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PCM > Approach to Hypersensitivity and Autoimmune Conditions > Flashcards

Approach to Hypersensitivity and Autoimmune Conditions Flashcards

1
Q

Type 1 Immediate Hypersensitivity

A

antigen exposure
IgE cross-linking on mast cell/basophil surfaces
histamine, leukotriene, prostaglandin, tryptase (mediators) release
symptoms of urticaria, rhinitis, wheezing, diarrhea, vomiting, hypotension, and anaphylaxis within minutes of exposure
*may have symptom return 4-8 hours after exposure

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2
Q

examples of type 1 hypersensitivity

A

pollen allergies, dust mite allergy, bee sting

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3
Q

Type 2 Cytotoxic Hypersensitivity

A

IgM or IgG antibody destroys cells by

  • opsonization
  • complement-mediated lysis
  • antibody-dependent cellular cytotoxicity
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4
Q

examples of type 2 cytotoxic hypersensitivity

A

ABO mismatch, Grave’s disease, myasthenia gravis

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5
Q

treatment for type 1

A

antihistamines

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6
Q

treatment for type 2

A

acetylcholinesterase inhibitors, plasmapheresis

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7
Q

Type 3 Immunocomplex Hypersensitivity

A

antigen-antibody complex formation
complexes activate complement and neutrophil infiltration of tissue
tissue inflammation leading to fever, urticaria, generalized lymphadenopathy, arthritis, glomerulonephritis, vasculitis

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8
Q

examples of type 3

A

systemic lupus erythematosus, rheumatoid arthritis, farmer’s lung

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9
Q

treatment of type 3

A

supportive and avoidance of antigen

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10
Q

Type 4 Cell-Mediated Hypersensitivity

A

antigen exposure activates sensitized T-cells

T-cell activation leads to tissue inflammation 48-96 hours after exposure to antigen

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11
Q

examples of type 4

A

poison ivy rash, PPD testing for TB

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12
Q

type 4 treatment

A

symptomatic, steroids (rxn is result of T-cell activation, not histamine)

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13
Q

rheumatoid arthritis mechanism

A

systemic inflammatory disease affecting synovial membranes
granulation tissues develops in joint spaces and erodes into articular cartilage and bone
females moreso
genetic component

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14
Q

rheumatoid arthritis presentation

A

joint swelling, warmth, erythema, and decreased ROM
morning stiffness >1 hour
PIP, MCP, wrist, knees, and ankles are most commonly affected

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15
Q

rheumatoid arthritis treatment

A

disease-modifying anti-rheumatic drugs (DMARDs), NSAIDs, steroids, physical therapy

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16
Q

rheumatoid arthritis treatment risks

A

increased risk of infection from immunosuppression, 2x increase in incidence and mortality from leukemia or lymphoma, increased risk of CVD

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17
Q

juvenile idiopathic arthritis mechanism

A

collagen vascular disorder with persistent inflammation in 1 or more joints for 6 or more weeks in pt <16 y/o
onset at 1-3 y/o
females>males

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18
Q

juvenile idiopathic arthritis presentation

A

pauciarticular - large joints, asymmetric, iridocyclitis, uveitis
polyarticular - large and small joints, symmetric
systemic (Still’s disease) - recurrent high fevers, myalgias, pericarditis, lymphadenopathy, anemia, leukocytosis

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19
Q

juvenile idiopathic arthritis treatment

A

NSAIDs, steroids, methotrexate, anti-TNF therapy, stretching, morning baths, weight-bearing exercises

20
Q

complications of juvenile idiopathic arthritis

A

pauciarticular - 70% of pts go into remission after several years
polyarticular - symptoms wax and wane
systemic - 50% develop destructive arthritis, complete resolution is rare

21
Q

systemic lupus erythematosus

A

inflammatory disease
females moreso, especially African American
recurrent exacerbations and remissions, secondary to autoantibody formation and immune complex deposition (type 3 hypersensitivity)
genetic component, HLA-DR2 and -DR3

22
Q

systemic lupus erythematosus presentation

A

pleuritis, pericarditis, myocarditis
oral aphthous ulcers
arthritis
photosensitivity
hemolytic anemia, thrombocytopenia, leukopenia, lymphopenia
proteinuria or urinary cellular casts
positive ANA
positive anti-dsDNA, anti-SM, antiphospholipid
lupus cerebritis, seizures, psychosis
malar rash (photosensitive butterfly rash)
discoid rash

23
Q

diagnosis of SLE

A

at least 4 of manifestions

24
Q

differences between SLE and RA

A

ESR and CRP highly elevated in untreated RA
erosions are common in RA
morning stiffness lasts for hours in RA, but only minutes in SLE
RA commonly deforms

25
Q

SLE treatment

A

depends on manifestations
steroids for flares
disease-modifying antirheumatic drugs (DMARDs)

26
Q

SLE prognosis

A

survival with treatment is 90-95% at 2 years, 75% at 20 years
mortality from end-organ damage (renal failure)
opportunistic infections secondary to immunosuppression

27
Q

Psoriasis

A

chronic, hyperproliferative inflammatory disorder characterized by thick adherent scales
females/males affected equally

28
Q

psoriasis presentation

A

mild pruritis, salmon-pink plaques, extensor surface involvement, bilateral, nail pitting, genetic component

29
Q

psoriasis diagnosis

A

history and physical exam
Auspitz sign - pinpoint bleeding after removal of scale
biopsy

30
Q

psoriasis treatment

A

topical steroids, topical vitamin D analogs, other topicals, UV light, systemic immunosuppression

31
Q

psoriasis prognosis

A

higher frequency of CVD, malignancy, diabetes, hypertension, metabolic syndrome, inflammatory bowel disease, serious infections, other autoimmune disorders
-psoriatic arthritis present in 7-48% of pts

32
Q

multiple sclerosis

A

demyelinating disorder of CNS
females>males
peak incidence 20-40 y/o

33
Q

MS presentation

A

vision changes, vertigo, weakness, numbness/tingling/pain, urinary incontinence or retention
Lhermitte’s sign = electrical sensation running down the spine and lower extremities with neck flexion

34
Q

MS diagnosis

A

MRI, CSF

35
Q

MS treatment

A

immunomodulatory, immunosuppressive, IV steroids for acute exacerbations, physical therapy

36
Q

MS prognosis

A

15 years after diagnosis:
20% have no functional limitations
70% limited or unable to perform major ADLs
75% are unemployed

37
Q

Primary Immunodeficiencies

A

t-cell specific
b-cell specific
t-cell/b-cell combined
phagocytic disorders

38
Q

clinical signs suggestive of primary immunodeficiency disease

A

positive family history, infections in multiple locations, increasing frequency/severity of infections with age, unusual and common pathogens

39
Q

t-cell primary immunodeficiency

A

present in first 3-4 months of life
disseminated intracellular diseases
ex: DiGeorge syndrome

40
Q

b-cell primary immunodeficiency

A

present after 6 months of age (maternal antibodies disappear)
sinopulmonary and GI infections
ex: common variable immunodeficiency (CVID)

41
Q

t-cell/b-cell combined primary immunodeficiency

A

combined features

ex: severe combined immunodeficiency (SCID)
- onset at 3 months of age
- diarrhea, pneumonia, otitis, sepsis
- failure to thrive
- treat with antibiotics, recombinant adenosine deaminase, bone marrow transplant

42
Q

phagocytic primary immunodeficiency

A

sinopulmonary and soft tissue infections

ex: chediak-higashi syndrome
- defect in microtubular function – decreased phagocytosis
- partial oculocutaneous albinism, progressive neuropathy
- treat with antibiotics, bone marrow transplant

43
Q

HIV/AIDS

A

spread almost exclusively through body fluids
5 million new pts worldwide annually
more prevalent in males

44
Q

HIV/AIDS presentation

A

initially asymptomatic, flu-like symptoms

myalgias, fever, anorexia, headache, fatigue, pharyngitis

45
Q

HIV Diagnosis

A

ELISA screen, Western blot confirmation, HIV RNA viral load

46
Q

HIV Treatment

A

recommendation to screen all pts between ages 13-64 at least once, depends on CD4 count, highly active antiretroviral therapy (HAART), prophylaxis of opportunistic infections

47
Q

AIDS diagnosis

A

CD4 count <200 cell/mm3
or
presence of an AIDS-defining illness (cytomegalovirus, mycobacterium avium-intracellulare, candidal esophagitis)

PCM (7 decks)

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