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Phase 3 > Week 9 - endocrine > Flashcards

Week 9 - endocrine Flashcards

1
Q

Define diabetes mellitus.

A

A metabolic disorder of multiple aetiology characterized 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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2
Q

What are the symptoms of hyperglycaemia?

A

Tiredness, weakness, weight loss, difficulty concentrating, polyuria, polydipsia, thirst, dry mucous membranes, postural hypotension, blurred vision.

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3
Q

What are some of the different ways that diabetes mellitus presents?

A

Ketone production - nausea, vomiting, abdominal pain, heavy/rapid breathing, acetone breath, drowsiness, coma.
Depletion of energy stores - weakness, polyphagia, weight loss, growth retardation in young.
Complications (T2DM) - macrovascular, microvascular, neuropathy, infection.

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4
Q

What is the criteria for a diagnosis of diabetes?

A

One abnormal value + symptoms OR Two abnormal values without symptoms.
Fasting plasma glucose of ≥7mmol/L

Random plasma glucose of ≥11.1 mmol/L
HbA1c ≥48 mmol/mol

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5
Q

What HLA variants are present in 90% of those diagnosed with type 1 DM?

A

HLA DR3, HLA DR4

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6
Q

What autoantibodies are commonly present in those with T1DM?

A

GAD, ICA, ZnT8, IA2

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7
Q

What is the pathogenesis of Type 1 diabetes mellitus?

A

Chronic metabolic disorder characterised by hyperglycaemia and the absence of insulin secretion. Results from autoimmune destruction of the insulin producing beta cells in the islets of Langerhans. Occurs in genetically susceptible individuals and triggered by one or more environmental agents.

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8
Q

What environmental factors are thought to increase risk of T1DM?

A

Viral infections i.e. enterovirus, early introduction to cow’s milk, obesity.

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9
Q

What is the pathogenesis of type 2 diabetes mellitus?

A

Chronic progressive metabolic disorder characterised by insulin resistance and insulin deficiency. Associated with obesity. Combination of genes and environmental factors.

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10
Q

What is the inheritance pattern of MODY?

A

Autosomal dominant.

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11
Q

What are the risk factors of gestational diabetes mellitus (GDM)?

A

High BMI, previous macrosomic baby or gestational diabetes, family history, ethnic prevalence.

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12
Q

Name 3 causes of secondary diabetes.

A

Disease of exocrine pancreas - i.e. pancreatitis/carcinoma. Immunosuppressive agents - i.e. glucocorticoids.
Endocrinopathies i.e. acromegaly.

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13
Q

Describe the process by which insulin is released from the pancreatic beta cells.

A

Glucose enters the beta cell through GLUT2 transporter.
Glucose is phosphorylated to form ATP.
ATP causes potassium ion channels to close, leading to increase in intracellular potassium concentration and cell depolarisation.
This results in calcium channels opening and calcium flooding into the cell.
This triggers insulin containing granules to be released out of the cell by exocytosis and into nearby blood vessels.

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14
Q

Glargine(Lantus), detemir and degludec (Tresiba) are all what type of insulin? How often would you take them?

A

Long acting insulin analogue

Once daily

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15
Q

Novorapid, actrapid and Humulin S are all what type of insulin? How often would they be taken?

A

Short/rapid acting (bolus)

With every meal.

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16
Q

Novomix 30, Humulin M3 and Humalog Mix 25/50 are what type of insulin?

A

Mixed

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17
Q

What guidance is there surrounding hypos and driving? Do diabetics need to notify the DVLA? When would a diabetic not get to keep their license?

A

Diabetics should check blood glucose before driving. If <5 mmol/L they should not drive and if feeling hypo they should not drive. They should only drive for 2 hours at a time.
Must notify DVLA of diabetes.
If they are not aware of when they are getting hypo.

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18
Q

Diabetic ketoacidosis is a life threatening complication of diabetes, typically seen in T1DM. How does it cause mortality in the young and adults?

A

Young: cerebral oedema
Adults: severe hypokalaemia, ARDS, illness causing decompensation.

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19
Q

What is the pathophysiology of DKA?

A

Insulin deficiency leads to profound hyperglycaemia because insulin is not being taken up into cells and remains in the blood stream and gluconeogenesis occurs uninhibited. Cells are starved of energy and so lipolysis occurs and ketones are produced as a by product. Osmotic diuresis and acidosis leads to dehydration.

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20
Q

What are the clinical features of DKA?

A 
Weight loss
Dehydration
Breathlessness (Kussmaul breathing)
Abdominal pains 
Leg cramps
Nausea and vomiting 
Confusion
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21
Q

What different factors can precipitate diabetes mellitus?

A

Acute illness (i.e. MI, trauma), new-onset DM, insulin omission, infections, eating disorder.

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22
Q

How is DKA treated?

A

IV 0.9% sodium chloride fluids with 10% dextrose IV insulin
Potassium
Treat the precipitant i.e. infection

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23
Q

What are some of the differences between DKA and HHS?

A

DKA - usually T1DM, patient usually young and slim, sudden onset, significant ketoacidosis.
HHS - usually T2DM, patient usually elderly, insidious onset, no ketoacidosis, very hypovolaemic.

24
Q

How is HHS treated?

A

Fluid - 0.9% sodium chloride, aim for positive fluid balance of 3-6 L by 12 hours. Rate of fall in sodium should not exceed 10mmol in 24 hours.
Insulin only started if glucose not falling with fluid alone.
LMWH, foot protection.

25
Q

Which electrolytes are especially important to monitor in DKA and HHS?

A

DKA - potassium (add to fluid bag if hypokalaemic)

HHS - sodium (do not exceed fall in more than 10mmol in 24 hours)

26
Q

What are the microvascular and macrovascular complications of diabetes?

A

Retinopathy, nephropathy, neuropathy/foot disease, CVD (i.e. stroke, MI, hypertension, claudication).

27
Q

How are diabetic complications managed?

A

Annual screening: retinal, foot, kidneys.

Control of hypertension and cholesterol.

28
Q

Describe the incretin effect.

A

Insulin response is greater following oral glucose than IV glucose, despite similar plasma glucose concentrations.

29
Q

How does metformin work to treat T2DM?

A

Increases activity of AMPK which inhibits gluconeogenesis and reduces insulin resistance.

30
Q

How do sulphonylureas work to treat T2DM? Give an example of one.

A

Bind to the SUR receptor and promote insulin release from the beta cells of the pancreas.
Gliclazide

31
Q

How does pioglitazone work to treat T2DM?

What are the side effects?

A

Stops inappropriate deposition of lipid in non-lipid tissue, improving insulin sensitivity.
Weight gain and fluid retention.

32
Q

How do incretin based therapies exanatide and sitagliptin work to treat T2DM?
What are some of the pros of incretin based therapies?

A

Exanatide - GLP-1 agonist (mimics the action of GLP-1)
Sitagliptin - DPP4 antagonist (inhibits DPP4 which inactivates GLP-1)

(GLP-1 is an incretin which lowers blood glucose levels).

Can cause weight loss, less risk of hypos.

33
Q

How do SGLT-2 inhibitors work to treat T2DM? Give an example of one of these drugs. What are the side effects?

A

Stop reabsorption of glucose in the proximal tubule.
Dapagliflozin
Genital infections i.e. thrush

34
Q

Name the 6 hormones that are produced by the anterior pituitary and the 2 produced by the posterior pituitary.

A

Anterior: ACTH, TSH, FSH, LH, GH, prolactin.
Posterior: Oxytocin, ADH

35
Q

Name three causes of hypopituitarism.

A

Tumours
Radiotherapy
Infarction/haemorrhage

36
Q

Name three causes of high prolactin.

A

Prolactinomas
Physiological i.e. lactation or pregnancy
Drugs that block dopamine i.e. tricyclics or antiemetics.

37
Q

What size are pituitary tumours considered ‘micro’ and ‘macro’?

A

Micro: <1 cm
Macro: >1 cm

38
Q

What are the clinical features of a prolactinoma?

A

Galactorrhoea
Headaches
Visual field defect
Amenorrhoea/erectile dyfunction

39
Q

How is a prolactinoma diagosed and treated?

A

Diagnosis: serum prolactin >6000
MRI pituitary
Treatment: dopamine agonists, if this fails surgery

40
Q

What is acromegaly and what are its features?

A

Acromegaly: disorder of excessive levels of growth hormone after puberty.
Features: Increased hand and feet size, alteration of facial features, sweats and headaches, visual impairment, cardiomyopathy, increased inter dental space.

41
Q

How is acromegaly diagnosed?

A

Diagnosis: glucose tolerance test (should suppress GH) and measure insulin like growth factor 1.
then MRI scan.

42
Q

How is acromegaly treated?

A

First line: surgery
Drugs: somatostatin analogue, dopamine agonist, GH receptor agonist.
Radiotherapy

43
Q

What is cushing’s syndrome?

How is it diagnosed?

A

Excessive production of cortisol.

Dexamethasone suppression testing.

44
Q

How would you diagnose and treat diabetes insipidus?

A

Diagnosis: water deprivation test
Treatment: underlying cause, DDAVP (desmopressin).

45
Q

What is the biochemical threshold for hypoglycaemia in patients with DM? What is it for patient’s without hypoglycaemia?

A

<4 mmol/L - DM

<3 mmol/L - non DM

46
Q

What are some of the symptoms of hypoglycaemia? (split into autonomic and neuroglycopaenic)

A

Autonomic - sweating, palpitations, pallor, tremor, nausea, irritability, hunger.
Neuroglycopaenic - inability to concentrate, confusion, drowsiness, personality change, slurred speech, incoordination, weakness, dizziness, vision impairment, headache, seizures, coma.

47
Q

What is Whipple’s triad?

A

Symptoms consistent with hypoglycaemia.
Low plasma glucose.
Relief of symptoms once plasma glucose is raised.

48
Q

How is non-DM hypoglycaemia investigated?

A

Post-prandial investigations: mixed meal test.
72 hour fast.
Measure:
- glucose
- insulin
- C peptide
- SU screen
- BHOB (low in insulinoma)
- Pro insure (low with exogenous insulin)
- insulin antibodies (can be taken at any time)

49
Q

What studies can you do to localise the source of hypoglycaemia?

A

Radiology - CT, MRI, EUS of the pancreas
Arterial Calcium Stimulation - injection of calcium gluconate into gastroduodenal, superior mesenteric or splenic artery and sample hepatic venous insulin levels.

50
Q

Describe the male gonadal pituitary axis.

A

GnRH produced in the hypothalamus, stimulates the pituitary to produce LH and FSH. LH stimulates the Leydig cells to produce Testosterone. FSH stimulates the Sertoli cells to produce Inhibin and androgen binding protein. Testosterone and Inhibit negatively feedback to the hypothalamus and pituitary and suppress release of GnRH and LH and FSH.

51
Q

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

A

Slow growth in teens, no pubertal growth spurt, small testes and penis, lack of secondary sexual development.

52
Q

What are the clinical features of hypogonadism in adults?

A

Low mood, poor libidp, erectile problems, poor muscle bulk, poor energy, sparse body/facial hair, gynoid weight gain, full head hair, short phallus, small testes.

53
Q

Clinical history is extremely important in diagnosing hypogonadism. What should be included? What clinical examination tool can be used?

A

Height, weight, growth, family, sexual, drug and social history.
Orchidometer.

54
Q

How is hypogonadism tested for?

A

Testosterone - early morning, free testosterone. total testosterone, SHBG.
LH and FSH
Semen analysis

55
Q

What is hypogonadotrophic hypogonadism? What are the causes?

A

Hypogonadism caused by a problem with the hypothalamus or pituitary, resulting in low FSH and LH and low testosterone.
Hypopituitarism i.e. pituitary tumour, pituitary surgery/radiotherapy, genetic syndromes, head injury, cerebellar ataxia, Kallman’s syndrome.

56
Q

What is the pathophysiology of Kallman’s syndrome? What is the genetic cause?

A

Failure of GnRH cells to migrate to the hypothalamus from the olfactory placode. Causes isolated gonadotrophin deficiency, resulting in delayed or absent puberty and reduced sense of smell.
Lack of KAL genes: 1, 2 or 3.

57
Q

What are the causes of primary gonadal failure? What would you expect the testosterone, gonadotoph and prolactin levels to be?

A

Testosterone: low
LH and FSH: normal/high
Prolactin: Normal

Phase 3 (14 decks)

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