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NSG 356 - Clinical Applications & Reasoning II > [M3] Autoimmune Conditions > Flashcards

[M3] Autoimmune Conditions Flashcards

1
Q

What is an acute illness?

A

rapid onset with short duration, usually returning to previous level of function after treatment

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2
Q

What is a chronic illness

A

prolonged with no cure; results in irreversible changes, possible disability and requires rehab and/or long term medical management and nursing care

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3
Q

What are the 7 tasks of chronic illness?

A
  1. Prevent and manage crises
  2. Carry out prescribed treatment regimen
  3. Control symptoms
  4. Reorder time
  5. Adjust to changes in course of disease
  6. Prevent social isolation
  7. Attempt to normalize interactions with others
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4
Q

What is Primary Prevention for chronic illness? Provide example(s).

A

measures that prevent the occurrence of a specific disease

diet, exercise, immunizations

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5
Q

What is Tertiary Prevention for chronic illness? Provide example(s).

A

activities that limit disease progression or return patient to optimal function

rehab

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6
Q

What is Secondary Prevention for chronic illness? Provide example(s).

A

actions aimed at early detection of disease that can lead to intervention to prevent disease progression

screenings

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7
Q

Autoimmune diseases may result in what?

A

destruction of body tissue, abnormal growth of an organ, or changes in organ function

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8
Q

What are some risk factors for autoimmune conditions?

A

genetics, weight, smoking

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9
Q

What can cause an autoimmune condition?

A

exact cause is unknown, but triggers include bacteria/viruses, medications, or chemical/environmental irritants

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10
Q

What is rheumatoid arthritis?

A

chronic, systemic, autoimmune condition resulting in inflammation of connective tissue in synovial joints

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11
Q

How does RA manifest in early stages?

A

fatigue, weight loss, anorexia, generalized stiffness

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12
Q

How does RA manifest in late stages?

A

symmetric small joint pain, stiffness, limited motion, tenderness, and warmth to touch, spindle shaped fingers,

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13
Q

What are the common groups of people affected with RA?

A

women of all ethnic groups; peaks between ages 30 - 50

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14
Q

Explain the etiology/pathophysiology of RA.

A

combination of genetics and environmental triggers; an antigen (bacteria/virus) triggers formation of abnormal immunoglobulin G (IgG); autoantibodies (rheumatoid factor) develop against the abnormal IgG

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15
Q

Patients with RA often experience what?

A

joint stiffness after inactivity and morning stiffness lasting 60 mins to several hours

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16
Q

What is tenosynovitis?

A

inflammation of the tendons around wrists producing symptoms of Carpal Tunnel

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17
Q

Explain the manifestations as RA progresses.

A

inflammation and fibrosis may cause deformity and disability, muscle atrophy and tendon destruction can cause subluxation, and walking disabilities can manifest along with hand deformities

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18
Q

Name this deformity.

A

ulnar drift

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19
Q

Name this deformity.

A

boutonniere’s deformity

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20
Q

Name this deformity.

A

hallux valgus

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21
Q

Name this deformity.

A

swan neck

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22
Q

What are the non-drug therapy methods for RA treatment?

A
  • balance of rest and activity
  • heat and cold application
  • relaxation techniques
  • joint protection
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23
Q

How is RA often diagnosed? Any labs?

A
  • history and physical
  • ESR and anti-CCP levels
  • synovial fluid analysis

ESR increase shows inflammation; anti-CCP and RF helps with early dx

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24
Q

Why/When is cold application beneficial for RA?

A

relieves pain and muscle spasms during periods of disease activity

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25
Why/When is **heat** application beneficial for RA?
relieves chronic stiffness
26
What are some common **drug** therapies for RA?
- NSAIDs - DMARDs - corticosteroids
27
What are **DMARDs**?
disease-modifying anti-rheumatic drugs
28
Why are DMARDs beneficial for RA treatment?
may slow disease progression and decrease risk for joint erosion and deformity
29
What are some examples of DMARDs?
*Methotrexate* and *Hydroxychloroquine*
30
Why are corticosteroids and NSAIDs beneficial for RA treatment?
both reduce acute inflammation to decrease pain and improve function
31
What are biologics in RA treatment? Why are they beneficial?
medications derived from a living organism, offering powerful and highly targeted treatment to slow RA progression
32
What should be taught to a patient with RA regarding lifestyle modifications? Why?
- alter routine to place less stress on joints - rest periods throughout the day to help relieve fatigue and pain - use assistive devices to help simplify tasks and use joint–protective devices whenever possible - encourage light exercise (walking, swimming) and gentle ROM exercises to keep joints functional - ensure adequate nutrition due to drug therapies and/or increased fatigue
33
What is **Systemic Lupus Erythematosus**?
a chronic progressive inflammatory disease of connective tissue that results in organ failure with alternating periods of remission and exacerbation
34
Explain the pathophysiology of SLE.
the body creates antibodies that cause inflammation and damage leading to vasculitis; depletes oxygen and blood supply to organs
35
How does SLE manifest?
no characteristic pattern occurs in the progression; general problems such as fever, weight loss, joint pain, and fatigue may occur due to affected tissues (skin and muscle, linings of the lung, heart, nervous tissue, and kidneys
36
What are the early signs of SLE?
polyarthralgia with morning stiffness and butterfly rash
37
What is an important consideration regarding a patient with SLE?
patients are at increased susceptibility to infections due to the impaired ability to eliminate invading bacteria, deficient production of antibodies, and immunosuppressive effect of many anti-inflammatory drugs
38
What are some functional nutritional health patterns of SLE?
weight loss, ulcers, nausea/vomiting, dry mouth, dysphagia, photosensitivity, and infections due to decreased metabolism
39
How does SLE affect the skin?
patients may develop alopecia, dry scalp, butterfly rash, hives, erythema of nails, or petechiae
40
What are some standouts in patient's medical history when suspecting SLE?
- exposure to UV light, drugs, chemicals, or viruses - stress - increased estrogen activity - pattern of remissions and flares
41
What are some **drug** therapies for SLE management?
- NSAIDs - antimalarial drugs - corticosteroids - immunosuppressive drugs
42
Why are NSAIDs beneficial for SLE treatment?
treats mild joint pain
43
Why are antimalarial drugs beneficial for SLE treatment?
reduces flares and treats fatigue and skin/joint problems
44
Why are immunosuppressive drugs beneficial for SLE treatment?
suppresses immune system and decreases end-organ damage
45
What should a patient with SLE be taught?
- avoid triggers (UV lights) - adjust lifestyle to accommodate disease and reduce fatigue/pain - pregnancy options; plan when disease activity is minimal and stop harmful drug therapies
46
What is **Inflammatory Bowel Disease**?
chronic inflammation of the GI tract with periods of remission and exacerbation; classified as ulcerative colitis (UC) or Crohn’s disease based on manifestations
47
What is the difference between **Ulcerative Colitis** and **regional enteritis (Crohn's)**?
UC: development of cancer common, primarily effects the mucosa layer, rarely have fistulas, strictures, or abscesses, rectal bleeding COMMON Crohn’s: cobblestone appearance, rare to develop cancer, fistulas, strictures, and abscesses, can affect all layers, rectal bleeding RARE
48
Which IBS condition is at higher risk of developing cancer later in life?
Ulcerative Colitis
49
What causes IBD?
environmental or bacterial triggers cause an overactive, inappropriate, sustained immune response in genetically susceptible people; inflammation causes widespread tissue destruction
50
What are some environmental causes for IBD?
diet, smoking, and stress alter microbial flora, and poor nutrition
51
What are some drug associations with IBD development?
NSAIDs, antibiotics, and/or oral contraceptives
52
Who is commonly affected by IBD?
teens or early adults with a second peak in 60s; those with a genetic link or family history are at higher risk
53
What are **local** complications of IBD?
complications that are local only to the GI tract hemorrhage, strictures, perforation (with possible peritonitis), abscesses/fistulas, CDI, toxic megacolon
54
What is important for those diagnosed with IBD?
regular cancer screening due to increased risk of colon cancer (UC) and small intestine cancer (Crohn's)
55
What are some systemic complications of IBD?
malabsorption, liver disease, and osteoporosis
56
How is IBD diagnosed?
- history and physical - labs - imaging - colonoscopy - stool exam
57
**True or False**: Most chronic illnesses may be viewed as having steady phases that are usually in crisis.
False. ## Footnote Most CIs may be viewed as a trajectory with overlapping phases, in which a person moves from a level of optimum functioning, with the illness in good control, to a period of instability where they may need assistance.
58
You suspect your patient has IBD. What blood work do you conduct? Why?
- CBC - to detect anemia, toxic megacolon, or perforation - serum electrolyte levels - due to diarrhea - albumin - due to poor nutrition - ESR/C-reactive protein - inflammation - WBCs - inflammation
59
What imaging can be done to diagnose IBD?
double–contrast barium enema study, small bowel series, CT, transabdominal ultrasound, and MRI
60
What are the goals of treating IBD?
- rest the bowel - control inflammation - combat infection - correct malnutrition - relieve symptoms - improve quality of life
61
What **drug** therapies are used to treat IBD?
- 5-Aminosalicylates (5-ASA) - antimicrobials - corticosteroids - immunomodulators
62
Explain why 5-Aminosalicylates are beneficial for IBD treatment.
decreases inflammation
63
What is the first-line drug treatment for RA?
DMARDs
64
Explain why antimicrobials are beneficial for IBD treatment.
prevents/treats secondary infection
65
Explain why corticosteroids are beneficial for IBD treatment.
prevents or decreases inflammation in the intestinal mucosa
66
Explain why immunomodulators are beneficial for IBD treatment?
suppresses the immune response and turns down inflammation
67
Drug selection for IBD depends on what?
severity and location of inflammation
68
What is the **Step-Up Approach** for treating IBD?
using less toxic therapies and working toward more toxic if initial treatments don't work
69
What is the **Step-Down Approach** for treating IBD?
using immunosuppressant and biologic therapies first
70
What causes nutritional deficiencies in IBD? How can they be fixed?
- decreased oral intake - try to reduce diarrhea by increasing appetite - blood loss - iron- deficiencies and zinc deficient patients need oral supplementation and/or parental nutrition - malabsorption of nutrients - depends on location of inflammation, but decreases absorption of cobalamin and bile acids - drug therapies (*Sulfasalazine* and corticosteroids)
71
What are the main goals of diet management for IBD patients?
- adequate nutrition without exacerbating symptoms - correct and prevent malnutrition - replace fluid and electrolyte losses - prevent weight loss
72
How can IBD drug therapy-induced nutritional deficiency be fixed?
- *Sulfasalazine* - increase folic acid intake/supplementation - corticosteroids - calcium supplements to prevent osteoporosis; potassium supplements
73
Why are liquid enteral feedings preferred during acute IBD exacerbations?
- high in calories and nutrients - lactose free - easily absorbed - help achieve remission and improve nutrition
74
What are common **non-drug** therapies for Crohn's disease?
- mind-body medicine (to reduce stress) - surgery - smart, healthy food choices
75
What should a patient with IBD be taught?
- importance of rest and diet management - perianal care (to reduce infection risk) - symptoms of recurrence - when to seek medical care - stress reduction strategies

NSG 356 - Clinical Applications & Reasoning II (4 decks)

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