Lecture 4

Question 1

Hypersensitivity disorders

Answer 1

increased or inappropriate immune response to the presence of an antigen that results in tissue destruction due to the host immune response itself

Question 2

Allergen

Answer 2

special class of antigens that elicits an allergic response

Question 3

Rapidity of immune response categories

Answer 3

Immediate = occur within minutes of exposure
Late phase = persist for hours-days after allergens are removed
Delayed = occurs after sensitization to antigens, several days later

Question 4

Type 1 hypersensitivity

Answer 4

immediate, called atopic conditions. examples include hay fever, hives, asthma, anaphylaxis

Question 5

pathogenesis of type 1 hypersensitivity

Answer 5

some people in response to antigens have hereditary predisposition to produce IgE instead of IgG in response to common environmental agents
IgE bind to mast cells, when allergen combines with mast cells, histamine is produced

Question 6

Local reactions of type 1 hypersensitivity

Answer 6

nose because IgE combines to mast cells to release histamine

Question 7

Serious systemic reactions of type 1 hypersensitivity

Answer 7

anaphylaxis = widespread histamine release occurs
causes widespread vasodilation, bronchospasm, increased mucus production, edema, irticaria, rhinorrhea

Question 8

Edema

Answer 8

accumulation of plasma in interstitial tissue

Question 9

Type 2 hypersensitivity

Answer 9

antibody mediated
examples: cross-reaction between pathogen and body tissue, like rheumatic fever/blood transfusion reactions

Question 10

Pathogenesis type 2 hypersensitivity

Answer 10

antibodies that attack antigens on the surface of cells
process starts by binding of antibodies to tissue specific antigens
activation of complement occurs, leading to clumping and phagocytosis of pathogens
body can misinterpret its own cells during immune response to pathogen

Question 11

Type 3 hypersensitivity

Answer 11

immune complex mediated disease
excessive immune complexes in circulation are cleared by complement and phagocytic cells
if IC are able to deposit in tissues, complement system is activated, leads to inflammation and local tissue injury
results in vasculitis (inflammation of blood vessels), which damages tissues

skin = urticaria
joints = arthritis
kidneys = nephritis
lungs = pleuritis

Question 12

Type 4 hypersensitivity

Answer 12

cell-mediated immunity, delayed
developed later in adulthood
includes contact dermatitis, latex sensitivity, transplant rejections

Question 13

Pathogenesis Type 4 hypersensitivity

Answer 13

tissue damage results from delayed cellular reaction to an antigen
slow onset/offset begins 24 hr exposure and last up to 14 days
primary antibody involvement is absent
antigen is processed by macrophages and presented to helper t cells
T cells secrete cytokines, helps to recruit lymphocytes, monocytes, macrophages, neutrophils

Question 14

Autoimmune disorers

Answer 14

failure in distinguishing self from non self
usually present in connective tissue
shared findings = HLA types, WBC counts, presence of autoantibodies
differentiation/diagnosis are often quite difficult
treatment is difficult, trying to quiet immune system while helping it function

glucocorticoids are the most helpful

Question 15

Lupus Erythematosus

Answer 15

chronic inflammatory autoimmune disorder
Types: SLE, discoid lupus (affects only skin), drug induced (stops when drug is stopped)
no recent estimates of prevalence and incidence

Question 16

Risk factors for lupus

Answer 16

young female
non-caucasian women
infection with epstein barr virus

Question 17

Pathogenesis of lupus

Answer 17

exact cause is unknown
multifactorial: immunological, genetic, hormonal, environmental
generalized autoimmune disease
causes deposition of antibody antigen complexes
the body makes antibodies against anything cellular

Question 18

Immune complex

Answer 18

bonded connection of antibody with antigen

Question 19

Clinical presentation of lupus

Answer 19

flares
signs/symptoms usually develop at intervals, rather than all at once
many organ systems can be affected

musculoskeletal = arthralgia, arthritis
renal = renal failure, anemia
cutaneous = butterfly rash

Question 20

Treatment of lupus

Answer 20

there is no cure
goals are to decrease autoimmune and inflammatory processes, prevent flare ups, achieve remission
pharamacological management

NSAIDs, antimalarial drugs, immunotherapy, glucocorticoids

Question 21

Patient education

Answer 21

rest is necessary
practice energy conservation (perform activities during peaks, reduce energy for task, analyze task before completing it)
photoprotection is vital
medication adherence
stress reduction is beneficial
avoid smoking
dietary consult
exercise is vital

Question 22

Prognosis of lupus

Answer 22

outlook of most people has become increasingly favorable due to early diagnosis and treatment
significant morbidity and mortality
illness pursues relapsing and remitting course. natural history varies
15 year survival rate
mortality is caused by CVD, infections, renal disease

Question 23

Complication of Lupus

Answer 23

Avascular necrosis
Renal problems
Adverse drug reactions

Question 24

Avascular necrosis

Answer 24

when blood supply to bone diminshes
tiny breaks in bone occur, leading to collapsed bone
can be due to lupus or medication
most common in the hip, increased pain with weightbearing

Question 25

Renal problems

Answer 25

note any new or increased HTN or edema and alert MD immediately

Question 26

Adverse drug reactions

Answer 26

occur in patients taking systemic glucocorticoids
cushing syndrome (thinning of skin, thin extremities, poor wound healing, easy bruising)