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3rd Year Conditions > Endo > Flashcards

Endo Flashcards

1
Q

What is diabetes insipidus?

A

Lack of ADH production or lack of response to it

Prevents kidney from concentrating the urine leading to polyuria and polydipsia

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2
Q

What are the causes of diabetes insipidus?

A

Nephrogenic - drugs especially lithium, mutations in the AVPR2 gene for ADH receptor, intrinsic kidney disease, hypokalaemia, hypercalcaemia

Cranial - idiopathic, brain tumour, head injury, brain malformation, brain infection, brain surgery or radiotherapy

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3
Q

Signs and symptoms of diabetes insipidus

A

Polyuria, polydipsia, dehydration, postural hypotension, hypernatraemia

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4
Q

Investigations for diabetes insipidus

A

Urine test to check osmolality - would be low

Serum osmolality - would be high

Water deprivation test - no fluid for 8 hours, measure urine osmolality, then give desmopressin. Measure urine osmolality after 8 hours again. In cranial osmolality will go up, in nephrogenic it’ll stay low.

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5
Q

How to manage diabetes insipidus

A

Treat underlying cause

Desmopressin for cranial diabetes insipidus
High dose desmopressin and thiazides diuretic for nephrogenic

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6
Q

What is Cushing’s syndrome? How is it different to Cushing’s disease?

A

signs and symptoms that develop as a result of abnormal elevation of cortisol

  • the disease is specifically when it’s caused by a pituitary adenoma secreting excessive ACTH
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7
Q

Aetiology/risk factors for Cushing’s syndrome

A
  • exogenous steroids
  • Cushing’s disease
  • Adrenal adenoma
  • Paraneoplastic Cushing’s (excessive ACTH released from a cancer other than the pituitary, usually small cell lung cancer)
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8
Q

Presenting signs and symptoms of Cushing’s syndrome

A
  • central obesity
  • fatigue
  • muscle weakness
  • hirsutism
  • acne
  • moon face
  • thin skin
  • poor wound healing
  • buffalo hump (fat pad on upper back)
  • bruises
  • hypertension
  • cardiac hypertrophy
  • hyperglycaemia
  • depression
  • insomnia
  • pink striae on abdomen/breasts/thighs
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9
Q

Investigations for Cushing’s syndrome

A
  1. Blood test to confirm hypokalaemic metabolic alkalosis
  2. Dexamethasone suppression test, no suppression of morning cortisol (low dose 1mg, then high dose 8mg)
  3. 24hr urinary free cortisol is alternative to suppression test
  4. MRI for pituitary adenoma
  5. Chest CT for lung cancer
  6. Abdominal CT for adrenal tumours
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10
Q

How can we use the dexamethasone suppression test to find the cause of Cushing’s syndrome?

A
  • confirm Cushing’s with low dose test
  • Cushing’s disease, the 8mg will suppress cortisol due to negative feedback so low cortisol and low ACTH
  • Adrenal adenoma, the 8mg doesn’t affect the cortisol release from the tumour but it will suppress the ACTH release from the pituitary so low ACTH, high cortisol
  • in ectopic ACTH release, the cortisol will be high and ACTH will be high
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11
Q

How is Cushing’s syndrome treated?

A
  • treat the underlying cause
  • remove the tumour
  • use metyrapone or ketoconazole to inhibit cortisol synthesis (if unfit for surgery or pre-operatively)
  • trans-sphenoidal removal of pituitary adenoma
  • surgical removal of adrenal tumour
  • surgical removal of tumour producing ectopic ACTH
  • radiotherapy after surgery if not cured
  • replacement steroids for life is both adrenals need to be removed
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12
Q

Possible complications of Cushing’s syndrome

A
  • diabetes
  • osteoporosis
  • hypertension
  • pre-disposition to infections
  • surgery complications:
  • CSF leakage
  • meningitis
  • sphenoid sinusitis
  • hypopituitarism
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13
Q

What is hyperthyroidism and what are the different causes?

A
  • over-production of thyroid hormone
  • Primary is due to thyroid pathology
  • Secondary is due to pituitary or hypothalamus pathology
  • Grave’s disease is autoimmune disease where TSH receptor antibodies cause primary hyperthyroidism
  • Toxic multinodular goitre (Plummer’s) is where nodules of thyroid gland act independently of the normal feedback system
  • Thyroiditis
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14
Q

What are the universal features of hyperthyroidism?

A
  • anxiety and irritability
  • sweating and heat intolerance
  • tachycardia
  • weight loss
  • fatigue
  • frequent loose stools
  • sexual dysfunction
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15
Q

Unique features of Grave’s disease

A

All due to presence of TSH receptor antibodies

  • diffuse goitre
  • exophthalmos
  • pretibial myxoedema
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16
Q

What is de Quervain’s thyroiditis?

A
  • viral infection with fever, neck pain and tenderness, dysphagia and features of hyperthyroidism
  • hyperthyroid phase
  • hypothyroid phase
  • NSAIDs and beta blockers used to treat it
17
Q

What is a thyroid storm?

A
  • rare presentation of hyperthyroidism
  • thyrotoxic crisis
  • pyrexia
  • tachycardia
  • delirium
  • fluid resuscitation, anti-arrhythmic medication and beta-blockers
  • other medication same as other hyperthyroid conditions
18
Q

How is hyperthyroidism investigated?

A
  • TFTs to identify cause
  • Autoantibodies
  • Imaging (US, uptake scan)
  • Inflammatory markers - CRP for thyroiditis
19
Q

How is hyperthyroidism managed?

A
  1. Carbimazole with levothyroxine 1st line - anti-thyroid drug
  2. Propythiourcail with levothyroxine 2nd line - similar but can cause hepatic reactions
  3. Radioactive iodine kills some thyroid cells but can result in hypothyroid and will require levothyroxine
    - mustn’t be pregnant within 6 months
    - avoid contact with children and pregnant women
  4. Beta blockers to stop symptoms, use propnaolol for thyrotoxicosis
  5. Surgery with levothyroxine for life
20
Q

What are the causes of hypothyroidism?

A
  • Hashimoto’s Thyroiditis - autoimmune inflammation caused by antithyroid peroxidase antibodies and antithyroglobulin antibodies (goitre then atrophy)
  • Iodine deficiency as iodine is needed to make thyroid hormone
  • Secondary to hyperthyroidism treatment
  • Lithium inhibits production of thyroid hormone and so does amidarone (amidarone can also cause thyrotoxicosis)
  • Secondary hypothyroidism (hypopituitarism)
21
Q

How does hypothyroidism present?

A
  • weight gain
  • fatigue
  • dry skin
  • coarse hair and hair loss
  • fluid retention
  • heavy/irregular periods
  • constipation
22
Q

Investigations for hypothyroidism

A
  • TFTs
  • Primary = low T3/4 and high TSH
  • Secondary = both low
23
Q

How is hypothyroidism managed?

A
  • Chronic = levothyroxine and adjust dose until TSH levels are normal
24
Q

What are the types of hyperparathyroidism and what causes each one?

A
  1. Primary = tumour of gland causing hypercalcaemia and high PTH
  2. Secondary = CKD or low vitamin D, high PTH in response to hypocalcaemia
  3. Tertiary = after secondary is treated, glands still secrete lots of PTH due to prolonged hyperplasia, high PTH and hypercalcaemia
25
Q

What are the affects of PTH and when is it secreted?

A
  • when blood calcium needs to be raised
  • increased osteoclast activity
  • increased calcium absorption in the gut
  • increased calcium absorption in the kidneys
  • increased vitamin D activity
26
Q

Signs and symptoms of hyperparathyroidism

A

Primary: sign of hypercalcaemia

  • polyuria
  • polydipsia
  • renal calculi
  • bone pain
  • abdominal pain
  • nausea
  • constipation
  • lethargy

Secondary: signs of hypocalcaemia or the underlying cause

  • paraesthesia
  • muscle spasms
  • cramps
  • tetany
  • seizures

3rd Year Conditions (16 decks)

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