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Dannys Medicine Finals > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

DIABETES

Associated autoantibodies?

A

Anti - GAD antibodies

HLA-DR3/4
ICA,IAA, IA-2A

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2
Q

DIABETES

Clinical features?

A 
Polyuria
Polydipsia
weight loss
lethargy 
dehydration 
vomiting
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3
Q

DIABETES

DKA features?

A 
CRAVATS KD
Confusion
Reduced urine output / GCS
Acidosis
Vomiting
Abdo pain
Tachycardia
Shock/ coma

KUSSMAUL breathing
Dehydration

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4
Q

DIABETES

3 types of insulin regime?

A

Basal - bolus (rapid before meals, long acting for basal)

1,2,3, injections daily (biphasic)

Continuous insulin infusion via pump (regular rapid/short acting)

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5
Q

DIABETES

What should you be careful of when starting insulin

A

Hypokalaemia

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6
Q

DIABETES

BG targets for waking, before meals and post meals?

A

waking - 5-7
before meals - 4-7
after meals - 5-9

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7
Q

DIABETES

Complications that need to be monitored?

A 
Retinopathy
nephropathy (eGFR + ACR)
Diabetic foot
CVS risks
Thyroid disease
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8
Q

DIABETES

what should be given alongside insulin if BMI over 25?

A

Metformin

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9
Q

DIABETES

‘sick day’ rules?

corrective dose amount?

A

Aim for fluid intake of at least 3 litres
extra monitoring + measure ketones

total daily insulin dose divided by 6 (maximum 15 units)

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10
Q

DIABETES

How does diabetic retinopathy occur?

A

1) Damage to retina leads to ischaemia

2) ischaemia causes release of VEGF which causes growth of weak vessels prone to haemorrhage

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11
Q

DIABETES

DKA diagnosis?

A

1) Hyperglycaemia (>11.1)
2) Ketosis (ketones >3)
3) Acidosis (pH <7.3 / bicarb <15)

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12
Q

DIABETES

Treatment of DKA?

A 
FIGPICK
Fluids (1litre isotonic saline in 1st hour then add K every 2/4 hours after) 
Insulin (0.1unit/kg/hr infusion) 
Glucose
Potassium (never infuse >10mmol hour) 
Infection
Chart fluid balance
Ketones (monitor)
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13
Q

DIABETES

WHen should DKA be resolved?

A

both the ketonaemia and acidosis should have been resolved within 24 hours. If this hasn’t happened the patient requires senior review from an endocrinologist

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14
Q

DIABETES

why should you be careful with fluid replacement?

A

Cerebral oedema if overused

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15
Q

DIABETES

test to distinguish between T1 and T2?

A

C-peptide levels (low in T1)

Diabetes specific antibodies in T1

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16
Q

DIABETES

what drugs should be avoided?

A

Thiazides and beta blockers as these may cause insulin resistance, impair secretion and alter autonomic response to a hypo

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17
Q

DIABETES

Describe method of action and side effects of the following drug:

Insulin

A

Direct replacement of insulin

SE: Hypoglycaemia, weight gain, lipodystrophy

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18
Q

DIABETES

Describe method of action and side effects of the following drug:

Glucagon like peptide 1 (GLP-1)

A

Increase insulin secretion and reduce glucagon secretion

SE:
Weight loss (could be beneficial) 
N+V
Dizziness
Pancreatitis
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19
Q

DIABETES

Describe method of action and side effects of the following drug:

Metformin

A

Increase insulin sensitivity and decrease hepatic gluconeogenesis

SE: GI upset and Lactic Acidosis
“do not use if eGFR <30”

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20
Q

DIABETES

Describe method of action and side effects of the following drug:

Sulfonyureas

A

Stimulate pancreatic beta cells to secrete insulin

SE:
Hypoglycaemia 
Weight gain
Hyponatraemia
SiADH
Increase CV risk/MI
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21
Q

DIABETES

Describe method of action and side effects of the following drug:

Thiazolidinediones

A

agonists to the PPAR-gamma receptor and reduce peripheral insulin resistance.

SE:
Weight gain
fluid retention
fractures
bladder cancer
liver impairment
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22
Q

DIABETES

Describe method of action and side effects of the following drug:

DPP-4 inhibitors (Gliptins)

A

Increase incretin levels which inhibit glucagon secretion

SE:
Increase risk of pancreatitis
GI upset

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23
Q

DIABETES

Describe method of action and side effects of the following drug:

SGLT-2 inhibitors

A

They reversibly inhibit sodium-glucose co-transporter 2 (SGLT-2) in the renal PCT to reduce glucose reabsorption and increase urinary glucose excretion.

SE: glucoseuria
Increased risk of UTIs

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24
Q

Give examples of

GLP-1

A

GLP-1 - Exenatide and Liraglutide

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25
Q

Name some Sulfonyureas

A

Gliclazide

Glimepiride

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26
Q

Name Thiazolidenediones

A

Pioglitazone

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27
Q

Name DPP-4 inhibitors

A

Gliptins

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28
Q

Name SGLT-2 drugs

A

Drugs ending -glifozin

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29
Q

T2DM

HbA1c targets?

A

48 if newly diagnosed

53 for diabetics moved beyond metformin

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30
Q

T2DM

When should another medication be added?

A

If HbA1c >58mmol/L (7.5%)

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31
Q

T2DM

Metformin is first line treatment. what is the stepwise treatment after this

A 
2nd - 
\+ gliptin
\+ sulfonyurea
\+ pioglitazone
\+ SGLT-2 inhibitor

3rd (any 2 but not gliptin with pioglitazone or SGLT-2)

M + Sulf + G
M + Sulf + P
M + Sulf + SGLT-2
M + P + SGLT-2

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32
Q

T2DM

Final medical stepwise treatment?

A

Metformin + Sulfonyurea + GLP-1 mimetic

if BMI over 35 and insulin contraindicated

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33
Q

T2DM

Stepwise treatment if Metformin not tolerated

A

1st - Gliptin, Pioglitazone or Sulfonyurea

2nd - Any two of above combined

3rd - Insulin

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34
Q

Diagnosis of gestational diabetes

A

Fasting >5.6
2hr >7.8

(5678 rule)

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35
Q

when should insulin be immediately given in gestational diabetes?

A

IF fasting glucose >7mmol/L

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36
Q

IF diabetic patients are pregnant what should be given?

A

1) Folic acid 5mg for 12 weeks
2) Aspirin from 12 weeks to reduce risk of pre-eclampsia
3) Anomaly scan at 20 weeks
4) Only metformin and insulin allowed

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37
Q

Glucose targets for pregnant women?

A

Fasting : 5.3

2 hours after meal : 6.4

1 hour after meal: 7.8

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38
Q

What could be given if insulin / metformin contraindicated or refused in Gestational DM?

A

Glibenclamide

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39
Q

when is DKA pronounced resolved

A

Bicarb >15
pH >7.3
blood ketones <0.6mmol/L

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40
Q

What are the treatment targets (hourly) for DKA

A

Ketones falling by 0.5mmol/hr

Bicarb rise by 3mmol/hr

Glucose falls by 3mmol/hr

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41
Q

Complications of DKA?

A 
Arrhythmias 
ARDS
AKI
Cerebral Oedema (rapid correction of fluids) 
Hypophosphataemia
VTE
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42
Q

Cerebral Oedema clinical features and what should be done if suspected?

A

Headache with reduced GCS + rapid decrease in osmolality

CT head if suspected (children are most vulnerable)

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43
Q

How does Diabetic foot occur?

A

Peripheral arterial disease reduces blood supply - reduced pulses and ABPI

Neuropathy means loss of sensation

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44
Q

HYPERGLYCAEMIC HYPEROSMOLAR STATE (HSS)

What is it?

A

Hyperglycaemia and hyperviscosity of blood

Hyperglycaemia = osmotic diuresis with Na/K loss

Hyperviscosity = due to hypertonicity - increased risk of MI / stroke / thromboses

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45
Q

HYPERGLYCAEMIC HYPEROSMOLAR STATE (HSS)

Early signs and later signs?

A

Early - polydipsia, polyuria

Late - Dehydration, focal neuro signs, reduced consciousness / hypotension, altered mental status, N+V

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46
Q

HYPERGLYCAEMIC HYPEROSMOLAR STATE (HSS)

Diagnosis?

A

Hypotension

Hyperglycaemia >30mmol/L without significant ketonaemia or acidosis

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47
Q

HYPERGLYCAEMIC HYPEROSMOLAR STATE (HSS)

Treatment?

A

IV 0.9% NaCl - fluid restoration (0.45% if osmolarity not decreasing)

3-6L in 12hrs (50% in 1st 12hrs)

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48
Q

HYPERGLYCAEMIC HYPEROSMOLAR STATE (HSS)

When is rising sodium a concern?

A

Only a concern if osmolality not declining concurrently

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49
Q

HYPERGLYCAEMIC HYPEROSMOLAR STATE (HSS)

When is insulin given?

A

Only give if significant ketonaemia is present

> 1mmol/L

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50
Q

HYPERGLYCAEMIC HYPEROSMOLAR STATE (HSS)

Treatment targets?

A

Osmolality decrease by 3-8mosm/kg/hr

Glucose decrease by 5mmol/L/hr

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51
Q

HYPERGLYCAEMIC HYPEROSMOLAR STATE (HSS)

What should be given prophylactically?

A

LMWH - due to high risk of thrombotic complications

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52
Q

What is IRMA

A

Intra retinal microvascular abnormalities

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53
Q

Types of Diabetic Retinopathy?

A

Non proliferative and proliferative

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54
Q

DIABETIC RETINOPATHY

Describe mild and severe NDPR

A

Mild - 1 microaneursym

Severe - blot haemorrhages and microaneurysms in 4 quadrants
IRMA in at least 1 quadrant
venous beading in at least 2 quadrants

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55
Q

DIABETIC RETINOPATHY

Describe Proliferative

A

Retinal neovascularisation due to vascular endothelial growth factor (creating new weak vessels) which are prone to haemorrhage

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56
Q

HYPERTHYROIDISM

Autoantibodies?

A

TSH receptor antibodies (Graves - 90/100%)

Anti thyroid peroxidase (TPO) - 75%

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57
Q

HYPERTHYROIDISM

What are TSH receptor antibodies

A

They mimic TSH and stimulate thyroid gland

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58
Q

HYPERTHYROIDISM

Secondary causes?

drug causes?

A

Increased TSH due to hypothalamus pituitary dysfunction

Amiodarone

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59
Q

HYPERTHYROIDISM

Second most common cause?

typical features and treatment

A

Toxic multinodular Goitre - continously producing thyroid hormone with no feedback

> 50 year olds with firm nodules on palpation and patchy uptake on nuclear scintigraphy

Treatment = Radioiodine therapy

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60
Q

HYPERTHYROIDISM

Specific Graves features?

A

Exopthalmos - eye bulging

Pretibial myxoedema - waxy oedematous deposits of mucin under skin

Thyroid Acropachy Triad

1) Clubbing
2) Soft tissue swelling
3) Periosteal new bone formation

+ DIFFUSE GOITRE

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61
Q

Universal Thyroid signs?

Hyperthyroid

A

General - Heat intolerance, weight loss, manic restlessness

Cardio - palpitations

Skin - increased sweating, pretibial myxoedema, acropachy (clubbing)

GI - Diarrhoea

Gynae - oligomenorrhoea

Neuro - anxiety, tremor

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62
Q

Universal Thyroid signs?

Hypothyroid

A

General - Cold intolerance, weight gain, lethargy

Cardio - Bradycardia

Skin - Dry skin, dry coarse hair, non pitting oedema

GI - Constipation

Gynae - Menorrhagia

Neuro - Decreased tendon reflexes, carpal tunnel syndrome

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63
Q

what is De quervains thyroiditis?

Triad of symptoms?

A

Painful swelling in thyroid due to Viral infection. Hyperthyroid phase to hypothyroid phase then back to normal

triad of :

  • Fever
  • Neck pain tenderness
  • Dysphagia
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64
Q

Treatment of De Quervains thyroiditis?

A

NSAIDs for pain

Beta blockers for symptom relief in hyperthyroid phase

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65
Q

Treatment of De Quervains thyroiditis?

A

NSAIDs for pain

Beta blockers for symptom relief in hyperthyroid phase

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66
Q

Signs of Thyroid Storm?

Precipitants of thyroid storm?

A

pyrexia, tachycardia, agitation, confusion, N+V in already established thyrotoxicosis patients

precipitants: Trauma, infection, surgery, acute iodine load (CT contrast media)

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67
Q

Treatment of Thyroid Storm?

A

IV propanolol

Dexamethasone converts T4 to T3

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68
Q

HYPERTHYROIDISM

Treatment?

A

1st line - Carbimazole

2nd - Propylthiouracil

+ beta blockers propanolol (block adrenaline symptoms)

Alternative - active radio iodine (avoid in pregnant and children)

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69
Q

HYPOTHYROIDISM

most common causes?

A

Hashimoto’s Thyroiditis

Iodine deficiency (in developing world)

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70
Q

HYPOTHYROIDISM

Medication causes?

A

Lithium and Amiodarone

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71
Q

HYPOTHYROIDISM

Autoantibodies?

A

Anti-TPO antibodies and anti- thyroglobulin antibodies

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72
Q

HYPOTHYROIDISM

Causes of secondary?

A

Hypopituitarism due to tumour, infection or Sheehan Syndrome

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73
Q

HYPOTHYROIDISM

Treatment and its side effects?

What does it interact with?

A

Levothyroxine

SE:
Reduced bone mineral density
worsening of angina and AF
interacts with iron and calcium carbonate

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74
Q

HYPOTHYROIDISM

Signs on thyroid testing?

A

Primary - TSH = high T3/T4 = low

Secondary - TSH / T3 / T4 = low

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75
Q

HYPERTHYROIDISM

Pregnancy treatment?

A

1st trimester = Propylthiouracil

2nd onwards = Carbimazole

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76
Q

Hypothyroidism

Changes when pregnant?

A

Increase dose of thyroxine by up to 50%

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77
Q

Types of Thyroid Cancer and their % incidence?

A 
Papillary - 70%
Follicular - 20% 
Medullary - 5%
Anaplastic - 1% (not responsive to tx/chemo) 
Lymphoma - rare
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78
Q

What is Medullary cancer of the thyroid?

A

Cancer of parafollicular cells

increased calcitonin - part of MEN-2 disorder

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79
Q

Treatment of Papillary and Follicular Thyroid Cancer?

A

Thyroidectomy following by radio iodine to kill residual cells

Every year over thyroglobulin levels tested to detect any recurrent disease

80
Q

Described MEN-1 disorder and what it consists of

A

hereditary condition associated with endocrine tumours

3Ps :

  • Primary hyperparathyroidism
  • Pituitary
  • Pancreas
81
Q

Described MEN-2 disorder

A

2Ps + M

  • Primary hyperparathyroidism
  • Pheochromocytoma
  • Medullary thyroid cancer
82
Q

Myxoedema Coma

What is it and what are the signs?

A

the extreme manifestation of (usually untreated) hypothyroidism.

Confusion + hypothermia

83
Q

Myxoedema Coma

Treatment?

A

IV thyroid replacement and fluids

IV corticosteroids (once adrenal insufficiency excluded)

84
Q

Myxoedema Coma

Treatment?

A

IV thyroid replacement and fluids

IV corticosteroids (once adrenal insufficiency excluded)

85
Q

Rare complication of Hypothyroid?

A

MALT Lymphoma

86
Q

Most common cause of CKD and glomerular pathology?

A

Diabetic nephropathy

87
Q

How is glomerulosclerosis caused by Diabetes and what is the key feature

Treatment?

A

High levels of glucose passing through glomerulus
Protein/glucoseuria

ACE-I (BP control)

88
Q

Hypercalcaemia symptoms?

A 
Bones (bone pain)
Stones (renal calculi)
Groans (abdo pain) 
Thrones (polyuria) 
Psychiatric moans (altered mental status)
89
Q

What produces PTH?

A

Parathyroid gland Chief cells in response to low calcium

90
Q

Functions of PTH? (4)

A

1) Increase calcium absorption from intestines
2) Increase reabsorption from kidneys
3) Increase osteoclast activity (resorption)
4) Convert Vit D to active form

91
Q

Symptoms of Hypercalcaemia?

A

Thirst
Polyuria
Constipation

92
Q

HYPERPARATHYROIDISM

Primary cause and treatmentr?

A 
Solitary adenoma (80%)
Hyperplasia (15%)

Removal of tumour

93
Q

Two main causes of Hypercalcaemia and how does it affect an ECG?

A
  • Primary hyperparathyroid

- Malignancy (squamous cell LC, bone mets, myeloma)

94
Q

other causes of hypercalcaemia?

A 
Acromegaly
Vit D intoxication 
Addisons
Sarcoidosis
Thyrotoxicosis/ Thiazides

Dehydration

95
Q

Treatment of Hypercalcaemia?

A

Saline rehydration (3-4L daily)

Bisphosphonates / Calcitonin

96
Q

Cause of secondary Hyperparathyroidism?

A

Reduced vitamin D/ CKD = reduced calcium absorption / reabsorption - Hypocalcaemia

97
Q

Cause of Tertiary Hyperparathyroidism?

A

Prolonged secondary - PT hyperplasia so baseline PTH increases lots

98
Q

PTH, Calcium and Phosphate levels for all 3 types of Hyperparathyroidism?

A

Primary - High PTH, High calcium, Low phosphate

Secondary - high PTH, low/normal calcium, high phosphate

Tertiary - High PTH, High calcium. Low or normal phosphate

99
Q

Why is phosphate high in secondary Hyperparathyroidism

What does phosphate cause

treatment of high phosphate?

A

its normally excreted by kidneys but isnt properly due to CKD.

high phosphate causes osteomalacia as the phosphate ‘drags out’ calcium from bones

Treatment? reduce phosphate in diet

100
Q

Signs on X-ray of Primary Hyperparathyroidism?

A

‘pepperpot skull’ characteristic x-ray sign

101
Q

Hypoparathyroidism cause and treatment?

PTH,Ca,Phosphate levels?

A

Primary - secondary to thyroid surgery

Tx - Alfacalcidol

PTH - low Cal - low Phos - high

102
Q

features of Hypoparathyroid / Hypocalcaemia?

on ECG?

A

(due to neuromuscular excitability)

Muscle spasm / twitch (tetany)

Perioral parasthesia

Prolonged QT interval

103
Q

Characteristic signs of Hypocalcaemia?

A

Trosseau’s sign - Carpal spasm if brachial artery occluded by BP cuff and maintains pressure above systolic BP

Chvostek’s sign - tapping over parotid causes facial muscles to twitch

104
Q

Causes of Hypocalcaemia?

A

CRAMP + VIt D deficiency

CKD 
Rhabdomyolysis 
Acute Pancreatitis 
Magnesium deficiency / massive blood transfusion 
Psuedohypoparathyroid / hypoparathyroid
105
Q

Acute treatment of Hypocalcaemia?

A

IV Calcium gluconate (10l of 10% solution of 10 mins)

106
Q

What is Pseudohypoparathyroidism?

Characteristic appearance?

PTH, Ca, Phosphate levels?

A

When target cells are insensitive to PTH

Low IQ, short stature with shortened 4th/5th metacarpals (abnormality of G protein)

PTH - high
Calcium - low
Phosphate - high

107
Q

Diagnosis of Hypoparathyroid?

A

Urinary cAMP and phosphate following PTH infusion

In HPT - increase in cAMP and phosphate

In PHPT - no increase in phosphate

108
Q

What is Pseudopseudohypoparathyroidism?

A

Similar phenotype to PHPT but normal biochemistry

109
Q

Causes of Hypomagnesaemia?

A 
Alcohol
Diarrhoea
Drugs (diuretics / PPIs)
Hypercalcaemia
Hypokalaemia
110
Q

Features of Hypomagnesaemia?

A

Similar to hypocalcaemia (tetany)

ECG similar to hypokalaemia

111
Q

Treatment of Hypomagnesaemia?

A

<0.4mmol - IV Mg sulphate (40mmol over 24hrs)

> 0.4mmol - Mg salts (can cause diarrhoea)

112
Q

HYPOKALAEMIA

Causes with Hypertension?

A

Cushings
Conn’s
Liddles syndrome

113
Q

HYPOKALAEMIA

Causes without Hypertension?

A 
Diuretics 
Thiazides 
GI loss (D+V)
Renal Tubular Acidosis
Gitelman / Bartters syndrome
114
Q

HYPOKALAEMIA

Causes with alkalosis?

A

Thiazides
GI loss (vomiting)
Conn’s
Cushing’s

115
Q

HYPOKALAEMIA

Causes with acidosis?

A 
GI loss (diarrhoea) 
Renal tubular acidosis (types 1+2) 
Acetazolamide
116
Q

HYPOKALAEMIA

Features?

A

Hypotonia
Muscle weakness

ECG - (U have no Pot, No T but long PR/QT)

117
Q

Describe the RAAS and how aldosterone is released

A

1) Low BP in juxtoglomerular cells causes renin secretion
2) Renin acts on Angiotensinogen (liver) to become Angiotensin I
3) Angiotensin I converted to Angiotensin II by ACE (lung)
4) Angiotensin II causes Aldosterone release

118
Q

Aldosterone function electrolyte wise?

A

Increase sodium reabsorption

Increase potassium and hydrogen secretion

119
Q

Causes of Primary Hyperaldosteronism?

A

(Conn’s)

Adrenal gland Increase due to:

1) Bilateral adrenal hyperplasia (70%)
2) Adrenal Adenoma (30-40%)

120
Q

Why does renin decrease in Primary Hyperaldosteronism?

A

Increase in BP

121
Q

Secondary cause of Primary Hyperaldosteronism?

A

Excess Renin when kidney BP > rest of body BP due to:

1) Renal artery stenosis
2) renal artery occlusion
3) Heart failure

122
Q

How is renal artery stenosis confirmed?

A

Confirmed with doppler US or CT angiogram / MRA

123
Q

Hyperaldosteronism

Investigations?

A

Renin / aldosterone ratio 1st Line

2nd - CT abdo (suspected tumour)

3rd - adrenal venous sampling

124
Q

Renin and aldosterone levels in primary and secondary Hyperaldosteronism?

A

Primary = low renin. high aldosterone

Secondary = high renin, high aldosterone

125
Q

What is the purpose of adrenal venous sampling?

A

Distinguish between unilateral adenoma and bilateral adrenal hyperplasia

126
Q

Features of Hyperaldosteronism?

A

Hypertension

Hypokalaemia e.g muscle weakness, paraesthesia

127
Q

Management of Hyperaldosteronism?

A
  • Aldosterone antagonists (Epleronone, Spironolactone)

- Surgical removal of tumour

128
Q

Management of Renal artery stenosis?

A

Percutaneous renal artery angioplasty (enter through femoral artery)

129
Q

CUSHING’S

What is ^ syndrome?

A

SIgns and symptoms after prolonged elevaterd cortisol

130
Q

CUSHING’S

What is ^ disease?

A

ACTH secreting pituitary adenoma causing adrenal hyperplasia (80% cause of Cushing’s syndrome)

131
Q

CUSHING’S

ACTH dependant causes?

A

Cushing’s disease

Ectopic ACTH (from small cell LC) 5-10%

132
Q

What is Pseudo Cushing’s?

A

mimics cushing’s, normally due to alcohol excess

causes false positive dexamethasone suppression test or 24 hr urinary free cortisol

133
Q

How to differentiate between Cushings and Pseudo?

A

insulin stress test

134
Q

CUSHING’S

ACTH independent causes?

A

Adrenal adenoma

Steroid overuse

135
Q

CUSHING’S

Symptoms?

A

Easily bruised
Fatigue
Depression
Sexual dysfunction

136
Q

CUSHING’S

Signs?

A 
Central Obesity 
Hump / hyperpigmentation in dependant causes
Abdominal striae
Moon face
Proximal limb muscle wasting/weakness
137
Q

CUSHING’S

blood signs?

A

Hypokalaemic metabolic acidosis

138
Q

CUSHING’S

how to differentiate between ectopic and pituitary secretion of ACTH?

A

Petrosal sinus sampling

139
Q

CUSHING’S

Treatment?

A

Surgically remove tumour (transphenoidal removal of pituitary tumour)

140
Q

CUSHING’S

describe diagnosis/ localisation test

A

DEXAMETHASONE SUPPRESSION TEST

1) Initially low dose Dexa given (1mg) at 10pm

2) Measure cortisol levels in morning. 
Low cortisol = normal
High cortisol (not suppressed) = Cushing's Syndrome

3)high dose Dexa given (8mg)
If low cortisol and low ACTH = Pituitary source (Cushing’s disease)

If High/normal cortisol and high ACTH = Ectopic ACTH (e.g. SCLC)

If high/normal cortisol but low ACTH = Adrenal Adenoma

141
Q

What to do if adrenal adenoma suspected?

A

CT adrenal gland

142
Q

What should be given to someone with Addison’s?

A

Steroid card and emergency ID tag so no doses are missed / emergency services know patient is on lifelong steroids

143
Q

ADDISON’S

Primary cause?

A

Autoimmune destruction of adrenal glands (80%) resulting in decreased cortisol and aldosterone

144
Q

ADDISON’S

Secondary cause?

A

Inadequate ACTH e.g. damage to pituitary post surgery

OR

Sheehans - pituitary necrosis after childbirth blood loss

145
Q

ADDISON’S

Tertiary cause?

A

CRH/ Hypothalamus suppression due to long term oral steroids

146
Q

ADDISON’S

Features?

Particular feature in primary?

A

Fatigue, Nausea, Cramps, Reduced libido

Bronze hyperpigmentation - in primary as ACTH causes melonocytes to release melanin

147
Q

Serum ACTH in primary / secondary addisons?

A

Primary - high (no negative feedback)

Secondary - low

148
Q

ADDISON’S

Electrolyte abnormalities?

A

Hyperkalaemia and Hyponatraemia causing

METABOLIC ACIDOSIS

and Hypoglycaemia

149
Q

ADDISON’S

Definitive investigations?

A

Short synacthen test

150
Q

What is Synacthen?

A

Synthetic ACTH

151
Q

ADDISON’S

Adrenal autoantibodies?

A

Adrenal cortex antibodies

21-hydroxylase antibodies

152
Q

ADDISON’S

What do the following serum cortisol levels infer?

> 500 nmol/l
< 100 nmol/l
100-500 nmol/l

A

> 500 nmol/l makes Addison’s very unlikely
< 100 nmol/l is definitely abnormal
100-500 nmol/l should prompt a ACTH stimulation test to be performed

153
Q

ADDISON’S

Treatment?

A

Glucocorticoid (replace cortisol) and Mineralocorticoid (replace aldosterone)
(hydrocortisone and fludrocortisone)

154
Q

How is hydrocortisone given in Addisons?

A

dose is split with most taken in first half of day (20-30mg daily)

155
Q

ADDISON’S

How should steroid doses be changed when you’re ill?

A

Double hydrocortisone dose

Keep fludrocortisone dose the same

156
Q

ADDISONIAN CRISIS

What is it? Triggers?

A

Acute severe addisons triggered by:

SSS
Sepsis
Surgery
Stopping long term steroids suddenly

157
Q

ADDISONIAN CRISIS

Presentation? Electrolytes abnormalities?

A

1) Reduced consciousness

4 hypo 1 hyper
Hypotension
Hyponatraemia
Hypoglycaemia
Hyperkalaemia
158
Q

ADDISONIAN CRISIS

Treatment?

A

Hydrocortisone IM/IV 100mg stat then 100mg every 6hrs if still unstable

1L saline over 30-60 mins

Add dextrose if hypoglycaemic

159
Q

ACROMEGALY

What is and what are the causes?

A

excess growth hormone due to

Pituitary adenoma (95%)

Rarely lung/ pancreatic cancer secreting ectopic GnRH/GH

160
Q

ACROMEGALY

Space occupying features?

How are these features caused?

A

Headache and Bitemporal Hemianopia

Bitemporal Hemianopia due to pituitary increasing in size and putting pressure on nearby optic chiasm

161
Q

ACROMEGALY

Features in terms of tissue overgrowth?

A

Frontal bossing
Large facial features/ hands/ feet/ tongue

Protruding jaw (Prognathism)

Excess sweating due to sweat gland hypertrophy

162
Q

ACROMEGALY

Other features organ related?

A

Hypertrophic heart
Arthritis from imbalance of joint growth
T2DM
Hypertension

163
Q

ACROMEGALY

Associated cancers?

A

Colorectal cancer

Thyroid Cancer

164
Q

ACROMEGALY

Medical treatment?

A

Somatostatin Analogues (Octreotide)

Pegvisomant (GH antagonist)

Dopamine Antagonists (Bromocriptine)

165
Q

ACROMEGALY

Why are somatostatin analogues better than Dopamine agonists

A

Dopamine agonist block GH but not a potent as somatostatin analogues

166
Q

ACROMEGALY

Definitive treatment?

A

Removal of tumour

167
Q

ACROMEGALY

Investigations?

A

1st - Serum IGF-1 levels

2nd - OGTT to confirm diagnosis

168
Q

ACROMEGALY

Imaging to look at suspected pituitary adenoma?

A

MRI pituitary

169
Q

ACROMEGALY

What % have Multiple Endocrine Neoplasia? (MEN1)

A

6%

170
Q

Carcinoid Syndrome

What is it?

A

Mets in the liver release serotonin and can secret ACTH/GHRH resulting in cushings

171
Q

Features of Carcinoid syndrome?

Investigation of Carcinoid syndrome?

A

Flushing, Diarrhoea, Bronchospasm

Urinary 5-HIAA

172
Q

Treatment of Carcinoid Syndrome?

A

Somatostatin Analogue (Octreotide)

173
Q

What is Octreotide brand name?

A

Sandostatin

174
Q

Why should Hyponatraemia be treated slowly?

A

To prevent Central Pontine Myelinolysis (brain has adapted to low osmolality and correction too quickly will mean major water loss from the brain) - no more than raised by 4 to 6 mmol/l in a 24-hour period

175
Q

Causes of Hypernatraemia?

A

dehydration
osmotic diuresis e.g. hyperosmolar non-ketotic diabetic coma
diabetes insipidus
excess IV saline

176
Q

Treatment of Hypernatraemia

A

Fluids but corrected SLOWLY by no more than 0.5 mmol/hour as to prevent cerebral oedema

177
Q

Hyponatraemia causes?

A

water excess or sodium depletion

178
Q

Causes of pseudohyponatraemia?

A

hyperlipidaemia (increase in serum volume) or a taking blood from a drip arm

179
Q

How is a Hyponatraemia diagnosis confirmed?

A

Urinary sodium and osmolarity levels

180
Q

Water excess causes?

A

Water excess (patient often hypervolaemic and oedematous)
secondary hyperaldosteronism: heart failure, liver cirrhosis
nephrotic syndrome
IV dextrose
psychogenic polydipsia

181
Q

Causes of sodium depeltion; extra renal loss?

A

diarrhoea, vomiting,
sweating
burns,
adenoma of rectum

182
Q

Causes of Sodium depletion, renal loss?

A

(patient often hypovolaemic)
diuretics: thiazides, loop diuretics
Addison’s disease
diuretic stage of renal failure

183
Q

Euvolaemic hyponatraemia causes?

A

SiADH

Hypothyroidism

184
Q

Worry if hyponatraemia untreated?

A

Cerebral Oedema - can in turn cause brain herniation

185
Q

Treatment of Hyponatraemia if:

Hypovolaemia suspected?

A

normal, i.e. isotonic, saline (0.9% NaCl)

186
Q

Treatment of Hyponatraemia if:

Euvolaemic cause suspected?

A

fluid restrict to 500–1000 mL/day
consider medications:
demeclocycline
vaptans

187
Q

Treatment of Hyponatraemia if:

a hypervolemic cause is suspected?

A

fluid restrict to 500–1000 mL/day
consider loop diuretics
consider vaptans

188
Q

Treatment of Acute Hyponatraemia?

A

Hypertonic Saline (3% NaCl)

189
Q

What is Phaeochromocytoma?

A

Phaeochromocytoma is a rare catecholamine secreting tumour

190
Q

Test for Phaeochromocytoma?

A

24 hr urinary collection of metanephrines (sensitivity 97%*)

191
Q

Treatment for Phaeochromocytoma?

A

Surgery is the definitive management. The patient must first however be stabilized with medical management:

1) alpha-blocker (e.g. phenoxybenzamine), given before a
2) beta-blocker (e.g. propranolol)

192
Q

Phaeochromocytoma triad of features?

A

Sweating, headaches and palpitations

+ hypertension

193
Q

How to estimate serum osmolality?

A

Serum osmolality can be estimated using

(2 x Na+) + glucose + urea

194
Q

Causes of hypoglycaemia?

A 
Exogenous drugs (typically sulfonylureas or insulin)
Pituitary insufficiency
Liver failure
Addison's disease
Islet cell tumours (insulinomas)
Non-pancreatic neoplasms
195
Q

What conditions can reduce HbA1c levels?

A

Sickle-cell anaemia and other haemoglobinopathies such as:

  • hereditary spherocytosis
  • G6PD deficiency

Treduce RBC lifespan and hence can artificially lower HbA1c levels.

196
Q

What conditions can increase HbA1c levels?

A

Vitamin B12/folic acid deficiency
Iron-deficiency anaemia
Splenectomy

197
Q

Treatment for MODY and what is it?

A

Maturity Onset Diabetes of the Young

Autosomal dominant mutation in the HNF -1 alpha (70%)

Sensitive to sulfonyureas

Dannys Medicine Finals (9 decks)

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