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PLAB 1 August 2024 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is the cause of acromegaly?

A
  • Excessive secretion of growth hormone.
  • Usually due to pituitary adenomas.
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2
Q

Symptoms of acromegaly?

A
  • Hands and feet enlargement
  • Coarse facial features
  • Macroglossia
  • Enlargement of jaw (prognathism)
  • DM2
  • Hypertension
  • Headaches
  • Sweating
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3
Q

What is the investigation done in acromegaly?

A

Initial test and for monitoring
- Insulin growth factor (IGF-1).

Confirmation of diagnosis
- Oral glucose test.

Others
- MRI scan of pituitary (adenomas).

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4
Q

What is the treatment of acromegaly?

A

- Trans-sphenoidal surgery
- GH receptor antagonist: Pegvisomant
- Somatostatin analogues: octreotide
- Radiotherapy

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5
Q

What is the physiology of Addison’s disease?

A
  • AKA primary adrenal insufficiency;
  • The adrenal gland (kidney) cannot produce adequate levels of cortisol (glucocorticoids) and aldosterone (mineralocorticoids) due to autoimmune destruction.
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6
Q

What is the cause of primary Addison’s disease?

A
  • Autoimmune.
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7
Q

What are the symptoms of primary adrenal disease?

A
  • Fatigue
  • Weakness
  • Weight loss
  • Postural hypotension
  • Hyperpigmentation (due to ACTH raised)
  • Salt cravings
  • Hypoglycaemia
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8
Q

What are the investigations done in primary Addison’s disease?

A
  • Electrolytes: Hyponatraemia & Hyperkalaemia.
  • Early morning cortisol: low
  • ACTH: high
  • Synacthem / ACTH stimulation test: cortisol does not rise.
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9
Q

What is the cause of SECONDARY adrenal insufficiency?

A
  • Hypothalamic and pituitary failure.
  • Long term steroid medication (suspension of hypothalamic-pituitary-adrenal axis)
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10
Q

What is the investigation of secondary adrenal insufficiency?

A

- ACTH: low
- Cortisol (early morning): low
- ACTH stimulation test / Synacthem: cortisol does not rise.

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11
Q

DDx between:
- Addison’s disease (primary adrenal insufficiency)
- Secondary adrenal insufficiency

A

• Primary adrenal insufficiency
- Autoimmune destruction of adrenal gland, leads to low cortisol and low aldosterone.
- Low cortisol leads to negative feedback to the pituitary which leads to high levels of ACTH which leads to hyperpigmentation.
- Low aldosterone leads to hyponatraemia and hyperkalaemia.

• Secondary adrenal insufficiency
- Inadequate pituitary or hypothalamic stimulation, leads to low ACTH, which leads to low cortisol.
- Aldosterone levels are normal hence normal Na and K.

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12
Q

What is the DDx between:
- Conn’s syndrome
- Addison’s disease

A

Conn’s syndrome
- Hypernatraemia
- Hypokalaemia
- Hypertension

Addison’s disease
- Hyponatraemia
- Hyperkalaemia
- Hypotension
- Hypoglycaemia

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13
Q

What are the causes of Addisonian crisis?

A
  • Withdrawal of chronic steroid therapy
  • Infection or stress (corticosteroids needs will be raised)
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14
Q

What are the symptoms of Addisonian crisis?

A
  • Shock: postural hypotension, tachycardia, oliguria
  • Abdominal pain
  • Hypoglycaemia
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15
Q

What are the investigations of Addisonian crisis?

A
  • Cortisol
  • ACTH levels
  • Blood sugar
  • FBC, U&Es, Cultures
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16
Q

What is the treatment of Addisonian crisis?

A
  • IV hydrocortisone 100 mg
  • IV fluids if shocked
  • IV glucose if hypoglycaemia
  • Improvement after 72h oral steroids
  • If adrenal pathology identified: fludrocortisone.
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17
Q

What is the Rx for DM₂?

A

First line:
- Metformin

Check HbA1c in 3-6 months
If HbA1c > 58 mmol/mol
- Reinforce lifestyle advice
- Add another drug.

If added cardiovascular risk:
- Metformin
AND
- SGLT-2 inhibitors

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18
Q

DM2

Describe the adjustements of biguanides in relation to kidney injury.

A

Example: Metformin

Renal imparment adjustments
- eGFR < 45: reduce dose
- eGFR < 30: discontinue

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19
Q

DM2

Describe the pharmacology of SGLT-2 inhibitors (AKA gliflozins).

A

Example:
- Dapagliflozin
- Canagliflozin
- Empagliflozin

Benefits
- Cardioprotective
- Renal protective
- Weight loss

Risks
- DKA at moderately raised glucose (< 14 mmol/L).

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20
Q

DM2

Describe the pharmacology of Sulphonylurea.

A

Example:
- Gliclazide

Risks
- Hypoglycaemia
- Weight gain

Not to be given to lorry, ambulance, heavy machinery drivers due to hypoglycaemia.

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21
Q

DM2

Describe the pharmacology of DDP4 inhibitors (AKA sitagliptin).

A

Example:
- Sitagliptin

Risks
- Pancreatitis

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22
Q

DM2

Describe the pharmacology of Pioglitazone.

A

Contraindicated in:
- Heart failure
- Bladder cancer
- Fractures (women)

Risks
- Weight gain

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23
Q

DM2

Describe the pharmacology of Repaglinide.

A

Risks
- Hypoglycaemia
- Weight gain
- Avoid in liver disease

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24
Q

DDx between:
- Osteoporosis
- Paget’s disease
- Osteomalacia

A

Osteoporosis
Calcium: Normal
Phosphate: Normal
Alkaline phosphatase: Normal

Paget's disease
Calcium: Normal
Phosphate: Normal
Alkaline phosphatase: High

Osteomalacia
Calcium: Low
Phosphate: Low
Alkaline phosphatase: High

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25
Q

Define what is Conn's syndrome / primary hyperaldosteronism?

A

Condition due to excessive production of aldosterone by the adrenal glands.

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26
Q

What are the symptoms of Conn's syndrome / primary hyperaldosteronism?

A
  • Hypertension: Due to ⬆︎ aldosterone ➝ hypernatraemia which causes water retention.
  • Hypokalaemia: causes muscles weakness.
  • Hypernatraemia
  • Metabolic alkalosis

Aldosterone acts on the convulted tubules to:
- ↑ Na⁺ reabsortion
- ↑ K⁺ excretion
- ↑ H⁺ excretion

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27
Q

What is the cause of Conn's syndrome / primary hyperaldosteronism?

A
  • Adrenal adenoma
  • Adrenal hyperplasia
  • Adrenal carcinoma
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28
Q

What are the investigations done in Conn's syndrome / primary hyperaldosteronism?

A

Renim - Aldosterone ratio
- Renim: low
- Aldosterone: High

CT scan / MRI
- Searching for adenomas, carcinomas, etc.

Renim is low because:
- The kidneys juxtaglomerular cells are responsible for sensing the BP coming to the kidneys.
- If the BP is low, they release renim
- Renim converts angioteninogem (produced by the liver) into angiotensin I
- Angiotensin 1 is then converted (in the lungs) into angiotensin 2 (by angiotensin converting enzymes)
- Angiotensin 2 acts on the adrenal gland to produce aldosterone increasing the BP ➝ lowering renim.

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29
Q

What is the treatment of Conn's syndrome / primary hyperaldosteronism?

A

Aldosterone antagonist:
- Spironolactone

Surgery:
- Adrenalectomy

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30
Q

Define what is Cushing's syndrome?

A

Condition caused by prolongued exposure of endogenous or exogenous glucorticoids leading to excessive cortisol on the body.

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31
Q

Describe the adrenal axis physiology.

A
  1. Hypothalamus releases CRH hormone
  2. CRH acts on the anterior pituitary gland
  3. Anterior pituitary releases ACTH hormone
  4. ACTH acts on the adrenal gland
  5. Adrenal gland releases cortisol
  6. Cortisol does the following:
    ◆ Inhibits the immune system;
    ◆ Inhibits bone formation;
    ◆ ⬆︎ blood glucose
    ◆ ⬆︎ metabolism
    ◆ ⬆︎ alertness
  7. ⬆︎ Cortisol sends a negative feedback to the anterior pituitary and to the hypothalamus, and they ⬇︎ the production of their hormones.
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32
Q

What are the causes of Cushings syndrome?

A

◉ ACTH dependent disease
◆ Cushings disease: Pituitary adenoma;
◆ Ectopic ACTH: small lung carcinoma

◉ Non-ACTH dependent
◆ Adrenal adenoma/carcinoma
◆ Exogenous steroids

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33
Q

What are the symptoms of Cushings syndrome?

A

◆ Round face
◆ Buffalo hump
◆ Abdominal obesity
◆ Purple abdominal striae
◆ Muscle weakness
◆ Osteoporosis
◆ Depression and insomnia

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34
Q

How is the diagnosis of Cushings syndrome done?

Investigations done to diagnose it.

A

1. 24h urinary free cortisol;
2. Dexamethasone suppression test (low dose).

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35
Q

Cushings syndrome

Explain how the low dose dexa supression test is done and its clinical relevance.

A

1. 1mg of Dexa is giving at midnight.
2. Cortisol (plasma) is measured the next day at 9 am.

➜ If positive for Cushings:
◆ 1mg of dexa won't be enough to supress the hypothalamus (CRH) or the anterior pituitary (ACTH), as the body is used to ⬆︎ levels of cortisol.

➜ If negative for Cushings:
◆ Cortisol < 50 nmol/L.
◆ 1mg of dexa will be enough to supress the hypothalamus and the anterior pituitary.

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36
Q

Cushings syndrome

After positive dexa supression test (low dose), what is the next step?

A

◉ Differentiate the causes of Cushings by doing:
➜ High dose dexamethasone supression test.

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37
Q

Explain how the high dose dexa supression test is done and its clinical relevance.

A

◘ 8mg of dexa is administered.

➔ Cushing disease/pituitary adenoma:
◆ ACTH ⬇︎
◆ Cortisol ⬇︎
◆ 8 mg would supress the ACTH/adenoma

➔ Adrenal adenoma:
◆ ACTH ⬇︎
◆ Cortisol ⬆︎
◆ 8 mg would supress the pituitary but the source of the ↑ cortisol is on the kidney itself.

➔ Ectopic ACTH (lung carcinoma):
◆ ACTH ⬆︎
◆ Cortisol ⬆︎
◆ The source of the ↑ cortisol is elsewhere even though the pituitary is supressed.

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38
Q

Diabetes

Describe the Dawn phenomenom.

A

It is a rise in glucose levels in the early hours (2 - 8 AM) in diabetic patients.

Especially DM1.

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39
Q

Diabetes

What is the Rx of the Dawn phenomenom?

A

⬆︎ night time dose of long acting insulin.

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40
Q

What is the cause of diabetes insipidus?

A

1. ⬇︎ production of ADH (antidiuretic hormone).
2. ⬇︎ response to ADH.

ADH is produced by the hypothalamus and stored in the pitituitary.

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41
Q

Diabetes insipidus

What is the function of ADH (antidiuretic hormone)?

A
  • Acts on the collecting ducts on the kidneys ⟶ Reabsportion of H₂O from urine (urine becomes concentrated due to lack of water)

On diabetes insipidus:
- ⬇︎ ADH
- Prevents urine from becoming concentrating due to excessive water in urine
- Polyuria (excessive amount of urine)
- Polydipsia (thirst caused by blood being concentrated)

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42
Q

What are the symptoms of diabetes insipidus?

A
  • Polyuria: excessive amount of urine due to ⬆︎ water in the urine
  • Polydipsia: thirst caused by blood being concentrated
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43
Q

What is the classification of diabetes insipidus?

A

Nephrogenic:
- Collecting ducts don’t respond to ADH (resistance to ADH)

Cranial:
- ⬇︎ production of ADH by the hypoothalamus.

44
Q

What are the causes of NEPHROGENIC diabetes insipidus?

A

Nephrogenic:
- Collecting ducts don’t respond to ADH (resistance to ADH)
- Example of causes:
◆ Lithium
◆ Genetics
◆ Kidney disease
◆ Electrolyte imbalances (↓K⁺, ↑Ca⁺)

45
Q

What are the causes of CRANIAL diabetes insipidus?

A

Cranial:
- ⬇︎ production of ADH by the hypoothalamus.
- Example of causes:
◆ Idiophatic
◆ Brain tumor
◆ Head injury
◆ Brain malformations
◆ Surgery
◆ Radiotheraphy

46
Q

What is the investigations done in diabetes insipidus?

A
  • Water deprivation test
  • Urine osmolality: low (due to water excess)
  • Plasma osmolality: high
47
Q

Define what is thyrotoxicosis?

A

⬆︎ levels of the thyroid hormone in the body / plasma.

48
Q

Define what is Primary hyperthyroidism?

A

It occurs when:
- The thyroid gland itself is responsible for ⬆︎ thyroid hormone production.

49
Q

Define what is Secondary hyperthyroidism?

A

It occurs when:
- ⬆︎ levels of TSH released by the pituitary
- TSH will act on the thyroid hormone and ⬆︎ thyroid hormone production

The problem might be in the pituitary or the hypothalamus.

50
Q

Describe what is hyperprolactinaemia.

A

⬆︎ levels of prolactin on the blood.

  • Prolactin is produced by the anterior pituitary.
  • It primarly regulates lactation.
51
Q

Define what is Graves disease?

A
  • Autoimune disease
  • TSH receptor antibodies cause the hyperthyroidism
  • These antibodies mimic TSH and stimulate the TSH receptors on the thyroid
  • TSH receptors cause the thyroid gland to secrete ⬆︎ thyroid hormone.
52
Q

Describe the syndrome of galactorrhoea-amenorrhoea.

A
  • ⬆︎ ` prolactin levels **⟶** prevents the hypothalamus from secreting luitenising hormone (LH) and follicle stimulating hormone (FSH) **⟶** disruption of normal menstrual cycle` .
53
Q

What are the symptoms of Graves disease?

A
  • Exophtalmos
  • Proptosis
  • Eyelid lag
  • Pretibial myxoedema
54
Q

What are the pathological causes of hyperprolactinaemia?

A
  • Prolactinoma (tumour)
  • Hypothyroidism
  • Antipsycotics: Risperidone, haloperidol, domperidone.
  • Brain injury
55
Q

What is the treatment of Graves disease?

A

First line
- Carbimazole
- Propylthiouracil

Others
- Radioiodine
- Thyroidectomy

56
Q

What are the symptoms of hyperprolactinaemia?

A

Females
- Inhibition FSH & LH causes amenorrhoea and galactorrhoea

Males
- Secondary hypogonadism
- ⬇︎ libido
- Gynaecomastia
- Erectile dysfunction

Neurological symptoms (prolactinomas)
- Bilateral hemianopia
- Headaches

57
Q

What are the causes of hyperthyroidism?

A

↑ T4 & ↓ TSH

Causes
- Autoimmune (graves disease)
- Toxic nodular goitre
- De Quervain’s thyroiditis (infectious)
- Drugs (exogenous thyroid hormone)

58
Q

What are the investigations done in hyperprolactinaemia?

A
  • Prolactin level
  • MRI (pituitary)
  • Visual field testing
59
Q

What is the treatment of hyperprolactinaemia?

A

First line
Dopamine agonists
- Cabergoline
- Bromocriptine

Others
-Surgery
- Radiotheraphy

60
Q

What are the symptoms of hyperthyroidism?

A

Gastro
- ↑ appetite
- Weight loss
- Diarrhoea

Cardio
- Palpitations
- Tachycardia

Others
- Heat intolerance
- Oligomenorrhea
- Irritability
- Weakness

61
Q

What is the treatment of hyperthyroidism?

A

↑ T4 & ↓ TSH

First line
- Carbimazole
- Propylthiouracil

Others
- Radioiodine
- Thyroidectomy

62
Q

DDx between:
- Clinical hyperthyroidism
- Subclinical hyperthyroidism

A

Clinical hyperthyroidism
T4: High
TSH: Low

Subclinical hyperthyroidism
T4: Normal
TSH: Low

63
Q

What are the causes of thyrotoxic storm?

A
  • Radioidine (treatment)
  • Thyroid surgery
  • Myocardial infarction
  • Infection
64
Q

What are the symptoms of thyrotoxic storm?

A
  • Altered mental status
  • Coma
  • Agitation
  • Hyperthermia
  • Atrial fibrillation
  • Tachycardia
  • Diarrhoea
  • Vomiting
65
Q

What are the investigation done in thyrotoxic storm?

66
Q

What is the Rx of thyrotoxic storm?

A

Counteracting the peripheral effects of thyroid hormone
- Beta blockade: propranol
- Digoxin (once adequately beta blocked)

Inhibiting thyroid hormone synthesis
- Propylthiouracil
- Lugol iodine

Treat the causes

Propylthiouracil prefered over carbimazole in emergencies as rapid onset.

67
Q

What are the causes of hypercalcaemia?

A
  • Primary hyperparathyroidism
  • Malignancy (multiple myeoloma, bone metastasis)
  • Sarcoidosis
  • Hyperthyroidism
  • Prolongued immobilization
  • Thiazides
68
Q

What are the symptoms of hypercalcaemia?

A
  • Gastro (Moans): Constipations due to ↓ bowel activity;
  • Renal (Stones): Kidney stones & nephrolithiasis due to calcium deposits in kidney. Polyuria & polydipsia due to induction of diabetic insipidus;
  • Neuro & Psych (Groans): Lethargy, confusion and depression;
  • Bone pain (Bones): seen in hyperthyroidism.
69
Q

What is the management of hypercalcaemia?

A
  1. Hydration with (3-4L) of NaCl 0.9% to induce urinary output and excretion of calcium;
  2. Bisphosphonates IV (Zoledronic acid or pamidronate);
  3. In sarcoidosis: steroids;
  4. 2ry hyperparathyroidism: Cinalcet hydrochoride;
  5. Renal failure: hemodialysis;
70
Q

DDx of hypercalcaemia?

A

Primary hyperparathyroidism
Ca⁺: High
PTH: High

Secondary hyperparathyroidism
Ca⁺: Low
PTH: High

Primary hypoparathyroidism
Ca⁺: High
PTH: High

PTH independent hypercalcaemia
Ca⁺: High
PTH: Low

71
Q

What is the classification of hyperparathyroidism?

A

1. Primary hyperparathyroidism

2. Secondary hyperparathyroidism

3. Tertiary hyperparathyroidism

72
Q

Explain the physiology of the parathyroid glands.

A
  • There are 4 parathyroid glands on the 4 corners of the thyroid gland.
  • The parathyroid glands function is to produce PTH hormone in response to low serum Ca²⁺ levels.
  • PTH ↑ Ca²⁺ reabsortion from the intestines, kidneys, and breaking down Ca²⁺ from the bones (to be released in the plasma)

◉ VITAMIN D
- Is a hormone produced by the body in response to sunlight and food.
- It acts on the intestines, kidneys and bones to increase the reabsortion of Ca²⁺.
- PTH also acts on vitamin D to enhace its action on Ca²⁺ reabsortion

Low Vit D causes hypocalcaemia.

73
Q

Describe what is primary hyperparathyroidism:
- Causes
- Investigations

A

➜ Abnormal levels of PTH acts on the kidneys, guts and bones to ⬆︎ Ca²⁺ ➔ Hypercalcaemia.

Causes:
- Parathyroid adenoma
- Hyperplasia
- Carcinoma

Investigations
- ↑ PTH (could be normal)
- ↑ Ca²⁺
- ↓ Phosphate

PTH increases phosphate excretion by the kidneys.

74
Q

Describe what is secondary hyperparathyroidism:
- Causes
- Investigations

A

➜ There is a reduced reabsortion of Ca²⁺ from the kidneys, guts and bones ➔ Hypocalcaemia.

Causes:
- ↓ Vitamin D
- CKD (there’s abnormal absorption of Ca²⁺ in the guts due to ↓ production of an active form of Vit D by the kidneys).

Investigations
- ↑ PTH
- ↓ Ca²⁺ (could be normal)
- ↑ Phosphate in CKD

75
Q

Describe what is tertiary hyperparathyroidism:
- Causes
- Investigations

A

➜ Occurs after prolongued 2ndary hyperparathyroidism.
➜ Hyperplasia of the glands occurs.
➜ ↑ baseline release of PTH
➜ After treatment of 2ndary hyperparathyroidism, the glands remain big and still secrete ⬆︎ levels of PTH ⟶ Hypercalcaemia.

Causes:
- Prolongation of 2nd hyperparathyroidism

Investigations
- ↑ PTH
- ↑ Ca²⁺
- ↑ Phosphate

76
Q

What is the Rx for secondary hyperparathyroidism?

A

Vitamin D supplementation
- Cholecalciferol
- Alfacalcidol (in patients with severe renal impairment)

77
Q

Describe what is pseudoHYPOparathyroidism:

A

Disorder where there is a resistance to PTH hormone in the body.

  • Ca²⁺ will not get absorbed by the kidneys, gut and bones.
  • Phosphate will not be excreted by the kidneys.

Symptoms
- ↓ Ca²⁺
- ↑ phosphate
- ⬆︎ PTH

PTH increases phosphate excretion by the kidneys.

78
Q

DDx of:
- ALP (alkaline phosphatase)
- Ca²⁺

A

⬆︎ ALP + ⬆︎Ca²⁺
- Bone metastasis
- Hyperparathyroidism

⬆︎ ALP + ⬇︎ Ca²⁺
- Osteomalacia:
◆ Vit D deficiency
◆ Renal failure
◆ Anticonvulsants

79
Q

Describe what is hypothyroidism and its classification.

A

Inadequate secretion of the thyroid hormones by the thyroid gland.

  • Primary hypothyroidism (issue on the thyroid itself)
  • Secondary hypothyroidism (insufficiency of TSH secretion by the pituitary/hypothalamus)
80
Q

What are the causes of:
- Primary HYPOthyroidism
- 2ndary HYPOthyroidism

A

Primary hypothyroidism causes:
- Autoimunne inflammation /. Hashimoto thyroiditis.
- Iodine deficiency (essential for T3, T4 production)
- Treatment for hyperthyroidism
- Lithium (inhibits T3, T4 production)
- Amiodarone

Secondary hypothyroidism
- Pituitary disorder/Hypothalamic disorder:
◆ Sheehans syndrome
◆ Tumors
◆ Radiation

81
Q

What are the labs features of hypothyroidism?

A

Primary hypothyroidism:
- ⬆︎TSH
- ⬇︎T3, T4

Secondary hypothyroidism
- ⬇︎TSH
- ⬇︎T3, T4

82
Q

What are the symptoms of hypothyroidism?

A
  • Weight gain
  • Cold intolerance
  • Tiredness
  • Dry skin
  • Menstrual abnormalities
83
Q

What is the Rx of hypothyroidism?

A

Levothyroxine.

84
Q

What are the features of SUBCLINICAL hypothyroidism?

A

- TSH High
- T4 normal

Primary hypothyroidism:
- ⬆︎TSH
- ⬇︎T3, T4

Secondary hypothyroidism
- ⬇︎TSH
- ⬇︎T3, T4

85
Q

What is the management of SUBCLINICAL hypothyroidism?

A
  • Repeat blood tests in 3 - 6 months.

1. ⬆︎TSH but < 10 miU/L
- On 2 tests 3 months apart
- Symptomatic
- < 65 years
➜ Consider levothyroxine

2. ⬆︎TSH > 10 miU/L
- On 2 tests 3 months apart
➜ Consider levothyroxine

86
Q

What are the causes of hypopituarism?

A

➜ Lost of function of the pituitary gland

Causes
- Pituitary adenoma
- Sheehan’s syndrome
- Tumous
- Infection
- Stroke
- Radiotheraphy
- Trauma

87
Q

What are the symptoms of hypopituarism?

A

↓LH, ↓FSH
- Amenorrhoea
- Infertility

↓GH
- No symptoms in adults

↓TSH
- Hypothyroidism symptoms

↓ACTH
- Fatigue
- Hyponatraemia
- Hypotension

↓Prolactin
- Absent lactation

1st two are the main ones to be affected first.

88
Q

Define LADA (latent autoimmune diabetes of adulthood)

A

A type of DM1 thar develops much slower and is diagnosed in adults.

89
Q

DM1

What is the investigation in LADA?

A

GAD antibody testing.

90
Q

What is the Rx for hyperthyroidism in pregnancy?

A

First trimester:
- Propylthiouracil

2nd and 3rd trimester:
- Carbimazole
- Partial thyroidectomy if carbimazole is not effective.

Postpartum:
- Carbimazole

91
Q

DDx between:
-Toxic nodular goitre
-Non-toxic goitre

A

Toxic
- Large goitre
- Produces ⬆︎ amount of thyroid hormones

Non-toxic
- Large goitre
- Produces normal amount of thyroid hormones.

92
Q

Rx of:
-Toxic nodular goitre
-Non-toxic goitre

A

Toxic
1. FNAC: rule out malignancy
2. Carbimazole
3. Radioidine: definitive treatment
4. Thyroidectomy

Non-toxic
1. FNAC: rule out malignancy
2. Thyroidectomy: if compression symptoms
3. Radioidine: if surgery is not an option (elderly).

93
Q

What are the symptoms and labs features of osteomalacia?

A
  • Bone pain
  • Ca²⁺: low
  • Serum phosphates: low
  • ALP: high
94
Q

What is the cause and treatment for Osteomalacia?

A
  • Cause: Vit D insufficiency, renal failure
  • Treatment: calcium & vit D supplements
95
Q

What are the causes of osteoporosis?

A
  • Corticoisteroids (long term)
  • Low BMI
  • Premature menopause w/out Rx
  • Immobillity
  • Smoking
  • Heavy alchool
96
Q

In osteoporosis, what is the step by step management for assessment and prevention?

A

Risk of osteoporosis
1. Fracture risk assessment;
2. If risk ≥10% of osteoporotic; fracture than step 3;
3. Dexa scan;
4. T-score <-2.5 ➝ offer Rx.

≥ 50 years & has a fragility fracture
- Dexa scan
- T-score <-2.5 ➝ offer Rx.

97
Q

Osteoporosis

Describe Klinefelter syndrome.

A
  • ⬇︎ bone mass and and density
  • Caused by ⬇︎ testoterone levels.

Treatment
- If ⬇︎ testosterone: testotorene therapy
- If not sure of cause: Look for other cause, Vit D perhaps.

98
Q

DDx between:
- Osteomalacia
- Osteoporosis
- Paget’s disease

A

Osteoporosis
- Ca²⁺: normal
- Serum phosphate: normal
ALP: normal

Paget's disease
- Ca²⁺: normal
- Serum phosphate: normal
ALP: ⬆︎

Osteomalcia
- Ca²⁺: ⬇︎
- Serum phosphate: ⬇︎
ALP: ⬆︎

99
Q

What is the treatment for 1ry hyperparathyroidism?

A

1. Cinalcet
2. Bisphosphonates: if risk of fractures
3. Parathyroidectomy

100
Q

What is the treatment for prolactinomas?

A

Tumour < 10mm
Restore function with dopamine agonists
- Cabergoline
- Bromocriptine

Tumour > 10mm
1. Restore function with dopamine agonists
- Cabergoline
- Bromocriptine
2. Reduce tumour size
- Surgery (if medical Rx fails)

101
Q

Describe what is Sheehan’s syndrome.

A

Necrosis of the pituitary gland secondary to massive haemorrhage and leading to hypopituitarism.

102
Q

What are the symptoms of Sheehan’s syndrome?

A
  • Failure to lactate
  • Amenorrhea / oligoamenorrhea
  • Hypothyroidism
  • Adrenal insufficiency
103
Q

What are the labs features of Sheehan’s syndrome?

A

↓LH & ↓FSH
- Failure to lactate and oligo/amenorrhea

↓TSH, ↓T3, ↓T4
- Hypothyroidism

↓ACTH & ↓Cortisol
- Adrenal insufficiency

104
Q

What are the labs features of SIADH secretion?

ADH is produced by the hypothalamus and stored in the pituitary.

Acts on the collecting ducts to induce water reabsorption.

A

- ADH: High
- Urine osmolality: High
- Urine sodium: High
- Serum sodium: Low
- Plasma osmolality: Low

105
Q

What is the Rx of SIADH secretion?

A
  • Treat the cause
  • Fluids restriction (500 - 1L/24h)
  • Demeclocycline (induces nephrogenic DI)
  • Vaptans (in severe hyponatraemia)

PLAB 1 August 2024 (32 decks)

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