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Year 4 > Endocrinology and clinical biochem > Flashcards

Endocrinology and clinical biochem Flashcards

1
Q

What is type I diabetes

A

Auto-immune desrtruction of beta-cells in the islets of langerhans of the pancreas causing insulin insufficiency and hyperglycaemia

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2
Q

What is the typical presentation of type I diabetes

A
  • polydipsia
  • polyuria
  • haematuria
  • proteinuria
  • weight loss
  • personal/family history of autoimmune disease
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3
Q

What fasting glucose is indicative of DM

A

> 7mmol/L

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4
Q

What random glucose is indicative of DM

A

> 11mmol/L

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5
Q

What HbA1c is indicative of DM

A

> 48mmol/L

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6
Q

What lifestyle modifications can be advised for T2DM

A
  • weight loss
  • ecerxise
  • smoking cessation
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7
Q

What is the most widely prescribed drug for T2DM

A

metformin

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8
Q

What is a serious possible side effect of metformin

A

lactic acidosis

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9
Q

How does metformin work

A

It is a type of biguanide and is anti-hyperglycaemic

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10
Q

Does metformin carry a risk of hypoglycaemia

A

Not if taken alone as it doesn’t increase insulin secretion

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11
Q

Ehat are the names of some sufonylureas

A

Gliclazide, glipizide

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12
Q

What is a possible side effect of sulfonylureas (eg gliclazide)

A

hypoglycaemia

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13
Q

What should you look for when examining the skin of a patient who injects subcut insulin

A

lipohypertrophy

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14
Q

what can you advise the patient to do to prevent lipohypertrophy

A

Switch injection sites regularly

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15
Q

What happens to insulin levels when a patient continues injecting in a site with lipohypertrophy

A

The insulin uptake is poorer

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16
Q

What are the two categories of diabetes complications

A

macrovascular and microvascular

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17
Q

What are the ultra fast-acting subcut insulins

A

humalog and novorapid

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18
Q

What are the long-acting recombinant human insulin analogues

A

insuline detemir

insulin glargin

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19
Q

What is first line for long-acting basal insulin therapy

A

insulin detemir

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20
Q

What are some common insulin regimens

A
  • basal-bolus
  • biphasic
  • insulin pump
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21
Q

Describe the basal-bolus regimen

A

One or more separate doses of intermediate- or long-acting insulin with short-acting bolus injections before or right after meals

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22
Q

What should insulin-dependent diabetics remember when they are sick eg with the flu?

A
  • insulin requirement often increases
  • maintain calorie intake
  • monitor blood glucose and ketonuria
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23
Q

When would you admit a patient who is a insulin-dependent with the flu

A

if they are vomiting, dehydrated, ketotic, a child or pregnant

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24
Q

What is the target blood pressure for diabetic patients

A

<135/85mmHg

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25
Q

What are some macrovascular complications of diabetes?

A
  • coronary artery disease
  • peripheraly artery disease
  • stroke
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26
Q

How should you manage macrovascular risk in diabetes?

A
  • lifestyle advice
  • atorvastatin
  • manage complications individually
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27
Q

What are some microvascular diabetes complications

A
  • retinopathy
  • cataracts
  • nephropathy
  • neuropathy
  • diabetic foot
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28
Q

What are the types of diabetic neuropathy?

A
  • autonomic neuropathy
  • painful diabetic neuropathy
  • sensory loss
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29
Q

What are some types of autonomic diabetic neuropathy?

A
  • gastroparesis
  • bladder emptying issues
  • erectile dysfunction
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30
Q

How might diabetes result in the diabetic foor?

A

diabetic neuropathy and vascular disease

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31
Q

How do you tell the difference between vascular cause of diabetic foot and neuropathic cause

A
  • Vascular may be pulseless
  • Neuropathic will have decreased sensation
  • Neuropathic may be more likely on pressure points
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32
Q

How do you screen for diabetic retinopathy?

A

diabetic eye screening programme

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33
Q

How do you treat diabetic nephropathy

A

ACE-inhibitors or angiotensin II receptor blockers if not tolerated

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34
Q

What is gestational diabetes

A

Glucose intolerance intolerance that is first recognised during pregnancy

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35
Q

What trimester is most common for diagnosis of gestational diabetes?

A

Third trimester

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36
Q

What are the risks to the mother of gestational diabetes

A
  • pre-eclampsia
  • increased risk of developing T2DM
  • increased risk of developing cardiovascular disease
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37
Q

What are the risks to the foetus of gestational diabetes

A
  • miscarriage
  • pre-term labour
  • congenital malformations
  • macrosomia
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38
Q

What is macrosomia

A

A baby that is much larger than normal

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39
Q

Describe the treatment options for gestational diabetes

A
  • lifestyle changes
  • metformin
  • insulin
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40
Q

What is secondary diabetes

A

Diabetes that results as a consequence of another medication, endocrine disease or hereditary disease

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41
Q

Give some examples of diseases that cause of secondary diabetes

A
  • pancreatitis (acute/chronic)
  • pancreatic cancer
  • other endocrine disorders eg Cushing’s and acromegaly
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42
Q

What is the most common drug cause of secondary diabetes

A

steroids

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43
Q

What are the two main forms of monogenic diabetes

A
  • neonatal diabetes

* maturity-onset diabetes of the young (MODY)

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44
Q

What is monogenic diabetes

A

rare forms of diabetes that result from mutations or changes in a single gene

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45
Q

What are the main diabetic emergencies?

A
  • DKA
  • hypoglycaemia
  • HHS
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46
Q

What does HHS stand for

A

Hyperosmolar hyperglycaemic state

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47
Q

What is diabetic ketoacidosis

A

A consequence of insulin deficiency where there is breakdown of free fatty acids into ketone bodies which causes acidosis

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48
Q

What are ketones?

A

An energy substrate made in starvation or insulin deficiency

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49
Q

What is the classic presentation of diabetic ketoacidosis

A
  • polyuria
  • polydipsia
  • Kussmaul breathing
  • sweet smelling breath
  • reduced GCS
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50
Q

What is Kussmaul breathing? What is it indicative of?

A

Deep rapid breathing indicative of patient trying to ‘blow off’ CO2 in acidosis

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51
Q

What investigations should be undertaken in an unwell diabetic?

A
  • blood glucose
  • venous blood gas
  • blood ketones
  • urine dipstick
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52
Q

What blood results (including VBG) would indicate ketosis?

A
  • glucose >11mmol/L
  • ketones >3mmol/L
  • VBG signs of metabolic acidosis
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53
Q

How is DKA managed?

A
  • Fluids!
  • IV insulin infusion
  • eventually give glucose in fluids
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54
Q

Why would you start giving glucose in fluids in DKA?

A

because the insulin reduces the ketones but can cause hypoglycaemia at the same time

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55
Q

What is HHS?

A

Hyperosmolar hyperglycaemic state is a hyperglycaemic state of hypovolaemia

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56
Q

What is the predominant problem in HHS

A

dehydration

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57
Q

What is the pathogenesis of HHS

A

Patients with T2DM may have enough insulin to stop ketone body production, but glucose still accumulates in the blood, leading to an osmotic diuresis

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58
Q

What is the onset period for HHS compared to DKA

A

Can be over many days, whereas DKA is a few hours or days

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59
Q

What is the management of HHS like

A
  • fluid replacement

* insulin infusion, although lower rates than in DKA

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60
Q

When do symptoms of hypoglycaemia start to appear? What glucose level?

A

<3.4mmol/L

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61
Q

What are some symptoms of hypoglycaemia?

A
  • hunger
  • pallor
  • sweating
  • palpitations
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62
Q

What severe symptoms of hypoglycaemia might a patient present with?

A
  • seizures
  • unconsciousness
  • death
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63
Q

What treatment should unconscious patients with hypoglycaemia receive?

A
  • IM glucagon or IV glucose infusion
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64
Q

What are some primary causes of hypothyroidism

A
  • iodine deficiency
  • hashimoto’s thyroiditis
  • surgery or medication
65
Q

What are some symptoms of hypothyroidism?

A
  • cold sensitivity
  • weight gain
  • lethargy
  • constipation
  • menstrual disturbances
66
Q

What is the emergency that hypothyroidism might result in

A

myxoedema coma

67
Q

What is the metabolically active form of thyroxin

A

T3

68
Q

What are the bloods like in primary hypothyroidism

A
  • high TSH

* low T3/T4`

69
Q

How is hypothyroidism treated

A

levothyroxine (T4)

70
Q

What are symptoms of hyperthyroidism

A
  • palpitations
  • sweating
  • heat intolerance
  • weight loss
  • anxiety
  • diarrhoea
  • a goitre
71
Q

What are some complications of hyperthyroidism?

A
  • heart failure
  • atrial fibrillation
  • Graves’ ophthalmopathy
  • thyrotoxicosis
72
Q

What is the main cause of primary hyperparathyroidism

A

Graves’ disease

73
Q

What blood results indicate hyperthyroidism

A

Low TSH

Elevated T3/T4

74
Q

What drug therapy can be given for hyperthyroidism

A
  • caribomazole

* thyroxine may be required

75
Q

What non-pharmacological therapy can be given for hyperthyroidism

A
  • surgery

* radioactive iodine

76
Q

Why would radioactive iodine be contraindicated

A

in patients with Graves’ ophthalmopathy it makes it worse

77
Q

What is a possible complication of thyroid surgery

A
  • hypothyroidism
  • hypoparathyroidism
  • bleeding
78
Q

What is a toxic thyroid goitre?

A

A goitre associated with hyperthyroidism

79
Q

How are thyroid goitres treated

A
  • treat underlying pathology

* surgery

80
Q

What may be found on examination of a goitre in Graves’? Why?

A

a bruit may be heard because the goitre becomes very vascular

81
Q

What would a diffusely enlarged and smooth goitre without bruit indicate?

A

Iodine deficiency

82
Q

Does a thyroid goitre need to be investigated in pregnancy if there are no symptoms?

A

Not neccessarily, because the thyroid may enlarge for increased demand and then will receed after pregnancy

83
Q

What investigation should be done for a nodular goitre?

A

fine needle aspiration and TFTs

84
Q

What are causes of thyroid lumps?

A
  • thyroid cysts
  • follicular adenoma
  • malignancy
  • nodule of multinodular goitre
85
Q

What is multinodular goitre

A

enlarged thyroid that contains many nodules of varying sizes

86
Q

How is thyroid carcinoma treated?

A
  • radioactive iodine
  • radiotherapy
  • chemotherapy
  • surgery
87
Q

What causes PTH release?

A

Low calcium levels

88
Q

What does PTH do

A
  • triggers bone resorption
  • causes kidney reabsorption of Ca
  • causes kidney production of calcitriol
89
Q

What does calcitriol do

A

increases GI absorption of calcium

90
Q

What elecrolyte abnormalities are found in hyperparathyroidism

A

hypercalcaemia

hypophosphataemia

91
Q

What are symptoms of hyperparathyroidism

A
  • painful and fragile bones
  • kidney stones
  • cardiac arrhythmias
  • confusion
  • muscle weakness
  • dehydration
92
Q

What is the most common cause of hyperparathyroidism

A

parathyroid gland adenoma

93
Q

What are malignant tumours of the parathyroid gland often associated with?

A

MEN (multiple endocrine neoplasia)

94
Q

How is hyperparathyroidism investigated

A
  • PTH levels
  • serum calcium and phosphate
  • U&Es
  • x ray
95
Q

What LFT might be elevated in hyperparathyroidism

A

Alk Phos

96
Q

What medications may cause hypercalcaemia

A
  • lithium

* thiazide diuretics

97
Q

What treatment can be given for primary hyperparathyroidism

A
  • surgery

* bisphosphonates, calcitonin, cinacalcet

98
Q

What medical therapy can be used for primary hyperparathyroidism

A
  • calcitonin
  • cinacalcet
  • bisphosphonates
99
Q

What are complications of surgical removal of parathyroid glands

A
  • hypocalcaemia
  • recurrent laryngeal nerve injury
  • bleeding
100
Q

What causes secondary hyperparathyroidism

A

conditions that cause hypocalcaemia will result in increased PTH secretion, which if prolonged can cause the glands to enlarge

101
Q

Give an example of a condition that causes hyperparathyroidism

A
  • vitamin D deficiency or malabsorption

* renal failure

102
Q

What is tertiary hyperparathyroidism

A

If secondary hyperparathyroidism persists, the level of calcium required to inhibit PTH production is reset to a higher level which causes autonomous parathyroid gland activity

103
Q

What is treatment of tertiary hyperparathyroidism

A

surgery

104
Q

What condition often causes tertiary hyperparathyroidism

A

chronic kidney failure

105
Q

What are the main causes of hypoparathyroidism

A
  • surgery
  • congenital deficiency - digeorge syndrome
  • idiopathic hypoparathyroidism
106
Q

What are the symptoms of hypoparathyroidism

A
  • hand and feet parasthesia
  • muscle cramps
  • depression
  • cardiac arrhythmias
107
Q

What is Trousseau’s sign? What condition causes it?

A

Blood pressure cuff on arm causes carpopedal spasm due to tetany of muscles in hands
Hypocalcaemia/hypoparathyroidism

108
Q

What would the elecrolytes show in hypoparathyroidism

A

hypocalcaemia

hyperphosphataemia

109
Q

What are some causes of hypocalcaemia you should investigate

A 
Hypoparathyroidism
Acute pancreatitis
Renal failure
Vitamin D3 deficiency
Alkalosis
Rhabdomyolysis
Drugs (eg bisphosphonates)
110
Q

Does adrenal cortex insufficiency usually affect a specific layer?

A

It tends to affect the whole adrenal cortex rather than specific layers

111
Q

What causes increased skin pigmentation in adrenal insufficiency?

A

increased ACTH levels

112
Q

What effect does cortisol have on glucose

A

increases blood glucose levels

113
Q

What triggers cortisol release

A

ACTH from the pituitary

114
Q

What triggers aldosterone release

A

renin

115
Q

What effect does aldosterone have

A
  • increases sodium
  • decreases potassium
  • increases blood pressure
116
Q

What does loss of aldosterone cause

A
  • hyponatraemia
  • hyperkalaemia
  • hypovolaemia
  • low blood pressure
  • metabolic acidosis
117
Q

What drugs are given in primary adrenal insufficiency?

A

hydrocortisone and fludrocortisone

118
Q

What hormoen does fludrocortisone replace

A

aldosterone

119
Q

What hormone triggers ACTH release

A

corticotrophin releasing hormone from the hypothalamus (CRH)

120
Q

What are causes of primary adrenal insufficiency

A
  • autoimmune (addisons)
  • TB
  • malignancy
121
Q

What are symptoms of primary adrenal insufficiency

A
  • fatigue
  • confusion
  • postural hypotension
  • abdominal pain
  • nausea and vomiting
  • skin hyperpigmentation (especially around joints)
122
Q

What are symptoms of an addisonian crisis

A
  • back/abdo/leg pain
  • vomiting and diarrhoea
  • dehydration
  • loss of consciousness
  • hypotension
  • hypoglycaemia
123
Q

What is an addisonian crisis

A

When a trigger (often illness) causes chronic adrenal insufficiency to become acute

124
Q

How is primary adrenal insufficiency diagnosed

A
  • synthetic ACTH

* cortisol levels monitored do not increase with ACTH

125
Q

What would be the issue if synthetic ACTH did trigger appropriate cortisol levels were observed?

A

secondary adrenocortical insufficiency

126
Q

What is the most common cause of hypopituitarism

A

treatment for hyperpituitarism

127
Q

What are some causes of hypopituitarism

A
  • compression
  • infarct
  • haemorrhage
  • tumour
128
Q

What is treatment for hypopituitarism

A

hormone replacement with careful monitoring

129
Q

What investigations are required for hypopituitarism

A
  • cranial nerve exam (for any focal deficits caused by compression)
  • CT/MRI head
  • hormone levels
  • stimulation tests
130
Q

What is the most common cause of Cushing’s disease (if not taking cortisol)

A

pituitary adenoma

131
Q

What are the possible causes of Cushing’s (if not on exogenous cortisol)

A
  • pituitary adenoma
  • paraneoplastic syndrome
  • adrenal tumour
132
Q

What investigations should be undertaken for Cushing’s

A
  • CT/MRI head for pituitary adenoma
  • PET-scan for other malignancies
  • dexamethasone suppression test
133
Q

What would results from a dexamethasone suppression test tell you?

A
  • reduced ACTH indicates adrenal tumour

* elevated ACTH = pituitary adenoma or paraneoplastic syndrome and requires imaging

134
Q

How is Cushing’s disease treated

A

surgery

135
Q

What is a complication of surgery for Cushing’s disease pituitary adenoma?

A

panhypopituitarism

136
Q

What is acromegaly

A

excessive growth after skeletal epiphyseal closure due to increased growth hormone

137
Q

What usually causes acromegaly

A

benign pituitary adenoma

138
Q

What causes morbidity and mortality in untreated acromegaly

A
  • cardiovascular disease
  • cerebrovascular disease
  • malignancy
139
Q

What are some symptoms of acromegaly

A
  • sweating
  • headache
  • clothes fit tightly
  • amenorrhoea or impotence
  • deep voice and slow speech
140
Q

What is the most common functioning adenoma of the anterior pituitary gland

A

prolactinoma

141
Q

How do prolactinomas present in females

A
  • oligomenorrhoea
  • amenorrhoea
  • infertility
  • galactorrhoea
142
Q

How do prolactinomas present in males

A
  • headache
  • visual field defect
  • erectile dysfunction
143
Q

Why would prolactinomas cause visual field defects?

A

compression of optic chiasm

144
Q

What can be given as a test to suppress GH secretion

A

oral glucose

145
Q

What is PCOS

A

a condition of hyperandrogenism, oligo-/an-ovulation, and polycystic ovaries

146
Q

What causes PCOS

A

raised LH levels

147
Q

What are symptoms of PCOS

A
  • oligo/amenorrhoea
  • hirsutism or male pattern baldness
  • infertility
  • obesity
  • insulin resistance
148
Q

What dermatological finding is associated with PCOS

A

acanothosis nigricans

149
Q

What tests and results are diagnostic of PCOS

A
  • increased LH:FSH ratio
  • increased androstenedione levels
    • 5 cysts found on ultrasound of ovaries
150
Q

What are causes of gonadal failure in males

A
  • Klinefelter
  • cryptorchidism
  • testicular torsion
151
Q

What are causes of gonadal failure in females

A
  • Turners

* autoimmune ovarian failure

152
Q

What is Klinefelter’s?

A

46XXY

153
Q

What is a phaeochromocytoma?

A

a rare cathecholamine-producing tumour of the adrenal medulla

154
Q

What do phaeochromocytomas do?

A

secrete adrenaline and noradrenaline causing headaches and high blood pressure

155
Q

Apart from the adrenal medulla, where might phaeochromocytomas occur?

A

the sympathetic ganglia beside the abdominal aorta

156
Q

What is Conn’s syndrome

A

An adenoma causing hyperaldosteronism

157
Q

What are the effects of hyperaldosteronism?

A
  • hypernatraemia
  • hypokalaemia
  • fluid retention
  • alkalosis
  • hypertension
158
Q

What triad of symptoms should make you suspicious of Conn’s?

A
  • hypokalaemia
  • hypertension
  • alkalosis
159
Q

What would be different in blood tests between hyperaldosteronism and renal artery stenosis?

A

renin would be raised in renal artery stenosis but low in hyperaldosteronism

Year 4 (13 decks)

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