Immune system Flashcards

1
Q

the immune system (what, involves, ______ & ______ critical to maintaining health and preventing disease)

A
  • the body’s defense mechanism against invasion and allows a rapid response to foreign substances in a specific manner
  • involves: inflammation, immunity to work w/ other defenses in providing protection from harmful microorganisms and cells
  • inflammation and immunity are critical to maintaining health and preventing ds.

TIP: immune system involves (nervous, GI, endocrine)

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2
Q

immunocompetent

A
  • when all the different parts and functions of inflammation and immunity are working well, giving the individual maximum protection against infection
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3
Q

2 types of immunity

A

1) natural (innate): non specific immunity, present at birth
- first line of hose defense following antigen exposure, because it protects the host without remembering prior contact with an infectious agent

2) acquired (adaptive): specific immunity, develops after birth
- usually develops as a result of prior exposure to an antigen through immunization (vaccination) or by contracting a disease

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4
Q

natural immunity (innate immunity) (what, immunity, mechanism of action, includes 5)

A
  • AKA inflammation
  • provides immediate protection (short term) against the effects of tissue injury and invading foreign proteins
  • innate-native immunity: natural protective feature of a person
  • barrier to prevent organisms from entering the body OR can be an attacking force that eliminates organisms that have already entered the body
  • includes: skin, mucosa, cilia of respiratory tract (cough, sneeze), acidic gastric secretions (enzymes -> destroys invading organisms), antimicrobial chemicals on the skin (barrier)

TIP:
- burn to hand, bacteria middle ear -> inflammation -> how severe/intense depends on level of exposure

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5
Q

acquired (adaptive) immunity (what, responses are, type (2))

A
  • internal protection that results in long-term resistance to the effects of invading microorganisms
  • responses are not automatic, body has to learn to generate specific immune responses when it is infected by or exposed to specific organisms (may take wks -> months)
  • types:
    1) active acquired immunity: immunologic defenses developed by the person’s own body
    2) passive acquired immunity: temporary immunity transmitted from a source outside the body that has developed immunity through previous disease or immunization (transfer antibiotics mother -> infant (womb, breastfed, IG injections)
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6
Q

review: IgG (appears, role, etc.)

A
  • appears: serum, tissues (interstitial fluid)
  • major role: bloodborne and tissue infections
  • activates complement system
  • enhances phagocytosis
  • crosses PLACENTA
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7
Q

review: IgA (appears, what (3))

A
  • appears: bodily fluids (blood, saliva, tears, breast milk, pulmonary/GI/prostatic/vaginal)
  • protects against respiratory, GI, GU infections
  • prevents absorption of antigens from food
  • passes to neonate in breast milk for protection
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8
Q

review: IgM (appears, what)

A
  • appears: intravascular system
  • appears: first immunoglobulin produced in response to bacterial/viral infections
  • activates complement system
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9
Q

review: IgD (appears, what)

A
  • appears: small amounts in serum
  • possibly influences B-lymphocyte differentiation, role is UNCLEAR
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10
Q

review: IgE (appears, what)

A
  • appears: serum
  • takes part in ALLERGIC, some hypersensitivity reactions
  • combats PARASITIC infections
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11
Q

autoimmunity (what, _______ directed against ______, mgmt, pharm)

A
  • process whereby person develops an inappropriate immunity
  • antibodies/lymphocytes are directed against healthy normal cells and tissues (attack on self)
  • mgmt: depends on organ/organs affected, NO CURE
  • anti-inflammatory drugs, immunosuppressive drugs: commonly used along with symptomatic treatment to suppress the excess immunity
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12
Q

immunity changes w/ aging: inflammation (3)

A
  • reduces neutrophil function
  • leukocytosis does NOT occur during acute infection
  • older adults may NOT have a fever during inflammatory or infectious episodes
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13
Q

immunity changes w/ aging: antibody mediated immunity (2)

A
  • total # colony forming B-lymphocytes and ability of these cells to mature into antibody secreting cells are diminished
  • decline in natural antibodies, decreased response to antigens, and reduction in the amount of time the antibody response is maintained
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14
Q

immunity changes w/ aging: cell mediated immunity

A
  • number of circulating T-lymphocytes decreases
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15
Q

Human immune deficiency virus (what, patho, high potency)

A
  • retrovirus transmitted through direct contact with HIV infected body fluids, such as blood, semen, genital secretions, or from HIV infected mother -> child during pregnancy, birth, or breastfeeding, and attacks the body’s immune system
  • patho: HIV has to enter a cell, take over the cell, force the cell into making more copies of the virus (viral particles), these new viral particles then are shed and look for additional cells to infect, repeating the cycle
  • high potency: blood, breast milk, vaginal secretions
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16
Q

physical assessment techniques immune system (neuro, resp, cardio, GI, musck, integument, lymph, V/S)

A
  • neuro: cognitive dysfunction, hearing loss, visual changes, headaches, ataxia, tetany
  • resp: changes in RR, cough, abnormal lung sounds, rhinitis, bronchospasm
  • cardio: hTN, tachycardia, dysrhythmia, vasculitis, anemia
  • GI: hepatosplenomegaly, colitis, vomiting/diarrhea
  • musculoskeletal: joints mobility, edema, pain
  • integumentary: lesions, dermatitis, purpura, urticaria, inflammation, discharge
  • lymph: lymph nodes are palpated for location, size, consistency, tenderness
  • VS: temp. recorded (MAIN), chills/sweating
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17
Q

recommendations for “standard precautions” to prevent spread HIV

A
  • perform hand hygiene
  • wear PPE
  • handle soiled patient care equipment appropriately with gloves
  • follow procedures for environmental control
  • handle textiles and laundry in a manner that prevents transfer
  • handle needs and other sharps appropriately
  • use devices during patient resuscitation
  • prioritize patient placement as needed
  • educate on proper respiratory hygiene and cough etiquette
  • reduce number of sexual partners + abstain from exchanging sexual fluids
  • latex condoms
  • avoid unprotected sex with another HIV seropositive person (cross infection with that person’s HIV can increase severity of the infection)
  • not donate blood, plasma, body organs, or sperm
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18
Q

s/sx acute HIV infection (7)

A
  • fever
  • night sweats
  • chills
  • headache
  • muscle aches
  • sore throat
  • rash

TIP: 4 wks before infection s/sx

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19
Q

stages of HIV (0-3)

A

1) stage 0:
- interval between the appearance of detectable HIV RNA and the first detection of antibodies
- about 40-80% of patients develop clinical symptoms of a nonspecific viral illness (eg. fever, fatigue, rash) lasting 1-2 weeks

2) stage 1: CD4+ t-cell count of greater than 500 cells/mm3 with NO AIDS defining

3) stage 2: CD4+ t-cell between 200-499 cells/mm3 with NO AIDS defining

4) stage 3: CD4+ t-cell count less than 200 cells/mm3 with AIDS DEFINING ILLNESS, or a person who has higher CD4+ t-cell counts but as an AIDS defining illness (severe development of immune diseases (3 year prognosis)
-s/sx: fevers, chills, wt. loss, sweats, lymph glands, weakness
- opportunistic infections

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20
Q

acquired immune deficiency syndrome (AIDS) (what, diagnosis)

A

diagnosis of AIDS requires that the person can be HIV positive and have either:
- CD4 T-cell count of less than 200 cells/mm3
- an opportunistic infection

  • once AIDS is diagnosed, even if the patient’s t cell count goes higher than 200 cells/mm3 of the infection is successfully treated, the aids diagnosis remains tand the patient does not revert to being just HIV positive

TIP:
- disease mortality (60% adults)
- beginning (development takes months -> years, depends on how acquired, other health illness, interventions)

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21
Q

s/sx AIDS (5)

A

1) immunologic manifestations: lymphadenopathy, fatigue
2) integumentary manifestations: dry skin, poor wound healing, skin lesions, night swears
3) respiratory manifestations: cough, SOB
4) GI manifestations: diarrhea, weight loss, N/V
5) CNS manifestations: confusion, dementia, headache, fever, visual changes, memory loss, personality changes, pain, seizures

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22
Q

HIV/AIDS diagnostic labs (5)/tests (0)

A

1) diagnostic labs:
- antibody tests (detects abx, might miss HIV in stage 0)
- antigen/antibody tests (detect HIV)
- nucleic acid (RNA) tests (detect HIV)
- viral load testing (detects presence of HIV viral genetic material/protein)
- CD4+ t-cell count (800-1000, lymphocytes 30-40% diff) (CD4/CD8 = 2:1 ratio)

2) diagnostic tests: NONE

tip:
- blood (faster detection than oral)
- antibodies increased in blood

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23
Q

HIV/AIDS interventions (8)

A

1) prevention is KEY (education)
2) pre-exposure prophylaxis: truvada (emtricitabine, tenofovir) for HIV negative sexual partners of known HIV positive people to reduce HIV transmission
3) highly active antiretroviral therapy (HAART):
- reduces viral load to help reduce transmission
- improves CD4+ t-cell counts and restores immunologic function
- slows disease progression and reduces HIV associated morbidity/mortality
4) screening for adherence:
- every health care encounter should be used as an opportunity to briefly review the treatment regimen, identify any new issues, and reinforce successful behaviors
- lab tests evaluate whether ART is effective for a specific patient
- viral load should be measured at baseline and on a regular basis thereafter because viral load is the most important indicator of response to ART
5) pain mgmt: NSAIDs, Lyrica, TCAs, Neurotin (BAGA), dilantin, opioids
6) enhancing nutrition: high calorie/high protein diet, good mouth care, drink 2-3L fluids per day, appetite stimulants
7) monitor and treat opportunistic infections: know s/sx, self mgmt
8) comfort measures and supportive care: hydrotherapy, massage, heat or cold

tip:
- viral load below level detection (optimal protection)
- RNA (decrease 20-85 copies)
- figure 32.8 + 32.10

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24
Q

monitor for AIDS manifestations and opportunistic infections (resp., gi., oncological)

A

1) respiratory infections:
- pneumocystis jiroveci pneumonia (PCP): SOB, cough, chest pain, fever
- TB: cough, night sweats, wt. loss, hemoptysis

2) GI infections:
- candidasis: oropharyngeal, esophageal painless creamy white plaque like lesions
- HIV wasting syndrome: loss of more than 10% body weight with diarrhea or weakness and fever for more than 30 days

3) oncological:
- kaposi sarcoma: variable course from brownish-pink to deep purple cutaneous lesions to multiple organ system involvement

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25
Q

hypersensitivity/allergy (what, 4 types)

A
  • excessive inflammation occurring in response to the presence of an antigen (foreign protein or allergen) to which the patient usually has been previously exposed (occurs with reexposure)
  • 4 types:
    1) immediate
    2) cytotoxic
    3) immune complex mediated
    4) delayed
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26
Q

hypersensitivity/allergies diagnostic labs (3)/tests

A

diagnostic labs:
- CBC: excess immunity with allergic response (increased eosinophils)
- ELISA for serum IgE: increased with allergies
- skin testing: which allergens are cause, OTC allergy/antihistamines suppress skin tests) - stop 48-90 hours before, most accurate

diagnostic tests: NONE

27
Q

type 1 rapid hypersensitivity reaction (what, common, responsible, reactions occur in, other reactions involve)

A

AKA atopic allergy
- most common type of hypersensitivity from excess immunity
- primary chemical mediators are responsible for the symptoms of type 1 hypersensitivity bc of their effects on the skin, lungs, and GI tract
- some reactions occur just in the areas exposed to the antigen, such as mucous membranes of nose/eyes, causing symptoms of rhinorrhea, sneezing, and itchy red watery eyes
- other reactions may involve all blood vessels and bronchiolar smooth muscle causing widespread blood vessel dilation, decreased cardiac output, and bronchoconstriction

TIP:
- histamine: short acting biochemical
- antigen specific IgE (basophils, mast cells)
- first exposure -> IGE created -> bind to basophils/mast cells -> histamine release -> sensitized to allergen

28
Q

type 1 rapid hypersensitivity reactions examples (4)

A

1) inhaled: plant pollens, fungal spores, animal danger, house dust, grass, ragweed
2) ingested: foods, food additives, drugs
3) injected: bee venom, drugs, biologic substances such as contrast dyes
4) contaced: latex, pollens, foods, environmental proteins

29
Q

allergic rhinitis s/sx (6)

A
  • rhinorrhea: clear/white drainage, nasal mucosa is swollen and pink
  • itchy, watery eyes
  • mouth breathing
  • nasal voice quality
  • headache or sinus pressure
  • dry, scratchy or sore throat
30
Q

interventions for allergic rhinitis (2, pharm (6)

A
  • avoidance therapy
  • desensitization therapy/immunotherapy (steroid/non-steroid to decrease allergic response)

pharmacologic:
- antihistamines
- corticosteroid nasal sprays
- adrenergic agents
- mast cell stabilizers
- steroids
- leukotriene modifiers

31
Q

anaphyaxis (what, affects, common causes)

A

1) most life threatening example of a type 1 hypersensitivity reaction, it occurs rapidly and systemically
- affects many organs within seconds to minutes after allergen exposure (faster onset -> more severe reaction)
2) common causes:
- acute care setting: drugs and dyes
- community setting: food, insect stings/bites

TIP:
- some patients must carry emergency anaphylaxis kit or epinephrine injector (EpiPen) or medical bracelet

32
Q

anaphylaxis s/sx mild (8)

A
  • peripheral tingling
  • sensation of warmth
  • sensation of fullness in the mouth and throat
  • nasal congestion
  • periorbital swelling
  • pruiritis
  • sneezing
  • tearing of the eyes
33
Q

anaphylaxis s/sx moderate (6)

A
  • some mild symptoms + flushing
  • warmth
  • anxiety
  • itching
  • bronchospasm and edema of the airways or larynx with dyspnea
  • cough and wheezing
34
Q

anaphylaxis s/sx severe (12)

A
  • some moderate symptoms + abrupt onset with rapid bronchospasm
  • laryngeal edema
  • severe dyspnea
  • cyanosis
  • hTN
  • dysphagia
  • abdominal cramping
  • vomiting
  • Diarrhea
  • seizures
  • coma
  • cardiac arrest
35
Q

anaphylaxis interventions (8, pharm (5))

A
  • assess ABCs
  • call RRT
  • apply oxygen using high flow non-rebreather mask at 90-100%
  • remove allergen if possible
  • be prepared to administer epinephrine IV or IM (constrict BV, increase cardiac contraction, dilate bronchiols)
  • administer NS
  • position the patient w/ HOB elevated 10-45 degrees and raise feet/leg
  • stay w/ the patient

pharm:
- sympathomimetics (first line): epinephrine
- antihistamines (second line): benedryl
- corticosteroids (oral, low dose post anaphylaxis contracted): decadron, solumedrol, prednisone
- vasopressors: levophed, dopamine
- IV fluids/ volume expanders

TIP:
- most deaths r/t dysrhythmias, shock, CPR r/t treatment delay
- IV med: stop med, DONT remove IV ACCESS

36
Q

type 2 cytotoxic reactions (what, examples (4))

A
  • body makes autoantibodies directed against self cells that have some form of foreign protein attached to them
  • autoantibody binds to self cell and forms an immune complex, the self cell is then destroyed along w/ attached protein

examples:
- immune hemolytic anemias
- immune thrombocytopenic purpura
- hemolytic transfusion reactions
- drug induced hemolytic anemia

37
Q

type 2 cytotoxic reactions interventions (4)

A
  • discontinuing the offending drug or blood product
  • plasmapheresis to remove autoantibodies may be beneficial
  • symptomatic
  • monitor for complications: hemolytic crisis/kidney failure
38
Q

type 3 immune complex reactions (what, trigger, examples)

A
  • excess antigens cause immune complexes to form in the blood that usually lodge in small blood vessel walls of the kidneys, skin, and joints
  • complexes trigger inflammation, and tissue or vessel damage/permeability results

examples:
- rheumatoid arthritis
- systemic lupus erythematosus (SLE)

39
Q

type 3 immune complex reactions s/sx (7)

A
  • fever
  • arthralgia (joint pain)
  • rash
  • malaise (discomfort)
  • lymphadenopathy
  • polyarthritis (multiple joint inflammation)
  • nephritis (inflamed tissue in kidneys, issue filtering waste from blood)
40
Q

type 3 immune complex reactions interventions (what, pharm (3))

A
  • supportive care

pharm:
- antihistamines (itching)
- aspirin (arthralgia)
- prednisone (manifestations are severe)

41
Q

type 4 delayed hypersensitivity reactions (4, examples)

A
  • reactive cell is the T-lymphocyte (t-cell), antibodies and complement are NOT involved
  • sensitized T-cells (from previous exposure) respond to an antigen by releasing chemical mediators and triggering macrophages to destroy the antigen
  • typically occurs 24-48 hours after exposure
  • consists of edema, induration, ischemia, tissue damage at the site

ex:
- positive purified protein derivative (PDD) test for TB
- contact dermatitis
- poison ivy skin rashes
- local response to insect stings
- tissue transplant rejections
- sarcoidosis

42
Q

type 4 delayed hypersensitivity reactions interventions (3, pharm (2))

A
  • removal of the offending antigen is the major focus of mgmt
  • reaction is self limiting in 5-7 days
  • patient is treated symptomatically

pharm:
- diphenhydramine (benedryl): not useful for type 4 reactions d/t histamine NOT main mediator
- corticosteroids: reduce discomfort and help resolve reaction more quickly

tip:
- monitor reaction site (distal-circulation)
- IGE (not type of reaction, desensitization can’t reduce response)

43
Q

transplant rejection (patho)

A
  • natural killer (NK) cells and cytotoxic/cytolytic t-cells destroy cells from other people or animals
  • although this action is normal and usually helpful, it is also responsible for rejection of tissue grafts and transplanted organs (aka grafts)
  • because the solid organ transplanted into the recipient is seldom a perfectly identical match of HLAs between the donated organ and the recipient host, the patient’s immune system cells recognize a newly transplanted organ as non-self
  • without intervention, the recipient’s immune system starts inflammatory and immunologic actions to destroy or eliminate these non-self cells -> causes rejection of the transplanted organ
  • rejection can be hyperacute, acute, or chronic
44
Q

hyperacute reaction (begins, what, s/sx)

A

begins immediately on transplantation and is an antibody mediated response
- antigen/antibody complexes form in the blood vessels of the transplanted organ. widespread clotting occludes blood vessels and leads to ischemic necrosis, massive cellular destruction within the transplanted organ and graft loss
-s/sx: apparent within minutes of attachment, organ becomes mottled/cyanotic, organ fails

tip:
- mostly transplanted kidneys
- risl: received ABO blood type organ, hx of mult. pregnancy, previous transplants, mult. blood transfusions
- transplanted organ needs to be removed immediately

45
Q

acute rejection (what, first mechanism, second mechanism, s/sx, tx.))

A

first occurs within 1 wk to 3 months after transplantation; two mechanisms are responsible
- first mechanism: antibody mediated, results in vasculitis within the transplanted organ
- second mechanism: cellular, recipient cytotoxic t-cells and NK cells enter the transplanted organ and starts an inflammatory response that causes lysis of the organ cells
- s/sx: pain/tenderness of the organ/site, general discomfort, uneasiness, or ill feeling, flu like sx., organ dysfunction
- tx: medication mgmt

46
Q

chronic rejection (what (3, s/sx, tx.)

A

similar to chronic inflammation and scarring
- smooth muscles of blood vessels overgrow and occlude the vessels, donated organ tissues are replaced w/ fibrotic, scar like tissue. bc this fibrotic tissue is not organ tissue, the transplanted organ’s function is reduced in proportion to the amount of normal tissue that is replaced by fibrotic tissue
- although good control over the recipient’s immune function can delay this type of rejection, the process probably occurs to some degree with all transplanted solid organs
- s/sx: pain/tenderness of the organ site, general discomfort, uneasiness, or ill feeling, flu like symptoms, organ dysfunction
- tx: retransplantation

47
Q

transplant rejection interventions (2)

A

1) maintenance therapy is continuous immunosuppression
- drug used for routine therapy after solid organ transplantation are combinations of a calcineurin inhibitor, corticosteroid, antiproliferative agent)

2) rescue therapy is used to treat rejection episodes
- drug categories for this purpose are the monoclonal and polyclonal antibodies
- drugs used for maintenance are often also used during rejection episodes at much higher dosages than for maintenance

tip:
- drug depends on the tx. type and health issue (PO meds)
- tx: increased risk bacterial/fungal infection, cancer development

47
Q

rheumatoid arthritis (what (4))

A
  • chronic, progressive, systemic inflammatory autoimmune disease process that affects primarily the synovial joints
  • transformed autoantibodies (rheumatoid factors RF) are formed that attack healthy tissue, especially synovium, causing inflammation
  • the disease then begins to involve the articular cartilage, joint capsule, and surrounding ligaments and tendons
  • characterized by natural remissions and exacerbations
48
Q

s/sx RA early (joint (2), systemic (5))

A

1) joint:
- symmetric joint pain
- inflammation and stiffness (esp. in morning)

2) systemic:
- low grade fever
- fatigue
- weakness
- anorexia
- paresthesias

49
Q

s/sx RA (joint (7), systemic (9))

A

1) joint:
- deformities (eg. swan neck, ulnar deviation)
- moderate to severe pain
- morning stiffness
- swelling
- warmth
- erythema
- lack of function

2) systemic:
- fever
- wt. loss
- fatigue
- anemia
- lymph node enlargement
- subcutaneous nodules
- peripheral neuropathy
- pericarditis
- cardiovascular disease

50
Q

RA interventions (nonpharm, pharm, sugery)

A

1) nonpharm:
- ice
- heat
- proper positioning
- adequate rest
- proper diet
- hot shower in the morning

2) pharm:
- anti-inflammatory/analgesics: NSAIDs, COX2 inhibitors, glucocorticoids
- immunosuppressives/DMARDs: methotrexate, hydroxchloroquine (plaquenil)

3) surgery:
- synovectomy
- total joint replacement: RA early dx/ can delay long term joint deformity (remission)

tip:
- med mgmt: DMAR (slow progression of the disease, monitor LIVER/KIDNEY function)

51
Q

systemic lupus erythematosus (what, subtype (2), involves, onset)

A
  • what: inflammatory, autoimmune disorder that affects nearly every organ in the body
  • lupus nephritis: subtype of lupus d/t autoimmune complexes in SLE tend to be most attracted to the glomeruli of the kidneys
  • discoid lupus erythematosus: subtype of lupus that primary affects the skin on the face
  • involves chronic states where sx. are minimal or absent and acute flare ups
  • onset: childbearing (20-40 years)
52
Q

systemic lupus erythematosus s/sx (skin, renal, cardiac, pul., neuro, GI, musk, other)

A

1) skin: inflamed red rash (butterfly rash), discoid lesion, oral ulcers
2) renal: nephritis, kidney failure
3) cardiac: pericarditis, myocarditis, HTN, dysrhythmias, atherosclerosis, raynaud’s phenomenon
4) pulmonary: pleural effusions
5) neuro: psychosis, cognitive impairment, seizures, neuropathies, stroke
6) Gi: abdominal pain
7) musculoskeletal: joint inflammation, arthralgia, polyarthitis
8) other: fever, fatigue, anorexia, wt. loss

53
Q

systemic lupus erythematosus interventions (what, pharm (6))

A
  • supportive care: avoid prolonged exposure (fluorescent light)

pharm:
- topical cortisone preparations (decrease inflammation, promote fade skin lesions)
- analgesics
- anti-malarial agent: hydroxychloroquine (plaquenil)
- steroids (tx. systemic disease)
- immunosuppressive agents: methotrexate (rheumatrex), axathiprine (imuran)
- biologic/monoclonal antibody: belimumab (benlysta)

tip:
- plasmapharesis (3 days, if not response to meds mgmt well, kidney transplant)
- mild soap, avoid harmful perfumes, psychosocial support, smoking cessation

54
Q

sjorgen’s syndrome (3)

A
  • systemic autoimmune disease that progressively affects the lacrimal and salivary glands of the body
  • problems include: keratoconjunctivitis sicca (insuff. tear production), xerostomia (dry mouth d/t salivary gland activity: tooth decay, oral nasal infection), dry vagina (RA, lupus, infection)
  • problems are caused by autoimmune destruction (excess immunity) of the lacrimal, salivary, and vaginal mucus producing glands
55
Q

sjorgren’s syndrome s/sx (8)

A
  • dry eyes
  • blurred vision, burning, itching of the eyes
  • thick mattering in the conjunctiva
  • dry mouth, difficulty swallowing
  • changes in taste
  • epistaxis
  • frequent upper respiratory infections
  • vasculitis, arthralgia (joint stiffness), neuropathy
56
Q

sjorgren’s syndrome intervention (nonpharm (3), pharm (2))

A

1) nonpharm:
- artificial tears, artificial saliva, humidifiers, lubricants, moisturizers
- eat small frequent meals omitting spicy, salty, and irritating food
- avoiding smoking, excessive alcohol use, drugs with aCH side effects

2) pharm:
- rituximab
- interferone

57
Q

gout (types, incidence, _____ acid, rigger)

A

type of inflammatory arthritis and systemic disease in which urate crystals deposit in the joints and other body tissues, causing inflammation
- incidence of gout increases with age, body mass index, alcohol consumption, hypertension, and diuretic use (hydrochlorothizaide)
- uric acid: by product of purine metabolism, purines are basic chemical compounds found in high concentrations in meat products
- trauma, alcohol ingestion, dieting, medications, surgical stress, or illness may trigger the acute attack

58
Q

gout s/sx (7)

A
  • joint inflammation (most common)
  • painful to touch
  • swelling
  • redness
  • warmth
  • tophi (chronic, articular, ostycous, soft, cartilage tissue
  • renal calculi (renal dysfunction)

tip:
- change in urinary output

59
Q

gout diagnostic labs (3)/tests

A

labs:
- serum uric acid
- ESR (increased d/t inflammation)
- arthrocentesis

tests: NONE

tips:
- synovial fluid aspiration -> detect crystals in joint, characteristics of gout

60
Q

gout interventions (nonpharm, acute attacks (3), chronic (2))

A

1) nonpharm:
- low purine diet: avoid red meats, shellfish, oily fish with bones, ETOH, aspirin, diuretics

2) acute attacks: inflammation subside 3-10 days (most cannot tolerate pain) - take for 4-7 days
- colchicine
- NSAIDs
- corticosteroids

3) chronic gout:
- allopurinol: xanthan oxidate inhibitor (prevent xanthine convert to uric acid, take with water to decrease GI distress)
- febuxostat

61
Q

fibromyalgia (what, trigger, %, predisposing factors)

A

chronic pain syndrome (NOT INFLAMMATORY DISEASE) where pain, stiffness, and tenderness are located at specific sites in the back of the neck, upper chest, trunk, low back, and extremities
- tender points (trigger points) can typically be palpated to elicit pain in a predictable, reproducible pattern (burning, growing pain, increase muscle tenderness )
- between 25-65% of patients with fibromyalgia have other rheumatologic conditions
- there are a number of predisposing factors or pain, including anxiety, depression, physical trauma, emotional stress, sleep disorder, and viral infection

62
Q

fibromyalgia s/sx (8)

A
  • chronic fatigue
  • generalized muscle aching
  • stiffness
  • sleep disturbances
  • functional impairment
  • forgetfulness
  • concentration problems
  • pain/tenderness (come and go, worse w/ stress, weather condition changes)
63
Q

fibromyalgia interventions (supportive care (3), pharm (3))

A

1) supportive care:
- limit caffeine, etoh, exercise regularly, establish regular sleep pattern
- physical therapy
- cognitive behavioral therapy

2) pharm:
- antidepressants: TCAs, SNRIs, SSRIs
- analgesics: NSAIDs, muscle relaxants, tramadol (ultram)
- anticonvulsants: gabapentin, pregabalin