Endocrine 🔁 Flashcards
F
1
Q
What is refeeding syndrome?
A
An imbalance of electrolytes that is potentially fatal when a severely malnourished patient begins to reintroduce food
2
Q
What electrolyte abnormalities are seen in refeeding syndrome?
A
Low phosphate
Low potassium
Low magnesium
Hyperglycaemia
3
Q
What symptoms can low phosphate cause?
A
Muscle weakness
Respiratory failure
Delirium
Seizures
4
Q
What symptoms can low magnesium cause?
A
Neuromuscular excitability
Muscle weakness
Cardiac arrhythmias
5
Q
What symptoms can low potassium cause?
A
Muscle weakness
Paralysis
Potentially fatal cardiac arrhythmias
6
Q
What symptoms can hyperglycaemia cause?
A
Polyuria
Polydipsia
Fatigue
Blurred vision
7
Q
What is the management of refeeding syndrome?
A
Monitoring of potassium, magnesium and phosphate levels
Slow reintroduction of food
Thiamine replacement for at risk patients to prevent Wernicke’s encephalopathy
8
Q
Why does refeeding syndrome occur?
A
In starvation mode, circulating insulin levels drop, and intracellular phosphate is depleted
When refeeding occurs, insulin levels suddenly rise, and phosphate is taken up into cells
9
Q
What are the risk factors for refeeding syndrome?
A
Dehydration
Fasting for more than 5 days
BMI < 16
Excessive exercise
Rapid weight loss
10
Q
What is adrenal insuffiency?
A
Where the adrenal glands do not produce enough of the steroid hormones cortisol and aldosterone
11
Q
What is primary adrenal insuffiency?
A
Where damage to the adrenal glands results in a lack of cortisol and aldosterone
12
Q
What is the most common cause of primary adrenal insuffiency?
A
Autoimmune conditions
13
Q
What is secondary adrenal insuffiency?
A
A lack of ACTH leads to a lack of stimulation of the adrenal glands, and less cortisol.
It is usually as a result of damage to the pituitary gland
14
Q
What is tertiary adrenal insufficiency?
A
Tertiary adrenal insufficiency is a result of a lack of CRH (corticotrophin releasing hormone) from the hypothalamus
15
Q
What is the most common cause of tertiary adrenal insufficiency?
A
Long term steroid use causes suppression of the hypothalamus
16
Q
Why does tertiary adrenal insufficiency occur with long term steroid use?
A
When steroids are withdrawn, the hypothalamus cannot make endogenous steroids quick enough
17
Q
What is the presentation of adrenal insufficiency?
A
Fatigue
Muscle weakness
Muscle cramps
Thirst and salt craving
Dizziness
Weight loss
Abdominal pain
Depression
18
Q
What are the physical signs of adrenal insufficiency?
A
Bronze pigmented skin
Hypotension (specifically postural hypotension
19
Q
Why does adrenal insufficiency cause bronze pigmented skin?
A
Excessive ACTH stimulated melanocytes to produce melanin
20
Q
What biochemical findings may be seen in adrenal insufficiency?
A
Hyponatraemia
Hyperkalaemia
Hypoglycaemia
Raised creatinine and urea (dehydration)
Hypercalcaemia
21
Q
What is the investigation of choice for diagnosis of adrenal insufficiency?
A
Short synacthen test
22
Q
What antibodies may be present in primary adrenal insufficiency?
A
Adrenal cortex antibodies
21-hydroxylase antibodies
23
Q
How is the short synacthen test performed?
A
Synthetic ACTH (synacthen) is given - blood cortisol is tested after 30 and 60 minutes
Failure of cortisol levels to double indicates primary adrenal insufficiency (or secondary insufficiency that has caused significant adrenal atrophy)
24
Q
What is the first line management of adrenal insufficiency?
A
Hydrocortisone to replace cortisol
Fludrocortisone to replace aldosterone
25
What is the management of an addisonian crisis?
IV hydrocortisone 100mg
1 litre normal saline over 30-60 minutes
Dextrose if hypoglycaemic
Continue hydrocortisone until stable
No fludrocortisone required
26
What is acute hyponatraemia?
Develops over a period of less than 48 hours
27
What is chronic hyponatraemia?
Develops over a period of more than 48 hours
28
What is mild hyponatraemia?
130-134mmol/L
29
What is moderate hyponatraemia?
120-129mmol/L
30
What is severe hyponatraemia?
<120mmol/L
31
What are the early symptoms of hyponatraemia?
Headache
Lethargy
Nausea
Vomiting
Dizziness
Confusion
Muscle cramps
32
What are the late symptoms of hyponatraemia?
Seizures
Coma
Respiratory arrest
33
What is the management of chronic hypovolaemic hyponatraemia?
Normal saline (0.9% NaCl)
34
What is the management of acute hyponatraemia with severe symptoms?
Hypertonic saline (3% NaCl)
35
What is the management of euvolemic hyponatraemia?
Fluid restrict to 500-1000ml/day
Consider
- Demeclocycline
- Vaptans (vasopressin)
36
What is the management of hypervolemic hyponatraemia?
Fluid restrict to 500-1000ml/day
Consider loop diuretics
Consider vaptans
37
What are the causes of hypovolaemic hyponatraemia?
Diuretic stage of renal failure
Diuretics
Addisonian crisis
38
What are the causes of euvolemic hyponatraemia?
SIADH
39
What are the causes of hypervolemic hyponatraemia?
Heart failure
Liver failure
Nephrotic syndrome
40
What is osmotic demyelination syndrome?
A complication of hyponatraemia treatment. It happens due to over-correction of severe hyponatraemia
41
What is the pathophysiology of osmotic demyelination syndrome?
In chronic hyponatraemia there is the loss of active organic osmolytes from astrocytes. These provide protection against cerebral oedema.
Organic osmolytes cannot be replaced quickly enough when the brain volume begins to shrink in response to correction of hyponatraemia
42
What are the symptoms of osmotic demyelination syndrome?
Dysarthria
Dysphagia
Paraparesis
Seizures
Confusion
Coma
43
What is the presentation of hypercalcaemia?
'Bones, stones, groans and psychic moans'
- Renal stones
- Bone pain
- Nausea and vomiting, poor appetite, constipation
- Fatigue and confusion
44
What are the two main causes of hypercalcaemia?
Primary hyperparathyroidism
Malignancy
45
What are the other causes of hypercalcaemia?
Sarcoidosis
Vitamin D intoxication
Acromegaly
Thiazide diuretics
Addison's disease
Dehydration
46
What investigation is important to carry out in hypercalcaemia?
ECG due to risk of arrhythmias
47
What is the first line management of hypercalcaemia?
IV normal saline
48
What is the second line management of hypercalcaemia?
IV bisphosphonates
49
What is the action of parathyroid hormone?
Increased osteoclast activity
Increases calcium reabsorption in the kidneys
Increases vitamin D activity
50
What action does vitamin D have on calcium?
Vitamin D increases calcium absorption from the intestines
51
What is primary hyperparathyroidism?
Uncontrolled parathyroid hormone production by a tumour of the parathyroid hormone glands
52
What is secondary hyperparathyroidism?
Insufficient vitamin D or chronic kidney disease reduced calcium absorption from the intestines, kidneys and bones.
Low calcium results in the parathyroid secreting more PTH
53
What is tertiary hyperparathyroidism?
When secondary hyperparathyroidism continues for an extended period, after which the underlying cause is treated (due to hyperplasia of the parathyroid hormone as they adapt to producing a higher baseline of PTH)
54
What is the treatment of primary hyperparathyroidism?
Removal of the parathyroid gland tumour
55
What is the treatment of secondary hyperparathyroidism?
Treatment of the underlying cause
56
What is the treatment of tertiary hyperparathyroidism?
Partial surgical removal of the parathyroid gland
57
What is calcitonin?
Calcitonin is a hormone secreted by the parafollicular cells of the thyroid
58
What is the action of calcitonin?
It acts to reduce serum calcium levels
59
What medication can be used in conservative management of hyperparathyroidism?
Cinacalcet (a calcium mimetic)
60
What is the action of cinacalcet?
It mimics the action of calcium on tissues - negative feedback on the parathyroid gland results in a decrease in PTH levels, and a decrease in calcium
61
What blood results would be seen in primary hyperparathyroidism?
Raised calcium
Low phosphate
PTH may be raised or normal
62
What investigations are used in the diagnosis of hyperparathyroidism?
Serum calcium, phosphate and PTH
Technetium-MIBI substraction scan
X-ray
63
What blood results would be seen in secondary hyperparathyroidism?
Elevated PTH
Low or normal calcium
Elevated phosphate
64
What blood results would be seen in tertiary hyperparathyroidism?
Normal or high calcium
Elevated PTH
Decreased or normal phosphate
Raised ALP
65
What is the presentation of hyperparathyroidism?
Polydipsia
Polyuria
Depression
Anorexia
Nausea
Pancreatitis
Bone pain
Renal stones
Hypertension
66
What is acromegaly?
An excess of growth hormone
67
Where is growth hormone produced?
Anterior pituitary gland
68
What is the most common cause of acromegaly?
A pituitary adenoma
69
What are the other causes of acromegaly?
Secondary to cancer (GHRH or GH secreting tumours)
70
What visual field defect can occur with a pituitary adenoma?
Bitemporal hemianopia
71
What is the presentation of acromegaly?
Prominent forehead
Coarse, sweaty skin
Large nose
Large tongue
Large hands and feet
Large protruding jaw
A space occupying pituitary tumour can also cause:
- Headaches
- Bitemporal hemianopia
72
What conditions are associated with acromegaly?
Hypertrophic heart
Hypertension
Type 2 diabetes
Carpal tunnel syndrome
Arthritis
Colorectal cancer
73
What is the first line investigation for acromegaly?
Serum IGF-1 levels
74
What investigation will confirm acromegaly?
OGTT
75
What OGTT results will be seen in a patient with acromegaly?
Growth hormone will not be suppressed after OGTT
76
How is a OGTT for acromegaly carried out?
A 75g glucose drink is consumed, and growth hormone levels are tested at baseline and 2 hours following the drink
77
What is the first line treatment of acromegaly?
Trans-sphenoidal resection of pituitary adenoma
78
What medications can be used to manage acromegaly?
Somatostatin analogue - ocreotide (first line medical management)
GH receptor antagonists - pegvisomant
Dopamine agonists - bromocriptine
79
What is somatostatin?
Growth hormone-inhibiting hormone. It is secreted by the brain, GI tract, and pancreas
80
What is Cushing's syndrome?
High levels of glucocorticoids in the body
81
What is the primary glucocorticoid produced by the body?
Cortisol
82
What is Cushing's disease?
Cushing's syndrome as a cause of a pituitary adenoma - the pituitary adenoma secretes excess ACTH that results in excessive cortisol
83
What is the most common cause of Cushing's syndrome?
Cushing's disease - ACTH secretion from a pituitary adenoma
84
What are the other causes of Cushing's syndrome?
Ectopic ACTH production e.g small cell lung cancer
Steroids
Adrenal adenoma
Adrenal carcinoma
85
What is pseudo-Cushing's?
Conditions that mimic Cushing's - often caused by severe depression or alcohol excess
86
What test can differentiate between Cushing's and pseudo-Cushing's
Insulin stress test - in patients with psuedo-Cushing's, cortisol levels will rise in response to hypoglycaemia
87
What are the features of Cushing's syndrome?
Round face
Central obesity
Abdominal striae
Buffalo hump
Proximal limb muscle wasting
Hirsutism
Easy bruising
Hyperpigmentation of skin
Mood changes
Menstrual irregularity
Reduced libido
88
What metabolic conditions are associated with Cushing's syndrome?
Hypertension
Type 2 diabetes
Dyslipidaemia
Osteoporosis
89
What investigation is used to diagnose Cushing's?
Dexamethasone suppression test
90
What are the three types of dexamethasone suppression test and what are they used for?
Low dose overnight test - used as a screening test to exclude Cushing's
Low dose 48-hour test - used in suspected Cushing's
High dose 48-hour test - used to determine the cause in patients with confirmed Cushing's syndrome
91
What is a normal dexamethasone suppression test?
Cortisol is suppressed
92
What is the action of dexamethasone on cortisol?
Dexamethasone negatively feeds back to the hypothalamus - this reduced corticotropin-releasing hormone output, which reduced ACTH output
Reduced ACTH results in a low cortisol level
93
What other investigations may be useful in diagnosis of Cushing's syndrome?
24 hour urinary free cortisol
FBC - high white cells
U&Es
MRI brain for pituitary adenoma
CT chest for small cell lung cancer
CT abdomen for adrenal tumours
94
What is the treatment of Cushing's disease?
Treatment of underlying problem:
- Trans-sphenoidal resection of pituitary adenoma
- Surgical removal of adrenal tumour
- Surgical removal of ectopic ACTH tumour
95
What are the results of high dose dexamethasone test in Cushing's disease?
Low dose DST - cortisol is not suppressed
High dose DST - cortisol is suppressed
96
What are the results of high dose dexamethasone test in an ectopic ACTH source?
Low dose DST - cortisol is not suppressed
High dose DST - cortisol is not suppressed
97
What is SIADH?
Increased release of ADH from the posterior pituitary
98
What is the impact of too much ADH?
Water reabsorption from the urine is increased (in the collecting ducts of the kidneys) - this causes hyponatraemia
99
What are the two potential sources of excess ADH?
Increased production by the posteior pituitary
Ecoptic ADH, most commonly from small cell lung cancer
100
What is serum and urine osmolality like in SIADH?
Low serum osmolality
High urine osmolality
101
What is the presentation of SIADH?
Headache
Fatigue
Muscle cramps
Confusion
Reduced consciousness (severe hyponatraemia)
Seizures (severe hyponatraemia)
102
What are the possible causes of SIADH?
Post-op after major surgery
Lung infection
Brain pathologies - head injury, stroke, meningitis
Medications - SSRIs, carbamazepine
Small cell lung cancer
HIV
Hypothyroidism
103
What are the diagnostic criteria for SIADH?
Low plasma osmolality - <275
High urine osmolality > 100
High urine sodium > 30 mmol/L
Clinical euvolaemia
Exclusion of glucocorticoid deficiency
104
What is the managment of acute SIADH?
Acute SIADH < 48 hours - treatment of hyponatraemia
- Hypertonic 3% saline
105
What is the management of chronic SIADH (> 48 hours)?
Maximum increase of 10mmol/L per day of sodim
- Fluid restriction for mild cases
- Demeclocycline or ADH receptor antagonists (tolvaptan) for severe cases
106
What are the complications of SIADH?
Cerebral oedema
Central pontine myelinolysis (due to rapid correction of sodium)
107
What is central pontine myelinolysis?
Demyelination (typically of the pontine white matter tracts) following rapid correction of hyponatraemia
108
What is the presentation of central pontine myelinosis?
Tremors
Dysarthria
Quadriplegia
Seizures
Extrapyramidal symptoms
Locked in syndrome
109
How is diagnosis of central pontine myelinolysis confirmed?
MRI
110
What is mild hypothermia?
32-35 degrees body temperature
111
What is moderate or severe hypothermia?
<32 degrees body temperature
112
What are the causes of hypotheramia in the elderly?
Exposure to cold in the environment
Inadequate insulation in the operating theatre
Cardiopulmonary bypass
113
What are the risk factors for hypothermia?
General anaesthesia
Substance abuse
Hypothyroidism
Impaired mental status
Homelessness
Extremes of age
114
What are the signs of hypothermia?
Shivering
Cold and pale skin
Slurred speech
Tachypnoea
Respiratory depression
Bradycardia
Confusion
115
What are the investigations for hypothermia?
12 lead ECG
Temperature
FBC
Blood glucose
ABG
Coagulation factors
CXR
116
What would be seen on an ECG in hypothermia?
Acute ST elevation
J wave
117
What might be seen on bloods in someone with hypothermia?
Elevated haemoglobin and haematocrit
Hypokalaemia
118
What is the initial management of hypothermia?
Remove patient from environment
Remove wet blankets or clothing
Warm the body with blankets
Secure the airway and monitor breathing
Warm IV fluids or passing warm air over the patient
119
What is the definition of hyperthermia?
Body temperature of more than 40 degrees
120
What features of the elderly make them more susceptible to hyperthermia?
Reduced cardiac output
Chronic volume depletion
Normal deficiencies in heat shock protein
121
What are the features of hyperthermia?
Agitation
Lethargy
Seizures
Hot dry skin
Elevated core body temperature
Intense thirst
Weakness
Syncope
Headache
Tachypnoea
Tachycardia
122
What are the risk factors for hyperthermia?
Age > 65
Pre-existing dehydration
Obesity
Environmental factors
Diabetes
Cardiovascular disease
Congenital disorders
Drug and alcohol misuse
Medications
- Diuretics
- Beta blockers
- Anticholinergics
- Antidepressants
- Antihistamines
123
What investigations should be performed in someone with hyperthermia?
FBC
LFTs
Renal function
Rectal temperature
Glucose
U&E
ABG
Creatinine Kinase
Urinalysis
ECG
124
What electrolyte abnormalities might be seen in hyperthermia?
Hypokalaemia
Hyponatraemia
125
What other blood tests results might be seen in hyperthermia?
Elevated CK
Elevated urea
Elevated ALT and AST
126
What is the management of hyperthermia?
Remove excess clothing
Rapid active cooling:
- Wetting and fanning the skin
- Wetted ice packs
Oxygen
IV fluids
Small dose benodiazepines
127
What temperature should patients with hyperthermia be cooled to?
No less than 39 derees
128
Why are IV benzodiazepines sometimes given in hyperthermia?
IV benzos increase shivering, which causes heat gain and makes cooling less effective
- this ensures that patients are not cooled too much or too quickly
129
What is thyrotoxicosis?
Abnormal and excessive quantity of thyroid hormomes (due to any cause)
130
What is subclinical hyperthyroidism?
T3 and T4 levels are normal, but TSH is suppressed
131
What is the most common cause of primary hyperthyroidism?
Graves' disease
132
What are the causes of hyperthyroidism?
GIST
G - graves' disease
I - inflammation
S - solitary toxic thyroid nodule
T - toxic multinodular goitre
133
What clinical picture does thyroiditis often present with?
Causes an initial period of hyperthyroidism, followed by under-activity of the thyroid gland
134
What are the causes of thyroiditis?
De Quervian's thyroiditis
Hashimoto's thyroiditis
Postpartum thyroiditis
Drug-induced thyroiditis
135
What is the presentation of hyperthyroidism?
Anxiety and irritability
Sweating and heat intolerance
Tachycardia
Weight loss
Fatigue
Insomnia
Frequent loose stools
Sexual dysfunction
Menstrual irregularity
136
What are the signs specific to Graves' disease?
Diffuse goitre
Graves' eye disease including exophthalmos
Pretibilar myxoedema
Thyroid acropachy
137
What investigations are used in the diagnosis of hyperthyroidism?
TFTs - first line
Antibodies - anti-TSH receptor positive in patients with Graves' disease
Thyroid ultrasound
Technetium radionuclide scan
ECG - AF
138
What TFT results will be seen in primary hyperthyroidism?
High T4
Low TSH
139
What TFT results will be seen in subclinical hyperthyroidism?
Normal T4
Low TSH
140
What TFT results will be seen in secondary hyperthyroidism?
High T4
Normal TSH
141
What is the first line treatment for hyperthyroidism?
Carbimazole - taken for 12 to 18 months
Once the patient is euthyroid:
- Carbimazole is titrated OR
- A higher dose blocks all production, and levothyroxine is added and titrated
142
What is the second line treatment for hyperthyroidism?
Propylthiouracil (due to hepatotoxicity)
143
What is the treatment of hyperthyroidism during pregnancy?
Propylthiouracil is used in the first trimester, and then switched to carbimazole
144
What is the first line treatment for severe Graves' disease or toxic multinodular goitre?
Radioiodine treatment
145
What is radioiodine treatment?
A single dose of radioactive iodine is drank
- The thyroid takes this up, and the emitted radiation destroys a proportion of the thyroid cells
146
What are the strict rules of radioiodine treatment?
Women should not be pregnant, and should not conceive within 6 months of treatment
Men should not father treatment within 4 months of treatment
Limit contact with people after the dose
147
What is De Quervian's thyroiditis?
Temporary inflammation of the thyroid causes three phases:
- Thyrotoxicosis
- Hypothyroidism
- Return to normal
148
What is the management of De Quervian's thyroiditis?
NSAIDs
Beta blockers for symptoms of hyperthyroidism
Levothyroxine for symptoms of hypothyroidism
149
What is the presentation of a thyroid storm?
Fever
Tachycardia
Delirium
Hypertension
150
What is the management of a thyroid storm?
Beta blockers - IV propranolol
Anti-thyroid drugs - methimazole or propylthiouracil
Dexamethasone
151
What is the most common cause of hypothyroidism?
Hashimoto's thyroiditis
152
What is primary hypothyroidism?
The thyroid produced inadequate thyroid hormones
- Negative feedback is absent, resulting in increased production of TSH
153
What TFTs would be seen in primary hypothyroidism?
Low T3/T4
High TSH
154
What is secondary hypothyroidism?
The pituitary behaves abnormally and produces inadequate TSH, resulting in under stimulation of the thyroid
155
What TFTs are seen in secondary hypothyroidism?
Low TSH
Low T3/T4
156
What are the other causes of hypothyroidism?
Iodine deficiency
Treatment for hyperthyroidim
Lithium
Amiodarone
157
What are the clinical features of hypothyroidism?
Weight gain
Cold intolerance
Lethargy
Dry skin
Constipation
Menorrhagia
Coarse hair and hair loss
Fluid retention
Bradycardia
Goitre
158
What are the causes of secondary hypothyroidism?
Pituitary adenoma
Surgery to the pituitary
Radiotherapy
Sheehan's syndrome
Trauma
159
What are the primary investigations used to diagnose hypothyroidism?
TFTs
Antibodies - anti-TPO associated with Hashimoto's thyroiditis
Inflammatory markers - raised in Dequervain's thyroiditis
160
What is the management of primary hypothyroidism?
Levothyroxine
- Offer with regular review of symptoms
- TSH every 3 months
161
What are the complications of hypothyroidism?
Cardiovascular disease
Carpal tunnel syndrome
Peripheral neuropathy
Myxoedema coma
Thyroid lymphoma
162
What are the side effects of thyroxine?
Hyperthyroidism
AF
Osteoporosis
Angina
163
What TFTs would be seen in subclinical hypothyroidism?
High TSH
Normal T3/T4
164
When should subclinical hypothyroidism be treated?
If the TSH level is >10 on 2 separate occasions, 3 months apart
165
What is sick euthyroid syndrome?
Low T3/T4 levels alongside a normal TSH, in a patient that is acutely unwell
166
What is the management of sick euthyroid syndrome?
Changes are reversible upon recovery from illness, therefore no treatment is needed
167
What is diabetes insipidus?
An inability of the body to concentrate urine
It is caused by a lack of ADH, or a lack of response to ADH
168
What is cranial diabetes insipidus?
Where there is insufficient vasopressin release from the hypothalamo-pituitary axis
169
What is nephrogenic diabetes insipidus?
Where the collecting ducts of the kidneys do not respond to ADH
170
What are the causes of cranial diabetes insipidus?
Brain tumours
Brain injury
Brain surgery
Brain infections
Genetic mutations in ADH gene
Wolfram syndrome
171
What are the causes of nephrogenic diabetes insipidus?
Medications - lithium
Genetic mutations in the ADH receptor gene
Hypercalcaemia
Hypokalaemia
Kidney diseases e.g PCKD
172
What is primary polydipsia?
Excessive intake of fluid, that leads to reduced serum osmolality, and the suppression of ADH
This causes polyuria
173
What are the clinical features of diabetes insipidus?
Polyuria
Nocturia
Polydipsia
Fatigue
Dry mucous membranes
Reduced skin turgor
Tachycardia
Hypotension /postural hypotension
Hypernatraemia
174
What are the primary investigations used in the diagnosis of diabetes insipidus?
Urine and serum osmolality
- High serum osmolality
- Low urine osmolality
U&Es
- Sodium may be raised
- Deranged potassium and calcium may suggest nephrogenic DI
Serum glucose
- Exclude diabetes
24 hour urine output
Water deprivation test
175
What is a water deprivation test?
The patient is deprived of water for 8 hours
- Serum and urine osmolality are measured hourly
176
What is a positive water deprivation test?
Water deprivation causes low urine osmolality and high serum osmolality
177
What test differentiates between cranial and nephrogenic DI?
Desmopressin suppression test
178
How does the desmopressin suppression test differentiate between cranial and nephrogenic diabetes insipidus?
After desmopressin:
- Urine osmolality remains low in nephrogenic DI, as the body still cannot respond to ADH
- Urine osmolality is high in cranial DI, as the body is able to respond to ADH
179
What is the management of cranial DI?
Desmopressin
Monitor serum sodium
Manage fluid balance
180
What is the management of nephrogenic diabetes insipidus?
Manage fluid balance
Treat underlying cause
Sodium restriction
Thiazide diuretics - can reduce urine output in nephrogenic DI
181
What are the causes of primary hyperaldosteronism?
Adrenal hyperplasia
Adrenal adenoma - Conn's syndrome
Adrenal carcinoma
182
What are the causes of secondary hyperaldosteronism?
Excessive renin - caused by disproportionately lower blood pressure in the kidneys due to:
- Renal artery stenosis
- Heart failure
- Liver cirrhosis
183
What is the clinical presentation of hyperaldosteronism?
Lethargy
Mood disturbance
Paraesthesia
Muscle cramps
Refractory hypertension
184
What is refractory hypertension?
Where blood pressure remains high despite taking >5 different anti-hypertensives
185
What is the first line diagnostic investigation for hyperaldosteronism?
Aldosterone/renin ratio
Primary hyperaldosteronism
- High aldosterone
- Low renin
Secondary hyperaldosteronism
- High aldosterone
- High renin
186
What other investigations are useful in the diagnosis of hyperaldosteronism?
U&Es - hypokalaemia and hypernatraemia
CT abdomen
Adrenal venous sampling - to determine if there is unilateral or bilateral disease
Renal artery imaging
187
What is the first line management of primary hyperaldosteronism?
For unilateral adrenal hyperplasia or adenoma
- Laparoscopic adrenalectomy
For bilateral adrenal hyperplasia or adenoma
- Spironolactone or eplerenone
188
What is the most common cause of secondary hypertension?
Hyperaldosteronism
189
What is DKA?
A medical emergency characterised by hyperglycaemia, acidosis and ketonaemia
190
What situations does DKA commonly present in?
Initial presentation of T1DM
An existing diabetic who is unwell
An existing diabetic who is not adhering to insulin regime
191
What is the presentation of DKA?
Polyuria
Polydipsia
Nausea and vomiting
Acetone smell to breath
Dehydration
Weight loss
Hypotension
Altered consciousness
Kussmaul respiration (deep hyperventilation)
192
What is the pathophysiology of DKA?
A net reduction in insulin leads to reduced entry of glucose into cells
Lipids are metabolised as an alternative energy source, which leads to elevated free fatty acids and ketones
193
What investigations are performed in the diagnosis of DKA?
Urine dip - ketonuria and glycosuria
Bedside ketone and capillary glucose
ABG/VBG
U&Es
FBC and CRP
194
What is the criteria for diagnosis of DKA?
Hyperglycaemia - >11mmol/L
Ketosis > 3mmol/L
Acidosis - pH < 7.3 and/or HCO3 < 15mmol/L
195
What is the management of DKA in adults?
IV fluid resuscitation
Insulin
Glucose
Potassium
Treat any underlying infection
Monitor glucose, ketones, pH, bicarbonate and electrolytes
196
What fluid resuscitation is given in DKA?
If systolic < 90 - 500ml 0.9% NaCl given over 15 minutes
If systolic > 90:
1 litre 0.9% NaCl given over 1 hour
1 litre 0.9% NaCl with KCl given over next 2 hours
1 litre 0.9% NaCl with KCl given over next 2 hours
1 litre 0.9% NaCl with KCl given over next 4 hours
1 litre 0.9% NaCl with KCl given over next 4 hours
1 litre 0.9% NaCl with KCl given over next 6 hours
197
When is glucose started in DKA?
An infusion of 10% dextrose should be started at 125ml/hour when blood glucose is < 14 mmol/L
198
What alterations are made to a patient's regular insulin in DKA?
Long acting insulin is continued, short acting insulin should be stopped
199
What is required for insulin and fluid to be stopped in resolving DKA?
Ketosis and acidosis is resolved
Patient is eating and drinking
Patient has started their regular subcut insulin (short acting insulin)
200
What are the complications of treatment for DKA?
Hypoglycaemia
Hypokalaemia
Cerebral oedema
Pulmonary oedema secondary to fluid overload
201
What are the complications of DKA?
Gastric stasis
Thromboembolism
Arrhythmias secondary to hyperkalaemia
AKI
202
What is the pathophysiology of diabetic neuropathy?
Chronic hyperglycaemia leads to peripheral nerve damage through inflammatory pathways, oxidative stress and advanced glycation end products
203
What are the types of diabetic neuropathy?
Distal symmetrical sensory neuropathy
Small-fibre predominant neuropathy
Diabetic amyotrophy
Mononeuritis multiplex
Autonomic neuropathy
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What is distal symmetrical sensory neuropathy and how does it present?
The most common form of DPN - results from loss of large sensory fibres
- It presents with sensory loss in a glove and stocking distribution
- Affects touch, vibration and proprioception
205
What is small fibre predominant neuropathy and how does it present?
Diabetic neuropathy due to the loss of small sensory fibres
- Loss of pain and temperature sensation in a glove and stocking distribution
206
What is diabetic amyotrophy and how does it present?
Diabetic neuropathy originating from inflammation of the lumbosacral plexus or cervical plexus
- Presents with severe pain around the thighs and hips, with proximal weakness
207
What is mononeuritis multiplex?
Mononeuritis multiplex is a neuropathy involving two or more distinct peripheral nerves
208
What is autonomic neuropathy and how does it present?
Occurs when the nerves that control autonomic body function are damaged
- Presents with postural hypotension, gastroparesis, constipation, urinary retention, arrhythmias and erectile dysfunction
209
What are the differentials of diabetic neuropathy?
Vitamin B12 deficiency
Alcohol induced peripheral neuropathy
CIDP
Hypothyroidism
210
What investigations are indicated in suspected diabetic neuropathy?
Neurological examination
Nerve conduction studies
Blood tests:
- Glucose levels
- HbA1c
- B12 levels
- TFTs
- LFTs
211
What is the management of diabetic neuropathy?
First line - amitriptyline, duloxetine, gabapentin or pregabalin
Pain management clinic
Tramadol - rescue therapy for exacerbations
212
What are the complications of autonomic neuropathy?
Gastroparesis
- Presents with erratic blood glucose control, bloating and vomiting
- Management with metoclopramide, domperidone or erythromycin (prokinetics)
213
Where is insulin produced?
Insulin is produced in the beta cells of the Islets of Langerhans in the pancreas
214
Where is glucagon produced?
Glucagon is produced in the alpha cells in the Islets of Langerhans in the pancreas
215
What are the symptoms in initial presentation of T1DM?
Polyuria
Polydipsia
Weight loss
216
When do the symptoms of T1DM typically present?
1 to 6 weeks before the onset of DKA
217
What investigations are performed in a newly diagnosed type 1 diabetic?
FBC
Renal profile
HbA1c
TFTs, TPO antibodies
Anti-TTG antibodies
Insulin antibodies, anti-GAD antibodies and islet cell antibodies
218
What is the criteria for diagnosis of type 1 diabetes?
One of the following is sufficient for diagnosis:
Random glucose > 11.1 or fasting plasma glucose > 7
2 hour glucose tolerance test > 11.1
HbA1c > 48
219
What type of regime is insulin typically administered using?
Basal-bolus regime
- Long acting insulin to give constant background insulin during the day
- Short acting insulin before meals
220
What are the blood glucose goals for before meals, and before bed?
Pre-meal blood glucose - 4-7 mmol/L
Bedtime blood glucose - 6-10 mmol/L
221
What are the long term macrovascular complications of T1DM?
Coronary artery disease
Peripheral ischaemia - diabetic foot
Stroke
Hypertension
222
What are the microvascular complications of T1DM?
Peripheral neuropathy
Retinopathy
Glomerulosclerosis
223
What are the infection related complications of T1DM?
UTIs
Pneumonia
Skin and soft tissue infections
Fungal infections - oral and vaginal candidiasis
224
How often is HbA1c monitored in T1DM patients?
Every 3 to 6 months
225
What are the sick day rules for type 1 diabetics?
Increase blood glucose monitoring to every 3-4 hours
Do not stop insulin treatment
Check ketone levels regularly (every 3-4 hours)
Maintain normal meal battern
If unable to eat, or vomiting, replace meals with carbohydrate containing drinks
226
What are the main causes of hypoparathyroidism?
Surgical removal of parathyroid gland
Autoimmune destruction of the parathyroid gland
227
What is the pathophysiology of hypoparathyroidism?
Decreased PTH production or function leads to decreased calcium absorption from the intestines, reduced bone resorption, and impaired renal reabsorption of calcium
228
What is the clinical presentation of hypoparathyroidism?
Hypocalcaemia related symptoms:
- Muscle cramps
- Paraesthesia
- Tetany
Neuropsychiatric symptoms:
- Anxiety
- Depression
- Cognitive impairment
Dental enamel hypoplasia and tooth discolouration
229
What are the differentials of hypoparathyroidism?
Hypocalcaemia due to other causes e.g renal failure
Vitamin D deficiency
Neuromuscular disorders
Psychiatric conditions
230
What investigations are performed in the diagnosis of hypoparathyroidism?
Serum calcium - low
Serum phosphate - high
PTH levels - low/inappropriately normal
Vitamin D levels
Urinary calcium - low
ECG - detection of long QT due to hypocalcaemia
231
What is the management of hypoparathyroidism?
Calcium and vitamin D supplementation
Regular monitoring of calcium levels and PTH
232
What is the management of acute severe hypocalcaemia?
IV calcium
233
What are the complications of hypoparathyroidism?
Seizures
Cardiac arrhythmias
Kidney stones - increased urinary calcium excretion
Impaired renal function
Cataracts
234
What is pseudohypoparathyroidism?
A rare genetic disorder where the bone, kidney and gut fail to respond to normal levels of PTH
235
What is the pathophysiology of psudoparathyroidism?
A mutation of the FNAS1 gene lead to defects in the PTH receptor.
236
What is a carcinoid tumour?
A type of slow growing neuroendocrine tumour
237
What hormone do carcinoid tumours most commonly secrete?
Serotonin
238
Where do carcinoid tumours typically originate?
Appendix
Small intestine
239
What are the symptoms of a carcinoid tumour?
Abdominal pain
Diarrhoea
Flushing
Wheezing
Pulmonary stenosis
240
What are the differentials of a carcinoid tumour?
IBS
IBD
Mastocytosis
241
What investigations are used in the diagnosis of carcinoid tumours?
Hormone levels - level of 5-HIAA (a breakdown product of serotonin)
CT, MRI or ocreotide scan
Tissue biopsy
242
What is the primary management of carcinoid tumour?
Ocreotide
Surgical resection of tumour
243
How does ocreotide work against a carcinoid tumour?
Ocreotide is a somatostatin analogue, which can inhibit production hormones by the tumour
244
What is hyperosmolar hyperglycaemic state?
A complication of diabetes, characterised by hyperglycaemia and hyperosmolality of the blood, in the absence of ketones
245
What is the clinical definition of hyperosmolar hyperglycaemic state?
Marked hyperglycaemia (>30mmol/L), without significant ketosis (<3 mmol/L), or acidosis (pH>7.3)
Osmolality 320 mosmol/kg or more
246
What are the risk factors for hyperosmolar hyperglycaemic state?
Poorly controlled diabetes
Advanced age
Infections or other illnesses
Medications that affect glucose metabolism
247
What are the symptoms of hyperosmolar hyperglycaemic state?
Profound dehydration
Dry mucous membranes
Altered mental status
Neurological symptoms - seizures or focal neurological deficits
Hypotension
Tachycardia
248
What investigations are used in the diagnosis of hyperosmolar hyperglycaemic state?
Blood glucose levels
Serum osmolality
U&Es
Urinalysis for ketones
249
What is the management of hyperosmolar hyperglycaemic state?
Fluid resuscitation 0.9% NaCl
Insulin can be given if blood sugars stop falling with fluids alone
250
What are the complications of hyperosmolar hyperglycaemic state?
Hypovolaemic shock
Cerebral oedema
Thromboembolic events
AKI
Cardiac arrhythmias
Respiratory failure
Long term neurological effects
251
What is a pituitary adenoma?
A pituitary adenoma is a benign tumour of the pituitary gland
252
What visual field defect is most common with a pituitary tumour?
Bitemporal hemianopia
253
What is the most common type of pituitary tumour?
Pituitary adenoma
254
What is the typical presentation of a pituitary adenoma?
Headache
Visual field defects - bitemporal hemianopia
255
What is the cause of a bitemporal hemianopia that affects predominantly the upper quadrants?
An inferior chiasmal compression (pituitary tumour)
256
What is the cause of a bitemporal hemianopia that predominantly affects the inferior quadrants?
Superior chiasmal compression - commonly a craniopharyngioma
257
What investigations are used in the diagnosis of a pituitary adenoma?
Brain MRI - diagnostic
Visual field defect screening
Hormone tests - if tumour is suspected of being a functioning adenoma
258
What is the primary management of a pituitary adenoma?
Transphenoidal resection of the pituitary adenoma
259
What additional treatments may be used in the management of pituitary adenoma?
Radiotherapy
260
What is the most common hormone secreting pituitary tumour?
Prolactinoma
261
What are microadenomas and macroadenomas?
Microadenoma = <10mm
Macroadenoma = >10mm
262
What is the presentation of prolactinoma in women?
Oligomenorrhoea or amenorrhoea
Galactorrhoea
Vaginal dryness
Headaches
Visual field defects
263
What is the presentation of prolactinoma in men?
Erectile dysfunction
Reduced facial hair growth
Headaches
Visual field defects
264
What investigations are used in the diagnosis of prolactinoma?
MRI brain
Serum prolactin
265
What is the medical management of prolactinoma?
Dopamine agonists e.g cabergoline
HRT
266
What is the definitive management of prolactinoma?
Trans-sphenoidal resection of the tumour (when medical treatment fails to manage the tumour)
267
What is multiple endocrine neoplasia?
A group of inherited disorders characterised by the development of neoplasms in multiple endocrine organs
268
What is the inheritance of multiple endocrine neoplasia?
Autosomal dominant
269
What genes are affected in multiple endocrine neoplasia?
MEN-1 is caused by mutations in the MEN1 gene
MEN-2a and MEN-2b are caused by mutations in the RET gene
270
What glands are affected in MEN-1?
Parathyroid
Pancreas
Pituitary
271
What glands are affected in MEN-2a?
Thyroid (medullary thyroid cancer)
Adrenal (phaeochromocytoma)
Parathyroid
272
What glands are affected in MEN-2b?
Thyroid (medullary thyroid cancer)
Adrenal (phaeochromocytoma)
Parathyroid
Mucosal neuromas
273
What investigations are involved in the diagnosis of MEN?
Genetic testing
Hormonal assays
Imaging - CT/MRI
274
What is the management of MEN?
Surgical intervention for removal of tumours
Hormonal therapies
Lifelong surveillance for early detection of new tumours
