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TAS > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What are the two types of cell surface receptors?

A

tyrosine kinase
G-protein coupled

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2
Q

Which hormones are hydrophilic and which are lipid soluable?

A

hydrophilic- insulin, catecholamines, pituitary hormones
lipid- thyroid, steroid

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3
Q

what hormones bind to tyrosine kinase cell receptors?

A

insulin, insulin-like growth factor-1, epidermal growth factor, fibroblast and platelet-derived growth factor)

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4
Q

What glucose test results suggest diabetes?

A

A random or two hour glucose test > 11mmol/L
A fasting glucose >7 mmol/L

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5
Q

What to do if uncertainty around T1 or T2 diabetes?

A

formal oral glucose tolerance test with measurement ofinsulin and c eptide. High concentrations of insulin and c-peptide on baseline and two hour blood samples would indicate the presence of T2D.

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6
Q

What antibody titres are raised in T1DM?

A

glutemate decarboxylase

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7
Q

What is T1 DM? and when do symptoms emerge?

A

T cell-mediated autoimmune damage to pancreatic β-cells
After destruction of > 90% of β-cells

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8
Q

What HLA types are associated with T1dM?

A

DQA, DQB and DRB

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9
Q

When can’t you used hbA1c monitoring for diabetes? what use instead?

A

haemaglobinopathies
continuous glucose monitoring or fructosamine

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10
Q

How does metformin work?

A

suppresses hepatic gluconeogenesis.

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11
Q

How do sulfonylureas work?

A

bind to the potassium channel on the pancreatic β-cell, precipitating membrane depolarization, calcium influx and insulin release

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12
Q

What are patients with T2DM linked with developing

A

polycystic ovaries

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13
Q

What is MODY?

A

maturity-onset diabetes of the young
ususally mild mutation in transcription facors in beta cells of pancreas casuing varying insulin release but it still works

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14
Q

characterise MODY

A

mild asymptomatic hyperglycaemia in non-obese children, often with a strong autosomal dominant family history of ‘diabetes’ associated with low or non-existent risks of complications

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15
Q

hypoglycaemia + hepatosplenomegaly suggests what?

A

Glycogen storage disorder

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16
Q

hypoglycaemia + tall stature and excess weight suggests what?

A

hyperinsulinism

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17
Q

hypoglycaemia + optic atrophy suggests what?

A

septo-optic dysplasia

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18
Q

hypoglycaemia + Cranial midline defects, short stature, microgenitalia suggest what?

A

Pituitary disorder

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19
Q

hypoglycaemia + Increased skin/ buccal pigmentation and hypotension

A

Addison’s disease

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20
Q

hypoglycaemia + Abnormal ear-lobe creases, macroglossia, umbilical hernia, hemihypertrophy suggests what?

A

Beckwith-Wiedemann syndrome

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21
Q

What are genes commonly implicated in congenital hyperisnulinism?

A

sulphonylurea receptor (ABCC8) and associated potassium inward rectifying channel (KCNJ11).

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22
Q

What is the treatment for congeital hyperinsulinism?

A

chlorothiazide and diazoxide-induces hyperpolarization, decreased calcium influx and reduced insulin secretion.
somatostatin analogue may be used to exert a direct receptor-mediated inhibition of insulin release.

23
Q

What types of cells produce calcitonin?

A

parafollicular cells in the thyroid

24
Q

Where is most T3 produced?

A

converted from T4 by Type II deiodinase in peripheral tissues

25
Q

What antibody is present in graves/ hashimoto’s thyroiditis?

A

Thyroid peroxidase

26
Q

What antibody is present in excess in graves disease?

A

TSH receptor antibodies (TRAb)

27
Q

What does raised plasma calcitonin suggest in the context of thyroid lump?

A

Medullary thyroid cancer

28
Q

Describe Activating mutation of the TSH receptor gene

A

A.D.
TSH low but T4+ T3 high. need surgical correction

29
Q

What are the normal values for fasting serum adn urine osmolality?

A

Serum osmolality of 275–295 mOsmol/kg
Urine osmolality > 850 mOsmol/kg

30
Q

What are the values of fasting serum and urine osmolality in Diabetes insipidus?

A

Inappropriately diluted urine.
i.e. hyper osmolar blood- Serum osmolality >290mOsmol/Kg but inappropriately dilute urine urine osmolaity < 750 mosmol/kg

31
Q

What is the treatment for diabetes insipidus; cranial and nephrogenic?

A

Cranial- desmopression, give cautiously!
Nephrogenic - Thiazuide diuretic to inc salt excretion in urine

32
Q

Define Cranial Diabetes insipidus + nephrogenic diabetes insipidus

A

cranial - insufficient production of ADH
nephrogenic- renal irresponsive to ADH

33
Q

What are the causes of Renal Diabetes Insipidus

A

Commonest is X-linked condition a/w polydipsia, polyuria and hypernatraemia

34
Q

What is vasopressin also known as, and where is it produced?

A

Antidiuretic hormone (ADH)
Posterior pituitary

35
Q

Describe SIADH

A

Inappropriate ADH secretion causing inappropriate retention of fluid. Therefore hyponatraemia and hypervolaemia

36
Q

What are the symptoms of SIADH?

A

May be mild, (restless, fatigue weakness) if NA+ >125
If <125 headache, vomiting reduced level of consciousness,
seizures and death

37
Q

What drugs can cause SIADH?

A

Carbamezapine, cyclophosphomide, sodium valproate

38
Q

What is the treatment for SIADH?

A

Treat underlying condition
inc sodium by no more than 8mmol/l in 24h

39
Q

what hormones are produced in the anterior pituitary?

A

Prolactin
FSH, LH
Thyroid stimulating horomone, Growth Hormone
Adrenocorticotrophic hormone (ACTH)

40
Q

What congenital condition is characterised by significant hypothalamic-pitutiary issues, featuring short growth and obesity from 2 years of age

A

Prader-Willi Syndrome

41
Q

What are the lab findings of pseudohypoparathyroidism?

A

Low Ca2+, high Po4-, high PTH

42
Q

What physiological sign is pathagnomic for primary adrenal insufficiency?

A

Increased generalised pigmentation of the skin, especially parts of the body which are not exposed to the sun

43
Q

How do neonates present with adrenal insufficiency?

A

2-3 weeks of life. Poor weight gain, vomiting , increased pigmentisation, virilised females

44
Q

What enzyme deficiency commonly causes CAH?

A

21-hydroxylase deficiency

45
Q

What are the laboratory features of an adrenal crisis?

A

Low Na+ , High K+, Low Ca2+, low glucose
metabolic acidosis
Low aldosterone, low cortisol

46
Q

What is the test for CAH?

A

17alpha-hydroxyprogesterone levels
+/- karyotyping if ambiguous genitalia

47
Q

What is addison’s disease and how does it present?

A

Autoimmune destruction of adrenal cortex
Adrenal insufficiency + increased pigmentation

48
Q

What is the test for Addison’s diease?

A

Short Synacthen test. Low cortisol despite ACTH stimulation.

49
Q

How is an addisonian/ adrenal crisis treated?

A

Hydrocrotisone IV, Fluid resucitation with 0.9% saline and 10 % dextrose

50
Q

What are the inital investigation done to confirm hypercortisolism?

A

24 hour urinary free cortisol excretion- pos if high
serum cortisol circadian rhythm study (0900 h, 1800 h and midnight when asleep) - pos no change with circadian rythm
overnight dexamethasone suppression test with 1 mg dexamethasone- pos if not suppressed

51
Q

What is commonest form of CAH?

A

21-hydroxylase deficiency

52
Q

hypertension and hyperkalaemia and ambiguous genitalia suggest what?

A

11-beta-hydroxylase deficiency CAH
with normal genitalia it would have been Conns

53
Q

delayed puberty and hypertension suggests what

A

17-alpha-hydroxylase deficiency

TAS (18 decks)

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