Random Review Part 3 Flashcards
Observational Studies summary
Cross-sectional: Group of people with a disease, lets see if they have a gene present. Can’t establish causality
Case-control (only retrospective): Group of people with COPD. What were the odds they were smokers for each group? Odds ratio
Cohort (pro or retrospective): Group of smokers, what is the risk of getting COPD?
Clinical trials: Is it safe? Does it work? Is it better? Can it stay?”
Select biases/effects
Berkson bias - study population selected from hospital
Pygmalion effect - researchers believe in efficacy of treatment which affects the outcome
Hawthorn effect - Participants knowledge of being studied affects outcome
Disease prevention
Primary = preventing Secondary = screening Tertiary = treating
Lymph node structure
Follicle = B cell Medulla = reticular cells + macrophages Paracortex = T-cells
Spleen structure
Periarteriolar lymphatic sheeth = T cells Follics = B-cells Marginal zone (between red and white) = APCs
Cell markers
CD16 (binds Fc) or CD56 = NK cells
CD3/CD4/CD25/FOXP3 = Treg
CD14 (recognizes LPS) = macrophages
CD34 = hematopoietic stem cell
Th1 cells activate:
Macrophages (IFN-y)
Cytotoxic T-cells (IL-12)
To activate Th1 or Th2 cells:
Th1 by IL-12
Th2 by IL-4
Turn down immune response
TGF-B, IL-10
Septic shock and cachexia
TNF-a
X-linked agammaglobulinemia
Manifestations after 6 months due to IgG from mother still in circulation
IL-12 Receptor Deficiency
Decreased IFN-y (due to decreased TH1 response). Often presents after BCG vaccine w/disseminated mycobacterial infection. Also fungal infection.
Hyper-IgE syndrome
Deficient Th17 cells (STAT3 mutation) –> neutrophils not recruited to sites of infection
FATED: Facies (coarse) Abscesses (staph) Teeth (retained primary ) IgE Derm problems (eczema)
SCID causes
IL-2R defective (most common, X-linked) ADA deficiency (AR)
Chediak Higashi Syndrome
Lysosomal trafficking regulator gene. Microtubule dysfunction. Partial albinism. Peripheral neuropathy. Giant granules in granulocytes and platelets.
Immunosupressants
Cyclosporine –Binds cyclophilin, blocks calcineurin, no NFAT, no IL-2 transcript
Tacrolimus – Binds FKBP, same as above, no IL-2 transcript
Sirolimus (Rapamycin) – Binds FKBP, inhibits mTOR, prevents IL-2 response
Daclizumab, basiliximab – blocks IL-2R
Glucocorticoids – Inhibits NF-kB
Bcl-2 inhibits:
BAX/BAK and Apaf-1
CD11/CD18 (LFA-1/Mac-1)
Let’s fuck mac daddy, Im 18 now. Integrins on leukocyte. defective in LAD type I (effects tight binding). ICAM, VCAM (POV, vag cam) to film it. The endothelial sites for tight binding.
If you have decreased Sialyl Lewis to initiate the whole process, thats LAD type 2 (effects margination and rolling)
Wound healing factors
PDGF - smooth muscle cell migration, fibroblast growth for collagen synthesis
FGF - Stimulates angiogenesis
EGF - Cell growth via tyrosine kinases
TGF-B - angiogenesis, fibrosis, cell cycle arrest
TNF-a
Important in maintaining granulomas
Amyloidosis
Cardiac atria - ANP
Thyroid - Calcitonin
Pancreatic islets - Islet amyloid polypetitde (Amylin)
Cerebrum - B-amyloid
Pituitary - Prolactin
Old age - transthyretin (esp in myocardium)
Dermatomyosites malignancy
Think GU
c-kit
GIST
NF1 vs NF2 gene
NF1 = Ras GTPase, neurofibromin
NF2 - Merlin (schwannomin) protein
p16
Melanoma
VHL
Inhibits hypoxia inducible factor 1a
PO2 of umbilical vein
pretty low, at 30mmHg
Fetal flow of blood (IVC vs SVC)
IVC - FO
SVC - PA to ductus
Remnants
allaNtois –> mediaN umbilical vein
umbiLical arteries –> mediaL umbilical ligaments
umbilical vein –> ligamentum teres hepatis inside falciform ligament
Most peripheral resistance is from which vessel:
arterioles
When graphing cardiac vs vascular function curves
Inotropy changes cardiac function slow
Venous tone changes x intercept
TPR changes both curves at same time, but maintains same meeting point at the x axis (vasopressors, exercise)
Heart sounds summary
Systolic - aortic/pulmonic stenosis, mitral/tricuspid regurg, VSD, MVP
Diastolic - aortic/pulmonic regurg, mitral/tricuspid stenosis
Holosystolic murmurs (2 of them)
MR/TR vs VSD – high pitched blowing at apex vs harsh-sounding at LSB
Opening snap/S2 length
Less = worse because over time LA develops more force and is able to open it quicker.