Exam 2 Flashcards

1
Q

What are the ways HIV can be transmitted?

What are the risks (%) of transmission through a transfusion?

A
  • Blood
  • Semen
  • Vaginal secretions
  • Breast milk: also through pregnancy and delivery

Only 1% risk of infection through a blood transfusion.

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2
Q

How long is the window between exposure and when antibodies show up?

What is the percentage of risk for healthcare workers after a needle stick?

What % of babies are born from untreated infected mothers who get HIV?

A

A few weeks.

0.3 - 0.4%

25% : Risk decreases to only 2% in those receive ART.
The biggest risk is delivery.

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3
Q

How long can infants test positive for HIV antibodies after delivery?

A

Up to 18 months.

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4
Q

What does PEP mean?

What do we test for when we are at risk for transmission?

What does PPE mean?

A

Post-Exposure Prophylaxis.
This should be started within hours of possible transmission.

We are tested for HIV, HBV (hep B), and HCV (hep C)

PPE: Personal Protective Equipment

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5
Q
Duration/frequency of contact
Volume of fluid
Virulence of organism
Host immune status and
Viral load of fluid are all factors that affect what?
A

Transmission depends on these factors.

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6
Q

What kind of receptors are needed in order for the HIV to infect cells?

How many CD4-T cells are killed each day?

What parts of the body initially replace these with?

A

CD4 receptors.

About a billion CD4-T cells are killed/day.

The thymus and bone marrow initially replace.
Thymus = produce and mature T cells
Bone marrow = stem cells -> T cells -> thymus for maturity.

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7
Q

What is the normal range for CD4 cells?

A

500 - 1500 cells/mm3

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8
Q

What are the stages of HIV infection?

A
  1. Acute - primary (or initial) HIV infection (about 2-4 weeks): begin to develop “off” feelings, similar to flu/mono/palsy/meningitis. Also seroconversion occurs.
  2. Chronic - 6 months or longer: low viral load. With ART, this stage can last up to 40 years.
  3. Late stage or AIDS - CD4 count 200 or below. Opportunistic infections.
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9
Q

During this stage, there is an undetectable viral load and many may think they are “cured.”

Where are the latent reservoirs located?

A

Chronic stage.

There are latent reservoirs where the virus “hang out” undetected. Means that ART is working.

Reservoirs: 
Blood
Brain
Lymph
GI
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10
Q

If the patient does not manage their HIV infections strictly, what may happen?

S/S of dz progression?

A
  1. Resistance
  2. Dz progression

S/S

  • Increased viral load
  • CD4 drops below 500 (200-499)
  • Symptomatic progression
  • Opportunistic infections and CA’s
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11
Q
Oral hairy leukoplakia,
Shingles,
Candida,
Herpes outbreaks (oral/genital),
Bacterial infections, and 
Kaposi sarcoma are all examples of what?
A

Opportunistic infections.

FYI: Oral hairy leukoplakia (luke-oh-play-key-uh) is from the Epstein-Barr virus (same as mono).

May also see some cervical dysplasia… abnormal cells that progress into CA.

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12
Q

What is the difference between antiviral drugs and antiretroviral drugs?

A

AntiVIRAL:
Target diverse group of viruses such as herpes, hepatitis, and influenza viruses.

AntiRETROviral:
Used to fight retrovirus infections which mainly include HIV. Different classes of antiretroviral drugs act on different stages of the HIV life cycle.

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13
Q

What level of CD4 indicates AIDS?

What happens to the viral load at this time?

A

Under 200.

Viral load is pretty high.

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14
Q

What are some common complications involved with AIDS?

A
  • Dementia
  • Wasting Syndrome
- Opportunistic infections: 
Candidiasis in bronchi and below
Cytomegalovirus (CMV)
Toxoplasmosis
Tuberculosis
Invasive cervical CA
Kaposi's sarcoma (KS)
Cryptococcal meningitis
Mycobacterium avium complex (GI s/s)
Non-Hodgkins Lymphoma
Pneumocystis carinii pneumonia (PCP)
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15
Q

Which opportunistic infection is big with AIDS and has a high mortality?

s/s?

Tx?

A

Pneumocystis carinii pneumonia (PCP)

1 in 10 hospitalized HIV pts have PCP

s/s

  • Nonproductive cough, wheezing
  • SOB (esp with exertion)
  • low grade fever
  • fatigue
  • chest pain when breathing

Tx: Pentamidine, an antifungal and antiprotozoal agent

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16
Q

What is Pentamidine used for?

What are it’s side affects?

How is it administered?

A

Pentamidine is used to treat Pneumocystis carinii pneumonia (PCP).

It is an antifungal and antiprotozoal agent.

It’s side affects include:

  • Severe hypotension (significant enough that this drug is given while the patient is lying down)
  • Arrhythmias (on cardiac monitor)
  • Nephrotoxic
  • Extravasation and tissue damage

Administered by IV

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17
Q

What virus is responsible for Kaposi’s sarcoma?

A

Related to human herpes virus 8 (HHV-8)

Develops when infected cells that line lymph or blood vessels begin to divide without stopping and spread into surrounding tissues. Whereas most cancers begin in one part of the body and may later spread to other areas, KS can start in several parts of the body at the same time.

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18
Q

What do we call weakness and wasting of the body due to severe chronic illness?

A

Cachexia.

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19
Q

What are the following symptoms signs of?

Chronic diarrhea for more than 30 days.
Greater than 10% weight loss
Chronic weakness/fever
Cachexia and malnutrition
GI malnutrition
A

Wasting Syndrome

Not helped by increased protein or calories.

May be due to mycobacterium avium500

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20
Q

What are some other signs that the body is shutting down?

A
  • Neutropenia (under 500)
  • Anemia
  • Thrombocytopenia
  • Altered liver functions (AST/ALT enzymes)
  • Hep B or C
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21
Q

How do we diagnose HIV?

A
  • Test for HIV antibodies (HIV antibody assay; Not detectable for about 2 months)
  • Rapid testing can be done in 20 minutes
  • HIV antibodies can be found in the blood, urine, and saliva (the virus is NOT in the saliva, just antibodies)
  • All infants born to HIV+ moms will be antibody positive for up to 18 months.
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22
Q

Where can HIV antibodies be found?

A

Blood, urine, and saliva.

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23
Q

How many positive tests are needed for dx?

If you have a + rapid test, which test is next?

If you have a + EIA and a negative Western blot, then what do you need to test for?

A

Need 2-3 positive tests.

If you have a positive rapid then it is followed with a Western blot test.

If you have a positive Enzyme Immunoassay (EIA) and a negative Western blot, then you need to test for HIV RNA

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24
Q

How are we to interpret the positive HIV test?

A
  • HIV antibodies are present in the blood
  • HIV is active in the body, is transmittable
  • Does not necessarily have AIDS
  • Not immune to AIDS - still may/will develop if non-compliant.
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25
Q

Goals of HIV treatment include:

Lowering the viral load to < 50 copies, maintain CD4T cells at >350, delay development of symptoms… and what else?

A
  • Prevent development of viral resistance to the therapy drugs (strict compliance is needed)
  • Maintain quality of life
  • Protect others
  • Support person in coping with disease and dying
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26
Q

What does ART mean?

What is HAART?

What is the difference?

A

ART = Antiretroviral Drug Therapy

HAART = Highly Active ART

HAART is newer and doesn’t require the same level of strict-regimen.

These drugs delay the dz progression, reducing the viral load thereby reducing transmission risks.

Drug therapy is a combination of drugs that attack the virus in different ways and at different times in the replication cycle = lowers risk of resistance.

Very expensive = $1300/month w/out insurance
Usu. many pills to take at specific times of the day

Can reduce viral load by 90-99%

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27
Q

What are some typical ART drugs?

A

Saquinavir

Abacvir

Dolutegravir

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28
Q

What are some common antiviral drugs?

A

Acyclovir (herpes)

Oseltamivir (influenza)

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29
Q

Why is strict compliance so imperative with ART?

A

If the adherence to the schedule is not upheld, resistance can happen rapidly. (use alarms, pill minders, etc)

Some ART users will not respond to tx, these individuals will progress through the dz to AIDS.

Some may not be able to use: $, side effects, inability to adhere to schedule (we shouldn’t make decision), many ART drugs interact with OTC and other Rx drugs (making it more complicated)

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30
Q

When should ART be started?

When in pregnancy?

A
  • Start when CD4 is down to 350 and keep it above 350.
  • ART will decrease transmission to uninfected partners by 96%
  • The newest therapy (2012) you start ASAP, preferably at the time of dx, regardless of the CD4 levels.
  • Pregnancy: ART should be started in the 1st trimester.
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31
Q

PEP versus PrEP

A

PEP is Post-Exposure Prophylaxis

PrEP is Pre-Exposure Prophylaxis

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32
Q

What is PrEP used for?

What is the common Rx for PrEP?

A

PrEP is used for at-risk persons (partners of HIV +)

Truvada is the Rx (tenofovir disoproxil fumarate/emtricitabine)

This is the first ART drug to be given prophylactically

  • Must be HIV neg and retested every 3 months.
  • Must consult with MD and add other drugs to Truvada if HIV positive

Effective to decrease new infections by 75%
Cost: $15,600/year (that’s 1300/month)

33
Q

Management of HIV includes:
Treatment of opportunistic infections
Vaccinations (avoiding live in AIDS)
Avoidance of infections… and what else?

A

Improving immune function: rest and exercise, stress reduction, nutrition therapy, reduce alcohol/tobacco/drugs

Antidepressants

Psychological counseling

Social counseling

Handling of blood and possibly infected excretions: appropriate PPE, wash hands, standard precautions, don’t share possibly contaminated objects.

34
Q

What vaccines are super important for HIV patients to have?

A

Not live vaccines if AIDS

Hep B
Flu
Pneumococcal (pneumonia)
Tetanus, diphtheria, and pertussis (Tdap). Booster of Td every 10 years. Td = tetanus and diphtheria

35
Q

Nursing Care of HIV patients:

  • Promote skin integrity (1st defense)
  • Promote usual bowel habits
  • Prevent infection
  • Improve activity intolerance
  • Maintain thought processes
  • Listen, listen, listen…. and?
A
  • Improve airway clearance
  • Relieve pain and discomfort
  • Improve nutritional status
  • Decrease sense of isolation
  • Cope with grief
36
Q

All studies show progression to AIDS and death, risk increasing with age.

A

Lifespan greatly increased with EARLY use of ART drugs… approaching 35-40 years from time of infection.

37
Q

What are some risk-reducing activities for HIV patients?

A
  • Treat all HIV + clients with ART (90-99%)
  • Barriers (condoms: male 80-90%, female 94-97%)
  • Male circumcision (50-60% in hetero)
  • Cleaning drug equipment
  • Standard precautions
  • Safety needles, sharp boxes
  • PEP / PrEP
38
Q

What are the 4 types of immune hypersensitivity?

A

Type I: IgE mediated: anaphylaxis, atopic dermatitis, allergic rhinitis

Type II: Cytotoxic/cytolytic, IgG/M direct bind: hemolytic transfusion reactions, good pasture syndrome.

Type III: Immune Complex reaction, IgG/M: autoimmune disorders (lupus, etc)

Type IV: Delayed Hypersensitivity, T lymphocytes: contact dermatitis; happens on a delayed response.

39
Q

What does cytotoxic mean?

What does cytolytic mean?

A

Cytotoxic: Toxic to living cells

Cytolytic: Dissolution or destruction of a cell

40
Q

Which 2 drugs are big for causing an autoimmune reaction?

What other factors can cause an autoimmune disorder?

A
  1. Methyldopa (Aldomet)
  2. Procainamide (Pronestyl)

Autoimmune causes:

  • Inherited susceptibility
  • Triggers (infections/ trauma)
  • Drugs
  • Gender (female)/ hormones (puberty, pregnancy)
41
Q

Name 3 systemic autoimmune disorders:

A
  1. SLE: Systemic Lupus Erythematosus (An inflammatory disease)
  2. Scleroderma (Chronic hardening and tightening of the skin and connective tissues.)
  3. Rheumatoid Arthritis (RA) (chronic inflammatory disorder affecting many joints)
42
Q

What autoimmune affects the CNS?

The Muscles?

The heart?

The GI?

Endocrine?

A

CNS: Guillain-Barre and Multiple Sclerosis

Muscles: Myasthenia gravis

Heart: Rheumatic fever

GI: Celiac and Ulcerative Colitis

Endocrine: Type I Diabetes Mellitus

43
Q

What are some treatment options for autoimmune disorders?

A

Apheresis: a medical technology in which the blood of a person is passed through an apparatus that separates out one particular constituent and returns the remainder to the circulation.

… When antibodies are building up in the body = issues/damage occur.

  • Plateletpheresis (removes platelets)
  • Leukocytopheresis (removes WBCs)
  • Plasmapheresis (removes plasma components)
44
Q

What is the difference between primary and secondary immunodeficiency disorders?

A

Primary:
Cells are deficient/absent/malformed from birth. What cells? Phagocytic cells, B cells (secrete antibodies), and T cells (attack cells invaded by virus, and sometimes bacteria).

Secondary: Induced by some other means…

  • Drug induced immunosuppression
  • Malnutrition
  • Disorders such as AIDS, Hodgkin’s Lymphoma, SLE, Radiation, Chemo, Steroids and Chronic Stress
45
Q

What is the Human Leukocyte Antigen System?

What do transplants use?

A

How we associate w/ autoimmune diseases… antigens on the 6th chromosome that are highly variable and pass on specific genes…

Genes involved: A, B, C, D, and DR

Transplants use A, B, and DR for compatibility

46
Q

Common TISSUES for transplantation:

  • Corneas
  • Skin
  • Bone Marrow
  • Heart Valves
  • Bone
  • Connective tissue
A

Common ORGANS for transplantation:

  • Heart: 4 month wait
  • Lung: 4 month wait
  • Liver : 11 month wait
  • Kidney : 5 YEAR wait
  • Pancreas: 2 YEAR wait
  • Intestine

Can also have partial organ donation
A kidney/pancreas special only waits 1.5 years.

47
Q

What is HLA typing (for tissue typing)?

A

HLA = Human Leukocyte Antigen

Check A, B, and DR genes

48
Q

This version of tissue typing is able to detect preformed antibodies:

A

Panel of Reactive Antibodies (PRA)

Looking for sensitivities before transplant… mix blood with random donor’s lymphocytes to see any reaction.

49
Q

This version of tissue typing takes lymphocytes from living donor or cadaver and mixed with recipient serum with a result of negative or positive:

A

Crossmatch

Negative result = Transplant, no cytotoxic antibodies
Positive = Absolute contraindication to transplant

Repeated again just before transplant.

50
Q

3 types of transplant rejection:

A
  1. Hyperacute: occurs within minutes to hours of procedure. The organ must be removed. This is now rare d/t crossmatching protocol before transplant
  2. Acute: seen within the first 6 months. Recipient lymphocytes are activated; antibodies develop to transplanted organ; not uncommon to have at least one episode. Tx: increase in immunosuppressive therapy.
  3. Chronic: within months to years of the transplant. Organ infiltrated with B and T cells. Fibrosis and scarring result. Tx: Supportive care, try immunosuppressive therapy, will probably need another transplant at some point.
51
Q

Types of immunosuppressive therapy:

A
  • Corticosteroids: Not being used as much d/t SE
  • Suppresses inflammatory response
  • Inhibits cytokine production
  • Inhibits T cells
  • Calcineurin Inhibitors: Foundation of immunosuppression
  • Does NOT cause bone marrow suppression
  • Tacrolimus is a medication that is nephrotoxic but still a good choice for this kind of therapy.

Cytotoxic Drugs:

  • Suppresses T and B lymphocytes
  • Sirolimus is the main one
  • Mycophenolate Mofetil: GI toxicities
52
Q

What is a cytokine?

What does calcineurin do?

A

Cytokines are any number of substances, such as interferon, interleukin, and growth factors, that are secreted by certain cells of the immune system and have an effect on other cells… they are small proteins that are important in cell signaling. Their release has an effect on the behavior of cells around them.

Calcineurin is a calcium and calmodulin dependent serine/threonine protein phosphatase, it activates T cells.

53
Q

What drug is a calcineurin inhibitor?

A

Tacrolimus

- This drug is nephrotoxic but still considered a good choice for immunosuppressive therapy. Risk vs Benefit.

54
Q

Which two drugs are Cytotoxic drugs that are used in immunosuppressive therapy?

A
  • Sirolimus is the main one.
  • Mycophenolate Mofetil
    • This drug has GI toxicities
55
Q

What is GVHD?

A

Graft Versus Host Disease

This is when the donor tissue rejects the host tissue.

This occurs within 7-30 days after transplant

S/S:
Skin - Itchy, rashy
Liver - Jaundice, ALT/AST
GI - possible bleeding, diarrhea

Tx: We try to prevent this with immunosuppression medications… nothing else we can do.

56
Q

Which autoimmune has S/S of:

  • Numbness, tingling
  • Fatigue
  • Muscle spasms
  • Pain
  • Walking difficulty?
A

Multiple Sclerosis.

Onset: Insidious = medical attention is delayed

Chronic progressive deterioration to remission and exacerbation.

57
Q

How is Multiple Sclerosis diagnosed?

A

No definitive diagnostic test…

Take into consideration their history, and clinical manifestations

Must have:

  • MRI plaques
  • At least 2 inflammatory demyelinating lesions in 2 different locations in the CNS
  • Damage/attack 1 month or greater apart.

All other possibilities must be ruled out.

58
Q

What’s the patho of MS?

What are some factors that may cause it?

What gender and climate are higher risk?

A

Unknown. Activation of T cells leads to chronic inflammation, antigen-antibody reaction occurs in the CNS that causes an inflammatory response which leads to scarring in the CNS

Factors:
Genetics
Infection
Smoking
Emotional Stress
Excessive Fatigue
Pregnancy
Physical injury

High risk age 20-50, women 2-3 x more than men
More often in temperate climates (45-65 degree latitude)

59
Q

How is MS treated?

What teaching may be involved?

A
Collaborative Care:
Drugs:
- Immunomodulators
- Immunosuppressors
- Corticosteroids (during periods of exacerbation)

Symptom management:

  • cholinergics and anticholinergics for spastic/flaccid bladder
  • Muscle relaxers for spasms
  • Nerve conduction enhancers to help with nerve signals

Surgery
- Implant electrical simulator

  • Exercise improves daily function, PT

Teaching: How to avoid triggers, Prevent complications, and resistance to illness through vaccines, exercise, etc.

60
Q

This is an autoimmune disease of the neuromuscular junction and affects the acetylcholine receptor sites:

Who’s at risk?

What are the s/s?

What is the course of progression?

What are factors that exacerbate?

A

Myasthenia Gravis

Affects childbearing women and men ages 50-70.

S/S:
- Fluctuating weakness increased by the end of the day; some relief with rest.

Progression is variable:

  • Exacerbations/ remissions (like MS)
  • Progressive
  • Weakness stabilizes, pt gets better.

Factors that exacerbate:
- Stress, illness, trauma, pregnancy, drugs, and temperature extremes.

61
Q

What is Myasthenic Crisis and what can trigger/cause it?

A

An acute exacerbation of muscle weakness.

Triggers:
Infection, surgery, emotional distress, drug OD, inadequate drug

Many times these patients are hospitalized.

62
Q

How is Myasthenia Gravis diagnosed?

How is it treated?

A
  • H and P (history and physical)
  • Electromyogram
  • Tensilon IV (anticholinesterase)
  • CT chest (to assess thymus: tumor/hyperplasia)

Treatment:
* Anticholinesterase
* Alternating days of corticosteroids (prednisone).
* Immunosuppressants:
Pyridostigmine is a big one, increases ACH
Imuran, Cell-Cept
* Surgery (removal of thymus: antibodies)
* Plasmapheresis
* IV immunoglobulin G (decreases antibody production)

63
Q

What opportunistic infections will you see in the chronic stage of HIV?

A
  • Candida of the mouth or vagina
  • Shingles
  • Herpes of the mouth or genitalia
  • Oral hairy leukoplakia
  • Bacterial infections
  • Kaposi sarcoma
64
Q

What opportunistic infections will you see in the late stage, or AIDS?

A
  • Candida in bronchi and below
  • Cytomegalovirus
  • Toxoplasmosis
  • Tuberculosis
  • Invasive cervical cancer
  • Kaposi’s sarcoma
  • Cryptococcal meningitis
  • Mycobacterium Avium complex (GI s/s)
  • Non-Hodgkins Lymphoma
  • Pneumocystis carinii pneumonia (PCP)
65
Q

Any of several drugs that prevent destruction of the neurotransmitter acetylcholine:

A

Anticholinesterase

By the enzyme acetylcholinesterase within the nervous system.

66
Q

This is the most common form of joint disease in North America. It has a slow progression where cartilage destruction begins between the ages of 20 and 30 but symptoms do not manifest until after age 50-60:

A

Osteoarthritis.

Noninflammatory disorder of the diarthrodial joints.

Where rheumatoid arthritis has a thickening of the cartilage d/t RF depositing in the synovial joints = inflammation = thickening of cartilage, osteoarthritis has the destruction of the cartilage, and it is noninflammatory.

This is not a normal part of the aging process.

67
Q

What is a diarthrodial joint?

A

The most common and movable type of joint which is characterized by the presence of a layer of fibrocartilage or hyaline cartilage that lines the opposing bony surfaces, as well as a lubricating synovial fluid within the synovial cavity.

68
Q

What causes osteoarthritis?

What are the risk factors?

S/S?

Tx?

A

Either direct damage or instability.

  • Age
  • Estrogen reduction at menopause
  • Obesity
  • Injury (job / sports)
  • Frequent kneeling / stooping

S/S:
- Joint pain (which is many times relieved by rest)
- Stiffness (many times resolves shortly)
- Crepitus and deformity can occur
No systemic involvement r/t non inflammatory

Tx:
Encourage to exercise and rest
Heat and cold application
Obese = decrease their weight

69
Q

This disease is a chronic systemic autoimmune disease. It has periods of remission and exacerbation and affects the connective tissue in diarthrodial (synovial) joints:

Risk factors?

A

Rheumatoid Arthritis.

This disease has extraarticular manifestations = systemic. Several systems are impacted, esp the heart, CNS, hematological.

Incidence increases with age
Peaks between 30 and 50 yo
Women more than men
Theory of genetics and environment that trigger

Can be very debilitating = mobility aids, joint reconstruction (deformity)

70
Q

What are the S/S of Rheumatoid Arthritis?

How is it diagnosed?

How is it treated?

A

S/S: Nonspecific manifestations:

  • Fatigue
  • Weight loss
  • General stiffness (similar to osteoarthritis but lasts much longer)

Dx:

  • Criteria: how much joint involvement is happening? What are the levels of RF? CRP and ESR (inflammation)?
  • H and P
  • Labs
  • Other studies… x rays

Tx:

  • Drug therapy: steroids, DMARDs, BRMs, NSAIDs
  • Patient education: dz process/stages (early, moderate, severe, terminal)
  • Home management strategies: rest, decrease joint stress, alternating heat and cold
71
Q

DMARDs: meaning and use

A

Disease Modifying Anti-Rheumatic Drugs

They slow the progression of the disease and decrease joint deformity.

Ex: Methotrexate (nephrotoxic, risk vs benefit)

72
Q

BRMs: meaning and use

A

Biological Response Modifiers

They also decrease the progression of Rheumatoid Arthritis. They can be used with DMARDs or in place of them if the pt cannot tolerate them.

73
Q
This autoimmune disease has hallmark s/s of:
Butterfly rash
Arthritis / pain in joints
Kidney damage (glomelular nephritis then ESRD)
A

Systemic Lupus Erythematosus

This is a chronic inflammatory autoimmune disease with alternating exacerbation and remission phases.

It has complex factors: Genetic, Hormonal, Environmental (UV light, chemical exposure, certain meds), Immunologic.

74
Q

Which drug can cause SLE?

What systems are affected by SLE?

A

Procainamide

  • Skin
  • Joints
  • Serous membranes: Pleura and Peridardium
  • Renal system
  • Hematologic system
  • Neurologic system
75
Q

What is the etiology of SLE?

A

Antibodies attack cell nucleus, DNA.

Immune complexes deposited in basement membranes of capillaries in the kidneys, heart, skin, brain, and joints

Inflammation and tissue damage

Often will have impaired immune system r/t impaired phagocytosis and use of immunosuppressants

76
Q

How is SLE treated?

A
  • NSAIDs for pain and inflammation
  • Antimalarial drugs for fatigue, skin, and joints.
  • Steroid-sparing drugs like methotrexate
  • Corticosteroids maybe, limited by side effects
  • Immunosuppressive drugs, used for organ involvement, when there’s more systems involved.

Promotion of early diagnosis and tx through education of both health professionals and the community to control pain, symptoms, and prevention of organ damage.

77
Q

This pain syndrome is not an autoimmune disorder. It involves an abnormal processing in the CNS leading to an increased pain perception:

What are some possible causes?

A

Fibromyalgia

It’s a chronic disorder that is a widespread and non-articular musculoskeletal pain and fatigue and has multiple tender points.

  • Genetic
  • Recent illness
  • 75 - 90% are women (hormones)
78
Q

S/S of fibromyalgia:

Complications:

A
    • Fluctuating widespread burning pain
  • Can accompany TMJ dysfuncion
  • Tenderness points (11 of 18 are dx)
  • Cognitive effects: difficulty concentrating/memory, feelings of being overwhelmed
  • Migraine HA

finish complications