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133 Cards in this Set
- Front
- Back
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Hypersensitivities what test would it be positive?
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positive coombs test
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what are the 4 types of hypersensitivities?
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Type 1: Anaphylaxis
Type 2: Atopy Cytotoxic Type 3: Immune Complex Type 4: Delayed/Cell mediated |
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examples of anaphylaxis?
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Urticaria "hives"
Anaphylaxis Food allergies Angioedema |
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5 examples of cytotoxic
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autoimmune
Hemolytic anemia Goodpasture's Graves Rh/ABO |
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examples of immune complex (4)
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SLE ( exception)
RA (exception) Serum sickness Cryoglobulinemia |
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examples of Delayed /Cell mediated (4)
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Contact dermatitis
TB skin test Sarcoidosis Chronic transplant rejection· |
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Cell responsible for Type I
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Mast cell
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cell reponsible for type II
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TK and MAC
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cell reponsible for type IV
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Langerhans cell
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Mediator: type I
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IgE
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mediators for type 2 hypersensitivity
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IgG/IgM
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mediators for type 3 hypersensitivity
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Ag-Ab
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mediators for type 4 hypersensitivity
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hapten
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pathophysiology of type 1 hypersensitivity
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1) Ag=> IgE to bind
mast cell 2) Ag crosslinks IgE >> mast cell release |
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pathophysiology of type 2 hypersensitivity
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Fix complement deliberately:
Ag binds Ab => recruit killers |
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pathophysiology of type 3 hypersensitivity
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Fix complement accidentally:
Ag-Ab ppts=> RBCs take to spleen |
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pathophysiology of type 4 hypersensitivity
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Hapten binds Langerhans-MHCII to lymph: TH1 to skin:
1) INFy => MP 2) CD8 => Tk |
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why do we need the Complement Cascade?
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Need complement to destroy encapsuated organisms
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what are the 2 complement pathways?
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I) Classic Pathway:
II) Alternative pathway: |
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Classic Pathway: what does it need to get activated?
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uses Ag-Ab
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Alternative pathway: what does it use to get activated?
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uses IgA
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what is the alternative pathway?
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C-3 ⇨ C3b ⇨ C3 and C5 convertase
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what is the first complement to disappear during the classical pathway?
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(C4 is the first to disappear=> can test for this)
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which of the complement "coats encapsulated organisms"
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C3 "opsonin- coats encapsulated organisms"
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which complement is part of the MAC complex
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C5: part of MAC complex
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what are the anaphylatoxin?
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C3a and C5a
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what is the mac attack complex
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MAC attack: C5B-C9
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function of C8
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aligns capsule for destruction (holds 'em down)
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function of C9
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perforates the capsule (kills 'em)
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describe the classical pathway
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1) Ag-Ab: activates C1 ⇨C1q
2)C1q cuts (via C1 Esterase): • C4 => C4a + C4b • C2 => C2a + C2b forms "C3 convertase": C4b2a forms "C5 convertase": C4b2a3b 3) Use C3 and C5 convertase 4) MAC attack: C5B-C9 |
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C5-9 Deficiency: clues (2) and tx
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>encapsulated infections (Neisseria= biggest)
>Recurrent meningitis, trunk petechiae • Tx: Vancomycin + Ceftriaxone (Dexamethasone if hypotensive) |
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Hereditary Angioedema
mode of inheritance pathogenesis what complement is low? |
>(AD)
>C1 Esterase Inhibitor deficiency, low C4 |
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Hereditary Angioedema:
presentation cogenital and acquired |
Recurrent facial swelling
Primary: in kids, born with deficiency Secondary: in adults, usually due to ACE-I. |
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Hereditary Angioedema: prophylaxis and tx
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• Prophylaxis: Androgens
• Tx: Metoprolol/Epinephrine (no ACE-I) |
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Hereditary Angioedema: Anaphylaxis Tx:
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1) Epinephrine (1:1 ,000)- O.5mL q15min x 3
2) Benadryl - 5Omg IV 3) Steroids - will take 8-12hr to work 4) Dopamine |
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Angioedema with throat swelling or vocal cord edema
tx |
Tx: intubate, steroids, racemic Epi
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ACEI
tx MOA effects (3) what is it made up of? |
⇧K, have sulfur, ⇩heart failure mortality, ⇩DM proteinuria
tx CHF |
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ACE side effects
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>Inhibit the C1 Esterase inhibitor => facial swelling (angioedema)
>⇧Bradykinin => dilate veins "venodilate" (⇩preload), cough >⇩ATII => dilate arteries "vasodilate" (⇩afterload) |
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what are the ACEI
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Captopril
Enalopril Lisinopril Rinilopril |
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Sulfur Drugs: SE
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Urticaria, SJ, G-6PD hemolysis
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what are the drugs that contain sulfur?
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"SAD TLC"
ACEI Celecoxib Thiazides Loop diuretics Sulfonylurea Dapson |
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ATII receptor blockers: advantage
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no cough
Losartan Valsartan Irbesartan candysartan |
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Losartan
what is this a tx for? what does it do? |
pee out uric acid
(tx HTN with gout) |
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Warm hemolysis ab
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Anti-Rh Ab:
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ITP Ab
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Anti-platelet Ab
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Ab: Pernicious anemia
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Anti-IF Ab
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Ab: Type A Gastritis
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Anti-parietal cell Ab
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Anti-gliadin.Ab
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Celiac sprue ''
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Ab: Celiac sprue (3)
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Anti-reticulin Ab
Anti-tissue transglutaminase Ab Anti-gliadin Ab |
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Anti-tissue transglutaminase·Ab:
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Celiac sprue
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Ab: Dermatitis herpetiformis
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Anti-endomysial Ab
anti-BMZ |
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Ab: 1° Biliary Cirrhosis
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Anti-mitochondrial Ab
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p-ANCA Ab (3)
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Poylarteritis Nodosa,
1° Sclerosing Cholangitis ulcerative colitis |
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c-ANCA Ab
another name for what type of antibody |
anti-proteinase Ab
Wegener's |
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Ab: MPGN type II
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Anti-C3 convertase Ab:
nephritic factor |
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Nephritic factor
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MPGN type II
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Ab: Post-Strep
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ASO•Ab
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Ab: Goodpasture's
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Glomerulonephritis
Anti-GBM Ab |
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Ab: Grave's
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Anti-TSH receptor Ab
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Ab: Guillain-Barre
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Anti-ganglioside Ab
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Anti-microsomal Ab
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Hashimoto's
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Ab: Hashimoto's (3)
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Anti-thyroglobulin Ab
Anti-microsomal Ab Anti-peroxidase Ab |
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Ab: Hashimoto's
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Anti-peroxidase Ab "TP0"
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Ab: CREST
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Anti-centromere Ab
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Ab: Mixed connective tissue disease
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Anti-RNP Ab
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Ab: Scleroderma (2 names)
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Anti-topo I "Anti-Scl 70" Ab
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Ab: Drug induced SLE
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Anti-histone Ab:
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SLE sensitive
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ANA:
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Ab: SLE specific
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Anti-Smith Ab
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Ab: SLE w/ renal dz
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Anti-ds DNA
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Ab: SLE cerebritis
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Anti-neuronal Ab
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Ab: Neonatal SLE (heart block)
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Anti-SSA "Rho" Ab
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Anti-cardiolipin Ab: cause and tx
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repeat miscarriages, false(+) VRDL
(Tx: ASA or Heparin if pregnant) |
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Ab: Dermatomyositis
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Anti-Jo-1 Ab
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Ab: Vitiligo
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Anti-melanocyte Ab
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Ab: Dermatitis herpeteformis (2)
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Anti-BMZ Ab
anti-endomysial ab |
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Ab: Pemphigus vulgaris
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Anti-desmosome Ab:
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Ab: Bullous pemphigoid
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Anti-hemidesmosome Ab:
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Ab: Multiple sclerosis
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Anti-myelin Ab
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Ab: Myasthenia Gravis
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Anti-Ach receptor Ab
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Ab: Lambert-Eaton syndrome
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Anti-Calcium channel Ab:
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Ab: Sjogren's
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Anti-SSB "La" Ab
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Rheumatoid arthritis Ab
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Rheumatoid Factor (IgM against IgG Fc):
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Ab: Autoimmune hepatitis type I (females)
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Anti-SM Ab
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Ab: Autoimmune hepatitis type II (kids)
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Anti-LKM Ab
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Ab: EBV Mononucleosis
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Heterophile Ab
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Ab: DM type I
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Anti-GAD Ab
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Ab: paroxysmal cold autoimmune hemolysis
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Donath-Landsteiner Ab:
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what is the most common Transplants?
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Blood
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Syngeneic
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Twin ⇨ Twin
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Autograft
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Self ⇨Self
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Allograft
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Human ⇨ Human
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Xenograft:
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1 species ⇨ another species (Ex: pig ⇨ human)
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What are the Blood Transfusion Reactions:
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1) Febrile
2) Anaphylaxis 3) Incompatibility |
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Febrile Blood Transfusion Reaction:
presentation what is it due to? tx |
⇧temp
• Due to donor RBC • Tx: Acetaminophen |
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Anaphylaxis Blood Transfusion Reaction:
presentation what is it due to? tx |
itch/wheeze
• Due to host plasma proteins • Tx: Epi/ Steroids/ Anti-histamines |
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Incompatibility Blood Transfusion Reaction:
presentation what is it due to? tx |
hypotension/ back pain
• Due to human error • Tx: IVF, stop transfusion |
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what is a good match for HLA typing? therefore who is a good match?
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HLA Typing: Good match: > 60%
• Sibling: best chance • Parents: not good donors b/c they won't match > 50% |
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RBC Agglutination studies:
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RBc<-> normally repel each
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Coombs test: define
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= > Ab involved
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Direct Coombs test
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on surface => hemolytic anemias
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Indirect Coombs test
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in serum
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RBC Phenotype
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=> Pt Ag
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Ab screening
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= > Pt Ag
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Crossmatch
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=> Pt pre-formed Ab against Donor Ag (past transfusion)
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Mixed lymphocyte reaction
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Pt reaction against donor's lymphocytes
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Type and cross
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you know you can use that blood, save it for specific pt
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Type and match
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type it and wait
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Forward typing
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uses Ab to detect Ag "Fabulous"
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Backward typing
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uses Ag to detect Ab
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Transfusion Infxns:
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• HIV
• Hep B,C,D • CMV • EBV • Syphilis • Malaria • Babesiosis |
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Who is not the father? (4)
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1) ABO=> who is not the daddy
2) Rh· 3) Minor antigens 4) Immunoglobulin allotypes |
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ABO Blood Typing: what are they?
how does one acquires them? |
• These Ag are sugars
• You inherit the enzyme that attaches the sugar on your RBCs |
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Blood type A
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=>Have A Ag
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Blood type O
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= no Ag "universal donor"
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Blood type AB
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= both Ag "universal recipient"
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Rh(+):
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has D Ag => "D"
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Rh(-):
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not have D Ag => "d"
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Hemolytic Disease of Newborn:
when is it a concern pathogenesis |
Worry about Rh(-) Mom with Rh(+) Dad
Placenta tears, baby's blood ⇨ Mom ⇨ Ab ⇨ attacks fetus |
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Hemolytic Disease of Newborn:Test:
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Indirect Coomb's (if Mom has high titer Rh Ab, then it's too late)
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Hemolytic Disease of Newborn:
management when is Rhogam given (4) |
>RHOGAM = anti-D IgG
1st Dose: 28 wk gestation 2nd Dose: 72 hrs post -delivery (if baby is Rh +) >Other Dose: Amniocentesis, Spontaneous abortion, Ectopics, Trauma |
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Mom=OO, Dad=AB: problem
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If Mom=OO, Dad=AB =>Mom will have Ab to baby's blood
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Hemolytic Disease of Newborn (HDN) Tx:
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intra-uterine blood transfusion
⇨ Phenobarbital (breaks down fetal bilirubin) Kleihauer-Betke test: # fetal RBCs in Mom => Rho-Gam dosage (or 300 μg if Mom bleeds <30mL) |
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Transplant Rejection: 4 types
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Hyperacute
Acute Chronic Graft vs. Host |
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Hyperacute: describe, cells involved and tx
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within hours (preformed Ab)
• Tx: Remove organ |
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Acute: describe, cells involved and tx
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within weeks (T-cells, MP)
Tx: Prednisone, Cyclosporine, anti-lymphocyte Ab, FK-506 |
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Chronic:describe, cells involved and tx
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within months-years (Fibroblasts)
• Tx: Remove organ |
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Graft vs. Host: describe and cells involved
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bone marrow transplants (TK,MP):
"The Lone Lymphocyte gets revenge" |
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Transplant Problems:
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• Viral infection: CMV, EBV, HPV =>genital warts
• Cyclosporine =>gout • Graft arteriosclerosis |
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Type A:
Glycoprotein Ag Ab Genotype |
Glycoprotein: Galactosamine Transferase
Ag: A Ab: anti-B Genotype: AAorAO |
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Type B:
Glycoprotein Ag Ab Genotype |
Galactose Transferase
B anti-A BB or BO |
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Type O:
Glycoprotein Ag Ab Genotype |
Fuctose
None anti-A, anti-B OO |
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Type AB:
Glycoprotein Ag Ab Genotype |
Both transferases
A,B None AB |
