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Med 2 Life Cycle > Develop > Flashcards

Develop Flashcards

1
Q

Breastfeeding by Rebecca Miles

Impact of not breastfeeding

*LOB: List the benefits of breastfeeding

A

Infant
Reduced immune protection, brain and gut development, educational attainment
Higher risk of SIDS, Necrotising Enterocoloitis (NEC)
Higher incidence of obesity, diabetes, dental decay

Mother/ Birthing Person
Breast and ovarian cancer
Postnatal depression
Diabetes

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2
Q

Breastfeeding by Rebecca Miles

Anatomy of Breast

A
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3
Q

Breastfeeding by Rebecca Miles

Lactogenesis

*LOB: Describe the endocrine regulation of lactation

A

Lactogenesis 1
Proliferation of lobulo-alveolar
Development of myoepithelial cells
Placental lactogen and prolactin promote breast development
Progesterone and oestrogen stimulate mammary growth
Stimulate prolactin, inhibit milk secretion

Lactogenesis 2
Fall in progesterone and oestrogen reduces inhibition to milk production
Suckling stimulus releases prolactin driving milk synthesis
Releases oxytocin driving milk ejections
Some autocrine inhibition from duct cells

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4
Q

Breastfeeding by Rebecca Miles

Prolactin

*LOB: Describe the endocrine regulation of lactation

A
  • Tells lactocytes to make milk
  • Produces calmness and reduces stress
  • Stimulates mothering behaviour
  • Triggered through touch
  • Needs to be stimulated early and frequently to ensure
  • long term production
    *
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5
Q

Breastfeeding by Rebecca Miles

Oxytocin

*LOB: Describe the endocrine regulation of lactation

A
  • Works on muscle cells to expel milk
  • Pulsatile action
  • Induces feeling of love and well-being
  • Levels are higher when baby is near
  • Can be temporarily inhibited by stress
  • Creates a feeling of wellbeing
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6
Q

Breastfeeding by Rebecca Miles

Feedback Inhibitior of Lactation

*LOB: Describe the endocrine regulation of lactation

A
  • FIL is secreted as part of milk
  • Build-up of FIL blocks milk production
  • Removing FIL allows milk production
    *
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7
Q

Breastfeeding by Rebecca Miles

Effect of drugs

*LOB: Describe the endocrine regulation of lactation

A

Suppress lactation
decr prolactin secretion
dopamine agonists
e.g. bromocriptine, cabergoline

Augment lactation
incr prolactin secretion
dopamine antagonists
e.g. domperidone, metoclopramide

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8
Q

Breastfeeding by Rebecca Miles

Components of breastmilk

*LOB: State the components of breastmilk

A
  • Nutrients - macronutrients and trace elements (low “solute
  • load”)
  • Immunoglobulin (secretory IgA)
  • Cells (macrophages & lymphocytes)
  • Non-specific immune components
  • Growth factors
  • More than just food
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9
Q

Breastfeeding by Rebecca Miles

Immunity from breastmilk

*LOB: State the components of breastmilk AND List the benefits of breastfeeding

A

Instant protection in the broncho-mammary pathway and the entero-mammary pathway

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10
Q

Breastfeeding by Rebecca Miles

Benefits

*LOB: List the benefits of breastfeeding

A

Improves gastric emptying
Prevents NEC
Cognitive improvement
Human milk oligosaccharides block bacterial antigens and feed “helpful” bacteria- better microbiome
Less SIDS
Reduced allergic disease
REduced diabetes
Better BP

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11
Q

Breastfeeding by Rebecca Miles

Transfer and Error in breastfeeding

*LOB: Describe the processes by which milk is transferred from mother to baby and how it can go wrong

A

Ineffective attachment
Respond to food cues
Breastfed infants cannot be overfed or spoiled!
Sore nipples, mastitis, low production, MH
Feeding frequently, poor weight gain, jaundice, hypernatraemia

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12
Q

Switching on and maintaining a fuel supply in the newborn by Dr Rooy

What is the difference in the growth trajectory of a newborn vs a child?

*LOB: To provide an understanding of neonatal metabolic adaptation

A
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13
Q

Switching on and maintaining a fuel supply in the newborn by Dr Rooy

Neonatal metabolic adaptation

*LOB: To provide an understanding of neonatal metabolic adaptation

A

From anabolic (build from mums nutrients)
To catabolic (break stores to build)

=SWITCH ON ENZYMES

Note: Cerebral metabolic rate of glucose is low at birth increases quickly.

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14
Q

Switching on and maintaining a fuel supply in the newborn by Dr Rooy

Catabolic (counteregulatory ) enzymes

*LOB: To provide an understanding of neonatal metabolic adaptation

A

ANABOLIC= insulin
Opposite: Glucagon, adrenaline, (cortisol), (growth hormone)

Release glucose from tissue stores for body tissues which are obligate glucose users
Break down fats for energy

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15
Q

Switching on and maintaining a fuel supply in the newborn by Dr Rooy

Catecholamine surge

*LOB: To provide an understanding of neonatal metabolic adaptation

A

ACTIVATES CATABOLIC ENZYMES

Birth is accompanied by a surge in adrenergic hormones.
This prompts a rise in Glucagon secretion
Cutting the cord will cause an abrupt fall in blood glucose
The rise in Glucagon opposes the actions of insulin, and activates gluconeogenesis and glycogenolysis.

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16
Q

Switching on and maintaining a fuel supply in the newborn by Dr Rooy

During a postnatal fast..

*LOB: To provide an understanding of neonatal metabolic adaptation

A

The baby will need to utilise stores to provide glucose as an energy source for the tissues.
Gluconeogenesis is the process of providing glucose from stores – muscle (amino acids and glycogen) and fat via substrates such as lactate, pyruvate, alanine and glycerol.
Glycogenolysis is the breakdown of glycogen to Glucose from body stores
Ketogenesis is the process of providing ketone bodies (which act as a fuel) from the breakdown of fat

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17
Q

Switching on and maintaining a fuel supply in the newborn by Dr Rooy

Supply: Energy stores

*LOB: To provide an understanding of neonatal metabolic adaptation

A

The term baby is (by weight):
about 1% glycogen
about 16% fat

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18
Q

Switching on and maintaining a fuel supply in the newborn by Dr Rooy

Fasting (post-absorptive) state

*LOB: To provide an understanding of neonatal metabolic adaptation

A

Substrates are mobilised peripherally through action of counter-regulatory hormones.
Catecholamines
Cortisol
Glucagon
Insulin is opposed

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19
Q

Switching on and maintaining a fuel supply in the newborn by Dr Rooy

Fed (post-prandial) state.

*LOB: To provide an understanding of neonatal metabolic adaptation

A

Infant diet is 50% fat and 40% carbohydrate
CHO is mainly lactose
Breast milk contains a lipase

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20
Q

Switching on and maintaining a fuel supply in the newborn by Dr Rooy

Babies who have problems

*LOB: inborn error

A

Demand exceeds supply
Hyperinsulinism
Counter-regulatory hormone deficiency
Inborn errors of metabolism

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21
Q

Switching on and maintaining a fuel supply in the newborn by Dr Rooy

The extremely small preterm baby:

*LOB: inborn error

A

High demands
Small nutrient stores
Immature intermediary metabolism
Establishment of enteral feeding delayed
Poor fat absorption

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22
Q

Switching on and maintaining a fuel supply in the newborn by Dr Rooy

The extremely small preterm baby:

*LOB: inborn error

A

High demands
Small nutrient stores
Immature intermediary metabolism
Establishment of enteral feeding delayed
Poor fat absorption

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23
Q

The IUGR baby

A

High demands (especially brain)
Low stores (liver, muscle, fat)

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24
Q

Infant of the diabetic mother

A

High maternal glucose
 high fetal glucose
Fetal and neonatal hyperinsulinism
Neonatal macrosomia and hypoglycaemia.

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25
Q

Other deficiencies of Counterregulatory hormones:

A

Hypothalamic-pituitary-adrenal insufficiency:
Septo-optic dysplasia
Waterhouse- Friederichsen:
Severe adrenal haemorrhage with adrenal gland dysfunction secondary to sepsis or hypoxia

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26
Q

Causes of refractory hypoglycaemia

A
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27
Q

Inborn errors of metabolism

A

Causes of neonatal hypoglycaemia include:
Glycogen storage disease (usually Type 1)
Galactosaemia
MCAD (medium chain acyl-coA dehydrogenase deficiency)

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28
Q

Galactosaemia

A

Lactose in milk is broken down to Galactose and Glucose.
Galactose is then converted to Glucose by Galactose-1-phosphate Uridyl Transferase (Gal-I-put)
This enzyme is missing in Galactosaemia, leading to toxic levels of galactose-1-phosphate.
Presents with:
Hypoglycaemia
Jaundice and liver disease
Poor feeding and vomiting
Cataracts an brain damage
E Coli sepsis

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29
Q

MCADD – Medium Chain acyl-CoA dehydrogenase deficiency

A

Can present with hypoglycaemia induced by fasting
most prevalent in individuals of Northern European Caucasian descent.

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30
Q

Cardiorespiratory Adaptation at Birth by Sandeep Shetty

Lung Growth Stimuli:

*LOB: Factors Preparing Fetal Lung for Postnatal Gaseous Exchange:

A

Mechanical Stretch: Fetal breathing movements stimulate lung growth and development.

Chemical Factors: Hormones like cortisol from the mother, thyroid hormones, and growth factors promote lung growth.

Oxygen Tension: Hypoxic conditions in utero stimulate vascular and alveolar development.

Time of onset is crucial for lung development.
before 16 weeks, structural damage could lead to potentially permanent reduction in alveoli numbers.

Structural pathology such as congenital diaphragmatic hernia, lung cysts, malnutrition, and smoking can impact lung development irreversibly.

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31
Q

Cardiorespiratory Adaptation at Birth by Sandeep Shetty

Production and Role of Pulmonary Surfactant:

*LOB: Factors Preparing Fetal Lung for Postnatal Gaseous Exchange:

A
  • Surfactant is produced by type II pneumocytes in the late stages of fetal development.
  • It reduces surface tension, preventing alveolar collapse during expiration.
  • Enhances lung compliance and prevents atelectasis.
  • Critical for the transition to air breathing at birth.
  • Lung liquid pathology includes conditions like oligohydramnios and early rupture, which can adversely affect lung development.
  • surfactant reduces surface tension in the alveoli, preventing collapse.
  • Composition includes phospholipids like surfactant phosphatidylcholine (PC) and proteins (SP-A, SP-B, SP-C, SP-D).
  • Surfactant maturation is influenced by factors like glucocorticoids, thyroid hormones, insulin, and delayed pulmonary maturation can lead to respiratory distress.
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32
Q

Cardiorespiratory Adaptation at Birth by Sandeep Shetty

Foetal Lung Liquid Secretion:

*LOB: Describe the role of foetal lung liquid secretion and the mechanism by which the liquid is removed at birth

A
  • Produced by lung epithelial cells and glands, filling the airways in utero.
  • Aids in lung growth and development by maintaining patency of the airways.
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33
Q

Cardiorespiratory Adaptation at Birth by Sandeep Shetty

Removal at Birth:

*LOB: Describe the role of foetal lung liquid secretion and the mechanism by which the liquid is removed at birth

A
  • During labor and delivery, mechanical compression expels the liquid.
  • Hormonal changes, such as increased catecholamines, reduce lung liquid secretion.
  • Establishment of air-breathing leads to absorption of remaining fluid via lymphatic and vascular systems.
  • Cooling stimulates the first breath, along with other sensory stimuli.
  • After birth, air replaces fluid within minutes, with most of the fluid absorbed into lymphatics and capillaries.
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34
Q

Cardiorespiratory Adaptation at Birth by Sandeep Shetty

Oxygen Transfer:

*LOB: Explain the functional adaptations of foetal haemoglobin that promote oxygen transfer from maternal to foetal blood and its developmental changes

A
  • Higher affinity for oxygen compared to adult hemoglobin (HbA).
  • Facilitates efficient oxygen transfer from maternal to fetal blood at the placenta.
  • Maintains oxygen saturation of fetal blood despite lower partial pressure in the uterine environment.
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35
Q

Cardiorespiratory Adaptation at Birth by Sandeep Shetty

Developmental Changes:

*LOB: Describe the role of foetal lung liquid secretion and the mechanism by which the liquid is removed at birth

A
  • Gradual decline in fetal hemoglobin (HbF) and increase in adult hemoglobin (HbA) after birth.
  • Transition to extrauterine life prompts the switch to HbA.
    *
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36
Q

Cardiorespiratory Adaptation at Birth by Sandeep Shetty

Structural Adaptations:

*LOB: Describe the anatomical and functional adaptations in the foetal circulation

A
  • Presence of shunts like ductus arteriosus and foramen ovale to bypass non-functional lungs and liver.
  • High pulmonary vascular resistance to divert blood flow away from lungs.
    *
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37
Q

Cardiorespiratory Adaptation at Birth by Sandeep Shetty

Functional Adaptations:

*LOB: Describe the role of foetal lung liquid secretion and the mechanism by which the liquid is removed at birth

A
  • Right-to-left shunting of blood at the level of the foramen ovale and ductus arteriosus.
  • High levels of fetal hemoglobin to facilitate oxygen transport.
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38
Q

Cardiorespiratory Adaptation at Birth by Sandeep Shetty

Peri-natal Transition:

*LOB: Describe the peri-natal (transition) and post-natal changes in circulation and understand the consequences if these fail (patent ductus arteriosus and pulmonary hypertension)

A
  • Closure of shunts (ductus arteriosus, foramen ovale) due to changes in pressure gradients and oxygen levels.
  • Failure in closure leads to conditions like patent ductus arteriosus (PDA) and persistent pulmonary hypertension of the newborn (PPHN).
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39
Q

Cardiorespiratory Adaptation at Birth by Sandeep Shetty

Post-natal Changes:

*LOB: Describe the peri-natal (transition) and post-natal changes in circulation and understand the consequences if these fail (patent ductus arteriosus and pulmonary hypertension)

A
  • Increase in pulmonary blood flow due to lung expansion and decrease in pulmonary vascular resistance.
  • Establishment of independent pulmonary circulation.
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40
Q

Cardiorespiratory Adaptation at Birth by Sandeep Shetty

Consequences of Failure:

*LOB: Describe the peri-natal (transition) and post-natal changes in circulation and understand the consequences if these fail (patent ductus arteriosus and pulmonary hypertension)

A
  • Failure of closure of the ductus arteriosus can lead to patent ductus arteriosus (PDA), causing left-to-right shunting and potential heart failure.
  • Persistent pulmonary hypertension of the newborn (PPHN) can result from failure of pulmonary vascular resistance to decrease, leading to inadequate oxygenation and potential cardiovascular compromise.
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41
Q

Cardiorespiratory Adaptation at Birth by Sandeep Shetty

Temperature Control:

A
  • Neonates are at increased risk of heat loss due to factors like lack of brown fat, conduction, convection, evaporation, and radiation.
  • Thermogenesis, primarily through brown fat, helps maintain body temperature.
  • Non-shivering thermogenesis
  • Highly vascular
  • Sympathetic innervation
  • ↑ Mitochondrial content
  • Can double heat production
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42
Q

Cardiorespiratory Adaptation at Birth by Sandeep Shetty

Fluid Balance:

A
  • Neonates have a limited ability to concentrate urine and are at risk of fluid loss due to immature kidneys and increased surface area.
  • Fluid balance is crucial for maintaining homeostasis and preventing dehydration.
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43
Q

Cardiorespiratory Adaptation at Birth by Sandeep Shetty

Pulmonary Vascular Resistance Falls

A

Lung expansion
Pulmonary stretch receptors
Increased Oxygen tension
8-10x rise in blood flow

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44
Q

Cardiorespiratory Adaptation at Birth by Sandeep Shetty

Abnormal Circulation

A
  • Transition may not be permanent
  • Pulmonary arterioles very reactive and constrict to certain stimuli
  • Hypoxia
  • Hypercarbia
  • Acidosis
  • Cold
  • Rise in PVR and Right to Left shunting: foetal circulation
    *
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45
Q

Implantation

*LOB: Describe the process of implantation of the blastocyst:

A

Differentiation of the trophoblast: Trophoblast cells undergo differentiation to form syncytiotrophoblast and cytotrophoblast layers.

Trophoblastic invasion of decidua and myometrium: Trophoblast cells invade the decidua and later the myometrium, facilitating implantation and establishment of placental circulation.

Remodeling of the maternal vasculature in the utero-placental circulation: Maternal blood vessels undergo remodeling to accommodate increased blood flow to the placenta.

Development of vasculature within the trophoblast: Blood vessels form within the trophoblast to support nutrient and gas exchange between maternal and fetal circulation.

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46
Q

Implantation and placentation M5

Implantation

*LOB: Describe the process of implantation of the blastocyst:

A

Differentiation of the trophoblast: Trophoblast cells undergo differentiation to form syncytiotrophoblast and cytotrophoblast layers.

Trophoblastic invasion of decidua and myometrium: Trophoblast cells invade the decidua and later the myometrium, facilitating implantation and establishment of placental circulation.

Remodeling of the maternal vasculature in the utero-placental circulation: Maternal blood vessels undergo remodeling to accommodate increased blood flow to the placenta.

Development of vasculature within the trophoblast: Blood vessels form within the trophoblast to support nutrient and gas exchange between maternal and fetal circulation.

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47
Q

Hormone production essential for normal development and growth:

*LOB: Describe the process of implantation of the blastocyst:

A

βHCG (human chorionic gonadotropin): Produced by trophoblast cells, maintains the corpus luteum to sustain progesterone production, crucial for maintaining pregnancy until placental steroidogenesis is established.

Progesterone: Produced by the corpus luteum under the influence of βHCG, essential for decidualization and maintaining uterine quiescence.

Estrogens (E1, E2, E3): Produced by the placenta and maternal adrenals, contribute to uterine hypertrophy, metabolic changes, cardiovascular adaptations, and breast development.

Placental CRH and cortisol:Increase from the second trimester onwards, impacting metabolic changes, fetal lung maturity, and possibly involved in labor initiation.

Human placental lactogen (HPL): Similar to growth hormone, induces metabolic changes and may play a role in lactation.

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48
Q

Hormone production essential for normal development and growth:

*LOB: Explain how the embryo signals its presence to the maternal system:

A

βHCG (human chorionic gonadotropin): Produced by trophoblast cells, maintains the corpus luteum to sustain progesterone production, crucial for maintaining pregnancy until placental steroidogenesis is established.

Progesterone: Produced by the corpus luteum under the influence of βHCG, essential for decidualization and maintaining uterine quiescence.

Estrogens (E1, E2, E3): Produced by the placenta and maternal adrenals, contribute to uterine hypertrophy, metabolic changes, cardiovascular adaptations, and breast development.

Placental CRH and cortisol:Increase from the second trimester onwards, impacting metabolic changes, fetal lung maturity, and possibly involved in labor initiation.

Human placental lactogen (HPL): Similar to growth hormone, induces metabolic changes and may play a role in lactation.

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49
Q

Explain how the embryo signals its presence to the maternal system:

A
  • The embryo signals its presence primarily through the production of βHCG, which serves as the “maternal recognition of pregnancy.”
  • This hormone helps maintain the corpus luteum, ensuring continued progesterone production necessary for pregnancy maintenance until placental steroidogenesis is established.
  • Additionally, placental hormones such as CRH, cortisol, and human placental lactogen also contribute to signaling and modulating maternal physiology during pregnancy.
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50
Q

Placenta

*LOB: Define the functions of the extra-embryonic structures and describe the key steps in their development:

A
  • Extra-embryonic structures, including the placenta and its associated membranes, play crucial roles in supporting embryonic/fetal development
  • The trophoblast differentiates into syncytiotrophoblast and cytotrophoblast layers, facilitating implantation and forming the placenta.
  • The placenta serves as the interface for nutrient and gas exchange between maternal and fetal circulation. Additionally, the amnion and chorion provide protection and support for the developing embryo/fetus.
  • *
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51
Q

Complications of pregnancy

Outline common complications of pregnancy in each trimester

*LOB: Outline common complications of pregnancy in each trimester

A

First Trimester: Miscarriage, ectopic pregnancy, hyperemesis gravidarum.

Second and Third Trimesters (Maternal): Urinary tract infections, anemia, pre-eclampsia, gestational diabetes, antepartum hemorrhage.

Second and Third Trimesters (Fetal): Premature labor, intrauterine growth restriction, macrosomia.

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52
Q

Miscarriage

*LOB: Relate pathological conditions of pregnancy to normal physiology with reference to anaemia, gestational diabetes and pre-eclampsia

A
  • Occurs in approximately 15% of pregnancies, though the percentage may vary.
  • Can happen due to various reasons, including chromosomal abnormalities in the embryo, maternal health conditions, uterine abnormalities, hormonal imbalances, infections, and lifestyle factors like smoking or substance abuse.
  • Symptoms of miscarriage may include vaginal bleeding, abdominal cramping, and passage of tissue from the vagina.
  • Management of miscarriage depends on several factors, including the stage of pregnancy, the cause of miscarriage, and the patient’s overall health, and may involve expectant management, medication, or surgical intervention.
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53
Q

Gestational diabetes

*LOB: Relate pathological conditions of pregnancy to normal physiology with reference to anaemia, gestational diabetes and pre-eclampsia

A
  • Occurs in about 5% of pregnancies, marked by glucose intolerance first recognized during pregnancy.
  • GDM is characterized by glucose intolerance, resulting in elevated blood sugar levels.
  • Risk factors for GDM include obesity, advanced maternal age, family history of diabetes, and previous history of gestational diabetes.
  • Women with GDM are at increased risk of complications such as macrosomia (large birth weight), birth trauma, neonatal hypoglycemia, and increased likelihood of cesarean delivery.
  • Management of GDM involves dietary modifications, regular physical activity, monitoring blood glucose levels, and in some cases, insulin therapy. Close monitoring of maternal and fetal well-being throughout pregnancy is essential to reduce the risk of complications.
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54
Q

Pre-eclampsia

*LOB: Relate pathological conditions of pregnancy to normal physiology with reference to anaemia, gestational diabetes and pre-eclampsia

A
  • Affects around 3-4% of pregnancies, characterized by hypertension and proteinuria after 20 weeks of gestation.
  • Pre-eclampsia is a multisystem disorder characterized by new-onset hypertension (blood pressure ≥ 140/90 mmHg) and proteinuria (≥ 300 mg of protein in a 24-hour urine collection) occurring after 20 weeks of gestation in a previously normotensive woman.
  • Other signs and symptoms of pre-eclampsia may include headache, visual disturbances, upper abdominal pain, edema (swelling), and decreased urine output.
  • Pre-eclampsia can progress to eclampsia, a severe complication characterized by seizures, and may lead to complications such as placental abruption, HELLP syndrome (hemolysis, elevated liver enzymes, low platelet count), renal failure, and fetal growth restriction.
  • Management of pre-eclampsia involves close monitoring of maternal and fetal well-being, blood pressure control, and delivery of the fetus and placenta, often necessitating early induction of labor or cesarean section
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55
Q

Relate pathological conditions of pregnancy to normal physiology with reference to anaemia, gestational diabetes and pre-eclampsia

A
56
Q

Labour

Physiology and Mechanism of Normal Labour:

*LOB: Describe the physiology and mechanism of normal labour

A

Labour is the process by which the uterus contracts and the cervix dilates to allow the delivery of a viable fetus (>24 weeks), placenta, and membranes. The onset of labour involves a complex interplay of hormonal, neural, and mechanical factors, though the exact mechanisms are not fully understood.

57
Q

Labour

Physiology and Mechanism of Normal Labour:

*LOB: Describe the physiology and mechanism of normal labour

A

Labour is the process by which the uterus contracts and the cervix dilates to allow the delivery of a viable fetus (>24 weeks), placenta, and membranes. The onset of labour involves a complex interplay of hormonal, neural, and mechanical factors, though the exact mechanisms are not fully understood.

58
Q

Labour

Stages of Labour:

Define and describe the three stages of labour

A

First Stage: Begins with regular, painful uterine contractions and ends with full cervical dilation.
Second Stage: Starts with full cervical dilation and ends with delivery of the fetus.
Third Stage: Involves delivery of the placenta and membranes.

59
Q

Labour

First Stage of Labour:

*LOB: Describe the physiology and mechanism of normal labour

A

Latent Phase: Characterized by cervical effacement and dilation from 3 cm to <0.5 cm, can take 6-8 hours in nulliparous women and 4-6 hours in multiparous women.

Active Phase: Involves cervical dilation from 3 to 10 cm, typically progresses at an average rate of 1 cm/hour.

60
Q

Second Stage of Labour:

A

Physiological changes include vulval bulging, anal dilatation, urge to push, increased respiratory rate, and restlessness.

61
Q

Third Stage of Labour:

A

Active management involves administering intramuscular Syntometrine with the delivery of the anterior shoulder, controlled cord traction, examination of the placenta and membranes for completeness, estimation of blood loss, and management of any tears with local anaesthetic and sutures if required.

62
Q

Management of Labour:

A

Admission in Labour: Involves assessment of risk status, team management, and apportionment of care. The definitive diagnosis of labour may require observation.

Management of Active Phase: Essential components include reassurance, one-to-one support, hydration, and adequate pain relief.

63
Q

Failure to Progress:

Common Complications and Their Management:

A

Intervention may be required if labour progresses slower than expected. This can involve reassessment, augmentation of labour with oxytocin, or consideration of alternative delivery methods such as cesarean section.

64
Q

Postpartum Haemorrhage (PPH):

A

Defined as blood loss >500 ml within 24 hours of vaginal birth or >1000 ml after cesarean section. Management includes early recognition, administration of uterotonics, controlled cord traction, examination for retained placental tissue, and surgical intervention if necessary.

65
Q

Anaemia in Pregnancy

A

Physiology: Increase in plasma volume leads to hemodilution. Increased iron demand for fetal/placental development may outpace intake, causing relative iron deficiency.

Pathology: Anaemia occurs when plasma volume increase outpaces red blood cell volume, causing dilutional effect on hemoglobin levels. Symptoms: fatigue, weakness, pallor

66
Q

Anaemia in Pregnancy

A

Physiology: Increase in plasma volume leads to hemodilution. Increased iron demand for fetal/placental development may outpace intake, causing relative iron deficiency.

Pathology: Anaemia occurs when plasma volume increase outpaces red blood cell volume, causing dilutional effect on hemoglobin levels.

Symptoms: fatigue, weakness, pallor

67
Q

Gestational Diabetes

A

Physiology: Hormonal changes lead to insulin resistance, allowing maternal glucose to be shunted to fetus. Pancreas increases insulin production.

Pathology: Excessive insulin resistance leads to impaired glucose tolerance, resulting in elevated blood sugar levels.

Symptoms: increased thirst, frequent urination, fatigue.

68
Q

Pre-eclampsia

A

Physiology: Changes in vascular function and immune response to support fetal growth. Placental factors contribute to maternal endothelial dysfunction, increased vascular permeability.

Pathology: Abnormal vascular changes, vasoconstriction, endothelial dysfunction lead to hypertension, proteinuria.

Symptoms: headache, visual disturbances, upper abdominal pain, edema.

69
Q

Principles of Growth by Dr Fatima

Detail the factors affecting pre-natal growth: Intrinsic

A

Genetic variations can influence factors such as birth weight, length, head circumference, and susceptibility to certain diseases.

Hormone Function such as insulin-like growth factors (IGFs) are essential for promoting cell proliferation and differentiation, while thyroid hormones are crucial for brain development and metabolism

70
Q

Principles of Growth by Dr Fatima

Detail the factors affecting pre-natal growth: Intrinsic

*LOB: Detail the factors affecting pre-natal growth

A

Genetic variations can influence factors such as birth weight, length, head circumference, and susceptibility to certain diseases.

Hormone Function such as insulin-like growth factors (IGFs) are essential for promoting cell proliferation and differentiation, while thyroid hormones are crucial for brain development and metabolism

71
Q

Principles of Growth by Dr Fatima

Detail the factors affecting pre-natal growth: Extrinsic

*LOB: Detail the factors affecting pre-natal growth

A
  • placenta
  • maternal anatomy (uterine size, shape, and vascularization)
  • nutrition
  • exposure to teratogens such as maternal diabetes mellitus, gestational infections
  • chemical or physical agents like hyperthermia or ionizing radiation.
72
Q

Principles of Growth by Dr Fatima

First Trimester

*LOB: Detail the factors affecting pre-natal growth

A

rapid growth and differentiation of organs with the formation of embryonic disk:

ectoderm (skin, hair, brain, nerves)
endoderm (cardiac, skeletal, renal, bloods)
mesoderm (lung, gut, thyroid, pancreas)

73
Q

Principles of Growth by Dr Fatima

Second and Third Trimester

*LOB: Detail the factors affecting pre-natal growth

A

Cell hyperplasia in the second trimester (week 9-16 growth in length)
Cell maturation in the third trimester (week 17-38 weight increase)

Second and third trimesters:
Cellular hyperplasia and a peak foetal length velocity of 2.5 cm per week

Third trimester:
Cellular hypertrophy and maturation of organs
produces a substantive weight gain, mainly related to subcutaneous brown fat tissue near term

74
Q

Principles of Growth by Dr Fatima

Zygote is characterised

*LOB: Detail the factors affecting pre-natal growth

A

by an increase in cell number with no increase in mass (day 1-3 post conception)

75
Q

Principles of Growth by Dr Fatima

Postnatal growth is regulated by

*LOB: Describe the endocrinological regulation of postnatal growth and understand the Karlsberg ICP model of growth:

A

growth hormone and sex hormones

76
Q

Principles of Growth by Dr Fatima

What is Karlbergs ICP model?

*LOB: Describe the endocrinological regulation of postnatal growth and understand the Karlsberg ICP model of growth:

A
  • Infancy, Childhood and Puberty (the ICP-model) breaks down growth mathematically
  • The model provides an improved instrument for detecting and understanding growth failure
  • It emphasizes the influence of genetics and environmental factors, particularly nutrition, on growth trajectories.
  • Infancy is characterized by rapid weight gain
  • childhood by relatively constant growth rates influenced by thyroid and growth hormone
  • and puberty by a growth spurt driven by sex hormones.
77
Q

Principles of Growth by Dr Fatima

Karlbergs ICP model: Infancy

*LOB: Describe the endocrinological regulation of postnatal growth and understand the Karlsberg ICP model of growth:

A

Weight easiest parameter to use for evaluating growth during infancy
birth 3/3.5 Kg
doubled at 4-5months
3 -fold weight gain at one year (9kg)

Height:
20 cm/year at birth
10-12cm/year at 12months

78
Q

Principles of Growth by Dr Fatima

What is Canalisation

*LOB: Define canalisation and explain the principles of catch-up and catch-down growth:

A

infants and children stay within one or two growth centiles
crossing of height centiles always warrants further evaluation.

Crossing of centiles is a normal event in child development, though in a clinical setting crossing centiles should still be taken seriously

Waddington in 1957

79
Q

Principles of Growth by Dr Fatima

What is Catch down growth?

*LOB: Define canalisation and explain the principles of catch-up and catch-down growth:

A
  • Starts off at a high percentile in early infancy, over time, reduced then stay on a lower percentile
  • starts at 3–6 months of age and is completed by 9–20 months old
  • Infant of diabetic mother
  • Overfed infant
  • Future constitutional delay in growth
  • a fall of more than 2 major percentiles warrants investigations
80
Q

Principles of Growth by Dr Fatima

What is Catch up growth?

*LOB: Define canalisation and explain the principles of catch-up and catch-down growth:

A
  • height velocity above the limits of normal for age for at least 1 year after a transient period of growth inhibition
  • baby born IUGR
  • child with hypothyroidism received thyroxine
  • Future early maturer
  • Can be complete or incomplete (mean final height vs mean target height)
  • Typically occurs between birth and 6–18 months of age)
81
Q

Principles of Growth by Dr Fatima

What is Catch down growth?

*LOB: Define canalisation and explain the principles of catch-up and catch-down growth:

A
  • Starts off at a high percentile in early infancy, over time, reduced then stay on a lower percentile
  • starts at 3–6 months of age and is completed by 9–20 months old
  • Infant of diabetic mother
  • Overfed infant
  • Future constitutional delay in growth
  • a fall of more than 2 major percentiles warrants investigations
82
Q

Principles of Growth by Dr Fatima

Mean Predicted Parental Height

*LOB: Define canalisation and explain the principles of catch-up and catch-down growth:

A

A way to determine the child’s genetic growth potential
Boys: [(mum + dad) + 13 ]/2
Girls: [(mum + dad) – 13] /2

+/- 5 cm for +/- 1 SD and +/- 10 cm for +/- 2 SD

83
Q

Principles of Growth by Dr Fatima

Skeletal growth

*LOB: Describe the physiological processes of skeletal growth

A
  • Osteogenesis starts week 6-7 of life
  • intramembranous ossification (flat bones)
  • endochondral ossification (long bones)
84
Q

Principles of Growth by Dr Fatima

Intramembranous ossification

*LOB: Describe the physiological processes of skeletal growth

A
  • Mesenchymal cells group into clusters, and ossification centers form
  • Secreted osteoid traps osteoblasts, which then become osteocytes
  • Trabecular matrix and periosteum form
  • Compact bone develops superficial to the trabecular bone, and crowded blood vessels condense into red marrow.
85
Q

Principles of Growth by Dr Fatima

Endochondral Ossification

*LOB: Describe the physiological processes of skeletal growth

A
  • Mesenchymal cells differentiate into chondrocytes
  • The cartilage model of the future bony skeleton and the perichondrium form
  • Capillaries penetrate cartilage. Perichondrium transforms into periosteum. Periosteal collar develops. Primary ossification center develops
  • Cartilage and chondrocytes continue to grow at ends of the bone
  • Secondary ossification centers develop
  • Cartilage remains at epiphyseal (growth) plate and at joint surface as articular cartilage
    *
86
Q

Principles of Growth by Dr Fatima

How do bones grow in length ?

*LOB: Describe the physiological processes of skeletal growth

A
  • Epiphyseal plate is composed of four zones of cells and activity
  • Bones grow in length at the epiphyseal plate under the influence of growth hormone with the addition of sex hormones at puberty
  • On the epiphyseal side of the epiphyseal plate, cartilage is formed.
  • On the diaphyseal side, cartilage is ossified, and the diaphysis grows in length.
  • The longitudinal growth of bone is a result of cellular division in the proliferative zone and the maturation of cells in the zone of maturation and hypertrophy.
87
Q

Principles of Growth by Dr Fatima

Childhood Growth

*LOB: Describe body composition changes and gender differences during growth

A

Length/height
Influenced by puberty start but…
Double at 2 y
Triple at 13 y

25 cm in the first year
12.5 cm in the second year
5-7.5 cm/year until puberty

Weight
2 kg/year between 2 to 6 years
3 kg/year 7years to puberty
6 kg/year during puberty

88
Q

Principles of Growth by Dr Fatima

Childhood growth sex differences

*LOB: Describe body composition changes and gender differences during growth

A
  • Girls grows slightly faster than boys until 4 years then few differences in the height velocities between the sexes before puberty
  • Skeletal maturity slightly more advanced in girls than boys.
  • Active change in body proportion
  • legs growing faster than the trunk and head
89
Q

Principles of Growth by Dr Fatima

Puberty growth

*LOB: Describe body composition changes and gender differences during growth

A
  • Upper segment to lower segment ratio dips below 1 during puberty and then returns to 1 when pubertal growth complete
  • In both genders, oestrogens, not androgens, cause the bone age to advance
  • F
  • Peak growth spurt: beginning to mid puberty
  • End point: menarche (slows down and stop)
  • Linear growth essentially complete when bone age is 15.5 years
  • M
  • Growth spurt starts: mid/late puberty with 6-10 ml testes
  • Peak height velocity: 10-12 mls testes (average 14 years)
  • Linear growth essentially complete when bone age is 18 years
    *
90
Q

Principles of Growth by Dr Fatima

Body Composition

*LOB: Describe body composition changes and gender differences during growth

A
91
Q

Principles of Growth by Dr Fatima

Society and Growth

*LOB: Identify social influences on growth

A

Nutritional impairment
Prolonged chronic illness affecting energy consumption or hormonal and growth factor influences.
Absence of a secure and caring environment

Growth patterns respond to environmental pressures
E.g. excessive training, anorexia, emotional deprivation

Psychosocial dwarfism- extreme stress reduces growth

Insulin resistance could predispose to DM2 and CVD

92
Q

Growth Charts and Their Uses by Dr Fatima

Why monitor growth?

*LOB: Understand the importance of monitoring growth in childhood

A
  • Essential for prescribing
  • Assessment of overall health
  • Nutrition
  • Deviation from expected normal may indicate variety of conditions
  • For diagnosis or monitoring of conditions
  • May indicate social concerns that require support
  • May indicate safeguarding concerns
  • Screening
  • Surveillance
    *
93
Q

Principles of Growth by Dr Fatima

Measuring Growth

*LOB: Be familiar with the different growth charts in use in the UK

A

Regular monitoring in infancy
All children in the UK have height and weight measured – National Child Measurement Programme- 4-5 years (reception)- 10-11 years (year 6)Primarily to monitor trends in obesity

Length <2 yrs
Height- >2 yrs – standing height

Head circumference

94
Q

Principles of Growth by Dr Fatima

Growth Charts

*LOB: Be familiar with the different growth charts in use in the UK

A

UK-WHO growth charts
Based on WHO Child Growth Standards
Bands on the growth charts denote standard deviations from the mean
Single growth parameter should not be assessed in isolation
Serial measurements used to show the pattern

No lines between birth and 2 weeks – normal to lose weight during this time- though weight loss of >10% requires assessment - 80% of infants regain birth weight by 2 weeks

Length / height centiles change at 2 years as the spine squashes a little on standing

95
Q

Principles of Growth by Dr Fatima

Mid-parental centile (MPC)

*LOB: Plot and interpret simple measurements on a growth chart

A
  • Assess growth in context of the child’s family
  • Heights from both biological parents should be used to calculate the MPC
  • Or calculate mean of father’s and mother’s height and add 7cm for a boy, subtract 7cm for a girl.
  • Most children have a height centile within two centile spaces of the MPC.
96
Q

Principles of Growth by Dr Fatima

Centile Space

*LOB: Be familiar with the different growth charts in use in the UK

A

A Centile Space is the distance between two centile lines (e.g. C)

Can also be used to describe where two points are both midway between centiles (e.g. D)

Falls or rises should be described in terms of centile spaces (e.g. a fall through 2 ½ centile spaces).

97
Q

Principles of Growth by Dr Fatima

Preterm infants

*LOB: Be familiar with the different growth charts in use in the UK

A
  • Specific growth charts for preterm infants born <32 weeks, for close monitoring
  • If between 32 and 37 weeks – plot in the preterm section until 42 weeks
  • Thereafter, plot measurements at actual age (dot), but also correct for gestational age (the arrow)
  • Continue correcting until at least 1 year of age (2 if very preterm)
    *
98
Q

Principles of Growth by Dr Fatima

Other Charts

*LOB: Be familiar with the different growth charts in use in the UK

A

Down syndrome
Turner syndrome
Williams syndrome
Prader- Willi syndrome

99
Q

Principles of Growth by Dr Fatima

Growth Concerns

*LOB: Understand what is meant by faltering growth, short stature, underweight, overweight and obesity and how to recognise these

A

Rapid weight loss (or gain)
Unexplained short stature
Signs of an underlying disorder
Safeguarding concerns
Dropping centiles

100
Q

Principles of Growth by Dr Fatima

Faltering growth

*LOB: Understand what is meant by faltering growth, short stature, underweight, overweight and obesity and how to recognise these

A

Often defined as a fall in weight of two or more major centile linesor weight centile two or more below length/heightor OFC or weight centile below 2nd centile for ageNeeds serial measurements

101
Q

Principles of Growth by Dr Fatima

Short stature:

*LOB: Understand what is meant by faltering growth, short stature, underweight, overweight and obesity and how to recognise these

A

Height below the 2nd centileConsider familial, constitutional delay of growth and puberty, genetic disorders, nutritional, general health and endocrine causes

102
Q

Principles of Growth by Dr Fatima

BMI terminology

*LOB: Understand what is meant by faltering growth, short stature, underweight, overweight and obesity and how to recognise these

A
  • From 2 years
  • UnderweightBMI under 2nd centile
  • OverweightBMI over 91st centile
  • ObesityBMI over 98th centile (and if over 99.6th centile – severely obese)
103
Q

Psychomotor Development by Georgina Ndukwe

Formation of the CNS

*LOB: Outline the theory of neurodevelopment

A
  1. Formation of the neural tube
  2. Development of the prosencephalon (the primitive forebrain)
  3. Neuronal proliferation, migration and organisation
  4. Myelination
104
Q

Psychomotor Development by Georgina Ndukwe

Formation of the Neural Tube

*LOB: Outline the theory of neurodevelopment

A

Day 16 – neural plate forms from the ectoderm
Day 18 – neural groove
Day 22 – neural tube
Day 27 – neural tube closed, brain and spinal cord differentiation begin

Molecules released by the notochord are programmed to genetically initiate the differentiation of cells to become neural tissue.
These molecules are chordin, noggin and follistatin in the cranial region and WNT3a and FGF in the hindbrain and spinal cord.

105
Q

Psychomotor Development by Georgina Ndukwe

Abnormal formation of the CNS

*LOB: Outline the theory of neurodevelopment

A

Failure of the correct folding and closure can result in:
* Anencephaly
* Encephalocoele
* Chiari malformation
* Spina bifida

Causes:
* Px: retinoic acid, anticonvulsants or lithium which all have teratogenic effects
* alcohol, cocaine and opiates
* ionising radiation, dioxins, heavy metals, organic solvents
* diabetes, low folate levels, hyperthermia and TORCH infections

106
Q

Psychomotor Development by Georgina Ndukwe

Development of the prosencephalon (the primitive forebrain)

*LOB: Outline the theory of neurodevelopment

A

takes place between the 5th and 10th gestational weeks
4th wk: forebrain, midbrain and hindbrain)
6th wk: differentiation of cerebral hemispheres

107
Q

Psychomotor Development by Georgina Ndukwe

Abnormal evelopment of the prosencephalon

*LOB: Outline the theory of neurodevelopment

A

Holoprosencephaly (trisomy 13)
Corpus callosum agenesis
Dandy Walker syndrome

108
Q

Psychomotor Development by Georgina Ndukwe

Neuronal proliferation, migration and organisation

*LOB: Outline the theory of neurodevelopment

A

The proliferation starts between the 10th and 20th week of pregnancy

From 2-5 months gestation:
Cell differentiation into neurons and supporting cells
Cell proliferation
Neuronal migration and organisation

Neuroblasts proliferate in the germinal matrix between 7 and 8 weeks of gestation, from here cells migrate peripherally to form the brain

neuronal migration and this happens between 12 and 24 weeks of gestation

109
Q

Psychomotor Development by Georgina Ndukwe

Synaptogenesis

*LOB: Outline the theory of neurodevelopment

A

Synapses each maximum density at 6-12 months after birth

110
Q

Psychomotor Development by Georgina Ndukwe

Abnormalities in neuronal migration and organisation include:

*LOB: Outline the theory of neurodevelopment

A
  • Heterotopias – migration problem
  • Microcephaly -– growth and proliferation problem
  • Polymicrogyria : migration and organisation problem
  • Agyria-pachygyria no gyri, broad gyri
  • Lissencephaly- : smooth brain surface
    *
111
Q

Psychomotor Development by Georgina Ndukwe

Myelination

*LOB: Outline the theory of neurodevelopment

A

At birth:
Cerebral cortex primitive
Neurons poorly connected

Changes around and after birth:
Myelination of nerves
Increase of number of connections between cells

Myelination progresses:
Nervous control of various functions improve
Continues throughout childhood

112
Q

Psychomotor Development by Georgina Ndukwe

Dysmyelinating disorders:

*LOB: Outline the theory of neurodevelopment

A

Dysmyelinating disorders:
White matter disorders - laying down of abnormal myelin
Leukodystrophies (genetically determined diseases of white matter) such as:
Krabbe disease
Metachromatic leukodystrophy
X-linked adrenoleukodystrophy

113
Q

Psychomotor Development by Georgina Ndukwe

Influences on Development

*LOB: Recognise causes of delayed development

A
114
Q

Psychomotor Development by Georgina Ndukwe

Causes of developmental problems…

*LOB: Recognise causes of delayed development

A
115
Q

Psychomotor Development by Georgina Ndukwe

Gross Motor Function Development

*LOB: Apply your understanding of developmental milestones in a clinical scenario
*LOB: Detail the normal patterns of development for gross motor function, fine motor function and vision, speech and hearing, and social development

A
116
Q

Psychomotor Development by Georgina Ndukwe

Fine Motor Function Development

*LOB: Apply your understanding of developmental milestones in a clinical scenario
*LOB: Detail the normal patterns of development for gross motor function, fine motor function and vision, speech and hearing, and social development

A
117
Q

Psychomotor Development by Georgina Ndukwe

Vision and Speech Function Development

*LOB: Apply your understanding of developmental milestones in a clinical scenario
*LOB: Detail the normal patterns of development for gross motor function, fine motor function and vision, speech and hearing, and social development

A
118
Q

Psychomotor Development by Georgina Ndukwe

Social Development

*LOB: Apply your understanding of developmental milestones in a clinical scenario
*LOB: Detail the normal patterns of development for gross motor function, fine motor function and vision, speech and hearing, and social development

A
119
Q

Psychomotor Development by Georgina Ndukwe

What is delay?

*LOB: Explain how developmental delay may be diagnosed

A

Failure to acquire a particular developmental skill at an age when 95% of peers have

Global and Specific Delay

120
Q

Psychomotor Development by Georgina Ndukwe

Diagnosing Delay

*LOB: Explain how developmental delay may be diagnosed

A
121
Q

Paediatric Pharmacology by Dr Sara Griffiths

What makes pharmacology different in children

*LOB: Recognise the differences in pharmacokinetics for the paediatric p

A

Lack of data/evidence
Medicines used “off-label”
Prescribing by weight
Huge range in age/weight/surface area
Children grow and develop very quickly
Practical/behavioural problems

122
Q

Paediatric Pharmacology by Dr Sara Griffiths

A – Absorption (enteral)

*LOB: Recognise the differences in pharmacokinetics for the paediatric

A

-Gastric pH – higher in neonates (6-8) but reaches adult levels by age 3

  • Acid labile drugs (eg amoxicillin) more easily absorbed
  • Weak organic acids (eg phenytoin) decreased absorption
  • Basic drugs – absorbed more rapidly
  • Gastric emptying – slow and linear in neonates – adult levels at 6-8 months
  • Intestinal transit – prolonged in neonates, reduced older infants
  • Bile and pancreatic fluid – immaturity -> reduced absorption of fat soluble vitamins
  • Variable microbial colonizaton
123
Q

Paediatric Pharmacology by Dr Sara Griffiths

A – Absorption (IM)

*LOB: Recognise the differences in pharmacokinetics for the paediatric

A
  • Decreased blood flow to muscle
  • Reduced muscular mass
  • Painful
124
Q

Paediatric Pharmacology by Dr Sara Griffiths

A – Absorption (rectal)

*LOB: Recognise the differences in pharmacokinetics for the paediatric

A
  • pH alkaline in children (neutral in adults)
  • Variations in rectal venous drainage
  • Differences in absorption of paracetamol in preterm/term neonates
  • Differences in absorpton of tramadol in children vs adults
  • Absorption unpredictable
    *
125
Q

Paediatric Pharmacology by Dr Sara Griffiths

A – Absorption (percutaneous)

*LOB: Recognise the differences in pharmacokinetics for the paediatric

A
  • Greater body surface area related to weight
  • Increased permeability (100-1000x greater <30 weeks gestation)
  • Systemic toxicity eg lidocaine, steroids
126
Q

Paediatric Pharmacology by Dr Sara Griffiths

D – Distribution – body composition

*LOB: Recognise the differences in pharmacokinetics for the paediatric

A

Neonates/young infants –
high total body water (80-90%)
low body fat (10-15%)
Higher volume of distribution of water-soluble drugs (Eg gentamycin)
Similar or lower for fat-soluble drugs (eg diazepam)

127
Q

Paediatric Pharmacology by Dr Sara Griffiths

D- Distribution – plasma protein binding

*LOB: Recognise the differences in pharmacokinetics for the paediatric

A

Reduced concentration of binding proteins in neonates
Increased concentration of “free” drug
Increased efficacy/toxicity

128
Q

Paediatric Pharmacology by Dr Sara Griffiths

D- Distribution – membrane permeability

*LOB: Recognise the differences in pharmacokinetics for the paediatric

A

Blood-brain barrier more permeable
Brain disproportionately large in young children

129
Q

Paediatric Pharmacology by Dr Sara Griffiths

M- Metabolism

*LOB: Recognise the differences in pharmacokinetics for the paediatric

A

-Phase 1 – modification - Cytochrome p450
– CYP3A4
- CYP1A2
Phase 2 – conjugation
glucuronidation
sulfation.

CYP3A4 activity is very low in neonates

130
Q

Paediatric Pharmacology by Dr Sara Griffiths

E- Excretion

*LOB: Recognise the differences in pharmacokinetics for the paediatric

A
  • Variable Glomerular filtration rate
  • Neoate 30-40% adult values
  • Toddlerhood - exceeds
  • Tubular secretion and resorption also maturing
  • Decreased renal blood flow
  • Urinary pH – lower in young children – increased resorption of weak acids
    *
131
Q

Paediatric Pharmacology by Dr Sara Griffiths

IV chloramphenicol - Grey baby syndrome

A
  • Abdominal distension, hemodynamic collapse, ashen-gray skin discoloration
  • Immature liver enzymes - reduced glucuronidation
  • Reduced renal excretion
  • Impaired myocardial contractility -> cardiovascular collapse
  • Chloramphenicol displaces unconjugated bilirubin
  • Increased permeability of BBB -> kernicterus
  • *
132
Q

Paediatric Pharmacology by Dr Sara Griffiths

Toxicity + Adverse drug reactions

*LOB: Explain the significance of therapeutic drug monitoring in childre

A

Toxicity on developing organs
Corticosteroids – growth suppression
Sulphonamide – kernicterus
Ceftriaxone + calcium solutions – calcium precipitation in lungs

133
Q

Paediatric Pharmacology by Dr Sara Griffiths

Drug Errors

*LOB: Explain the significance of therapeutic drug monitoring in childre

A

Potentially harmful errors 3x higher in paediatrics
6 major themes;
Children’s fundamental differences
Individualised dosing and calculations
Medication formulations
Communication with children
Experience working with children

134
Q

Paediatric Pharmacology by Dr Sara Griffiths

Therapeutic drug monitoring

*LOB: Recognise the differences in pharmacokinetics for the paediatric

A
  • Weak correlation between the dose administered and concentration reached
  • Quantitative relationship between concentrations and side effects
  • Therapeutic concentration range is narrow
  • Results can be used to adjust treatment
  • Small blood volume
  • Difficulty obtaining blood samples
  • Diminished ability to tolerate/recognize or communicate drug effects
  • Accuracy of dose administration and preparation
  • Compliance
135
Q

Paediatric Pharmacology by Dr Sara Griffiths

Drug Route

*LOB: Appreciate the importance of the route of drug administration in c

A

Availability of suspension/elixars
Palatabilty
Measuring Errors – small dosing
Adherence
Intravenous – difficult to obtain, painful, infection risk
Intramuscular – variable muscle mass/blood flow, painful
Rectal – dosage difficult/ not always popular/convenient
Intraosseous - critically unwell patients/resuscitation

Med 2 Life Cycle (4 decks)

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