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RACP Written Exam Cram Series > Endo Cram > Flashcards

Endo Cram Flashcards

1
Q

Adrenal cortex zones and products?

A

Zona Glomerulosa - produces aldosterone regulated by ECF concentration of K+ and angiotensin II
Zona Fasciculata - produces cortisol regulated by ACTH
Zona Reticularis - produces DHEAS -> androgens regulated by ACTH

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2
Q

Regulators and effects of mineralocorticoids?

A

Up-regulated by Angiotensin II (most powerful) and high K+
Down-regulated by atrial naturetic peptide
Increases Na channel in collecting duct
Increases Na and K+ excretion
Increases blood volume and blood pH

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3
Q

Regulators and effects of glucocorticoids?

A

ACTH stimulation produces cortisol
Highest on waking, lowest asleep
Increases gluconeogenesis and increases insulin resistance
Decreases B cells and lowers immune function
Increases bone resorption and lowers Ca = low BMD
Decreases fibroblasts (bruising, poor wound healing)
Increases adrenal androgens

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4
Q

Products of the adrenal medulla?

A

Dopamine
Norepinephrine
Epinephrine

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5
Q

Effects of Angiotensin II?

A

Vasoconstriction of efferent arterioles to increase resorption of sodium and water
Systemic vasoconstriction
Thirst
ADH release - water retention
Aldosterone release - sodium respiration and potassium excretion
Heart remodelling

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6
Q

Primary adrenal insufficiency

A

Deficiency of glucocorticoids and mineralocorticoids

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7
Q

Central adrenal insufficiency

A

Deficiency of glucocorticoids ONLY
Secondary - pituitary defect
Tertiary - hypothalamic

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8
Q 
Low cortisol
High ACTH
Hypertension
HypOnatremia & hypERkaelaemia
High plasma renin
A

Primary adrenal insufficiency

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9
Q

Low cortisol
Low ACTH
Fasting hypoglycaemia

A

Secondary adrenal insufficiency

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10
Q

Synacthen test?

A

ACTH stimulation test
Normal in primary adrenal insufficiency
Low in secondary adrenal insufficiency
Low in tertiary adrenal insufficiency

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11
Q

Who to consider adrenal crisis in?

A

Primary adrenal insufficiency
Hypopituitarism
Previous or current prolonged steroid therapy

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12
Q

Presentation of adrenal crisis?

A 
Hypotension & shock
Hyponatremia
Hyperkalaemia
Hypoglycaemia 
Metabolic acidosis
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13
Q

Sign of primary adrenal failure?

A

Hyperpigmentation due to ACTH excess stimulating melanocortin1 receptor

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14
Q

Steroid replacement in adrenal crisis?

A

50-100mg/m2 IV hydrocortisone

If mineralocorticoid deficiency fludrocortisone can be started once oral intake is being tolerated

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15
Q

Causes of primary adrenal insufficiency?

A

CAH - infancy
Autoimmune - childhood
APECED - childhood
Adrenoleukodystrophy - childhood

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16
Q 
Low cortisol
High ACTH
HypOnatremia/HypERkalaemia
HIGH renin
Hyperandrogenism - ambiguous genitalia in females
A

21-Hydroxylase deficiency
Autosomal recessive
CYP21A2

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17
Q

Ambiguous genitalia in females or increased penile length in boys
Hypertension
HypOkalemia
LOW renin

A

11B-Hydroxylase deficiency

CYP11B1

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18
Q

Ambiguous genitalia in males
Pubertal delay
Hypertension

A

17a-hydroxylase deficiency

CYP17A1

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19
Q

Weakness/spasticity

Blindness

A

Adrenoleukodystrophy
X-Linked
ABCD1

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20
Q

Craniofacial malformation
Growth failure
Developmental delay

A

Smith-Lemli-Opitz

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21
Q

Hypothalamic haemartoblastoma
Hypopituitarism
Imperforate anus
Gelastic seizures

A

Pallister-Hall

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22
Q

Non-classic 21-hydroxylase CAH presentation?

A

Premature pubarche

Advanced bone age

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23
Q

Cushing syndrome VS disease?

A 
Syndrome = prolonged glucocorticoid excess
Syndrome = pituitary adenoma secreting ACTH
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24
Q

Investigation findings in Cushing’s?

A

High midnight cortisol
High urinary cortisol
Elevated after low dose dexamethasone suppression test

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25
Q

Purpose of 2 step Dex suppression test?

A

Differentiate ACTH dependant or independant
Cortisol not suppressed if ACTH independant
Cortisol suppressed in pit adenoma

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26
Q

Causes of ACTH independant Cushing?

A

Iatrogenic
Adrenal adenoma
McCune-Albright/Primary Pigmented Nodular Adrenocortical Disease

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27
Q

HypERnatremia
HypOkalaemia
Hypertension
Low renin

A

Conn’s Syndrome

Primary Aldosteronism

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28
Q

Familial cancer syndromes associated w adrenocortical tumours?

A

Li Fraumeni (TP53)
Multiple Endocrine Neoplasia (MEN1)
Familial adenomatous polyposis (APC)
PRKAR1A gene

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29
Q

Headache
Sweating
Tachycardia

A

Phaeochromocytoma

  • von Hippel-Lindau
  • MEN2A MEN2B
  • NF1
  • TS
  • Sturge Weber
  • Ataxia Telangiectasia
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30
Q

Hormone production of alpha, beta and gamma pancreatic cells?

A

Alpha - secretes glucagon
Beta - secretes insulin
Gamma - secretes somatostatin

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31
Q

Earliest sign of beta cell dysfunction?

A

Loss of insulin secretion pulsatility

Diabetes clinically evident when 90% of beta cells lost

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32
Q

Site of action of glucagon?

A

Liver

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33
Q

Glucose maintenance mechanism in fasting periods?

A

2-4 hrs dietary glucose
Glycogenolysis stimulated by glucagon 10-12hrs
Gluconeogenesis stimulated by cortisol 12-24hrs
Lipolysis stimulated by GH 18-36hrs

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34
Q

Genes associated w T1DM?

A

85% NO FHx

HLA-DR3/4 and HLA-DQ2/8

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35
Q

Risk factors for T1DM?

A

Viral infections (40% congenital rubella)
Diet - BF protective, cows milk risk
High SES
Vit D def

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36
Q

Presentation of T1DM

A 
Polyuria
Polydipsia
Weight loss
Perineal canidiasis
Visual disturbance (osmotic millieu of lens)
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37
Q

Antibodies assoc w T1DM?

A

Islet cell cytoplasmic antibodies - 70%
Anti-insulin antibodies - first apparent, disappear w insulin
Anti-GAD - 70-80%
Anti-IA2 - best predictor of T1DM development
Anti-zinc transporter - 99% specific

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38
Q

Autoimmune associations of T1DM?

A

Autoimmune thyroid disease 5% hypothyroid, 1% hyperthyroid
Celiac - increased risk if younger age of onset
Adrenal disease
Gastric autoimmunity
Vitiligo

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39
Q

Side effects of insulin?

A 
Formation of antibodies
Hypoglycaemia
Insulin resistance
Weight gain
Local reaction
Lipohypertrophy at injection site
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40
Q

Diabetic retinopathy screening and management?

A

1-2yearly from age 9/2yrs diabetic
Cotton-wool/soft exudates
Laser photocoagulation or photocoagulation

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41
Q

Diabetic nephropathy screening and management?

A

Annually from age 9/2yrs diabetic
Alb:Cr ratio
Improve BSL control, BP control, ACE-inhibitor, reduced protein diet

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42
Q

Diabetic neuropathy screening and management?

A

Annually from age 9/2yrs diabetic

Vibration/proprioception

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43
Q

Dwarfism
Delayed puberty
Hepatomegaly with steatosis
Cushingoid features

A

Mauriac Syndrome

Chronic underinsulinisation

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44
Q

DKA diagnostic criteria?

A

Hyperglycaemia
Metabolic acidosis (pH <7.3)
Ketonuria

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45
Q

Fluid and electrolyte replacement in DKA?

A

NS bolus if hypoperfused
NS + K+ for first 6hrs
Na will self-correct
K+ needs active replacement with correction of acidosis
BICARB NOT RECOMMENDED - paradoxical CNS acidosis

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46
Q

Risk factors for cerebral oedema?

A

1% of DKA presentations
1st presentation, long hx of poor control, age <5
Risk period is first 6-12 hrs after therapy initiation
-> treat w mannitol and fluid reduction

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47
Q

When to suspect T2DM?

A

Strong FHx
Obesity/central adiposity
Acanthosis nigricans, skin tags
No insulin requirement after honeymoon phase

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48
Q

Who to screen for T2DM?

A 
Overweight PLUS
 - FHx
 - Hispanic/polynesian/indian/chinese
 - acanthosis/HTN/dyslipidaemia/PCOS
SCreening test îs fasting plasma glucose
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49
Q

Most common presentation of T2DM?

A

Symptomatic - polyuria, polydipsia, fatigue

10% present in DKA; 10% hyperglycaemia hyperosmolar

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50
Q

Treatment of choice for T2DM?

A

Metformin monotherapy

Insulin if HbA1C >9%

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51
Q

SEs of metformin?

A

Abdo pain, diarrhoea, lactic acidosis

Assists in weight loss

52
Q

Biguanide (metformin) mechanism?

A

Reduce hepatic glucose production
Reduce glucose uptake from stomach
Increase insulin sensitivity

53
Q

Sulfonylureas (gliclazide) mechanism?

A

Increase insulin secretion from pancreatic beta-cells

54
Q

Thiazolidinediones (-azones) mechanism?

A

Increase insulin sensitivity

55
Q

Acarbose mechanism?

A

Reduce glucose absorption from GI tract

56
Q

SLGT2 inhibitor (-pagliflozins) mechanism?

A

Promotes glycosuria reducing BGL

57
Q

Hyperosmolar hyperglycaemia?

A

Severe hyperglycaemia without ketosis
Dehydration +++++
Needs more fluid Jesus than DKA, less insulin

58
Q

Non-insulin dependant diabetes
Diagnosis <25
No auto-antibodies
Strong FHx (>2 generations)

A

MODY
Autosomal dominant
Treat w sulfonylureas

59
Q

Most common MODY genes?

A

HNF1-alpha 50-65% (treat w sulfonylureas)

GCK 15-30% (treat w diet)

60
Q

Which area of brain most susceptible to hypoglycaemia in neonatal period?

A

Occipital - visuospatial impairment

61
Q

Determinants of growth in early childhood vs later childhood?

A

Genetic/chromosomal at all ages is most important factor
First 3 years of life - nutrition main driver, also IGF2
Later childhood growth hormone, nutrition, thyroid, vitamin D, steroids

62
Q

Female vs male peak growth velocity?

A

Females 11-12

Males 13-14

63
Q

Bone age normal range?

A

Up to 1yr/20% difference to chronological age considered normal

64
Q

Conditions to consider if equal reduction in height and weight?

A

Chromosomal/TORCH

65
Q

Conditions to consider if height more affected?

A

Endocrinopathies/skeletal dysplasia

66
Q

Conditions to consider if weight more affected and HC normal?

A

Malnutrition

67
Q

Precocious puberty in girls vs boys?

A 
Girls = unlikely pathological
Boys = brain tumour until otherwise proven
68
Q

Delayed puberty in girls vs boys?

A 
Girls = Turners until otherwise proven
Boys = likely to be normal
69
Q

Cause of short stature in Turners?

A

SHOX (short stature homeobox) insufficiency

70
Q

Cause of short stature in renal failure?

A

IGF-1 deficiency

Renal disease = high GH and low/normal IGF-1

71
Q

Features of constitutional growth delay?

A 
Short child with normal height parents
Slow growth
Delayed puberty 
Delayed bone age
Has good height prognosis
72
Q

Features of familial short stature?

A

Child short and parents shirt
Normal growth and puberty
Normal bone age
Has poor height prognosis

73
Q

Hypoglycaemia
Micropenis
Jaundice

A

Growth Hormone Deficiency

74
Q

Causes of growth hormone deficiency?

A

GH1 mutation
Post-radiotherapy
Trauma
Infection (meningitis), inflammation, histiocytosis

75
Q

Causes of growth hormone insensitivity?

A

GH Release Hormone mutation
GH Receptor mutation
IGF-1/IGF-1 receptor mutations

76
Q

Complications/AEs of growth hormone replacement therapy?

A 
Primary/central hypothyroidism
T2DM
Pseudotumour cerebrii
Gynaecomastia
SUFE
Adenotonsillar hypertrophy/worsens OSA
Possible link to leukaemia/brain tumours
77
Q

Factors affecting onset of puberty?

A

Genetics

Increased BMI

78
Q

Testosterone production?

A

Produced by Leydig cells and synthesised in tissues by 5-alpha reductase

79
Q

In males FSH stimulates?

A

FSH stimulates Sertoli cells and results in spermatogenesis

80
Q

In males LH stimulates?

A

LH stimulates Leydig cells and produces testosterone

81
Q

In females FSH stimulates?

A

FSH stimulates follicular thecae cells and produces oestrogen/progesterone

82
Q

When is greatest % of bone mass accrued?

A

Puberty - 50% of total bone mass

83
Q

Hormone profile in central precocious puberty?

A

High LH and FSH (even post GnRH stimulation test)

High estradiol and testosterone

84
Q

Hormone profile in combined central/peripheral precocious puberty?

A

Low then normal FSH and LH

High estradiol and testosterone

85
Q

Hormone profile in peripheral precocious puberty?

A

Low LH/FSH

High estradiol and testosterone

86
Q

Causes of central precocious puberty in girls?

A 
Idiopathic (80%)
Brain lesions - hypothalamic harmatoma or brain injury (radiation, hydrocephalus)
Hypothyroidism
NF1
MKRN3 - most common genetic cause
87
Q

Precocious puberty and slow growth?

A

Hypothyroidism

88
Q

Precocious puberty
Cafe au lait/coast of Maine lesion
Fibrous dysplasia

A

McCune Albright

89
Q

Causes of peripheral precocious puberty in boys?

A

Hepatoblastoma

Germ cell tumours/gonadal or adrenal tumours

90
Q

Solitary maxillary incisor

A

GH deficiency

91
Q

Short stature
Frontal bossing, triangular face
Short incurved 5th fingers
SGA and FTT

A

Russell-Silver

92
Q

Rapid growth in early childhood with no endocrine disorder found

A

Sotos Syndrome

93
Q

TSHR antibody

A

Graves disease

94
Q

Anti-Tg antibody

A

Autoimmune thyroiditis

95
Q

Anti-TPO antibody

A

Autoimmune thyroiditis

96
Q

Hypothyroidism

Absence of thyroid uptake on radio nucleotide scan?

A

Agenesis (most common)
Maternal thyroid blocking antibodies
Iodine trapping defect

97
Q

Hypothyroidism

Increased thyroid uptake on radio nucleotide scan?

A

Dyshormonogenesis

Iodine exposure

98
Q

Hyperthyroidism

Reduced thyroid uptake on radio nucleotide scan?

A

Exogenous T4
Subacute thyroiditis
Hashimoto’s

99
Q

Hyperthyroidism

Increased thyroid uptake on radio nucleotide scan?

A

Graves

Multinodular/toxic nodule

100
Q

Defect of thyroid binding globulin?

A

Not associated with clinical disease and requires no treatment
X-linked dominant

101
Q

Congenital hypothyroidism causes?

A

85% thyroid dysgenesis

15% hereditary mutation of thyroid hormone synthesis

102
Q

Hypothyroidism
Sensorineural deafness
Goitre
Temporal bone abnormality

A

Pendred syndrome

103
Q

Most common cause of acquired hypothyroidism?

A

Hashimoto’s thyroiditis

104
Q

Autoimmune acquired hypothyroidism causes?

A 
Hashimoto's
T21
Turner's
T1DM
Kleinefelter
105
Q

Difference between transient hypothyroxinaemia and transient hypothyroidism?

A

Both affect press
Both have Low T4
Transient hypothyroxinaemia has a normal TSH but hypothyroidism has a high TSH
No need to treat hypothyroxinaemia, hypothyroidism needs treatment

106
Q

Syndromes associated w Hashimoto’s?

A 
APS1/2
IPEX
Turner
T21
Kleinefelter
107
Q

Genes associated w increased risk of Graves?

A

HLA-B8 and HLA DR3

108
Q

AEs of carbimazole?

A 
Agranulocytosis
ANCA vasculitis
Pancreatitis
Hepatotoxicity
Cholestatic jaundice
Lupus like syndrome
Glomerulonephritis
Teratogen
109
Q

PTH actions?

A

Increased bone resorption within minutes
Increased intestinal absorption of calcium within days
Decreased urinary calcium excretion from distal tubule within minutes
Increased urinary phosphate excretion from proximal tubule

110
Q

Anatomic locations in Vit D synthesis?

A

7-dehydroxycholesterol -> cholecalciferol in SKIN
Colecal -> 25OHD LIVER
25 OHD -> 1,25OHD KIDNEY

111
Q

Hypocalcaemia and low PTH?

A

Hypoparathyroidism

HypoMg

112
Q

Hypocalcaemia with normal PTH?

A

Abnormal calcium sensing receptor

113
Q

Hypocalcaemia with high PTH?

A

Vit D deficiency
Pseudohypoparathyroidism
Renal failure

114
Q

Hypocalcaemia
Hyperphosphataemia
High PTH

A

Pseudohypoparathyroidism

115
Q

Causes of hypercalcaemia?

A 
William's Syndrome
Primary hyperparathyroidism
Vit D excess
Subcutaneous fat necrosis
Renal disease
116
Q

Medications that inhibit Vit D?

A

Glucocorticoids
Anti-epileptics
Anti-fungals
Anti-TB

117
Q 
Bone pain
Muscle cramps
Delayed dentition
Delayed fontanelle colsure
Bowed legs
Hypocalcaemia
118
Q

Radiographic findings of rickets?

A 
Best seen at growth plate of rapidly growing bones - ulna/knee
Metaphyseal widening, fraying
Osteopenia
Fractures
Trabecular bone
119
Q

Phosphopenic rickets

A

Renal phosphate wasting - Fanconi
Hereditary
Presents with short stature and PROFOUND skeletal bowing

120
Q

Posterior pituitary hormones?

A

ADH (vasopressin)

Oxytocin

121
Q

46XY

Female genitalia

A

Complete androgen insensitivity

122
Q

Anosmia

Delayed/absent puberty

123
Q

Learning disability
Tall, long legs
Mitral valve prolapse
Small testes, penis

A

Kleinefelter

47XXY

124
Q

Bioavailability of sex hormone (oestrogen/testosterone) depends on what?

A

Level of sex hormone binding globulin

125
Q

Cryptophthalmos
Ambiguous genitalia
Craniofacial anomalies

A

Fraser syndrome

RACP Written Exam Cram Series (19 decks)

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