Endocrine Flashcards

1
Q

Where are the 3 main places that glucose is stored and what is it stored as?

A

1) Muscle as glycogen
2) Adipose tissue as triglycerides
3) Liver as glycogen

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2
Q

At what blood glucose concentration would you expect to find glucose in your urine after a glucose load?

A

Over 11mmol/l as this is the renal threshold after which glucose is lost in the urine. This is because SGLT-2 becomes saturated, can’t transport anymore glucose so it is lost in the urine.

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3
Q

How does adrenaline effect blood glucose levels?

A

It acts rapidly to increase blood glucose levels by increasing glycolysis and gluconeogenesis in the liver.

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4
Q

What tissues are totally dependent on glucose as an energy source and why?

A
  • Erythrocytes as they don’t have any mitochondria to generate ATP.
  • Retina, has a barrier.
  • Brain, has a barrier, BBB. Makes a lot of neurotransmitters that are made from intermediates of glucose.
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5
Q

Why do patients with diabetes mellitus tend to have nocturnal polyuria?

A

They regularly exceed the renal threshold so there is loss of glucose. Glucose takes water with it in osmotic diuresis. This is noticed more at night though hyperglycaemia may also be more common at night.

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6
Q

Why do patients with T1DM lose weight whilst eating plenty?

A

They have a lack of insulin but an excess of glucagon. This causes the body to go into catabolism and break down muscle proteins.

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7
Q

What is Sheehan’s syndrome?

A

Also known as postpartum pituitary gland necrosis, is hypopituitarism (decreased functioning of the pituitary gland), caused by ischemic necrosis due to blood loss and hypovolemic shock during and after childbirth.

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8
Q

Define ‘Diabetes Mellitus’

A

A metabolic disorder of multiple aetiology characterised by chronic hyperglycaemia with disturbances of carbohydrate, protein and fat metabolism resulting from defects in insulin secretion, insulin action, or both.

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9
Q

Symptoms of hyperglycaemia?

A

Tiredness, weight loss, polyuria, polydipsia, dry mucous membrane, postural hypotension, blurred vision.

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10
Q

What do DM patients get blurred vision?

A

They get swollen ocular lenses due to glucose shifts.

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11
Q

Plasma ketone levels

A

Below 0.6mmol/L is normal. 0.6 to 1.5mmol/L indicates the development of a problem. Above 1.5mmol/L in the presence of hyperglycaemia indicates risk of diabetic ketoacidosis.

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12
Q

What is MODY?

A

Mature onset diabetes of the young. 1-2% of DM. Caused by change in a single gene. Autosomal dominant. HNF1-A gene accounts for 70% of MODY.

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13
Q

What is Gestational diabetes mellitus?

A

Carbohydrate intolerance with onset, or diagnosis, during pregnancy.

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14
Q

What is secondary diabetes?

A

A diabetic condition that develops after the destruction of the beta-cells in the pancreatic islets and/or the induction of insulin resistance by an acquired disease (e.g. endocrinopathies) or others.

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15
Q

What is the basal rate of endogenous insulin secretion under fasting conditions?

A

40 microgram/h

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16
Q

Why is insulin released in a biphasic manner?

A

First release is the insulin storage in granules, the second release is the insulin which has just been synthesised, processed and secreted whilst blood glucose levels are high.

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17
Q

How is insulin administered to DM patients?

A

Insulin is a peptide so cannot be given orally. Given as a subcut injection.

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18
Q

Advantages of insulin pens versus vial and syringe

A
  • More convenient
  • More accurate doses
  • Easier to use for those with impairments in visual and fine motor skills
  • Less injection pain
  • Can be used without being noticed.
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19
Q

What is CSII?

A

Continuous subcutaneous insulin infusion-an insulin pump.

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20
Q

Complications of CSII?

A

Continuous subcut insulin infusion. Reactions/infections at cannula site, tube blockage and pump malfunction.

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21
Q

What is the curative treatment for T1DM?

A

Islet cell transplant of pancreatic transplant.

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22
Q

Whipple’s Triad

A

1) Symptoms of low blood glucose.
2) Measured plasma glucose <2.8mm-normal. <4.0mmol-insulin treated.
3) Better after glucose

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23
Q

What is the diagnostic criteria for DKA?

A

1) Metabolic acidosis
2) Plasma glucose >13.9mmol/l
3) Urinary/plasma ketones present

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24
Q

What are the clinical features of DKA?

A

Osmotic symptoms, weight loss, breathlessness (Kussmaul respiration), abdominal crmaps, leg cramps, N&V, confusion

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25
Q

What are the precipitating factors to DKA?

A

Acute illness, new-onset DM, insulin omission, infections.

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26
Q

What is the treatment of DKA?

A

1) Fluid-first saline to restore volume then dextrose
2) Potassium
3) Insulin

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27
Q

Precipitating factors of DKA.

A
5 I's of DKA:
Infection
Ischemia
Infarction 
Intoxication 
Insulin missed
28
Q

Precipitating factors of Hyperglycaemic hyperosmolar state (HHS)?

A

Infection, poor compliance and drugs.

29
Q

Causes of hypopituitarism?

A

Tumours, radiotherapy, infacrtion/haemorrhage, infiltration (eg. sarcoid), trauma, lymphocytic hypophysitis.

30
Q

Causes of high prolactin?

A

Prolactinomas, physiological (lactation/pregnancy), drugs (that block dopamine) eg. tricyclics, antiemetics, antipsychotics, “stalk” effect- due to loss of inhibitory dopamine.

31
Q

What drugs block dopamine and so could cause high prolactin levels?

A

Tricyclics, antiemetics, antipsychotics.

32
Q

What are some of the clinical features of prolactinoma?

A
  • Galactorrhoea
  • Headaches
  • Mass effect
  • Visual field defect
  • Amenorrhea/erectile dysfunction
33
Q

Features of acromegaly

A
  • Sweat and headaches
  • Alteration of facial features
  • Increased hand and feet size
  • Visual impairment
  • Cardiomyopathy
  • Increased inter-dental space
34
Q

Cushing’s disease

A

Pituitary tumour releasing ACTH. One of the causes of Cushing’s syndrome.

35
Q

What is primary amenorrhoea?

A

Failure of menses to start by age 16. Can be due to genitourinary abnormalities, chromosomal abnormalities, secondary hypogonadism.

36
Q

What is secondary amenorrhoea?

A

When a woman who has had normal menstrual periods stops getting her periods for 6 months or longer.

37
Q

What is hirsutism?

A

Excess hair growth in a male pattern due to increased androgens and increased skin sensitivity to androgens.

38
Q

Presentation of PCOS

A

Anovulation with associated symptoms of hyperandrogenism (hirsutism, acne, alopecia).

39
Q

What artery supplies the parathyroid glands?

A

Inferior thyroid artery.

40
Q

What controls secretion of parathyroid hormone?

A

Calcium sensing receptor

41
Q

What is the commonest cause of hypercalcaemia in hospitalised patients?

A

Malignancy. Solid organ tumours and haematological mechanisms.

42
Q

What are ‘brown tumours’ and what are they found in?

A

Found in hyperparathyroidism. They are not neoplastic but are the results of excess osteoclast activity, collection of osteoclasts, poorly mineralised bone and fibrous tissue. “brown” because of appearance- haemosiderin deposition.

43
Q

What are some of the complications of parathyroidectomy?

A

Vocal cord paresis, haematoma causing tracheal compression. Transient hypocalcaemia.

44
Q

What is “hungry bones”?

A

Uncommon complication of parathyroidectomy. Occurs in patients with significant bone disease pre-op or elevated PTH. Sudden withdrawal of PTH leads to imbalance between bone formation and resorption-marked net increase in uptake of calcium, phosphate and magnesium by bone.

45
Q

Causes of Vit. D deficiency?

A

Poor sunlight exposure (elderly or housebound), malabsorption, gastrectomy, enzyme inducing drugs eg. anticonvulsants, renal disease.

46
Q

How do we treat vit D deficiency?

A

Cholecalciferol (D3) given to restore body stores, correct metabolic disturbance and heal bony abnormalities. Alfacalcidol (active vit D) given to patients with renal impairment or hypoparathyroidism.

47
Q

What is the commonest ‘secondary’ cause of hypertension?

A

Primary aldosteronism (40% adenoma, 60% bilateral hyperplasia).

48
Q

What is the saline suppression test and what is it for?

A

Test for hyperaldosteronism. 2L of saline over 4 hours. 4h aldosterone >270 pmol/l highly suspicious.

49
Q

What are the causes of Cushing’s syndrome?

A
ACTH dependent
-pituitary adenoma
-ectopic ACTH
-ectopic CRH
ACTH independent
-adrenal adenoma
-adrenal carcinoma
-nodular hyperplasia
50
Q

Signs and symptoms of phaechromocytoma?

A

Hypertension (intermittent in 50%), episodes of headache, palpitations, pallor and sweating. Also tremor, anxiety, N&V, chest or abdo pain. Crises last 15 mins, often well between crises.

51
Q

Diagnosis of adrenal insufficiency eg. Addison’s disease

A

Suspicious biochem.-decreased NA, increased K. Hypoglycaemia. Short synACTHen test-measure plasma cortisol before and 30 minutes after IV ACTH injection. Normal: baseline >250nmol/l, post ACTH>480.

52
Q

What do the bloods look like in Osteomalacia?

A
  • Low Ca
  • Low phosphate
  • High alk phos
  • Low vit D
  • Elevated PTH
53
Q

High calcium and high PTH?

A

Primary hyperthryoidism until proven otherwise.

54
Q

What is phaeochromocytoma?

A

Tumour of the adrenal medulla.

55
Q

What enzyme turns testosterone into dihydrotestosterone (the active form)?

A

5 alpha reductase

56
Q

What do sertoli cells do?

A

Form the blood-testis barrier. Secretes androgen binding protein to hold testosterone in the testis. Also produce inhibin B.

57
Q

What are the clinical features of hypogonadism in children/young adults?

A

Slow growth in teens-no pubertal growth spurt. Small testes and phallus, lack of secondary sexual development.

58
Q

What are the clinical features of hypogonadism in adults?

A

Depression/low mood, poor libido, erectile problems, poor muscle bulk/power, poor energy. Sparse body/facial hair, gynaecomastia, gynoid weight gain, short phallus, small testes (abnormal consistency), great hair.

59
Q

What is an orchidometer?

A

Instrument used to measure the volume of the testes.

60
Q

How do you test for hypogonadism?

A

Test for sex steroid deficiency, early morning testosterone. Fertility, semen analysis-1-3 days after last ejaculation, 2-5ml volume, 50% progressive motility, 20x10^6 sperm/ml. Over 30% with normal morphology. Can used LH and FSH to work out whether it is a possible pituitary cause.

61
Q

What is Kallmann’s syndrome?

A

A condition characterised by delayed or absent puberty and an impaired sense of smell. This disorder is a form of hypogonadotropic hypogonadism, which is a condition resulting from a lack of production of certain hormones that direct sexual development.

62
Q

What are the side effects of androgen replacement therapy?

A
  • Mood issues (aggression/behaviour changes)
  • Libido issues
  • Increased haematocrit
  • Possible prostate effects
  • Acne, sweating
  • Gynaecomastia
63
Q

What is a mixed meal tolerance test?

A

A test to look for post prandial non-diabetic hypoglycaemia. Patient is given a meal/drink high in proteins/fats/sugars. This causes body to make more insulin. patient is monitored over a period of 5 hours or so with BG measured every 30 mins or so.

64
Q

What is a selective arterial calcium stimulation test and how does it work?

A

Used to localise insulinomas causing hypoglycaemia. Calcium gluconate is injected into the gastroduodenal, splenic, superior mesenteric arteries then there is sampling of hepatic venous insulin levels as calcium promotes insulin production. Allows localisation of the tumour.

65
Q

What 3 arteries supply the pancreas?

A

Gastroduodenal (head), superior mesenteric (uncinate process) and splenic (tail).