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* DIT each session > Day 2.3 Immuno > Flashcards

Day 2.3 Immuno Flashcards

1
Q

What HPS types are Ab-mediated?

A

Type I
Type II
Type III
(Type IV is Tcell mediated)

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2
Q

How are Type II and Type III different in terms of Ab?

A

Type II has Ab against self. This induces macrophages to eat the self and causes tsu dmg.
Type III has Ab against non-self, and it’s the Ab-Ag complex that gets deposited into tissues. This induces macrophages to eat the complexes and cause dmg.
In both cases, the dmg is due to macrophages.
Note: Some disorders which feature Type III and Type IV HPS have anti-self Ab. Just bc there is anti-self Ab doesn’t mean the rxn will be Type II.
But, all Type II rxns are mediated by anti-self Ab.

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3
Q

How long does it take for…
Type I HPS?
Type III?
Type IV?

A

Type I = 15 min
Type III = 5-12 hrs
Type IV = 24-48 hrs (delayed)

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4
Q

Type I HPS

A

Anaphylactic and atopic.
Free Ag cross-links IgE on presensitized mast cells and basophils- these degranulate and rls vasoactive amines that act at post-capillary venules (histamine).
Causes edema.
Rapid

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5
Q

How do you test for Type I HPS?

A

Scratch test (scratch back and put Ag there, wait for 15 min to see well-defined wheal and flare.

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6
Q

What is wheal and flare?

A 
Wheal = hive
Flare = red
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7
Q

Examples of Type I HPS

A

Anaphylaxis: bee sting, food/drug allergy
Allergic/Atopic: rhinitis, hay fever, eczema*, hives, asthma
Even tho eczema is Tcell mediated, it is a Type I bc it’s fast!

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8
Q

Type II HPS

A

Antibody mediated- IgM, IgG bind to fixed Ag on “enemy cell” (which is actually self!), leading to lysis by complement, or to phagocytosis.
Cy-2-toxic.
Ab and complement lead to MAC.
Dz is usually specific to the tsu/site where Ag is found

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9
Q

What are the 3 mechanisms of a Type II HPS rxn?

A
  1. Ab opsonize cells or activate complement
  2. Ab recruit neutrophils and macrophages that incite tsu dmg
  3. Ab bind to normal cellular receptors and interfere w functioning.
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10
Q

What is the test for Type II HPS?

A

Coombs (direct and indirect)

Use a known marker that binds to Ab to see if the Ab are there.

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11
Q

What is a direct Coombs test?

A

Anti-Ig antibody is added to the patient’s RBC agglutinate to see if RBCs are coated with Ig.

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12
Q

What is an indirect Coombs test?

A

Normal RBCs are added to the patient’s serum agglutinate to see if the serum has anti-RBC surface Ig

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13
Q

Ex of Type II HPS rxn

A

Auto-immune hemolytic anemia
Pernicious anemia
ITP (Ab against plts)
Erythroblastosis fetalis (Rh incompatibility)
Acute hemolytic txfsn rxns (wrong blood type)
Rheumatic Fever
Goodpasture’s synd (vasculitis)
Bullbous pemphigold
Pemphigus vulgaris
Graves’ dz (Ab against TSH receptor- stim the receptor –> hyperthyroidism)
Myasthenia Gravis (Ab against Ach receptor)

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14
Q

Type II HPS: What is pernicious anemia?

A 
Have Ab against intrinsic factor (IF) so Vit B12 can't be absorbed in the ilieum.
B12 deficiency (neurologic problems)
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15
Q

Type II HPS: What is erythroblastosis fetalis?

A

Maternal Ab to a fetal RBC Ag. (Fetus is Rh+ but mom is Rh-, so mom makes Ab against fetus since it’s “foreign”).
Neonate has:
anemia d/t hemolysis of fetal RBC by maternal Ab
jaundice (Hb was broken down, so excess bilirubin –> jaund)
Hydrop fetalis (generalized fetal edema- fluid in lungs, peritoneum, tsus)
IU death.

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16
Q

Rh- moms don’t have Rh-D on the surface of the blood cells. When should they get anti-Rh-D Ig?

A

28 weeks (bc fetus can be born after this time)
Any traumatic event in which mom might be exposed to fetal RBC (ex: MVA)
W/in 3 days of delivery
Abortion or miscarriage

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17
Q

For which pregnancies will the mom’s anti-Rh Ab have an effect?

A

All pregnancies after the 1st one. (Incl if the first one ended in abortion/miscarriage).
The Ab develop in the 1st pregnancy, but are not in lg enough quantity to cause harm until 2nd pregnancy.

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18
Q

Type II HPS:

What is bullous pemphigoid and pemphigus vulgaris?

A

Bullous pemphigoid = Ab against hemidesmosomes
Pemphigus vulagaris = Ab against desmosomes / desmoglien
Both of these are Ab against epithelium, so they manifest in skin.

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19
Q

Type III HPS

A

Ab against non-self Ag, form Ag-Ab immune complexes and get deposited into tsu.
Ag-Ab (IgG) complexes activate complement, which attracts neutrophils.
Neutrophils rls lysosomal enz.
Imagine immune complex as 3 things stuck together: Ag-Ab-complement
5-12 hrs

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20
Q

What are 2 special kinds of Type III HPS?

A

Serum sickness

Arthus reaction

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21
Q

What is the mechanism of serum sickness?

A

Type III immune complex dz in which Ab to foreign proteins are produced (takes 5 days). Immune complexes form and are deposited in membranes, where they fix complement and cause dmg to the tsu.
In past before Abx, gave lots of Ab to the dz, so it would mk complexes and deposit in vessel walls (so, “serum” sickness). Now, it’s usually caused by drugs.

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22
Q

Symptoms of serum sickness?

A

Type III immune complex dz.
Fever, urticaria, arthralgias, proteinuria (and glomerulonephritis), and lymphadenopathy.
Occurs 5-10 days after Ag exposure, bc Ab to the Ag have to be produced.

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23
Q

What is the mechanism of Arthus reaction?

A

Type III HPS, local, sub-acute, Ab-mediated.
Intradermal injection of Ag (eg tetanus vaccine) induces Ab, which form Ag-Ab complexes in skin.
Test for it w. immunofluroescent staining.

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24
Q

Symptoms of Arthus rxn?

A

Type III HPS
Edema, necrosis, activation of complement.
5-12 hrs after intradermal injection of Ag.

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25
Q

Ex of Type III HPS

A 
SLE
Rheumatoid arthritis
Polyarteritis nodosa
Post-strep glomerularnephritis
Serum sickness
Arthus rxn
HPS pneumonia (farmer's lung)
Can be assoc'd with vasculitis and systemic manefestations
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26
Q

Type IV HPS

A

Delayed, T-cell mediated.
Sensitized Tcells encounter Ag and then rls lymphokines which lead to macrophage activation.
No Ab are involved.
24-48 hrs.
Bc it’s cell mediated, it is not transferable by serum.
Test: patch test (e.g. PPD for TB)

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27
Q

What are the 4 T’s of Type IV HPS?

A

T-lymphocytes (Tcell mediated)
Transplant rejections
TB skin tests
Touching (contact dermatitis)

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28
Q

Mnemonic for HPS rxns: ACID

A 
ACID:
Anaphylactic and Atopic = Type I
Cytotoxic (Ab-mediated) = Type II
Immune complex = Type III
Delayed (Tcell mediated) = Type IV
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29
Q

Ex of Type IV HPS

A 
DM Type I
MS
Guillian-Barre Synd
Hashimoto's Thyroiditis
Graft v Host dz
PPD (test for M. TB)
Contact dermatitis
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30
Q

What are ex of contact dermatitis (Type IV delayed HPS)

A

Poison ivy, oak

Nickel allergy- watch, belt buckle, sandal buckle

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31
Q

Anti-nuclear Ab (ANA)

A 
SLE 
but also many other things:
Sjorgrens
Scleorderma
Polymyositis
Dermatomyositis
Rheumatoid arthritis
Juvenile arthritis
MCTD
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32
Q

Anti-dsDNA, Anti-Smith

A

Specific for SLE

dsDNA = even more specific for renal dz in SLE

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33
Q

Anti-histone

A

Drug-induced lupus

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34
Q

Anti-IgG (Rhematoid Factor)

A

Rhematoid Arthritis.

This is IgM Ab attacking IgG

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35
Q

Anti-centromere

A

CREST Scleroderma

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36
Q

Anti-Scl70 (Anti-DNA topoisomerase I)

A

Diffuse Scleroderma

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37
Q

Anti-mitochondrial

A

Primary biliary cirrhosis

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38
Q

Anti-gliadin, Anit-endomysial

A 
Celiac dz (malabs syndrome where villi of gut are severely atrophied)
Gliadin - component of wheat
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39
Q

Anti-basement mbr

A

Goodpasture’s synd (renal dz, lung dz)

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40
Q

Anti-desmoglien

A

Pemphigus vulgaris

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41
Q

Anti-microsomal, anti-thyroglobulin

A

Hashimoto’s thyroiditis

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42
Q

Anti-Jo-1

A

Polymyositis

Dermatomyositis

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43
Q

Anti-SSA (Anti-Ro)

A

Sjogren’s

SLE

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44
Q

Anti-SSB (Anti-La)

A

Sjogren’s

SLE

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45
Q

Anti-U1 RNP (ribonucleoprotein)

A

MCTD (mixed CT dz)

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46
Q

Anti-smooth muscle

A

Autoimmune hepatitis

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47
Q

Anti-glutamate decarboxylase (Anti-glutamic acid decarboxylase)

A

DM Type I

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48
Q

c-ANCA (Anti-neutrophil cytoplasmic An)

A

Wegener’s granulmatosis

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49
Q

p-ANCA

A

Vasculitis:
microscopic polyangitis
Chrug-Strauss

50
Q

mpo-ANCA (myeloperoxidase)

A

Pauci-immune crescentic glomerulonephritis

51
Q

Anti-TSH receptor

A

Graves’ Dz (HYPERthyroidism- the receptor is stimulated)

52
Q

Anti-ACh receptor

A

Myasthenia Gravis

53
Q

Illnesses with elevated ESR

A 
Polymyalgia rhenmatica
Temporal arthritis
Disease activity in RA and SLE
Infection, Inflammation, Malignancy
Osteoarthritis- infection of bone, can be subclinical. if high ESR, increased suspicion; if not, can rule it out.
54
Q

22q11 deletion syndromes

A

Due to aberrant devt of 3rd and 4th brachial pouches
CATCH-22:
Cleft palate
Abnormal facies
Thymic aplasia (–> Tcell deficiency)
Hypocalcemia (secondary to parathyroid aplasia)

DiGeorge = thymic, parathyroid, cardiac defects
Velocardiofacial syndrome = palate, facial, cardiac defects

55
Q

Which immune deficiencies are B-cell disorders?

A

Bruton’s agammaglobulinemia
Hyper-IgM Syndrome
Selective Ig deficiency
CVID- common variable immunodeficiency

56
Q

Which immune deficiencies are T-cell disorders?

A

Thymic aplasia (DiGeorge)
IL-12 receptor deficiency
Hyper IgE Syndrome (Job)
Chronic mucocutaneous candidiasis

57
Q

Which immune disorders are combined B-cell and T-cell disorders?

A

SCID - severe combined immunodeficiency
Ataxia-telangiectasia
Wiskott-Aldrich syndrome

58
Q

Which immune disorders are due to phagocyte dysfunction?

A

Leukocyte adhesion deficiency (Type I)
Chediak-Higashi syndrome (MT fn)
Chronic granulomatous dz (NADPH oxidase deficiency)

59
Q

Which immunodeficiencies are X-linked?

A

WBC:
Wiskott-Aldrich
Bruton’s Agammaglobulinemia
Chronic Granuolmatous Dz (sometimes X-linked, not always)
Also one of the 3 types of Hyper-IgM Syndrome is X-linked (the type with no CD ligand)

60
Q

What are the 3 types of Hyper-IgM syndrome?

A

Hyper-IgM = lots of IgM but low amts of other Ig’s.

  1. X-linked (no CD ligand)
  2. Autosomal Recessive (no CD40)
  3. NEMO deficiency
61
Q

What is the defect in Bruton’s agammaglobulinemia?

A

X-linked recessive, so moreso in Boys (one of the WBC X-linked)
Defect in BTK, a tyrosine kinase gene –> blocks Bcell differentiation and maturation –> low levels of all Ig’s.

62
Q

Px of Bruton’s agammaglobulinemia

A

Recurrent bacterial infections after 6 months (decreased maternal IgG) due to opsonization defect.
Low levels of all Ig’s so get lots of infections.

63
Q

Labs for Bruton’s agammaglobulinemia

A

Normal pro-B
Decreased maturation, # of B cells
Decreased Ig of all classes

64
Q

Defect in Hyper-IgM syndrome

A

Defective CD40L on Thelper cells –> inability of B cells to class switch because need CD40-CD40L binding to signal it. So, all Ig’s are stuck as IgM

65
Q

Px of Hyper IgM syndrome

A

Severe pyogenic infections early in life.

66
Q

Labs for Hyper IgM

A

Lots of IgM
very low IgG, IgA, IgE
No CD40L on flow cytometry for Tcells

67
Q

Defect in Selective Ig Deficiency

A

Defect in isotype switching –> deficiency in a specific class of immunoglobulins. (Can be any, but IgA deficiency most common)

68
Q

Px of Selective Ig Deficiency

A

Most pts are healthy, may not know.
Sinus/lung infections
Milk allergies and diarrhea
Assocd w atopy (allergy predisposition), asthma
Imp: Anaphylaxis on exposure to blood products with IgA.
Occurs in 1/600 pts of European descent

69
Q

Labs for Selective Ig Deficiency

A

IgA deficiency is most common.
Failure to mature into plasma cells.
Decreased secretory IgA.

70
Q

Defect in CVID (common variable immunodeficiency)

A

Defect in B cell maturation.

D/t many causes

71
Q

Px of CVID

A

Can by acquired in 20s-30s

Increased risk of autoimmune dz, lymphoma, sinopulmonary infections.

72
Q

Labs for CVID

A

Normal number of B cells but decreased plasma cells and Ig

73
Q

Defect in DiGeorge Syndrome (thymic aplasia)

A

22q11 deletion

failure to develop 3rd and 4th brachial pouches

74
Q

Px DiGeorge

A

No Thymus - no mature Tcells = recurrent viral, protozoal, fungal infections
No Parathyroid - no PTH - low Ca2+ = tetany
Congenital heart and great vessel defects
Facial abn - cleft palate, low ears, smooth phitrum, micrognathia (chin)

75
Q

Labs DiGeorge

A

No thymus, parathyroid, so decreased T cells, decreased PTH, decreased Ca2+
No thymic shadow on CXR

76
Q

What are the 2 signs for low Ca2+?

A

Chovstek’s sign- tap cheek- when facial nerve is tapped, facial muscles will contract (tetany)
Trosseau’s sign- Carpal spasm when tighten BP cuff (tetany)

77
Q

Defect, Px, Labs in IL-12 receptor deficiency

A

Defect: Decreased Th1 response
Px: Disseminated mycobacterial infections
Labs: Decreased IFN-gamma (bc Th1 are not secreting it)

78
Q

Defect in Job’s Syndrome (Hyper IgE)

A 
Th cells fail to produce IFN-gamma
So PMNs (neutrophils) don't respond to chemotactic stimuli (C5a, LTB4, IL-8)
79
Q

Px of Job’s syndrome (IgE)

A 
Triad:
Eczema
Recurrent cold abscesses (S. aureus)
Course facial features: broad nose, frontal bossing of forehead, deep eyes, doughy skin.
Also can have retained primary teeth- 2 rows of teeth!
Job was FATED:
Facies
Abcesses (cold- noninflamed)
Teeth retained
E (hyper-IgE)
Dermatologic (eczema)
80
Q

What is the defect, Px, and Rx for chronic mucocutaneous Candidiasis?

A

Defect: Tcell dysfn
Px:
C. albicans infections of skin and mucous mbr
Rx: Ketoconazole (anti-fungal)

81
Q

What is the defect in SCID?

A

Defect is in early stem cell differentiation (No Bcells, Tcells)
Can be caused by >7 diff gene defects.
Most common:
Adenosine deaminase deficiency (purine salvage pathway)
Defective IL-2 receptor (X-linked defect)
Failure to synth MHC-II Ag
Only defense is NK cells.

82
Q

Px of SCID

A 
Triad:
1. Recurrent infections- viral, bacterial, fungal, protozoal due to both B and T cell deficiency (chonic mucocutaneous candida, RSV, VZV, HSV, measles, flu, parainfluenza, PCP pneumonia)
2. Chronic diarrhea
3. FTT
Plus no thymus on CXR (like DiGeorge)
83
Q

Rx for SCID

A

Bone marrow txplt (no allograft rejection)

84
Q

Labs for SCID

A 
Decreased IL-2R (decreased Tcell activation)
Increased adenine (toxic to B and T cells)- decreased dNTPs, decreased DNA synth.
85
Q

What is ADA deficiency (Adenosine deaminase)

A

ADA converts Adenosine to Inosine in the purine salvage pathway.
Defective ADA means accumulation of deoxyadenosine, which leads to excess ATP and dATP. This causes imbalance in nucleotide pool, d/t fdbk inhibition of ribonucleotide reductase. This prevents DNA synth and therefore decreases lymphocyte count.
Mjr cause of SCID.

86
Q

What is the defect in Ataxia-Telangiectasia?

A

Defect in DNA repair enz and IgA deficiency.

87
Q

Px of Ataxia-Telangiectasia

A

Triad:
1. Cerebellar defects (ataxia) plus poor smooth pursuit of moving target w eyes
2. Spider angiomas (telangiectasia) when >5yo
3. IgA deficiency
Also have increased CA risk (lymphoma, acute leukemia) and radiatiion sensitivity (avoid xray)
Die at 25yo

88
Q

If you see a 1 yo with poor smooth pursuit, how should you check for Ataxia-Telangiectasia?

A

Increased alpha-fetoprotein (in kids >8mo)

89
Q

Defect in Wiskott-Aldrich syndrome

A

X-linked recessive (it’s an x-linked Wbc)

Progressive deletion of Bcells and Tcells

90
Q

Px of Wiscott-Aldrich

A 
WAITER:
Wiscott
Aldrich
Immunodeficiency/Infection
Thrombocytopenic purpura
Eczema (unusual bc it's trunkal eczema)
Recurrent pyrogenic infections- no IgM against capsular bacteria
91
Q

Labs for Wiscott-Aldrich

A

Low IgM

High IgA, IgE

92
Q

Defect in Leukocyte Adhesion Deficiency (Type 1)

A

Defect in LFA-integrin protein (CD18) on phagocytes. This means phagocytes can’t exit circulation. (Can’t “integrate” into tsu’s)

93
Q

Px of Leukocyte adhesion deficiency (Type I)

A

Recurrent bacterial infections, absent pus formation

Delayed separation of umbilicus

94
Q

Labs for Leukocyte adhesion deficiency (type 1)

A

Neutrophilia (high amt of neutrophils in blood)

95
Q

Defect in Chediak-Higashi syndrome

A

Autosomal recessive
Defect in microtubular function with decreased phagocytosis
Defective LYST gene (lysosomal txprt)- can’t get the enz which degrade things into the lysosomes.
Defective phagocyte lysosome- see giant cytoplasmic granules in PMNs (can engulf, but can’t degrade once engulfed)

96
Q

What is a PMN?

A 
Polymorphonuclear Leukocytes (PMN, PML) aka granulocytes.
There are three types of granulocytes:
Neutrophils
Eosinophils
Basophils
All have granules and lobed nuclei.
97
Q

Px of Chediak-Higashi

A

Triad:
Partial albinism
Recurrent respi and skin infections (esp pyogenic infections by Staph and Strep)
Neurologic disorders- peripheral neuropathy

98
Q

Defect in Chronic Granulomatous Dz

A

NADPH oxidase deficiency. Therefore phagocytes can’t generate ROS (e.g. superoxide and free radicals). Absent respiratory burst in neutrophils.

99
Q

Px of Chronic Granulomatous Dz

A 
Increase susceptibility to catalase+ organisms:
Staph (esp S. aureus)
E. coli
Klebsiella
Aspergillis
Candida
100
Q

Dx of Chronic Granulomatous Dz

A

Nitroblue tetrazolium dye test is negative.
Normal phagocytes engulf NBT dye and oxidize it, turning it from yellow to blue-black.
Pts w CGD can’t oxidize- so don’t see blue-black color.

101
Q

Rx for Chronic Granulomatous Dz

A

Prophylactic TMP-SMX (bactrin)

INF-gamma can also help.

102
Q

Where is the thymus derived from embryologically?

A

The 3rd and 4th brachial pouches, which are ENDODERM.

103
Q

What are the type of grafts (allo, auto, etc)

A

Autograft- from self
Syngeneic graft - from identical twin or clone
Allograft - from nonidentical pt of same species
Xenograft- from different species

104
Q

What are the 4 types of txplt rejection?

A

Hyperacute
Acute
Chronic
Graft-vs-Host dz

105
Q

What is Hyperacute rejection?

A

Ab-mediated (Type II HPS)
Due to presence of pre-formed anti-donor Ab in the txplt recipient.
W/in minutes after txplt

106
Q

What is Acute rejection?

A

Tcell-mediated d/t Cytotoxic Tcells reacting against foreign MHCs.
Weeks after txplt.
Reversible with immunosuppressants

107
Q

What immunosuppressants can reverse Acute Rejection?

A

Cyclosporine

OKT3

108
Q

What is Chronic rejection?

A

Tcell and Ab-mediated vascular dmg (obliterative vascular fibrosis)
Months-years after txplnt, Irreversible
The non-self MHC-I is seen by Cytotoxic Tcells as self MHC-I which is presenting foreign Ag, so it attacks.
Take immunosuppresants after txplt to delay this.

109
Q

What is Graft-vs-Host dz?

A

Grafted immunocompetent Tcells proliferate in the immunocompromised host and reject foreign (to them) cells- which are the host’s cells.
Causes severe organ dysfn.
Mjr sympt: maculopapular rash, jaundice hepatosplenomegaly, diarrhea.

110
Q

What does the Long Thoracic N innervate

A

Serratus Anterior

scapular winging if lesioned

111
Q

What does the Suprascapular N. innervate?

A 
Infraspinatus M (lateral rotator)
Supraspinatus M (1st 10degrees of arm abduction)
112
Q

What does the Lateral Pectoral Nerve innervate?

A

Pectoralis Mjr M.

113
Q

What does the Upper Subscapular N. innervate?

A

Subscapularis M. (medial rotator)

114
Q

What does the Thoracodorsal nerve innervate?

A

Latissimus Dorsi M.

115
Q

What does the Lower Subscapular N. innervated?

A

Teres Mjr M. (medial rotator, extender, ADductor)

116
Q

What does the Musculocutaneous N. innervate?

A

Flexor muscles:
Biceps brachii
Coracobrachialis
Brachialis

117
Q

What does the Axillary N. innervate?

A

Deltoid m

118
Q

What does the Radial N. innervate?

A

Extensors of forearm

Triceps

119
Q

What does the Median nerve innervate?

A

Pronators.

Causes Pope’s blessing, Ape hand

120
Q

What does the Ulnar N innervate

A

Interosseous, Lumbricals

Causes claw hand

121
Q

What is Cori’s disease?

A

Deficiency in glycogen debranching enz.
Glycogen is stored in the liver. With debranching enz deficiency, it can’t undergo glycogenolysis (glycogen breakdown) to turn it into glucose.
With no glucose except from diet, there is hypoglycemia.
This leads to FTT.

122
Q

What is Von Gierke’s Disease?

A

Glycogen storage disease- no glucose-6-phoshatase enz, so liver can’t make glucose from glycogen or from gluconeogenesis

* DIT each session (34 decks)

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