RDA Flashcards
1
Q
How man Carnegie Stages of Human Development are there?
A
1-23
2
Q
What percentage of identifiable structures of the adult body have appeared by Carnegie stage 23?
A
90 percent
3
Q
What is PF?
A
Post-fertilisation
Approx. 2 weeks less than gestational age, GA
4
Q
What is oxygen tension in the fetus and placenta in the first trimester?
A
Before week 3= 3%
By week 10 PF= 8%
5
Q
What happens in the 3rd week of pregnancy?
A
Formation of trilaminar disc (mesoderm), CNS and somites
Blood vessel initiation
Initiation of placental villi
(3mm)
6
Q
What happens in the 4th week of pregnancy?
A
Closure of neural tube Heart, face, arm initiated Umbilical cord elaboration of placental villi (4mm)
7
Q
What happens in the 5th week of pregnancy?
A
Face and limbs continue
5-8mm
8
Q
What happens in the 6th week of pregnancy?
A
Face, ears, hands, feet, liver, bladder, gut, pancreas
10-14mm
9
Q
What happens in the 7th week of pregnancy?
A
Face, ears, fingers, toes
17-22mm
10
Q
What happens in the 8th week of pregnancy?
A
Lungs, liver, kidneys
Placental elaboration continues, development of villi
Placental endocrinology becomes dominant
Cytotrophoblast plugs in spiral arteries lost over next 2 weeks
(28-30mm)
11
Q
How much does a fetus weigh by the end of week 12?
A
50g
12
Q
How much does a fetus weigh by the end of week 28?
A
1050g
13
Q
How much does a fetus weigh by the end of week 40?
A
2100g
14
Q
When does most growth in the fetus occur?
A
Mostly 2nd and 3d trimester
Before 2nd= 50g, after 3rd= 2100g
15
Q
How can you see changes in the first 4 weeks PF?
A
Microscopy
16
Q
What size is a blastocyst at 9 days?
A
0.1cm
Early stage of implantation
17
Q
What size is an embryo at 5-6 weeks?
A
1cm
Can see yolk sac (very red area= liver)
18
Q
What size is a 3 month old fetus?
A
7cm
19
Q
What is the conceptus?
A
Everything produced from fertilised egg
20
Q
When is the embryonic genome activated?
A
Between Day 2 and 3
Between 4 and 8 cells
21
Q
When do you call a fertilised egg an embryo?
A
After week 1
Expanded blastocyst has hatched
22
Q
How do cells proliferate in the embryo?
A
Changes in response to GFs
Changes in receptor expression
May be due to changes in cell survival
All paracrine or autocrine regulation (embryo doesn’t have blood vessels so can’t have endocrine processes)
23
Q
How do chemo-attractants cause movement in embryos?
A
Local production
Paracrine effects
24
Q
What are cognate receptors expressed on?
A
Target cells
25
Why are proteases and inhibitors important in movement in embryos?
Production and activation of movement
26
Why is the ECM important in movement of embryos?
Re-modelling of tissues
27
How does differentiation happen in embryo movement?
Paracrine regulation
Receptor expression (necessary in target cells)
Loss of proliferation (not necessarily)
28
What controls cell loss in an embryo? Give examples of this
Apoptosis
Controlled mainly by paracrine factors
Stops webbing between digits and loses tail
29
How do concentration effects affect regulation of cells?
Cells are exposed to different combinations of regulators
Leads to different responses
Gradients of factors important
Temporal changes in factors or responses to them
E.g. limb bud from proliferation in 3 dimensions causing finger-like projection
30
What kind of cell regulators operate on embryos?
Proliferation
Differentiation
Chemo-attraction
Can operate individual or together
31
What are main models of embryos?
```
Chicks= limb, mainly wing
Fish= eye
Mouse= KO or KI, tissue specificity
```
Gene families involved in development are same in many species
32
Give an example of genes having a similar effect in animals and in humans?
Piebaldism in mouse and boy (mutation of KIT receptor)
33
What do Hox genes do?
Establish A-P axis
Differences in the vertebrae
CNS divisions
Pattern the limbs
34
What controls Hox genes?
```
Retinoic acid (derivative of vitamin A)
Environment important (especially mothers health and diet)
```
35
Describe the bilaminar disc 9 days PF
Found within decidualising endometrium
```
(TOP TO BOTTOM)
Syncytiotrophoblast
Amnion
Bilaminar embryonic disc= epiblasts and hypoblasts
Yolk sac
Cytotrophoblast
```
36
What happens in gastrulation (day 15/16)?
Forms a 3 layer embyro
Becomes elongated
Buccopharyngeal membrane (prechordal plate) at head end
Primitive streak at other end
Surrounded by cut edge of amnion and then wall of yolk sac around
37
What is the primitive streak? What happens in gastrulation
Depression where epiblast cells are proliferating and then undergo differentiation
These then move into layer between epiblast and hypoblast
Form germ layer
Proliferation, differentiation, movement and apoptosis happen at same time
38
What happens to mesoderm cells that bump into the hypoblast (rather than forming germ layer)?
Form exoderm (possibly)
39
What are the 3 germ layers?
Ectoderm (epiblast)
Mesoderm
Endoderm (hypoblast)
40
What is the fate of the germ layers?
Endoderm-> gut, liver, lungs
Mesoderm-> skeleton, muscle, kidney, heart, blood
Ectoderm-> skin, nervous system
Very few tissues are just one type
41
What happens in neurulation?
By 21 days
Neural plate forms with notochordal process in it
Primitive streak lengthens and develops
Newly added cells to both
Oropharyngeal membrane at top
Cloacal membrane at bottom
Notochord deep to neural groove
Surrounded by neural fold which close
Somite around neural groove
42
What is the relationship between the developing umbilical cord and yolk sac?
Between 21 and 28 days= closure of body cavity
Developing umbilical cord is directly adjacent to yolk sac
Gap in body wall for this= belly button
43
What kinds of folding occur between day 17 and 28?
Head to tail folding and lateral folding
44
When does a fetus start looking human?
By day 56
45
When does CNS development begin?
Week 3
46
When does heart development begin?
Week 3
| Starts outside main embryo
47
When does limb development start?
Week 4
48
When does the urogenital system development start?
Week 3
| Link between urinary and gonadal/tubular systems linked
49
When do the lungs start to develop?
Week 3
| Continues during rest of pregnancy and after birth
50
When does face development start?
Week 4
| Throughout first trimester
51
How does the CNS develop?
22 days= fusion of tissues
Somites attach
Neural fold surrounded by otic placode, then pericardial bulge (anterior end), then amnion edge
23 days= elaboration
Anterior neuropore forms
Posterior neuropore forms
25 days
Pharyngeal arches start to form
Yolk sac develops
```
28 days
Lens
Otic placode
Pharyngeal arches develop
Limb ridges begin
Heart bulge forms
Umbilical cord forms
Closure of neuropores
```
52
What causes spina bifida?
If posterior neuropore doesn't close (failure of caudal fusion)
Should close by 28 days
Faulty neurulation
53
What happens in spina bifida?
Range of effects
Depends on type and severity
```
Neurogenic bowel/bladder incontinence
Lower limb paralysis
Fractures
Joint contractures
Developmental deformities
Learning impairment
Hydrocephalus and meningitis
```
Surgery helps anatomical, but not functional problems
54
What are the types of spina bifida?
Spina bifida occulta= doesn't go through skin, patch of hair
Meningocele= spinal cord protrudes through child's back (meninges don't)
Myelomeningocele= spinal cord and meninges protrude through child's back
55
How often do anencephaly and spina bifida occur?
```
SB= 1-2 per 1,000 pregnancies
A= 1-8 per 10,000
```
Anencephaly more severe but less common than spina bifida (particularly in female babies)
56
When should folic acid be given to avoid spina bifida and anencephaly?
Before pregnancy
Problem present within 4 weeks of fertilisation
Less sure about effects of FA on A than on SB
57
What causes anencephaly and what happens?
Literally 'lack of head'
Caused by anterior neuropore not closing (failure of rostral fusion)
Under-developed brain
Abnormally developed skull line
58
How does the heart develop?
Between week 2 and 7
Cardiogenic area with primitive blood vessels around day 18
Initial formation of the heart as a muscular tube, which can pump blood
- Heart tube fusion
- Heart tube begins to beat
A complex pattern of folding forms the basic structure of the heart (LOOPING)
- C-shaped loop and S-shaped loop
Separation into the four main chambers by septae and valves
Connection of specific arteries and veins to each chamber of the heart
- Rotation of arteries and veins (connections between precursor tissues)
- If under pressure-> bends and makes corkscrew shape
Closure of the ductus arteriosus and foramen ovale at birth convert the single-cycle flow of the fetus into a figure-of-eight loop
- Very limited blood to lung (don't need lungs until birth)
Heart tube structures seen only near head end
59
What are the main changes in the heart after birth (vs before)?
```
FETAL HEART
Open ductus arteriosus
Open foramen ovale
Minimal blood to lungs (and deoxygenated blood from lungs)
Get oxygenated blood also from placenta
```
HEART AFTER BIRTH
Closed ductus arteriosus
Closed foramen ovale
All deoxygenated blood now flows to lungs
60
How do limbs develop?
Forelimb bud appears at d27/28
Hindlimb bud appears at d29
Grow rapidly out of lateral plate mesoderm
Fully formed by d56
61
What courses Achrondroplasia?
Gain of function mutation in FGFR3
Stops switch of cartilage to bone
Bones remain short
62
What does thalidomide cause?
Interferes with blood vessel development
Variable pattern typical
More common in boys
Affects upper limbs more
Can also cause deformed eyes and hearts, deformed alimentary and urinary tracts, blindness and deafness
63
What can thalidomide be used to treat?
Leprosy and some cancer treatments
| Was used for morning sickness
64
What regulates limb development?
Sonic hedgehod (Shh)- zone of polarizing activity
Fibroblast-like growth factor-8 (Fgf8) in chick- apical ectodermal ridge
65
What is polydactyly?
Addition digits
66
How is the kidney developed?
Pronephros develops first (precursor tissue that directs formation of mesonephros)
Metanephros/permanent kidney appears by the 5th week
Develops from the metanephric mesoderm
```
Ureteric bud (outgrowth of cloaca) leads to collecting ducts of the permanent kidney
- Bud penetrates metanephric tissue and gives rise to ureter, renal pelvis, calyces and collecting tubules
```
Newly formed collecting tubule is covered at its end by a metanephric tissue cap
Kidney ascent (by end of week 9)
67
What happens in kidney ascent?
Kidneys initially form near the tail of embryo
Vascular buds from the kidneys grow toward and invade the common iliac arteries
Kidney position changes relative to adrenal glands and gonads
Kidneys then send out new cranial branches and then induce the regression of the more caudal branches
68
How is the bladder formed?
Mostly endodermal (except the trigone, mesodermal) which develops from the mesonephric duct
Trigone signals filing of the bladder to the brain
69
What happens if development of the kidneys goes wrong?
```
Renal agenesis
Abnormal shaped kidneys
Abnormal ureter
Pelvic or horseshoe shaped kidney (enlarged renal pelvis)
Bladder exstrophy
```
70
What is renal agenesis?
Early degeneration of ureteric bud
Unilateral (L more than R)
NB. bilateral= Potter's syndrome (oligohydramnios)- baby doesn't produce enough urine
71
How do gonads and other reproductive tissues developed?
Gonads arise from intermediate mesoderm within urogenital ridges of the embryo
Primordial germ cells are the precursors of all gametes
Genital ducts arise from paired mesonephric and paramesonephric ducts
- Mesonephric ducts give rise to MALE genital ducts
- Paramesonephric ducts give rise to FEMALE genital ducts
Differentiation happens after 7 weeks
72
What causes sexual differentiation?
The gonads and reproductive tracts are indifferent up until 7 weeks
Differentiation is determined largely by the presence or absence of SRY (on the Y chromosome)
```
SRY+= development proceeds along the male path (7 weeks onwards)
SRY-= development proceeds along the female path (9 weeks onwards)
```
73
How does the male reproductive tract develop?
SRY expression= gonad develops into a testic containing spermatogonia, Leydig cells and Sertoli cells
Leydig cells produce testosterone (support growth of mesonephric ducts)
Some testosterone converted to DHT which supports development of prostate gland, penis and scrotum
Sertoli cells produce anti-mullerian hormone (AMH) which induces regression of the paramesophric ducts
74
What do the following embryonic features lead to (in men)?
Ureteric bud
Mesonephric ducts
Urogenital sinus
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
75
How does the female reproductive tract develop?
In absence of SRY, gonad develops into an ovary with oogonia and stromal cells
Since no testosterone= mesonephric (Woolfian) ducts regress
No AMH so Mullerian (paramesonephric) ducts persist and give rise to oviducts, uterus and upper third of vagina
Urogenital sinus contributes to formation of bulbourethral glands and lower 2 thirds of vagina
76
What do the following embryonic features lead to (in women)?
Ureteric bud
Paramesonephric ducts
Urogenital sinus
Ureteric bud= ureter
Paramesonephric ducts= oviducts, uterus and upper third of vagina
Urogenital sinus= bulbourethral glands and lower 2 thirds of vagina
77
What ducts are in male and female fetuses?
Male= mesonephric, Woolfian
Female= paramesonephric, Mullerian
78
When does hCG peak?
Week 8 after LMP
79
When do the testes descent?
Testes arise in lumbar region
Descent is due to tethering of the testes to the anterior body wall by the gubernaculum
Descend into pelvic cavity and through the inguinal canal to end up in the scrotum (due to growth and elongation of embryo and shortening of gubernaculum)
80
What happens if there are undescended testes?
Stuck in inguinal canal (don't go through superficial inguinal ring)
Increased risk of cancers
Abnormal function
81
What happens to development of genitalia if there is no testosterone?
Female structures will form
82
What is hypospadia?
Structurally abnormal development of reproductive systems
Fusion of urethral folds is incomplete so urethra exits the penis other than at the tip
83
What Mullerian duct abnormalities are there?
Fusion of mullerian ducts is altered
Affect uterine structure
May affect fertility
84
What happens in Persistent Mullerian Duct syndrome?
Occurs in genetic males with mutations in AMH or the AMH receptor
Testosterone and DHT are produced leading to normal male external genitalia and male (Wolffian) genital ducts
No inhibition so 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
85
What is Androgen Insensitivity Syndrome?
Androgen insensitivity= testicular feminization
Occurs in genetic males (XY) with mutations in the androgen receptor (AR)
Androgens have no effect
Errors in production or sensitivity to testes hormones lead to a predominance of female characteristics under the influence of maternal and placental estrogens
Relatively normal female external genitalia (no functional androgens) but undescended testes
Mesonephric ducts are rudimentary or lacking due to loss of testosterone signaling
Normal production of MIS from Sertoli cells causes Mullerian duct regression, so no oviducts, uterus, or upper third of vagina
86
What is congenital adrenal hyperplasia?
Female homology to AIS
Genetic females with decreased or lacking 21-hydroxylase enzyme activity essential for cortisol synthesis
Leads to increased production of weak androgenic hormones from the adrenal gland which results in weak virilization of external genitalia
- Male features with enlarged clitoris and partial or complete fusion of labia majora
Internal genitalia are female
- Testes absent (no SRY)
- No mesonephric ducts
No AMH so Mullerian duct structures develop
87
How does the face develop?
Formation of face as two separate halves
5-10 weeks
Eyes move from side to front (front and inwards)
Medial nasal prominences merge
Facial symmetry especially attractive
88
What causes a cleft lip and palate?
Failure of tissues to fuse
89
Why is surgery to fix cleft lips and palates so successful?
Cells proliferate quickly
Heal very quick
Minimal scarring
90
What can be caused by a cleft lip and palate?
These disorders can result in feeding problems, speech problems, hearing problems, and frequent ear infections
91
How do lungs develop before birth?
```
Conducting zone (weeks 3-16)
WEEKS 3-8
Embryonic= bronchi
```
WEEKS 5-17
Pseudoglandular= bronchioles then terminal bronchioles
Lobes begin to form
Transitional and respiratory zone (weeks 16-38)
WEEKS 16-27
Canalicular= respiratory bronchioles
WEEKS 24-36
Saccular= alveolar ducts (AND SURFACTANT)
WEEKS 26 and after birth
Alveolar= alveolar sac
92
What happens to lungs from 26 weeks to childhood?
Saccular period= 26 weeks to birth
| Alveolar period= 8 months to childhood
93
What causes Respiratory distress syndrome (RDS)?
```
Surfactant levels are low or absent
Alveoli collapse (surfactant normally keeps low surface tension in alveoli)
```
94
What is surfactant comprised of? How can it be produced artificially?
Lipids, proteins and glycoproteins
Know composition
Half life 5-10 hours
Can increase production in utero (1 injection of glucocorticoids)
95
Why is premature delivery dangerous for lungs?
Before 24 weeks, surfactant not produced
96
What are teteratogens?
Factors which dysregulate patterning
Cause congenital anomalies defects in development (affect normal patterning and lead to maldevelopment)
Interfere with embryonic or fetal organogenesis, growth or cellular physiology
97
What factors can act as teratogens? When do they have their main effects?
Illegal drugs, medications, radiation, infections
Main effects in first trimester of pregnancy
98
When do most miscarriages occur?
Before 23 weeks of gestation
| Mostly within 13 weeks
99
When is considered term?
37-41 weeks
100
What percentage of term babies are delivered by elective Caesarean?
25%
101
What are preterm babies?
Born 23-37 weeks of gestation
| Either by labour or emergency Caesarean
102
What is the approximate size of a baby at term?
Head close to adult hand size
Body close to adult forearm size
Between 6-9 pounds
103
What happens in labour?
Cervical ripening and effacement (increasing)
Coordinated myometrial contractions (increasing)
- Fundally dominant
Rupture of fetal membranes
- Fetal membrane remodelling
- Lower segment relaxation
Delivery of infant
Delivery of placenta
Contraction of uterus
104
When does labour happen?
Latent stage approx 8 weeks e.g. Braxton hicks contractions (practise)
Labour 12-48 hours
- PHASE 1= many hours (contractions, cervical changes
- PHASE 2= hours (baby)
- phase 3= 30 mins (placenta)
105
What can initiate preterm labour?
```
Intrauterine infection
Intrauterine bleeding
Multiple pregnancy
Stress (maternal)
Others
```
106
What happens in cervical ripening and effacement in labour?
```
Change from rigid to flexible structure
Remodelling (loss) of extracellular matrix
Recruitment of leukocytes (neutrophils)
Inflammatory process (PGE2, IL8)
```
107
What happens in co-ordinated myometrial contractions in labour?
Fundal dominance
Increased co-ordination of contractions
Increased power of contractions
Key mediators
- PG F2α (E2) levels increased from fetal membranes
- Oxytocin receptor increased
- Contraction associated proteins
108
What happens in rupture of fetal membranes in labour?
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
Inflammatory process in fetal membranes
109
What is NFKB involved in?
A pro-inflammatory transcription factor
Involved in labour too (almost all pro-labour genes have NFKB binding domains in their promoters, seems to be key regulator)
110
How does inflammation relate to labour?
NFKB in both
Inflammatory changes are strongly linked with labour
NB. Differs in term and pretem labour
Activators of inflammation are readily linked with preterm labour (e.g. intrauterine infection)
PGE2 involved in term labour induction
CRH and PAF can upregulate inflammatory pathways in fetal membranes (and initiate labour)
111
What is the role of platelet-activating factor in the fetus?
```
Part of lung surfactant
Surfactant proteins and complexes
Produced by maturing lung, before birth
Levels in amniotic fluid increase near term
Fetal signal of maturity
```
112
What happens to CRH in pregnancy?
CRH upregulated in maternal circulation and CRH binding proteins fall at end of pregnancy
Anything that increases CRH may predispose to labour (stress, multiple infants)
113
What can predispose to labour?
Increased CRH (stress, multiple infants)
Increased muscle contraction (stretch of uterus)
Activation of inflammatory cascades
Intrauterine infection, bleeding, twins
114
What is the role of progesterone in human pregnancy?
Needed to sustain pregnancy
Levels very high until after delivery of placenta
There is a mutually negative interaction between NFKB and progesterone
Can switch of many pathways involved in labour biochemistry
115
What does the progesterone receptor mediate?
PR-B mediates the main effects of progesterone via gene expression
PR-A is less able to mediate these effects
Ratio of PR-A : PR-B increases at term
Loss or change in PR may lead to ‘functional progesterone withdrawal’ (e.g. during labour)
116
What is development?
Increase in understanding, acquisition of new skills and more sophisticated responses and behaviour
Gain ability to respond and adapt to environment in a planned, organised and independent manner
Dynamic process
Bidirectional transactional process (between genetic and environmental factors)
Process by which child evolves from helpless infancy to independent adult
117
What are the ANTENATAL environmental causes of damage to brain development?
Early maternal infections e.g. rubella, toxoplasma, cytomegalovirus
Late maternal infections e.g. varicella, malaria, HIV
Toxins e.g. alcohol, pesticides, radiation, smoking
Drugs e.g. cytotoxics, antiepileptics
118
What are the POSTNATAL environmental causes of damage to brain development?
Infections e.g. meningitis, encephalitis, cytomegalovirus
Metabolic disorders e.g. hypoglycaemia, hyponatraemia or hypernatraemia, dehydration
Toxins e.g. lead, mercury, arsenic, chlorinated organic compounds, solvents
Trauma e.g. especially head injury
Severe understimulation, maltreatment or domestic violence
Malnutrition e.g. iron defiency, folate deficiency, vitamin D
Maternal mental health disorders (depression)
119
When are the periods of susceptibility to teratogens?
Greatest sensitivity= 3-8 weeks
Highest risk around week 5 (embryonic period)
Each organ will also have a period of peak sensitivity
Lethality may occur before 2 weeks
(Decreasing sensitivity= after 9 weeks, period of functional maturation)
120
What happens to the baby if the mother has rubella in the first trimester?
Congenital rubella in baby
Cataracts, glaucoma, heart defects, hearing loss, tooth abnormalities, pneuomonitis, splenomegaly, blueberry rash muffin or petechial, bone abnormalities, jaundice, hepatomegaly, virus in urine, microcephalus, intracerebral calcification, hydrocephalus, growth restriction
Lose red reflex
121
What happens to the baby if the mother has cytomegalovirus?
Microcephaly, visual impairment, intellectual disability, fetal death
122
What happens to the baby if the mother has herpes simplex virus?
Microphthalmia, microcephaly, retinal dysplasia
123
What happens to the baby if the mother has varicella virus?
Skin scarring, limb hypoplasia, intellectual disability, fetal dysplasia
124
What happens to the baby if the mother has toxoplasmosis?
Hydrocephalus, cerebral calcifications, microphthalmia
125
What happens to the baby if the mother has syphilis?
Intellectual disability, hearing loss
126
What medications can be dangerous for pregnant women?
```
Valproic acid
Trimethadione
Lithium
SSRIs
Amphetamiines
Warfarin
ACE inibitors
Mycophenylate
Alcohol
```
127
What does maternal valproic acid cause in babies?
Neural tube defects
| Heart, craniofacial and limb anomalies
128
What does maternal alcohol cause in babies?
```
Fetal alcohol syndrome (FAS)
Short palpebral fissures
Maxillary hypoplasia
Heart defects
Intellectual disability
Dysmorphic features
```
129
What maternal hormone conditions can lead to child developmental displays?
Androgenic agents
DES
Maternal diabetes
Maternal obesity
130
What does maternal diabetes cause in babies?
Various malformations
Heart and neural tube defects most common
Large for gestational age baby (uterus is too small, can get stuck and have hypoxia)
Particularly bad if uncontrolled during pregnancy
131
What can cause folate deficiency?
Nutritional
| Inhibitors of folate synthesis
132
What are the domains of child development?
Gross motor
Vision and fine motor
Hearing, speech and language
Social, emotional and behavioural
133
What is a milestone? How are they estimated?
Acquisition of a key performance skill
Normal range of attainment varies widely
Estimations based on median age when half of a standard population of children achieve that level
Limit ages= age by which they should be reached
Correct for prematurity until age 2
134
What are the shared features of development between children?
Remarkably constant pattern
Varies in rate
135
How can you check gross motor and posture?
```
Standing
Walking
Running
Kicking a ball
Climbing stairs
Peddling a tricycle
```
136
How does lying/sitting change in the first 8 months?
Newborn= lying down, limbs flexed, symmetrical posture
= marked head lag on pulling up
6-8 weeks= raises head to 45 degrees in prone
6 months= sits without support, round back
8 months= sits without support, straight back
137
How does crawling/standing change in the first 15 months?
8-9 months= crawling (commando crawl, on all fours or bottom shuffling)
10 months= cruises around furniture
12 months= walks unsteadily, broad gait hands apart
15 months= walks steadily
138
Why do babies have primitive reflexes?
Protective and survival value
Promote proper orientation
Promote postural support and balance
Should be present from birth to 4 or 6 months
139
Give examples of primitive reflexes
```
Stepping
Moro
Grasp
Asymmetric tonic reflex
Rooting
```
140
What is the downward parachute reflex and when does it occur?
5 months
When held and rapidly lowered the infant extends and abducts both legs
Feet are plantigrade
141
What is the sideward protective reflex and when does it occur?
6 months
Infant puts arms out to save if tilted off balance
142
What is the forward protective reflex and when does it occur?
7 months
Arms and hands extend on forward descent to ground
143
What is the backward protective reflex and when does it occur?
9 months
Backward protective extension of both arms when pushed backwards in sitting position
144
What are the protective or righting responses?
Downward parachute reflex
Sideward protective reflex
Forward protective reflex
Backward protective reflex
145
What is the moro reflex?
Almost drop the baby (back a few inches)
| Baby should put arms to try and protect itself
146
What is the asymmetric tonic reflex?
Turn baby to one side
They extend their limbs on that side
Fencing posture
147
How can you study fine motor and vision in a child?
Looks at hand function and hand-eye coordination
```
Can also give some information of cognitive function:
Holding objects
Picking up objects
Pointing
Waving
Throwing/catching
```
148
What is object permanence?
Cognitive ability
Infant realizes that out of sign doesn't mean object has disappeared
Happens around 8-9 months
149
What happens to vision and fine motor over the first 5 years?
6 weeks= follows moving object or face by turning the head (relatively blind compared to adults)
4 months= reaches out for toys
4-6 months= grasps toys (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 building (develops)
2-5 years= ability to draw without seeing how it's done
Can copy 6 months earlier
150
What happens if there is normal hearing in a baby?
Normal speech develops
Babbling
Words
Sentences
Social communication
Language is birectional
151
How does speech develop over the first 3 years?
Newborn= startles to loud noises
3-4 months= vocalises alone or when spoken to (coos or laughs)
7 months= Manchester rattle test (turns to soft sounds out of sight)
7 months= At 7 months, sounds used indiscriminately
10 months= At 10 months, sounds used discriminately to parents
12 months= two to three words (other than dada and mama)
18 months= 6-10 words, shows two parts of the body
20-24 months= uses two or more words to make simple phrases
2.5-3 years= talks constantly in 3-4 word sentences
152
What can you study to evaluate a child's social behaviour and play?
```
Looks at interaction with others and self care skills
Stranger awareness
Play
Feeding, toileting and dressing
Social interaction
```
153
How does the social, behaviour and play of a child change in the first 3 years?
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
2.5-3 years= parallel play, interactive play evolving, takes turn
154
What are the key features of speech and language skills?
Vocalization
Words
Understanding
Imaginative play
155
What are the key features of social skills?
Social interaction
Stranger reaction
Eating skills
Dressings
156
What are the key features of gross motor skills?
```
Position
Head tag
Sitting
Walking
Running
```
157
What are the key features of fine motor skills?
```
Uee of hands
Grasp and fine pincer
Bricks
Crayon
Puzzles
```
158
What is a limit age of milestones?
Limit ages= latest age by which a child should have achieved a milestone
2 standard deviations from the mean
159
When should children have their first steps?
```
25% by 11 months
50% by 12 months
75% by 13 months
90% by 15 months
97.5% by 18 months
```
160
When should a child walk independently?
18 months
161
When should a child fix and follow visually?
3 months
162
When should a child join words?
2 years
163
When should a child engage in symbolic play?
2-2.5 years
164
What is developmental delay?
Slow acquisition of skills
May be in one or more domains
165
What is a development disorder?
Maldevelopment of a skill
166
What is it called if:
1 domain is affected by delay
2 domains affected by delay
1 domain is affected by delay= domain-specific
| 2 domains affected by delay= global
167
What is consonant delay?
All domains affected to same extent
168
What is dissonant delay?
Domains affected to different extent (most delay starts dissonant, rate differs)
169
What are the patterns of developmental delay?
Slow but steady
Plateau
Regresses
170
What causes GLOBAL developmental delay?
```
Idiopathic severe learning disability
DS
Other dysmorphic and chromosomal abnormalities
Meningitis
Trauma
FAS
Abuse and neglect
Neurodegenerative disorders
Neurocutaneous disorders
```
171
What causes TALKING delay?
```
Stammering
Hearing deficit
Maturational delay
Environmental factors
Learning disabilities
Autism
Language disorders
```
172
What causes WALKING delay?
Maturational delay
Severe learning disabilities
Cerebral palsy
Duchenne muscular dystrophy
173
How do children present with developmental problems?
Routine child health surveillance
Identified risk factors (such as prematurity)
Parents may be worried
Professionals in a nursery or day care setting concerned
Concerns may be detected opportunistically at health contacts
174
What questions should be asked to identify and then treat a child with developmental problems?
Routine child health surveillance
Identified risk factors (such as prematurity)
Parents may be worried
Professionals in a nursery or day care setting concerned
Concerns may be detected opportunistically at health contacts
175
What are the clinically approaches to treating developmental delay?
History= risk factors, reported milestones
Physical examination
Developmental assessment
Differential diagnosis and identification of co-morbidities
Targeted tests
176
What needs to be considered in the history to study a developmental delay?
```
ANTENATAL
Illnesses and infections
Medications
Drugs
Environmental exposure
```
BIRTH
Prematurity
Prolonged and complicated labour
NNU stay and problems
POSTNATAL
Illnesses and infections
Trauma
CONSANGUINITY
FAMILY AND SOCIAL HISTORY
MILESTONES
Developmental milestones from parents
177
What needs to be considered in the physical exam to study a developmental delay?
Growth parameters= height, weight and head circumference
Dysmorphic features= face, limb, body proportions
Skin= neurocutaneous stigmata, injuries
Central nervous exam= power, tone, reflexes and any asymmetry
Systems exam e.g. cardiac= related to different syndromes and chromosomal abnormalities
Formal developmental assessment= SOGS II, Griffiths, Denver, Specialised
178
What is SOGS II?
Schedule of growing skills assesment
```
Considers:
Passive postural skills
Active postural skills
Locomotor skills
Manipulative skills
```
179
What is the Griffiths Mental Development?
Birth to 2 years (GMDS 0-2)
Used to measure the rate of development of infants and young children
180
What is the Denver scale?
DDST is a widely used assessment
Examines the developmental progress of children from birth until the age of six devised
181
What investigations can be used to consider for developmental delay?
Cytogenetic= chromosome karyotype, fragile x, DNA FISH analysis
Metabolic= thyroid function tests, LFTs, bone chemistry, urea and electrolytes, amino acids, creatine kinase, blood lactate etc.
Infection= congenital infection screen
Imaging= cranial ultrasound in newborn, CT and MRI, skeletal survey and bone age
Neurophysiology= EEG, EMG, nerve conduction studies, ERG, VEP
Histopathology and histochemistry= Nerve and muscle biopsy
Other= hearing, vision, cognitive assessment, therapy assessment, child psychiatry, dietician, nursery reports
182
What is the Child Development Service?
Multidisciplinary (health professionals and social worker)
Multi-agency (health, social services, education, volunteers, parent support groups)
Coordinated service
Monitor children up to 25 years
Emphasises children's needs within community
Often has nominated key worker for a child
183
What is cerebral palsy?
Disorder of movement and posture due to a non-progressive lesion of motor pathways in the developing brain
The clinical manifestations emerge over time, reflecting the balance between normal and abnormal cerebral maturation
The most common cause of motor impairment in children
184
What causes cerebral palsy?
80% of cases antenatal due to genetic syndromes and congenital infection
10% of cases are thought to be due to hypoxic-ischaemic injury at birth
10% are postnatal in origin (e.g. in meningitis, encephalitis, encephalopathy, head trauma, symptomatic hypoglycaemia, hyperbilirubinaemia)
185
How does cerebral palsy present?
Abnormal limb tone and limb 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
186
What are the classifications of cerebral palsy?
Spastic (70%)
Ataxic hypotonic (10%)
Dyskinetic (10%)
Mixed pattern (10%)
187
What problems are associated with cerebral palsy?
```
Learning difficulties
Epilepsy
Squints
Visual impairment from errors of refraction and cortical damage
Hearing impairment
Speech and language disorders
Behaviour disorders
Feeding problems
Joint contractures, hip subluxation, scoliosis
```
188
What is autism spectrum disorder characterised by? When does it present and how does it happen?
Neurobiological disorder characterised by
- Qualitative impairment of social interaction
- Qualitative impairments in communication
- Restricted, repetitive, and/or stereotyped patterns of behaviour, interests and activities
Boys>girls
Usually presents 2-4 years of age
Screening and diagnostic assessment tools are available
Intensive support required for child and family
Prognosis depends on severity
189
What are the main features of autism?
IMPAIRED SOCIAL INTERACTION
Doesn't seek comfort, share pleasure, form close friendships
Prefers own company
No interest in others
Gaze avoidance
Socially and emotionally inappropriate behaviour
Doesn't appreciate that others have thoughts and feelings
Lack of appreciation of social cues
SPEECH AND LANGUAGE DISORDERS
Delayed development, may be severe
Limited use of gestures and facial expression
Formal pedantic language, monotonous voice
Impaired comprehension with over-literal interpretation of speech
Echoes questions, repeats instructions
Can have superficially good expressive speech
IMPOSITION OF ROUTINES WITH RITUALISTIC AND REPETITIVE BEHAVIOUR
On self and others, with violent temper tantrums
Unusual stereotypical movements e.g. gait and hand flapping
Concrete play
Poverty of imagination in play and general activities
Restriction in behaviour repertoire
CO-MORBIDITIES
General learning and attention difficulties
Seizures
190
What are learning disability?
Classified as mild, moderate, severe and profound
May present:
As part of a recognizable syndrome
Failure to meet milestones
Dysmorphic features with associated problems
191
What causes learning disabilities?
```
Chromosome disorders
Identifiable syndromes
Cerebral palsy, infantile spasms, post-meningitis
Metabolic or degenerative diseases
Idiopathic (25%)
```
192
How do you manage learning disabilities?
```
Identify a possible cause
MDT
School= statementing required
Associated problems= vision, hearing, epilepsy
Specific diagnosis=specific problems
```
193
How can education be affected by learning difficulties?
Education Acts= provide children with Special Educational Needs and Disability with additional support to integrate in mainstream schools
Early identification and intervention maximises progress and potential
Children identified are notified to the Local Education Authority (LEA)
194
What is ADHD?
Attention Deficient Hyperactivity Disorder
A persistent pattern (> 6 months) of inattention with or without hyperactivity-impulsivity that
Interferes with functioning or development to a degree that is inconsistent with developmental level and that
Negatively impacts directly on social, academic and occupational activities
Are not solely a manifestation of oppositional behaviour, defiance, hostility or failure to understand tasks or instructions
Were present prior to age 12 years
Are present in two or more settings
195
How can you assess ADHD?
Questionnaires (strengths and difficulties, Connors)
Exclude medical causes e.g. hyperthyroidism, iron deficiency anaemia
Hearing deficits
Identify risk factors and co-morbidities
196
What is the SDQ?
Strengths and Difficulties Questionnaire
Brief behavioural screening questionnaire about 3-16 year olds
Exists in several versions to meet the needs of researchers, clinicians and educationalists
197
What is the Connors questionnaire?
ADHD Connors test
Doctors can assess what type of behaviour has been observed by parents over time
198
What is the recommended management for ADHD?
```
Pyschotherapy
Family therapy
Medication e.g. methylphenidate, other
Co-morbidities e.g. medical management
Diet modification
CAMHS for more complex cases
```
199
What are the main themes of development?
Physical
Cognitive
Emotional
Social
200
What are the developmental stages of adolescence?
Early adolescence= 11-14
Middle adolescence= 14-17
Late adolescence= 18-21
201
What are the gender differences in adolescence?
Girls grow taller earlier than boys
Girls start puberty earlier than boys
Girls are physically mature in general 2 years earlier
202
Outline the pubertal changes in girls?
8-13 years= breast budding
8-14 years= growth of pubic hair
9.5-14 years= growth spurt (peaks 11-13.5)
10-16 years= menarche
10.5- 16.5 years= growth of underarm hair
11-15.5 years= change in body shape
12.5-16.5= adult breast size
203
Outline the pubertal changes in boys?
10.5-17 years= growth of scrotum and testes
10.5-18 years= change in voice
11-15 years= lengthening of penis
11-14= growth of public hair
12-17 years= growth spurt (peaks 13-15)
11-17 years= change in body shape
13-18= growth of facial and underarm hair
204
What are early maturing girls and late maturing boys are at higher risk of?
```
Depression
Substance abuse
Disruptive behaviour/ delinquency
Eating Disorder
Bullying
```
205
What happens in the brain during puberty?
Developmental curves peak at at 12 years (frontal and parietal lobes) and at 16 years (temporal lobes)
PFC increases in density of GM up to puberty and then after puberty decreases GM density
From puberty= increases density cortical WM
Dorsolateral PFC= late in reaching adult levels cortical thickness
Cellular changes too (synaptogenesis, axonal myelination and fine tune PFC and other cortical regions)
206
What are the executive functions?
```
Working memory
Cognitive flexibility
Selective attention
Planning
Inhibition and abstract reasoning
```
207
What happens in the brain to cellular processes?
Synaptogenesis followed by pruning (synapse elimination)
Axonal myelination (speeds up nerve conduction)
Fine tune prefrontal cortex and other cortical regions
208
What are Piaget's 4 stages of cognitive development?
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 and 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
209
What is Kohlberg's theory of moral development?
Moral reasoning (basis for ethical behaviour), has 6 developmental stages, each capable of responding to moral dilemmas than its predecessor
Sequence is fixed,three broad stages
Many people never obtain highest level
Pre-conventional, conventional and post-conventional
210
What are the stages of Kohlberg's theory?
Level 1 and 2: PRE-CONVENTIONAL
- Obedience and punishment orientation (how can I avoid punishment?)
- Self-interest orientation (what's in it for me?)
Level 3 and 4: CONVENTIONAL
- Interpersonal accord and conformity (social norms)
- Authority and social-order maintaining order morality (law and order morality)
Level 5 and 6: POST-CONVENTIONAL
- Social contract orientation
- Universal ethical principles (principle conscience)
211
What influences self-concept?
Intellectual development leads to more complex self-concept
Pubertal and social changes leads to self concept
Adolescence leads to struggle to understand self
212
What are the 8 dimension of self-concept according to Harter?
```
Scholastic competence
Job competence
Athletic competence
Physical appearance
Social acceptance
Close friendships
Romantic appeal
Conduct
```
213
What is the structure of self-concept according to Shavelson, 1976?
Need academic, social, emotional and physical
Academic and non-academic self- concept
Evolution of behaviour
214
What are the clinical implications of good self-esteem?
70-80% adolescents
Self-confidence
Leadership
215
What are the clinical implications of low self-esteem?
20-30% adolescents
```
Depression
Anxiety
Poor school performance
Social isolation
Feeling not respected
```
216
What is important in identity formation in adolescence?
Search for identity important at this stage
Coincides with physical growth
Need for important life decisions
Resolution may be through “crisis”
217
What are Erikson's 8 life-span stages?
Trust vs mistrust (infancy, first year)
Autonomy vs shame and doubt (infancy, 1-3 years)
Initiative vs guilt (early childhood, 3-5 years)
Industry vs inferiority (middle and late childhood)
Identity vs confusion (adolescence 10-20 years)
Intimacy vs isolation (early adulthood, 20s and 30s)
Generativity vs stagnation (middle adulthood, 40s and 50s)
Integrity vs despair (late adulthood, 60s+)
218
What is identity formation according to Marcia?
Identity diffusion= not yet experienced crisis, no commitment to cation/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 experiences crisis, resolved on own terms
219
What is identity associated with?
```
Achievement
Moral reasoning
Career maturity
Social skills
Lower anxiety
```
220
How do cultural minorities develop ethnic identity?
Integration= retain cultural traditions, develop and maintain relationships with mainstream culture
Assimilation= high involvement and relationships with mainstream culture, low maintenance cultural traditions
Separation= retains cultural traditions, low identification mainstream culture
Marginalisation= low both dimensions
221
How do family relationships contribute to adolescence?
Development of autonomy and continuation close relationships
Social domains - adolescents and parents may have different views about who has final say depending on “domain” friendships, clothes, career etc.
Mid-adolescence: most intense negotiations
222
How does conflict with parents affect adolescents?
Most adolescents report good relationships parents
Get on well with mother 86% and father 80%
High confiding to mothers
Disagreements around dress, music choice, leisure activities, time of coming home, tidying bedrooms
223
What does family connectedness manifest as?
Joint activities, mealtimes etc.
High confiding
Parental surveillance: parents communicates with adolescent, knows where they are, etc.
224
What are the benefits of family connectedness?
Associated with reduced risk behaviours (early and unprotected sex, drug, alcohol, cigarette consumption, fighting)
Higher adolescent self-esteem
225
What happens in primary school (7-11 years) in friendships (peer development)?
Friends shared activities
Main goal- acceptance by same gender group
Prefer same gender friends
Loyalty build on earlier interactions
226
What happens in 11-13 year olds in friendships (peer development)?
Expect genuineness, intimacy, self-disclosure, common interests
Emergence of cliques
227
What happens in 13-16 year olds in friendships (peer development)?
Friendship goal= understanding self
Beginning cross gender relationships
Development of larger groups
228
What happens in 16-18 year olds in friendships (peer development)?
Expects friends to provide emotional support
| Increased dyadic romantic ties
229
What happens to children rejected in friendships?
In less satisfying friendships
230
What are the gender differences in peer development?
```
Girls= close relationships, more confiding, more brittle
Boys= less intimate, less disclosing, friendships more embedded in larger circle
```
231
What do parents have more influence than peers on?
Academic choices
Job preferences
Future aspirations
232
What do peers have more influence than parents on?
Interpersonal style
Friendships selection
Fashion and entertainment
233
How do parental and peer influences interact in marijuana consumption?
If friends don't use and parents use= 17% use
If friends use and parents don't= 56% use
If friends and parents use= 67% use
234
What online opportunities are present to the digital generation?
Social networking
Peer contact
Obtain information/learning
IT expertise
235
What online risks are present to the digital generation?
```
Illegal
Unhealthy content e.g. self-harm or pro-anorexia
Cyber-bullying
Abuse personal information
Amount of time online or sedentary
```
236
What do adolescents usually use the internet for?
5-7 year olds= mostly playing games
8-11 year olds= mostly school work and homework
12-15 year olds= mainly school work, homework and social networking
237
Why is school important in developing an adolescent's behaviour?
Teacher effects expectancy and positive attitude
Classroom rules teach about structure, cooperation, competition
School ethos teaches about attainment and behaviour
238
Who is most likely to do well in school?
5 or more A*-C grades
- Higher if upper social class
- Ethnic variation (chinese, indian, white, bangladeshi, pakistani, black)
239
What is the ICD 10 criteria of anorexia nervosa?
```
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 be other weight loss behaviours
```
240
List endocrines disturbances that may result from anorexia nervosa?
Amennorrea in women
Loss of sexual interest in men
Puberty may be delayed
241
What is the ICD 10 criteria of bulimia nervosa?
Persistent preoccupation with eating and binges
Weight losing behaviours (purging by vomiting, laxatives, diuretics, stimulants, excessive exercise)
Psychopathology- morbid dread of fatness, aims for weight lower than premorbid or healthy
242
What is the DSM 5 criteria of bulimia nervosa?
Recurrent episodes of binge eating
Sense of lack of control over eating during episode
Recurrent inappropriate compensatory behaviour to prevent weight gain (purging by vomiting, laxatives, diuretics, stimulants, excessive exercise)
Binge eating and compensatory behaviours both occur and last at least 1 week for 3 months
Self evaluation is unduly influenced by body shape and weight
243
What happens if boys have early pubertal development?
Satisfaction related to height and musculature
Feel more attractive
More popular and relaxed
Advantages may persist e.g. better at sport
244
How does puberty affect girl's feelings about herself?
Associated with increased height and body fat (dissatisfaction related to weight and fat- being slim perceived as desirable)
Ambivalent attitude to menarche
245
How does fashion and media influence girls during puberty?
Slimmer body shapes attractive (e.g. models, mannequins, magazines)
Hard to prove direction of causality
246
True or false; girls 'feeling fat' decreases between ages 12 and 17?
False
| Increases (and increase in dieting)
247
True or false; boys 'feeling fat' decreases between ages 12 and 17?
False
Boys feel fattest around 14 years
Many want to gain weight (particularly by age 17)
248
What race is most associated with seeing self as fat overweight in girls and boys?
GIRLS
White, asian, black
BOYS
White, asian (similar to white), black
249
What are the best ways to predict that a girl may develop eating problems?
Earlier pubertal maturation and higher body fat
Concurrent psychological problem e.g. depression (7x)
Dieting over 6 months at severe level (16x) or moderate level (5x)
Family history (twin studies 50% heritable)
Personality (perfectionist, obsessional)
250
Outline the epidemiology of anorexia nervosa
Female 10x more than men
Onset teenage usually
Dieting
More in certain subcultures e.g. ballet schools, Western affluence societies
251
What are the possible mechanisms of distorted body image in AN?
Somatosensory cortex
252
What are the possible mechanisms of increased anxiety in AN?
Amygdala
253
What are the possible mechanisms of obsessional drive in AN?
Basal ganglia
254
What are the possible mechanisms of enhanced sense of reward in AN?
Nucleus accumbens
255
What are the possible mechanisms of visuo-spatial deficits in AN?
Parietal cortex
256
What are the possible mechanisms of executive impairments in AN?
Frontal lobe
257
What happens if you have weak central coherence in EDs?
Poorer global processing-> weak central coherence (limit ability to understand context or see big picture)
258
What family factors are important in developing AN?
Parental negative attitudes to body fat and shape
Maternal dieting and eating disorders
Family interaction
Dissatisfaction with family life
259
What adverse experiences are important in developing AN?
Sexual abuse
Death
Other adverse life events
260
What sociocultural factors are important in developing AN?
Ethnic group (less in Afro-caribbeans in UK)
Institutions e.g. ballet school
Media (role unclear)
Anorexia in higher social class
261
How does anorexia present?
Self starvation, weight loss, abnormal growth
Symptoms related to self starvation e.g. nausea, abdominal distension, fainting and dizziness
Selective eating e.g. fat avoidance
Other weight controlling strategies e.g. vomiting, exercising, laxatives
Low mood, irritability
Later may have withdrawal, poor concentration, sleep disturbance
262
How do you assess a patient with AN?
Family interview (structure, EDs, illness, psych issues, siblings, parental authority in attitude to treatment)
Individual interview with child or adolescent
- Social adjustment
Physical exam and investigations
- Eating and weight history
- Psychosexual (menstruation and puberty)
- Past medical histroy
- Mental state exma
Data on growth
263
What are the differential diagnose for AN?
PHYSICAL
GI disorder e.g. Crohns
Metabolic e.g. diabetes
Pituitary
```
PSYCHIATRIC
Bulimi nervosa
Depression
Psychosis
OCD
```
264
How is AN treated?
Admission for weight restoration in minority of cases
Family therapy
Nutritional counselling
CBT (to reduce weight preoccupations and challenge faulty cognitions)
265
What does family therapy to treat AN include?
Parents supervise eating, ensure weight gain
Discussion of family relationships
Family life-cycle issues
Most adolescents are significantly helped by family treatments
Initially weight gain, then improvement in eating attitudes and mood
Family conflict reduces and warmth between parents increases, relationships become more harmonious
Important problems in treatment are drop-out, depression, poor treatment progress, low weight
266
How does family therapy lead to a patient's recovery?
Initial focus of adolescents= need to eat
(Parents and carers to supervise)
Adolescent gradually assumes more control of eating (graded improvement in social function)
Address other developmental, relationship and life cycle issues
267
What is CBT?
Cognitive behavioural therapy
Can be individual, groups or self-help
Can be with other treatments (sequenced or concurrent)
```
Involves:
Psychoeducation
Self-monitoring
Behavioural goals
Modify abnormal cognitions
```
268
What is the prognosis for AN?
Only can study the half that present for treatment
50% recover after 5 years
30% weight far below average
Many don't have menstruation
76% recover after 15 years
30% developed binge eating
5-15% mortality after 20 years
269
What kind of model is needed for AN?
Multifactorial
Psychosocial factors mediate between pubertal development and onset of unhealthy eating with weight controlling behaviours
270
What developmental features characterise adolescence?
Cognitive and emotional
Family
Peers
Biology
271
What cognitive and emotional changes happen in adolescence?
Emotional change (including increased intensity of mood states)
More abstract reasoning (sophisticated)
Ability to consider alternative outcomes, consequences, ambiguity (what if?)
Greater knowledge and awareness of the world
Identity (of self, family, ethnicity)
- Autobiographical memory develops (can get sense of self across time)
- Care about how others view them (reputation with peers)
272
What family changes happen in adolescence?
Relationships transformed
Challenging rules
Discipline needs reasoning
Less confiding and intimacy in parents
Shift from time with family to autonomy and independence
273
What peer changes happen in adolescence?
Peer activities and confiding
Sexual relationships
Peer group influences values and behaviour
Over time, peers become more important and take up more time
More exposure to other social factors e.g. media, experimentation
Tend to choose friends with similar values to our parents
274
What biological changes affect behaviour in adolescence?
Puberty and endocrine changes
Physical growth
Brain maturation
275
Who defines the following?
Anti-social behaviour
Delinquency or offending
Conduct disorder
Anti-social behaviour= defined by society
Delinquency or offending= defined by law
Conduct disorder= defined by psychiatry
276
What is the ICD 10 definition of conduct disorder?
Repetitive and persistent (>6 months) pattern of dis-social, aggressive or defiant behaviour
Frequency and severity beyond age appropriate norms
(DSM 5 also says impaired everyday functioning- social, acadmeic or occupational)
277
What behaviours are typical in conduct disorder?
```
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
```
278
What is cyberbullying?
Can be from one incidence (single posting can repeatedly injure individual)
Impact is often delayed
Anonymity and disinhibition can lead people to be more aggressive
Aggressors don't receive communication from their victims that might otherwise moderate behaviour
Forms of cyber bullying evolved with technology
279
What is the epidemiology of conduct disorder?
Higher in London (2x)
4% 5-10 year olds
6% 10-15 year olds
Higher in boys (2x)
Anti-social behaviour can be limited to adolescence of persist for life
Anti=social behaviour is increasing
280
What factors are important int the aetiology of conduct disorder?
Individual child factors e.g. ADHD, Callous-Unempotional traits, physical or developmental healthy problems, difficulties at school or with friends
Family factors e.g. inadequate parenting, poor family communication, parental personality and mental health
School factors e.g. poor organisation, teacher satisfactors and cooperation, deviant peers,
Societal factors e.g. socioeconomic status, neighbourhood
281
What are the risk factors for conduct disorder?
Interaction of factors (individual, family, school and society)
Cumulative factors
Protective factors insufficient
282
What is the impact of conduct disorder?
Affects the individual child e.g. exclusion, imprisonment
Affects the family
Affects innocent victim (antisocial behaviour)
Huge financial costs to society
283
How can you treat conduct disorder?
```
Begin at early age
Deal with major modifiable risk factors
Treat comorbidity e.g. underlying hyperactivity, LD, depression
Parenting programmes
Cognitive problem-solving skills
Interventions at school
Multi-systemic therapy
```
284
What do parenting programmes (for parents of children with CD) include?
Play and good times together
Praise and recognition for good behaviour
Clearly expressed expectations
Consistent and calm consequences for misbehaviour
Planning ahead to avoid trouble
285
What is cognitive problem-solving skills training?
For adolescents with CD
Techniques to develop more accurate perceptions (people with CD may have distorted attributions of aggressions in other people)
Teaching problem-solving skills using range of options and their consequences
286
What kind of interventions for conduct disorder are there?
Parenting programmes
Cognitive problem-solving skills training
Interventions at school
Multi-systemic therapy
287
What interventions at school can help a child with conduct disorder?
Teaching teachers how to manage disruptive behaviour
| Increasing reading ability
288
What multi-systemic therapy can be used for conduct disorder?
Targets causes of youth anti-social behaviour
```
Intensive package to improve:
Parent-adolescent relationship
Parent skills and understanding
Decrease deviant peer associations
Enhance school and occupational performance
Develop support network for family
```
289
What is the prognosis for conduct disorder?
40% of 7 and 8 year olds with CD become a convicted, reoffending criminal as teenagers
90% of recidivist juvenile delinquents had CD
Also predicts alcohol, drug dependence, unemployment and relationship difficulties
290
How has the concept of depression changed?
Used to be yes or no (coding system categorically)
| Now seen as more of spectrum
291
True or false; increased symptoms leads to increased impairment in depression?
True
292
What are the symptoms of depression disorder?
1 OR MORE OF THESE:
Persistent sadness or low mood
Loss of interests or pleasure (anhedonia)
Fatigue or low energy
```
ASSOCIATED WITH (at least 2 weeks, most days)
Disturbed sleep
Poor concentration, indecisiveness and libido
Low self confidence
Change in appetite and weight
Suicidal thoughts or acts
Agitation and slowing of movements
Guilt or self-blame
```
293
How can you define the degree of depression?
<4 symptoms= not depressed
4 symptoms= mild depression
5-6 symptoms= moderate depression
7 or more symptoms= severe depression (with or without psychotic symptoms)
Symptoms pervasive, impairing and present for at least 2 weeks
294
What are the associated problems of depression?
Increased risk of self-harm
Association with anxiety disorders, EDs and conduct problems
Familial aggregation (genetic and learning)
295
How does childhood depression present?
```
Persistent safness
Anhedonia
Boredom or irritability (functionally impairing)
Unresponsive to pleasurable activities
Functional impairment
```
296
What are the 2 main types of pre-pubertal depression?
```
1
More common
Co-morbid behavioural problems
Resembles children with conduct disorder
No increased risk of recurrence in adult life
```
2
Less common
Highly familial (multigenerational loading)
High rates of anxiety and bipolar disorder
Recurrences of depression in adolescence and adulthood
297
How can you tell the difference between normal adolescent angst vs psychiatric disorder?
NORMAL
Mastering the tasks of development (social, physical, cognitive, emotional, moral)
PSYCHIATRIC
Symptoms lead to severe suffering and impairment
Personal, family, peers, education and work
298
What is adolescent depressive disorder?
Irritability instead of sadness and low mood (especially in boys)
Somatic complaints and social withdrawal are common
Psychotic symptoms rare before mid-adolescence
299
What are the outcomes over time for adolescent depressive disorder?
SHORT TERM
High rates of persistence and recurrence
LONG TERM
Significant continuity into adulthood
Impaired relationships and educated in adulthood
300
What is the epidemiology of adolescent depressive disorder?
No different pre-puberty between girls and boys
By 15, F 2x as likely as M
Cumulative probability by late adolescence 10-20%
Rate of depressive disorders may be increasing over time
301
What is the amine hypothesis?
In depression
| Results for hypo-activity of monoamine neurotransmitter reward systems
302
What are the factors contributing to cognition, emotion, mood and pain? What is the neurotransmitter that relates to this?
DA= Pleasure, drive, energy
NE= Vigilance
5-HT= Impulsivity
303
What happens in puberty that contributes to depression?
Gonadal hormones increase which has a direct CNS effect (estradiol)
Low levels of estrogen in women associated with premenstrual syndrome, postnatal depression and post-menopausal depression
Changes in body shape can be negative experience (especially for girls)
- Timing important
304
What happens in the brain that leads to cognitive and emotional changes in adolescence?
PFC= synaptic pruning, myelination, changes in GM and WM
Lots of new connections in the brain-> development of dopaminergic system
305
How can mild depression be treated?
CBD (individual or group)
| Interpersonal psychotherapy for adolescents
306
How can moderate-severe depression be treated?
Anti-depressants e.g. SSRIs e.g. fluoxetine
| Could be SSRI and CBT (combined therapy)
307
What is the theory CBT is based on? How does CBT work?
Based on Beck theory that depressed individuals show distortions in their thinking and info processing
I.e. they emphasise the negative aspects and under-emphasise the positive (leads to depressed mood and maladaptive behaviours)
CBT aims to interrupt this cycle
I.e. change feelings and thoughts to change body sensations and behaviour
308
What is interpersonal psychotherapy?
Conceptualises depression as occurring within an interpersonal matrix and tries to get rid of interpersonal stress
E.g. loss, role disputes, role transitions, interpersonal skills deficits, adjustment to single parent family
Starts by taking an interpersonal inventory of important relationships
Aims to replace conflictual, unfulfilling relationships with meaningful lower-conflict relationships
309
Is TCA (ticyclic AD) beneficial for treating depressioni in adolescents?
No better than placebo
Can have efficacy with SSRIs especially fluoxetine (adolescents and younger adults seem to respond better to serotonergic agents)
E.g. March et al, 2004 TADS study
310
What is the difference between biological and chronological age?
Biological= age organs etc. seem
Chronological= age
311
What is life expectancy?
Statistical measure of how long a person can expect to live
Increasing in most countries
312
What are the 2 key drivers of population ageing?
Falling fertility rates
| People living longer
313
Why do people age?
Programmed ageing
| Damage to error theories
314
What happens to cause programmed ageing?
Hayflick limit (cells in culture would only undergo a certain number of divisions and then stop)
Seems to be controlled by cell being able to count (organism can reach maturity and reproduce)
Evidence mixed
- Some older people have more active telomerase which repairs telomeres
- Possible role of insulin and IGF-1
315
What are free radicals?
Oxidative stress due to reactive oxygen species exceeds antioxidant capacity
O-, H202, H-, NO-
316
Where do most free radicals come from?
Mitochondria
- Contain own DNA, repair mechanisms less robust and eventually DNA damaged repair-> mitochondrion die-> cells die
Chronic inflammation and chronic infections
- Macrophages
- Peroxisomes
- Cytochrome P45-
Lifestyle options
- Smoking
- Skin damage
- Diet (best to have micronutrients, <1500)
317
Should people take antioxidant multivitamins?
No
| No evidence for cancer, CV disease, DM, ARMD, cataracts, AD
318
How do free radicals cause DNA damage?
Frequent damage to DNA whilst it’s being transcribed-> DNA polymerase can’t repair all of it-> damage accumulates and contributes to missing proteins and cellular apparatus etc -> eventually to cell death
319
How does protein glycation lead to oxidative stress?
Contributes to neurofibrilliary tangles
Involved in AD, atherosclerosis and cataracts
320
What challenges does society face as a result of population ageing?
Outdated and ageist beliefs and assumptions
Working life and 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
321
What makes us age differently?
Genetic inheritance (and epigenetic factors)
Sex and ethnicity
Lifestyle (where? behaviour? access to health care? education? social position? wealth?)
322
Why is it important to invest in healthy ageing?
Older people make contribution to society
Bring benefits to older people and returns for society as a whole
323
What does social care comprise of?
```
Financial assessment
Home carers
Sheltered housing
Care home= residential, nursing
Personal budgets
```
324
What is frailty?
Loss of biological reserve across multiple organ systems
Leads to vulnerability to physiological decompensation and functional decline after a stressor event
Cycle involving weight loss, declined activity, decreased strength, decreased walking speed and falling energy and VO2 max
325
What alters the presentation of disease with age?
Frailty
| Non-specific presentations
326
Summarise the difficulties in managing disease in older people?
```
Multimorbidity
Polypharmacy
Iatrogneic harm
Compprehensive geriatric assessment
Rehabilition
```
327
What does frailty lead to?
Increased risk of falls
Worsening disability
Care home admission
Death
328
How can frailty be treated?
Exercise
Nutrition
Possibly drugs
Prevention is better than cure
329
What are the non-specific presentations of frailty?
```
Instability
Immobility
Incontinence
Intellectual impairment
Iatrogenic harm
```
Older people less likely to have common symptoms e.g. chest pain in ACS and pleuritic chest pain and haemoptysis in PE
More likely to have shortness of breath and syncope
330
Define: multimorbidity
2 or more chronic conditions
Impact on one another
NB. Treatments may impact each other
331
What are the negative effects of multi-morbidity?
Worse QoL so more likely to be depressed
Increased functional impairment
Burden of treatment
Polypharmacy
332
Why do older people take more drugs?
```
Comorbidities
Guidelines, QOF and NICE (almost always single disease, don’t take burden of treatment into account, don’t consider other conditions)
Undetected non adherence
Infrequent review
Poor communication
```
333
What is polypharmacy associated with bad outcomes?
Falls
Increased length of stay
Delirium
Mortality
334
What is iatrogenic harm?
Iatrogenesis refers to any effect on a person, resulting from any activity of one or more persons acting as healthcare professionals or promoting products or services as beneficial to health, that does not support a goal of the person affected
335
What nosocomial conditions cause iatrogenic harm?
```
Infections
Pressure sores
Constipation
Deconditioning
Delirium
Malnutrition
Incontinence
```
336
Which drug is most likely to be the cause of a hospital admission?
NSAID 30%
Warfarin 10%
Antidepressant 7%
Opioid 6%
Digoxin 3%
337
Why are older people at increased risk of hospital admission?
```
Reduced physiological reserve
Impaired compensation mechanisms
Comorbidities
Polypharmacy
Cognitive impairment
```
338
What is the CGA?
Comprehensive geriatric assessment
Medical, function, social and psychological assessment
Problem list and plan developed
CGA IN THE COMMUNITY
Reduce admissions to institutional care
Reduce falls
Most benefit in mild or moderate frailty
CGA FOR FRAIL INPATIENTS
Reduces inpatient mortality
Reduces functional and cognitive decline
Reduces admission to institutional care
339
What is the aim of rehabilitation for the elderly?
To restore or improve functionality
Multidisciplinary
Rehabilitation alongside acute illness (preventing deconditioning)
Prehabilitation
340
What do you look for on an MRI of an ageing brain to check cognition?
Grey matter reductions- mainly in size and number of connections between neurons (not in neuron numbers)
White matter reduction
341
What are normal cognitive changes in older people?
Processing speed slows
Working memory slightly reduced
Simple attention ability preserved, but reduction in divided attention
Executive functions generally reduced
No change in non-Wdeclarative memory
No change in visuospatial abilities
No overall change in language (some reduction in verbal fluency)
342
What is dementia?
```
Decline in all cognitive functions, not just memory
Impairment of function
Progressive
Degenerative
Irreversible
```
343
What can cause dementia?
HIV
Progressive multifocal leukencephalopathy (PML)
Post encephalitis
Neuro syphilis
Thiamine deficiency
Pellagra (niacin def)
Hypothyroidism
Alcohol
```
Huntingdon’s
Multiple sclerosis
Progressive supranuclear palsy (PSP)
Corticobasal degeneration (CBD)
Posterior cortical atrophy
Creutzfeld-Jakob disease (CJD)
```
Normal pressure hydrocephalus
344
What is the difference between dementia and delirium?
```
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
```
345
What cognitive assessments are used e.g. looking for dementia?
SCREENING
AMT
4AT
DIAGNOSTIC AND MONITORING
Mini Mental State Examination (MMSE)
Montreal Cognitive Assessment (MOCA)
Addenbrooke’s Cognitive Examination (ACE)
346
What is AMT?
Abbreviated mental test
```
10 questions:
DOB
Age
Current place
Year
Time (to nearest hour)
Dates of WW2
Monarch or PM
Count 20-1
Recognise 2 people
Remember 3-item address (“42 West Street”)
```
Score out of 10 (no half points)
>8 is normal
347
What are the problems with AMT?
Very orientation focused (orientation can be well preserved in some forms of dementia)
Assumes cultural knowledge and interest (WW2, PM)
Assumes numeracy
Monarch or PM could give different results
No time limit on 20-1 (can count very slowly, shows processing time)
Person recognition can be difficult in hospital
348
What are the problems with cognitive assessments?
Most assumes some basic cultural knowledge
Most assume numeracy and literacy
Depression can masquerade as dementia
Ceiling effects in highly educated/intelligent
Interpret them in context
