Equations/Pharm/Biostat Flashcards
Filtration Fraction?
GFR/RPF = Cr Clear/PAH Clear
Drugs with zero order kinetics?
“PEAs shaped like zero” Phenytoin, Ethanol, Aspirin
Vd?
Vd= Amount of Drug Given/Concentration of Drug in Serum Nb: most of the time Vd will be given in L/Kg therefore you need to multiply by the mass of person
Clearance?
Cl=0.7*Vd/half life
Loading dose?
Loading Dose=Vd * Conc at steady state
Maintenance dose
Maintenance dose=Clearance * conc at steady state
Hardy Weinberg: NB: Frequencies in an x-linked rec trait?
p+q=1 p^2 + 2pq + q^2 = 1 Males=q; females q^2
Cyp P450 Inhibitors and inducers?
PICCKEGS (cimetidine and cipro)
Protease Inhibitors, INH, Cimetindine AND CIPRO, Ketoconazole, Erythromycin, Grapefruit Juice, Sulfonamides
BCG PQRS (phenytoin/phenobartibtol is inducer)
-Barbiutes, Carbemezepine, Griseofulvin, Phenytoin, Quinidine, Rifampin, St John’s Wart, Crhonic ETOH
Confidence interval formula?
CI=Mean+- Z*SEM (Z usually ~2 for 95%) SEM: STDEV/sqrt(sample size)
Case Control vs Cohort?
Case control: Group based on disease and look at risk factors: ODDS RATIO
Cohort: Group based on risk factors and look at disease outcome: RELATIVE RISK
Cross sectional Study?
Snap shot of population at a particular time. Tells you prevelance, cannot tell you incidence or causality (but can infer some risk factor association with it)
Clincal Trial phases?
1) Is it safe?
2) Does it work?
3) Is it better?
4) Survalience for unknown SEs.
Bias of a Meta-analysis?
Selection bias based on what studies the examiners decide to inclue/throw out
Screen test is good to have a high?
Sensitivity
As frequency of disease change what variables change?
PPV and NPV.
Sens and spec do not as these characteristics are inherent to the test
Sens
Spec
PPV
NPV
Sens: TP/(TP+FN)
Spec: TN/(TN+FP)
PPV: TP/(TP+FP)
NPV: TN/(TN+FN)
Calculating Incidence?
New cases/Population at risk during time period
NB: need to subtract out people with disease from denominator…its people without the disease but at risk to get disease NOT total population
Odds ratio used in
Case-control studies
Relative risk used in
Cohort studies
What is used Case-control studies? What’s the formula?
Odds ratio (“start with disease”):
(a/c)/(b/d)
this also equals: ad/bc
Odds ratio approximates relative risk if the disease prevelance is not very high
What is used in Cohort studies? Formula?
Relative risk (“start with risk factor”):
a/(a+b)
c/(c+d)
Attributable risk?
Absolute risk reduction?
AR:
a/(a+b) - c/(c+d)
this is Relative risk but differnce btwn the two rather than ratio
ARR:
c/(c+d) - a/(a+b)
NNT?
NNH?
1/ARR
1/AR
1) Berkson Bias
2) Confounding Bias
3) Pygmalion Effect
4) Hawthorn Effect
1) Looking only at inpatients of hospitals
2) Third variable affecting disease/risk interaction: asbestos miners more likley to smoke (increases lung cancer rates)
3) Self fulfilling prophecy: Dr believes so much in therapy they unconciously bias outcome
4) Measurement bias where people who know they are being watched act differently: washing you hands more cuz you know your in a trial
Positive Distribution vs Negative distribution in mean median and mode?
+: Peak is to the left: “ameoba creeping towards the positive end”
Mean > Median > Mode
-: Peak is to the left
Mode > Median > Mean
Single most preventable cause of death in the US?
Smoking.
Pathways that use cAMP?
FLAT ChAMP
FSH, LH, ACH, TSH, CRH, hCG, ADH (V2), MSH, PTH
and calcitonin, GHRH, glucagon
Endocrine pathways that use IP3
GOAT HAG
GnRH, Oxytocin, ADH (V1), TRH, Histaimine, Angiotensin II, Gastrin
Steroid Receptors?
VETTT CAP
Vitamin D, Estrogen, Testo, T3, T4
Cotrisol Aldo, P4
Drugs with anticholinergic effects that aren’t anticholinergics per se?
H1 blockers, TCAs, Typical Neuroleptics.
Amantidine
Gq GCPR subunit mechanism and ANS receptors using it?
“cue-tsie” Q–>Ca–>PLC–>PKC
HAVe 1 M&M
H1, A1, V1 (vasopressin), M1, and M3***
just gotta remember M3 (bladder, eyes, exocrine secretion)
Gi subunit mechanism?
Receptors?
Gi inhibits AC which decreases cAMP
“MAD 2’s”
M2, alpha2, D2 (dopamine)
1) Tyrosine Kinase Receptor? What binds it?
2) JAK STAT pathway?
1) “Growth Factors”
Insulin, IGF, FGF, PDGF, EGF
Think about tyrosine kinase receptor inhibitors used to stop cancer cuz you want to stop the growth factor signal
2) Prolactin, Immunomodulators (Interleukins), Growth Hormone (NOT PDGF***), EPO
- Epi?
- NE?
- Isoproterenol?
- DA?
- Dutamine?
- Phenyleprine?
- Alubterol?
- B>A (alpha wins at high doses, thus use for septic shock) EBA
- a1>a2>b1 Increases BP but decreases Renal Perfusion NAAB (dont use in septic shock cuz A1 agonism causes too much vasoconstriction which decreases CO)
- ONLY BETA IBB
- D1=D2>B>A DADBA
- Low doses: increased GFR and renal excretion (D1/D2) (good for renal’s!)
- High doses increase inotropy (B1) and vasoconstriction (A1)
- B1>B2, alpha thus Ionotrophic > Chronotropic DBBA (give in acute Heart failure)
- Stronger inotrope than chronotrope
- a1>a2 Vasconstriction PAA
- B2>B1
Drugs used for:
Anphalyctic shock
Cardiogenic shock
Septic Shock
Epi
Dubatamine
NE
Drug induced lupus:
Antibody?
Metabolism type? Why?
Anti-Histone Antibody
Acetylation—studies show slow acetylators are more likely to develop drug induced SLE, suggesting the parent drug is more likely to cause the reaction
Receptor for:
Pupillary Dilation?
Uterine Relaxation?
Bladder Internal Urethral Contraction?
Alpha 1
Beta 2
Alpha 1
ADPKD chromos?
ADPKD systemic issues and other manifestations?
1) PKD1 is 16
PKD2 is 4 (4^2=16)
2) Renal failure=uremia, HTN, anemia (no EPO) etc
“Cysts in Kidneys, Brain (berries), liver, and heart (papillary muscles=mitral valve prolaspe)”
ARPKD
Infatile presentation.
If severe Potter’s Sequence.
Associated with congenital hepatic fibrosis.
Kids that survive have HTN, portal HTN and progressive renal insuf
2 Common Lithium SEs?
1) Diabetes Insipidus
2) Hypothyroidism
Which AChEI pass thru BBB which does not?
P-hysostigmine P-asses
N-eostigmine does N-ot
(nor does edrophonium)
