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Endocrinology Flashcards

1
Q

Give 4 causes of hyperthyroidism

A
  • G : Graves
  • I : Inflammation
  • S : Single toxic thyroid nodule
  • T : Toxic multinodular goitre
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1
Q

What are the general 7 symptoms of hyperthyroidism?

A
  • Weight loss
  • Anxiety
  • Diarrhoea
  • Menstrual and sexual disturbances
  • Fatigue
  • Sweating and heat intolerance
  • Insomnia
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2
Q

What are the 6 general signs of hyperthyroidism?

A
  • Tachycardia
  • Brisk reflexes on examination
  • Hyperkinesia
  • AF
  • Tremor
  • Dilated warm peripheries
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3
Q

Define primary and secondary hyperthyroidism

A
  • Primary hyperthyroidism : low TSH with raised T3/T4
  • Secondary hyperthyroidism : raised T3/T4 with raised TSH
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4
Q

What is the cause of Grave’s?

A
  • Autoimmiune
  • TSH receptor antibodies cause primary hyperthyroidism by stimulating thyroid to release T3 and T4
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5
Q

Give 4 Grave’s specific signs of hyperthyroidism

A
  • Exophthalmos, opthalmoplegia
  • Pretibial myxoedema
  • Thyroid acropachy (digital clubbing, swelling of hands and feet, periosteal new bone formation)
  • Diffuse goitre = increased homogenous uptake in a radioactive iodine uptake test
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6
Q

What autoantibodies are found in Grave’s?

A
  • TSH receptor stimulating antibodies
  • Antithyroid peroxidase antibodies
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7
Q

What is the first line management of hyperthyroidism ?

A
  • Carbimazole (40mg) -> blocks the action of thyroid peroxidase
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8
Q

What is a risk associated with carbimazole use ?

A
  • Acute pancreatitis
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9
Q

If a patient presents with a sore throat and is taking carbimazole, what is the life-threatening cause ?

A
  • Agranulocytosis - low white blood cell count
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10
Q

What can be used 1st line for symptoms control in hyperthyroidism

A
  • Propanolol -> non selectively blocks adrenalin related symtoms
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11
Q

If carbimazole doesn’t control symptoms of hyperthyroid, what can be done?

A
  • Radioactive iodine treatment
  • CI = pregnant or breastfeeding and must not be pregnant within 6 mnths of treatment), <16, thyroid eye disease
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12
Q

What is the definitive management of hyperthyroid?

A
  • Thyroidectomy
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13
Q

What is thyrotoxicosis and a resultant thyroid storm ?

A
  • Thyrotoxicosis : effects of abnormal and excessive thyroid hormone
  • Thyroid storm : life threatening complication of thyrotoxicosis often precipitated by thyroid surgery, trauma, infection of acute iodine overload.
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14
Q

Features of a thyroid stome ?

A
  • Fever > 38.5ºC
  • Tachycardia
  • Confusion and agitation
  • N&V
  • HTN
  • HF
  • Abnormal liver function test - jaundice may be seen clinically
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15
Q

How is thyroid storm management

A

-1st line = IV propanolol
- Paracetamol for symptoms
- Anti-thyroid drugs (e.g. methimazole, propylthiouracil)

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16
Q

what is De Quervain’s thyrodisitis and it’s 3 stages ?

A
  • Subacute thyroditis
  1. Thyrotoxicosis
  2. Hypothyroidism
  3. Return to normal
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17
Q

How does the thyrotoxic phase of de quervain’s present and how is it managed

A
  • Thyroid swelling and tenderness, flu like illness and raised CRP/ESR
  • Self limiting : NSAIDS for pain, BB for hyperthyroidism and levothyroxine for hypothyroidism
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18
Q

Briefly explain thyroid hormone synthesis

A
  • Blood supplies iodine
  • Transported into follicular cells of thyroid
  • Here, thyroidperoxidase converts iodine to iodide
  • Iodide then attaches to tyrosine residues on thyroglobulin forming T3 and T4
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19
Q

Define primary and secondary hypothyroidism

A
  • Primary : thyroid produces inadequate T3 and T4, leading to raised TSH
  • Secondary : inadequate TSH release leading to low T3 and T4
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20
Q

Give 5 causes of primary hypothyroidism

A
  • Hashimoto’s thyroiditis (most common)
  • Iodine deficiency
  • Lithium
  • Amiodarone
  • Hyperthyroidism treatment
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21
Q

Give 5 causes of secondary hypothyroidism

A
  • Pituitary adenomas
  • Pituitary surgery
  • Radiotherapy
  • Sheehan’s syndrome : post-partum haemorrhage cause avascular necrosis of pituitary gland
  • Trauma
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22
Q

Give the general features of hypothyroidism

A
  • General : weight gain, cold intolerance, fatigue
  • Skin : dry skin, coarse scalp hair, loss of lateral aspect of eyebrow
  • GI : constipation
  • Gynae : menorrhagia
  • Neuro : decreased tendon reflexes, carpal tunnel
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23
Q

What is the mainstay of treatment for hypothyroidism and its SE

A
  • Levothyroxine
  • SE : hyperthyroid, reduced bone mineral density, worsening of angina, AF
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24
Q

What is Hashimoto’s thyroiditis

A
  • Autoimmune condition causing inflammation of the thyroid gland
  • Is associated with anti-thyroid peroxidase (TPO) and anti-thyroglobulin (Tg) antibodies
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25
Q

What are the features of Hashimoto’s and what is it associated with ?

A
  • Hypothyroidism, firm and non tender goitre
  • Associated with : other autoimmune conditions and MALT lymphoma
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26
Q

What is the most common cause of acromegaly

A
  • Pituitary adenoma
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27
Q

what rarely causes acromegaly

A
  • Ectopic GHRH or GH release by cancer (lung/pancreatic)
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28
Q

What are the general features of acromegaly (6)

A
  • Frontal bossing
  • Coarse sweaty skin
  • Large nose
  • Macroglossia
  • Large hands and feet
  • Large protruding jaw
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29
Q

What are the mass effects of a pituitary adenoma causing acromegaly ?

A
  • Headache
  • Bitemporal hemianopia
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30
Q

What are the investigations for acromegaly ?

A
  1. IGF-1 levels (produced by the liver).
  2. Growth hormone suppression test - no suppression of GH to <2mu/L after 75g glucose drink
  3. Pituitary MRI to determine presence of pituitary adeoma
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31
Q

What is the 1st line management of acromegaly

A
  • Trans-sphenoidal surgery to remove a pituitary adenoma
  • +/- external radiotherapy
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32
Q

What are the medical manegement options of acromegaly

A
  1. Pegvisomant : SC injection, GH receptor antagonist.
  2. Somatostatin analogue (ocreotide) - blocks GH release from pituitary.
  3. Dopamine agonist (bromocriptine) : inhibits GH release from pituitary, less effect than ocreotide.
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33
Q

Give 5 complications of acromegaly

A
  • HTN
  • T2DM
  • Cardiomyopathy (hypertrophic)
  • Colorectal cancer
  • Bilateral carpal tunnel
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34
Q

Define Cushing’s syndrome and Cushing’s disease

A
  • Syndrome : features of prolonged high levels cortisol
  • Disease : prolonged raised cortisol due to pituitary adenoma secreting ACTH
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35
Q

What are the possible causes of cushing’s syndrome

A
  • ACTH dependent : cushing’s disease, ectopic ACTH product (SCLC)
  • ACTH independent : iatrogenic steroids, adrenal adenoma/carcinoma
  • Pseudo cushing’s : due to alcohol excess or severe depression
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36
Q

What are the features of cushing’s syndrome (7) ?

A
  • ‘Full moon’ face
  • ‘Buffalo hump’
  • Muscle wasting in the extremeties
  • Easy bruising and poor skin healing
  • Abdominal striae
  • Central obesity
  • Hyperpigmentation in Cushing’s disease due to raised ACTH
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37
Q

What are the metabolic effects of Cushing’s syndrome

A
  • HTN
  • T2DM
  • Osteoporosis
  • Cardiac hypertrophy and increased risk of CVD
  • Dyslipidaemia
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38
Q

Where is cortisol released from

A
  • Zona fasciculata in the adrenal cortex
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39
Q

How is Cushing’s syndrome investigated ?

A
  • 1st line = Low dose overnight dexamethasone suppression (screening to exclude cushing’s)
  • Low dose 24 hour (used in suspected cushing’s)
  • High dose 24 hour (used to determine cause)
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40
Q

Explain the dexamethasone suppression tests

A
  1. Overnight : dexamethasone (1mg) given at night. Check cortisol 9am. No suppression = further assessment.
  2. Low dose 24 hr : dexamethasone (0.5mg) every 6 hrs for 8 doses. Cortisol checked at 9am on day 1 and 9am day 3. No suppression = cushing’s syndrome
  3. High dose 24hr. Same as above but dose at 2mg. Cushing’s syndrome = cortisol will be suppressed. Adrenal adenoma or ectopic ACTH = no suppression.
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41
Q

What is the primary treatment of Cushing’s syndrome ?

A
  • Treat underlying cause :

~ Trans-sphenoidal removal of pituitary adenoma
~ Surgical removal of adrenal tumour
~ Surgical removal of tumour producing ectopic ACTH

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42
Q

What is Nelson’s syndrome

A
  • Development of ACTH-producing pituitary tumour after sugical removal of both adrenal glands due to lack of cortisol and negative feedback
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43
Q

What medical treatment can be used to reduce production of cortisol in adrenals?

A
  • Metyrapone
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44
Q

What does adrenal insufficiency result in a lack of ?

A

Steroid hormones - cortisol and aldosterone

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45
Q

What is the most common primary cause of adrenal insuficiency ?

A
  • Addison’s : autoimmune destruction of the adrenal glands resulting in a lack of cortisol and aldosterone
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46
Q

What is secondary adrenal insufficiency and 5 causes ?

A
  • The pituitary produces a lack of ACTH
  1. Pituitary tumour
  2. Radiotherapy
  3. Sheehan’s
  4. Surgery to pituitary
  5. Trauma
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47
Q

What is tertiary adrenal insufficiency and the most common cause?

A
  • Lack of CRH from the hypothalamus
  • Long term oral steroid use = hypothalamus suppression. Once expogenous steroids are stopped the hypothalamus doesn’t ‘wake up’ and leads to a lack of endogenous steroid release.
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48
Q

How does adrenal insufficiency present ?

A
  • Fatigue
  • Muscle weakness
  • Weight loss
  • Thirst and salt craving
  • N&V
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49
Q

What is a sign of adrenal insufficiency caused by Addison’s?

A
  • Bronze hyperpigmentation of the skin, particularly in the palmar creases.
  • Due to excess ACTH stimulating melanocytes to produce melanin.
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50
Q

What biochemical findinds are seen in adrenal insufficiency and why ?

A
  • Hyponatraemia and hyperkalaemia : aldosterone increases Na+ reabsoprtion and K+ secretion. A lack of it causes this.
  • Hypoglycaemia
  • Raised creatinine and urea due to dehydration
  • Hypercalcaemia
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51
Q

What is the investigation of choice for diagnosing adrenal insufficiency

A
  • Short Synacthen test
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52
Q

What is the short synacthen test ?

A
  • Synthetic ACTH is given and blood cortisol measured 30 and 60 mins after the dose
  • Cotrisol level should at least double.
  • Failure = adrenal insufficiency
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53
Q

Once adrenal insufficiency is established how is primary or secondary insufficiency determined?

A
  • ACTH level
  • It will be high in primary and low in secondary
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54
Q

How is adrenal insufficieny managed ?

A
  • Replace steroids : hydrocortisone and fludrocortisone
  • Give steroid carrd, ID tag and emergency letter.
  • Double glucocorticoid dose in acute illness.
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55
Q

how many an adrenal crisis present ?

A
  • Reduced consciousness
  • Hyperkalaemia and hyponatraemia
  • Hypoglycaemia
  • Hypotension
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56
Q

How is an adrenal crisis managed ?

A
  • Hydrocortisone 100 mg IM or IV. Then 6hrly until stable
  • IV fluids (1L normal saline) over 30-60 mins or with dextrose if hypoglycaemic
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57
Q

Define hyperaldosteronism and Conn’s syndrome

A
  • Hyperaldosteronism = raised aldosterone
  • Conn’s = raised aldosterone due to an adrenal adenoma producing too much aldosterone
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58
Q

Explain the role of the renin-angiotensisn-aldosterone system in blood pressure

A
  • Juxtaglomerular cells in the affterent arterioles of the kidney detect a low BP
  • They release renin
  • Renin converts angiotensinogen produced by the liver to angiotensin I
  • ACE in the lungs converts angiotensin I to angiotensin II
  • Angiotensisn II stimulates aldosterone release from the adrenal glands - zona glomerulosa
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59
Q

What is the role of aldosterone in low BP?

A
  • Increases sodium resorption from distal tubule
  • Increases potassium secretion from. distal tubule
  • Increases hydrogen secretion from collecting ducts
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60
Q

What is primary hyperaldosteronism and give 3 causes

A
  • Adrenal glands produce too much aldosterone.
  • Renin is low as suppressed due to high BP.
  1. Bilateral adrenal hyperplasia.
  2. Conn’s - adrenal adenoma
  3. Familial
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61
Q

What is secondary hyperaldosteronism and 3 causes

A
  • Excessive renin stimulates release of aldosterone
  1. Renal artery stenosis
  2. HF
  3. Liver cirrhosis and ascites
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62
Q

What is the screening test for hyperaldosteronism

A

Aldosterone-to-renin ratio

~ High aldosterone with low renin = primary
~ High aldosterone with high renin = secondary

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63
Q

what investigations are used to determine underlying cause of hyperaldosteronism ?

A
  • High resolution CT for adrenal tumour or adrenal hyperplasia and adrenal vein sampling to differentiate adenoma and bilateral hyperplasia
  • Renal artery imaging for renal artery stenosis
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64
Q

what is the medical management of hyperaldosteronism ?

A
  • Adenoma : laparoscopic adrenalectomy
  • Hyperplasia :Aldosterone antagonists : eplerenone, spironolactone
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65
Q

What is SIADH ?

A
  • Increased release of ADH (vasopressin) from the posterior pituitary
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66
Q

What is the action of ADH

A
  • Increases water resorption form the collecting ducts of the kidneys
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66
Q

What are the 2 possible sources of excessive ADH release?

A
  • Increased secretion by the posterior pituitary
  • Ectopic ADH release by a SCLC
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66
Q

What is the result of excessive ADH release ?

A
  • Increased water resorption
  • This dilutes the blood
  • Causes hyponatraemia
  • Excessive fluid doesn’tm usually cause fluid overload = euvolaemic hyponatraemia
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66
Q

what is the effect on the urine in SIADH

A
  • It becomes more concentrated
  • High urine osmolality
  • High urine sodium
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66
Q

If not asymptomatic how migh SIADH present ?

A
  • Headache, fatigue, muscle aches and cramps, confusion
  • Severe = seizures and reduced consciousness
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66
Q

What are 3 more common causes of SIADH

A
  • Post operative
  • Ectopic ADH release from SCLC
  • Medications (SSRI’s / carbamazepine)
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66
Q

What are the 5 clinical features of SIADH ?

A
  • Euvolaemia
  • Hyponatraemia
  • Low serum osmolality
  • High urine osmolality
  • High urine sodium
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67
Q

How is SIADH managed?

A
  • Admission (If Na+ <125)
  • Tx underlying cause
  • Fluid restriction (750-1000ml per day)
  • Vasopression receptor antagonists (tolvaptan) -> block ADH receptors
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67
Q

Why does the sodium need to be corrected slowly in SIADH

A
  • Risk of osmotic demyelination syndrome
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68
Q

what is the cause of T1DM?

A
  • Pancreas unable to produce adequate insulin
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69
Q

Explain where insulin is produced and it’s role

A
  • Anabolic hormone , acts to reduce blood glucose
  • Beta cells in the islets of langerhans of the pancreas
  • Cells to take up glucose
  • Liver and muscle to convert glucose to glycogen (glycogenesis)
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70
Q

Explain where glucagon is produced and its role

A
  • Catabolic hormone, acts to increase blood glucose
  • Alpha cells, islets of langerhans
  • Causes liver to breakdown glycogen to glucose (glycogenolysis)
  • Causes liver to convert protein and fats to glucose (gluconeogenesis)
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71
Q

Explain where and why ketones are produced

A
  • Produced by the liver when there is inadequate glucose and depleted glycogen stores
  • Fatty acids - ketones
  • Acidic properties of ketones buffered by the kidneys
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72
Q

In what 2 ways can T1DM present ?

A
  • DKA
  • Signs of hyperglycaemia and dehydration (polyuria, polydipsia, weight loss)
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73
Q

What is the diagnostic criteria for T1DM

A
  • If symptomatic : fasting glucose > or equal to 7.0mmol/l OR random glucose > or equal to 11.1mmol/L
  • If asymptomatic, above needs to be demonstrated on 2 separate occassions.
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74
Q

When may autoantibodies or serum c-peptide be used for diagnosis of T1DM?

A
  • When there is doubt between T1DM & T2DM.
  • C peptide is a measure of inuslin production : it will be LOW in T1DM
  • T1DM autoantibodies are : anti-islet cell, anti-GAD and anti-insulin
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75
Q

What is required for a diagnosis of DKA

A
  • Hyperglycaemia (>11mol/l) or known DM
  • Ketones (>3mmol/L) or +2 on dipstick
  • pH <7.3 or bicarbonate <15mmol/l (metabolic acidosis )
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76
Q

How does DKA present

A
  • Abdo pain
  • Polyuria, polydipsia, dehydration
  • Kussmaul respiration
  • Acetone ‘pear drop’ smelling breath
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77
Q

why does DKA cause dehydration

A
  • Hyperglycaemia eventually overwhelms the kidneys
  • Glucose is lost in urine
  • This causes water to be lost in the urine leading to polyuria and severe dehydration
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78
Q

Explain the patholphysiology behind the potassium imbalance in DKA

A
  • Insulin is required to draw K+ into cells
  • Without it, total body potassium is low
  • This can lead to hypoklaemia was treatment begins
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79
Q

What are the principles of treatment in DKA

A
  • F : fluids
  • I : insulin
  • G : glucose
  • P : potassium
  • I : infection (treat if underlying)
  • C : chart fluid balance
  • K : ketones
80
Q

How are the fluids given for DKA

A
  • IV normal saline
  • 1L in first hour
  • Followed 1L every 2 hours
81
Q

How is insulin given in DKA

A

Fixed rate at 0.1unit/kg/hour

82
Q

When is glucose given in DKA management

A
  • Added to infusion when levels reach less than 14mmol/l
83
Q

Give 4 key complications during treatment of DKA

A
  • Hypoglycaemia
  • Hypokalaemia
  • Cerebral oedema (rapid fluid)
  • Pulmonary oedema (sec. to fluid overload or acute resp distress)
84
Q

what monitoring is involved for a patient with T1DM?

A

-HbA1c measure every 3-6 months
- Capillary blood glucose monitoring at least 4 times daily

85
Q

what are the blood glucose targets of someone with T1DM?

A
  • 5 to 7 mmol/l on waking
  • 4 to 7 mmol/l before meals and at other times.
86
Q

What is the basal-bolus regime for managing T1DM ?

A
  • Background, long acting insulin injected once daily
  • Short acting insulin injected 30 mins before consuming carbs
87
Q

what needs to be considered when injected insulin

A
  • Not injecting same site every time, can cause lipodystrophy
88
Q

Give 2 short term complications of T1DM

A
  • Hypoglycaemia
  • HYperglycaemia and DKA
89
Q

What are the macrovascular long term complications of T1Dm

A
  • Coronary artery disease
  • Peripheral ischaemia lading to poor skin healing and foot ulcers
  • Stroke
  • Hypertension
90
Q

What are the microvascular long term complications of T1DM

A
  • Peripheral neuropathy
  • Retinopathy
  • Kidney disease, esp glomerulosclerosis
91
Q

Give 4 infection-related complications of T1DM

A
  • UTI
  • Pneumonia
  • Skin and soft tissue infections, esp in the feet
  • Fungal infections, es oral and vaginal candidiasis
92
Q

Give 3 non modifiable RF for T2DM

A
  • Older age
  • FHx
  • Ethnicity (black afran, caribeean, south asian)
93
Q

Give 3 modifiabke RF for T2DM

A
  • Obesity
  • High carb diet
  • Sedentary lifestyle
94
Q

what is required for a diagnosis of T2DM

A
  • If asymptomatic :

~ HbA1c > 48mmol/l
~ Fasting glucose greater than or equal to 7.0 mmol/l
~ Random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)

If asymptomatic the above needs demonstrating on 2 separate occasions

95
Q

Give 6 presenting symptoms of T2DM

A
  • Tiredness
  • Polyuria and polydipsia
  • Unintentional weight loss (rare)
  • Opportunistic infections
  • Slow wound healing
  • Glucose in urine (on dipstick)
96
Q

What skin sign can be seen in someone with T2DM?

A
  • Acanthosis nigricans - thickening and darkening of the skin at the neck, axilla and groin.
  • Associated within insulin resistance
97
Q

what HbA1c level suggest pre diabetes

A

42-47

98
Q

What is the first line management of T2DM ?

A

metformin

99
Q

what is the first line management of T2DM if :

  • There is a high risk of CVD or established CVD or chronic HF
A

Metformin :

Once established add SGLT-2 inhibitor (e.g. dapagliflozin)

100
Q

what is second line management of T2DM ?

A

Metformin +

  • sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor (if NICE criteria met)
101
Q

What is the third line management of T2DM?

A
  • Triple therapy with metformin + second line drugs

OR

  • Insulin therapy (initiated by specialist diabetic nurse)
102
Q

what is the HbA1c target for someone being managed for T2Dm

A
  • Just lifestyle : 48mmol/mol
  • Lifestyle + metformin : 48 mmol/l
  • Any drug which may cause hypoglycaemia : 53mol/mol
103
Q

what is the HbA1c target for someone already on medication but HbA1c still rising

A
  • Already on one drug, but HbA1c has risen to 58 mmol/mol : target is now 53mmol/mol
104
Q

What kind of medication is metformin and how does work ?

A
  • Biguanide
  • Increases insulin sensitivity and decreases glucose production by the liver.
105
Q

Does metformin cause weight gain or hypoglycaemia ?

A
  • No weight gain
  • No hypoglycaemia
106
Q

What are the notable side effects of metformin ?

A
  • GI symptoms : pain, nausea and diarrhoea
  • Lactic acidosis (secondary to AKI)
  • Modified release metformin can be used in people with GI side effects.
107
Q

How do SGLT-2 inhibitors work ?

A
  • They act on the sodium-glucose co-transporter 2 protein in the proximal tubules of the kidney.
  • By blocking it, it causes more glucose to be excreted in the urine.
108
Q

Doe SGLT-2 inhibitors cause weight gain or hypoglycaemia ?

A
  • Causes hypoglycaemia and WEIGHT LOSS
109
Q

Give 2 notable SE of SGLT-2 inhibitors

A
  • Increased frequency of UTI’s and genital thrush due to glucose passing through urine.
  • DKA
110
Q

what kind of medication is pioglitazone and how does it work ?

A
  • Thiazolidinedione
  • Increases insulin sensitivity and decreases liver production of glucose
111
Q

Does pioglitazone cause hypoglycaemia or weight gain?

A
  • Causes WEIGHT GAIN
  • Not typically hypoglycaemia
112
Q

Give 4 SE of pioglitazone

A
  • Weight gain
  • HF
  • Increased risk of bone fractures
  • Small increased risk of bladder cancer
113
Q

Give an example of a sulfonylurea and how does it work ?

A
  • Gliclazide
  • Stimulate insulin release from the pancreas
114
Q

Does gliclazide cause weight gain or hypoglycaemia ?

A

BOTH

115
Q

What are incretins and how do they reduce blood sugar ?

A
  • Hormones produced by GI tract
  • Secreted in response to large meals and :

-Increase insulin secretion
- Inhibit glucagon production
- Slow absorption by GI tract

116
Q

How do DPP-4 inhibitors work ?

A

They inhibit dipeptidyl, an enzyme which inhibits incretins

117
Q

Give 2 examples of DPP-4 inhibitors and their 2 most notable SE

A
  • Sitagliptin and alogliptin
  • Headaches and a low risk of pancreatitis Does
118
Q

Do DPP-4 inhibitors cause hypoglycaemia

A

NO

119
Q

How do GLP-1 mimetics work and give 2 example

A
  • Glucagon-like peptide (GLP-1) is an incretin
  • exenatide and liraglutide mimic the incretin action
  • They as SC injections
120
Q

Give 3 notable SE of GLP-1 mimetics

A
  • WEIGHT LOSS
    -Reduced appetite
  • GI symptoms
121
Q

What is HHS

A
  • HYperosmolar hyperglycaemia state
  • Complication of T2DM in which there is hyperosmolality, hyperglycaemia but absence of ketones
122
Q

Hoes HHS present

A
  • Polyuria and polydipsia
  • Weight loss
  • Dehydration
  • Tachycardia
  • Hypotension
  • Confusiojn
123
Q

How is HHS managed ?

A

Fluids

124
Q

Give 8 complications of T2DM

A
  • Infections (e.g., periodontitis, thrush and infected ulcers)
  • Diabetic retinopathy
  • Peripheral neuropathy
  • Autonomic neuropathy
  • Chronic kidney disease
  • Diabetic foot
  • Gastroparesis (slow emptying of the stomach)
  • Hyperosmolar hyperglycemic state
125
Q

what is used 1st line for management of HTN in any patient with T2DM

A
  • ACE inhibitors
126
Q

what advice is given to people with T2DM during ramadan ?

A
  • Try and and eat a meal containing long-acting carbohydrates prior to sunrise.
  • Given a blood glucose monitor to allow them to check their glucose levels, particularly if they feel unwell
  • For patients taking metformin the expert consensus is that the dose should be split one-third before sunrise (Suhoor) and two-thirds after sunset (Iftar)
  • Expert consensus also recommends switching once-daily sulfonylureas to after sunset.
  • For patients taking twice-daily preparations such as gliclazide it is recommended that a larger proportion of the dose is taken after after sunset
  • No adjustment is needed for patients taking pioglitazone
127
Q

what are the 3 sick days rules for patients with diabetes ?

A
  • Increase frequency of blood glucose monitoring to four hourly or more frequently.
  • Encourage fluid intake aiming for at least 3 litres in 24hrs.
  • Struggling to eat may need sugary drinks to maintain carbohydrate intake
128
Q

Explain the 3 types of hyperparathyroidism

A
  1. Primary : tumour of parathyroid leads to excess secretion. Most likley solitary adenoma
  2. Secondary : insufficient vit D or CKD leads to low Ca2+. As a result, more parathyroid is secreted.
  3. Tertiary : prolonged secondary hyperparathyroidism leads to hyperplasia of parathyroid gland.
129
Q

Give the levels of PTH and calcium in each type of parathyroidism.

A
  1. Primary : Ca2+ and PTH high. (PTH could be normal)
  2. Secondary : PTH high, calcium low or normal
  3. Tertiary : Both high.
130
Q

Where is PTH produced and in response to what ?

A
  • Chief cells in the 4 parathyroid glands
  • Released in response to low blood calcium
131
Q

Give 3 actions of PTH

A
  1. Increase osteoclast activity in the bones (resorbing calcium)
  2. Increasing calcium absorption in the kidneys.
  3. Increasing vit D activity, resulting in increased Ca2+ absorption in intestines.
132
Q

How does parathyroid act on vitamin D

A
  • Converts it into its active form, vitamin D then increases calcium absorption from. the intestines
133
Q

Give 4 symptoms of hypercalcaemia

A

STONES, BONES, GROANS, MOANS

  • Kidney stones
  • Painful bones
  • Abdominal groans (constipation, N&V)
  • Psychiatric moans (fatigue, depression, psychosis).
  • Polydipsia, polyuria
134
Q

Other than hyperparathyroidism, what else can cause hypercalcaemia

A
  • Malignancy
  • calcium will be high, PTH is low but parathyrpid hormone related peptide may be raised
135
Q

give 3 causes of primary hypoparathyroidism

A
  • Decrease PTH secretion
    e.g. secondary to thyroid surgery*
  • Low calcium, high phosphate
    Treated with alfacalcidol
136
Q

Give 5 signs of hypoparathyroidism

A

MOSTLY SECONDARY TO HYPOCALCAEMIA

  • Tetany: muscle twitching, cramping and spasm
  • Perioral paraesthesia
  • Trousseau’s sign: carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic
  • Chvostek’s sign: tapping over parotid causes facial muscles to twitch
  • If chronic: depression, cataracts
137
Q

what is seen on ECG in hypocalcaemia ?

A

Prolonged QT interval

138
Q

What is pseudohypoparathyroidism

A
  • Target cells are insensitive to PTH
    due to abnormality in a G protein.
  • Associated with low IQ, short stature, shortened 4th and 5th metacarpals
  • Low calcium, high phosphate, high PTH
  • Diagnosis is made by measuring urinary cAMP and phosphate levels following an infusion of PTH.
  • In hypoparathyroidism this will cause an increase in both cAMP and phosphate levels. In pseudohypoparathyroidism type I neither cAMP nor phosphate levels are increased whilst in pseudohypoparathyroidism type II only cAMP rises.
139
Q

What are the two causes of diabetes insipidus

A
  • Cranial : lack of ADH secretion
  • Nephrogenic : insensitivity to ADH in collecting duct of kidney.
140
Q

What are the causes of cranial diabetes insipidus

A
  • Brain tumours
  • Brain injury
  • Brain surgery
  • Brain infections (e.g., meningitis or encephalitis)
  • Genetic mutations in the ADH gene (autosomal dominant inheritance)
  • Wolfram syndrome (a genetic condition also causing optic atrophy, deafness and diabetes mellitus)
  • Haemochromatosis
141
Q

What are the cause of nephrogenic diabetes insipidus

A
  • Genetic:
    more common form affects the vasopression (ADH) receptor
    less common form results from a mutation in the gene that encodes the aquaporin 2 channel
    electrolytes
  • Hypercalcaemia
  • Hypokalaemia
  • Medications : lithium
  • Demeclocycline
  • Tubulo-interstitial disease: obstruction, sickle-cell, pyelonephritis
142
Q

what are the features of DI and why ?

A
  • Polyuria
  • Polydipsia
  • Dehydration
  • Postural hypotension
  • Lack of ADH = lack of water resoprtion in the kidneys.
143
Q

What do the investigations show in DI

A
  • Low urine osmolality (lots of water diluting the urine)
  • High/normal serum osmolality (water loss may be balanced by increased intake)
  • More than 3 litres on a 24-hour urine collection
144
Q

what is the investigation of choice for diagnosing DI

A
  • Water deprivation test
145
Q

what is the water deprivation test ?

A
  • Pt avoids fluids for 8 hours.
  • Urine osmolality measured.
  • Desmopression is given and urine smolality measured 2-4 hrs later
146
Q

what is the result of the water deprivation test in cranial DI?

A
  • Low prior to desmopression, high after
147
Q

what is the result of the water deprivation test in nephrogenic DI?

A
  • Low prior to desmopression, low after
148
Q

what is the result of the water deprivation test in primary polydipsia

A

High urine osmolality, therefore desmopression not given

149
Q

How is cranial DI managed ?

A

desmopression : vasopressin V2 receptor agonist

150
Q

How is nephrogenic DI managed ?

A
  • Ensuring access to plenty of water + low salt/protein diet
  • Thiazide diuretics
  • NSAIDs
  • High-dose desmopressin
151
Q

How is BMI calculated

A

weight (kg) / height (m)

152
Q

what are the classifications based on BMI/

A
  • Underweigh : < 18.49
  • Normal : 18.5 - 25
  • Overweight : 25 - 30
  • Obese class 1 : 30 - 35
    Obese class 2 : 35 - 40
    Obese class 3 : > 40
153
Q

what is the stepwise management of obesity

A
  • Conservative: diet, exercise
  • Medical : orlistat, liraglutide
  • Surgical
154
Q

what is the criteria for orlistat use in obesity

A
  • BMI of 28 kg/m^2 or more with associated risk factors, or
    BMI of 30 kg/m^2 or more
  • Continued weight loss e.g. 5% at 3 months
  • orlistat is normally used for < 1 year
155
Q

How does orlistat work and what are it’s SE

A

-Pancreatic lipase inhibitor.
- SE : faecal urgency/incontinence and flatulence

156
Q

what is liraglutide and how is it used

A
  • (GLP-1) mimetic
  • SC injection
157
Q

what is the criteria for liraglutide use

A
  • Person has a BMI of at least 35 kg/m²
  • Prediabetic hyperglycaemia (e.g. HbA1c 42 - 47 mmol/mol)
  • Can be given as an adjuncr to orlistat
158
Q

What is the definitive management of hyperparathyroidism

A

Total parathyroidectomy

159
Q

What is the conservative management of hyperparathyroidism

A
  • Cinacalcet
  • A calcimimetic
160
Q

what is seen on a blood gas in cushing’s?

A

hypokalaemic metabolic alkalosis

161
Q

What is a phaeochromocytoma ?

A

Tumour of the adrenal glands -> leading to excessive release of catecholamines (adrenaline)

162
Q

Where is adrenaline produced

A
  • Chromaffin cells in the medullla of the adrenal gland
163
Q

what 3 genetic conditions are associated with phaeochromocytomas ?

A
  • Multiple endocrine neoplasia type 2 (MEN 2)
  • Neurofibromatosis type 1
  • Von Hippel-Lindau disease
164
Q

How does a phaeochromocytoma present ?

A

Intermittent episodes related to bursts of adrenaline release :

  • Anxiety
  • Sweating
  • Headache
  • Tremor
  • Palpitations
  • Hypertension
  • Tachycardia
165
Q

How is phaeochromocytoma investigated ?

A
  • Initial : 24 hr urine metanephrines
  • CT/MRI for tumour
  • Genetic testing
166
Q

How is a phaeochromocytoma managed ?

A
  • Initially establish patient on an alpha blocker (phenoxybenzamine) then BB (propanolol)
  • Then surgery to remove adrenal adenoma
  • Surgery is then definitive management
167
Q

How is hypercalcaemia managed

A
  • Initially rehydrate with normal saline
  • Following rehydration, bisphosphonates
168
Q
A
  • Vitamin D deficiency (osteomalacia)
  • CKD
  • Hypoparathyroidism
  • Pseudohypoparathyroidism
  • Magnesium deficiency
  • Massive blood transfusion
  • Acute pancreatitis
169
Q

how is severe hypocalcaemia managed

A

IV calcium gluconate, 10ml of 10% solution over 10 minutes

170
Q

what is seen on ECG in hypercalcaemia ?

A

Shortened QT interval

171
Q

Give 6 causes of hyperkalaemia

A
  • AKI
  • Drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, heparin**
  • Metabolic acidosis
  • Addison’s disease
  • Rhabdomyolysis
  • Massive blood transfusion
172
Q

what is seen on ECG in hyperkalaemia ?

A
  • Peaked or ‘tall-tented’ T waves (occurs first)
  • Loss of P waves
  • Broad QRS complexes
  • Sinusoidal wave pattern
  • Ventricular fibrillation
173
Q

what are the stages of hyperkalaemia ?

A
  • Mild: 5.5 - 5.9 mmol/L
  • Moderate: 6.0 - 6.4 mmol/L
  • Severe: ≥ 6.5 mmol/L
174
Q

what is management of severe hyperkalcaemia

A
  • IV calcium gluconate: to stabilise the myocardium
  • Insulin/dextrose infusion: short-term shift in potassium from ECF to ICF
175
Q

what causes hypokalaemia with alkalosis ?

A
  • Vomiting
  • Thiazide and loop diuretics
  • Cushing’s syndrome
  • Conn’s syndrome (primary hyperaldosteronism)
176
Q

what causes hypokalaemia with acidosis ?

A
  • Diarrhoea
  • Renal tubular acidosis
  • Acetazolamide
  • Partially treated diabetic ketoacidosis
177
Q

what are the features of hypokalaemia ?

A
  • Muslce weakness, hypotonia
178
Q

what are. 4ECG features of hypokalaemia ?

A
  • U waves
  • small or absent T waves
  • Prolonged PR interval
  • ST depression
  • Long QT
179
Q

what are carcinoid tumours ?

A
  • A neuroendocrine tumour
180
Q

what is carcinoid syndrome

A
  • A collection of symtpoms that occur when people have a neuroendocrine tumour
181
Q

what are the most common causes of carcinoid syndrome ?

A
  1. Metastases in the liver releasing serotonin into the systemic circulation.
  2. Lung carcinoid
182
Q

Give 7 features of carcinoid syndrome

A
  • Flushing (often the earliest symptom)
  • Diarrhoea
  • Bronchospasm
  • Hypotension
  • Right heart valvular stenosis (left heart can be affected in bronchial carcinoid)
  • Other molecules such as ACTH and GHRH may also be secreted resulting in, for example, Cushing’s syndrome
  • Pellagra can rarely develop as dietary tryptophan is diverted to serotonin by the tumour
183
Q

what investigations are done in carcinoid syndrome

A
  • Urinary 5-HIAA
  • Plasma chromogranin A y
184
Q

what is the management of carcinoid syndrome

A
  • Somatostatin analogues e.g. octreotide
  • Diarrhoea: cyproheptadine may help
185
Q

what can be seen on routine bloods on someone taking steroids (e.g. prednisolone)

A

Neutrophilia

186
Q

When is gradual withdrawal of systemic corticosteroids (over weeks, not days) indicated ?

A
  • Received more than 40mg prednisolone daily for more than one week
  • Received more than 3 weeks of treatment
  • Recently received repeated courses
187
Q

How should a patient with addisons adjust medications when suffering from an intercurrent illness ?

A

Double the glucocorticoids, keep fludrocortisone dose the same

188
Q

What kind of diuretic can cause hypercalcaemia ?

A
  • Thiazides (e.g. bendroflumethiazide)
189
Q

Explain the difference in goitre seen in hashimotos and de Quervain’s thyroiditis

A
  • Hashimoto’s = firm and non tender
  • De Quervain’s = tender
190
Q

what is a risk of opver replacement in hypothyroidism ?

A

osteoporosis

191
Q

what side effect can occur in men taking digoxin ?

A
  • Drug induced gynaecomastia
192
Q

What changes need to be made in pregnancy in women with hypothyroidism ?

A
  • Increase their thyroid hormone replacement dose by up to 50% as early as 4-6 weeks of pregnancy
193
Q

First line management of hyperhidrosis

A

Topical aluminium chloride

194
Q

Low T3/T4 and normal TSH in the context of acute illness

A

Sick euthyroid syndrome
Repeat TFTs in sick weeks at GP

195
Q

what metabolic abnormalities are seen in cushing’s

A

Hypokalaemia
Hypernatraemia

196
Q

Most important modifiable risk factor for development of thyroid eye disease

A

Stop smoking

197
Q

Treatment of choice for toxic multinodular goitre

A

Radioactive iodine therapy

198
Q

4 features of DKA

A
  • Abdominal pain
  • Polyuria, polydipsia, dehydration
  • Kussmaul respiration (deep hyperventilation)
  • Acetone-smelling breath (‘pear drops’ smell)
199
Q

Initial management of DKA

A

IV 0.9% sodium chloride

200
Q

Following initial fluids, management of DKA

A
  • Insulin infusion at 0.1 unit/kg/hr
  • Once blood glucose is < 14 mmol/l an infusion of 10% dextrose should be started at 125 mls/hr in addition to the 0.9% sodium chloride regime
201
Q

Important complication of fluid resuscitation in DKA

A

Cerebral oedema

202
Q

Effect of excess parathyroid hormone on calcium and phosphate

A

EXCESS PARATHYROID + EXCESS PHOSPHATE EXCRETION

= High calcium
= Low phosphate

203
Q

hypothyroidism in pregnancy

A

Increase dose by up to 50% in first 4-6 wks of pregnancy

204
Q

Acromegaly increases the risk of what cancer

A

colorectal

205
Q

Management of prolactinoma

A
  • Dopamine agonists (bromocriptine, cabergoline)
  • Surgery for those who can’t tolerate of fail to repsond.
206
Q

Excess prolactin in women

A

Amenorrhoea
Galactorrhoea
Infertility

207
Q

Excess prolactin in men

A

Impotence
Loss of libido
Galactorrhoea

208
Q
A

Finals (92 decks)

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