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Conditions + definitions > Endocrine - paeds + others > Flashcards

Endocrine - paeds + others Flashcards

1
Q

What are the puberty stages?

A 
Breast development 1-5 (girls)
Genital development 1-5 (boys)
>Scrotum + penile length + thickening
>Testicular volumes 2-20ml
Pubic hair 1-5
Axillary hair 1-3

1 - prepuberty
2 - start of puberty
5 - adult

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2
Q

What are the different assessments in child growth?

A 
Height/length/weight
	Growth charts and plotting
	MPH + target centiles
	Growth velocity
	Bone age
Pubertal assessment
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3
Q

What is a bone age scan?

A

X-ray of hand + wrist
Looks at 20 different bones
Indication of how long left until fully fused
Puberty + Xray collerate

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4
Q

What stages define puberty in boys and girls?

A

Breast budding T stage B2 in girl
Testicular enlargement T G2 (T3-4ml) in boy
Boy doesn’t start growth spurt for a year after this stage, girl growth spurt now

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5
Q

What effect does puberty have on growth?

A

In children obesity makes taller to start with
Puberty tends to be earlier in obese people
So obese may not be taller afterward

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6
Q

What are the indications for referring a child to a growth specialist?

A 
Extremely tall/short stature
	Height below target
	Abnormal height velocity
	History of chronic disease
	Obvious dysmorphic syndrome
Early/late puberty
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7
Q

What are the common causes of short stature?

A

Familial
Constitutional
If constitutional do a bone age scan as probably behind
SGA/IUGR

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8
Q

What are the common pathological causes of short stature?

A 
Undernutrition
Chronic illness
Iatrogenic (steroids)
Psychological + social
Hormonal (GHD, hypothyroidism)
Syndromes (Turner, P-W)
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9
Q

What does a child look like if they have growth hormone deficiency?

A

Correct proportions, just small stature

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10
Q

What does a child look like with a thyroid hormone deficiency?

A

The bones don’t mature and they stop growing
Then put on weight as slowed metabolism
Thus look “short and fat”

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11
Q

When is a boy’s puberty early, and when delayed?

A

Early less than 9,

Delayed older than 14

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12
Q

When is a girl’s puberty early and when delayed?

A

Early less than 8,

Delayed greater than 13

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13
Q

What is central precocious puberty?

A

Early development + secondary sexual characteristics in growing child
Usually idiopathic in girls, but look for pathological cause in boys
Will have advanced bone age scan + growth spurts with sexual characteristics
Often gonadotrophin independant with abnormal sex steroid secretion

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14
Q

What is the procedure with a baby with ambiguous geniltalia?

A

DO NOT guess sex
Involve a multidisciplinary team + karyotype
First exclude congenital adrenal hyperplasia
>Otherwise risk of adrenal crisis

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15
Q

What is the most common cause of acquired hypothyroidism in children?

A

Autoimmune thyroiditis

AKA hashimotos disease

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16
Q

What is the clinical picture of hypothyroidism in children?

A

Overweight/obese
High risk of diabetes (1/3)
>Often have black pigmentation on neck showing insulin reistance

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17
Q

What syndromes can cause hypothyroidism in children?

A

Prader Willi syndrome
Laurence-Moon-Biedel syndrome
Pseudohypoparathyroidism
Down’s

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18
Q

How do you treat hypothyroidism in children?

A

Insulin
Steroids
Antithyroid drugs (if autoimmune)

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19
Q

What are the symptoms of diabetes in children?

A 
Thirsty
Thinner
Tired
Toilet more
		Test immediately - finger prick test! >11mM = diabetes, other cause otherwise
	Also bet wetting after being dry
Same day review if positive test!
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20
Q

What are the symptoms of diabetes in the under 5s?

A 
Heavier than usual nappies
Blurred vision
Candidiasis
Constipation
Recurring skin infections
Irritability, behaviour changes
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21
Q

What are the symptoms of DKA in children?

A 
Nausea + vomitting
Abdo pain
Sweet smeling breath
Drowsiness
Rapid, deep "sighing" respiration
Coma
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22
Q

What is the aetiology of type 1 diabetes?

A

Autoimmune attack on islet cells (eg Anti-GAD)

Lymphocyte infiltration of islets (insulitis) - destruction of B cells

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23
Q

What is the effect of the destruction of the B cells?

A

Genes + environment leads to destruction in B cells

Destruction of islets leading to decreased insulin (increased glucose)

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24
Q

What is the Aetiology of type 2 diabetes?

A

Expanded upper body visceral fat mass
>Due to increase in food intake + lack of exercise resutls in more FFAs in blood
»Overwight adipocytes release fatty acids

These fatty acids lead to decrease in receptor sensitiity to insulin
Need more insulin to get same amount of glucose into cells
>Causes decreased removal of glucose from blood

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25
Q

How does diabetes accelerate atherosclerosis?

A

Glucose attaches to LDL, stopping it from attaching to its receptor (on liver cells)
Leads to not being removed by liver cells and so it stays in the blood (hyperlipidaemia) –> atherosclerosis

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26
Q

What is the mechanism of athersclerosis in arterioles in diabetes?

A

Molecules flux into subendothelial space but find it difficult
Leads to build up of trapped molecule
>Especially damaging in peripheral tissues (feet) eyes + arterioles supplying nerves
High risk of amputation, end stage renal disease + blindness

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27
Q

How does diabetes lead to small vessel disease?

A

Gluose added to proteins - glycosylation
Non enzymatic, reversible at first.
Irreversible if covalent bonds (advanced glycosylation end products (AGEs)
Collagen is glycosylated
Normally, collagen doesn’t bind to albumin, but glycosylated collagen does
>Leads to accumulation of subendothelial space of aterioles
Proteins get cross linked
>Difficult to remove and persistence of proteins in arteriole walls

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28
Q

What are the diagnostic criteria for diabetes?

A

One diagnostic lab glucose + symptoms

Or TWO diagnostic lab glucose / HbA1c levels without symptoms

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29
Q

What are the lab glucose results for diabetes?

A

Diagnostic glucose levels (venous plasma) fasting ≥ 7.0 mmol/l, random ≥ 11.1 mmol/l
OGTT (oral glucose test) 2h after 75g CHO ≥ 11.1 mmol/l
Diagnostic HbA1c ≥ 48 mmol/mol

Intermediate hypergycaemia
>Impaired fasting glucose 6.1-7 mmol/l
>Impaired glucose tolerance 2h glucose ≥7.8 and <11mmol/l

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30
Q

What is HbA1c?

A

Glycated haemoglobn - gives indication of blood glucose levels after over last 8-12 weeks
Glucose + haemoglobin –> glycohaemoglobin

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31
Q

When can you not use HbA1c?

A

After transfusion
Newly diagnosed
Any other reason causing errant results

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32
Q

What are the risk factors for type 2 diabetes?

A

Overweight
Family history
Over age 30 years if Maori ⁄ Asian (Indian subcontinent)
⁄ Pacific Island descent
Over age 40 years if European
Previous history of diabetes in pregnancy (Gestational Diabetes)
Had a big baby (more than 4 kg)—not in immediate post-natal period
Inactive lifestyle, lack of exercise
Previous high blood glucose ⁄ impaired glucose tolerance

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33
Q

What are the other types of diabetes (other than mellitus)?

A

Genetic syndromes - MODY
Gestational diabetes
Secondary diabetes

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34
Q

What is MODY?

A

An autosomal dominant disease
Causes glucokinase or transcription factor mutations
Results in slightly higher blood glucose than rest of population

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35
Q

How does the treatment/disease vary depnding on what MODY mutation you have?

A

Glucokinase is stable hyperglycaemia
>Treat with diet often sufficient
>Complciations rare

Transcription factors progressive hyperglycaemia
>Often need insulin/other drugs on top of diet
>Complications frequent

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36
Q

What is secondary diabetes?

A

Due to either drug therapy (corticosteroids for example)
Or due to pancreatic destruction/removal
>CF, chronic pancreatitis, haemochromatosis
Or rare endocrine disorders
>such as cushings, acromegaly, phaeochromocytoma

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37
Q

What is gestational diabetes?

A

Increased insulin resistance during pregnancy
Associated with family history of diabetes
Often develops in 2nd/3rd trimester
More common if overweight/innactive
Increases risk of type 2 diabetes later in lief

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38
Q

What can gestational diabetes lead to in the neonate?

A

Macrosomia
Respiratory distress
Neonatal hypoglycaemia

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39
Q

How do you reduce CVS risk in diabetics?

A

Control BP to £ 130/80
HbA1c target of 52mmols/mol
Statin therapy - any patient over 40 with diabetes
Lifestyle, smoking cessation

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40
Q

What is peripheral artery disease?

A

A diffuse dsease, often more sital
Calcification of arteries
>Only disease where this happens.
>Therefore shows in x-rays

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41
Q

How do you prevent retinopathy?

A

Good glucose control
Tight BP control
Early detection & intervention

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42
Q

What retinal abnormalities can occur in diabetes?

A

Microaneurysms (dots)
Blot haemorrhages
Hard exudates
Cotton wool spots

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43
Q

How do you treate proliferative retinopathy?

A

Laser photocoagulation
>Destruction of peripheral ischaemic retina leads to reduction of endothelial growth factors and regression of new vessels
Vitrectomy

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44
Q

What is diabetic maculopathy? What does it lead to?

A

Exudates and blot haemorrhages at macula
>Macular ischaemia then develops
>Macular oedema deforms the macula
Leads to decrease in Visual acuity - common in type 2 diabetes

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45
Q

What is the risk increase for cataracts in diabetic patients?

A

2x more likely in diabetics to get a cataract

Increased if poor control

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46
Q

What is peripheral neuropathy in diabetics?

A 
nerves of peripheries die off  - Affects mainly feet
>Feet inensitive to trauma
>Unpleasant chronic symtpoms 
>May be asymptomatic
>Small musce wasting
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47
Q

How do you manage peripheral neuropathy?

A 
Early detection
Self care education
Protection of feet
Pain relief
>Capsaisin cream 
>Amitriptyline, gabapentin, duloxetine
48
Q

How do you prevent uclers in diabetics?

A

Foot screening and risk scoring
Patient education on foot care
Regular podiatry for those at high risk
Trauma avoidance /fitted footwear

49
Q

What is acute sensory peripheral neuropathy, how serious is it?

A 
Rapid onset of neuropathic symptoms 
Precipitating factors
>Rapid tightening of control
>Acute metabolic upset
May be very severe – gradual recovery
"Temporary insult"
50
Q

Who gets proximal motor neuropathy and what is the presentation?

A 
Elderly men type 2
Legs mostly
Wasting of thigh muscles
Weight loss
Painful but good prognosis
51
Q

What is diabetic nephropathy?

A

Damage to structure and function of the capillaries which make up the glomerulus
Reduction in ability to filtrate blood
Earliest screening test - albumin in urine
Then protein in urine
Then impaired renal function

52
Q

How do you test for microalbinurea?

A

SCREENING TEST - first morning urine sample
DEFINITIVE TEST- timed overnight urine collection for albumin excretion rate (AER)
Normal < 20μg/min
Microalbuminuria 20-200μg/min

53
Q

What is the normal albumin/creatine ratio?

A

Normal albumin/creatinine ratio

Male <2.5 mg/mmol; Female <3.5

54
Q

How do you treat diabetic nephropathy?

A

Optimise glucose control
BP control
ACEI slows progression
Cardiovascular risk factor management

55
Q

What is the proposed sequence for getting an autoimmune disease?

A 
Initiating event + genetic susceptibility
>Leads to break down of self tolerance
>Leads to autoreactivity
>can be Humoral +/- cellular 
>Leads to tissue damage
56
Q

What is the pathogenesis of autoimmune disease?

A
  • Antibody mediated
  • Cell mediated
  • Complement mediated
    -Phagocytes, cytokines, Natural Killer cells etc.
    Combinations of above
57
Q

What is the aetiology of autoimmune disease?

A

1) Genetic factors
2) Immune regulatory factors
3) Hormonal factors
4) Environmental factors -
5) ‘Other’ factors

58
Q

What antibody stimulates grave’s disease?

A

TSH

59
Q

What autoantibody causes hashimotos disease?

A

TSH
Thyroglobulin
Peroxidase

60
Q

What autoantibodies cause addison’s diseae?

A

Adrenal cortex antibodies

>Either 21 or 17 hydroxylase

61
Q

What is grave’s disease?

A

Goitre & thyroid hyperfunction
TSH receptor stimulating antibodies
Class 2 HLA expression on thyroid epithelial cells

62
Q

What are the complications with grave’s disease?

A

Associated ophthalmopathy found in 25-50 % of cases.
>Increased fat and retrobulbar muscle size due to fibroblast stimulation
>results in release of stimulating cytokines from activated T cells directed against TSH receptor-like autoantigens on orbital fibroblasts.
Stimulating antibodies may also be partly responsible.

63
Q

What is the mechanism of grave’s disease?

A

Mostly humoral
But T cells present in thyroid gland
>clearly involved in helping autoantibody production and in pathogenesis of eye disease.

64
Q

Who is more likely to get grave’s disease?

A

Women 7:1 men

65
Q

What genes are associated with graves disease?

A

HLA-B8

DR3

66
Q

Who is most likely to get hashimoto’s disease?

A

females 4:1 males

67
Q

What gene is related to hashimoto’s disease?

A

HLA-DR5

68
Q

What is hashimoto’s disease?

A
  • Goitre & thyroid gland hypofunction
  • Dense lymphocytic infiltrate of thyroid (B cells, CD4 & CD8 T cells)
  • TSH receptor destroyed
69
Q

What happens in hashimoto’s disease?

A

The primary agents cause two things
>thyroid growth stimulating antibody
>And sensitisation of T cells to thyroid surface (autoantigens)
Together these cause the secondary effects
?Growth
>Tissue damage
>Thyroglobulin autoantibodies + peroxidase antibody

70
Q

What is primary myxoedema?

A
  • TSH receptor growth & metabolism epitope blocking antibodies
  • Lymphocytic infiltration of thyroid
  • thyroid gland atrophy
71
Q

Who is more likely to get primary myxoedema?

A
  • F>M

- People with HLA-DR3 gene

72
Q

What is the mecahnism of hashimoto’s disease?

A

Mechanism of disease: Humoral (goitre) + Cellular (tissue destruction –> gland hypofunction)
Antibodies produced against thyroid peroxidase and thyroglobulin
> useful as disease markers.

73
Q

When is the peak onset of type 1 DM?

A

puberty

74
Q

What is the evidence for that type 1 diabetes is driven by autoimmune causes?

A

Hereditary factors
Environmental influences (such as after colds, based on geographical location)
Direct/indirect evidence of autoreactivity
>Islet cell antibodies
>lymphocytic infiltrate in islts
>Evidence of resonse to immunosupressive therapy

75
Q

What is the pathogenesis of autoimmune type 1 diabetes?

A

Trigger + genetics
Leads to damage to beta islet cells
Releases beta cell autoantigen
>Causes sensitisation of autoreactive islet cell antigen
+inappropriate HLA expression on islet cells
>Leads to T cell recognition of autoantigen
>then B-cell destruction

76
Q

What genes are associated with autoimmune polyendocrine syndromes?

A

HLA-B8

DR3

77
Q

What are type one autoimmune polyendocrine disorders?

A

adrenal + parathyroid disease along with chronic candidal infection of nails or mucous membranes

78
Q

What are type two autoimmune polyendocrine disorders?

A

autoimmune disease of adrenal & thyroid + Type 1 DM

79
Q

What are type three autoimmune polyendocrine disorders?

A

autoimmune thyroid disease + one of

a) Type 1 DM
b) gastric autoimmune disease (e.g. atrophic gastritis)
c) non-endocrine autoimmune disease (e.g. RA, SLE)

80
Q

What can cause differences in endocrine samples?

A

Posture
Timing
Diet
Drugs

81
Q

When can hypokalaemia be disguised as hyperkalaemia?

A

When high levels of glucose causes acidosis
>In order to maintain neuraility of acid/base balance potassium leaves the cell
This results in high serum levels, but low body levels of potassium

82
Q

What is multinodular goitre?

A

Iodine deficiency leads to impaired synthesis of thyroid hormones
Leads to raised TSH
Leads to hypertrophy and hyperplasia of thyroid

83
Q

How does multinodular goitre look?

A

Crowded follicles
Distended colloid filled follicles
Haemorrhage, fibrosis, cystic change
Nodular appearance

84
Q

What are the type of thyroid tumours?

A

Follicular adenoma

Carcinoma (5% of nodules)
Differentiated thyroid carcinoma
Papillary carcinoma              75-85%
Follicular carcinoma             10-20%
Anaplastic carcinoma                5%
Medullary carcinoma                 5%
   (lymphoma)
85
Q

What is follicular carinoma?

A

Rare, usually solitary
Malignant cells breach capsule
Metastases – blood, bones

86
Q

What is papillary carcinoma?

A

BRAF mutation or RET/PTC gene rearrangement
Associated with exposure to ionizing radiation
Spreads via lymphatics…

87
Q

What is the prognosis of papillary carcinoma of thyroid?

A

Excellent prognosis - 95% survival (esp <45yrs 99% at 1yr

88
Q

What does papillary carcinoma of thyroid look like?

A

Papillary projections
Empty nuclei
Psammoma bodies
May be cystic

89
Q

What is thyroid medullary carcinoma?

A

A malignant tumour of C cells

Produces lots of calcitonin

90
Q

What causes parathyroid hyperfunction?

A 
Mostly primary causes
	Sporadic or familial (MEN-1)
	• Adenoma (85-95%
	• Hyperplasia (5-10%)
	• Carcinoma (rare)
	2ry hyperparathyroidism
Physiological response to  ↓ Ca2+ renal failure
91
Q

How do the cells stain in the pituitary gland?

A 
3 major cell types:
pink ACIDOPHILS
> secrete GH and PRL
dark purple BASOPHILS         
> secrete ACTH, TSH, FSH, LH
pale CHROMOPHOBES
92
Q

How does pituitary adenoma appear?

A

soft, well-circumscribed lesion
small microadenomas may be incidental eg at post mortem
cells of same appearance as normal gland
classified by hormone(s) produced by the neoplastic cells - detected by immunohistochemical stains

93
Q

What are teh types of multiple endocrine neoplasia?

A

MEN 1

Or MEN 2 (2, 2a, 2b )

94
Q

What is MEN1?

A

Tumour suppresion gene mutation resulting in defect in menin protein
Results in parathyroid hyperpasia + adenomas
>Primary Hyperparathryoidism
Pancreatic + duodenal endocrin tumours
>Results in ulcers + hypoglycaemia
Pituitary adenoma

95
Q

What is men 2?

A

RET proto-ongogene mutations
Medullary carcinoma of thyroid
Primary hyperparathryroidism
Phaeochromocytoma

96
Q

What is men 2A?

A

Men2 +:
Parathyroid hyperplasia
Extracellular domain auto dimerisation of RET receptor

97
Q

What is MEN 2B?

A

MEN 2+:
+ Neuromas of skin &mucous membrane, skeletal abnormalities
+ Younger patients, aggressive
Autoactivation of tyrosine kinase pathway

98
Q

What can cause pituitary hypofunction?

A

Compression by tumours
Trauma
Infection
Ischaemic necrosis

99
Q

What syndromes accur from adrenal cortical hyperfunction?

A

Cushings - hypercortisolism
Conn’s - hyperaldosteronism
Adrenogenital syndromes

100
Q

What are the types of cushing’s disease?

A 
Exogenous (steroids)
ACTH dependent
>Due to pituitary adenoma, or ectopic ACTH
ACTH independent
>Functional adrenal adenoma cause
101
Q

What can cause conn’s syndrome?

A

Bilateral idiopathic hyperplasia
Functioning adrenal adenoma
Secondary hyperaldosteronism caused by kidneys

102
Q

What are the androgenital syndromes?

A

Functioning adrenal tumour
Pituitary tumour Cushings disease
Congenital adrenal hyperplasia – steroid enzyme deficiency

103
Q

What are the acute features of hypocalcaemia?

A 
Neuromuscular irritability (tetany)
>Muscle twitching
>Seizures etc
Cardiac
>Proonged QT
>Heart failure
>Hypotension
>Arrythmia
Papilloedma
104
Q

What are the chronic features of hypocalacaemia?

A 
Ectopic calcification
Parkinsons
Dementia
Ataracts
Abnormal dentition
105
Q

What is torsseau’s sign?

A

After sphyg is applied and inflated on upper arm

Forearm goes into spasm within 4 minutes

106
Q

What is chovstek’s sign?

A

Relax facial muscles
Tap facial muscle anterior to earlobe + below zygomatic arch

Positive is twitching of mouth/facial muscle spasm depending on severity of hypocalcaemia

107
Q

What can cause hypocalcaemia?

A 
Disruption of parathyroid glands
	Severe vit D deficiency
	Mg deficinecy
	Cytotoxic drugs
Pancreatitis, blood transfusions
108
Q

What can cause hypoparathyroidism?

A

agenesis (e.g. DiGeorge syndrome)
destruction (neck surgery, autoimmune disease)
Infiltration (e.g. haemochromatosis or Wilson’s disease)
reduced secretion of PTH (neonatal hypocalcaemia, hypomagnesaemia)
Resistance to PTH (psuedohypoparathyroidism)

109
Q

What is pseudohypoparathyroidism?

A

Where target organ is unresponsive to PTH
Presents in childhood
Can lead to albrights hereidarty osteodystrophy

110
Q

What is Albright’s heriditary osteodystrophy (ABO)?

A

Leads to shortening of metacarpal bones
Can also occur without calcium abnormalities
Psuedo-psuedohypoparathryoidism

111
Q

What is pseudoparathyroidism characterised by?

A

Characterised by
Hypocalcaemia
Hyperphosphatemia
+ elevated rather than reduced PTH concentrations

112
Q

How do you treat mild hypocalcaemia?

A

Mild hypocalcaemia (>1.9mmol/l, asymptomatic)
Oral tablets
If Vit D deficient, Vit D
If magnesium low, replace and stop lowering drugs

113
Q

How do you treat severe hypocalcaemia?

A 
Medical emergency
IV calcium gluconate
Initial -
>10-20ml 10% calcium gluconate in 50-100ml of 5% dextrose IV over 10 minutes with ECG monitoring
Treat the underlying cause
114
Q

What are the causes of hypercalcaemia?

A 
Primary hyperparathyroidism
	Inherited conditions
	Renal failure
	Meidcations
Malignancy
115
Q

What are the clinical features of hypercalcaemia?

A 
"Bones, stones, groans and pyschihc moans"
	Polyuria, polydipsia
	Nephrolithiasis
	Anorexia
	Nausea/vomiting
	Constipation
	Muscle weakness
	Decreased concentration
Shortening of QT
116
Q

How do you treat hyperparathyroidism?

A

Generous fluid intake
Cinacalcet (acts as a calcimetic, i.e. mimics the effect of calcium on the calcium sensing receptor on Chief cells, this leads to a fall in PTH and subsequently calcium levels)

117
Q

How do you treat hypercalcaemia?

A

Rehydration

IV biphosphonates

Conditions + definitions (68 decks)

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