Endocrinology Flashcards
T1 diabetes definition
Metabolic disorder characterised by hyperglycaemia due to absolute insulin deficiency
How common is T1 diabetes
Accounts for about 5-10% of all patients with diabetes
Most commonly diagnosed in childhood/ puberty
Who does T1 diabetes affect
Mostly young people <20
Risk factors of T1 Diabetes
Geographical region
Weak: genetic predisposition, infectious agents, dietary factors
Symptoms and signs of T1 diabetes
Presence of risk factors
Polyuria
Polydipsia - getting up at night to drink
Young age, weight loss, blurred vision, nausea and vomiting, abdominal pain, tachypnoea, lethargy, coma
Differentials of T1 diabetes
Monogenic diabetes: maturity onset diabetes of the young
Neonatal diabetes
Latent autoimmune diabetes in adults (LADA)
Type 2 diabetes
Investigations to confirm T1 diabetes ,
1st line:
Random plasma glucose: >11mmol/L confirms diagnosis in the presence of symptoms of polyuria, Polydipsia and unexplained weight loss.
Fasting plasma glucose: > 6.9mmol/L
2 hour plasma glucose: >11mmol/L plasma glucose is measured 2 hours after 75g oral glucose load
Plasma or urine ketones: medium or high quantity
Hb1Ac: >48mmol/mol- ref,eats degree of hyperglycaemia over the preceding 3 months
Consider: fasting c-peptide -> low or undetectable
Autoimmune markers -> glutamic acid decarboxylase,
Insulin, is,et cells etc. -> positive
Management of T1 diabetes
1st line: basal bolus insulin e.g. insulin glargine: injected subcutaneously once daily
If pregnant- give insulin isophane human (NPH) subcut twice daily
2nd line: fixed dose insulin e.g. isophane human/ insulin neutral, injected subcut twice daily
Prognosis of T1 diabetes
Dependant on whether it is treated
Untreated can be fatal due to DKA
Poorly controlled T1 diabetes is a risk factors for chronic complications e.g. CKD
Complications of T1 and T2 diabetes
Macrovascular - CAD, strokes, PVD
Microvascular - CKD, Retinopathy, Neuropathy
Metabolic- DKA, HHS
T2 diabetes definition
Progressive disorder defined by deficits in insulin secretion and action that leads to abnormal glucose metabolism related metabolic derangements
How common is T2 diabetes
Global prevalence is 2.8%
Causes of T2 diabetes
Combination of insulin resistance/ insensitivity and insulin deficiency
This balance of the two varies between people
Risk factors for T2 diabetes
Older age Overweight/ obese Gestational diabetes Pre- diabetes Family history of T2 diabetes African, Hispanic, south Asian or Native American ancestry Hypertension Dyslipidaemia CVD Physical inactivity
Symptoms of T2 diabetes
Presence of risk factors
Asymptomatic
Candida infections: most commonly vaginal, penile or in skin folds
Skin infections e.g. cellulitis or abscesses
UTIs e.g? Cystitis or pyelonephritis
Fatigue
Blurred vision
Signs/ examination of T2 diabetes
Often no physical signs, although lymphadenopathy signs of a pleural effusion, lobar collapse or unresolved pneumonia may be present
Differential diagnosis of T2 diabetes
Pre- diabetes Diabetes mellitus LADA Monogenic diabetes Ketosis prone diabetes Diabetes gestational
T2 diabetes investigations
1st line
- Hb1Ac: confirm with a repeat Hb1Ac or another diagnostic test, also used to monitor glycemic control, usually every 3 months
- fasting plasma glucose: order after a minimum 8 hour fast
- 2 hour post load glucose after 75g glucose: more costly and inconvenient than fasting plasma glucose or Hb1Ac
Management of T1 diabetes
1st line - lifestyle, diet changes
Acute:
- hyperglycaemia: 1st line - basal bolus insulin + cardiovascular risk reduction / lifestyle measures
- HbA1c above goal at diagnosis: 1st line - metformin + cardiovascular risk reduction/ lifestyle measures
- pregnant: 1st line: diet + basal bolus insulin
Prognosis of T2 diabetes
Increases the likelihood of major cardiovascular events and death but varies between pts
Definition of primary hypothyroidism
A clinical state resulting from underproduction of the thyroid hormones T3 and T4
How common is primary hypothyroidism
More common in the developing world due to iodine deficiency is a major cause of hypothyroidism
Autoimmune thyroiditis (Hashimoto’s disease) is the most common cause of primary hypothyroidism —> lymphocytic infiltration and destruction of thyroid tissue with secondary antibodies to thyroid peroxidase, thyroglobulin, and other thyroid antigens
Prevalence of primary hypothyroidism
Higher in woman and increased with age
Causes of primary hypothyroidism
- T4 is the main hormone produced by the thyroid gland
- It is converted to T3 in target tissues
- T3 mediates the amin actions of thyroid hormone, which includes stimulation of cellular oxygen consumption and energy generation, by binding to nuclear receptors and modulating gene expression
- Through a negative feedback mechanism, failure of the thyroid to produce its hormones stimulates the pituitary to increase production of TSH
Risk factors for primary hypothyroidism
Iodine deficiency Female Middle age Fx of autoimmune thyroiditis Autoimmune disorders Graves’ disease Radiotherapy Aminodarone use Lithium use MS Primary pulmonary hypertension
Symptoms/ signs of primary hypothyroidism
Presence of risk factors Weakness Lethargy Cold sensitivity Constipation Weight gain Depression Menstrual irregularity Myalgia Dry or coarse skin Eyelid and facial oedema Thick tongue Coarse hair Bradycardia Deep voice Diastolic hypertension Goitre Delayed relaxation of tendon reflexes
Differential diagnosis of primary hypothyroidism
Central or secondary hypothyroidism
Depression
Alzheimer’s dementia
Anaemia
Investigations for primary hypothyroidism
1st line - serum TSH: normal is 0.5 to 5 - levels are elevated
Consider
Free serum R4, serum cholesterol, FBC, fasting blood glucose, serum CK, serum sodium, anti thyroid peroxide antibodies
Management of primary hypothyroidism
1st line: levothyroxine e.g. 1.6micrograms/kg/day orally
Adjust dose in increments of 12.5or 25 micrograms to normalise TSH, start on full replacement dose
Prognosis of primary hypothyroidism
Generally excellent with full recovery upon adequate replacement of thyroid hormones
Complications of primary hypothyroidism
Angina, complications in pregnancy, AF, osteoporosis, myxoedema coma, resistant hypothyroidism
Secondary/ tertiary hypothyroidism definition
- It results from a deficiency of thyroid hormones, which results in a generalised slowing of metabolic processes
- Results of anterior pituitary hypofunction or thalamic hypofunction
- It is characterised by decreased thyroid-stimulating hormone secretion in turn causing decreased thyroid hormone synthesis and release
How common is secondary/ tertiary hypothyroidism
Rare, only accounts for less than 1% of hypothyroid cases
Pituitary adenomas are the most common cause of secondary hypothyroidism
Causes of secondary/ tertiary hypothyroidism
CENTRAL HYPOTHYROIDISM: caused by a deficiency of TSH because of hypothalamic and/or pituitary dysfunction, can occur as a result of deficient stimulation of the anterior pituitary by TRH, deficient synthesis and secretion of TSH by the anterior, or secretuib of biologically ineffective TSH as in some genetic diseases
T3 and T4 mechanism
- TSH is glycoprotein that is produced and secrered by the anterior pituitary
- TASH stimulates thyroidal biosynthesis and secretion of thyroid hromones T3 and T4
- TSH secretion is regulated by the TRH as well as by thyroid hormones
- TRH is a tripeptide released into the hypothalamic-pituitary portal vessels and transported to the anterior piruitarym where it promotes synthesis and secretion of TSH
- T3 and T4 act on the anterior pituitary in a ngetaive feedback loop, inhibiting the synthesis and secretion of TSH
- T3 and T4 also act at the hypothalamic level to inhibit the secretion of TRH
Risk factors for secondary/ tertiary hypothyroidism
Multiple endocrine neoplasia (MEN) type 1
Head and neck irradiation
Traumatic brain injury (TBI)
Weak: sarcoidosis, histiocytosis, haemochromatosis, pregnancy, Fx of central hypothyroidism
Symptoms / signs of secondary/ tertiary hypothyroidism
Presence of risk factors Weakness Fatigue Cold intolerance Decrease memory Muscle cramps Weight gain Depression Dry coarse skin Bradycardia Reduced body and scalp hair
Differential diagnosis of secondary/ tertiary hypothyroidism
Primary hypothyroidism Non-thyroid also illness Iodine deficiency Chronic fatigue syndrome De Quervain’s thyroiditis Depression Fibromyalgia
Investigations for secondary/ tertiary hypothyroidism
1st line
TFTs
- serum free thyroxine (T4): low
- serum TSH: inappropriately low to normal TSH in the setting of low serum free T4
Consider: MRI of brain, Ct head, prolactin (PRL), 9a.m, serum cortisol
Management of secondary/ tertiary hypothyroidism
1st line - levothyroxine
If adrenal hormone deficiency -> add corticosteroids e.g. hydrocortisone orally
Prognosis of secondary/ tertiary hypothyroidism
Risk for recurrent pneumothoraces
Complications of secondary/ tertiary hypothyroidism
Re-expansion pulmonary oedema
Talc plaurodesis- related ARDS
Hyperthyroidism definition
Also known as thyrotoxicosis
The clinical effect of excess thyroid hormone, usually from gland hyperfunction
Causes of hyperthyroidism
Graves’ disease
- The most common cause
- Thyroid stimulating antibodies (IgG) bind to TSH receptors and stimulate the thyroid
- Thyroid gland hypertrophies and becomes diffusely enlarged
- The autoimmune process leads to mucopolysaccharide infiltration of the extra-ocular muscles and may lead to exophthalmos
TSH secreting pituitary adenoma
- T3 T4 secreting site in the thyroid (nodule in a multinodular goitre, adenoma or (very rarely) carcinoma
Thyroiditis
- Large amounts of preformed hormones are released after the destruction of follicles, with transient thyroid toxicosis
Exogenous intake of thyroid hormones (factitious thyrotoxicosis)
Risk factors for hyperthyroidism
Female
Tobacco use
Weak: high iodine intake, lithium therapy, biological agent and cytokine therapies, radiation, radioiodine therapy for benign modular goitre, stress
Symptoms of hyperthyroidism
Diarrhoea Weight loss Increased appetite Sweats Heat intolerance Palpitations Tremor Irritability Labels emotions Oligomenorrhoea +/- infertility
Signs of hyperthyroidism
Bradycardia Irregular pulse Warm moist skin Fine tremor Palmar erythema Thin hair Lid lag Lid retraction Exophthalmos May be a goitre, thyroid nodules or bruit depending on the cause
Differential diagnosis of hyperthyroidism
Pleural thickening
Pulmonary collapse and consolidation
Elevated hemidiaphragm
Pleural tumours/ extrapleural fat
Investigations for hyperthyroidism
1st line: TFTs - TSH suppressed and T4 & T3 increased
2nd line: autoantibodies - most commonly seen in Graves’ disease e.g. anti micro Somali antibodies against thyroid peroxidase, anti- thyroglobulin antibodies, TSH receptor antibodies
3rd line: thyroid USS and thyroid uptake scans when cause is unknown
Consider: CRP and ESR (raised)
Management for hyperthyroidism
Thyroid storm: high dose antithyroid drugs, corticosteroids, beta blockers and iodine solution with supportive care
Symptomatic but not pregnant: prolonged antithyroid drug therapy (carbimazole, orally) OR radioactive iodine + hydrocortisone OR surgery ( patients need to be returned to euthyroid state before surgery)
Pregnant: propylthiouracil (causes liver failure so only give 1st line in pregnancy and thyroid storm)
Prognosis for hyperthyroidism
• Relaspes and remittances, spontenous remission is seen in <10%
Complications of hyperthyroidism
• Heart failure, angina, AF, osteoporosis, ophthalopathy, gynaecomastia
Thyroid lump (goitre and thyroid nodule) definition
Goitre - enlargement of the thyroid gland
Thyroid nodule - lump in an otherwise normal thyroid gland
Goitres may consist of many nodules (multi-modular goitre) and solitary nodules may exist within a goitre
Nodules may be cystic, colloid, hyperplastic, adenomatous or cancerous
How common is Thyroid lump (goitre and thyroid nodule)
24.8 cases per 100,000 adults
Affects mainly adults
What causes Thyroid lump (goitre and thyroid nodule)
Can be physiological or pathological in origin
Diffuse:
- physiological (puberty or pregnancy)
- autoimmune (graves or hashimotos)
- acute viral thyroiditis (de Quervains thyroiditis)
- Iodine deficiency (endemic goitre) -> most common, dyshormonogenesis
- goitrogens e.g. sulphonylureas
Nodular:
- multinodular goitre
- solitary nodule
- fibrotic (Riedell’s thyroiditis)
- Cysts
Tumours - adenoma, carcinoma, lymphoma
Miscellaneous - sarcoidosis, TB
Characteristics of thyroid cancer
- Papillary (70%): young people, spreads locally, good prognosis
- Follicular (20%): middle age, spreads to the lung/bone. Prognosis usually good
- Medullary cell (5%): often familial (MEN1), spreads locally and via mets. Poor prognosis
Anaplastic <5%, aggressive, spreads locally, very poor prognosis
Symptoms of Thyroid lump (goitre and thyroid nodule)
Often asymptomatic and noticed by family members or seen in the mirror
Sometimes can cause pain and rarely present with features of compression of the trachea
Ask about previous radiation
Signs of Thyroid lump (goitre and thyroid nodule)
• Ask the patient patient to drink some water and note the thyroid moves as the pt swallows
• Note enlargement or asymmetry
• Stand behind a seated pt and use the second and third fingers of both hands to eamine the gland as they swallow again
• Note lumps, asymmetry, size and tenderness
- check for regional lymphadenopathy
Red flags
Stridor associated with a thyroid mass
Unexplained hoarseness or voice changes associated with goitre
Painless thyroid mass enlarging rapidly over a period of a few weeks
Palpable cervical lymphadenopathy
Differential diagnosis of Thyroid lump (goitre and thyroid nodule)
Non- toxic (simple) goitre - non functioning nodules, TFTs are normal
Toxic multi nodular goitre - functioning nodules, abnormal TFTs
Retrosternal goitre (usually multi nodular)
Hyperplastic nodule. ( single nodule or part of a multinodular goitre)
Colloid nodule
Thyroid adenoma
Thyroid cyst
Thyroid carcinoma
Graves - diffusely overactive thyroid gland
Hashimoto’s thyroiditis- autoimmune destruction of the gland may cause diffuse enlargement
Investigations for Thyroid lump (goitre and thyroid nodule)
1st line: TFTs • 1st LINE: TFTs – those with abnormal TFTs and no suspicious features should be referred to an endocrinologist
• 2ND LINE: USS – highly sensitive for detection and characterisation of thyroid nodules
• 3RD LINE: FNA – fine needle aspiration gives tissue for cytology
Management of Thyroid lump (goitre and thyroid nodule)
- Usually not required apart from introducing euthyroidism if necessary
- Surgical intervention is required for the cosmetic effects of large goitres, pressure effects on the trachea or oesophagus, or confirmed or possible malignancy
Prognosis and complications of Thyroid lump (goitre and thyroid nodule)
Dependant on cause
Cushing’s syndrome definition
Clinical manifestation of pathological hypercortisolism from any cause
How common is Cushing’s syndrome
Occurs 4 times more commonly in women than men
Relatively uncommon in the general population
Causes of Cushing’s syndrome
ATH secreting pituitary tumours by autonomous adrenal cortisol overproduction and, rarely by ectopic ACTH secreting tumours
Risk factors for Cushing’s syndrome
Exogenous corticosteroid use Pituitary adenoma Adrenal adenoma Adrenal carcinoma WEAK: neuroendocrine tumours, thoracic or bronchogenic carcinoma
Symptoms / signs for Cushing’s syndrome
Presence of risk factors
Facial plethora
Moon face
Pathological fractures ( especially vertebrae and ribs)
Supraclavicular fullness Violaceous striae Absence of pregnancy Menstrual irregularities Absence of malnutrition, alcoholism and of physiological stress Linear growth deceleration in children Decreased libido Acne Facial rounding
Differential diagnosis of Cushing’s syndrome
Obesity
Metabolic syndrome
Investigations for Cushing’s syndrome
- urine pregnancy test
- serum glucose : elevated
- late night salivary cortisol: elevated
- 1mg overnight dexamethasone suppression test: morning cortisol > 50 nanomol/L
- 24 hour 2mg (low dose) dexamethasone suppression test: morning cortisol >50nanomol/L
Management for Cushing’s syndrome
1st line: transsphenoidal pituitary adenomectomy - removes the causative pituitary adenoma
2nd line: repeat transsphenoidal pituitary adenomectomy
3rd line: pituitary radiotherapy
4th line: bilateral adrenalectomy
Prognosis for Cushing’s syndrome
Without treatment, hypercortisolism persist and in many patients worsens
Untreated disease carries a dismal survival rate at 50% at 5 years
Complications for Cushing’s syndrome
Adrenal insufficiency CVD Hypertension Osteoporosis Diabetes mellitus
Definition for Addison’s Disease (Primary Adrenal Insufficiency)
Disorder that affects the adrenal glands causing decreased production of adrenocrotical hormones (cortisol, aldosterone, and dehydroepiandrosterone)
Characterised by hyponatreamia, hypercalcaemia, and hyperkalaemia
How common is Addison’s Disease (Primary Adrenal Insufficiency)
5-10% of all patients with diabetes
Most commonly diagnosed under 20 years of age
Affects mostly young people <20 years
What causes Addison’s Disease (Primary Adrenal Insufficiency)
Decreased production of adrenalcortical hormones as a result of either destruction of the 3 layers of the adrenal cortex (the glomerulosa, fasciculate, and reticularis or destruction of hormone synthesis
Infiltrating diseases such as TB or metastasis can also cause destruction of the adrenal medulla
Primary: destruction or dysfunction of the adrenal gland
Secondary: inadequate pituitary adrenocroticotophic hormone (ACTH) and subsequent cortisol production
Tertiary: inadequate hypothalamic corticotropin- releasing hormone and subsequent ACTH release
Risk factors for Addison’s Disease (Primary Adrenal Insufficiency)
Female Adrenocortical abs Adrenal haemorrhage TB Non-TB bacterial infection
Symptoms for Addison’s Disease (Primary Adrenal Insufficiency)
Presence of risk factors Fatigue Anorexia Weight loss Hyperpigmentation - present in mucosa and sun-exposed areas, more pronounced in cloak are creases, areas of friction and scars
Signs for Addison’s Disease (Primary Adrenal Insufficiency)
Hyponatreamia
Hypercalcaemia
Hyperkalaemia
Differential diagnosis for Addison’s Disease (Primary Adrenal Insufficiency)
Adrenal suppression due to corticosteroid therapy Haemochromatosis Hyperthyroidism Occult malignancy Anorexia nervosa
Investigations for Addison’s Disease (Primary Adrenal Insufficiency)
1st line:
- SERUM ELECTROLYTES: not routinely required for diagnosis but findings are typical -> low sodium, elevated potassium, elevated calcium
- BLOOD UREA: may be elevated
- FBC: anaemia, eosinophilia
- MORNING SERUM CORTISOL: blood should be drawn between 8am and 9am when cortisol levels leak -> of <83 nanomols/ L
- ACTH STIMULATION TEST: should be ordered when morning serum cortisol does not confirm or exclude adrenal insufficiency -> serum cortisol <497 nanomols/L
- ADRENAL CRISIS- GLUCOCORTICOID AND SUPPORTIVE THERAPY: hydrocortisone sodium succinct IV
- ONGOING- GLUCOCORTICOID PLUS MINERALCORTICOID: cortisone or hydrocortisone or prednisone + fludrocortisone
With use of orenusolone it avoids the peaks and troughs which may occur with hydrocortisone
Prognosis for Addison’s Disease (Primary Adrenal Insufficiency)
Patients should receive treatments for life
Complications of Addison’s Disease (Primary Adrenal Insufficiency)
Secondary Cushing’s syndrome
Osteopenia/ osteoporosis
Treatment related hypertension
Parathyroid adenoma definition
- Benign tumour on one your parathyroid glands
- These are 4 very small glans located near or at the back of your thyroid gland
- Generally causes hyperparathyroidism
How common is parathyroid adenoma
1% incidence rate
Who does parathyroid adenoma affect
Prevalence is highest among post menopa women, with 1:500 possible being affected
Causes of parathyroid adenoma
Associated with the overexpression of cyclic D1 gene and MEN syndromes
Risk factors for parathyroid adenoma
MEN gene
Cyclin D1 gene
Symptoms of parathyroid adenoma
- Bone fractures
- Urinary calculi
- Mental changes: depression, lethargy or confusion
- Nausea
- Vomiting
- Pain in your muscles or abdomen
Signs of parathyroid adenoma
- Polyuria, polydipsia and nocturia are also common symptoms
- More than half of patients report no specific symptoms and accept it as getting older
- Hypercalcaemic crisis can occur in patients with PHPT exposed to severe dehydration (diarrhoea, vomiting)
- In severe cases, patients can present in a coma
Differential diagnosis of parathyroid adenoma
Monogenic diabetes: maturity onset diabetes of the young
Neonatal diabetes
Latent autoimmune diabetes in adults (LADA)
Type 2 diabetes
Investigations for parathyroid adenoma
1st line
- SERUM CALCIUM: increased corrected SC is highly suggestive if unexplained but not diagnostic
- SERUM PTH: increased PTH in the presence of hypercalcaemia confirms the diagnosis (e.g. bone mets. (Breast renal, thyroid carcinoma) have a low PTH concs )
- USS: high resolution may identify tumours
- SESTAMIBI (Radioisotope): scanning used to localise adenomas and is accurate in 50% of cases
Management for parathyroid adenomas
• 1st LINE:
- PARATHYROIDECTOMY: if tumour location is known
- IF UNKNOWN: bilateral neck exploration and removing the enlarged ones has been standard tx
Prognosis and complications for parathyroid adenomas
Surgery cures 95% of patients
Complications include paralysis of the voice box, permanent low calcium levels in the blood
Primary hyperparathyroidism definition
- PHPT is an endocrine disorder in which autonomous overproduction of PTH results in derangement of calcium metabolism
- In approx. 80% of cases, over-production of PTH is due to a single parathyroid adenoma
How common is Primary hyperparathyroidism
• 1 in 500 women and 1 in 2000 men aged over 40
Affects post menopausal women
What causes Primary hyperparathyroidism
- Low serum calcium ordinarily stimulates PTH secretion, whereas high calcium levels suppress PTH secretion
- In PHPT, PTH secretion is not suppressed (as would typically be expected) by high calcium levels
- Excessive PTH leads to over-stimulation of bone resorption, with cortical bone affected more than cancellous bone
- PTH also stimulates the kidneys to reabsorb calcium and to convert 25-hydroxyvitamin D3 to its more active form of 1,25-dihydroxyvitamin D3
- This active vit d is responsible for GI absorption of calcium
- Over-stimulation of PTH receptors, specifically type-2 PTH receptors is thought to play a role in the subjective neurocognitive and affective symptoms
- Hypercalcuria may also lead to nephrolithiasis
Risk factors for Primary hyperparathyroidism
Female Over 59 Treatment MEN 1,2A or 4 Hyperparathyroidism- jaw tumour syndrome Hx of head and neck irradiation
Symptoms for primary hyperparathyroidism
- Hx of osteoporosis or osteopenia
- Fx of PHPT
- Nephrolithiasis
- Bone pain
- Fatigue, anxiety, depression, memory loss
- Bones: Aches/pains localised in larger joints
- Stones: Calcium based renal stones
- Moans: Psychological/psychiatric symptoms (lethargy, depressed mood)
- Groans: Non-specific GI symptoms (abdominal pain, constipation)
DDx of primary hyperparathyroidism
- Familial hypocalciuric hypercalaemia
- Humoral hypercalcaemia of malignancy
- Multiple myeloma
- Milk-alkali syndrome
- Sarcoidosis
- Hypervitaminosis D
Investigations for primary hyperparathyroidism
1st line:
- SERUM CALCIUM: from high-normal to raised
- SERUM INTACT PTH WITH IMMUNORADIOMETRIC OR IMMUNOCHEMICAL ASSAY: from high-normal to elevated
- PARATHYROIDECTOMY: if asymptomatic with surgical indications or symptomatic inc. over 50, inability to ensure appropriate follow-up, serum calcium >0.25 abover normal reage, creatinine clearance <60, T-score<2.5 at lumbar spine, total hip, femoral neck or distal third of radius
- If asymptomatic with no surgical indications: monitor (1st), parathyroidectomy when indicated (2nd line)
Prognosis for primary hyperparathyroidism
• Parathyroidectomy has a cure rate of over 95%
Complications for primary hyperparathyroidism
Osteoporosis
Bone fractures
Nephrolithiasis
Pneumothorax and/ or hypocalcaemia following surgery, neck haematoma following surgery
Secondary hyperparathyroidism definition
Manifestation of abnormalities of calcium, phosphorus, PTH or vit D metabolism, abnormalities in bone turnover, mineralisation, volume, linear growth or strength, vascular or other soft tissue calcification
How common is secondary hyperparathyroidism
• Most commonly associated with CKD or vit d deficiency (which may arise from malabsorption syndromes or chronic lack of exposure to sunlight)
Commonly affects Caucasians
Causes of secondary hyperparathyroidism
- Any disorder that results in hypocalcaemia will elevated PTH levels and can serve as a cause of secondary hyperparathyroidism
- 3 principal aetiologies that may lead to this situation are CKD, malabsorption syndromes or chronic inadequate exposure to sunglight
- CKD: there is loss of 1-alpha-hydroxylase in the kidney, which results in a decreased conversion of 25-hydroxyvitamin D to the active 1,25-dihydroxyvitamin D, this then causes hyperphosphataemia and hypocalcaemia with a consequent rise in PTH
- in conditions such as Crohn’s disease, coeliac disease, chronic pancreatitis or Whipple’s disease or following gastric bypass surgery there is fat malabsorption that contributes to reduced absorption of vit d and dietary calcium ultimately leading to hypocalcaemia and an increase in PTH
- for most people, exposure to sunlight enables them to synthesis 90-95% of the vit d they require
Risk factors for secondary hyperparathyroidism
Ageing
Chronic renal failure
Bit D deficiency: inadequate sunlight exposure or malabsorption
Nutritional deficiency ( especially absence of dairy products and fish)
Symptoms of secondary hyperparathyroidism
Presence of risk factors
Features of chronic renal failure
Features of underlying malabsorption syndrome
Muscle cramps and bone pain
Signs of secondary hyperparathyroidism
- Chvostek’s sign: tapping on the face ant to the ear and seeing a twitching of muscles around the mouth
- Trousseau’s sign: inflating blood-pressure cuff above diastolic for about 3 minutes causes muscular flexion of the wrist, hyperextension of the fingers and flexion of the thumb
Differential for secondary hyperparathyroidism
Primary hyperparathyroidism
Investigations for secondary hyperparathyroidism
• 1st LINE:
- SERUM CALCIUM: first line for diagnosis <2.1 mmol/L
- SERUM INTACT PTH: first line and definitive test >88 nanograms/L
- SERUM CREATININE
- SERUM UREA NITROGEN
Management for secondary hyperparathyroidism
• 1st LINE:
- LACK OF SUNLIGHT: UV radiation exposure and vit d/calcium supplementation
- MALABSOPRTION-RELATED: optimised management of underlying disease
Prognosis and complications for secondary hyperparathyroidism
Dependant on cause
Complications include osteodystrophy, osteoporosis, uraemia
