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MSRA > Endocrine and Metabolic Disturbance > Flashcards

Endocrine and Metabolic Disturbance Flashcards

1
Q

What is the difference between primary and secondary endocrine disease?

A

Primary - target organ dysfunction

Secondary - pituitary dysfunction

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2
Q

What are mineralocorticoids and where are they produced?

A

Function is to influence salt and water balance

Produced in the zona glomerulosa in the adrenal cortex.

eg. aldosterone

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3
Q

What are glucocorticoids and where are they produced?

A

Function is to reduce inflammation and suppress the immune system. Affect carbohydrate, lipid and protein metabolism.

Produced in the zone fasciculate in the adrenal cortex.

eg. cortisol

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4
Q

What are androgens and where are they produced?

A

Sex hormones, produced in the zona reticularis in the adrenal cortex (also in the reproductive organs)

eg. testosterone

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5
Q

What is produced in the adrenal medulla?

A

Epinephrine, norepinephrine and dopamine

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6
Q

What is Cushing’s syndrome?

A

Clinical state produced by chronic glucocorticoid excess and loss of the normal feedback mechanisms of the hypothalamo-pituitary-adrenal axis.

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7
Q

What causes Cushing’s syndrome?

A

Exogenous:
- Oral steroids

Endogenous:

  • Adrenal tumour (benign/malignant - low ACTH)
  • Pituitary tumour secreting ACTH (Cushing’s disease)
  • Ectopic ACTH secreting tumours (SCLC, carcinoid)
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8
Q

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

A

Central obesity (lemon on a stick), moon face, striae, plethora, buffalo hump, thin skin/hair/nails, hirsutism, acne, depression, bruising, DM

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9
Q

How is Cushing’s syndrome investigated primarily? (what is diagnostic)

A
  1. 24 hour urinary free cortisol excretion (levels >280) AND
  2. Overnight dexamethasone suppression test (no cortisol suppression as loss of feedback
  3. 48h dexamethasone suppression test (measure at 0 and 48h, failure to suppress cortisol)

Bloods may show hypokalaemic metabolic acidosis - this is because cortisol at high levels can simulate the effects of aldosterone > increased sodium > potassium excretion > bicarbonate resorption

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10
Q

How can you localise the cause of Cushing’s syndrome?

A
  1. Do plasma ACTH levels:
    - Low ACTH = adrenal tumour (do CT/MRI)
    - High ACTH = pituitary/ectopic tumour
  2. Ectopic ACTH suspected - administer metyrapone (inhibits cortisol synthesis), if cortisol is still high the ACTH is coming from an ectopic source
  3. High dose dexamethasone test:
    - <90% drop in urinary cortisol = ectopic ACTH
    - >90% drop in urinary cortisol = pituitary adenoma (cushings disease)
  4. Then do corticotrophin releasing test, cortisol will rise with pituitary disease but not ectopic.
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11
Q

What is Cushing’s disease?

A

Bilateral adrenal hyperplasia from an ACTH-secreting pituitary adenoma.

Plasma cortisol not suppressed on low dose dexamethasone test only high dose.

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12
Q

What can cause ectopic ACTH production? What are the specific features?

A
  • Small cell lung cancer
  • Carcinoid tumours (slow-growing, neuroendocrine)

Pigmentation, hypokalaemic metabolic acidosis, weight loss, hyperglycaemic. Tend to not have classical Cushing’s syndrome features.

Even high dose dexamethasone fails to suppress cortisol production.

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13
Q

Which adrenal tumours can cause Cushing’s syndrome?

A
  • Adrenal adenoma/malignancy (no cortisol suppression in low/high dose)
  • Adrenal nodular hyperplasia (as above)
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14
Q

How is Cushing’s disease managed?

A

MEDICAL (often adjunct to surgery)

  • Somatostatin analogue (pasireotide)
  • Steroidogenesis inhibitor (metyrapone)

SURGICAL

  • Pituitary adenectomy
  • Patients may need post-surgery steroid replacement to avoid adrenal crisis
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15
Q

How is ectopic ACTH managed?

A

MEDICAL (adjunct)

  • Mifepristone
  • Paseireotide
  • Metyrapone

SURGICAL
- Resection or ablation of tumour

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16
Q

How is adrenal disease managed?

A

MEDICAL (adjunct)

  • Mifepristone
  • Paseirotide
  • Metyrapone

SURGICAL

  • Unilateral/bilateral adrenalectomy (depending on if tumour or hyperplasia)
  • May need permanent steroid replacement
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17
Q

What causes hypoadrenalism?

A

Primary - Autoimmune destruction of adrenals aka Addison’s (glucocorticoid and mineralocorticoid deficiency)

Secondary - ACTH pituitary deficiency (only glucocorticoid deficiency as mineralocorticoids controlled by RAAS), usually due to long-term steroid use and withdrawal

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18
Q

What are the clinical features of hypoadrenalism?

A

Malaise, weight loss, nausea and vomiting, abdo pain, postural hypotension, hypoglycaemia, mood disturbance, adrenal crisis

‘Lean, tanned, tired, tearful’

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19
Q

How can you distinguish between primary and secondary causes of hypoadrenalism?

A

Do short syncathen test (synthetic form of ACTH) - measure baseline cortisol, give 250 micrograms IM syncathen and measure cortisol at 0,30,60 mins

Healthy - cortisol levels should double

Primary - subnormal response to ACTH as problem lies within adrenal gland

Secondary - dramatic increase in cortisol levels (>550NM/L) as problem lies within pituitary ACTH defieicney

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20
Q

What is Addison’s disease?

A

Autoimmune destruction of the adrenal cortex leading to mineralocorticoid and glucocorticoid deficiency. Always have at the back of your mind bc it is very non specific!

Symptoms may include:
- lethargy, weakness, weight loss, salt craving
- hyperpigmentation (as ACTH has same precursor molecule as melanocyte stimulating hormone)
- collapse/shock

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21
Q

What do investigations show in Addison’s disease?

A
  • Low sodium, high potassium
  • Low glucose
  • High urea and calcium
  • Anaemia
  • High ACTH
  • Positive 21-hydroxylase adrenal autoantibodies
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22
Q

How is Addison’s disease managed?

A

Steroid replacement with hydrocortisone and fludrocortisone

Must warn against abruptly stopping steroids as could precipitate an adrenal crisis - give steroid card! Double glucocorticoids if unwell, keep fludrocortisone the same

Follow up with BP, U&Es yearly

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23
Q

How is secondary adrenal insufficiency managed?

A
  • Dont abruptly withdraw steroids!
  • Replace glucorticoids with hydrocortisone

(nb there is no hyper pigmentation as ACTH is low)

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24
Q

What are the features of an adrenal crisis?

A

Hypovolaemic shock, abdo pain, vomiting, hypoglycaemia, confusion and fever

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25
Q

How is an adrenal crisis managed?

A
  1. 1 litre 0.9% saline STAT
  2. 100mg IV hydrocortisone STAT then 200mg/24hr
  3. Correct hypoglycaemia

Monitor BP, fluid status and electrolytes

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26
Q

What are the 3 ways in which aldosterone secretion is managed?

A
  1. RAAS - levels rise in response to low BP and renin release
  2. Potassium - directly stimulated aldosterone secretion
  3. ACTH - this is minor!!
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27
Q

What is primary hyperaldosteronism?

A

Excess production of aldosterone, independent of RAAS causing sodium and water retention (polydipsia/uria, hypertension, hypokalaemia)

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28
Q

What causes primary hyperaldosteronism?

A
  1. Solitary aldosterone-producing adenoma (Conns syndrome)

2. Bilateral adrenocortical hyperplasia

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29
Q

What are the characteristic bloods in primary hyperaldosteronism?

A
  • Hypokalemia (but not always!)
  • Hypomagnesia
  • Metabolic alkalosis
  • Aldosterone/renin ratio high
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30
Q

How is primary hyperaldosteronism managed?

A

Conn’s - laparoscopic adrenalectomy with post-op spironolactone

Hyperplasia - spironolactone, amiloride or eplenerone

Carcinoma - surgery and post-op adsrenolytic therapy with mitotane

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31
Q

What causes secondary hyperaldosteronism?

A

Any condition which increases renin production!! eg. renal artery stenosis, HF, liver failure, nephrotic syndrome Barrters syndrome Gitelmanns syndrome

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32
Q

What is Bartters syndrome?

A

Congenital (AR) salt wasting via a sodium and chloride leak in the loop of Henle due to a defective channel.

Presents with failure to thrive, polyuria, polydipsia. Normal BP!

Sodium loss leads to volume depletion causing increased renin and aldosterone production (low K, metabolic alkalosis)

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33
Q

How is Bartter’s syndrome managed?

A
  • Potassium replacement

- NSAIDS and ACE-is

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34
Q

What is a phaeochromocytoma?

A

Tumour found in the adrenal medulla that produces CATECHOLAMINES (dopamine, norepinephrine, epinephrine)

Follow the 10% rule - 10% malignant, 10% extra-adrenal, 10% bilateral, 10% familial

Symptoms precipitated by exercise, stress, certain drugs

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35
Q

What are the symptoms of phaeochromocytoma?

A

Classical triad of:

  1. Episodic headache
  2. Sweating
  3. Tachycardia

Tend to have a very high BP!!!

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36
Q

Which cancer syndromes are phaeochromocytomas sometimes related to?

A

Thyroid
MEN2A,B
Neurofibromatosis
von Hippel-Landau syndrome

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37
Q

How is phaeochromocytoma investigated?

A
  1. Do plasma and 3x24h urinary test for met adrenaline and normetadrenaline (3x normal upper limit)
  2. Abdo CT/MRI or meta-iodobenzylguanidine scan to localise tumour
  3. Genetic testing to investigate cancer syndromes
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38
Q

How is phaeochromocytoma managed?

A
  1. Alpha/beta-blockers (ensure hydration and high salt diet after to avoid hypotension) eg. phenoxybenzamine then propranolol
  2. Surgical excision of tumour (if appropriate)
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39
Q

How is a hypertensive crisis managed?

A

Phentolamine IV (alpha blocker)

Must manage quickly as risk of cerebral haemorrhage, cardiac arrhythmias, MI, HF

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40
Q

What is the use of adrenal vein sampling?

A

Used to investigate hyperaldosteronism

If aldosterone levels are >3x higher in one vein than the other, indicates a unilateral adenoma that can be surgical excised

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41
Q

Which hormones does the anterior pituitary produce?

A

ACTH, TSH, FSH/LH, Prolactin, GH

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42
Q

Which hormones does the posterior pituitary produce?

A

ADH, oxytocin

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43
Q

What causes panhypopituitarism?

A

This is deficiency of all anterior hormones due to irradiation, surgery or tumour

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44
Q

What causes hypopituitarism at the level of the hypothalamus?

A
  1. Kallmans syndrome
  2. Tumour
  3. Inflammation
  4. Infection (TB, meningitis)
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45
Q

What is Kallmans syndrome?

A

Delayed/absent puberty and impaired sense of smell due to HYPOGONADOTROPHIC HYPOGONADISM

This is X-linked recessive and caused by ANOS1 gene mutations

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46
Q

What causes hypopituitarism at the level of the pituitary stalk?

A
  1. Trauma
  2. Surgery
  3. Mass lesion eg. craniopharygioma
  4. Meningioma
  5. Carotid artery aneurysm
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47
Q

What causes hypopituitarism at the level of the pituitary?

A
  1. Tumour
  2. Irradiation
  3. Inflammation
  4. Autoimmunity
  5. Infiltration (haemochromatosis, amyloid, mets)
  6. Ischaemia (pituitary apoplexy, sheehan’s syndrome, DIC)
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48
Q

What is pituitary apoplexy?

A

Infarction/haemorrhage of the anterior pituitary (usually due to tumour) causing headache, collapse, visual loss (bitemporal quadrantopia) and death.

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49
Q

How is pituitary apoplexy diagnosed and managed?

A

Diagnose with MRI and blood tests

If severely unwell requires surgery. If milder, urgent IV steroids and fluid balance

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50
Q

What are the symptoms of hypopituitarism?

A

Depends on whichever hormone is lacking:

  1. GH - obesity, dry, low strength, osteoporosis
  2. FSH/LH - no menses, los of fertility, erectile dysfunction, low libido, hair changes
  3. Thyroid - think hypothyroidism
  4. ACTH - adrenal insufficiency but no pigmentation!
  5. Prolactin - rare, absent lactation
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51
Q

How is hypopituitarism investigated?

A

BLOODS - LH, FSH, testosterone, oestrogen, prolactin, IGF-1, U&E, FBC

SPECIAL - short synacthen, insulin tolerance test, growth hormone tests

IMAGING - MRI to look for lesion

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52
Q

How is hypopituitarism managed?

A
  1. TREAT UNDERLYING CAUSE

2. REPLACE DEFICIENT HORMONES

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53
Q

What is Sheehan’s syndrome?

A

Postpartum pituitary gland necrosis - caused by blood loss and hypovolaemic shock during and after childbirth

Classic early symptoms are agalactorrhoea, hypothyroidism and amenorrhea

If severe can see pituitary halo ring sign on CT/MRI (halo around empty sella turtica)

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54
Q

What can cause a raised prolactin?

A

the p’s:

pregnancy
prolactinoma
physiological
PCOS
primary hyperthyroidism
phenothiazine, metoclopramide, domperidone

Presents as impotence, loss of libido, amenorrhoea, galactorrhoea

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55
Q

How is prolactin quantified?

A

Raised prolactin = PRL>390mU/L

If >5000 likely to be a prolactinoma

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56
Q

What are the symptoms of hyperprolactinaemia?

A

Females: amenorrhoea, infertility, galactorrhea, loss of libido, weight gain, dry vagina

Males (present later): ED, loss of hair, glacrotthoea, osteoporosis

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57
Q

What is a prolactinoma and how is it treated?

A

Benign lactotroph adenoma expressing and secreting prolactin - usually due to a mutation in the lactotroph causing it to divide uncontrollably

Management:
1st line - dopamine agonists eg. bromocriptine, cabergoline
2nd line - trans-sphenoidal hypophysectomy

58
Q

What are the symptoms of a prolactinoma?

A
  1. Symptoms of prolactinoma (incl subfertility and osteoporosis)
  2. Symptoms of mass effect (headaches, visual loss, seizures)

Men/post-menopausal women tend to present later with macro-adenomas (as no menstrual irregularity)

59
Q

What is a microadenoma and how is it managed?

A

Micro (<10mm on MRI)

Management may not be needed unless affecting fertility. Dose titration of DA (bromocriptine/cabergoline), give at night due to hypotension

60
Q

What is a macroadenoma and how is it managed?

A

Macro (>10mm on MRI)

More likely to cause pain from meninges compression and ocular symptoms (bitemporal hemianopia) as near the optic chiasm.

Manage with cabergoline, consider radiotherapy or surgical resection if severe

61
Q

Why can prolactinomas affect fertility?

A
  1. Inhibits GnRH and decreases FSH/LH

2. Less oestrogen/testosterone produced

62
Q

What is acromegaly?

A

Increased secretion of growth hormone due to a pituitary tumour or hyperplasia

63
Q

What is the normal role of growth hormone?

A

Stimulates bone and soft-tissue growth through secretion of IGF-1

64
Q

What are the signs and symptoms of acromegaly?

A
  • Acroparaesthesia
  • Amenorrhoea
  • Loss of libido
  • Headache
  • Sweating
  • Arthralgia/back age
  • Growth of hands
  • Coarse features
  • Skin darkening and acanthuses nigricans
  • OSA
  • Goitre
  • Any symptoms of mass effect from pituitary mass
65
Q

What are the complications of acromegaly?

A
  • Impaired glucose tolerance and DM
  • Vascular complications (IHD, arrhythmias, stroke)
  • Neoplasia (colon cancer)
66
Q

What do investigations show in acromegaly?

A

BEDSIDE: ECG/echo to look for cardiac complications, visual fields, ask for old photo for comparison

BLOODS: raised glucose, calcium, phosphate, IGF1

SPECIAL: failure to suppress GH ( >1 microgram/L) in oral glucose tolerance test

IMAGING: MRI may show tumour

67
Q

How is acromegaly secondary to pituitary tumour managed?

A
  1. Transphenoidal surgery
  2. Somatostatin analogue (eg. pasireotide)/ growth hormone antagonist
  3. Radiotherapy
68
Q

What is a somatostatin analogue?

A

Drugs that stop hormone production, used in neuroendocrine tumours

Naturally occurring somatostatin also control emptying of stomach and bowel (so may cause GI side effects)

69
Q

Describe the physiology of the thyroid

A
  1. Hypothalamus secretes TRH
  2. TRH stimulates TSH release from anterior pituitary
  3. Thyroid produces T4 (mostly) and T3
  4. T4 converted to T3 peripherally
  5. Most T4/3 bound to TBG making it inactive
  6. Active T4/3 increase cell metabolism and vital in growth and development
70
Q

Why is free T4/3 used to quantify thyroid disease?

A

Total T4/3 are bound to TBG - TBG is increased in pregnancy, HRT and hepatitis and decreased in nephrotic syndrome and malnutrition

Free T4/3 therefore gives a better idea of thyroid function alone

71
Q

What do the following bloods signify:

a) high TSH, low T4
b) high TSH, normal T4
c) high TSH, high T4
d) high TST, high T4, low T3

A

a) Hypothyroidism
b) Treated/subclinical hypothyroidism
c) TSH secreting tumour/thyroid hormone resisitance
d) slow conversion of T4 to T3

NB - in hypO thyroidism, T3 usually not needed

72
Q

What do the following bloods signify:

a) low TSH, high T4/T3
b) low TSH, normal T4/T3
c) low TSH, low T4
d) low TSH, low T4/T3
e) normal TSH, abnormal T4

A

a) Hyperthyroidism
b) Treated/subclinical hyperthyroidism
c) Central hypothyroidism (hypothalamic/pituitary disorder)
d) Sick euthyroidism
e) Amiodarone, assay interference, pituitary TSH tumour

73
Q

What is sick euthyroidism?

A

TFTs may become deranged in systemic illness - causes everything to be low. Repeat tests after recovery.

74
Q

What other special tests can be performed in thyroid disease?

A
  • Autoantibodies
  • Receptor antibody
  • Serum thyroglobulin
  • Ultrasound
  • Isotope scan (looks at hot and cold nodules)
75
Q

What are the signs and symptoms of hyperthyroidism?

A

Symptoms: diarrhoea, weight loss, anxiety, palpitations, increased appetite, sweating, heat intolerance, mood

Signs: irregular pulse, tremor, erythema, thin hair, lid lag, goitre, nodules

76
Q

What causes hyperthyroidism?

A
  • Graves disease
  • Toxic multi nodular goitre (iodine deficient, elderly)
  • Toxic adenoma (hot nodule)
  • Ectopic thyroid tissue (metastatic cancer)
  • Exogenous thyroid production (iodine excess)
77
Q

What is Graves disease and what are the specific signs?

A

Autoimmune IgG disorder causing smooth thyroid enlargement and increased hormone production.

  1. Eye disease (esp if smoker)
  2. Pretibial myxoedema (swelling)
  3. Thyroid acropachy (clubbing)
78
Q

How is hyperthyroidism managed?

A
  1. B-blockers (propanolol) for symptoms relief
  2. Carbimazole for thyroid blocking
  3. Radioiodine with thyroxine replacement
  4. Thyroidectomy with thyroxine replacement

Pregnancy:
1st trimester - prophylthiouracil
2nd trimester - switch to carbimazole

79
Q

How is carbimazole initiated and what are the major side effects?

A

Start at 40mg and reduce gradually to maintain euthyroidism, usually continued for 12-18 months

AGRANULOCYTOSIS - need urgent FBC if signs of infection and ulcers

80
Q

How does eye disease manifest in Graves disease and how is it managed?

A

Eye discomfort, grittiness, diplopia, EXOPTHALMOS, PROPTOSIS, conjunctival oedema, loss of colour vision, OPTHALMOPLEGIA

Consider IV steroids/surgical decompression for severe disease

81
Q

What are the features of a thyrotoxic storm?

A

Agitation, confusion, coma, tachycardia, AF, goitre, jaundice bruit, acute abdomen, heart failure, collapse

Precipitated by recent surgery/radioiodine, infection, MI, trauma

82
Q

How is thyrotoxic storm managed?

A
  1. IV access, fluids, NG
    2 Treat underlying precipitating event
  2. IV propanolol (cardiac specific beta blocker like atenolol/metoprolol/esmolol or dilitiazem if asthma/poor cardiac output)
  3. Digoxin to slow heart
  4. Propylthiouracil/methimazole IV
  5. Lugols iodine
  6. Dexamethasone IV to prevent T4-T3 conversion
  7. Co-amoxiclav IV if suspected infection
  8. Plasma exchange if treatment refractory
83
Q

What are the signs and symptoms of hypothyroidism?

A

Symptoms: Tired, low mood, weight gain, cold intolerance, weight gain, constipation, menorrhagia

Signs: reflexes poor, ataxia, dry hair/skin, drowsy, cold, ascites, immobile

84
Q

What causes hypothyroidism?

A
  • Iodine defiency (main cause worldwide)
  • Autoimmune (primary atrophic, hashimotos - main cause in UK)
  • Post-thyroidectomy
  • Subacute (de Quervain’s) - triphasic course of transient thyrotoxicosis, hypothyroid and euthyroidism post viral infection
  • Drug-induced (amiodarone, lithium, iodine)
85
Q

What are the 2 autoimmune causes of hypothyroidism?

A
  1. Hashimotos - goitre, common in women, may have transient thyrotoxicosis in acute phases, positive TPO/Tg antibodies, associated with development of MALT lymphoma (slow growing NHL)
  2. Primary atrophic - no goitre
86
Q

What are the complications of hypothyroidism in pregnancy?

A

Eclampsia, anaemia, prematurity, low birthweight, stillbirth - measure every 6 weeks in pregnanct patients

87
Q

How is hypothyroidism managed?

A

Levothyroxine
- start 25mcg OD in pts with IHD/over 50yo/severe hypothyroidism
- otherwise start on 50-100mcg OD

Therapeutic goal is to normalise TSH - check TFTs 8-12 weeks after starting treatment

Pregnant women should have dose increased by 25-50 micrograms

SE: hyperthyroid, poor BMD, angina, AF
Interactions: iron, calcium carb > give 4h apart

88
Q

What is a myxoedema coma?

A

Severe hypothyroidism causing hypothermia, hyporeflexia, low glucose, bradycardia, coma, seizures

May have psychotic symptoms just before the coma

89
Q

How is myxoedema coma managed?

A
  1. Admit, IV
  2. Send bloods T3/T4/TSH, FBC, U&E, cultures, cortisol, glucose, ABG
  3. Correct hypoglycaemia
  4. Give T3 (liothyronine) IV
  5. Hydrocortisone IV (due to possibility of coexisting adrenal insufficiency)
  6. Cefuroxime IV
  7. Active warming blankets

Careful with fluid resuscitation! May need inotropes

90
Q

How are subclinical thyroid states managed?

A

Recheck bloods in 2-4 months

Hypo - treat if TSH>10, autoantibodies, past graves or other autoimmune disease

Hyper - treat on individual basis (usually if TSH<0.1 and symptoms)

Recheck 6 monthly

91
Q

What is parathyroid hormone?

A

A hormone secreted in response to low calcium levels, which acts to:

  1. Increase osteoclast activity to release calcium and phosphate from bone
  2. Increased calcium and decrease phosphate reabsorption in the kidney
  3. Increase vitD3 production

The 4 parathyroid glands are situated posterior to the thyroid.

92
Q

What is primary hyperparathyroidism?

A

High PTH (may be normal), high calcium

Non-specific signs, may be weak, tired, depressed, pain, fractures, osteoporosis. Increased BP!

Due to pathology within the parathyroids - solitary adenoma (80%), hyperplasia (20%) or cancer

Treat surgically

93
Q

What is secondary parathyroidism?

A

Low calcium, High PTH

High PTH due to low levels of calcium in the blood, this may be due to low vitamin D or chronic renal failure

Treat by treating underlying cause

NB - tertiary parathyroidism comes from hyperplasia of parathyroid glands due to secondary causes, and is when the glands remain large and produce excess PTH despite resolution of underlying cause. Causes high PTH and high Ca

94
Q

How is familial hypercholesterolaemia diagnosed ?

A

Simon Broome criteria:
- In adults TC >7.5mmol/l and LDL-C >4.9 mmol/l or children TC > 6.7 mmol/l and LDL-C >4mmol/l +
- for definite FH: tendon xanthoma/DNA based evidence
- for possible FH: family hx of MI <50 yo in 2nd degree relative or <60yo in 1st degree relative, or FH of hypercholesterolaemia

95
Q

How is familial hypercholesterolaemia managed?

A
  • Dont use QRisk as not valid
  • Use high dose statins (atorvastatin 20mg or rosuvastatin 10mg) or ezetimibe 10mg/bile acid sequestrant if CI
  • Screen 1st degree relatives (including children <10yo if one affected parents)
  • Discontinue statins 3 months prior to conception in child-bearing women
96
Q

What are the symptoms and signs of hypocalcaemia?

A

Symptoms:
- Tetany
- Perioral paraesthesia
- Depression,cataracts

Signs:
- Prolonged QT on ECG
- Trousseau’s sign; carpal sapsm if brachial artery occluded by inflating BP cuff (wrist flexion and finger drawn together)
- Chvostek’s sign; tapping over parotid causes facial muscles to twitch

97
Q

What are the symptoms and signs of hypercalcemia? How is it managed?

A

Symptoms:
Bones, abdo groans, stones, thirst

Signs:
Short QT

Causes:
- Primary hyperparathyroidism
- Malignancy
- Sarcoidosis
- Acromegaly
- Thyrotoxicosis
- Drugs (thiazides)
- Dehydration
- Addisons
- Pagets disease f the bone

Management:
1. IV saline (3-4L daily)
2.Bisphosphonates/calcitonin/steroids

98
Q

What are the signs and symptoms of hypokalemia?

A

Symptoms:
Weakness, fatigue, cramps, parasthesia, palpitations, SOB

Signs:
ECG - tall p waves, prominent J waves, ST depression, long QT, VT, torsades de pointes, long PR

99
Q

What are the signs and symptoms of hyperkaelaemia?

A

Symptoms:
Heart palpitations, SOB, chest pain, N&V, weakness

Signs:
ECG changes - small p waves, wide QRS, deep t waves, tall tented t waves

100
Q

What is SIADH?

A

SIADH is characterised by hyponatraemia secondary to the dilutional effects of excessive water retention.
ADH aka vasopressin is produced by hypothalamus and stored in the pituitary gland
Its role is to regulate water balance by acting on the collecting ducts in the kidney

Features:
- Patients are typically euvolaemic
- Causes include SCLC, stroke, SAH, meningitis, TB, pneumonia, drugs, PEEP, porphyrias
- High urine osmolality >100 (concentrated), low serum osmolality. High urinary Na >40.

101
Q

How is SIADH managed?

A
  • SLOW CORRECTION to avoid central pontine myelinolysis
  • Fluid restriction
  • Demelocycle (reduced responsiveness of collecting tubule cells to ADH)
  • ADh receptor antagonists
102
Q

Where are insulin and glucagon produced?

A

Both hormones are secreted by islet of langerhans cells in pancreas

Insulin - beta cells
Glucagon - alpha cells

103
Q

How does insulin work?

A
  1. High levels of blood glucose causes insulin release
  2. Insulin binds to insulin receptors in muscle cells and adipose tissue
  3. Vesicles containing glucose transporters from inside the cell, fuse with the cell membrane allowing glucose to be transported into the cell
104
Q

How does glucagon work?

A
  1. Low levels of blood glucose cause release of glucagon from IoL
  2. Glucagon promotes gluconeogenosis in liver
  3. It also promotes glycogen break down to release glucose into the blood (glycogenolysis)
105
Q

What is the mechanism of T1DM?

A

Type 1 - Body doesn’t make enough insulin due to cell mediated immune response in which a persons own T cells attack the beta cells in the pancreas.

106
Q

Why do you get weight loss and hunger in someone with uncontrolled T1DM?

A

Body breaks down fat in adipose tissue, and protein in muscle tissue, as it is unable to break down glycogen

107
Q

Why do you get polyuria in T1DM?

A

High levels of glucose in the urine which has an osmotic effect, pulling water out > this then leads to thirst (polydipsia)

108
Q

What is the diagnostic criteria and mechanism of DKA?

A

Lipolysis causes ketone production which increases the acidity of the blood causing a high anion gap

Diagnostic criteria:
- Glucose >11 or known DM
- Blood ketones >3 or urinary ketones >2
- pH <7.3 or HC02 <15

109
Q

How can stress precipitate DKA?

A

Release of epinephrine > release of glucagon > increase blood glucose > dehydration > need for alternative energy > generation of ketone bodies > DKA

110
Q

How is DKA managed?

A
  1. IV fluids 0.9% NaCl +/-KCl (if K 3.5-5.5) (tends to be 1L over 1h, 1L over 2h, and so on apart from children who are more at risk of cerebral oedema)
  2. Fixed rate insulin of 0.1units/kg/hr with ongoing long acting SC insulin at patients usual dose and time
  3. Once CBG <14, add glucose 10% to FRII

Resolution is defined as venous pH >7.3 and blood ketones negative. If pt E&D change to SC insulin and stop FRII/glucose.
If pt not E&D switch to variable rate insulin.

When restarting SC insulin give short acting insulin with meal and stop insulin infusion 30-60 minutes later.

All pts should be seen by DNS prior to discharge, and should be seen by endocrine if not resolved within 24h.

111
Q

How is T1DM usually diagnosed?

A

If symptomatic:
- Fasting glucose >= 7
- Random glucose >=11
If asymptomatic must have above diagnostic criteria on two seperate occasions

Can also look at:
- C-peptide (LOW as it is made when insulin is broken down)
- anti-GAD (present in 80%)
- islet cell antibodies (present in 80%)
- insulin autoantibodies (more common in young children)

Note HbA1c is NOT HELPFUL as it may not reflect a recent rise in serum glucose

112
Q

How is T1DM managed?

A

Insulin therapy:
- Offer multiple daily injection basal-bolus insulin regimen
- Mixed (biphasic) regimen
- Continueous insulin infusion
Consider adding metformin if BMI >=25

Pts should self monitor at least 4 times daily but more frequently if hx of hypos, illness, pregnant etc. Blood glucose targets:
5-7 on waking
4-7 before meals and other times of day

113
Q

What are the causes of hypoglycaemia?

A
  • Self administration of insulin/sulphonylureas
  • Liver failure
  • Addison’s disease
  • Insulinoma
  • Alcohol (causes increased insulin secretion)
  • Nesidioblastosis
114
Q

What are the symptoms of hypos?

A

Glucose <3.3 - sweating, shaking, hunger, anxiety, nausea

Glucose <2.8 - weakness, visual changes, confusion, dizziness

115
Q

How are hypos managed?

A

Conscious:
- Oral glucose 10-20g or glucogel

Unconscious:
- SC/IM injection of glucagon or IV 20% dextrose

116
Q

What is the mechanism of T2DM?

A

Acquired insulin resistance due to:
- excess of adipose tissue (causes inflammation and resistance)
- genetics

As a result the body produces MORE insulin due to beta hyperplasia/hypertrophy. Overtime these cells shrink and die, causing hyperglycemia.

117
Q

How is T2DM diagnosed?

A
  1. Glucose tests
    If symptomatic:
    -Fasting glucose >= 7
    - Random glucose >= 11
    If asymptomatic, must be demonstrated on two seperate occasions
  2. HbA1c >48mmol is diagnostic of diabetes (42-47 is prediabetes)

A fasting glucose between 6-7 imples impaired fasting glucose - these pts should be offereed an oral glcuose tolerance test, if value between 7.8-11.1 they have impaired glycose tolerance)

118
Q

What is HHS?

A

Hyperosmolar hyperglycaemic state = High glucose pulls in water from the cells > polyuria and dehydration > electrolyte deficiencies

No specific diagnostic criteria but will generally see:
- Hypovolaemia
- Glucose >30
- Serum osmolarity > 320
- Normal or mildly raised ketones
- No significant acidosis

119
Q

How is T2DM managed?

A
  1. Metformin
    - uptitrate as necessary
  2. SGLT-inhibitor eg. dapagliflozin/empagliflozin
    - if high HbA1c (>58) on max metformin or established CVD
  3. Add DPP-4 inhibitor/pioglitazone/sulfonylurea OR start insulin therapy
  4. If triple therapy not effective consider switching one frug for a GLP1 mimetic eg. exenatide, dulaglutide

Check HbA1c every 3-6 months until stable then 6 monthly

NOTE PTS ON METFORMIN + HYPOGLYCAEMIC DRUG SHOULD AIM HBA1C 53 AND ONLY ADJUST MEDS IF HBA1C 58 OR MORE

119
Q

How is HHS managed?

A
  • IV fluids (0.5-1L hrly) +/- K replacement
  • VTE thromboprophylaxis

Do not given insulin unless hypoglycaemic!

120
Q

If metformin is contraindicated, how is T2DM managed?

A

High risk CVD > SGLT-2 monotherapy

Low risk CVD > DPP-4 inhibitor (-gliptin) OR pioglitazone OR sulfonylurea

121
Q

How is insulin started in T2DM?

A
  • Tends to be third line therapy
  • Should continue metformin alongside
  • Start with human NPH insulin (isophane, intermediate acting) at bedtime or BD
122
Q

What are the pros and cons of metformin?

A

Pros: low cost, oral, no hypos
Cons: risk of lactic acidosis, GI side effects

Metformin works by reducing hepatic glucose production > leads to weight loss

123
Q

What are the pros and cons of sulphonylureas eg. gliclazide?

A

Pros: low cost, oral route
Cons: risk of hypos, weight gain, drug interactions, cant use in breastfeeding/pregnancy

SFs work by increasing insulin secretion (and therefore glucose storage > weight gain) and hence are only effective if functional B-cells are present

124
Q

What are the pros and cons or thiazolidinediones eg. pioglitazone?

A

Pros: oral, no hypos
Cons: slow onset of action, contraindicated in cardiac (fluid retention) /liver failure (LFT derangement), weight gain, risk of bladder cancer

PPAR-gamma receptor agonists - reduce peripheral insulin resistance

125
Q

What are the pros and cons of SGLT-2 inhibitors?

A

Pros: oral, no hypo, also used in HF
Cons: Risk of UTI and deydration

126
Q

What are the pros and cons of DPP4 inhibitors?

A

Pros: oral, no hypos
Cons: risk of acute pancreatitis

127
Q

What are the pros and cons of GLP-1 receptor agonists?

A

Pros: Weight loss, no hypos, reduced insulin requirement
Cons: SC injections, GI side effects, risk of acute pancreatitis

Note NICE prefers patients to achieve 11mmol reduction in HbA1c and 3% weight loss in 6 months to justify ongoing prscription

128
Q

What are the microvascular complications of diabetes?

A

Retinopathy
- cotton wool spots, microhaemorrhages, macular thickening

Neuropathy
- peripheral
- autonomic (gastroparesis, resting tachycardia, urinary frequency, ED as the nerves respond more slowly to a change in your body)

Nephropathy
- glomerluosclerosis (scarring of glomerulus)
- pyelonephritis

129
Q

What are the macrovascular complications of diabetes?

A

Coronary heart disease:
- chest pain
- congestive heart failure
- dyspnoea

Cerebrovascular:
- haemorrhage
- cerebral infarcts
- memory problems

Peripheral vascular:
- atherosclerosis
- gangrene
- ulceration

130
Q

How does hyperglycaemia cause vascular disease?

A
  • Glucose enters endothelial cells of vessels
  • Stimulates growth factors including ROS, PKC
  • Toxic diabetic metabolism, endothelial dysfunction and vascular inflammation
  • Formation of foam cells from macrophages and hyperlipidema
  • Foam cells deposit in the tunica intima causing thrombosis/atherosclerosis
131
Q

In which patients can HbA1c not be used to diagnose diabetes?

A

Sickle cell anaemia
GP6D deficiency
Hereditary spherocytosis
Haemodilaysis
Vitamin B12/folic acid deficiency
Splenectomy

This is because HbA1c (glycosylated haemoglobin) is dependent on blood glucose concentration and red blood cell lifespan, therefore anything that affects RBC lifespan will effect it

132
Q

Which diabetic drugs cause hypoglycaemia?

A
  • Sulfonylureas (gliclazide, glimepiride)
  • Insulin

Think - any drug which secrets insulin independently of plasma glucose concentrations

133
Q

How is diabetic neuropathy managed?

A

Glove and stocking distribution

1st line - amitriptyline, duloxetine, gabapentin, pregabalin

Can use tramadol for exacerbation or topical capsaicin for localised neeruopathic pain

134
Q

How is gastrointestinal autonomic neuropathy managed?

A

Prokinetic agents - metoclopramide, domperidone, erythromycin

135
Q

What does annual diabetic foot disease screening entail?

A

Ischaemia - palpate both dorsalis pedis and posterior tibial artery

Neuropathy - 10mg monofilament on various parts of foot

Any patients with any problems other than simple calluses should be followed up regularly by the local diabetic foot centre

136
Q

How is subacute (De Quervain’s) thyroiditis managed?

A

Conservative management with NSAIDs for painful goitre

137
Q

What do the following HbA1c’s represent:
a) 48
b) 53
c) 58

A

a) Target for patients managed by lifestyle or a single drug
b) Target for patients on multiple agents or if on hypo causing drug
c) Threshold for changing medications

138
Q

How is gastroparesis managed?

A

Metoclopramide, domperidone or erythromycin
(prokinetic agents)

139
Q

What is Waterhouse-Friderichsen syndrome?

A
  • Disease of the adrenal glands most commonly caused by the bacterium Neisseria meningitidis
  • Leads to massive haemorrhage into one or both adrenal glands
  • Disseminated DIC + adrenocortical insufficiency
140
Q

What is congenital adrenal hyperplasia?

A
  • Autosomal recessive metabolic disorder related to enzymatic defects in the biosynthesis of cortical steroids
  • Due to 21-hydroxylase deficiency causing DEFICIENCY IN CORTISOL AND/OR ALDOSTERONE PRODUCTION
  • Resulting adrenocortical hyperplasia due to increased ACTH secretion
  • Manage with lifelong hydrocortisone and fludrocortisone

MSRA (24 decks)

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