Flashcards in Immunology Deck (117)
To what nodes do the rectum and anus respectively drain?
Rectum - internal iliac, anus - superficial inguinal
What do the right lymphatic duct and thoracic duct drain respectively?
RLD - right arm and right half of head, thoracic duct - everything else (left side, trunk, and right leg)
Where are the T and B cells found in the spleen?
T cells - PALS (white pulp), B cells - Follicles (white pulp)
Salmonella, S pneumoniae, H flu, N meningitidis
What is seen on a blood smear postsplenectomy?
Howell-Jolly bodies (nuclear remnants), Target cells, Thrombocytosis
HLA subtype associated with hemochromatosis
Disorders associated with HLA-B27 (4)
Psoriasis, Ankylosing Spondylitis, IBD, Reiters
HLA subtype associated with Graves
HLA subtype associated with MS, hay fever, SLE, and Goodpastures
HLA subtype associated with DM
DR3 and DR4
HLA subtype associated with RA
HLA subtype associated with pernicious anemia and hashimotos
What cytokines enhance NK cell activity?
IL-12, IFN-B and IFN-A
Which cytokine increases Th1 development and what cytokines are mainly produced by Th1 cells
IL-12. They make IL-2 and IFN-G. Th1 response mainly increases cell-mediated response (CD8 functioning)
Which cytokine increases Th2 and which cytokines are mainly produced by Th2 cells?
IL-4. They make IL-4 and IL-5. Th2 mainly supports humoral responses (IgE more than IgG)
What cells are developing T cells checked for reaction against in the process of negative selection?
Thymic medullary epithelial and dendritic cells
Interaction of what two molecules is responsible for signal 2 in the process of helper t cell activation?
B7 (APC) and CD28 (CD4 cell)
What cytokine (produced by Th cells) needs to be present when a CD8 cell decides to kill a virus infected cell?
What two molecules interact when a Th cell activates a B cell (in addition to the cytokines the Th cell is secreting)?
CD40L (Th2 cell) and CD40 (B cell)
What cyotkines inhibit the Th1 and Th2 responses respectively?
Th1 inhibited by IL-10 (from Th2 cells), Th2 inhibited by IFN-g (from Th1 cells)
What are the two main things that bind to the Fc portion of Ig?
Complement and Macrophages (macrophages bind closer to the base, complement higher up)
Where does isotype switching occur?
Lymph node follicles
Which two Igs activate the classic complement pathway?
IgG and IgM
Which complement component is most important in opsonization?
Which Ig is most important in opsonization?
What is contraindicated in C1 esterase inhibitor deficiency?
Susceptibility to what is increased in C3 deficiency?
Type 3 hypersensitivity reactions (C3 clears immune complexes)
What is given to patients lacking IL-12R and why?
IFN-G to help them mount a better granulomatous response
List the cytokines secreted by each of the following - macrophages, all T cells, Th1 cells, and Th2 cells
Macrophages - IL-1, IL-6, IL-8, IL-12, TNF-a. All T Cells - IL-3. Th1 - IL-2, IFN-G. Th2 - IL-4, IL-5, IL-10
What two cytokines are important in inhibiting inflammation?
TGF-B and IL-10
How do interferons improve antiviral efforts?
They stimulate uninfected cells to produce ribonuclease that inhibits viral mRNA
What is the main role of platelet activating factor?
It is chemotactic for neutrophils
What cell surface marker is typically used to identify macrophages?
What cell markers are present on NK cells?
CD16 (binds Fc of IgG) and CD56 (unique to NK)
Give the CD ranges which typically correspond to each of the following - T-cells, Myeloid cells, B cells
T - 1 to 8, Myeloid - 11 to 15, B - 19 to 23
Two main bacteria with superantigens
Strep pyogenes and Staph aureus
What is the action of LPS?
Directly stimulates macrophages by binding CD14
Preformed antibodies are given after exposure to what entities?
Tetanus toxin, Botulinum toxin, HBV, Rabies virus
List live attenuated vaccines
MMR, polio (sabin), varicella, yellow fever
List killed vaccines
Cholera, flu, Hep A, polio (Salk), Rabies
About how long does serum sickness take to develop and what will be found?
Around 5 days. Will find low C3 levels
Most common cause of serum sickness and findings
Bactrim. Fever, urticaria, arthralgias, proteinuria, lymphadenopathy (5-10 days after exposure)
PBC, also gallbladder GVHD
Anti-U1 RNP antibodies
Mixed connective tissue disease
Anti-smooth muscle antibodies
Anti-glutamate decarboxylase antibodies
What is the main fungal or parasitic infection seen in pts with no B cells and why?
GI Giardiasis (due to lack of IgA)
Defect and genetics of Brutons agammaglobulinemia
X recessive. Defect in BTK, a tyrosine kinase prevents pre-B cells from becoming immature B cells
Recurrent bacterial infections, intact thymus, decreased number of B cells and Ig of all classes
Defect of Hyper-IgM syndrome
Severe pyogenic infections early in life, high IgM and low other Igs
Sinus and lung infections, milk allergies and diarrhea, anaphylaxis on exposure to blood products with IgA, decreased secretory IgA
Selective Ig deficiency
Which B cell disorder can be acquired in 20s or 30s?
What is the defect in common variable immunodeficiency?
Failure of B-cells to mature. Normal numbers of b-cells found but decreased plasma cells and Ig
Genetics and embryology of DiGeorge
22q11 deletion. Failure of 3rd and 4th pharyngeal pouches to develop
Defects in DiGeorge besides hypocalcemia and immunodeficiency
Congenital heart and great vessel defects
Hyper-IgE due to Th cells failing to produce IFN-g (neutrophils cant respond to chemotactic stimuli)
Coarse facies, non-inflammed staph abscesses, retained primary teeth, eczema
Jobs syndrome (Hyper Ig-E due to Th cell failure)
Two major causes of SCID, which is more common, and the pathogenesis of each
Defective IL-2R (more common) - decreased T-cell activation, and ADA deficiency - Buildup of adenosine, which is toxic to B and T cells, decreased DNA synthesis
Cerebellar defects, spiger angiomas, IgA deficiency
Ataxia-telangiectasia (defect in ATM gene, which codes for DNA repair enzymes)
Defect and genetics of Wiskott-Aldrich
X recessive. Deletion of B and T cells
Thrombocytopenic purpura, Infections, Eczema. High IgE and IgA with low IgM
Defect and genetics of Chediak-Higashi
AR. Defect in lysosomal regulator trafficking gene
Recurrent infections, partial albinism, peripheral neuropathy (nystagmus)
Lab finding in chronic granulomatous disease
Negative nitroblue tetrazolium dye reduction test (due to lack of respiratory burst in neutrophils)
Findings in GVHD
Skin, liver, intestine - Maculopapular rash, jaundice, hepatosplenomegaly, diarrhea. Most common in BM and liver transplants.
Main targets of chronic rejection
Recipient CD8 cells target blood vessels. Exception is chronic lung rejection, where small airways are targeted, causing bronchiolitis obliterans
Blocks differentiation and activation of T cells by inhibiting calcineurin (preventing production of IL-2 and IL-2R). Nephrotoxic, causes gout
Inhibits calcineurin (and thus IL-2 and IL-2R production). Causes nephrotoxicity, peripheral neuropathy, HTN, pleural effusion, hyperglycemia
Inhibits mTOR (thus inhibiting T-cell proliferation in response to IL-2)
Monoclonal antibody for IL-2R on activated T cells
Antimetabolite precursor of 6-MP (interferes with nucleic acid synthesis). Watch with allopurinol
Monoclonal antibody to CD3
IL-2 analog. Use in RCC, metastatic melanoma
Uses of IFN-a
Hep B and C, Kaposi, Leukemia, Malignant melanoma
Uses of IFN-B
Uses of IFN-G
Chronic granulomatous disease
IL-11 analog, use in thrombocytopenia
Antibody to TNF-a. Use in Crohns, RA, psoriatic arthritis, ankylosing spondylitis
Antibody to TNF-a. Use in Crohns, RA, psoriatic arthritis
Antibody to IIb/IIIa. Use in unstable angina and percutaneous coronary intervention
Antibody to ERB-B2. Use in Her-2 expressing breast cancer
Antibody to CD20. Use in B-cell NHL
Antibody to IgE. Last line for severe asthma
Type of hypersensitivity used to kill helminths
Type 2. IgE antibodies coat the eggs, Eosinophils recognize and release major basic protein
Markers for Reed-Sternberg cells
CD15 and CD30
Marker for ALL
CD10 (also called CALLA)
Most common pathogen in cellulitis
Group A Strep (pyogenes)
What metal is required by the enzyme that converts granulation tissue (Collagen type 3) to scar tissue (Collagen type 1)?
What can chronically draining sinuses predispose to?
Squamous cell carcinoma
What cells are the main players in type 4 hypersensitivity?
Helper T cells and Macrophages
Two portions of the tubule most susceptible to hypoxia
Straight portion of the proximal tubule and medullary portion of the thick ascending limb
Main disease associated with cryoglobulins
Irritation of what receptor leads to dyspnea in heart failure?
The J receptor in the lungs
Three major causes of lymphedema
Mastectomy, W Bancrofti, Chlamydia Trachomatis (lymphogranuloma venarium)
Quick way to estimate serum osmolarity
Double sodium and add 10
Tonicity of normal saline
What is a good general rule for interpreting low serum sodium levels?
If serum sodium is below 120 it is very likely to be SIADH
What drugs produce SIADH?
Oral sulfonylureas (eg chlorpropramide)
What is the usual tonicity of diarrhea?
In babies it is hypotonic, in adults it is isotonic
What is the tonicity of sweat?
Non pharmacologic treatment for edematous states and SIADH respectively
Edematous state - Restrict salt and water, SIADH - restrict water
Treatment for hypovolemic shock
Give normal saline until BP normal. Then replace what they lost (sweating - half normal saline, adult diarrhea - isotonic saline, DI - 5 percent dextrose)
Most common cause of shock in the hospital
Septic shock from E coli due to indwelling urinary catheters
Formula for O2 content
(1.34 x Hb x O2saturation) + pO2
Mixed venous oxygen content in the different types of shock
Septic shock - High, Cardiogenic and hypovolemic - Low
TPR in the different types of shock
Septic - low. Cardiogenic and hypovolemic - high
LVEDV in the different types of shock
Septic - low, Hypovolemic - low, Cardiogenic - high
Young African American woman comes in with microscopic hematuria. First step in management?
Get a sickle cell screen. O2 tension is low enough in renal medulla to cause sickling in sickle trait patients
What effect do progesterone and estrogen have on respiration?
Cause a respiratory alkalosis due to overstimulation of respiratory center. Pregnant women have AV fistulas in lungs which go away after delivery
Respiratory status in endotoxic shock
Respiratory alkalosis (endotoxins stimulate resp center)
Acid base status in salicylate overdose
Mixed. Respiratory alkalosis due to overstimulation of resp center and metabolic acidosis due to acid ingestion. Similar to endotoxic shock (mixed Ralk with Macid)
What should you associate inspiratory stridor in a child with?
H flu (epiglottitis)