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4th Year Exam > Endocrinology ILOs > Flashcards

Endocrinology ILOs Flashcards

1
Q

Define T1DM and give its Aetiology

A

Metabolic disorder characterised by hyperglycaemia due to absolute insulin deficiency

Destruction of pancreatic beta cells by immune-mediated mechanism

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2
Q

Give 2 symptoms and 2 risks of T1DM

A

Polyuria + polydipsia

Young age + HLA DR3 and HLADR4 genes

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3
Q

Outline the pathophysiology of T1DM

A
  • Subclinical until 90% beta cells destroyed

- Long-term hyperglycaemia = complications

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4
Q

Give 4 investigations for T1DM

A

Fasting blood glucose >/= 7.0mmol/L

Random plasma glucose >/= 11.1mmol/L

Ketone testing +/- bicarbonate

Pancreatic auto-antibodies

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5
Q

Give 3 treatment options for T1DM

A

Basal bolus insulin
BD mix regime
CHO counting

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6
Q

Define T2DM

A

Deficits in insulin secretion and action leading to abnormal glucose metabolism and related metabolic derangement

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7
Q

Give 3 predisposing factors for T2DM

A

Ageing
Physical inactivity
Obesity

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8
Q

Give 2 symptoms and 2 risks of T2DM

A

S: Frequent infection + fatigue

R: Obesity + Black/Hispanic

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9
Q

Outline the pathophysiology of T2DM

A
  • More free fatty acids interfere with downstream insulin signalling
  • insulin gets to receptor but glucose cannot be taken into muscles
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10
Q

Give the diagnostic criteria for T2DM

A

2 of:

  • Fasting plasma glucose >6.9mmol/L
  • HbA1c 48 or greater
  • Random plasma glucose >11.1
  • Plus symptoms of hyperglycaemia
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11
Q

What are the 3 microvascular complications of diabetes?

A
  • Neuropathy
  • Nephropathy
  • Retinopathy
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12
Q

Give 2 symptoms and 2 risks of diabetic neuropathy

A

S: Pain + loss of sensation

R: poorly controlled hyperglycaemia + reduced ankle reflexes

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13
Q

Give 2 treatments for diabetic neuropathy

A

Glycaemic control

Pregabalin

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14
Q

What pathology occurs in diabetic nephropathy?

A

Alteration in glomerular BM permeability and increase in intraglomerular pressure

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15
Q

What 2 things may be seen on blood tests in diabetic nephropathy?

A

Raised albumin

Reduced eGFR

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16
Q

Give 3 treatment options in diabetic nephropathy

A

Diabetic control
ACEI/ARB
Smoking cessation

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17
Q

What pathological processes occur in diabetic retinopathy?

A

Loss of retinal supporting cells, BM thickening and blood flow changes

Ultimately retinal detachment and vision loss

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18
Q

Give one treatment of diabetic retinopathy

A

Intravitreal Anti-VEGF therapy

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19
Q

Give 3 macrovascular complications of diabetes and how they occur

A

MI, stroke, PAD

Hyperglycaemic causes increased vascular smooth muscle cells and decreased blood capacity

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20
Q

Define DKA

A

Mostly occurring in T1DM (can be 1st presentation), medical emergency in which there is absolute insulin deficiency

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21
Q

What causes DKA?

A

Trigger

Insulin deficiency

Hyperglycaemia and ketone
bodies formed by free fatty acids from the liver

Acidosis

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22
Q

Give 3 symptoms of DKA

A

Polydipsia
Acetone breath
Kussmaul breathing

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23
Q

What happens to K+ during DKA?

A

Insulin normally activates Na/K ATPase but this is reduced = K moving into bloodstream

Excess K then excreted by kidneys

Serum K looks normal but body is actually deplete

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24
Q

Give the 3 parameters used to diagnose DKA

A
  • Diabetes (blood glucose >11 or known diabetes)
  • Acidosis (pH <7.3 or H+>45 or Bicarb <15)
  • Ketonaemia (blood ketone >3 or urine ketone ++)
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25
Q

Give 3 triggers of DKA

A

Infection
Alcohol
MI

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26
Q

Give the 4 main management options in DKA

A

IV Fluid
IV Insulin
IV Dextrose
Correct hypokalaemia

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27
Q

Give 3 complications of DKA

A

Death
VTE
Cerebral oedema

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28
Q

Define HHS

A

Profound hyperglycaemia (glucose >30mmol/L), hyperosmolality and volume depletion in absence of significant ketoacidosis, commonly in T2DM

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29
Q

Give 3 causes of HHS

A

Infection
Acute illness e.g. stroke
Drugs e.g. beta blockers

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30
Q

What significant electrolyte abnormality occurs in HHS

A

Hypernatremia

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31
Q

Outline pathology of HHS and give 2 risks

A

Metabolic derangement due to insulin deficiency and increased counterregulatory hormones, residual insulin is present

Age >65
Infection

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32
Q

Give 3 investigations of HHS

A

Blood glucose high

Blood ketones negative or low

VBG = mild acidosis

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33
Q

Give 3 treatment options for HHS

A

IV fluid

Fixed rate insulin infusion

Potassium replacement

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34
Q

Give 2 treatments of mild hypoglycaemia

A

15-20g quick acting carbs

Glucotabs

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35
Q

Give 2 treatments of moderate hypoglycaemia

A

Swallow glucogel squeezed between teeth and gums

Glucagon 1mg IM

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36
Q

Give 2 treatments of severe hypoglycaemia

A

100ml 20% glucose IV

150ml 10% glucose IV

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37
Q

Define gestational diabetes and give the cause

A

Glucose intolerance in pregnancy, usually 24-28 weeks

Resistance to insulin action normally increases during pregnancy but some women’s beta cells cannot compensate

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38
Q

Give 3 causes of secondary diabetes

A

CF
Cancer
Pancreatectomy

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39
Q

Why is there a higher risk of hypoglycaemia in secondary diabetes?

A

Loss of alpha cells producing glucagon as well as beta cells

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40
Q

What is monogenic diabetes?

A

Monogenic (change in single gene), autosomal dominant occurring age <25 with negative pancreatic autoantibodies

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41
Q

Define hypothyroidism and give 2 causes

A

Underproduction of T4 and T3 (active form) mainly due to primary hypothyroidism

  • Hashimoto’s thyroiditis
  • Thyroidectomy
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42
Q

Give 4 symptoms of hypothyroidism

A
  • Cold sensitivity
  • Menorrhagia
  • Weight gain
  • Dry skin
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43
Q

Give 2 risk factors for hypothyroidism

A
  • Iodine deficiency

- Female

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44
Q

What 3 things may be seen on blood tests in hypothyroidism?

A

High TSH
Low T3/T4
+ thyroid antibody

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45
Q

What is the main treatment for hypothyroidism?

A

Levothyroxine

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46
Q

Give 3 causes of hyperthyroidism

A
  • Grave’s disease
  • Thyroid nodules
  • Drugs e.g. Amiodarone
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47
Q

Give 4 symptoms of hyperthyroidism

A
  • Sweating
  • Oligomenorrhoea
  • Tremor
  • Diffuse goitre
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48
Q

Give 3 investigations for Grave’s disease

A

Low TSH
High T3/T4
Diffuse uptake on isotope scan

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49
Q

Give 3 treatments for Grave’s disease

A

Carbimazole
Beta blockers
Radioactive iodine

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50
Q

What is a diffuse goitre vs a nodular goitre?

A

Diffuse: swollen and smooth

Nodular: Nodular and irregular

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51
Q

Define toxic multinodular goitre

A

Multiple functioning nodules resulting in hyperthyroidism, function independently of thyroid and are almost always benign

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52
Q

Give 3 investigations of a goitre

A

Neck exam
TSH
Thyroid US

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53
Q

Give 4 types of thyroid cancer

A

Follicular
Papillary
Anaplastic
Medullary

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54
Q

Give 3 risks for thyroid cancer

A

Head and neck irradiation
Female
30-40 years

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55
Q

Give 2 treatments for thyroid cancer

A

Surgery

Radioiodine

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56
Q

Give 3 features of thyroid eye disease

A

Lid lag
Exophthalmos
Proptosis

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57
Q

Define hyperparathyroidism and give 2 causes

A

Autonomous overproduction of PTH resulting in hypercalcaemia

  • Parathyroid adenoma
  • Inherited e.g. MEN1
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58
Q

Give 2 symptoms and 2 risks of hyperparathyroidism

A

Bone pain and poor sleep

Female, age >50

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59
Q

Outline the pathophysiology of hyperparathyroidism

A

Normally high serum Ca would supress PTH but this does not happen and excessive PTH = over-stimulation of bone resorption with cortical bone more effected

60
Q

Give 3 blood tests used in the investigation of hyperparathyroidism

A 
Serum Ca (high)
Vitamin D (low)
ALP (raised)
61
Q

Give 3 treatments for hyperparathyroidism

A

Parathyroidectomy
Vitamin D supplementation
Bisphosphonate

62
Q

What is secondary hyperparathyroidism?

A

Any condition resulting in hypocalcaemia will elevate PTH levels

63
Q

Define primary hypoparathyroidism

A

Relative or absolute deficiency of plasma PTH synthesis and secretion (low serum Ca, high serum phosphate)

64
Q

Give 2 causes of hypoparathyroidism

A

Post surgical

Genetic e.g. DiGeorge syndrome

65
Q

Give 3 symptoms of hypoparathyroidism

A

Dry hair
Poor memory
Diarrhoea

66
Q

How does hypoparathyroidism occur?

A

Hypocalcaemia results from deficient actions of PTH to reabsorb calcium from urine

67
Q

Give 2 investigations of hypoparathyroidism

A 
Serum Ca (low) - indicates Primary 
ECG (prolonged QT)
68
Q

Define secondary hypoparathyroidism

A

Physiological state in which PTH levels are low due to primary process that causes hypercalcaemia

69
Q

Give 2 treatments for hypoparathyroidism

A

Calcium + calcitriol

Diuretic

70
Q

Define Addison’s disease

A

Primary adrenal insufficiency causing decreased adrenal hormones of autoimmune cause

71
Q

Give 3 symptoms of Addison’s

A

Fatigue
Anorexia
Hyperpigmentation

72
Q

What two electrolyte abnormalities may be seen in Addison’s?

A

Hyponatraemia

Hyperkalaemia

73
Q

What test is commonly used in Addison’s and what happens during it?

A

Short Synthacthen test: plasma cortisol measured before and 30 mins after IV ACTH

74
Q

What is the treatment of Addison’s disease?

A

Glucocorticoid plus mineralocorticoids

Androgen replacement

75
Q

Define hypopituitarism and give 2 causes

A

Partial or complete deficiency of one or more pituitary hormones

  • Pituitary adenoma
  • Inflammatory lesion
76
Q

Give 3 symptoms of hypopituitarism

A

Headache
Failure to thrive
Infertility

77
Q

Give 4 tests used to investigate hypopituitarism

A

Na (low in ACTH/TSH deficiency, high in diabetes insipidus)

8am cortisol and ACTH (low)

TFTs

FSH and LH level

78
Q

Give 2 treatments for hypopituitarism

A

Tx correctable causes

Hormone replacement (start with cortisol if all axes affected)

79
Q

Define Cushing’s syndrome

A

Clinical manifestation of hypercortisolism from any cause

80
Q

Give 1 ACTH dependent and 1 ACTH independent cause of Cushing’s

A

Dependent: Pituitary adenoma

Independent: Adrenal adenoma

81
Q

Give 4 symptoms of Cushing’s

A
  • Buffalo hump
  • Thin skin
  • Striae
  • Moon face
82
Q

Give 4 investigations for Cushing’s

A
  • 24hr urinary free cortisol
  • Urine cortisol:creat ratio
  • Dexamethasone supression test (normal = undetectable)
  • Late night salivary cortisol (normal = undetectable)
83
Q

Give 2 treatment options for Cushing’s

A
  • Reduce/stop steriods

- Tumour resection

84
Q

Define acromegaly and give it’s main cause

A

Chronic, progressive disease caused by excessive secretion of GH

Pituitary somatotropin adenoma

85
Q

Give 3 features of acromegaly

A

Coarse facial features
Enlarged tongue
Visual field loss

86
Q

Outline the pathology of acromegaly

A

Tumour chronically secretes excessive GH, stimulating insulin-like growth factor 1 producing = majority of symptoms

87
Q

Give 3 investigations for acromegaly

A

Glucose tolerance test (glucose load fails to supress GH)

IGF-1 level elevated

Pituitary MRI – macroadenoma >1cm, invades surrounding structures

88
Q

Give 2 treatments for acromegaly

A

Transsphenoidal surgery (non-curative)

Pituitary radiotherapy

89
Q

Give 2 causes and 2 symptoms of hyperprolactinaemia

A

Causes:

  • Prolactinoma
  • Traumatic sectioning of pituitary stalk

Symptoms:

  • Vaginal dryness
  • Irregular periods
90
Q

Give 2 investigations of hyperprolactinaemia

A

Prolactin level

Pituitary MRI

91
Q

Define PCOS and give 3 symptoms

A

Hyper-andorgenism and hyper-androgenaemia of unknown cause

  • Oligo/anovulation
  • Hirsutism
  • Infertility
92
Q

Give the 3 main pathological mechanisms involved in PCOS

A

Gonadotrophins (increased LH, decreased FSH)

Androgens (increased androgens and decreased SHBG)

Insulin (increased resistance)

93
Q

Give 3 tests to investigate PCOS

A
  • Serum 17-hydroxyprogesterone
  • TFTs
  • Serum prolactin
94
Q

Give 3 PCOS treatments

A

Weight loss
Metformin
Clomifene (anti-oestrogen to inhibit -ve feedback and increase FSH)

95
Q

Define primary gonadal failure in men and give 2 causes

A

Clinical syndrome that comprises symptoms and/or signs, along with biochemical evidence of testosterone deficiency

  • Klinefelter’s
  • Cryptorchidism
96
Q

Give 2 symptoms of primary gonadal failure in children and adults (men)

A

C: Slow growth + lack of secondary sexual characteristics

A: poor libido + depression

97
Q

Outline the pathophysiology of primary gonadal failure in males

A

Injury to Leydig cells results in decreased testosterone production, while seminiferous tubule involvement results in decreased or absent spermatogenesis

98
Q

Give 2 investigations and 2 treatments for primary gonadal failure in males

A

Testosterone level and semen analysis (1-3 days after ejaculation)

Androgen replacement + fertility Tx

99
Q

Define primary gonadal failure in females and give 2 causes

A

Cessation of menses for more than 1 year before 40 years of age secondary to loss of ovarian function

  • AI disease
  • Genetic
100
Q

Give 3 symptoms of primary gonadal failure in females

A

Hot flushes
Sleep disturbance
Vaginal dryness

101
Q

Give 2 tests and 2 treatments of primary gonadal failure in females

A
  • Serum FSH/LH + Serum estradiol

- Combined hormone replacement + vaginal oestrogen

102
Q

Define Klinefelter’s syndrome and give 2 symptoms

A

Commonest genetic cause of hypogonadism in men, caused by XXY sex chromosomes clinically manifesting at puberty

Delayed puberty
Azospermia

103
Q

Give 2 management options for Klinefelter’s syndrome

A

Androgen replacement

Fertility support

104
Q

Define phaeochromocytoma and give 2 symptoms

A

Catecholamine producing tumour of chromaffin cells of adrenal medulla

  • Headache
  • Palpitations
105
Q

Give 2 tests and 2 management options for pheochromocytoma

A

24hr urine catecholamines + plasma catecholamines

Alpha blocker then beta blocker

106
Q

Define primary hyperaldosteronism and give 2 symptoms

A

Aldosterone production exceeds body’s need, commonest secondary cause of HTN

HTN + polyuria

107
Q

Give 2 tests and 2 treatments for primary hyperaldosteronism

A
  • Aldosterone-renin-ratio
  • Saline suppression test

Tx:

  • Unilateral adrenalectomy
  • MR antagonists
108
Q

What BMI defines obesity?

109
Q

Give 2 causes and 2 risks for obesity

A

A: genetic + behavioural

R: hypothyroidism + hypercortisolism

110
Q

Give 3 pathological mechanisms involved in obesity

A

Appetite

Leptin (secreted by adipose when substrate is plentiful, obese people in state of leptin resistance)

Hypothalamus (appetite regulation)

111
Q

Give 4 management options for obesity

A
  • Diet
  • Exercise
  • Orlistat (inhibits lipases)
  • Bariatric surgery
112
Q

Define hyperkalaemia and give 2 cause

A

Plasma K+>5.5mmol/l

  • AKI
  • CKD
113
Q

Give 1 symptom and 1 sign of hyperkalaemia

A

Weakness

Depressed/absent tendon reflexes

114
Q

Outline why the kidneys are commonly implicated in hyperkalaemia

A

Kidneys responsible for 90% K excretion via GI tract so renal impairment is one of most common causes

115
Q

Give 3 ECG changes seen in hyperkalaemia

A

Tall tented T waves
Wide QRS
Prolonged PR

116
Q

Give 4 treatments for hyperkalaemia

A
  • Calcium gluconate IV (10mls 10% in 10 mins)
  • Insulin-glucose infusion
  • Salbutamol
  • Calcium Resonium
117
Q

Define hypokalaemia and give 2 causes

A

Plasma K+ <3.5mmoll/L

  • GI losses
  • Diabetes insipidus
118
Q

Give 2 symptoms of hypokalaemia

A

Weakness

Muscle cramps

119
Q

Give 2 ECG changes seen in hypokalaemia

A

U waves

T wave flattening

120
Q

Give 2 medical management options for hypokalaemia

A

Oral K+Cl- (Sando-K)

IV Potassium

121
Q

Define hypernatraemia and give 2 causes

A

Serum sodium >145mmol/L

  • Severe diarrhoea
  • Dehydration
122
Q

Outline the pathology of hypernatraemia

A

Represents deficit of water relative to sodium, always associated with serum hyperosmolality

123
Q

What is the common treatment of hypernatraemia?

A

Oral/IV fluid

124
Q

Define hyponatraemia and give its three main, broad causes

A

Serum Na+ <135mmol/l

  • Hypovolaemia
  • Euvolaemia
  • Hypervolaemia
125
Q

Outline the pathology of hypovolaemia

A

Sodium falls due to excess water in the body due to retention and/or water intake relative to sodium

126
Q

Give one treatment for Hypovolaemia hyponatraemia and one for eurovolaemic/normovolaemic

A

Hypo: NaCl 0.9% IV

Euvo/Normo: Fluid restrict

127
Q

Define hypercalcaemia and give 2 causes

A

Serum Ca > 2.6mmol/L

  • Hyperparathyroidism
  • Myeloma
128
Q

How is hypercalcaemia usually managed?

A

IV saline 0.9% at varying rate depending on severity

129
Q

Define hypocalcaemia and give 2 causes

A

Serum Ca <2.2mmol/l

  • Hypoparathyroidism
  • Hypomagnesaemia
130
Q

Give 2 symptoms of low calcium

A

Tetany

Seizures

131
Q

Give 2 treatments of hypocalcaemia

A

Oral Ca salts

IV Ca in tetany

132
Q

Define hypermagnesaemia and give one cause

A

Serum magnesium >1.1mmol/l

  • Renal impairment
133
Q

Give 2 symptoms of hypermagnesaemia

A

Nausea

Flushing

134
Q

How is hypermagnesaemia treated?

A

Mainly asymptomatic so no Tx needed

135
Q

Define hypomagnesaemia and give 1 cause

A

Serum magnesium <0.7mmol/L

GI loss

136
Q

Give 2 symptoms of hypomagnesaemia

A

Tremor

Tetany

137
Q

Give 2 treatment options for hypomagnesaemia

A

Oral supplement

IV magnesium sulphate

138
Q

Give 2 causes of respiratory acidosis

A

Opiates

Asthma

139
Q

Give 2 causes of respiratory alkalosis

A

Anxiety

Hypoxia (increased RR)

140
Q

Give 2 causes of metabolic acidosis

A

More acid production

Renal bicarbonate loss

141
Q

Give 2 causes of metabolic alkalosis

A

Vomiting

Diarrhoea

142
Q

What is the normal anion gap range?

A

4-12mmol/L

143
Q

What does an increased anion gap indicate?

A

Increased acid production

Acid ingestion

144
Q

What does an decreased anion gap indicate?

A

Decreased acid production

HCO3 loss

145
Q

What happens in mixed picture acidosis/alkalosis?

A

CO2 and HCO3 move in opposite directions

4th Year Exam (20 decks)

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