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MD3002 > Week 10 > Flashcards

Week 10 Flashcards

1
Q

What is the EPOR model (4 phases of human sexual response)?

A
  1. EXCITEMENT: sexual arousal
  2. PLATEAU: intensification of arousal
  3. ORGASM: involuntary muscular contractions in both sexes
  4. RESOLUTION: detumescence & re-arousal is impossible (may not be true of women)
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2
Q

What phases in women cycle are varied/fixed in time?

A
  • Luteal phase FIXED at approx 14days
  • Follicular phase VARIES
  • Menstrual phase VARIES
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3
Q

How long is sperm viable for?

A

24-72hrs

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4
Q

How long is oocytes viable for?

A

12-24hrs

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5
Q

When must coitus occur for fertilisation to occur?

A

No more than 3 days before ovulation & no more than 1 day after

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6
Q

What is coitus?

A

Sexual intercourse

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7
Q

How long are sperm capable of fertilising an egg?

A

4-6days

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8
Q

How long does an ovulated egg remain viable for?

A

Approx 24-48hrs

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9
Q

Describe the trimesters of pregnancy?

A
  • 1ST (weeks 1-12): most miscarriages occur
  • 2ND (weeks 13-28): at 24weeks 50% survival rate for early prematurity
  • 3RD (weeks 29-40): parturition at ~40weeks from LMP
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10
Q

How likely are women to conceive (study of women <35yrs in china & europe)?

A
  • 50% pregnant after 2 cycles
  • 85% pregnant after 6 months
  • 1/2 remaining were pregnant after 1yr
  • ~5% subfertile
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11
Q

What % of pregnancies miscarry?

A

10-15%

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12
Q

What is a spontaneous abortion?

A

Pre-implantation & post-implantation failure occurring frequently

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13
Q

What % of unprotected intercourse will result in blastocyst stage?

A

20%

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14
Q

What % of blastocysts fail to implant?

A

8-20%

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15
Q

What % of clinically detected pregnancies will fail in the 1st 12 weeks?

A

15-20%

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16
Q

What is the cause of abnormalities?

A

Chromosomal caused by non-disjunction (aneuploidy), sperm DNA shows high rates of mutation because they lack DNA repair system

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17
Q

What are the 3 stages of the embryonic period (8weeks)?

A
  1. Preimplantation embryo
  2. Implantation
  3. Differentiation & development of organ systems
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18
Q

What are the 2 stages of the foetal period (8-40weeks)?

A
  1. Differentiation continues

2. Growth

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19
Q

What 2 things happen at ovulation?

A
  1. Egg extruded onto surface of ovary

2. Smooth muscle of fimbriae cause them to pass over ovary while cilia beat in waves towards interior of duct

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20
Q

What is the purpose of Cumulus cells?

A
  • Aid transport from surface of the ovary
  • Sticky cells cling to claimed surface of fimbriae
  • Transported by ciliary current (& perhaps peristalsis) to ampulla
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21
Q

Describe intercourse & sperm transport?

A
  • Ejaculation deposits semen into vagina
  • Passage into cervical mucus dependent on oestrogen-induced changes in mucus consistency
  • Movement through uterus & fallopian tubes via sperm’s own propulsions & uterine contractions
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22
Q

Why do several 100 million to 100-200 sperm die when travelling from vagina to fallopian tubes?

A
  • Vaginal environment is acidic

- Length & energy requirements of trip are large

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23
Q

What does capacitation of sperm cause?

A
  • Change from wavelike beats of tail to whip-like action to propel sperm
  • Sperm’s plasma membrane altered so its capable of fusing with surface membrane of egg (acrosome reaction)
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24
Q

How does capacitation destabilise sperm’s surface membrane to enhance fusion with oocyte?

A
  • Increase in Ca2+ permeability (rise in intracellular Ca2+)
  • Removal of membrane proteins (glycoproteins)
  • Change in surface charge
  • Depletion of cholesterol
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25
Q

When does fertilisation usually occur?

A

Few hrs after ovulation & within 24-48hrs of ovulation

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26
Q

What are the 8 processes which occur in fertilisation?

A
  1. Sperm cell weaves past follicular cells & binds to zone pellucida
  2. Rise in [Ca2+]i triggers exocytosis of acrosome
  3. Hydrolytic enzymes released, dissolving zona pellucida
  4. Head of sperm lying sideways, microvilli on oocyte surround sperm head, membranes fuse
  5. Rise [Ca2]i occyte triggers cortical reaction
  6. Rise [Ca2+]i ooctye induces completion of oocytes 2nd meiotic division & formation of 2nd polar body
  7. Sperm head enlarges to become male pronucleus
  8. Male & female pronuclei fuse
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27
Q

Describe the Acrosome reaction which occurs during the 2nd step of fertilisation?

A
  • Fusion of acrosome plasma membranes
  • Releases contents of acrosome (hydrolytic enzymes in acrosomal cap)
  • Causes more Ca2+ entry
  • Sperm digests a path through zona pellucida (proteolytic enzymes)
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28
Q

What induces the acrosome reaction?

A

Sperm head contacting the zona pellucida & binding to glycoproteins ZP2 & ZP3

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29
Q

Describe the Cortical reaction which occurs during the 5th step of fertilisation?

A
  • Exocytosis of granules that previously lay immediately beneath the plasma membrane
  • Enzymes released lead to changes in zona pellucida proteins = harden, preventing entry of other sperm
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30
Q

Describe the male & female pronuclei fusion which occurs during the 8th step of fertilisation?

A
  • Sperm contributes its nuclear material & centrioles
  • All other organelles are present in oocyte cytoplasm
  • Mitochondrial DNA inherited exclusively via maternal route
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31
Q

What happens 2-4 days after LH peak?

A

Cell division to ~32 cells in fallopian tube

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32
Q

What happens 5 days after LH peak?

A

Blastocyst enters uterine cavity

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33
Q

What happens 6-7 days after LH peak?

A

Implantation at the uterus

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34
Q

What happens 9-10 days after LH peak?

A

Human chorionic gonadotropin (hCG) from implanted blastocyst (trophoblast cells) rescues corpus luteum, located at trophoblast –> maternal ovary

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35
Q

How is conceptus “held” in fallopian tube?

A

Oestrogen maintains contraction of smooth muscle near where fallopian tube enters wall of uterus

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36
Q

Describe the process of cell division to ~32 cells?

A
  • Conceptus undergoes number of mitotic cell divisions ie. cleavage & morula formed
  • Unusual as no cell growth occurs before each division, therefore conceptus reaching uterus is same size as original fertilised egg
  • Cells are totipotent
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37
Q

What are totipotent cells?

A
  • Can form all the cell types in a body, plus the extraembryonic, or placental, cells.
  • Embryonic cells within the 1st couple of cell divisions after fertilisation are the only cells that are totipotent
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38
Q

What are pluripotent cells?

A

Can give rise to all of the cell types that make up the body (embryonic stem cells)

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39
Q

What are multipotent cells?

A

Can develop into more than 1 cell type, but are more limited than pluripotent cells (adult stem cells & cord blood stem cells)

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40
Q

Why are blastocyst removed for screening?

A

They are pluripotent so a cell can be removed for testing without damage to the embryo

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41
Q

Describe how the conceptus/blastocyst enters the uterine cavity?

A
  • Plasma progesterone rise 3-4days after fertilisation, smooth muscle relax
  • 4-5days after fertilisation, cavities develop
  • ~3days, conceptus/blastocyst lies free in uterine cavity supported by uterine secretions
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42
Q

What does trophoblast of the blastocyst give rise to?

A

Placenta

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43
Q

What does inner cell mass of the blastocyst give rise to?

A

Form embryo

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44
Q

What happens to blastocyst at day 6?

A

Attaches to endometrium adjacent to inner cell mass (embryonic pole)

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45
Q

What does the trophoblast differentiate into?

A
  • Inner cytotrophoblast

- Outer syncytiotrophoblast (loses cell boundaries)

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46
Q

Where are the different sites which metabolism occurs?

A
  • Gut lumen
  • Gut wall
  • Plasma
  • Lungs
  • Kidneys
  • Nerves
  • Liver
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47
Q

What are the 2 phases of metabolism which mainly occur in the liver?

A
  • PHASE I: oxidation, reduction or hydrolysis. Reveal/introduce reactive group “functionalisation”, produces more reactive
  • PHASE II: synthetic, conjugative reactions. Hydrophilic, inactive compounds generated
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48
Q

What happens to hydrophilic drug molecules during metabolism?

A

Hydrophilic molecules –> kidney –> urine

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49
Q

What happens to hydrophobic drug molecules during metabolism?

A

Hydrophobic molecules –> hydrophilic metabolite –> kidney –> urine
OR…
Hydrophobic molecules –> conjugate –> bile –> intestines –> faeces

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50
Q

What 6 reactions occur during Phase I (functionalisation) metabolism?

A
  • Oxidation
  • Reduction
  • Hydrolysis
  • Hydration
  • Dethioacetylation
  • Isomerisation
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51
Q

What 8 reactions occur during Phase II (conjugative) metabolism?

A
  • Glucuronidation/glucosidation
  • Sulfation
  • Methylation
  • Acetylation
  • Amino acid conjugation
  • Glutathione conjugation
  • Fatty acid conjugation
  • Condensation
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52
Q

Give examples of oxidation reactions in Phase I metabolism?

A
  • Mixed-function oxidase system (cytochrome P450)
  • Alcohol dehydrogenase
  • Xanthine oxidase
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53
Q

Give examples of reduction reactions in Phase I metabolism?

A
  • Ketone reduction

- Anaerobic cytochrome P450 metabolism

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54
Q

Give examples of Hydrolysis reactions in Phase I metabolism?

A
  • Ester hydrolysis (ie. cholinesterases)

- Amide hydrolysis

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55
Q

Describe Mixed-function oxidase systems (CYP450s)?

A
  • Microsomal (ER) enzymes
  • Consists of cytochrome P450, NAPDH-CYP450 reductase, lipid
  • Requires molecular oxygen, NADPH
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56
Q

What does Phase II metabolism usually produce?

A

Detoxified, water-soluble, easily secreted products suitable for excretion in bile or urine

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57
Q

What are the 3 causes of variation in drug metabolism?

A
  1. Many enzymes capable of metabolising drugs
  2. Potential for competition & saturation
  3. Issues of variation/induction/inhibition
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58
Q

In what 2 ways are drugs eliminated?

A
  1. Unchanged

2. As metabolites

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59
Q

In general, hydrophilic drugs are eliminated _____ than lipophilic drugs?

A

MORE

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60
Q

Give examples of the possible sources of excretion for drugs?

A
  • Urine
  • Faeces
  • Breath
  • Milk
  • Saliva
  • Perspiration
  • Hair
  • Bile
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61
Q

What is the most important organ involve in elimination of drugs & their metabolites?

A

Kidneys

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62
Q

What 3 things transfer drugs from plasma to bile?

A
  1. Organic cation transporters (OCTs)
  2. Organic anion transporters (OATs)
  3. P-glycoproteins (P-GP)
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63
Q

What can happen to the drug concentrated in bile once delivered to the intestines?

A
  • Hydrophilic drug conjugates (ie. glucuronides)
  • Hydrolysis of conjugate can occur
  • Reabsorption of liberated drug
  • Enterohepatic circulation
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64
Q

Describe the Enterohepatic circulation?

A

Conjugate in liver –> conjugate in bile –> conjugate in intestines (excretion in feces) –> drug in intestine –> drug in blood (renal excretion)

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65
Q

Describe glomerular filtration of drug?

A
  • Filters drugs below 20kDa mol. weight

- Not filtered if drug bound to plasma albumin

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66
Q

Describe Tubular secretion of drug?

A
  • OATs & OCTs
  • OATs transport against electrochemical gradient
  • Cleared even if bunch to plasma albumin
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67
Q

How much of the drug is reabsorbed if the renal tubule is freely permeable?

A

99%

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68
Q

What happens to lipophilic & polar drugs in the renal tubule?

A
  • Lipophilic excreted poorly

- Polar remain in lumen

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69
Q

What causes weak acids to be more rapidly excreted?

A

Alkaline urine

oposite for weak bases

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70
Q

Describe Zero order kinetics?

A
  • Few drugs
  • Rate of metabolism is constant
  • Does NOT vary with amount of drug present
  • Enzyme saturation (alcohol dehydrogenase)
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71
Q

Describe 1st order kinetics?

A
  • Most drugs
  • Constant fraction metabolised/unit time
  • Increases proportionately to drug
  • More drug, faster metabolism
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72
Q

Describe the metabolism of Salicylic acid (hydrolysis of aspirin)?

A
  • Non-linear kinetics

- High doses saturate

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73
Q

What is the Apparent volume of distribution (Vd)?

A

Total amount of drug in body/ Blood plasma conc. of drug

L or L/kg

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74
Q

What is the clearance of a drug (CL)?

A

Sum of all routes of elimination (ie. metabolism + excretion)
(L/h)

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75
Q

Describe the relationship between t1/2 (half-life), Vd & CL of a drug?

A

t1/2 depends on Vd & inversely on CL of drug from the body

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76
Q

What are the 4 different factors that can affect metabolism?

A
  1. Age: decreases as age increases
  2. Genetic variation: wide range of CYP phenotypes, race
  3. Disease: need proper liver function, adequate essential amino acid, severe burns
  4. Other Medication: induction of metabolic enzymes, inhibition of metabolic enzymes
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77
Q

What 3 phases develops an anatomical link between the mother & foetus?

A
  1. Invasion
  2. Decidualisation
  3. Placentation
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78
Q

What makes the maternal portion of placenta?

A

Endomertium underlying the chorion

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79
Q

How is the endometrium around villi changed?

A

Changed by enzymes & paracrine agents so each villi is surrounded by a pool/sinus of maternal blood

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80
Q

Describe the maternal blood supplying the placenta?

A
  • Enters placental sinuses/pools via uterine artery
  • Flows through sinuses
  • Exits via uterine veins
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81
Q

Describe the foetus blood supplying the placenta?

A

Flows into capillaries of choronic villi via umbilical arteries & back to foetus via umbilical vein

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82
Q

What connects the foetus to placenta?

A

Umbilical cord

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83
Q

What happens to the blastocyst at day 6/7 (end of week 1)?

A
  • Leaves zona pelucida & is bathed by uterine secretions for 2 days
  • Progesterone prepares supportive uterine environment increasing glandular tissue
  • Oestrodiol is required to release glandular secretion
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84
Q

Describe the Attachment & Implantation of Blastocyst which occurs at the end of week 1?

A
  • Limited time window
  • Syncytiotrophoblast cells “flow” into endometrium
  • Causing oedema, glycogen synthesis & increased vascularisation (decidualisation)
  • Pregnant endometrium is now termed the decidua
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85
Q

Describe the implantation which occurs at day 13 (time woman expects her next period)?

A
  • Syncytiotrophoblast erode through the walls of maternal capillaries, bleed into the spaces (primitive placental circulation).
  • Nutrition depends on uterine secretion & tissues
  • Breakthrough bleeding may occur
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86
Q

What resides in the core of the villus?

A

Fetal capillary loop, dilated at the tip (slow flow rate)

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87
Q

What eventually happens to the chorionic villi?

A

Become localised at embryonic pole & present a huge surface area for exchange of O2, nutrients & waste products

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88
Q

When does the maternal side of the placental circulation begin to function?

A

10-12 weeks

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89
Q

What separates maternal & fetal circulations?

A

Placental membrane, no mixing!

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90
Q

What are syncytiotrophoblasts bathed in?

A

Maternal blood

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91
Q

How thick should the endometrium be for successful implantation?

A

Atleast 8mm

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92
Q

How is the trophoblastic lacunae formed?

A
  • Syncytiotrophoblast forms a network of interconnected cords invading endometrium & eroding the maternal capillaries
  • Expanded uterine spiral arteries connect with trophoblastic lacunae
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93
Q

What 2 things make up the primary villus?

A

Core of cytotrophoblast covered by multinucleated syncytiotrophoblast

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94
Q

What 3 things make up the secondary villus?

A
  1. Inner core of extra embryonic mesoderm
  2. Middle cytotrophoblast layer
  3. Outer syncytiotrophoblast layer
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95
Q

How long does LH support the steroid secretion of the corpus luteum?

A

10-12days

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96
Q

What is the function of hCG (human chorionic gonadotropin)?

A

Mimics action of LH & supports steroid synthesis (progesterone) of corpus luteum & therefore prevent menstruation & any further follicular development

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97
Q

What secretes hCG?

A

Syncytiotrophoblasts soon after implantation (peaks ~8-10 weeks)

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98
Q

When can hCG be detected in maternal blood by immunoassay?

A

From day 6-7

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99
Q

When can commercial kits detect hCG in urine?

A

After ~14days

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100
Q

What are the placental functions in the 1st 3 months?

A
  • 1st month: villus formaiton
  • 2nd month: increasing surface area & circulation
  • 3rd month: growing, becoming increasingly efficient
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101
Q

What are the 4 “organ-like” functions of the placenta?

A
  1. “Gut”: supplying nutrients
  2. “Lung”: exchanging O2 & CO2
  3. “Kidney”: regulates fluid volumes & disposing of waste metabolites
  4. “Endocrine”: synthesises steroids & proteins that affect maternal & foetal metabolism
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102
Q

Why must be have progesterone for the maintenance of pregnancy?

A
  • Suppresses follicular growth & ovulation
  • Suppresses immune response
  • Maintenance of endometrium
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103
Q

When does the placenta secrete all steroid hormones required for pregnancy?

A

4-5weeks

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104
Q

what is the substrate for progesterone production?

A

Cholesterol from the maternal circulation

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105
Q

What is the main oestrogen in pregnancy?

A

Oestriol

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106
Q

What are the 4 functions of oestrogen in pregnancy?

A
  1. Stimulates growth of uterine myometrium
  2. Stimulates growth of ductal tissue of breast
  3. Along with relaxin, relaxes & softens maternal pelvic ligaments & symphysis pubis allowing expansion of uterus
  4. Stimulate LDL cholesterol uptake & P450 enzyme activity
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107
Q

What does oestrogen levels measure?

A

Foetal well being & placental function

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108
Q

Describe the nutrient exchange across the placenta?

A
  • Rapid, increases as pregnancy advances
  • H20 & electrolytes diffuse freely
  • Glucose via facilitated diffusion
  • Amino acids actively transported
  • Lipids cross as free fatty acids
  • Vitamins
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109
Q

What can be stored for postnatal requirements?

A

Glycogen in liver

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110
Q

Babies from what type of mothers are typically heavier than normal range?

A

Diabetic mothers

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111
Q

Describe gas exchange across the placenta?

A
  • Simple diffusion of gases close to efficiency of lungs
  • Concentration gradients influenced by blood flow rates
  • Quantity of O2 reaching foetus flow limited
  • End of pregnancy exchange capacity decreases & placenta less able to meet demands
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112
Q

What has a greater affinity for O2- adult or fetal haemoglobin?

A

Fetal haemoglobin

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113
Q

Where are 95-97% of ectopic pregnancies found?

A

Ampulla/isthmus of the tube

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114
Q

What can rupture of the fallopian tube cause?

A

Blood loss that may be lifer threatening to mother & fatal for embryo

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115
Q

What can symptoms of ectopic pregnancy be confused with?

A

Appendicitis

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116
Q

What is the definition of “Genetic counselling” according to the Task Force of National Society of Genetic Counsellors (2006)?

A
  • Process of helping people understand & adapt to the medical, psychological & familial implications of genetic contributions to disease
  • Families get a “crash course” in medicine”
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117
Q

What 3 things does the process of Genetic counselling integrate?

A
  1. Interpretation of family & medical histories to assess chance of disease occurrence/recurrence
  2. Eduction of inheritance, testing, management, prevention, resources & research
  3. Promote informed choices & adaptation to the risk or condition
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118
Q

Describe the newborn screening programme for Cystic fibrosis?

A
  • Heel-prick immunoreactive trysinogen (IRT) level = stressed pancreas
  • Raised IRT test using CF mutation kit
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119
Q

When is cystic fibrosis suspected in newborn testing?

A

Raised IRT & 1 pathogenic mutation found

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120
Q

When is cystic fibrosis confirmed in newborn testing?

A

2 pathogenic mutations found

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121
Q

Describe the “mild” mutation R117H?

A
  • 2nd mutation in 1.85% of Scottish CF patients
  • 9% of CF mutations identified on postnatal screen
  • Majority do NOT present with CF in childhood
  • Effect varies to Intro 8 splice site efficiency
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122
Q

What CFTR Intron 8 variant is the most common in population?

A

7T

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123
Q

Describe the 5T CFTR Intron 8 variant?

A

Poor splicing resulting in exon 9 skipping, its not producing much full length protein (10% of normal CRTR)

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124
Q

What new drug artificially opens the chloride channel in G551D mutation?

A

Ivacaftor

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125
Q

What is R117H associated with?

A

Male Infertility

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126
Q

What is the risk of Spinal Muscular Atropy if a couple has already had an affected child?

A

1 in 4 recurrence risk

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127
Q

Describe cleavage stage biopsy?

A
  • Need lots of embryos
  • Remove 1 cell day 5
  • Whole genome amplification
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128
Q

Why not look directly for mutation?

A
  • Single cell, very low copy number DNA
  • Problem with contamination (false +)
  • Allele drop out (false - from failure to amplify)
  • Expensive
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129
Q

What tests would be done for a mother who has had recurrent previous miscarriages?

A

Ultrasound at week 8 (earlier than normal, usually bad news if abnormalities detected at 13 weeks)

130
Q

What is Trisomy 13 also known as?

A

Patau syndrome (associated with renal defects)

131
Q

What is the pre-symptomatic testing protocol?

A
  • Full information on test & limitations (non-directive)
  • Opportunity for facilitated decision making
  • Meet 2-3x before test to ensure understanding
132
Q

What are the 3 issues with pre-symptomatic testing?

A
  1. Insurance company cannot use results to increase premium
  2. Employment
  3. Relationships
133
Q

What are the 4 key points for genetic counselling?

A
  1. Good family history (atleast 3 generations)
  2. Genetic diseases can be associated with different phenotypes
  3. Diagnosis in 1 family member will often have implications for other family members
  4. Lab tests should be interpreted in light of clinical features
134
Q

What is Cascade testing?

A
  • Rest of extended family may be worried, can test them all.
  • Not as necessary for autosomal recessive disorders, unless very worried
  • Other sibling may be a carrier
135
Q

What should you remember regarding sequencing?

A

Reveals the sequence of total DNA, so both chromosomes are mixed together not each chromosome separately

136
Q

What is Haplotyping?

A
  • Group of genes within an organism that was inherited together from a single parent
  • Look at inheritance of chromosome markers around site of disease associated mutation
137
Q

What is the mutation for early onset of Alzheimers disease?

A
  • Substitution mutation in exon 7 of PSEN-1 gene changing codon 214 from CAC to TAC
  • Replaces histidine with tyrosine in the PSEN-1 protein (missense)
138
Q

When is the fundus of the uterus palpable abdominally?

A

From 13 weeks gestation

139
Q

Where does the uterus reach at term?

A

Xyphoid process (thorax widens as ribs flare to accommodate organs)

140
Q

What anatomical changes does the mother experience during pregnancy?

A
  • Changes centre of gravity causing accentuated lumbar lordosis (backache)
  • Relaxin causes softening of ligaments (sacroiliac & symphysis pubis pain)
141
Q

Describe the average weight gain a pregnant woman has?

A
  • ~7-14kg total
  • 6kg uterus, foetus & breast
  • 3kg fat reserves for lactation
  • Remainder is fluid
142
Q

Why are pregnant woman prone to varicose veins & ankle oedema?

A

Pressure on IVC esp when lying down will impede venous return fro lower limbs & may impair function of valves

143
Q

Describe physiological anaemia of pregnancy?

A
  • Haematopoiesis is increased (up 30%)

- Plasma volume increase (up 50%) means haematocrit, red cell count & haemoglobin concentration decrease

144
Q

What are the other circulatory adaptations (blood volume & composition) during pregnancy?

A
  • Small increase in WBC
  • Unchanged platelet count, but more reactive
  • Increase in clotting factors with thromboembolism risk
145
Q

Describe the uteroplacental circulation?

A

High volume, low resistance flow as uterine spiral arteries & arterioles lose capacity to vasoconstrict

146
Q

What do pregnancy hormones do to the woman sensitivity to pressor agents?

A

Reduce sensitivity (ie. angiotensin), hence peripheral vasodilatation (heat-intolerance)

147
Q

What does reduced TPR trigger in pregnancy?

A

Renin-angiotensin-aldosterone system increasing blood volume

148
Q

What additional factors favour vasodilation, maintaining normal (low) blood pressure?

A
  • Oestrogen increases vascular endothelial growth factor (VEGF) & nitric oxide (NO)
  • Endothelial cells release prostacyclin (prostaglandin I2 or PGI2)
149
Q

What happens to the woman’s cardiac output (CO) during pregnancy?

A
  • Increases by 30-50% between weeks 6-28 (~6L)

- In late pregnancy, CO sensitive to posture (hypotension/fainting when lying flat)

150
Q

What happens to Heart Rate (HR) & Stroke Volume (SV) during pregnancy?

A
  • HR: increases 70/min to 80-90/min

- SV: increases ~10%

151
Q

When does the woman’s Cardiac Output (CO) return back to pre-pregnancy condition?

A

6 weeks post-partum

152
Q

How is the pregnant woman’s blood pressure (BP) measured?

A

Semi-recumbent using Korotkoff phase 5 for diastolic

153
Q

Describe a pregnant woman’s blood pressure?

A
  • Although CO increases, BP normally falls in 2nd trimester
  • Systolic falls ~5-10mmHg
  • Diastolic falls ~10-15mmHg
154
Q

Describe Pre-eclampsia?

A
  • Placental problem involving increase in BP, proteinuria & oedema
  • May involve failure of 2nd wave of trophoblast invasion that normally impairs capacity of material spiral arterioles to constrict (12-16weeks)
155
Q

How common is pre-elcampsia?

A

~2-8% of pregnancies, more common in 1st pregnancy

156
Q

What 3 things does increased vascular resistance in placenta during pre-elclampsia cause?

A
  • Decrease blood to placenta
  • Hypertension in mother
  • Renal arteriolar endothelial damage causes oedema, glomerular damage & proteinuria (acute atherosis)
157
Q

Describe Eclampsia?

A
  • Potentially fatal, Extreme hypertension (ie. 180/120)
  • Increased intracranial pressure, seizures, coma
  • Significant risk of cerebral haemorrhage
158
Q

What % of maternal mortality does eclampsia cause?

A

~8-36%

159
Q

What are 4 interventions for eclampsia?

A
  1. Magnesium sulphate
  2. Antihypertensives
  3. Rapid delivery
  4. Careful fluid balance
160
Q

What happens to the woman’s respiratory system during pregnancy?

A
  • Progesterone increases sensitivity of central CO2 receptors
  • Deep ventilation
  • Increase tidal vol by ~40%
  • Rate unchanged
161
Q

What happens to the woman’s renal system during pregnancy?

A
  • Increased glomerular filtration rate (GFR), due to increase CO
  • Decreased plasma urea, creatinine & uric acid
  • Ureters dilated, predisposing to infection
162
Q

What is the most useful renal marker in pregnancy & why?

A

Uric acid as it rises before creatinine in response to renal impairment (ie. pre-eclampsia)

163
Q

Why do pregnant women urinate frequently & urgently?

A

Bladder is compressed

164
Q

What happens to the total body water (TBW) in pregnant women?

A
  • Increases by ~6-8L

- ECF increases by ~3L, split between plasma & interstitial fluid (ISF)

165
Q

What happens to the osmolality in pregnant women?

A
  • Falls by ~10mOsm/kg

- Decreased urea & creatinine

166
Q

What 3 GI system problems do pregnant woman commonly suffer with & why?

A
  1. Morning sickness esp 12-14weeks: parallels HCG levels
  2. Constipation: pressure on rectum & lower colon, decreased motility (progestognenic effect)
  3. Gastric acid reflux, heartburn: relaxation of lower oesophageal sphincter, pressure of uterus, worse lying down, aspiration risk
167
Q

How much should a woman’s daily calorie intake increase when pregnant?

A

~15%, so 200-300kcal/day extra

168
Q

Describe the physiological changes that occur in early pregnancy?

A
  • ~3kg fat laid down for energy source in final trimester when growth is rapid
  • Maternal tissues more sensitive to insulin
  • increased protein synthesis
169
Q

When does the growth of foetus peak?

A

30-36 weeks

170
Q

Describe the physiological changes that occur in later pregnancy?

A
  • Relative insulin resistance, predisposing to “high-normal” glucose
  • Increase lipolysis
  • Increase circulating triglycerides stored in mammary tissue
  • Increased requirement for protein
171
Q

What were the findings for Gestational weight gain (GWG)?

A
  • Median 13.7kg

- Different variations can all lead to a healthy outcome, weight gain doesn’t matter

172
Q

Describe gestational diabetes?

A
  • Spectrum from normal to “impaired glucose tolerance” to actual diabetes
  • Predictor of future type 2 diabetes
  • Associated with foetal macrosomia (increase insulin resistance, high glucose)
173
Q

What are the 3 risk factors for gestational diabetes?

A
  1. Race
  2. Obesity
  3. Family history
174
Q

What are the vitamin requirements for a pregnant woman?

A
  • Folic acid needed for neural tube fusion
  • Vegetarians may need increase B12 intake
  • High levels of vit A may lead to foetal abnormalities
  • Vit D supplementation
175
Q

What are the mineral requirements for a pregnant woman?

A
  • Calcium (calcification of skeleton)
  • Maternal gut absorption increases (vit D3)
  • Urinary loss decrease (parathyroid hormone)
  • Increase in release of calcium from bone
  • Active transport across placenta
176
Q

Why do pregnant woman need Zinc?

A
  • Important in many metabolic processes
  • Protein synthesis
  • Nucleic acid synthesis
  • Synthesis/activity of insulin
  • Increased dietary need, esp Vegans
177
Q

When would pregnant women supplement Iron?

A
  • If dietary iron low (maternal iron deficiency)

- NOT when normal iron stores as it may increase oxidative stress

178
Q

What are the endocrine secretions from the placenta during pregnancy?

A
  • hCG: role in maintaining pregnancy

- Other placental proteins & steroids

179
Q

What are the endocrine secretions from the mother during pregnancy?

A
  • Increased growth hormone
  • Decrease FSH & LH
  • Increased prolactin
  • Increased parathyroid hormone
  • Pituitary increases size
  • Thyroid increases size due to hCG
180
Q

What are the physiological post-natal changes that the woman’s body undergoes?

A
  • Uterine involution/shrink by 6 weeks
  • Amenorrhoea if breast feeding
  • Coagulation system changes reversed by longer than week 6
  • Glucose tolerance normalises very rapidly
181
Q

What can be the cause of 1. small babies 2. big babies?

A
  1. Small: pre-eclampsia

2. Big: gestational diabetes

182
Q

What is the Estimated Date of Delivery (EDD)?

A
  • 40 weeks/ 280 days from the 1st day of last menstrual period (LMP)
  • Actual fetal age will be 14 days less than EDD
183
Q

What is delivery “at term”?

A

Between 37-42 completed weeks

184
Q

What is delivery “pre-term”?

A

Before 37 completed weeks

185
Q

What is delivery “post-term”?

A

Beyond 42 weeks

186
Q

How do you estimate gestational age in 1st trimester?

A
  • Gestation sac volume for very early gestation

- Crown-rump length

187
Q

How do you estimate gestational age in 2nd trimester?

A
  • Head circumference
  • Biparietal diameter
  • Abdominal circumference
  • Femur length
188
Q

What is ultrasound biometry for in late pregnancy?

A

Growth not gestational age

189
Q

What 3 things maintain the pregnant state?

A
  1. Uterine quiescence: gap junction down regulated, oxytocin receptors down regulated, relaxin
  2. Anatomical arrangement of the cervix: collagen fibres over smooth muscle, glycosaminoglycan
  3. Amnion & chorion membranes are intact: low prostaglandin biosynthesis
190
Q

How is labour initiated?

A
  • Increased oestrogen encouraging uterine contractions
  • Increased PG
  • Increased cytosol-free calcium needed for muscular contraction
  • Oxytocin
191
Q

Describe cervical ripening during initiation of labour?

A
  • Prostaglandin biosynthesis increases
  • Increasing water content of glycosaminoglycan matrix
  • Myometrial activity results “effacement” & thinning of cervix
  • Relaxin upregulates matrix metalloproteinases
192
Q

Describe uterine contractions during initiation of labour?

A
  • Initially un co-ordinated, non painful “Braxton Hicks”

- Progressively regular, frequent, co-ordinated & painful

193
Q

What are the 4 stages of cervical effacement & dilation?

A
  1. Not effaced, no dilation
  2. Fully effaced, 1cm dilated
  3. 5cm dilation
  4. Fully dilated at 10cm
194
Q

How long does labour take on average for Primiparous & Multiparous?

A
  • Primiparous: 14hrs

- Multiparous: 8hrs

195
Q

Describe the 1st stage of labour?

A
  • “Latent phase”: painful contractions 5-10min intervals, cervical ripening & effacement, slowing dilating 3-4cm
  • Active phase: cervix dilated 0.5-1cm/hr, increase in frequency & strength of contractions, cervical dilatation, descent of presenting part, membrane rupture
196
Q

Describe the 2nd stage of labour?

A
  • Cervix fully dilated (10cm)
  • Contractions stronger 2-5mins
  • Presenting part descends
  • Urge to bear down
  • “Ferguson reflex” of perineal stretching
  • Deliver
  • ~1hr long
197
Q

Describe the 3rd stage of labour?

A
  • Expulsion of placenta & membranes
  • Separation due to forceful uterine contraction, reduces size of placental bed which reduces bleeding
  • ~5mins
198
Q

What are 2 ways of managing the 3rd stage of labour?

A
  1. Expectantly (traditional or physiological)

2. Actively: oxytocic drugs (ergotamine), coupled with physically pulling umbilical cord

199
Q

What are 5 factors influencing uterine contractions?

A
  1. Prostagladins
  2. Oxytocin
  3. Relaxin
  4. Stretch response
  5. Positive feedback
200
Q

Describe what prostaglandins (PGF2α & PGE2) do?

A
  • Paracrines released from uterine decidual cells
  • Stimulate uterine contractions
  • Soften, thin & dilate cervix
  • Potentiate contractions induced by oxytocin
  • Increase gap junction numbers
201
Q

Describe what oxytocin (posterior pituitary hormone) does?

A
  • Triggers phospholipase C cascade & release of intracellular Ca2+ from smooth muscle SR (receptors on smooth muscle cells)
  • Stimualtes PGF2α production
  • Constricts uterine blood vessels at site of placenta
202
Q

What does fetal oxytocin moving to maternal circulation do?

A

Onset of labour

203
Q

What does maternal oxytocin do?

A

Released in bursts as a consequence of dilation of the cervix (Ferguson reflex)

204
Q

What produces relaxin?

A
  • Corpus luteum
  • Placenta
  • Decidua
205
Q

What does relaxin do?

A
  • Uterine quiescence
  • Softens & helps cervix dilate during labour
  • Affects collagen metabolism & soften ligaments
206
Q

What are pregnant woman vulnerable to?

A

Ligamentous strain of relaxin

207
Q

Describe the positive feedback influencing uterine contractions?

A
  • Contraction stimulate prostaglandin release –> increases contraction intensity
  • Contractions stretch cervix –> oxytocin release & stimulates further contractions
208
Q

Describe engagement of the fetal head during labour & delivery?

A
  • 2-4 weeks prior to delivery in primiparous
  • May not happen in multiparous
  • Presenting part descends into pelvis
209
Q

What are the 4 stages of fetal delivery?

A
  1. Engagement & flexion of head
  2. Internal rotation
  3. Delivery by extension of head, nose scrapes blanket
  4. Delivery of shoulders
210
Q

Describe the “lie” delivery presentation?

A
  • Longitudinal (spines of mother & baby parallel)

- Transverse would be abnormal more common in preterm & multiple pregnancies

211
Q

Describe the “attitude” delivery presentation?

A
  • Baby normally lies in “fetal” position (head tucked into chest)
  • Crown of head/verte presents 1st (neck extended would be abnormal)
212
Q

What % of delivery presentations are cephalic, breech, shoulder?

A
  • Cephalic 97%
  • Breech is buttock 1st 3%
  • Shoulder 1%
213
Q

What is External cephalic version (ECV)?

A

Manipulation of foetus through abdomen from breech to cephalic presentation from 36 weeks nulliparous or 37 weeks multiparous

214
Q

What is the success rate of external cephalic version (ECV)?

A

~50%, >5% revert to breech

215
Q

What can you use to relax the uterus?

A

Tocolysis (salbutamol or terbutaline)

216
Q

What maternal intrapartum monitoring can you do?

A
  • Vital signs, increasing in frequency as labour progresses

- Progress “partography”

217
Q

What fetal intrapartum monitoring can you do?

A
  • Auscultation of fetal heart rate & pattern with Pinard stethoscope/hand held doppler/electronic monitoring with cardiotocography (CTG)
  • Inspection of liquor once membranes are ruptured
218
Q

Describe what you look at for Partograph?

A
  • Fetal HR
  • Rate of cervical dilatation
  • Descent of fetal head
  • Contraction characteristics
  • Membrane ruptured- colour of amniotic fluid
  • Volume of maternal urine
  • Record of medications
  • Maternal vitals
219
Q

Describe the 3 layers to the anatomy of the uterus?

A
  1. Perimetrium (serosa): thin outer layer of epithelium
  2. Myometrium: thick middle layer of smooth muscle
  3. Endometrium: inner layer with glands, blood vessels, lymphatics & epithelial cells
220
Q

What are uterine contractions dependent on?

A

Gap junctions for phasic propagation of depolarisation (connexin 43 protein)

221
Q

Describe the gap junctions in uterine smooth muscle?

A
  • Inducible (especially hormonally)

- Fundal dominance during labour may arise from anatomical arrangement of expressed gap junctions

222
Q

What are the 2 receptor types effecting sympathetic outflow of the uterus?

A
  • alpha-adrenoceptors: contraction
  • beta-adrenoceptors: relaxation

(hormones influence the ratio of these receptors)

223
Q

What are the posterior pituitary hormones which stimulate contraction of the uterus?

A
  • Antidiuretic hormone (ADH)
  • Vasopressin
  • Oxytocin
    (9 amino acid peptides, 2 amino acids different)
224
Q

What is the effect & receptor numbers of oxytocin influence by?

A

Sex hormone levels

225
Q

Describe the effect of oxytocin on uterine motility?

A
  • Smooth muscle sensitive prior to labour due to increase oxytocin receptors
  • Stimulates increasingly regular, co-ordinated contractions that travel from fundus to cervix
  • Uterus relaxes between contractions
226
Q

What is the purpose of uterine stimulants (oxytocics)?

A
  • Induce abortion
  • Induce & accelerate labour
  • Contract the uterus after delivery to control postpartum haemorrhage (PPH)
227
Q

What is the purpose of uterine relaxants (tocolytics)?

A
  • Treat menstrual cramps
  • Prevent preterm labour
  • Facilitate obstetric manoeuvres
  • Counteract (iatrogenic) uterine hyperstimulation
228
Q

What are 3 oxytocic drugs used to stimulate uterine contractions?

A
  1. Oxytocin (IV infusion to induce labour, IV or IM injection after delivery to control PPH)
  2. Ergometrine
  3. E & F series prostaglandins
229
Q

Describe the use of Ergometrine oxytocic drug?

A
  • Main use in obstetric haemorrhage (PPH)
  • Bleeding early pregnancy (miscarriage)
  • Causes sustained powerful uterine contractions
230
Q

What is the drug Syntometrine?

A

Combination of Oxytocin & Ergometrine for 3rd stage of labour

231
Q

What 3 places in the uterus has a significant prostaglandin synthesising capacity?

A
  1. Endometrium
  2. Decidua
  3. Myometrium
232
Q

Describe the difference classes of prostaglandins?

A
  • Prostaglandin F2a (PGF2a): large amounts
  • Prostaglandin I2 (PGI2)/ Prostacyclin: occur naturally
  • Prostaglandin E2 (PGE2): occur naturally
  • F series: vasoconstrictor
  • E series: vasodilator
233
Q

What are the 4 prostaglandin drugs & what are the equivalent to?

A
  1. Dinoprostone: PGE2, naturally occurring
  2. Carboprost: synthetic analogue PGF2a
  3. Gemeprost: synthetic analogue PGE1
  4. Misoprostol: synthetic analogue PGE1
234
Q

What is Misoprostol (PGE1 analogue) used for?

A
  • Room temp
  • Treatment/prevention of peptic ulcers
  • Medical abortion
  • Induction of labour
  • Control of postpartum haemorrhage (PPH) secondary to uterine atony
  • Oral, vaginal, sublingual or rectal route
235
Q

What are 5 examples of uterine relaxants (tocolytics)?

A
  1. β2-agonists
  2. Calcium channel blockers
  3. Nonsteroidal anti-inflammatory drugs (NSAIDS)
  4. Oxytocin receptor antagonist
  5. Nitrates
236
Q

Give 3 examples of β2-agonists and describe how they are used?

A
  • Ritodrine, Terbutaline, Salbutamol
  • Increase cAMP in smooth muscle
  • Adverse effects: tachycardia, hypertension, hyperglycaemia
237
Q

Give 2 examples of calcium channel blockers and how they are used?

A
  • Nifedipine
  • Magnesium sulphate
  • Prevent intracellular Ca2+ increase in smooth muscle
238
Q

Give an example of an NSAID and how they are used?

A
  • Indomethacin

- Inhibit prostaglandin biosynthesis

239
Q

Give an example of an oxytocin receptor antagonist?

A

Atosiban

240
Q

Give 2 examples of nitrates used for uterine relaxants (tocolytics)?

A
  • Nitric oxide (NO) donors

- Nitroglycerine patch

241
Q

What does an imbalance of Prostaglandin E vs Prostaglandin F in endometrium cause?

A

Dysmenorrhoea & menorrhagia (excessive blood loss)

242
Q

Why can NSAIDS be used to treat menstrual symptoms?

A
  • Pain relief

- May reduce blood loss by ~10%

243
Q

What are the consequences of pre-term birth?

A
  • Respiratory distress
  • Hypothermia
  • Cerebral palsy (Intraventricular haemorrhage)
  • Hypoglycaemia
  • Jaundice
  • Sepsis
244
Q

Who owns your body & its parts while you are alive?

A

Limited property rights as we don’t have ownership but a “weaker package of limited property rights”

245
Q

What is the key issue with saying we own & have property over our own bodies?

A
  • You can typically transfer property (car, house etc) to someone else
  • We have weak property right in that we can donate an organ, but don’t have strong property right to sell
246
Q

Who owns your body & its parts once you have died?

A

There is NO property in a corpse, so nobody owns it

247
Q

Describe what happened in the Alder Hey hospital organ scandal in late 1990?

A
  • Children dying of cardiac surgery had their organs stored
  • Aborted or stillborn foetuses were kept
  • Parents had consented to a post-mortem, but not to retention
248
Q

What was the doctor at the centre of the Alder Hey Hospital scandal?

A

Professor Dick van Velzen (specialist in cot death)

249
Q

How did Professor Dick van Velzen back up his illegal and unethical act?

A

“Children are too precious to die without using every scrap of information which could help the next child”

250
Q

Describe the John Moore’s spleen case?

A
  • John Moore was diagnosed with hairy cell leukemia
  • Attended UCLA medical centre, & was under the care of David Golde
  • Moore had spleen removed & returned to UCLA from Seattle several times to have blood & samples taken
  • Golde had patented cell line derived from Moore’s T-cells & products & was working in collab with pharma company making ~£15million
251
Q

What did Moore do once finding out the truth about Golde using his samples for his own research without consent?

A
  • Took him to court
  • Asserted “continuing property interest” (conversion)
  • Said he did not give informed consent & Golde had breached ethical duty
252
Q

What was the conclusion from the court case between Moore & Golde?

A
  • No property interest (removed spleen was not his property)
  • Golde did breach ethical duty by not acting for patients benefit & should have ensured Moore was fully informted (financial fain was conflict of interest)
253
Q

What is a “Continuing property interest” (conversion)?

A

“Where property belonging to one person is wrongly disposed of or converted to the use of another, to the detriment of its rightful owner” (Talbot, 2012)

254
Q

Describe the Hagahai & T-cell case?

A
  • US researchers collected samples

- Created T-cell line and applied for a patent

255
Q

What is a patent?

A

Government authority or licence conferring a right or title for a set period, esp the right to exclude others from making, using, or selling an invention

256
Q

What ethical issues did the Hagahai & T-cell case raise?

A

Raises issues of “biopiracy”, need for prior consent, discussion of benefit-sharing

257
Q

What does the Tissue Act (Scotland) 2006 legally state?

A

Requires authorisation for use of organs, tissues & samples from the deceased

258
Q

What legislation regulates the use of tissues from the living in Scotland?

A

NHS Scotland accreditation scheme (2011), now under Healthcare Improvement Scotland

259
Q

What legislation regulates DNA analysis?

A

Consent as detailed in Human Tissue Act 2004 (England, Wales & N Ireland), there is an offence known as “DNA theft”

260
Q

Describe how the Canavan gene patent controversy arose?

A
  • Greenberg family affected by Canavan disease, father got scientist to look into disease, allowing his childrens tissues to be used
  • Canavan gene testing price increased because patented by a hospital
  • US supreme court “We hold that a naturally occurring DNA segment is a product of nature & not patent-eligible merely because it has been isolated”
261
Q

What are the 2 main gene defects identified in familial breast cancer?

A
  • BRCA1

- BRCA2

262
Q

Describe BRCA1 gene defect?

A
  • Large families with breast & ovarian cancer
  • Autosomal dominant
  • Lifetime risk 50-80%
  • Increases ovarian risk 40-50%
263
Q

What is the Knudson hypothesis?

A

Two-hit hypothesis: cancer is the result of accumulated mutations to a cell’s DNA

264
Q

What does BRCA1 do?

A
  • Human tumor suppressor gene
  • Mutations mean protein shorter than normal
  • C-terminus involved in DNA repair and binds to RAD50/51
  • Stabilises the double strand break for BRCA2 to repair it
265
Q

Describe the DNA damage response?

A
  • If damage cells, BRCA1 location changes & overlaps with other proteins known to respond to damage
  • When laser passed through nucleus, only region passed through will be damaged
266
Q

Describe BRCA2 gene defect?

A
  • > 400 mutations
  • Most result in truncated protein
  • Founder effect
  • Increases risk of prostate cancer & breast cancer
267
Q

What does BRCA2 do?

A
  • Binds to RAD51 protein

- Responds to DNA damage, cells without BRCA2 particularly sensitive to DNA damaging agents

268
Q

Describe the steps of Homology directed repair of DNA double strand breaks?

A
  1. dsDNA break
  2. Resection by exonuclease
  3. Base-pairing with unwound DNA of undamaged sister chromatid
  4. Strand extension
  5. Disengage and pair
  6. Fill in gaps, restore wild-type helix
269
Q

Describe the steps of BRCA2 & DNA damage response?

A
  1. BRCA2 recruits Rad51 to sites of DNA damage
  2. BRCA2 promotes nucleation of Rad51 filament
  3. BRCA2 stimulates Rad51-mediated strand exchange & D-loop formation
270
Q

What are the 6 factors to consider in referral for genetic counselling?

A
  1. Numer of family members affected
  2. What generations?
  3. Age of onset
  4. Ethnic background
  5. Breast cancer susceptibility genes have low penetrance
  6. Polygenic disease?
271
Q

How can you reduce the risk of breast cancer?

A
  • Genetic testing
  • Refer for screening (mammography/MRI)
    i) Breast cancer
  • tamoxifen 53%
  • mastectomy >90%
  • oophorectomy up to 68%
    ii) Ovarian cancer
  • Oophorectomy 96%
  • Oral contraceptives 60%
272
Q

What are 3 implications for treatment in potential breast cancer?

A
  1. DNA damaging agents
  2. DNA double strand breaks
  3. Replication fork stalling
273
Q

What is synthetic lethality?

A

2 genetic mutations are independently compatible with life BUT together cause mortality

274
Q

What is PARP & what does it do?

A
  • Poly ADP-ribose polymerase

- Repairs single-strand DNA breaks by sending a signal to recruit other proteins

275
Q

What is resistance in breast cancer?

A
  • Over time small number of cells became resistant to PARP inhibitor
  • Normal cells start to arise from resistant cell line
  • Cell line starts off truncated with BRCA2 mutation.
  • Small proportion repair some DNA (faulty)
  • Instead of creating truncated protein, create essentially more functioning protein then started off with
276
Q

What 3 things make you more susceptible to sporadic breast cancer?

A
  • Early menarche
  • Late menopause
  • 1st child after 30 years
277
Q

What % of tumours are oestrogen receptor (ER) positive?

A

~60%

278
Q

Describe the hormone therapy of Tamoxifen?

A
  • Prodrug
  • Antagonist of oestrogen receptor
  • Prevents expression of genes which would otherwise be stimulated by oestrogen
  • Prophylactic after surgery for early stage breast cancer
  • Side effect: hot flushes
279
Q

What % of tumours are epidermal growth factor receptor 2 (HER2/erbB2) positive?

A

20-30%

280
Q

What does HER2/erbB2 do?

A

Binds to growth factor receptor found on plasma membrane & causes signal transduction cascade which results in cells division

281
Q

Describe Trastuzumab (Herceptin) treatment?

A
  • “Humanised” monoclonal antibody to HER2
  • Prevents signalling
  • Suppresses HER2+ cancer cell growth & angiogenesis
  • Cell mediated cytotoxicity
282
Q

Describe when & why you would use Dozetaxel (Taxotere) as breast cancer treatment?

A
  • Drug stabilises microtubules (key component of spindle)
  • Promotes apoptosis
  • Many tumours are aneuploid, may be because mitotic checkpoint isn’t working
283
Q

What are the risk factors for STI’s?

A
  • Young age
  • Failure to use barrier contraceptives
  • Non-regular sexual relationships
  • Homosexuality
  • IV drug use
  • African origin (Sub-Saharan Africa)
  • Social Deprivation
  • Prostitution
  • Poor access to advice & treatment of STIs
284
Q

Describe Human Papillomavirus (HPV)?

A
  • Induces hyperplastic epithelial lesions (genital warts)
  • Types exhibit tissue/cell specificity
  • Incubation period 1-6months
285
Q

What are the different types of HPV warts which have varying potential to cause malignancy?

A
  • Cervical carcinoma
  • Urogenital warts
  • Laryngeal papillomas
  • Common, flat & plantar warts
286
Q

What is the treatment for HPV?

A
  • Podophyllum
  • Cryo (freezing)
  • Laser
  • Surgery
287
Q

What are the 2 killed vaccines available for HPV protection?

A
  • Cervarix (bivalent)

- Gardasil (quadrivalent)

288
Q

Describe the HPV vaccine?

A
  • Based on VLP1 (papillomavirus-like particle) a major capsid protein
  • Given to girls 12-13yrs
  • Protects against most cervical cancers
289
Q

Describe Chlamydia trachomatis?

A
  • Obligate, Intracellular, gram negative
  • A,B,C serotypes: trachoma
  • D-K serotypes: genital infection
  • L1,L2,L3 serotypes: lymphogranuloma venereum cancer
290
Q

What is a Trachoma?

A

Contagious bacterial infection of the eye, causing inflamed granulation on the inner surface of the lids, leads to fibrosis which causes the eyelids to contract & tighten causing it to be permanent (blindness)

291
Q

What are the female & male symptoms for Chlamydia infection?

A
  • FEMALE: discharge, abdominal & pelvic tenderness, infertility, Reiter’s syndrome
  • MALE: discharge, prostatitis, epididymal tenderness, Reiter’s syndrome
292
Q

What are the possible investigations you can do to test for Chlamydia?

A
  • Urine: NAATs
  • Endocervical swab: cell culture
  • Antigen detection or EIAs
293
Q

How do you treat Chlamydia infection?

A

Azithromycin & Tetracycline (doxycycline)

294
Q

Describe Candida albicans?

A
  • Vaginal discharge
  • Yeast
  • Normal microbiota of vagina
295
Q

Describe thrush (UK) / Yeast infection (USA)?

A
  • Intensely itchy vaginitis
  • Present as UTI
  • Diagnosed by microscopy/culture
  • Recurrence common in women
  • Rarely symptomatic in men
296
Q

What is the treatment for Thrush (UK)/ Yeast infection (USA)/ Candida albicans?

A

Oral fluconozole & topical nystatin

297
Q

Describe Trichomonas vaginalis?

A
  • Anaerobic, single cell, flagellated protozoa
  • Attaches to squamous epithelium
  • Incubation 4d-3wk
  • Infects vagina & urethra
  • Causes trichomoniasis
  • Yellowish vaginal discharge
  • Diagnosed by dark-phase microscopy
298
Q

How would you treat Trichomonas vaginalis infection?

A

Metronidazole

299
Q

What are the 2 different types of Herpes Simplex Virus?

A
  • HSV type 1 (HSV-1): oral region & causes cold sores
  • HSV type 2 (HSV-2): genital infection (penis, anus, vagina)
    CAN BOTH INFECT MOUTH &/OR GENITALS
300
Q

Describe what happens in a person with Herpes Simplex virus?

A

Commonly asymptomatic but still shedding virus & infectious (responsible for most new infections)

301
Q

What can neonatal herpes simplex virus infection cause?

A

Disseminated infection often involving CNS (severe neurological deficit)

302
Q

Describe the primary infection of genital herpes (typically HSV-2)?

A
  • Fever flu-like prodrome (5-7days)
  • Tingling neuropathic pain in buttock, genitals, legs
  • Bilateral crops of painful blisters/ulcers in genitals, vagina & cervix
  • Tender lymph nodes
  • Local oedema
  • Dysuria
  • Vaginal or urethral discharge
303
Q

What do you treat genital herpes with?

A

Aciclovir

304
Q

Why does recurrence of genital herpes occur?

A
  • Following primary infection, virus becomes latent in local sensory ganglia
  • Periodic reactivation
  • Episodes usually shorter (<10days)
  • Attacks become less frequent over time
305
Q

What is the median recurrence rate after a symptomatic 1st episode in HSV-1 & HSV-2?

A
  • HSV-1: ~1 attack in the subsequent 12 months

- HSV-2: ~4 attacks in the subsequent 12 months.

306
Q

How do you diagnose Herpes simplex virus?

A
  • Clinical appearance
  • Viral culture
  • DNA detection using NAAT of swab from base of ulcer/vesicle fluid
  • Serology to identify asymptomatic infection & distinguish between 2 types
307
Q

How long may it take for HSV to become antibody positive after primary infection?

A

Upto 12 weeks

308
Q

Describe Neisseria gonorrhoeae?

A
  • Gram negative
  • Intracellular diplococcus
  • Infects epithelial cells of mucous membrane of GU tract/rectum
  • Development of localised infection with production of pus
  • Asymptomatic carriage in women
309
Q

Describe the symptoms of Gonorrhoea in male & female?

A
  • Acute inflammation & discharge in male
  • Cervical discharge in female
  • Rectal infections in male homosexuals
  • Oral pharyngitis
  • Disseminated infection (septic arthritis)
310
Q

What is Ophthalmia neonatorum?

A
  • Conjunctivitis contracted by newborns during delivery
  • Mother infected with N. gonorrhoeae or C. trachomatis
  • Can cause blindness without treatment
311
Q

What lab diagnosis can you do for Gonorrhoea?

A
  • Light microscopy of gram-stained genital specimens to look for gram-negative diplococci
  • NAAT (urine)
  • PMN in urethral pus
312
Q

What are the 3 possible treatments for confirmed, uncomplicated gonococcal infection in adults?

A
  • Ceftriaxone 250mg IM
  • Cefixime 400mg oral
  • Ciprofloxacin 500mg oral (if beta lactam allergy)
313
Q

What antibiotic do most strains of gonorrhoea respond to?

A

Ceftriaxone

314
Q

What may be given to treat patients with gonorrhoea & concomitant chlamydial infection?

A

Doxycyline

315
Q

Describe Treponema pallidum?

A
  • Gram negative spirochete

- Causes syphilis

316
Q

Describe the primary stage of syphilis?

A
  • Hard genital or oral ulcer (chancre) at site of infection after about 3 weeks
  • Asymptomatic for upto 24 weeks
317
Q

Describe the secondary stage of syphilis?

A
  • Red maculopapular rash (highly infectious) anywhere & pale moist papules in urogenital region & mouth (condylomas)
  • Latent for 3-30 years
318
Q

Describe the tertiary stage of syphilis?

A

Degeneration of nervous system, aneurysms & granulomatous lesions in liver, skin & bones (gumbos) in about 40% of patients

319
Q

Describe congenital syphilis from mother to baby?

A
  • Placental transfer after 10-15weeks of pregnancy
  • Infection can cause death/spontaneous abortion of foetus
  • Survivors develop secondary syphilis symptoms
320
Q

How can you diagnose syphilis?

A
  • Lesions or infected lymph nodes in early syphilis
  • Dark field microscopy
  • Direct fluorescent antibody (DFA) test
  • NAAT
  • EIA (can be for IgM in early infection, or IgG at 5 weeks or both)
321
Q

Describe Haemophilus ducreyi?

A
  • Causes chancroid
  • Gram negative bacteria
  • Painful genital ulcers
  • Diagnosed by microscopy/culture
322
Q

How do you treat Chancroid STI?

A
  • Macrolide (ie. erythromycin)

- Ceftriaxone

MD3002 (15 decks)

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