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General Surgery > Endocrine disorders > Flashcards

Endocrine disorders Flashcards

1
Q

What is the action of PTH?

A

Increase [Ca2+] in the blood:

  • Bone: osteoclasts break down bone, release Ca2+
  • Kidney: calcium reabsorption
  • GIT: absorption increased (activate vitamin D)

Decrease [phosphate] in the blood (small net decrease):

  • Kidney: increased excretion/reduced reabsorption
  • GIT: increased uptake (vitamin D)
  • Bone: increased osteoclast activity –> release into blood
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2
Q

What is the action of calcitonin?

A

Decreases serum Ca2+

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3
Q

Where is calcitonin secreted?

A

C-cells/parafollicular cells of the thyroid gland

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4
Q

What is primary hyperparathyroidism?

A

Increased PTH due to intrinsic abnormality of the parathyroid glands: usually a single adenoma –> hypercalcaemia
Most common cause of hypercalcaemia in non-hospital population

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5
Q

Causes of hypercalacaemia?

A
  • Disorders of parathyroid gland: primary hyperparathyroidism, long term lithium Rx
  • Malignancy: haematological, bone mets, paraneoplast syndrome
  • Vit D disorders: hypervitaminosis D
  • High bone turnover: Thyrotoxicosis, long-term bed rest, thiazides, multiple myeloma, vitamin A
  • Renal disorders: Tertiary hyperparathyroidism
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6
Q

Clinical features of hypercalcaemia?

A
  • Bones: pathological fractures, musculoskeletal pain, radiological/densitometric abnormalities
  • Stones: Renal calculi
  • Groans: Abdominal pain (renal stones)
  • Moans: Depression, apathy/tiredness, confusion, delirium
  • Asymptomatic
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7
Q

What is secondary hyperparathyroidism?

A

Physiological/appropriate secretion of excess levels of PTH due to hypocalcaemia, most commonly secondary to chronic kidney disease and hypovitaminosis D (lack of sunlight exposure, or dietary intake)

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8
Q

What is tertiary hyperparathyroidism?

A

Long-standing secondary hyperparathyroidism which has progressed to an autonomous hyperplastic parathyroid gland/s, which continue to secrete PTH at high levels following resolution of secondary cause

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9
Q

What are the islet cell tumours of the pancreas (in order of incidence)?

A

Insulinoma - B cells
Gastrinoma - D cells
Gulcagonoma - A cells

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10
Q

Which cells may undergo neoplastic change to form a gastrinoma?

A

Gastrin-producing cells of the pancreas and duodenum, but NOT the antrum of the stomach

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11
Q

What is the classic triad of features of Zollinger-Ellison syndrome?

A
  • Recurrent peptic ulceration
  • Marked acid secretion
  • Gastrinoma
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12
Q

How to diagnose Zollinger-Ellison syndrome?

A

Elevated serum gastrin + raised basal fasting acid secretion

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13
Q

Features suggestive of Z-E syndrome?

A

MURDR MEN:

  • Multiple ulcers
  • ulcers in Unusual sites
  • Recurrent ulcer
  • ulcer + Diarrhoea
  • Refractory ulcer
  • ulcer + MEN syndrome
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14
Q

Causes of hypoglycaemia?

A
  • Anti-diabetic medications
  • Liver disease
  • Alcohol
  • Post-gastrectomy dumping
  • Insulinoma
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15
Q

MEN 1 syndrome?

A
  • Pituitary: acromegaly/prolactinoma
  • Pancreas: insulinoma/gastrinoma
  • Hyperparathyroidism
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16
Q

MEN 2a syndrome?

A
  • Medullary thyroid cancer
  • Phaeochromocytoma
  • Hyperparaythroidism
17
Q

MEN 2b syndrome?

A
  • Medullary thyroid cancer
  • Phaeochromocytoma
  • Marfanoid habitus
  • Mucosal neuromas
18
Q

Clinical features of Cushing’s syndrome?

A
  • Central obesity
  • Weakness/proximal myopathy
  • Hypertension
  • Skin changes: bruising/thin skin, acne, hirsuitisn, striae
  • Psychiatric changes: mental slowing, depression
  • Oligo-/amenorrhoea/impotence
  • Osteoporosis
  • Thirst/polyuria
  • Glucose intolerance
19
Q

Common causes of Cushing’s disease?

A
  • Steroid administration/iatrogenic - common
  • Cushing’s Disease (pituitary) - 70%
  • Ectopic ACTH (paraneoplastic) - 10%
  • Adrenal ademona/carcinoma - 20%
20
Q

What is Cushing’s syndrome caused by, hormonally?

A

Excess adrenal cortical hormones - cortisol

21
Q

What is Conn’s syndrome?

A

Aldosterone-secreting adenoma of the adrenal cortex causing hypokalaemia and hypertension

22
Q

What are carcinoids?

A

Indolent neuroendocrine tumours

Found anywhere in the GIT (particularly the ileum, appendix), lung, thymus, ovaries

23
Q

What is carcinoid syndrome?

A

When carcinoid tumour metastasizes past the liver (metabolic filter) and secretes metabolic products, causing systemic effects

24
Q

Clinical features of carcinoid syndrome?

A

Excessive production of a range of hormones, most notably serotonin, causing:

  • Flushing (episodic, lasts 30 seconds, involves face, neck, chest, turning red/purple, mild burning sensation)
  • Severe diarrhoea
  • Wheezing
  • Abdominal cramping
  • Peripheral oedema
25
Q

Causes of flushing?

A

Physiological: menopause, anxiety, anaphylaxis
Drugs: alcohol, levo-dopa
Metabolic: carcinoid, phaeochromocytoma, medullary thyroid carcinoma, renal cell carcinoma

General Surgery (15 decks)

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