H I V
Retrovirus
Spread by direct contact with infected blood and body fluids
Blood, semen, vaginal secretions, cerebrospinal fluid
Not spread by casual contact
4
Q
The Patient with H I V Infection
Behavioral risk factors
A
Behavioral risk factors Unprotected anal intercourse Heterosexual intercourse Injection drug use Needle and paraphernalia sharing Small occupational risk of health care providers
5
Q
Manifestations of H I V
A
May be overlooked by healthcare providers Delay in care and treatment Asymptomatic to severe immunodeficiency Multiple opportunistic infections Fever Sore throat Malaise Arthralgias and myalgias Headache Rash
6
Q
Manifestations of AIDS
A
H I V progresses to AIDS CD4-T cell count <200 mcL General malaise Fever Fatigue Night sweats Involuntary weight loss Skin dryness, rashes, diarrhea, oral lesions (hairy leukoplakia, candidiasis, gingival inflammation and ulcerations)
7
Q
Neurologic Effects of H I V
HAND
A
H I V-associated neurocognitive disorders (H A N D)
Complex neurologic manifestations of H I V
Motor function and cognitive function affected
8
Q
Neurologic Effects of H I V
A
Inflammatory, demyelinating, degenerative changes
9
Q
Neurologic Effects of H I V
HAD
A
H I V-associated dementia (H A D; formerly AIDS dementia complex) Late complication of H I V Fluctuating memory loss Confusion Apathy (lack motivation to do anything or just don't care about what's going on around you) Diminished motor speed Lethargy Difficulty concentrating
10
Q
Opportunistic Infections Associated with H I V
A
Most common manifestations of AIDS
Risk predictable by C D4 T-cell count
<200/m c L opportunistic infections and cancer likely
11
Q
Opportunistic Infections Associated with H I V
Most common
A
Pneumocystis pneumonia (serious infection caused by the fungus Pneumocystis jirovecii. Most people who get PCP have a medical condition that weakens their immune system, like HIV/AIDS, or take medicines (such as corticosteroids) that lower the body's ability to fight germs and sickness.) Most common opportunistic infection
12
Q
Opportunistic Infections Associated with H I V
Tuberculosis
A
Tuberculosis
Reactivation of prior infection
Leading cause of death among those with H I V
13
Q
Opportunistic Infections Associated with H I V
Other
A
Other infections
Toxoplasma gondii
Cryptococcus neoformans
Candida albicans
14
Q
Secondary Cancers to H I V Kaposi Sarcoma (K S)
A
Kaposi Sarcoma (K S)
Seen in fewer than 1% of patients with H I V due to antiretroviral therapy (A R T)
Herpes virus transmitted through sexual contact
Vascular macules, papules, or violet lesions
15
Q
Secondary Cancers to H I V
Lymphomas
A
Lymphomas
Malignancies of lymphoid tissue
Late manifestation of H I V
16
Q
Secondary Cancers to H I V
Cervical Cancer
A
Cervical Cancer
Frequently develops in women with H I V
Pap smear every 6 months
17
Q
Other Conditions Associated with H I V/AIDS
Cardiovascular
A
Cardiovascular complications
Coronary heart disease
Dyslipidemia
18
Q
Other Conditions Associated with H I V/AIDS
Hepatic
A
Hepatic complications
90% of patients with H I V are also infected with H B V
A R T may have negative affects on liver
19
Q
Other Conditions Associated with H I V/AIDS
nephropathy
A
H I V - a s s o c i a t e d nephropathy
Disproportionately affects African-Americans and Hispanic/Latinos
Excessive protein in urine, nitrogen in blood
Glomerular lesions
20
Q
Diagnosis of H I V
H I V rapid antibody test
A
H I V rapid antibody test: finger prick used to provide blood sample for antigen test strip; turns color if positive antibody present and takes <30 minutes.
21
Q
Diagnosis of H I V
Enzyme-linked immunosorbent assay (E L I S A)
A
Enzyme-linked immunosorbent assay (E L I S A): Most common screen test. Only detects antibodies, not virus. Can have false negative if done prior to 13 weeks from infection
22
Q
Diagnosis of H I V
Western blot antibody testing
A
Western blot antibody testing: Blood serum mixed with HIV proteins to detect antibody/antigen reaction. 99.9% sensitive if done with ELISA test
23
Q
Diagnosis of H I V
viral load testing
A
H I V viral load testing: Measures amount of active replicating HIV. Correlates with disease progression/treatment effectiveness
24
Q
Diagnosis of H I V
C B C
A
C B C: checks for anemia, leukopenia, and thrombocytopenia
25
Diagnosis of H I V
| Absolute C D4 lymphocyte count
Absolute C D4 lymphocyte count: Most widely used test to monitor disease progress and guide therapy. AIDS defined as CD4 cell counts <200/mm3 or CD4 lymphocytes <14% regardless of an opportunistic infections present.
26
Diagnosis of H I V
| H I V drug-resistance testing
H I V drug-resistance testing: Test to determine the sensitivity or resistance of virus in relation to current medication regimen.
27
CDC Recommendations Recommendations for Testing
Voluntary and confidential
Should involve counseling
All Healthcare settings should provide routine, voluntary screening for HIV
STI and TB treatment should include HIV screening
Patients and prospective partners should be tested prior to new sexual relationships
Annual HIV screening should be performed annually for high risk individuals
28
Medications for Treatment of H I V
| ART
Antiretroviral therapy (A R T)
Expensive
Wholesale between $1931 and $3057 for a 30-day supply
Not including drugs for opportunistic infections/complications
Goals: suppress infection, provide prophylaxis of opportunistic infections, and decrease symptoms and prolonging life.
29
Medications for Treatment of H I V
Combination therapy
| Three or more drugs from at least 2 different classes
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Medications for Treatment of H I V
| Nucleoside Reverse Transcriptase Inhibitors (N R T I)
Nucleoside Reverse Transcriptase Inhibitors (N R T I)
Mainstay of A R T
Inhibits action of viral reverse transcriptase
Acts as chemical decoy, preventing RNA from being copied to DNA.
Nursing: allergic reaction, nausea, headache, peripheral neuropathy, anemia, neutropenia, assess CBC/Chemistry for liver and pancreas involvement.
31
Medications for Treatment of H I V
| Protease inhibitor
Protease inhibitor
Block function of protease
Combined with other drugs, may be effective in eliminating virus
Nursing: Assess for liver and cardiovascular disease and Diabetes, lipodystrophy, creatinine clearance and flank pain, Nausea, intestinal distress, headache, periph. neuropathy common
32
Medications for Treatment of H I V
| Nonnucleoside Reverse Transcriptase Inhibitors (N N R T I)
Nonnucleoside Reverse Transcriptase Inhibitors (N N R T I)
High incidence of cross-resistance to N R T I s, Only one used at a time, Risk for liver toxicity
Nursing: Assess for hx liver disease, PO, assess for skin rash, kidney function, anemia, and liver function.
33
Medications for Treatment of H I V
| Entry Inhibitors
Entry Inhibitors
Prevention of viral entry into host cells
Injection 2x daily, expensive, candidate if resistant to ART
Nursing: Respiratory infection risk, cough, fever, URI, abdominal pain, dizzy, rash
34
Medications for Treatment of H I V
| H I V integrase Strand Transfer Inhibitor
H I V integrase Strand Transfer Inhibitor
Targets enzyme that integrates viral genetic material into human D N A
Approved for patients resistance to ART
Nursing: nausea, diarrhea, and headache
35
Medications for Treatment of H I V
| Adherence
Patient adherence most important factor
Interruptions in A R T correlate with rapid viral load increases
Increased risk for rapid disease progression
Referral to H I V/AIDS specialist recommended
36
HIV Nutritional Guidelines
Poor Food Preparation and Storage can make people sick
Wash hands before and after prepping food and clean workspaces
Rinse fruits and veggies with clean water
Thaw out foods in refrigerator and not at room temperature
Cook meats well done (165-212 degrees)
Do not eat raw, soft-boiled or over easy eggs
No sushi, raw meats, or unpasteurized milk or dairy products
Refrigerate leftovers and throw out food refrigerated more than 3 days
37
HIV Nutritional Guidelines
| Weight
Patients with HIV may have trouble maintaining weight related to their disease or medications causing reduced appetite, poor tasting food, poor absorption, mouth sores, nausea, vomiting, and fatigue.
To maintain weight: add more protein (meats, fish, beans, dairy products, nuts) and calories (fats and carbs: butter, sour cream, cheese, avacodos, breads, oatmeal, pasta, potatoes and rice)
38
Interprofessional Care of the Patient with H I V
| Goals of Care
Goals of Care:
Early identification of infection and treatment
Promotion of health maintenance
Prevention of opportunistic infections
Treatment of disease complications
Provide emotional and psychosocial support
39
The Patient with Leukemia
Ratio of red to white blood cells is reversed.
normal ratio is 1 WBC for every 600-700 RBC
Characteristics
Replacement of bone marrow by malignant immature W B C s
Abnormal immature circulating W B C s
Infiltration of these cells into the liver, spleen, and lymph nodes
40
Physiology Review
Myeloblasts
**DO NOT NEED TO MEMORIZE
Myeloblasts
Granular leukocytes (granulocytes)
Neutrophils- most numerous, phagocytes, first to arrive at injured tissue
Eosinophils- allergic response and parasitic infections
Basophils- inflammatory response (histamine release)
41
Physiology Review
Monoblasts
**DO NOT NEED TO MEMORIZE
Monoblasts
Monocytes- phagocytic cells, dispose of foreign and waste material
Macrophages- phagocytic cells, dispose of foreign and waste material
42
Physiology Review
Lymphoblasts
**DO NOT NEED TO MEMORIZE
Lymphoblasts
Lymphocytes- smallest WBCs, important piece of immune system
B cells- humoral response and antibody production
T cells- Part of cell-mediated immune response
43
Pathophysiology of Leukemia
Leukemia begins with malignant transformation of a single stem cell that multiplies slowly and differentiates abnormally.
Cells do not function as mature WBC’s and are ineffective in the inflammatory and immune responses
Leukemia results in severe anemia, infection, and bleeding
Fatal without treatment
44
Manifestations of Leukemia
The general manifestations of leukemia, regardless of type, results from anemia, infection, and bleeding
Anemia: pallor, fatigue, tachycardia, malaise, lethargy, and dyspnea on exertion
Infection: fever, night sweats, oral ulcerations, and frequent or recurrent respiratory, urinary, integumentary, or other infections.
Bleeding: bruising, petechiae, bleeding gums, and bleeding within specific organs or tissues
45
Classifications of Leukemia
| Major types
Acute lymphoblastic leukemia (A L L)
Chronic lymphocytic leukemia (C L L)
Acute myeloid (myeloblastic) leukemia (A M L)
Chronic myeloid leukemia (C M L)
46
Classifications of Leukemia
| Acute lymphoblastic leukemia (A L L)
Acute lymphoblastic leukemia (A L L)
Malignant transformation of B cells, rapid onset, most common in children/young adults
Immature cells
47
Classifications of Leukemia
| Chronic lymphocytic leukemia (C L L)
Chronic lymphocytic leukemia (C L L)
Proliferation/accumulation of small, abnormal, mature lymphocytes in bone marrow, peripheral blood, body tissues
Gradual onset
48
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Classifications of Leukemia
Acute myeloid (myeloblastic) leukemia (A M L)
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Acute myeloid (myeloblastic) leukemia (A M L)
Uncontrolled proliferation of myeloblasts and hyperplasia of bone marrow/spleen
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49
Classifications of Leukemia
| Chronic myeloid leukemia (C M L)
Chronic myeloid leukemia (C M L)
| Abnormal proliferation of all bone marrow elements
50
Incidence of Leukemia
Diagnosed 10 times more often in adults than in children
Highest incidence in the United States, Canada, Sweden, New Zealand
Men affected more frequently
Unknown cause
51
Risk factors of Leukemia
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Risk factors
Cigarette smoking
Chemicals such as benzene
Exposure to ionizing radiation
Down's syndrome higher risk
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52
Leukemia Diagnosis
C B C with differential
Evaluates cell counts, hemoglobin and hematocrit levels, and the number, distribution, and morphology (size and shape) of WBC’s
Platelets
Identifies thrombocytopenia secondary to leukemia and the risk of bleeding
Bone marrow examination
Provides information about cells within the marrow, type of erythropoiesis, and maturity or erythropoietic and leukopoietic cells
53
Leukemia Treatment and Therapy
Chemotherapy
Single or combination chemotherapy
Radiation therapy
Damages cellular D N A so that cell cannot divide, multiply
Bone marrow transplant (B M T)
Often used in conjunction with or following chemotherapy or radiation
Allogenic (donor) or Autologous (patient's own)
54
The Patient with Malignant Lymphoma
Hodgkin Disease- Reed-Sternberg Cells; most curable cancer
Non-Hodgkin Lymphoma- T-Cells, B-Cells, or macrophages; more common than Hodgkin Disease
Malignancies of lymphoid tissue
Characterized by proliferation of lymphocytes, histocytes, and precursors or derivatives
55
Manifestations of Malignant Lymphoma
| Hodgkin Lymphoma
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Hodgkin Lymphoma
Manifestations
Painlessly enlarged lymph nodes in cervical or subclavicular region
Persistent fever
Night sweats
Fatigue, malaise
Weight loss
Pruritus
Anemia
Enlarged spleen
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56
Manifestations of Malignant Lymphoma
| Non-Hodgkin Lymphoma
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Non-Hodgkin Lymphoma
Manifestations
Painless lymphadenopathy localized or widespread
Persistent fever
Night sweats
Fatigue, malaise
Weight loss
Abdominal pain, nausea, vomiting
Headaches
Altered Mental Status
Seizures
CNS involvement
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57
Pathophysiology
| Hodgkin lymphoma
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Hodgkin lymphoma
Develops in a single lymph node or chain of nodes, spreads to adjoining cells
Reed-Steinberg cells
Immune system impairment
Etiology unknown
Contributing factors
Epstein-Barr virus
Genetic factors
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58
Pathophysiology
| Non-Hodgkin lymphoma
Non-Hodgkin lymphoma
Does not contain Reed-Steinberg cells
Etiology unknown
Viral infections can play a role, EBV and HIV, genetics
Manifestations
Early, similar to Hodgkin disease
Fever, night sweats, fatigue, and weight loss are less common
59
Course of Lymphoma
| Stages 1-4
Disease Staging
Stage I: Involvement of a single lymph node region or lymphoid structure
Stage II: Involvement of two or more lymph node regions on the same side of the diaphragm
Stage III: Involvement of lymph node regions or structures on both sides of the diaphragm
Stage IV: Involvement of an extranodal site
60
Course of Lymphoma
| Prognosis
Prognosis determined by
Stage of disease
Presence of systemic manifestations
Factors such as age
Prognosis good when localized to one or two node regions
Anemia, thrombocytopenia, and older age reduce likelihood of cure
61
Treatment of Lymphoma
Chemotherapy
Followed by radiation therapy
Choice of drug combination depends on patient's age, stage of disease
Immunotherapy
Rituximab
Alone or with cyclophosphamide, vincristine, and prednisone (C V P)
Radiation therapy
May be primary treatment for early-stage Hodgkin
Stem cell transplant
Autologous peripheral blood stem cell transplant (P B S C T)
Complications of treatment
Permanent sterility
Secondary cancer a late adverse effect
62
The Patient with Multiple Myeloma
| what is it
Malignancy in which plasma cells multiply uncontrollably
63
The Patient with Multiple Myeloma
| Pathophysiology
Pathophysiology
Cells infiltrate bone marrow, lymph nodes, and spleen
Affected bones are weakened
Pathologic fractures
64
The Patient with Multiple Myeloma
| Incidence and Risk Factors
Incidence and Risk Factors:
Affects African Americans nearly twice as often as Caucasian Americans, men more than women
Unknown cause
65
Manifestations of Multiple Myeloma
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Bone pain
Rapid bone destruction
Hypercalcemia
Manifestations of neurologic dysfunction
Recurrent infections
Renal failure- Bence Jones Protein
Pancytopenia (low blood count for all three types of blood cells)
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66
Diagnosis and Staging of Multiple Myeloma
X-rays: reveal ”punched out” lesions in bones
Bone marrow examination: ↑ immature plasma cells
C B C: anemia with ↑ ESR
Protein electrophoresis: ↑ IgG antibody
Serum calcium, creatinine, uric acid, and B U N levels: all are often elevated
Urinalysis: Bence Jones Protein
Biopsy of myeloma lesions confirms diagnosis
67
Diagnosis and Staging of Multiple Myeloma
| Based on?
Staging: Based on hemoglobin, serum calcium levels, amount of abnormal protein present, and degree of bone involvement
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Treatment of Multiple Myeloma
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No cure
Induction chemotherapy
Stem cell transplant
Maintenance chemotherapy
Combination chemotherapy
Localized radiation therapy
Plasma exchange therapy
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