Immuno Flashcards
lack of all B cells
bruton x linked agammaglobulinemia
cause of bruton
deficiency in (bruton) Tyrosine Kinase
lack of Pus formation
LAD
infection with catalase + organisms
chronic granulomatous disease
albinism
chediak higashi
deficiency of CD40L on T cells
Hyper-IgM. Class switching defect
MHC are encoded by _______ and found on _________
HLA genes
MHC1: all nucleated cells
MHC2: APC’s
present antigen fragments to T cells and bind TCRs
MHC
Needs release of invariant chain for peptide loading
MHC2
Stating that there is a difference when none exists
Type 1 (alpha) error
alpha (epi) is the probability of ____________
making a Type 1 error (False positive)
what does p
there is less than a 5% chance that the data will show a difference/effect that is not actually there (FP)
T cell development: produced in BM and then travel to thymus: explain Cortex, Medulla
Cortex:
Arrive as double negative (no cd4 or cd8)
–>DNA rearrangement –>become Double Positive. POSITIVE selection = those that bind self MHC can survive. go to medulla
Medulla: now those that bind self too tightly die= NEGATIVE selection
Positive (1st) and Negative selection(2nd) T cell
Cortex…Positive selection: When Double Positive T cells bind self MHC, its a positive thing and they survive
Medulla…Negative selection: Now they are Single Positive. Those that bind self too strongly are killed. So binding self strong is a Negative thing.
TB: Cord factor and sulfatide
Cord Factor: prevents MQ maturation and induces TNF release (which forms granuloma)
Sulfatide: “the tide is too strong for phagolysosome fusion)
Superantigen and Cachexia cytokines:
TNF alpha; IFN gamma; IL-1, IL-6.
Alpha is 1, Gamma is 6.
Whats the link between Fluticasone/Budenoside (Pulm Corticosteroids) and TNF alpha?
These drugs inhibit NF-KB, which is the TF that induces TNF alpha production
Radiation therapy causes what kind of damage?
Free radical formation and double stranded DNA breakage
FAS:
9-5 job would kill me FASt (Fas aka Fas-R = CD95)
If its looking autoimmune, we want to kill it FASt (negative selection–>thymic medulla)
whats difference btwn apopotosis and necrossi (basic)
Necrosis = INFLAMMATION
Apopotosis is NOT inflammatory. Note: Apoptosis requires ATP.
Coagulative vs Liquefactive necrosis
Coag: Ischemia;
–>Proteins Denature, and then Enzymatic Degradation
Liquef: ABSCESSES and Brain infarct
- ->Enzymatic degradation first, then Proteins Denature
- ->Neutrophils release lysosomal enzymes that digest the tissue
Order: remember liquefactive is E-P-L: Enzymes first and then Proteins degraded in Liquefactive.
Whats EPL?
Reminds us that order of degradation is Enzymes and then Proteins in Liquefactive necrosis (vs opp order in coag)
renal zones most susceptible to ischemia (and thus ischemic ATN)
Proximal Tubule and Thick Ascending Limb
PCT and TAL nigga
(Red)Hemorrhagic Infarct: Location
where there is dual blood supply
LUNGS, LIVER, INTESTINE
–>can get Reperfusion injury here
Pale Infarcts
Heart/Kidney/Spleen since there is only a single blood supply (Ischemic/anemic infarct)
Angiogenesis mediators (3)
FGF and VEGF and TGFbeta
PDGF does vascular remodeling
Wound Healing: which mediator sticks around the longest?
So macrophages are important for granulation tissue/scar formation
its the FIBROBLASTS that stick around for over 6 months after wound for REMODELING –> Tpe 3 collagen replaced by Type 1 collagen = INCREASE TENSILE STRENGTH
age related (senile) amyloidosis:
Deposition of normal TRANSTHYRETIN in heart and elsewhere.
LOOK FOR SIGNS OF RESTRICTIVE CARDIOMYOPATHY AKA S4 (BECAUSE WE KNOW AMYLOIDOSIS DOES THIS)
reflex is to dismiss this since its THYroxine (t4) and RETINOL but AGE RELATED CHANGE SONNY BOY
Amyloidosis in diabetes
Islet Amyloid polypeptide (IAPP): From AMYLIN deposition in Pancreatic Islets
Type 2 because they still have islets
Yellow and brown “wear and tear” pigment associated with normal aging (from autophagocytosed organellar membrane)
Lipofuscin
–>product of free radical injury/oxidation/lipid peroxidation
dont confuse with hemosiderin (a brown and gold granular pigment)
Have Neoplastic cells invaded intact basement membranes?
NO!!! These are the cells of carcinoma in-situ
What do cells use to invade basement mem in invasive carcinomas?
Collagenases and hydrolases = metalloproteinases
–>cell-cell contacts lost by inactivation of E-cadherin
causes Multidrug resistance, expressed by cancers, and functions to pump out toxins (including chemotherapy so lower response to therapeutics)
p-glycoprotein
Is dysplasia reversible?
Yes.
Neoplasia is not (can be benign or malignant)
Carcinoma vs Sarcoma
Carcinoma: Epithelial; Spreads by LYMPHATICS
Sarcoma: Mesenchyma; Spreads HEMATOGENOUSLY
whats the name for ectopic gastric tissue seen in Meckels?
Choristoma: Normal tissue in a foreign location
Adenoma and Papilloma
the rest (blood vessels/cells, smooth/striated muscle, connective tissue/bone/fat
Epithelium derived
this is what MESENCHYME is.
So for example you can have Adenocarcinoma –>EPI
or Osteosarcoma/Angiosarcoma/Leiomyosarcoma: MES
Malignant tumors upregulate what to prevent chromosome shortening and cell death?
TELOMERASE
Paraneoplastic indicator of visceral malignancy, that is also associated with insulin resistance
Acanthosis Nigricans
–>Diabetes, Cushings, Obesity, or Gastric AdenoCA
