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Met3 > Endocrinology:Endocrine Hypertension and Calcium Disorders > Flashcards

Endocrinology:Endocrine Hypertension and Calcium Disorders Flashcards

1
Q

State the 4 grades of hypertensive retinopathy

A

Grade 1 – silver (copper) wiring
Grade 2 – arteriovenous nipping
Grade 3 – flame shaped haemorrhages + exudates
Grade 4 - papilloedema

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2
Q

Name a cardiac cause of secondary hypertension [1]

A

Coarctation of the aorta(differential BP between upper and lower limb and arms; radio-radial delay)

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3
Q

Name three renal causes of secondary hypertension [3]

A
  • CKD
  • Glomerulonephritis
  • Renovasculardisease
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4
Q

Name 4 endocrine causes of secondary hypertension [4]

A
  • Conns
  • Cushings
  • Phaeochromocytoma
  • Acromegaly
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5
Q

What grade of retinopathy is depicted? [1]

A

Grade 4

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6
Q

Label A

A

Optic disc swelling

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7
Q
  • 35y/0 man admitted with headaches
  • c/o muscle weakness, frequent urination
  • O/E BP210/100mmHg
  • Grade 4 retinopathy
A

Conn’s syndrome (Hyperaldosteronism - indicated by low K and hypertension; not Cushings as you would expect other clinical signs)

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8
Q

Conn’s syndrome refers to an [] producing too much aldosterone.

A

Conn’s syndrome refers to an adrenal adenoma producing too much aldosterone.

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9
Q

Conn’s syndrome refers to an adrenal adenoma producing too much aldosterone.

What are the two options that this could be caused by? [2]

Which is more likely? [2]

A

Solitary aldosterone producing adenoma
* 2/3rds

Bilateral adrenocortical hyperplasia
* 1/3rd

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10
Q

What is the key presenting feature of hyperaldosteronism? [1]

A

Hyperaldosteronism may be present in 5-10% of patients with hypertension.

Hypertension is the key presenting feature, and many patients are otherwise asymptomatic. It may cause non-specific symptoms such as headaches, muscle weakness and fatigue.

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11
Q

You suspect a ptx with Conns syndrome; how would you expect their blood gas to appear after investigation? [1]

A

Hypokalaemic alkalosis (XS aldosterone causes increased K+ secretion and Na+ absorption)

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12
Q

You suspect a patient has Conn’s syndrome due their refractory BP.

Name a differential diagnosis that is more common cause of this [1]

A

Renal artery stenosis

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13
Q

Apart from investigating electrolytes, what further tests (and results) would you conduct for a ptx suspected to have hyperaldosteronism? [4]

A

Hyperaldosteronism investigations:
- Plasma renin: suppressed
- Elevated serum aldosterone
(these tests are conducted together: paired renin/aldosterone level)
- CT adrenals
- Adrenal vein sampling to differentiate unilateral from bilateral adrenal disease

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14
Q

What are clinical presentations of Conn’s syndrome? [6]

A
  • Often asymptomatic
  • cramps
  • muscle weakness
  • hypotonia
  • reduced reflexes
  • Hypertension (often have resistant HTN or severe HTN)
  • 40-60 years old
  • Hypokalaemic (but NOT always present, so can’t rely on this for diagnosis)

often the signs are due to hypokalaemia

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15
Q

What is the management of unilateral adrenal adenoma? [1]
What is the management of bilateral adrenal hyperplasia? [2]

A

Unilateral adrenal adenoma: Surgery (laparoscopic adrenalectomy)

Bilateral adrenal hyperplasia: aldosterone antagonist
- eplerenone
- spironolactone

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16
Q

What is the 10% rule for phaeochromocytoma? [4]

A

 10% extra adrenal
 10% malignant
 10% familial (endocrine neoplasia syndromes)
 10% bilateral

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17
Q

Presentation of phaeochromocytomas? [5]

A

Classic triad:
* Tachycardia
* Sweating
* Episodic headache

Others:
* Tremor
* Anxiety
* Palpitations
* Hypertension
* Tachycardia

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18
Q

*

Why does prescribing beta blockers worsen symptoms for patients with phaeochromocytoma? [2]

A

Inhibits B2 receptor action (vasodilatation);

Causes unparalleled action of A1 and A2 receptors (vasoconstriction)

Can cause severe hypertensive crisis

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19
Q

Which drugs would you prescribe for symptoms of phaeochromocytoma? [2]

What is an alternative management? [1]

A

Always give alpha blockers first (otherwise can cause hypertensive crisis; then beta blockers)

Alpha blockers:
Doxazosin
Phenoxybenzamine

Beta blockers (if heart disease or tachycardic)
Propranolol
Atenolol

and / or

Surgical resection of the lesion
(Patients have their symptoms controlled medically before surgery to reduce the anaesthesia and surgery risks)

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20
Q

Initial tests for diagnosing phaeochromocytoma include? [4]

A
  • Elevated plasma free metanephrines (breakdown products of the catecholamines epinephrine (adrenaline) and norepinephrine)
  • Elevated 24-hour urine catecholamines (not as accurate as measuring metanephrines)
  • Image adrenals (CT/MRI)
  • MIBG (radionucleotide scan of Iodine-123)
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21
Q

Describe the treatment options for acromegaly [3]

A
  • 1st line: trans-sphenoidal surgery

Medical management of acromegaly:

  • Somatostatin analogues: Octreotide
  • Growth hormone receptor antagonist:: Pegvisomont
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22
Q

What is the MoA of Pegvisomont? [1]

A

Used to treat acromegaly: GH Receptor antagonist

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23
Q

Serum Ca2+ is mainly controlled by which hormones? [2]

A

parathyroid hormone (PTH) and vitamin D

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24
Q

PTH has many actions - all serving to increase plasma Ca2+ levels.

State what they are [5]

A
  • Increasing osteoclastic resorption of bone - occurs rapidly
  • Increasing intestinal absorption of Ca2+ - slow response
  • Activation of 1,25-dihydroxyvitamin D (calcitriol) in the kidney
  • Increasing renal tubular reabsorption of Ca2+
  • Increasing excretion of phosphate
25
Q

What is the name for the active form of vitamin D? [1]

Name 3 causes of active vitamin D secretion [3]

A

Calcitriol:

  • Low plasma Ca2+
  • Low plasma phosphate
  • PTH
26
Q

State 4 roles of calcitriol [4]

(active form of vitamin D)

A
  • Increased Ca2+ and phosphate absorption in the gut
  • Increased Ca2+ and phosphate reabsorption in the kidney’s
  • Inhibits PTH release - negative feedback
  • Enhanced bone turnover by increasing numbers of osteoclasts
27
Q

What is the role of calcitonin? [2]
Where is it produced? [1]

A

Lowers Ca2+ & P levels by:
- Inhibits Ca2+ absorption by intestines
- Inhibits Ca2+ reabsorption in kidney
- Promotes osteoblasts, inhibits osteoclasts

Secreted by C cells of thyroid

28
Q

Hypercalcaemia has what effect on urine and thirst? [1]

A

Causes polyuria and polydipsia

29
Q

Give three differential diagnoses for polyuria and polydipsia [3]

A

DM
Diabetes insipidus
Hypercalcaemia

30
Q

How should you manage acute hypercalcaemia? [1]
What drug should you prescribe if Ca2+ remains elevated? [1]

A
  1. Give IV saline alone
  2. If Ca still high - give bisphosphinates; pamidronate: prevent bone resorption by inhibiting osteoclast activity
31
Q

Describe dosing of pamidronate for acute hypercalcaemia [1]

Name 2 SEs [2]

A

Single dose of (4mg) will will normalise serum Ca2+ levels with a week

SEs:
- Bone pain
- Decresed PO4-
- Myalgia
- N & V
- Ca2+ decreasing

32
Q

Describe the causes of [3]

Primary hyperparathyroidism
Secondary hyperparathyroidism
Tertiary hyperparathyroidism

A

Primary hyperparathyroidism:
- is caused by uncontrolled parathyroid hormone production by a tumour of the parathyroid glands
- this leads to a raised blood calcium (hypercalcaemia)

Secondary hyperparathyroidism:
- is where insufficient vitamin D or chronic kidney disease reduces calcium absorption from the intestines, kidneys and bones.
- this result in low blood calcium (hypocalcaemia).
- The parathyroid glands react to the low serum calcium by excreting more parathyroid hormone.
- The serum calcium level will be low or normal, but the parathyroid hormone will be high.

Tertiary hyperparathyroidism:
- when secondary hyperparathyroidism continues for an extended period, after which the underlying cause is treated
- hyperplasia (growth) of the parathyroid glands occurs as they adapt to producing a higher baseline level of parathyroid hormone
- Then, when the underlying cause of the secondary hyperparathyroidism is treated, the baseline parathyroid hormone production remains inappropriately high.
- In the absence of the previous pathology, this high parathyroid hormone level leads to the inappropriately high absorption of calcium in the intestines, kidneys and bones, causing hypercalcaemia. Treatment is surgically removing part of the parathyroid tissue to return the parathyroid hormone to an appropriate level.

33
Q
A
34
Q

State the most likely cause of:

Primary hyperparathyroidism [2]
Secondary hyperparathyroidism [2]
Tertiary hyperparathyroidism [1]

A

Primary hyperparathyroidism
* Solitary adenoma (80%)
* Hyperplasia (20%)

Secondary hyperparathyroidism
* Vit D deficiency (reduced intake)
* CKD - difficulty making Vit D

Tertiary hyperparathyroidism
- Secondary hyperparathyroidism

35
Q

If you investigate raised hypercalcaemia and find PTH to be undetactable, what would this indicate? [1]

Give three causes of the above [3]

A

Malignancy: PTH related Peptide (PTHrP) causes the increased Ca2+ levels, but itself is undetectable

E.g. squamous cell lung cancers; breast, renal cell carcinomas

36
Q

How would you investigate for hypercalcaemia if PTH is high? [1]

How would you investigate for hypercalcaemia if PTH is low? [1]

A

PTH high: indicates hyperparathyroidism
- USS
- SestaMibi Scan
- Parathyroid venous sampling

PTH low: indicates cancer:
- test for PTH related Peptide (PTHrP) - but can’t measure this - so do local body signs of cancer and further tests

37
Q

Give differential diagnosis of primary hyperparathyroidism [3]

A

Thiazide like diuretics [1]
Lithium [1]
Tertiary hyperparathyroidism [1]

38
Q

What blood tests would you use to investigate primary hyperparathyroidism [2]

A
  • Ca2+ and PTH raised
  • ALP raised (due to bone activity)
    *
39
Q

Describe a radiographical sign of hyperparathyroidism [1]

A

Pepper pot skull: extensive resorption bone in the skull in combination with cystic areas of osteopenia are termed pepper pot skull.

40
Q

What are clinical presentations of Conn’s syndrome? [4]

A
  • Often asymptomatic
  • Hypertension: often have drug resistant or severe HTN
  • 40-60 years old
  • Hypokalaemic (but NOT always present) - therefore signs of hypokalameia
41
Q

How do you treat hyperparathyroidism?
- Surgically? [1]
- Therapeutically? [1]

A

Parathyroidectomy
Cinacalcet directly lowers parathyroid hormone levels by increasing the sensitivity of the calcium sensing receptors to activation by extracellular calcium, resulting in the inhibition of PTH secretion. Indicated in patients with:
- Chronic renal failure
- Tertiary hyperparathyroidism

42
Q

When is cinacalcet indicated for treatment of hypeparathyroidism? [2]
What is the MoA? [1]

A
  • Used for patients with chronic renal failure and tertiary hyperparathyroidism
  • Increases the sensitivity of parathyroid cells to Ca2+ thereby causing less PTH secretion
43
Q

Which drug class should you avoid with patients suffering from primary hyperparathyroidism causing hypercalcaemia? [1]

A

Avoid THIAZIDE DIURETICS and high Ca2+ and vitamin D intake

44
Q

Acute severe hypercalcaemia is a MEDICAL EMERGENCY.
State how you would treat a ptx suffering from acute severe hypercalcaemia [4]

A
  • Rehydrate with IV 0.9% saline fluids - to prevent stones
  • Furosemide: loop diuretic that increases Ca2+ excretion
  • Give bisphosphonates (to prevent bone resorption by inhibiting osteoclasts) after rehydration e.g. IV PAMIDRONATE
  • Measure serum U&E’s daily and serum Ca2+ 48hrs after initial treatment
  • Can give glucocorticoid steroids e.g. ORAL PREDNISOLONE in myeloma, sarcoidosis and vitamin D excess
45
Q

What is the name of this sign? [1]
When does it occur? [1]
What does it indicate? [1]

A

Trousseau sign: hypocalcemia
The hand adopts a characteristic posture when the sphygmomanometer cuff is inflated above the systolic blood pressure within 3 minutes.

46
Q

What is the name of this sign? [1]
How do you illicit this sign? [1]
What does it indicate? [1]

A

Chvostek’s Sign:

  • This clinical sign refers to a twitch of the facial muscles that occurs when gently tapping an individual’s cheek, in front of the ea
47
Q

How do you treat ptx with hypocalcaemia:

With < 1.9 Ca2+, no symptoms? [2]
With < 1.9 Ca2+, symptoms? [2]

A

 < 1.9 with no symptoms
-  Oral calcium supplements
-  If due to severe vitamin D def, treat with high dose vit D (Calcitriol)

 < 1.9 with symptoms
-  IV calcium gluconate

48
Q

State 5 causes of hypocalcaemia [5]

A

 Thyroid / parathyroidectomy
 Severe vitamin D deficiency
 Magnesium deficiency (PPI induced - PPIs needed for PTH to work)
 Pancreatitis
 Cytotoxics

49
Q

What pathology is this a sign of? [1]

Explain

A

Pseudohypoparathyroidism is a rare genetic metabolic bone disease caused by a defect in the GNAS1 protein that leads to a decreased response to PTH.

Patients present with characteristic findings of short 4th and 5th metacarpals, round facies, short stature, and symptoms of hypocalcemia.

50
Q

How does renal artery stenosis cause HTN? [2]

A
  • Atherosclerosis or fibromuscular dysplasia most causes narrowing of the renal arteries
  • The chronic ischemia produced by the obstruction of renal blood flow leads to adaptive changes in the kidney which include the formation of collateral blood vessels and secretion of renin by juxtaglomerular apparatus
51
Q

What are the radiological investigations of suspected Conn’s syndrome and phaeochromocytoma? [1]

A

Use MIBG scan: Iodine-123

52
Q

[] is used to diagnose patients with primary hyperaldosteronism (Conn’s syndrome) when the adrenal CT scan does not show a tumor

A

Adrenal vein sampling is used in patients with primary hyperaldosteronism (Conn’s syndrome) when the adrenal CT scan does not show a tumor

53
Q

Hypercalcaemia is RARELY the FIRST PRESENTING SYMPTOM of
malignancy

Therefore, hypercalcaemia in an otherwise well outpatient is most likely to be due
to []

A

hypercalcaemia in an otherwise well outpatient is most likely to be due
to primary hyperparathyroidism

54
Q

Explain why CKD is the most common cause of hypocalcaemia [2]

A

Results from inadequate production of active vitamin D and renal phosphate retention
Resulting in micro-precipitation of phosphate in the tissues

55
Q

State the overarching causes of hypocalcaemia [8]

A
  • Secondary to increased serum phosphate levels: CKD
  • Severe vitamin D deficiency
  • Reduced PTH production:
    Primary hypoparathyroidism
    & Secondary hypoparathyroidism
  • Radiation
  • Hypomagnesaemia - Mg is required for PTH secretion
  • Pseudohypoparathyroidism: failure of target cell response to PTH due to owing to a mutation in the Gs alpha-protein (GNAS1), which is coupled to the PTH receptor
  • Pseudopseudohypoparathyroidism: Same phenotypic defects as pseudohypoparathyroidism e.g. short stature; but without any abnormalities of Ca2+ metabolism
  • Drugs: Calcitonin - decreases plasma Ca2+ and phosphate; Bisphosphonates - reduce osteoclast activity resulting in reduced Ca2+
  • ACUTE PANCREATITIS
56
Q

Describe the causes of primary and secondary hypoparathyroidism [2]

A

Primary hypoparathyroidism:
- caused by autoimmune DiGeorge syndrome (Congenital familial condition in which the parathyroid glands fail to develop;
- idiopathic hypoparathyroidism

Secondary hypoparathyroidism
- After parathyroidectomy or thyroidectomy surgery. most common cause)

57
Q

Clinical presentation of hypocalcaemia? [6]

A
  • Increase excitability of muscles and nerves
  • Parathesiae (numbness and tingling) around the mouth and in the extremities, followed by cramps, tetany
  • Convulsions and death if untreated
  • Chvostek’s sign: (tapping over the facial nerve in the region of the parotid gland causes twitching of the IPSILATERAL facial muscles
  • Trousseau’s sign: carpopedal spasm induced by inflation of sphygmomanometer cuff to a level above systolic blood pressure
  • papilloedema and a prolonged QT on ECG (severe hypocalcaemia)
58
Q

How would differentiate unilateral from bilateral adrenal disease? [1]

A

Adrenal vein sampling

Met3 (52 decks)

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