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(OMS1) PCM II Final > Approach to Hypersensitivity/Autoimmune Topics > Flashcards

Approach to Hypersensitivity/Autoimmune Topics Flashcards

1
Q

Type I Hypersensitivity Steps

A

Ag exposure

IgE cross link on mast cells

Histamine, leukotrienes, prostaglandins, tryptase released

symptoms of urticaria, rhinitis, wheezing, diarrhea, vomit, hypotension & anaphylaxis (w/ in min of exposure)

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2
Q

When does the reaction occur in type 1 hypersenstivity?

A

immediate, w/ in min of expsoure

symptoms can return 4-8 hrs after exposure

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3
Q

What are some examples of type 1 hypersensitivities?

A

pollen allergies, dust mite allergy, bee sting

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4
Q

What helps to treat type 1 rxns?

A

anti-histamines

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5
Q

What is type 2 cytotoxic hypersensitivity?

A

IgM or IgG antibody destroys cells by:

opsonization
complement-mediated lysis
AB depend cell cytotoxicity

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6
Q

What are examples of type 2 hypersensitivity?

A

ABO mismatch, Grave’s disease, myasthenia gravis

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7
Q

What is the pathology of myesthenia gravis?

A

antibodies to ACH receptor which prevents Ach from binding (type 2)

IgM or IgG causing destruction

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8
Q

Steps for Type 3 Hypersensitivity

A

Ag-Ab complex formation

Complexes activate complement & neutrophil infiltration of tissue

Tissue inflammation

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9
Q

What are symptoms of tissue inflammation in type 3?

A

fever, urticaria, lymph node swelling, arthritis, glomerulonephritis, vasculitis

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10
Q

What are the steps of Type 4 hypersensitivity?

A

Ag exposure activates T cells

T cell activation leads to tissue inflammation

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11
Q

When do symptoms start in Type 4?

A

48-96 hours after exposure to antigen

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12
Q

What are examples of type 4?

A

poison ivy rash, PPD testing for TB

delayed reaction

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13
Q

What is an autoimmune condition?

A

characterized by an immune response against something that is normally found in the body

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14
Q

What is rheumatoid arthritis?

A

systemic inflammatory disease affecting synovial membranes

granulation tissues develops in joint spaces & erodes into articular cartilage/bone

females>males

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15
Q

How does RA present?

A

joint swelling, warmth, erythema, decreased ROM

morning stiffness > 1 hr

PIP, MCP, wrist, knees & ankles affected

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16
Q

How do you differentiate RA from OA?

A

symptoms of RA: affects metacarp joints, no Herbeden’s nodes, joints are soft & warm, stiffness worse after resting

symptoms of OA: distal joints affected, present w/ Herbeden’s nodes, joints are hard & bony, stiffness worse w/ effort

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17
Q

What is common in RA?

A

MCP joint swelling w/ boutonniere deformities bilaterally

erosions of joints on X rays

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18
Q

What are complications assoc w/ RA?

A

increased risk of infection from immunosuppression

2x increase in incidence/mortality from leukemia or lymphoma

increased risk of CVD

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19
Q

What is juvenile idiopathic arthritis?

A

collagen vascular disorder w/ persistent inflammation in 1 or more joints for 6 or more week sin pts<16 yo

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20
Q

How does pauciarticular JIA present?

A

affects large joints, asymmetric

inflammation involves ciliary body

uveitis (eye inflammation)

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21
Q

How does polyarticular JIA present?

A

large & small joints, symmetric

22
Q

How does systemic JIA present?

A

recurrent high fevers

myalgias, pericarditis, lymphadenopathy

anemia, leukocytosis

23
Q

What is a complication of systemic JIA?

A

50% pts develop destructive arthritis (complete resolution is rare)

24
Q

What is SLE?

A

inflammatory disorder that females>males

recurrent exacerbations & remissions secondary to auto-AB formation & immune complex deposition (type 3)

25
Q

What is the genetic component of SLE?

A

HLA DR2 & DR3

26
Q

How does SLE present & what is needed for diagnosis?

A 
Pleuritis
Oral ulcers
Arthritis 
Photosensitivity
Hemolytic anemia
Proteinuria/urinary cell casts
Positive ANA
Postivie anti-dsDNA
Lupus cerebritis/seizures
Malar rash
Discoid rash

need at least 4 of manifestations

27
Q

How do you distinguish between RA & SLE?

A

in SLE, erosions in joints are rare & morning stiffness only lasts few min & deforming arthritis is uncommon

in RA, ESR & CRP are SIGNIFICANTLY elevated

28
Q

What usually causes mortality in SLE pts?

A

end organ damage

opportunistic infections secondary to immunosuppression

29
Q

What is psoriasis?

A

chronic, hyper-proliferative inflammatory disorder characterized by thick adherent scales

30
Q

How does psoriasis present?

A 
mild pruritus
salmon pink plaques w/ adherent silver-white scale
extensor surface involvement
nail pitting
*genetic component
31
Q

How do you diagnose psoriasis?

A

history & PE (Auspitz sign w/ pinpoint bleeding after removal of scale)

32
Q

What are complications assoc w/ psoriasis?

A 
CVD
malignancy
diabetes
HTN
metabolic syndrome
IBD
serious infections
other autoimmune disorders
33
Q

What is MS?

A

demyelinating disorders of CNS, females>males & develops from 20-40yo

34
Q

How does MS present?

A 
vision changes (1st sign)
vertigo
weakness
numbness/tingling/pain
urinary incontinence/retention
Lhermitte's sign
35
Q

What is Lhermitte’s sign?

A

electrical sensation running down spine & LE w/ neck flexion

+ for MS

36
Q

How is MS diagnosed?

A

MRI

CSF (spinal tap)

37
Q

What are examples of primary immunodeficiencies?

A

T cell specific
B cell specific
T/B cell combined
Phagocytic disorders

38
Q

What are clinical signs that suggest primary immunodeficiency disease?

A

+ family history
infections in many anatomical locations
increasing frequency & severity of infections w/ age
recurrent serious infections w/ common pathogens
serious infections w/ unusual pathogens

39
Q

T cell primary immunodef

A

disseminated intracellular disease that presents in 3-4 months of life

DiGeorge syndrome

40
Q

B cell primary immunodef

A

present @ 6 months of age when maternal antibodies disappear, show sinopulmonary & GI infections

CVID

41
Q

T/B cell combined primary immunodef

A

combo of T cell & B cell features

SCID

42
Q

DiGeorge Syndrome presentation

A

22q11 deletion

thymic aplasia (absent thymic shadow on Xray)

hypoparathyroidism & hypocalcemia (tetany & seizures)

43
Q

CVID presentation

A

defect in B cell maturation

present w/ lymphadenopathy & splenomegaly

44
Q

SCID presentation

A

onset @ 3 months of age w/ diarrhea, pneumonia, otitis, sepsis

failure to thrive

45
Q

Phagocytic primary immunodef

A

sinopulmonary & soft tissue infections

Chediak Higashi syndrome

46
Q

Chediak Higashi syndrome

A

defect in microtubular function that leads to decreased phagocytosis

partial oculocutaneous albinism, progressive neuropathy

47
Q

HIV/AIDS pathogenesis & presentation

A

spreads thru transmission of body fluids

initially asymptomatic & then have flu-like symptoms:

myalgias
fever
anorexia
headache/fatigue
pharyngitis
48
Q

How is HIV/AIDS diagnosed?

A

ELISA screen
Western blot confirmation
HIV RNA viral load

49
Q

What is important to ask about in new patient appointment?

A

ask about past HIV screen b/c all pts btwn ages 13-64 need to be screened for HIV at least once

50
Q

How is AIDS diagnosed?

A

CD4 count<200 cells

presence of an AIDS-defining illness

51
Q

What are AID defining illnesses?

A

cytomegalovirus
mycobacterium avium-intracellulare
candidal esophagitis

(OMS1) PCM II Final (9 decks)

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