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Year 3 - Met3b > Endocrine Hypertension and Calcium Disorders > Flashcards

Endocrine Hypertension and Calcium Disorders Flashcards

1
Q

What target organs are damaged by hypertension

A
  • Heart
  • Kidneys
  • Eyes
  • Brain
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2
Q

How is the heart affected by hypertension

A
  • can cause left ventricular hypertrophy
  • lead to heart failure
  • puts it at risk of MI
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3
Q

How is the kidney affected by hypertension

A
  • Small shurnken kidneys

- proteinuira

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4
Q

How are the eyes affected by hypertension

A
  • hypertensive retinopathy

- palipoedema

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5
Q

How are is the brain affected by hypertension

A
  • intracerebral haemorrhage
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6
Q

What are the grades of hypertensive retinopathy

A

 Grade 1 – silver (copper) wiring
 Grade 2 – arteriovenous nipping
 Grade 3 – flame shaped haemorrhages + exudates
 Grade 4 - papilloedema

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7
Q

What are the secondary causes of hypertension

A

 Cardiac:
- Coarctation

 Renal:
- CKD, 
- glomerulonephritis,
- renovascular disease(renal
artery stenosis) - might hear a renal bruit

 Endocrine:

  • Conns,
  • Cushings,
  • Phaeochromocytoma
  • Acromegaly
  • Hypothyroidism
  • Hyperparathyroidism
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8
Q

What are the risk factors for secondary hypertension

A

 Younger Age

 Strong Family History

 Requirement for multiple anti-hypertensives (due to resistant hypertension)

 Physical signs of secondary hypertension:
- Renovascular, endocrine

 Other factors: Electrolytes, glucose, calcium

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9
Q

What is conns syndrome (primary hyperaldosteronosim)

A
  • excess production of aldosterone, independent of the RAAS system causing increase in sodium and water retention and decreases renin release
  • hyperaldosteronism which leads to hypertension and hypokalemia
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10
Q

What are the causes of conns syndrome

A
  • adrenal adenoma

- bilateral adrenal hyperplasia

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11
Q

What investigations should you do when investigating conns syndrome

A

 Electrolytes:
- hypokalaemic alkalosis

do a paired renin aldosterone level
 Elevated serum aldosterone
 Suppressed plasma renin

 Image the adrenals with CT

 Adrenal
vein sampling to differentiate unilateral from bilateral adrenal disease

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12
Q

what age group does conn’s disease occur in

A
  • Aged 40-60 years old
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13
Q

describe the hypertension experienced by conns disease

A

 Resistant hypertension: more than 3 agents

 Severe hypertension: >160 mmHg systolic or 100 mmHg diastolic

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14
Q

Patients with conns disease are not…

A

always hypokalaemic

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15
Q

How do you manage conns disease

A

 Unilateral adrenal adenoma:
- Surgery

 Bilateral adrenal hyperplasia:
- aldosterone antagonist
▪ eg eplerenone, spironolactone

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16
Q

how can cushing syndrome present in hypertension

A

Exogenous
- prednisolone therpay

Endogenous

  • Cortisol excess
  • ACTH - dependant
  • ACTH - independant
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17
Q

What happens in a phaecytochroma

A

excess catecholamines

-tumour of adrenal medulla

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18
Q

What is the adrenal medulla regulated by

A

Adrenal medulla is regulated by direct cholinergic input from the splanchnic nerve

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19
Q

What do chromaffin cells secrete

A

Chromaffin cells secrete adrenaline > noradrenaline > dopamine

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20
Q

What do catecholamines activate

A

 Tachycardia
 Vasoconstriction
 Hypertension
 Fight, fright, flight response

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21
Q

What is the 10% rule in phaechromocytoma

A

 10% extra adrenal
 10% malignant
 10% familial endocrine neoplasia syndromes

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22
Q

List what is the types of familial endocrine neoplasia syndromes

A
  • Von hippel lindau disease
  • MEN 2
  • SDH mutation
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23
Q

Describe Von hippel lindau disease

A
  • cerebellar haemangioma
  • retinal angiomata
  • renal cell carcinoma
  • phaeochromocytoma
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24
Q

Describe MEN2

A
  • Medullary carcinoma thyroid
  • Phaeochromocytoma
  • hyperparathyroidism
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25
Q

What diseases are associated with an increased risk of phaeochromocytoma

A
  • Von hippel lindau disease
  • MEN 2
  • SDH mutation
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26
Q

What does A1 and A2 alpha receptors do

A

 A1: vasoconstriction

 A2: vasoconstriction

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27
Q

What do B1 and B2 receptors do

A

 B1: increased heart rate,
increased cardiac contractility
 B2: vasodilatation, increase hepatic glucose production, increase renin secretion

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28
Q

name some alpha receptor blockers

A

 Doxazosin

 Phenoxybenzamine

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29
Q

Name some beta receptor blockers

A

 Propranolol

 Atenolol

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30
Q

What investigations do you do for a phaeochromocytoma

A

 24 hour collection (3 times) urine catecholamines / metanephrines
 Imaging of the abdomen CT or MRI
 MIBG scan
 (Screening for endocrine neoplasia syndromes)

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31
Q

How do you manage a phaeochromocytoma

A

Surgery

  • alpha blockage pre-op: phenoxybenzamine (used before beta blocker to avoid crisis from unopposed alpha-adrenergic stimulation) + beta blocker if heart disease or tachycardia
  • malignant cases: Chemotherapy and therapeutic MIBG
  • post-op: do 24 hour urine metanephrine 2 weeks post op, monitor blood pressure

Follow up
- lifelong malignant recurrence may present late; genetic screening

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32
Q

what hormone does GH counteract the effective of

A

GH is a stress hormone and counters the effects of insulin

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33
Q

what adenoma can cause growth hormone excess

A
  • Secretory adenoma of the pituitary somatotroph cells
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34
Q

What investgiations do you do to investigate growth hormone excess

A

 Oral glucose tolerance test
 Failure of suppression of growth hormone after 75 grams of
glucose

 IGF-1

 MRI pituitary fossa

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35
Q

What is the management of growth hormone excess

A

 Trans-sphenoidal resection

 Post op radiotherapy

 Medical management
 Somatostatin analogues
  ▪ Octreotide
 Growth hormone receptor antagonist
  ▪ Pegvisomont
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36
Q

What happens with serum calcium falls

A
  • PTH increases
  • leads to increase in activation of vitamin
  • increase in movement of calcium from the bones into the blood
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37
Q

What is the differential diagnosis of polyuria and polydipsia?

A
  • diabetes mellitus
  • diabetes inspedius - can be cranial or nephrogenic
  • hypercalemia
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38
Q

if serum PTH is risen in a high calcium what does that mean

A

hyperparathyroidism

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39
Q

what happen if serum PTH is low and there is high calcium

A
  • most likely not related to the parathyroid gland and can be due to malignancy
  • due to excess PTHrp produce by the tumour
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40
Q

How do you manage hypercalcaemia

A
  1. Give 5% dextrose
  2. Give IV saline and pamidronate
  3. Give IV saline alone
  4. Give 5% dextrose and pamidronate
  5. Give IV saline and calcitonin
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41
Q

How do you investigate hyperparathyroidism

A

Localise the parathyroid adenoma using

  • USS
  • SestaMibi Scan
  • Parathyroid venous sampling
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42
Q

How do you manage cancer

A

 Treat cancer

 Bisphosphonates

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43
Q

Where is phosphate predominantly found

A
  • Predominantly bound in bone (85%) and some in the serum
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44
Q

What happens to phosphate at the kidney

A

When it is in the blood and not bound to protein it is filtered by the kidney and it is either:

  • reabsorbed at the PCT
  • reabsorbed via the Na/PO4 co-transporter in the loop of Henle
  • excreted as a urinary buffer
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45
Q

How does PTH reduce the phosphate reabsorption in the loop of Henle

A
  • PTH inhibits the Na/PO4 co transporter

- this reduces phosphate reabsorption in the loop of Henle

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46
Q

Where is calcium in the body

A
  • most in the bone 99.9%
  • ## rest in the serum - 50% protein bound, 40% ionised, 10% in complexes with phosphate/citrate
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47
Q

How much of calcium is biologically active

A

2.2-2.6mmol/L

48
Q

How is calcium filtered in the kidney

A
  • most is reabsorbed at the PCT
  • further absorption in the thick ascending loop of Henle where some potassium leaks back into the lumen via Na/K/2Cl co-transporter
  • the resulting electrochemical gradient drives paracellular absorption of sodium, magnesium and calcium
49
Q

what do loop diuretics cause in terms of calcium

A
  • Hypocalcaemia
50
Q

What do thiazide diuretics cause in terms of calcium

A
  • hypercalcaemia

- increases calcium reabsorption in DCT useful for treating idiopathic hypercalciuria and stone formation

51
Q

How does PTH affect calcium reabsorption

A
  • increase calcium reabsorption in the DCT
52
Q

What happens to calcium in acidaemia

A
  • decrease binding to protein so there is an increase in ionised calcium
53
Q

What happens to calcium in alkalaemia

A
  • increase binding to protein therefore there is a decrease in ionised calcium
54
Q

What is parathyroid hormone secreted in response to

A
  • secreted in response to decreased ionised calcium
55
Q

Where is parathyroid hormone produced

A
  • from 4 parathyroid glands behind the thyroid
56
Q

What controls parathyroid hormone

A
  • controlled by negative feedback of calcium
57
Q

What is the function of parathyroid hormone

A
  • increases osteoclast activity this releases calcium and phosphate form the bones
  • increases calcium and decreases phosphate reabsorption in the kidney
  • increases 1,25-dihydroxyvitamin D3 production
58
Q

Where is calcitonin produced

A
  • secreted by parafollicular cells (C-cells) of the thyroid
59
Q

what is calcitonin released in response to

A

increased ionised calcium

60
Q

What does calcitonin do

A
  • counteracts the effects of PTH and increase secretion of sclerotin by osteocytes
61
Q

describe how vitamin D is produced

A
  • 7-dehydrocholesterol is turned into provitamin D from the skin and UV radiation
  • vitamin D is then converted into 25-hydroxyvitamin D (liver) unregulated
  • 25-hydroxyvitamin D is turned to 1,25-dihydroxyvitamin D in the kidney and this is regulated
62
Q

What are the actions of 1,25-dihydroxyvitamin D

A
  • intestine - increases calcium and phosphate absorption
  • Kidney - increases calcium and phosphate reabsorption
  • Bone - stimulates osteoclast to increase bone reabsorption to calcium and phosphate
63
Q

How does hypercalcaemia present

A
  • Bones - pain
  • stones - renal biliary
  • abdomen groans - abdominal pain, nausea and vomiting, constipation
  • psychic moans - confusion, cognitive dysfunction, depression, anxiety, insomnia, lethargy, coma, hyporeflexia
  • thrones - polyuria, polydipsia
64
Q

What does hypercalcaemia look like on an ECG

A
  • Short QT interval
65
Q

What are the causes of hypercalcaemia

A

Hyperparathyroidism

  • primary
  • secondary
  • tertiary
  • malignant
  • familial hypocalciuric hypercalcaemia
  • excess action of vitamin D
  • excess calcium intake
  • drugs
  • thryotoxicosis
  • Addison’s disease
66
Q

What is the most common cause of hypercalcaemia

A

primary hyperparathyroidism

67
Q

What causes primary hyperparathyroidism

A
  • solitary adenoma
  • hyperplasia of all glands
  • parathyroid cancer
68
Q

What causes secondary hyperparathyroidism and what happens in it

A
  • reduced vitamin D intake and CKD (no Hypercalcaemia)

- decreased calcium and increased PTH

69
Q

What happens in tertiary hyperparathyroidism

A

Prolonged secondary hyperparathyroidism

  • glands act autonomously due to hyperplasia/adenoma
  • causes increase calcium from increased secretion of PTH unlimited by negative feedback control
70
Q

What cancers can cause malignant hyperparathyroidism

A
  • squamous cell cancer
  • breast cancer
  • renal cell cancer
71
Q

describe how malignant hyperparathyroidism happens

A
  • parathyroid-related protein (PTHrP) is produced by the tumour, this mimics PTH resulting in increased calcium
  • PTH is decreased as PTHrP is not detected in assay
72
Q

What does familial hypocalciruic hypercalcaemia due to

A
  • autosomal dominat mutation in calcium sensing receptors in PTH glands and cells in thick ascending limb
  • this lead to increase in serum calcium and decrease in excretion
  • the increase inc calcium is detected as normal due to defect of the receptors so PTH increases due to loss of negative feedback
73
Q

what can cause excess action of vitamin D

A
  • Iatrogenic or self-administered excess
  • granulomatous diseases such as sarcoidosis, tuberculosis
  • lymphoma
74
Q

What causes excessive calcium intake

A
  • milk-alkali syndrome
75
Q

What drugs cause hypercalcaemia

A
  • thiazide diuretics
  • vitamin D analogues
  • lithium
  • Vitamin A
76
Q

What do bloods look like in

  • calcium
  • PTH
  • phosphate
  • ALP

for

  • primary hyperparathyroidism
  • secondary hyperparathyroidism
  • tertiary hyperparathyroidism
  • malignant hyperparathyroidism
  • familial hypocalciuric hypercalcaemia
A

Primary Hyperparathyroidism

  • calcium = raised
  • PTH = raised
  • phosphate = decreased
  • ALP = raised

Secondary hyperparathyroidism

  • calcium = lowered
  • PTH = raised

Tertiary hyperparathyroidism

  • calcium = raised
  • PTH = double raised

Malignant hyperparathyroidism

  • Calcium - raised
  • PTH - lowered

familial hypocalciuric hypercalcaemia

  • Calcium = raised
  • PTH = raised
77
Q

What does a DEXA scan look like in hypercalemia

A
  • subperiosteal erosions or cysts
  • brown tumours of phalanges
  • Acro-osteolysis
  • Pepper pot skull
78
Q

What does end organ damage to hypercalaemia look like

A
  • Bone – osteoporosis
  • Renal – calculi, impairment, nephrocalcinosis
  • Joints – chondrocalcinosis, pseudogout
  • Pancreas – pancreatitis
79
Q

Acute hypercalcaemia is greater than..

A

> 3.5mmol/L

80
Q

How do you manage acute hypercalcaemia

A
  1. IV saline and a loop diuretic
  2. Bisphosphonates IV -e.g. pamidronate
  3. Calcitonin - if no response to IV bisphosphonates
  4. glucocorticoids - prednisolone 40mg/day
81
Q

How do you treat mild hyperparathyroidism

A
  • increase fluid intake to prevent stones
  • avoid thiazides
  • high calcium and vitamin D diet
  • review 6 monthly
82
Q

What surgery can you do for hyperparathyroidism

A

Excision of adenoma or partial/total parathyroidectomy

83
Q

What are the indications for surgery in hyperparathyroidism

A
  • increase in serum or urinary calcium
  • bone disease
  • osteoporosis
  • renal calculi
  • decreased renal function
  • aged less than 50 years
84
Q

What are the complications that result from surgery in hyperparathyroidism

A
  • hypoparathyroidism
  • recurrent laryngeal nerve damage (hoarse voice)
  • symptomatic hypocalcaemia
  • recurrence of adenoma
85
Q

What is the medical treatment in hyperparathyroidism

A
  • HRT
  • bisphosphonates to inhibit bone reabsorption
  • calcium sensing receptor agonists - to reduce PTH secretion
86
Q

What are the side effects of calcium sensing receptor agonists

A
  • myalgia

- decrease testosterone

87
Q

How does hypocalcaemia present

A
  • Chvostek’s and Trousseau’s signs
  • hyperreflexia
  • spontaneous twitching
  • muscle cramps
  • tingling and numbness
  • anxiety
  • tetany
88
Q

What is the ECG of hypocalcaemia

A
  • Long QT interval

- Small T waves

89
Q

Name the causes of hypocalcaemia

A
  • hypoparathyroidism
  • drugs
  • CKD
  • vitamin D deficiency
  • acute pancreatitis - inhibition of bone reabsorption
  • low plasma albumin - liver disease and malnutrition
90
Q

Describe how primary hypoparathyroidism causes hypocalcaemia

A
  • due to gland failure e.g. autoimmune, congenital (DiGeorge syndrome), idiopathic
91
Q

Describe how secondary hypoparathyroidism causes hypocalcaemia

A
  • radiation
  • thyroidectomy
  • parathyroidectomy
  • severe hypomagnesaemia (PPI-induced, magnesium is required for PTH secretion)
92
Q

Describe how Pseudo hypoparathyroidism causes hypocalcaemia

A
  • failure of target cell response to PTH

- e.g. overactivity of calcium receptor may lead to desensitisation

93
Q

What are the signs of pseudo hypoparathyroidism

A
  • 4th and 5th metacarpals
  • round face
  • short stature
  • calcified basal ganglia
94
Q

What are drugs that cause hypocalcaemia

A
  • Calcitonin – inhibition of bone resorption
  • Bisphosphonates – inhibition of bone resorption
  • Phosphate therapy – increased phosphate levels
95
Q

Describe what can cause vitamin D deficiency leading to hypocalcaemia

A
  • intestinal malabsorption - e.g. coeliac disease
  • diet
  • inadequate sunlight exposure
96
Q

What investigations do you use in hypocalcaemia

A
  • History and serum calcium - usually diagnostic

Other blood tests

  • phosphate
  • ALP
  • U&Es
  • PTH
  • parathyroid Abs
  • 25-hydroxyvitamin D
  • magnesium

Other tests - X ray of metacarpals (pseudoparathyroidism)

97
Q

What does primary and secondary hypoparathyroidism look like in blood

  • calcium
  • PTH
  • phosphate
  • ALP
A
  • calcium = decreased
  • PTH = decreased
  • phosphate = increased or normal
  • ALP = normal
98
Q

What does psuedohypoparathyrodism look like in

  • calcium
  • PTH
  • phosphate
  • ALP
A
  • calcium = decreased
  • PTH = increased
  • ALP = increased or normal
99
Q

What is the difference between chronic and acute hypocalcaemia

A
  • Chronic hypocalcaemia = <1.9mmol/L without symptoms

- Acute hypocalcaemia = <1.9mmol/L with symptoms

100
Q

how do you mange chronic hypocalcaemia

A
  • calcium supplements

- calcitriol

101
Q

How do you manage acute hypocalcaemia

A
  • IV calcium gluconate

- alpha- calcidiol

102
Q

What is the blood supply of the adrenal gland

A
  • Superior, middle and inferior adrenal arteries anastomose underneath the capsule
  • Medulla - supplied by long cortical arteries which drain blood from the cortex and therefore the blood may contain corticosteroids that influence that medulla’s production of adrenaline
  • cortex- supplied by short cortical arteries
103
Q

What are the zones of the adrenal cortex

A

Zona glomerulosa – mineralocorticoids – aldosterone
- Na+ and K+ retention by the kidneys

Zona fasciculata – glucocorticoids – cortisol
- Glycogen, protein and fat breakdown into glucose; Suppression of immune system (prostaglandins)

Zona reticularis – androgens – dehydroepiandrosterone
- Sex steroids which have weak effect until peripheral conversion to testosterone and dihydrotestosterone

104
Q

What causes secondary hyperaldosteronism

A
  • due to increase renin from decreased renal perfusion e.g. renal artery stenosis, accelerated hypertension, diuretics, CCF, hepatic failure
105
Q

what are the symptoms of Conns disease

A
  • often asymptomatic
  • hypokalaemia
  • weakness
  • cramps
  • paraesthesiae
  • polyuria
  • polydipsia
  • hypertension (not always)
106
Q

What are the causes of hyperaldosteronism

A
  • 2/3- Conn’s syndrome: solitary aldosterone-producing adenoma
  • 1/3- bilateral adenocortical hyperplasia
  • rare causes - adrenal carcinoma, glucocorticoid-remediable aldosteronism (GRA)
107
Q

What is the management of hyperaldosteronism

A
  • Conn’s - laparoscopic adrenalectomy + 4 weeks pre-op spironolactone - 25-100mg/24 hour PO (to decreases BP and increase potassium)
  • hyperplasia - medically: spironolactone or amiloride
  • GRA-1) dexamethasone 1mg/25hour PO for 4 weeks (normalities biochemistry but not always BP) OR 2) Spironolactone if blood pressure still raised
  • adrenal carcinoma - surgery +/- post-operative adsrenolytic therapy with mitotane (prognosis is poor)
108
Q

What is phaechromocytoma

A
  • rare catecholamine-producing tumours arising fro sympathetic chromatin cells
109
Q

What is the classic triad of phaechromocytoma

A
  • episodic headache
  • swelling
  • tachycardia

blood pressure can be decreased, increased or normal

110
Q

What are the features of phaechromocytoma

A
  • Heart = tachycardia, palpitations/VT, dyspnoea, faints, angina, MI/LVF, cardiomyopathy
  • CNS - headache, visual disorder, dizziness, tremor, numbness, fits, encephalopathy, Horner’s syndrome, subarachnoid/CNS haemorrhage
  • Psychological - anxiety, panic, hyperactivity, confusion, episodic psychosis
  • Gut - D&V, abdominal pain over tumour site, mass, mesenteric vasoconstriction
  • others - sweats/flushes, heat intolerance, pallor, fever, backache, haemopytsis
111
Q

What does the ECG say in phaechromocytoma

A
  • Signs of LVF
  • raised ST segment
  • VT
  • Cardiogenic shock
112
Q

What are the precipitating factors of phaechromocytoma

A
  • straining
  • exercise
  • stress
  • abdominal pressure
  • surgery
  • drugs (beta blockers, IV contrast agents, TCAs)
  • sexual intercourse
  • parturition
  • defecation
  • micturition
113
Q

In what three cases should you think Conn’s disease in hypertension

A
  • Hypertension associated with hypokalaemia
  • Refractory hypertension, eg despite ≥3 antihypertensive drugs
  • Hypertension occurring <40yrs of age (especially in women)
114
Q

Describe how Conn’s syndrome leads to hypertension

A
  • normally when BP or blood volume decreased, angiotensinogen is converted into angiotensin I (by renin in kidney)
  • angiotensin I is converted to angiotensin II
  • angiotensin II stimulates the release of CRH which stimulates ACTH release
  • angiotensin II + ACTH + increase in potassium leads to aldosterone secretion
  • in Conn’s aldosterone secretion occurs pathologically in excess and its effects are:
  • decrease in sodium and water excretion
  • increase in potassium excretion
  • renin suppression

This results in an increase in blood volume and pressure

115
Q

Describe how renal artery stenosis leads to hypertension

A
  • juxtaglomerular apparatus releases renin in reponse to lowered blood pressure in the afferent arterioles
116
Q

describe how pheochromocytoma leads to hypertension

A
  • Juxtaglomerular apparatus releases renin in reponse to sodium (excess from tumour)

Year 3 - Met3b (26 decks)

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