Devendra Block 2 Flashcards

Question

Transcription Factor (Steroid)

Answer 1

* **DNA binding domain=**Zinc finger * **Response element=**HRE * **Fnx=**Steroid response

Answer 2

* **DNA binding domain:** Leucine zipper * **Response element:** CRE * **Fnx:** Response to cAMP

Answer 3

Hox: * **DNA binding domain:** Helix turn Helix * **FNX:** Development of tissue/limbs MyoD: * **DNA binding domain:** Helix turn helix * **FNX:** myogenic reg-morphogenesis

Answer 4

* Synpolydactyly * **Heterozygotes=**Interphalangeal webbing & extra digits hands/feet * **Homozygotes=**Similar symptoms & bone abnormalities in hands, wrists, feet, ankles * Expansion of polyalanine tract in amino terminal domain

Answer 5

* **Cells comm w/each other develop proper spatial arrangement**s of tissues (receptor-ligand interactions=paracrine) * _Fibroblast growth factors receptor abnormalitie_s=Achondroplasia & cranisynostosis (JAK-STAT =GF help in diff) * Bone growth factors, DISORDERS-mutations of FGFR3 genes * _Sonic hedge hog loss_=holoprosencphaly (dorsal/ventral diff) * **Notochord-induces/organizes diff types of cell & tissues** in developing brain/SC * Limb bud zone, polarizing activity generate asymmetrical pattern of digits

Answer 6

* Failure of midface & forebrain to develop, cleft lip/palate, hypertelorism (wide spaced eyes) * _Variable expressivity=_based on amount of SHH protein * **SHH receptor defect=Gorlin syndrome** * cysts of jaw, basal cell carcinoma * _Mutation=PATCHED gene_

Answer 7

* Involved in specifications of dorsal/ventral axis & formation of brain, muscle, gonads, kidneys * **Homozygotes for mutation=absence of 4 limbs** * Abnormal signaling=Tumor formation

Answer 8

* Organized in particular positiions w/particular polarities * Kidney epithelial cells (polysistin 1 & 2) * Need apical & basal sides * _Polycysitc kidney disease_=Loss of fnx of polysistin 1/2 * Failure to sense fluid flow=c**ells continue to proliferate=CYSTS**

Answer 9

* Cells assist in moving particular areas to carry out fnxs * **Lissencephaly (Miller-Dieker)=**Deletion of L1S1 gene="smooth brain" * **Waardenburg syndrome=**Defect in migration of neural crest cells (melanocytes), SEE (sensory hearing loss, 2 diff colored iris, hair hypopigmentation forelock) _Dystopia canthorum_ (eyes-nose WIDE) * **Hirschsprung disease=**Cells from neural crest _Doesn't form Auerbach's plexus,_ CHRONIC constipation in newborns

Answer 10

* Cell Death required to remodel or form appropriate tissues * Normal positioning of aortic & pulmonary vessels * Separation of indivdual digits * Perforation of anal membrane * Comm between uterus & vagina * _Eliminate lymphocyte lineages that react to self (Defect=auto immune_) * **Thymus breakdown lymphocytes**

Answer 11

1. Provide informed choice 2. Termination of pregs 3. Allow option for appropriate manage for birth of child w/genetic disorder * Psycholigical prep * Pregs/delivery management * Post natal care

Answer 12

* Advanced maternal age (35+) * Previous child w/aneuploidy * Structure abnormalality in 1 of the parents (Roberstonian Translocation) * Family history of genetic disorders * Family history of X-linked disorders * Abnormal maternal serum screening * Risk of neural tube defects

Answer 13

* **_Chronic Villus Sampling:_** (_ADVANTAGE diagnosis 1st trimester)_ * Biopsy of chorionic tissues from chorionic frondosum (placenta) * 10-12 weeks * Fetal trophoblastic cells=direct karotyping * RISK=1-2% inducing abortion * **_Amniocentesis_**: * Aspiration of amniotic fluid under ultrasound guidance * 15-16 weeks * **Use of alpha-fetoprotein to screen for neural tube defects** * RISK=inducing miscarriage, leakage of fluid, infection

Answer 14

* **_Cordocentesis:_** * used for _blood disorders (anemia) & detection of Rh isoimmunization_ * ALSO detect infections=_Toxoplasmosis & rubella(virus measles)_ * If blood order detected can use blood transfusions to fetus & medication directly to fetus * **HIGHEST risk for spontaneous abortion **

Answer 15

* **_Maternal serum Alpha-fetoprotein:_** * Detect neural tube defects & aneuplodies * _Values HIGHER than normal_=possible defect @ 16 weeks * Used to prevent neural tube defects w/folic acid through pregs * Produced in fetal yolk sac & fetal liver-enters maternal blood VIA placenta

Answer 16

* **_Elevated in:_** * Multiple pregs * fetal death * abdominal wall defects * **neural tube defects** * renal anomalies * GI tract anomalies * **_Decreased in:_** * ANEUPLODIES

Answer 17

* **_1st trimester: _** * Pregs associated plasma protein A (PAPP-A) * Human chorionic gonadtophin (Beta-HCG) * **_2nd trimester:_** * MSAFP, beta-HCG, unconj estriol = _TRIPLE SCREENING_ * **Triple screening + inhibin A = quadruple screening = BEST**

Answer 18

* **_Trisomy 21:_** * INCREASED=nuchal transluceny (back of neck of fetus), free-beta HCG, inhibin A * DECREASED=_PAPP-A_, uncon E3, AFP * **_Trisomy 18:(Edward)_** * INCREASED=nuchal transluceny * DECREASED=_PAPP-A_, free beta hCG, uncon E3, AFP * **_Trisomy 13:(Patau)_** * INCREASED=nuchal transluceny * DECREASED=_PAPP-A_, Free beta hCG, Uncon E3, AFP

Answer 19

* **_Unconj Esteriol (Uncon E3):_** * Synth in fetal liver * **Decreased in=**Trisomy 18,21, Triploidy, Fetal demise, Cong adrenal hypoplasia * **_Human chorionic gonadotropin:_** * Secreted by corpus luteum (maintains pregs) * **Elevated LVLs=**Hydotiform moles & down syndrome * **Decreased LVLs**=Trisomy 13,18 * **_Inhibin A:_** * Secreted by granulosa & sertoli cells (fetoplacental unit) = INHIBITS FSH & menstrual cycle * **Increased LVLS=**down syndrome & ovarian cancer

Answer 20

* Confirm pregs * Determine fetal age * ID multiple pregs * Fetal Assessment & determination of morpholocial anomalies * MID-trimester=determine detal sex & screen for X-linked recessive cond. * 2 types: 1. **Transabdominal** =simple 2. **Transvaginal**=More sensitive & specific (early predictor)

Answer 21

* Source from maternal circulation * Problems: Mosacism (presence of 2 or more cell lines) * **True mosacism=**detected in multiple tissue samples and or cultures * **Pseudomosaicism=**single unusual cell line detected, involving several colonies of cells in SINGLE primary culture, OR contamination from maternal cells * **Confined placental mosaicism=**trisomy rescue, uniparentaldisomy

Answer 22

* **Labile cells=**Continually cycling (epithelial & stem cells) * **Stable cells=**exit G1 to G0 metab active BUT NOT proliferating (skin fibroblasts, hepatocyctes) RE-enter G1 if stimulated * **Permanent cells=**non dividing cells (neurons, cardiamyocytes, beta cells of pancreas)

Answer 23

* **_Regulation: _** * Cell cycle response to extracell growth factors & intracellular (cell size) signals * NO growth factor=enter G0

Answer 24

1. **GI restriction point =** deactivate of nutrients & signals (Cyclin D, CDK 6&4) * _Cyclin D (CD K 6,4)=phospho of Rb gene_ 1. **G1/S check point=**Check for DNA damage (Cyclin E, CDK-2) * _Prevented by retinoblastoma protein_ 1. **S check point**=Check for DNA damage & replication defects (cyclin A, CDK-2) 2. **G2/M check point**=prevent mitosis until replication completed (CyclinB, CDK-1) 3. **Spindle assembly check points**=make sure chromosomes are aligned properly

Answer 25

* **Cyclin dependent Kinases (CDK)-**Protein kinases play prom. role in cell cycle progeression reg. (phosphor active sites) * **Activation**=phosphor of threonine-160-attachment of cyclins * **Inhibition**=phosphor of threonine-14 & tyrosine 15, CKI's (CDK inhibitors) * **Stimulation=**Activates RAS, RAF, ERK, MEK pathways-\>stims cyclin D1 synthesis * **_D1=_**Complexes w/CDK 4&6 to phosphor Rb protein

Answer 26

1. **CKI's-**P21, P27, P57=block cell cycle by binding to cyclin E, A, B, CDK2 & 1 complexes 2. **INK4-**P16, P15, P14 (REG 1st step): Inhibit Rb gene phosphorylation by binding to CDK4, 6 & cyclin D 3. **ARF-**Increases P53 by inhibiting MDM-2 * **Cyclins=**Reg subunits req for catalytic activity of CDKs * **GF=**Control progression through G1 restriction pnt

Answer 27

* **Oncogenes:** Drive cell proliferation=Mutations LEAD to increased cell prolif - **Gain of function** * **Related GF=**Ras, Raf, Cyclins, Ret, Myc

Answer 28

* Act as BREAKs in cell cycle * **Loss of Fnx** leads to INCREASED cell prolif * Related to=Rb protein, P53, ATM

Answer 29

* **_Normal:_** Dephosphor, binds to E2F (transcription factor) & keeps inactive * **Phosphorylation by CDK6,4 & cyclin D**=release E2F-\>Activation of target genes & INCREASE in cyclin E synthesis * **CDK/Cyclin E complex=**Allow G1 to S transition-\>Activate MCM helicase=replication inititation & entry into S phase

Answer 30

* **_ATM:_** Reg the G2-Mphase-\>ID double stranded DNA breaks-\>Activates ATM to phosphorylate check point kinases * **MUTATION in ATM=**ataxia telangeictasia (++ of broken strands)

Answer 31

* Commonly involved in Cancers * Causes cell arrest & apoptosis * Stims apoptosis=**BAX gene** * Regulates BY _MDM-2 (feedback)_ * Ubiquitin protein ligase(MDM2)=_low conc of P53_ * **DNA damage**=INK4/ARF (**INK** inhibit Rb phosopho binding & **ARF** inhibits MDM-2) _activated=\>phophorylates_ MDM=_INCREASED P53_=INCREASED CIP/KIP-\>_INHIBITs G1/S transition_ * Main control pnt for G1/S phase

Answer 32

1. **_G0=_**Post miotic, senescent stage, permanent for fully differentiated cells * Interphase (prep stage) 1. **G1=**1st growth stage * End of previous mitosis to begin DNA synthesis * I**ncreased biosynthetic activity in cells**=Synthesize enzymes for S phase * Duration 10-12hrs

Answer 33

1. **_S=Synthetic phase_** * DNA synthesis-_Double DNA content (replication)_ * LOW protein synthesis (histones) * 6-8 hours 1. **_G2=2nd growth factor_** * _Microtubule formation_ * 2-4hours 1. **_M phase=mitosis_**

Answer 34

* Needed in proper development - ex. separation of fingers & toes, sloughing off of uterus, perforation of orifices (anus) * Irreversible adjustments to body

Answer 35

1. Withdrawal of + signs (GF & interleukin 2-control WBCs) 2. Receives - signals = trigger apoptosis binding to death receptors * Increased LVLs of oxidants * DNA damage * Death activators= - TNF-alpha (tumor necrosis factor alpha) - TNF-beta (Lymphotoxin) - FasL (fas ligand)

Answer 36

1. **Pyknosis** (irreversable cond of chromatin) 2. **Karryorhexis** (Nuclear fragmentation) 3. **Karyolysis** (Complete dissolution of chormatin) * **_Blebbing:_** 1. Allows formation of controlled apoptotic bodies 2. recognized & phagocytosed 3. Trigger cytochrome C moving it out of mitochondria = START of apoptosis

Answer 37

1. **signal intiation:** FAS ligand, hormone withdrawl, P53 gene, cell injury, cytotoxic T cell 2. **Control & integration of process:** Via BCL-2 family (reg. death by apoptosis or continue cell life)-_BCL2: inhibit_ & _BAX promotes_ 3. **Execusion**: Via capsases 4. **Phagocytosis**

Answer 38

* **Intrinsic:** involves MITOCHONDRIA comp-cytochrome C is released-Activates Caspases (executioner proteins) **_Pathway=_** 1. **DNA damage** = P53 activation 2. Mitochondrial cytochrome C release 3. I_nitator capase 9_ 4. _Effector capase 3=_ **APOPTOSIS**

Answer 39

* **_Extrinsic:_** Ligands bind to death receptors (_independent of BCL family)_ * _**Pathway:** _ 1. Death ligand bind to death receptor 2. _Activate Capase 8_ 3. _Effector capase 3_ 4. Apoptosis

Answer 40

* Proteases, _cysteine, residues in active site_, cleave after _aspartate residues in substrate proteins_ * **_Key target proteins:_** DNAase, Nuclear lamins, Cytoskeletal proteins * Made as inactive precursors-\>require activation by proteolytic cleavage * **ACTIVATED by binding to APaf-1** & cytochrome C = apoptosome * _Apoptosome_-cleaves & activated effector capases (3/7) = CELL DEATH (**instrinsic pathway**)

Answer 41

* _Initiator caspases:_ 6, **_8, 9_**, 12 * _Effector caspases_: 2, **_3_**, 7

Answer 42

* **_BCL-2 Family - Catalytic :_** * Form oligomers on mitochondrial outer membrane-\>act as pores-\>release cytochrome C = **ACTIVE CASPASES** * **BCL-2/BCL-x:** favor cell survival (antipoptic) * **Bax/Bak:** favor cell apoptosis (multi domain) * **BH3**: PROapoptotic-\>form pores (1 domain)

Answer 43

* IAP = Inhibit Caspases * Activation of apoptosis= - DNA damage - ATM senses damage - **Activates CHK1/2** - Phosphorylates P53 (cytosol) - Intiates transcription of **PUMA & Noxa** - Trigger release of proapoptotic factors

Answer 44

* PIP-3 (auto-phosophorylates) activates mTOR * mTOR activates AKt * AKt phosphorylates BAD * **Cell survival** * AKt phosphorylates FOXO-\>sequesters Bam=**Cell survival** * AKt phophorylates MDM2=inactive

Answer 45

* **Phosphatidyl serine marker** (normally inside) * **Exposed to outside** of apoptotic bodies * Bodies recognized by **macrophages**

Answer 46

* **Somatic=**sporadic mutations * **Germline=**familial transmission of cancer

Answer 47

* Mutant forms of **proto-oncogenes** * Affect proteins in signaling pathways * _Abnormal stimulation of cell division & proliferation_ (gain of fnx mutation)

Answer 48

* **SIS activation**=glioma (tumor started from glial cells)-_GF_ * **Myc activation**=Burkitt lymphoma-_Transcription Factor_ * **Bcl2 activation**=Chronic lymphocytic leukemia-_Inhibit apoptosis_

Answer 49

* _Tyrosine Kinase receptor_ (**Ret gene**)=multiple endocrine adenomatosis 2 * _Cytoplasmic tryosine kinase_ (**Abl gene)**=Chronic myelogenous leukemia * _G protein signaling_ (**K-Ras2**)=pancreatic cancer * _Phosotidylinostiol 3 kinase_(**PTEN gene**)=Breast cancer, glioma

Answer 50

* Pnt mutation activation=**MEN-2** * Multiple endocrine adenomatosis * _**Type 2a: **Sipple syndrome_=medullary thyroid cancer & pheochromocytoma * **_Type 2b:_** 2a & neuromas & marfanoid habitus (tumor in NS & marfran like symptoms) * Cause=**Pnt mutation in RET proto-oncogene** * Gain of fnx mutation * Normally encodes tyrosine kinase receptors = _activation of receptor w/o GF_ * Auto-phosphorylates=**PROLONGED activity**

Answer 51

* **Hirschprung disease:** Loss of fnx in RET-proto oncogene * Hereditary papillary renal carcinoma (multiple kidney tumors)

Answer 52

* **_Chronic myelogenous leukemia:_** * Increased & unregulated growth of predom. **myeloid cells in BONE marrow** * _Proliferation_ of mature _granulocyctes_ (neutrophils, eosinophils, basophils) * **Hepatosplenomegaly** DUE to ++ of myeloid cells in blood * Caused by **Philadelphia chromosome** (translocation of 9q & 22q) * _UNregulated tyrosine kinase activity_

Answer 53

* **_Burkitt Lymphoma:_** * _B-cell tumor on Jaw_ (Epstein barr virus implicated-Herpes) * Starry sky appearance of cells (Lipids) * **Translocation of 8 & 14** * Increased transcription of MYc = HIGHER cell growth

Answer 54

* **_Follicular B-cell lymphoma:_** * _Translocation of 14 & 18_ * BCL-2 goes from **18 to promoter region of IgH on 14** * Overexpression of BCL-2 = antiapoptotic effect on lymphocytes * _MASSIVE expansion of B-cells_ (**NO apoptosis**)

Answer 55

* **Loss of function**=Cancer * _**RB1**=cell cycle reg_ * Controls G1-S checkpnt by binding to E2F=**Hyperphospho** ALLOWS transition to S phase * Loss of Rb eliminates G1 checkpnt

Answer 56

* **_Familial Retinoblastoma:_** * Malignant tumor of retina * Inherited as AD w/ incomplete penetrance (second hit) * 400 x greater risk after radiation exposure * **_Sporadic Retinoblastoma:_** * Small cell lung carcinoma, breast cancer * Majority are sporadic

Answer 57

* Loss of P53=decreased production of Cip/Kip mols - avoidance of apoptosis * **_Familial Li Fraumeni syndrome(majority)_** * Diff types of cancers in diff members of family early in life * Bone, soft tissue, breast cancer, brain, leukemia * Due to Loss of fnx TP53 gene * **_Sporadic Li Fraumani syndrome_** * Lung cancer, breast cancer, etc..

Answer 58

* Decreases cell survival in the absence of survival signs * Associtated w/**Sporadic colorectal cancer**

Answer 59

* part of cytoplasmic destruction complex * Inhibits induction of Blood vessel growth w/ O2 present * **_Familial Von-Hippel Lindau syndrome:_** * benign cyst-like tumors * **_Sporadic clear cell renal carcinoma:_**

Answer 60

* responsible for _detecting & repairing mutations, maintaining genomic integrity_ * Loss of Fnx=**mutations ++**=INDIRECTLY leads to cancer * **_Neurofibromatosis:_** Mutation in TSG of neurofibromin 1 (chr 17) * Schannomas, cafe-au-lait spots, neurofibromas, freckles & lisch nodules * **NF1 normally acts w/RAS** to regulate proliferation (inactivate RAS)

Answer 61

* Chromosome repair in response to double strand breaks * **_Familial breast cancer & ovarian cancer:_** * Dom mendelian inheritance * **_BRCA 1=_** 50% AD (chromsome 17) * Increased risk of ovary cancers, prostate, colon * **_BRCA2=_**33% AD (chromsome 13) * Increased risk of MALE breast cancer, ovarian, melanomas, pancreatic tumors * **_Sporadic Breast & ovarian_**

Answer 62

* Repair nucleotide mismatches between strands of DNA * **_Familial hereditary nonpolyposis colon cancer_** * Mutations in microsat repeat regions * Onset early adulthood * Males=90% chance of 2nd hit * Females=70% chance of 2nd hit (also ovarian cancer) * **_Sporadic colorectal cancer_** * Many associated genes * AD

Answer 63

* All autosomal recessive * **_Ataxia Telangiectasia:_** * Double strand breaks * LOF mutation @ ATM gene on chr 11 * **Presentation early in life**=cerebellar ataxia, ocular apraxia, telangiectasia(spider veins @ mucous membranes), immunodef. & lymphoid cancers

Answer 64

* **_Fanconi Symdrome:_** * Double strand breaks=NO activation of DNA repair mech * Skeletal malformations, uninary tract, GI, heart, & CNS malformations (triad) * Bone marrow failure (low prod of RBCs)

Answer 65

* **_Bloom syndrome:_** * Double strand breaks=NO fnx of REcQ (unwinds DNA) * Ineffective DNA repair * Short stature, long face, micrognathia (small jaw), butterfly rash (sunexposed area), hypogonadism (azospermia)

Answer 66

* **_Xerodermapigmentosa:_** * Nuceotide excision repair defect * ++ of pyrimidine dimers DUE to **defective exinuclease** * Extreme UV light sensivity, Excessive freckling, multiple skin cancers, **corneal ulcerations**

Answer 67

* Gene amplifications * promoter mutations * point mutations * **MiRNAs (microRNAs)=**RNA mediated inhibition of gene expression by inducing degradation of target mRNAs OR blocking translation * **Oncomirs=**OVER or under expressed miRNAs - 10% of ALL cancers * Chromosome translocations * + or - function mutations

Answer 68

* **Reverse Transcriptase**=Normally maintains ends of DNA * Presistant in Stem cells & rapidly multi cells = _Upregulated by oncogenes_ * **_Mutation initiated=_**++ of additional genetic damage through mutation in caretaker genes (cancer stem cells)

Answer 69

* Dominant * **_Sporadic=_**mutation in 1 copy=deletion in other copy= Tumor PROgression * **_Familial=_**Inherit germline mutation=deletion in other copy=Tumor PROgression * _2nd hit always due to mutation_ * **Epigenetic role=**Methylation of functional gene=causes transcriptional inactivation

Answer 70

* Activated by ATM after ID damage * **_NHEJ pathway=_**requires Ku protein & DNA dependent protein kinase * **_HR pathway=_**Requires RAD 51,52 & BRCA-1 * Occurs late S & G2 phase

Answer 71

* **APC tumor supressor gene** **mutation**=Familial colon cancers * _Loss of APC=_Beta catenin dephosphor acts as transcription factor * **_Adenomatous polyposis coli:_** * AD=Loss of heterozygosity * Numerous adenomatous polyps by 10 * **_Gardner syndrome:_** * AD, LOH=Familial colon * See polyps, osteomas of jaw & desmoid tumors

Answer 72

* Rate @ which body absorbs, transports, metabolizes/excretes drugs or metabolites * Hydrophobic to hydrophilic * **_Mitochondrial =_** conversion of chelosterol to steroids, bile acid synthesis, hydroxylation of Vit D * **_Microsomal =_** detox of drugs, carcinogens, petroleum products, pesticides, etc...

Answer 73

* **Exclusively in Liver** * _Phase 1 metab:_ * Hydrophoic to hydrophilic * enzymes are monooxygenase group * Heme containing * Use of NADPH as electron donor

Answer 74

* _Wild type: Normal fnx_ * **Reduced:** low activity due to missense mutation * **Absent:** no activity due to frameshift, splicing mutations * **Increased:** elevated activity due to copy # polymorphisms-_ Have to provide higher amounts of drugs to a given blood conc_ (faster metab of drugs)

Answer 75

* Codine coverted into morphine * **Ultrafast metab =** risk overdose due to standard higher dose * Poor metab = No benefit

Answer 76

* With polymorphism = **toxicity to camptothecin** (topoisomerase inhibitor in chemo) * _Type 1 topoisomerase:_ inhibited by **topotecan & irinotecan** * _Type 2 topoisomerase:_ inhibited by **etoposide, teneposide** * _Gyrase_ (relieves strain while DNA is being unwound): inhibited by **quinolone antibiotics** (bacterial) - Cipro

Answer 77

* **NAT 2 gene** shows polymorphic variation * INH=Treatment for tuberculosis * _SLOW acetylators_ = peripheral neuropathy * _FAST acetylators_ = more drug to maintain response

Answer 78

* common affect of anti-cancer drugs (leukemia) * **Increase effectiveness or render toxic** (dose dependent) - hair loss, bone marrow * Common polymorphisms in mehtyltransferases

Answer 79

* Diff rates of metab of cholinergic drugs * related to methylation * Ex: Succinyl choline used for skeletal paralysis * **_BCHE=_**lower activity-stronger effect of drug-prolonged paralysis

Answer 80

* X linked * common in malaria endemic areas * **Require NADPH to maintain glutathione in reduced states** * Stress to system w/oxidative drugs * Ex. **Primaquine** (antimalaria) & **sulfonamides** (antibacterial)

Answer 81

* AD * _Adverse rxn to halothene_ (anesthetic) or _succinyl choline_ (relaxes muscle) * Life threatening fever, muscle contractions, & hyper catabolism * DUE to: _increased intracell Ca+2_ * **Defective ryanodine receptors** (ca+2 induced ca+2 induced) or dihydropyridine Ca+2 channels * Treatment=**Dentrolene Sodium**

Answer 82

* _Inhibits Vit K epoxide reductase_ complex * Treatment of thrombolic phenomenon=Blocks clotting factors **2, 7, 9, 10** * **_2 haplotypes:_** * _AA = least dosage_ * _BB = most dosage_ * **Detox via CYP2C9** (phase 1 cytochrome p450 system)

Devendra Block 2 Flashcards

(106 cards)