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LCRS Year 2 MEGAN > Reproduction, Development and Ageing > Flashcards

Reproduction, Development and Ageing Flashcards

1
Q

What is the conceptus?

A

Everything produced from the fertilized egg

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2
Q

What causes regulation of cells during proliferation and differentiation of the developing foetus?

A

Paracrine and autocrine effect of hormones

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3
Q

How long is a normal pregnancy?

A

37-41 weeks

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4
Q

What is gastrulation? What is the result?

A

Formation of a 3-layer embryo Results in 3 germ layers - Ectoderm - Mesoderm - Endoderm

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5
Q

What is the fate of the different germ layers?

A

Endoderm: gut, liver, lungs Mesoderm: Skeleton, muscle, kidney, heart, blood Ectoderm: skin, nervous system

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6
Q

How is the CNS formed during neurulation?

A

Formed from the ectoderm Neural groove does not undergo differentiation. Cells move and fuse to form the CNS

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7
Q

When does closure of the body cavity occur?

A

Begins at 21 days Closes around 28 days

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8
Q

What development occurs in the second month PF?

A
  • Limbs develop days 28-56 - Face develops - Internal tissues develop (heart and lungs, gut) - Looks like a foetus by day 56
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9
Q

What is the difference between PF and GA

A

Gestational age: Measured from day of last period Post-fertilisation: Fertilisation occurs 2 weeks after the last day of period

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10
Q

What causes spina bifida?

A

When there is failure to complete neurulation; formation of a posterior neuropore - Usually occurs towards the bottom of the spine - Contents and location determines the outcome - Vertebrae do not form correctly about the maformation. Neural tissue directs bone formation Incidence: 1-2 per 1000 pregnancies Surgery can hep anatomical but not functional problems

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11
Q

What are the different types of spina bifida?

A

Spina bifida occulta: Vertebrae do not form correctly. Superficially there are hairs above that part of the spine Spina bifida meningocele: Pocket of CSF Spina bifida myelomeningocele: More severe; part of the neural cord contained within the pocket

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12
Q

What is the incidence of anencephaly?

A

1-8 per 10,000 births Female > male

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13
Q

How does the heart develop in utero?

A
  • Heart tubes are at the greater edge of the blastocyst. - Greater fold pushes heart tubes underneath and towards the cranial edge of the embryo - The two heart tubes fuse to form the primitive heart tube - Primitive atrium rotates around the primitive ventricle, whilst the primitive ventricle grows in size, until the atrium is sat behind the ventricle - New connection forms between right atrium and ventricle
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14
Q

What is the ductus arteriosus?

A

Connection between aorta and pulmonary artery allows blood to bypass the lungs until birth

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15
Q

What changes occur to the heart after birth?

A

Before - Deoxygenated blood from the upper body and oxygenated blood from the placenta enter the right atrium - Goes to right ventricle - Minimal blood goes to the lungs and most goes through the ductus arteriosus into the aorta - Small amount of blood returns from lungs into right atrium, into ventricle then into the aorta After - Blood into right atrium is no longer a mix of oxygenated and deoxygenated, as no oxygen from placenta - Ductus arteriosus closes so all blood from right ventricle goes to the lungs

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16
Q

How do the limbs develop?

A
  • Forelimb bud appears at day 27/28 - Hindlimb bud appears at day 29 - Grow out from lateral plate mesoderm rapidly under control of special signalling regions - Fully formed and patterned by day 56
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17
Q

What causes acondroplasia?

A

Gain of function mutation in FGFR3

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18
Q

What is Thalidomide? What effect does it have on foetal development?

A
  • A drug used ~1958-1962 to treat morning sickness - Currently used to treat leprosy and cancer - Typically caused poor development of upper limbs - In addition caused deformed eyes and heart, deformed alimentary and urinary tracts, blindness and deafness - Interferes with blood vessel development (Morning sickness peaks at 8 weeks- same time as limb development)
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19
Q

What is polydactyly?

A

Malformation of the hand causing 5 fingers and a thumb. Cells direct development of each digit, extra cell present No functional problems

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20
Q

How do the kidneys develop in utero?

A

Pronephros develops first. Precursor tissue that directs formation of the Mesonephros which connects to the cloaca. There are limited excretory functions. Early fourth week: Uretetic bud appears Sixth week: Metanephric blastema (metanephros = definitive kidney) Eighth week: Differentiating metanephric tissue ascends

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21
Q

How do the kidneys ascend?

A
  • The kidneys initially formed near the tail end of the embryo - Vascular buds from the kidneys grow toward and invade the common iliac arteries - Kidney position changes relative to: a) adrenal glands b) gonads - Rather than “drag” their blood supply with them as they ascend, the kidneys send out new and slightly more cranial branches and then induce the regression of the more caudal branches
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22
Q

What does the bladder develop from in utero?

A

Mostly endodermal, except the trigone (mesodermal) which develops from the mesonephric duct (Trigone signals filling of the bladder to the brain)

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23
Q

What are the possible outcomes if development of the kidneys goes wrong?

A
  • Renal agenesis - Abnormal shaped kidneys - Abnormal ureter - Pelvic or horseshoe-shaped kidneys - Bladder exstrophy
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24
Q

What causes renal agenesis?

A
  • Early degeneration of ureteric bud - Unilateral renal agenesis 1:1000 L>R - Bilateral - Potter’s syndrome (oligohydramnios)
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25
Q

How do the gonads develop in utero?

A
  • The gonads arise from intermediate mesoderm within the urogenital ridges of the embryo - Primordial germ cells are the precursors to all gametes - The genital ducts arise from paired mesonephric and paramesonephric ducts - The mesonephric ducts give rise to MALE genital ducts (Wolffian duct) - The paramesonephric ducts give rise to FEMALE genital ducts (Mullerian duct)
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26
Q

At what point does sexual differentiation occur in utero?

A

The gonads and reproductive tracts are indifferent up until 7 weeks of development; differentiation is determined largely by the presence or absence of SRY (on the Y chromosome) Normally: - If SRY+, then development proceeds along the male path (~7 weeks onwards) - If SRY-, then development proceeds along the female path (~9 weeks onwards) - If male is dysfunctional then female will take over

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27
Q

How does the male reproductive tract develop?

A
  • SRY expression: a gonad develops into a testis containing spermatogonia, Leydig cells and Sertoli cells - Leydig cells produce testosterone, which support growth of the mesonephric ducts (without testosterone, they regress) - Some testosterone is converted into Dihydroxytestosterone (DHT), which supports development of the prostate gland, penis, and scrotum - Sertoli cells produce anti-mullerian hormone (AMH, or mullerian inhibiting substances MIS), which induces regression of the paramesonephric ducts (absence of MIS, the paramesonephric ducts will persist)
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28
Q

What does the male genitalia differentiate from in utero?

A
  • Ureteric bud: ureter - Mesonephric ducts: rete testis, efferent ducts, epididymis, vas deferens, seminal vesicle, trigone of bladder - Urogenital sinus: bladder (except trigone), prostate gland, bulbourethral gland, urethra
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29
Q

How does the female reproductive tract develop?

A
  • In the absence of SRY, the gonad develops into an ovary with oogonia and stromal cells - Since no testosterone is produced, the mesonephric (Wolffian) ducts regress - Since there is also no AMH (MIS), the Mulleria (paramesonephric) ducts persist to give rise to the oviducts, uterus, and upper ⅓ of the vagina - The urogenital sinus contributes to the formation of the bulbourethral glands and the lower ⅔ of the vagina
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30
Q

What does the female genitalia differentiate from in utero?

A
  • Ureteric bud: ureter - Mesonephric ducts: trigone of bladder - Paramesonephric ducts: oviduct, uterus, upper ⅓ of vagina - Urogenital sinus: bladder (except trigone), bulbourethral gland, urethra, lower ⅔ of the vagina
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31
Q

What causes the decent of the testes?

A

Due to tethering of the testes to the anterior body wall by the gubernaculum. With growth and elongation of the embryo coupled with shortening of the gubernaculum, the testes are pulled through the body wall, then the inguinal canal, and finally into the scrotum

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32
Q

What are the risks associated with undescended testes?

A
  • Increased risk of cancer - Do not function normally
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33
Q

How does external genitalia form?

A
  • Male structures form under the control of testosterone - In the absence of testosterone, female structures will form
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34
Q

What is hypospadias?

A
  • Fusion of urethral folds is incomplete, so the urethra exits the penis other than at the tip. Primarily a structural complication
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35
Q

What is persistent Mullerian duct syndrome?

A
  • Occurs in genetic males with mutations in AMH/MIS or the AMH/MIS receptor - Because testosterone and DHT are produced, there are normal male external genitalia and male (Wolffian) genital ducts - Because there is no inhibition, the paramesonephric ducts persist, i.e. there is a small uterus and paired fallopian tubes - The testes may lay either in what would be the normal position for ovaries (i.e. within the broad ligament) or one or both testes may descend into the scrotum
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36
Q

What is androgen insensitivity syndrome?

A
  • Occurs in genetic males (XY) with mutations in the androgen receptor (AR) - Lack of virilisation of due to inability of AR to bind testosterone or DHT, so androgens have no effect - Relatively normal female external genitalia (no functional androgens) but undescended testes - Mesonephric ducts are rudimentary or lacking due to loss of testosterone signalling - Normal progression of MIS from Sertoli cells causes Mullerian duct regression, so no oviducts, uterus, or upper ⅓ of vagina
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37
Q

What is Congenital Adrenal Hyperplasia?

A
  • A female homologue to AIS - Genetic females with decreased of lacking 21-hydroxylase enzyme activity, essential for cortisol synthesis - Lack of cortisol feedback to pituitary causes overproduction of ACTH, and overactivity of the adrenal gland - This leads to increased production of weak androgenic hormones from the adrenal gland, which results in weak virilisation of external genitalia, some male features: - Enlarged clitoris - Partial of complete fusion of labia majora - The internal genitalia are female
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38
Q

During what time does formation of the face occur in embryogenesis?

A

Between 5 and 10 weeks

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39
Q

How does development of the lungs occur in utero?

A

Embryonic phase (~2-8 weeks) Pseudoglandular phase (~5-17 weeks) Canalicular phase (~16-27 weeks) Saccular phase (~24 weeks-birth) Alveolar phase (36 weeks-post-partum) 0-16 weeks: conducting zone: bronchi, bronchioles, terminal bronchioles 16 weeks+: transitional and respiratory zones: respiratory bronchioles, alveolar ducts, alveolar sacs Surfactant production begins at 25 weeks and increases past birth

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40
Q

What causes Respiratory Distress Syndrome?

A

Babies born prematurely, before they have produced surfactant (1% of all births) - ~100% at GA 24 weeks - ~50% at GA 26-28 weeks - ~25% at GA 30-31 weeks Can be treated with artificial surfactant or supplemental oxygen

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41
Q

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

A
  • ~40-45% DP-PC - ~40-45% other phospholipids, mainly other PC - ~5% surfactant-associated proteins - ~5% other proteins - Cholesterol - Trace components Half-life: 5-10 hours Source: Type II cells (pneumocytes) Primary function: low surface tension in alveoli
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42
Q

What are teratogens?

A

Many different factors can act as teratogens (illegal drugs, medications, radiation, infections), but they all exert their main effects in the first trimester of pregnancy

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43
Q

What can be impacted the whole way through pregnancy by teratogens?

A

CNS

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44
Q

What is labour?

A
  • Fundally dominant contractions (Starting at the top of the uterus and pushing down) - Cervical ripening and effacement (changes from rigid to soft) - Fetal membrane remodelling - Lower segment relaxation
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45
Q

What is the process of labour? What are the phases?

A

Cervical ripening and effacement (increasing) - Rigid to flexible structure - Loss of ECM - Recruitment of leukocytes (neutrophils) - Inflammatory process (prostaglandin E2, local (paracrine) change in IL-8 Co-ordinated myometrial contractions (increasing) - Fundal dominance - Increased co-ordination of contractions - Increased power of contractions - Key mediators (Prostaglandin F2α (E2) levels increased from fetal membranes; oxytocin receptor increased; contraction associated proteins) Rupture of fetal membranes - Loss of strength due to changes in amnion basement component - Inflammatory changes, leukocyte recruitment (exacerbated in preterm labour) - Increased levels and activity of MMPs - Inflammatory process in fetal membranes - Delivery of infant - Delivery of placenta - Contraction of uterus Phase 1 (many hours): Contractions, cervical changes Phase 2 (hours): Baby delivered Phase 3 (30 mins): Placenta delivered

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46
Q

What causes preterm initiation of labour?

A
  • Intrauterine infections - Intrauterine bleeding - Multiple pregnancies - Stress (maternal) - Others
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47
Q

What is the main pro-inflammatory factor associated with labour? What evidence supports this?

A

NF-𝜅B Almost all pro-labour genes have NF-𝜅B binding domain as their promoter

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48
Q

What is thought to control term labour?

A

CRH or PAF can upregulate inflammatory pathways i fetal membranes

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49
Q

What is the hypothesis for parturition?

A
  • CRH from placenta causes release of ACTH from fetal pituitary, which then acts on adrenals to stimulate release of cortisol - Cortisol stimulates the lungs to produce surfactant - PAF in surfactant stimulates IL to activate prostaglandins, which induces labour
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50
Q

What effect does progesterone have on pregnancy?

A

Progesterone is needed to sustain pregnancy - Progesterone receptor blockade: pregnancy loss - Placenta produces high levels of progesterone

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51
Q

What is development?

A

Growth, increase in understanding, acquisition of new skills and more sophisticated responses and behaviour

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52
Q

What infectious agents can affect a foetus in utero?

A

T - Toxoplasmosis O - Others (syphilis, HIV etc) R - Rubella C - Cytomegalovirus H - Herpes simplex virus

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53
Q

What are the complications associated with spina bifida cystica?

A
  • Neurogenic bowel incontinence - Neurogenic bladder incontinence - Lower limb paralysis - Fractures - Joint contractures - Developmental deformities - Learning impairment - Hydrocephalus ↔︎ meningitis
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54
Q

What are the different domains of child development?

A
  • Gross motor - Vision and fine motor - Hearing, speech and language - Social, emotional and behavioural
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55
Q

What is a limit age for development? How is it different in prematurity?

A

The age by which a child should have achieved a milestone (2 standard deviations from the mean) Must be corrected for prematurity until 2 years of age (must subtract the number of months premature from the milestone)

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56
Q

What is the development of gross motor and posture in a child?

A

Newborn - limbs flexed, symmetrical posture - marked head lag on pulling up 6-8 weeks - raises head to 45° in prone - sits without support (at 6 months with round back, at 8 months with straight back) 8-9 months - crawling 10 months - cruises around furniture 12 months - walks unsteadily - broad gait, hands apart 15 months - walks steadily

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57
Q

What are the primitive reflexes?

A
  • Stepping - Moro - Grasp - Asymmetric tonic reflex (turn babies head one way and they will extend their limbs on that side, other sides remains flexed) - Rooting (stroke next to mouth- baby will turn to face that side) They should disappear by 4-6 months
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58
Q

When are the different protective reflexes developed in childhood?

A

Downward parachute reflex: 5 months Sideward protective reflex: 6 months Forward protective reflex: 7 months Backward protective reflex: 9 months

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59
Q

What is the development of fine motor and vision in a child?

A

6 weeks - follows moving object or face by turning the head 4 months - reaches out for toys 4-6 months - palmar grasp 7 months - transfers toys from one hand to another 10 months - mature pincer grip 16-18 months - makes marks with a crayon 14 months-4 years - tower of 3 blocks (18 months) - tower of six blocks (2 years) - tower of eight or a train with four bricks (2½ years) - bridge (from a model) (3 years) - steps (after demonstration) (4 years) 2 to 5 years - line (2 years) - circle (3 years) - cross (3½ years) - square (4 years) - triangle ( 5 years - Ability to draw without seeing how it is done - Can copy 6 months earlier

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60
Q

What is the development of language and hearing in a child?

A

Newborn - startles to loud noise 3-4 months - vocalises alone or when spoken to, coos and laughs 7 months - turns to soft sounds out of sight (Manchester rattle test) 7-10 months - at 7 months, sounds used indiscriminately - at 10 months, sounds used discriminately to parents 12 months - two to three words other than ‘dada’ or ‘mama’ 18 months - 6-10 words. Shows two parts of the body 20-24 months - uses two or more words to make simple phrases 2½-3 years - talks constantly in 3-4 word sentences

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61
Q

What is the development of social, behaviour and play in a child?

A

6 weeks - smiles responsively 6-8 months - puts food in mouth 10-12 months - waves bye-bye, plays peek-a-boo 12 months - drinks from a cup with two hands 18 months - holds spoon and gets food safely to mouth 18-24 months - symbolic play* 2 years - dry by day, pulls off some clothing 2½-3 years - parallel play. Interactive play evolving. Takes turns* *Affected in autism

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62
Q

What are the concerns if a child does not meet their development milestone by the limit age in the different domains?

A

Vision and fine motor development: occipital blindness or cataracts Hearing, speech and language: If cannot join two words together- must assess hearing Social: could be autism

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63
Q

What are the different types of delay in development of a child?

A

Consonant delay: all domains affected to same extent Dissonant delay: domains affected to different extent

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64
Q

What causes cerebral palsy in children?

A

∼80% of cases antenatal - genetic syndromes and congential infection ∼10% of cases are thought to be due to hypoxic-ischaemic injury at birth ∼10% are postnatal in origin - rise in survival of extremely preterm infants meningitis / encephalitis / encephalopathy - head trauma, symptomatic hypoglycaemia, hyperbilirubinaemia

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65
Q

What is the clinical presentation of cerebral palsy?

A
  • Abnormal limb tone and/or trunk posture in infancy with delayed motor milestones may be accompanied by slowing of head growth - Feeding difficulties, with oromotor incoordination, slow feeding, gagging and vomiting - Abnormal gait once walking is achieved - Asymmetric hand function before 12 months of age - Primitive reflexes may persist and become obligatory
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66
Q

What are the types/classification of cerebral palsy?

A
  • Spastic (70% stiff) - Ataxic hypotonic (10% muscular tone is low) - Dyskinetic (10% abnormal movements) - Mixed pattern (10%)
67
Q

What other problems are associated with cerebral palsy?

A
  • Learning difficulties (∼60%) - Epilepsy (40%) - Squints (30%) - Visual impairment from errors of refraction and cortical damage (20%) - Hearing impairment (20%) - Speech and language disorders (due to hearing loss, oromotor incoordination and learning difficulties) - Behaviour disorders - Feeding problems - Joint contractures, hip subluxation, scoliosis
68
Q

What is autism spectrum disorder?

A

A neurobiological disorder: - Qualitative impairment of social interaction - Qualitative impairments in communication - Restricted, repetitive and/or stereotypes patterns of behaviour, interests and activities Boys > Girls

69
Q

What are the different classifications of a learning disability? How does it present?

A

Classified as mild, moderate (30/1000), severe (4/1000) and profound May present: - As part of a recognisable syndrome - Failure to meet milestones - Dysmorphic features with associated problems

70
Q

What are the possible causes of learning disabilities?

A
  • Chromosome disorders (30%) - Other identifiable syndromes (20%) - Cerebral palsy, infantile spasms, post-meningitis (20%) - Metabolic or degenerative diseases (<1%) - Idiopathic (25%)
71
Q

What is ADHD?

A

Attention Deficit Hyperactivity Disorder Persistent pattern (>6 months) of inattention and/or hyperactivity-impulsivity that: - interferes with functioning or development to a degree that is inconsistent with developmental level - negatively impacts directly on social and academic/occupational activites - not solely a manifestation of oppositional behaviour, defience, hostility, or failure to understand tasks or instructions - present prior to 12 years of age

72
Q

What are the developmental stages of adolescence?

A

Early adolescence: 11-14 Middle adolescence: 14-17 Late adolescence: 18-21

73
Q

What are the gender differences in puberty?

A
  • Girls grow taller earlier than boys - Girls start puberty earlier than boys - Girls are physically mature in generally, 2 years earlier
74
Q

What are the pubertal changes that occur in girls and the age at which they occur?

A

Breast budding (8-13 years) Growth of pubic hair (8-14 years) Growth spurt (9½-14½ years) First period (10-16 years) Growth of underarm hair (10½-16½ years) Change in body shape (11-15½ years) Adult breast size (12½-16½ years)

75
Q

What are the pubertal changes that occur in boys and the age at which they occur?

A

Growth of scrotum and testes (10½-17 years) Change in voice (10½-18 years) Lengthening of the penis (11-15 years) Growth of pubic hair (11-14 years) Growth spurt (12-17 years) Change in body shape (12-17 years) Growth of facial and underarm hair (13-18 years)

76
Q

What are early maturing girls and late maturing boys at higher risk of?

A
  • Depression - Substance abuse - Disruptive behaviour/delinquency - Eating disorder - Bullying
77
Q

What changes occur in the brain during adolescence?

A
  • Grey matter volumes decrease from 6 years-adolescence - Linear increase in white matter - 20 years - Developmental curves peak at: - ∼12 years: frontal and parietal lobes - ∼16 years: temporal lobes - Prefrontal cortex: increase in density of grey matter up to puberty; after puberty decrease in grey matter density - early adulthood - From puberty: increase in density of cortical white matter [connections between neurones] - Dorsolateral prefrontal cortex: late in reaching adult levels cortical thickness - Synaptogenesis followed by pruning (synapse elimination) - Axonal myelination - Fine tune prefrontal cortex and other cortical regions Cortical function becomes fine-tuned with development Brain regions associated with more basic functions such as sensory and motor processes mature first, followed by association areas involved in top-down control of behaviour
78
Q

What are Piaget’s 4 stages of cognitive development?

A

Birth-2 years SENSORIMOTOR STAGE: Infant constructs an understanding of the world by coordinating sensory experiences with physical actions 2-7 years PREOPERATIONAL STAGE: Begins to represent the world with words and images. This reflects an increased symbolic thinking 7-11 years CONCRETE OPERATIONAL STAGE: Child can now reason logically about concrete events and classify objects into different sets 11-15 through adulthood FORMAL OPERATIONAL STAGE: The adolescent reasons in more abstract idealistic and logical ways

79
Q

What is Kohlberg’s theory of moral development?

A

Level 1: Pre-conventional 1. Obedience and punishment orientated 2. Self-interest orientation Level 2: Conventional 3. Interpersonal accord and conformity 4. Authority and social-order maintaining orientation Level 3: Post-conventional 5. Social contract orientation 6- Universal ethical principles

80
Q

What are the risks associated with low self esteem?

A
  • Depression - Anxiety - Poor school performance - Social isolation - Feeling not respected
81
Q

What is Marcia’s theory of identity formation?

A

Identity diffusion: Not yet experienced crisis; no commitment to vocation/beliefs Identity foreclosure: Not yet experienced crisis; committed to goals, beliefs; largely result of choices made by others Moratorium: Individual not resolved struggle over identity actively searching to achieve identity Identity achievement: Individual experienced crisis, resolved on own terms; committed to occupation, ideology, choice of social rules

82
Q

What is a person’s identity associated with?

A

Highest: - Achievement - Moral reasoning - Career maturity - Social skills - Lower anxiety

83
Q

What are the different types of ethnic identity in cultural minorities?

A
  1. Integration Retain cultural traditions; develop and maintain relationships with mainstream culture 2. Assimilation High involvement/relationships with mainstream culture; low maintenance cultural traditions 3. Separation Retains cultural traditions, low identification mainstream culture 4. Marginalisation Low both dimensions
84
Q

What is family connectedness? What are the benefits?

A
  • Joint activities, mealtimes etc - High confiding - Parental surveillance: parents communicate with adolescent, knows where they are etc Benefits Associated with reduced risk behaviours (early/unprotected sex; drug, alcohol, cigarette consumptions, fighting). Higher adolescent self-esteem
85
Q

What is the main goal of peer development in primary school (7-11 years)?

A

Main goal: acceptance by same gender group - Stable preference for same gender friends - Loyalty built on earlier interactions

86
Q

How does peer development change from 11 to 18 years old?

A

11-13: Expect genuineness, intimacy, self-disclosure, common interests. Emergence of cliques 13-16: Friendship goals: understanding self; beginning cross-gender relationships. Development of larger groups 16-18: Expect friends to provide emotional support; increase dyadic romantic ties

87
Q

What is the difference between friendships in girls and boys during adolescence?

A

Girls: close relationships, more confiding, more brittle Boys: less intimate, less disclosing, friendships more embedded in larger circle

88
Q

What do parents and peers infuence more during adolescence?

A

Parents: - Academic choices - Job preferences - Future aspirations Peers: - Interpersonal style - Friendships selection - Fashoin/entertainment

89
Q

What are the benefits and risks associated with adolescent internet use?

A

Opportunities: - Social networking - Peer contact - Obtain information/learning - IT expertise Risks: - Illegal - Unhealthy content (self-harm/pro-anorexia) - Cyber bullying - Abuse personal information - Amount of time online/sedentary

90
Q

What factors affect school attainment and behaviour?

A

Teacher effects: - Expectancy - Positive attitude/self efficacy Classroom management: - Order/structure - Cooperative/competitive School effects: - Attainment and behaviour (e.g. truancy rates) - More inclusive school may reduce risk behviours (e.g. early teenage pregnancy)

91
Q

What are the social variables affecting attainment of 5 or more GCSEs A*-C?

A
  • Higher chance in upper social schools - Girls achieve better than boys - Ethnic variation: Chinese>Indian>White> Bangladeshi>Pakistani>Black
92
Q

What is the ICD 10 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 - May also be other weight loss behaviour
93
Q

What is the DSM 5 criteria of anorexia nervosa?

A
  • Persistant restriction of energy intake leading to significantly low body weight (expected for age, sex, development and physical health) - Either an intense fear of gaining weight or of becoming fat, or persistent behaviour that interferes with weight gain - Disturbance in the way one’s body weight/shape is experienced, undue influence of body shape and weight on self-evaluation, or persistent lack of recognition of the seriousness of the current low body weight Sub-types: - Restricting type - Binge-eating/purging type
94
Q

What is the ICD 10 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
95
Q

What is the DSM 5 criteria for bulimia nervosa?

A
  • Recurrent episodes of binge eating: - Eating in a discrete period of time (e.g. within any 2-hour period) - An amount of food that is definitely larger than most people would eat - A sense of lack of control over eating during the episode - Recurrent inappropriate compensatory behaviour to prevent weight gain: self-induced vomiting, misuse of laxatives, diuretics/other medications, fasting, or excessive exercise - The binge eating and compensatiory behaviours both occur, at least 1/week for 3 months - Self-evaluation is unduly influenced by body shape and weight - The disturbance does not occur exclusively during episodes of AN
96
Q

What are adolescent eating problems associated with?

A
  • Earlier pubertal maturation and higher body fat - Concurrent psychological problem (e.g. depression)
97
Q

What is the epidemiology of anorexia nervosa?

A

Female:Male 10:1 Onset typically teenage years Dieting More in certain subcultures e.g. ballet schools, West Europeans/North American affluent societies Uncertain importance - Social class

98
Q

What increases the risk of eating disorder in female adolescents?

A

Dieting over 6 months at: - severe level 16x - moderate level 5x greater chance of developing an eating disorder than non-dieters Psychiatric comorbidities 7x

99
Q

What is the aetiology of anorexia nervosa?

A

Genetic - heritability bay be 50% Puberty - Increase in body fat (8% mid-childhood to 22% after puberty) - Negative attitudes to puberty - Late maturing girls at lower risk of eating disorders Personality - perfectionist, obsessional Neuropsychology - Distorted body image (somato-sensory cortex) - Increased anxiety (amygdala) - Obsessional drive (basal ganglia) - Enhanced sense of reward (Nucleus accumbens) - Visuo-spatial deficits (parietal cortex) - Executive impairments (frontal lobe) - Association with Autism Spectrum Disorder - Poorer global processing → weak central coherence Family factors - Parental negative attitudes to body fat/shape - Maternal dieting and eating disorder - Family interaction Adverse experiences - Sexual abuse and other adverse life events Sociocultural factors - ethnic group - institutions - Media-role unclear

100
Q

What is the presentation of an eating disorder?

A
  • Self-starvation, weight loss, abnormal growth - Symptoms related to self starvation e.g. nausea, abdominal distention, 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
101
Q

What assessments are carried out on a patient with an eating disorder?

A
  • Family interview - Individual interview with child/adolescent - Physical examination and investigations - Data on growth
102
Q

What are the differential diagnoses for anorexia nervosa?

A

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

103
Q

What is the treatment for anorexia nervosa?

A
  • Admission for weight restoration in a minority of cases - Family therapy* - Nutritional counselling - Cognitive behaviour therapy (CBT) - Treatment of persistent depression etc *Best treatment
104
Q

What are the principles of family therapy used to treat anorexia nervosa?

A
  1. Initial focus of adolescents need to eat. Parents/carers to take charge/supervise 2. Adolescent gradually assumes more control of eating. Graded improvement in social function 3. Address other developmental/relationship/life cycle issues
105
Q

What is involved in CBT used to treat anorexia nervosa?

A
  • Psychoeducation - Self-monitoring - Behaviour goals - Modify abnormal cognitions - Context - CBT with individuals, groups, or self-help - With other treatments - Sequenced or concurrent
106
Q

What is the prognosis of anorexia nervosa?

A

Community - < half of adolescents with AN present for treatment - 50% recover after 5 years 30% weight far below average Clinic 1 year follow up - 37%recovered - 25% weight gain and amenorrhoea - 37% underweight and amenorrhoea 10-15 year follow up - 76% recovered - 30% developed binge eating within 5 years of initial assessment Mortality (e.g. at 20 year follow-up): 5-15%

107
Q

What developmental features characterise adolescence?

A

Cognitive/emotional changes - Emotional change - Reasoning - more abstract - Greater knowledge/awareness of world - Identity - of self, family, ethnicity Peers - Peer activities/confiding - Sexual relationships - Peer group influences values and behaviour (pro/anti-social) Biology - Puberty/endocrine changes - secondary sexual characteristics - Physical growth - Brain maturation Family - Challenging rules - Discipline needs reasoning - Less confiding and intimacy in parents

108
Q

What defines antisocial behaviour?

A

Defined by society

109
Q

What defines delinquency/offending?

A

Defined by the law

110
Q

What defines conduct disorder?

A

Defined by psychiatry

111
Q

What is conduct disorder?

A
  • Repetitive and persistent (>6 months) pattern of dis-social, aggressive or defiant behaviour - Frequency and severity beyond age appropriate norms - DSM 5 - impairment in everyday functioning
112
Q

What behaviours are associated with conduct disorder?

A
  • Oppositional behaviour, defiance - Tantrums - Excessive levels of fighting or bullying, assault - Cruelty to animals - Running away from home - Truancy - Stealing - Destructiveness to property - Fire-setting
113
Q

What are the effects of cyberbullying?

A
  • Does not need to be repetitive impact on victim. Single post can repeatedly injure that individual - Individuals are separated in space and time, so impact is often delayed - Anonymity and disinhibition can lead people to be more aggressive than face-to-face - Aggressors don’t receive communication from their victims that might otherwise moderate behaviour - Forms of cyber bullying evolves with the technology
114
Q

What is the epidemiology of conduct disorder?

A

Common disorder of childhood - 1 year prevalence = 3% - 2 x in London - 4% in 5-10 years; 6% in 10-15 years - Boys:Girls 2:1 Antisocial behaviour - Adolescent-limited - Life course persistent

115
Q

What is the ecological framework or aetiology of conduct disorder?

A

Individual child factors (e.g. ADHD) Family factors (e.g. inadequate parenting) School factors (e.g. poor organisation) Societal factors (e.g. socioeconomic status)

116
Q

What individual factors contribute to conduct disorder?

A
  • Genetic - Personality Callous-unemotional traits - low empathy, guilt, callousness (increases heritability from 0.3 to 0.8) - Hyperactivity/impulsivity - Physical health problems - Developmental problems - Difficulties with friends/school
117
Q

What familial factors contribute to conduct disorder?

A

Parental approach - poor supervision - inconsistent, harsh discipline - parental disharmony - persistent criticism/rejection of the child - low involvement in the child’s activities - abuse Family communication Parental personality and (mental) health

118
Q

What social and neighbourhood factors contribute to conduct disorder?

A

Schools - Poorly organised and run-down - Poor teacher satisfaction, cooperation, clarity of rules - Deviant peer groups Socio-economic class Neighbourhood - inner cities - overcrowding - high crime - high unemployment

119
Q

What is the impact of conduct disorder?

A

Affects the individual child - e.g. school exclusion, imprisonment Affects the family Affects innocent victims - long-term emotional cost - can affect functioning - Neighbourhoods blighted by antisocial behaviour Huge financial cost to society

120
Q

What is the difference in cost to society of children-28 years with conduct disorder compared to those without?

A

Conduct disorder: £70,019 No conduct disorder: £7,423

121
Q

What is the intervention for conduct disorder?

A
  • Should be targeted at major modifiable risk factors and should begin at an early age - Treat comorbidity (e.g. underlying hyperactivity, learning disabilities, depression) - Parenting programmes - Cognitive problem-solving skills training - Interventions at school - Multi-systemic therapy
122
Q

What are the key aspects of parenting programmes to treat conduct disorder?

A
  1. Play and good times together 2. Praise and recognition for good behaviour 3. Clearly expressed expectations 4. Consistent and calm consequences for misbehaviour 5. Planning ahead to avoid trouble
123
Q

What is cognitive problem-solving skills training used to treat conduct disorder?

A
  • Adolescents with conduct disorder may have distorted attributions of aggressive intentions in other people - Techniques to develop more accurate perceptions - Teaching of problem-solving skills including range of options and their conseqences
124
Q

What school interventions can treat conduct disorder?

A
  • teaching teachers management of disruptive behaviour - increasing reading ability
125
Q

What is multi-systemic therapy used as an intervention in conduct disorder?

A

Targets causes of youth anti-social behaviour Intensive package that seeks to improve: - parent-adolescent relationship - parent skills and understanding - decrease deviant peer associations - enhance school/occupational performance - develop support network for family

126
Q

What is the prognosis of conduct disorder?

A
  • 40% of 7 and 8 year olds with conduct disorder became recidivist delinquents as teenagers - Over 90% of recidivist juvenile delinquents had conduct disorder as children Predictor of: - Antisocial PD in adulthood (~50%) - Alcoholism and drug dependence - Unemployment and relationship difficulties Intergenerational transmission
127
Q

What are the symptoms of depression?

A
  • Persistent sadness or low mood; and/or - Loss of interests or pleasure (anhedonia) - Fatigue/low energy (anergia) At least 1, most days, most of the time for at least 2 weeks + associated symptoms: - Disturbed sleep ↑/↓ - Poor concentration or indecisiveness + libido - Low self-confidence - Appetite/weight ↑/↓ - Suicidal thoughts or acts - Agitation/slowing of movements - Guilt or self-blame Not depressed (<4 symptoms) Mild depression (4 symptoms) Moderate depression (5 to 6 symptoms) Severe depression (7+ symptoms, with or without psychotic symptoms - Symptoms impairing - Presenting for at least 2 weeks - Symptoms and impairment → distinguish mild, moderate and severe
128
Q

What problems are associated with depression?

A
  • Increased risk of self-harm - Association with anxiety disorders; eating disorders [females]; conduct problems - Familial aggregation (genetic and learning)
129
Q

What is the clinical presentation of childhood depression ?

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
130
Q

What are the different types of pre-pubertal depression?

A

1st: - More common presentation is with co-morbid behavioural problems, parental criminality, parental substance abuse and family discord - Course of this resembles that of children with conduct disorder - No increased risk of recurrence in adult life 2nd - Less common - Highly familial with multigenerational loading for depression - High rates of anxiety and bipolar disorder - Recurrences of depression in adolescence and adulthood

131
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 Short term - High rates of persistence and recurrence Long term - Significant continuity adolescence → adulthood - Adolescent depressive disorder - 40-70% recurrence in adult hood - 2-7x increased risk as an adult - Impairment relationships/education in adulthood
132
Q

What is the epidemiology of depression?

A

Point prevalence - Pre-pubertal = 1-2% - Adolescents = 3-8% Cumulative probability by late adolescence 10-20% Time trends: suggestions that rate of depressive disorders may be increasing over time

133
Q

What it the heritability of depression?

A

Family history of major affective disorders, usually depression

134
Q

What is the amine hypothesis of depression?

A

Suggests that depression results from hypoactivity of monoamine neurotransmitter reward systems

135
Q

What pubertal changes are associated with depression?

A

↑ gonadal hormones → low levels oestrogen in women associated with: - premenstrual syndrome - postnatal depression post-menopausal depression Change in body shape (early/late developer)

136
Q

What is the treatment for mild depression?

A
  • CBT (individual or group) - Interpersonal psychotherapy for adolescents
137
Q

What is the treatment for moderate to severe depression?

A
  • Antidepressants (e.g. SSRI’s: Fluoxetine) - Can use SSRI’s and CBT
138
Q

What is the rational for using CBT to treat depression?

A
  • Based on the theory that depressed individuals show “distortions” in their thinking and information processing - Emphasise the “negative” aspects and under-emphasise the “positive” Focus is on interrupting this cycle of: - negative thinking - depressed mood - maladaptive behaviours
139
Q

Typically what problems are targeted using interpersonal psychotherapy? What is the goal?

A

Targets: - Loss - Role disputes - Role transitions - Interpersonal skills deficits - Adjustment to a single parent family Goal - Replace conflictual, unfulfilling relationships with meaningful lower-conflict relationships

140
Q

What medication is used to treat depression?

A

SSRI (Serotonin reuptake inhibitors) - Fluoxetine

141
Q

How will the number of people over 60 years of age change from 2015 to 2050?

A

2015: 900 million (12%) 2050: 2 billion (22%) (of total world population)

142
Q

What are the two key drivers of population ageing?

A
  • Falling fertility rates - People living longer overall
143
Q

Why do people age?

A
  • Programmed ageing (shortening of telomeres) - Damage or error theories (free radicals- sources primarily mitochondria: DNA repair mechanisms less robust than nuclear ones so becomes damage, mt die, so cell dies)
144
Q

What are the different rates at which a person ages?

A
  • Chronological age - Biological age
145
Q

How can ageing be prevented?

A
  • Don’t smoke - Don’t drink a lot of alcohol - Exercise - Eat healthily
146
Q

What challenges does society face as a result of population ageing?

A
  • Outdated and ageist beliefs/assumptions - Working life/retirement balance - Medical system designed for single acute diseases - Extending healthy old age not just life expectancy - Inadequate or absent services - Lack of accessibility for people with disabilities
147
Q

What factors impact health in older age?

A
  • Genetic inheritance - Who we are (sex, ethnicity, occupation, educational attainment and wealth) - Where we live (transportation options, healthcare systems, long-term care systems) - Our health behaviour - Our access to healthcare
148
Q

What is frailty?

A

Loss of biological reserve across multiple organ systems, leading to physiological decompensation and functional decline after a stressor event

149
Q

What is frailty associated with?

A
  • Increased risk of falls - Worsening disability - Care home admission - Death
150
Q

What are the non-specific presentations in the ageing population?

A
  • Instability - Immobility - Incontinence - Intellectual impairment - Iatrogenic harm
151
Q

Why do older people take more drugs?

A
  • Comorbidities - Guidelines/QOF/NICE - Undetected non-adherence - Infrequent review - Poor communication
152
Q

What percentage of prescriptions in the ageing population are inappropriate? What is polypharmacy associated with?

A

40% - Falls - Increased length of stay - Delirium - Mortality

153
Q

What iatrogenic harm occurs in the ageing population?

A

Adverse reactions to medications Nosocomial conditions - Infections - Pressure sores - Constipation - Deconditioning - Delirium - Malnutrition - Incontinence Falls Psychological/cognitive damage

154
Q

What are the uses and outcomes of Comprehensive Geriatric Assessment?

A

In the community - Reduce admissions to institutional care - Reduce falls - Most benefit in mild or moderate frailty For frail inpatients - Reduced inpatient mortality - Reduced functional and cognitive decline - Reduced admission to institutional care

155
Q

What is involved in a Comprehensive Geriatric Assessment?

A

Multidisciplinary assessment - Medical - Functional - Social - Psychological/psychiatric Problem list Plan

156
Q

What are the normal cognitive changes in older people?

A
  • Processing speed slows - Working memory slightly reduced - Simple attention ability preserved, but reduction in divided attention - Executive functions generally reduced - No change in non-declarative memory - No change in visuospatial abilities - No overall change in language (some reduction in verbal fluency)
157
Q

What is dementia?

A

Decline in al cognitive functions, not just memory Impairment of function Progressive Degenerative Irreversible

158
Q

What are the different types of dementia?

A
  • Alzheimer’s disease - Vascular dementia - Mixed dementia - Dementia with Lewy bodies - Parkinson’s dementia - Frontotemporal dementia
159
Q

What is the difference between dementia and delirium?

A

Dementia - Chronic (months-years) - Gradual progression - No change in conscious level - Irreversible Delirium - Acute (hours-days) - Fluctuating - Main problem with alertness and attention - Usually reversible - Usually precipitated by something - People with dementia are at higher risk

160
Q

What are the different cognitive assessments?

A

Screening tests: - AMT - 4AT Diagnostic and monitoring assessments - Mini mental state examination (MMSE) - Montreal cognitive assessment (MOCA) - Addenbrooke’s Cognitive Examination (ACE)

161
Q

What are the problems with the AMT?

A
  • Very orientation focused - Orientation can be well preserved in some forms of dementia - Assumes cultural knowledge/interest (WW2 or prime minister) - Assumes numeracy - Monarch or PM could give different results - No time limit on counting back from 20 - Person recognition can be difficult in a hospital
162
Q

What are the problems with cognitive assessments?

A
  • Most assume some basic cultural knowledge - Most assume numeracy and literacy - Depression can masquerade as dementia - Ceiling effects in highly educated/intelligent - Interpret them in context
163
Q

After what Carnegie stage is the embryo considered a foetus?

A

Stage 23

164
Q

What is the length and weight of the developing foetus at the end of each trimester?

A

Trimester 1 Length: 5-8cm Weight: 50g Trimester 2 Length: 24-27cm Weight: 1050g Trimester 3 Length: 35-36cm Weight: 2100g

LCRS Year 2 MEGAN (6 decks)

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