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Endocrinology Flashcards

1
Q

What is the presentation of T1DM?

A

Diabetic ketoacidosis - dehydration, lethargy, confusion, polyuria/polydipsia, weight loss, abdominal pain

Triad of hyperglycaemia:
Polyuria, polydipsia, weight loss

Secondary enuresis
Recurrent infections

Toilet, thirst, tiredness, thinner

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2
Q

What are the investigations when a new diagnosis of T1 DM is established?

A

FBC, renal profile, lab glucose
Blood cultures
HbA1c
TFTs
Thyroid peroxidase antibodies
Tissue transglutaminase anti TTG for coeliac
Insulin antibodies, anti GAD antibodies and islet cell antibodies

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3
Q

What does long term management of T1 DM involve?

A

Insulin -

Basal bolus regime e.g. Lantus in evening to give constant background then Actrapid 3x day before meals, injected according to carbs

Insulin pumps - tethered or patch pumps

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4
Q

What are the short term complications of T1DM?

A

Hypoglycaemia - hunger, tremor, sweating, irritability, dizziness, pallor
Treat with rapid acting glucose and slow carbs
If coma - IV dextrose and IM glucagon

Hyperglycaemia
DKA

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5
Q

What are some other causes of hypoglycaemia?

A 
Hypothyroidism
Glycogen storage disorders
Growth hormone deficiency
Liver cirrhosis
Alcohol and fatty acid oxidation defects
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6
Q

What are some of the long term complications of T1 DM?

A

Macrovascular
CAD, peripheral ischaemia causes poor healing, ulcers, diabetic foot
Stroke
Hypertension

Microvascular Complications
Peripheral neuropathy
Retinopathy
Kidney disease, glomerulosclerosis

Infection related complications
UTIs, pneumonia
Skin and soft tissue infections
Fungal infections, oral and vaginal candidiasis

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7
Q

What is the pathophysiology of DKA?

A

Cells think they have no fuel, so initiate ketogenesis
Ketone levels rise, bicarbonate used to buffer this is used up, so Ketoacidosis occurs

Hyperglycaemia overwhelms kidneys, glucose filtered into urine
Draws water out causing osmotic diuresis
Wees a lot, so then thirsty

Insulin normally drives potassium into cells
without it total body potassium low and serum potassium high in DKA

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8
Q

What is a dangerous consequence of DKA in children?

A

Risk of developing cerebral oedema
Dehydration and high blood sugar concentration causes water to move into extracellular space

Look for headaches, altered behaviour, bradycardia
changes to consciousness

Slow IV fluids, IV mannitol, IV hypertonic saline

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9
Q

What is the presentation of DKA?

A 
Polyuria
Polydipsia
Nausea and vomiting
Weight loss
Acetone smell to their breath
Dehydration and subsequent hypotension
Altered consciousness
Symptoms of an underlying trigger (i.e. sepsis)
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10
Q

What is the criteria to diagnose DKA?

A

Hyperglycaemia (i.e. blood glucose > 11 mmol/l)
Ketosis (i.e. blood ketones > 3 mmol/l)
Acidosis (i.e. pH < 7.3)

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11
Q

What is the principle of management of DKA in children?

A

Correct dehydration evenly over 48 hours - corrects dehydration, dilutes hyperglycaemia and ketones, correcting faster increases risk of cerebral oedema

Give a fixed rate insulin infusion

Avoid fluid boluses
Treat underlying triggers e.g. abx for sepsis
Prevent hypoglycaemia with IV dextrose if falls below 14
Add potassium to IV fluids
Monitor for signs of cerebral oedema
Monitor glucose, ketones and pH

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12
Q

What is the classification of diabetes?

A

Type 1 - most childhood diabetes, due to destruction of beta cells, autoimmune

Type 2 - insulin resistance, obesity related

Type 3 - maturity onset diabetes of the young, genetic defects, drugs, pancreatic exocrine insufficiency e.g. CF, neonatal diabetes, chromosomal e.g. Down’s or Turners

Type 4 - gestational

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13
Q

What is a sign of insulin resistance?

A

Acanthosis nigricans

Velvety dark skin on the neck or armpits

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14
Q

What are other signs of type 2 diabetes?

A

Family history
Severely obese children
Skin tags
PCOS

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15
Q

What factors can increase blood glucose levels?

A 
Omission of insulin
Food, esp refined carbs
Illness
Menstruation - shortly before onset
Growth hormone
Corticosteroids
Sex hormones at puberty
Stress of an operation
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16
Q

What factors can decrease blood glucose levels?

A 
Insulin
Exercise
Alcohol
Some drugs
Marked anxiety/excitement
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17
Q

What is important in a regular assessment of a child with diabetes?

A 
Any episodes of hypos, DKA, hospital admission
Awareness of hypos
Absence from school
Insulin regimen, blood glucose results
Diet
Lipohypertrophy

BP, renal disease, eye screening, coeliac, thyroid, annual flu vaccine

Becoming self reliant, sport and exercise, smoking, alcohol

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18
Q

What are causes of hypoglycaemia beyond the neonatal period?

A

Insulin excess
Medication, tumours, autoimmune, Beckwith syndrome

Without hyperinsulinaemia
Liver disease, ketotic hypoglycaemia, inborn errors of metabolism, inborn errors of metabolism
Hormonal deficiency e.g. GH, ACTH, Addison’s

Reactive/non-fasting
Galactosaemia
Fructose intolerance
Maternal diabetes
Hormonal deficiency
Aspirin/alcohol poisoning
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19
Q

How can hypoglycaemia be treated?

A

IV infusion of glucose
10% dextrose

Avoid giving excess volume
Corticosteroids may be used if there is a possibility of hypopituitarism or hypoadrenalism

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20
Q

Who should hypoglycaemia be excluded in?

A

Sepsis
Seriously ill
State of prolonged seizure or altered state of consciousness

Don’t Ever Forget Glucose

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21
Q

What are causes of congenital hypothyroidism?

A

Maldescent of thyroid and athyrosis
Dyshormonogenesis - inborn error of thyroid hormone synthesis
Iodine deficiency
Hypothyroidism due to TSH deficiency

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22
Q

What are the features of congenital hypothyroidism?

A 
Usually asymptomatic
Picked up on screening
Failure to thrive
Feeding problems
Prolonged jaundice
Constipation
Pale, cold, mottled dry skin
Coarse facies
Large tongue
Hoarse cry
Goitre - occasionally 
Umbilical hernia
Delayed development
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23
Q

What are the features of acquired hypothyroidism?

A 
Females > males
Short stature/growth failure
Cold intolerance
Dry skin
Cold peripheries
Bradycardia
Thin, dry hair
Pale, puffy eyes
Loss of eyebrows
Goitre
Slow relaxing reflexes
Constipation
Delayed puberty
Obesity
Slipped upper femoral epiphysis
Deterioration in school work, learning difficulties
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24
Q

How is congenital hypothyroidism detected?

A

Neonatal. blood screening. - Guthrie test

Raised TSH in the blood

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25
Q

What is the treatment for congenital hypothyroidism?

A

Oral replacement of thyroxine - levothyroxine

Titration of dose to maintain normal growth, TSH, and T4 levels

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26
Q

What is the cause of hyperthyroidism in children?

A

Graves disease

Secondary to production of thyroid stimulating immunoglobulins

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27
Q

What are the clinical features of hyperthyroidism?

A

Eye features less common
Low TSH, high T3/T4

Anxiety, restlessness
Increased appetite
Sweating, diarrhoea, weight loss, rapid growth in height
Tremor, tachycardia
Goitre
Learning difficulties
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28
Q

What is the treatment for hyperthyroidism?

A

Carbimazole or propylthiouracil - interferes with thyroid hormone synthesis
Beta blockers for symptomatic relief

Risk of neutropenia - seek help if sore throat and high fever

Treatment given for 2 years, many relapse

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29
Q

What is the cause of hypoparathyroidism in children?

A

Congenital deficiency - Di George syndrome

Associated with thyme aplasia, defective immunity, cardiac defects, facial abnormalities

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30
Q

What are the types of adrenal insufficiency?

A

Primary - Addison’s, adrenal glands damaged

Secondary - inadequate ACTH stimulating glands - congenital hypoplasia, surgery, infection, loss of blood flow, radiotherapy

Tertiary adrenal insufficiency - inadequate CRH release from hypothalamus, due to long term steroids

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31
Q

What are the features of adrenal insufficiency in babies?

A 
Lethargy
Vomiting
Poor feeding
Hypoglycaemia
Jaundice
Failure to thrive
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32
Q

What are the features of adrenal insufficiency in older children?

A

Nausea and vomiting
Poor weight gain or weight loss
Reduced appetite (anorexia)
Abdominal pain
Muscle weakness or cramps
Developmental delay or poor academic performance
Bronze hyperpigmentation to skin in Addison’s caused by high ACTH levels. ACTH stimulates melanocytes.

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33
Q

What are the investigations for adrenal insufficiency?

A 
U&Es - hyponatraemia, hyperkalaemia 
Blood glucose - hypoglycaemia
Cortisol
ACTH
Aldosterone
Renin
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34
Q

What are the results of investigations if Addison’s is the diagnosis?

A

Low cortisol
High ACTH
Low aldosterone
High renin

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35
Q

What are the results of investigations if secondary adrenal insufficiency is the diagnosis?

A

Low cortisol
Low ACTH
Normal aldosterone
Normal renin

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36
Q

What is the short synacthen test?

A

Used to confirm adrenal insufficiency
Given synacthen, blood cortisol measured baseline and then 30-60 mins after
Synthetic ACTH should stimulate adrenal glands to produce cortisol, if not - less than double - primary insufficiency

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37
Q

What is the treatment of adrenal insufficiency?

A

Replacement steroids
Hydrocortisone = cortisol
Fludrocortisone = aldosterone

Steroid card, do not miss a dose
Dose increased during acute illness

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38
Q

What is the presentation of an Addisonian crisis?

A

Reduced consciousness
Hypotension
Hypoglycaemia, hyponatraemia, hyperkalaemia

Can be first presentation, triggered by infection, trauma or acute illness

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39
Q

What is the management of Addisonian crisis?

A

Intensive monitoring if unwell
Parenteral steroids e.g. IV hydrocortisone
IV fluid resuscitation
Correct hypoglycaemia
Careful monitoring of electrolytes and fluid balance

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40
Q

What is congenital adrenal hyperplasia?

A

Congenital deficiency of hydroxylase enzyme causing underproduction of cortisol and aldosterone
Overproduction of androgens from birth

Inherited in autosomal recessive pattern

41
Q

What is the pathophysiology of CAH?

A

No conversion of progesterone to aldosterone and cortisol
Conversion to testosterone does not rely on this enzyme

So low aldosterone, low cortisol and abnormally high testosterone

42
Q

What is the presentation of CAH in severe cases?

A

Ambiguous genitalia
Enlarged clitoris due to high testosterone
Hyponatraemia, hyperkalaemia, hypoglycaemia

Poor feeding, vomiting
Dehydration
Arrhythmias

43
Q

What is the presentation of CAH in mild cases?

A

Symptoms tend to be related to high androgen levels
Hyperpigmentation because pituitary responds to low cortisol by producing ACTH

Tall for age, facial hair
Absent periods
Deep voice
Early puberty

Large penis, small testicles

44
Q

What is the treatment of CAH?

A

Cortisol replacement - hydrocortisone
Aldosterone replacement - fludrocortisone
May require corrective surgery

45
Q

What are the types of growth hormone deficiency?

A

Congenital - disruption of growth hormone axis at hypothalamus or pituitary
Due to genetic mutation

Acquired growth hormone deficiency - secondary to infection, trauma, interventions

46
Q

What is the presentation of growth hormone deficiency?

A

In birth/neonates:
micropenis, hypoglycaemia, severe jaundice

Older children:
Poor growth - stopping/slowing age 2-3
Short stature
Slow development of movement and strength
Delayed puberty
47
Q

What are the investigations for growth hormone deficiency?

A

Growth hormone stimulation test - response to medications normally stimulating release of GH e.g. glucagon, insulin, arginine, clonidine

Test for associated deficiencies e.g. thyroid, adrenal
MRI brain - pituitary or hypothalamus abnormalities
Genetics e.g. Turners, P-W
X-Ray usually of wrist or DEXA scan to determine bone age and final height

48
Q

What is the treatment of GH deficiency?

A

Daily subcutaneous injections of growth hormone - somatropin
Treatment of other associated hormone deficiencies
Close monitoring of height and development

49
Q

What is diabetes insipidus?

A

Lack of ADH
or lack of response to ADH
Prevents kidneys from concentrating urine, leads to polyuria and polydipsia

50
Q

What is nephrogenic diabetes insipidus?

A

Collecting ducts do not respond to ADH

Drugs - lithium in BAD
Genetic mutations coding for the ADH receptor
Intrinsic kidney disease
Electrolyte disturbances - hypokalaemia, hypercalcaemia

51
Q

What is cranial/central diabetes insipidus?

A

Hypothalamus does not produce ADH for pituitary glands to secrete
Can be idiopathic or:

Brain tumours, malformations
Head injury
Infection - meningitis, encephalitis, TB
Brain surgery, radiotherapy

52
Q

What is the presentation of diabetes insipidus?

A 
Polyuria
Polydipsia
Dehydration
Postural hypotension
Hypernatraemia
53
Q

What are the investigations for diabetes insipidus?

A

Low urine osmolality
High serum osmolality

Water deprivation test - desmopressin stimulation test:

No fluids for 8 hours
Urine osmolality measured
Synthetic ADH - desmopression administered
8 hours later measured again

In central - patient lacks ADH, so when given osmolality is high as kidneys now respond and reabsorb water concentrating urine

If nephrogenic - will remain low

54
Q

What is the management of diabetes insipidus?

A

Desmopression to replace ADH

Treatment of underlying cause e.g. if due to drugs stop, treatment of electrolyte disorder

55
Q

What causes Vitamin D deficiency?

A

Deficient intake or defective metabolism
Causes low serum calcium
Triggers secretion of PTH and demineralises bone

56
Q

What is the presentation of Vit D deficiency?

A

Bony deformity, rickets

Symptoms of hypocalcaemia - seizures, neuromuscular irritability/tetany, apnoea, stridor

57
Q

What is the clinical manifestation of rickets?

A

Ping pong ball sensation over the skull - craniotabes
Elicited by pressing on occipital/parietal bones
Wrists and ankles widened
Harrison sulcus on chest
Delayed closure of anterior fontanelle

Misery
Failure to thrive

58
Q

What are the causes of rickets?

A 
Nutritional - primary rickets
Living in northern latitudes 
Dark skin
Decreased exposure to sun
Diets low in calcium, phosphorous, Vit D

Intestinal malabsorption
Coeliac, CF, liver disease
High phytic acids in diet e.g. chapattis

Defective production of 25 (OH)D2, increased metabolism, defective productive of active VitD

59
Q

How is a diagnosis of rickets made?

A

Dietary history for vit and calcium intake
Blood tests
x-ray of wrist joint - shows cupping and fraying of the metaphases, widened epiphyseal plate

60
Q

What is the management of rickets?

A

Advice on balanced diet
Correction of risk factors
Daily administration of Vit D3 - cholecalciferol
Healing takes 2-4 weeks, monitored by lowering alkaline phosphatase

61
Q

What are some of the complications of obesity?

A 
Orthopaedic - SUFE, bow legs, abnormal foot structure
Idiopathic intracranial HTN
Hypoventilation syndrome, sleep apnoea
Gallbladder disease
PCOS
T2 DM
HTN
Abnormal blood lipids
Other medical and psychological sequelae
62
Q

What centile defines a child as overweight or obese?

A

> 91st centile overweight

>98th centile obese

63
Q

What is the management of obesity?

A

Treat endogenous cause
Healthier eating
Increase in habitual physical activity
Reduce physical inactivity e.g. small screen time to less than 2h per day

Drug treatment
Orlistat reduces absorption of dietary fat, produces steatorrhoea
Metformin if any evidence of insulin insensitivity

64
Q

What are the phases of growth?

A

First 2 years - rapid growth driven by nutritional factors
From 2 years to puberty: steady slow growth
During puberty - rapid growth spurt driven by sex hormones

65
Q

What defines faltering growth?

A

One or more centile spaces if their birthweight was below the 9th centile
Two or more centile spaces if their birthweight was between the 9th and 91st centile
Three or more centile spaces if their birthweight was above the 91st centile

66
Q

What are the causes of failure to thrive?

A 
Inadequate nutritional intake
Difficulty feeding
Malabsorption
Increased energy requirements
Inability to process nutrition
67
Q

What can cause inadequate nutritional intake and subsequently failure to thrive?

A 
Maternal malabsorption if breastfeeding
Iron deficiency anaemia
Family or parental problems
Neglect
Availability of food
68
Q

What can cause difficulty feeding and failure to thrive?

A

Poor suck e.g. cerebral palsy
Cleft lip or palate
Genetic conditions
Pyloric stenosis

69
Q

What can cause malabsorption and failure to thrive?

A 
CF
Coeliac disease
Cows milk intolerance
Chronic diarrhoea
IBD
70
Q

What can cause an increase in energy requirements and failure to thrive?

A

Hyperthyroidism
Chronic disease e.g. congenital heart disease and CF
Malignancy
Chronic infections e.g. HIV, immunodeficiency

71
Q

What can cause an inability to process nutrients properly?

A

Inborn errors of metabolism

Type 1 diabetes

72
Q

What defines short stature?

A

More than 2 standard deviations below average for age and sex

73
Q

What are some of the causes for short stature?

A

Familial short stature
Constitutional delay in growth and development
Malnutrition
Chronic diseases e.g. coeliac, IBD, congenital heart disease
Endocrine e.g. hypothyroid
Genetic conditions e.g. Downs
Skeletal dysplasia e.g. achondroplasia

74
Q

What occurs in constitutional delay in growth and puberty?

A

Delayed bone age - x-ray assesses size and shape of bones and growth plates

75
Q

What can cause delayed puberty with short stature?

A

Turner’s
Prader Willi
Noonan’s

76
Q

What can cause delayed puberty with normal stature?

A

PCOS
Androgen insensitivity
Kallman’s syndrome
Klinefelter’s

77
Q

When is it defined as late-onset puberty?

A

When physical changes e.g. breast and testicular development have not begun before the age of 14

78
Q

What is adrenarche?

A

Increased production of androgens in adrenal glands, in girls
converted to oestrogen

Leads to increased sebaceous gland activity
Acne, sweating
Hair growth
Body odour

79
Q

What is the staging of pubertal development?

A

Tanner Staging

80
Q

When does menarche occur?

A

Average age is 12.9

Usually coincides with Stage 3 of breast development

81
Q

What occurs in testicular development?

A

Testicular enlargement, measured with an orchidometer
Increased pigmentation
Scrotal thickening
Penile growth and thickening

82
Q

What is a common side effect of puberty in boys?

A

Gynaecomastia

Initial imbalance of oestrogen and androgens at onset

83
Q

What are the types of precocious puberty?

A

True - early activation of hypothalamic pituitary axis

False - gonadotrophin independent, isolated development of one pubertal characteristic

84
Q

What are the causes of hypogonadotropic hypogonadism?

A

Deficiency of LH and FSH
Deficiency of testosterone and oestrogen as gonads not stimulated

Previous damage e.g. radiotherapy
Growth hormone deficiency
Hypothyroidism
Hyperprolactinaemia 
Serious chronic conditions
Excessive exercise/dieting
Constitutional delay in growth and development 
Kallman syndrome
85
Q

What is hypergonadotrophic hypogonadism and its causes?

A

Where gonads fail to respond to stimulation
No negative feedback, so AP produces more and more LH/FSH

Previous damage to gonads
Congenital absence of testes or ovaries
Kleinfelter’s
Turner’s XO

86
Q

What are the investigations for delayed puberty?

A

Girl - 13, boy - 14 if no evidence of any changes
History, height, weight

FBC, ferritin - anaemia
U&Es - CKD
Anti-TTF, anti-EMA

Early morning serum FSH and LH, TFTs, GH, PL

Microarray for
Kleinfelter’s, Turner’s

Imaging
X-ray of wrist - bone age
Pelvic US - ovaries
MRI - pituitary pathology

87
Q

What is the definition of precocious puberty?

A

Development of secondary sexual characteristics before 8 years in females, 9 in males
More common in females

88
Q

What are the causes of true gonadotrophin dependent precocious puberty?

A

Central malformation or damage e.g. hydrocephalus, neurofibromatosis

Acquired - post-sepsis, surgery, radiotherapy, trauma

Brain tumours

89
Q

What are the causes of false gonadotrophin dependent precocious puberty?

A 
Increased adrenal activity
Congenital adrenal hyperplasia
Gonadal tumour
Hypothyroidism
McCune Albright syndrom
90
Q

What is McCune Albright syndrome?

A

Not inherited
Due to random somatic mutation

Precocious puberty
Cafe au lait spots
Polyostotic fibrous dysplasia
Short stature

91
Q

What are some causes of tall stature?

A

Familial tall stature

Endocrine disorders:
Precocious puberty
Hyperthyroidism
Glucocorticoid resistance
GH excess
Nonendocrine disorders:
Exogenous obesity
Klinelter's
47,xxy
Marfan
Homocystinuria
Neurofibromatosis type 1
Beckwith-Wiedemann Syndrome - overgrowth disorder, increase of childhood cancer
92
Q

What are baseline investigations for tall stature?

A 
Karyotype
T4, TSH
IGF-1
Bone age assessment
Predication of final height
Serum LH, FSH
Testosterone
Glucose suppression for GH
Visual field examination
MRI of pituitary
Serum cortisol
Serum prolactin
93
Q

What is gigantism?

A

Abnormal linear growth due to growth hormone excess
Leads to IGF-1 synthesis, cell growth and proliferation
Tall stature
Growth of distal limbs
Tumour mass symptoms - hypopituitarism
Progressive macroencephaly
Coarse facial features

94
Q

What tests confirm gigantism?

A

Raised serum IGF-1
Raised GH after oral glucose tolerance test

MRI can show pituitary mass
CT if MRI negative - exclude other GH secreting tumours e.g. pancreas, adrenal glands, ovarian, bronchial

95
Q

What is the difference between gigantism and acromegaly?

A

GH hyper secretion before fusion of long bone epiphysis, acromegaly is after fusion leading to large extremities and characteristic facies

96
Q

What is the treatment of gigantism?

A

Transsphenoidal surgery - pituitary adenoma excision
Somatostatin analogs
GH receptor antagonists

97
Q

What is Marfan’s syndrome?

A

Autosomal dominant connective tissue disorder

Defect that codes for protein fibrillin -1

98
Q

What are the features of Marfan’s?

A

Tall stature
Arm span to height ratio >1.05
High arched palate
Arachnodactyly
Pectus excavatum
Pes Plans
Scoliosis >20 degrees
Heart - dilation of aortic sinuses - aortic aneurysm, aortic dissection, aortic regurgitation
Lungs - repeated pneumothoraces
Eyes - upwards lens dislocation, blue sclera, myopia
Dural ectasia - ballooning of the dural sac

Paediatrics (17 decks)

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