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McGill Note- General > Immunology > Flashcards

Immunology Flashcards

1
Q

Q: What are the 5 antigen presenting cells of the body [?]

A
  • Monocyte
  • Macrophage
  • Dendritic cell
  • Langerhans cell
  • B-cell
    • Also, Microglia (brain) and Kupfer cells (liver)
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2
Q

Q: Discuss cell-mediated immunity [?]

A
  • Type of adaptive cell immunity
  • Major Histocompatibility Complex proteins:
    Class I – present on all nucleated cells, binds to CD8+
    Class II – present on APC’s, bind to CD4+ -
  • T-cell subclasses:
    1-Helper cells (TH) – Express CD4+, recognizes class II MHC’s (signal 1) and requires CD28 activation (signal 2) = secretes IL2 (autocrine-based proliferation); 2 subsets:
    TH1 (cell mediated) stimulates IgM, IgG and IgA 􏰁 macrophages CD8+ T cell activation & increases CMI response,
    TH2 (humoral); activate B cells (IgE > IgG)
    2- Cytotoxic (TC) – Express CD8+, recognizes antigen expressed with Class I MHC
    3- Suppressor (TS)
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3
Q

Q: Discuss humoral immunity [?]

A
  • B-cells bear surface receptors (Fc) similar to Ig’s
  • T-dependent activation: Antigen is bound, processed and expressed on MHC II; primed CD4 TH2-cell (turned on from same Ag from different cell) binds to B-cell CD40, which causes cell proliferation and plasma cell differentiation
  • T-independent activation – strong Ags (bacterial capsule / cell wall); Inefficient, provides mainly IgM
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4
Q

Q: Discuss Immunoglobulins: Structure; subtypes [?]

A
  • Structure – 2 Light chains (2 types = kappa & lambda), 2 Heavy chains (5 types, determine class of antibody= M, A, G, E, D)
  • IgM – Predominates in early immune response; Pentameric, IgM & IgD main Ig’s expressed on B-cell surface
  • IgA – Predominates in bodily secretions; primary defense against local mucosal infection, dimeric with a secretory component bound to it
  • IgG – 75% of total serum antibodies; 4 subtypes, crosses placenta to protect fetus, can fix complement - IgE – Binds to mast cells & basophils, triggers inflammatory mediator release
  • IgD – Found in serum; monomeric, main function unknown
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5
Q

Q: Discuss Complement: Activation pathways (2), 4 activities [?]

A
  • Primary humoral mediator of antigen-antibody reactions
  • 2 Activation Pathways:
    Classical (activated by IgG/IgM, C1 –> C4b,2b)
    Alternative (PAMPs (pathogen associated molecular patterns), C3 –> C3b,Bb)
  • 4 Biologic activities (COAL)
    Chemotaxis
    Opsonization,
    Cell Activation (neutrophils & macrophages)
    Cell Lysis through the membrane attack complex (MAC)
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6
Q

Q: Describe the allergic reaction at the cellular level [?]

A
  • Early response (~5 minutes post-exposure) – mediated by Mast cells & Basophils; IgE binds to FceR on mast cell, crosslinking of IgE triggers activation = Degranulation of mast cell’s preformed mediators (histamine, heparin, tryptase, beta-glucosaminidase, eosinophil & neutrophil chemotactic factors), and Synthesis of mediators from membrane bound phospholipids (PGs, LTs, PAF)
  • Late response (~4 hours post exposure) – mediated by neutrophils & eosinophils, reaction secondary to cytokines
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7
Q

Q: Describe 3 phases of allergic rhinitis [?]

A
  • Acute – due to Histamine and other preformed/newly synthesized mediators; causes sneezing, itchy eyes, nose and throat, nasal discharge
  • Intermediate or transitional – due to recruitment and activation of leukocytes into nasal tissue, asymptomatic
  • Late phase – 4-6 hours post exposure, due to leukocytes in nasal tissue; main symptom is nasal congestion
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8
Q

Q: Gell and Coombs Type Hypersensitivity Reactions (ACID) [?]

A
  • Type I – Allergy (immediate); TH2 / IgE (Allergic rhinitis, anaphylaxis, asthma)
  • Type II – Cytotoxic, Ab-dependent; TH1 / Cytotoxic IgG or IgM antibody mediated (goodpasture)
  • Type III – Immune complex mediated, Ag-Ab-Complement (serum sickness, Arthus reaction)
  • Type IV – Delayed type hypersensitivity, T-cell mediated CD8+ (TB test, contact dermatis)
  • Type V – Receptor-stimulating Ig (Pasha)
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9
Q

Q: Four cellular effects of histamine [?]

A
  • Vasodilation
  • Increases capillary permeability
  • Bronchoconstriction
  • Tissue edema
  • Main mediator of early allergic reaction
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10
Q

Q: Five proteins found in eosinophils [?]

A
  • Major basic protein (MBP)
  • Eosinophil cationic protein (ECP)
  • Eosinophil peroxidase (EPO)
  • Charcot Leyden crystal
  • Neurotoxin
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11
Q

Q : Discuss HIV: diagnostic tests, clinical categories (including definition of AIDS) [?]

A
  • Acquired immunodeficiency syndrome
  • Family retroviridae (subfamily = lentivirus) - Strong disease correlation with CD4 counts
  • Three clinical categories
    A – Asymptomatic, PGL, or Acute HIV infection
    B – Symptomatic condition attributable to HIV infection and associated defects in CMI, but not in A or C
    C – AIDS (diagnosis = CD4+ <200 cells/uL, or HIV+ with AIDS defining disease (H&N: NHL, Kaposi, Candidiasis, oral HSV, Mycobacterium, PC, TB)
  • Stratification by CD4 counts - >500 cells/uL, 200-499 cells/uL, <200 cells/uL
  • H&N Manifestations: Oralcavity/oropharynx (oral candidiasis) > cervical LAD > rhinosinusitis >
    CSOM
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12
Q

Q (DO): Definition of AIDS?

A

CD4+ < 200 cell/uL + AIDS defining disease

AIDS defining disease?
1. Candidiasis of bronchi, trachea, or lungs
2. Candidiasis esophagea
3. Coccidioidomycosis, disseminated or extrapulmonary
4. Cryptococcosis, extrapulmonary
5. Cryptosporidiosis, chronic intestinal for longer than 1 month
6. Cytomegalovirus disease (other than liver, spleen or lymph nodes)
7. Cytomegalovirus retinitis (with loss of vision)
8. Encephalopathy (HIV-related)
9. Herpes simplex: chronic ulcer(s) (for more than 1 month); or bronchitis, pneumonitis, or
esophagitis
10. Histoplasmosis, disseminated or extrapulmonary
11. Isosporiasis, chronic intestinal (for more than 1 month)
12. Kaposi’s sarcoma
13. Lymphoma, Burkitt’s
14. Lymphoma, immunoblastic (or equivalent term)
15. Lymphoma, primary, of brain
16. Mycobacterium avium complex or Mycobacterium kansasii, disseminated or
extrapulmonary
17. Mycobacterium, other species, disseminated or extrapulmonary
18. Mycobacterium tuberculosis, any site (extrapulmonary)
19. Pneumocystis jirovecii pneumonia (formerly Pneumocystis carinii)
20. Progressive multifocal leukoencephalopathy
21. Salmonella septicemia (recurrent)
22. Toxoplasmosis of the brain
23. Tuberculosis, disseminated
24. Wasting syndrome due to HIV

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13
Q

Q: Pathologies associated with low CD4 counts and prophylaxis [?]

A
  • <400 cells/uL = TB
  • <200 cells/uL = NHL (including sinonasal), PCP – Septra
  • <150 cells/uL = Fungal sinusitis
  • <100 cells/uL = Kaposi sarcoma, Cryptococcal meningitis, Toxoplasmosis
  • <50 cells/uL = Aspergillus, Cryptosporidiosis, CMV, Mycobacterium – Azithromycin - Hodgkin’s is associated with a wide range of CD4
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14
Q

Q: Eight Indications for open biopsy of lymphadenopathy in HIV [?]

A

1- FNA that suggests Malignancy
2- FNA negative for malignancy with any of: [
- Enlarging node
- Nodes >2cm
- Asymmetric, localized, unilateral adenopathy
- Significant mediastinal or abdominal lymphadenopathy
- Failed antibiotic trial
- Low CD4 with new lymphadenopathy
- B symptoms – Fever, night sweats, weight loss

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15
Q

Q: Ddx of cervical disease in HIV; most common [?]

A
  • Persistent generalized lymphadenopathy (PGL, 12-45%)
  • Mycobacterium tuberculosis
  • Pneumocystis (carnii)jirovecii pneumonia (PCP)
  • Lymphoma
  • Kaposi sarcoma (Human Herpes Virus 8)
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16
Q

Q: DDx of skin manifestations of HIV (6) [?]

A
  • Molluscum contagiosum (watery warts; caused by MCV)
  • Bacillary angiomatosis (found in immunicompromised pts wth Bartonella Henselae infection) - KS
  • HSV
  • Herpes Zoster
  • Cryptococcus
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17
Q

Four Indications for Treatment of Localized Kaposi sarcoma [?]

A

KS = HHV-8

  • Cosmesis
  • Reduction of symptom
  • Improved local control
  • ?Functional compromise?
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18
Q

Q: Five Treatment modalities for small localized Kaposi sarcomas [?]

A

CONSERVATIVE
- Observe/do nothing

MEDICAL

  • Radiation (only if localized obstruction)
  • Chemotherapy: interferon, vinblastine (impair mitotic spindle)
  • Topical immunomodulators
  • Topical retinoic acid

SURGICAL

  • Laser excision
  • Cryotherapy
  • Surgical excision (cosemesis, functional compromise, local control, reduction of symptoms)
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19
Q

Q: Three Indications for Treatment of Systemic Kaposi sarcoma [?]

A
  • Visceral disease
  • Pulmonary disease
  • Extensive mucocutaneous involvement (>10 new in 1 month)
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20
Q

Q: Treatment options for Systemic Kaposi sarcoma [?]

A

HAART (as per emedicine)

  • Liposomal Doxo- or Daunorubicin +/- Combination Vinblastine-Bleomycin
  • Systemic Etoposide and Paclitaxel
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21
Q

-Q: Oral hairy leukoplakia: Cause, chance of AIDS, 4 other oral findings in AIDS [?]

A

Due to EBV (herpes family) infection

  • Chance of HIV - AIDS: 50% at 15mos, 80% at 30mos, 100% at 60mos
  • White, vertically corrugated asymptomatic lesion on anterolateral tongue
  • Oral Findings in HIV/AIDs:
  • Fungsl: candidiasis, crptococcus, histoplasmosis
  • VIRAL: CMV, VZV HSV, HPV
  • Neoplastic: Kaposi sarcoma, lymphoma
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22
Q

Q: Describe this condition [?]

A

black hairy tongue , aka Lingual Villosa Nigra

  • Occurs on the anterior surface of the tongue, anterior to circumvillate papillae
  • RF: (i) smoking, (ii) poor oral hygiene (iii) xerostomia, (iv) soft diet
  • Histology: elongation of filliform papillae, hyperkeratosis, bacteria
  • Rx: good oral hygiene, add roughage to diet, +/- keratolytics or anti-fungals; surgical
    debridement (laser, electrodesiccation, cold steel) if other options fail
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23
Q

Q: Discuss MS: Clinical, Charcot’s triad, Diagnosis, 4 types, & Treatment [?]

A
  • Immune mediated inflammatory disease attacking myelin of CNS in young adults
  • DDx: ALS, MG, HIV encephalopathy, Lyme disease, TIA/RIND/CVA
  • Dx:
  • Labs: autoimmune workup, FTA-Abs, lyme dz, CBC, ESR, CRP
  • Imaging: MRI (demyelined foci in white matter), Evoked potentials, LP = elevated protein/glucose/IgG

*Charcot’s triad – nystagmus, scanning speech, intention tremor
Subtypes: (1) primary progressive, (2) secondary progressive, (3) relapsing-remitting, (4) progressive-relapsing
*Rx: Acute = steroids, plasma exchange (plasmapharesis)/ Chronic - disease modifying agents for MS (interferon-beta, peginterferon-beta, natalizumab)

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24
Q

Q: Discuss Myasthenia Gravis: DDx; Pathophysiology, Causes, Dx, Treatment [?]

A

Autoimmune disease against the Ach nicotinic postsynaptic receptors of the NMJ

  • DDx: MS, ALS (EOMs preserved!), basilar artery thrombosis, Lambert-Eaton (Abs against presynaptic Ca Channels releasing ACh, can be associated with lung cancer, better with repetition)
  • Diagnosis – History, Tensilon test (edrophonium = short active AchE inhibitor), 85% positive anti-AChR Ab, Anti-MuSK, anti lipoprotein related, anti-agvin, anti-striational, EMG (repetitive stimulation test, single fiber EMG)
  • Types – MGFA Class I (only ocular) to Class V (intubated)
  • Treatment – Thymectomy, Acetylcholinesterase inhibitors – Edrophonium (Tensilon), Neostygmine, Pyridostigmine (Mestinon), IVIG, plasmapheresis
  • Triggers of exacerbation: surgery, immunizations, infection, extreme sunlight, menstruation, drugs (Ag, Lithium, beta-blockers)
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25
Q

Q: Define Sluder syndrome [?]

A

Sphenopalatine ganglion neuralgia that results in constellation of neural, motor, sensory, and gustatory manifestations
CF:
- Localized facial pain (orbit, nose/V1, V2
- Vasomotor abN (lacrimation, rhinorrhea, salivation

26
Q

Q: Discuss the boundaries of the sella turcica/pituitary [?]

A
  • Superior – Diaphragma sellae & optic chiasm
  • Anterior – Tuberculum sellae
  • Inferior – Sphenoid sinus
  • Lateral – Cavernous sinuses
  • Posterior – Dorsum sellae
27
Q

Q: Discuss the components of the pituitary gland [?]

A
  • Adenohypophysis (Anterior) – Derived from Rathke’s pouch (ectoderm); secretes ACTH, FSH/LH, GH, PRL, TSH
  • Neurohypophysis (Posterior) – Axons of cell bodies from supraoptic & paraventricular nuclei of hypothalamus; secretes Oxytocin & ADH
28
Q

Q: Classification of pituitary adenomas [?]

A
  • Class I – Microadenoma (<10 mm)
  • Class II – Macroadenoma (>10 mm)
  • Class III – Partial destruction of sellar floor
  • Class IV – Total destruction of sellar floor
29
Q

Q: Describe Carcinoid syndrome [?]

A
  • Endogenous secretion of mainly serotonin and kallkrien from carcinoid tumour→ resulting in an array of symptoms including flushing, diarrhea, bronchoconstriction, and CHF
  • Most common “APUDoma”
  • A = amine (high amine content)
  • PU = precursor uptake (high content of amine precursor)
  • D = decarboxylase (high content of enzyme amino acid decarboxlylase; concerts precursor to amine)
  • Dx: 24 hour urine collection of 5-HIAA, CT/MRI of suspected site. 5-HIAA = hydroxyindoleacetic acid = main metabolite of seratonin
  • Rx: Surgery, pharmacotherapy
30
Q

Q: What does APUD stand for [?]

A

APUD Cells:

  • Amine Precursor Uptake - for high uptake of amine precursors
  • Decarboxylase - for high content of the enzyme amino acid decarboxylase (for conversion of precursors to amines)
31
Q

Q: Describe ANCAs [?]

A
  • Anti-Neutrophil Cytoplasmic Antibody
  • c-ANCA - cytoplasmic; binds proteinase 3 (PR3) located in neutrophil cytoplasm (Wegner’s, microscopic polyangitis, Goodpastures)
  • p-ANCA - perinuclear; binds myeloperoxidase (MPO) in neutrophil nuclei (Churg Strauss, PAN, Crohn;s Kawasaki, CF, PTU, Goodpastures)
32
Q

Q: Churg-Strauss: Definition, Dx Criteria [?]

A

aka Eosiniphilic Granulomatosis with polyangitis OR allergic granulomatosis vasculitis
Affects small-medium sized vessels

Diagnosis: At least 4/6 of PEANUT
○ Paranasal sinus abnormality
○ Eosinophils > 10%
○ Asthma
○ Neuropathy
○ Unfixed (non-fixed) pulmonary infiltrates
○ Tissue biopsy: Extravascular eosinophils

33
Q

Q: Churg-Strauss: Phases, DDx, Ix, Rx [?]

A

Phases:

  • 1st: Prodromal: allergic rhinitis, polyps, asthma
  • 2nd: Loeffler Syndrome: hypereosinophilia in peripheral blood and tissues
  • 3rd: systemic necrotizing vasculitis

DDx: WG, Goodpasture, sarcoidosis, PAN, hypereosinophilia syndrome
Ix: pANCA (50%), ESR, CRP, RA, CBC, biopsy
Tx: high dose steroids, cyclophophosphamid

34
Q

Q: Ddx of non-neoplastic, non-traumatic, and non-infectious subglottic stenosis in adults [?]

A

Aka autoimmune or systemic causes

  • Sarcoidosis
  • Wegener’s granulomatosis (Granulomatosis with polyangitis/GPA)
  • Amyloidosis
  • Relapsing polychondritis
  • Idiopathic
35
Q

Q: Amyloidosis: What is deposited? Most common sites, Ix, Dx, Tx [?]

A
  • Deposition of extracellular deposition of fibrillar proteins
  • Classification: (i) primary vs. secondary OR (ii) localized vs. systemic
  • Dx: bifringerence in polarized light
  • Primary and/or Myeloma → light chain Ig
  • Secondary → amyloid associated protein

MC sites: Primary: tongue > orbit > larynx (TVC, ventricle, FVC)> trachea)

  • Ix: (i)Biopsy of lesion (congo red stain)
    (ii) bone marrow biopsy for plasma cells (MM)
    (iii) serum protein electrophoresis, urine protein electrophoresis
  • Rx: conservative, removal of depositions (fxnal compromise), steroids +/- chemo +/- colchicine
36
Q

Q: Amyloidosis: subtypes [?]

A

Primary Localized: 9%
Primary systemic: 56% → mesenchymal organs (heart, tongue, GIT)

Myeloma associated: 26%

Secondary systemic: 8%; due to destructive dz (TB, RA, osetomyelits → kidney, spleen, liver, adrenals)
Secondary localized (Alzheimers, Parkinson, Huntingtons)
37
Q

Q: Histopathological tests for Amyloid [?]

A
  • Congo Red (apple-green birefringence under polarized light)
  • Crystal violet
  • Thioflavin T
38
Q

Q: Ten H&N manifestations of SLE [?]

A
  1. Malar skin rash (50%)
  2. Telangectasias of H&N
  3. Acute parotid enlargement (10%)
  4. Chronic Xerostomia
  5. Painful oral ulcers
  6. TVF thickening
  7. SGS
  8. CA joint arthritis
  9. Cranial neuropathy (15%)
  10. Septal perforation and ulcers (3-5%)
39
Q

Q: Diagnostic criteria of SLE [?]

A

≥4/11 of: “SOAP BRAIN MD”

  1. Serositis (pericarditis, pleuritis)
  2. Oral ulcers
  3. Arthritis
  4. Photosensitivity
  5. Blood disorders
  6. Renal involvement (proteinuria, cellular casts)
  7. ANA
  8. Immunologic phenomenon (anti-Smith, anti-phospholipid, anti dsDNA)
  9. Neurological disorders
  10. Malar rash
  11. Discoid rash
40
Q

Q: Treatment options for SLE [?]

A
  • Disease modifying antirheumatic disease (DMARDs): retuximab, belubimab
  • non-DMARDs: MTX, cyclophosphamide
  • Antiinflammatories: NSAIDs, steroids
  • Anti Malarials: hydroxychloroquine
41
Q

Q: Diagnostic Criteria of Rheumatoid Arthritis [?]

A

> 4/7 for > 6 weeks + observed by a physician

  1. Morning stiffness > 1h
  2. 3+ joint swelling
  3. Hand joint swelling
  4. Symmetrical joint swelling
  5. Subcutaneous rheumatoid nodules
    • RF on serology
  7. X Ray finds of joint osteopenia + erosion
42
Q

Q: Four H&N manifestations of Rheumatoid Arthritis [?]

A 
Neck: cervical arthritis, pain reduced ROM
TMJ dysfunction (pain and tenderness overlying muscles0
Throat #1: Cricoarytenoid joint arthritis →arytenoid edema, decreased mobility, fixed cords in adduction, dysphonia, stridor, dyspnea
Throat #2: TVF nodules = bamboo nodules,
Ear: ossicle fixation (tympanogram = As/decreased compliance with normal pressures)
43
Q

Q: Bechet’s syndrome [?]

A

Multisystem disease of unknown etiology
Dx: Recurrent Oral Ulcers (≥3 episodes / yr) AND 2 of:
1. Genital ulcers
2. Eye lesions (uveitis)
3. Skin lesions (erythema nodosum)
4. Positive pathergy test (papular/pustular response to skin trauma)

Also get Progressive SNHL
DDx: IBD, Reiter’s, Pemphigus, Viral (HSV/EBV/HIV/Cox), aphthous, Trauma, SCC, SLE
Treatment – Corticosteroid cream for ulcers, Colchicine or Dapsone PO, myadriatics and
corticosteroid drops for eyes

44
Q

Q: Sarcoidosis (definition, ethnicity, Tx) [?]

A

Idiopathic multi-system non-caseating granulomatous disease; affects mainly black females
Clinical Features:
1. Cervical LAD (40%)
2. Supraglottic mass
3. VC paralysis
4. Nasal or orbital mass
5. Septal perforation
6. Pulmonary hilar LAD (most common presenting system)
7. Heptatic, renal, splenic, bone and nerve involvement

Rx: steroids

45
Q

Q: Sarcoidosis (Dx, associated syndromes) [?]

A

Diagnosis:
1. Labs: elevated (i) ACE, (ii) calcium, (iii) ALP, (iv) hypercalciuria, (v) SPEP
2. Imaging: CXR → stages sarcoidosis
Stage 0: no CXR findings
Stage1:bilateralhilarLAD
Stage2:BilateralhilarLAD+pulmonaryinfiltrates(parenchymal)
Stage 3: Bilateral infiltrates (parenychymal)
Stage 4: Fibrosis
3. Biopsy: non-caseating granulomatous dx of Langerhan giant cells
Schaumman bodies: calcium+protein within Langerhan giant cells
Asteroidbodies: located within Langerhan giant cells

Ass syndromes

  • Heerfordt Syndrome: uveopartoid fever → parotitis, uveitis, fever, VII paralysis
  • Lofgren Syndrome: polyarthralgias, erythema nodosum, bilateral hilar LAD
  • Lupus Pernio: cutaneous lesion pathognomonic for sarcoid; chronic, violaceous cutaneous lesions with a predilection for cold-sensitive areas such as the nose, cheeks, ears, and fingers
46
Q

Q: Head and Neck manifestations of Sarcoidosis [?]

A
  • Eye – Episcleritis, uveitis, conjunctivitis, orbital mass
  • Salivary glands – Parotid swelling (bilateral)
  • Neck – Cervical lymphadenopathy
  • Oropharynx – Tonsillar hypertrophy
  • Nose – Lupus pernio, inflammation, septal perforation, nasal crusting
  • Larynx – Epiglottic swelling (turban epiglottis) and subglottic stenosis, supraglottic mass
  • Neuropathies – CN VIII (sudden SNHL), CN VII (unilateral or bilateral facial palsy), CN X (VC paralysis
47
Q

Q: Diagnostic criteria of Sjogren’s [?]

A

Require 4/6 for diagnosis; one of which must be positive labs or biopsy:

  • Ocular Symptoms:
    » Dryeyes>3months
    » FBsensation
    »Use of tear lubrication >TID
  • Glandular Symptoms:
    »Drymonth
    »Recurrent swollen salivary glands
    »Use of liquids to aid swallowing
  • Ocular Signs:
    »Rose-Bengalscore>4
    » SchirmerTest:<5mmin5min
  • Glandular Signs:
    » Salivary scintinography: reduced uptake in Tech99m scan
    » Salivary sialography: diffuse sialectasis, punctate (<1mm)/globular (1-2mm) contrast collections
    » Sialometry: unstimulated flow < 1.5cc/15 min (<0.1cc/min)

** Positive lip biopsy: Focus score ≥1 = ≥50 lymphocytes in 4 mm2 of glandular tissue
(must have normal mucosa and ≥5 MSGs separated by connective tissue)
** Positive serology: anti-Ro (SS-A) or anti-La (SS-B) antibodie

48
Q

Q: Discuss Wegener’s Granulomatosis (definition, CP, DDx, Ix, and Tx) [?]

A

AKA GPA

Idiopathic autoimmune disease involving necrotizing granulomatous inflammation and vasculitis of small & medium chain vessels
Occurs in upper respiratory tract, lungs, kidneys
* DDx: Churg-Strauss, NK/T cell or DLBC lymphoma; Goodpasture’s
*Clinical:
- Eyes: uveitis, episcleritis, conjunctivitis, proptosis, NLD obstruction
- Ears: MEE, hearing loss (CHL)
- Nose: saddle deformity, rhinitis, epistaxis, nasal crusting, nasal mass
- Oro: ulcers, strawberry gingival hypertrophy
- Throat: SGS
- Lungs: infiltrates, cough, dyspnea
- MSK: arthralgias, arthritis
- Kidney: necrotizing GN, RF

  • Ix: (1) CBC (anemia),
    (2) c-ANCA,
    (3) PR-3
    (4) Imaging: sinuses, lungs, renal
    (5) BUN/Cr/urinalysis
    (6) biopsy = necrotizing granulomas, vasculitis
  • Rx: Prednisone (1mg/kg/day x 4 weeks, then taper), Cyclophosphamide (2mg/kg/day for 6- 12 months); if hemorrhagic cystitis occurs may use Methotrexate or Azathioprine; Septra, IVIG in immunosuppresion nonresponders
49
Q

Q: Subtypes of GPA [?]

A

1) Limited = E (for ENT)
2) Systemic = EL (ENT and lung)
3) Widely disseminated = ELK (ENT, lung and kidney)

50
Q

Q: Diagnostic Criteria for GPA [?]

A

4/6 of GUNC
○ Granuomatous inflammation on biopsy
○ Ulcers (oral) and nasal discharge
○ Nephritis urinary sediments (red cast cells ou >5 RBC per HPF)
○ CXR findings: nodules, fixed infiltrates or cavities

51
Q

Q: Head & Neck symptoms of Wegener’s granulomatosis [?]

A
  • Nasal (90%) : Crusting, epistaxis, obstruction, septal perforation, saddle nose
  • Otologic (25%) : CHL, suppurative OM, SNHL (can be bilateral & profound), VII paralysis
  • Oral : strawberry Gingival hyperplasia & gingivitis
  • Laryngeal : Laryngeal ulceration & edema (25%), subglottic stenosis (8.5%)
52
Q

Q: Five histologic findings in Wegener’s [?]

A

Necrotizing granulomatous vasculitis “SINGA!”

  • Small & medium vasculitis
  • Infiltration of inflammatory cells (macrophages, lymphocytes, langerhans, histiocytes multinucleated giant cells)
  • Necrotizing granulomas
  • Geographic necrosis
  • Angioinvasion
53
Q

Q: Sjogren’s syndrome: Complications, and Treatment [?]

A

Sjogren’s = chronic autoimmune disease involving lymphocytic infiltration of exocrine glands

Complications:

  • Eyes: corneal ulcers, blindness, conjunctivitis
  • Oral: dental caries, candidiasis (chronic atrophic), angular chelitis
  • Nose epistaxis, hyposmia, CRS
  • Lymphoma risk = 40x

Treatment: symptomatic

54
Q

Q: Subtypes of Sjogren’s syndrome [?]

A

􏰀 Subtypes:

  • Primary: sicca complex (xerostomia, xerophthlamia, keratoconjunctivitis)
  • Secondary: involves other autoimmune dz (i.e. RA> SLE >scleroderma/CREST > PBC)

􏰀 Sicca Syndrome: involvement of exocrine glands without evidence of autoimmune disease

55
Q

Q: Histopathology of Sjogren’s syndrome [?]

A

Need to biopsy minor salivary glands x 4 ; “LAMP”

  • Lymphocyte and histiocyte infiltration
  • Acinar cell atrophy
  • Metaplasia and hyperplasia of ductal epithelium
  • Prominent myoepithelial components as ductal lumens disappear
56
Q

Q: Five Risk factors for lymphoma in Sjogren’s [?]

A
  • Primary Sjogren’s
  • Constant parotid enlargement
  • Lymphadenopathy
  • Splenomegaly
  • Decreased IgM
57
Q

Q: Discuss Relapsing Polychondritis ( Def, and CP) [?]

A

Autoimmune dz of unknown etiology involving recurrent episodic inflammation of cartilaginous structures; especially ears, nose, and laryngotracheobronchial tree.

Clinical Features:
- Eyes: scleritis, uveitis conjunctivitis, decreased vision, diplopia, eyelid swelling
- Ears: inflammation of CNVIII → otalgia, OM, HL, vertigo, lobule-sparing auricular
chondritis, tinnitus, collapse/loss of structure
- Nose: swelling, inflammation, saddle nose deformity, epistaxis
- Throat: laryngeal swelling, laryngomalacia, tracheomalacia, stenosis
- CVS, MSK, systemic, kidney

58
Q

Q: Diagnostic criteria of Relapsing Polychondritis [?]

A
59
Q

Q: Whats the diagnosis and what’s the Most common HN presentation, overall finding, and laryngeal finding [?]

A

Uveoparotid fever (Heerfordt’s disease)

● Most common HN presentation = Cervical lymphadenopathy
● Most common overall finding: Hilar adenopathy
● Most common laryngeal finding: Supraglottic submucosal mass (epiglottis)

60
Q

Q: What’s the diagnosis [?] [Path]

A

Sarcoidosis

Above Schaumann bodies (calcium and protein inclusions within a Langerhan cell)

Below. Asteroid bodies (cytoplasmic inclusions within a Langerhans cel)

61
Q

Q: What’s the diagnosis and name the subtypes [?][Path]

A

Lichen Planus

Types: Playa ARUBA (Plaque, Annular, Reticular, Ulcerative, Bullous, Atrophic)

McGill Note- General (4 decks)

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