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Year 2 LCRS RDA > All of RDA > Flashcards

All of RDA Flashcards

1
Q

Summaris the hormonal axis of the male repoductive system

A

GnRH

LH/FSH

  • LH stimmulates Testosterone production from the Leydig cells
  • FHS together with Testosterone acts on Sertori cells
    • produce Sperm from Germ cells
    • produce inhibin

Both Testosterone and Inhibin have a -ve feedback on Hypothalamus and Pituitary

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2
Q

What is the epidymis?

A

Part where Sperm Are stored before being ejeculated

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4
Q

Where does spermatogenesis occur?

What are the main cells involved?

A

It takes place in the Seminiferous tubule, cells pass from outsid to in for ripe sperm cells

  • Sertoni cells= grey
  • Leydic cells= associated
  • spermatogonia are the visible cells
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5
Q

Explain the cyclical changes in the feedback loop of the femaly reproducive system

A

Oestrogen has an

  • inhibiting role in first part of cycle
  • enhancing (+ve feedback) for mid cycle (triggers ovulation)

And Progesterone has generally

  • -ve feedback on hypothalamic Pituitary axis
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7
Q

Explain the process of male ejaculation

A

At ejaculation

  1. sperm pass from epidymis through
  2. the two Vas Deferens (which are contractile),
  3. mixed with fluid from the seminal vesicles
  4. leaves the ejaculatory duct,
  5. and passes into the urethra where it
  6. mixes with secretions from the prostate gland.
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8
Q

Summarist the circulating steroid hormonal changes and LH/FSH changes in the female cycle

A
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9
Q

Explain the changes in the endometrial lining during the menstrual cycle

A
  1. Thickening from 2-3mm to 7-16mm in first 3/4 (Etrogen only)
    1. imlantation happens at maximal thickness
  2. Menstruation (shedding of Endometrium) –> E2+ Progesterone
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10
Q

Summarist the stages of Follicuogenensis and its timing

A
  1. Primary follicle with primary oocyte starts to form
  2. Growing follicle
  3. Antral Ovum
  4. Oculation
  5. Formation of Corpus Luteum
  6. Degradation of Corpus Luteum

Happens over 3 Months! Several eggs in both ovaries

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13
Q

Which neuroendocrine system is involved in Reward and pleasure?

A

The mesolimbis dopaminergic pathway

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14
Q

Which neuroendocrine system is involved regulation of fertility and parenting?

A

Hypothalamus to pituitary

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15
Q

Explain the role of FSH in femal reproduction

A

•FSH stimulates (some) development of ovarian follicles & 17b-estradiol synthesis

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16
Q

Explain the role of LH in female reproduction

A

•LH stimulates progesterone production

+ acts on thecal cells to stimmulate androgen production (converted to oestregen by granulosa cells under influence of FSH)

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20
Q

Explain the precess of oogenesis

A
  1. 1st mitotic devison happens in utero
  2. Cell reusmes with 2nd mitotic devision when it ripenes –> 2 month before Menstrutation
  3. BUT: stops at Metaphase II at ovulation
  4. Only resume with Fertilisation!
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21
Q

Differentiate between sexual reproduction, sexual intercourse and biological sex

A

Definitions

Sexual reproduction – produce genetically different offspring.

Sexual intercourse – required for – sexual reproduction, sexual activity, sexual pleasure, human bonding.

Biological sex – identifies gender, a result of chromosomes, produces different gametes.

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24
Q

What are the changes to the penis that occur during erection?

A
  • Initiated by: increased parasympathetic activity to smooth muscle of pudendal artery
  • increase in NO
  • NO–> increases cGMP –> dilatation of arterial smooth muscle.
  • counteracts sympathetic-maintained myogenic tone
  • increases blood flow in corpus cavernosum
  • which compresses the dorsal vein, restricting the outflow of blood
  • The urethra is protected from increased pressure by surrounding corpus spongiosum (less turgid)
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25
Q

What are the Risk of pregnancies in the first trimester?

A

There is a high risk of miscarriage, often due to

  • placental abnormalities
  • chromosomal abnormalitiesof the foetus
    *
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26
Q

What are the features of the first trimestern in pregnancy for the mother?

A
  • Altered brain function [1st & later]
  • Altered emotional state [1st & laterr
  • due to: Altered hormones [1st & later]
  • Altered appetite (quantity and quality) [1st & later] – GI imbalance
  • Altered immune system [1st & later]
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27
Q

What are the main changes that happen to the mother during the 2nd trimester of pregnancy?

A
  • Altered fluid balance [2nd & later]
  • Increased blood volume [2nd & later]
  • Increased blood clotting tendency [2nd & later]
  • Decreased blood pressure [2nd]

+ all changes from 1st trimester

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28
Q

What are the main maternal changes in the 3rd trimester?

A

Increased weight [3rd]

Altered joints [3rd]

–> plus symptoms from 1st and 2nd trimester

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29
Q

Explain the differentiation and characteristics of the trimesters of pregnancy

A
  1. 0-13 Weeks
    • High risk of miscarriage
  2. 13-26 Weeks
    • (Barely) no viability if delivery before that
  3. 26-40 Weeks
    • Term, viable outside uterus
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30
Q

Summarise the hormonal changes during Pregnancy

A

Overall: very very high hormone levels

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32
Q

What are the main maternal risks of Pregnancy?

A

Generally: Low risk except delivery itself (risk of bleeding)

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33
Q

What is a conceptus?

A

Conceptus – everything resulting from the fertilised egg (baby, placenta, fetal membranes, umbilical cord)

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34
Q

What is an embryo?

A

Embryo – the baby before it is clearly human Ca. 0-9ssw

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35
Q

What is a fetus?

A

Fetus – the baby for the rest of pregnancy (clearly human and not just an embryo)

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36
Q

When does Pregnancy start?

A

Normally counted as the first day of the last menstrual cycle

  • because ovulation is difficult to determine (expecially with infrequent periods etc)

But embryologist would start at time of conception/fertilisation

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37
Q

What is the source of the high levels of progesterone in pregnancy?

A

0-8 Weeks: Corpus Luteum

After 10 Weeks: Placental produces all progesteone

–> Called: ‘luteo-placental shift’

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38
Q

Steroidogenesis: recognise pregnancy as a three-way interaction between mother, fetus and placenta with steroidogenesis as an example of this

A

The human placenta does not express the enzyme (Cytochrome P450 17A1, or CYP 17, or Cytochrome P450 17,20-lyase) that converts pregnenolone to androgens, so this part of biosynthesis takes place in the fetal adrenals (which are large and well-developed even in the first trimester). The weak androgen produced (dehydroepiandrosterone, DHEA) is sulphated as well to give DHEA-S, which is inactive. Hence a female fetus is not exposed to an androgen during development. The DHEA-S circulates to the placenta, where it is converted to 17beta-oestradiol as shown.

In human pregnancy, very high levels of oestriol are found, which are produced by a parallel mechanism (Figure 3.5), which includes hydroxylation of DHEA-S in the fetal liver to produce the precursor 16OH-DHEA-S.

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39
Q

What are the sources of the high oestrogen levels in pregnancy?

A

Early Weeks: Corpus Luteum

Then: Shift to

  1. Maternal adrenals
  2. Placenta
  3. And Fetal Adrenals/Liver
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41
Q

Explain the immunological changes durig pregnancy

A

Need to tolerate foreign Baby

  • downregulation of maternal immune system
  • HLA (almost invariant) expression on Placenta
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42
Q

What is the implication of the different counting of pregnancy (fertilisation and LMB)

A

Normally not relevant at full term but important in early development (or when deciding, whether fetus viable or not)

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43
Q

What is the main structural (and functional) unit of the placenta?

A

Cotyledons (structural SU with groovs inbetween that are filled with maternal tissue)

  • One cotyledon can have one or several villi (placental villous trees)
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44
Q

Explain the basic structure of a placental villous tree

A

Structure that allows exchange between maternal and fetal circulation

  • it has one main branch
  • with many small branches coming off again
  • complex blood supply, including arterial and venous vessels, connected to smaller capillaries in the terminal portions of each villus
    • huge surface area
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45
Q

What is the state of the placenta 9 days post fertilisation?

A

The conceptus is almost fully implanted

  • Placenta will form from Cytotrophoblast
  • Proliferate under layer of syncytiotrophoblast, which contain fluid-filled lacunae
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46
Q

What happens to placental development after implantation?

A

cytotrophoblast proliferate into the syncytium

  1. first a columnar structure is formed (cytotrophoblast column),
  2. which then undergoes branching (villous sprouts).
    1. At the centre of each villus are mesenchymal (extra-embryonic mesoderm) cells, from which the villus vascular system develops.
  3. –> Further Branching later in pregnancy
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47
Q

What is the cytotrophoblast shell?

A

Shell that is formed around the developing fetus that minimised exchange between Fetus and Mother

  • To protect fetus (e.g. from free oxygen radicals) (fetus is cery vulnerable during that time)
    • Achieved via cytotrophoblast plugs that block spiral arteries
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48
Q

What are Spiral arteries?

A

Are modulated wide, maternal arteries without SM layer or endoethelial layer but replacement with cytotrophoblast cells –> no contraction and allows constant high Blood flow to Baby

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49
Q

What is a Teratogens

A

A substance that can interfere with normal embryological development

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50
Q

What are the functions of the placenta?

A
  • Exchange
    • of nutrients (maternal to fetal) and waste products (fetal to maternal)
    • Between the vascular systems of the mother and embryo or fetus.
  • Connection (or anchorage)
    • ​to keep the fetus and the connection to maternal blood vessels intact
  • Separation
    • e.g. to not cause rejection, etc.
  • Biosynthesis
    • very active, e.g. in hormone production etc.
  • Immunoregulation
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57
Q

What is the main nutritional supply of the fetus in the first 10 Weeks of Pregnancy? How does it change after that?

A

First 10 Weeks

  • via decidual glands (hypertrophy) –> supply with glands: histotrophic nutrition

After 10 Weeks:

  • Maternal blood (haemotrophic nutrition) will supply nutrients
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58
Q

What might happen during the junction of the fetal and maternal circulation?

A

There is an increased risk of miscarriage (late first trimester) due to

  • the placenta is not fully anchored to maternal decidua but
  • the increase in pressure as it is exposed to the maternal arterial supply can detach the placenta
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59
Q

How is regulation of placental growth achieved?

A

Autocrine regluation by Placenta itself

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60
Q

What are the consequences of placental mal-development?

A
  • Miscarriage (late first trimester + 2nd trimester)
  • Pre-eclampsia (early delivery)
  • Fetal growth restriction (small infant)
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61
Q

What is Stillbirth?

A

Stillbirth refers to the death of an infant within the uterus, so that it is delivered without any signs of life

Hard to define (age wise), viability can be used as indicator (before that: miscarriage)

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62
Q

What are counted as term deliveries?

A

Deliveries between 37 and 41 Weeks of Pregnancy

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63
Q

When do post-term deliveries take place?

A

After 42 Weeks of pregnancy

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64
Q

When do pre-term deliveries take place?

How can you differentiate?

A

Pre-term= deliveries between 22-37 weeks

  • Extremely preterm
    • 22-28 weeks
  • Very preterm
    • 28-32 weeks
  • Moderate to late preterm
    • 32-36 weeks
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65
Q

What are misscarriages?

How can you distinguish between them?

A

Miscarriage: Less than 22 weeks (non viable infant delivered).

  • Early miscarriage
    • First trimester (common, often due to problems in anchoring and vascular formation)
  • Late miscarriage
    • Second trimester less than 22 weeks
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66
Q

What are the key tissues involved in Labour?

A
  • The mxometrium
  • Cervix and the
  • Fetal membranes
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67
Q

What is the clinical definition of labour?

A

Fundally dominant contractions

  • coordinated contraction of the myometrium combined with

Cervical ripening & effacement

  • change in cervical structure –> softens

Also involved:

  • Rupture of fetal membranes
  • Delivery of infant
  • Delivery of placenta
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68
Q

What is the latent stage (of labour?)

A

It is the stage about 8 weeks prior to delivery myometrial remoddeling (+ practice contractions) happen

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69
Q

What happens in the three stages of labour?

How long do they take?

A
  1. Stage 1= Contractions, cervical changes (usually rupture of fetal membranes) (variable, many hours)
  2. Stage 2= Baby delivered (hours)
  3. Stage 3= delivery of placenta (around 30 min)
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72
Q

What are factors that might trigger preterm initiation of labour?

A
  • Intrauterine infection
    • activation of inflammatory cascade (NF-kß)
  • Intrauterine bleeding
  • Multiple pregnancy
  • Stress (maternal)
  • Others
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73
Q

Which factors initiate full term labour in humans?

A

–Not really sure!!!

–Estrogens; low progesterone?; CRH?; oxytocin?

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74
Q

What happens during cervical ripening and effacement in labour?

A

It is an inflammatory change!!

  • Change from rigid to flexible structure
  • Remodelling (loss) of extracellular matrix
  • Recruitment of leukocytes (neutrophils)
  • Inflammatory process
    • Prostaglandin E2, interleukin-8
    • Local (paracrine) change in IL-8
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75
Q

Explain the key characteristics and that happen to the endometrium during labour and the most important mediators

A
  • Fundal dominance
  • Increased co-ordination and power of contractions
  • Key mediators
    • Prostaglandin F2a (E2) levels increased from fetal membranes
    • Oxytocin receptor increased
    • Contraction associated proteins
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76
Q

What is involution?

What is its significance?

A

It is tue poweful contraction of the uterus after delivery of the placenta

–> prevents mother from bleeding to death

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77
Q

What happens to the fetal membranes during labour?

What are the key mediators?

A

Also Inflammatory

  • Rupture of fetal membranes
    • Loss of strength due to changes in amnion basement component
  • Inflammatory changes, leukocyte recruitment
    • Modest in normal labour, exacerbated in preterm labour
    • Increased levels and activity of MMPs (matrix Metalloproteases)
    • PGs and interleukins
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78
Q

Explain the role of Platelet-activating factor

A

It is a fetal signal of maturity that might lead to initiation of Labour (via upregulation of inflammatory processes)

  • Part of lung surfactant
  • Produced by maturing lung, before birth
  • Increased levels before birth
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79
Q

Explain the role of CRH in labour

A

CRH up-regulate inflammatory pathways in fetal membranes via stimmulation of Progesterones and IL

  • Maternal CRH causes production of fetal corticosteroids leading to
    • +ve feedback of CRH production in the placenta
    • Production of Estrogens (leading to further modulation e.g. in oxytocin receptors)
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80
Q

Explain the role of Progesterone in labour

A

Thought to possibel initiate labour

  • High levels are needed to keep pregnancy
  • High levels of Progesterone Receptors inhibit NF-kB during pregnancy leading to
    • lower levels of inflammation
  • At term: less of Progesterone Receptors B (that are the main mediators of levels of progesterone in comparison to PR A can mediate the reponse less)
    • Activation of NF-kB
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81
Q

Which biochemical pathways of labour are affected by progesterone?

A

Via the increase expression of NF-kB

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82
Q

Explain how examination of the cervix is used to assess the progress of labour

A
  • The cervix must be 10 cm dilated and 100% effaced (thinned out) for delivery (can be felt)
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83
Q

What is the role of NF-kß in labour?

How is it activated?

A

Seems to be activated by many initiators of laborur

And is the main regulator, driver of labour

  • +ve feedback loop (causes inflammation and inflammation causes expression of NF-kß)
    *
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84
Q

What does activation of NF-kB lead to?

A

It is a Transcription factor

  • binds to promoters of pro-labour gene
    • upregulation of these genes and driving of inflammation leading to expression of
      • COX-2 (prostaglandins - PGs),
      • IL-8, IL-1b,
      • MMPs,
      • Oxytocin and PG
      • contraction-associated proteins
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85
Q

Explain the role of Platelet-activating factor

A

It is a fetal signal of maturity that might lead to initiation of Labour (via upregulation of inflammatory processes)

  • Part of lung surfactant
  • Produced by maturing lung, before birth
  • Increased levels before birth
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86
Q

Explain the role of CRH in labour

A

CRH up-regulate inflammatory pathways in fetal membranes via stimmulation of Progesterones and IL

  • Maternal CRH causes production of fetal corticosteroids leading to
    • +ve feedback of CRH production in the placenta
    • Production of Estrogens (leading to further modulation e.g. in oxytocin receptors)
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87
Q

Explain the role of Progesterone in labour

A

Thought to possibel initiate labour

  • High levels are needed to keep pregnancy
  • High levels of Progesterone Receptors inhibit NF-kB during pregnancy leading to
    • lower levels of inflammation
  • At term: less of Progesterone Receptors B (that are the main mediators of levels of progesterone in comparison to PR A can mediate the reponse less)
    • Activation of NF-kB
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88
Q

Which biochemical pathways of labour are affected by progesterone?

A

Via the increase expression of NF-kB

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89
Q

Explain how examination of the cervix is used to assess the progress of labour

A
  • The cervix must be 10 cm dilated and 100% effaced (thinned out) for delivery (can be felt)
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90
Q

What are the cellular processes that happen in embryology?

A

They overall function the exact same as other cells

Everything also happens via

  • proliferation
  • differentiation
  • reorganisation and
  • apoptosis
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91
Q

What happes during the first two month of human development?

A

Mainly lay down of all important organs

After 8 Weeks: mainly growth and elaboration of the structures that develop during the first two months

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92
Q

What happens to the fertilised egg in the Preimplantation state?

A

Preimplantation about 6 days

  1. Serious of cleavage –> Every time doubeling the cell number
  2. Egg develops into a Morula (=ball of undifferentiated cells)
  3. Differentiates so outer cells differ from inner cells
  4. Develops into a Balastocyte
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93
Q

Explain the structure of a Blastocyst

A

structure that has an

outer layer of trophectoderm (surrounded by zona pellucida)

, an inner cell mass,

and a fluid-filled cavity.

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96
Q

What is gastulation?

When does it occur?

A

14-18 days postfertilisation

which converts the bilayer of hypoblast and epiblast cells into a trilaminar embryo,

containing the three layers of Germ Cells

  • (Ectoderm,
  • Mesoderm and
  • Endoderm),
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97
Q

Explain the process of gastrolation

A
  1. Epiblast cells proliferate and differentiate to form mesoderm cells
  2. These cells move to space between hypoblast and epiblast
  3. Mesoderm Cells differentiate and replace the hyoblast cells with endoderm cells
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99
Q

When does implantation take place?

How does is happen?

A

The blastocyst seperates from outer zona pellucida and merges with the uterine lining (finished at day 10)

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100
Q

How does a Blastocyst differentate further (during implantation)?

A

The inner cell mass ot blastocyte becoms a bilayer disk, composed of

  • hypoblast and
  • epiblast cells

–> This bilayer disk gives rise to all the tissues of the human fetus

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101
Q

What is Neurolation

What is it controlled by?

A

It is formation of the Neural tube (Brain + Spinal Chord) controlled by the Notocord (in the mesoderm)

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102
Q

Explain the earyl process of neurolation

A
  1. Development of the neural plate
  2. It develops two folds
  3. They grow and meet over the neural groove
  4. to form the neural tube
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103
Q

When does the neural tube close?

A

Closing continues in Week four

  • Cranial End about 22 days
  • Rostral End about 23/24 days
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104
Q

Explain the process of embryological folding

When does this happen?

A

3-4 Weeks

  • Tissues fold laterally and fuse in the ventral midline
  • In anteroposterior direction
  • Folds the primordial germ cells (PGCs) from caudal end into hindgut and heart progenitor cells under head of embryo
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105
Q

What is the state of the embryo at the End of Week 4?

A

Precursor of all internal organs have been laid down

External structures start to develop

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107
Q

Summarist the embryological development of the limbs

A

Occurs over a number of weeks

  • Forelimb bud appears at d27/8
  • Hindlimb bud at d29
    • Grow out from lateral plate mesoderm rapidly under control of special signalling regions (+rotation etc)
    • Fully formed and patterned by d56.
  • develop further (finger differentiation)
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108
Q

What controlls the pattern of digit development?

A

By the sonic Hedgehodge SHH protein in the:

The ZPA = Zone of Polarising activity

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109
Q

Explain the use of thalidomide (historically and present) and its complications

A

Historically: was used as treatment against morning sickenss in first trimester of pregnancy –> caused many deformations (not just limbs but also more organ systems)

  • Now: As cancer treatment+ against leprosy
  • it damages developing blood vessels, thus depriving the adjacent cells of nutrients and preventing their proper growth and development –> most seen in upper limb development
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110
Q

Summarist the development of the kidneys?

A

Closly interconected with genital formation

  1. Will develop from urogenital ridge in Mesoderm at around Week 4
    1. Pronephrons
      1. Week 4
      2. in cervical region of embryo
      3. get degraded around Week 6
    2. Mesonephrons
      1. develops caudally to pronephrons
      2. Month 2
    3. Metanephrons
      1. adult type of Kidney
      2. Apperars in 5th week of kidney, fully functional at 12th week
      3. Ascent from pelvic region to abdomen

–> Sequential development and degradation of pronephrons, mesonephrons and metanephrons

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112
Q

Explain the formation of the male reproducitve system

A
  1. Primordial germ cells migrate to the genital ridge on the nephrogenic chord (intermediated mesoderm)
  2. Form gondads, attached to mesonephric duct (Wolffian)
  3. surrounded by paramesonephric duct

​Up to this point: sex is indistinguishable

Then

  1. SRY+ (on y chromosome)
  2. Maternal hCG binds to leydig cells –> induction of production of testosterone and Anti-mullerian Hormone
    1. AMH= regression of mullerian (paramesonephric) + formation of wolffian (mesonephric) system
  3. External Genitalia: Tostesterone
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113
Q

Explain the formation of the Female reproductive system

A
  1. Primordial germ cells migrate to the genital ridge on the nephrogenic chord (intermediated mesoderm)
  2. Form gondads, attached to mesonephric duct (Wolffian)
  3. surrounded by paramesonephric duct (Müllerian system)

Up to this point: indistinguishable

  • Absence of SRY- and Testosterone
  • formation of female tract of the pararmesonephric ducts and female external genitalia
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114
Q

What kind of tissues to mesoderm cells differntiate?

A

muscles, blood, skeleton, heart and kidney

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115
Q

What kind of tissues to ectoderm cells differntiate to?

A

Skin and CNS

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116
Q

Summarise the embryological development of the heart

A
  1. two heart tubes form which fuse to give rise to
  2. single heart tube (21 days post fertilisation)
  3. Complex Looping/Folding of Heart
    4.
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117
Q

Explain the fetal circulation

A

Blood recieved from umbilical chord

goes through ductus venosus into IVC

to Right atrium

can go to left atrium via foramen ovale

Ductus arteriosum connects “pulmonary artery” directly to aorta

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118
Q

What are the most common cardiac abnormalities in developmen

A

Relativly common but can be severe

  • often structual –> can be cured by surgery
  • Most important: Septal defects
  • But rare but might also occur: transposition of blood vessels
    • e.g. aorta attached to right ventricle, pulmonary artery attahced to left ventricle
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119
Q

Which tissues to endoderm differentiate to?

A

Into

  • Gut
  • Lung
  • Liver

But: Muscular and vascular tissue are generally of mesodermal origin, so tissues are normally a mixture of germ layer types (e.g. muscle in the skin and gut).

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121
Q

Summarist the process and timing of embryological facial development

A

Most structures are formes in first 5 Weeks (bilaterally!

Migrate and meet in centre (over a period of about 5 Weeks)

  • Movement thought to happen via
    1. Cleft formation and loss of tissue
    2. Filling of cleft with migrating tissue
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122
Q

Explain the formation of a cleft lip

A
  1. Usually unilateral upper lip and palate
  2. Might be bilaterally (cleft lip)
  3. Or symmetrical (palatine cleft)
    1. because of the way they come together (picture)
  4. Developmental Error about Week 10
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123
Q

Identify the five stages of lung development and Identify the changes in structure that occur in these stages.

A
  1. Embryonic
    1. Bronchi form
  2. Pseudoglandular
    1. Bronchioles and terminal bronchioles form
  3. Cannicular
    1. Respiratory bronchioles form
  4. Saccular
    1. alveolar ducts form
  5. Alveolar stage
    • alveolar sacs form
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128
Q

As overview: what happens during Month 2 of embryological develompent?

A

Mostly elaborate the tissues formed in first weeks

  • urogenital
  • cardiac
  • facial
  • lung development

+

  1. Limbs
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133
Q

Summarise the development of the gonads

A

Develop from: The gonads arise from intermediate mesoderm within the urogenital ridges of the embryo

  • The genital ducts arise from paired mesonephric and paramesonephric ducts (up to 7 Weeks: no differentiation)
  • Differential development of the male reproductive system is dependent on the activity of sex-determining region Y (SRY) protein, coded for by the SRY gene on the Y chromosome.
  • The mesonephric ducts give rise to MALE genital ducts
  • The paramesonephric ducts give rise to FEMALE genital ducts
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136
Q

What are the main causes that might lead to abnormal development of the male reproductive system?

A
  1. inability to produce Testosterone/ AMH (anti-mullerian hormone)
  2. inability of tissues to respond to the stimmuli
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137
Q

Name examples of disorders of the reproductive system

A
  1. Androgen Insensitivity Syndrome Variable phenotypes
    • genetic mutation in androgen receptor
    • external genitalia: female
    • Internal genitalia
      • mesonephric (Woolffian) ducts are rudimentary/ lacking
      • no descending of testicles
      • But: AMH normal: no female structures possible
  2. Congenital Adrenal Hyperplasia
    • enzyme deficiency (endo) of cortisol production
      • high ACTH
      • overstimmulation of adrenals
      • androgen production
    • Partial virilisation of the external genitalia
    • Internal genitalia: female
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141
Q

Explain the time and formation and risk factors of spina bifida

A

Defect in closing of neural tube (around day 21/22)

Occurs early in development

–> Many cases can be prevented with supply with folate acid

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142
Q

What is anencephaly?

When does this developmental defect originate?

A

No closure of the anterior neuropore

–> open skull and lack of part of the brain

Also at around 22 after fertilisation

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146
Q

When does surfactant production start?

What is its role in delivery and delivery of premature babies?

A

Production begins in early 3rd trimester of pregnancy and increases

  • production needed for normal lung function at birth
  • Can be accelerated by glucocorticoid injection
  • ofte therefore: preterm babies suffer from lung complications (low surfactant production)
    • might lead to Respiratory Destress syndrome
      *
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147
Q

Where is most historical data about fetal growth from?

What is used today?

A

Historically: from miscariages (but problem: often fetus that have growth restiction are more likely to die)

Now: ultrasound

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148
Q

How does fetal growth (e.g. measured crown-rump length) change during pregnancy?

A

Growth is essentially a - exponential curve

  • Very fast at first and then gets slower and slower
149
Q

How does fetal weight change during pregnancy?

A

Curve: historical data differnet from the actual numbers (because derived from miscarriages)

Actual numbers:

  • 14-15 wks: 5g /day
  • 20 wks: 10 g/day
  • 32-34 wks: 30-35g/day –> Mainly in 3rd trimester
  • >34 wks: growth rate decreases
152
Q

What is fetal growth?

A

Increase in mass that occurs between the end of embryonic period and birth

153
Q

What are the 2 components that determine fetal growth?

A

2 components

  1. Genetic potential
    1. genetics from parents
    2. (mediated through growht Factors e.g. insulin)
  2. Substrate supply
    • essential to achieve genetic potential
    • derived from placenta which is dependent upon both uterine and placental vascularity
154
Q

How is normal growth assessed once all the important parameters are assesed?

A

Via Percentiles:

  • allows normal minitoring of differnet sized that are still normal

What would be problematic: shift in percentile

155
Q

What are the three phases in normal fetal growth?

A
  1. Cellular hyperplasia (4-20W)
  2. Hyperplasia and hypertrophy (20-28 Weeks)
  3. Hypertrophy alone (28-40W)
156
Q

Explain the role and assessment of abdominal palpation and dating of pregnancies and assesment of fetal growth

A

Dating: With Symphysis fundal height (via abdnominal palpation

  • 1cm about 1 Week (+/-)
  • But: not very acurate so dating should now be perfomed on US measurements
    • limitations: wrong last menstrual period date, the baby in a transverse lie, or complications including oligohydramnios (low levels of amniotic fluid) or a baby that is small for gestational age (SGA)
157
Q

What are the differnet parameters that are used to assess fetal growth?

A

Via ultrasound measured

  • Biparietal diameter (BPD),
  • Head Circumference (HC),
  • Abdominal Circumference (AC) and Femur Length (FL)

They are combined to give the Estimated Fetal Weight (EFW).

158
Q

How shoud pregnancies be dated now?

What other measurements could also be used?

A

Now: Should be dated via Crown rump lengh

Because other ways of dating can be inaccurate

  • Last Menstrual Period: irregular periods; abnormal bleeding; oral contraceptives, breastfeeding)
160
Q

Explain the role and use of customised fetal growth charts

A

Percentile curves altered to give more accurate prediction of what is normal based on

  • fetal weight curves for normal pregnancies, free from pathological factors (e.g. smoking, diabetis)
  • adjusted maternal variation e.g. maternal height, weight, ethnicity, parity.
162
Q

What are the advantages and disadvanatges of mearuign SFH

A

Symphisis Fundal Height

Pro:

  • Simple
  • Inexpensve

Con:

  • Low detection rate: 50-86%
  • Great inter-operator variability
  • Influenced by a number of factors (BMI, fetal lie, amniotic fluid, fibroids)
164
Q

Which factors influence fetal growth?

A

There are Maternal and feto-placental factors that influence fetal growth

165
Q

What are the maternal factors that influence fetal growth?

A
  • Poverty
  • Age (healthy 16-35)
  • Drug use
    • Smoking/Nicotine
    • Alcohol
  • Diet
  • Weight
  • Disease
    • hypertension
    • diabetes
    • coagulopathy
  • Prenatal depression
  • Environmental toxins
166
Q

Which fetal factors influence fetal growth?

A

Feto-placental

  • Genotype: genetic potential
  • Gender (B>G)
  • Hormones
    • somatotrophin
    • FHS/LH
    • Insulin
    • Thyorid
    • Andorgens
  • Previous pregnancy
167
Q

Why is the correct dating of a pregnancy important?

A
  • preventing inappropriately identified as Large or Small for gestational age.
  • Right Clinical decisions about delivery timings and methods (induction or Caesarean section)
  • Decision over glucocorticoids are given prior to preterm delivery to enhance lung surfactant production and subsequent lung function.
168
Q

Explain the role of hormones in fetal growth

A

Very important in growth

  • https://medlearn.imperial.ac.uk/repro-dev-ageing-1920/session-pages/feto-placental-factors-influencing-fetal-growth/
  • Important: Cortisone, IGFI, Thytoxine,
  • GH not influence!
169
Q

What is Small for gestational Age? (SGA)?

A

he infant has a birth weight <10th centile (also called ‘Small for dates’).

170
Q

What is IntraUterine growth resticion (ICGR)?

A

Failure of the infant to achieve its predetermined (genetic) potential for a variety of reasons

171
Q

Define Low Birth weight

A

Less than 2,500g at delivery. Currently ~7% of live births (UK).

172
Q

Define Very low birth weight

A

Less than 1,500g at delivery. Currently ~1% of live births (UK).

173
Q

Define Extremetly low birht weight

A

Less than 1,000g at delivery. Currently ~0.2% of live births (UK).

174
Q

When trying to define babies with IUGR, which percintiles to you use as guidance?

A

Depending on what you want

  1. 10th centile: high sensitivity (will pick up all babies) but also many healthy
  2. 3rd centile: highly specific but will miss IUGR babies
175
Q

How can IUGR be assessed?

A

should only be used for fetuses with definite evidence that growth has altered

–> Percentile deviation from series of observations should be used!

178
Q

What are the different outcomes that might happen from IUGR

A

Widely increases change of stillbirth

  • subsequent pregnagncies might also be affected and have an increased riks
  • increased numer of complications:
    • short term
    • medium term
    • long term
179
Q

What are the short term probems of IUGR?

A
  • Respiratory distress
  • Intraventricular haemorrhage
  • Sepsis
  • Hypoglycaemia
  • Necrotising enterocolitis
  • Jaundice (when loosing weight)
  • Electrolyte imbalance
180
Q

What are the medium-term consequences of IUGR?

A
  • Respiratory problems
  • Developmental delay
  • Special needs schooling
181
Q

What are the long term problems of IUGR?

A

Fetal programming –> might still have problems in adut life

182
Q

When do IUGR ususally develop?

A

Usually in 2nd and 3rd trimester (where most growht happens)

183
Q

What are the main categories of factors that can influence IUGR

A
  1. Maternal Behaviour
  2. Maternal Medical factors
  3. Fetal factors
  4. Placental Factors
184
Q

Which maternal medical factors might lead to the developent of IUGR?

A
  • Chronic hypertension
  • Connective tissue disease
  • Severe chronic infection
  • Diabetes mellitus
  • Anaemia
  • Uterine abnormalities
  • Maternal malignancy
  • Pre-eclampsia
  • Thrombophilic defects
185
Q

What is pre-eclampsia?

What is the consequence

A

Condition that is characterised by

  • development of Maternal HTN
  • And Proteinuria
  • After 20 weeks
  • Cause unknown but
    • fibrous spiral arteries –> abnormal placenta
      • leading to inflammation –>
      • endothelial alteraltion of maternal organs leading to vasoconstriction
  • Might lead to IUGR and miscarriage, displacement of placenta
186
Q

What are maternal behavioural factors that might cause IUGR?

A
  • Smoking
  • Low booking weight (<50 kg)
  • Poor nutrition
  • Age <16 or >35 years at delivery
  • Alcohol
  • Drugs
  • High altitude
  • Social deprivation
187
Q

What are fetal factors that might lead to IUGR?

A
  • Multiple pregnancy
  • Structural abnormality
  • Chromosomal abnormalities
  • Intrauterine (congenital) infection
  • Inborn errors of metabolism
188
Q

What are placental factos that might lead to IUGR?

A
  • Impaired trophoblast invasion
  • Partial abruption or infarction
  • Chorioamnionitis
  • Placental cysts
  • Placenta praevia
189
Q

Explain the sequence of events in IUGR that might lead to Fetal Death

A
190
Q

Explain the effects of Hypoxia in the fetus

A
191
Q

What is the Ductus Venosus?

How might it be used in prediction of IUGR?

A

Longitudinal through upper abdomen
• Parallel, anterior to the right of the aorta • Receives 40% of umbilical venous flow
• Directs oxygenated blood to the L ventricle

  • Change its Doppler screening in Hypoxia/Acidosis
192
Q

Compare early vs late IUGR

A
193
Q

How is pre-eclampsia managed?

A

Very hard to treat so main aim:

  • Monitor and
  • Time the right time for delivery
    • ggf. consider corticosteroids to help development of fetus
194
Q

Which factors are monitored in pre-eclapsia and considered to time the right time for delivery?

A

Doppler assessment of Arteries

  • uterine artery
  • umbilical artery
  • fetal middle cerebral artery
  • ductus venosum
    • Are also indicators of metabolic status

Fetal movements (reduction might precede fetal death)

  • done by Cardiff Kick chart and/or
  • CTG
195
Q

Explain the sequence of events in IUGR that might lead to Fetal Death

A
196
Q

Explain the effects of Hypoxia in the fetus

A
197
Q

What is the Ductus Venosus?

How might it be used in prediction of IUGR?

A

Longitudinal through upper abdomen
• Parallel, anterior to the right of the aorta • Receives 40% of umbilical venous flow
• Directs oxygenated blood to the L ventricle

  • Change its Doppler screening in Hypoxia/Acidosis
198
Q

Compare early vs late IUGR

A
199
Q

What are common measurements taken in children to dermine growth?

A
  • head circumference
    • = indicator of brain development
  • weight
  • height/length
  • leg length
  • BMI
  • growth velocity
200
Q

Explain the generation and meaning of centile charts

A

Just mean what is average:

In 50 percentile: 50% of children will be smaller, 50% will be taller

Being in low/high centiles does not have to mean to be abnormal

201
Q

Explain how growth velocoty changes through childhood

A
  1. Very fast in early childhood
  2. Decreases and stabelises in later childhood
  3. Accelerates at puberty
202
Q

How is growth velocety calculated and expressed?

A

In cm/ year

Intervals for measurement (if you are keen) are about every 6 months

206
Q

Explain the endocrine controll of growth

Which factors influenct the secretion of that hormone?

A

Via Growth hormone that produces IGF1

  • •Pulsatile secretion

–Influenced by nutrition, sleep, exercise, stress.

207
Q

What are the different phases of growth?

A
  1. Antenatal
  2. Infancy
  3. Childhood
  4. Puberty
208
Q

When is the antenatal phase of growth?

What are the most important influencing factors?

A

Before birth- most rapid phase of brith

Influenced mainly ba maternal health and placental status

209
Q

What are the sexual differnences in growth in puberty?

A

Up to puberty: only very little difference

  • In puberty
  • Girls
    • growth spurt is at the begining of puberty
    • puberty is earlier
  • Boys
    • growth spurt is at the end of puberty
    • puberty is later
210
Q

What are the characteristics of the infancy phase of growth?

Which factors influence growth?

A
  1. Continuation of fetal growth (up to about 9-12 Month)
  2. Nutrition dependant (not hormonal)
    1. GH influence after 9-12 Months
  3. Rapid initial growth ( 23-25 cm in first year)
211
Q

What are the characteristics of the childhood phase of growth?

Which factors influence growth?

A
  • Post infancy to adolescence
  • Growth rates in boys and girls similar
  • GH/IGF-1 axis drives growth
  • Nutrition less impact (in western world where there is no starvation)
212
Q

What are the characteristics of growt in puberty?

Which factors influence growth?

A

Hormonally driven:

  • sex steroids and GH
    *
214
Q

When do you stop growing?

A

At the end of puberty (most epiphysis close)

  • final part of growth occurs in spine
  • at the pelvis
215
Q

How would you spot “abnormal” growth?

A

Low/ high percentiles don’t have to be abnormal!

  • Growth pattern is the most important thing
    • most children settle in centile by age 2 and follow it
    • A child who falls significantly in centile position is not growing normally, whatever their height
216
Q

List causes of short stature

A
  1. Genetic
  2. Pubertal and growth delay
  3. IUGR/SGA
  4. Dysmorphic syndromes
  5. Endocrine disorders
  6. Chronic paediatric disease
  7. Psychosocial depravation
217
Q

Explain how genetics and IUGR can influence short stature

A
  1. Parental height can influence short stature
    1. just having “small genes”
  2. Genetic syndromes
    1. E.g. Turners
    2. Downs
    3. Or Skeletal dyslasias (anchondroplasia)
  3. IUGR children not always catch up completely
218
Q

Why is obesity in childhood a problem?

A

It increases the risk of death and developing many comorbidities

  • Type 2 diabetes
  • Orthopaedic problems
  • Polycystic ovarian disease
  • Cardiovascular risk
  • psychological problems
  • Cancer
  • Respiratory difficulties
219
Q

Summarise the hormonal axis of Growth Hormone

A
220
Q

What is the defninition of obesity in children and adulats?

A

For adults BMI of over 25 kg/m2 is overweight and over 30 kg/m2 is obese.

Children are different! Have lower BMIs!!!

(assessed via BMI centile posistion)

221
Q

Explain endocrine problems that might lead to short stature

A

Endocrine problems

  1. hypothyroidism
  2. growth hormone deficiency
  3. steroid excess
222
Q

Explain how chronic illnesses in childhood can influence growth

A

Many reasons e.g. Inflammatory diseases

  • inflammatory mediatiors disrupt intracellular GH signaling –> reduced production of IGF1
223
Q

Which chornic pedriatric diseases can e.g. lead to short stature?

A
  1. Severe forms of
    • Asthma
    • Sickle cell
    • Cystic fibrosis
  2. Inflammatory diseases
    • Juvenile chronic arthritis
    • Inflammatory bowel disease
      • Crohns disease
      • Coeliac disease
  3. Organ failures
    • Renal failure
    • Congenital heart disease
224
Q

What are causes of tall stature?

A

tall parents

early puberty

Or rarer:

  • syndromes eg Marfans
  • growth hormone excess
228
Q

What are the causes of obesity?

A

Normally: multigenic + environmental influence

  • very rare monogenic inherited syndromes
  • normally involved in appetite regulation
    • –Leptin deficiency

–Leptin receptor deficiency

–POMC deficiency

–PC-1 deficiency

–MC4R deficiency

229
Q

What are the four domains of childhood develoment?

A
  1. Speech and Language
  2. Gross motor skills
  3. Fine Motor skills
  4. Social skills
230
Q

What are the possible patterns of abnormal development

A
  1. Slow but steady
  2. Plateau (no further development)
  3. Or regression
233
Q

Which factors influece a developmental delay?

A
234
Q

What are the different types of developmental delay?

A

They can be

  1. Global
    1. affectinv every domain of development or
  2. Specific
    1. affecting only one/several domains of development
      1. language
      2. motor
      3. social/cognitive
      4. sensual
235
Q

What does developmental progress depend on?

A

Combiation of biological and environmental influecnes

236
Q

When are developmental abnormalities in children normally picked up?

A

(i) identification of antenatal or postnatal risk factors; (ii) developmental screening; or (iii) concerns raised by parents or other healthcare professionals. Thus, these children may present at any age.

239
Q

What are possible causes of global developmental delays?

A
  • Chromosomal abnormalities
    • e.g. Down’s syndrome, Fragile X
  • Metabolic
    • e.g. hypothyroidism, inborn errors of metabolism
  • Antenatal and perinatal factors
    • Infections, drugs, toxins, anoxia, trauma, folate def
  • Environmental-social issues
  • Chronic illness
240
Q

Explain the approact to assess develpmental delays

A
  1. History taking
    1. family history
    2. birth history
    3. parental anxiety
  2. PMHX
    1. preceding milestones
    2. expected milestones for age
  3. Examination
    1. developmental assessment + general neurological examination
    2. further investigations
241
Q

What is Cerebral palsy?

A

learning difficulties, epilepsy, visual impairment, hearing loss, feeding difficulties, poor growth, and respiratory problems.

  • 0.1-0.2% incidence
  • most causes: antenatal
  • non-progressive lesion in the brain before the age of 2
242
Q

Summarise the main features and characteristics about autism spectrum disorders

A
  • Prevalence is 3-6 per 1000 live births
  • Boys>girls
  • Usually presents between 2 – 4 years of age
  • Features include
    • (1) impaired social interaction;
    • (2) speech and language disorder; and
    • (3) imposition of routines with ritualistic and repetitive behaviour.
  • Comorbidities include learning and attention difficulties, and epilepsy
243
Q

Explain the role of MDTs in abnormal develpment of children

A

Needed for

  • Assessment
  • Diagnosis and disclosure
  • Development of Management programme
  • Social support
244
Q

Summarise the main features and characteristics of ADHD

A

Attention deficit hyperactivity disorder

Diagnosted via

  • (1 )Inattention;
  • (2) Hyperactivity;
  • (3) Impulsivity;
  • (4) Lasting > 6 months;
  • (5) commencing < 7 years and inconsistent with the child’s developmental level
  1. Boys more common than girls
  2. associated with other onduct disorder, anxiety disorder & aggression
  3. Adults: are more likely to become antisocial + more criminal and ilicit drug use
245
Q

Summarise the management of ADHD

A
  • Psychotherapy – Behavioural therapies
  • Family therapy
  • Drugs – If behavioural therapy alone insufficient; stimulants, e.g. methylphenidate (Ritalin), amphetamines (dexamphetamine)
  • Diet – Some children benefit noticeably from exclusion of certain foods from their diet, e.g. red food colouring
246
Q

Summarise the main facts about lerning disabilities

A

Classified as mild, moderate, severe and profound

Prevalence: Moderate: 3%, severe 0.4%

Causes

  • 25% not identifiable
  • 30% chromosomal
  • 20% other identifiable syndromes
  • 20% postnatal cerebral insults
  • 1% metabolic/degenerative

Presentation

  • reduced intellectual functioning,
  • delay in early milestones,
  • dysmorphic features, ± associated problems (epilepsy, sensory impairment, ADHD)
247
Q

What are the main developmental warning signs?

A
  • Different patterns of develpment
    • slow but steady
    • REgression
    • Plateau
  • persistance of primitive reflexes
249
Q

What are the objectives of management of developmental delays in children?

A

Maximise mobility

Minimise discomfort

Promote speech and language

Promote social and emotional health

250
Q

What are the main milestones in gross motor develppment of children?

A
  1. Usupported sitting at 9 Month
  2. Crawling 9 Monts
  3. Walking at 1 year
251
Q

What is adolescence?

When is it?

A

phase between childhood & adulthood

  • Start: may be begining of puberty
  • end: artificially (curtural dependant) about 18 (new definition: 10-25)
252
Q

What is Adrenarche?

When and why does it start?

A

Precursor of Puberty (role is still uncertain)

  • Starts
    • Females: 6-9 years
    • Males: 7-10 years
  • Rise in adrenal 19- carbon steroid production, dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEAS).
  • Manifests clinically as the appearance of axillary and pubic hair, usually about age 8.
253
Q

What are the main physical changes in adolescence in females?

A
  • growth of pubic hair
  • growth spurt
  • menarche (first period)
  • development of breastsa
  • change in body shape
254
Q

What are the main physical changes in adolescence in males?

A
  • growth of pubic and underarm hair
  • development of testicles and penis
  • beard growth
  • growth spurt
  • Change in body shape
  • change in voice
    *
257
Q

What are the main endocrine changes associated with puberty?

A
  1. Adrenarche
    1. production of sex steroids in adrenals driven by ACTH production
  2. Pruberty
    1. sex steroid production in gonads driven by GnRH secretion
      1. increase in estrogen
      2. increase in androgens
258
Q

Explain growth patterns in girls and boys in puberty

A

Normally: Girls have growth spurt earlyer at begining of puberty

Boys have growth spurt later in puberty

259
Q

What is the normal onset of adolescence in boys and girls

A

often = begin of puberty (but might be 10-25)

  • Begining
    • Girls: 8-13
    • Boys 10-13 1/2
260
Q

Explain how and why there was a change in onset of puberty in boys and girls

A

It decreased

  • main factor thought to be: nutrition
261
Q

Explain the development mismatch hypothesis (in puberty)

A
  • There is a constant development cognitice regulation and control
  • But a fast development of dopaminergic activity and sensation seeking

–> Leads to risky behaviour due to miscalculation of risk

264
Q

Explain the Etiology of Anorexia Nervosa

A

Many factors are involved!

  • Genetics and prenatal factors (e.g. hormones) influence trait and cognigitve style. Expecially endangered if
    • obsessionality
    • perfectionalist
    • deficits in social cognition
    • inflexibility
  • Leading to dieting behaviour, weight loss, starvation, and an increase in anxiety and depression
265
Q

What are the main psychological changes in puberty?

A

Cognition e.g. morality
Identity
Increased self-awareness
Affect expression and regulation

And also

  • social changes
    *
266
Q

What are the normal social changes puberty?

A

Decrease of family and increase in importance of peer group (+wider social peer group)

  • Peers have a higher influence which can also go wrong if teenagers experience rejection
  • Teenagers also develop social role, occupatione etc.
268
Q

Explain the biological changes in the brain of teenagers

A
  1. Thickening of Cortex
  2. Thinning of cortex
    1. –> transformaiton of grey to white matter with use of neurons
269
Q

What are the main features of Anorexia Nervosa?

A
  1. Restriction of energy intake –> significantly low body weight in the context of age, sex, developmental trajectory and physical health
  2. Fear of gaining weight or becoming fat
    • does not have to be vocalised (behaviour is enough)
  3. Lack of recognition of low body weight and disturbane in shape/weight perception
271
Q

What is the aetiology of depressions in adulthood?

A
272
Q

Explain the outcome and treatment for anorexia nervosa

A
  • 80% recover after 5 years
  • 20% chronic type
  • High mortality rate: 5-10% of which 1 in 5 is suicide
  • Treatment
    • Family intervention
    • For abnormal eating attitudes and depression: cognitive behavioural therapy.
    • Small % need admission for weight restoration
273
Q

Summarise the range of mood dirsorders in adolescence

A
  1. Depression
    1. Low mood/sadness
    2. Loss of enjoyment (anhedonia)
    3. Loss of energy
      1. Seen in
        * changes to appetite, sleep, concentration, libido, self esteem etc.
  2. Many Subtypes
    1. repressive episode (only once) vs recurrent depression
    2. bipolar depression
    3. Psychotic depression, Atypical depression, Seasonal affective disorder (SAD), Inflammatory subtype
274
Q

What are the associated problems with depression in adolescence?

A
  • Increased risk of self-harm
  • Association with anxiety disorders; eating disorders [females];conduct problems; substance misuse
  • Familial aggregation (genetic and learning)
275
Q

What are the two types of pre-pubertal depression?

A
  1. No recurrent risk in adult life
    • common to present with co-morbit behavioural problems
    • no familar connection
  2. Risk of Recurrence in adult life
    • less common
    • highly familiar pattern
    • high rates of anxiety and bipolar disorders
276
Q

What is adolescent depressive disorder?

A
  • Irritability instead of sadness/low mood Especially in boys
  • Somatic complaints and social withdrawal are common
  • Psychotic symptoms rare before mid-adolescence
277
Q

What are the different types of adolescent depressive disorder?

A

Defined by time-frame

  • short term
    • High rates of persistence and recurrence (20% in 1 yr)
  • long term
    • Significant continuity to adolescence and adulthood (40-70%)
      • Impairment relationships/education in adulthood
279
Q

Summarise the treatment plan for depression

A
  • Mild depression
    • Cognitive behavioural therapy [Individual or group]
    • Interpersonal psychotherapy for adolescents
    • Brief Psychosocial Intervention
  • Moderate-Severe Depression
    • Antidepressants e.g. SSRI’s: fluoxetine • Could be SSRI + CBT
    • Combined treatment–> highest rate of symptomatic remission in 37% combined vs 20% fluoxetine alone (March et al., 2004)
280
Q

What are possible causes for depression?

A
  • Familial aggregation; genetic factors known
  • Effects of family interaction e.g. criticism
  • Life events, adversities
    • physical closeness
    • peers, rejection, bullying
    • exams
  • Endocrine disorders
281
Q

What are other terms for conduct disorders?

A

Persistent failure to control behaviour appropriately within socially defined rules.

  • antisocial behaviour
  • offending
282
Q

Name some examples of signs of conduct disorders

A
  • Oppositional behaviour, defiance
  • Tantrums
  • Excessive levels of fighting or bullying, assault Running away from home
  • Truancy
  • Cruelty to animals
  • Stealing
  • Destructiveness to property
  • Fire-setting
283
Q

What are the developmental factors that have to be taken into consideration in a child with conduct disorders?

A
  • Changes in family relationships – less direct surveillance, physical closeness, joint activities
  • Peers – increased involvement with peers; may amplify antisocial behavior
  • Experimentation and risk taking – rule violation, drugs & alcohol, petty offending frequent.
284
Q

Summarise the epidemiology of conduct disorders

A
  • 4% at ages 5-10 years; 6% at ages 10-15 years; overall 5% at ages 5-15 years.
  • Higher in deprived inner-city areas
  • Boys: girls 3:1
  • Age of onset may vary

Associated with

  • Larger family size
  • lower socio-economic status
285
Q

Summarise the possible cuases for conduct disorders

A
  • Genetic – weak
  • Child – difficult temperament
  • Environment:
    • Family
      • poor parenting, discord, lack warmth, inconsistent discipline, coercive interaction, aggression
    • Wider environment
      • poor schools
      • neighbourhoods
286
Q

What are the outcomes of Conduct disorders?

A
  • poorer outcome with more problems in child, and family
  • Risk of antisocial personality disorder in males
  • Range of emotional and personality disorders in females
287
Q

How can someonw interve in a child/ teenager with conduct disorder?

A
  • For child – problem solving skills.
  • Parent training
  • Family intervention
  • Address problems across contexts e.g. in school
288
Q

What is Ageing?

A

Ageing is the process of growing older

It has 3 different main domains:

  • Biological
  • Psychological/cognitive
  • Social
289
Q

What is Life expectancy?

A

Life expectancy is a statistical measure of how long a person can expect to live

290
Q

Why did life expectancy increase in the past 100 years

A

Many factory but mainly

  1. better public health (sanitation, hygene etc) but also:
    1. better nutrition
    2. less violence
    3. adnancaes in medicine and
    4. better education
291
Q

How does the nature of the ageing population changes?

A
  • Increasing numbers of BAME (black asian, minority ethnicity) older people
  • Increasing education of older people
  • Reduction in poverty
  • More people are working for longer
  • More complex/nuanced retirement process
292
Q

What are the two main groups of Ageing theories?

A
  1. Programmed ageing
  2. Damage or error theories

But:

  • no know theory/application there are no anti-ageing treatments in medicine
  • people age at different rates
293
Q

Explain the main thesis of “programmed ageing” theory

A

Aged because it is programmed in DNA

  • e.g. telomers get shorther
  • –> cells count the number they are deviding and at some point stop deviding
294
Q

Explain the “Damage of error theories” as a rationale behind ageing

A

In theory: could live forever but cells get damage appears that cause ageing

295
Q

What are the big challanges for society in a ageing population?

A
  • Working life/retirement balance - dependency ratio
  • Extending healthy old age not just life expectancy
  • Caring for older people, the sandwich generation
  • Outdated and ageist beliefs/assumptions
  • Medical system designed for single acute diseases
296
Q

Explain the role of the dependency ration as a challenge of ageing

A

Working life/retirement balance - dependency ratio

  • number of depemdance of people in society (older people in pansion and children)
  • vs number of people that work
    • being able to pay pansion to people!
297
Q

Explain the role of extending healthy old age not just life expectancy in a challange of ageing

A

Extending healthy old age not just life expectancy

  • aim: to reduce disease time and increase life expectancy
    • but currently: mainly life expectancy went up but disease free time did not
299
Q

Which factors influence health and (disease free) life expectancy?

A
  • where we live (e.g. pollution)
  • genetic
  • health behaviour
  • access to healthcare
  • who we are (gender etc.)
300
Q

Explain the challenge of Caring for older people, the sandwich generation

A

3% of over 65 live in a carehome

  • is expensive for working “sandwich” generation
    • caring for an older relative
    • whilst bringing up children
  • not paied by government for vast majority of people
  • leading to
    • decreased workforce and
    • underpaied workers, delayed and worse care
301
Q

Explain the consequences of the increased age on the healthcare system

A
  • Increasing demand for primary, secondary and tertiary health care
  • Increasing complexity
  • Navigating the health and social care divide
302
Q

Which factors influence Frailty?

A

It is dependant on

  • Environmental and
  • Genetic factors
  • Leading to
    • accumulative damage to cells and molecular damage (Ageing)
    • reduced physilogical reserve (in all organ systems)
      • influenced by nutritional status and exercise
303
Q

What is frailty?

A

Loss of biological reserve

  • across multiple organ systems
  • leading to vulnerability to physiological decompensation and
  • functional decline

after a stressor event

–> having decreased resources to deal with a stressor event so that a minor stressor (e.g. mild infection) have a big impact (need for care afterwards, admission to long-term care and hospital

305
Q

What does a stressor event in a fragile person lead to?

A

It leads to (more) severe response/effects like

  1. falls
  2. Delirium
  3. Fluctuating disability

Leading to

  • increased care needs
  • admission to hospital
  • admission to long-term care
306
Q

What are the characteristics of

  • mild
  • severe frailty
A
  • Mild
    • living on their own, dependant on some help
  • severe
    • dependant on others and help of others (often living in care home)
307
Q

Can frailty be prevented?

A

Yes, with lifestyle choices

  • exercise
  • nutrition
  • no smoking
  • no drinking
308
Q

Can frailty be treated?

A

Yes but it is difficult

  • Exercise
  • Nutrition
  • Drugs (possibly)

Prevention is better than cure

309
Q

What are the non-specific presentations of fraiglty?

A
  • Falls
  • Reduced mobility
  • Recurrent infections
  • Confusion
  • Weight loss
  • “Not coping”
  • Iatrogenic harm

–> Not diagnosis but syndromes that make people come into hospital

310
Q

How does presentation of a disease in old people change?

A

They are less likely to have a “textbook presentation” of symptoms but are more likely to show additional symptoms

  • ACS
    • Less likely to have chest pain
    • More Likely to have SOB
  • PE
  • Less likely to have pleuritic chest pain
  • Less likely to have haemoptysis
  • More likely to have syncope
311
Q

What is the impact of multimorbidity in age?

A

Because: conditions of conditions impact on one another

  1. directly
  2. viat the treatment of one condition
  3. Leading to
    • Worse Quality of Life, more likely to be depressed
    • Increased functional impairment
    • Burden of treatment
    • Polypharmacy
312
Q

Why do older people take more drugs?

A
  • more conditions (multimorbidity)
  • infrequent review
  • guidelines
    • only on single condition and not on multimoriditions that might be treated differently
  • undetected non-adherence
  • poor communication
313
Q

What is the result of Potentially inappropriate polypharmacy (PIP) ?

A

E.g. Long-term perscription of opioids,

  • Falls
  • Increased length of stay
  • Delirium
  • Mortality
314
Q

What is the iatrogenic harm?

A

Harm caused by the medical treatment

iatrogenic illness or death caused purposefully or by avoidable error or negligence on the healer’s part

315
Q

What are the possible effects of iaterogenic harm?

A
  • Adverse reactions to medications
  • Nosocomial conditions
    • Infections
    • Pressure sores
    • Constipation
    • Deconditioning
      • in hosptial e.g. moving too little in Hospital Bed
    • Delirium
    • Malnutrition
    • Incontinence
  • Falls
  • Psychological/cognitive damage
316
Q

Why are older people more suspectible to ADRs?

A
  • Reduced physiological reserve
  • Impaired compensation mechanisms
  • Comorbidities
  • Polypharmacy
  • Cognitive impairment
317
Q

What is a CGA?

A

Comprehensive geriatric assessment

318
Q

How is a CGA made?

A
  • It is a Multidisciplinary assessment of
    • Medical
    • Functional
    • Social
    • Psychological/psychiatric needs
  • Then: coming up with a Problem list and a
  • Treatment Plan
319
Q

What are the advantages of a CGA?

A

In the community

  • reduces hospital admissions
  • and falls
    • benefit in mild or moderate frailty

In hospital:

  • reduces mortality
  • reduced functional and cognitive decline
  • reduces hospital/care home admission
320
Q

What are the goals of Rehabilitation?

A
  • Aim is to restore or improve functionality
  • Multidisciplinary
  • Rehabilitation alongside acute illness
  • Preventing deconditioning
  • Prehabilitation
321
Q

What are the biological changes in the brain that occur with ageing?

A
  • Enlargement of the ventricles
  • loss of supporting matter + connection between neurons
    • in grey+ white matter
322
Q

What are the normally cognitive functions that decline with age?

A

Reduction of

  • cognitive speed, working memory
  • executive function e.g. probling solving abilits
  • devided attention
323
Q

Name some cognitive abilities that do not physiologically change with age?

A

No change (decline) in

  1. simple (on one thing) attention
  2. nondeclerative memory
  3. visuospatial abilities
  4. language (some reduction in verbal fluency)
324
Q

What is dementia?

A

•Decline in all cognitive functions, not just memory

  • Impairment of function
  • Progressive
  • Degenerative
  • Irreversible
325
Q

Can dementia can be prevented?

A

YES (at least lifestle has some influence)

  • stop smoking
  • exercise
  • diet
  • alcohol
326
Q

What is the AMT?

A

It is a brief assessment (10 point) of cognitive function

The Abbreviated mental test score (AMTS)

327
Q

Explain the process of testing the MOCA test

A

MOCA= Montreal Cognitive Assessment

–> normally 30 min for exam (realistically 15-20)

328
Q

What are possible screening test cognitive function?

A
  • AMT–> 10 point questions used in clinical practice
  • Clock drawing test (try the patients to show time with their fingers)
    • both used tas brief screening for cognitive impairment
  • MMSE (Minimal Mental Stater Examination) not used in clincal practice anymore
  • MOCA (Montreal Cognitive Assessment) –> has replaced MMSC as brief screening test (screening test that is a bit more detailed thatn first two)
329
Q

What are possible diagnositc test that can test cognitive function?

A
  1. Addenbrooke’s Cognitive Examination (ACE)
    1. 100 qestions, 20-50 mins
  2. Detailed neuropsychometric testing
    1. hours, done by psychology
331
Q

What are the adantages of a MOCA screeming test?

A
  • Covers a variety of domains of cognitive function
  • Brief to administer (10 mins)
  • Validated in a range of populations
  • Available in translated versions
  • Widely used –> good comparisons available
332
Q

What are the disadvantages of the MOCA test?

A
  • Education level will affect results
  • Language level will affect results
  • Floor and ceiling effects
    • with good education –> education but still dement and high score
  • Can be poorly administered (if people don’t have the training)
  • Possibly practice/coaching effects
333
Q

What are possibilities to differentiate between dementia and delirium?

A

Confusion Assessment Method (CAM)

4AT

are tools to help distinguish between delirium and dementia

334
Q

What are general problems with cognitive tests?

A

Just interpret test in the context of the patient!

  • Physical problems may limit testing
    • also hearing + seeing
    • e.g. can’t hold a pen
  • Education may limit testing
    • most need: numeracy and literacy
    • and some basic cultural knowledge
  • Depression can masquerade as dementia
  • Not valid in acute illness (acute confusion)
  • Normal cognitive changes (slower processing speed, slower reaction times) may affect administration
335
Q

What are the implications of the two main theories of ageing on treatment?

A
  1. Damage theories
    • if damage could be prevented/ repaired this could stop ageing
  2. Programmed ageing theories
    • if genetic modification
336
Q

What are the “giants of geriatric medicine”?

A

The reasons why old people come into hospital

  • immobility
  • intellectual impairment
  • instability
  • incontinence
  • iatrogenic problems.
337
Q

What are possibilities to differentiate between dementia and delirium?

A

Confusion Assessment Method (CAM)

4AT

are tools to help distinguish between delirium and dementia

Year 2 LCRS RDA (11 decks)

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