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2a - SBCS > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Give 2 examples of water-soluble hormones

A

Peptides and monoamines

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2
Q

How do water soluble hormones get into a cell

A

Bind to cell surface receptors

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3
Q

Are water soluble hormones stored in vesicles or synthesised on demand

A

Stored in vesicles

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4
Q

Give an example of a fat soluble hormones

A

Steroids e.g. cortisol

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5
Q

Are fat soluble hormones stored in vesicles or synthesised on demand

A

Synthesised on demand

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6
Q

Give examples of an amine hormone

A

Adrenaline and noradrenaline

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7
Q

Describe the pathway of noradrenaline synthesis

A

Phenylalanine -> L-tyrosine -> L-dopa -> dopamine -> NAd and Ad.

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8
Q

Name 2 enzymes that break down catecholamines.

A

MAO and COMT.

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9
Q

Give 5 ways in which hormone action is controlled.

A
  1. Hormone metabolism.
  2. Hormone receptor induction.
  3. Hormone receptor down-regulation.
  4. Synergism e.g. glucagon and adrenaline.
  5. Antagonism e.g. glucagon and insulin
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10
Q

What is the posterior pituitary derived from?

A

The floor of the ventricles.

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11
Q

Where are posterior pituitary hormones synthesised?

A

They are synthesised in the para-ventricular and supra-optic nuclei.

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12
Q

Name 2 hormones secreted from the posterior pituitary

A

Oxytocin and ADH.

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13
Q

Does the posterior pituitary produce hormones

A

NO
It stores and secretes hormones produced in the hypothalamus

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14
Q

What is the function of ADH?

A

It acts on the collecting ducts of the nephron and increases insertion of aquaporin 2 channels -> there is H2O retention.

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15
Q

Give 2 functions of oxytocin.

A
  1. Milk secretion.
  2. Uterine contraction
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16
Q

What are hypophysiotropic hormones

A

hormones that control secretion of anterior pituitary hormones

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17
Q

Name the 6 hormones secreted from the anterior pituitary

A

FSH
LH
adrenocorticotropic releasing hormone
TSH
Prolactin
GH

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18
Q

What secretes glucagon

A

Alpha cells of the islets of Langerhans

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19
Q

What secretes insulin

A

Beta cells of the islets of Langerhans

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20
Q

Apart from glucagon, name other counterregulatory hormones of insulin

A

Adrenaline
Cortisol
Growth hormone

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21
Q

Diagnostic fasting glucose value for diabetes

A

above 7mmol/L.

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22
Q

What would a person’s random plasma glucose be if they were diabetic?

A

more than 11.1mmol/L

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23
Q

What might someone’s HbA1c be if they have diabetes?

A

> 48mmol/mol

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24
Q

What is type 1 diabetes mellitus

A

Autoimmune destruction of pancreatic beta cells leading to complete insulin deficiency.

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25
Q

Explain the pathogenesis of type 1 DM

A
  • No insulin production means cells of the body can’t take glucose from the blood
  • Level of glucose in the blood keeps rising as cells think the body has no glucose supply
    = hyperglycaemia
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26
Q

At what age does T1DM usually present?

A

Often people with Type 1 diabetes will present in childhood (age 5 to 15)

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27
Q

Describe the pathophysiological consequence of impaired insulin secretion

A
  • Glycogenolysis, gluconeogenesis and lipolysis are not suppressed and there’s reduced peripheral glucose uptake
  • perceived stress leads to increased Ad and cortisol
  • progressive catabolic state and increase levels of ketones
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28
Q

Give 3 signs of T1DM

A
  • Polydipsia - extreme thirstiness
  • Polyuria - excessive urination
  • Unexplained weight loss
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29
Q

Investigation of T1DM

A
  • Random plasma glucose of >11.1mmol/L
  • Fasting plasma glucose >7mmol/L
  • Oral glucose tolerance test: results as above
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30
Q

What is type 2 DM

A

Combination of peripheral insulin resistance and impaired insulin secretion

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31
Q

Is ketoacidosis associated with T1 or T2 DM

A

T1 due to absence of insulin

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32
Q

Treatment of T2DM

A
  • Lifestyle modification
  • Metformin
  • Sulfonylurea E.g gliclazide
  • SGLT2 inhibitor - e.g. canagliflozin, empagliflozin
  • Insulin
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33
Q

Function of SGLT2 inhibitors in T2DM
Give 2 SE

A

Inhibits reabsorption of glucose in the kidney i.e. glucose excreted in urine
E.g. canagliflozin
* SE: UTI, weight loss

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34
Q

How does sulfonylurea work in treating T2DM?

A

Stimulates insulin secretion by binding to beta cell receptors

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35
Q

Give 2 side effects of Sulfonylurea (e.g. gliclazide) for the treatment of T2DM.

A

Can cause hypoglycaemia and weight gain

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36
Q

Describe the mechanism of action of Biguanide (metformin)

A

Decreased gluconeogenesis in the liver and increased cell sensitivity to insulin

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37
Q

What are potential side effects of taking metformin for T2DM

A

GI disturbances - anorexia, nausea and diarrhoea

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38
Q

Give 4 risk factors of T2DM

A

Obesity
Hypertension
Above 40 years old
Ethnicity: Afro-Carrib, SA

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39
Q

How does T2DM present

A
  • Polydipsia - thirstiness
  • Polyuria - excessive urination
  • Polyphagia - excessive hunger
  • Glucosuria - excessive glucose in urine
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40
Q

Explain the pathophysiology of T2DM

A
  • Repeated exposure to high levels of glucose and insulin makes the cells in the body become resistant to the effects of insulin
  • Over time, the pancreas (beta cells) becomes fatigued and damaged by producing so much insulin and they start to produce less
  • Continued high levels of glucose on the body in light of insulin resistance and pancreatic fatigue leads to chronic hyperglycaemia
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41
Q

Investigation of T2DM

A
  • GS: HbA1c test - tells average BG for last 3m
  • HbAc1 > 48mmol/mol = diabetes
  • Blood tests: random and fasting plasma glucose
  • Oral glucose tolerance test
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42
Q

Describe the lifestyle modifications suggested for T2DM

A

Dietary advice - high complex carbs, low fat
Weight loss
Decrease alcohol intake

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43
Q

What is diabetic ketoacidosis

A

When complete lack of insulin results in high ketone production

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44
Q

What is the triad for DKA diagnosis

A

Hyperglycaemia
Ketosis ( blood ketones over 3)
Acidosis (pH less than 7.3)

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45
Q

Causes of DKA

A

Untreated T1DM
Infection/ illness
Myocardial infarction

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46
Q

State some ways DKA presents

A

Acetone-smelling breath (Pear drops)
Nausea and vomiting
Drowsy/confused
Hyperventilation

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47
Q

Explain the pathophysiology of DKA

A

Unrestrained production of glucose and decreased peripheral glucose uptake = hyperglycaemia —-> osmotic diuresis = dehydration

Peripheral lipolysis —> ^FFA —-> oxidised to acetyl CoA —-> ketones = acidosis

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48
Q

Give 3 microvascular complications of DM

A

Peripheral neuropathy
Retinopathy
Nephropathy

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49
Q

Give 4 macrovascular complications of DM

A

Coronary artery disease
Peripheral artery disease
Hypertension
Stroke

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50
Q

How is hypocalcaemia investigated

A

Ca levels - <8.5mg/dL
ECG - prolonged QT interval
Parathyroid function

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51
Q

Give 3 complications of hypocalcaemia

A

Seizures
Muscle spasm
Cardiac arrest

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52
Q

State the 2 signs that commonly present in both hypocalcaemia and hypoparathyroidism

A

Chvostek’s sign and Trousseau’s sign

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53
Q

Describe Chvostek’s sign

A

tapping over the facial nerve induces spasm of facial muscles

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54
Q

Describe Trousseau’s sign

A

Inflating bp cuff to 22mmHg above systolic pressure for 5 mins causes wrist to flex and fingers to draw together

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55
Q

Give 3 causes of hypocalcaemia

A

Hypoparathyroidism
Vit D deficiency
Malignancy

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56
Q

Give some symptoms of hypocalcaemia and hypoparathyroidism

A

CATS go Numb:
Convulsions
Arrhythmias
Tetany - involuntary contraction
Spasm
Numbness

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57
Q

Treatment for hypocalcemia

A

IV calcium gluconate, 10ml of 10% solution over 10 mins (slow)
Vit D supplements

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58
Q

What are the causes of primary hypoparathyroidism

A

Parathyroid gland failure:
* Congenital diseases (DiGeorge)
* Autoimmune destruction

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59
Q

What are the causes of secondary hypoparathyroidism

A

Damage to the parathyroid glands during surgery or receiving radiotherapy
Mg deficiency ( required for PTH secretion)

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60
Q

What is the typical bone profile of someone with hypoparathyroidism

A

Low calcium
Normal/ high phosphate
Low PTH

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61
Q

What is pseudohypoparathyroidism

A

This is when the body is resistant to parathyroid hormone

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62
Q

What is hypoparathyroidism

A

Reduced PTH production

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63
Q

Give some causes of hypercalcaemia

A

Primary hyperparathyroidism
Malignancy
Sarcoidosis
Thiazides
Thyrotoxicosis
Dehydration
Addisons
Acromegaly

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64
Q

Symptoms of hypercalcaemia

A

Bones - pain
Stones - kidney
Groans - nausea
Moans - depression

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65
Q

Give an ECG change seen in hypercalcaemia

A

short QT

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66
Q

Investigation of hypercalcaemia

A
  • Fasting serum Ca and phosphate - confirm mild hypercalcaemia
  • Serum PTH and Ca - raised
  • Ultrasound
  • 24h urinary Ca
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67
Q

Treatment for hypercalcaemia

A
  • rehydration with normal saline
  • bisphosphonates
  • Loop diuretics such as furosemide
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68
Q

Symptoms of hyperparathyroidism

A

Hypercalcaemia:
Bones - painful
Kidney stones
Abdominal - constipation and nausea
Depression and lethargy

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69
Q

Give 3 complications of untreated DKA

A

Coma
Cerebral oedema
Thromboembolism

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70
Q

How is DKA managed

A
  1. ABC management
  2. Replace fluid with IV 0.9% NaCl
  3. IV insulin and glucose (prevent hypoglycaemia)
  4. Restore electrolytes e.g K+
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71
Q

How can insulin treatment for DKA cause hypokalaemia

A

Insulin decreases K+ levels in the blood by redistributing it into cells via increased Na/K pump activity causing low serum K+ levels = Hypokalaemia

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72
Q

What are 2 differences in the presentation of T2DM compared to T1DM

A

T2DM can often display Central obesity and slower onset

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73
Q

What is a serious complication of uncontrolled T2DM

A

Hyperosmolar hyperglycaemic state

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74
Q

Describe the diagnosis and characteristics of HHS

A

Severe hyperglycaemia (>30mmol/L)
Hyperosmolality (>320 mmol/kg)
Mild/ no ketosis
Urine dipstick: Glucosuria

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75
Q

Describe the pathophysiology of HHS

A

Decreased insulin levels are:
• insufficient to inhibit gluconeogenesis (hyperglycaemia -> osmotic diuresis)
but
• sufficient enough to inhibit ketogenesis
Severe volume depletion -> raised serum osmolarity -> hyper viscosity of blood

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76
Q

Give 3 signs and symptoms of HHS

A

Confusion and reduced mental state
Severe dehydration
Lethargy

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77
Q

Treatments of HHS

A

1st line: Fluid replacement - 0.9% saline IV
Restore electrolyte loss (K+)
Low molecular weight heparin (LMWH) to decrease risk of thromboembolism
Give insulin

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78
Q

What is a functioning tumour

A

When a tumour derived from endocrine tissue produces hormones of the original tissue

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79
Q

What is a common structure affected by a pituitary tumour

A

optic chiasm

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80
Q

A pituitary tumour is pressing upwards on the optic chiasm; this compresses the nasal fibres. What visual field defect will be seen

A

Bitemporal hemianopia

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81
Q

If a pituitary tumour applies pressure on the cavernous sinus what could happen

A

cranial nerve palsies

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82
Q

How does a 3rd nerve palsy present

A

Depression and abduction of eye
Drooped eyelid

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83
Q

What can cause a raised prolactin level

A

Stress
Antidopaminergic drugs (anti-psychotics)
Lactotroph adenoma

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84
Q

Signs and symptoms of prolactinomas

A

Amenorrhea - absence of periods
Galactorrhoea - Milky nipple discharge
Low libido
Infertility
Visual field defect

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85
Q

Treatment for prolactinoma

A

1st line: Dopamine agonists e.g. cabergoline
2nd line: combined oral contraceptive
Trans-sphenoidal surgery for men and post-menopausal women

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86
Q

What is prolactinoma

A

Lactotroph cell tumour of the pituitary producing excess prolactin which initiates lactation and breast development

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87
Q

What investigations are done to diagnose prolactinoma

A

prolactin levels
Pituitary MRI

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88
Q

What is cushing syndrome

A

Refers to the signs and symptoms that develop after Long term exposure to excessive cortisol

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89
Q

Signs and symptoms of cushings syndrome

A

Stretch marks
Thin skin (bruising)
Central obesity
Round moon face
Depression

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90
Q

What is cushings syndrome and cushings disease

A

Disease: caused by a pituitary adenoma secreting excess ACTH
Syndrome: high cortisol of any cause

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91
Q

4 causes of Cushing’s syndrome

A

Iatrogenic - steroid use (most common)
Adrenal adenoma secreting cortisol
Cushing’s disease
Ectopic ACTH

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92
Q

What is ectopic ACTH

A

ACTH secreting tumour outside of the pituitary and adrenal glands e.g. small cell lung cancer

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93
Q

Describe the diagnosis process for cushing’s syndrome

A

First exclude oral steroids
1st line: Random plasma cortisol: if high do further tests
Gold standard: Overnight dexamethasone suppression test: cortisol should be low in a healthy patient
Other: Positive urinary cortisol (24h) - doesn’t show underlying cause
MRI brain
abdomen and chest CT

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94
Q

What is the treatment for cushing’s caused by a pituitary adenoma

A

Transsphenoidal surgery

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95
Q

What is the treatment for cushing’s caused by an adrenal adenoma

A

adrenalectomy

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96
Q

What is the treatment for cushing’s that has an latrogenic cause

A

Stop medication if possible

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97
Q

Give 4 complications associated with cushing’s

A

CV disease
Hypertension
DM
Osteoporosis

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98
Q

Give 3 complications of prolactinoma

A

Infertility
Sight loss
Raised intracranial pressure

99
Q

What is acromegaly

A

Release of excess growth hormone causing overgrowth of all systems

100
Q

Causes of acromegaly

A

Pituitary adenoma (most common)
Ecoptic GH production from small cell lung cancer

101
Q

Describe the pathophysiology of acromegaly

A

GH acts directly on tissues such as liver, muscle, bone or fat, as well as indirectly through induction of insulin like growth factor (ILGF-1)

102
Q

Give 3 complications of acromegaly

A

Sleep apnea - overgrowth of pharynx
T2DM
Heart disease

103
Q

State 5 presenting features of acromegaly

A

Large hands, nose, tongue and feet
Prominent forehead and brow
Profuse sweating
Increased jaw size
Visual field defects

104
Q

What is the 1st line investigation for acromegaly

A

Insulin like growth factor 1 test. Raised with acromegaly

105
Q

Why is testing random serum GH not a reliable way to diagnose acromegaly

A

Levels of GH vary throughout the day for normal people and increases when stressed, pregnant and during puberty

106
Q

Describe the gold standard method for acromegaly diagnosis

A

Oral glucose tolerance test
In a healthy subject: glucose is given and this suppresses GH
In a patient with acromegaly, GH is not suppressed

107
Q

What is the 1st line treatment for acromegaly

A

Transsphenoidal resection surgery (if cause is adenoma)

108
Q

What 3 different drugs are used to treat acromegaly

A

Somatostatin analogue - octreotide (longer half-life)
GH receptor antagonists - pegvisomant
Dopamine agonist - cabergoline

109
Q

What are common symptoms of hypoglycaemia

A

Shaking
Sweating
Palpitations
Poor concentration
Nausea

110
Q

What plasma glucose level is classed as hypoglycaemia

A

Less than 3.9 mmol/l (70mg/dl)

111
Q

Symptoms of severe hypoglycaemia

A

Reduced consciousness
Coma
Death

112
Q

What causes hypoglycaemia

A

Long duration of diabetes
increasing age
Addison’s
Drugs - SE sulfonylureas or excess insulin

113
Q

How is hypoglycaemia treated

A

Fast acting glucose (lucozade) and slow acting carb (biscuits)
Unconscious: IV dextrose and IM glucagon

114
Q

Give 3 characteristics of pseuodohypoparathyroidism

A

Mild learning difficulties
Short 4th metacarpals
Obesity

115
Q

Causes of primary hyperparathyroidism

A

Single benign adenoma (80%)
Hyperplasia of all glands

116
Q

What is primary hyperparathyroidism

A

Tumour/ hyperplasia of parathyroid gland produces excess PTH

117
Q

What is secondary hyperparathyroidism

A

Increased secretion of PTH to compensate hypocalcaemia
High PTH, low CA

118
Q

What causes secondary hyperparathyroidism

A

Chronic kidney failure or Low Vit D leads to low absorption of Ca = hypocalcaemia

119
Q

What is tertiary hyperparathyroidism

A

Autonomous secretion of PTH even after correction of calcium deficiency due to CKD

120
Q

Causes of tertiary hyperparathyroidism

A

Develops from prolonged secondary hyperparathyroidism
Parathyroid glands become hyperplastic to further increase excess PTH secretion

121
Q

How does PTH increase Ca

A

PTH increases Calcium through bone resorption, gut absorption, renal reabsorption and activating Vit D

122
Q

What is the typical PTH/bone profile of someone with primary hyperparathyroidism

A

high PTH, high calcium low phosphates

123
Q

how is hyperparathyroidism investigated

A

•PTH, Ca, Phosphate levels
• DEXA scan - bone density
• Xray - pepperpot skull
• Ultrasound for renal stones

124
Q

How is hyperparathyroidism treated

A

primary - parathyroidectomy
Ca correction - treat Vit D deficiency (ergocalciferol) or kidney transplant for CKD

125
Q

What are the treatments for hypoparathyroidism

A

IV Calcium gluconate
oral Calcitriol
Synthetic PTH

126
Q

What is goitre

A

Swelling or nodules that develop on the thyroid gland

127
Q

What is hyperthyroidism

A

Excess thyroid hormone:
Primary - abnormal increased thyroid function
Secondary - abnormal increased TSH production

128
Q

Causes of hyperthyroidism

A

Graves disease (75-80%)
Toxic multinodular goitre
De Quervain’s thyroditis
Iodine excess

129
Q

Signs and symptoms of hyperthyroidism

A

Hot and sweaty
Diarrhoea
Tachycardia
Weight loss

130
Q

Risk factors of hyperthyroidism

A

Smoking
Young/ middle aged women (20-40)
Stress

131
Q

Describe the pathophysiology of hyperthyroidism

A

Increased T3 increases metabolic rate, CO, bone resorption and activates SNS

132
Q

Investigations of hyperthyroidism

A
  • Thyroid function tests: high T4
    Primary (thyroid pathology) = low TSH
    Secondary (overstimulation by TSH) = inappropriately high TSH
133
Q

Describe the drug management for hyperthyroidism

A

1st line: Carbimazole - blocks synthesis of T4 (SE= sore throat)
2nd line: Propylthiouracil - alternative in first trimester of pregnancy
Propranolol - control thyrotoxic symptoms

134
Q

Excluding drugs, what are the treatments for hyperthyroidism

A

Radioiodine - beta particles cause ionisation of thyroid cells
Thyroidectomy

135
Q

What is thyrotoxicosis

A
  • clinical syndrome that results when tissues are exposed to high levels of circulating thyroid hormone
  • Thyroid storm is the severe end of the spectrum
136
Q

Symptoms of thyroid storm

A
  • Fever
  • CV dysfunction
  • Profuse sweating
  • Nausea and vomiting
137
Q

Explain the pathophysiology of graves disease

A

IgG autoantibodies bind to and activate TSH receptors causing the autonomous production of T4/T3
They also react with orbital autoantigens

138
Q

Give symptoms of graves disease

A

Thyroid eye disease: eyelid retraction and periorbital swelling (exophthalmos)
Pretibial myxoedema - orange peel texture on legs
Thyroid acropachy

139
Q

3 features of thyroid acropachy

A

Digital Clubbing
swelling of hands and feet
New Bone growth

140
Q

What is a supporting investigation done to confirm whether a patient has graves

A

Positive TSH receptor antibodies

141
Q

Why is PTU used instead of carbimazole to treat hyperthyroidism in young women hoping to get pregnant

A

Carbimazole is teratogenic - causes fetal abnormalities

142
Q

Define hypothyroidism

A

Lack of thyroid hormone
1- abnormal decreased thyroid function
2 - abnormal decreased TSH production

143
Q

Causes of primary hypothyroidism

A

Hashimotos thyroiditis - most common
De Quervain’s thyroiditis
Drug therapy
Iodine deficiency

144
Q

Give 2 drugs that can cause hypothyroidism

A

Lithium toxicity
Amiodarone - high iodine content

145
Q

Causes of secondary hypothyroidism

A

Pituitary failure - not enough TSH - Hypopituitarism

146
Q

5 Clinical features of hypothyroidism

A

Weight gain
Fatigue
Constipation
Dry, coarse scalp
Cold intolerance

147
Q

Investigations for hypothyroidism

A

TFT: low T3/4
High TSH in primary, Low TSH in secondary

148
Q

What Ab are found in almost all patients with autoimmune hypothyroidism

A

Thyroid peroxidase and thyroglobulin antibodies

149
Q

Treatment for hypothyroidism

A

Levothyroxine (synthetic T4)

150
Q

Complications of hypothyroidism

A

Heart disease
Pregnancy problems
Myxoedema coma

151
Q

Give 3 autoimmune diseases associated with thyroid autoimmunity

A

T1DM
Addison’s disease
Vitiligo

152
Q

What is hashimoto’s thyroiditis

A

autoimmune disease
thyroid gland is attacked via cell and antibody-mediated immune processes causing inflammation and dysfunction

153
Q

Explain the pathophysiology of hashimoto’s thyroiditis

A

formation of antithyroid antibodies that attack the thyroid tissue, causing progressive fibrosis

154
Q

What is De Quervain’s thyroiditis

A

Self-limited inflammation of thyroid gland

155
Q

Cause of DQ’s thyroiditis

A

Often occurs following a viral infection

156
Q

Explain the pathophysiology of DQ’s thyroiditis

A

4 phases:
Phase 1- lasts 3-6 weeks: hyperthyroidism, painful goitre, Raised ESR
Phase 2- Lasts 1-3 weeks: Euthyroid (normal function)
Phase 3- weeks to months: Hypothyroidism
Phase 4- Thyroid structure and function goes back to normal

157
Q

State the 4 main types of thyroid cancer

A

Papillary
Follicular
Medullary
Anaplastic

158
Q

What is the treatment for T1DM

A

Patient education - monitoring carb intake and blood sugar levels
Subcutaneous insulin:
* basal: detemir (2x)
* bolus: lispro injected 30mins before meals

159
Q

What is basal insulin

A

Long acting insulin
Used to maintain stable insulin level throughout the day

160
Q

What is bolus insulin

A

Faster acting insulin
Taken 30 mins pre-meal to give insulin spike

161
Q

What is MODY

A

Maturity onset diabetes of youth
Rare auto dom diagnosed < 25y

162
Q

Treatment for MODY

A

sulfonylurea

163
Q

Complications of a total thyroidectomy

A

Increased risk of recurrent laryngeal nerve damage or hypoparathyroidism

164
Q

What is Conn’s syndrome

A

Primary hyperaldosteronism due to an aldosterone producing adrenal adenoma

165
Q

What is primary hyperaldosteronism

A

Adrenal dysfunction causing raised aldosterone levels
- serum renin will be low as it is suppressed by high bp

166
Q

What is secondary hyperaldosteronism

A

Inappropriate activation of the RAAS = raised renin which = raised aldosterone

167
Q

Explain the pathophysiology of Conn’s syndrome

A

Excess production of aldosterone independent of RAAS results in:
- high Na and water retention
- increased K+ excretion from kidneys
- low renin release

168
Q

Presentation of Conn’s syndrome

A

Often asymptomatic
Possible:
Hypertension
Headaches
Hypokalaemia
Weakness

169
Q

What investigation are used in the diagnosis of Conn’s

A
  • Aldosterone-renin ratio: high (>70%)
  • Low plasma K+
  • CT/MRI to locate adrenal lesions
  • selective adrenal venous sampling ( gold standard )
170
Q

What is the first line treatment for Conn’s

A

Aldosterone antagonists - control BP and K+ levels (Spironolactone)

171
Q

What is the gold standard treatment for Conn’s

A

Surgical removal of adenoma

172
Q

Define cranial diabetes insipidus

A

ADH deficiency: Hypothalamus doesn’t produce ADH for the post pituitary to secrete

173
Q

Define nephrogenic diabetes insipidus

A

ADH resistance/insensitivity: collecting ducts of kidney don’t respond to ADH

174
Q

Define SIADH

A

syndrome of inappropriate secretion of ADH

175
Q

Presentation of DI

A

Polyuria
Polydipsia
Dehydration
(NO GLUCOSURIA)

176
Q

State 3 causes of cranial DI

A

Brain tumours - craniopharyngioma
head trauma
Infections - TB, meningitis

177
Q

Give 4 causes of nephrogenic DI

A

Inherited - mutation in ADH receptor
Drugs - lithium
Systemic disease - chronic kidney disease
Electrolyte disturbance - hypokalaemia, hypercalcaemia

178
Q

Describe the diagnosis and investigations for DI

A

• GS: water deprivation test
• Urine osmolality - low (<200)
• Serum osmolality - high (>300)
• Serum Na - norm/high
• Serum glucose - exclude DM if glucosuria not seen

179
Q

What is the gold standard test for DI and why

A

Water deprivation test
Can distinguish between cranial and nephrogenic

180
Q

Describe the water deprivation test

A

1) Used to confirm DI
Deprived of fluid for 8 hours
Urine osmolality is measured hourly.
* Urine still dilute indicates DI (dehydration = normal response)

2) distinguish between cranial and nephrogenic DI
Desmopressin is administered IM.
8 hours later urine osmolality is measured again

181
Q

Describe the results of a water deprivation test for a patient with cranial DI

A

Patients with cranial DI respond to desmopressin with a reduction in urine output and an increase in urine osmolality to >750 mmol/kg

182
Q

Describe the results of a water deprivation test for a patient with nephrogenic DI

A

Don’t respond to desmopressin
No or little reduction in urine output and no increase in urine osmolality (as they are insensitive to ADH)

183
Q

Treatment for cranial DI

A

Desmopressin - high activity at V2 receptor

184
Q

Treatment for nephrogenic DI

A

Thiazide diuretics (Bendroflumethiazide) - offset water losses
NSAIDs - reduce urine output

185
Q

What is a complication of DI

A

Hypernatremia

186
Q

Give 2 causes of hyponatraemia

A

Excess water - most common
Salt loss

187
Q

What would be the serum Na of someone with hyponatraemia

A

<135 mmol/l
(norm = 135-144)

188
Q

Give 3 symptoms of hyponatraemia

A

Headache
Nausea
Confusion

189
Q

Treatment for hyponatraemia

A

Stop hypotonic fluids
Assess underlying causes

190
Q

Give 4 causes of SIADH

A

Meds - thiazide diuretics, carbamazepine, SSRI
Malignancy - SCLC
TB
Stroke

191
Q

Explain the pathophysiology of SIADH

A
  • Excessive ADH = excessive water reabsorption in collecting ducts
  • Water dilutes Na in the blood = hyponatraemia
  • Water reabsorption isn’t significant enough to cause fluid overload = euvolemic hyponatraemia
  • Urine more concentrated - high urine osmolality & high urine Na
192
Q

Symptoms of SIADH

A

Largely due to hyponatraemia:
Headache
Fatigue
Muscle aches

193
Q

Describe the diagnosis and investigation of SIADH

A

Usually diagnosed by exclusion
- Euvolaemia
- U+E = hyponatraemia
- low serum osmolality
- high urine and Na osmolality

194
Q

Treatment of SIADH

A

Establish and treat cause
Fluid restriction (<1L/24h) - correct hyponatraemia
Vasopressin receptor antagonist (Tolvaptan)

195
Q

What is a complication of SIADH

A

Central pontine myelinolysis - correct Na slowly to avoid this

196
Q

What is adrenal insufficiency

A

Where the adrenal glands don’t produce enough steroid hormones particularly aldosterone and cortisol

197
Q

Define primary adrenal insufficiency (Addison’s disease)

A

When the adrenal glands have been damaged resulting in reduced cortisol and aldosterone

198
Q

Give 2 common causes of Addison’s disease

A

Autoimmune adrenalitis (inflammation) - most common in developed countries
TB - most common worldwide

199
Q

What is secondary adrenal insufficiency

A

Inadequate adrenocorticotropic hormone stimulating the adrenal glands resulting in low levels of cortisol release

200
Q

Give 2 causes of secondary adrenal insufficiency

A

Radiotherapy
Pituitary macroadenoma

201
Q

What is tertiary adrenal insufficiency

A

Result of inadequate CRH release by the hypothalamus

202
Q

Causes of tertiary adrenal insufficiency

A

Usually the result of patients being on long term oral steroids (>3w) causing suppression of the HPA axis

203
Q

Presentation of Addison’s

A
  • Hyperpigmentation especially in the palmar creases - only in primary AI
  • lethargy, weight loss,
  • Postural hypotension and hypoglycaemia
  • vitiligo and loss of pubic hair
204
Q

Give 3 biochemical indicators of adrenal insufficiency

A
  • Low Na, high K (SIADH)
  • Eosinophilia
  • Borderline elevated TSH
205
Q

Investigations for AI

A
  • Renin/ Aldo: elevated renin and low aldo in Addison’s
  • Low cortisol
  • low Na, high K
  • High ACTH in primary, Low/ normal ACTH in secondary
  • Short synacthen test
206
Q

State and explain the gold standard test for AI

A

Short synacthen test: ideally in the morning
* Patient injected with synthetic ACTH (synacthen)
* cortisol measured at baseline, 30 & 60 mins
* failure of cortisol to rise (less than double baseline) indicates addison’s

207
Q

What is an adrenal crisis

A

This is when the level of cortisol drops significantly and symptoms of AI worsen

208
Q

How is an adrenal crisis treated

A
  • Immediate hydrocortisone 100mg IV/IM
  • Fluid resuscitations (saline)
  • Continued hydrocortisone until recovered 6 hourly
  • Wean dose to normal when stable
209
Q

Treatment for AI

A

Hydrocortisone (15-25mg divided into 2-3 doses) - replace cortisol
Fludrocortisone - replace aldosterone

210
Q

When should the dose of hydrocortisone be doubled

A

If unwell with fever/flu like illness as cortisol is needed for stress response

211
Q

What is MODY

A

Maturity onset diabetes of youth
Rare auto dom diagnosed < 25y

212
Q

What is pheochromocytoma

A

neuroendocrine tumour of the chromaffin cells found in the adrenal medulla
causes excessive release of adrenaline and noradrenaline

213
Q

Causes of pheochromocytomas

A

Usually inherited
Neurofibromatosis
Multiple endocrine neoplasia syndrome

214
Q

Signs and symptoms of pheochromocytoma

A

Headache
hypertension
Palpitations
Tremor
Pallor

215
Q

Investigations for pheochromocytoma

A
  • Increased plasma metanephrines and normetanephrines ( longer 1/2 life than Adr & NAd)
  • CT - tumour
  • 24h Urinary catecholamines
216
Q

Treatment for pheochromocytoma

A

1st line: alpha blockers (phenoxybenzamine)
* Surgery to remove tumour

217
Q

What is a complication of pheochromocytoma and how is this treated

A

HTN crisis ( 180/120 bp)
Treated with ant hypersensitive agent: phentolamine

218
Q

What is carcinoid syndrome

A

Occurs due to release of serotonin into the systemic circulation from a carcinoid tumour

219
Q

Where do carcinoid tumours commonly arise from

A

GI tract (SI)
Lungs
Liver - most common for metastasis
Ovaries
Thymus

220
Q

How does carcinoid syndrome present

A

Flushing
Diarrhoea
Abdo cramps

221
Q

Define hypokalaemia

A

Serum K level <3.5 mmol/L

222
Q

What causes hypokalaemia with alkalosis

A

Vomiting
Thiazide and loop diuretics
Cushing’s syndrome
Conn’s

223
Q

What causes hypokalaemia with acidosis

A

Diarrhoea
Renal tubular acidosis
Partially treated DKA
Decreased intake

224
Q

How does hypokalaemia present

A

Muscle weakness
Hypotonia
Arrhythmias
Hyporeflexia

225
Q

Describe the ECG presentation of someone with hypokalaemia

A

Small/ inverted T wave
Prominent U wave
Long PR interval
ST depression

226
Q

Investigations for hypokalaemia

A

Decreased [K+]
Urine electrolytes - differentiate between renal and non-renal causes of hypokalaemia
ECG

227
Q

Treatment for hypokalaemia

A

Mild: oral K+ replacement
Severe (<2.5mmol/L): IV replacement 40mmol KCl in 1L 0.9 NaCl

228
Q

Give 2 complications of hypokalaemia

A

Long QT syndrome
Chronic heart failure

229
Q

Define hyperkalaemia

A

Serum K value >5.5mmol/L

230
Q

Causes of hyperkalaemia

A

Acute kidney injury
Addison’s
DKA
NSAIDs
ACEi

231
Q

Symptoms of hyperkalaemia

A

Fast irregular pulse (AF)
Muscle aches and pains
Chest pain
Ventricular fibrillation

232
Q

Describe the typical ECG presentation of hyperkalaemia

A

Tall tented T waves
Small/ absent p waves
Wide QRS

233
Q

Diagnosis and investigations of hyperkalaemia

A

U+E - high [K+]
ECG

234
Q

Treatment for hyperkalaemia with ECG changes

A

Stabilise cardiac membrane via IV Ca gluconate/chloride

235
Q

Treatment for hyperkalaemia if no cardiotoxic changes are seen

A

Shift K+ ECF to ICF by giving combined insulin and dextrose infusion with nebulised salbutamol

236
Q

What can be used to remove potassium from the body

A

Calcium resonium
Loop diuretics
Dialysis

237
Q

Define severe hyperkalaemia

A

Serum K value > 6.5mmol/L

238
Q

Describe the dexamethasone suppression test

A

Low dose test: 1mg dexamethasone given
* normal response = low cortisol
* Cushing’s syndrome = normal/high cortisol
High dose test: 8mg dexamethasone given
* low cortisol = Cushing’s disease
Normal/high cortisol:
* low ACTH = adrenal adenoma
* high ACTH = ectopic ACTH

239
Q

What are normal levels of blood glucose

A

Between 3.5-8.0mmol/L

240
Q

What are the effects of T3/T4 on the body

A
  • Increases basal metabolic rate
  • Anabolic (form) effects at low serum levels and catabolic (breakdown) effects at higher levels
  • Increases release and effect of GH and IGF-1
  • Increases HR and contractility through increasing sensitivity to catecholamines
241
Q

Which part of the adrenal gland secretes catecholamines (e.g Adr)

A

Adrenal medulla

242
Q

Describe the layers of the adrenal cortex and state which hormone is secreted

A
  • Zona glomerulosa - secretes mineralocorticoids e.g. aldosterone
  • Z. fasciculata - secretes glucocorticoids e.g. cortisol
  • Z. reticularis - secretes androgens (sex hormones)
243
Q

Action of aldosterone

A
  • Works on kidneys to increase blood volume and BP
  • Can cause hypernatremia
244
Q

Action of cortisol

A
  • Suppresses immune system
  • Inhibits bone formation
  • Increases metabolism - protein catabolism, lipolysis, gluconeogenesis
  • Increases alertness

2a - SBCS (9 decks)

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