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Endocrinology Flashcards

1
Q

Differentials for gynaecomastia

A
  • Normal in puberty
  • Syndromes with androgen deficiency = Kallman’s, Klinefelter’s
  • Testicular failure = mumps
  • Liver disease
  • Testicular cancer
  • Ectopic tumour secretion
  • Hyperthyroidism
  • Medications
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2
Q

Medications causing gynaecomastia

A

o Spironolactone
o Cimetidine
o Digoxin
o Cannabis
o Finasteride
o GnRH agonists: goserelin, buserelin
o Oestrogens, anabolic steroids

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3
Q

Causes of hypokalaemia with hypertension

A
  • Cushing’s
  • Conns
  • Liddle’s syndrome
  • 11-beta hydroxylase deficiency
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4
Q

Causes of hypokalaemia WITHOUT hypertension

A
  • Diuretics
  • GI loss
  • Renal tubular acidosis
  • Bartter’s syndrome
  • Gitelman syndrome
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5
Q

What is acromegaly?

A

Increase secretion of growth hormone from pituitary tumour

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6
Q

Causes of acromegaly

A
  • MEN-1 (multiple endocrine neoplasia-1)
  • Pituitary adenoma
  • Hyperplasia (rare)
  • Secondary to cancer (lung, pancreatic) = secretes ectopic GHRH/GH
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7
Q

Presentation of acromegaly

A
  • Headaches (very common)
  • Increased size of hands and feet
  • Increase weight
  • Excessive sweating
  • Visual deterioration
  • Fatigue
  • Deep voice
  • Decreased libido
  • Arthralgia and backache
  • Acroparaesthesia = pain, tingling and numbness of extremities
  • Maxillofacial changes
  • Hypogonadal symptoms = Amenorrhea
  • Bitemporal hemianopia
  • Skin darkening
  • Coarsening face with large tongue, nose, protruding jaw
  • Prognathism
  • Big supraorbital ridge
  • Interdental separation
  • Goitre
  • Curly hair
  • Oily large pored skin
  • Scalp folds
  • Carpal tunnel syndrome (50%)
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8
Q

1st line investigation for acromegaly

A

Insulin-like Growth factor 1 raised

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9
Q

Gold standard investigation for acromegaly

A

Oral glucose tolerance test = high glucose normally suppressed by GH

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10
Q

Management of acromegaly

A
  • 1st line = Trans-sphenoidal removal of pituitary tumour
  • Surgical removal of ectopic secreting cancers
  • SC Pegvisomant daily = GH antagonist
  • Somatostatin analogues (ocreotide) = inhibits GH release
  • Dopamine agonist (bromocriptine) = weakly control IGF-1
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11
Q

Complications of acromegaly

A
  • Impaired glucose tolerance (40%)
  • Diabetes mellitus (15%)
  • Sleep apnoea = excess soft tissue in larynx
  • Hypertension, left ventricular hypertrophy, cardiomyopathy, arrhythmias, ischaemic heart disease, stroke
  • Colon cancer
  • Arthritis
  • Cerebrovascular events and headache
  • Enlargement of joints and soft tissues
  • Decreased life expectancy
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12
Q

What is diabetes insipidus?

A

Reduced ADH secretion from posterior pituitary or impaired response to ADH

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13
Q

Cranial causes of diabetes insipidus

A

o Brain Tumour = metastases, posterior pituitary tumour
o Head Trauma
o Brain malformations
o Brain Infections = TB, encephalitis, meningitis
o Brain surgery or radiotherapy
o Infiltrative disease = sarcoidosis
o Vascular = aneurysm, infarction, sickle cell
o Inflammatory = neurosarcoidosis, Guillain Barre, granuloma

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14
Q

Nephrogenic causes of diabetes insipidus

A

o Drugs = lithium chloride, glibenclamide
o Familial = mutation AVPR2 gene on X chromosome
o Intrinsic kidney disease
o Electrolyte disturbance = Hypokalaemia and Hypercalcaemia

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15
Q

Presentation of diabetes insipidus

A
  • Polyuria
  • Polydipsia
  • Dehydration
  • Postural hypotension
  • Hypernatraemia = lethargy, weakness, irritability, confusion, coma and fits
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16
Q

Investigation for diabetes insipidus

A
  • Water deprivation test
    o Serum and urine osmolality, urine volume and body weight are measured hourly for up to 8 hours during fasting and without fluids
    o Normal response = serum osmolality remains within normal range while urine rises
    o DI = serum osmolality rises without adequate conc of urine
    o Then desmopressin administered and urine osmolality measured 8 hours later
    o Cranial DI (kidneys still respond to ADH) = urine osmolality high
    o Nephrogenic DI (can’t respond to ADH) = low urine osmolality
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17
Q

Management of diabetes insipidus

A
  • Treat underlying cause
  • Desmopressin (synthetic ADH) = cranial DI
  • Nephrogenic DI
    o Thiazide diuretics = oral Bendroflumethiazide
    o NSAIDs
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18
Q

What is SIADH?

A

Continued secretion of ADH despite plasma being very dilute

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19
Q

Causes of SIADH

A
  • Post-operative from major surgery
  • Infection = atypical pneumonia and lung abscesses, TB
  • Medications = thiazide diuretics, carbamazepine, vincristine, cyclophosphamide, antipsychotics, SSRIs, NSAIDs
  • Malignancy = small cell lung cancer, pancreas, prostate
  • Neurological = Meningitis/encephalitis, SAH, SDH, stroke, head injury
  • Pulmonary lesions = pneumonia, TB, CF, asthma
  • Alcohol withdrawal
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20
Q

Presentation of SIADH

A
  • Headache
  • Fatigue
  • Muscle aches and cramps
  • Confusion
  • Seizures and reduced consciousness = severe hyponatraemia
  • Anorexia and nausea
  • Irritability
  • Unstable gait/falls
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21
Q

Investigations for SIADH

A
  • Dilutional hyponatraemia = excessive water retention
  • Euvolaemia = normal blood vol
  • High urine Na+ > 30 mmol/L
  • Negative short synacthen test = exclude adrenal insufficiency
  • 1-2L or 0.9% Saline = sodium depletion will respond but SIADH won’t
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22
Q

Management of SIADH

A
  • Treat underlying cause
  • Fluid restriction = 500ml-1L
  • ADH receptor blockers (tolvaptan) = close monitoring
  • Demeclocycline = tetracycline Abx inhibits ADH
  • Hypertonic saline
  • Salt and loop diuretic = oral furosemide
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23
Q

Complication of SIADH

A

Central pontine myelinolysis = brain swelling

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24
Q

What is Conn’s syndrome?

A

Primary hyperaldosteronism from adrenal adenoma

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25
Q

Causes of primary hyperaldosteronism

A
  • Adrenal adenoma (Conn’s syndrome)
  • Bilateral adrenocortical hyperplasia
  • Familial hyperaldosteronism type 1 and 2
  • Adrenal carcinoma
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26
Q

Presentation of primary hyperaldosteronism

A
  • Often asymptomatic
  • Weakness/cramps
  • Paraesthesia, polyuria and polydipsia
  • Hypertension = severe increase in blood volume
  • Hypokalaemia
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27
Q

Investigations for primary hyperaldosteronism

A
  • Plasma aldosterone: renin ratio
    o High aldosterone and low renin = primary hyperaldosteronism
    o High aldosterone and high renin = secondary hyperaldosteronism
  • Increased plasma aldosterone levels not suppressed with 0.9% saline infusion or fludrocortisone administration = diagnostic
  • ABG = alkalosis
  • Hypokalaemic ECG = Flat t waves, ST depression, long QT
  • CT or MRI adrenals to differentiate adenomas from hyperplasia
  • Renal doppler ultrasound = renal artery stenosis or obstruction
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28
Q

Management of primary hyperaldosteronism

A
  • Aldosterone antagonists = Oral spironolactone
  • Laparoscopic adrenalectomy
  • Percutaneous renal artery angioplasty = renal artery stenosis
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29
Q

Complications of primary hyperaldosteronism

A

Renal, cardiac and retinal damage

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30
Q

What is addison’s disease?

A

Autoimmune damage to adrenal glands causing reduction in secretion of cortisol and aldosterone (Primary adrenal insufficiency)

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31
Q

Causes of primary adrenal insufficiency

A
  • Autoimmune adrenalitis
  • TB
  • Adrenal metastases
  • Long term steroid use
  • Adrenal haemorrhage/infarction = meningococcal septicaemia
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32
Q

Presentation of Addison’s disease

A
  • Toned = lean build, anorexia, weight loss
  • Tanned  Pigmentation of skin (increased ACTH) cross reacts with melanin receptors
  • Tired = lethargy
  • Tearful = depression, low mood and self esteem
  • Nausea and vomiting
  • Diarrhoea, constipation and abdominal pain
  • Impotence/amenorrhea
  • Dizzy, syncope
  • Headache
  • Cramps
  • Reduced libido
  • Vitiligo = white patches and loss of body hair due to loss of adrenal androgens
  • Dehydration
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33
Q

Investigations of primary adrenal insufficiency

A
  • Short synACTHen test (ACTH stimulation)
    o Measure plasma cortisol before and 30 mins after IM tetracosactide
    o Addison’s excluded if 30 mins cortisol >550nmo/L Hyponatraemia and Hyperkalaemia
  • Adrenal autoantibodies  adrenal cortex antibodies and 21-hyroxylase antibodies
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34
Q

Electrolyte abnormalities in Addison’s disease

A

hyperkalaemia, hyponatraemia, hypoglycaemia, metabolic acidosis

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35
Q

Management of primary adrenal insufficiency

A
  • Oral hydrocortisone = glucocorticoid replacement
  • Oral fludrocortisone = mineralocorticoid replacement
  • Steroid card and emergency ID tag
  • Hydrocortisone dose doubled during acute illness
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36
Q

Complications of primary adrenal insuffiency

A
  • Critical deterioration = shock, raised temp, coma
  • Adrenal crisis
    o Nausea, vomiting, abdominal pain, muscle cramps and confusion
    o IV hydrocortisone immediately
  • CVD risk increased
  • Osteoporosis
37
Q

Causes of secondary adrenal insufficiency

A
  • Loss or damage to pituitary gland = hypopituitarism
  • Surgery to remove pituitary tumour
  • Infection
  • Loss of blood flow
  • Radiotherapy
  • Long term steroid therapy
  • Hypothalamic-pituitary disease
38
Q

Causes of hypercalcaemia

A
  • Long term immobility
  • Hyperparathyroidism (primary, secondary, tertiary)
  • Malignant hyperparathyroidism
  • Excess Ca2+ intake
  • Drugs = thiazide diuretics, vit D analogies, lithium administration
39
Q

Presentation of hypercalcaemia

A
  • Can be asymptomatic if mild
  • Stones = renal colic, biliary stones
  • Bones = Pain, fractures, osteomalacia/osteoporosis
  • Groans = abdo pain, N+V
  • Psychic moans = Depression, anxiety, cognitive dysfunction, insomnia and coma
  • Thrones: Polyuria and polydipsia, Constipation
  • Other: Weakness, fatigue, muscle symptoms, Anorexia and weight loss
  • Hypertension
40
Q

Investigations for hypercalcaemia

A
  • High serum Ca2+, High 24 hr urinary Ca2+, raised ALP (malignancy), raised PTH
  • Low renal function = 2nd/3rd
  • AXR  renal calculi or nephrocalcinosis
  • Skull XR  pepper-pot
  • Hand XR  subperiosteal erosions in middle/terminal phalanges
  • Parathyroid ultrasound  insensitive for small tumours
  • Radioisotope scanning = 90% sensitive for detecting adenoma
  • High res CT/MRI malignancies around body
  • DEXA bone density scan
41
Q

Management of acute severe hypercalcaemia

A

o Rehydrate with IV 0.9% saline fluids = prevent stones
o Bisphosphonates after rehydration (IV pamidronate)
o Oral prednisolone = myeloma, sarcoidosis and vit D excess

42
Q

Management of primary hyperparathyroidism

A

o Parathyroid adenoma/hyperplasia = surgical removal
o Calcimimetic = increases sensitivity of parathyroid cells to Ca2+
o Avoid thiazide diuretics, high Ca2+ and vit D intake

43
Q

Causes of hypocalcaemia

A
  • CKD
  • Severe vit D deficiency (Osteomalacia)
  • Drugs = calcitonin, bisphosphonates
  • Acute pancreatitis
  • Massive blood transfusion
  • Rhabdomyolysis
  • Magnesium deficiency
44
Q

What is primary hypoparathyroidism

A

Low PTH due to parathyroid gland failure
o Ca2+ is low and phosphate high

45
Q

Presentation of hypocalcaemia

A
  • Parathesiae (numbness and tingling) around mouth and extremities
  • Cramps, tetany
  • Diarrhoea
  • Anxious, irritable, irrational
  • Wheeze = muscle tone increases in smooth muscle
  • Orientation impaired and confusion
  • Dermatitis ± Impetigo herpetiformis
  • Chvostek’s sign = Tapping over facial nerve causes twitching of ipsilateral facial muscles
  • Trousseau’s sign = Carpopedal spasm induced by inflammation of sphygmomanometer cuff to level above systolic pressure
  • Papilloedema, Cataract
  • Cardiomyopathy
46
Q

Investigations of hypocalcaemia

A
  • Bloods = Low serum Ca2+, eGFR, creatinine, urine, low Mg, low vit D
  • PTH absent or low in hypoparathyroidism but high in other causes of hypocalcaemia
  • Parathyroid antibodies = present in idiopathic hypoparathyroidism
  • X-rays of metacarpals = short 4th metacarpal in pseudohypoparathyroidism
  • ECG  prolonged QT interval
47
Q

Management of hypocalcaemia

A
  • Give IV calcium gluconate 10ml of 10% every 10 mins over 30 mins with ECG monitoring
  • Vit D deficiency = Oral colecalciferol/adcal
  • Hypoparathyroidism = Calcium supplements and calcitriol (active vit D)
48
Q

Difference between Cushing’s disease and Cushing’s syndrome

A
  • Syndrome = Too much cortisol
  • Disease = pituitary adenoma secretes excess ACTH leading to increased cortisol
49
Q

Risk factors for Cushings

A

Depression
Obesity
Pregnancy

50
Q

Causes of Cushings

A
  • Oral steroids = glucocorticoid therapy (most common)
  • Pituitary adenoma (Cushing’s disease)
  • Adrenal adenoma
  • Paraneoplastic Cushing’s = small cell lung cancer
  • Alcohol pseudo-Cushing’s syndrome
51
Q

Presentation of Cushings

A
  • Central obesity (trunk, abdomen and neck) = weight gain
  • Ruddy and swollen with moon face
  • Bruising
  • Thin skin
  • Gonadal dysfunction (irregular periods and erectile dysfunction)
  • Acne
  • Failure for children to grow tall despite excess weight
  • Recurrent non healing ulcers
  • Hirsutism  Excess hair in chin and moustache area
  • Lethargy
  • Striae = Purply stretch marks on abdomen, breasts and thighs
  • Buffalo hump = fat pad on upper back
  • Proximal limb muscle wasting + weakness
  • Malaise, depression, psychosis, insomnia
52
Q

Investigation for Cushings

A
  • Overnight dexamethasone suppression test
    Low dose
    o If low cortisol then normal
  • if high/normal then Cushings

High dose
If low then Cushings disease
If high/normal then check ACTH
ACTH low = adrenal cushings
ACTH high = ectopic ACTH

53
Q

What is T1DM?

A

Insulin deficiency from autoimmune destruction of pancreatic insulin-secreting Beta cells in islets of Langerhans

54
Q

Risk factors for T1DM

A
  • Family history (HLA DR3/4)
  • Other autoimmune diseases = autoimmune thyroid, coeliac disease, Addison’s disease, pernicious anaemia
  • Environment = Dietary constituents, Enteroviruses, Vit D deficiency
55
Q

Presentation of T1DM

A
  • Thirsty (polydipsia)
  • Polyuria and nocturia
  • Weight loss/lean
  • Fatigue
  • Glycosuria
  • Breath smelling of ketones
  • Persistent hyperglycaemia = Despite diet and medications
  • Ketonuria
56
Q

Investigations for T1DM

A
  • Random plasma glucose >11.1mmol/L
  • Fasting plasma glucose >7mmol/L = One abnormal value is diagnostic in symptomatic individuals and 2 in asymptomatic individuals

C-peptide levels low
Metabolic acidosis

57
Q

Antibodies in T1DM

A

o Anti-GAD
o Islet cell antibodies
o Insulin autoantibodies
o Insulinoma-associated 2 autoantibodies

58
Q

Management of T1DM

A

Lifelong insulin therapy

59
Q

Advice for T1DM

A
  • Must inform DVLA = Advise not to drive if severe hypoglycaemic spells
  • Good control to educate to self-adjust doses
  • Can phone for support 24/7 nurse
  • Can modify diet wisely and avoid binge drinking
  • Abort hypoglycaemia with sugary drinks
  • Finger pricking glucose
    o Before meal = inform long-acting insulin doses
    o After meal = inform short-acting insulin doses
60
Q

Complications of T1DM

A
  • Diabetic Ketoacidosis
  • Insulin treatment
    o Hypoglycaemia
    o Injection site = lipohypertrophy
    o Insulin resistance
    o Weight gain
  • Coronary artery disease
  • Peripheral neuropathy
    o Tx: amitriptyline, duloxetine, gabapentin, pregabalin
  • Gastrointestinal autonomic neuropathy
    o Gastroparesis  erratic blood glucose control, bloating, vomiting
    o Chronic diarrhoea
    o GORD
  • Retinopathy
61
Q

What is T2DM

A

Decreased insulin secretion with/out increased insulin resistance

62
Q

Organic causes of T2DM

A
  • Combination of insulin resistance and less severe insulin deficiency
  • Drugs = steroids, anti-HIV drugs, new antipsychotics, thiazides
  • Pancreatitis, pancreatic surgery, trauma, pancreatic cancer
  • Cushing’s disease, acromegaly, hyperthyroidism
  • Pregnancy
  • Congenital lipodystrophy, glycogen storage diseases
63
Q

Investigations of T2DM

A
  • Random plasma glucose >11.1mmol/L, Fasting plasma glucose >7mmol/L
  • HbA1c >48mmol/mol
64
Q

Pharmacological management of T2DM

A

Oral metformin
Add SGLT-2 inhibitors
Add sulfonyluriea (gliclazide)
Add pioglitazone
Add sitagliptin
Add insulin therapy

65
Q

Side effects of metformin

A

diarrhoea, abdo pain, lactic acidosis

66
Q

Side effects of sulfonylurea (gliclazide)

A

weight gain, hypoglycaemia, increased CVD/MI risk, liver dysfunction

67
Q

Side effects of pioglitazone

A

weight gain, fluid retention, anaemia, heart failure, liver dysfunction, fractures

Contraindicated in heart failure

68
Q

Side effects of SGLT-2 inhibitors (empahlifozin)

A

urinary and genital infection, Fournier’s gangrene, normoglycaemic ketoacidosis, increase risk of lower limb amputation

69
Q

Positive effects of SGLT-2 inhibitors

A

Improve outcomes for patients with CVD
Weight loss

70
Q

Complications of T2DM

A
  • Atherosclerosis = stroke, IHD, MI and peripheral vascular disease (gangrene)
  • Diabetic Retinopathy
  • Diabetic Polyneuropathy = Diabetic foot ulceration
  • Erectile dysfunction
  • CKD (10%) = Diabetic nephropathy
  • Infections (6%)
71
Q

Causes of hyperthyroidism

A
  • Grave’s disease
  • Toxic multi nodular goitre
  • Toxic adenoma (benign)
  • Ectopic thyroid tissue
  • Drug-induced hyperthyroidism = amiodarone, iodine, lithium
  • Thyroiditis (De Quervain’s)
  • Hashimoto’s, postpartum
72
Q

Presentation of hyperthyroidism

A
  • Palpitations, tachycardia
  • Heat intolerance = sweating
  • Anxiety
  • Diarrhoea (Frequent loose stools)
  • Weight loss and increased appetite
  • Oligomenorrhea (infrequent periods) and infertility
  • Irritability/ behavioural change
  • Sexual dysfunction
  • Goitre
  • Hyperkinesis = muscle spasm
  • Proximal myopathy and muscle wasting
  • Lymphadenopathy and splenomegaly
  • Hands = palmar erythema, warm moist skin and fine tremor
  • Lid lag and stare
73
Q

Investigations for hyperthyroidism

A
  • TFTs  serum TSH low, T4/T3 high
  • Raised ESR and CRP = thyroiditis
  • Thyroid peroxidase (TPO) and thyroglobulin antibodies = 80% of Graves’ but all normal hyperthyroidism
  • Ultrasound of thyroid = differentiate Graves’ from toxic adenoma
  • TSH receptor stimulating antibodies = Graves’ specific
74
Q

Management of hyperthyroidism

A
  • Anti-thyroid drugs
    1. Oral Carbimazole
    2. Propylthiouracil
  • Radioactive iodine = destroys portion of thyroid cells
    o Treatment of choice to toxic multinodular goitre
  • BB (propranolol) = rapid control of symptoms
  • Surgery (thyroidectomy) = Large goitre, poor response to drugs and have drug side-effects
  • Thyroid pain  aspirin/NSAIDs
75
Q

Complications of hyperthyroidism

A

Thyroid crises/storm

76
Q

Presentation of thyroid storm

A

fever > 38.5ºC
tachycardia
confusion and agitation
nausea and vomiting
hypertension
heart failure
abnormal liver function test - jaundice may be seen clinically

77
Q

Management of thyroid storm

A

symptomatic treatment e.g. paracetamol
treatment of underlying precipitating event
beta-blockers: typically IV propranolol
anti-thyroid drugs: e.g. methimazole or propylthiouracil
Lugol’s iodine
dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3

78
Q

What is Grave’s disease?

A

Autoimmune condition where TSH receptor antibodies cause primary hyperthyroidism

79
Q

What features are specific to Grave’s disease

A

Grave’s ophthalmopathy = protruding eye and proptosis, eye discomfort, corneal ulceration, paralysis of eye muscles

Grave’s dermopathy = pretibial myxoedema

TSH receptor stimulating antibodies

80
Q

What are the different types of thyroid cancers?

A

Papillary = young, well differentiated, good prognosis

Follicular = middle age, well differentaited, good prognosis

Anaplastic = aggressive, very undifferentiated, poor prognosis

Lymphoma

Medullary cell

81
Q

Presentation of thyroid cancers

A
  • Dysphagia
  • Hoarse voice = tumour compression on surrounding structures (oesophagus and laryngeal nerve)
  • Thyroid nodules (90%)
  • Cervical lymphadenopathy or with lung, cerebral, hepatic or bone metastases
  • Thyroid gland = large, hard, irregular
82
Q

Investigations for thyroid cancers

A
  • Fine needle aspiration cytology biopsy = benign or malignant nodules
  • Ultrasound of thyroid = Differentiate between benign or malignant

Blood test (TFT)
o Check if hyperthyroid or hypothyroid = treated before carcinoma surgery
o T3, T4, TSH, thyroid autoantibodies

  • CXR = Tracheal goitres, mets
83
Q

Management of thyroid cancers

A
  • Thyroidectomy
  • Radioactive Iodine  Locally irradiate and destroy cancer with little radiation damage to other surrounding structures
  • Levothyroxine (T4)  Keep TSH reduced (growth factor for cancer)
  • Chemotherapy  Reduce risk of spread and treats micro-metastases that have been undetected
84
Q

Causes of hypothyroidism

A
  • Hashimoto’s thyroiditis (developed world)
  • Iodine deficiency (developing world)
  • Post-thyroidectomy/ radioiodine/ anti thyroid drugs
  • Post-partum thyroiditis
  • Drug induced = Carbimazole, lithium, amiodarone, interferon Secondary hypothyroidism (reduced TSH from anterior pituitary)
  • Hypopituitarism = tumours, infection, vascular, radiation
  • Other autoimmune disease
85
Q

Presentation of hypothyroidism

A
  • Weight gain
  • Hoarse voice
  • Goitre
  • Constipation
  • Menorrhagia
  • Myalgia, weakness
  • Low mood, dementia
  • Myxoedma
  • Bradycardia
  • Reflexes relax slowly
  • Ataxia (cerebellar)
  • Dry, thin hair/skin
  • Yawning/drowsy/coma
  • Cold hands (temp drop)
  • Ascites (Fluid retention = oedema, pleural effusions)
  • Round puffy face
  • Defeated demeanour
  • Immobile (ileus)
  • Congestive cardiac failure
86
Q

Investigations for hypothyroidism

A
  • Thyroid function tests
    o Serum TSH high (primary hypothyroidism)
    o Serum TSH low (secondary hypothyroidism)
    o Serum free T4/T3 low (both)
  • TPO antibodies  Hashimoto’s
  • Raised serum aspartate transferase levels from muscle and/or liver
  • Increase serum creatinine kinase levels (myopathy)
  • Hypercholesterolaemia
  • Hyponatraemia = increase in ADH and impaired free water clearance
87
Q

Management of hypothyroidism

A

Lifelong oral levothyroxine

88
Q

Complications of hypothyroidism

A
  • Myxoedema coma
    o Severe hypothyroidism = rarely present with confusion and coma
    o Hypothermia, cardiac failure, hypoventilation, hypoglycaemia and hyponatraemia
    o Medical emergency  IV/oral T3 + glucose infusion as well as gradual rewarming
  • Dyslipidemia
  • Metabolic syndrome
  • CHD and stroke
  • HF
  • Neurological and cognitive impairments
  • MALT lymphoma (Hashimoto’s)

Finals (23 decks)

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