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Phase 2a > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Cheat sheet for these diseases?

Diabetes =

Thyroid disorders =

Cushing’s =

Acromegaly =

Conn’s syndrome =

Addison’s =

A

Diabetes = too much blood glucose / not enough insulin

Thyroid disorders = too much or too little thyroid hormone

Cushing’s = too much cortisol

Acromegaly = too much growth hormone

Conn’s syndrome = too much aldosterone

Addison’s = too little cortisol and too little aldosterone

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2
Q

Cheat sheet for these diseases?

Diabetes insipidus =

SiADH =

Hyperkalaemia =

Hypercalcaemia =

Parathyroid disorder =

A

Diabetes insipidus = not enough ADH

SiADH = too much ADH

Hyperkalaemia = too much potassium

Hypercalcaemia = too much calcium

Parathyroid disorder = too much or too little parathormone

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3
Q

Describe the pituitary gland?

A

Lies just inferior to the optic chiasm

Connected to the hypothalamus via pituitary stalk

Formed of separate anterior and posterior parts

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4
Q

Describe the anterior pituitary?

A
  • Recieves blood from portal venous circulation of hypothalamus
  • Contains 5 types of hormone producing cell which together produce 6 hormones
  • Hormone production is stimulated by the hypothalamus
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5
Q

Describe the CRH axis?

A

Hypothalamus > CRH > Ant. pituitary > ACTH > Adrenal cortex > glucocorticoids (cortisol)

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6
Q

Describe the GRH axis?

A

Hypothalamus > GRH > Ant. Pituitary > LH/FSH > gonads > various effects inc production of testosterone and oestrogen

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7
Q

Describe the GHRH axis?

A

Hypothalamus > GHRH > Ant. Pituitary > GH > Liver > IGF-1

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8
Q

Describe the TRH axis?

A

Hypothalamus > TRH > Ant. Pituitary > TSH > thyroid > T3 and T4

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9
Q

Describe the dopamine axis?

A

Hypothalamus > Dopamine > Ant. Pituitary > DECREASED prolactin

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10
Q

Describe the posterior pituitary?

A

Hormones are produced in the hypothalamus and stored in the posterior pituitary for release

The only two hormones are:

  1. Oxytocin
  2. ADH (vasopressin)
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11
Q

Symptoms of hyperthyroidism?

A

Symptoms:
Diarrhoea

Weight loss

Sweats

Heat intolerance

Palpitations

Tremor

Anxiety

Menstrual disturbance

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12
Q

Signs of hyperthyroidism?

A 
Tachycardia
Thin hair
Lid lag
Onycholysis
Lid retraction
Exophthalmos
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13
Q

Investigation of hyperthyroidism?

A

Thyroid function tests
Primary = low TSH, high T3/T4
Secondary = high TSH, high T3/T4

Thyroid autoantibodies

Radioactive iodine isotope uptake scan

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14
Q

Treatment for hyperthyroidism?

A

Beta blockers for rapid symptom control
Carbimazole = antithyroid drug
Radioiodine therapy
Thyroidectomy

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15
Q

Pathology and aetiology of Graves disease?

A

aetiology: Associated with other autoimmune diseases
pathology: Increased levels of TSH Receptor Stimulating Antibody (TRAb) - causes excess TH secretion from the thyroid

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16
Q

What is Graves’ Ophthalmology?

A
  • Extraocular muscle swelling
  • Eye discomfort
  • lacrimation
  • Diplopia
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17
Q

What is the investigation and treatment for Graves’ disease

A

Same as normal hyperthyroidism but with emphasis on TRAb (Ix)

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18
Q

Aetiology of hypothyroidism?

A

Hashimoto’s thyroiditis
Iodine deficiency
Previous radioiodine therapy
Over-treatment of hyperthyroidism

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19
Q

Symptoms of hypothyroidism

A 
Fatigue 
Cold intolerance 
Weight gain 
Constipation 
Myalgia 
Constipation 
Menorrhagia
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20
Q

Signs of hypothyroidism?

A

Bradycardic

Bradycardia
Reflexes relax slowly 
Ataxia 
Dry thin hair/skin 
Yawning 
Cold Hands 
Ascites 
Round puffy face 
Defeated demeanor 
Immobile 
Congestive HF
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21
Q

What is is acromegaly?

A

Increased production of growth hormone occurring in adults after fusion of epiphyseal plates

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22
Q

What is gigantism?

A

Increased production of growth hormones occurring in children

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23
Q

Aetiology of acromegaly?

A

Mainly a pituitary adenenoma

Very slow insidious onset over many years

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24
Q

Signs of acromegaly?

A 
Massive growth of hands and feet 
Big tongue and widely spaced feet 
Darkening skin 
Obstructive sleep apnoea 
Deep voice
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25
Q

What is acroparaesthesia?

A

pins and needles

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26
Q

What are the symptoms of acromegaly?

A 
Acroparaesthesia
Sweating 
Headache 
Arthralgia 
Decreased libido
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27
Q

Investigation of acromegaly?

A

Not a random gH test because GH is a pulsatile protein and levels may vary throughout the day

ORAL GLUCOSE TOLERANCE TEST

  • normally a rise in blood glucose will suppress GH levels
  • Give glucose then test GH, if still high this is diagnostic for acromegaly

MRI the pituitary fossa for adenomas

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28
Q

Treatment for acromegaly?

A

Transphenoidal surgery to remove the adenoma

GH antagonist e.g. pegvisomant

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29
Q

Define: hyperaldosteronism

A

Excess production of aldosterone independent of the RAAS system

Aldosterone works in the kidney to cause potassium loss, excess causes hypokalaemia and sodium and water retention

2/3 - conns syndrome
1/2 - bilateral adrenocortical hyperplasia

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30
Q

Symptoms of hyperaldosteronism?

A

Symptoms of hyperaldosteronism = symptoms of hypokalaemia

  • constipation
  • weakness and cramps
  • paraesthesia
  • polyuria and polydipsia

Also causes hypertension due to increased bv

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31
Q

Investigation of hyperaldosteronism?

A

U&E

  • decreased renin
  • increased aldosterone

ECG flat T, long PR, long QT, U waves

Adrenal CT

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32
Q

Treatment of hyperaldosteronism?

A

Conn’s: laproscopic adrenalectomy

Spirolactone - aldosterone anatagonist

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33
Q

Describe the action of PTH?

A

Increased bone resorption by osteoclasts
Increased intestinal calcium absorption
Activates 1,25 dihydroxyVD in kidney
Increased calcium reabsorption and phosphate excretion in the kidney

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34
Q

Aeitology of hyperparathyroidism?

A

80% solitary adenoma
20% = parathyroid hyperplasia
rare = parathyroid cancer

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35
Q

Symptoms of hyperparathyrodism?

A

Symptoms of hyperparathyroidism = symptoms of hypercalcaemia

Bones stones groans moans

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36
Q

Investigation of hyperparathyroidism?

A

Bloods:

Primary: ↑PTH, ↑Ca, ↓Phosph

Secondary: ↑PTH, ↓Ca, ↑Phosph

Tertiary: ↑everything (progression of secondary)

Increased 24hr urinary calcium excretion DEXA bone scan for osteoporosis

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37
Q

Treatment of hyperparathyroidism?

A

Fluids, surgically treat underlying cause, bisphosphates

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38
Q

Aetiology, S+S and Tx of hypoparathyroidism?

A

Aeitology: autoimmune destruction of PT, congenital, surgical removal (secondary) Mg/VD deficiency

S+S = hypocalcaemia = SPASM

Tx = Ca supplement, calcitriol, synthetic PTH

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39
Q

Pseudohypoparathyroidism

A

Decreased response to PTH
Bloodwork shows low Ca, high PTH
Treat as normal hypoparathyroid

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40
Q

The initial treatment for someone having a thyrotoxic storm is:

a )IV 0.9% saline

b) Propanolol
c) Salbutamol
d) Carbimazole
e) Omeprazole

A

B) propanolol

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41
Q

Which autoantibody will be present in Graves’ disease?

a) Thyroid Peroxidase (TPO)
b) TSH Receptor Stimulating Antibody (TRAb)
c) Graves Related Thyroid Antibody (GRTA)
d) Eutonic Auto Thyroid-Fascicle Automatic Renal Thyroid (EAT-FART)
e) T3 Mimicking antibody (TMA)

A

b) TSH Receptor Stimulating Antibody (TRAb)

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42
Q

Describe hypokalemia?

A

[K+] <3.5 mmol/L

Which causes…
- Low K+ in the serum (ECF) causes a water concentration gradient out of the cell (ICF)

  • Increased leakage from the ICF causing hyperpolarisation of the myocyte membrane
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43
Q

Investigation of hypokaelemia?

A

ECG!

U got no Pot and you got no T but a long PR and and long QT

U waves
No T waves
Long PR
long QT

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44
Q

Treatment of hypokalemia?

A

Not enough potassium - give some

Mild = oral K+ 
Severe = IV K+
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45
Q

Hyperkalemia investigation?

A

ECG

Tall tented ECG
Small P
Wide QRS

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46
Q

Treatment of hyperkalemia?

A

non urgent - polystyrene sulphonate resin - binds the K+ in the gut decreasing uptake

urgent - calcium gluconate - decreases VF risk in the heart
Insulin - drives K+ into the cells

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47
Q

Things that cause

HYPOkalemia

HYPERkalemia

A

HYPOkalemia - fasting, anorexia

HYPERkalemia - excessive consumption at a fast rate: IV fluids

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48
Q

Hyperokalemia on muscles?

A

Smooth- constipation
Skeletal - weakness/cramps
Cardiac - arrhythmias and palpitations

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49
Q

Hyperkalemia on muscles?

A

Smooth - cramping
Skeletal - weakness/flaccid paralysis due to overcontraction of muscles becoming totally drained of energy
Cardiac - arrhythmias and arrest

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50
Q

Potassium excretion issues?

A

HYPO (high secretion) = high aldosterone

HYPER (low secretion) = low aldosterone, adrenal insufficiency
AKI decreased filtration rate so more K+ os maintained in the blood

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51
Q

Describe hypokalemia internal balance issues?

A

insulin = excess
pH = alkalosis
B2 receptor = B2 agonists

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52
Q

Describe hyperkalemia internal balance issues?

A 
insulin = deficiency 
pH = acidosis 
B2 = beta blocker
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53
Q

Where is calcium stored?

A

99% of calcium is stored in bone calcium as calcium phosphate

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54
Q

What is calcium balance controlled by?

A

Parathyroid: PTH
Thyroid: Calcitonin

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55
Q

What causes hypocalcaemia?

A

HAVOC

hypoparathyroidism
acute pancreatitis 
vit D deficiency 
osteomalacia 
chronic kidney disease
56
Q

Symptoms and signs of hypocalcaemia?

A

SPASM

spasms 
peripheral paraethesia 
anxious 
seizures 
muscle tone increase
57
Q

Investigation and treatment of hypocalcaemia?

A

ECG= long QT interval

Tx:
mild - adcal
severe - calcium gluconate

58
Q

Aetiology of hypercalcaemia?

A

90% is due to primary hyperparathyroidism

59
Q

Symptoms of hypercalcaemia?

A

bones stones groans moans

painful bones
kidney stones
abdominal groans
psychiatric moans

60
Q

Investigation of hypercalcaemia?

A
  1. Find cause - corrected calcium levels and PTH

2. Identify damage - U&E renal damage, Xray

61
Q

What would the correct calcium and PTH levels show if hypercalcaemia was being caused by hyperparathyroidism?

A

Corrected calcium - mild increase

PTH - high

62
Q

What would the corrected calcium and PTH levels show if hypercalcaemia was being caused by cancer?

A

Correct calcium - severe increase

PTH - low

63
Q

How do you calculate corrected calcium levels?

A

Corrected calcium = total serum calcium +0.02 * (40 – serum albumin)

64
Q

What is Cushing’s syndrome?

A

Excess cortisol + loss of hypothalamic pituitary axis feedback + loss of circadian rhythm

65
Q

What is Cushing’s disease?

A

Excess cortisol + loss of hypothalamic pituitary axis feedback + loss of circadian rhythm + CAUSED BY PITUITARY ADENOMA

66
Q

What as some ACTH independent causes of excess cortisol?

A

Oral steroids = iatrogenic !!

Adrenal adenomas

67
Q

What are some ACTH dependent causes of excess cortisol?

A

Cushing’s disease - bilateral adrenal hyperplasia due to ACTH hypersecretion by pituitary adenoma

Ectopic Cushing’s Syndrome- due to paraneoplastic syndrome e.g. small cell lung cancer prpducing ACTH

68
Q

Signs of Cushing’s?

A

CUSHING

Cataracts 
Ulcers 
Striae 
HTN
Infections 
Necrosis
Glucosuria
69
Q

Aesthetic symptoms of Cushing’s?

A 
Truncal obesity 
Moon face 
Buffalo hump 
Acne 
Hirsutism (excess hair)
Wt gain
70
Q

Investigations for Cushing’s?

A

NOT a random plasma cortisol rest as levels change with stress, time of day, etc

DEXAMETHASONE SUPRESSION TEST - usually supresses cortisol level, failure to suppress over 24hr period is diagnostic of Cushing’s

Check 24hr urinary free cortisol - if normal Cushing’s unlikely

71
Q

Describe the treatment of Cushing’s?

A

If iatrogenic - stop steroids

Cushing’s disease - transphenoidal removal of pituitary adenoma

Adrenal adenoma - adrenalectomy, radiotherapy

Ectopic ACTH - surgery to remove tumour if location known

72
Q

Epidemiology and aetiology of type 2 diabetes?

A

Epi = old, obese, asian, male

Aeti = insulin resistance, B cell dysfunction

73
Q

Risk factors of type 2 diabetes?

A

Lack of excercise
High calorie intake
Fx or PHM of T2DM

74
Q

Presentation of T2DM?

A

Asymptomatic

75
Q

How is T2DM diagnosed?

A

WHO criteria:

Symptomatic
+
1 abnormal glucose result
(fasting / random)

OR

Asymptomatic
+
2 separate abnormal glucose result (fasting / random / 2hpostprandial)

OR

Abnormal HbA1c

76
Q

What is HBA1c

A

HBA1c is glycated Hb that is covalently bound to glucose

77
Q

Treatment of T2DM?

A

Prediabetic = lifestyle

Diabetic = lifestyle, then:

1st line - meformin

2nd = duel therapy eg. metformin + DPP4 inhibitor

3rd - triple therapy e.g. metformin + DPP4 + SU

4th - insulin / metformin / SU / GLP 1 mimetic

78
Q

What diabetic emergencies present with T2DM?

A

Hypoglycaemia

Hyperglycaemic hyperosmolar state

79
Q

Epidemiology and aetiology of T1DM?

A

Epi = young

Aeti = Autoimmune b cell destruction

80
Q

Risk factors of T1DM?

A

Fx or PMH of autoimmune disease

81
Q

Presentation of T1DM?

A

Weight lost
Polyuria
Polydipsia

82
Q

Treatment of T1DM?

A

Insulin

83
Q

What diabetic emergencies present with T1DM?

A

Hypoglycaemia

Diabetic Ketoacidosis

84
Q

Complications of T1DM and T2DM?

A

Microvascular: diabetic neuropathy(leg), diabetic retinopathy(eye) diabetic nephropathy (kidney)

Macrovascular: Stroke, MI

85
Q

Describe the pharmacology of biguanides?

A

Drug class: Biguanide

Example: Metformin

Mechanism: Reduces gluconeogenesis in liver

Side effects: GI disturbances, weight loss, can cause lactic acidosis (rare)

86
Q

Describe the pharmacology of sulfonylureas?

A

Drug class: Sulfonylurea

Example: Gliclazide

Mechanism: Stimulates B cells to secrete insulin

Side effects: hypoglycaemia, weight gain (appetite stimulation)

87
Q

Describe the pharmacology of DP4 inhibitors?

A

Drug class: DPP4 inhibitors

Example: sitagliptin

Mechanism: Inhibits DPP4, so increased incretins (GLP-1 and GIP), increasing insulin

Side effects: do not weight gain/loss

88
Q

What is an incretin?

A

A group of hormones released after eating and augment the secretion of insulin

e.g. GLP-1 and GIP

89
Q

Describe the pharmacology of glitazones?

A

Drug class: Glitazone

Example: Pioglitazone

Mechanism: Enhance the uptake of fatty acids and glucose

Side effects: fluid retention and fat gain - weight gained

90
Q

Describe the weight changes for the following drugs:

Metformin
Gliclazide
Sitagliptin
Pioglitazone

A

Metformin = lost
Gliclazide = gain
Sitagliptin = no change
PioGlitazone (glitazones) - gain

G is for gain
S is for same
M is for mini

91
Q

What is Addisons disease?

A

Primary Adrenal Insufficiency

Impairment of adrenal gland, low cortisol and aldosterone

Opposite of Cushing’s

92
Q

What is the commonest cause of primary adrenal insufficiency in the world?

A

TB

93
Q

What is the commonest cause of primary adrenal insufficiency in the UK?

A

Addison’s disease

94
Q

Describe the signs and symptoms of Addison’s?

A

Look= Lean and tanned
Mood = Depressed and tearful
GI: abdominal pain

95
Q

Investigation for addision’s?

A

Short ACTH stimulation test: give ACTH (synacthen) then measure cortisol levels - in Addisons cortisol remains low

Test from 21-hydrolyase (+Ve in 80%)

Bloods will show Na+ low and K+ high due to low aldosterone

96
Q

Treatment of Addisons?

A

Hydrocortisone to replace cortisol

Fludrocortisone to replace aldosterone

97
Q

Emergencies with Addisons?

A

Addisonian crisis:

Patients present with shock
Treat with fluid and hydrocortisone

98
Q

Diabetic ketoacidosis:

How?
Aetiology?

A

How - insufficient insulin

Aetiology - More ketones due to less glucose available, more ketones produced

99
Q

Signs and symptoms of diabetic ketoacidosis?

A
  • Fruity breath
  • Vomiting and abdominal pain
  • Signs of dehydration
  • Kussmaul breathing
100
Q

Diagnosis of DKA?

A

Acideamia (blood pH)
Hyperglycaemia
Ketonaemia/ketoniuria

101
Q

Management of DKA?

A

Fluid

Insulin

102
Q

Hypoglycaemia:

How?
Aetiology?

A

How - Too much insulin / oral hypoglycaemic agents

Aetiology - Insufficient glucose to brain

103
Q

Signs and symptoms of hypoglycaemia?

A

Odd behaviour
Sweating
Raised pulses
Seizures q

104
Q

Diagnosis of hypoglycaemia?

A

Blood glucose level

105
Q

Treatment of hypoglycaemia?

A

Glucose

Glucagon

106
Q

Hyperglycaemic Hyperosmolar State:

How?
Aetiology?

A

Insufficient oral hypoglycaemic agents

Aetiology - no ketogenesis, just hyperglycaemia

107
Q

Signs and symptoms of hyperglycaemic HS?

A

Signs of dehydration

108
Q

Diagnosis of hyperglycaemic HS?

A

Blood glucose level

109
Q

Treatment of hyperglycaemic HS?

A

LMWH prohpylaxis
Fluid
Insulin if severe

110
Q

What is diabetes insipidus?

A

Too little ADH from the posterior pituitary gland (cranial DI)

Kidney not responding to ADH (nephrogenic DI)

111
Q

Causes of diabetes insipidus?

A

Cranial DI: Head trauma, pituitary tumour

Nephrogenic: drugs e.g. lithium

112
Q

Signs and symptoms of DI?

A

Water deprivation test

  1. Restrict fluid
  2. Measure urine osmolarity (+ve for DI if urine osmolarity is low)
  3. Desmopressin (ADH analogues) to differentiate cranial or nephrogenic
113
Q

Treatment of diabetes insipidus?

A

Cranial: desmopressin

Nephrogenic: bendroflumethiazide, NSAIDs

114
Q

What is SIADH?

A

Syndrome of inappropriate ADH secretion

Too much ADH

115
Q

Causes of SIADH?

A

Malignancy
Drugs
CNS disorder

116
Q

S&S of SIADH?

A

Confusion
Anorexia
Nausea
Concentrated urine

117
Q

Diagnosis of SIADH?

A

Measure urine and plasma osmolarity

118
Q

Treatment of SIADH?

A

Treat the underlying cause
Restrict fluid
Vasopressin receptor antagonists

119
Q

Actions of PTH?

A
  1. Increased bone resorption by osteoclasts
  2. Increased intestinal calcium resorption
  3. Activates 1.25dihydroxyVD in kidney
  4. Increased calcium reabsorption and phosphate excretion in the kidney
120
Q

What might the thyroid function tests show in SECONDARY hyperthyroidism

a) Low TSH, High T3/T4
b) High TSH, High T3/T4
c) Normal TSH, High T3/T4
d) High TSH, Low T3/t4
e) High TSH, Normal T3/T4

A

b)High TSH, High T3/T4

In secondary hyperthyroidism, something is triggering high levels of TSH, which in turn causes high T3/T4

121
Q

What might the thyroid function tests show in PRIMARY hyperthyroidism

a) Low TSH, High T3/T4
b) High TSH, High T3/T4
c) Normal TSH, High T3/T4
d) High TSH, Low T3/t4
e) High TSH, Normal T3/T4

A

a)Low TSH, High T3/T4

122
Q

What is the best blood test for acromegaly?

a) Random plasma growth hormone test
b) IGF-1 conversion test
c) Glucose tolerance test
d) Serum GHRH tolerance test
e) Random plasma glucose

A

c)Glucose tolerance test

You cannot do a random GH test because GH is pulsatile

Best blood test is to check if glucose is suppressing GH levels as it should do

123
Q

Spironolactone is a…

a) Loop diuretic
b) Potassium – losing diuretic
c) Renin agonist
d) Aldosterone antagonist
e) Calcium channel blocker

A

d)Aldosterone antagonist

Spironolactone is a potassium SPARING diuretic, but its main action is as an aldosterone antagonist

124
Q

Give 4 causes of hypocalcaemia?

A 
H- hypoparathyroidism
A- Acute pancreatitis
V- Vitamin D Deficiency 
O- Osteomalacia
C- Chronic Kidney Disease
125
Q

In acidosis, how would the blood potassium level be?

A

Hyperkalemia

126
Q

What does a high Plasma ACTH but negative response to methotrexate suppression test indicate about the cause of a patients Cushing’s?

A

High ACTH so dependant and negative response to dexamethasone suppression test so paraneoplastic e.g. small cell lung cancer

127
Q

Which of the following ECG findings is indicative of Hypokalemia?

Tented T, short QT
Long QT, U waves
Tented T, no P
Long QT

A

Long QT

128
Q

Lara Williams, a 16yr old female, presents to A&E with her mother after feeling vey weak and experiencing some palpitations. Her mother is concerned that her daughter is very skinny, you check her BMI and it is 16.What is the most likely cause of her condition?

Hypokalaemia
Hyperkalaemia
Hypocalcaemia
Hypercalcemia

A

Hypokalemia

Anorexic - BMI

129
Q

Jim Bob a 73 year old gentleman presents to his GP for some routine tests following a recent diagnosis of tertiary hyperparathyroidism. All the results get mixed up in the pile which one is Jims?

A) Calcium high, Phosphate high, ALP high
B) Calcium low, phosphate low, ALP low
C)Calcium low, Phosphate high, ALP high
D) Calcium low, phosphate low, ALP high

A

B) Calcium low, phosphate low, ALP low

130
Q

Jim Bob a 73 year old gentleman presents to his GP for some routine tests following a recent diagnosis of secondary hyperparathyroidism. All the results get mixed up in the pile which one is Jims?

A) Calcium high, Phosphate high, ALP high
B) Calcium low, phosphate low, ALP low
C)Calcium low, Phosphate high, ALP high
D) Calcium low, phosphate low, ALP high

A

A) Calcium high, Phosphate high, ALP high

131
Q

Jim Bob a 73 year old gentleman presents to his GP for some routine tests following a recent diagnosis of primary hyperparathyroidism. All the results get mixed up in the pile which one is Jims?

A) Calcium high, Phosphate high, ALP high
B) Calcium low, phosphate low, ALP low
C)Calcium low, Phosphate high, ALP high
D) Calcium low, phosphate low, ALP high

A

D) Calcium low, phosphate low, ALP high

132
Q

A 29yo man presents with 4-week history of polyuria and extreme thirst. The urine is very dilute. The patient does not have any weight loss and maintains a good diet. No findings are found on urine dipstick. The most appropriate invevstigation is:

Serum osmolality
Fasting plasma glucose 
Urinary electrolytes 
MRI head 
Water deprivation test
A

Water deprivation test

133
Q

A 50yo Asian man is referred to the diabetes clinic after presenting with polyuria and polydipsia. His BMI = 30, BP = 137/88, Fasting plasma glucose = 7.7mmol/L (high). The most appropriate first-line treatment is:

Dietary advice and exercise
Sulphonylurea
Exenatide
Thiazolidinediones
Metformin
A

Dietary advice and exercise

Metformin = first line drug but not first line treatment

134
Q

A 6yo girl presents to accident and emergency with severe abdominal pain, nausea and vomiting. Patient has a sweet (fruity) odour from her breath and is breathing fast (tachypnoeic). The most likely diagnosis is:

Diabetic ketoacidosis
Hyperglycaemia hyperosmolar state 
Gastroenteritis (Infection of intestine) 
Pancreatitis
Addisonian crisis
A

Diabetic ketoacidosis

135
Q

A 57yo woman presents with dull grey-brown patches in her mouth and the palms of her hand which she has noticed in the last week. She has also noticed she gets very dizzy when rising from a seated position and is continually afraid of fainting. The most likely diagnosis is:

SIADH
Hyperthyroidism 
Hypothyroidsim 
Addison’s disease 
Diabetes insipidus
A

Addison’s disease

PIGMENTATION

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