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RCPCH TAS/ AKP > Endocrinology & Diabetes > Flashcards

Endocrinology & Diabetes Flashcards

1
Q

Effects of increased cortisol in the body

A

Increased BP
Increased gluconeogenesis, lipolysis, proteolysis
Anti-inflammatory
Reduced bone function, immunity

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2
Q

Which areas of the adrenal gland produce which hormone?

A

Medulla: Adrenaline, noradrenaline

Cortex: (out to in)
- Glomerulus - Mineralocorticoids (aldosterone)
- Fasiculata - Glucocorticoids (cortisol)
- Reticular - Sex (androgens)
Go Find Rex, Make Good Sex

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3
Q

What controls calcium homeostasis in the body?

A
  1. Low calcium
  2. Parathyroid releases more PTH
  3. Acts in 3 places:
    -Bones - osteoclasts break down bone
    - Kidneys - retain Ca2+ and Vit D
    - Intestines - absorb more Ca2+

Mg2+ also regulates PTH release

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4
Q

What controls the release of sex hormones?

A
  1. Hypothalamus releases GnRH
  2. Ant. Pituitary releases LH / FSH
  3. In males –> LH –> Testes release Testosterone and FSH stim. sperm maturation
  4. In females –> LH and FSH –> ovaries release estradiol and progesterone
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5
Q

What biochemical changes would you see in different types of Hypothyroidism?

A
  1. Primary = High TSH, low T3/T4
  2. Secondary = Low TSH, T3/4
  3. Treated / subclinical= High TSH, normal T3/4
    Rising TSH indicates poor compliance
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6
Q

What biochemical changes would you see in different types of Hyperthyroidism?

A
  1. Primary= Low TSH, high T3/4
  2. Secondary = High TSH, T3/4
  3. Treated / subclinical = low TSH, normal T3/4
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7
Q

Presentation of congenital hypothyroidism

A

D5 Guthrie. Sx 6-12w
Protruding tongue
Hoarse cry
Delayed growth and development
Pale
Prolonged jaundice
Umbilical hernia

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8
Q

Congenital hypothyroidism cauases

A

Maternal iodine def.
Thyroid agenesis
Inborn error thyroid hormone synthesis
Pituitary dysfunction

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9
Q

Presentation of acquired hypothyroidism

A

Weigh gain / short
Thin skin / hair
Cold intolerance
Poor conc. / LD
Bradycardia
Goitre eg AI/ Hashimoto’s
Constipation
Low iodine

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10
Q

Presentation acquired hyperthyroidism

A

Weight loss, tall
Tachycardia
Diarrhoea
Reduced Conc.
Goitre
Eyes - Exophthalmos, opthalmoplegia, lid retraction, lid lag
Pre-tibial myxoedema

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11
Q

Causes of acquired hyperthyroidism

A

Mainly primary. More girls.
Graves’ - AI thyroiditis. TRAB Ab
Thyroiditis
Thyroid nodules
De Quervain’s thyroiditis - post-viral. Painful. Self-limiting.

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12
Q

Treatment for acquired hyperthyroidism

A
  1. Carbimazole - block thyroxine synthesis (SE neutropenia)
  2. ?2nd course
  3. Radical - thyroidectomy, radioactive iodine
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13
Q

Symptoms of hypocalcaemia

A

Tetany
Cramps
Paraesthesia
Stridor
Diarrhoea
Seizures

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14
Q

Biochemistry in hypoparathyroidism

A

Low PTH
Low Calcium
High Phosphate
Normal Alk Phos

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15
Q

Causes of hypoparathyroidism

A

DiGeorge
Magnesium deficiency
Genetic mutation of calcium sensing gene
AI

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16
Q

Presentation and biochemistry of pseudohypoparathyroidism

A
  • Presentation: Short, obese, LD, SC nodules, short 4th metacarpal
  • Biochemistry: Increased PTH and Phosphate, low Calcium, normal Alk Phos
    = end organ resistance to PTH (defect in G protein signalling)
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17
Q

Symptoms of hypercalcaemia

A

Constipation
Lethargy
Polyuria
Anorexia
Polydipsia

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18
Q

Causes of hyperparathyroidism in children?

A

Rare
William’s
Later - adenoma, MEN

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19
Q

What hormones are affected in adrenal insufficiency?

A

LOW CORTISOL
LOW ALDOSTERONE

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20
Q

Causes adrenal insufficiency

A

AI - Addison’s
CAH
Haemorrhage / infarct
Infective - TB
X-linked adrenoleukodystrophy
Removal of long term steroids (Low ACTH / CRH)

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21
Q

Presentation of adrenal insufficiency

A

LOW SODIUM, HIGH POTASSIUM
Weight loss
Abdo pain / vomiting/ dehydration
Lethargy
Pigmentation
Infant - salt losing crisis
Crisis - Low BP, low GCS, N+V

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22
Q

What tests for adrenal insufficiency?

A

Short Synacthen test
ACTH stimulation

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23
Q

Treatment for adrenal insufficiency

A

Acute - IVT, glucose, hydrocortisone
Chronic - Hydrocortisone / fludrocortisone
Double steroids if unwell

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24
Q

Presentation of congenital adrenal hyperplasia

A

Virilisation of genitalia esp girls
Salt losing crisis
Hypoglycaemia
High 17-OHP at 72 hours

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25
Q

Genetics of CAH

A

Autosomal recessive
HLA on Ch 6 –> defect in enzyme for steroidogenesis

26
Q

Presentation of adrenal excess

A

Short and fat + striae
Prox muscle weakness/ wasting
Bruising
Thin skin
OP
Red cheeks
Hirutism

27
Q

Causes of adrenal excess (high cortisol)

A
  • Low ACTH = Adrenal adenoma, arenal nodular hyperplasia, steroids
  • High ACTH = Cushing’s disease, pituitary adenoma, ectopic ACTH (paraneoplastic)
28
Q

What test would you do for adrenal excess

A
  1. Low dose Dex suppression test –> Cushing’s = no suppression
  2. High dose suppression test –> Cushing’s disease suppressed at 8mg, ectopic ACTH / adrenal adenoma not suppressed

Undetectable ACTH = adrenal tumour

29
Q

Presentation of phaeochromocytoma

A

Episodic:
Headache
HTN
Tachycardia
Flushing/ sweating

30
Q

Causes of Phaeochromocytoma

A

Adrenal medullary tumour
Raised adrenaline / noradrenaline

Increased risk in NF1

31
Q

Ix Phaeochromocytoma

A

Urine catecholamines / metanephrines
Blood metanephrines
CT Abdo

32
Q

Which hormones are secreted from the anterior pituitary gland?

A

TSH
ACTH
GH
Prolactin
LH
FSH

33
Q

Which hormones are released from the Posterior pituitary gland?

A

ADH
Oxytocin

34
Q

Presentation of growth hormone deficiency

A

Faltering growth after 6 months of age
Maxillary hypoplasia
Forehead prominence

35
Q

Test for GH deficiency

A

GH provocation test
Random GH not useful

36
Q

How does growth hormone cause growth?

A

Acts on IGF-1 at growth plate –> proliferation of chondrocytes

37
Q

Causes of Diabetes Insipidus

A
  1. Neurogenic = Inadequate release ADH. Idiopathic, AI, pituitary disease
  2. Nephrogenic = Inadequate renal response ADH (defect vasopressin-2 reception or aquaporin-2). Drugs (lithium), CRF, post-obstructive uropathy, High glucose / Na+ / Ca2+
38
Q

Diabetes Insipidus investigations

A

-Low urine osmolality, High serum Osmolality
- Hypernatraemia
- Water deprivation test - urine conc. <600 –> give desmopressin –> concentrates only in neurogenic. SE desmopressin = water retention –> hold when unwell.
- MRI head

39
Q

Causes of SIADH

A
  • CNS - meningitis, encephalitis, trauma, hypoxia
  • Haemorrhage
  • Guillain-Barre
  • Resp - LRTI, TB
  • Tumours - Thymoma, lymphoma, Ewing’s
  • Drugs
40
Q

What is Kallmann syndrome?

A

Defective GnRH release from hypothalamus
- Anosmia
- Colour blindness
- Delayed puberty

41
Q

Presentation of pituitary apoplexy

A

Headache
Meningism
Low GCS
Visual field defect
Ophthalmoplegia

42
Q

Physiological response to hypoglycaemia

A

Increased glucagon
Increased adrenaline –> Palp, tremor, sweating, pallor

43
Q

How is mid-parental height calculated?

A

(Mum+Dad)/2 –> +7 in boys
- 7 in girls

44
Q

Define Short stature

A

Height <2nd centile
2 SD away from mean

45
Q

Causes of Short stature

A
  • Familial
  • Constitutional delay
  • Iatrogenic eg steroids
  • Nutritional
  • Chronic disease (low IGF-1)
  • Foetal alcohol syndrome
  • Genetics - Russell- Silver, Turner’s, Noonan’s, Skeletal dysplasia, Prader-Willi, Trisomies, SHOX gene
  • Endocrine - thyroid, GH, cortisol
46
Q

Causes of Tall Stature

A
  • Nutritional - same final height
  • Genetic- Klinefelter’s, Marfan’s, Beckwith-Wiedemann, Sotos, NF
  • Metabolic - Homocystinuria
  • Endocrine - Hyperthyroid, precocious puberty, CAH, excess growth hormone
47
Q

What is defined as precocious puberty?

A

Onset of puberty before
- 8 years in girls
- 9 years in boys

48
Q

Causes of precocious puberty

A
  • Gonadotrophin dependent (High LH and FSH) = Pituitary mass (bitemoporal hemianopia), brain injury. More common in girls.
  • Gonadotrophin independent (Low FSH and LH) - adrenal tumours, CAH
49
Q

Investigations precocious puberty

A
  • LHRH stiulation test
  • LH, FSH, testosterone / oestradiol
  • L wrist xray
  • Pelvic USS
  • MRI brain
50
Q

What can be used to delay precocious puberty?

A

Ig Gonadotrophin dependent, can use GnRH analogues eg Leuprorelin –> decreases LH / FSH

51
Q

Causes of delayed puberty (>13y in girls, >14y in boys)

A
  • General - illness, malnutrition, steroids
  • Constitutional delay (more in boys)
  • Systemic causes low gonadotrophin = CF, asthma, Crohn’s
  • HPA disorder causing low gonadotrophin eg pituitary tumour, Kallmann, hypothyroid
  • High FSH / LH and low androgens: Turner’s, Klinefelter’s, gonadal damage eg surgery, radio
52
Q

Treatment of delayed puberty

A
  • Girls = Oestradiol
  • Boys = IM testosterone
53
Q

Genetic association of Type 1 DM

A

HLA D3/4

54
Q

Which auto-antibodies are associated with T1DM?

A

GAD
ZnT8
IA-2
T cell mediated damage to beta cells

55
Q

Glargine mechanism of action

A

Molecular changes –> shifts isoelectric point –> slow release of bioactive molecules

56
Q

Definition of severe DKA

A

pH <7.1
HCO3- <5

57
Q

When is insulin started in DKA and at what dose?

A

1 hour after rehydration
0.05 - 0.1 units/kg/hr

58
Q

Complication of rapid fluid correction in DKA

A

Cerebral oedema
Headache, agitation, irritability
Tx: Mannitol / hypertonic saline

59
Q

Pathophysiology PCOS + Tx

A

-Excess LH –> stim ovarian androgen production and hyperinsulinaemia upregulates 17-alpha-hydroxylase + synthesises androgen precursors.
-High level of uninhibited oestrogen –> endometrial hyperplasia.
-Tx: OCP corrects hormonal imbalances –> suppress ovarian stimulation by suppressing release of LH / FSH.

60
Q

What does low c-peptide levels mean?

A

Low endogenous production of insulin

61
Q

Diabetic retinopathy - signs on fundoscopy

A

Microaneurysms
‘Dot-and-blot’ haemorrhages
Venous bleeding ‘Cotton wool’ spots.

62
Q

Management of CF related DM

A

-Continue high calorie diet + exercise
-Start insulin and monitor blood glucose levels.

RCPCH TAS/ AKP (20 decks)

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