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Year 2: LCRS > Human Life Cycle > Flashcards

Human Life Cycle Flashcards

1
Q

What is the definition of foetal growth?

A

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

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2
Q

What 2 components does foetal growth depend on?

A

1) Genetic potential
- derived from both parents
- mediated through growth factors e.g. insulin like growth factors
2) Substrate supply
- essential to achieve genetic potential
- derived from placenta which is dependent upon both uterine and placental vascularity

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3
Q

What 3 phases in normal foetal growth characterised by?

A

1) Cellular hyperplasia
2) Hyperplasia and hypertrophy
3) Hypertrophy alone

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4
Q

What is the foetal growth velocity between 14-15 weeks?

A

5g/day

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5
Q

What is the foetal growth velocity at 20 weeks?

A

10g/day

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6
Q

What is the foetal growth velocity at 32-35 weeks?

A

30-35g/day

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7
Q

How does the foetal growth velocity change at >34 weeks?

A

Growth rate decreases

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8
Q

What is symphysis fundal height?

A

Distance over the abdominal wall from the symphysis to the top of the uterus

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9
Q

Where is the fundal height landmark at 12 weeks?

A

Symphysis pubic

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10
Q

Where is the fundal height landmark at 20 weeks?

A

Umbilicus

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11
Q

Where is the fundal height landmark at 20-34 weeks?

A

Gestational age +/- 2 cm

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12
Q

Where is the fundal height landmark at 36-38 weeks?

A

Gestational age +/- 3 cm

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13
Q

Where is the fundal height landmark at >38 weeks?

A

Gestational age +/- 4 cm

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14
Q

For what reasons could a baby be measuring as having a small fundal height?

A
  • Wrong dates
  • Small for gestational age
  • Oligohydramnios
  • Transverse lie
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15
Q

For what reasons could a baby be measuring as having a larger fundal height?

A
  • Wrong dates
  • Molar pregnancy
  • Multiple gestation
  • Large for gestational age
  • Polyhydramnios
  • Maternal obesity
  • Fibroids
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16
Q

What are the pros and cons of symphysis fundal height?

A 
Pros:
- Simple 
- Inexpensive 
Cons:
- Low detection rate: 50-86%
- Great inter-operator variability 
- Influenced by a number of factors (BMI, foetal lie, amniotic fluid, fibroids)
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17
Q

Why is dating by last menstrual period inaccurate?

A
  • Irregular periods
  • Abnormal bleeding
  • Oral contraceptives
  • Breastfeeding
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18
Q

Why is correct dating important?

A
  • Small for gestational age or large for gestational age confusion
  • Inappropriate inductions
  • Steroids in preterm deliver
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19
Q

How should all pregnancies be dated?

A

Crown Rump Length

- EXCEPT IVF pregnancies

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20
Q

When is head circumference dating used?

A

If the first scan is done after 14 weeks (CRL>84mm)

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21
Q

Which 4 biometrical parameters assess foetal growth when using an ultrasound?

A

1) Biparietal diameter
2) Head circumference
3) Abdominal circumference
4) Femur length

Combination = Estimated foetal weight

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22
Q

How are normaltive growth curves constructed from ultrasound measurements expressed?

A

Centiles

- Used clinically to identify a normal intrauterine growth and detect risk of obstetric and neonatal complications

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23
Q

What maternal factors influence foetal growth?

A
  • Poverty
  • Age
  • Drug use
  • Weight
  • Disease (hypertensiom, diabetes, coagulopathy)
  • Smoking and nicotine
  • Alcohol
  • Diet
  • Prenatal depression
  • Environmental toxins
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24
Q

What foeto-placental factors affect foetal growth?

A
  • Genotype (genetic potential)
  • Gender (B>G)
  • Hormones
  • Previous pregnancy
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25
Q

What are the foetal hormones and from where are they secreted?

A 
Pituitary
- Somatrophin 
- Prolactin 
- FSH/LH 
Pancreas- Insulin 
Adrenals - Androgens 
Gonads- Androgens 
Thyroid- Iodothryonines
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26
Q

By which principles does the customised growth charge define individual foetal growth potential?

A

1) Adjusted to reflect maternal constitutional variation. Maternal height, weight, ethnicity, parity
2) Optimised by presenting a standard free from pathological factors such as diabetes and smoking
3) Based on foetal weight curved derived from normal pregnancies

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27
Q

What is covered in obstetric ultrasound examination?

A
  • Assessment of foetal ‘wellness’ not just size
  • Looking at trends in growth
  • Predicting foetal metabolic compromise
  • Anticipating the need to deliver prematurely
  • Liaising with neonatal services
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28
Q

When is a foetus considered small for gestational age (SGA)?

A

Birth weight

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29
Q

What is the definition of foetal growth restriction (FGR)?

A

Failure of the foetus to achieve its predetermined growth potential for various reasons

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30
Q

What is a severe SGA ( small for gestational age)

A

EFW or AC

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31
Q

What is considered a low birthweight?

A

less than 2500 g

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32
Q

What is considered a very low birthweight?

A

less than 1500 g

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33
Q

What do epidemiological studied use?

A
  • Use birth weight alone, not gestastional age
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34
Q

What is the increase in perinatal mortality in FGR babies?

A

3-10 fold increase

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35
Q

When choosing centiles, which is the most sensitive and which is the most specific?

A 
Sensitive= 10th 
Specific= 3rd
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36
Q

Why will you get a number of false positives with the tenth centile?

A

It captures all babies with FGR but will also include those babies that are just small for gestational age

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37
Q

Why will you get a number of false negatives with the third centile?

A

All babies recorded using the third centile will have FGR, but some FGR babies may be missed

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38
Q

What are the short term problems of LBW/FGR/ Prematurity?

A
  • Respiratory distress
  • Intraventricular haemorrhage (cannot fight infection)
  • Sepsis (cant fight infaction)
  • Hypoglycaemia
  • Necrotising enterocolitis
  • Jaundice
  • Electrolyte imbalance
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39
Q

What are the medium term problems of LBW/FGR/Prematurity?

A
  • Respiratory problems
  • Developmental delay ( brain damage)
  • Special needs schooling
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40
Q

How will premature babies with electrolyte imbalance appear?

A

Have thin porous skin, not fat

approx 34 weeks

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41
Q

Why would premature babies be jaundice?

A

Immature liver pathways

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42
Q

What is the long term problem with LBW/FGR/Prematurity?

A

Foetal programming

IHD, CHD, diabetes are more common due to compensatory pathways initiated due to poor growth

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43
Q

What are the differential diagnoses of smallness?

A
  • Not small at all
  • Normal small
  • Abnormal small
  • Starved small
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44
Q

What is the type of growth seen in abnormal small fetuses?

A

Symmetrical or asymmetrical

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45
Q

What is preeclampsia?

A
  • Normal pregnancy: spiral arteries that reside in the endometrium open to form a funnel which allows trophoblasts to invade the maternal vascular system
  • In preeclampsia, this doesn’t happen. The placenta is not perfused properly therefore the mother compensates by throwing blood down the arteries at higher and higher pressure. The mother therefore becomes increasingly ill whilst their is no growth in the foetus
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46
Q

What maternal medical factors are associated with FGR and SGA foetus?

A
  • Chronic hypertension
  • Connective tissue disease
  • Severe chronic infection
  • Diabetes mellitus
  • Anaemia
  • Uterine abnormalities
  • Maternal malignancy
  • Pre-ecamplsia
  • Thrombophilic defects
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47
Q

What foetal factors are associated with FGR and SGA foetus?

A
  • Multiple pregnancy
  • Structural abnormality
  • Chromosomal abnormalities
  • Intrauterine (congenital) infection
  • Inborn errors of metabolism
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48
Q

What maternal behavioural factors are associated with FGR and SGA foetus

A
  • Smoking
  • Low booking weight (35 years at delivery
  • Alcohol
  • Drugs
  • High altitude
  • Social deprivation
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49
Q

What placental factors are associated with FGR and the SGA foetus?

A
  • Impaired trophoblast invasion
  • Partial abruption or infarction
  • Chorioamnionitis
  • Placental cysts
  • Placenta praevia
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50
Q

When is the period of placentation?

A

10-12 weeks

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51
Q

What are the functions of the placenta?

A
  • Maintains immunological distance between mother and the foetus
  • Special endocrine organ: produces protein-peptides and steroid hormones and functions as a ‘transient hypothalamo-pituitary-gonadal axis’
  • Responsible for exchange of nutrients, gases and metabolic waste products between maternal and foetal circulation
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52
Q

What does preeclampsia result from?

A

A combination of impaired trophoblast differentiation and invasion during the first trimester.
Results in the failure of trophoblast cells to destroy the muscularis layer or the spiral arterioles which causes the development of a poorly perfused placenta

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53
Q

Where do spiral arteries sit in non-pregnant women?

A

Within the endometrium

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54
Q

What is seen in pre-eclampsia?

A
  • Hypertension
  • Oedema
  • Proteinuria
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55
Q

What is the definition of pre-eclampsia?

A

Gestational hypertension of at least 140/90 mmHg on two separate occasions > 4 hours apart
- Significant proteinuria of at least 300 mg in a 24- hour collection of urine, arising de novo after the 20th week of gestation in a previously normotensive woman and resolving completely by the 6th postpartum week

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56
Q

What foetuses need growth monitoring?

A

Those with bad obstetric history
- Previous maternal hypertension
- Previous FGR
- Stillbirth
- Placental abruption
Those with concerns in index pregnancy as they arise
- Abnormal serum biochemistry
- Reduced symphysis fundal height
- Maternal systemic disease e.g. hypertension, renal, coagulation
Antepartum haemorrhage
Multiple pregnancy e.g. monochorionic twins

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57
Q

Why may foetal movement counting be of value?

A

A reduction in foetal movements may precede foetal death by a day or more

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58
Q

What is the most used method for foetal movement counting?

A

Cardiff kick method

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59
Q

What is needed for women who report a reduction or absence of foetal movements?

A

Cardiotocography

and/or ultrasounds assessment of the foetus to reassure the mother and ensure foetal wellbeing

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60
Q

What is the use of the Doppler ultrasound?

A

To determine the pattern of waveforms on the umbilical artery

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61
Q

Where is the ductus venosus?

A
  • Longitudinal through upper abdomen

- Parallel, anterior to the right of the aorta

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62
Q

What is the purpose of the ductus venosus?

A
  • Receives 40% of umbilical venous flow

- Direct oxygenated blood to the left ventricle

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63
Q

Which maternal risk factors may contribute to a foetus becoming growth restricted?

A
  • Poor obstetric history
  • Primips
  • Obese
  • Afro-Carribean/ African
  • Strong family history
  • Essential hypertension
  • Diabetes/impaired glucose tolerance
  • Systemic vascular disease
  • Renal disease
  • Thrombophilias
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64
Q

What should be administered at gestations

A

Corticosteroids

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65
Q

What does the mode of delivery depend upon?

A
  • Gestation of the pregnancy
  • Condition of the pregnancy
  • State of the cervix
  • Presentation of the foetus
  • Other factors: oligohydramnios (labour may be poorly tolerated due to cord compression)
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66
Q

What stage is a blastocyte?

A

9 days

Approx 0.1cm

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67
Q

What stage is an embro?

A

5-6 weeks

Approx 1 cm

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68
Q

What stage is a foetus?

A

3 months

Approx 7cm

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69
Q

What is the concentration of oxygen in the first trimester?

A

3%

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70
Q

What occurs in the 3rd week of the first trimester?

A
  • Formation of the trilaminar disc (mesoderm)
  • CNS and somites
  • Blood vessel initiation
  • Initiated of placental villi (3mm)
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71
Q

What occurs in the 4th week of the first trimester?

A
  • Closure of the neural tube
  • Heart, face and arm initiated
  • Umbilical cord
  • Elaboration of placental villi (4mm)
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72
Q

What occurs in the 5th week of the first trimester?

A
  • Face and limbs continue

5-8mm

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73
Q

What forms in the 6th week of the first trimester?

A

Face, ears, hands, feet, liver, bladder, gut, pancreas

10-14mm

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74
Q

What forms in the 7th week of the first trimester?

A

Face, ears, hands, fingers, toes

17-22mm

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75
Q

What forms in the 8th week of the first trimester?

A

Lungs, liver, kidneys
28-30mm
- Placental elaboration continues, development of villi
- Placental endocrinology becomes dominant

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76
Q

How does foetal nutrition change at 10 weeks GA?

A

Maternal enters placental intervillous spaces

- Increase in oxygen tension to approx 8 %

77
Q

At which week is the foetus 50g?

A

12-13 weeks

78
Q

At which weeks is the foetus 1050g?

A

28-29 weeks

79
Q

At which weeks is the foetus 3000g?

A

37-40 weeks

80
Q

How does the embryo develop in week 1 (pre-implantation development)?

A 
Day 1- I cell is fertilised
Cleavage stages: 
Day 2- 2 cells to 4 cells 
Day 3- 8 cells 
Compactation and differentiation:
Day 4- Morula 
Cavitation:
Day 5- Blastocyte
81
Q

What happens on day 6 of embryonic development?

A

Attachment of blastocyst to decidualising endometrial epithelium

82
Q

What happens on day 8-9 of embryonic develoment?

A

Implantation and formation synctiotrophoblast contact with maternal tissue

83
Q

What happens of day 12- 13 of embryonic development?

A

Synctiotrophoblast invasion and contact with maternal capillaries (2mm)

84
Q

When does the foetal genome become pluripotent?

A

Day 4

85
Q

What changes occur during cell proliferation?

A
  • Changes in response to growth factors
  • Changes in receptor expression
  • May be due to changes in cell survival
  • All paracrine or autocrine regulation
86
Q

What causes movement of cells?

A

1) Chemo-attractants
- Local production
- Paracrine effects
2) Cognate receptors
- Expressed on target cells

87
Q

What causes the production and activation of proteases?

A 
Matrix metalloproteinases (MMP)
Tissue Inhibitor of metalloproteinases (TIMPs)
88
Q

How is differentiation regulated

A

Paracrine regulation

- Receptor expression which is necessary in target cells

89
Q

What controls apoptosis?

A

Paracrine factors

90
Q

What is cleft lip and palate?

A

Failure to correctly form the face

- Defects mostly in the mouth and nasal area

91
Q

How do cleft lip and palate differ?

A

Cleft lip= One side of the face or the other. Or both

Palate= Mostly central

92
Q

When do cleft lip and palate defects happen?

A

Carnegie stage 18

93
Q

How does the face form?

A

As two separate halves, they move and fuse during developments
- Cleft lip and palate reflect failures in this process

94
Q

What is spina bifida?

A

Birth defect where there is incomplete closing of the backbone and membranes around the spinal cord
CNS defect

95
Q

When does neurulation begin?

A

Week 3 post fertilisation

96
Q

When does spina bifida present as a problem?

A

Within 4 weeks of fertilisation

97
Q

What is the primary problem which causes spina bifida?

A

Failure to complete neurulation ( closure of posterior neuropore)

98
Q

What are the different types of spina bifida?

A

Occulta
Meningocele
Myelomeningocele

99
Q

What is anencephaly?

A

Absence of a major portion of the brain, skull that occurs during embryonic development

  • Female babies are affected more commonly than male
  • Folic acid shows benefit which implies similar causes to spina bifida
100
Q

How can spina bifida be prevented?

A

Give folic acid to help the closure of the neuropore

101
Q

What is the meaning of spina bifida?

A

2 spines

102
Q

What is spina bifida occulta?

A

‘Hidden’
There is a defect in the formation of the spine but the defect is modest
- Mostly internal

103
Q

What may signal spina bifida occulta on the surface of the skin?

A

A patch of hair towards the base of the spine

104
Q

What is spina bifida meningocele?

A

The membrane over the spinal column have bulged out.
The bulge mostly contains liquid- CSF, not much neural tissue
- Effects are limited

105
Q

What is spina bifida myelomeningocele

A
  • The neural tissue bulges out

- Nervous system function is deranged as is not connected to peripheral nerves

106
Q

What are the different phases in lung development?

A

Embryonic Pseudoglandular (6-16 weeks)
Canalicular (16-26 weeks)
Saccular (26 weeks-birth)
Alveolar (8 months-childhood)

107
Q

What precautions are taken to detect FGR?

A

Foetal movements count
CTG
Serial growth scans
Foetal Dopplers and liquor volume

108
Q

How do the lungs develop in weeks 3-4?

A

Simple outgrowth from the pharynx as the lung develops
Trachea starts to divide off
Tracheoesophageal septum (days 18-28)

109
Q

How do the lungs develop in weeks 5-8?

A

5 weeks) Lung buds
6 Weeks) become more elaborate with bronchi
8 Weeks) Lungs mostly formed

110
Q

What is respiratory distress syndrome?

A

When surfactant levels are low or absent

111
Q

How can production of surfactant be increased in utero?

A

By 1 injection of glucocorticoids (2-3 days)

- May be better to delay delivery in premature so glucocorticoid can have time to take effect

112
Q

What does surfactant consist of?

A 
Lipids 
Proteins 
Glycoproteins
40-45% DP-PC 
40-45% phospholipids, other PC 
5% surfactant associated proteins 
5% other proteins 
Cholesterol 
Trace components
113
Q

What is the half life, source and primary function of surfactant?

A

Half life: 5-10 hours
Source: Type II cells (pneumocytes)
Primary function: low surface tension in alveoli

114
Q

What are the layers of the bilaminar disc of the blastocyst?

A

Outer layer= Epiblast that consists of columnar cells
Inner layer= Hypoblasts that consists of cuboidal cells

  • Bilaminar disc forms 9 days post fertilisation
115
Q

What is gastrulation?

A
  • When the embryo changes from having a bilaminar disc to a trilaminar disc
  • Occurs at day 15/16 post fertilisation
  • Primitive streak on epiblast surface through which cells move
116
Q

What happens inside the embryo during gastrulation?

A
  • Epiblast proliferates and differentiates to give rise to mesoderm cells (gives rise to most tissues in our bodies)
  • Mesoderm cells replace hypoblast cells (apoptosis) and become endoderm cells
  • Proliferation, differentiation, movement and apoptosis
117
Q

What 3 layers does gastrulation result in and what are their fates as organs?

A

Ectoderm - skin, nervous system
Mesoderm - skeleton, muscle, kidney, heart, blood
Endoderm - gut, liver, lungs

118
Q

What is the notochord?

A

Tube of cells which directs the formation of the central nervous system

119
Q

What do Hox genes control?

A
  • Establish A-P axis
  • Differences in the vertebrae
  • CNS divisions
  • Pattern in the limbs
120
Q

What signal controls the activation of Hox genes?R

A

Retinoic acid

- A derivative of Vitamin A

121
Q

How do limbs develop?

A
  • Forelimb bud appears at day 27/28
  • Hindlimb bud at day 29
  • Grow out from lateral plate mesoderm rapidly under control of special signalling regions
  • Fully formed and patterned by day 56
122
Q

What regulates limb development

A 
Sonic hedgehog (Shh) 
Fibroblast-like growth factor-8
123
Q

What did thalidomide deform?

A
  • Limbs
  • Deformed eyes and hearts
  • Deformed alimentary and urinary tracts
  • Blindness and deafness
  • Used in some leprosy and cancer treatments
124
Q

What is the most rapid phase of growth?

A

Antenatal growth

- Important influences are the placenta and maternal nutrition

125
Q

What are the variables in growth?

A
  • Starting point
  • Speed of growth
  • Time over which growth occurs
126
Q

How is height velocity calculated?

A

height now - height last visit/

age now-age last visit

127
Q

What determines adult height?

A
  • Genetic contribution: parental height and inherited conditions
  • Events during growth: nutrition, illness
128
Q

What factors influence growth?

A
  • Nutrition
  • Hormones: growth hormone, thyroxine, sex steroids
  • Illnesses: inflammation
  • Drugs: steroids: etc
129
Q

What is increased growth velocity related to?

A

GH and sex steroids

Sex steroids stimulate increased GH secretion

130
Q

In what order to parts of the body stop growing?

A
  • Hands and feet stop, then long bone
  • Last growth in height is in the spine
  • Last epiphyses to fuse are in the pelvis
131
Q

How is growth hormone secretion controlled?

A
  • Controlled by somatostatin and GHRH from the hypothalamus
  • Individual pulses of secretion will return to baseline in return
  • Influenced by a range of factors including day and night, nutrition and stress
  • Secretion falls as we get older
  • Most of its action is through IGFI
132
Q

How does Insulin like growth factor I act?

A
  • Action of GH stimulates IGFI secretion in many cells of the body
  • Acts as a paracrine hormone as well as a circulating endocrine hormone
  • At least 6 different binding proteins modulate the action
133
Q

How do sex steroids stimulate growth?

A
  • Both oestrogen and testosterone stimulate growth
  • Sex steroids also stimulate GH secretion
  • Oestrogen is responsible for fusion of the epiphyses in both sexes
134
Q

What are the causes of short stature with normal patterns of growth?

A
  • Genetic (short parents)
  • Random variation
  • Low birth weight
  • Medical or nutrition problems in the neonatal period or infancy
135
Q

What are the causes of short stature with abnormal growth pattern- growing too slowly?

A
  • Chronic medical conditions
  • Hormone deficiency- GH, thyroid, IGF I
  • Skeletal abnormality
136
Q

What deficient hormone can cause short stature?

A
  • GH deficiency
  • Hypothyroidism impairs GH secretion
  • Leads to a failure to generate IGF I
137
Q

What are the consequences of GH deficiency?

A
  • Reduced growth velocity
  • GH secretion is reduced in standard tests
  • Severe deficiency will present in the first year
  • Some have normal pituitary MRIs and other pituitary hormones, or it can be associated with pituitary developmental disorders
  • Stimulation test to diagnose
138
Q

How is growth hormone deficiency treated?

A

With recombinant GH- daily injection are needed throughout growth

139
Q

What are the causes of short stature with skeletal abnormality?

A

Genetic conditions

  • Achondroplasia
  • Turner syndrome
  • Down syndrome
140
Q

What are the characteristics of Turner syndrome

A

Many girls show features

  • Webbed neck
  • Wide carrying angle of arms
  • Hypoplastic nails
141
Q

What is Turner syndrome?

A
  • Causes by absence of one complete or partial copy of the X chromosome in some or all of the cells
  • 45XO Karyotype or mosaic of this
  • Short stature with normal growth hormone
  • Ovarian failure resulting in failure to progress in puberty
142
Q

What are abnormal causes of tall stature?

A
  • Marfan syndrome and a few other syndromes

- Pituitary tumours are rare causes of tall stature

143
Q

What treatments are available for growth problems?

A
  • Treat underlying non endocrine medical problems
  • Thyroxine in hypothyroidism
  • GH in GH deficiency and some other growth disorders
  • IGF I in GH insensitivity
144
Q

What is GH treatment used for?

A
  • GH deficiency
  • Turner syndrome
  • Prader Willi syndrome
  • Short stature secondary to low birth weight
  • Short stature secondary to renal failure
  • SHOX deficiency
  • Requires daily injections throughout the growing period
145
Q

What intrauterine environment factors affect height?

A
  • Low birth weight

- Preterm delivery

146
Q

What is leptin?

A
  • Hormone secreted by fat with receptors in the hypothalamus
  • Increased fat mass correlates with increased leptin concentrations
147
Q

Alleles of what gene are associates with risk of obesity?

A

FTO

148
Q

What is Prader Willi syndrome?

A
  • Syndrome associated with development delay and poor muscle tone
  • Loss of function of a number of paternally imprinted genes on chromosome 15
  • Associated with an increased appetite
149
Q

How do patients with Prader Willi syndrome act with regards to food?

A
  • Increased interest in food and food seeking
  • Tantrums in denied food
  • Will eat without boredom and will eat raw, frozen and discarded food
  • Stealing, hiding and hoarding food
  • Risk of gastric rupture and necrosis as well as of obesity
150
Q

What are the complications and associated features of obesity?

A
  • Acanthosis nigricans
  • Impaired glucose tolerance/type 2 diabetes
  • Orthopaedic problems
  • Polycystic ovarian disease
  • Cardiovascular disease
  • Psychological problems
151
Q

What is Acanthosis nigricans?

A
  • Marker of insulin resistance

- Acanthosis nigricans means that insulin levels will be high- but no acanthosis does not mean that insulin is normal

152
Q

What are the risk factors for type 2 diabetes?

A
  • Obesity
  • Family history
  • Ethnic origins
  • PCOS
  • Low birth weight
153
Q

What is seen in polycystic ovarian disease?

A
  • High androgens, Hyperinsulinaemia, elevated LH levels
  • Amenorrhoea or irregular periods
  • Infertility
  • Hirsutism
  • Acne
  • Male pattern baldness
  • Increase risk of diabetes, hypertension, heart disease
154
Q

How can obesity be managed?

A
  • Information and education
  • Making healthy choices more available
  • Public attitudes
  • School and local initiatives
  • Changes in food manufacture and advertising
155
Q

How is obesity medically managed?

A
  • Bariatric surgery

- Psychological input, dietary advice, risk factor screening

156
Q

What are the possible investigations into short stature?

A
  • Thyroid function
  • Coeliac screen
  • Full blood count, CRP, serum iron
  • IGF 1
  • Bone age
157
Q

Why is measurement of frailty important?

A

Frailty predicts:

  • Falls
  • ED visits and hospitalisation
  • Entry into residential care
  • Death
158
Q

Why does frailty occur?

A

No single process has been identified

  • Comorbities are important, but 25% of frail have no identified chronic disease
  • Sarcopaenia (decreased muscle mass)
  • Inflammatory markers, hormones, coagulation factors are important
  • 10% to 30% of frail people are obese
159
Q

How can frailty be treated?

A
  • Improve physical functions
  • Improve nutrition
  • Ameliorate deficits
  • Treat disease
  • Improve physiological reserve
160
Q

What are the hyper-acute frailty syndromes?

A
  • Immobility
  • Falls
  • Delirium
  • Fluctuating disability
  • Incontinence
161
Q

What is the comprehensive geriatric assessment?

A

A multidimensional and usually interdisciplinary diagnostic process designed to determine a fail older person’s medical conditions, mental health, functional capacity and social circumstances.
- The purpose is to plan and carry out a holistic plan for treatment, rehabilitation, support and long term follow up.

162
Q

What are the domains of the comprehensive geriatric assessment?

A

1) Medical
- Active medical problems
- Significant past medical problems
- Surgical history
2) Functional
- Physical function
- Gait and mobility
- Sensory impairments
3) Psychosocial
- Cognitive and effective state
- Living situation/social supports
- Financial issues

163
Q

What is age associated with?

A
  • Normal ageing processes resulting in the loss of physiological reserve
  • Increasing number of co-morbidities
  • Polypharmacy
  • Problems with communication
  • Late presentation
164
Q

What does it mean when a person is ‘frail’?

A

Loss of physiological reserve that makes a person susceptible to disability from minor stresses
- Weakness, weight loss, muscle wasting, exercise, intolerance, frequent falls,, immobility, incontinence, instability of chronic diseases

165
Q

What are the possible conditions a patient may be suffering from when presenting with weakness, lethargy, confusion, agitation?

A
  • Myocardial infarction, congestive cardiac failure
  • Pneumonia, urinary tract infection, biliary disease
  • Bacteraemia
166
Q

What are the possible conditions a patient may be suffering from when presenting with fall/collapse?

A
  • Osteoarthritis, proximal myopathy, visual problem

- Stroke, atherosclerosis, heart block

167
Q

What is the Montreal Cognitive Assessment?

A
  • Precise in measuring cognitive impairment
  • Sensitive in order to detect early stages of impairment for the most common neurodegenerative conditions such as Alzheimer’s disease
  • Specific so that it would not falsely label someone who is normal as being impaired
168
Q

What is the criteria for anorexia nervosa?

A
  • Body weight at least 15% below expected
  • Avoidance of fattening foods
  • Psychopathology-morbid dread of fatness, aims for weight lower than premorbid or healthy
  • Endocrine disturbance
169
Q

What is the criteria for bulimia nervosa?

A
  • Persistent preoccupation with eating, binges
  • Weight losing behaviours
  • Purging: by vomiting, taking a laxative, diuretic or stimulant and/or excessive exercise
  • Psychopathology: morbid dread of fatness, aims for weight lower than premorbid or healthy
170
Q

What are the characteristics of pubertal development in boys?

A
  • Associated with increase increase in height and muscle development
  • Dissatisfaction related to height and musculature
  • Early maturing boys feel more attractive, more popular and relaxed
171
Q

What are the characteristics of pubertal development in girls?

A
  • Associated with increase in height and body fat
  • Ambivalent attitude to menarche (first menstruation)
  • Dissatisfaction strongly related to weight and fat
  • Puberty may lead to lower self-esteem
  • Being slim perceived as desirable
172
Q

What is the aetiology of anorexia nervosa?

A

1) Genetic
2) Puberty
- Increase in body fat
- Negative attitudes to puberty
- Late maturing girls at a lower risk of eating disorders
Personality)
- Perfectionist
- Obsessional

173
Q

What are the possible mechanisms of anorexia nervosa with regards to neuropsychology?

A

1) Distorted body image- somato-sensory cortex
2) Increased anxiety- amygdala
3) Obsessional drive- basal ganglia
4) Enhanced sense of reward- nucleus accumbens
5) Visuo-spatial deficits- parietal cortex
6) Executive impairments- frontal lobe

174
Q

What are the environmental factors which contribute to anorexia nervosa?

A

1) Family factors
- Parental negative attitudes to body fat/shape
- Maternal dieting and eating disorders
- Family interaction
2) Adverse experiences
- Sexual abuse and other adverse life events
3) Sociocultural factors
- Ethnic group
- Institutions
- Media-role unclear

175
Q

How do patients with anorexia nervosa present?

A
  • Self starvation, weight loss, abnormal growth
  • Symptoms related to self starvation e.g. nausea, abdominal distension, fainting and dizziness
  • Selective eating- fat avoidance
  • Other weight controlling strategies e.g. vomiting, exercising, laxatives
  • Low mood, irritability
  • Later: withdrawal, poor concentration, sleep disturbance
176
Q

What are the differential diagnosis of anorexia nervosa?

A

1) Physical
- Gastro-intestinal disorder e.g. Crohn’s disease
- Metabolic e.g. diabetes
- Pituitary
2) Psychiatric
- Bulimia nervosa
- Depression
- Psychosis
- Obsessive compulsive disorder (OCD)

177
Q

How is anorexia nervosa treated?

A
  • Admission for weight restoration in a minority of cases
  • Family therapy
  • Nutritional counselling
  • Cognitive behaviour therapy (CBT)
  • Treatment of persistent depression etc
178
Q

What are the principles of cognitive behavioural therapy?

A
  • Psychoeducation
  • Self-monitoring
  • Behavioural goals
  • Modify abnormal cognitions
179
Q

What are the symptoms of depression?

A
  • Persistent sadness or low mood
  • Loss of interests of pleasure (anhedonia)
  • Fatigue/low energy (anergia)
    And associated symptoms:
  • Disturbed sleep
  • Poor concentrations or indecisiveness and libido
  • Low self-condifence
  • Appetite/weight
  • Suicidal thoughts or acts
  • Agitation/slowing of movements
  • Guilt or self blame
180
Q

How is the degree of depression defined?

A

The degree of symptoms experienced

- Not depressed ( symptoms with or without psychotic symptoms)

181
Q

How does childhood depression clinically present?

A
  • Persistent and pervasive sadness
  • Anhedonia
  • Boredom or irritability that is functionally impairing
  • Relatively unresponsive to pleasurable activities, interactions and attention from other people
  • Functional impairment is an important distinguishing factor from the normal mood fluctuations of childhood
182
Q

What are the types of pre-pubertal depression?

A

Type 1:
- More common
- Presentation is with co-morbid behavioural problems, parental criminality, parental substance abuse and family discord
- No increased risk of recurrence in adult life
Type 2:
- Less common
- Highly familial with multigenerational loading for depression
- High rates of anxiety and bipolar disorder
- Recurrences of depression in adolescence and adulthood

183
Q

How does normal adolescent angst differ from the psychiatric disorder?

A
  • Normal adolescent angst involves mastering the tasks of development, physical, cognitive, social, emotional and moral changes
  • Psychiatric disorders involves symptoms of serious suffering/impairment relating to person life, family, peers and education/work
184
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
185
Q

What are the biological factors contributing to depression?

A

1) Genetics
- Family history of major affective disorders, usually depression
2) Biochemical changes
- Anime hypothesis suggests that depression results from hypo-activity of monoamine neurotransmitter reward systems

186
Q

How can puberty affect mood?

A

1) An increase in gonadal hormones can have a direct CNS effect.
Low levels of oestrogen in women is associated with
- Premenstrual syndrome
- Postnatal depression
- Post-menopausal depression
2) Change in body shape can be a negative experience
3) The timing of puberty

187
Q

How can cognitive and emotional developmental changes affect mood?

A

1) Brain development
- Prefrontal cortex: synaptic pruning, myelination, changes in grey matter (cell bodies) and white matter (axones)
2) Cognitive changes:
- Thoughts more logical, abstract, reasoning
- Alternative outcomes, consequences, ambiguity
- Ability to ruminate and ask ‘what if’
3) Establishment of identity
- Reflect on own thoughts and perspectives in relation to others
- Sense of self across time
- Reputation with peers
4) Increase intensity of mood states

188
Q

How do developments in social relationships affect mood

A

1) Family
- Relationship transformed
- Shift to autonomy and independence
- Less time with family
- Cognitive: discussion/arguments
- Question rules
2) Peers
- Spend more time and they become more important
- Romantic and sexual relationships
3) Social world
- Exposure to media stereotypes

189
Q

How is depression treated?

A

1) Mild depression
- Cognitive behavioural therapy (CBT)
- Interpersonal psychotherapy for adolescents
2) Moderate-severe depression
- Antidepressants e.g. SSRIs- FLUOXETINE
- Could be SSRI and CBT

Year 2: LCRS (8 decks)

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