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STEP1-FirstAid > Immunology > Flashcards

Immunology Flashcards

1
Q

A woman presents with an anaphylactic reaction. Which interleukin (cytokine) is responsible for the antibody(ies) responsible for the hypersensitivity reaction?

Who/what produces this cytokine?

A

Antibody= IgE

Cytokine= IL-4

IL-5 is produced by Th2 cells

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2
Q

These two cytokines serve to downregulate the activity of all T-cells?

How/where are these two cytokines produced?

A

IL-10 and TGF-B

Treg produce IL-10
Th2 produce IL-10 and TGF-B (along with IL4 and 5)

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3
Q

Two primary roles of IL-5

What/who produces IL-5?

A

IL-5 produced by Th2 cells

1) IgA isotype switching “league of its own”
2) Stimulating growtha and differentiation of eosinophils

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4
Q

Which factor induces differentiation into Th2 cells?

Which cells produces this factor?

A

IL-4
-also promotes growth of B-cells
(isotype switching to IgE and IgG)

PRODUCTION:
IL-4 is produced by Th2…lol

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5
Q

The lower duodenum, jejunum, ileul, colon, and splenic flexure drain into whch lymph node cluster?

A

Superior mesenteric

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6
Q

Which organs drain into the inferior mesenteric artery?

A

Colon (from splenic felxure to upper rectum)

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7
Q

This factor promotes growth of all types of T-cells, and NK cells?

Who produces this factor?

A

IL2 is produced by ALL T-cells and works in an autocrie fashion

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8
Q

This factor functions like GM-CSF and stimulates differentiation into the myeloid lineage

A

IL-3

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9
Q

This factor promotes differntiation of T-cells into Th1 cells. It also activated NK-cells

Who/what produces this factor?

A

IL-12

secreted by macrophages and also secreted by B-cells

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10
Q

To which lymph node cluster do the following organs drain into?

  • Lower rectum to anal canal (above the pectinate line)
  • Bladder
  • Vagina (middle 3rd)
  • Prostate
A

Internal iliac

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11
Q

Which organs drain into the para-aortic lymph node cluster?

-Name 4

A

Testes
Ovaries
Kidneys
Uterus

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12
Q

Head and neck drain into this lymph node cluster

A

Cervical

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13
Q

Inside the spleen, where are the T-cell rich regions and where is the B-cell rich region?

A

T-cells:
around the PALS which surround the single splenic artery in the white pulp

B-Cells:
-in the germinal centers in the white pulp
PS: both are in the white pulp

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14
Q

Where are the APC cells found inside the spleen and what other cells are found in this region?

A

The marginal zone!! an area between the white pulp and the red pulp

Other cells found there: specialized B-cells

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15
Q

What are the 4 functions of IFN-gamma?

Who/what produces IFN-gamma?

A

FUNCTIONS:

  1. activation of macrophages into incredible Hulk
  2. activation of NK cells into cytotoxic cells for virus-infected cells
  3. increases MHC expression and antigen presentation into all cells
  4. Has antiviral and antitumor properties (just like INF-a and IFN-b which are produced by macrophages)

PRODUCTION:
-produced by Th1 cells

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16
Q

Inside a lymph node, where are the T-cells and B-cells located?

A

B-CELLS:

  • -found in follicles in the CORTEX
  • forms germinal center when activated

T-CELLS:
—found in the paracortex i.e. region between medulla and cortex

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17
Q

What is the function of the red pulp of the spleen?

What structures are found there?

A

Sinusoids of the spleen are found in the Red Pulp and this is where blood is filtered. The Reticular endothelial System is found here.

Hence numerous macrophages are present to sequester old RBCs and engulf opsonized antigens.

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18
Q

The Hilar lymph node cluster drains which organs?

A

Lungs,

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19
Q

This cytokine induces the following:

  • Mediates septic shock
  • Activates endothelium
  • Causes leukocyte recruitment and vascular leak.

Who produces this cytokine?

A

TNF=alpha is produced by Th1 cells

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20
Q

The celiac lymph node cluster drains which organs?

-Name 5

A 
Liver
Stomach
Spleen
Pancreas
Upper Duodenum
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21
Q

From which pharyngeal pouch did the thymus arise from?

–Where are the mature T-cells and where are the immature Tcells located inside the thymus?

–What structures are present in the Hassall’s Corpuscle?

A

DERIVED: epithelium of 3rd pharyngeal pouch

Mature T-cells: medulla (pale)
Immature T-cells: Cortex (dense)

Hassal’s Corpuscle: Epithelial Reticular Cells

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22
Q

This factor promotes differntiation into the lympoid lineage

A

IL-7

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23
Q

An indiviual has a history of infections with organisms such as:

Strep Pneumo
Hemophilus B
Neisseria Meningiditis
Ecoli
Staph Aureus
Klebsiella Pneumo
Salmonella
Group B Strep

What do you expect to find if you did who-body imaging?

A

Missing Spleen (or splenic dysfunction)…most likely sickle-cell patient because they usually undergo autosplenectomy

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24
Q

This factor is the major chemotactic factor for neutrophils

–Who/what produces this factor?

A

IL-8

produced by macrophages

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25
Q

Cells making up the innate system and those making up the adaptive system?

A

INNATE:

  • neutrophils
  • macrophages/monocytes
  • NK cells
  • dendritic cells
  • complement

ADAPTIVE:

  • T-cells
  • B-cells
  • Circulating antibodies from plasma cells
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26
Q

What kind of receptors does the innate immunity use to recognize antigens?
-Give an example of what these receptors recognize

A

Toll-Like Receptors, which recognize PAMPs and DAMPs

–PAMPs include: LPS from GNB, flagellin from bacteria, and ssRNA from viruses

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27
Q

What is found in the medulla of the lymph node?

A

Contains Medullary Cords and Medullary Sinuses

CORDS:
-packed with lymphocytes and plasma cells

SINUSES:
-comuictae iwth efferent lymphatics

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28
Q

This cytokine is an endogenous pyogen that causes fever and promotes production of acute-phase reactants by the liver.

Who/what produces this factor?

A

IL-6

produced by Th2 cells

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29
Q

This cytokine is an endogenous pyogen that causes fever and acute inflammation. Unlike a similar endogenous pyogen, this one induces endothelial cells to express chemokine molecules and produce chemokines that recruit leukocytes.

Who/what produces this factor?

A

IL-1 a.k.a. osteoclast activating factor

produced by Macrophages

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30
Q

Anal Canal (below pectinate line) and skin below the umbilicus (except popliteal territory) drains into which lymph node cluster?

A

Superfiial Inguinal

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31
Q

Which HLA molecular markers are found on MHC Class II molecules and which ones are found on class I MHC?

A

MHC I= HLA-A, HLA-B, and HLA-C
—present endogenous antigens to CD8+

MHC II= HLA-DP, HLA-DQ, HLA-DR
—-present exogenous antigens to CD4+

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32
Q

The Upper Limb, breast and skin above umbilicus drain into which lymph node cluster

A

Axillary

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33
Q

This molecule is responsible for loading a peptide onto MHC-I in the RER

A

TAP protein transporter

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34
Q

This molecule prevents loading of a peptide onto MHC-II in the RER

A

Invariant Chain

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35
Q

The trachea and esophagus drain into which lymph node cluster?

A

Mediastinal

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36
Q

A famly is found to express the HLA-DQ2/DQ8 in many of its family members. Which disease is family high predisposed to?

A

Celiac Disease

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37
Q

Which parts of the body drain into the R.Lymphatic duct and which ones go into the Thoracic Duct?

A

RLD:
-right side of the body above the diaphragm

Th.Duct:
-everything else not drained by the RLD.

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38
Q

Into whoch vessel does that thoracid duct drain into?

A

Drains into the junction of the left subclavian and the internal jugular vein

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39
Q

Patients with Diabetes Mellitus type I, SLE, Graves disease most likely have which common HLA subtypes?

A

DR3

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40
Q

Which organs drain into the popliteal lymph node cluster?

-Name 2

A

Dorsolateral Foot

Posterior Calf

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41
Q

Which diseases are associated with the DR5 subtype of HLA genes?

A

1) Pernicious Anemia (which then causes megaloblastic anemia through Vit-B12 shortage)
2) Hashimoto Thyroiditis

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42
Q

Which chemicals are presentt in the granules of NK-cells?

What are the 2 mechanisms by which NK cells carry out their cytotoxic function?

A

Perforin and Granzymes
-which induce apoptosis of virally-infected and tumor cells…NO granuysin in NK cells!! only in CD8+ cells

MECHANISMS:
1) when exposed to a non-specific signal in the absence of MHC-I

2) Antibody-dependent cell mediated cytotoxicity
- -binds to Fc portion of IgG (or IgE if parasite)

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43
Q

What is positive and negative selection in regards to T-cell maturation?

Which one of these processes happens first?

A 
POSITIVE SELECTION(thymic cortex):
----removal of T-cells that do not recognize MHC molecules. Prior to this, cell is CD4+/CD8+

NEGATIVE SELECTION (thymic medulla):

  • —removal of T-cells that bind too strongly to self-antigens
  • ***otherwise these Tcells would increase risk of autoimmunity
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44
Q

What are the 3 requirements of T-cell activation?

A

1) ANTIGEN: small peptide presented by either
MHCI or II
2) Co-stimulatory interaction with the APC: i.e
CD28 on naive Tcell and B7 on the APC cells

3) T-cell produces cytokines after being activated

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45
Q

What do patients with Goodpastures disease, SLE, M.Sclerosis, and Hay Fever have in common?

A

Usually carry the DR2 subtype of HLA

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46
Q

A patient has both RA and DMtype1. Which HLA haplotype is she likely to posess?

A

DR4

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47
Q

The A3 subtype of HLA genes is commonly associated with which disease?

A

Hemochromatosis?

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48
Q

Which cytokines promote activation of NK cells?

A

IL-2
IFN-beta
IL-12
IFN-alpha

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49
Q

What are the 4 signals/players that are required for B-cell activation and subsequent isotype class switching?

A

1) ANTIGEN bound to by the “naive B antibody” i.e.
IgM

2) Presentation of antigen to CD4+ T-cell in a manner similar to (APC vs T-cell) except APC= B cell in this case

3) Co-stimulatory interation between CD40 ligand on CD4+ cell and CD40 Receptor on the B-cell
NB: CD8+ does not have CD40L

4) Depending on antigen type, T-cell will produces cytokines that promote isotype switching (usually IL4 and IL4)

NB: Lack of CD40Ligand on T-cells leads to Hyper IgM Syndrome

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50
Q

Which diseases are usually associated with the HLA-B27 subtype?

A

mnemonic = “P.A.I.R.”
**occurs more often in men than women

  • Psoriatic Arthritis
  • Ankylosing Spondylitis
  • arthritis of IBD
  • Reactive Arthritis (Reiter’s Syndrome)
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51
Q

Which factors promote differentiation of Th1 cells and which signals inhibit?

What are the productis of Th1 cells?

A

SYNTHESIS:
-IL-12 produced by macrophages and B-cells

INHIBITION:
-IL4 and IL10 which are both produced by Th2
(IL10 also produced by Treg)
-Also inhibited by TGF-B

PRODUCTS:

  • IFN-gamma
  • TNF-alpha
  • IL-2
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52
Q

Which factors promote differentiation of Th2 cells and which signals inhibit?

What are the productis of Th2 cells?

A

SYNTHESIS:
-IL4

INHIBITION:
-IFN-gamma from Th1 cell

PRODUCTS:

  • IL4
  • IL5
  • IL-6
  • IL13
  • TGF-b
  • IL10
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53
Q

Function of IFN-gamma

A
  • inhibit Th2 cells
  • activate Macrophages into incredible hulk
  • also activates CD8+ and NK-cells
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54
Q

Which molecules are present in the granules of CD8+ cells?

-name 3

A

1) PERFORIN–which punches holes into the infected cell
2) GRANZYMES–which are serine proteases that induce apoptosis in host cell
3) GRANULYSIN—an antimicrobial that also induces apoptosis

NB: NK cells only have the first 2

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55
Q

Which Transcription factor UPREGULATES expression of T-reg cells?

What are the 3 surface markers used to identify T-reg cells?

A

FOXP3!!! = transcription factor

SURFACE MARKERS:
-CD3
-CD4
-CD25 (apha chain of IL-2 receptor)
NB:::: FOXP3 is also expressed inside these cells
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56
Q

Which enzyme is responsible for adding nucleotides to DNA during VDJ recombination in B and T-cells?

A

TdT (terminal deoxynucleotide transferase)

Enzyme is only expressed on pre-B and T-cells so it’s used to distinguish Acute Myelogenous Leukemia (AML) from ALL—blasts onto which it will be present

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57
Q

Most abundant antibody isotype in the serum?

A

IgG

IgE is the least concentrated

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58
Q

Antbody with the highest:

a) avidity?
b) affinity?

A

Affiity: IgG
Avidity: IgM

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59
Q

Four functions of IgG

A

1) Neutralization & Opsonizaton (C3b is the other major opsonin–AND CRP in chronic inflammation) of bacteria
2) Passive immunity to fetus and and first 6 months of neonate…only antibody that can cross the placenta
3) Fixes Complement (along with IgM)–responsible for classical complement pathway
4) Aslo activates NK cells via its Fc portion in ADCC

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60
Q

At what point and where does somatic hypermutation take place?

A

It occurs when a B-cell encounters and antigen and this process only happens in B-cells

SHM: Introduction of somatic mutations in the VDJ region and this takes place in secondary lymphoid tissue such as B-cells

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61
Q

What is the diff between thymus-independent antigens and thymus dependent antigens?

A

Thy.Independent Antigens: They lack a peptide component and thus, cannot be presented to T-cells. They can only elecit B-cells
and if used as vaccines, they tend to require a booster as memory and immunogenicity is not as good

Thy.Dependent Antigen: Carry a peptide component and can, thus be presented to T-cells.

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62
Q

An Rh- mother gives birth to a baby with erythroblastosis fetalis…which antibody is responsible for the hemolytic disease of the newborn?

A

IgG

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63
Q

Which acute-phase reactants are upregulated and which ones are donwregulated during inflammation?
-Name 7 total

A

UPREGULATED:
-Hepcidin-inhibits absoprtion of Fe2+ from gut and
release from macrophage..inhibits ferriportin
transporter. Causes ACD
-Amyloid A…can lead to amyloidosis if prolonged
-CRP…acts as an opsonin to facilitate
phagocytosis
-Ferritin
-Fibrinogen

DOWNREGULATED:

  • Transferrin
  • Albumin
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64
Q

Major functions of complement?

Name 4

A

1) C3a, C4a, and C5a act as “anaphylotoxins” that can mediate anaphylaxis without IgE involvements
2) C3b= major opsonin
3) C5a = neutrophiil chemotactic factor (also IL8)
4) C5b-9= cytolysis by the MAC

65
Q

A young boy has a history of URIs and sometimes gets bacteria too. Which antibody is he deficient in?

A

IgA…for mucosal surfaces
-antibody prevents attachment of bacteria and
virus to mucosal surfaces

66
Q

This antibody is released into secretions (tears, saliva, mucus, and early breast milk[colostrum]) and it crosses epithelial surfaces by transcytosis?

In what form is this antbody when secreted and in what form is it in circulation?

A

IgA

Secreted as a dimer but circulates as a monomer
–so when secreted, the valence =4 since each antbody monomer can bind 2 identical antigens

67
Q

Antibody relased in primary response to antigen?

A

IgM

-released as a pentamer so has a valence of 10 ince each antbody monomer can bind 2 identical antigens

68
Q

Antibody with the lowest concentration in serum?

A

IgE

IgG is the most abundant

69
Q

This antibody cross-links when exposed to allergen and it mediates Type I HSRs.

To which kinds of cells does it bind to?
Name 2

A

IgE

–Binds mast cells and basophils

It also mediates immuity to parasites by activating eosinophils

70
Q

What are the three ways to activate the complement pathway?

A

1) CLASSICAL PATHWAY:
Antigen and Antibody (IgG/IgM) form complexes that recruit complement

2) ALTERNATIVE PATHWAY
this is spontaneous, and its usually just a “benign” microbial surface trigerring the pathway eading to formation of C3b

3) LECTIN PATHWAY
- sugars on bacteria e.g. mannose trigger the pathway

71
Q

What substance does IgA pick up from an epithelial surface and why?

A

Substance = “SECRETORY COMPONENT” which protects the antibody from mucosal degradation

72
Q

A cell is positive for CD16 and CD56; what is the cell?

A

NK cell!!!

Unique marker for the cells is CD56+

73
Q

Do all T-Cells express the CD40Ligand?

A

No! Only CD4+ because its the one that needs to bind with the CD40 on B-cells during activation and isotype-swithcing of B-cells.

NB: It’s the Th2 cells that would produce the necessary cytokines needed to switch isotypes.

NB: CD40 is also expressed on macrophages

74
Q

Which cell-surface markers are common to the 2 major types of T-cells?

A
  • CD28 (binds B7 on APC)
  • CD3 = co-receptor which is used to transduce signals into the cell
  • TCR: the receptor to which MHC presents
75
Q

What are the 2 inhibitors of complement?

Which diseases result when these inhibitors are missing?

A

1) Decay- accelerating factor DAF = CD55 and CD59
* **leads to Paroxysmal Nocturnal Hemoglobinuria if defective

2) C1-Esterase inhibitor: Helps prevent complement activation on self cells
* *Causes hereditary Angioedema
* **ACE Inhibitors are contra-indicated

76
Q

A 3 year old girl has a history of severe, recurrent pyogenic sinus and respiratory tract infections. And she has increased susceptibility to Type III HSR. Her IgA levels are normal and she is negative for p-ANCA.
What is the cause of her illness?

A

She has C3 deficiency (in the complement pathway)
—-which is a profound lacking because it affects both pathways… Patients present with angioedema: severe swellig of mouth, tonhue, etc because complement is overactive.

**Other descriptions rule out IgA deficiency and Churg-Strauss

77
Q

What is the term given to autoreactive T-cells become non-reactive without costimulatory molecule?

A

ANERGY!!

B-cells also become anergic, but tolerance is less complete than in T-cells

78
Q

What are the cell-surface markers expressed on macrophages?

A 
CD14
CD40 
MHCII
MHCI
B7 (binds to CD28 on T-cells)
Fc and C3b  receptors (for enhanced phagocytosis)
79
Q

A 2 year old patient presents with swelling, particularly of the face and airways, and abdominal cramping. 2 of his uncles had the same condition and he has a cousin with the same symptoms.

What is likely missing in this yound man?

A

Diagnosis: Hereditary Angioedema

Cause: missing/defective “C1 Esterase Inhibitor” so he is unable to turn off complement

NB: Ace Inhibitors are contraindicated!!

80
Q

What is the main function of IFN-a and IFN-beta?

Who/What produces them?

A

glycoproteins that work to fight RNA and DNA viruses.

–They are produced by innfected cells—>spilled onto neighboring uninfected cells and then that whole are is “primed” for viral defense

BOTTOMLINE: they both lead to apoptosis

81
Q

Which 2 enzymes are activated by viral dsRNA and work in conjunction with IFN-a and IFN-b?

What are the functions of each of those two enzymes

A

RNAase L activated by viral dsRNA
FUCTION—->degrades viral/host mRNA

Protein Kinase…activated by viral dsRNA too
FUNCTION—->inhibits viral/host protein synthesis

BOTTOMLINE: they both lead to apoptosis

82
Q

An 18 year old men has presented to you with Neisseria infection. In the last 6 months, he has had 3 similar episodes? What is the underlying cause of his illness?

A

C5-C9 deficiencies. He has unable to form MAC complex

83
Q

A 60 year old man presents with dark urine in the morning which progressively clears during the day. What treatment will you give him?

A

Eculizimab= Rx!!!

He has a deficiency in DAF (CD55/CD59) and is sufferig from PNHemoglobinuria.—>which causes intravascular hemolysis.
The antibody above donregulates complement

84
Q

A patient presents with Fever, Rash and Shock. What is the most likely microbe that caused this?

A

This is the TRIAD for toxic shock syndrome (TSS):
Fever, Shock, and Rash!!

Caused by S.Aureus or S.Pyogenes.==Superantigens

85
Q

How do the following bacteria produce antigenic variation?

  • Neiserria Gonorrhea?
  • Samonella?
  • Borrelia?
A
  • Neiserria Gonorrhea: pilus protein
  • Samonella: 2 flagellar variants
  • Borrelia: Relapsing Fever
86
Q

How does the Influenza virus produce antigenic variation?

–Name the 2 classic Methods

A

Major = Shift
“two or more different strains of a virus, or strains of two or more different viruses, combine to form a new subtype having a mixture of the surface antigens of the two or more original strains.”

Minor=Drift
“natural mutation over time of known strains of
influenza (or other things, in a more general
sense) which may lead to a loss of immunity”

87
Q

How do parasites such as Trypanosomes produce antigenic variation?

A

programmed rearrangment

88
Q

In which 4 major infections/exposures to we give patients preformed antibodies?

A

1)Tetanus Toxin
2)Botulinum toxin
3)Hepatitis B: (combined passive and active
usually given)
4)Rabies: (combined passive and active usually
given)

mnemonic: “To Be Healed Rapidly”

89
Q

Examples of Live Attenuated vaccines?

A

-Measles, Mumps, Rubella
-Polio (Sabin)
-Influenza (Intranasal)
-Varicella
Yellow Fever

mnemonic = “VIMPY”

**THEY MAY ELICIT CELLULAR IMMUNITY

90
Q

Examples of Inactivated/Killed Vaccines?

A

Cholera
Rabies
Influenza (injection)
Hepatitis A

mnemonic = “CRIP-A”

**THEY MAY ELICIT HUMORAL IMMUNITY

91
Q

A patient presents with Fever, Rash and Shock.

Describe the mechanism of this presentation.

A

This is TSS due to Superantgens!!! Triad of fever, rash and shock.

S.Pyogenes and S.Aureus are SUPERANTIGENS

—They produce bacterial toxins, which crosslink the B-region of many polyclonal T-cells with the MHC-II molecule leading to over-activation of Tcells and a cytokine storm production.

BOTTOMLINE: A superantigen binds to T-cells non-specifically such that many many many POLYCLONAL T-cells are activated resulting in excess: IL-2 and IFN-y being produced

92
Q

Major antibody active in Type I HSR?

What is the major pathogenesis in Type I?

A

IgE

First encounter is sensitization, but on re-exposure…antigen binds to activated IgE and trigger mast cells and basophil degranulation

93
Q

Of the influenza vaccines: which one is live attenuated and which one is inactivated, killed?

A

LIVE/ATTENUATED: Intranasal

KILLED/INACTIVATED: Injection

94
Q

Distinguish between Serum Sickness and Arthus Reaction?

both are Type III HSR

A

SERUM SICKNESS:
-antibodies to foreign proteins are produced and form complexes that are deposited in membranes
E.G. a person injected with anti-venom toxin and 5 days later appear with fever and proteinuria

ARTHUS REACTION:

  • much more localized and less common than Serum Sickness
  • The same method as serum sickness but here the complexes happen in skin (e.g. at site of injection)
95
Q

Which test is used to determine the Arthus Reaction?

A

Immunofluorescent Staining.

96
Q

Which Coombs test is more specific?

A

Indirect is more specific but requires more steps

97
Q

Pathogenesis of Type II versus Type III?

A

Type II: Antibodies react with stationary non-moving tissue (EXCEPT for RBC acute hemolysis which is circulating )

Type III: Antibdy binds to circulating/moving antigen…form a complex and then the complex activates complement.
Eventually, this “tri-mer” will deposit into tissue and damage tissue e.g. RA (IgM targets Rheumatoid Factor [IgG] and then go to deposit in the tissue)

98
Q

In a type IV HSR (DTH), which cell types do you expect to be abundant at site of reaction?

A

ACTIVATED MACROPHAGES!!

  • -Reaction delays while T-cells are being activated and then once activated, Th1 release IFN-y which turns macrophages into incredible hulk
  • **NO ANTIBODIES FOUND AT SITE
99
Q

Major cause of Serum sickness? [Type III]

—Approx how many days after antigen exposure will this take place?

A

Drugs acting as haptens, e.g. a-methyldopa in Coombs+ hemolytic reaction

~5 days after exposure

***Symptoms include Fever, Urticaria, Arthralgia, Proteinuria, Lymphadenopathy

100
Q

Of the two polio vaccines, which one is live attenuated and which one is inactivated, killed?

A

LIVE/ATTENUATED: Sabin

KILLED/INACTIVATED: Salk

MNEMONIC” Salk Sucks!!

101
Q

A patient des of a bronchoconstriction after being bitten by a bee and developing. What type of hypersensitivit reaction is this classified as?

Which cells are the major players here?

A

Type I

IgE mediated…and activation of basophils and mast cells.

102
Q

What is common to Graves Disease and Myaesthenia Gravis?

What is different?

A

COMMON:
–both are Type II HSR in which antibodies attack
the host cells

DIFFERENT:
—In MG, the antbodies results in loss of function of the post-synaptic Ach receptors, but in
GD; antibodies alter function, but don’t lead to loss of function. Specifically, the autoantibodies (IgG) in GD stimulate the TSH receptor on thyroid gland, hence leading to HYPERthyroidism!!!

Bottomline: One is a gain of function and another is a loss of function

103
Q

What type of immune reaction leads to post-streptococccal glomerulonephritis?

b) Which bacterin cause PGN

A

Type III Hypersensitivity Reaction

b) caused by Group A strep

104
Q

Which 3 antibodies do you expect to see in Polymyositis and Dermatomyositis?

A
  • Anti-Jo1
  • Anti-SRP
  • anti-Mi-2
105
Q

A patient develops autoimmune hemolytic anemia 5 days after taking alpha-methyldopa (hapten in this case).
a) What type of an immune reaction is this? Be specific

A

Dx: Serum Sickness

=Type III HSR

Specifically, these are warm agglutinis that are involved (IgG)

106
Q

What kind of immune reaction is Type II diabetes?

Who is attacking who in this disease?

A

Type II HSR

Auto-Antibodies are attacking the insulin receptor

107
Q

After suffering with a viral illness, a 3 year old girl develops thrombocytopenia and a bone marrow biopsy shows increased number of megakarocytes?

a) What is the diagnosis
b) If the disease is immune-related (what type of an immune reaction is it?)

A

a) Dx= Immune Thrombocytopenia

b) Cause: Type II HSR with antibodies targeting platelets

108
Q

Anti-SSA (anti-Ro) and Anti-SSB (anti-La) antibodies are found in which disease

A

Sjoren’s Syndrome

109
Q

In primary biliary cirrhosis, what antibodies do we expect to see?

A

anti-mitochondrial

110
Q

A 5 year old girl comes to your clinic. Clinical records indicate she has chronic rhinitis, eczema and asthma?
What test would you administer to determine the nature of her illness? i.e.what would you look for specifically and where?

A

Perform a skin test specific for IgE.

Her symptoms are an example of a Type I HSR

111
Q

anti-TSG receptor antibodies are classically found in which disease?

A

Graves Disease

112
Q

Which two specific antibodies are commonly found in RA?

A

1) Rheumatoid Factor (IgM attacking Fc portion of
IgG)

and

2) anti-CCP

113
Q

With regards to the following, what are the consequences of having no T-cells. I..E assume a patinet has no T-cells, what do you expect with regards to the following:

a) Bacteria
b) Virus
c) Fungi/Parasites

A

a) BACTERIA:
- sepsis is common

b) VIRUS
-common infections with CMV, EBV, JCV,
VZV and chronic infection with respiratory/GI
viruses

c) FUNGI/PARASITES:
- Candida and PCP are common infections

114
Q

After a man is involved in an accident, he is transfused with blood and almost immediately, he develops fever, hypotension, tachypnea, tachycardia, flank pain, and develops hemoglobinuria

1) What is the diagnosis?

A

Acute Hemolytic Transfusion Reaction (hence causing autoimmune hemolytic anemia)

It’s intravascular hemolysis due to Type II hypersensitivity reaction

Cause: ABO blood group incompatibility

115
Q

In the followiing vasculites, which ones are p-ANCA positive and which one are c-ANCA positive?

1) Microscopic Polyangiitis
2) Wegener’s Granulomatosis
3) Churg-Strauss Disease

A

c-ANCA:
-Wegener’s Granulomatosis

p-ANCA:

 - Microscopic Polyangiitis
 - Churg-Strauss Disease
116
Q

After a young girl suffers massive bleeding after playing sportt she is transfused with blood and 2 days later, she develops jaundice

1) What is the diagnosis?

A

Type II hypersensitivity reaction causing Acute Hemolytic Transfusion Reaction

CAUSE: Host antibody reaction against foreign antigen on donor RBC

Jaundice: Shows that its extravascular hemolysis

117
Q

What do the following diseases have in common?

  • RA
  • Lupus
  • Polyarteritis Nodosa
A

Type III HSR!!!

118
Q

In a patient who develops acute hemolytic anemia after a transfusion, what is the difference in pathogenesis in a patient who develops

a) intravascular hemolysis vs
b) extravascular hemolysis?

A

a) intravascular hemolysis:
- due to ABO blood group incompatibility

b) extravascular hemolysis?
-usually due to host antibodies reacting against
foreign antigens on host RBCs

NB: Both are Type II HSR

119
Q

After a 40 year old man receives bloos transfusion, he develops Urtcaria, pruritis, wheezing, and fever?

How would you treat him and why?

A

Give him Benadryl (OR equivalent anti-histamine)

This is a Type 1 allergic reaction against plasma proteins in transfused blood.

In an anaphylactic reaction (severe allergic reaction); paitient would have dyspnea, bronchospasm, hyPOtension, respiratory arrest and shock

120
Q

After a 36 year old human heals from a campylobacter infection, she starts to experience numbness that starts at her fingertips and has been progressing up her arms?

A) What is the diagnosis
B) What type of an immune reaction is going on?

A

A) Guillain-Barre

B) Type IV HSR (DTH)

121
Q

Bullous Pemphigoid and Pemphigas Vulgaris are 2 types of dermatologic diseases.

Who is attacking who in these diseases and what kind of immune reactions are they?

A

Both are Type II HSR

B.Phemphigoid:
IgG against hemidesmosomes leading to tense bullae formation with negative Nikolsky sign

P.Vulgaris:
IgG targeting desmoglein (part of desmosomes) leading to falccid intradermal bullae wiith Positive Nikolsky sign.
***More severe/sicker than bullous pemphigoid

122
Q

3 days after a 4 year old comes into contact with a wild plant at pre-school, the child develops a wet-looking rash. What types of cells do you expect to find in the skin of the child if you bisopsy the “strange rash”?

A

This a type IV HSR (DTH) that has caused CONTACT DERMATITIS.

Expect to see Macrophages because the Th1 cells activated produce IFN-y which turns macrophages into incredible hulk

123
Q

With regards to the following, what are the consequences of having no B-cells. I..E assume a patient has no B-cells, what do you expect with regards to the following:

a) Bacteria
b) Virus
c) Fungi/Parasites

A

a) BACTERIA:
- common infections with encapsulated bacteria

b) VIRUS
- enteroviral encephalitis
- Poliovirus (live vaccine is contraindicated)

c) FUNGI/PARASITES:
- GI giardiasis (because there is no IgA)

124
Q

What is common to both Rheumatic Fever and Post-Strep Glomerulonephritis?
What is different?

A

COMMON:
—They are both caused following infection with
Group A Strep

DIFFERENT:

 - RF=====>Type II HSR
 - PGN====> Type III HSR
125
Q

3 days after receiving a blood transfusion, a woman develops Fever, Headaches, Chills and Flushing?
What is going on?

A

Dx: Febrile nonhemolytic transfusion reaction

A Type II HSR

Cause: Host antibodies against HLA antigens and leukocytes

126
Q

Erythroblastosis Fetalis and Goodpastures disease are what type of immune reactions?

A

Type II HSR

127
Q

Which diseases are associated with the following antibodies:

A) anti-Centromere

B) anti-Cardiolipin

C) anti-Glutamate decarboxylase

A

A) anti-Centromere:
-Liited Scleroderma (CREST SYNDROME)

B) anti-Cardiolipin:

   - SLE 
   - anti phospholipid syndrome

C) anti-Glutamate decarboxylase
-Type 1 diabetes

128
Q

Which antibodies do you expcect to find in the following diseases?

A) drug-induced lupus
-name 1

b) Hashimoto Thyroditis
- name 2

A

A) drug-induced lupus
-anti-Histone

b) Hashimoto Thyroditis
- antimicrosomal
- antithyroglobulin

129
Q

Which antibodies do you expect to find in limited scleroderma and which ones in diffuse scleroderma?

A

LIMITED: anticentromere

DIFFUSE: anti-Scl-70
i.e. anti DNA topoisomerase I

130
Q

With regards to the following, what are the consequences of having no granulocytes. I..E assume a patient has no granulocytes, what do you expect with regards to the following:

a) Bacteria
b) Virus
c) Fungi/Parasites

A

a) BACTERIA:
-common infections with Staphylococcus,
Burkholderia Cepacia, Serratia, Nocardia

b) VIRUS
N/A

c) FUNGI/PARASITES:
- Candida, Aspergillus

131
Q

In mixed CT diseae, which antibodies do we normally see?

A

anti-U1 RNP (ribonucleoprotein)

132
Q

anti-smooth muscle antibodies are seen in which disease?

A

Autoimmune hepatitis

133
Q

The following two anti-bodies are seen in which disease?

1) IgA antiendomysial
2) IgA anti-tissue transglutaminase

A

Celiac Disease

134
Q

A 6 year old child presents with a Candiida infection.
She has had prior infections with Serratia and Pseudomonas. A dihydrorhodamine test on flow cytometry is abnomal. What is the diagnosis?

A

Chronic Granulomatous Disease due defect in NADPH oxidase.

135
Q

A young male patients presents with a positive Romberg sign, spider angiomas and multiple URIs.

What genes is likely defective and what lab findings would a nurse expect?

A

Dx= Ataxia-Telengiectasia

CAUSE: defective ATM gene leading to DNA double strand breaks and hence, cell-cycle arrest.

FINDINGS:

  • Increased AFP in utero
  • Low IgA, IgG, and IgE
  • Lymphopenia
  • Cerebellar Atrophy
136
Q

A 13 year old girl with a history of ear infections, sinusitis, and/or pneumonia has been hospitalized.
What is the number one item on the differential?

What lab findings/measurements do you expect to find?

A

Dx= Selective IgA deficiency…hence infections in all the mucosal surfaces

Labs: Significantly reduced or totally absent IgA but all other antibodies at normal levels

NB: patients can be asymptomatic and
2) when exposed to blood products with Iga, anaphylactic reactions result and usually, they develop antibodies to IgA

137
Q

A 9 month old baby boy has recurrent bacterial and enteroviral infections. On physical exam, his tonsils are missing even though he has never had surgery. His lymph noodes are also difficut to palpate.
What is the diagnosis and if genetic, what is the mode of inheritance?

A

X-linked (Bruton) Agammaglobulinemia [XLA] which is due to a defect in a BTK (a tyrosine kinase needed to allow B-cells to mature)

Findings show decreased levels of antibodies of all classes, usually after 6 months when maternal IgG have fallen

138
Q

A 7 year old boy with very pale blue eyes and sensitive skin to the sun presents with a 3rd illness of pneumonia in 2 months. Today he has come because he is starting to experience numbeness and tingling on his thumb.

a) what 3 findings do you expect in his peripheral blood spear?
b) What is the underlying cause of his illness?

A

Dx= Chediak-Higashi Sydrome

Blood Smear:

- Pancytopenia
- Mild Coagulation Defects
- Giant granules in neutrophils

CAUSE:
-defect in lysosomal traffickig regulator gene
(LYST) therefore limiting phagocytosis

139
Q

An 8 month baby presents with abnormal movements and has persistent rhinorrhea.
When he was 2 months old, he had an infection with Candida.
a) What other physical exam and lab abnormalities do you expect?
-Name 5
b) what is the diagnosis?

A

Dx= Thymic Aplasia (Di-George Syndrome)

CAUSE:
22q11 deletion and failure of he 3rd and 4th pharyngeal pouches

OTHER FINDINGS:
-absent thymic shadow
-No T-cells
-No PTH
-Low Calcium (causes tetany described in vignette)
-Deletion detect by FISH
-Viral/Fungal Infections (described in vignette)
-Conotruncal abnormalities:
eg tetralogy of fallot, truncus arteriosus

140
Q

A child presents with an infection and lab tests yield a negative tetrazolim test. What is the mechanism of inheritance of the underlying disease?

A

X-LIKED

Dx= Chronic Granulomatous Disease due to NADPH oxidase deficiency

141
Q

Mode of inheritance of Chediak-HigashI Syndrome

A

autosomal-recessive

142
Q

A 3 month old baby presents with a historyof recurrent bacterial infections since birth and the mother repports that the baby’s umbilical cord took longer to separate compared to the baby’s 2 older siblings. You biopsy one of the skin lesions. Which cells do you expect to find?

b) what do you expect to fing in the peripheral blood smear?
c) What is the diagnosis?

A

Dx= Leaukocyte Adhesion Deficiency Type 1

CAUSE: defect in LFA-1 integrin (CD28) on phagocytes resulting in impaired migration and chemotaxis

BIOPSY: absence of neutrophils at infection sites

BLOOD SMEAR: increased leukocytes, since they don’t chemotaxis

143
Q

A 14 month old baby has recurrent noninvasive Candida Albicans infections on his skin, ears, mouth and sinuses. Lab tests done show absent in vitro T-cell proliferation in response to candida antigens and also absent cutaneous reaction to candida.

What is the diagnosis and cause of his presentation?

A

Dx= Chronic Mucocutaneous Candidiasis

CAUSE:
-T-Cell dysfunction due to many causes

144
Q

A pale-looking and tiny 16 month old baby come to the clinic. Her mother says the baby almost always passes loose stool. You examine the baby and notice the tongue is covered in white exudate and the baby has persistent rhinorrhea. You look at the baby’s chart and notice that he has been previously admitted for several episodes of pneumonia.

What is the diagnosis?
How would you treat the baby?

A

Dx= SCID!!!

CAUSE: No B and T-cells due to several kinds of mutation e.g. defects in the Rag genes needed for VDJ recombination or

b) defective IL2-R gama chain (most common) or
c) adenosine deaminade deficiency

TREATMENT: BMarrow Transplant (no risk of rejection)

Bottomline: Baby is affected by virus, fungi, protozoa, bacteria, and virtually ANYthing!
Presents with failure to thrive

145
Q

A baby born in Harare has just received her first BCG vaccine at birth. Later she develops disseminated bacterial and mycobacterial infections.

What is most likely deficient in this baby?
What do you expect to find from lab test?

A

Dx= 1L-12 Receptor Deficiency
hence decreased Th1 response

LAB FINDINGS: decreased IFN-y

INHERITANCE: autosomal recessive

146
Q

A 3 year old child presents with a history of severe pyogenic infections. In her prior visit, she tested positive for CMV and 2 months before then, she had been admitted for infections with Cryptosporidium and Peumocystis [double hit]
Lab findindings very high levels of IgM.

What is the mode of inheritance of the disease?

A

Dx= Hyper IgM Syndrome which is due to lack f CD40Ligand on CD4+ cells and hence, no class-switching

INHERITANCE: X-linked recessive

147
Q

An 11 year old girl with very coarse facial features and eczema on her flexor surfaces comes to your clinic. Her primary teeth are still intact and she has several abscesses on her limbs. Which gene is likely mutated?

When you look at her blood sample, what findings do you expect?
-name 2

A

Dx= Autosomal dominant hyper-IgE Syndrome (Job Syndrome)

CAUSE:Deficiency of Th17 cells due to STAT3 mutation

FINDINGS: very high IgE and low IFN-y

148
Q

A 26 year old woman suddenly develops autoimmune conditions like hemolytic anemia due to anti-phospholipid syndrome and even 6 months later she is diagnosed with lymphoma and bronchiectasis. Just when she though the worst was over, she developed pneumonia and she has come to see you this morning.

Exam findings show that her plasma levels are low and she has reduced immunoglobins in her system?

What is the diagnosis?

A

Dx= Common variable immunodeficiency which is due to defects in B-cell differentiation (many causes)

Can be acquired in 20s-30s

149
Q

A 14-month old boy presents to your cliic with multiple purplish patches on arms and pneumonia. You notice that he has eczema on his flexor surfaces and when you look at his blood smear, you notice that the platelets are significantly reduced and they look smaller than normal.

a) Which gene is likely mutated and what is the mode of inheritance?

A

Dx= Wiskott-Aldrich Syndrome:

Triad= Thrombocytopenic purpura
Eczema
Reccurrent infections
-an dincreased risk of autoimmune diseases

CAUSE: mutated WAS gene and inability to
reorganize actin cytoskeleton
X-linked recessive

150
Q

What is the name for a graft from an identical twin?

A

Isogeneic OR Syngeneic

151
Q

A surgeon is just beginning to suture abdominal incisions he made while implanting a kideny into a 24 year old woman. Suddenly the patient experriences widespread thrombosis and some of her vital organs start to look ischemic when the surgeon reopens the abdomen.
What cells are responsible for this unfortunate event?

A

Dx= Hyperacute transplant rejection

CAUSE: preformed antibodies in the woman have reacted to the donor antigens and activated complement (Type II HSR)

152
Q

A graft from another donor who is not your twin is called?

A

Allograft

153
Q

Which parts of the immune system are involved in both Acute and Chronic transplant rejection?

How is the management of these two different?

A

Both Cellular and Humoral componets.

Management:

  • Acute rejection (weeks to months) can be prevented or reversed with immunosuppressants
  • Chronic rejection is irreversible really
154
Q

What are the organs-specific manifestations of chronic transplant rejection for the following:

  • Heart
  • Lung
  • Liver
  • Kidney
A

Lungs: bronnchiolitis Obliterans

Heart: atherosclerosis

Liver: Vanishing Bile Ducts

Kidney: Vascular Fibrosis, Glomerulopathy

155
Q

A woman with a history of kidney transplant perfored 10 years ago presents with jaundice, maculopapular rash, hepatosplenomegaly and diarrhea.
What is the diagnosis?

A

Graft-versus-host Disease

156
Q

Ian Smith has an eye that was dervied from a goat. What kind of graft do we call that?

A

Xenograft

157
Q

These to gram-positive cocci cause toxic shock syndrome by formation of superantigens?

A

S.Pyogenes

S.Aureus

158
Q

A patient with a recent infection and antibiotic treatment of with a cephalosporin presents with the following symptoms:

1) Fever
2) Pruritis
3) Arthropathy (“bones hurt”)

What is the DDx and treatment?

A

SERUM SICKNESS!! Type III HSR

Treat with prednisone and diphenhydramine (anti-histmaine) for symptomatic relief

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