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.
PDA
congenital rubella
U wave
Hypokalemia
Drugs that prolong QT
Some risk meds can prolong QT
Sotalol, risperidone, macrolides, chloroquine, protease inhibitors, quinidine, thiazides/TCAs
Also ondansetron and haldol
Congenital long QT
1) Romano-Ward (AD), most common
2) Jervell and Lange-Nielsen syndrome (AR), +sensorineural deafness [2 names, 2 problems]
Rate and rhyhtm control drugs
Rate: B-blockers, digoxin, non-dhp Ca2+ blockers
Rhythm: IC or III
Nesiritide
recombinant BNP (think, nesa has no brain)
Baro/chemoreceptors transmit to:
solitary nucleus of medulla
Free wall rupture due to
macrophage mediated structural degradation (days 3-14)
All septal leads =
Anterior (LAD)
I, aVL, V5-V6
Lateral (LCX)
II, III, aVF
Inferior (RCA)
Post MI pericarditis
Fibrinous - 1-3 days after
Dressler syndrome - autoimmune, 2+wks after
Loffler syndrome
Endomyocardial fibrosis w/eosinophilic infilitrate
heart failure cells
pulmonary edema can cause hemosiderin laden macrophages over time
endocarditis on heart valve cause
s. epidermidis
Cardiac tumors
Mxyoma most often in left atrium
Rhabdomyomas associated with tuberous sclerosis
Kaposi vs bacillary angiomatosis
lymphocytic vs neutrophilic infilitrate
Polyarteritis nedosa
Associated with HBV
Does not involve pulmonary arteries
Immune complex mediated
Transmural inflammation w/fibrinoid necrosis
Microscopic polyangiitis
Like Wegeners but without the nasopharngeal involvement, no granulomas, and instead p-ANCA mediated
Churg-Strauss
associated with peripheral neuropathy and wrist/foot drop
Nitroprusside caution
Cyanide toxicity, tx w/sodium thiosulfate
Fenoldopam
D1 agonist that decreases BP and increases natriuresis
Class I drugs
IB is Best post-MI, IC is Contraindicated post-MI (and structural/ischemic disease)
Related hormones
Alpha subunit: TSH, FSH, LH, hCG
Stim by CRH: ACTH, MSH, B-endorphin
Stim by TRH: TSH, prolactin
Cortisol effects
- Upregulates a-1 receptors on arterioles to increase sensitivity to norepi and epi
- Can find aldo receptors at high levels
- Decrease osteoblast activity
PTH and VitD
Very similar, including feedback regulation. Only diff is that VitD stims absorption of both Ca and phos
Mg and Ca
Decreased Mg increases PTH seceretion, but severely depleted Mg decreases PTH because its needed as a cofactor. Thus patients resistant to Ca correction must first have Mg fixed.`
cAMP hormones
FLAT ChAMP
FSH, LH, ACTH, TSH, CRH, ADH (V2), MSH, PTH
Thyroid hormone functions
Increase B1 receptors in heart
Increase Na/K-ATPase activity
Riedel thyroiditis
Thyroid replaced by fibrous tissue, can mimic anaplastic carcinoma. Related to IgG4 systemic disease (autoimmune pancreatitis, retroperitoneal fibrosis, noninfectious aortitis)
Increased cAMP in urine
PTH
cyclists nerve injury
Ulnar
Denosumab
Monoclonal ab against RANK-L
Von Gierke
Glycogen storage disease (g6phostase) but can also present with excessive uric acid
Reactive arthritis after:
Post-GI (dysentery causers), or post-chlamydia infections
Poly/dermatomyositis histology + immuno
Polymositis = CD8 endomysial Dermatomyositis = CD4 perimysial
Lichen planus
6Ps: Pruritic, purple, polygoal, planar, papules
Associated w/HCV
-dronates
bisphosphonates. pryophosphate analogs. bind hydroxyapatite, inibiting osteoclast activity
Spinda bifida occulta AFP
normal. the other NTD have increased
Not protected by BBB
Area postreme, OVLT (osmotic sensing), neurohypohysis
Phases of sleep
Awake (Eyes open) B Awake (Eyes closed) A N1 T N2 S(sleep spindle/kcomplex) N3 D REM B
Lateral Medullary Syndrome
Nucleus ambiguous effects (specific to this syndrome)
PICA
-Don’t pick a (PICA) horse (hoarseness) that can’t eat (dysphagia)
Lateral pontine syndrome
Facial nucleus effects (specific to this syndrome)
-Facial dronyu op means the AICAs pooped
Friedreich ataxia
Friedreich is fratastic (frataxin), hes always stumbling around and falling, but he has a big sweet heart. Chromosome 9
Cavernous Sinus components
Occular movements + V1, V2 (III, IV, V1, V2, VI)
Postganglionic sympathetic pupillary fibers –> horner syndrome
Curtain drawn down vision
retinal detachment
Butorphanol
mu partial agonist, kappa agonist –> good for migraie or labor, causes less respiratory depression
Tramadol
Extremely weak opiod agonist, also blocks 5HT and NE reuptake [tram it all]
Caution: serotonin syndrome
Local anesthetics
Amides have 2 I’s in the name, esters have 1. Esters more likely to produce allergy. Block inner portion of Na channel
Amantadine
Used to be used for influenza A, but now used to increase dopamine release and decrease reuptake for parkinsons.
Selegiline
Preferentially blocks MAO-B, which mostly degrades dopamine and not NE or 5HT
