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PCM2 Midterm > Immunopathology > Flashcards

Immunopathology Flashcards

1
Q

Type 1 Hypersensitivity

A

IgE Ab mediated: allergy or antiparasite activity

Activation of Mast Cells: increase vascular permeability

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2
Q

Atopy

A

familiar predispostion to developing a particular allergen

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3
Q

Signs and Sx of Type 1 HS

A

Allergic conjuctivitis
Allergic Rhinitis
Atopic dermatitis (eczema)
diarrhea and cramping

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4
Q

Hypersensitivity to wasp/bee/hornet sting

A

Type 1:
Anaphylaxis to bee sting
urticarial swelling, wheezing, laryngeal swelling, obstruction
Tx: immediate SQ injection of Epi

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5
Q

Type II: Cytotoxic HS Disorder

A

Ab mediated cytotoxic reaction involving complement activation
causing lysis, recruitment of immune cells, NK cells, Autobs agains receptors

Examples of causes: ABO mismatch, transplant rejection, Goodpasture syndrome, Rheumatic fever, Newborn Rh hemolytic disease, Myasthenia Gravis, Graves disease

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6
Q

Type III: Immunocomplex Hypersensitivity Disorder

A

deposition of circulating complexes of Ag bound to IgG or IGm in target tissue with subsequent complement activation:
–neutrophils and macrophage damage tissues
*arthus reaction
Farmers lung
Serum Sickness

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7
Q

Arthus Reaction

A

Type 3 HS

-local immunocomplex deposition causing vasculitis

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8
Q

Serum Sickness

A

Type 3 Hs

fever, urticarial rash, generalized lymphadenopathy, arthritis, glomerulonephritis, vasculitis

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9
Q

Farmer’s Lung

A

Type 3 HS
exposure to actinomyces antigen in the air causing antibodies to form in the lungs

-Re-exposure produces local immunocomplex formation in lung intersitium
granulomatous inflammation occurs later: Type 4 HS

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10
Q

Type 4 HS

A

T cell mediated: cellular immunity:

  • AB not required in any of these reactions
  • -Allergic contact dermatitis: pre-exposed then reexposed
  • -PPD skin test for TB
  • -cell mediated response to intracellular pathogens with granuloma formation: late phase farmer’s lung
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11
Q

Rheumatoid Arthritis

A
  • Typical onset: Age 30-50
  • Risk factors: women, smokers, family hx
  • typical presentation: pain and stiffness in multiple joints, typically wrists and joints of hand
  • DIPS usually not impacted by RA
  • *Morning Stiffness lasting more than 1 hour suggests inflammatory etiology

ROS : fatigue, weight loss, anemia

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12
Q

Differential Dx for RA

A

Systemic lupus erythematosus, systemic sclerosis, psoriatic arthritis, sarcoidosis, crystal arthropathy, and spondyloarthropathy

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13
Q

RA Tx

A

first line: Methotrexate
(Methotrexate my not be appropriate for patients with increased risk of hepatotoxicity: alcohol abuse and fatty liver disease)
DMARDS: leflunomide, plaquenil, sulfasalzine

glucocorticoids if disease activity is high
-lowest possible dose of prednisone

**Treat Early
Goal to Tx: remission ro lowers disease activity

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14
Q

Juvenile Rheumatoid Arthritis

A

Children present w/ painless joint inflammation
normal results with rheumatologic tests
-present with limp
must last 6 weeks in at least 1 joint and exclusion of other symptoms in a person under age 16
morbidity: idopathic inflammatory eye disease

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15
Q

JRA Dx

A

diagnosis of exclusion
r/o lyme disease, leukemia, infection of bone or joint, psoriasis, IBD, Strep

lab tests don’t help you…clinical judgement

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16
Q

Systemic Lupus Erythematosus

A

Risk factors: black person, female
recurrent sx: with periods of flares
*fatigue, weightloss, fever, arthralgia, myalgia

ROS: skin, MSK, renal, neuropsychiatric, hemotologic,

Less common signs and sx:
Malar rash, new onset raynaud phenomenon, mouth sores, photosensitivity, pleuritic chest pain

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17
Q

Typical signs and sx for SLE

A 
discoid "coin shaped' rash
malar rash
Unexplained seizures or psychosis 
photosensitivity 
positive ANA
Non-erosive arthritis involving 2 or more joints
persistent proteinuria 
serositis
18
Q

If you suspect SLE

A

4 ACR criteria and Check ANA

if ANA positive: get a CBC, Urinalysis, with differential

19
Q

Tx for SLE

A
  • Hydroxychloroquinine reduces arthritis pain associated with SLE
  • combination of glucocorticoid plus immunosuppressant is more effective than glucocorticoids alone in preserving renal function

-glucocorticoid and cellcept achieves SLE nephritis

20
Q

SLE

A

female, black, episodic illness, fatigue, arthralgia, weight loss myalgia, fever without a focal infection

Exam findings:
discoid rash, malar rash, unexplained seizure or psychosis
photosensitivity, ANA, Anti-dSDNA, Anti-SM, anti cardiolipin

21
Q

Psoriasis

A

inflammatory skin condition
onset between 15-30 years
smoking increases risk of psoriasis and severity
1/3 of psoriasis patients have 1st degree relative with condition
-physiologic stress associated with onset and worsening of condition
direct skin trauma can trigger psoriasis

worsens with HIV

22
Q

Dx of Psoriasis

A

scaly skin lesions with additional manifestations in the nails and joints. plaque psoriasis is the most common

23
Q

Psoriasis exam

A

consider a joint exam if you see a rash and pitting of the nails

24
Q

Psoriasis Tx

A

topical corticosteroids, vitamin D analongs and tazarotene

systemic biologic therapies for moderate to sever psoriasis

TNF inhibitor for psoriatic arthritis

25
Q

Grave’s Disease

A

Chronic Autoimmune thyroid disorder
Thyroid stimulating antibodies activate TSH receptors which triggers increased TH synthesis to amplify catacholamine signaling thru increased bAr recptors

Risk factors: female, family hx of autoimmune disorder

Signs and Sx: palpitations, heat intolerance, diaphoresis, tremor stare, hypermetabolism

26
Q

Tx for Graves Disease

A

beta blockers, Anti-thyroid medication

27
Q

Hashimoto’s Thyroiditis

A

Chronic Autoimmune thyroid disoder
immune cells attack the thyroid to limit its production
Present: hypothyroidism with an elevated TPO Ab level

risk factors: female, family history of autoimmune disorder

signs and sx: fullness in the neck, fatigue, weight gain, thyroiditis, diffuse muscle pain

Tx: levothyroxine

28
Q

Dx for Hashimotos

A

A frank elevation in TPO Ab level

Measure TSH Levels

29
Q

Primary Immunodeficiency in children

A

antibody, combined b cell and cell, phagocytic, complement disorders

  • positive family history
  • infections in multiple anatomic locations
  • increase frequency and severity of infections with age
  • recurrent serious infections with common pathogens
  • serious infections with unusual pathogens
30
Q

Antibody disorders

A

majority of primary imunodeficiency
presentation: unusually severe and recurrent infection with common organisms
broadly characterized as absence or presence of B cells

if B cells present: are they of normal quantity or quality

31
Q

Agammmaglobulineima

A

(X linked bruton tyrosine kinase deficiency)
-born absent of b cells in peripheral and umbilical blood
-tonsils and lymph nodes may be absent
All Ig subclasses are decreased with absence of B cell lymphocyte subset analysis

32
Q

Hypogammaglobulinemia

A

low or deficient levels of any of the Igs or abnormal response of immunoglobulins to vaccinations
most reported CVID…in CVID at least 2 subsets of Igs are low

persists after 3 months
ear, sinus, pulmonary infections
GI problems also occur in CVID

33
Q

T cell disorders

A

t cells are important to normal function of b cell so most t cell deficiency leads to combined T cell and B cell disorder

SCID is the the most serious

34
Q

SCID

A

presents at life threatening infection as an infant
T cell disorder
diarrhea, failure to thrive, opportunistic infection, sever routine infections in children younger than 3 months

35
Q

Phagocytic Disorder

A

abnormalities in neutrophils or monocytes
usually diagnosed by age 5

characterized by pneumonia, abscesses, supprative adentis, GI infections
*first sign is omphalitis in infants

Infections related to inability to kill catalase postive organisms including staph aureus, candida

invasive fungal infection

36
Q

Complement Disorders

A

rare in regards to primary immunodeficiency disease
disorders involves encapuslated organisms
deficiency of C3 is associated with pyogenic infections of strep pneumoniae and H influenzae
C5-C9 deficiency is associated with N. Meningitidis

37
Q

How will primary immunodeficiency disease present?

A

Recurrent ear, sinus, pulmonary infections, diarrhea, failure to thrive

  1. positive family history for immunodisease
  2. Diagnosis of sepsis treated with IV antibiotics
  3. Failure to thrive
38
Q

Recurrent infection in 1 anatomic location

A

more likely to have anatomic defect than immunodeficiency …if infection is present in 2 or more sites we should suspect immunodeficiency

39
Q

HIV

A

acute hiv infection occurs before seroconversion
some people are asymptomatic
OR: transient symptoms related to high levels of HIV with viral replication

*often misdiagnosed with influenza

Signs and Sx: mucocutaneous ulcerations, rash, myalgia, arthralgia, anorexia, weight loss, fever, CNS manifestations, fatigue, headache, lymphadenopathy, pharyngitis, GI distress

40
Q

HIV differential

A

Epstien Barr, Influenza, Strep Pharyngitis, Viral URI, Acute viral hepatitis, drug reaction, secondary syphillius

41
Q

Acute HIV illness

A

1-4 weeks after transmission
presents as mononucleus or influenza like
clinically resembles a T cell immunodeficiney disorder

42
Q

Test for HIV

A

HIV Viral RNA load–11-12 days
P24 antigen (core protein in HIV virus)–14-15 days
HIV Elisa–3 to 8 weeks

PCM2 Midterm (8 decks)

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