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Final Year - ICSM > Endocrinology_Medicine > Flashcards

Endocrinology_Medicine Flashcards

1
Q

Hyponatremia - Sx? Ix & Approach? What happens if you correct Na too fast?

A

Sx: confusion, altered GCS, headaches, seizures, encephalopathic

Ix: fluid status, U&E, paired osmolalities (urine, serum)

Fluid status:

  • HYPOvolaemic (dehydrated) - WASTING (diarrhoea/vomiting, diuretics) –> IV fluids
  • EUvolaemic (normal) - ENDOCRINE (SIADH, hypothyroidism, Addison’s) –> fluid restrict + Tx underlying cause
  • HYPERvolaemic (fluid overload) - FAILURE (liver, renal, heart) –> fluid restrict + Tx underlying cause

Urine Na:

  • <20 mmol/L –> hypovolaemia (increased Na reabsorption in kidneys –> increasing H20 retention –> reducing urine Na)
  • >20 mmol/L –> SIADH (BUT if on diuretics, urine Na can’t be interpreted) –> fluid restrict

Na corrected too fast (>10) = osmotic demyelination syndrome (central pontine myelinolysis) –> pseudo-bulbar palsy, paraparesis, locked-in syndrome

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2
Q

Potassium homeostasis - areas involved? Hypo/hyper? Appearance on ECG? Hyper Tx?

A

Areas involved:

  1. Dietary intake
  2. Absorption in GI tract
  3. Adrenals & kidneys - regulate serum K concentration

HYPOkalaemia:

  • Poor dietary intake, vomiting/diarrhoea
  • Diuretics - loop/thiazide (block channels causing K reabsorption)
  • Hyperadrenalism (Conn’s, bilateral adrenal hyperplasia, Cushing’s)
    • Conn’s/BAH - excess aldosterone - NOTE: Aldosterone promotes reabsorption Na, excretion K
    • Cushing’s = excess cortisol –> off-target effect on mineralocorticoid receptors –> mimics aldosterone

HYPERkalaemia:

  • false = HAEMOLYSIS –> repeat sample
  • Kidney failure e.g. on dialysis (kidneys = main route to remove K)
  • Anti-HTN/diuretics
    • ACEi/ARB - reduce kidney hyperfiltration, mainly a risk if CKD
    • K+-sparing diuretics e.g. spironolactone/amiloride
  • Addison’s disease (failure - can’t produce enough cortisol/aldosterone)
  • NOTE: appearance on ECG = tented T-waves, broad QRS, prolonged PR interval

Hyperkalaemia Tx:

  • Protect heart - IV 10-30ml 10% Ca Gluconate (repeat /15m, x5 MAX)
  • Reduce K+:
    • 1st line - 10U Actrapid (insulin > drive K into cells) AND 100mL 20% glucose (to prevent hypo)
    • 2nd line - 5mg Salbutamol NEB (b-agonist)
  • Ix cause: drug chart, U&E (kidney funct), short SynACTHen test (Addison’s)
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3
Q

Calcium homeostasis?

Hyper Sx? Ix & causes? Mx?

Hypo Causes? Sx? Ix? Mx?

A

Hormone production:

  • Parathyroid gland - PTH –> INCREASE Ca:
    • Bone resorption
    • GI absorption
    • Kidney - decreased excretion, increases 1alpha-hydroxylation (vitD activation)
  • Vit D3 aka cholecalciferol (UV)/ergocalciferol (diet)
    • In Liver –> 25-OH(D) aka calcidiol
    • In Kidney + 1alpha-hydroxylase –> 1,25-OH2(D) aka Calcitriol (activated vitD) –> INCREASE Ca
      • GI absorption
      • Kidney - decreased excretion

HYPERcalcemia ​

  • Sx:
    • Stones - urinary tract calculi
    • Bones - fractures
    • (Abdo) moans - dyspepsia
    • Thrones - polyuria, constipation
    • (Psych) overtones - depression, psychosis
  • Ix - check PTH:
    • Low - hypercalcemia of malignancy (PTH axis is functioning normally) - bone mets, PTHrP (released by lung SCC), myeloma (CRAB)
    • Normal/high - primary hyperparathyroidism (as if serum Ca high, PTH should be low) - adenoma, hyperplasia, MEN 1&2
    • Other:
      • Fluid status, ECG (short QT), protein electrophoresis, 24hr urinary Ca (familial hypocalciuric hypercalcemia)
      • Bloods - bone profile (Ca, PO4), U&E
      • Imaging: CXR
  • Mx:
    • IMMEDIATE = aggressive IV 0.9% fluid resus (4-6L over 24krs), repeat Ca
    • Tx underlying cause:
      • Parathyroid adenoma - minimally invasive surgery (subtotal/total parathyroidectomy)
      • Malig - Zalendronate/Pamidronate (inhibit osteoclast activity), slow infusion
      • Other:
        • If bone mets –> bisphosphonates
        • If renal failure –> Cinacalcet (reduce PTH)
    • Recheck serum Ca @day 2 –> 4

HYPOcalcaemia

  • Causes:
    • Hypoparathyroidism (PO4 high, PTH low)
    • Pseudohypoparathyroidism (PO4 high, PTH high) = PTH resistance
    • CKD (high PO4, PTH high, ALP high)
    • Vit D def (rickets/osteomalacia, low/normal PO4, high PTH, high ALP)
    • Hypomagnesaemia (low/normal PO4, low/normal PTH, normal ALP)
  • Presentation:
    • Peri-oral numbness, digital paraesthesia, dermatitis
    • +ve Trousseau’s (BP cuff 20 over SBP for 3mins –> salt bae hand), Chovstek signs (tap over the masseter muscle in the inferior pre-auricular area)
    • Laryngospasm (wheeze, dysphagia, muscle cramps)
    • Confusion, seizures, prolonged QT
  • Ix: serum Ca, PO4, Mg, PTH, U&E, Vit D
  • Mx: PO/IV replacement of Ca
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4
Q

If a patient has metformin & CKD when to stop metformin?

A

eGFR <30

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5
Q

If on insulin - what to do about driving?

A

Inform DVLA, must be able to record CBG every 2hrs

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6
Q

Tired, thirsty and irritable, wees alot (very pale) - Dx?

What is there Serum Sodium lvl?

A

Diabetes insipidus

Ix: hypernatraemia

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7
Q

Large hands + jaw + bitemporal hemianopia - Dx?

A

Acromegaly (anterior pituitary macroadenoma)

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8
Q

Young female, resistant HTN, hypokalaemia - Dx?

A

Conn’s syndrome (hyperaldosteronism)

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9
Q

Headache, sweating, tachy, HTN - Dx?

A

Phaeochromocytoma

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10
Q

Hyperparathyroidism sub-categories?

A
  • Primary - PTH secretion from primary parathyroid tumour/ectopic secretion from another tumour (high Ca, high PTH)
  • Secondary - PT hyperplasia to maintain control of hypocalcemia, normally from CKD (low Ca, high PTH, normal -ve feedback)
    • CKD –> bone profile, parathyroid hormone lvl every 3-6 months
  • Tertiary - prolonged secondary, becomes irrepressible by serum Ca lvls. Mostly kidney transplant patients (high Ca, very high PTH)
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11
Q

Hoarse voice post-thyroidectomy - why?

A

Recurrent laryngeal nerve injury

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12
Q

Low Ca, high PO4, high PTH, short fingers

A

Pseudohypoparathyroidism (similar features to secondary hyperparathyroidism - consider if CKD or vit D deficiency does not explain the presentation)

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13
Q

Facial twitching when tapping anterior to the tragus - sign?

A

Chvostek sign (hypocalcaemia)

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14
Q

Diabetes: presentation? RFs? types? criteria for Dx? Mx? Complications?

A

Presentation: polyuria, polydipsia, dehydration

  • Ketosis - malaise, vomiting
  • FHx, other endo disorders
  • If known DM:
    • Previous DM control (hyp/hyper)
    • Micro/macrovascular complications
    • Diabetic eye disease (Dx & Tx)

RFs: overweight, FHx (DM), PMHx (GDM), PCOS, HTN, dyslipidemia, CVD

Criteria for Dx (repeat test needed for Dx):

  • Fasting plasma glucose of ≥7.0 (normal ≤6)
  • OGTT (BM 2hours after 75g glucose-load)/ Sx + random plasma glucose of ≥11.1mmol/l (normal <7.8)
  • HbA1c ≥48mmol/mol (≥6.5%) - not for young/T1DM, acutely ill, haem disease, preg, iatrogenic

T1DM Mx: exogenous insulin to avoid DKA & long-term complications

  • Diet - lower fat, higher carbs = counting carbs (adjust insulin around diet rather than limiting eating)
  • Diabetic specialist nurse - EDUCATE:
    • Self-adjust dose - DAFNE course for T1DM (D for DM)
    • Fingerprick glucose
    • Calorie intake & carb counting
    • Phone support
  • Don’t stop insulin during acute illness, maintain calorie intake
  • Insulin regimens:
    • 1st line - Basal-bolus regimen
      • Basal (background) - BD insulin detemir (or Levemir/Lantus/Tresiba) as basal insulin
      • Bolus (before meals) - analogue rapid-acting insulin e.g. insulin Lispro (Humalog)/Aspart (Novorapid)/Neutral (Actrapid)
    • Other:
      • BD biphasic (premixed insulin, hypos common) e.g. Novomix, Humulin M3, Humalog Mix
      • OD before bed long-acting (for T2DM)
      • NOTE: intermediate-acting insulin e.g. Humulin I, Insulatard

T2DM Mx:

  • 1st line - Lifestyle changes - DESMOND course for T2DM (D for DM), dietician input, self-BM monitoring (individual HbA1c target <6.5)
    • HbA1c targets:
      • No hypoglycaemics - 48mmol/mol
      • Hypoglycaemics - 53mmol/mol
      • Escalate Tx - 58mmol/mol
  • Medication:
    • 2nd - Metformin (SEs: diarrhoea, LA - avoid if eGFR <30)
    • 3rd - ADD Sulphonylurea e.g. Gliclazide (SEs: hypoglycaemia, weight gain)
    • 4th - ADD other DM med:
      • Pioglitazone (SEs: hypoglycaemia, weight gain, oedema, fractures in elderly)
        • C/I in HF, bladder cancer
      • SGLT-2 inhibitor e.g. Empagliflozin (SEs: Hypoglycaemia, weight loss, UTI)
        • Not recommended in impaired renal funct
      • DPP-4 inhibitor e.g. Linagliptin (APPROVED FOR USE IN CKD, weight neutral)
      • GLP-1 analogues e.g. Exenatide/Liraglutide (SE: weight loss - useful if BMI >35; vomiting)
        • Not recommended in impaired renal funct
    • 5th - If on triple therapy & not providing control –> commence insulin
  • CVD risk Mx - anti-HTN, anti-lipid, QRISK-3 score
  • Diabetic nephropathy Mx:
    • Monitor albumin-creatinine ratio (ACR)
    • Consider ACEi/ARB early
  • Diabetic neuropathy Mx:
    • Annual Sx review (erectile dysfunction, autonomic neuropathy - orthostatic hypotension, gastroparesis, bladder emptying difficulties)
    • Annual foot screen + specialist foot Mx, monitor for diabetic foot/ulcers ± amputation
  • Diabetic retinopathy: retinal screen annually (age ≥12yrs)
    • Background: need to tighten control
      • Venodilation, microaneurysms (dots), hard exudates (lipid deposits)
      • Tx: tighten glycaemic control, refer if near macula
    • Pre-proliferative (mild) - soft exudates (cotton wool spots e.g. infarcts)
    • Proliferative - neovascularization (+ floaters, reduced acuity)
      • Tx: pan-retinal photocoagulation
    • Diabetic maculopathy - hard exudates, oedema (+ blurred vision, reduced acuity)
      • Tx: intravitreal triamcinolone acetonide decreases macula oedema
    • NOTE: Pre-diabetic –> refer to diabetes prevention programme (DPP)

Diabetes complications:

  • Microvascular:
    • Eye - diabetic retinopathy (± cataracts, glaucoma)
    • Kidney - diabetic nephropathy
    • Neuropathy - damage to PNS –> diabetic neuropathy (peripheral neuropathy - glove & stockings distribution) –> diabetic ulcers/gangrene
  • Macrovascular:
    • Brain - stroke/TIA/cog impairment
    • Heart - coronary heart disease
    • Extremities - PVD, diabetic ulcers/gangrene
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15
Q

Acromegaly cause? presentation? Ix? Mx? Complications?

A

Cause: macroadenoma in anterior pituitary

Presentation: coarse facial features

  • Skin (acanthosis nigricans - thick & dark in creases), sweating, carpal tunnel syndrome (bilateral)
  • Arthropathy, sleep apnoea, reduced sexual functioning, visual field defects (bitemporal hemianopia)
  • Assoc: DM, HTN, MEN type 1 (15%)

Ix:

  • Bedside: CN VI palsy, urine dip (glucose), ECG (cardiomyopathy)
  • Bloods: elevated IGF-1, GH lvl during OGTT (not suppressed in acromegaly)
  • Imaging: MRI brain (macroadenoma), sleep studies, colonoscopy (screening), visual field testing (driving)

Mx:

  • Transsphenoidal hypophysectomy (curative)
  • Medical: somatostatin analogue (octreotide)
  • External pituitary radiotherapy (long-term 5-10yrs)

Complications:

  • General: HTN, DM, carpal tunnel syndrome, sleep apnoea, colorectal cancer, LVH/cardiomyopathy/IHD
  • Anterior pituitary hypofunction: hypogonadism
  • Local compressive: bitemporal hemianopia
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16
Q

Perioperative DM Mx?

A

Variable insulin infusion for 30-60 mins after starting SC insulin to avoid iatrogenic DKA

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18
Q

SGLT2 inhibitors (dapagliflozin) S/E?

A

Increased yeast/UTIs, hypoglycaemia, weight loss

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19
Q

Pioglitazone S/E? C/Is?

A

hypoglycaemia, weight gain, fluid retention (oedema), assoc with bladder cancer, osteoporosis (elderly - fractures)

C/Is: HF, bladder cancer

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20
Q

Sulphonylureas (oral) or insulin (sc) S/E?

A

Weight gain & hypoglycaemia

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21
Q

Diabetic patient having surgery:

  • What to do if high HbA1c?
  • What to do if long surgical period (missing 2 meals)?
  • What to do if short surgical period if taking insulin/other diabetic meds?
  • What to do the day before admission and day after surgery?
A

If poorly controlled DM (HbA1c ≥69) or long starvation period (≥2 missed meals) –> variable rate insulin infusion + IV maintenance fluids (5% glucose in 0.45% saline)

If on insulin:

  • If using variable rate insulin infusion - stop all insulin until eating/drinking normally and has been 30mins since first post-op insulin dose
  • Basal (background insulin) always maintained to prevent ketosis - dose reduced by 20% to avoid hypoglycaemia
  • Bolus (before meals) avoided:
    • If AM surgery - omit morning & lunch dose
    • If PM surgery - omit lunch dose

If on diabetic medications:

  • Stop ALL if variable-rate insulin infusion used - apart from GLP-1, which can be maintained
  • Insulin & sulphonylureas (glipizide) - dose must be reduced as they lower BM –> hypoglycaemia
    • AM surgery - omit morning dose
    • PM surgery - omit morning and afternoon dose
  • Metformin, GLP-1 analogues (liraglutide), DPP-IV inhibitors (linagliptin), SGLT2 inhibitors (dapagliflozin) - rarely cause hypoglycaemia while fasting (only reduced if other concerns)
    • SGLT2 inhibitors - omit morning dose if AM/PM surgery

NOTE: take all as normal day before admission, take as normal day after surgery

22
Q

Hyperosmolar Hyperglycaemic State

  • What does insulin do? Pathophysiology of HHS?
  • HHS criteria? HHS Mx? HHS Mx Targets?
A

Insulin:

  • High level of insulin –> reduces serum BM (pushes into surrounding tissues & hepatic glucose store)
  • Low level of insulin –> switches off ketone production

Pathophysiology:

  • HHS = complication of T2DM
  • In HHS have enough insulin to switch of ketone production but not enough to reduce BM lvls
  • High glucose - osmotically active –> polyuria –> dehydration

HHS criteria:

  • Hypovolaemia
  • Glucose >30mmol/L
  • NO ketonaemia
  • Serum osmolality >320mOsmol/kg

Mx: REHYDRATE = IV 0.9% NaCl (3-6L by 12hrs, deficit 110-220mL/kg)

  • Targets:
    • Reduce Na by less than 10mmol/L/day (otherwise risk osmotic demyelination syndrome)
    • Reduce BM by over 5mmol/L/hr
    • NOTE: if targets not met by 0.9% saline –> 0.45% instead
  • If fluid alone are not enough –> 0.05 units/kg/hr fixed-rate insulin infusion
23
Q

SIADH - pathophysiology? criteria? causes?

A

Criteria:

  • True hyponatraemia
  • High urine osmolality
  • Clinically euvolemic
  • Dx of exclusion (9am cortisol + TFTs must be normal)

Causes:

  • Malig (small cell lung cancer, breast cancer)
  • CNS disorders (encephalitis, abscess)
  • Chest disease (pneumonia, TB)
  • Drugs (opiates, SSRIs, carbamazepine)
24
Q

Hypernatremia - breakdown into different causes? Mx?

A

Causes:

  • Hypovolaemia (H20 loss > Na loss) - most common
    • GI loss: D&V
    • Skin loss: excessive sweating, burns
    • Renal loss: diabetes insipidus (DI), osmotic diuresis (glucose/mannitol), loop diuretics, kidney disease
  • Euovolaemia - Resp (tachypnoea), skin (sweating, fever), renal (DI)
  • Hypervolaemia
    • Mineralocorticoid excess – Conn’s syndrome
    • Inappropriate saline

Causes thirst –> most people self-correct UNLESS: failure to ingest water (Elderly/dementia, fasting (e.g., for surgery), excess loss)

Mx: SLOW Hartmann’s (rapid correction –> cerebral oedema)

25
Q

Calcium, PTH, Vit D, ALP levels in hyperparathyroidism & relevant differentials

26
Q

Diabetes insipidus - Sx? Types? Ix? Tx?

A

Sx: hypernatremia (lethargy, thirst, irritable, confusion, coma, fits), polyuria, urine plasma osmolality <2 (very dilute)

Types:

  • Central (lack of ADH prod in hypothalamus) – pituitary surgery, irradiation, trauma, infarction
  • Nephrogenic (resistance to ADH effects) – hypercalcaemia, hypokalaemia, meds (lithium)

Ix: rule out DDx (BM, review drugs, K/Ca lvls)

  • U&E, Ca, BM, serum & urine osmolarities
  • Dx: 2-step fluid deprivation test = give desmopressin (DDAVP):
    • Normal/primary polydipsia –> urine concentrates on fluid deprivation (>600)
    • Cranial DI - giving desmopressin allows ADH prod –> urine conc
    • Nephrogenic DI: urine never concentrates
    • NOTE: DI excluded if urine to plasma (U: P) osmolarity ratio >2:1
  • Cranial MRI - if suspect cranial DI

NOTE: Fluid deprivation test process:

  • Baseline urine osmolality
  • Fluid deprivation for 8hrs, take urine osmolality
  • Give desmopressin, wait 8hrs, take urine osmolality

Tx:

  • Nephrogenic DI –> fluids (+ monitor UO) + thiazide diuretics (hydrochlorothiazide - weird/does not make sense)
  • Central DI –> fluids + desmopressin
27
Q

Hypokalaemia - causes? features? Ix? Mx?

A

Causes:

  • GI loss (D&V)
  • Redistribution into cells: insulin (refeeding syndrome (KPMg), insulinoma), b-agonist (salbutamol), metabolic alkalosis (pump out H, pump in K)
  • Renal loss:
    • Alkalosis: Conn’s, loop diuretics/Barter’s syndrome, thiazide diuretics/Gitelman syndrome (diuretics –> K not reabsorbed)
    • Renal tubular acidosis: T1 (reduced H+ excretion), T2 (reduced bicarbonate reabsorption), T4 (aldosterone def/resistance – hyperkalaemia)

Clinical features: muscle weakness, cardiac arrhythmia, polyuria/dipsia (nephrogenic DI)

Ix: ECG, cardiac monitor (risk of VF/arrhythmia), aldosterone: renin ratio

Mx:

  • Mild: SandoK (2 tablets TDS for 3 days, monitoring)
  • Severe: IV KCl (<10mM/hr)
  • Treat cause, correct Mg
28
Q

Hyperkalaemia - causes? Ix? Mx?

A

Causes:

  • Spurious sample
  • Excessive intake: oral, parenteral, stored blood transfusion
  • Transcellular mov (ICF>ECF):
    • Acidosis, insulin shortage (DKA - high glucose, high ketones, metabolic acidosis)
    • Tissue damage/catabolic state (rhabdomyolysis) – CK very high
  • Decreased excretion:
    • AKI (oliguric phase)/CKD (late)
    • Drugs (spironolactone – K-sparing diuretic, ACEi/ARB/NSAID)
    • Addison’s (mineralocorticoid def)

Ix:

  • Repeat sample (VBG to also look for acidosis)
  • CK, Creatinine & Urea
  • AM Cortisol/Short synACTHen test
  • ECG
    • Loss of p-waves, tall, tented T-waves, broad QRS (+ bradycardia)
    • If severe & untreated –> ECG forms ‘sine wave’

Mx (if >5.5 w/ ECG changes OR >6.5):

  • IV 10mls 10% calcium gluconate (cardioprotective, doesn’t lower K)
    • If on Digoxin – IV Ca causes arrhythmias – cardiac monitoring
  • IV 10ml 20% dextrose + 10 units short-acting insulin e.g., Actrapid (insulin drives K into cells, dextrose prevents hypo)
  • Neb salbutamol adjunct + treat cause
29
Q

Thyroid disease - types? presentations? causes? Mx? What is a thyroid storm?

A

Hypothyroidism:

  • Causes:
    • Primary:
      • Hashimoto’s thyroiditis - most common hypothyroidism
        • Goitre, AI disease (vitiligo, pernicious anaemia, T1DM, Addison’s)
        • Elderly females
        • May be initial ‘Hashitoxicosis’
        • +++ Autoantibody titres
          • Antithyroid peroxidase (TPO) & antithyroglobulin (TG)
      • Atrophic AI thyroiditis
        • No goitre, anti-TPO/TSH
      • Iodine def, meds (carbimazole, lithium), thyroid surgery
    • Secondary: pituitary gland fails to produce TSH
      • Tumour, vascular (Sheehan syndrome), radiation, inf
  • Ix:
    • Bedside: ECG (pericardial effusion, ischaemia)
    • Bloods: FBC, U&E, TFTs, Lipids, Prolactin, Anti-TPO/TG
    • Imaging: CXR (effusions, HF)
  • Mx: thyroid replacement therapy (levothyroxine)
    • Monitor with serum TSH, careful with dose in elderly (prone to IHD)
    • Myxoedema coma - A-E & active warming, T3 slow IV, hydrocortisone IV
  • Associated complications:
    • Cardiac - HF
    • Serous effusions (pleural, peritoneal, pericardial, joint)
    • Neuro - carpal tunnel, proximal myopathy, cerebellar dysfunction, myxedema coma
    • Systemic - dyslipidemia, anaemia

Hyperthyroidism:

  • Presentation:
    • Weight loss, increased appetite
    • Heat intolerance, tremor, sweating, palpitations
    • Mood (anxious, irritable)
    • Bowel habit (diarrhoea), menses (oligomenorrhoea)
    • Goitre
    • Eye Sx (watering, gritty, red)
    • Other AI disease (vitiligo)
    • Signs:
      • Lid lag (eyes)
      • Palmar erythema
      • Brisk reflexes
      • Sinus tachy/AF
  • Ix: TSH low, T3/4 high, TPO (may be raised), anti-TSHr ab (in Graves), technetium 99m uptake scan (diffuse/reduced)
  • Causes:
    • High-uptake:
      • Graves’ disease: MOST COMMON, autoantibodies ++ (anti-TSH-R ab),
        • Eye signs: proptosis –> exophthalmos, diplopia, visual loss
        • Peripheral signs: pretibial myxoedema, thyroid acropatchy, onycholysis, bruit over thyroid
      • Toxic multinodular goitre aka Plummer’s disease: hot nodules, painless
      • Toxic adenoma: 5%, single ‘hot nodule’ on isotope scan (1 area of uptake)
    • Low-uptake:
      • Subacute De Quervains (viral) thyroiditis: self-limiting post-viral painful goiter. Initially hyperthyroid, then hypothyroid
        • Tx: NSAIDs
      • Postpartum thyroiditis (like De Quervain’s but postpartum)
  • Mx:
    • Conservative: lifestyle changes, corneal lubricants
    • Medical:
      • Sx relief – B-blockers
      • Antithyroid meds - Carbimazole (or propylthiouracil)
        • SEs: rashes, agranulocytosis - monitor​
      • Radioiodine:
        • acts slowly, effective, best Tx for toxic multinodular goitre
        • Risk of permanent hypothyroidism (10%)
        • CI in preg/lactating women
    • Surgical: subtotal thyroidectomy (in large goitre/relapse)
    • Monitoring with TFTs annually
    • Thyroid storm: acute state of shock, pyrexia, confusion, vomiting
      • HDU/ITU support
      • Propylthiouracil 600mg –> 200mg QDS
      • Stable iodine (Lugol’s iodine) ≥1hr later
      • Propranolol, dexamethasone & IV fluids
30
Q

Thyroid neoplasia types?

A

Papillary (>60%)

  • 30-40yrs,
  • Psammoma bodies on histology
  • Very good prognosis
  • Surgery +/- radioiodine, thyroxine (to ↓TSH)

Follicular (35%)

  • Middle age, well-differentiated but spreads early
  • Surgery + RI + thyroxine

Medullary (5%)

  • Originates in parafollicular “C” cells – linked to MEN2
  • Produce calcitonin (monitoring levels is useful to detect recurrence)

Lymphoma (5%)

  • MALT origin
  • RFs: chronic Hashimotos (lots of lymphocytes that proliferate)
  • Good prognosis

Anaplastic

  • Rare, elderly, poor response to all treatments
31
Q

Multiple endocrine neoplasia (MEN) - what are these?

A

Group of 3 inherited disorders (AD) –> predisposition to endocrine cancers

  • MEN1 (3Ps): Pituitary, Pancreatic (e.g., insulinoma), Parathyroid (hyperparathyroidism)
  • MEN2a (2Ps, 1M): Parathyroid, Phaeochromocytoma, Medullary thyroid
  • MEN2b (1P, 2Ms): Phaeochromocytoma, Medullary thyroid, Mucocutaneous neuromas (& Marfanoid)
32
Q

Adrenal disease breakdown? Causes? Presentations? Ix? Mx?

A

Cushing’s #HighCortisol

  • Causes:
    • ACTH-dependent:
      • Pituitary tumour (85%) = “Cushing’s disease”
      • Ectopic ACTH-prod tumour (5%) - SCLC/carcinoid tumour
    • ACTH-independent:
      • Adrenal tumour (10%)
      • Iatrogenic steroid use
  • Presentation:
    • Thin skin, easy bruising, proximal myopathy, obesity (moon face, buffalo hump), other (hirsutism, acne)
    • Exam: vertical abdo striae
    • HTN, DM, osteoporosis (back/bone pain)
  • Ix:
    • Exclude pseudo-Cushing’s - depression, alcohol excess, chr inf (no muscle weakness)
    • Confirm Dx: low-dose dex suppression test - fail to suppress cortisol in all
      • Overnight dexamethasone suppression test (1g @11pm) OR
      • 48hr low-dose 0.5mg/6h PO dexamethasone supression test OR
      • 24-hr urinary free cortisol (test x3 as low sensitivity)
    • Plasma ACTH measured:
      • High - CRH test identifies if pituitary or ectopic
        • Could also do bilateral inferior petrosal sinus sampling –> if no mass –> CT contrast CAP for ectopic
      • Low - adrenal tumour –> CT/MRI adrenal glands –> if nothing –> adrenal vein sampling
  • Mx: treat underlying disease e.g. withhold steroids or surgical removal of the lesion
    • Cushing’s disease (pituitary tumour) –> trans-sphenoidal hypophysectomy (complications - DI, hypopituitarism)
      • 2nd - pituitary radiotherapy (also used if still high cortisol post-surgery) –> progressive anterior pituitary failure
      • Metyrapone & ketoconazole - sometimes before/after surgery
      • 3rd - laparoscopic bilateral adrenalectomy in refractory (but require lifelong glucocorticoid/mineralocorticoid replacement + risk of Nelson’s syndrome (increased skin pigment from high ACTH

Hypoadrenalism

  • Causes:
    • AI: Addison’s disease (>70%)
    • Malig: mets (lung, breast. kidney)
    • Inf: TB (>10%), HIV (CMV adrenalitis), Fungal
    • Infiltration: granulomatous disease, hemochromatosis, amyloidosis
    • Iatrogenic: ketoconazole, rifampicin, phenytoin, bilateral adrenalectomy
    • Congenital: congenital adrenal hyperplasia (late-onset)
  • Presentation:
    • Anorexia/weight loss, fatigue/weakness, postural dizziness, reduced libido, sweating
    • N&V, diarrhoea, salt craving
    • Signs: hyperpigmentation in skin creases/lip/mouth, vitiligo, sparse axillary/pubic hair
  • Ix:
    • Bedside - postural hypotension, IGRA (TB inf)
    • Bloods - FBC, U&E (↑ K+, ↓ Na+), low glucose, serum Ca, AI/auto-ab screen, plasma renin & aldosterone, short snACTHen 250mcg IM test (not Addison’s if 30min cortisol rises >550nmol/L
    • Imaging: CXR (past TB), adrenal CT (for TB/mets)
  • Mx:
    • Addisonina crisis: Tx underlying cause, ICU input & alert bracelet
      • Ppt factors: inf, trauma, surgery, missed steroid doses
      • Ix: Cortisol, ACTH, U&E
      • Mx: IV hydrocortisone + IV fluids ± fludrocortisone (if primary adrenal lesion)
        • Monitor BM ± IV dextrose
        • Bloods, urine, sputum culture ± abx
    • Chronic: hydrocortisone + fludrocortisone (Na homeostasis), education (compliance, increase steroid dose if ppt factors, follow-up

Hyperaldosteronism (incl. Conn’s)

  • Primary (HTN, ↑ Na+ ↓ K+):
    • ​Conn’s - aldosterone-secreting adrenal adenoma
    • Bilateral adrenal hyperplasia
  • Secondary - decreased renal perfusion (high renin –> Na reabsorption –> HTN) - RAS, HF, liver failure
  • Ix: aldosterone-renin ratio (ARR), CT/MRI adrenals, adrenal vein sampling
    • Conn’s is very high (high aldosterone, low renin) VS BAH has both high (high aldosterone, high renin)
  • Mx: spironolactone, unilateral adrenalectomy (for Conn’s)

PHaeochromocytoma #HighCatecholamines

  • Cause: adrenal medulla tumour –>↑ catecholamines (adrenaline/NA)
  • Presentation: episodic headache, sweating, tachycardia, hypertension, arrhythmias, death if untreated
  • 10% exta-adrenal, 10% bilateral, 10% malignant
  • Ix: ECG (LVF, increased ST seg, VT), 24hr urinary metanephrines, abdo CT/MRI
  • Mx: specialist endo centre - alpha blockade = PHenoxybenzamine then beta-blockade –> then surgery when BP controlled (after 4-6wks)
33
Q

Mx of obesity?

A
  • Conservative measures
  • Medical (none proven to provide sustainable weight loss)
    • Orlistat (gut lipase inhibitor, SEs: profound flatus, diarrhoea)
  • Surgical – bariatric surgery (BMI >40 OR >35 w/ comorbidity assoc w/ obesity)
    • Needs extensive screening + commitment to long-term follow-up
34
Q

Hyperprolactinaemia - causes? presentation? Ix? Mx

A

Causes:

  • Prolactinoma (macroprolactinoma >6000)
  • Adenoma (non-funct pituitary adenoma 1000-5000, from compression & DA lvls)
  • DA antagonist (metoclopramide, anti-psychotics, methyldopa)
  • Hypothyroidism (increased TRH stimulates prolactin prod)
  • Physiological (pregnancy, breastfeeding)

Presentation: irreg periods, decreased libido, galactorrhoea

  • Bilateral hemianopia

Ix:

  • Bedside - pregnancy test, visual fields assessment
  • Bloods - serum prolactin, TFTs, U&E
  • Imaging - pituitary MRI

Mx:

  • Asymptomatic pre-menopausal/post-menopausal with microadenoma - observation
  • Symptomatic pre-menopausal/macroadenoma post-menopausal/male:
    • Dopamine agonist (Cabergoline/Bromocriptine), 2nd line - COCP (not if want pregnancy)
    • Trans-sphenoidal surgery (if visual Sx/pressure effects refractory to medical Tx)
    • Follow-up: monitor prolactin, check visual fields
35
Q

DDx for tiredness & lethargy? Ix?

A

DDx:

  • Anaemia - PUD, altered bowel habit? occult blood loss?
  • Thyroid disease - thyroiditis?
  • DM - polyuria, polydipsia, weight loss
  • Adrenal insufficiency
  • Primary hyperparathyroidism - constipation, urinary stones, abdo pain, depression
  • Hypopituitarism
  • Anxiety & depression - sleep disturbances, poor appetite, recent stress

Ix:

  • FBC, U&E, LFTs, CRP, bone profile, HbA1c, TFTs, haematinics
  • CXR
36
Q

DDx for weight loss?

A

DDx:

  • Thyrotoxicosis - heat intolerance, palpitations, SoB, mood (irritable/anxious), bowel habit, menses, goitre, exophthalmos, recent pregnancy
  • GI-related conditions (IBD, upper GI pathology, coeliac disease, chr pancreatitis) - dysphagia, vomiting, regurgitation, abdo pain, altered bowel habit
  • Eating disorders (Anorexia nervosa) - reduced eating, compulsive exercise
  • Systemic conditions (malignancy) - FLAWS

Ix:

  • FBC, U&E, CRP, LFTs, fasting BM, bone profile, TFTs, anti-TTG, IgA levels, haematinics
  • CXR
37
Q

What are the causes of goitre?

A

Diffuse: Graves’ disease, Hashimoto’s thyroiditis, De Quervain’s thyroiditis

Nodular: Multinodular goitre, adenoma, carcinoma

38
Q

Addison’s + T1DM - Dx?

A

Schmidt’s syndrome

39
Q

What is subclinical hypothyroidism?

A

High TSH but normal T4

Common in treated hyperT4/elderly

40
Q

Causes of secondary HTN? Stages? Ix?

A

Secondary HTN:

  • Renal - CKD, RAS
  • Endo - Conn’s, Phaeo, Cushing’s (thin skin, proximal myopathy, obesity), Primary hyperparathyroidism, acromegaly
  • Drugs - CS, OCP

Stages:

  • 1 - 140/90
  • 2 - 160/100
  • 3 - 180/120
  • Accelerated - 180/120 + retinal haemorrhages ± papilloedema

Ix:

  • Bedside: urine dip, PCR, ECG, fundoscopy, QRISK score
  • Bloods: FBC, U&E, BM, HBA1c, lipids, if young - renin-aldosterone ratio, plasma free metanephrines (phaeo)
  • Imaging: CXR (LVH, pul oedema), USS KUB, renal MR angiography (RAS)
41
Q

Causes of hypokalaemia?

A

GI - diarrhoea, laxatives

Endo - Conn’s, Cushing’s syndrome, Refeeding syndrome

Drugs - thiazides, loop diuretics, insulin, PPI, steroids, gentamicin

42
Q

Correcting hyperglycaemia in DM:

  • How much does 1 unit of rapid-acting insulin reduce BM by?
  • How much to adjust insulin dose by at one time?
  • Target insulin dose?
A

ASK PATIENT - rule of thumb is 100/total daily dose (TDD)

  • E.g. TDS Actrapid 7 units + 18U lantus = 39U TDD –> 100/39 = 2.5
  • Generally it is roughly 3mmol/L

10%

Target glucose: 4-10 (aim for 7-8)

43
Q

DPP-4 e.g. linagliptin - massive benefit in T2DM?

A

Approved for use in CKD

44
Q

Why use GLP-1 analogue e.g. exenatide/liraglutide for T2DM? Other SE? How is it given?

A

Induces weight loss (good for BMI >35, >30 + comorb)

Vomiting

SC inj

45
Q

Diabetic Ketoacidosis (DKA)

  • Normal glucose transport & during starvation?
  • The problem in insulin deficiency (diabetes)? How does this relate to Sx of DKA?
  • Ix? Dx criteria? Mx? Monitoring Tx & hourly targets?
A

Normal glucose transport: diet –> blood –insulin–> hepatic glucose store –GH, Cortisol, Adrenaline, Glucagon–> blood

  • During starvating - GH, Cortisol, Adrenaline, Glucagon make sure there is enough glucose in the blood BUT liver also produces ketones
  • Ketones can cross BBB providing an alternative source of fuel for the brain when low glucose
  • Pancreatic beta cells –> insulin prod –> reduces glucose (high glucose has–> feedback on pancreatic beta cells –> produce more insulin)
  • High insulin (associated with high glucose) –> -ve feedback on ketone prod

In insulin deficiency - high glucose but unable to produce insulin + no -ve feedback on ketone prod –> high glucose, high ketones

  • High glucose - osmotically active (moves along concentration gradient into urine –> pulling more water with it) –> POLYURIA –> DEHYDRATION
  • High ketones - acidic (metabolic acidosis) –> enzyme dysfunction –> COMA & DEATH

DKA Ix:

  • Bedside - urine dip, ECG, continuous cardiac monitoring
  • Bloods - VBG, FBC, U&E, BC, BM
  • Imaging - possibly CXR

DKA Dx:

  • BM: ≥11mmol/L
  • Ketones: ≥3mmol/L (serum) OR ≥2+ (urine)
  • Acidaemia: pH <7.3 OR Bicarb <15mmol (ketoacidosis)

DKA Mx: A-E assessment

  • IV FLUIDS (rehydrate)
    • ​Bolus –> 1L over 1hr –> 2hr –> 3hr –> 4hr
    • Add 40mmol KCL to fluids after bolus
  • 0.1 U/kg/hr fixed-rate INSULIN infusion (reduce ketones)
    • If BM <14 –> start 125ml/hr 10% dextrose
    • Insulin infusion continues until ketones normalise (not BM) ​
  • NOTE: follow local trust guidelines for DKA Tx as varies slightly between trusts

Monitor - BM, ketones, VBG (K conc)

  • Hourly targets:
    • Fall in BM ≥3
    • Fall in ketones ≥0.5
    • Rise in HCO3 ≥3
  • Continue until: blood ketones <0.6, pH >7.3, HCO3 >18
49
Q

Young patient, being Tx for DKA with reduced GCS, severe acidosis, relative bradycardia - what is going on?

A

Cerebral oedema

50
Q

Case:

  • A 52yrs male presents with hypercalcaemia (bones, stones, moans, thrones, overtones)
  • Bloods - corrected Ca high, PO4 low, ALP high, PTH normal

Dx?

A

Dx: primary hyperparathyroidism

  • In normal parathyroid with working -ve feedback –> PTH low due to high Ca (so here must be abnormal)
  • In tertiary - PTH very high, commonly in end-stage CKD on dialysis
51
Q

What do I need to check with Ca level?

A

Albumin to obtain the corrected Ca level as Ca in serum is bound to albumin so if hypo/hyperalbuminaemia then total Ca conc may not reflect free ionised Ca

52
Q

Osteomalacia vs osteoporosis - Ca, PO4, ALP, PTH?

A

Osteoporosis - everything normal as this is a problem of bone density

Osteomalacia - caused by vit D deficiency so low/normal Ca, high PTH, low/normal PTH –> soft bones

Final Year - ICSM (20 decks)

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