Immunology Flashcards
IL 4
Mediates class switching to IgE; “Four makes ya a whore–switching classiness” Secreted by Th2 cells
IL 5
Promotes Eosinophil Migration; FivE=Eosinophils
IL-6
Secreted by T-cells and Macros. Proinflam cytokine
Osteoblasts secrete to activate clasts.
IL 10
Stimulates Th2 cells, and Inhibits Th1 cells; “Ten to fight the bacteriem”
also tones down immune system along with Il17
IL-7
HSC, B, T and NK cell maturation factor (and general lymphoid cell survival)
IL-8
Recruits neutrophils
“clean up on ilse 8”
TH2 cells secrete
IL 4, 5, 10 (particuallary in allergic reactions)
4=IgE class switching
5=Eosinohpils
10=inhibiting Th1 and promoting Th2s
Why do you see hypercalcemia in granulomas (and what type of granulomas?)?
Expression of 1 alpha hydroxylase in noncaseating granulomas leading to Vitamin D activation
Prosthetic Heart Valves
Coagulase Negative Staph (tends to be Left heart Valves) HACEK bacteria: H aemophilus aphrophilus A ctinobaccilus actinoymycetemocomitans C ardiobacterium hominis, E ikenlla corrodens K ingella kingae
IVDA (intravenous drug users
Staph Aureus (virulent) TENDS TO BE RIGHT SIDE OF HEART, which can cause other pulm issues
Susceptible Organsims upon splenectomy
Encapsulated organisms: “S SHIN”: Salmonella, S. pneumoniae, H. Influenzae, N. meningitidis Post Splenectomy: Howell-Jolly Bodies, Target Cells, Thrombocytosis
HLA Subtype associations: A3 B27 B8 DR2 DR3 DR4 DR5 DR7
A3: Hemochomatosis
B27: Psoriasis, ankylosing spondylitis, inflammatory bowel disease, Reiter’s syndroeme (“PAIR”)
B8: Grave’s Disease “Gr8ves”
DR2: MS, Hay fever, SLE, Goodpasture’s
DR3: DM type 1 (“DR3 + DM1 = DR4”)
DR4: DM type 1, Rheumatoid arhtirtis
DR5: Pernicious anemia (B12 def), Hashtimoto’s thyroiditis (“Thy ~5”)
DR7: Steroid-responsive nephrotic syndrome (Minimal change disease)
Infections that affect fetus
TORCH: Toxoplasmosis, Other (syphillis, TB), Rubella (german measles), CMV, Herpes/HIV
Cryptococcus Neoformans
Meningitis in HIV/Immunocomp. Monomorphic fungus–Encapsulated yeast buds always
Blastomyces Dermatitidis
Broad-based budding yeasts (clinical non enviro form). Skin and bone lesions most common
Paracoccidioides Brasiliensis
Budding yeast in pilot’s wheel (clinical) Central and south america. Presents as primary pulmonary disease
Histoplasma Capsulatum
Intracellular yeast within macrophages NOT encapsulated. Primary pulm infection Bird Droppings
Aspergillus
Oppurtunistic infections Septate Hypahae with 45 degree angles Mengitis (cyrpto more common)
Coccidioides immitis
Fungal meningitis in immuno comp. Sonoran desert zone of US (san joaquiin valley fever)
Metronidazole
“GET GAP on the Metro” Giardia, Entameoba, Trichomonas, Gardnerella vaginalis, Anaerobes, h. Pylori
Drugs that inhibit P450 Enzymes
PICK EGS Protease inhibitors, Isonazid, Cimetidine, Ketoconazole, Erythromycin, Grapefruit Juice, Sulfanomides
Patients with Chronic Granulomatous Disease
Get Staph Aureus.
Encephalitis (6)
HSV1, HSV2, Rabies Virus, Arboviruses, T. Gondii, T. Brucei
Neonatal Meningitis (3)
S. Agalactiae, L. monocytogenes, E. coli
Meningitis 6 months to 6 yrs (3)
S. pneumoniae, N. meningitidis, H. Influenzae type B
Meningitis 6yrs to 60years (3)
N meningitidis, poliovirus, S. pneumoniae
Aseptic Menigidits(4)
Coxsackie Virus, Echovirus, Mumps Virus, Poliovirus
Fungal menigitidis
C. neoformans
Rheumatic Heart Disease
S. pyogenes
Myocarditis
Coxsackie type B, T. Cruzi, S. Aueus + E. faecalis (from endocarditis), C. Diphtheriae, B. Burgodrferi
Endocarditis: Native valve
Strep Viridans, S. Bovis, Strep Pyogenes (usually better known to cause the rheumatic fever that causes Type III hypersenstivity of heart damage)
Endocarditis: IV Drug Users
Staph Aureus, Strepococci, E. Faecalis, P. Aeruginosa. Candida Albicans***
Prosthetic Valve
S. Epi, S Aureus, Gram Negs, C. Albicans Subacturely: Streptococci
Protein A
Finds the Fc portion of IgG prevent Opsinization (eg Staph Aureus)
HIV
CD4+ Counts
800+ Healthy
600-800: Assymptomatic
400-600: Generalized Lymphadenopathy
200-400 Generalized Lympadenopathy and Thrush
Antibodies to the envelope continue to rise due to antigenic variaiton that need primary (nonCD4+) response. p24 antibodies (capsid) decline.
Asplenic Pateints are at risk for
Why?
What else can they do?
SHiNS SKI bacteria (S. pneumo, HiB, N. meningitidis, Salmonella, Klebsiella, Group B Strep).
Capuslated
Transformation–can take up DNA from environmnet
Drugs for Aids, Influenza, and Herpes
- avirs=for AIDs (A, A)
- ivirs for influenza (I, I)
- ovirs for herpes (O for ouch it hurts)
Common atpical pneumonias:
MLCV, My lungs can’t “vreethe”. Mycoplasma legionalla, chlamydia, viruses
Urease Positive Organisms
PUNCH
Proteus, Ureaplasma, Nocardia, Cryptococcus, Helicobacter pylori
Catalase Postive organisms (what condition leaves person susceptible to these bugs? How do you test for this condition?)
PLACESS (pseudomonas, listeria, aspergillus, candida, E. coli, S. aureus, Serratia)
NADPH deficiency. Nitroblue tetrazolium test will be negative (non blue) [it will be positvie/blue in MPO def).
MPO def is increased risk to candida infections.
What does Psuedomonas Cause?
PSEUDO:
Pneumonia (cf ppl), Sepesis, External otitis (swimmer’s ear=think water), UTI, Drug use and Diabetic Osteomyeltitis.
And hot tub folliculitis of course.
Ecthyma gangrenosum-necrotic cutanesoul lesions rapidly progressing; in immunocomp ppl
Tx: aminoglycoside with extended spectrum penicllin (P-iperacillin for P-suedo)
Transplant Rejection Stages
1) Hyperacute: preformed IgG causing T2HSR
2) Acute: Cell mediated T4HSR (and you have T2HSR with new antibody devo)
3) Chronic: Host T cells can interact with graft MHC 1’s however the grafts antigens that are presented on MHC 1’s are seen as foreign causing RXN
4) Graft vs Host disease: graft’s T-cells fight against immunocomprimised host
What cells participate in ADCC, what do they need?
Macrophages Positive for what CD’s what do they do?
Macrophages (C14/40+)/NK cells
CD16 which binds to the Fc portion of Igs
CD14 (TLR) used to bind Endotoxin
Severe Recurrent Pyogenic Infections?
C3 def particularly of upper resp tract:
Strep Pneumo and H Flu
Type of HSR:
Polyarteritis Nodosa?
Ecyzema?
Serum Sickness?
Arthrus Reaction?
3
1
3
3
X linked Immuno def?
“WBC”
Wiskott, Brutons (can be), Chronic Granulomatous (can be)
Kid with poor smooth pursuit, small malformed blood vessels on skin, and recurrent sicknesses
ATM
Three A’s A-taxia, Angiomas (teliectasias), IgA def
Lepramatous leprosy demonstrate weak what?
Tuberculoid Leprosy?
Weak cell mediated response thus decreased Th1, thus defective macros.
Better cell mediated thus higher Th1 CD8+
Interstitial Pneumonia in a lung transplant patient?
CMV***, will likely see intranuclear inclusions and GIANT cells (cytoMEGAlovirus)
Interferon for granuloma formation? For maintenance?
IFN Gamma for formation
TNF alpha for maintenance
B cell vs T cell immunodef presentations?
B-cell: Otits media (Strep pneumo, moraxella, H flu)
T-cell: mucocandidiasis infections and pneumocystis infections
2 factors that drive angiogenesis?
VEGF and FGF***
Blood characteristic seen commonly in chronic ETOH?
Macrocytosis
Occurs either from poor nutrition (B12/Folate) or by ETOH acting as direct toxin on marrow
Predisposing factor for hematogenous spread of candida albicans?
Superficial spread?
Low Neutrophils
Low CD4+ cells
Live attenuated vaccines better at?
Generating a prolonged immune reponse, thus have more IgG’s and mucosal IgA’s (A’s if the organism has a mucosal invasion component)
3*** things that are released from degranulating mast cells?
Histamine
Leukotrienes
TRYPTASE (specific to mast cells)
Fibrinoid Necrosis?
Fibrionid~Fibrin like telling you some immune component is present
Usually the result of type III complexes being deposited in endothelial wall (eg Polyarteritis Nodosa, Henoch Schonlein Purpura; can also be seen in malignant HTN/Preeclampsia)
Pertussis vaccine is what type?
H Flu is what type?
Acellular. Think DTaP as “acellular pertussis”
Hflu conjugated to diptheria toxin
Protein A vs IgA protease?
Protein A binds Fc Recptor preventing ospinization
IgA Protease allows for mucosal survival/penetration
UTIs
What does a leukocyte esterase test tell you?
Nitrite Test?
DD for Urease test?
L Esterase tells you its bacterial in origin
Nitrite tells you its a Gram Neg*****
Urease + prolly Proteus/Kleb
Urease - prolly E. coli or enteroccocus
