Endocrine II

Question 2

State the 4 grades of hypertensive retinopathy

Answer 2

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

Question 3

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]

Answer 3

Solitary aldosterone producing adenoma
* 2/3rds

Bilateral adrenocortical hyperplasia
* 1/3rd

Question 4

*

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

Answer 4

Inhibits B2 receptor action (vasodilatation);

Causes unparalleled action of A1 and A2 receptors (vasoconstriction)

Can cause severe hypertensive crisis

Question 5

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

What is an alternative management? [1]

Answer 5

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)

Question 6

Describe the treatment options for acromegaly [3]

Answer 6

• 1st line: trans-sphenoidal surgery

Medical management of acromegaly:

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

Question 7

What is the MoA of Pegvisomont? [1]

Answer 7

Used to treat acromegaly: GH Receptor antagonist

Question 8

Give differential diagnosis of primary hyperparathyroidism [3]

Answer 8

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

Question 9

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

Answer 9

 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

Question 10

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

Answer 10

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

Question 11

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

Answer 11

• 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

Question 12

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

Answer 12

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

Question 13

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

Answer 13

Chvostek’s Sign: - indiactes hypocalcaemia

• 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

Question 14

How do you treat ptx with hypocalcaemia:

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

Answer 14

 < 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

Question 15

What pathology is this a sign of? [1]

Explain

Answer 15

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.

Question 16

How does renal artery stenosis cause HTN? [2]

Answer 16

• 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

Question 17

State the overarching causes of hypocalcaemia [8]

Answer 17

• 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

Question 18

Describe the causes of primary and secondary hypoparathyroidism [2]

Answer 18

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)

Question 19

Clinical presentation of hypocalcaemia? [6]

Answer 19

• 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)

Question 20

Name and explain drugs may you suspect of a patient’s DH, who is displaying symptoms of thyrotoxicosis [3]

Answer 20

Amiodarone (treats afib): high levels of iodine
Lithium: can mimic iodine
ARVs

Question 21

Asides from TSHR-Ab, which other antibodies would you potentially test for in a ptx presenting with thyrotoxicosis? [1]

Answer 21

Thyroid Stimulating Immunoglobulin (TSI)

Question 22

Treatment for thyroid crisis / storm? [4]

Answer 22

• ORAL CARBIMAZOLE
• ORAL PROPRANOLOL
• ORAL POTASSIUM IODIDE (to block acutely the release of thyroid hormone from gland)
• IV HYDROCORTISONE (to inhibits peripheral conversion of T4 to T3)

Question 23

Describe the features of a myxoedema coma [5]

Answer 23

• hypothermia
• cardiac failure (bradycardia)
• hypoventilation
• hypoglycaemia
• hyponatraemia
• myxoedema (thickened, swelling of skin)

Question 24

How do you treat a patient presenting with myxoedema coma? [3]

Answer 24

• IV/ORAL T3
• IV fluid
• IV corticosteroids (until the possibility of coexisting adrenal insufficiency has been excluded)
• Glucose infusion
• Gradual rewarming

Question 25

Explain the 5 main types of thyroid carcinoma [5]

Answer 25

Papillary (70%):
* Most common, well differentiated
* Young people, local spread and good prognosis
* Arise from thyroid epithelium
* Lymph node metastasis predominate
* Usually contain a mixture of papillary and colloidal filled follicles
* Histologically tumour has papillary projections and pale empty nuclei

Follicular (20%):
* Middle age, spread to lung/bone, usually good prognosis
* 3x more likely in women
* Well differentiated, arise from thyroid epithelium
- Follicular adenoma: Usually present as a solitary thyroid nodule. Malignancy can only be excluded on formal histological assessment.
- Follicular carcinoma: Capsular invasion seen microscopically, and without this finding the lesion would be a follicular adenoma. Vascular invasion predominates unlike papillary which is lymph-node predominant

Anaplastic (< 5%):
* Very undifferentiated and arise from thyroid epithelium
* Aggressive, local spread but poor prognosis

Lymphoma (2%)
* Can be associated with Hashimoto’s

Medullary cell (5%):
* C cells derived from neural crest and not thyroid tissue
* Serum calcitonin levels often raised
* Both lymphatic and haematogenous metastasis are recognised, nodal disease is associated with a very poor prognosis.

Question 26

Which is the most common type of thyroid carcinoma? [1]

Answer 26

Papillary (70%)

Question 27

General treatment of thyroid carcinomas? [4]

Answer 27

• Administer lots of LEVOTHYROXINE (T4) to keep TSH reduced as this is a growth factor for the cancer!
• Iodine 131 ablation
• Thyroidectomy
• Chemotherapy helps to reduce risk of spread and treats micro-metastases that have been undetected

Question 28

TOM TIP: The MHRA issued a warning in 2019 about the risk of [] in patients taking carbimazole.

In your exams, look out for a patient on carbimazole presenting with symptoms of []

NB - not agranulocytosis

Answer 28

TOM TIP: The MHRA issued a warning in 2019 about the risk of acute pancreatitis in patients taking carbimazole.

In your exams, look out for a patient on carbimazole presenting with symptoms of pancreatitis (e.g., severe epigastric pain radiating to the back).

Question 29

TOM TIP: Both carbimazole and propylthiouracil can cause agranulocytosis, with a dangerously low white blood cell counts. Agranulocytosis makes patients vulnerable to severe infections.

[] is a key presenting feature of agranulocytosis. In your exams, if you see a patient with a sore throat on carbimazole or propylthiouracil, the cause is likely agranulocytosis. They need an urgent full blood count and aggressive treatment of any infections.

Answer 29

TOM TIP: Both carbimazole and propylthiouracil can cause agranulocytosis, with a dangerously low white blood cell counts. Agranulocytosis makes patients vulnerable to severe infections.

A sore throat is a key presenting feature of agranulocytosis. In your exams, if you see a patient with a sore throat on carbimazole or propylthiouracil, the cause is likely agranulocytosis. They need an urgent full blood count and aggressive treatment of any infections.