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Neuroscience > Year 3 - Endocrinology > Flashcards

Year 3 - Endocrinology Flashcards

1
Q

What Ix is done to confirm Addison’s disease?

A

SynACTH test.

Pregnancy and COCP may cause a false increase due to increased cortisol-binding globulin

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2
Q

What is the treatment for Addison’s disease?

A

Glucocorticoids (Hydrocortisone)

Mineralocorticoids (Fludrocortisone)

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3
Q

What are Addison’s patients advised to do if they become ill?

A

Double Hydrocortisone doses when ill

If having surgery or Vomiting/Diarrhoea then switch to IV/IM dosing.

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4
Q

What electrolyte changes are seen in Addisons disease (and what is the acid/base status?)

A

Hyponatraemia
Hyperkalaemia
Metabolic acidosis seen
(Also hypoglycaemia, raised urea, mild anaemia)

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5
Q

What is the treatment for an Addisonian crisis?

A

Urgent IV fluids + IV hydrocortisone (no fludrocortisone is required)

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6
Q

What are potential causes of an Addisonian crisis?

A

Steroid withdrawal
Adrenal haemorrhage (eg Waterhouse Friderichsen syndrome)
Sepsis
Surgery

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7
Q

Name 3 investigations for Cushing’s SYNDROME

A
  1. 24 hour urine free cortisol (will be elevated)
  2. Low dose dexamethasone suppression test (failure to suppress cortisol to <50nmol/L after LDDST)
  3. MRI pituitary gland = Pituitary adenoma
    (Possible late night salivary cortisol levels. Overnight dexamethasone suppression test)
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8
Q

Give 3 differentials for Cushing’s SYNDROME.

A
  1. Ectopic ACTH (eg small cell lung cancer)
  2. Cushing’s disease (pituitary adenoma)
  3. Adrenal tumour (low ACTH levels)
    Most common cause = exogenous steroids!
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9
Q

If MRI detects nothing, what is another Ix for Cushing’s DISEASE?

A

Inferior petrosal sinus sampling - shows gradient between central and peripheral ACTH levels after CRH injection.

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10
Q

How could you differentiate between Ectopic ACTH secretion and Cushings DISEASE?

A

High dose dexamethasone test.

Suppresses Cushings disease, doesnt suppress ectopic ACTH levels

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11
Q

In Cushing’s syndrome, how may we detect adrenal tumours?

A
  1. ACTH levels low and high cortisol levels
  2. CT/MRI of adrenal glands
  3. If no mass on CT/MRI&raquo_space; Adrenal vein sampling.
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12
Q

Name a MEDICAL treatment for Ectopic ACTH causes of Cushing’s SYNDROME?

A

Ketoconazole

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13
Q

What surgery is performed in Cushing’s disease?

A

Trans-sphenoidal removal of pituitary adenoma.

If unable to localise source = Bilateral adrenalectomy

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14
Q

What is Nelson’s syndrome?

A

Complication of bilateral adrenalectomy (possible treatment of Cushing’s disease.
High ACTH levels from enlarging pituitary tumour as removal of adrenals stops negative feedback = Increased skin pigmentation

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15
Q

What is the treatment for Adrenal tumours in Cushing’s DISEASE?

A

Laparoscopic adrenalectomy

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16
Q

Name some OTHER causes of diabetes mellitus.

A

Pancreas (Pancreatitis, Surgery, Haemachromatosis, Cystic Fibrosis)
Cushing’s disease, Acromegaly, Phaeochromocytoma

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17
Q

Name the microvascular complications of diabetes mellitus.

A

Retinopathy
Neuropathy
Nephropathy

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18
Q

Name the macrovascular complications of diabetes mellitus

A

Stroke, MI, Renovascular disease, Limb ischaemia

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19
Q

Give the venous glucose levels required to diagnose DM

A

Random >= 11.1mmol/L
Fasting >=7mmol/L
(HbA1C >48mmol/mol)

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20
Q

When should HbA1C NOT be used?

A

Pregnancy
Children
Type 1 Diabetes Mellitus
Haemoglobinopathies

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21
Q

Give some general management for DM

A 
Exercise increases insulin sensitivity.
Healthy eating (reduce saturated fats, reduce sugars, increase starch-carbohydrates, moderate protein)
Statin therapy (for vascular risks)
Control BP
Give foot care
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22
Q

What is Latent autoimmune disease in adults?

A

Form of Type 1 DM, slower progression to insulin dependence in later life.

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23
Q

Old patient develops diabetes, they are ketotic with poor response to oral hypoglycaemics. What condition are you considering?

A

Latent autoimmune disease in adults.

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24
Q

What autoantibodies are seen in T1DM

A

Islet cell antibodies

Anti-glutamic acid decarboxylase antibodies

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25
Q

What is the standard strength of insulin?

A

Insulin = 100units / 1mL

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26
Q

Name 3 typical insulin regimens.

A

BD ‘Biphasic regimen’ = twice daily premixed insulins by pen (eg Novomix 30)
QDS regimen = before meals ultra-fast insulin + bedtime long-acting analogue
Once-daily before-bed long acting insulin

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27
Q

When must ill insulin dependent diabetics be admitted?

A

Admit if vomiting, dehydrated or ketotic, a child or pregnant. (insulin requirements increase when ill, check BM >=4 times daily when unwell)

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28
Q

When are insulin pumps considered?

A

If a person has been unable to obtain HbA1C targets despite careful management.

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29
Q

What is the MoA of Metformin?

A

Increases insulin sensitivity

Reduces gluconeogenesis

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30
Q

When should Metformin be avoided?

A

If eGFR <30mL/min

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31
Q

What are the side effects of Metformin?

A

Lactic acidosis

GI upset

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32
Q

What is the MoA of Sulfonylurea’s (eg Gliclazide)

A

Increases insulin secretion (via action on Katp channels?)

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33
Q

What are the side effects of Sulfonylurea’s?

A

Hypoglycaemia
Weight gain
Hyponatraemia

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34
Q

What is the MoA of Sitagliptin?

A

Blocks DPP-4 (which normally destroys incretin) = increased incretin levels = inhibits glucagon secretion = increased insulin levels

35
Q

What is the side effect of Sitagliptin?

A

Pancreatitis

36
Q

Name a thiazolidamide drug

A

Pioglitazone

37
Q

What is the MoA of Thiazolidamide (eg Pioglitazone)?

A

Activates PPAR gamma receptors in adipocytes = promotes angiogenesis & fatty acid uptake.

38
Q

What are the side effects of Pioglitazone?

A

Fluid retention
Weight gain
Hypoglycaemia

39
Q

When is Pioglitazone contraindicated?

A

CI = Congestive cardiac failure

40
Q

What is the MoA of Empagliflozin?

A

Empagliflozin inhibits SGLT2 in the PCT of the kidney = inhibits reabsorption of glucose = urinate out glucose

41
Q

What is a side effect of Empagliflozin?

A

UTI/Thrush

42
Q

What is the mechanism of action of Exenatide?

A

GLP-1 analogue = Incretin mimetic = Inhibits glucagon secretion = Increased insulin secretion

43
Q

What are the side effects of Exenatide?

A

N&V

Pancreatitis

44
Q

How is Exenatide administered?

A

Given Subcutaneously

45
Q

What are the side effects of Insulin?

A

Hypoglycaemia
Weight gain
Lipodystrophy (suggest rotation of injection sites)

46
Q

What is Pre-diabetes?

A

When there is impaired glucose levels which are above the normal range but not high enough for DM.

47
Q

What is Impaired Glucose Tolerance (IGT)?

A

Fasting glucose <7mmol/L and OGTT 2h glucose >=7.8mmol/L but <11.1mmol/L
(Due to muscle insulin resistance)

48
Q

What is Impaired Fasting Glucose (IFG)?

A

Fasting glucose between 6.1-6.9mmol/L

Due to hepatic insulin resistance

49
Q

What is the Criteria for metabolic syndrome?

A

Central obesity (BMI >30 or Increased waist circumference) plus two of:

  • BP >= 130/85
  • Triglyceride >= 1.7mmol/L
  • HDL <= 1.03mmol/L for males; <=1.29mmol/L for females
  • Fasting glucose >=5.6mmol/L or T2DM
50
Q

What is the recommended target BP for T1DM?

A

Treat if BP >135/85mmHg

if albuminuria or 2+ features of metabolic syndrome 130/80mmHg

51
Q

What is the recommended target BP for T2DM

A

Target BP <140/80mmHg OR

If kidney, eye or cerebrovascular damage <130/80mmHg

52
Q

How are vascular risks controlled in diabetes?

A

BP control
Refer to smoking cessation services
Check plasma lipids - Statin therapy
(note aspirin is only offered as secondary prevention of CVS disease in T1DM)

53
Q

What are the signs of Diabetic Retinopathy?

A

Microaneurysms (dots)
Haemorrhages (blots)
Infarcts (Cotton wool spots)

54
Q

What is the treatment for Maculopathy or Proliferative retinopathy in diabetes?

A

Laser photocoagulation

55
Q

How do diabetic foot ulcers typically present?

A

Typically painless, punched-out ulcer in an area of thick callus. Possible superadded infection.
Cellulitis, Abscesses and Osteomyelitis are all possible

56
Q

What things might you want to assess with a diabetic foot ulcer?

A

Degree of Neuropathy
Presence of Ischaemia (Clinically + Doppler +/- Angiography)
Bony deformity (eg Charcot joint, Clinically + Xray)
Infection (swabs, blood cultures, xray for osteomyelitis, probe ulcers for depth)

57
Q

What are the signs of diabetic neuropathy?

A

Decreased sensation in ‘stocking’ distribution
Absent ankle jerks.
Neuropathic deformity (Charcot joint) = pes cavus, claw toes, loss of transverse arch, rocker-bottom sole

58
Q

Name some possible Diabetic neuropathies.

A

Symmetric sensory polyneuropathy
Mononeuritis multiplex (eg CN III & IV)
Amyotrophy = painful wasting quadriceps and other pelvifemoral muscles.
Autonomic neuropathy

59
Q

Name some presentations of Autonomic neuropathy seen in diabetic neuropathy

A

Postural BP drop.
Reduced cerebrovascular autoregulation.
Loss of respiratory sinus arrhythmia (vagal neuropathy).
Gastroparesis (early satiety, post-prandial bloating, N&V)
Urine retention
Erectile dysfunction

60
Q

Give some basic management of diabetic foot complications

A

Chiropody
Bed rest +/- Therapeutic shoes
Charcot joint = Bed rest/Crutches/Total contact cast until bony repair is complete. +/- Bisphosphonates
Cellulitis = IV antibiotics (local guidelines). Surgery may help

61
Q

What is the investigation for primary hyperaldosteronism?

A

Raised Aldosterone:Renin ratio is seen with Primary hyperaldosteronism

62
Q

Give 2 causes of Primary hyperaldosteronism.

A

Conn’s syndrome (Aldosterone producing adenoma)

Bilateral adrenocortical hyperplasia.

63
Q

What is the treatment for Conn’s syndrome?

A

Laparoscopic adrenalectomy.

Spironolactone is given for 4 weeks pre-op to control BP and K+ levels

64
Q

What is the cause of Secondary hyperaldosteronism?

A

Caused by reduced renal perfusion (eg Renal artery stenosis, Accelerated hypertension, Diuretics, CCF, Hepatic failure)

65
Q

What is Bartter’s syndrome?

A

Major cause of congenital (autosomal recessive) salt wasting&raquo_space; Sodium and Chloride leak in the loop of henle via mutations in channels and transport.
Rx = K+ replacement, NSAIDs, ACEi

66
Q

When should Conn’s syndrome be considered?

A

Hypertension associated with hypokalaemia
Refractory hypertension (despite >= 3 antihypertensives)
Hypertension occurring before 40 years of age.

67
Q

What are the investigations for Phaeochromocytoma?

A

24 hour urine metanephrines

Abdominal CT/MRI or MIBG scan to localise the tumour.

68
Q

Where are Phaeochromocytoma’s found?

A

90% in the adrenal medulla

10% as extra-adrenal tumours (paraganglioma)

69
Q

What is the classic triad of Phaeochromocytoma’s?

A

Episodic headache
Sweating
Tachycardia

70
Q

What is the treatment of Phaeochromocytoma’s?

A

Alpha blockade given first = Phenoxybenzamine
Beta blockade given after to prevent reflex tachycardia
Definitive = SURGICAL EXCISION

71
Q

What is the presentation of Non-functioning pituitary adneoma’s?

A

Visual field loss
Headache
Hypopituitarisim

72
Q

What hormones do Non-functioning pituitary adneomoa’s secrete?

A

Usually they don’t secrete anything.

They can secrete biologically INACTIVE LH and FSH

73
Q

What is the management for Non-functioning pituitary adenoma’s?

A

Surgery is indicated if visual field defects are present or there is a threat to vision (Surgery is performed trans-sphenoidally)

74
Q

What are the symptoms of Hypopituitarism?

A

Often non-specific symptoms of: (Think low testosterone)
Lethargy.
Weight gain.
Sexual dysfunction.

75
Q

How does an ACUTE hypo-adrenal crisis present?

A

Also called Addisonian Crisis =

Hyponatraemia + Hypotension

76
Q

How would you investigate hypopituitarism?

A

Prioritize excluding adrenal insufficiency

Secondary hypothyroidism = Low T4, Non-elevated TSH

Secondary hypogonadism = Low sex hormones + Non-elevated LH and FSH
(Low LH/FSH is a very good indicator in post-menopausal women)

77
Q

What condition is a Glucose tolerance test used for?

A

Acromegaly

78
Q

What is the investigations for suspected Diabetes Insipidus?

A

Water deprivation test

79
Q

What is the consequences of growth hormone deficiency?

A 
GH deficiency may give rise to:
Reduced QoL.
Reduced muscle and bone mass.
Increased fat mass.
Adverse cardiovascular profile.
80
Q

What is the use of Insulin tolerance testing?

A

Insulin causes a reduced blood glucose which causes stress.

Used to assess the Adrenal and GH axes (GH and Coritsol levels increase with stress)

81
Q

How might you localise a parathyroid adenoma?

A 
Parathyroid ultrasound (works 70-90% of the time)
SETAMIBI isotope scanning works alongside USS
82
Q

What are the 2 most common causes of primary hyperparathyroidism?

A 
Pituitary adenoma (80%) 
Parathyroid hyperplasia (if in >1 gland suggests genetic cause eg MEN)
83
Q

What condition must be excluded before treatment of Primary hyperparathyroidism?

A

Familial hypocalciuric hypercalcaemia must be excluded (via a low urine calcium:creatinine ratio)

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