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Endocrinology > Basics Endocrinology > Flashcards

Basics Endocrinology Flashcards

1
Q

What is Addison’s?

A
  • autoimmune destruction adrenal glands
  • most common cause hypoadrenalism
  • reduced cortisol and aldosterone
  • hyponatraemia, hyperkalaemia, hyperpigmentation, vitiligo, hypoglycaemia, hypotension, salt craving, weight gain etc.
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2
Q

How do you investigate Addison’s?

A
  • ACTH stimulation test
  • plasma cortisol 30 min before and after 250 ug IM synacthen
  • electrolyte abnormalities
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3
Q

How do you manage an Addisonian crisis?

A
  • hydrocortisone 100mg IM or IV
  • 1 litre normal saline or dextrose if hypoglycaemic
  • continue hydrocortisone 6 hourly until stable
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4
Q

Management of Addison’s

A

glucocorticoid and mineralocorticoid replacement therapy (hydrocortisone and fludrocortisone)

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5
Q

What is Acromegaly?

A
  • excess GH
  • 95% secondary due to pituitary adenoma
  • coarse facial features, prognathism, interdental spaces, increase shoe size, sweat gland hypertrophy, features of primary tumour
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6
Q

How do you investigate acromegaly?

A
  • GH vary so not diagnostic
  • serum IGF-1 levels first line
  • OGTT can help to confirm
  • Pituitary MRI
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7
Q

How do you manage acromegaly?

A 
-transphenoidal surgery 
if not:
-somatostatin analogue e.g. octreotide
-GH receptor antagonist e.g. pegvisomant
-dopamine agonist e.g. bromocriptine
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8
Q

What is Bartter’ syndrome?

A
  • autosomal recessive severe hypokalaemia due to defective chloride absorption at NKCC2 in ascending loop of Henle
  • normotensive
  • failure to thrive in childhood, polyuria, polydipsia, hypokalaemia, normotension and weakness
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9
Q

What are the causes of congenital adrenal hyperplasia?

A
  • autosomal recessive disorders
  • high ACTH in response to low cortisol
  • 21-hydroxylase deficiency
  • 11-beta-hydroxylase deficiency
  • 17-hydroxylase deficiency
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10
Q

What investigations for Cushing’s

A
  • hypokalaemic metabolic alkalosis
  • impaired glucose tolerance
  • ectopic ACTH leads to hypokalaemia
  • insulin stress test to distinguish pseudo
  • confirm with overnight dexamethasone suppression test and 24 hour urinary free cortisol
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11
Q

Explain the difference in results between normal, Cushing’s syndrome, disease and ectopic ACTH with low dose dexamethasone, high-dose and ACTH levels:

A
  • normal: decrease, decrease, no change
  • syndrome: no change, no change, decrease
  • disease: no change, decrease, increase
  • ectopic ACTH: no change, no change, increase
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12
Q

What is Liddle’s syndrome?

A
  • rare autosomal dominant cause of hypertension
  • hypokalaemic alkalosis
  • disordered increased sodium reabsorption
  • treat with amiloride or triamterene
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13
Q

MEN type I

A

-parathyroid
-pituitary
-pancreas
(adrenal and thyroid)
MEN1 gene

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14
Q

MEN type II

A

-medullary thyroid cancer
-parathyroid
-phaeochromocytoma
RET oncogene

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15
Q

MEN type III

A

-medullary thyroid cancer
-phaeochromocytome
-marfanoid body, habits, neuromas
RET oncogene

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16
Q

What is a myxoedema coma and how do you treat it?

A
  • decompensated hypothyroidism
  • confusion and hypothermia
  • IV thyroid replacement, IV fluids, IV corticosteroids, electrolyte imbalance correction
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17
Q

What is a phaeochromocytoma?

A
  • rare catecholamine secreting tumour
  • 10% familial: MEN type II, neurofibromatosis, von Hippel-Lindau
  • causes hypertension, episodic headaches, palpitations, sweating and anxiety
18
Q

How do you test for phaeochromocytoma?

A
  • 24hr urinary collection of metanephrines

- replaced 24hr collection of catecholamines

19
Q

How do you treat phaeochromocytoma?

A
  • surgery

- before surgery, stabilise with alpha blocker (phenoxybenzamine) and beta blocker (propranolol)

20
Q

What are some typical symptoms of pituitary adenomas?

A
  • symptoms due to excess or depletion of hormone
  • stretching of dura causing headaches
  • compression of optic chasm causing bitemporal hemianopia
21
Q

What are the investigations for pituitary adenomas?

A
  • pituitary blood profile: HG, prolactin, ACTH, FH, LSH, TFTs
  • formal visual field testing
  • MRI brain with contrast
22
Q

How can you treat pituitary adenomas?

A
  • hormonal therapy (bromocriptine)
  • surgery if progression in size
  • radiotherapy
23
Q

What are the features of primary hyperaldosteronism and what is it caused by?

A
  • adrenal adenoma, bilateral idiopathic adrenal hyperplasia and adrenal carcinoma
  • hypertension, hypokalaemia, alkalosis
24
Q

What are the investigations for primary hyperaldosteronism?

A
  • plasma aldosterone/renin (increased aldosterone, decreased renin due to negative feedback)
  • adrenal venous sampling
  • CT abdomen
25
Q

Treatment of hyperaldosteronism?

A
  • adrenal adenoma: surgery

- bilateral arden-cortical hyperplasia: aldosterone antagonist e.g. spironolactone

26
Q

Carbimazole ADR

A
  • agranulocytosis (sore throat, fever)

- crosses placenta so lower dose in pregnancy

27
Q

What type of activity do different corticosteroids have?

A
  • fludrocortisone: very high mineralocorticoid, low glucocorticoid
  • hydrocortisone: high mineralocorticoid, glucocorticoid
  • prednisolone: high glucocorticoid, low mineralocorticoid
  • betmethasone, dexamethasone: very high glucocorticoid, minimal mineralocorticoid
28
Q

Glucocorticoid ADR

A
  • endocrine: dysregulated glucose, hirsutism, hyperlipidaemia, increased appetite and weight gain
  • Cushing’s
  • MSK: osteoporosis, proximal myopathy, avascular necrosis
  • immunosuppression
  • psychiatric
  • peptic ulcers, pancreatitis
  • opthalmic: glaucome, cataracts
  • decreased growth children
  • neutrophilia
  • ICHTN
29
Q

Mineralocorticoid ADR

A
  • fluid retention

- HTN

30
Q

Growth hormone ADR

A
  • headache
  • ICHTN
  • fluid retention
31
Q

How does insulin stress test work and what are the contraindications?

A
  • to investigate hypopituitarism
  • IV insulin and measure cortisol and GH which should rise normally
  • CONTRA: ischaemic heart disease, epilepsy, adrenal insufficiency
32
Q

Features of insulinoma, diagnosis and treatment:

A
  • hypoglycaemia early in morning and before meal
  • weight gain, increased insulin, increased proinsulin:insulin and increased c-peptide
  • investigate with CT abdomen and prolonged fasting 72 hours
  • treat surgically or with diazoxide and somatostatin
33
Q

Meglitinides (MOA, examples and ADR)

A
  • increases pancreatic insulin secretion similarly to sulfonylureas (good for erratic lifestyle)
  • e.g. nateglinide, repaglinide
  • ADR: weight gain, hypoglycaemia
34
Q

Orlistat (MOA, ADR)

A
  • pancreatic lipase inhibitor for obesity
  • for >=28 with risk factors or 30kg/m2 BMI
  • ADR: faecal incontinence/urgency and flatulence
35
Q

SGLT-2 inhibitors (examples, ADR)

A

-dapagliflozin, empagliflozin, canagliflozin
ADR:
-urinary and genital infections (Fournier’s)
-increased risk lower limb amputations
-normoglycaemic ketoacidosis
-weight loss

36
Q

Sulfonylureas (MOA, ADR)

A

-binds to ATP independent K+ channel on pancreatic beta cells
-increases insulin secretion
ADR:
-weight gain
-hypoglycaemic
-hyponatraemia
-bone marrow suppression
-hepatotoxicity
-peripheral neuropathy
-AVOID in pregnancy and breast feeding

37
Q

Thiazolidinediones (MOA, ADR)

A 
-agonists of PPAR gamma receptor and decreased peripheral insulin resistance
ADR:
-weight gain
-liver impairement
-bladder cancer
-increased risk fractures
-fluid retention (contra in HF)
38
Q

Androgen insensitivity syndrome

A
  • x-linked recessive condition
  • defect in androgen receptor so end organ resistance to testosterone
  • male genotype and female phenotype (no uterus)
  • testosterone, oestrogen and LH elevated
39
Q

5-alpha reductase deficiency

A
  • autosomal recessive
  • inability to convert testosterone to dihydrotestosterone
  • ambiguous genitalia in newborn, hypospadias and virilisation at puberty
40
Q

Kallmann’s syndrome

A
  • cause of delayed puberty secondary to hypogonadotrophic hypogonadism
  • inherited x-linked recessive
  • failure of GnRH secreting neurones to migrate to hypothalamus
  • anosmia, decreased sex hormones, LH and FSH, normal or above average height, cleft lip/palate and visual/hearing defects
41
Q

Klinefelter’s syndrome

A
  • XXY
  • taller
  • lack of secondary sexual characteristics
  • small, firm testes
  • infertile
  • gynaecomastia
  • GnRH increased and testosterone decreased

Endocrinology (3 decks)

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