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Endocrine Flashcards

1
Q

What are the symptoms of hypothyroidism?

A
  • Constipation
  • Menorrhagia
  • Weight gain + loss of appetite
  • Lethargy + weakness
  • Cold intolerance
  • Infertility
  • Loss of libido
  • Poor memory/ cognition
  • Low mood
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2
Q

What are the signs of hypothyroidism?

A
  • Bradycardia
  • Delayed tendon reflex relaxation
  • Jaundice
  • Pitting oedema + ascites
  • Cold hands
  • Peripheral neuropathy
  • Myxoedema- puffy hands/ feet/ face
  • Pleural effusion
  • Overweight
  • Carpal tunnel
  • Goitre
  • Cerebellar ataxia
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3
Q

Causes of hypothyroidism

A
  • Primary (Low T3/4, High TSH)
    • Primary atrophic hypothyroidism (no goitre)
    • Hashimoto’s (goitre)
    • Iodine deficiency
    • Post-thyroidectomy/ radioactive iodine
    • Drug induced- antithyroid, amiodarone, lithium, iodine
  • Secondary (Low T3/4 and TSH) = hypothalamus/ pituitary dysfunction.
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4
Q

Ix and Tx of hypothyroidism

A
  • Ix- TFTs, autoantibodies, cholesterol/ triglycerides
  • Tx= levothyroxine. Start low (50 micrograms OD) and titrate up monthly. Once stable –> yearly bloods.
  • Elderly/ cardiac disease start 25 micrograms.
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5
Q

Presentation of myxoedema coma

A
  • Usually >65y
  • Hypothermia
  • Cyanosis
  • Hyporeflexia
  • Hypoglycaemia
  • Bradycardia
  • Coma/ seizures
  • Preceding psychosis (myxoedema madness)
  • Signs/ Sx of hypothyroid eg goitre. Prev radiodine/ thyroidectomy
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6
Q

Ix and Tx of myxoedema coma

A
  • Ix- ECG, TFTs, FBC, U+Es, cultures, cortisol, glucose, ABG. ??Cause
  • Tx: In ITU
    • ABCDE +/- O2 + cautious IVT
    • Warming blanket
    • Correct hypoglycaemia
    • T3 (liothyronine) IV 2-3d –> Levothyroxine PO
    • Hydrocortisone if ?pituitary
    • ABx if ?infection
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7
Q

Symptoms of hyperthyroid

A
  • Weight loss + increased appetite
  • Diarrhoea/ fatty stools
  • Sweats
  • Heat intolerance
  • Loss of libido
  • Oligomenorrhoea
  • Irritability
  • Tremor
  • Palpitations
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8
Q

Signs of hyperthyroid

A
  • Proximal myopathy
  • Osteoporosis
  • Fine tremor
  • Palmar erythema
  • Goitre
  • Thin
  • Exophthalmos/ ophthalmoplegia/ lid lag / lid retraction
  • Moist skin
  • Tachycardia
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9
Q

Causes of hyperthyroidism

A
  • Graves’ disease= AI. Thyroid enlargement and increased thyroid hormone production
  • Toxic multinodular goitre- Nodules secreting more thyroid hormone
  • Toxic adenoma- Solitary nodule secreting T3/T4. Hot on isotope uptake
  • Ectopic thyroid tissue eg metastatic thyroid cancer
  • Exogenous- iodine excess, levothyroxine, amiodarone, lithium
  • Thyroiditis- Destruction –> release hormones
    • de Quervain’s- self-limiting post-viral goitre. High temp/ESR. Decreased isotope uptake.
  • Post-partum
  • TB
  • Secondary- pituitary/ hypothalamus. RARE.
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10
Q

Hyperthyroid investigations

A
  • Bedside- ECG
  • Bloods- TFTs, FBC, ESR, calcium, LFTs, thyroid autoantibodies
  • Imaging- USS, isotope uptake scan
  • ? Eye testing
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11
Q

Treatment of hyperthyroid

A
  • Medical:
    • Beta blockers (rapid)
    • Titration- carbimazole titrated to TFTs
    • Block and replace- carbimazole + thyroxine
    • Graves’ Tx for 12-18 months –> stop. 1/2 relapse.
  • Radioiodine
  • Thyroidectomy (risk: recurrent laryngeal n.)
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12
Q

Presentation of thyroid storm

A
  • Signs/ Sx of hyperthyroid
  • Hyperthermia
  • Agitation
  • Confusion
  • Coma
  • Tachycardia
  • AF
  • D+V
  • Goitre
  • Thyroid bruit
  • HF
  • Acute abdo
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13
Q

Ix and Tx of thyroid storm

A
  • Ix- TFTs, culture, isotope uptake. Don’t delay Tx
  • Tx:
    • ABCDE + IVT
    • ?Sedate- chlorpromazine
    • Propranolol (diltiazem if asthma/HF)
    • ?Digoxin to slow heart
    • Antithyroid drugs- carbimazole (reduce after 5d) –> Lugol’s solution (iodine) for 7-10d.
    • Hydrocotisone/ dexamethaone
    • ?ABx
    • Cool fluid, paracetamol
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14
Q

Features and treatment of mild/ subclinical hypothyroid

A
  • Raised TSH, normal T3/T4, no obvious Sx
  • Recheck TFTs 2-4 months later to check persistence.
  • Tx if TSH >10/ autoantibodies/ past Tx Graves’/ other AI
  • TSH 4-10 –> trial Tx 6 months and stop if Sx don’t improve
  • No Tx –> monitor yearly TFTs
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15
Q

Features and Tx of mild/ subclinical hyperthyroid

A
  • Low TSH, normal T3/T4
  • Recheck TFTs 2-4months. Check for non-thyroid cause eg pregnancy, illness
  • TSH <0.1 Tx if Sx of hyperthyroid/ AF/ unexplained weight loss/ osteoporosis/ goitre
  • Tx- carbimazole, propylthiouracil
  • No Sx –> recheck 6 monthly
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16
Q

Signs of Graves’ Disease

A
  • Eyes- ophthalmoplegia, exophthalmos
  • Pre-tibial myxoedema
  • Thyroid acropachy (clubbing)
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17
Q

Goitre differentials

A
  • Diffuse
    • Iodine deficiency
    • Physiological- puberty, pregnancy
    • Congenital
    • AI- Graves’, Hashimoto’s
  • Nodular
    • Multinodular goitre
    • Cyst
    • Adenoma (hot)
    • Malignancy (cold)
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18
Q

Types of thyroid cancer + Tx

A
  • Papillary (60%). Younger. Tx- total thyroidectomy+ node excision + radioactive iodine + thyroxine
  • Follicular (25%). Older. Tx as above.
  • Medullary- MEN. Calcitonin. Thyroidectomy
  • Lymphoma- stridor/ dysphagia. chemo/ radio
  • Anaplastic- elderly. Poor response to Tx.
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19
Q

Hyperglycaemic symptoms

A
  • Polydipsia
  • Polyuria
  • Ketotic breath (pear drops)
  • Sweet smelling urine
  • Fatigue
  • Weight loss
  • Susceptible to infection eg thrush
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20
Q

What makes the Dx more likely to be T1DM and not T2DM?

A
  • T1DM= absolute insulin deficiency –> insulin
  • Young
  • Thin
  • Usually no FHx
  • Complications not usually present at Dx
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21
Q

What makes the Dx more likely to be T2DM and not T1DM?

A
  • Relative insulin deficiency
  • Gradual onset. Usually adults.
  • Obese.
  • Usually 1st degree relative.
  • Complications often present at Dx
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22
Q

Features of MODY

A
  • Genetic –> strong FHx
  • Present young but don’t always need insulin
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23
Q

Features of LADA

A
  • T1DM in adulthood.
  • Slower onset.
  • Rapid progression to insulin
  • May present with DKA
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24
Q

Secondary causes of DM

A
  • Pregnancy (GDM)
  • Cushing’s
  • Acromegaly
  • Pancreatitis
  • Hyperthyroid
  • Haemachromatosis
  • Steroids
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25
Q

What is metabolic syndrome?

A
  • Cluster of conditions:
    • Central obesity
    • BP >130/85
    • Fasting BM >5.6 mmol/L
    • High triglycerides and HDL
  • Increased risk of: DM, heart diease, stroke, gallstones, cancer.
  • Tx= usually diet and exercise.
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26
Q

WHO diagnostic criteria for DM

A
  • Sx of hyperglycaemia and 1x elevated venous blood glucose:
    • Fasting >7mmol/L
    • Random >11.1mmol/L
  • 2x elevated venous blood glucose (or OGTT 2h >11.1 mmol/L)
  • HbA1c >48 mmol/L (only T2DM)
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27
Q

Complications of DM

A
  • Macrovascular:
    • Heart- MI, angina, CHF, HTN
    • Brain- CVA, TIA, cognitive impairment
    • PDV- Ulcers, gangrene, claudication, amputation
  • Microvascular:
    • Kidney- nephropathy (frothy urine)
    • Eye- retinopathy, maculopathy, cataracts, glaucoma
    • Neuropathy
    • Erectile dysfunction
    • Ischaemic foot
  • Emergencies- Hypo, DKA, HHS
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28
Q

Causes of hypoglycaemia

A

EXPLAIN

  • EXogenous- insulin, gliclazide, alcohol, aspirin, ACEi, beta blockers
  • Pituitary insuffiency
  • Liver failure
  • AKI/ Addison’s
  • Islet cell tumours (insulinoma) + Immune Hypo
  • Neoplasm (non-pancreatic)
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29
Q

Presentation of hypoglycaemia

A
  • ‘Drunk’
  • ANS- sweating, palpitations, hunger, dizziness
  • Neuroglycopoenic- Coma, confusion, drowsiness, difficulty speaking, seizure, incoordination, visual disturbance
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30
Q

Emergency treatment of hypoglycaemia

A
  • ABCDE
  • Correct glucose
    • Can swallow- 10-20g glucose PO eg juice, biscuits, glucogel
    • Cannot swallow- 1mg glucagon IM/SC OR 100ml 10% glucose/ 50ml 20% glucose over 20mins
    • Repeat until glucose over 4mmol/L
  • Long acting carbs eg toast
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31
Q

Presentation of DKA

A
  • Drowsy/coma
  • Dehydration/ shock
  • Kussamul breathing (deep and laboured)
  • Ketotic breath
  • Abdo pain
  • Vomiting
  • Weakness
  • Hyperglycaemic Sx
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32
Q

Diagnosis of DKA

A
  • BM, urine, ABG
  • Glucose >15mmol/L
  • Raised urine/ blood ketones
  • pH <7.3
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33
Q

Management of DKA

A
  • ABCDE
  • IVT- 6L in 1st 24h. IL stat –> 1hour –> 2h –> 4h –> 8h
  • Sliding scale insulin actrapid- 0.1 units/kg/hour. Stop reg. short acting.
  • Hunt for trigger
  • K+ replacement after 1st bag (40mmol/L)
  • Monitor: BM, K+, VBG (pH, bicarb, glucose, K+)
  • BM <14 –> Add 10% glucose 125ml/h
  • Stop insulin when ketones <0.3, pH >7.3, bicarb >18mmol/L. Rapid acting –> stop 30mins later
  • LMWH
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34
Q

Presentation of HHS

A
  • Subacute- around 1w
  • Nausea
  • Dry skin
  • Profound dehydration
  • Reduced consciousness + confusion
  • Polyuria
  • Polydipsia
  • Lethargy
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35
Q

HHS Dx

A
  • Glucose >35mmol/L
  • Osmolality >340mosmol/kg
  • No acidosis
36
Q

HHS management

A
  • Slow IVT over 28h
  • Replace K+ when passed urine
  • Aim glucose to fall 5mmol/L/h –> if not, add 0.05units/kg/h insulin
  • LMWH
37
Q

Key features of diabetic retinopathy

A
  • Background- Microaneurysms, hard exudates, blot haemorrhages
  • Pre-proliferative- Blot haemorrhages, venous bleeding, cotton wool spots
  • Proliferative- new vessel formation. Risk of haemorrhage!
38
Q

Presentation of diabetic nephropathy

A
  • Most Asx
  • Proteinuria
  • Measure annually- urine dip, serum creatinine, eGFR
39
Q

Annual r/v of DM

A
  • HbA1c
  • Injection sites
  • Albumin:creatinine ratio
  • Fundoscopy
  • Check feet
  • LIpid profile
  • U+Es, urine dip
  • BP
  • BMI
  • Education
40
Q

Management of T1DM

A
  • Lifestyle- good diet, carb counting, courses
  • CVS risk control- statin, aspirin, ACEi
  • Insulin
    • Rapid acting eg novorapid
    • Short acting eg actrapid
    • Intermediate eg isophane
    • Long acting eg glargine
    • Mixed eg novomix
    • Regimes eg basal-bolus
  • Changes in insuline dose- increase by 10%, decrease by 20%
41
Q

Management of T2DM

A
  • Lifestyle
  • Manage glucose:
    • Metformin (gliclazide if thin/ poor renal function)
    • Metformin + gliclazide (or gliptin/ pioglitazone)
    • Metformin + gliclazide + gliptin/pioglitazone
    • Insulin
  • Manage BP- ACEi
  • Manage lipids + CVS risk- Statins, aspirin
  • ID + manage complications
42
Q

What is Cushing’s syndrome and how might it present?

A
  • ++ Cortisol. Loss of -ve feedback.
  • Presentation:
    • Buffalo hump
    • Moon face
    • Central obesity
    • Proximal muscle wasting
    • Plethora, bruising, striae
    • Osteoporosis
    • Skin/ muscle atrophy
    • Gynaecomastia
    • Mood change
43
Q

Causes of Cushing’s Syndrome

A
  • ACTH Dependent (raised):
    • Cushing’s disease- piuitary adenoma.
    • Ectopic ACTH eg SCLC. Sx- hyperpigmentation, weight loss, hyperglycaemia, hypokalaemia, metabolic alkalosis
    • Ectopic CRF production (thyroid/ prostate Ca)
  • ACTH Independent (Low):
    • Adrenal adenoma
    • Adrenal nodular hyperplasia
    • Iatrogenic **steroids**
44
Q

Ix of Cushing’s syndrome

A
  • Confirm cushing’s- raised serum cortisol
  • Low dose dexamethasone- Cushing’s = no suppression of cortisol.
  • 48h cortisol suppression test:
    • Cushing’s disease suppresses with 8mg –> pituitary MRI
    • Ectopic ACTH/ adrenal adenoma not suppressed.
  • Plasma ACTH
    • Undetected= adrenal tumour –> CT
    • Detectable = cushing’s disease/ ectopic ACTH. Do 48h suppression.
45
Q

What is Addison’s Disease and what might cause it?

A
  • Addison’s= destruction of adrenal cortex –> reduced cortisol and aldosterone
  • Primary= Addison’s disease. Destruction of adrenals –> no production of mineralo/glucocorticoids
  • Secondary= Common. Iatrogenic due to long term steroids. Present in crisis after removal of steroids
  • Causes: AI, TB, adrenal mets, opportunistic infection, adrenal haemorrhage, late onset congenital
46
Q

Presentation of Addison’s Disease

A
  • Mood change
  • Tired + tearful
  • Weight loss/ anorexia
  • Tanned
  • Myalgia/ arthralgia/ weakness
  • Hypogonadal
  • Changed distribution of body hair
  • GI disturbance- abdo pain, vomiting
47
Q

Addison’s Disease Ix

A
  • Bedside- BM (low)
  • Bloods- anaemia, hyponatraemia, hyperkalaemia, hypercalcaemia, uraemia, eosinophilia, autoantibodies, plasma renin-aldosterone
  • Imaging- AXR/CXR ?TB ?acute abdo
  • Special- short synacthen test:
    • Plasma cortisol before and 30mins after 250 micrograms tetracosactide
    • Addison’s exclused if 30 min cortisol >550 nmol/L
48
Q

Management of Addison’s Disease

A
  • Replace steroids!
    • 15-25mg hydrocortisone (+5-10 before exercise)
    • 50-200 micrograms fludrocortisone
    • Double steroids in febrile illness/ injury/ stress
  • Don’t stop abruptly!
  • Give steroid card
  • Follow up annually. BP, U+Es, look for AI disease
49
Q

Causes and presentation of Addisonian Crisis

A
  • Causes- infection/ trauma/ dehydration/ shock in someone with Addison’s. Missed steroid in someone on long term.
  • Presentation:
    • Intense fatigue/ weekness
    • Nausea ++
    • Confusion, headache, dizziness
    • Low GCS/ coma
    • Hypotension
    • Hypoglycaemia
    • ?Hyperkalaemia + hyponatraemia
50
Q

Ix and Tx of Addisonian Crisis

A
  • Don’t delay Tx if suspect!
  • Ix: Bloods- cortisol, ACTH, U+Es, glucose, cultures
  • Tx:
    • ABCDE + IVT resus
    • HYDROCORTISONE 100MG IV STAT –> PO after 72h
    • ?Fludrocortisone if adrenal disease
    • ?Glucose
    • Tx the cause
51
Q

What is hyperaldosteronism, what causes it and how might it present?

A
  • = excess aldosterone production –> Na+ and water retention
  • Causes: Adrenal adenoma (conn’s), adrenal hyperplasia.
  • Presentation:
    • Thirst ++
    • Polyuria
    • Weakness
    • Muscle spasms
    • Headaches
    • Hypertenison (in young, refractory)
52
Q

Ix and Tx of primary hyperaldosteronism

A
  • Ix-
    • U+Es (hypokalaemia, hypernatraemia)
    • ABG (metabolic alkalosis)
    • Plasma renin:aldosterone (high ald, low renin)
  • Tx:
    • Spironolactone 200-300mg/24h PO
    • ?Surgical resection of adenoma
53
Q

What causes secondary hyperaldosteronism?

A
  • Renal hypoperfusion
  • Eg diuretics, HF, liver failure, renal artery stenosis
  • Presents similarly, renin:aldosterone not high
  • Tx- spironolcatone, ACEi
54
Q

What is a phaeochromocytoma and what causes it?

A
  • = Excess catecholamine (noradrenaline) release from the adrenal medulla.
  • Caues= usually adrenal tumour. Rarely paraganglioma.
55
Q

Presentation of phaeochromocytoma

A
  • Triad: Epidodic headache, tachycardia, sweating.
  • Other Sx:
    • Episodic hypertension
    • Anxiety
    • Facial flushing
    • Chest tightness
    • SOB
    • Tremor
    • Palpitations
    • Abdo pain + vomiting
56
Q

Ix and Tx of Phaeochromocytoma

A
  • Ix
    • Bedside- 24h urine collection for creatinine, catecholamines, metanephrines.
    • Bloods- serum metanephrines
    • Imaging- CT abdo
    • Special- Genetic testing
    • Lifelong malignancy screening.
  • Tx:
    • Alpha blockers (phenoxybenzamine) –> beta blockers (propranalol)
    • Surgical resection of tumour
57
Q

What is acromegaly and how might it present?

A
  • = Excess growth hormone secretion from pituitary tumour/ hyperplasia
  • Large hands/ feet
  • Coarse facial features
  • Jaw protrusion
  • Headaches +/- bitemporal hemianopia
  • Macroglossia
  • Hyperglycaemia
  • Hypertenison
  • Sweating
58
Q

Ix and Tx of acromegaly

A
  • Ix
    • Bedside- ECG, BM, visual fields, BMI
    • Bloods- IGF-1, glucose, calcium, phosphate
    • Imaging- MRI pituitary
    • Special- OGTT
  • Tx
    1. Pituitary tumour resection
    2. Octreotide
    3. Pegvisomant
59
Q

Complications of acromegaly

A
  • DM
  • Vascular- HTN, LVH, cardiomyopathy, arrhythmias, CVA, IHD
  • Neoplasia- colon
60
Q

What hormones are produced by the pituitary?

A
  • Ant. Pituitary
    • TSH
    • ACTH
    • GH
    • Prolactin
    • LH
    • FSH
  • Post. Pituitary
    • ADH
    • Oxytocin
61
Q

Causes of Hypopituitarism

A
  • Hypothalamus- Kallman’s, tumour, inflammation, infection, ischaemia
  • Pituitary stalk- Trauma, surgery, mass lesion, meningioma, carotid arty aneurysm
  • Pituitary- Tumour, irradiation, inflammation, AI, infiltration (mets, haemachromatosis), ischaemia (apoplexy, Sheehan’s, DIC)
62
Q

What is Pituitary apoplexy, how might it present and how should it be treated?

A
  • = Rapid pituitary bleed and enlargement.
  • Sx- acut headache, meningism, low GCS, ophthalmoplegia, visual field defect
  • Tx= urgent hydrocortisone 100mg IV
63
Q

What is Kallman’s syndrome?

A
  • Loss of GRH
  • Colour blindness
  • Anosmia
  • Hypopituitarism
64
Q

Presentation, Ix and Tx of Hypopituitarism

A
  • Presentation depends on hormone- GH, FSH/LH, hypothyroidism, adrenal insufficiency, prolactin
  • Ix:
    • Bloods- LH, FSH, LSH, testosterone, oestradiol, cortisol, IGF-1, U+Es
    • Short synacthen
    • Imaging- MRI
  • Tx- Hydrocortisone, replace other hormones
65
Q

What is Diabetes Insipidus, what causes it, and how might it present?

A
  • = Failure to concentrate urine due to lack of ADH (neurogenic) or lack of renal respone (nephrogenic).
  • Causes:
    • Neurogenic- Idiopathic, traum, tumour/ mets, infection, haemorrhage
    • Nephrogenic- Lithium, CRF, post-obstructive uropathy
  • Presentation- Polydipsia ++, polyuria, diluted urine, dehydration
66
Q

Ix and Tx of Diabetes Insipidus

A
  • Ix:
    • Bedside- urine osmolality
    • Bloods- U+Es, calcium, glucose, serum osmolality
    • Water deprivation test- don’t drink water, monitor weight, fluid balance, urine+plasma osmolality over 8 hours
    • –> DI = failure to concentrate urine (<600mOsmol/Kg).
    • –> Give desmopressin –> concentrated in neurogenic not nephrogenic
  • Tx: Tx cause!
    • Neurogenic- desmopressin
    • Nephrogenic- bendroflumethiazide, NSAID
67
Q

Causes and presentation of hypokalaemia

A
  • Hypokalaemia= <3.5mmol/L
  • Intake- diet, IVT (need 1mmol/kg/hr)
  • Excretion- D+V, sweating, diuretics, Cushing’s Conn’s, renal (eg gittleman’s)
  • Intracellular shift- Alkalosis, insulin, salbutamol
  • Presentation- weakness, cramps, nausea, palpitations
68
Q

Ix and Tx of hypokalaemia

A
  • Ix:
    • ECG- flatted T waves, arrhythmias
    • U+Es (inc Mg)
    • ABG- ?alkalosis
  • Tx: (emergency = <2.5mmol/L)
    1. ABCDE
    2. Continuous ECG
    3. Access and bloods
    4. Replace 40mmol/L KCl in 1L 0.9 NaCl
    5. ABG
    6. Senior r/v
    • Non-emergency- Sando K, Mg replacement, 20-40mmol/L KCl
69
Q

Causes and presentation of hyperkalaemia

A
  • Hyperkalaemia= K+ >5.3 mmol/L
  • Intake- IVT
  • Excreation- Renal failure, Addison’s, spironolactone, amiloride, ACEi
  • Extracellular shift- Metabolic acidosis, non-selective Beta blockers, low insulin, tissue necrosis
  • Presentation- Palpitations, chest pain, dizziness
70
Q

Ix and Tx of Hyperkalaemia

A
  • Ix:
    • ECG- tall tented t waves –> broad QRS –> VF
    • U+Es
    • ABG- acidosis
  • Tx: Emergency= >7mmol/L
    1. ABCDE + ECG
    2. Access and bloods- U+Es
    3. 10mL 10% calcium gluconate over 2 mins
    4. 10 units actrapid in 50mL 50% glucose over 10 mins
    5. 5mg salbutamol NEBS
    6. ABG
    7. Senior r/v
    • Non-emergency- furosemide, ?dialysis. Stop nephrotoxic drugs
71
Q

Presentation of hyponatraemia

A
  • Anorexia
  • Nausea
  • Malaise
  • Headache
  • Irritability
  • Confusion
  • Weakness
  • Low GCS (cerebral oedema)
  • Seisures
  • ?HF/ Oedema
72
Q

Causes of hyponatraemia

A
  • Hypovolaemic:
    • Urine Na+ >20mmol/L = renal loss. Addison’s, diuretics, salt losing nephropathy
    • Urine Na+ <20mmol/L= non-renal loss. D+V, burns, SBO, heat
  • Hypervolaemia- nephrotic syndrome, HF< liver cirrhosis, renal failure
  • Euvolaemia:
    • Urine osmolality >100mmol/kg= Water overload, hypothyroid
    • <100mmol/kg = SIADH
73
Q

What is SIADH and how is it diagnosed?

A
  • Syndrome of Inappropriate ADH secretion from hypothalamus –> hyponatraemia
  • Diagnosis
    • Urine concentrated (osmolality >500mOsmol/kg), dilute plasma (<275mOsmol/kg)
    • No recent diuretics
    • Euvolaemic
    • Urine sodium >20mmol/L
    • Normal adrenal and thyroid function.
74
Q

Causes of SIADH

A
  • Malignancy- lung, pancreas, lymphoma
  • Lung/ CNS infection
  • Vascular events
  • Drugs- SSRIs, TCAs, carbamazepine, antipsychotics
  • Idiopathic
75
Q

Treatment of hyponatraemia

A
  • Correct fluid and Na+ at same rate lost (ie usually slowly)
  • Na+ rise no more than 10mmol/l/24h (risk of osmotic demyelination)
  • Acute- seizures/ coma or Na+ <120mmol/l –> rapid replacement with hypertonic saline 5mmol/L
  • Chronic Asx- fluid restriction +/- domecloclyline
  • Stop diuretics + NSAIDs
  • Hypovolaemia- replace lost fluid with 0.9% NaCl
76
Q

Causes and presentation of hypernatraemia

A
  • Causes:
    • Fluid loss- D+V, burns, DI, DM, Conn’s
    • ++ Na+- IVT, Conn’s
  • Presentation:
    • Thirst
    • Weakness/ lethargy
    • Irritability
    • Confusion
    • Seizures/ Coma
    • Signs of dehydration
77
Q

Ix and Tx of Hypernatraemia

A
  • Ix:
    • Urine osmolality (>400mOmol/kg = fluid loss)
    • Plasma osmolality
    • ?CT/ MRI if ?central cause
  • Tx:
    • Slow correction
    • Hypovolaemia- 0.9% NaCl 1L/6h
    • Normovolaemic- PO fluids/ 5% glucose 1L/6h
78
Q

Presentation of hypercalcaemia

A
  • Stones - renal stones
  • Bones - pain, osteoporosis, osteopoenia, arthritis
  • Groans - abdo pain, D+V, constipation, weight loss
  • Psychiatric Moans - depression, confusion
  • Thrones - polyuria + polydipsia
  • Signs- dehydration, arrhythmias, cachexia, HTN
79
Q

Causes of hypercalcaemia

A
  • Hyperparathyroidism- Primary (adenoma), tertiary (prolonged secondary and hyperplasia)
  • Malignancy- Boney mets, myeloma, AML, ALL, ectopic PTH-related peptide (SCLC, endometrial, breast, ovarian, renal)
80
Q

Ix and Tx of hypercalcaemia

A
  • Bedside- ECG, urine electrophoresis
  • Bloods- FBC, U+Es, Mg2+, Ca2+, PO43-, ALP, PTH, ESR, serum electrophoresis
    • Hyperparathyroidism- High calcium + PTH
    • Multiple myeloma- High calcium, high serum albumin
    • ALL- High calcium and phosphate
    • AML- variable calcium levels
    • Ectop PTH-r peptide- High calcium, low phosphate, variable albumin
  • Imaging- CXR, bone scan
  • Tx- IVT, bisphosphonates eg Zolendronic acid
81
Q

Presentation of Hypocalcaemia

A

SPASMODIC

  • Spasms
  • Perioral tingling
  • Anxious/ depressed
  • Seizures
  • Muscle tone (tetany + hyperreflexia)
  • Orientation impaired (confusion)
  • Dermatitis
  • Impetigo herpetiformis
  • Chvostek’s + cardiomyopathy
  • Others: arrhythmias, bradycardia/hypotension
82
Q

What are Trousseau’s and Chvostek’s signs and what do they indicate?

A
  • Trousseau’s= spasm of hand when inflating BP cuff
  • Chvostek’s= Unilateral twitching of face from tapping facial nerve
  • = Hypocalcaemia
83
Q

What are the causes of hypocalcaemia?

A
  • Vitamin D deficiency:
    • Malabsorption- Coeliac, CF, short bowel
    • Lack of sunlight
    • Renal disease
  • Hyperventilation
  • Hypomagnesia:
    • Drug induced- PPI, loop + thiazide diuretics, alcohol
    • Malabsorption- laxative abuse, crohn’s, UC, coeliac, short gut
  • Hypoparathyroidism- Post-surgical, Di-George
84
Q

Ix and Tx of hypocalcaemia

A
  • Ix:
    • Bedside- ECG (arrhythmias)
    • Bloods- U+Es, calcium, phosphate, magnesium, albumin, ALP, PTH, Vit D
  • Tx:
    • Hypoparathyroid- Acute= IV calcium gluconate. Chronic- PO calcium + calcitrol (vit D)
    • Hypomagnesia- Acute= IV magnesium sulphate replacement +/- IV calcium gluconate . Chronic- PO magnesium oxide
85
Q

Causes, Sx and Tx of Hypophosphataemia + Hyperphosphataemia

A

Hypo

  • Causes- Vit D def, alcohol withdrawal, refeeding syndrome, starvation, hyperparathyroidism, DKA
  • Sx: Muscle weakness, rhabdomyolysis, cardiac arrest, arrhythmias
  • Tx: PO/IV phosphase supplement

Hyper causes- CKD Tx with phosphate binders, tumour lysis

86
Q

Caues, Sx and Tx of hypomagnesaemia/ hypermagnesaemia

A

Hypo

  • Causes- diuretics, diarrhoea, ketoacidosis, alcohol, parenteral nutrition
  • Sx- Paraesthesia, seizures, tetany, arrhythmias
  • Tx= magnesium salts

Hyper

  • Renal failure, excessive antacids.
  • Sx- low bp/ hr, hyporeflexia, CNS/resp depression, coma
  • Tx only severe >7.5

Finals!!! (19 decks)

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