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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
What is the standard strength of insulin?
Insulin = 100units / 1mL
26
Name 3 typical insulin regimens.
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
27
When must ill insulin dependent diabetics be admitted?
Admit if vomiting, dehydrated or ketotic, a child or pregnant. (insulin requirements increase when ill, check BM >=4 times daily when unwell)
28
When are insulin pumps considered?
If a person has been unable to obtain HbA1C targets despite careful management.
29
What is the MoA of Metformin?
Increases insulin sensitivity | Reduces gluconeogenesis
30
When should Metformin be avoided?
If eGFR <30mL/min
31
What are the side effects of Metformin?
Lactic acidosis | GI upset
32
What is the MoA of Sulfonylurea's (eg Gliclazide)
Increases insulin secretion (via action on Katp channels?)
33
What are the side effects of Sulfonylurea's?
Hypoglycaemia Weight gain Hyponatraemia
34
What is the MoA of Sitagliptin?
Blocks DPP-4 (which normally destroys incretin) = increased incretin levels = inhibits glucagon secretion = increased insulin levels
35
What is the side effect of Sitagliptin?
Pancreatitis
36
Name a thiazolidamide drug
Pioglitazone
37
What is the MoA of Thiazolidamide (eg Pioglitazone)?
Activates PPAR gamma receptors in adipocytes = promotes angiogenesis & fatty acid uptake.
38
What are the side effects of Pioglitazone?
Fluid retention Weight gain Hypoglycaemia
39
When is Pioglitazone contraindicated?
CI = Congestive cardiac failure
40
What is the MoA of Empagliflozin?
Empagliflozin inhibits SGLT2 in the PCT of the kidney = inhibits reabsorption of glucose = urinate out glucose
41
What is a side effect of Empagliflozin?
UTI/Thrush
42
What is the mechanism of action of Exenatide?
GLP-1 analogue = Incretin mimetic = Inhibits glucagon secretion = Increased insulin secretion
43
What are the side effects of Exenatide?
N&V | Pancreatitis
44
How is Exenatide administered?
Given Subcutaneously
45
What are the side effects of Insulin?
Hypoglycaemia Weight gain Lipodystrophy (suggest rotation of injection sites)
46
What is Pre-diabetes?
When there is impaired glucose levels which are above the normal range but not high enough for DM.
47
What is Impaired Glucose Tolerance (IGT)?
Fasting glucose <7mmol/L and OGTT 2h glucose >=7.8mmol/L but <11.1mmol/L (Due to muscle insulin resistance)
48
What is Impaired Fasting Glucose (IFG)?
Fasting glucose between 6.1-6.9mmol/L | Due to hepatic insulin resistance
49
What is the Criteria for metabolic syndrome?
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
What is the recommended target BP for T1DM?
Treat if BP >135/85mmHg | if albuminuria or 2+ features of metabolic syndrome 130/80mmHg
51
What is the recommended target BP for T2DM
Target BP <140/80mmHg OR If kidney, eye or cerebrovascular damage <130/80mmHg
52
How are vascular risks controlled in diabetes?
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
What are the signs of Diabetic Retinopathy?
Microaneurysms (dots) Haemorrhages (blots) Infarcts (Cotton wool spots)
54
What is the treatment for Maculopathy or Proliferative retinopathy in diabetes?
Laser photocoagulation
55
How do diabetic foot ulcers typically present?
Typically painless, punched-out ulcer in an area of thick callus. Possible superadded infection. Cellulitis, Abscesses and Osteomyelitis are all possible
56
What things might you want to assess with a diabetic foot ulcer?
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
What are the signs of diabetic neuropathy?
Decreased sensation in 'stocking' distribution Absent ankle jerks. Neuropathic deformity (Charcot joint) = pes cavus, claw toes, loss of transverse arch, rocker-bottom sole
58
Name some possible Diabetic neuropathies.
Symmetric sensory polyneuropathy Mononeuritis multiplex (eg CN III & IV) Amyotrophy = painful wasting quadriceps and other pelvifemoral muscles. Autonomic neuropathy
59
Name some presentations of Autonomic neuropathy seen in diabetic neuropathy
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
Give some basic management of diabetic foot complications
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
What is the investigation for primary hyperaldosteronism?
Raised Aldosterone:Renin ratio is seen with Primary hyperaldosteronism
62
Give 2 causes of Primary hyperaldosteronism.
Conn's syndrome (Aldosterone producing adenoma) | Bilateral adrenocortical hyperplasia.
63
What is the treatment for Conn's syndrome?
Laparoscopic adrenalectomy. | Spironolactone is given for 4 weeks pre-op to control BP and K+ levels
64
What is the cause of Secondary hyperaldosteronism?
Caused by reduced renal perfusion (eg Renal artery stenosis, Accelerated hypertension, Diuretics, CCF, Hepatic failure)
65
What is Bartter's syndrome?
Major cause of congenital (autosomal recessive) salt wasting >> Sodium and Chloride leak in the loop of henle via mutations in channels and transport. Rx = K+ replacement, NSAIDs, ACEi
66
When should Conn's syndrome be considered?
Hypertension associated with hypokalaemia Refractory hypertension (despite >= 3 antihypertensives) Hypertension occurring before 40 years of age.
67
What are the investigations for Phaeochromocytoma?
24 hour urine metanephrines | Abdominal CT/MRI or MIBG scan to localise the tumour.
68
Where are Phaeochromocytoma's found?
90% in the adrenal medulla | 10% as extra-adrenal tumours (paraganglioma)
69
What is the classic triad of Phaeochromocytoma's?
Episodic headache Sweating Tachycardia
70
What is the treatment of Phaeochromocytoma's?
Alpha blockade given first = Phenoxybenzamine Beta blockade given after to prevent reflex tachycardia Definitive = SURGICAL EXCISION
71
What is the presentation of Non-functioning pituitary adneoma's?
Visual field loss Headache Hypopituitarisim
72
What hormones do Non-functioning pituitary adneomoa's secrete?
Usually they don't secrete anything. | They can secrete biologically INACTIVE LH and FSH
73
What is the management for Non-functioning pituitary adenoma's?
Surgery is indicated if visual field defects are present or there is a threat to vision (Surgery is performed trans-sphenoidally)
74
What are the symptoms of Hypopituitarism?
Often non-specific symptoms of: (Think low testosterone) Lethargy. Weight gain. Sexual dysfunction.
75
How does an ACUTE hypo-adrenal crisis present?
Also called Addisonian Crisis = | Hyponatraemia + Hypotension
76
How would you investigate hypopituitarism?
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
What condition is a Glucose tolerance test used for?
Acromegaly
78
What is the investigations for suspected Diabetes Insipidus?
Water deprivation test
79
What is the consequences of growth hormone deficiency?
``` GH deficiency may give rise to: Reduced QoL. Reduced muscle and bone mass. Increased fat mass. Adverse cardiovascular profile. ```
80
What is the use of Insulin tolerance testing?
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
How might you localise a parathyroid adenoma?
``` Parathyroid ultrasound (works 70-90% of the time) SETAMIBI isotope scanning works alongside USS ```
82
What are the 2 most common causes of primary hyperparathyroidism?
``` Pituitary adenoma (80%) Parathyroid hyperplasia (if in >1 gland suggests genetic cause eg MEN) ```
83
What condition must be excluded before treatment of Primary hyperparathyroidism?
Familial hypocalciuric hypercalcaemia must be excluded (via a low urine calcium:creatinine ratio)

Neuroscience (13 decks)

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