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Phase 2A Medicine > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is the role of calcium in the body?

A
  1. regulation of voltage-gated ion channels in neurones and muscle
  2. mineralisation and strengthening of bones
  3. facilitation of blood clotting
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2
Q

What are the causes of abnormalities in calcium homeostasis?

A

Dysregulation in:

  1. PTH production
  2. vitamin D production
  3. renal dysfunction
  4. metabolic bone disease
  5. gut dysfunction and dietary deficiency of calcium, phosphate or magnesium
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3
Q

What is the homeostatic response to a decrease in serum calcium?

A

Increased PTH production. Increased calcium reabsorption in nephrons. Increased bone resorption. Increased calcium absorption.

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4
Q

What measures can be taken to help prevent nocturnal hypoglycaemia?

A
  • take a bedtime snack regularly
  • patients that take twice daily mixed insulin can separate their evening dose and take the intermediate insulin at bedtime rather than before supper
  • reduce the dose of soluble insulin before supper since its effects persist well into the night
  • change to rapid-acting insulin analogue with a long-lasting insulin analogue at night
  • changing to an insulin infusion pump that can be programmed to deliver lower doses of insulin at time of night when a patient has been experiencing hypoglycaemia.
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5
Q

Why is there a poor correlation between urine tests and simultaneous blood glucose?

A
  • changes in urine glucose lag behind changes in blood glucose
  • mean renal threshold is around 10 mmol/L but the range is wide form 7 to 13. Threshold rises with age.
  • urine tests can give no guidance concerning blood glucose levels below renal threshold.
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6
Q

What is ketonuria?

A

Detectable ketone levels in the urine.

can occur in fasted non-diabetics

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7
Q

What is ketosis?

A

Elevated plasma ketone levels in the absence of acidosis.

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8
Q

What is diabetic ketoacidosis?

A

A metabolic emergency in which hyperglycaemia is associated with a metabolic acidosis due to greatly raised (>5 mmol/L) ketone levels. Seen in T1DM.

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9
Q

What is a hyperosmolar hyperglycaemia state?

A

A metabolic emergency in which uncontrolled hyperglycaemia induces a hyperosmolar state in the absence of significant ketosis. Seen in T2DM.

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10
Q

What is lactic acidosis?

A

A metabolic emergency in which elevated lactic acid levels induce a metabolic acidosis. In diabetic patients, it is rare and associated with biguanide therapy.

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11
Q

Briefly describe the pathogenesis of diabetic ketoacidosis.

A

Insulin deficiency leads to uncontrolled catabolism. Gluconeogenesis in the liver is no longer suppressed and hence there is increased glucose production. This causes hyperglycaemia and glycosuria leading to osmotic diuresis. Simultaneously, rapid lipolysis occurs forms more free fatty acids that are converted to ketones by hepatocytes. This leads to acidosis and vomiting. There is fluid and electrolyte depletion causing renal hypoperfusion and impaired excretion of ketones and hydrogen ions.

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12
Q

What are the clinical features of diabetic ketoacidosis?

A

prostration, hyperventilation (Kussmaul breathing), nausea, vomiting, abdominal pain, confusion, stupor, evidence of dehydration, ketone breath, low body temp, dry skin.

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13
Q

What are the principles of management of DKA?

A
  • replace fluid losses
  • replace electrolyte losses
  • restore acid-base balance
  • replace deficient insulin
  • monitor blood glucose closely
  • seek the underlying cause
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14
Q

Which hormone is affected in acromegaly and how?

A

Hypersecretion of growth hormone

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15
Q

What is the role of the growth hormone?

A

GH stimulates skeletal and soft tissue growth

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16
Q

What is an excess of growth hormone before puberty called?

A

Gigantism

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17
Q

What is an excess of growth hormone after puberty called?

A

Acromegaly

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18
Q

What happens to bone growth at puberty?

A

Epiphyseal fusion

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19
Q

Describe the onset of acromegaly in one word.

A

Insidious

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20
Q

What inhibits growth hormone?

A

Somatostatin

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21
Q

What factors stimulate growth hormone release?

A

Stress, sleep, exercise

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22
Q

What are the sporadic causes of acromegaly?

A
  1. Somatotroph adenoma
  2. Ectopic GH secretion
  3. Hyperplasia due to GHRH excess
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23
Q

What are the genetic causes of acromegaly?

A
  1. Familial acromegaly

2. Multiple endocrine neoplasia (MEN1)

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24
Q

What is familial acromegaly?

A

It is an autosomal dominant inherited form of acromegaly that has incomplete penetrance and leads to gigantism.

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25
Q

What are the symptoms of acromegaly?

A
  1. Change in facial appearance
  2. Headache
  3. Visual disturbance
  4. Deep voice
  5. Goitre
  6. Fatigue
  7. Daytime drowsiness
  8. Weight gain
  9. Sweating
  10. Arthralgia
  11. Amenorrhoea/oligomenorrhoea
  12. Impotence/ decreased libido
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26
Q

What are the signs of acromegaly?

A
  1. Prominent supraorbital ridge
  2. Prognathism
  3. Interdental separation
  4. Macroglossia
  5. Visual field defects
  6. Hirsutism
  7. Spade-like hands and feet
  8. Carpal tunnel syndrome
  9. Hypertension
  10. Proximal myopathy
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27
Q

What investigations would you do if you suspect acromegaly?

A
  1. GH levels (normal around 0.5)
  2. Oral glucose tolerance test (no suppression if positive so greater than 0.3)
  3. IGF-1 levels would be high
  4. Visual field exam- bitemporal hemianopia
  5. MRI pituitary fossa for lesion
  6. Test pituitary function
  7. Test PRL levels
  8. ECH, echo
  9. Compare with old photos
28
Q

What are the surgical treatment options for acromegaly?

A
  1. Trans-sphenoidal hypophysectomy for microadenoma

2. Trans-frontal for macroadenoma

29
Q

What is the disadvantage of adjuvant radiotherapy for acromegaly?

A

Can cause hypopituitarism

30
Q

What medications are available to treat acromegaly?

A
  1. Pituitary somatostatin receptor agonists- octreotide, lanreotide
  2. Dopamine (D2) agonists- Bromocriptin, cabergoline
  3. Growth hormone antagonists- pegvisomant
31
Q

Which is the most common pituitary tumour?

A

Benign adenoma

32
Q

What problems can a pituitary tumour cause?

A
  1. Local mass effects
  2. Hormone excess
  3. Hormonal deficiency
33
Q

Which local anatomical structures can a pituitary tumour affect by pressure or infiltration?

A
  1. Visual pathways causing field defects and vision loss
  2. Cavernous sinus causing cranial nerve palsy of 3, 4 and 6
  3. Bony structures and meninges around fossa causing headaches
  4. Hypothalamus causing altered appetite, thirst, wakefulness and precious puberty
  5. Ventricles causing interrupted CF flow leading to hydrocephalus
  6. Invasion of sphenoid sinus leading to CSF rhinorrhoea
34
Q

What are the differential diagnoses for a pituitary tumour?

A
  1. Other tumours like craniopharyngioma, meningioma, glioma, chondroma, primary pituitary carcinoma.
  2. Hypophysitis, sarcoidosis, Langerhans cells histiocytes
  3. Carotid artery aneurysm, arachnoid cyst, Rathke’s cleft
35
Q

Which visual field defects are usually caused by a pituitary tumour?

A

Bitemporal hemianopia and upper temporal quandrantanopia

36
Q

Give examples of secretory pituitary adenomas and how they differ histologically.

A
  1. Prolactinoma- chromophobe
  2. Acromegaly- acidophil
  3. Cushing’s disease- basophil
  4. Nelson syndrome- basophil
37
Q

What is hypopituitarism?

A

It is a diminished secretion of anterior pituitary hormones.

38
Q

In what order are anterior pituitary hormones affected in hypopituitarism?

A

Growth hormones- FSH/LH- PRL- TSH- ACTH

39
Q

What is panhypopituitarism?

A

It is a deficiency of all anterior hormones usually caused by irradiation, surgery or a pituitary tumour.

40
Q

What are the causes of primary hypopituitarism?

A
  • Pituitary tumour
  • Irradiation of pituitary
  • Pituitary inflammation- haemochromatosis, amyloidosis, cancer
  • Pituitary ischaemia- Sheehan’s syndrome, apoplexy
41
Q

What are the causes of secondary hypopituitarism?

A
  • Tumour, infection (meningitis, TB), inflammation, ischaemia of hypothalamus
  • Kallman’s syndrome (GnRH)
  • Trauma, surgery, meningioma, craniopharyngioma, carotid artery aneurysm affecting pituitary stalk
42
Q

What is the main principle of management for hypopituitarism?

A

Hormone replacement + treatment of underlying cause

43
Q

Which oral replacement drug would you give for secondary adrenal failure?

A

Hydrocortisone

44
Q

Which oral replacement drug would you give for hypothyroid?

A

Thyroxine

45
Q

Which hormone replacement would you give to induce fertility in someone suffering from hypopituitarism?

A

Human chorionic gonadotropin

46
Q

What is Cushing’s syndrome?

A

Cushing’s syndrome is the term used to describe the clinical state of increased free circulating glucocorticoid.

47
Q

What are the ACTH-dependent causes of Cushing’s?

A
  • Pituitary adenoma (Cushing’s disease)

- Ectopic ACTH-producing tumours

48
Q

What are the non-ACTH dependent causes of Cushing’s?

A
  • Adrenal adenomas
  • Adrenal carcinomas
  • Exogenous steroids
49
Q

What are the symptoms of Cushing’s?

A
  • Hirsuitism
  • Acne
  • (central) weight gain
  • Thin skin/easy bruising
  • Depression/psychosis/insomnia
  • Muscle weakness/back pain
  • Amenorrhoea/oligomenorrhoea
  • Poor libido/sexual dysfunction
  • Polyuria/polydypsia
50
Q

What is pseudo-Cushing’s?

A

It is when a person has a Cushingoid appearance due to excess alcohol consumption.

51
Q

What are the signs of Cushing’s?

A
  • Plethora
  • Moon facies
  • Hypertension
  • Buffalo hump
  • Central obesity
  • Thin skin and bruising
  • Poor wound healing
  • Abdominal striae
  • Proximal myopathy
52
Q

What investigations would you carry out to confirm a diagnosis of Cushing’s syndrome?

A
  1. Dexamethasone suppression test
  2. 24hr urinary free cortisol
  3. Midnight cortisol
  4. Plasma ACTH
  5. Adrenal CT/MRI
  6. Pituitary MRI
  7. Plasma potassium levels
  8. CRH test
  9. Chest X-ray or lung/mediastinal/ abdominal CT
  10. Radiolabelled Octreotide to locate ectopic ACTH sites
53
Q

How would you remove a tumour that is causing Cushing’s?

A

Trans-sphenoidal approach or a bilateral adrenalectomy

54
Q

What is Nelson syndrome?

A

It is the post-adrenalectomy development of locally aggressive pituitary tumour due to lack of negative feedback.

55
Q

What are the dynamic tests for Cushing’s?

A

Dexamethasone suppression test and CRH stimulation

56
Q

What is the dynamic test for acromegaly?

A

Oral glucose tolerance test to check GH suppression

57
Q

What is the dynamic test for a TSHoma?

A

TRH stimulation

58
Q

What are the dynamic tests for GH/ACTH deficiency?

A

Insulin-induced hypoglycaemia and the glucagon test

59
Q

What is the dynamic test for gonadotrophin deficiency?

A

GnRH stimulation

60
Q

True or False: excess inhaled steroids commonly cause Cushing Syndrome.

A

False

they commonly cause adrenal suppression and rarely cause Cushing.

61
Q

When does steroid therapy become problematic?

A

when therapy lasts longer than 3 weeks

when daily dose of prednisolone exceeds 5 mg

62
Q

What are the major adverse effects of corticosteroid therapy?

A
  • adrenal and/or pituitary suppression
  • increased BP
  • pancreatitis
  • polyuria, nocturia
  • depression, euphoria, psychosis, insomnia
  • weight gain
  • glycosuria/hyperglycaemia/diabetes
  • impaired growth
  • amenorrhoea
  • osteoporosis, proximal myopathy and wasting
  • skin thinning and easy bruising
  • cataracts
  • increased susceptibility to infections (esp fungal)
63
Q

What advice should be given to patients on steroid therapy?

A
  1. carry their steroid card at all times
  2. long-term therapy should not be stopped suddenly
  3. doses should be gradually reduced, with most given in the morning to minimise adrenal suppression
  4. doses need to be increased (doubled) during serious intercurrent illness
  5. other physicians, anaesthetists and dentists should be made aware
  6. possible side effects
64
Q

What are the various endocrine causes of hypertension?

A
  1. excessive renin (thus angiotensin II) production- renal artery stenosis, local renal disease, renin-secreting tumours
  2. excessive production of catecholamines- phaeochromocytoma
  3. excessive GH production - acromegaly
  4. excessive aldosterone production- adrenal adenoma (Conn syndrome), idiopathic adrenal hyperplasia, dexamethasone-suppressible hyperaldosteronism
  5. excessive production of other mineralocorticoids- Cushing syndrome, congenital adrenal hyperplasia, tumours producing other mineralocorticoids like corticosterone
  6. exogenous mineralocorticoids or enzyme inhibitors- liquorice ingestion inhibits 11beta-hydroxylase, misuse of mineralocorticoid preparations
65
Q

What are the four major stimuli to thirst?

A

Hypertonicity: Cellular dehydration acts via an osmoreceptor mechanism in the hypothalamus
Hypovolaemia: Low volume is sensed via the low pressure baroreceptors�in the great veins and right atrium
Hypotension: The high pressure baroreceptors in carotid sinus & aorta�provide the sensors for this input
Angiotensin II: This is produced consequent to the release of renin�by the kidney (eg in response to renal hypotension) which is also sensed by the subfornical organ and organum vasculosum in the lamina terminalis (OVLT) and used as a neurotransmitter from the SFO to the hypothalamus to initiate thirst.

66
Q

What is the initial treatment or someone who is having a thyroid storm?

A

beta blockers like propranolol

Phase 2A Medicine (16 decks)

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