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Clinical > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What are the types of MEN (multiple endocrine neoplasia)?

A

Men 1: pituitary tumour, parathyroid hyperplasia/adenomas, gastrinomas, insulinomas, prolactinomas.
Men 2a:medullary thyroid cancer, pheochromocytoma, parathyroid adenoma/hyperplasia.
Men2b: 2a + mucosal adenomas.

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2
Q

What are the signs of Diabetes Insipidus?

A

Polyuria, excessive thirst, raised serum osmolality (>296), low urine osmolality (<700).

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3
Q

What are the two types of Diabetes insipidus and how can you tell them apart?

A

Cranial: ADH not released. Giving desmopressin will increase urine osmolality.
Nephrogenic: kidneys don’t respond to ADH. Giving desmopressin will make no difference.

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4
Q

What are two drugs that can cause nephrogenic diabetes insipidus?

A

lithium, demeclocycline

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5
Q

Hyponatraemia, raised urinary Na, and decreased plasma osmolality is indicative of what?

A

SIADH.

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6
Q

How can you test for hypopituitarism?

A

Insulin tolerance test: injection of insulin
In a healthy person would cause blood sugar to drop and CRH to be released which will increase cortisol to compensate for low sugars..
In a pt with hypopituitarism, blood sugar will drop but CRH won’t be released to stimulate cortisol to compensate so cortisol won’t increase.

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7
Q

What is pituitary apoplexy? What are the Sx?

A

Bleeding into the pituitary gland causing sudden onset retro-orbital headache, nausea, and vomiting.
Happens in pts with pituitary tumours.

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8
Q

How do you diagnose pituitary apoplexy?

A

Give hydrocortisone and do an MRI to visualise pathology.

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9
Q

What is the definitive test for acromegally?

A

OGTT: will not suppress GH like it does in a healthy person

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10
Q

Female presenting with amenorrhoea, reduced libido, and galactorrhoea is indicative of what? What is this caused by?

A

Hyperprolactinaemia.
- Physiological: pregnancy, nipple stimulation, sleep, stress, etc
- Pharmacological e.g., dopamine antagonists - Prolactin is supressed by dopamine so low dopamine can cause elevated prolactin.
- Pathological: Pituitary tumours, hypothyroidism, renal insufficiency, etc

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10
Q

What is the most likely cancerous complication of Acromegally? Why?

A

Colorectal cancer due to high IGF-1 and GH causing raised VEGF and therefore growth of new blood vessels.

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11
Q

What is macroprolactin vs monomeric prolactin?

A

Macroprolactin isn’t biologically active.

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12
Q

What happens to calcium, PTH, and phosphate levels in primary hyperparathyroidism?
What is the most common cause?
How is this cause managed?

A

Raised calcium,
PTH high-normal,
Phosphate low (PTH reabsorption is reduced in PCT).
Most commonly caused by parathyroid adenoma (managed with cinacalcet or surgery).

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13
Q

What happens to calcium, PTH, and phosphate levels in secondary hyperparathyroidism?

A

Low calcium (increased excretion, malabsorption, or lack of vit d due to long term disease) raised PTH (to compensate for low calcium) and low phosphate (due to raised phosphate).

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14
Q

What happens to calcium, PTH, and phosphate levels in tertiary hyperparathyroidism?

A

Long-term secondary causes raised phosphate, PTH, and calcium.

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15
Q

What is the trigger for DeQuervian’s Thyroiditis? What are the sx of the thyrotoxic phase?

A

Viral infection.
Fever, malaise, fatigue, anorexia, body pains, tachycardia, sweating, restlessness, weight loss, neck pain and discomfort.

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16
Q

What is a thyroid storm? How does it present? How is it managed?

A

Untreated hyperthyroidism presents with restlessness, tremor, hyperthermia, palpitations, HeTN, confusions.
Very low TSH and high T3/4.
PTU, fluids, propranolol, steroids.

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17
Q

A pt presenting with a ‘painful fullness in their neck’, tremor, tachycardia, pretibial myxoedema, ophthalmoplegia, and tachycardia, is likely what?

A

Grave’s Disease.

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18
Q

What is sick euthyroid syndrome?

A

Low TSH and T3/4 during acute illness, resolves afterwards.

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19
Q

What is a myxoedema coma?

A

Complication of extreme hypothyroidism.
Signs include decreased consciousness, hypotension, bradycardia, hypothermia, periorbital myxoedema.

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20
Q

Subacute granulomatous thyroiditis (DeQuervian’s) comes in 3 stages, the first being the thyrotoxic phase, what are the following two?

A

2) hypothyroid phase: 2-6 months after 1st stage, there is now decreased levels of T3/4, variable quantity of thyroid reuptake, and increased ESR.
3) Euthyroid phase: normal thyroid will return in >90% pts.

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21
Q

Which antibody is associated with Hashimoto’s thyroiditis? What are the biochemical findings?

A

Anti TPO is +ve in 90% pts.
Raised TSH and low T3/4.

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22
Q

What are the symptoms of Hashimoto’s thyroiditis?

A

Cold intolerance, lethargy, queen Anne’s signs, bradycardia, cardiomegaly, carpal tunnel, slow relaxing reflexes, peripheral neuropathy, cerebellar ataxia.

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23
Q

Amiodarone induced thyrotoxicosis is split into what types?

A

1: high iodine content causes excess T3/4
2: destructive thyroiditis causes excessive releaseand therefore hgigh serum levels of high T3/4

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24
Q

What type of heart failure can hyperthyroidism cause?

A

Congestive high output cardiac failure (preserved EF, normal diastolic function).

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25
Q

What is the wolff-Chaikoss effect? How is this used medically?

A

Reduced thyroxine synthesis after unphysiologically high iodine exposure.
Used in Lugol’s iodine whereby high levels are used to treat thyroid cancer or thyroid storm to induce hypothyroidism.

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26
Q

Why can hypothyroidism cause hyperprolactinaemia?

A

Elevated TRH levels can cause lactotroph hyperplasia leading to pituitary gland enlargement and hyperprolactinaemia.

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27
Q

What are the sick day rules for insulin-dependent diabetics?

A

Never stop long-acting insulin, stop short acting if not eating and drinking.
Test sugars and ketones regularly.

28
Q

What are the components of DKA? What type of acidosis is casued?

A

Hyperglycaemia (>11.1)
Raised ketones (>3)
Acidosis (<7.3 or bicarb <15).
= Raised anion gap metabolic acidosis.

29
Q

What might happen to the WCC in DKA?

A

May increase.

30
Q

What are the signs of DKA?

A

N+V, ado pain, tachypnoeic (Kussmaul breathing), dehydration (polyuria).

31
Q

How is DKA managed?

A

Fluids (500 ml 0.9% NaCl over 15 minutes followed by 1L over 1 hour),
Insulin (continuous infusion @ 0.1 units/kg/hr alongside normal insulin regime).

32
Q

What complications can happen in DKA?

A

Hypo or hyperkalaemia
Hypoglycaemia
Cerebral oedema
Pulmonary oedema

33
Q

What are the pre-diabetic and diabetic levels for fasting glucose?

A

Normal: 3.9-5.6 mmol/L
Prediabetic: 5.7-6.9
Diabetic: >7.0

34
Q

What are the components of HHS (hyperglycaemic hyperosmolar state)?

A

Serum osmolality >325, volume depletion in the absence of acidosis, hyperglycaemia.

35
Q

How do we manage HHS?

A

Fluids, insulin, LMW heparin to prevent clots (stroke, DVT, PE, etc), correct electrolyte disturbances.

36
Q

What can happen if glucose, fluids, or insulin are corrected too quickly in HHS?

A

Glucose: Clots causing stroke, PE, DVT, etc.
Fluid: oedema
Insulin: hypos (tend to be very insulin sensitive)

37
Q

What is Diabetic Ketosis?

A

Raised ketones in the absence of acidosis

38
Q

What are the complications of Diabetes?

A

Microvascular: retinopathy, nephropathy, neuropathy
Macrovascular: CVD, PVD, cerebrovascular disease

39
Q

What are the main roles of mineralocorticoids vs gluccocorticoids?

A

M: e.g., aldosterone, cause increase reabsorption of water and Na in the kidneys.
G: anti-inflammatory chemicals with a role in glucose response

40
Q

Congenital adrenal hyperplasia is a deficiency in what?

A

21-hydroxylase deficiency, over production of ACTH, and deficiency of aldosterone and cortisol.

41
Q

What happens to Na and K in congenital adrenal hyperplasia?

A

Hyponatraemia and hyperkalaemia.

42
Q

What manifestations occur in the phenotype of people with congenital adrenal hyperplasia?

A

Development of exaggerated male type characteristics in females and precociously in males.

43
Q

What is Conn’s Syndrome?

A

Adrenal adenoma or bilateral adrenal hyperplasia causing hyperaldosteronism.

44
Q

What are the electrolyte abnormalities in Conn’s syndrome? Why?
What happens to the pH?

A

Hypernatremia (malignant HeTN), hypokalaemia.
Increased level of aldosterone = increased action on principle cells in the kidney causing increased reabsorption of Na and excretion of K.
You get a metabolic alkalosis

45
Q

How do you Test for Conn’s syndrome?

A
  • Aldosterone renin ratio (will be high)
  • High res CT or MRI to look for adrenal mass
46
Q

How do you manage Conn’s Syndrome?

A

1) spironolactone or eplerenone for aldosterone inhibition.
2) Phenoxybenzamine (non-specific alpha blocker) can manage HeTN, this can be used also before surgery to prevent spikes in BP.
3) If it is an adrenal adenoma, can be removed surgically (give metyrapone to normalise cortisol before surgery)

47
Q

What is Addison’s Disease? What are the sx?

A

Destruction of adrenal cortex causing defect in production of glucocorticoid (cortisol).
HoTN, fatgue, weakness, GIT sx, increased pigmentation (tanned).

48
Q

How do we investigate for Addison’s disease?

A

Synacthen test: inject ACTH then measure cortisol levels after 30 minutes. In a healthy person this would stimulate increase in cortisol, in Addison’s it won’t so cortisol will stay low.
9am cortisol <100 is suspicious if adrenal insufficiency.

49
Q

How do we manage Addison’s Disease?

A

Replacement of glucocorticoid using steroids.
Replacement dose of prednisolone is 4mg/day.

50
Q

What is an Addisonian Crisis? Mx?

A
  • Severe (often refractory to fluids) HoTN
  • Electrolyte disturbance (hyponatremia, hyperkalaemia)
  • Low glucose and cortisol levels
  • Can lead to coma and death
    Manage with IV hydrocortisone, IV fluids, IV glucose.
51
Q

What is Cushing’s Syndrome? What are the sx?

A

Excess cortisol.
- Central obesity, buffalo hump
- Easy bruising, striae
- Hirsutism
- ED in men
- Persistent HeTN
- Glucose intolerance
- Hypokalaemia, hypernatreamia

52
Q

What are the two types of Cushing’s?

A

ACTH Dependent: excessive ACTH = excessive cortisol
ACTH Independent: primary adrenal disease

53
Q

How do you test for Cushing’s?

A
  • Overnight dexamethasone suppression test and 9 am cortisol. This should cause cortisol to be <50, in Cushing’s this won’t happen.
  • 24 hour free urinary cortisol or late night salivary cortisol: will be raised.
54
Q

How is Cushing’s Syndrome Managed?

A

Medical: metyrapone, ketoconazole, mifepristone, and pasireotide are medications to help decrease cortisol production.
Surgical: if caused by a pituitary tumour, this can be removed.

55
Q

What is a Pheochromocytoma? What are the sx? How do we test for it?

A

Catecholamine-secreting, neuroendocrine tumour from chromaffin cells of the adrenal glands.
- HeTN
- Hyperglycaemia
- Headache
- Hypermetabolism
- Hyperhidrosis
Test for by measuring plasma metanephrines

56
Q

What are the biochemical abnormalities in PCOS?

A

Increased LH : FSH (LH increases but FSH stays normal).
High testosterone.
Low SHBG.

57
Q

What are the components of the Rotterdam Criteria for PCOS?

A
  • Hirsutism
  • Oligomenorrhoea
  • Polycystic ovaries
58
Q

What is hypergonadotrophic hypogonadism?

A

Low sex hormone (oestrogen/testosterone), bit elevated levels of LH and FSH due to negative feedback system.
Indicates a primary problem of ovaries/testes to produce enough sex hormone to reduce LH/FSH levels.

59
Q

What is Hypogonadotrophic hypogonadism?

A

Pituitary/hypothalamic problem meaning low LH and FSH which causes a low sex hormone level.

60
Q

What is Kleinfelter’s Syndrome?

A

Congenital hypergonadotropic hypogonadism in males.
Due to extra X chromosome - XXY karyotype.

61
Q

What is Turner’s Syndrome? What are the clinical features?

A

Congenital hypergonadotropic hypogonadism in females due to 45 XO karyotype (missing an X).
Signs include webbed necked, wide spaced nipples, primary amenorrhoea.

62
Q

What is Kallman’s Syndrome?

A

Congenital hypogonadotropic hypogonadism, accompanied by absence of smell.

63
Q

What is Androgen insensitivity syndrome? What are the characteristics?

A

XY chromosomes but the body does not respond to androgens for the development of male characteristics. Results in external female characteristics but no internal female organs.
Primary amenorrhoea, lack of secondary sexual characteristics (except breasts as testosterone can be turned into oestrogen in the peripheries), and short vagina (blind ending).

64
Q

What is the IV dose of glucose for someone who is hypoglycaemic?

A

100 ml of 20% glucose

65
Q

How would you investigate for an Insulinoma?

A

72 hour monitored fast

66
Q

MEN 2a+b are associated with which oncogene?

A

RET proto-oncogene (tyrosine kinase receptor).

67
Q

How can you manage a pathological hyperprolactinaemia?

A

Dopamine agonists such as cabergoline.

68
Q
A

Clinical (27 decks)

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