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MSRA 2 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What causes galactorrhoea-amenorrhoea syndrome?

A

Hyperprolactinaemia?

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2
Q

What are the pathological causes of hyperprolactinaemia?

A

Prolactinomas, drug-induced or hypothyroidism

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3
Q

How does hyperprolactinaemia present?

A

Galactorrhoea and amenorrhoea in women

Reduce libido and ED in men

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4
Q

How do we calculate anion gap?

A

(Na+ + K+) - (HCO3- + Cl-)

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5
Q

What is the normal range of an anion gap?

A

12-17

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6
Q

What is Waterhouse-Friderichsen syndrome?

A

Disease of the adrenal glands most commonly causes by N meningitidis, leading to massive haemorrhage in one or both adrenal glands

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7
Q

How does Waterhouse-Friderichsen syndrome present?

A

Meningococcemia, low BP, shock, DIC and adrenocortical insufficiency

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8
Q

What is Conn’s syndrome?

A

Increased aldosterone secretion from the adrenal glands due to adenoma, suppressed plasma-renin activity, hypertension and hypokalaemia

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9
Q

What causes primary hyperaldosteronism?

A

Unilateral aldosterone-producing adenoma (Conn’s syndrome)
Idiopathic hyperaldosteronism or bilateral adrenal hyperplasia

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10
Q

What is often seen on VBG in someone with Conn’s syndrome?

A

Hypokalaemic alkalotic htn

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11
Q

How do we treat Conn’s syndrome?

A

Laparoscopic adrenalectomy

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12
Q

What is thyroid storm?

A

Hyperthyroid crisis

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13
Q

How do we manage thyroid storm?

A

Cooling, IVI, resp support
Antithyroid meds, steroids, beta blockers, iodine soln

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14
Q

Why do we often see subclinical hypothyroidism in CF?

A

Reduced dietary absorption of iodine

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15
Q

How do we treat primary hypothyroidism in primary care?

A

T4 (do not treat with T3/T4 in community)

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16
Q

What is haemochromatosis?

A

Iron overload disorder

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17
Q

How does haemochromatosis present?

A

Cirrhosis, T2DM, skin pigmentation is the triad

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18
Q

What is the most common cause of secondary htn?

A

Conn’s

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19
Q

What electrolyte abnormality is associated with steroid use?

A

Hypokalaemia

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20
Q

In which population is Hashimoto’s thyroiditis most common?

A

Middle-aged females

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21
Q

Where do you see anti-TPO antibodies?

A

Hashimotos

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22
Q

How does De Quervain thyroiditis present?

A

Transient inflammatory disease characterised by pain and tenderness of the thyroid gland

23
Q

How does papillary thyroid carcinoma present?

A

Painless, hard thyroid mass with enlargement of cervical lymph nodes. Can invade local structures e.g. cause hoarseness/dysphagia

24
Q

How does Addison’s disease present?

A

Adrenocortical insufficiency

Collapse, low BMI, hx of autoimmune disease, hypotension, hyperkalaemia, hypona

25
Q

In which endocrinological conditions do you see hyperpigmentation?

A

Any with high ACTH e.g. Addisons, Cushing’s disease, ‘ectopic’ ACTH (ACTH made by a tumour outside of the pituitary e.g. the lung)

26
Q

How do we initially investigate Cushing’s syndrome?

A

Overnight dexamethasone suppression test

27
Q

What is the most common cause of SIADH?

A

Idiopathic

28
Q

What do we use parathyroid hormone levels for?

A

Can differentiate hypercalcaemia as PTH-mediated (primary hyperthyroidism, most common cause of hypercalc) or non-PTH-mediated (e.g. malignancy)

29
Q

Which blood test do we use for ? acromegaly?

A

IGF-1 (less variable than GH)

30
Q

Why do we not use HbA1c in HIV +ve pts?

A

Underestimates glycaemia

31
Q

What is arcus senilis?

A

Whitish-gray, opaque ring in the corneal margin

Seen in elderly people with hypercholesterolaemia

32
Q

What is the earliest marker for diabetic nephropathy?

A

Microalbuminaemia

33
Q

How do we investigate hypercalcaemia?

A

PTH

34
Q

Where do you see Chvostek’s sign?

A

Hypocalcaemia

35
Q

What is congenital adrenal hyperplasia?

A

Congenital adrenal hyperplasia is an autosomal recessive metabolic disorder related to enzymatic defects in the biosynthesis of cortical steroids. Majority of cases are attributed to 21-hydroxylase deficiency (95%). This results in deficient cortisol and/or aldosterone production and excess precursor steroids. In response, there is increased ACTH secretion from the anterior pituitary producing adrenocortical hyperplasia.

36
Q

How do we treat congenital adrenal hyperplasia?

A

Life-long replacement hydrocortisone and a salt-retaining steroid like fludrocortisone

37
Q

How does congenital adrenal hyperplasia present?

A
  1. Females are virilised at birth and post-pubertal amenorrhoea is common.
  2. Hyperpigmentation
  3. An adrenal crisis is characterised by salt loss and circulatory collapse. It usually occurs in the first few days of life and may be preceded by vomiting and poor weight gain. Cortisol and aldosterone are low or absent.
  4. Life-threatening hypoglycaemia may accompany cortisol deficiency due to omission of steroids or intercurrent illness.
38
Q

What does CN III innervate?

A

The third cranial nerve (CN III) innervates four extraocular muscles (which control elevation, depression, and adduction of the eye), the levator palpebrae superioris (which controls eyelid elevation), and the pupillary sphincter (which controls pupillary constriction).

39
Q

How do we calculate plasma osmolality?

A

Plasma Osmolarity = 2Na + Urea + Glucose

40
Q

What is the osmolar gap?

A

The difference between the measured and calculated plasma osmolarity is known as the osmolar gap and
normally is between 0 - 10 mmol/l.

41
Q

What is the normal range of osmolality?

A

For the purposes of the exam, it is worth remembering that the normal range is 285-295mmol/I and that plasma osmolarity should be higher than 290mmol/I in cases of DKA. If it is higher than 320mmol// and there is not significant ketonaemia/ketonuria, then HHS may be the diagnosis.

42
Q

How do we treat hypercalcaemia?

A

Rehydration
* Sodium chloride IV 0.9%

  • Loop diuretics not effective in lowering calcium & only to be used if fluid overload develops.
    • Dialysis may need to be considered in severe renal failure.
  • Bisphosphonates IV
  • E.g. Zoledronic acid or Pamidronate should be considered if further treatment is required after IV sodium chloride.
  • Second-line treatments
    • Considered on a case by case basis e.g. glucocorticoids as they inhibit 1,250H vitamin D production; calcimimetics e.g. cinacalcet; parathyroidectomy.
43
Q

How do we treat HHS?

A

For treatment of HHS, intravenous (IV) 0.9% sodium chloride solution is the principal fluid to restore circulating volume and reverse dehydration. Low dose IV insulin (0.05 units/kg/hr) should only be commenced once blood glucose is no longer falling with IV fluids alone OR immediately if there is significant ketonaemia.

44
Q

How does phaeochromocytoma present?

A

Phaeochromocytoma is a rare catecholamine-secreting tumour derived from chromaffin cells.
* The classic history of a patient with a phaeochromocytoma includes spells characterized by headaches, palpitations, and diaphoresis in association with severe hypertension. These 4 characteristics together are strongly suggestive of a phaeochromocytoma.
* The spells may vary in occurrence from monthly to several times per day, and the duration may vary from seconds to hours.
* Typically, they worsen with time, occurring more frequently and becoming more severe as the tumour grows.

45
Q

What is haemochromatosis?

A

Haemochromatosis is the abnormal accumulation of iron in the liver, heart, pancreas, pituitary, joints, and skin.

46
Q

How does haemochromatosis present?

A

The classic triad of cirrhosis, diabetes mellitus, and skin pigmentation occurs late in the disease

Other presentations include:
* arthralgia
* cardiomyopathy (congestive heart failure or arrhythmias)
* hypogonadism due to pituitary involvement by iron deposition (decreased libido and impotence)
* amenorrhoea and hypothyroidism may occur rarely.

47
Q

What is pseudohypoparathyroidism

A

Pseudohypoparathyroidism is caused by resistance to parathyroid hormone (PTH).
* It is characterised by hypocalcaemia, hyperphosphataemia, raised PTH levels, and an unusual collection of developmental and skeletal defects including short stature, rounded face, shortened fourth metacarpals and other bones of the hand and feet,
obesity, dental hypoplasia, and soft tissue calcifications/ossifications.

48
Q

What is diabetic sensory polyneuropathy?

A
  • This is the commonest form of diabetic neuropathy.
  • It consists of a distal symmetric polyneuropathy which develops insidiously and may be the presenting feature in type
    2 diabetes.
  • Sensory impairment is of a “glove and stocking” distribution. All forms of sensation may be affected.
  • Often initially asymptomatic and is only discovered on neurological examination or when secondary complications develop, but it may present with numbness, pain, & paraesthesiae, mainly distally in the lower limbs.
  • Autonomic neuropathy commonly coexists.
  • Minor distal motor involvement may be evident, but a significant distal motor neuropathy is uncommon.
  • Once established, diabetic sensory polyneuropathy is largely irreversible.
49
Q

What is lanugo?

A

She has Lanugo hair which usually grows on fetuses as a normal part of gestation, but is usually shed and replaced by vellus hair at about 33 to 36 weeks of gestational age.
* As the lanugo is shed from the skin, it is normal for the developing fetus to consume the hair with the fluid, since it drinks from the amniotic fluid and urinates it back into its environment. Subsequently, the lanugo contributes to the newborn baby’s meconium.

50
Q

Where else can you see lanugo, other than premature babies?

A

Lanugo can also be observed in patients with eating disorders and the malnourished. When found along with other physical findings,
lanugo can help a physician make a diagnosis of anorexia.

51
Q

What is the commonest cause of hypercalcaemia?

A

Primary hyperparathyroidism is the commonest cause of hypercalcaemia and usually presents as mild asymptomatic hypercalcaemia, due to excessive and inappropriate secretion of parathyroid hormone (PTH) secreted by the parathyroid glands. A solitary parathyroid adenoma is the cause in about 85% of cases.

52
Q

How does PTH increase calcium levels?

A

Increased secretion of PTH increases serum calcium by increasing bone resorption and renal calcium reabsorption, and indirectly by increasing intestinal calcium absorption.

53
Q

How does osteomalacia present?

A

Mildly affected patients may present with widespread bone pain and tenderness (especially low back pain and in the hips),
proximal muscle weakness and lethargy.
* Severely affected patients may have difficulty walking and may have a waddling gait or a change in gait from marked adductor spasm.
* Other signs include costochondral swelling (rachitic rosary), spinal curvature and signs of hypocalcaemia (e.g. tetany, carpopedal spasm) and tenderness over pseudofractures (which represent a lucent band of decreased cortical density).

54
Q

What is Conn’s syndrome?

A

Conn’s syndrome is characterized by increased aldosterone secretion from the adrenal glands, suppressed plasma renin activity,
hypertension, and hypokalaemia.

MSRA 2 (12 decks)

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