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Endocrinology Flashcards

الحقني يادكتور والله مابقدر عاينته وانا عيان وممنوع من السكر

1
Q

What hormones does the anterior pituitary gland release (6)

A

Theanterior pituitary glandreleases:

Thyroid-stimulating hormone(TSH)

Adrenocorticotropic hormone(ACTH)

Follicle-stimulating hormone(FSH) andluteinising hormone(LH)

Growth hormone(GH)

Prolactin

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2
Q

What hormones does the posterior pituitary gland release? (2)

A

Oxytocin

Antidiuretic hormone(ADH)

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3
Q

Explain the thyroid axis

A

Hypothalamus 💦 thyrotropin releasing hormone (TRH)

TRH 💥 anterior pituitary => 💦 thyroid stimulating hormone (TSH)

TSH 💥 thyroid => 💦 T3 (triiodothyronine) + T4 (thyroxine)

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4
Q

How does the thyroid axis self regulate

A

Negative feedback loop

T3 + T4 💥 hypothalamus + anterior pituitary => 🚫✋ TSH + TRH

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5
Q

What organ releases cortisol? How is cortisol released throughout the day?

A

secreted by adrenals

released in pulses and in response to stressful stimuli
peaks in early morning and lowest in late evening

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6
Q

Explain the adrenal axis

A

Hypothalamus 💦 CRH (corticotropin-releasing hormone)

CRH💥anterior pituitary => 💦ACTH (adrenocorticotropic hormone)

ACTH💥adrenal glands => 💦cortisol

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7
Q

How does the adrenal axis self-regulate?

A

Negative feedback loop

Cortisol 💥hypothalamus + anterior pituitary => 🚫✋CRH +ACTH

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8
Q

5 actions of cortisol within the body:

A
  • increases alertness
  • inhibits the immune system
  • inhibits bone formation
  • raises blood glucose
  • increases metabolism
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9
Q

Explain the Growth Hormone Axis

A

Hypothalamus 💦 GHRH (growth hormone-releasing hormone)

GHRH 💥anterior pituitary => 💦 growth hormone

Growth hormone 💥 liver => 💦IGF-1 (insulin-like growth factor 1)

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10
Q

Name 4 functions of growth hormone:

A
  • stimulates muscle growth
  • increases bone density and strength
  • stimulates cell regeneration and reproduction
  • stimulates growth of internal organs
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11
Q

Explain the Parathyroid axis:

A

(low serum calcium) 💥 4 parathyroid glands 💦 PTH (parathyroid hormone)

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12
Q

What is the role of parathyroid hormone?

A

increase serum Ca concentration

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13
Q

How does PTH increase serum Ca levels?

A
  • increases activity of osteoclasts in bone => reabsorption of calcium from bone into blood
  • stimulates calcium reabsorption in the kidneys (less Ca excreted in urine)
  • stimulates kidneys to convert Vit D3 into calcitriol (active vit D, which promotes Ca absorption from food)
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14
Q

How does the parathyroid axis regulate itself?

A

Negative feedback
When the serum calcium level is high, it suppresses the release of PTH

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15
Q

What is renin? Which cells/location is it released from?

A

Renin is an enzyme
Secreted by juxtaglomerular cells
in the afferent arterioles of the kidney

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16
Q

Explain the Renin-Angiotensin-Aldosterone System:

A

Low BP 💥 (juxtaglomerular cells) afferent arterioles in the kidney 💦 renin

Liver 💦 angiotensinogen

Angiotensinogen (+renin) => angiotensin I

(in lungs) angiotensin I + ACE (angiotensin-converting enzyme) => angiotensin II

Angiotensin II causes vasoconstriction

Angiotensin II 💥 adrenal glands 💦 aldosterone => hypertrophy of cardiac myocytes (cardiac remodelling)

Aldosterone 💥nephrons =>
- inc Na reabsorption from distal tubule (osmosis => inc intravascular volume)
- inc K secretion from distal tubule
- inc H secretion from collecting ducts

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17
Q

How does aldosterone work?

A

Aldosterone is a mineralocorticoid steroid hormone. It acts on the nephrons in the kidneys to:

  • Increase sodium reabsorption from the distal tubule
  • Increase potassium secretion from the distal tubule
  • Increase hydrogen secretion from the collecting ducts

When sodium is reabsorbed in the kidneys, water follows it by osmosis. This leads to increased intravascular volume and, subsequently, blood pressure.

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18
Q

What is the difference between primary and secondary hyperthyroidism? What lab results would correspond to each?

A

Primary - thyroid issue, produces excess T3/T4, suppressing TSH
⬆️ T3 ⬆️T4 ⬇️TSH

Secondary - pituitary issue, produces excess TSH
⬆️T3 ⬆️T4 ⬆️TSH

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19
Q

What is the difference between primary and secondary hypothyroidism? What lab results would correspond to each?

A

Primary - thyroid issue, produces inadequate T3/T4, leads to inc TSH
⬇️T3/T4 ⬆️TSH

Secondary - pituitary problem, produces inadequate TSH, so less T3/T4
⬇️T3/T4 ⬇️TSH

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20
Q

Name 3 thyroid antibodies. What diseases are they present in?

A

Anti-TPO (anti-thyroid peroxidase antibodies) - work against the thyroid gland
:: against autoimmune thyroid diseases e.g. Grave’s, Hashimoto’s

Anti-Tg (anti-thyroglobulin antibodies) - against thyroglobulin (protein produced by thyroid)
:: Grave’s :: Hashimoto’s :: thyroid ca

TSH receptor Ab’s - mimic TSH, bind to receptor, stimulate T3/T4 release
:: Grave’s disease

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21
Q

What imaging can be used in investigating thyroid pathology?

A

USS - diagnose thyroid nodules, distinguishes cystic and solid nodules, guides biopsies of a thyroid lesion

Radioisotope scans - investigate hyperthyroidism and thyroid cancer
:: radioactive iodine given IV or PO
:: gamma camera detects gamma rays emitted by I

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22
Q

How to interpret radioisotope thyroid scan results?

A

Diffuse high uptake = Grave’s disease

Focal high uptake = toxic multinodular goitre and adenoma

“Cold” areas (low uptake) = thyroid cancer

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23
Q

What is subclinical hyperthyroidism?

A

thyroid hormones (T3 and T4) are normal and thyroid-stimulating hormone (TSH) is suppressed (low). There may be absent or mild symptoms.

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24
Q

What is Grave’s disease?

A

autoimmune condition
TSH receptor Ab’s cause 1° hyperthyroidism
most common cause of hyperthyroidism

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25
Q

What is toxic multinodular goitre?

A

nodules on thyroid
unregulated by thyroid axis
continuously produce excess thyroid hormones
most common in >50 y/o

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26
Q

What is exophthalmos?

A

aka proptosis
bulging of eyes
caused by Grave’s disease
due to inflammation, swelling and hypertrophy of tissue behind eyeballs

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27
Q

What is pretibial myxoedema?

A

skin condition caused by deposits of glycosaminoglycans on pre-tibial area
discoloured, waxy, oedematous appearance
specific to Grave’s disease
reaction to TSH receptor Ab’s

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28
Q

Give 4 causes of hyperthyroidism (mnemonic)

A

GIST

Graves
Inflammation (thyroiditis)
Solitary toxic thyroid nodule
Toxic multinodular goitre

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29
Q

What are some causes of thyroiditis?

A

Thyroiditis can cause initial hyperthyroidism followed by hypothyroidism

Caused by:
- De Quervain’s thyroiditis
- Hashimoto’s thyroiditis
- Postpartum thyroiditis
- Drug-induced thyroiditis

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30
Q

Signs and symptoms of hyperthyroidism. Give 4 Grave’s specific features.

A

Symptoms:
:: anxiety/irritability :: sweating/heat intolerance :: weight loss :: fatigue :: insomnia :: loose stool :: sexual dysfunction ::

Signs:
:: tachycardia :: weight loss :: brisk reflexes

Grave’s specific:
:: diffuse goitre (not nodular) :: Grave’s eye disease :: peritbial myxoedema :: thyroid acropachy (hand swelling, finger clubbing)

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31
Q

What is solitary toxic thyroid nodule?

A

single abnormal thyroid nodule
release excessive thyroid hormone
usually benign adenoma

Tx: surgical removal

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32
Q

What is De Quervain’s thyroiditis? What are the treatment options? What is the prognosis?

A

aka subacute thyroiditis
temporary inflammation of thyroid, self-limiting

3 phases:
1. thyrotoxicosis
:: excess thyroid hormone :: flu-like illness :: thyroid swelling and tenderness :: ⬆️CRP
2. hypothyroidism
3. return to normal

Tx:
1) supportive: NSAIDs, Beta-blockers, levothyroxine

10% remain hypothyroid long-term

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33
Q

What is a thyroid storm? What is the management?

A

rare, severe, life-threatening presentation of hyperthyroidism

Presentation:
- fever
- tachycardia
- delirium

Tx:
- admit
- supportive treatment: IVI, beta-blockers

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34
Q

What are the pharmacological options for managing hyperthyroidism? (contraindications) Other management options?

A

1st) carbimazole (12-18m)
:: once euthyroid (4-6w) continue maintenance of carbimazole and either:
- titration-block of carbimazole
- higher dose block all thyroid production + levothyroxine (block and replace)
:::::::C/I in pancreatitis::::::::::
:::::::risk of agranulocytosis (low WCC) => severe infections (look out for sore throat):::::::::

2nd) propylthiouracil
::::::::risk of severe liver reaction inc death :::::
:::::::risk of agranulocytosis (low WCC) => severe infections (look out for sore throat):::::::::

3rd) radioactive iodine
drink single-dose of radioactive iodine. usually needs long-term levothyroxine
:::::::C/I: pregnancy or breastfeeding within 6 months of treatment, men must not father children within 4 months of treatment, limit contact with people (esp children and pregnant ::::::::

Adjunct: beta-blockers e.g. propranolol

Definitive: thyroidectomy + life-long levothyroxine

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35
Q

What is the difference between primary and secondary hypothyroidism? What labs markers (TFT) would correlate with either condition?

A

Primary = problem in thyroid.
⬇️T3/4 ⬆️TSH

Secondary = problem in pituitary
⬇️TSH ⬇️T3/4

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36
Q

What is the most common cause of primary hypothyroidism?

A

Hashimoto’s thyroiditis
autoimmune condition
assoc. w/ anti-thyroid peroxidase (anti-TPO) + anti-thyroglobulin (anti-Tg) ab’s

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37
Q

What is Cushing’s syndrome? What is Cushing’s disease?

A

Syndrome: Features of prolonged high levels of glucocorticoids in the body e.g. cortisol

Disease: a pituitary adenoma secreting excessive adrenocorticotropic hormone (ACTH), stimulating excessive cortisol release from the adrenal glands.
::::::high ACTH => hyperpigmentation

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38
Q

What are some physical features of Cushing’s?

A
  • Round face (known as a “moon face”)
  • Central obesity
  • Abdominal striae (stretch marks)
  • Enlarged fat pad on the upper back (known as a “buffalo hump”)
  • Proximal limb muscle wasting (with difficulty standing from a sitting position without using their arms)
  • Male pattern facial hair in women (hirsutism)
  • Easy bruising and poor skin healing
  • Hyperpigmentation of the skin in patients with Cushing’s disease (due to high ACTH levels)
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39
Q

What are some metabolic effects of Cushing’s?

A
  • Hypertension
  • Cardiac hypertrophy
  • Type 2 diabetes
  • Dyslipidaemia (raised cholesterol and triglycerides)
  • Osteoporosis
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40
Q

Causes of Cushing’s syndrome? (mnemonic)

A

CAPE

C – Cushing’s disease (a pituitary adenoma releasing excessive ACTH)
A – Adrenal adenoma (an adrenal tumour secreting excess cortisol)
P – Paraneoplastic syndrome e.g. SCLC
E – Exogenous steroids (patients taking long-term corticosteroids)

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41
Q

What is the 1st line investigation for Cushing’s?

A

Dexamethasone suppression test

Normal response : dex causes negative feedback on hypothalamus => less CRH => pituitary less ACTH => low cortisol

There are three types of dexamethasone suppression test:
- Low-dose overnight test (used as a screening test to exclude Cushing’s syndrome)
- Low-dose 48-hour test (used in suspected Cushing’s syndrome)
- High-dose 48-hour test (used to determine the cause in patients with confirmed Cushing’s syndrome)

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42
Q

What is the difference between low-dose and high-dose dexamethasone suppression tests?

A

Low overnight: 1mg ON. if cortisol is not suppressed => ?Cushing’s syndrome (needs further investigation)

Low 48-hr: 0.5mg QDS (8 doses). cortisol checked at 9am on day 1 and day 3.
:::::: no cortisol suppression => ?Cushing’s syndrome (needs further Inv)

High 48-hr: 2mg QDS (8 doses)
::::::suppression => Cushing’s disease (pituitary adenoma)
::::::no suppression => adrenal adenoma, ectopic ACTH

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43
Q

Dex suppression tests::::
low dose = ⬆️ cortisol,
high dose = ⬆️ cortisol,
low ACTH

Diagnosis?

A

adrenal adenoma

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44
Q

Dex suppression tests::::
low dose = ⬆️ cortisol,
high dose = ⬇️ cortisol,
high ACTH

Diagnosis?

A

pituitary adenoma

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45
Q

Dex suppression tests::::
low dose = ⬆️ cortisol,
high dose = ⬆️ cortisol,
high ACTH

Diagnosis?

A

Ectopic ACTH e.g. SCLC

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46
Q

What are some other investigations for Cushing’s disease (not dex)

A

24-hr urinary free cortisol

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47
Q

What are the treatments of Cushing’s syndrome?

A

Treat the underlying cause
- surgically remove the tumour
- surgically remove both adrenals and give life-long steroid replacement therapy
- metyrapone

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48
Q

How do cardiac symptoms present in acute hypokalaemia?

A

Patients may experience palpitations, angina-like chest pain, or syncopal episodes due to arrhythmias like ventricular tachycardia or fibrillation. On examination, signs of heart failure such as peripheral oedema and pulmonary crackles may be noted.

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49
Q

What muscular manifestations occur in acute hypokalaemia?

A

Muscle weakness, often affecting proximal muscles more than distal ones, is common. In severe cases, it can progress to flaccid paralysis. Deep tendon reflexes may also be diminished.

50
Q

What are the cardiac effects in chronic hypokalaemia?

A

Chronic hypokalaemia can lead to left ventricular hypertrophy and interstitial fibrosis, increasing the risk of arrhythmias. While patients might report palpitations, physical examination findings are often unremarkable.

51
Q

How does chronic hypokalaemia affect muscles?

A

Muscle weakness is milder compared to acute hypokalaemia. Patients may complain of fatigue, myalgia, or cramps, but muscle strength is generally preserved on examination.

52
Q

What renal manifestations are seen in chronic hypokalaemia?

A

Chronic hypokalaemia may lead to renal tubular acidosis (type I or II), nephrogenic diabetes insipidus, and chronic kidney disease. Patients may present with polyuria and nocturia, though these symptoms are often non-specific.

53
Q

What is the diagnostic serum potassium level for hypokalaemia?

A

Below 3.5 mmol/L.

54
Q

Which electrolyte disturbance is commonly associated with hypokalaemia and may exacerbate it?

A

Hypomagnesaemia

55
Q

What does a metabolic alkalosis on an ABG test suggest in the context of hypokalaemia?

A

Renal loss of potassium.

56
Q

What are the typical ECG changes seen in hypokalaemia?

A

ST depression, T wave flattening or inversion, prominent U waves, and prolonged QT interval.

57
Q

What medications can cause hypokalaemia?

A

Loop and thiazide diuretics
Corticosteroids
Beta-2-agonists

58
Q

What are common symptoms of acute hyperkalaemia?

A

Malaise, muscle weakness, and palpitations.

59
Q

What might be found during the physical examination of a patient with acute hyperkalaemia?

A

Reduced muscle power, reflexes, and in severe cases, flaccid paralysis or respiratory failure.

60
Q

What ECG changes occur as hyperkalaemia becomes more severe?

A

PR interval prolongation, QRS complex widening, and possibly a sine wave pattern.

61
Q

How can Addison’s disease lead to hyperkalaemia?

A

Due to decreased aldosterone production, causing potassium retention.

62
Q

Which medications can induce hyperkalaemia?

A

Potassium-sparing diuretics, ACE inhibitors, ARBs, and NSAIDs.

63
Q

How does insulin/dextrose infusion help in managing hyperkalaemia?

A

It causes a short-term shift of potassium from the extracellular to the intracellular compartment.

64
Q

What is the role of IV calcium gluconate in hyperkalaemia management?

A

It stabilizes the cardiac membrane but does not lower serum potassium levels.

65
Q

What potassium level is considered mild, moderate, and severe hyperkalaemia according to the European Resuscitation Council?

A

Mild: 5.5-5.9 mmol/L, Moderate: 6.0-6.4 mmol/L, Severe: ≥ 6.5 mmol/L.

66
Q

How is hyponatraemia categorized?

A

It can be categorized based on the patient’s volume status into hypovolaemic, euvolaemic, or hypervolaemic hyponatraemia.

67
Q

What are the potential severe neurological symptoms of hyponatraemia?

A

Seizures and coma due to cerebral oedema.

68
Q

How is acute symptomatic hyponatraemia managed?

A

With urgent treatment using hypertonic saline.

69
Q

What is the risk of overly rapid correction of sodium in hyponatraemia?

A

Osmotic demyelination syndrome, , which can result in dysarthria, quadriparesis, seizures, and locked-in syndrome.

70
Q

What are common medications that can cause hyponatraemia?

A

Thiazide diuretics and selective serotonin reuptake inhibitors (SSRIs).

71
Q

What is the clinical presentation of severe hyponatraemia?

A

Severe cases can present with cerebral oedema, causing seizures, respiratory arrest, coma, or death.

72
Q

What is pseudohyponatraemia?

A

A false low sodium level due to hyperlipidaemia or hyperproteinaemia.

73
Q

What condition is associated with euvolaemic hyponatraemia?

A

Syndrome of inappropriate antidiuretic hormone secretion (SIADH).

74
Q

How can you differentiate renal from non-renal causes of hyponatraemia?

A

By measuring urine sodium concentration: low levels indicate non-renal causes, while high levels suggest renal causes.

75
Q

What fluids are typically used for treating hypernatraemia?

A

Hypotonic fluids or dextrose solutions are used, with close monitoring of serum electrolytes.

76
Q

What are rare causes of hypernatraemia?

A

Hyperosmolar hyperglycaemic state and diabetes insipidus.

77
Q

What does a urine osmolality >600 mOsm/kg suggest in hypernatraemia?

A

It suggests an appropriate renal response to the hyperosmolar state.

78
Q

What does a urinary sodium concentration >20 mmol/L indicate?

A

It implies renal salt wasting.

79
Q

What conditions may contribute to hypovolaemic hypernatraemia?

A

Gastrointestinal losses (e.g., diarrhoea, vomiting), renal losses (e.g., diabetes insipidus), and cutaneous losses (e.g., sweating, burns).

80
Q

What conditions are associated with euvolaemic hypernatraemia?

A

Inadequate water intake and hypodipsia/adipsia (impaired thirst mechanism).

81
Q

What conditions can cause hypervolaemic hypernatraemia?

A

Sodium overload (e.g., excessive hypertonic saline) and mineralocorticoid excess (e.g., Conn’s syndrome, Cushing’s syndrome).

82
Q

What is the recommended rate of correction for hypernatraemia?

A

Serum sodium levels should be reduced gradually, not exceeding 10 mmol/L in a 24-hour period.

83
Q

What should be done for hypovolaemic hypernatraemia in terms of fluid management?

A

Immediate fluid resuscitation with isotonic saline is recommended.

84
Q

What are the most frequent causes of hypercalcaemia?

A

Primary hyperparathyroidism, malignancies such as lung and breast cancer, and multiple myeloma.

85
Q

What are common non-specific symptoms of hypercalcaemia?

A

Polyuria, polydipsia, constipation, nausea, fatigue, and cognitive impairment.

86
Q

What severe symptoms may occur in cases of hypercalcaemia?

A

Cardiac arrhythmias and coma.

87
Q

What can be seen on ECG in hypercalcaemia?

A
  • short QT interval
  • in severe hypercalcaemia, Osborn waves (J waves)
88
Q

How does hypervitaminosis D contribute to hypercalcaemia?

A

It leads to increased intestinal absorption and renal reabsorption of calcium.

89
Q

Which medications can contribute to hypercalcaemia?

A

Thiazide diuretics and lithium.

90
Q

What are the initial steps in managing hypercalcaemia?

A

Immediate stabilisation, rehydration with intravenous saline, and inhibition of bone resorption using bisphosphonates or corticosteroids.

91
Q

What is the mechanism of action of sulfonylureas?

A

increasing pancreatic insulin secretion and hence are only effective if functional B-cells are present. On a molecular level they bind to an ATP-dependent K+(KATP) channel on the cell membrane of pancreatic beta cells.

92
Q

What diabetic medication is recommended in patients with CVD risk (in addition to metformin or instead of metformin if C/I)?

A

SGLT-2 inhibitors e.g. dapagliflozin

93
Q

What is the most common cause of Cushing’s syndrome?

A

Prolonged use of exogenous corticosteroids (e.g., prednisolone or dexamethasone).

94
Q

What would ACTH levels show in different causes of Cushing’s syndrome?

A

Low ACTH: Adrenal adenoma or exogenous steroids

High ACTH: Pituitary adenoma (Cushing’s disease) or ectopic ACTH production

95
Q

What imaging techniques are used to investigate the causes of Cushing’s syndrome?

A

MRI of the brain for pituitary adenoma
CT of the chest for small cell lung cancer
CT of the abdomen for adrenal tumours

96
Q

What is Nelson’s syndrome, and what are its key features?

A

Nelson’s syndrome occurs after adrenalectomy when there is no cortisol feedback, leading to an ACTH-producing pituitary tumour. Symptoms include skin pigmentation, bitemporal hemianopia, and lack of other pituitary hormones.

97
Q

What is Addison’s disease?

A

Addison’s disease is primary adrenal insufficiency, where the adrenal glands are damaged, reducing cortisol and aldosterone secretion, most commonly due to autoimmune causes.

98
Q

What causes secondary adrenal insufficiency?

A

Inadequate ACTH from the pituitary gland due to pituitary tumours, surgery, radiotherapy, Sheehan’s syndrome, or trauma, leading to low cortisol production.

99
Q

What is tertiary adrenal insufficiency, and how is it caused?

A

Tertiary adrenal insufficiency results from inadequate CRH release by the hypothalamus, often caused by long-term steroid use that suppresses the hypothalamus. Sudden withdrawal of steroids can cause the condition.

100
Q

What are the symptoms of adrenal insufficiency?

A

Fatigue
Muscle weakness and cramps
Dizziness and fainting
Salt craving
Weight loss
Abdominal pain
Depression
Reduced libido

101
Q

What are the key signs of adrenal insufficiency on physical examination?

A

Bronze hyperpigmentation of the skin (especially in creases, scars, lips, buccal mucosa)
Hypotension (particularly postural hypotension)

102
Q

What are the key biochemical findings in adrenal insufficiency?

A

Hyponatraemia (low sodium)
Hyperkalaemia (high potassium)
Hypoglycaemia (low glucose)
Raised urea and creatinine (due to dehydration)
Hypercalcaemia (high calcium)

103
Q

What test is used to diagnose adrenal insufficiency?

A

The short Synacthen test (ACTH stimulation test), where synthetic ACTH is given, and cortisol levels are measured before and after to assess adrenal function.

104
Q

How does the short Synacthen test distinguish between primary and secondary adrenal insufficiency?

A

In primary adrenal insufficiency, cortisol fails to rise after Synacthen. In secondary insufficiency, cortisol may rise but still inadequately due to adrenal atrophy from low ACTH.

105
Q

What is the role of ACTH levels in diagnosing adrenal insufficiency?

A

High ACTH indicates primary adrenal insufficiency (e.g., Addison’s disease), while low ACTH suggests secondary adrenal insufficiency (due to pituitary pathology).

106
Q

How is adrenal insufficiency managed?

A

Replacement steroids: hydrocortisone for cortisol and fludrocortisone for aldosterone if necessary. Hydrocortisone doses are doubled during illness, and patients receive steroid cards, ID tags, and emergency instructions.

107
Q

What is an adrenal crisis (Addisonian crisis), and what are the symptoms?

A

An adrenal crisis is a life-threatening emergency where steroid hormones are critically low, leading to:

  • Reduced consciousness
  • Severe hypotension
  • Hypoglycaemia
  • Hyponatraemia and hyperkalaemia
108
Q

What is the emergency management of adrenal crisis?

A
  1. ABCDE approach
  2. Intramuscular or intravenous hydrocortisone (100mg initially)
  3. IV fluids for dehydration
  4. Correct hypoglycaemia (e.g., IV dextrose)
  5. Monitor electrolytes and fluid balance
109
Q

What is Conn’s syndrome?

A

Conn’s syndrome is a form of primary hyperaldosteronism where an adrenal adenoma produces too much aldosterone.

110
Q

What is the key presenting feature of hyperaldosteronism?

A

Hypertension is the key presenting feature, though many patients are asymptomatic. Symptoms, when present, include headaches, muscle weakness, and fatigue.

111
Q

What are the actions of aldosterone in the kidneys?

A

Aldosterone increases:

Sodium reabsorption from the distal tubule
Potassium secretion from the distal tubule
Hydrogen secretion from the collecting ducts

112
Q

What is primary hyperaldosteronism, and what are its causes?

A

Primary hyperaldosteronism occurs when the adrenal glands themselves overproduce aldosterone, typically due to:

  • Bilateral adrenal hyperplasia (most common)
  • An adrenal adenoma (Conn’s syndrome)
  • Familial hyperaldosteronism (rare)
113
Q

What is secondary hyperaldosteronism, and what causes it?

A

Secondary hyperaldosteronism results from excessive renin production, stimulating aldosterone release. Causes include:

  • Renal artery stenosis
  • Heart failure
  • Liver cirrhosis and ascites
114
Q

How is renal artery stenosis related to hyperaldosteronism, and how is it diagnosed?

A

Renal artery stenosis reduces blood flow to the kidney, leading to increased renin release and secondary hyperaldosteronism. It is diagnosed using:

  • Doppler ultrasound
  • CT angiogram
  • Magnetic resonance angiography (MRA)
115
Q

What does a high aldosterone-to-renin ratio (ARR) indicate?

A

High aldosterone and low renin suggest primary hyperaldosteronism.

High aldosterone and high renin suggest secondary hyperaldosteronism.

116
Q

What are the effects of hyperaldosteronism on blood tests?

A
  • Hypertension (raised blood pressure)
  • Hypokalaemia (low potassium)
  • Alkalosis (from increased hydrogen secretion)
117
Q

What imaging tests are used to investigate the cause of hyperaldosteronism?

A
  • CT or MRI for adrenal tumours or hyperplasia
  • Renal artery imaging (Doppler, CT angiogram, or MRA) for renal artery stenosis
  • Adrenal vein sampling to determine which adrenal gland is producing more aldosterone
118
Q

How is hyperaldosteronism medically managed

A

Aldosterone antagonists are used, including:

  • Eplerenone
  • Spironolactone
119
Q

What are the surgical treatments for hyperaldosteronism?

A
  • Surgical removal of the adrenal adenoma (for Conn’s syndrome)
  • Percutaneous renal artery angioplasty to treat renal artery stenosis
120
Q

How can C-peptide levels distinguish type 1 and type 2 diabetes?

A

Low in type 1, high in type 2

MSRA (16 decks)

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