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MBChB - year 2 > Week 4 Endocrine Lectures > Flashcards

Week 4 Endocrine Lectures Flashcards

1
Q

What are steroid hormones derived from?

A

The enzymatic modification of cholesterol

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2
Q

How is steroidogenesis regulated?

A

involves control of the enzymes which convert cholesterol into the steroid hormone desired

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3
Q

Where are enzymes which produce steroid hormones found?

A

mitochondria and smooth ER

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4
Q

What are the properties of steroid hormones?

A

They are lipid soluble and freely permeable to membranes

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5
Q

How are steroid hormones stored?

A

They are not stored but synthesized and immediately released

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6
Q

How are steroid hormones transported in the blood?

A

Since they are not water soluble they must be carried complexed to specific binding globulins

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7
Q

What carries cortisol in the blood?

A

Corticosteroid binding globulin

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8
Q

Where are the adrenal glands found?

A

In the abdomen above the kidney

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9
Q

Why are the adrenal glands yellow?

A

They have high cholesterol

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10
Q

What are the two parts of the adrenal glands?

A
  • Cortex -composed of zones, each of which has characteristic histology and secretes different hormone
  • Medulla –embryologically and histologically distinct
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11
Q

What is the blood supply to the adrenal glands?

A

The superior, middle and inferior suprarenal arteries

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12
Q

What is the venous drainage of the adrenal glands?

A

The medullary vein which emerges from the hilum of each gland before forming the suprarenal veins which eventually joins the inferior vena cava (RHS) and left renal vein (LHS)

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13
Q

What are the histological layers of the cortex of the adrenal gland?

A
  • zona glomerulosa
  • Zona fasciculata
  • Zona reticularis
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14
Q

What is the arrangement of the zona glomerulus of the adrenal gland?

A

Clusters of small cells.

Fewer lipids than other layers

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15
Q

What is the arrangement of the zona fasciculata of the adrenal gland?

A

Large cells arranged in cords

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16
Q

What is the arrangement of the zona reticularis of the adrenal gland?

A

Smaller cells in a haphazard arrangement

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17
Q

What is synthesised in the Zona glomerulosa of the adrenal gland?

A

Mineralocorticoids

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18
Q

What is synthesised in the Zona fasciculata of the adrenal gland?

A

Glucocorticoids

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19
Q

What is synthesised in the Zona reticularis of the adrenal gland?

A

adrenal androgens (DHEA and DHEAS)

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20
Q

How is the production of adrenal androgens in the Zona reticularis regulated?

A

ACTH

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21
Q

What are examples of glucocorticoids?

A

Cortisol or corticosterone

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22
Q

How is the production of glucocorticoids in the Zona Fasciculata regulated?

A

ACTH

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23
Q

What are glucocorticoids important for?

A

Carbohydrate regulation

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24
Q

How is the production of mineralocorticoids in the Zona glomerulosa regulated?

A

RAS

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25
Q

What are mineralocorticoids important for?

A

Sodium/BP homeostasis

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26
Q

What is the first enzymatic step of steroid hormone production?

A

The conversion of cholesterol to pregnenolone

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27
Q

What enzyme catalyses the conversion of cholesterol to pregnenolone?

A

Cytochrome P450 located in the inner mitochondrial membrane

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28
Q

What is the rate limiting step of the conversion of cholesterol to pregnenolone?

A

is the transport of free cholesterol from cytoplasm into mitochondria.

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29
Q

What enzyme carries out conversion of cholesterol to pregnenolone?

A

Steroidogenic Acute Regulatory Protein (StAR)

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30
Q

Where can cholesterol come from?

A

can be taken up from circulation or synthesised de novo from acetyl CoA or also taken up by the cell in the form of low-density lipoprotein (LDL).

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31
Q

What is the rate-limiting enzyme in cholesterol biosynthesis?

A

HMG-CoA reductase

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32
Q

What is LDL made up of?

A

cholesterol, phospholipids, triglycerides, and proteins (proteins and phospholipids make LDL soluble in blood)

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33
Q

How is LDL taken into cells?

A

via LDL receptors

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34
Q

How is LDL turned into cholesterol to synthesize steroid hormones?

A

broken down into esterified cholesterol, and then free cholesterol

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35
Q

what are the 6 domains of steroid receptors?

A

A-F

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36
Q

What do A/B domains on steroid receptors do?

A

N-terminal domain controls which gene is activated

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37
Q

What does the C domain on steroid receptors do?

A

DNA binding domain (Highly conserved) contains 2 zinc fingers which bind to specific sequences DNA (HREs)

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38
Q

What does the D domain on steroid receptors do?

A

Hinge region-controls movement of the receptor to nucleus

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39
Q

What does the E domain on steroid receptors do?

A

Ligand binding domain-binds steroid (Highly conserved)

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40
Q

What does the F domain on steroid receptors do?

A

C-terminal Domain

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41
Q

How do steroid hormones get into cells?

A

Diffuses through the plasma membrane

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42
Q

What is the mechanism of steroid hormones once they get inside the cell?

A
  • Binds to intracellular cytosolic receptor-member of steroid receptor superfamily
  • Receptor-hormone complex enters the nucleus and binds to a glucocorticoid response element (DNA Sequence) in 5’ flanking region of target genes
  • Binding initiates gene transcription to produce mRNA
  • mRNA is translated to protein which mediates the effects-target cell response
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43
Q

Where are mineralocorticoid receptors found?

A

Distal Nephron, Salivary glands, sweat glands, large intestine, Brain, vascular tissue, heart

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44
Q

What is the effect of cortisol on the liver?

A
  • Stimulates gluconeogenesis in liver. This results in the synthesis of glucose from non-hexose substrates such as amino acids and lipids
  • Permissive effect on glucagon (Glucagon causes the liver to convert stored glycogen into glucose)
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45
Q

What is the effect of cortisol on adipose tissue?

A

Stimulation of lipolysis in adipose tissue: fatty acids released are used for production of energy in tissues like muscle and the released glycerol provides another substrate for gluconeogenesis.

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46
Q

What do glucocorticoids do to insulin release?

A

They act as an insulin agonist and suppress the release of insulin

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47
Q

What effect does cortisol have on skeletal muscle?

A

Increased breakdown of skeletal muscle protein

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48
Q

What is the effect of aldosterone on the nephron?

A

causes Na+ reabsorption (and water which follows sodium) and concomitant K+ and H+ excretion.

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49
Q

Where does aldosterone act on the nephron?

A

mineralocorticoid receptors (MR) in the principal cells of the distal tubule and the collecting duct of the nephron

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50
Q

What happens when aldosterone binds to MR receptors in the nephron?

A
  • upregulates/ activates basolateral Na/K pumps
  • upregulates epithelial sodium channel (ENaC) increasing apical membrane permeability for Na+
  • stimulates the secretion of K+ into the lumen
  • stimulates secretion of H+ via the H+/ATPase in the intercalated cells of the cortical collecting tubules
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51
Q

What happens when ACTH binds to its receptor? (G-protein receptors)

A

Conformation changes in receptor stimulate adenyl cyclase, causing an increase in cAMP, activation of PKA and calcium influx

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52
Q

What is the long term effect of ACTH biding to its receptor?

A

Increased transcription of genes coding for steroidogenic enzymes e.g. 11B-hydroxylase

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53
Q

What is the rapid effect of ACTH binding to its receptor?

A

Stimulation of cholesterol delivery to the mitochondria

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54
Q

When is RAS activated?

A

In response to lowered blood pressure and potassium sodium levels

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55
Q

What does the activation of RAS lead to?

A

production of Angiotensin II

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56
Q

What is the direct effect on BP of angiotensin II?

A

vasoconstriction

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57
Q

What is the indirect effect on BP of angiotensin II?

A

aldosterone, thirst

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58
Q

What is the effect of angiotensin II binding to its receptor?

A
  • AngII binds to 7TMD G-protein coupled receptor
  • Activates phospholipase C
  • Hydrolyses phosphatidylinositol bisphosphate (PIP2) to form 2nd messengers inositol triphosphate (IP3) and diacyl glycerol (DAG).
  • IP3 causes stored Ca2+ to be released.
  • Rise in intracellular calcium ([Ca2+]i) activates Ca2+-calmodulin dependent protein kinases (CaMKs) which stimulate the transcription of StAR and cholesterol uptake into mitochondria
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59
Q

What happens in primary aldosteronism?

A
  • High levels of Aldosterone
    Increased sodium reabsorption, Volume expansion, Hypokalaemia (Potassium excretion), Alkalosis (hydrogen excretion), Low PRA, Hypertension
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60
Q

What are the most common causes of primary aldosteronism?

A

Aldosterone producing adenoma (unilateral)

Bilateral adrenal hyperplasia

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61
Q

What is Cushing’s syndrome?

A

High levels of cortisol

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62
Q

What are the signs and symptoms of Cushing’s syndrome?

A

Moon face, weight gain, High BP, Red face, extra fat around face, stretch marks

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63
Q

What are causes of Cushing’s syndrome?

A

ACTH producing adenoma (pituitary)

Cortisol producing adenoma (adrenal)

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64
Q

What is Addison’s disease?

A

Primary adrenal insufficiency or hypoadrenalism

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65
Q

What is the adrenal gland not making in Addison’s disease?

A

cortisol and aldosterone

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66
Q

What are the signs and symptoms of Addison’s disease?

A

Fatigue (lack of energy or motivation), Muscle weakness, Low mood, Loss of appetite and weight loss, increased thirst, pigmentation

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67
Q

What happens to aldosterone levels when potassium levels increase?

A

Increases

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68
Q

What is the osmolality of solution in the body maintained at the expense of?

A

Volume

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69
Q

How much of body fluid is intracellular?

A

2/3

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70
Q

What is plasma osmolality?

A

ratio of plasma solutes (sodium, glucose and urea) and plasma water

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71
Q

What is the most plentiful solute in plasma?

A

Sodium

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72
Q

How is the serum sodium concentration mainly determined?

A

By the amount of extracellular water in the body

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73
Q

What are the main mechanisms that regulate the extracellular water of the body?

A

Thirst and ADH

74
Q

What is the main role of ADH?

A

To regulate water status of the body

75
Q

What is ADH produced in response to?

A
  • Decreased plasma volume (sensed by baroceptors in atria/veins/carotids)
  • Increased plasma osmolality (sensed by osmoreceptors in hypothalamus)
76
Q

What receptor does ADH mainly act on?

A

AVP2

77
Q

Where is AVPR2 receptors found?

A

Basolateral membrane of kidney collecting ducts

78
Q

What happens when ADH binds to its receptor?

A

Aquaporin channels are inserted to increase renal water reabsorption

79
Q

What is the osmolality of solution in the body maintained at the expense of?

A

Volume

80
Q

How much of body fluid is intracellular?

A

2/3

81
Q

What is plasma osmolality?

A

ratio of plasma solutes (sodium, glucose and urea) and plasma water

82
Q

What is the most plentiful solute in plasma?

A

Sodium

83
Q

How is the serum sodium concentration mainly determined?

A

By the amount of extracellular water in the body

84
Q

What are the main mechanisms that regulate the extracellular water of the body?

A

Thirst and ADH

85
Q

What is the main role of ADH?

A

To regulate water status of the body

86
Q

What is ADH produced in response to?

A
  • Decreased plasma volume (sensed by baroceptors in atria/veins/carotids)
  • Increased plasma osmolality (sensed by osmoreceptors in hypothalamus)
87
Q

What receptor does ADH mainly act on?

A

AVP2

88
Q

Where is AVPR2 receptors found?

A

Basolateral membrane of kidney collecting ducts

89
Q

What happens when ADH binds to its receptor?

A

Aquaporin channels are inserted to increase renal water reabsorption

90
Q

What effect does aldosterone action have on the kidney?

A

increases sodium reabsorption and potassium excretion in the distal nephron. This increase in sodium status also increases plasma volume (where sodium goes water follows) and raises blood pressure

91
Q

When is someone classed as being hyponatraemic?

A

Serum sodium <135mmol/l

92
Q

What are the potential causes of SIADH?

A
  • Cancer: lung/lymphoma/ leukaemia
  • Chest disease: pneumonia
  • CNS disorders: infections, injury
  • Drugs: opiates, thiazides, anticonvulsants, proton pump inhibitors, anti-depressants
93
Q

How is a diagnosis of SIADH reached?

A
  • Hyponatraemia with inappropriate low plasma osmolality
  • Urine osmolality> plasma osmolality
  • Urine sodium> 30 mmol/l
  • Absence of adrenal, thyroid, pituitary or renal insufficiency
  • No recent use of diuretic agents
94
Q

What are the three classifications of causes of hyponatraemia?

A

Hypovolaemia
Euvolemia
Hypervolemia

95
Q

What happens in hypovolaemic hyponatraemia?

A

Decreased total body water

Decreased total body Na+

96
Q

What happens in euvolemic Hyponatraemia?

A

Total body water is increased as water is being retained

Na+ is normal

97
Q

What happens in hypervolemic Hyponatraemia?

A

Total body water is increased and Na+ is high as well but it is being diluted meaning the concentration is still low

98
Q

What are the renal causes of hypovolemic hyponatraemia?

A
  • Diuretic excess
  • Mineralocorticoid deficiency
  • Salt-losing nephritis
  • bicarbonaturia
  • Renal tubular acidosis
  • Ketonuria
  • Osmotic diuresis
99
Q

What are the extrarenal causes of hypovolemic hyponatraemia?

A
  • Vomiting
  • Diarrhoea
  • Pancreatitis
  • Traumatized muscle
100
Q

What are the causes of euvolemic hyponatraemia?

A
  • Glucocorticoid deficiency
  • Hypothyroidism
  • Pain
  • Psychiatric disorders
  • drugs
  • Syndrome of inappropriate ADH secretion
101
Q

What are the causes of hypervolemic hyponatraemia?

A
  • Nephrotic syndrome
  • Cardiac failure
  • Cirrhosis
  • Acute and chronic renal failure
102
Q

How is hypernatremia managed?

A
  • Treat underlying cause!
  • Estimate total body water deficit if possible
    • To guide fluid regimen
  • Avoid overly rapid correction
    • Aim for ↓ 10 mmol/l in 24 hours
    • Concern is cerebral oedema
  • Use IV 5% dextrose
103
Q

How is a diagnosis of SIADH reached?

A
  • Hyponatraemia with inappropriate low plasma osmolality
  • Urine osmolality> plasma osmolality
  • Urine sodium> 30 mmol/l
  • Absence of adrenal, thyroid, pituitary or renal insufficiency
  • No recent use of diuretic agents
104
Q

What happens in the brain when serum [Na] is low?

A

water moves into cells to increase plasma osmolality causing cell swelling

105
Q

What is the best way to correct hyponatraemia for the brain?

A

If corrected slowly then brain osmolality and volume are returned to normal

106
Q

What happens to the brain if there is a sudden drop in Na?

A

Cerebral oedema

107
Q

what happens if there is a sudden increase in Na?

A

Osmotic demyelination syndrome

108
Q

What are the clinical features of Hyponatraemia?

A

Can be asymptomatic but the symptoms worsen as plasma Na falls

  • Mild confusion
  • Gait instability
  • Marked confusion
  • Drowsiness
  • Seizures
109
Q

How is severe and acute hyponatraemia managed?

A
  • Unconscious or seizures
  • Give infusion of hypertonic (3%) saline – in small volumes (100ml or so)
  • Can increase quickly (but not quite back to normal) (5-10mmol/24hr)
110
Q

What is the effect of PTH on calcium and phosphate metabolism?

A

The net effect is an increase in plasma Ca concentration with no change or a decrease in plasma Phosphate concentration

111
Q

What are the main causes of hypernatremia?

A
  • Insensible/ Sweat losses ( severe burns/sepsis)
  • GI losses
  • Diabetes insipidus
  • Osmotic diuresis due to hyperglycaemia
112
Q

How is hypernatremia managed?

A
  • Treat underlying cause!
  • Estimate total body water deficit if possible
    • To guide fluid regimen
  • Avoid overly rapid correction
    • Aim for ↓ 10 mmol/l in 24 hours
    • Concern is cerebral oedema
  • Use IV 5% dextrose
113
Q

How is water deficit calculated?

A

Water deficit= current TBW x ((serum Na/140 ) -1).

TBW is 50-60% of lean body weight

114
Q

What are sources of calcium in the body?

A
  • GI tract
  • Bones
  • Kidney
115
Q

How is calcium obtained in the GI tract?

A

Absorbed throughout the small intestine from dietary sources (approx. 10% is absorbed)
This is dependent on vitamin D

116
Q

How are the bones a source of calcium?

A

Calcium reservoir

117
Q

How do the bones regulate plasma Ca?

A

Via action of osteoblasts and osteoclasts

118
Q

How much Ca is reabsorbed by the kidney?

A

97-99% of Ca is reabsorbed in the kidney

119
Q

What effect does vitamin D have on Ca?

A
  • Increases GI absorption
  • Increases bone resorption
    Increased renal reabsorption
120
Q

How is the cause of hypercalcaemia diagnosed?

A

Measure the PTH

If PTH is decreased then malignancy is likely

If PTH is normal or increased then the most likely cause is primary hyperparathyroidism

121
Q

What are the classic symptoms of hypercalcaemia?

A

Moans and bones, stones and groans

122
Q

What are the renal symptoms of Hypercalcaemia?

A
  • polyuria
  • Polydipsia
  • Nephrolithiasis
  • Nephrocalcinosis
  • Distal renal tubular acidosis
  • Nephrogenic diabetes insipidus
  • Acute and chronic renal insufficiency
123
Q

What are the GI symptoms of Hypercalcaemia?

A
  • Anorexia
  • Nausea and vomiting
  • Bowel hypomobility and constipation
  • Pancreatitis
  • Peptic ulcer disease
124
Q

What are the MSK symptoms of Hypercalcaemia?

A
  • Muscle weakness
  • Bone pain
  • Osteopenia/ Osteoporosis
125
Q

What are the neuro symptoms of Hypercalcaemia?

A
  • Decreased concentration
  • Confusion
  • Fatigue
  • Stupor, coma
126
Q

What are the ECG changes in hypercalcaemia?

A
  • Shortened QTC interval

- Bradycardia

127
Q

What can cause hypercalcaemia?

A
  • Primary hyperparathyroidism

- Malignancy

128
Q

How can primary hyperparathyroidism cause hypercalcaemia?

A

Increased bone resorption and Increased GI absorption

129
Q

How is hypocalcaemia treated?

A
  • Intravenous calcium replacement if tetany or cardiac manifestations
  • May also need magnesium infusion
  • Chronic management:
    • Vitamin D (D2 or D3)
    • Oral calcium salts
  • Treat underlying cause
130
Q

How is the cause of hypercalcaemia diagnosed?

A

Measure the PTH

If PTH is decreased then malignancy is likely

If PTH is normal or increased then the most likely cause is primary hyperparathyroidism

131
Q

How is hypercalcaemia managed with rehydration?

A
  • Patients often hypovolaemic
  • Hypovolaemia impairs renal clearance of calcium
  • Isotonic (0.9%) saline infusion corrects hypovolaemia
    • Be careful of fluid overload
  • Will not normalise calcium unless only mildly elevated
132
Q

How is hypercalcaemia managed with bisphosphonate therapy?

A
  • Inhibit bone resorption by inhibiting osteoclasts
    • Commonly used to treat osteoporosis
  • Agents of choice for treating hypercalcaemia of malignancy
    • Zoledronic acid is most commonly used
  • Delayed effect, maximal at 2-4 days after treatment
133
Q

What causes secondary adrenal insufficiency?

A
  • Lack of ACTH stimulation
  • -> pituitary/ hypothalamic disorders
  • exogenous steroid use
134
Q

What can happen with tetany in acute hypocalcaemia?

A
  • Increased neuromuscular excitability
  • Peri-oral numbness, muscle cramps, tingling of hands/feet
  • If severe: carpopedal spasm, laryngospasm, seizures
135
Q

What are the cardiac complications of acute hypocalcaemia?

A

Dysrhythmia

Hypotension

136
Q

What are the potential causes of hypocalcaemia?

A
  • Low PTH
  • High PTH
  • Dugs
  • Hypomagnesaemia
137
Q

When can low PTH cause hypocalcaemia?

A
  • After parathyroid surgery

- Autoimmune hypoparathyroidism

138
Q

Why can Hypomagnesaemia cause hypocalcaemia?

A

Leads to PTH resistance

139
Q

How is hypocalcaemia treated?

A
  • Intravenous calcium replacement if tetany or cardiac manifestations
  • May also need magnesium infusion
  • Chronic management:
    • Vitamin D (D2 or D3)
    • Oral calcium salts
  • Treat underlying cause
140
Q

What are examples of primary adrenal insufficiency?

A
  • Addison’s disease
  • Adrenal TB/ malignancy
  • Congenital adrenal hyperplasia (CAH)
141
Q

In adrenal insufficiency what are renin/ aldosterone levels expected to be?

A

Increased renin

Decreased aldosterone

142
Q

What does Congenital adrenal hyperplasia result in?

A

Deficiency of cortisol and aldosterone but increased adrenal androgens

143
Q

What causes secondary adrenal insufficiency?

A
  • Lack of ACTH stimulation

- -> pituitary/ hypothalamic disorders

144
Q

How much of the adrenal cortex is destroyed before people become symptomatic of Addison’s disease?

A

> 90%

145
Q

What other autoimmune diseases are associated with Addison’s disease?

A

Type 1 DM, Autoimmune thyroid disease, pernicious anaemia

146
Q

What are the clinical features of Addison’s disease?

A
  • Anorexia, Weight loss
  • Fatigue/ Lethargy
  • Dizziness and low BP
  • Abdo pain, vomiting, diarrhoea
  • Skin pigmentation
147
Q

How is adrenal insufficiency diagnosed?

A
  • ‘suspicious biochemistry’
  • Short synACTHen test
  • ACTH levels
  • Renin/aldosterone levels
  • Adrenal autoantibodies
148
Q

What constitutes ‘suspicious biochemistry’ when trying to diagnose adrenal insufficiency?

A

Decreased Na
Increased K
Hypoglycaemia

149
Q

What is the short synACTHen test?

A
  • Measure plasma cortisol before and 30 minutes after iv ACTH injection
  • Normal: baseline >250nmol/L, post ACTH >480
150
Q

In adrenal insufficiency what are ACTH levels expected to be?

A

Increased a lot (causes skin pigmentation)

151
Q

In adrenal insufficiency what are renin/ aldosterone levels expected to be?

A

Increased renin

Decreased aldosterone

152
Q

How is adrenal insufficiency managed?

A

Do not delay treatment until the diagnosis is confirmed

  • Hydrocortisone is given as a cortisol replacement
  • Fludrocortisone is given as an aldosterone replacement
  • Educate the patient on steroid treatment
153
Q

Why must patients on long term steroids have ID?

A

Steroid treatment cannot be stopped suddenly

154
Q

How do the clinical features of secondary adrenal insufficiency differ to those of Addison’s?

A

Skin is pale (no raised ACTH)

- Aldosterone production is intact

155
Q

How is Secondary adrenal insufficiency treated?

A

Hydrocortisone replacement

156
Q

What are the clinical features of cortisol excess?

A

Easy bruising, facial plethora, Striae, Proximal myopathy

157
Q

What are the two types of Cushing’s?

A

ACTH dependent and ACTH independent

158
Q

What can cause ACTH dependent Cushing’s?

A
  • Pituitary adenoma (68%) Cushing’s Disease
  • Ectopic ACTH 12% (carcinoid/ carcinoma)
  • Ectopic CRH <1%
159
Q

What can cause ACTH independent Cushing’s?

A
  • Adrenal adenoma 10%
  • Adrenal carcinoma 8%
  • Nodular hyperplasia 1%
160
Q

What are the steps of diagnosing Cushing’s syndrome?

A
  1. Establish cortisol excess

2. Establish source of excess

161
Q

How is cortisol excess determined when diagnosing Cushing’s disease?

A
  • Dexamethasone suppression testing
  • 24 hour urinary free cortisol
  • Late night salivary cortisol (should be low at bedtime)
162
Q

What are the surgical options for Cushing’s management?

A
  • transphenoidal pituitary surgery
  • Laparoscopic adrenalectomy
  • Removal of ACTH source
163
Q

What are the medical options for Cushing’s management?

A
  • Inhibit cortisol production - Metyrapone/ ketoconazole
164
Q

What is transphenoidal surgery?

A

Up through the nose and through the sphenoid sinus to the pituitary

165
Q

What is iatrogenic Cushing’s syndrome?

A

The most common cause of cortisol excess - due to prolonged high dose steroid therapy

166
Q

Why does long term steroid therapy cause iatrogenic Cushing’s syndrome?

A

Chronic suppression of pituitary ACTH production and adrenal atrophy

167
Q

What are the implications of adrenal suppression?

A
  • Unable to respond to stress (illness/surgery)
  • Need extra doses of steroid when ill/surgical procedure
  • Cannot stop treatment suddenly
  • Gradual withdrawal of steroid therapy if >4-6 weeks
168
Q

What is primary aldosteronism?

A

Autonomous productions of aldosterone independent of its regulators (angiotensin II/ potassium)

169
Q

What can cause primary aldosteronism?

A

Wither single adrenal adenoma or bilateral adrenal adenomas

170
Q

What are the clinical features of primary aldosteronism?

A
  • Significant hypertension
  • Hypokalaemia (in up to 50%)
  • Alkalosis
171
Q

How is Primary aldosteronism diagnosed?

A
  • Biochemistry
  • suppression testing
  • Adrenal CT
172
Q

What is the biochemistry like in primary aldosteronism?

A

Increased plasma aldosterone

Decreased plasma renin

173
Q

How is suppression testing used in the diagnosis of primary aldosteronism?

A

IV saline loading

174
Q

What is the surgical management of primary aldosteronism?

A
  • Unilateral laparoscopic adrenalectomy
  • Only if adrenal adenoma
  • Cure of hypokalaemia
  • Cures hypertension in 30-70% cases
175
Q

What is the medical management of primary aldosteronism?

A

In bilateral adrenal hyperplasia

  • Use MR antagonists (spironolactone (blocks receptor) or eplerenone)
  • Or amiloride (blocks Na reabsorption by kidney)
176
Q

What is a pheochromocytoma?

A

Catecholamine secreting tumour of the adrenal medulla

177
Q

What do pheochromocytomas cause episodes of?

A

headache, palpitations, pallor and sweating

178
Q

How is a pheochromocytoma diagnosed?

A
  • Measure urinary catecholamines and metabolites

- CT of adrenals

179
Q

How is a pheochromocytoma treated?

A

Adrenolectomy

180
Q

How is aldosterone secretion controlled?

A

By RAS and plasma K+

MBChB - year 2 (25 decks)

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