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Year 3 > Endocrinology: Passmed > Flashcards

Endocrinology: Passmed Flashcards

1
Q

Which electrolyte is important for parathyroid secretion?

A

Magnesium, which also mediates the action of PTH on target tissue. Reduction in magnesium can lead to hypocalcaemia, which is unresponsive to treatment with supplementation.

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2
Q

What is the role of prolactin?

A

Stimulates milk production and breast development and inhibits gonadal activity.

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3
Q

What is the primary hyperparathyroidism?

A

Typically caused by solitary adenoma and parathyroid carcinoma, characterised by:
-> High PTH and calcium
-> Low phosphate and low urine calcium and creatinine

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4
Q

What is the cause of secondary hyperparathyroidism?

A

Parathyroid gland hyperplasia due to low calcium, associated chronic renal failure. It is characterised by:
-> High PTH and phosphate
-> Low calcium and Vitamin D

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5
Q

What is tertiary hyperparathyroidism?

A

Hyperplasia of the thyroid gland after correction of the parathyroid glands, with hyperplasia of all 4 glands. It is characterised by:
High PTH and calcium and ALP
Decreased phosphate and Vitamin D

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6
Q

What is the cause of congenital adrenal hyperplasia?

A

Deficiency in 21-hydroxylase enzyme, which is important for the production of cortisol and aldosterone, but there is excess production of androgens. There is virilisation of the female genitalia, with precocious (early) puberty in males

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7
Q

How does insulin affect electrolytes?

A

Hypokalemia and hypernatremia due to increased activity of the sodium-potassium pump. It inhibits lipolysis and reduces muscle protein loss.

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8
Q

What happens to urine osmolality during a water deprivation test in healthy individuals?

A

Plasma osmolality begins low
Urine osmolality ends high
Urine osmolality remains high following administration of ADH.

-> High urine osmolality occurs in water deprivation due to ADH stimulating water and salt reabsorption. Final high urine osmolality indicates preserved kidney tubule function.

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9
Q

What happens to urine osmolality during a water deprivation test in patients with cranial diabetes insipidus?

A

Starting plasma osmolality is high
Final urine osmolality is low
Following administration of ADH, urine osmolality will be high

Deficiency of ADH causes excessive loss of water, therefore administration of synthetic ADH will correct this. Plasma osmolality is high due to dehydration.

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10
Q

What happens to urine osmolality during a water deprivation test in nephrogenic diabetes insipidus?

A

Plasma osmolality will be high
Final Urine osmolality will be low
Administration of ADH will cause final urine osmolality to be unchanged and remain low
-> This will occur due to reduced kidney tubule function reducing the ADH activity

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11
Q

How does PTH act?

A

Increases the activity of the 1-alpha-hydroxylase ENZYME for the activation of Vitamin D from 1,25 hydroxycholecalciferol for increased reabsorption of calcium from the small intestine.

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12
Q

What are the symptoms associated with excess glucorticoids?

A

Thinning of the skin
Osteonecrosis and osteoporosis
Sodium and water retention, causing hypernatremia and hypokalemia
Growth retardation in children

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13
Q

What is the action of cortisol?

A

Anti-inflammatory effects
Skeletal muscle breakdown
Stimulation of lipoplysis
Mineralcorticoid effects

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14
Q

What are the features of DKA?

A

Excessive uncontrolled lipolysis which results in accumulation of fatty acids, which causes nausea, vomiting, fruity-smelling breath and dehydration. This is triggered by infection or surgery. There is increased gluconeogenesis, with Kussmaul breathing and polyuria and polydipsia.

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15
Q

What is used for a differential diagnosis in primary aldosteronism?

A

Adrenal vein sampling, which can be used to differentiate between unilateral and bilateral adrenal hyperplasia, to take a blood sample and testing for hormone levels

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16
Q

What is the action of liraglutide?

A

GLP-1 agonist which promotes insulin release and reduces gastric emptying.

17
Q

Which hormones are increased post-operative period?

A

Glucocorticoids
Aldosterone
Growth hormone
ACTH

18
Q

What are the adverse effects of Sulphonylureas?

A

Hypoglycaemia and weight gain
-> It should be avoided in breastfeeding and pregnancy

19
Q

Which drug is used for patients with MODY?

A

Giclazide- a type of Sulphonylurea which binds to ATP K+ channel on pancreatic beta cells to promote insulin release.

20
Q

What is a risk with sudden stopping of corticosteroids?

A

Addisonian crisis

21
Q

Which diabetic medication causes glycosuria?

A

SGLT2 inhibitors, which have a lower risk of hypoglycaemia. It promotes weight loss, however there is normoglycaeic ketoacidosis.

22
Q

What is the action of carbimazole?

A

Carbimazole blocks thyroid peroxidase from coupling and iodinating the tyrosine residues on thyroglobulin → reducing thyroid hormone production

23
Q

How does Cushing’s affect potassium levels?

A

Cushing’s syndrome

24
Q

Which conditions cause hyperkalemia?

A

MACHINE
M- medications like NSAIDs and ACE inhibitors
A- acidosis
C- cellular destruction
H- Hyperaldosteronism/Haemolysis
I- Intake through diet
N- Nephrons
E- Excretion

25
Q

What is the main ketone body involved in diabetic ketoacidosis?

A

Acetoacetate and Betohydroxybutyrate, which is formed into the breakdown product acetone.
-> They are picked up by the extra-hepatic tissue and converted into acetylcoA

26
Q

What is the most common type of thyroid cancer?

A

Papillary carcinoma

27
Q

What inhibits insulin release?

A

Alpha adrenergic drugs/agonists
Beta blockers
Sympathetic nerves

28
Q

What are the features of postpartum thyroiditis?

A

Immediately following birth, there is hyperthyroidism followed by normal or decreased level of thyroid hormones.

29
Q

What are the adverse effects of fibrates?

A

GI side effects
Increased risk of thromboembolism

30
Q

Where is osmolality greatest in the kidney?

A

Tip of loop of Henle, prior to water reabsorption and following uptake of solutes.

31
Q

What can Potter sequence result in?

A

Potter sequence with bilateral renal agenesis and oligohydroamniosis.

32
Q

How does hyperacute rejection occur?

A

Type 2 hypersensitivity due to pre-formed antibodies against ABO or HLA which activates the coagulation cascade and causes thrombosis and occlusion of organ.

33
Q

What is Graft vs host disease?

A

Donor T cells mount a cell mediated response against host tissues causing cholestasis, jaundice and diarrhoea.

34
Q

What are the post operative complications?

A

Acute tubular necrosis of graft
Vascular thrombosis
UTI
Urine leakage

35
Q

What is the order of priority for graft failure?

A

HLA-DR
HLA-DB
HLA-DA

36
Q

How is acute graft failure mediated?

A

Less than 6 months and Occurs due to mismatched HLA, mediated by cytotoxic T cells or due to cytomegalovirus infection.

37
Q

Why does chronic graft failure occur?

A

Antibody and cell mediated damage cause fibrosis of the kidney, which may occur due to recurrence of original renal disease.

Year 3 (37 decks)

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