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IK6 - Exams > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What are the most likely causes of acromegaly?

A

GH secreting pituitary adenoma

GH secreting ganglioneuroma, GH-secreting bronchial CA or GH secreting pancreatic CA

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2
Q

What are some signs and symptoms of acromegaly?

A

sweating
headaches
carpal tunnel syndrome
thick, greasy skin
prominent eyebrow ridge + cheeks, thick lips, broad nose, large tongue, husky voice
enlarged feet

if due to pituitary adenoma -> bitemporal hemianopia

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3
Q

what are the pharmacological management options for patients wtih acromegaly?

A

subcut somatostatin analogues = octreotide, lanreotide

oral dopamine agonists = cabergoline, bromocriptine

GH antagonists = pegvisomant

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4
Q

what are the common causes of adrenal insufficiency?

A

iatrogenic (after stopping long term steroid therapy or bilateral adrenalectomy)

in developing worlds -> adrenal TB
in the UK -> primary due to addison’s (autoimmune)

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5
Q

what are RF for adrenal insufficiency?

A

autoimmune conditions
female
damage or pathology of adrenals
steroid therapy (long term)

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6
Q

what is an adrenal crisis?

A

an acute adrenal insufficiency attack precipitated by stress (infection, surgery, emotional)

leads to major haemodynamic collapse -> hypotensive shock, tachycardia, pale, cold, oliguria, clammy

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7
Q

A woman presents to the GP with a history of anorexia, weight loss, lethargy + weakness. She has had some dizzy episodes as well as diarrhea + vomiting with abdominal pain.

On examination you notice some increased pigmentation on her gums and hand creases. Her BP drops on standing indicating postural hypotension

what is the likely diagnosis?

A

adrenal insufficiency

possibly due to Addison’s (autoimmune)

KEY FEATURES: anorexia, weight loss, tired, weak, dizzy, diarrhoea and vomiting, abdo pain, depression, postural hypotension, skin pigmentation

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8
Q

what electrolyte abnormality might be seen on blood results from a patient with adrenal insufficiency?

A

hyponatraemia
hyperkalaemia

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9
Q

what investigations would you perform to diagnosis adrenal insufficiency?

A

9am serum cortisol (low)
short-synACTHen test -> no rise in cortisol
long synACTHen test -> just monitor for longer, no rise
bloods - autoantibodies (anti-21 hydroxylase), TFT, U&E

abdo CT, adrenal biopsy

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10
Q

how do you manage an addisonian crisis?

A
  1. rapid IV fluid rehydration
  2. 50mL 50% dextrose
  3. IV 200mg hydrocortisone - followed by 6hr 100ml bolus till BP is stable

treat underlying cause

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11
Q

how do you manage a patient with adrenal insufficiency in the long term?

A

replace glucocorticoids with HYDROCORTISONE

replace mineralocorticoids with FLUDROCORTISONE

advise: medic alert, increase dose in acute illness/stress

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12
Q

what is carcinoid syndrome?

A

where a carcinoid tumour secretes serotonin, histamine and/or bradykinin leading to excess of these hormones. these high levels lead to a cluster of symptoms

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13
Q

what symptoms do patients with carcinoid syndrome commonly experience?

A

diarrhoea
SOB
flushing
itching

often worse after alcohol and emotional stress

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14
Q

what is a carcinoid crisis?

A

PC: profound flushing, bronchospasm, tachycardia, fluctuating BP, pyrexial

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15
Q

what causes a carcinoid crisis?

A

tumour releases an overwhelming amount of the active substances usually due to tumour manipulation (e.g. surgery, biopsy) or in the induction of anaesthesia

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16
Q

What is the most common cause of Cushing’s syndrome?

A

exogenous corticosteroid exposure (steroid therapies)

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17
Q

ACTH dependent causes of Cushing’s?

A

cushing’s disease = ACTH secreting pituitary adenoma
ectopic ACTH production (small cell Lung CA or carcinoid tumours)

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18
Q

What are ACTH independent causes of Cushing’s?

A

adrenal adenoma/cancer
adrenal nodular hyperplasia
iatrogenic (steroid therapy)

carney complex and mccune-albright syndrome [RARE]

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19
Q

what are the features of cushings?

A

glucose intolerance, dyslipidaemia, weight gain (central obesity), striae, proximal myopathy, facial plethora, moon face

depression, easy bruising, hirsutism, lethargy

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20
Q

what investigations would you order if you suspect cushings?

A

bloods: glucose, U&Es
late night salivary cortisol (raised)

low dose dexamethasone suppression test
24 hour urinary free cortisol
scans for tumours

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21
Q

what medical therapies may be used to treat cushings?

A

stop steroids if possible

metyrapone or ketoconazole prevents cortisol synthesis

otherwise surgical intervention to remove tumour or radiotherapy

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22
Q

what is the management for cranial diabetes inspidus?

A

desmopressin

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23
Q

what is the management for nephrogenic DI?

A

salt +/- protein restriction
thiazide diuretics

stop any causative medications if possible e.g. lithium

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24
Q

how do you manage DKA?

A

give bolus insulin then use a sliding scale infusion until ketones are <0.3, pH > 7.3, bicarb >18

fluid resuscitation with saline
potassium replacement and monitoring

close monitoring, broad spec Abx if infection suspected, thromboprophylaxis

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25
Q

what is the pathophysiology of graves disease?

A

TSH receptor antibodies which stimulate the receptor causing T3 and T4 production

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26
Q

how do you manage acute hypercalcaemia?

A

IV fluids
avoid exacerbating factors e.g. thiazides or anything dehydrating

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27
Q

what medication can be used to increase parathyroid sensitivity to calcium?

A

cinacalcet

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28
Q

what order are the pituitary hormones lost?

A

Usually lost in this order: GH → gonadotrophins (FSH + LH) → ACTH and TSH

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29
Q

what order are the pituitary hormones lost?

A

Usually lost in this order: GH → gonadotrophins (FSH + LH) → ACTH and TSH

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30
Q

what are the signs of hypothyroidism?

A

BRADYCARDIC

Bradycardia
Reflexes relax slowly
Ataxia
Dry thin hair/skin
Yawn, drowsy, coma
Cold hands and low temperature
Ascites + non pitting oedema
Round puffy face, double chin, obese
Defeated demeanor (depression)
Immobile + ileus (constipation)
Congestive cardiac failure

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31
Q

what are some causes of hypothyroidism?

A 
autoimmune thyroiditis (hashimoto's disease) 
thyroidectomy/radiotherapy/iodine therapy for hyperthyroidism

amiodarone or lithium (iatrogenic)
secondary - Sheehan’s, pituitary apoplexy, head trauma

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32
Q

how do you treat hypothyroidism?

A

levothyroixine sodium to replace T4

if elderly or known heart disease start at a lower starting dose and titre up slowly to prevent exacerbating CVD

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33
Q

how do you treat myxoedema coma?

A

liothyronine sodium (T3 replacement)
hydrocortisone
correct glucose
fluids
if hypothermic warm slowly

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34
Q

what tumours are associated with MEN1?

A

parathyroid tumours
pituitary tumours
pancreatic tumours

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35
Q

what tumours are associated with MEN 2a?

A

parathyroid tumours
medullary thyroid cancer
phaeochromocytoma

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36
Q

what tumours are associated with MEN 2b?

A

medullary thyroid cancer
phaeochromocytoma

marfanoid appearance

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37
Q

what are the features of a phaechromocytoma?

A

episodes of sweating, palpitations and headaches
sporadic hypertension

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38
Q

what is osteomalacia?

A

a disorder of bone matrix mineralisation

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39
Q

what are RF for osteomalacia?

A

renal phosphate loss (excessive wasting)
vitamin D deficiency

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40
Q

what are the osteoporosis RF?

A

SHATTERED

Steroid use
Hyperthyroid, hyperparathyroid, hypercalciuria
Alcohol + tobacco
Thin
Testosterone low
Early menopause
Renal or liver failure
Erosive/inflammatory bone disease
Diet (low Ca2+), DM1

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41
Q

what is the origin of cells involved in a phaeochromocytoma?

A

catecholamine producing chromaffin cells
ADRENAL MEDULLA

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42
Q

what is Conn’s syndrome?

A

an aldosterone producing adenoma which leads to a primary hyperaldosteronism

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43
Q

what electrolyte imbalance are patients with primary aldosteronism vulnerable to?

A

hypokalaemia

may become hypernatraemic

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44
Q

what diuretic is appropriate for use in patients with primary aldosteronism?

A

a potassium sparing diuretic such as spironolactone

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45
Q

what medication is used to manage prolactinomas?

A

dopamine AGONISTS

e.g. cabergoline or bromocriptine

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46
Q

what is carbemazepine used for?

A

it is an anti-epileptic and to treat neuropathic pain

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47
Q

what is carbimazole used for?

A

carbimazole is used to treat hyperthyroidism

it acts by preventing iodination of molecules so reduces the amount of T3 and T4 produced

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48
Q

what is cabergoline used for?

A

to treat prolactinomas as it is a dopamine agonist

it may also be used to treat excess GH (i.e. acromegaly)

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49
Q

what are the features of SIADH?

A

inappropriate and excessive ADH

hypotonic hyponatraemia
concentrated urine
euvolaemic state

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50
Q

what are the causes of SIADH

A

drugs: SSRI, amiodarone, carbamazepine, amitriptyline, NSAIDs, chemo

infections or malignancy
porphyria, alcohol withdrawal

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51
Q

what would results would one expect from investigations for a patient with SIADH?

A

serum sodium < 135 (low)
serum osmolality < 280 {low}
urine osmolality > 100 and urine sodium > 40 if euvolaemic

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52
Q

What are other causes of hyponatraemia that must be ruled out prior a diagnosis of SIADH?

A

hypovolaemia
oedema
renal failure
adrenal insufficiency
hypothyroidism

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53
Q

what is the management of SIADH?

A

if severe hyponatraemia (<125) give hypertonic saline but only to stop seizures not to normalise sodium

fluid restriction
furosemide
vasopressin receptor antagonist (talvaptan)

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54
Q

what are the types of thyroid cancer?

A

papillary
follicular
anaplastic
medullar

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55
Q

what is the most common type of thyroid cancer?

A

papillary

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56
Q

where does a papillary thyroid cancer usually spread?

A

lymph nodes

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57
Q

how does a follicular thyroid cancer spread?

A

haematologically

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58
Q

what is the tumour marker for papillary and follicular thyroid cancer?

A

thyroglobulin

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59
Q

what is thyroglobulin a marker for?

A

follicular and papillary thyroid cancer

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60
Q

what is the marker for medullary thyroid cancer?

A

calcitonin

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61
Q

what is calcitonin a marker of?

A

medullary thyroid cancer

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62
Q

what are drugs that commonly cause drug-induced thyroiditis?

A

amiodarone, lithium and interferons

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63
Q

what is riedel’s thyroiditis?

A

chronic thyroiditis where normal thyroid tissue is replaced with fibrotic tissue

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64
Q

what are the complications of diabetes?

A

microvascular = retinopathy, neuropathy, nephropathy

macrovascular = MI, stroke, PVD

metabolic = DKA, HHS, hypoglycaemia

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65
Q

What drug is used to treat prolactinoma?

A

cabergoline

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66
Q

zones of adrenal + hormones produced

A

zone glomerulosa → aldosterone

zona fasciculata → cortisol

zone reticularis → sex steroid hormones

medullar → catecholamines (e.g. NA)

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67
Q

zones of adrenal + hormones produced

A

zone glomerulosa → aldosterone

zona fasciculata → cortisol

zone reticularis → sex steroid hormones

medullar → catecholamines (e.g. NA)

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68
Q

acromegaly - definition + causes

A

excess GH in adults leading to overgrowth of all organs, bones and soft tissue

causes:

  • pituitary adenoma
  • ectopic GH (rare)
  • ectopic GnRH (rare, ganglioneuroma, bronchia CA, pancreatic CA
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69
Q

key features of acromegaly presentation

A
  • headaches
  • sweating
  • carpal tunnel syndrome
  • visual disturbance - bitemporal hemianopia
  • thick greasy skin
  • prominent eyebrow ridge, broad nose bridge, prognathism
  • enlarged hands + feet
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70
Q

investigations for acromegaly

A
  • bedside
    • BP, ECG (LVH), CN/visual fields
  • bloods
    • IGF-1 (screening)
    • oral glucose tolerance test (diagnostic)
    • pituitary status - TFTs, LH + FSH, Test/Oes, prolactin
    • CoD screen - HbA1c/glucose, lipids, bone profile
  • imaging
    • MRI pituitary
    • CT chest - assess for CA ectopic cause
    • ECHO - LVH + cardiomegaly
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71
Q

complications of acromegaly

A

structural are usually irreversible so early treatment ESSENTIAL

  • HTN, cardiomyopathy (LVH)
  • OSA
  • colon + thyroid cancer
  • raised calcium, phosphate
  • raised lipids
  • DM/glucose intolerance
  • renal stones
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72
Q

treatment of acromegaly

A
  1. transphenoidal hypophysectomy
    1. CoM: nasoseptal perf, hypopituitarism, recurrence, infection. CSF leak
  2. medical Mx
    1. SC somatostatin analogue (octreotide)
    2. PO DA agonist (bromocriptine, cabergoline)
    3. GH antagonist (Pegvisoman)
  3. screening - monitor for DM/cardiac, colonoscopy if > 40 and every 5 years
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73
Q

definition and causes of adrenal insufficiency

A

inadequate production of cortisol + mineralocorticoids from adrenal cortex

primary - Addison’s disease (AI destruction of cortex)

secondary

  • infection - TB, post-meningococcal sepsis (Waterhouse-Friederichesen syndrome)
  • infiltration - mets, amyloidosis, lymphoma
  • infarction
  • inherited - ACTH receptor mutation
  • iatrogenic - bilateral adrenalectomy, long term steroid use
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74
Q

investigations for adrenal insufficiency

A
  • bloods
    • 9am cortisol - < 100nmol/L essential Ddx, 100-500 more tests, > 500 unlikely
    • autoAb - anti 21-hydroxylase, adrenal cortex Ab
    • U&Es, glucose
  • imaging
    • CT adrenals + contrast - infection/infiltration
  • specialist
    • short synACTH, < 550nmol at 30 = adrenal failure
    • adrenal biopsy
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75
Q

electrolyte abnormality in adrenal insufficiency

A

hyponatraemia

hyperkalaemia

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76
Q

acute management of adrenal insufficiency

A
  • fluid resuscitation 0.9% saline (bolus if needed or 1L in 1 hour)
  • IM 100mg hydrocortisone
    • another 100mg over 8 hours in 5% dextrose
  • treat hypoglycaemia
  • treat hyperkalaemia
  • treat precipitating cause
77
Q

what is carcinoid syndrome?

pathology + site

A

carcinoid tumours secreting vasoactive compounds e.g. serotonin

  • ⅔ of neuroendocrine gastroenteropancreatic tumours
  • most are serotonin producing enterochromaffin cells
  • most common sites is liver and small intestine
78
Q

presentation of carcinoid syndrome

A
  • paroxysmal flushing
  • diarrhoea
  • palpitations
  • sweating
  • wheeze
  • telangiectasis
  • right sided murmur
  • carcinoid crisis = profound flush, bronchospasm, tachy, fluctuating BP, pyrexia
79
Q

key carcinoid syndrome Ix

A
  • plasma chromagranin A - screening
  • 24 hour urine 5-HIAA collection (serotonin metabolic), > 25mg strong evidence
  • CT or MRI with radiolabelled somatostatin analogue (localise tumour)
80
Q

treatment of carcinoid syndrome

A
  1. surgical resection if possible
  2. somatostatin analogue - octreotide
81
Q

causes of cushing’s syndrome

A
  • ACTH dependent
    • Cushing’s disease → pituitary adenoma (suppressed with high dose)
    • Ectopic ACTH → SCLC, carcinoid tumour, high dose fails to suppress
  • ACTH independent
    • adrenal adenoma/cancer
    • adrenal nodular hyperplasia
    • iatrogenic/exogenous
    • Carney complex
    • McCune-Albright syndrome
82
Q

Key investigations for Cushings

A

diagnosis + cause

  • late night 11pm salivary cortisol - screening, raised abnormal
  • low dose dexamethasone suppression test (0.5mg, +ve > 50 nanomol/L)
  • inferior petrosal sinus sampling - confirm pituitary
  • pituitary adenoma
  • Adrenal CT
  • CXR/chest CT - ectopic lung CA

complications

  • BP - HTN
  • glucose, lipids, U&Es
  • DEXA scan
83
Q

treatment of Cushing’s syndrome

A
  • Iatrogenic → stop meds, reduce dose, steroid sparing
  • Medical treatment
    • Cortisol synthesis inhibition
      • Metyrapone or ketaconazole
        • Enzyme inhibitors, rapid effect
        • Usually ineffective long term in Cushing’s disease but bridge to surgery
      • Mitotane - adrenolytic drug
        • Delayed onset, long-lasting action, effective long-term
    • Optimise/manage any comorbidities
    • Osteoporosis preventing - calcium + vitamin D levels, consider bisphosphonates
  • Surgical treatment
    • Trans-sphenoidal resection of pituitary adenoma
    • resect/treat ectopic tumour
    • Bilateral adrenalectomy
      • Adrenal lesions
      • May require lifelong steroid hormone replacement
84
Q

causes of cranial DI

A
  • Surgery (pituitary)
  • Trauma
  • Tumours - primary or metastases (CNS, pituitary, breast mets)
  • Granulomatous infiltration
  • Vascular (aneurysm’s, Sheehan’s syndrome)
  • Inherited - AD mutation in vasopressin gene
85
Q

causes of nephrogenic DI

A
  • Inherited channelopathies (Rare)
  • Lithium
  • Demeclocycline
  • Hypercalcaemia
  • Post-obstructive uropathy
  • Pyelonephritis
  • DM - osmotic diuresis
86
Q

key feature of pathophysiology of diabetes insipidus

A

Failure to respond to ADH or to produce ADH → impaired water reabsorption in the kidneys → production of large amounts of dilute urine, concentrated serum.

87
Q

what electrolyte abnormality do DI patients have?

A

hypernatraemia (lethargy, thirst, irritable, confusion, coma, fits)

88
Q

key Ix for DI

A
  • urine osmolality - < 2, very dilute urine
  • 24 hour collection - > 3 hours
  • U&Es
  • plasma osmalality - raised
  • HbA1c - must exclude DM
  • calcium - must exclude high calcium
  • water deprivation test
    • restrict H2O for 8 hrs
    • normal - concentrate > 600 mOsmol/kg
    • primary polydipsia - 400-600
    • cranial - only after desmopression
    • nephrogenic - never concentrates
89
Q

management of cranial DI

A

DDVAP (desmopressin) replacement

  • monitor sodium every 1-3 months
90
Q

manage of nephrogenic DI

A
  • thiazide diuretic
91
Q

what is the sign of active Grave’s disease?

A

lid lag

92
Q

what is Grave’s disease?

A

Graves’ disease is an autoimmune condition whereby auto-antibodies bind to and stimulate the TSH receptors on the thyroid → overproduction of T3 and T4 → hyperthyroidism.

93
Q

what are the ophthalmological features of Grave’s?

A
  • exophthalmos (bulging eyes)
  • ophthalmoplegia (weakness/paralysis of eye muscles)
  • lid lag
  • gritty sensation in eyes
  • papilloedema, conjunctival oedema
94
Q

extra features of Grave’s (not usual hyperthyroid)

A
  • eye signs
  • proximal myopathy
  • pretibial myoedema (above lateral malleolus)
  • hyper-reflexia
  • thyroid acropachy (thick nails)
95
Q

key Ix of Grave’s

A
  • thyroid examine + eye examination
  • ECG
  • TFT - low TSH, high T4/T3
  • TSH-receptor antibodies
  • thyroid USS - enlarged and vascularised thyroid
  • technetium scan - raised uptake, not needed for diagnosis
96
Q

management of thyroid storm

A
  1. Admit + discuss with ITU/HDU
  2. Propranolol - 60mg QDS IV + digoxin
    1. Diltiazem if beta-blockers CI e.g. asthma
  3. Carbimazole - inhibits TPO, 15-25mg, QDS, PO
  4. Steroids - Hydrocortisone 100mg QDS IV or dexamethasone 2mg, QDS, PO
  5. Treat precipitant e.g. Abx for infection
  6. Supportive - as required consider cooling, IV fluids, further circulatory support
  7. Ongoing management
    • 4 hours after 1st carbimazole dose give Lugol’s iodine for 10 days (TDS)
    • After 5 days ↓ carbimazole to 15mg TDS, PO
    • After 10 days stop propranolol and iodine, adjust carbimazole as required
97
Q

management of Graves

A
  • refer to endo
  • symptom control - beta-blocker or CCB
  • radioactive iodine
    • 1st line in adults
    • realistically medical tried first
    • CI: compression concern, ?CA, pregnant, active thyroid eye disease
  • anti-thyroid drugs - 12-18 months, either block + replace, or dose titrate to TFTs
    • carbimazole
    • propylthiouracil - safe for pregnancy
    • monitor TFT every 6/52 until in range then very 3/12 rest of treatment
  • total thyroidectomy
    • 1st line if compression concern, ?CA, other methods CI/unsuccessful
98
Q

treatment of primary hyperparathyroidism

A
  • mild - increase fluid intake, thiazide diuretics
  • total parathyroidectomy
    • if high calcium (>2.85), bone disease, osteoporosis, renal stones, declining eGFR, < 50
  • conservative - not appropriate for surgery
    • Ca2+ < 2.85, > 50, no end organ damage
    • correct vitamin D
    • calcium lowering meds
      • calcitonin
      • cinacalcet (calcimimetic)
      • desonumab
      • bisphosphonates
99
Q

treatment of acute hypercalcaemia

A

treat if 3-3.5 + acute/symptomatic or > 3.4 even if asymptomatic

  1. IV fluids - 0.9% NaCl, 1L in 1st hour, 4-6L total in 24 hours
  2. Consider IV bisphosphonates (e.g. zoledronic acid 4mg over 15 minutes)
    • mainly used in malignancy related
  3. Address exacerbating factors e.g. thiazide diuretics
  4. Moderate calcium and vitamin D intake
100
Q

treatment of secondary hyperparathyroidism

A
  • calcium + vitamin D supplements as required
  • treat underlying cause
  • phosphate restriction + binders
  • cinacalcet (calcimimetic if ESRF and refractory to treatment)
101
Q

treatment of tertiary hyperparathyroidism

A
  • Total or subtotal parathyroidectomy
  • Cinacalcet
102
Q

biguanides

example medication

mechanism of action

A

metformin

complex mechanism but helps patient’s utilise insulin better

  • decreases hepatic glucose production
  • decreases intestinal absorption of glucose
  • improves insulin sensitivity by increasing peripheral glucose uptake and utilization
103
Q

metformin

class:

SE:

Cautions/risk:

benefit:

A

metformin

class: biguanide

SE: GI upset, altered taste, rare (hepatitis, skin reaction, reduced B12 absorption, lactic acidosis)

Cautions/risks: contraindicated → acute metabolic acidosis, eGFR < 30; caution → other RF for acidosis

benefit: cardio + renal protection, not linked with weight gain

104
Q

Empagliflozin, Dapaglifozin, etc

class:

SE:

Cautions/risk:

benefit:

A

Empagliflozin, Dapaglifozin

  • class: SGLT 2 inhibitors
  • SE:
    • serious - DKA
    • Common – thirst, urinary disorders, urosepsis, ↑ infection, hypo if + insulin or sulfonyl
    • Uncommon – dehydration, dizzy, hypotension, renal failure, syncope
  • Cautions/risk: DKA, increased risk of lower limb amputation, necrotising fasciitis of groin (Fournier’s)
  • benefit: weight loss, cardioprotective
105
Q

MOA of SGLT2 inhibitors and examples

A
  • Sodium-glucose co-transporter 2 inhibitor → reduced glucose resorption in kidney inducing glycosuria
  • “gliflozin”
    • Canagliflozin
    • Dapagliflozin
    • Empagliflozin
    • Ertugliflozin
106
Q

pioglitazone etc

class:

SE:

Cautions/risk:

A

pioglitazone etc

  • class: thiazolidinediones
  • SE:
    • weight gain (common)
    • # , infection, numbness visual impairment
  • Cautions/risk:
    • increased risk of HF, bladder cancer, bone #
      • avoid if other RF for this
107
Q

gliclazide etc

class:

SE:

Cautions/risk:

benefit:

A

gliclazide etc

  • class: sulphonylurea
  • SE:
    • hypoglycaemia
    • weight gain
    • GI disturbance
    • liver dysfunciton
    • agranulocytosis (rare)
  • Cautions/risk:
    • CI: high BMI, elderly, G6PD deficiency
108
Q

alogliptin, sitagliptin etc

class:

SE:

Cautions/risk:

benefit:

A

alogliptin, sitagliptin etc

  • class: DDP-4 inhibitor
  • SE: headache, constipation, dizzy, skin reaction
  • Cautions/risk:
    • CI - ketoacidosis
    • hypersensitivity reaction (SJS)
  • benefit:
    • weight loss
    • reduced CVD deaths
109
Q

Exenatide, liraglutide etc

class:

SE:

Cautions/risk:

benefit:

A

Exenatide, liraglutide etc

  • class: glucagon-like-peptide-1 mimetic (GLP-1 analogue)
  • SE:
    • GI disturbance
    • Interacts with warfarin
    • Common - ↓ appetite, dizzy, skin reactions
    • Uncommon – alopecia, drowsy, hyperhidrosis, renal impairment, change in taste
  • Cautions/risk:
    • Exenatide + liraglutide are weekly SC injection
    • CI – ketoacidosis, severe GI disease
    • Caution – elderly, pancreatitis
  • benefit:
    • prevents weight gain, may cause weight loss → good if BMI > 35
110
Q

Thiazolidinediones MOA and example

A

Bind to PPARs (PPAR-gamma) in adipocytes to promote adipogenesis and fatty acid take up

  • “glitazones”
    • Pioglitazone
111
Q

sulfonylurea MOA and examples

A
  • Insulin secretagon
    • Augment insulin secretion, requires some residual beta cell function
    • Bind + close ATP-sensitive channels so beta-cells depolarise opening Ca2+ channels and release of insulin granules
    • May inhibit hepatic glucose production
  • gliclazide
112
Q

MOA of DDP-4 inhibitors and examples

A

secretagon

Inhibitor DDP-4 which increases insulin secretion and decreases glucagon secretion by preventing DDP-4 breakdown of incretins (e.g. GLP-1)

  • “gliptin”
    • Alogliptin
    • Linagliptin
    • Saxagliptin
    • Sitagliptin
    • Vildagliptin
113
Q

what is the diagnostic criteria for DM?

A

Symptomatic + 1 biochemical test indicating hyperglycaemia

  • Fasting glucose > 7
  • Oral glucose tolerance test with 75g glucose - 2hr blood sugar > 11.1
  • Random glucose > 11.1
  • HbA1c > 48 (> 6.5%) → only for T2DM
    • Normal < 42, pre-diabetes is 42-47 (6-6.4%)

Asymptomatic + 2 biochemical tests indicating hyperglycaemia

114
Q

what are the genetic + autoantibody associations in T1DM?

A
  • Associated with HLA DR3 + HLA DR4
  • Associated autoantigens: glutamic acid decarboxylase (GAD), insulin, insulinoma-associated protein 2, efflux zinc transporter
115
Q

management of T1DM

A
  • Conservative
    • Structure education program (DAFNE course)
    • Advice: reduce CVD risk, foot care advice, DVLA
  • Medical
    • Aim for sugars of: 4-7 pre-meal, < 9 post-meal
    • Blood sugar monitoring - 1st and last thing in the day, prior to each meals.
    • Insulin therapy
      • Short acting - dose calculated using insulin unit: carbohydrate ratio
      • Long-acting
    • Optimise health - statins if ↑ lipids, anti-hypertensives if ↑ BP
  • Monitoring
    • HbA1c every 3-6 months
    • Annual review: retinopathy (annual), nephropathy, vascular disease, diabetic foot (at clinic), CVD risk factors
116
Q

Types of insulin regime

A
  • Types of regimes
    • Basal-bolus regime - 1st line
    • Twice daily regime - biphasic insulin given pre-breakfast and pre-evening meal
      • Mixed of intermediate acting with rapid or short acting
    • Pump therapy - continuous SC insulin infusion
117
Q

what are the target BM in DM if on insulin (T1DM mainly)?

A

Aim for sugars of: 4-7 pre-meal, < 9 post-meal

118
Q

management of hypoglycaemia

A

75ml 20% dextrose

150ml 10% dextrose

119
Q

when can HbA1c not be used for diagnosis of DM?

A

Inappropriate to use HbA1c in paediatrics, ?T1DM, < 2/12 of symptoms, medications impairing glucose metabolism, significant pancreatic damage, pregnancy

120
Q

epidemiology + RF of T2DM

A
  • UK prevalence is 5-10%
  • T2DM > T1DM
  • Asians, African, Hispanic, men and elderly are more commonly diagnosed.
  • RF - FHx, Afro-Caribbean, Black African, South Asian, HTN, overweight/obese
121
Q

stages and treatment of diabetic retinopathy

A
122
Q

Meeran’s guide for T2DM medical treatment (step 1+2)

A
  • Diet + exercise + lifestyle
  • Metformin = everyone unless CI
  • Step 2 → consult diabetes team for recommendation
    • Guidelines have changed to say you can use anything.
    • GLP-1 agonist if obese
      • Expensive, currently only injectable, but new ones coming orally
    • SGLT2 if ischaemic heart disease
      • Very good if heart failure
    • Gliclazide for everyone else/money important
      • Used to be gliclazide as always second line
123
Q

What are the NICE targets for T2DM?

A

NICE targets:

  • 48 mmol/mol HbA1c = diagnostic + target
  • if drug associated hypoglycaemia aim for 53 mmol/mol
  • If HbA1c not adequately controlled by single drug and rises to over 58 mmol/mol consider intensifying treatment and aim for < 53 mmol/mol
124
Q

what is the management of T2DM

A
  • conservative
    • education program
    • Advice: diet, exercise, reduce CVD risk, foot care, DVLA
  • medical
    • Conservative – diet and exercise advice, weight loss
    • Metformin - monotherapy
      • r/v if eGFR < 45, stop if < 30
      • CI: eGFR < 30, tissue hypoxia (MI, surgery), iodine contrast (stop 24 hrs prior → 48hrs after), alcohol abuse (relative)
    • dual therapy:
      • DDP-4 inhibitor (gliptins, e.g. sitagliptin) Good if overweight
      • pioglitazone (thiazolidinedione)
        • CI: HF, hepatic impairment, DKA, bladder cancer, un-Ix macroscopic haematuria
      • sulfonylurea (glibenclamide, gliclazide)
      • SGLT2 inhibitor (e.g. empagliflozin)
        • only if sulfonylurea CI/not tolerated or high risk of hypoglycaemia
    • triple therapy
      • can consider GLP-1 analogue if BMI > 35, or BMI < 35 with occupational consequences of insulin treatment
    • Insulin based treatment
      • continue metformin for cardio + renal protection

if metformin CI or not tolerated as 1st drug use another for mono → dual → insulin

125
Q

criteria for DKA

A
  • pH < 7.3 and bicarbonate < 15
  • Plasma glucose > 11mM
  • Blood ketones > 3 mM or ++ in urine
126
Q

treatment of DKA

A
127
Q

how do you calculate osmolarity?

A
  • Osmolarity = 2(Na+ + K+) + urea + glucose
  • Osmolarity is in mmol/L
128
Q

what is normal serum and urine osmolality?

A
  • Normal serum osmolality is 275-295 mmol/kg
  • Normal urine osmolality 50-1200 mmol/kg

osmolality is lab measure, osmolarity is calculated

129
Q

diagnostic criteria for HHS

A

Diagnostic criteria - patient is clinically hypovolaemic

  • pH > 7.3 (no acidosis)
  • Serum osmolarity > 320 mosmol/kg
  • Blood glucose > 30mM
130
Q

complications of HHS

A
  • Fluid overload, cerebral oedema, central pontine myelinosis
  • Ischaemic events including MI, cerebrovascular
  • VTE
  • ARDS, DIC, multi-organ failure, rhabdomyolysis
131
Q

Ix for HHS

A
  • Bedside
    • Weight - guide fluid resuscitation
    • GCS/AVPU
    • Urine dipstick - glucose +++, ketones may be mildly ↑ (+)
    • ECG
  • Bloods
    • VBG - ↑ glucose, normal pH (pH > 7.3, bicarbonate > 15)
    • Serum osmolality - > 320 mmol/L, normal 290 + 5
    • U&Es (Na+ often ↑)
    • FBC, CRP - exclude infection
    • CK - screen for rhabdo
  • Specialist or scoring
    • Calculate osmolarity
  • assessing for infection - urine/blood MC&S, CXR
132
Q

management of HHS

A
  1. Aggressive fluid replacement
    • 0.9% NaCL + K+ as indicted by U&Es
      • Swap to 0.45% NaCl if osmolality is not ↓ with adequate fluid resuscitation
      • Initial ↑ in Na+ is expected, should not prompt change of fluid
    • Aim for 3-6L by 12 hours depending on weight and extent of dehydration
    • Aim to ↓ glucose by no more than 5mM/h and sodium by 10mM/24 hours
    • Encourage oral intake as soon as safe to do so
  2. IV insulin infusion
    • Only required if glucose no longer falling with fluid resuscitation alone or significant ketonuria (++)
    • 0.05 IU/kg/hour fixed rate
  3. Treat the underlying precipitate
  4. VTE prophylaxis
  5. Monitoring - serial glucose, U&E, neuro obs
133
Q

indications for HDU in HHS

A

Consider HDU care for those with osmolality > 350, sodium > 160, PH < 7.1, K+ abnormalities, GCS < 12, ↓ O2 sats, SBP < 90, tachy or bradycardic, evidence of significant AKI.

Intubation and ventilation required for severely unwell especially if ↓ GCS

134
Q

what is hypopituitarism + it’s causes

A

Hypopituitarism is a deficiency in one or more pituitary hormones. The deficiency may be partial or complete.

Panhypopituitarism is a deficiency in all pituitary hormones.

causes

  • neoplastic - pit. adenoma (most common), craniopharyngioma (kids), mets (rare)
  • vascular - pituitary apoplexy, Sheehan’s, SAH, intrasellar aneurysm
  • inflammatory + infiltrative - haemochromatosis, sarcoid, TB
  • hypothalamic dysfunction - anorexia, starvation, over exercise
  • infection - abcess, TV, fungal (AIDS)
  • congenital
  • TBI
  • radiotherapy or pituitary surgery
135
Q

what are dynamic pituitary function tests?

A

Contraindications:

  • Ischaemic heart disease.
  • Epilepsy.
  • Untreated hypothyroidism (impairs the GH and cortisol response).

Procedure: Administration of LHRH (GnRH), TRH and insulin Measure the 0, 30, 60, 90 + 120 mins the pituitary hormones

Interpretation: Involves interpreting three aspects

  1. Insulin Tolerance test
    • Adequate cortisol response = ↑ greater than 170 nmol/l to above 500nmol/l.
    • Adequate GH response = ↑ greater than 6mcg/L
  2. Thyrotrophin Releasing Hormone Test
    • The normal result is a TSH rise to >5 mU/l (30 min value > 60 min value)
    • Hyperthyroidism = TSH remains suppressed
    • Hypothyroidism = exaggerated response.
    • With the current sensitive TSH assays basal levels are now adequate and dynamic testing is not usually needed to diagnose hyperthyroidism.
  3. Gonadotrophin Releasing Hormone Test
    • Normal peaks can occur at either 30 or 60 minutes
    • LH should > 10 U/l and FSH should > 2 U/l.
    • Gonadotrophin deficiency is diagnosed on the basal levels rather than the dynamic response.
136
Q

management of hypopituitarism

A

Acute pituitary failure

  • Resuscitation with IV fluids
  • IV hydrocortisone → IV infusion
  • Replacement of other hormones subsequently

Hormone replacement

  • Order of replacement therapy:
    • hydrocortisone → thyroxine → oestrogen/T → GH
  • Desmopressin - Central DI seen if pathology affects the posterior pit.

Surgical - apoplexy emergent decompression, SOL - resection

137
Q

causes of hypothyroidism

A
  • Primary hypothyroidism
    • Autoimmune thyroiditis (Hashimoto’s disease) is a common cause.
    • Thyroid atrophy
    • Congenital - thyroid aplasia or dysplasia
    • Thyroidectomy
    • radioactive iodine Tx
    • radiotherapy to head/neck
    • Severe iodine deficiency or iodine excess
  • Drug causes: lithium, amiodarone
  • Secondary: pituitary adenomas, sheehan’s syndrome, pituitary apoplexy, head trauma, surgical complication.
138
Q

Ix for hypothyroidism

A
    • Bloods
      • TFT - TSH will be ↑ or ↓ depending on whether primary or secondary, T3/4 ↓
      • Anti-TPO and anti-thyroglobulin antibodies
      • Lipids - often raised
      • HbA1c or fasting glucose
  • Imaging
    • Thyroid USS - if asymmetrical or suspicious thyroid mass
    • CT/MRI head - if suspicion of CNS cause
139
Q

management of myoxedema coma

A
  • Features: hypothermia, ↓ RR, ↓ Na+, ↓ glucose, heart failure, confusion, ↓ GCS/coma, hyporeflexia
  1. IV T3/T4) - loading dose + then maintenance
    • Loading doses - T4 500mch, T3 10mcg
  2. IV hydrocortisone (50-100mg)
  3. Supportive
    • Mechanical ventilation
    • Oxygen, warming blankets, fluid (cautiously), Abx if infective trigger
  4. Treat precipitant
140
Q

management of hypothyroidism

A

Clinical hypothyroidism

  • levothyroxine sodium (25-200mcg/day) replacement for T4.
    • 50-100mcg starting, increase till TSH in range or in secondary when T4 in mid-range
    • if CAD or > 60 start 25mcg
  • Monitoring
    • TFT 8-12 weeks after dose change
    • Aim to normalise TSH (0.5-2.5)
141
Q

management of subclinical hypothyroidism

A
  • ↑ TSH but normal T3/T4
  • TSH 4-10 and normal T4
    • < 65 and symptomatic - trial levothyroxine, stop if no improvement
    • Elderly - consider watch and wait approach
    • Asymptomatic - repeat TFT in 6/12
  • TSH > 10 and normal T4
    • Start levothyroxine regardless of symptom status if < 70 years
    • In 70+ consider conservative management and repeating TFTs
142
Q

causes of hyperthyroidism

A
  • primary
    • Graves, thyrotoxicosis, toxic adenoma, thyroiditis
    • amiodarone, lithium, exogenous iodine, levo overtreatment
  • secondary
    • TSH pit. adenoma, hCG secreting tumour (e.g. molar), gestational thyrotoxicosis
143
Q

what is the management of hyperthyroidism?

A
  • Sx - beta blocker
  • anti-thyroid
    • carbimazole or prophythiouracil
    • 2-3 weeks
    • block and replace or dose titration
    • assess if remission 18-24 months
  • radioiodine
    • takes 3-4 months
    • CI: pregnancy, no conception within 6 months
    • indicated: relapse, poor compliance, toxic nodular
  • surgery
    • if compression, failure of medical treatment
    • subtotal/total 98% cure rate
    • SE: haemorrhage, hypoparathyroidism, vocal cord paralysis, hypothyroidism (long-term)
144
Q

what are the classes of obesity?

A
  • BMI 25-29.9 - overweight
  • BMI 30-34.9 - obese (grade I)
  • BMI 35-39.9 - obese (grade II)
  • BMI > 40 - morbidly obese (grade III)
145
Q

medical management of obesity

A
  • Orlistat - pancreatic lipase inhibitor
    • Indicated: BMI > 28 with RF, BMI > 30, continued weight loss e.g. 5% in 3 months
    • SE: faecal urgency, incontinence, flatulence
  • Liraglutide - GLP1 receptor antagonist
    • Indicated: BMI > 30, BMI 27-30 with other weight related issues
    • Stop treatment after 12 weeks if weight loss < 5%
  • Consider vitamin and mineral supplements - esp. for elderly or growing adolescents
146
Q

definition of osteomalacia and causes:

A

Osteomalacia is a disorder of bone matrix mineralisation characterised by incomplete mineralisation of mature bone matrix following growth plate closure in adults

  • Dietary deficiency
  • Poor sunlight exposure
  • Malabsorption
147
Q

Ix of osteomalacia

A
  • Bloods
    • ABG - acutely unwell, exclude renal tubular acidosis
    • calcium (low or normal), phosphate (low), ALP (high) - bone profile
    • 25-hydroxy vitamin D
      • ↑ risk to bone health if < 25 nmol/L
      • Inadequate if 25-50nmol/L
      • > 50 is usually sufficient for most
    • PTH (high-secondary)
    • U&Es - assessment for CKD
  • Imaging
    • Limb x-ray - may be normal or may show osteopaenia.
      • Looser’s zone – wide, transverse lucencies traversing part way through a bone (usually at right angles)
148
Q

management of osteomalacia

A
  • Lifestyle
    • Advise about dietary source + safe sunlight exposure
  • Vitamin D and calcium replacement
    • Rapid correction - vitamin D
      • Indication: symptomatic, need correction prior to anti-resorptive treatment
      • consider combined calcium-vit D
    • Non-urgent correction vitamin D
      • 800-2000 IU daily, no requirement for loading
  • Monitor with serum calcium, phosphate, ALP, PTH - 1/12
    • no need to repeat vit D routinely
  • Treat any underlying cause.
149
Q

what causes osteoporosis?

A
  • primary
    • idiopathic, post-menopausal, age related
  • secondary
    • malignancy - myeloma, mets
    • Cushing’s, thyrotoxicosis, 1 hyperparathyroidism, hypogonadism
    • drugs - corticosteroid, heparin, PPI, SSRI, anti-epileptics, aromatase inhibitors
    • malabsorption syndromes
    • anorexia nervosa
    • ETOH, smoking
150
Q

what are the RF for osteoporosis?

A

Osteoporosis RF (secondary) SHATTERED

  • Steroid use >5mg/day of prednisolone
  • Hyperthyroidism, hyperparathyroidism, hypercacliuria
  • Alcohol and tabacco use
  • Thin < 22
  • Testosterone low
  • Early menopause
  • Renal or liver failure
  • Erosive/Inflammatory bone disease
  • Dietary low calcium or malabsorption, DM1
151
Q

what are the Ix for osteoporosis

A
  • Urinary bence-jones protein
  • Bloods
    • calcium, phosphate, Alk Phos, vitamin D (normal in primary osteoporosis)
    • TFTs
    • Testosterone
  • Imaging
    • X-ray
    • DEXA scan (gold standard): hip and lumbar spine usually
    • MRI spine - assess for vertebral #
  • Specialist or scoring
    • FRAX score - assess fracture risk
      • Used for those 40-90, with or without BMD values
    • Qfracture - 10 year predicted absolute fracture risk
      • Used for those 30-84, BMD cannot be incorporated
152
Q

how is FRAX score interpreted?

A
  • FRAX score - assess fracture risk
    • Used for those 40-90, with or without BMD values
    • Age, sex, secondary osteoporosis, alcohol intact, weight, height, previous fracture, parent hip #, smoking, glucocorticoid, RA, BMD
    • Results interpretation
      • Without BMD
        • Low risk - reassure
        • Intermediate - offer DEXA
        • High - offer bone protective treatment
      • With BMD
        • Low risk - reassure
        • Intermediate - consider treatment
        • High - strongly recommend treatment
153
Q

who should have a fracture risk score calculated?

A
  1. All men > 75
  2. All women > 75
  3. All men and women > 50 if they have:
    • FHx of hip #, falls Hx, previous fragility #, low BMI, ETOH > 4 units/day, are/were on steroids, disease associated with osteoporosis (coeliac, IBD, hyperparathyroidism)
154
Q

describe anti-resorptive medications available

A
  • Bisphosphonates - oral, alendronic acid, ibandronic acid, risedronate sodium
    • Indicated: 10 year # risk > 1%
    • Usually given weekly
    • MOA - incorporated into osteoclast cells and cause dysfunctional cell processes → non-functional + undergo apoptosis
  • Denosumab - Mab, RANK-L → prevents maturation and formation of osteoblasts
    • 6/12 SC injection
    • CI - low serum calcium
    • SE: joint and muscle pain in limbs
    • on stopping rapid ↓ BMD (prefer bisphos.)
  • Raloxifene - SERM → preserve BMD
    • For post-menopausal
    • Can worse menopausal Sx
    • ↓ risk of vertebral fractures and show to improve BMD
  • HRT - utilised in young women who have undergone premature ovarian insufficiency
  • Teriparatide - synthetic PTH, stimulates bone growth
155
Q

what is primary prevention of post-menopausal women for osteoporosis?

A
  1. Bisphosphonates
    • 10mg OD or 70mg once weekly
  2. Denosumab
    • SC injection once every 6/12
  3. Consider vitamin D and calcium supplement as required (AdCal)
156
Q

conservative management of osteoporosis

A
  • ↓ RF - stop smoking, ↑ diabetic control, ↓ ETOH
  • Diet - adequate vitamin D, calcium and protein intake
  • Regular weight bearing exercise
  • More information from National Osteoporosis society
  • Falls risk assessment
  • Hip protectors for elderly in care homes
157
Q

osteoporosis secondary prevention in post-menopausal women

A
  1. Bisphosphonates
  2. Raloxifen and teriparatide
    • Indicated - unable to comply with bisphosphonate, CI to bisphosphonate, combination of low T score + independent clinical RF for fracture
  3. Consider vitamin D and calcium supplements as required (AdCal)
158
Q

What is Paget’s disease

A

Condition characterised by increased bone turnover in focal bone regions resulting in abnormal bone structure and increased risk of fracture

  • controlled bone turnover
  • high osteoclast + osteoblast activity so disorganised bone breakdown and formation
159
Q

Paget’s complications

A
  • Disruption of anatomy
    • Pain
    • Deformity + #
    • Hearing loss - vestibulocochlear nerve compression or ossicle ossification
    • Spinal stenosis
    • Osteoarthritis
    • Nerve compression
  • Effects of abnormal metabolism
    • Osteosarcoma (<1%)
    • High output heart failure
160
Q

management of Paget’s disease

A
  1. Analgesia
  2. Supportive - orthotics, physiotherapy, hearing aids
  3. Bisphosphonates - alendronic acid, pamidronic acid + calcium and vitamin D as required
  4. Monitor every 6-12 for recurrence, ALP = marker
    • Indefinite due to risk of osteosarcoma
161
Q

define phaeochromocytoma and causes

A

Refers to a catecholamine producing tumour, usually originating from chromaffin cells in the adrenal medulla

causes

  • adrenal medullary tumour
  • sporadic (most)
  • familial - MEN2 (bilat), VHL, NF1, Paraganglioma syndromes
162
Q

rule of 10s for phaes

A
  • 10% bilateral
  • 10% malignant
  • 10% extra-adrenal
163
Q

investigations for phaechromocytomas

A
  • Bedside
    • BP + fundoscopy - HTN CoD
  • Bloods
    • Serum plasma free metanephrines, catecholamines and VMA
    • Glucose (often ↑), calcium (may be ↑), FBC (Hb may be ↑)
  • Imaging
    • CT CAP scan - assess for tumour
    • MIBG scan - if biochem +ve but CT -ve ,uses MIBG labelled with iodine
  • Specialist or scoring
    • Urinary metanephrines, catecholamines and VMA (vanillylmandelic acid)
    • Genetic testing
164
Q

management of phaeochromocytoma

A
  1. Alpha blockage - short acting → long-acting
  2. Beta blockage - propranolol
  3. Surgery - only once BP is controlled, usually 4-6 weeks after alpha-block to ensure full block
    • Resection
    • Repeat 24 hr urinary collection 2/52 to assess success
  4. + chemo/radiotherapy - indicated if on histology mass is malignant
165
Q

what is the diagnostic criteria of PCOS?

A
  1. Oligomenorrhea/irregular menses for 6 months
  2. Hyperandrogenism
    • Clinical evidence - hirsutism, male pattern alopecia
    • Biochemical - raised free testosterone
  3. Polycystic ovaries on USS
166
Q

investigations in PCOS?

A
  • USS of ovaries (TVUSS) - polycystic morphology defined as > 12 follicles 2-9mm or ovarian volume > 10mL (NICE)
  • LH and FSH - raised LH, ↑ LH:FSH ratio
  • Steroid hormone panel - raised androgens (↑ testosterone, ↑ androstenedione, ↓ SHBG)
  • Hormone levels to exclude other endocrine conditions
    • TFTs
    • prolactin,
    • 7-hydroxyprogesterone (CAH), 24-hr
    • urinary cortisol (Cushing’s)
    • DHEA-S and free androgen index (androgen secreting tumours)
  • Glucose tolerance test
  • Fasting lipid panel
167
Q

conservative management of PCOS

A
  • Reduce weight (5% loss can resume ovulation)
    • May reduce high insulin and androgen levels, ↓ DM and CVD risk, result in menstrual regularity and improve chances of falling pregnant
  • Dietary modification and exercise
  • Screening - for DM2 and CVD, at higher risk of developing
  • Advice
    • Inform them of ↑ risk of T2DM + GDM if they become pregnant, CVD and OSA
    • Smoking cessation
168
Q

management for PCOS patients who are fertility desiring

A
  • Clomiphene
    • Clomiphene (NICE)- antioestrogen (so ↑ FSH and LH
    • Given days 2-6 for follicle maturation
    • step wise 50mg → 100mg → 150mg
    • Letrozole (NICE) - recent medication, thought to be more effective in those with BMI < 30-35
    • Metformin - Add as adjunct if 3 cycles of clomiphene have failed
  • Gonadotrophins
    • For clomiphene resistant, daily SC FSH + LH
    • Start with a low dose, ↑ dose every 5-7 days until ovaries response, USS monitor
  • Laparoscopic ovarian diathermy (ovarian drilling)
    • Destroys some ovarian stroma, can induce more regular ovulation which may continue for years
  • IVF
169
Q

management of PCOS not desiring fertility

A
  • Oral contraceptive pill
  • Metformin - for subset with hyper-insulinaemia and CVS risk factors
    • off license use
  • Mechanical hair removal or topical treatments
    • Eflornithine topical → Slows hair growth
    • minoxidil topical → tx androgenic alopecia
  • Anti-androgen
    • For those with severe hirsutism or CI to hormonal contraception
    • 1st line - Spironolactone (block AR)
    • 2nd line - finasteride (5-alpha reductase inhibitor)
170
Q

causes of hyperaldosteronism

A
  • Adrenal adenoma → Conn’s syndrome, majority (70%)
  • Bilateral adrenal hyperplasia (2nd most common)
  • Familial hyperaldosteronism
  • Adrenal carcinoma (rare)
171
Q

Ix for hyperaldosteronism?

A
  • Bedside - BP, ECG
  • Bloods
    • VBG - alkalosis
    • U&Es - hypokalaemia, normal sodium usually
    • Aldosterone: renin ratio - ↑ ratio (↑ aldosterone, ↓ renin)
    • LFT, FBC, ESR, bone profile
  • Imaging
    • CXR
    • Adrenal CT with contrast - localise adrenal lesion
  • Specialist or scoring
    • Selective adrenal venous sampling - gold standard, helps to identify if the source of excess aldosterone is from one isolated adrenal (Conn’s) or from both (hyperplasia)
    • Saline suppression test
      • Failure of aldosterone levels to suppress after salt loading - confirms dx
172
Q

management of hyperaldosteronism - unilateral disease

A
  • Surgical → laparoscopic adrenalectomy - removal of affected adrenal gland
    • Spironolactone post-operatively for 4 weeks to control BP and K+
173
Q

management of bilateral hyperaldosteronism

A
  • Optimise HTN with anti-hypertensives
  • Potassium sparing diuretics - amiloride, spironolactone, eplerenone
    • Can help lower BP while promoting potassium retention
174
Q

causes of a high prolactin

A
  • Excess pituitary production
    • Pregnancy, breastfeeding
    • Hypothyroidism (↑ TRH, stimulates prolactin)
    • Prolactinoma
  • Compression of pituitary stalk (prevents DA inhibition)
    • Pituitary adenoma
    • Craniopharyngioma
  • Dopamine antagonists (most common cause of ↑ prolactin)
    • Anti-emetics - metoclopramide
    • Anti-psychotics - risperidone, haloperidol
175
Q

investigations for high prolactin?

A
  • Bedside
    • Visual field testing
    • Pregnancy test - exclude
  • Bloods
    • Prolactin - massively raised, > 6000
    • Hormones - GH/IGF-1, ACTH, FH + LSH (gonadotrophins)
    • TFTs - assess for hypothyroidism
  • Imaging
    • MRI brain w/ contrast
176
Q

management of prolactinoma

A

Medical

  • Dopamine agonist → 1st line, cabergoline, bromocriptine
    • Tx usually long term
  • Hormone replacement therapy → e.g. oestrogen
    • During period of hypogonadism, if fertility not issue

Surgery

  • Trans-sphenoidal hypophysectomy→ 2nd line
    • Indicated: significant SOL symptoms, failure of medical treatment

Radiotherapy - 2nd line, alternative to surgical management

177
Q

key biochemical features of SIADH

A

High urine osmolality (>100) + low serum osmolality + high renal sodium (>20mmol/L) + normal 9am cortisol and TFTs

178
Q

what must be excluded before SIADH is diagnosed?

A

Diagnosis of exclusion - must rule out Addison’s and abnormal thyroid function

  • 9am cortisol + TFTs
179
Q

management of SIADH

A
  1. Stabilisation - resuscitation if Sx + severe hyponatraemia (<125 mmol/L)
    • IV hypertonic saline - slow rate, monitor for neurological change
  2. Fluid restriction
  3. Treat underlying cause
  4. Demecycline, tolvaptan (vasopressin receptor antagonists) → induced DI state, but very expensive
180
Q

types of thyroiditis

A
  • Hashimoto’s thyroiditis
    • Autoimmune thyroiditis
    • Destruction of thyroid cells by auto-antibodies
  • De Quervain’s thyroiditis
    • Subacute granulomatous thyroiditis.
    • Thought to have a viral origin.
      • Associated with coxsackie
  • Post-partum thyroiditis
    • Affects 5% women giving birth every year.
    • 1 in 5 of those need long-term levo
  • Drug-induced thyroiditis
    • Damage from drugs
    • Common: interferons, amiodarone, lithium
  • Acute or infectious thyroiditis
    • Suppurative thyroiditis.
    • Infection by bacteria
      • e.g. S. aureus, S. pyogenes, S. pneumoniae, Klebsiella, H. Influenza
  • Riedel’s thyroiditis
    • Chronic form of thyroiditis, AI
    • Characterised by fibrosis and infiltration of IgG4 secreting plasma cells.
181
Q

-gliflozins Drug class

A

SGLT2 inhibitors

182
Q
  • glitazones
A

Thalizodinediones

183
Q
  • gliptin Drug class
A

DDP4 inhibitor Inhibit DDP4i which increases incretins like GLP-1 level (not metaglised ny DDP4) Causes rise in insulin secretion + inhibition of glucagon

184
Q
  • tide Drug class
A

GLP 1 agonists

185
Q

what are the pre-diabetes ranges - fasting glucose?

A

fasting 6.1-6.9

186
Q

what are the pre-diabetes ranges OGTT and random glucose?

A

7.8-11.1

187
Q

how to calculate the amount 1 unit of insulin will reduce someone’s blood sugar

A

correction factor = 100/total number daily units

correction factor is how much 1 unit of rapid acting insulin will lower BS

188
Q

alpha blocker used in phaeo

A

phenoxybenzamine

IK6 - Exams (24 decks)

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