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Phase 2a > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Epidemiology of type 1 DM

A

o Often starts before puberty, or <30 years
o Usually lean
o More common in Caucasian population

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2
Q

Epidemiology of type 2 DM

A

o Usually older patients, >30 years
o Usually overweight
o More common in South Asian population

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3
Q

Causes and risk factors for type 1 DM

A

o Autoimmune

o HLA DR3/4 affected in 90% (family history)

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4
Q

Causes and risk factors for type 2 DM

A

o Decreased insulin secretion and increased insulin resistance
o RFs: obesity, older, FH, South Asian ethnicity, HTN, hyperlipidaemia, alcohol excess
o Genetic susceptibility but not HLA link

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5
Q

Pathophysiology of type 1 DM

A

Autoimmune destruction of pancreatic beta cells in Islets of Langerhans, triggered by environmental antigens

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6
Q

Pathophysiology of type 2 DM

A

o Polygenic – environmental factors trigger
o Beta cell mass 50% of normal
o Low insulin secretion and peripheral insulin
resistance

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7
Q

Secondary causes of DM

A

o CF
o Chronic pancreatitis
o Acromegaly
o Cushing’s

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8
Q

Signs and symptoms of DM (hyperglycaemia)

A
  • Polyuria and polydipsia
  • Unexplained weight loss
  • Blurred vision
  • Genital thrush
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9
Q

Investigations for DM

A
  • Fasting glucose (>7mmol/L) or random plasma glucose (>11.1mmol/L)
  • HbA1c: >48mmol/mol
  • Oral GTT (glucose tolerance test)
  • C peptide goes down in type 1, persists in 2
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10
Q

Type 1 DM management

A

o Glycaemic control through diet and insulin (twice daily and with meals)
o Exercise encouraged

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11
Q

Type 2 DM management

A
  1. Lifestyle modification – diet, weight control, exercise, smoking cessation
  2. Monotherapy – 1st line standard release Metformin
  3. Dual therapy – Metformin + DPP4I (gliptins)/ glitazone/ sulphonylurea/ SGLTI
  4. If no change add insulin
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12
Q

Metformin mechanism

A

Increases insulin sensitivity and helps weight

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13
Q

Metformin SE’s and CI’s

A

SE’s: anorexia, D&V

CI’s: renal failure

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14
Q

Sulfonylurea mechanism

A

Opens channels in Beta cells so more insulin is produced

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15
Q

Sulfonylurea SE’s and CI’s

A

SE’s: hypoglycaemia and weight gain

CI’s: pregnancy and liver disease

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16
Q

DPP-4 receptors (gliptins) mechanism

A

Prevent breakdown of GLP-1, most effective if used early

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17
Q

Glitazone mechanism

A

Increases insulin sensitivity

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18
Q

Glitazone SE’s

A

Hypoglycaemia, fractures, fluid retention

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19
Q

Secondary prevention in DM

A

o Eye and foot screening
o BP checks and CV risk assessment – statins and BP lowering drugs if needed
o Kidney tests

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20
Q

Complications of DM

A
  • Diabetic nephropathy
  • Diabetic neuropathy
  • Diabetic retinopathy
  • Arterial disease
  • Diabetic ketoacidosis
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21
Q

Diabetic ketoacidosis pathophysiology

A

• Hallmark of type 1 DM
• Uncontrolled hyperglycaemia and catabolic state
• Body metabolites amino acids and triglycerides ->
ketones
• Renal hypoperfusion occurs due to osmotic diuresis
-> coma and circulatory failure -> death

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22
Q

Signs and symptoms of DKA

A 
o	Lethargy 
o	Polyuria and polydipsia 
o	Confusion 
o	Abdominal pain
o	Ketone smell in breath (fruity)
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23
Q

Investigations/diagnosis of DKA

A 
o	Acidaemia (pH <7.3)
o	Hyperglycaemia ( >11.0mmol/L) 
o	Ketonaemia or ketouria (dipstick)
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24
Q

Managament of DKA

A

o Fluid balance and rehydration
o Actrapid IV insulin
o Potassium replacement

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25
Q

Causes of hypothyroidism

A

o Primary hypothyroidism:
 Primary atrophic hypothyroidism
 Hashimoto’s thyroiditis (autoimmune)
 Post-thyroidectomy/radioiodine treatment
 Drug induced e.g. lithium
o Secondary hypothyroidism - hypopituitarism

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26
Q

Pathophysiology of primary hypothyroidism

A

Aggressive destruction of thyroid cells by various immune processes. Antibodies bind and block TSH receptors -> inadequate thyroid hormone production and secretion

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27
Q

Pathophysiology of secondary hypothyroidism

A

Reduced release or production of TSH -> reduced T3 and T4 release

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28
Q

Symptoms of hypothyroidism

A 
o	Hoarse voice
o	Constipation
o	Cold intolerance 
o	Weight gain 
o	Menorrhagia 
o	Weakness and tiredness 
o	Dementia
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29
Q

Signs of hypothyroidism

A 
o	Bradycardia
o	Reflexes relax slowly 
o	Dry thin hair/skin 
o	Yawning/drowsiness/coma
o	Cold hands 
o	Round, puffy face
o	Menorrhagia
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30
Q

Investigations for hypothyroidism

A

o Primary:
- Increased TSH and decreased T4
- TPO antibodies in Hashimoto’s
o Secondary - decreased TSH and T4

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31
Q

Management of hypothyroidism

A

o Levothyroxine (T4 replacement) – smaller does if
elderly as risk of angina or MI
o Primary – resect obstructive goitre
o Secondary – treat underlying cause

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32
Q

Conditions associated with hypothyroidism

A 
o   Autoimmune (T1DM, Addison’s, pernicious anaemia)
o   Inherited (Turner’s Down’s, CF)
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33
Q

Definition of hypothyroidism (thyrotoxicosis)

A

Lack of thyroid hormone

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34
Q

Definition of hyperthyroidism

A

Excess thyroid hormone, usually from gland hyperfunction

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35
Q

Causes of hyperthyroidism

A 
o   Grave’s disease 
o   Toxic multinodular goitre - elderly, iodine defficient
o   Toxic adenoma 
o   Ectopic thyroid tissue
o   Exogenous (iodine/T4 excess)
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36
Q

Symptoms of hyperthyroidism

A

o Palpitations
o Sweats, heat intolerance
o Weight loss, appetite increase
o Diarrhoea

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37
Q

Signs of hyperthyroidism

A 
o	Palmar erythema, moist, warm skin
o	Tachycardia
o	Thin hair
o	Goitre
o	Hyperreflexia
o	Amenhorrea
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38
Q

Investigations for hyperthyroidism

A 
o   Decreased TSH, increased T3/4
o   FBC (normocytic anaemia)
o   Raised ESR, Ca2+ and LFT
o   Autoantibodies
o   Visual fields, acuity, movements (thyroid eye)
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39
Q

Management of hyperthyroidism

A

o Beta-blockers (propranolol)
o Anti-thyroid medication (carbimazole)
o Radioiodine, thyroidectomy – SE: hypothyroidism,
CI: pregnancy

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40
Q

Carbimazole SE

A

Agranulocytosis

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41
Q

Graves’s disease pathophysiology

A

Thyroid stimulating Ig’s bind to TSH receptors -> stimulate T4 and T3 -> T4 receptors in pituitary gland activated by excess hormone -> reduce TSH release

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42
Q

Grave’s disease signs and symptoms

A 
o	Tachycardia
o	Tremor
o	Diffuse palpable goitre with audible bruit
o	Eye problems
o	Swelling of hands and fingers)
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43
Q

Investigations for Grave’s Disease

A

Bloods - high T4, low TSH

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44
Q

Definition of Cushing’s Syndrome

A

Chronic cortisol excess

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45
Q

ACTH dependant causes of Cushing’s Syndrome

A

o Cushing’s disease – ACTH-secreting pituitary adenoma

o Ectopic ACTH production – tumour

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46
Q

ACTH independent causes of Cushing’s syndrome (negative feedback causes low ACTH)

A

o Iatrogenic – steroids (common)
o Adrenal adenoma/cancer
o Adrenal nodular hyperplasia

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47
Q

What can cause pseudo-Cushing’s

A

Excessive alcohol

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48
Q

Symptoms of Cushing’s syndrome

A
  • Weight gain
  • Mood change
  • Proximal weakness
  • Gonadal dysfunction
  • Recurrent Achilles injury
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49
Q

Signs of Cushing’s syndrome

A
  • Fat distribution (central obesity, buffalo hump)
  • Skin changes (bruises, stretch marks)
  • Osteoporosis
  • Muscle atrophy
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50
Q

Investigations for Cushing’s syndrome

A

o Overnight dexamethasone supression test - no
suppression in Cushing’s syndrome
o Plasma and urine ACTH

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51
Q

Management of Cushing’s syndrome

A

• Iatrogenic – stop steroids
• Cushing’s disease/adenoma/carcinoma – trans-
sphenoid surgery
• Ectopic ACTH – surgery + cortisol-inhibiting drugs

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52
Q

Complications of Cushing’s disease

A
  • HTN
  • Obesity
  • Death
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53
Q

Acromegaly definition

A

Overall growth of all organ systems due to excess growth hormone

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54
Q

Causes of acromegaly

A

Pituitary tumour or hyperplasia

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55
Q

Pathophysiology of acromegaly

A
  • GH stimulates bone and soft tissue growth through increased secretion of insulin-like growth factor-1
  • If occurs before fusion of epiphyseal plates (children) -> gigantism
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56
Q

Symptoms of acromegaly

A
  • Acroparaesthesia
  • Amenorrhea and decreased libido
  • Headache
  • Excessive sweating
  • Snoring
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57
Q

Signs of acromegaly

A
  • Growth of hands, jaw and feet
  • Coarsening face, wide nose
  • Macroglossia (big tongue)
  • Puffy lips, skin and eyelids
  • Obstructive sleep apnoea
  • Carpal tunnel
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58
Q

Investigations and diagnosis of acromegaly

A
  • Raised glucose, calcium and phosphate
  • Raised IGF-I and oral GTT (gold standard)
  • MRI of pituitary fossa (pituitary adenoma)
  • Look at old photos
  • Visual acuity
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59
Q

Management of acromegaly

A
  1. Trans-sphenoidal resection surgery
  2. Radiotherapy or actreotide
  3. GH receptor antagonists (pegvisomant)
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60
Q

Complications of acromegaly

A
  • HTN and heart disease
  • Sleep apnoea
  • Arthritis
  • Type 2 diabetes
  • Cerebrovascular events and headaches
  • Blindness
61
Q

Conn’s syndrome definition

A

Excess production of aldosterone independent of RASS

62
Q

Conn’s syndrome pathophysiology

A

• Increased aldosterone -> increased reabsorption of
water and sodium + increased excretion of potassium
• Aldosterone also inhibits renin release

63
Q

Signs and symptoms of Conn’s syndrome

A

• Often asymptomatic or signs of hypokalaemia
(weakness, cramps, polyuria, polydipsia)
• Sometimes raised BP

64
Q

Causes of Conn’s syndrome

A
  • Conn’s disease – solitary aldosterone producing adenoma

* Bilateral adrenal hyperplasia

65
Q

Investigations for Conn’s syndrome

A

• Bloods – low renin, high aldosterone, U+E (high
sodium, low potassium)
• Don’t rely on low K+
• MRI scan

66
Q

Management of Conn’s disease

A

o Laparoscopic adrenalectomy

o Spironolactone pre-op

67
Q

Management of Conn’s syndrome caused by hyperplasia

A

Spironolactone (aldosterone antagonist)

68
Q

Definition of Addison’s disease

A

Adrenocorticoid insufficiency due to destruction of the adrenal cortex

69
Q

Pathophysiology of hyperpigmentation in Addison’s

A

destruction of adrenal cortex -> less cortical products -> excess ACTH stimulates melanocytes -> hyperpigmentation

70
Q

Definition of secondary adrenal insufficiency

A

Lack of ACTH (and therefore cortisol)

71
Q

Pathophysiology of secondary adrenal insufficiency

A

Inadequate pituitary of hypothalamic stimulation of the adrenal glands

72
Q

Causes of Addison’s disease

A

o Autoimmune
o TB
o Lymphoma
o Opportunistic infections in HIV

73
Q

Causes of secondary adrenal insufficiency

A

o Iatrogenic – steroids

o Hypothalamic-pituitary disease

74
Q

Symptoms of adrenal insufficiency

A
  • Nausea/vomiting, abdominal pain, constipation, weight loss
  • Tanned skin
  • Weakness, confusion, syncope
75
Q

Signs of adrenal insufficiency

A
  • Hyperpigmentation – Addison’s only
  • Postural hypotension
  • Dehydration, general wasting, alopecia
76
Q

Investigations for adrenal insufficiency

A

o Bloods - low Na+ and high K+ (Addison’s), low
glucose
o ACTH stimulation test:
- give synthetic ACTH
- measure cortisol and aldosterone produced
o ACTH raised in primary, low in secondary

77
Q

Management of adrenal insufficiency

A

• Replace steroids with hydrocortisone
• Fludrocortisone to replace mineralocorticoids –
Addison’s only

78
Q

SE of hydrocortisone

A

Insomnia if taken late

79
Q

Causes of hyperkalaemia

A 
Drugs - ACE-i, K+ sparing diuretics
Renal failure
Endocrine - Addison's
Artefacts
DKA
80
Q

Pathophysiology of hyperkalaemia

A

Renal impairment can lead to retention of potassium in the nephron, can also occur with K+ sparing diuretic

81
Q

Signs and symptoms of hyperkalaemia

A

o Fast irregular pulse, palpitations
o Chest pain
o Weakness, light-headedness

82
Q

Investigations for hyperkalaemia

A 
o	ECG:
       	Tall T waves
       	Wide QRS complex 
       	Ventricular fibrillation 
o	Bloods - Potassium >5.5 (consider artefact)
83
Q

Management of hyperkalaemia

A

o IV insulin with glucose
o salbutamol (CI tachycardic)
o review meds
o dialysis if severe

84
Q

Complications of hyperkalaemia

A

MI -> death

85
Q

Causes of hypokalaemia

A

o Diuretics
o Hyperaldosteronism/Conn’s
o D&V
o Cushing’s

86
Q

Pathophysiology of hypokalaemia

A

o Excessive loss of potassium in the kidneys in response to aldosterone or diuretics
o GI fluid loss -> less chloride -> ↑aldosterone -> ↓ potassium reabsorption

87
Q

Signs and symptoms of hypokalaemia

A

o Muscle weakness, hyporeflexia
o Palpitations, light-headedness (arrythmias)
o Constipation

88
Q

Investigations for hypokalaemia

A 
o	ECG:
       	Small T-waves 
       	Prominent U-waves (after T wave)
       	Long PR interval 
       	Depressed ST segments 
o	Bloods – low potassium (<3.5)
89
Q

Management of hypokalaemia

A 
o	Mild:
       	Oral K+ supplement 
       	Change thiazide diuretic to K+ sparing 
o	Severe - IV potassium cautiously 
o	Treat underlying cause
90
Q

Complications of hypokalaemia

A

Cardiac arrhythmia and sudden death

91
Q

Definition of SIADH

A

Continued ADH secretion despite normal plasma volume

92
Q

Pathophysiology of SIADH

A

Ectopic production increases ADH above mechanisms of control -> retention of water and hyponatraemia

93
Q

Causes of SIADH

A
  • Neurological - CNS disorders, trauma, meningitis
  • Chest disease – TB, pneumonia
  • Drugs – opiates, SSRI, anti-epileptics
94
Q

Signs and symptoms of SIADH

A
  • Nausea
  • Headache
  • Confusion
  • Fits and coma (hyponatraemia)
95
Q

Investigations for SIADH

A

• Bloods:

   - Dilutional hyponatraemia 
   - Low plasma osmolality
96
Q

Management of SIADH

A
  • Treat cause and restrict fluid
  • Vasopressin receptor antagonist (VRA)
  • Demeclocycline (ADH inhibitor)
97
Q

SE of demeclocycline

A

DI

98
Q

Physiology of central DI

A

Reduced ADH secretion from posterior pituitary

99
Q

Physiology of nephrogenic DI

A

Impaired response of kidney to ADH

100
Q

Causes of central DI

A 
o	Idiopathic 
o	Congenital
o	Tumour 
o	Neurosurgery 
o	Autoimmune
101
Q

Causes of nephrogenic DI

A

o Inherited
o Metabolic – hypokalaemia, hypercalcaemia
o Drugs – lithium
o Chronic renal disease

102
Q

Symptoms of DI

A
  • Polyuria
  • Polydipsia
  • Dehydration
  • Symptoms of hypernatraemia
103
Q

Investigations for DI

A 
•   Water deprivation test:
        - monitor urine output
        - high and dilute in DI
        - desmopressin response = central DI
•	MRI of hypothalamus
104
Q

Management of DI

A 
•   Central - desmopressin 
•   Nephrogenic:
       o   treat cause
       o   thiazides
       o   NSAIDs
105
Q

Causes of hypocalcaemia

A

o Vitamin D deficiency (actual or functional)
o Hypoalbuminaemia (artefact of)
o Hypoparathyroidism
o CKD

106
Q

Pathophysiology of hypocalcaemia caused by CKD

A

CKD -> increased serum phosphate -> microprecipitation of calcium phosphate in tissues -> low serum calcium

107
Q

Symptoms of hypocalcaemia

A

Increased excitability of muscles and nerves (numbness around mouth/extremities, spasms, cramps, tetany)

108
Q

Signs of hypocalcaemia

A

o Trousseau’s (facial nerve) and Chvostek’s (hand) signs

109
Q

Investigations for hypocalcaemia

A

o ECG – prolonged QT
o eGFR to check for CKD
o PTH high, vitamin D usually low (CKD)

110
Q

Management of hypocalcaemia

A

o Mild – calcium PO
o Acute/severe – IV calcium gluconate
o Persistent – Vit D supplement if deficient
o If CKD or hypoparathyroidism – alfacalcidol

111
Q

Causes of hypercalcaemia

A

o Malignancy

o Primary hyperparathyroidism

112
Q

Symptoms of hypercalcaemia

A

o Bones – pain
o Stones – kidney stones
o Groans – abdominal pain, nausea, constipation
o Moans – depression

113
Q

Signs of hypercalcaemia

A

o Polydipsia

o Polyuria

114
Q

Investigations for hypercalcaemia

A

o Bloods – raised calcium, raised PTH is hyperparathyroidism
o ECG – shortened QT

115
Q

Management of hypercalcaemia

A

o IV saline - for dehydration
o Bisphosphates - prevent bone resorption
o Loop diuretic - return calcium to normal
o Treat underlying cause

116
Q

Definition of hypoparathyroidism

A

Low levels of PTH

117
Q

Causes of hypoparathyroidism

A

o Parathyroidectomy
o Congenital – Di George syndrome
o Autoimmune
o Hypomagnesaemia

118
Q

Why does hypoparathyroidism cause hypocalcaemia and hyperphosphataemia?

A

o PTH stimulates activation of vit D -> intestinal calcium absorption, renal calcium absorption, calcium release from bone, inhibits phosphate reabsorption
o Low PTH levels -> hypocalcaemia + hyperphosphataemia

119
Q

Symptoms of hypoparathyroidism

A

o Increased excitability of muscles and nerves – spasms, paraesthesia around mouth/extremities, cramps, tetany, increased reflexes

120
Q

Signs of hypoparathyroidism

A

o Chvostek – corner of mouth twitches when facial nerve tapped over parotid
o Trousseau – when BP cuff inflated hand spasms

121
Q

Investigations for hypoparathyroidism

A

o Bloods – calcium and PTH low, phosphate high

o ECG – prolonged QT

122
Q

Management of hypoparathyroidism

A

o IV calcium – acute
o Vit D analogue – supplement if deficient
o Alfacalcidol if persistent

123
Q

Definition of hyperparathyroidism

A

High levels of PTH

124
Q

Causes of primary hyperparathyroidism

A

Solitary adenoma or hyperplasia

125
Q

Signs and symptoms of hyperparathyroidism

A

o Often asymptomatic

o Bones, stones, groans and moans

126
Q

Investigations for primary hyperparathyroidism

A

Bloods: hypercalcaemia, low phosphate, high PTH, phosphatase high

127
Q

Mangement of primary hyperparathyroidism

A

Surgical removal of adenoma

128
Q

Complications of parathyroid surgery

A

o Hypoparathyroidism

o Recurrent laryngeal nerve damage -> hoarse voice

129
Q

Causes of secondary hyperparathyroidism

A

o CKD
o Low vit D
o Malabsorption
o Any condition with hypocalcaemia

130
Q

Pathology of secondary hyperparathyroidism

A

Parathyroid gland becomes hyperplastic in response to chronic hypocalcaemia

131
Q

Investigations for secondary hyperparathyroidism

A

Bloods: low calcium, high PTH, high phosphate (renal disease)

132
Q

Management of secondary hyperparathyroidism

A

Correct causes and calcium correction

133
Q

Pathology of tertiary hyperparathyroidism

A

Glands become autonomous so produce excess PTH even after calcium correction

134
Q

Cause of tertiary hyperparathyroidism

A

CKD

135
Q

Investigations for tertiary hyperparathyroidism

A

Bloods: high PTH, high calcium, high phosphate (renal failure)

136
Q

Management of tertiary hyperparathyroidism

A

o Calcium mimetic (cinacalcet)

o Parathyroidectomy

137
Q

Causes of hyperprolactinaemia

A

o Prolactinoma
o Compression of the pituitary stalk, reducing local dopamine levels
o Dopamine antagonists

138
Q

Symptoms of hyperprolactinaemia

A

o Menstrual irregularity/amenorrhoea/infertility
o Galactorrhoea
o Low libido
o Low testosterone in men – decreased facial hair, erectile dysfunction
o Pressure effects from tumour

139
Q

Investigations for hyperprolactinaemia

A

o Test prolactin – CI antidopaminergic drugs

o Do pregnancy test

140
Q

Management of hyperprolactinaemia

A

o Dopamine agonists (first line) – cabergoline

o Trans-sphenoidal pituitary resection

141
Q

Definition of pheochromocytoma

A

Catecholamine (adrenaline) secreting tumour

142
Q

Signs and symptoms of pheochromocytoma

A

o Headaches
o Sweating
o Tremor
o Tachycardia

143
Q

Definition of carcinoid tumour

A

Serotonin secreting tumour (usually in gut, sometimes lungs)

144
Q

Causes of carcinoid tumour

A

MEN1 and MEN2 increase incidence

145
Q

Pathology of carcinoid syndrome

A

o Derived from enterochromaffin cells
o Secrete serotonin and Kallikrein -> increased
bradykinin if liver mets

146
Q

Signs and symptoms of carcinoid syndrome

A

o Bronchospasm (wheezing)
o Diarrhoea
o Skin flushing and
o Right sided heart lesions

147
Q

Investigations for carcinoid tumours

A

o Urine: high 5-hydroxyindoleacetic acid (serotonin
breakdown product)
o Liver US
o Octreoscan

148
Q

Management of carcinoid tumours

A

o Somatostatin analogue (octreotide)

o Surgical resection

149
Q

What is diabetes insipidus?

A

Secretion or response to ADH is impaired

Phase 2a (9 decks)

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