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Toxicology Final > Part 2 reproductive Tox > Flashcards

Part 2 reproductive Tox Flashcards

1
Q

What are the markers of physiologic damage for the Seminal Sperm tissue?

A

Sperm number, structure, motility, viability, agglutination, penetration, and egg interaction.

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2
Q

What are non reproductive tract fluids?

A

Blood, urine, saliva, and cerebrospinal fluid.

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3
Q

What is significant in temporal fluctuations?

A

blood

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4
Q

What is good for cumulative exposure?

A

Urine

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5
Q

What is an ultrafiltrate of plasma?

A

Saliva

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6
Q

What is limited by blood CSF/Brain barrier?

A

CSF

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7
Q

What shows the status of sperm/accessory organs?

A

Semen

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8
Q

What is cycle Specific and bacteria?

A

Vaginal Secretions

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9
Q

What 3 reproductive fluids are cycle-specific?

A

Cervical Secretions, Uterinel Luminal fluid, and tubal secretions.

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10
Q

What is only in stimulated cycles?

A

Follicular fluid

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11
Q

What is limited by autolysis?

A

Menstrual cycle.

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12
Q

What are the markers of physiologic damage of the testes tissue?

A

Histopathology

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13
Q

What are the markers of physiologic damage of seminal sperm?

A

Sperm number, structure, Motility, Viability, Agglutination, penetration, and egg interaction.

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14
Q

What are the markers of physiologic damage of other seminal parameters?

A

Physical characteristics, immature germ cells, chemical composition.

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15
Q

What are the seminal parameters of the chemical composition of sperm?

A

Normal and toxic materials, sertoli cells, leydig cells, and accessory glands.

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16
Q

What are the markers of physiologic damage of blood?

A

Hormone Levels

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17
Q

What are markers of physiologic damage for mother’s urine?

A

early pregnancy.

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18
Q

What are markers of genetic damage for testes (biopsy)?

A

Cytogenetic analyses of cells in mitosis and meiosis I, and II.

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19
Q

What are markers of genetic damage for Sperm?

A

Sperm cytogenetics, Sperm DNA and protein adducts, gene mutation, and sperm aneuploidy.

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20
Q

What are markers of genetic damage of Immature germ cells?

A

Spermatid Micronuclei

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21
Q

What are the markers of genetic damage for offspring tissue?

A

Cytogenetics, DNA sequencing, Protein mutations, Restriction-Length DNA polymorphism, RNAse digestion…

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22
Q

What are markers of genetic damage for mother’s urine?

A

Detection of early fetal loss.

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23
Q

What are potential markers for CNS?

A

Neurotransmitters.

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24
Q

What are potential markers for the pituitary?

A

LH, FSH,Prolactin, TSH, and growth hormone.

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25
Q

What are potential markers for steroids?

A

Estradiol, estrone, progesterone, testosterone, androstenedione.

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26
Q

What are potential markers for regulatory factors?

A

Relaxin, Prolactin, plasminogen activator, inhibinm oocyte maturation inhibitor, luteinization inhibitor.

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27
Q

What are potential markers for the fallopian tube?

A

Secretory proteins

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28
Q

What are the potential markers for the uterus?

A

Prolactin, Prostaglandins.

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29
Q

What are potential markers for the cervix?

A

mucus.

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30
Q

What are potential markers for the vagina?

A

Secretory proteins

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31
Q

What are the guideline for biomarkers in reproductive tox in regards to laboratory animals and humans?

A

Baseline values established.

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32
Q

Sensitivity and Specificity is a guideline for what?

A

biomarkers in reproductive toxicology.

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33
Q

What are the 4 factors that influence the toxicity of gonadotoxicants?

A

1) Pharmacokinetics/Toxicokinetics.
2) Biotransformation
3) Repair Mechanism
4) Alcohol and Drug Abuse.

34
Q

What are the pharmacokinetic/toxicokinetic considerations for absorption route?

A

Oral, Inhaling, dermal, vaginal.

35
Q

What are the pharmacokinetic/toxicokinetic considerations for absorption Ka?

A

Low-dose, Long-term exposure.

36
Q

What are the pharmacokinetic/toxicokinetic considerations for distribution property?

A

Lipophilicity

37
Q

What are the pharmacokinetic/toxicokinetic considerations for Distribution binding?

A

Tissue vs Plasma protein binding.

38
Q

What are the pharmacokinetic/toxicokinetic considerations for distribution barriers?

A

Blood-testis, blood-brain, blood placental.

39
Q

What are the pharmacokinetic/toxicokinetic considerations for distribution Vb?

A

Medium to large Vb

40
Q

What are the pharmacokinetic/toxicokinetic considerations for metabolism Detoxification?

A

Phase II conjugation and endogenous protective molecules.

41
Q

What are the pharmacokinetic/toxicokinetic considerations for metabolism bioactivation?

A

P450 system and epoxidase.

42
Q

What are the pharmacokinetic/toxicokinetic considerations for Elimination T (1/2)?

A

Reflects metabolism and excretion.

43
Q

What are the pharmacokinetic/toxicokinetic considerations for elimination clearance (CLs)?

A

Hepatic, renal, and placental.

44
Q

What occurs to absorption in regards to pharmacokinetic changes during pregnancy?

A

Increased Ventilation, peripheral blood flow.
Increased GI residence time
Decreased in GI motility

45
Q

What occurs to Distribution in regards to pharmacokinetic changes during pregnancy?

A

Increased cardiac output, plasma, and water volume.
Increased in body fat.
Decrease in Plasma proteins.

46
Q

What occurs to Metabolism in regards to pharmacokinetic changes during pregnancy?

A

Placental and Hepatic

47
Q

What occurs to Excretion in regards to pharmacokinetic changes during pregnancy?

A

Increased ventilation, renal blood flow, filtration rate.
Increased maternal-placenta-fetus exchange
Increased flow to uterus, placenta, fetal volume.
changes in pH gradient.

48
Q

In pregnant women what occurs to Vb and Vd?

A

Blood volume increases and Vd increases.

49
Q

In pregnant women what occurs to tissue volume and vd?

A

Vt increases and Vd increases

50
Q

In pregnant women ________ plasma protein binding leads to a _____ free fraction of chemical in blood.

A

Low, high

51
Q

What is Fb and Vd in low plasma protein binding leads to a high free fraction of chemical in blood?

A

increase in Fb and Increase in Vd

52
Q

In Valproic acid what is important to know in regards to Cmax and AUC?

A

Cmax is much more important that AUC for the valproic acid.

53
Q

What is the toxicity relevant to peak concentration?

A

Cmax

54
Q

What is the toxicity relevant to total exposure?

A

AUC

55
Q

What type of toxicants that the Cmax is more important than AUC?

A

Valproic Acid and Caffeine

56
Q

What type of toxicants that the AUC is more important than Cmax?

A

Cyclophosphamide, Retinoic acid, 2-methoxyacetic acid.

57
Q

VCH can metabolize through what?

A

P450 enzyme

58
Q

VCD effects the size of the ovary how?

A

It shrinks it/makes it smaller.

59
Q

Where is VCH mainly metabolized?

A

In the liver

60
Q

How does VCH get to the ovaries?

A

It’s metabolites are transported to ovaries and cause the damage.

61
Q

What is DNA repair mechanism?

A

Induce unscheduled DNA synthesis to repair damaged DNA

62
Q

What is the mechanism of protein replacement?

A

Increase protein production to replace the destroyed proteins.

63
Q

The use of illicit drugs by pregnant women may do what?

A

disrupt placental metabolism and exacerbate the effects of smoking.

64
Q

What uses lead that can lead to reproductive toxicity?

A

Construction material, alloys, pigments, batteries, plastics, electronic devices, etc…

65
Q

What is the gonadtoxicity in lead for males?

A

Reduced sperm count, compromised sperm motility, altered sperm morphology.

66
Q

What is the gonadtoxicity for lead induced toxicity in females?

A

Luteolysis, inhibition of implantation.

67
Q

What is the mechanism of gonadotoxicity?

A

Act on spermatogenesis processes, impair leydig cells, directly damage reproductive tract.

68
Q

What types usages are there for TCDD induced reproductive toxicity?

A

A contaminant in herbicides (DDT) Extremely toxic with LD50s of 0.022 and 0.045mg/kg for male and female rats, respectively.

69
Q

What is the gonadotoxicity in males for the TCDD induced reproductive toxicity?

A

Decrease testis weight and spermatogenesis, cause abnormal testicular morphology.

70
Q

What is the gonadotoxicity in females in regards to TCDD reproductive toxicity for females?

A

Reproduce fertility, alter menstrual cycle, and cause inability to conceive and carry a pregnancy.

71
Q

What is the general mechanism for gonadotoxicity for TCDD?

A

Inhibit testosterone biosynthesis and two antiestrogenic action.

72
Q

What is the first antiestrogenic action?

A

antagonize estrogen effect in target organs ( by a decrease in estrogen receptor number)

73
Q

What is the second antiestrogenic action?

A

Accelerate the metabolism of steroids ( by inducing P-450 in liver and target cells).

74
Q

What were the observation on ovary in regard to TCDD treatments?

A

Ovary was much smaller.

75
Q

What is an indication of sexual dysfunction?

A

Decreased libido; impotence.

76
Q

What is an indicator of sperm abnormalities?

A

Decreased number and motility; abnormal morphology

77
Q

What is an indicator of sub fecundity dysfunction?

A

Abnormal gonads, ducts of external genitalia: abnormal pubertal development; infertility of male or female origin; amenorrhea;anovulatory cycles;delay in conception.

78
Q

What is an indicator for dysfunction in illness during pregnancy and parturition?

A

toxemial hemorrhage.

79
Q

Early fetal loss to 28 weeks is an indicator of what?

A

possible reproductive dysfunction

80
Q

Late fetal loss after 28 weeks and still birth is an indicator of what?

A

a possible reproductive dysfunction.

81
Q

Intrapartum death/death in first week is an indicator of what?

A

possible reproductive dysfunction.

82
Q

What are markers of physiologic damage for the testes?

A

histopathology

Toxicology Final (7 decks)

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