Endocrine flashcards
Type 1 Diabetes
RF
Pathology
Symptoms
Investigations
Treatment
When the body has impaired ability to produce insulin due to autoimmune destruction of beta cells leading to hyperglycemia.
RF - Family history, HLA DR3 and DR4, Environmental infection (e.g. viral). (most common in 10-14 years and more common in europe)
PATHOLOGY
Autoimmune destruction of pancreatic beta cells –> leads to absolute insulin deficiency
- Hyperglycemia
- Low cellular glucose (less intake by muscles and adipose)
- Increased counter regulatory hormones –> leading to increased gluconeogenesis and glycogenolysis
SYMPTOMS
- Weight loss (lean patient)
- Polyuria
- Polydipsia
- Glycosuria
- Nocturia
Investigations
- Fasting plasma glucose - >7
- Random plasma glucose - >11.1
- Oral glucose tolerance test - > 11
- HbA1C - > 48 mmol/L or >6.5% (pre diabetes >42mmol/mol)
TREATMENT
Basal bolus insulin
Diabetic Ketoacidosis
RF
Pathology
Symptoms
Investigations
Treatment
Main complication of type 1 diabetes (due to poor management). Characterised by hyperglycemia, ketonaemia and metabolic acidosis
RF - pancreatitis, inadequate/inappropriate insulin treatment
PATHOLOGY
Absolute insulin deficiency + effect of counter regulatory hormones (increased lipolysis and gluconeogenesis) –> leads to excess free fatty acids being converted to ketone bodies.
Symptoms
DEHYDRATION
Polyuria
Polydipsia
Tachycardia
Delirium
Vomiting
Abdominal pain
Kussmaul’s breath - deep laboured breathing
(Fruity pear drop breath)
Investigations
Serum ketone - elevated
RPG - >11.0
Venous blood gas (metabolic acidosis) - pH <7.3 (or HCO3- <15mmol)
Treatment
1st line
Rehydration with IV fluids FIRST
then insulin infusion
(can give potassium to replenish K+ stores)
(can give glucose to prevent hypoglycemia)
Type 2 diabetes
RF
Pathology
Symptoms
Investigations
Treatment
A progressive disorder characterised by peripheral insulin resistance and partial insulin deficiency (amyloid deposits in the pancreas)
RF - Family history, obesity, hypertension, low physical activity (genetic link in T2DM is stronger than HLA link in T1DM)
PATHOLOGY
There is peripheral insulin resistance due to decreased GLUT 4 expression (on the liver, adipocytes and muscle) + pancreas pathology (removal, pancreatitis, amyloid deposits causing minor destruction)
–> Leads to hyperglycemia with increased insulin demand from a depleted beta cell population
SYMPTOMS
Typically an obese, hypertensive and older patient with:
- Polydipsia
- Polyuria
- Glycosuria
- Acanthosis nigricans –> dark pigmented skin folds due to insulin resistance)
INVESTIGATIONS
- Fasting plasma glucose - >7
- Random plasma glucose - >11.1
- Oral glucose tolerance test - > 11
- HbA1C - > 48 mmol/L or >6.5%
TREATMENT
First line - Lifestyle modifications (diet and exercise)
First line drug treatment
- Metformin
If HbA1C is above agreed threshold,
Other drugs include
- Sulphonylureas e.g. Gliclazide
- DPP4 inhibitors e.g. Gliptins
- SGLT 2 inhibitor e.g. Gliflozin
What are the functions and side effects of the 4 possible drugs for T2DM?
Metformin - (A biguinide)
- Reduces gluconeogenesis and increases glucose uptake by increasing insulin sensitivity
- Side effects of diarrhoea, abd pain, renal disease, heart failure, lactic acidosis
Sulphonylurea (Gliclazide)
- Stimulates insulin release by binding to beta cell receptors
- Side effect of hypoglycemia, hunger, weight gain
DPP4 inhibitors (Sitagliptin)
- DPP4 inhibition blocks incretin degradation which stimulates the release of insulin by beta cells
- GI side effects: Constipation, diarrhoea, vomiting, gastritis
SGLT 2 inhibitors (Empagliflozin)
- Prevents kidney from reabsorbing glucose via Cotransporter
- Side effects include: UTI, nausea, constipation, polyuria
Hyperosmolar hyperglycemic state
RF
Pathology
Symptoms
Investigations
Treatment
Main complication of type 2 diabetes. A state of hyperglycemia, hyperosmolality and volume depletion often precipitated with infection.
PATHOLOGY
- Due to elevations in serum glucose (due to insulin deficiency) and hyperosmolality (water loss leads to concentrated blood) –> there is excessive gluconeogenesis due to increased counter regulatory hormones.
SYMPTOMS
- Dehydration
- Cognitive impairment (disorientation, decreased consciousness, coma)
- Polyuria, polydipsia, glycosuria
INVESTIGATIONS
- Increased serum osmolality
- RPG > 11.1
- Serum ketones will not be elevated (eliminates DKA)
TREATMENT
- Intravenous fluid replacement (saline) FIRST
Followed by intravenous insulin
Hypoglycemia
RF
Pathology
Symptoms
Investigations
Treatment
Abnormally low blood glucose levels that have the potential to cause harm
- Mostly due to side effects of using drugs that treat diabetes.
(Non diabetic cause - liver failure, Addison’s disease)
SYMPTOMS
- Irritability
- Tremor
- Dizziness
- Hunger
- Falls and dislocation
INVESTIGATIONS
Fingerstick measurement of glucose to confirm diagnosis (<3.9mmol/L)
TREATMENT
IV Dextrose
(If no IV access then IM glucagon)
(Sometimes patient is awake and can swallow, they can treat with 15g fast acting carbohydrates e.g. Sweets, sugary soft drinks, jellies)
Examples of Monogenic diabetes
1) Maturity onset diabetes of the young –> Autosomal dominant gene defect altering beta cell function and insulin secretion –> T2DM in young people (<25 years)
2) Maternally inherited diabetes and deafness (MIDD) - mutation in mitochondrial DNA leading to loss of beta cell mass
3) Permanent neonatal diabetes - mutation in Kir 6.2 and SUR 1 subunits.
4) Latent autoimmune diabetes of adults (LADA)
- T1DM beginning in adulthood.
Hyperparathyroidism
RF
Pathology
Symptoms
Investigations
Treatment
Excess parathyroid hormone is secreted from the parathyroid gland
RF - Multiple endocrine neoplasia 1 (MEN 1), female, >50-60 years
PATHOLOGY
Primary (most common) –> Usually a parathyroid adenoma - Parathyroid gland over secreting PTH despite normal serum calcium –> leads to hypercalcemia
(Hyperparathyroidism leading to hypercalcemia)
Secondary –> Occurs due to a physiological response to a decrease in calcium e.g. Vitamin D deficiency, CKD (hypocalcemia leading to hyperparathyroidism)
Tertiary –> After a prolonged period of secondary hyperparathyriodism - In response to chronic PTH secretion, glands become hyperplastic and secrete PTH autonomously (Hyperparathyroidism regardless of high calcium)
SYMPTOMS
Bones, stones, groans, moans
Bones - Painful bones - osteitis fibrosa cystica
Stones - Kidney stones
Groans - Constipation
Moans - Depression, myalgia, anxiety (psychedelic moans)
INVESTIGATIONS
1st line - Serum calcium and PTH
Primary - High PTH, High Calcium, Low phosphate, High ALP
Secondary - High PTH, Low calcium, High phosphate
Tertiary - All high
Dexa scan - for bone density
ECG - Shows a short QT interval in Hypercalcemia
TREATMENT
Primary - Parathyroidectomy (removal of parathyroid adenoma)
If its secondary or tertiary, treat the cause
e.g. Bisphosphonates to prevent bone resorption
Rehydrate to prevent kidney stones
What cancers can lead to hyperparathyroidism?
Squamous cell lung cancer, breast cancer and renal cancer.
They secrete a protein called parathyroid hormone related protein (PTHrP) –> which shares structural similarities with PTH and can mimic its actions in the body
Complication of hyperparathyroidism
Severe hypercalcemia - treat with IV fluids and bisphosphonates
Hypoparathyroidism
RF
Pathology
Symptoms
Investigations
Treatment
Deficiency of parathyroid hormone synthesis or secretion
RF - Thyroid surgery, parathyroid surgery, hypomagnesaemia
PATHOLOGY
Primary
Parathyroid gland failure e.g. DI George syndrome
Secondary
Destruction of parathyroid gland due to surgery, radiation
Vitamin D deficiency
Hypomagnesaemia (required for production and release of PTH)
SYMPTOMS
- Paraesthesia, laryngospasm
(CATs go Numb)
- Convulsions, arrhythmia, tetany, numbness
– Chvostek’s sign (tapping on cheek causes twitching of facial muscle)
– Trousseau’s sign - upon inflating BP cuff above systemic pressure –> Carpopedal spasm (fingers come together)
INVESTIGATION
First - Serum calcium and PTH
Low PTH, Low calcium, High phosphate
ECG - Long QT interval (hypocalcemia)
TREATMENT
1st line - Oral calcium supplements and vitamin D3
Briefly what is pseudoparathyroidism
Body does not respond to PTH due to resistance (mutation in G alpha subunit of the receptor)
Results in short stature and short 4th/5th Metacarpal
Hypercalcemia
RF
Pathology - Main causes
Symptoms
Investigations
Treatment
Mostly caused by Primary hyperparathyroidism or malignancies
(Also caused by excess Vitamin D or calcium supplementation)
SYMPTOMS
- Bones, stones, groans, moans
Bones - Painful bones - osteitis fibrosa cystica
Stones - Kidney stones
Groans - Constipation
Moans - Depression, myalgia, anxiety (psychedelic moans)
INVESTIGATION
1st line - Serum PTH
ECG - Short QT interval
TREATMENT
IV fluids (rehydration) and IV bisphosphonates
- Surgical removal of parathyroid adenoma
2 checks to do when talking blood samples/investigating them.
Ensure that tourniquet is not on for too long (Concentration of electrolytes may be higher due to pooling below the tourniquet)
Ensure that sample is not old and haemolysed
Hypocalcemia
RF
Pathology - Main causes
Symptoms
Investigations
Treatment
Caused by:
- Hypoparathyroidism
- CHRONIC KIDNEY DISEASE
- Hypomagnesaemia
(Vitamin D deficiency)
SYMPTOMS
- Paraesthesia, laryngospasm
(CATs go Numb)
- Convulsions, arrhythmia, tetany, numbness
– Chvostek’s sign (tapping on cheek causes twitching of facial muscle)
– Trousseau’s sign - upon inflating BP cuff above systemic pressure –> Carpopedal spasm (fingers come together)
INVESTIGATIONS
Long QT interval on ECG.
Serum PTH and calcium
*Check for history of neck surgery - may point to parathyroid injury
TREATMENT
- Oral calcium and Adcal (Vit D3) supplements
(Severe - calcium gluconate)
Prolactinoma
RF
Pathology - Main causes
Symptoms
Investigations
Treatment
Hyperprolactinaemia - Benign adenomas which secrete prolactin (50% of pituitary adenomas)
RF - Women, 20-50 years (Child bearing age)
PATHOLOGY
Mainly caused by
- Prolactin secreting adenoma
- Drugs (e.g. Ecstasy)
(Increased Thyrotropin releasing hormone)
(Tumours that inhibit dopamine - by compression of the pituitary stalk, impeding its transport)
SYMPTOMS
- Galactorrhoea
- Amenorrhoea
- Infertility
- Loss of libido
Later presentations when tumour becomes locally invasive can lead to –> Visual disturbances, headaches
INVESTIGATIONS
1st line - Serum prolactin
GS - Pituitary MRI
TREATMENT
1st line - Cabergoline (Dopamine agonist), Bromocriptine
Definitive - Trans-sphenoidal surgical removal of pituitary tumour
Diabetes insipidus
RF
Pathology - Main causes
Symptoms
Investigations
Treatment
Arginine vasopressin deficiency - leading to an inability to concentrate urine.
RF
Central - Pituitary surgery, craniopharyngiomas, traumatic brain injury
Nephrogenic - CKD, LITHIUM THERAPY
PATHOLOGY
Central - REDUCED secretion of ADH
(Neurosurgery, idiopathic, ADH gene mutation, idiopathic)
Nephrogenic - Renal INSENSITIVITY to ADH (Drugs e.g Lithiun, CKD, mutation in ADH receptor)
Results in impairment in renal water reabsorption –> and thus hypotonic urine
SYMPTOMS
- Polyuria
- Polydipsoa
- Nocturia
- DEHYDRATION
- HYPERNATREMIA (can lead to confusion)
INVESTIGATIONS
1st line - Water deprivation (for 8 hours) and desmopressin test (Synthetic ADH)
Central - Urine osmolality is low before test and HIGH after test
Nephrogenic - Urine osmolality is low before and after test.
Measure urine volume - More than 3 litres a day.
Can investigate copeptin (fragment of precursor molecule for vasporessin)
Copeptin Low - Central DI (reduced vasopressin production)
Copeptin high - Nephrogenic DI (means reduced sensitivity is the cause)
TREATMENT
Central - Desmopressin (synthetic ADH)
Nephrogenic - Thiazides + treat underlying cause
Also ensure adequate water intake
Syndrome of inappropriate anti diuretic hormone (SIADH)
RF
Pathology
Symptoms
Investigations
Treatment
Characterised by concentrated urine, hyponatremia and a euvolemic state, caused by an increased ADH release (water retention)
RF - Pulmonary conditions, >50 years old
PATHOLOGY
Inappropriate release of ADH is caused by: SIADH (SCLC, infection, Abscess, Drugs, head trauma)
- Tumours - Small cell lung cancer, prostate)
- Drugs - carbamazapine
- Infections - Pneumonia, TB, meningitis
- Trauma to head
SYMPTOMS
Basically symptoms of HYPONATREMIA
- Nausea and vomiting
- Headache
- Decreased GCS
- Concentrated urine
- Irritability, dizziness, seizure, coma
INVESTIGATIONS
Combination of tests
Low serum sodium and high urine osmolality.
(Euvolemic Hyponatremia)
SHORT SYNACTHEN TEST TO EXCLUDE Adrenal Insufficiency (other cause of hyponatremia)
TREATMENT
1st - Fluid restriction (1L/day) - increases sodium concentration
For chronic cases –> Drugs e.g. Tolvaptan (vasopressin antagonist)
Demeclocycline - diminishes collecting ducts response to ADH (a tetracycline antibiotic)
Treat underlying cause - e.g tumour excision
Complication of SIADH
Central pontine myelinolysis
- Occurs due to overcorrection of treatment of hyponatremia
- It leads to the dehydration of brain tissue and demyelination of white matter
– Confusion, reduced alertness, tremors, slurred speech, weakness in the body
Acromegaly
RF
Pathology
Symptoms
Investigations
Treatment
Excessive secretion of growth hormone
Before epiphyseal fusion - children - Gigantism
After epiphyseal fusion - Adults - Acromegaly
RF - MEN-1
PATHOLOGY
Caused by a functional pituitary adenoma
Pituitary somatotroph adenomas chronically secrete excessive GH which stimulates IGF-1 production
SYMPTOMS
- Acral enlargement - Large hands, feet, headache
- Bitemporal hemianopia
- Sleep apnoea
- Carpal tunnel syndrome
- Arthralgia/backpain
- Large interdental gaps
- Oily, shiny skin
INVESTIGATIONS
1st - Serum IGF-1 - elevated
GS - Oral glucose tolerance test (impaired glucose tolerance)
TREATMENT
1st - Trans-sphenoidal pituitary surgery
Drug treatment:
Somatostatin analogue - Ocreotide
GH antagonist - Pegvisomant
Dopamine agonist - Cabergoline
Which diseases can lead to T2DM?
Acromegaly, Cushing’s syndrome and pheochromocytoma
Cushing’s syndrome
RF
Pathology
Symptoms
Investigations
Treatment
Clinical manifestation of hypercortisolism
RF - Exogenous corticosteroid use, pituitary adenoma, adrenal adenoma
Causes
ACTH independent causes - EXOGENOUS CORTICOSTEROID USE (most common cause)
ACTH dependent causes - Cushing’s disease (most common endogenous cause), ectopic ACTH (SCLC) - paraneoplastic
SYMPTOMS
- Moon face
- Central obesity
- Purple abdominal striae
- Easy bruising skin
- Plethoric complexion
- Muscle weakness
- Amenorrhoea
INVESTIGATIONS
1st line - Serum cortisol
GS- Overnight Dexamethasone suppression test (Dexamethasone given at 12am and readings taken at 8am)
If low dose dexamethasone suppresses cortisol levels - ACTH independent Cushing’s syndrome –> Adrenal cause
If high dose dexamethasone suppresses cortisol - ACTH dependent - Pituitary cause
High dose dexamethasone can suppress cortisol levels in Cushing’s syndrome but not due to adrenal adenoma/ectopic causes)
Plasma ACTH
ACTH low in adrenal adenoma, high in Cushing’s disease
MRI - for pituitary/adrenal adenoma
TREATMENT
Trans-sphenoidal resection of the pituitary gland
Unilateral adrenalectomy
(Also stop steroids)
Which pituitary hormone is released as part of a circadian rhythm?
ACTH (CRH –> ACTH –> Cortisol)
Pheochromocytoma
RF
Pathology
Symptoms
Investigations
Treatment
Adrenal medullary tumour that secretes catecholamines
PATHOLOGY
Some sporadic but can occur due to
- MEN 2a + 2b
- Neurofibromatosis Type 1 (tumours along nerve myelin sheath)
SYMPTOMS
- Hypertension
- Pallor
- Very sweaty
- Tachycardic
- Headache
INVESTIGATIONS
1st line and GS- Serum metanephrine and normetanephrine
CT scan of abdomen and pelvis for tumour
24 hour urinary catecholamines
TREATMENT
1st line - Alpha blocker (phenoxybenzamine) THEN beta blocker (atenolol)
Benign pheochromocytoma - Surgical excision of tumour
CAN LEAD TO HYPERTENSIVE CRISES
Complication of pheochromocytoma
Hypertensive crisis which you treat with phentolamine (reverses vasocontriction resulting from catecholamines)
Conn’s syndrome
RF
Pathology
Symptoms
Investigations
Treatment
Primary hyperaldosteronism - MOST COMMON SECONDARY CAUSE OF HYPERTENSION
PATHOLOGY
2/3 caused by - Adrenal adenoma (Conn’s syndrome
1/3 cause by - bilateral adrenal hyperplasia
Increased aldosterone –> Increased sodium + H2O, decreased potassium
(So, hypertension with hypokalemia)
SYMPTOMS
- Hypertension (that is not fixable with ace-i/bb)
- Hypokalemia - Muscle weakness, paraesthesia
- Polydipsia and polyuria
INVESTIGATIONS
1st line - Aldosterone:renin ratio (high)
(in secondary hyperaldosteronism, both will be elevated so the ratio will be low)
GS - Elevated serum aldosterone that is not suppressed with fludrocortisone
ECG - Hypokalemia - U waves, small/inverted T waves, long PR and QT interval + ST depression.
(Can lead to metabolic alkalosis due to increased aldosterone)
TREATMENT
First line - Oral spironolactone - Aldosterone antagonist (potassium sparing diuretic)
Primary hyperaldosteronism - Unilateral adrenalectomy
Adrenal insufficiency
RF
Pathology
Symptoms
Investigations
Treatment
Disease resulting in mineralocorticoid, glucocorticoid and androgen deficiency.
RF - Female, autoimmune disease, coeliac disease, adrenal haemorrhage
PATHOLOGY
Primary –> Addison’s disease (main cause in the developed world), TB (main cause in the developing world)
ADDISON’S –> Autoimmune mediated destruction of the adrenal cortex (Anti 21 hydroxylase antibodies, anti adrenal cortex antibodies)
Secondary –> Hypopituitarism - inadequate ACTH and lack of stimulation of adrenal glands (tumour, surgery, radiotherapy, trauma)
Tertiary –> Suppression of HPA axis, inadequate CRH release –> due to long term oral steroids
(So consider tertiary adrenal insufficiency in cases of recent steroid use)
SYMPTOMS
- Lethargy
- Weight loss
- Postural hypotension (decreased aldosterone)
- Vitiligo - pigment lost from areas of skin
- Bronze hyperpigmentation (only in Addison’s disease, haemochromatosis)
- Nausea and vomiting
(Symptoms of electrolyte imbalances)
INVESTIGATIONS
1st line and GS - Short synacthen test - test the cortisol producing function of the adrenal glands.
Serology for Anti 21 alpha hydroxylase antibodies (Addison’s disease)
Serum ACTH - elevated in primary, depressed in secondary
TREATMENT
1st line - Hydrocortisone for glucocorticoid deficiency (cortisol)
Fludrocortisone - for mineralocorticoid deficiency (aldosterone)
ENSURE PATIENTS CARRY A STEROID CARD
Doses are doubled during an acute illness, trauma, night shift work
Complication of adrenal insufficiency
(People who don’t follow sick day rules, stress, infection)
Adrenal crisis/Addisonian crisis–> Severe adrenal insufficiency with lack of cortisol
–> V+N, muscle cramps, confusion, renal failure, convulsions
Treat with immediate IV hydrocortisone and IV saline
Hypokalemia
RF
Pathology
Symptoms
Investigations
Treatment
PATHOLOGY
Caused by
- Inadequate potassium intake - anorexia, fasting
- Thiazide/loop diuretics
- GI loss e.g. vomiting, severe diarrhoea
- High levels of aldosterone (Conn’s)
SYMPTOMS
- Hypotonia
- Hyporeflexia
- Muscle weakness
- Constipation
- Arrhythmias (e.g. AF)
INVESTIGATIONS
1st line - Serum potassium - low
ECG - U waves, small/inverted T waves, ST depression, Long PR and QT interval
TREATMENT
- Oral potassium (Potassium chloride)
- Drugs: Spironolactone
Hyperkalemia
RF
Pathology
Symptoms
Investigations
Treatment
The amount in the blood determines the excitability of nerve and muscle cells –> potassium can cause cardiac arrhythmias and can lead to cardiac arrest.
PATHOLOGY
Caused by:
- Acute Kidney Injury
- Drugs - Spironolactone
- Addison’s disease
SYMPTOMS
- Fast irregular pulse (VF risk)
- Muscle weakness (usually decreased in the lower limbs)
- Chest pain
INVESTIGATIONS
1st - Serum potassium - elevated
ECG - (Go, Go tall, Go long, Go wide)
- Small/absent P waves
- Tall Tented T waves
- Prolonged PR interval
- Wide QRS
TREATMENT
If urgent and has heart problems - Calcium gluconate
Non urgent - Insulin and dextrose (glucose)
Hyperthyroidism
RF
Pathology
Symptoms
Investigations
Treatment
Overactive thyroid gland producing excessive thyroid hormone
RF - Females, HLA DR3/4, stress, smoking, amiodarone (releases iodine- increasing thyroid hormone production - it is used to treat arrhythmias)
PATHOLOGY
Main causes
1) Graves disease - Autoimmune condition where TSH receptor antibodies mimic TSH, resulting in OVERPRODUCTION of thyroid hormone
2) Thyroid/pituitary adenoma
3) Leakage of preformed hormone from the thyroid - due to injury, inflammation or trauma
4) Drugs - e.g. Amiodarone, levothyroxine
5) De Quervain’s thyroiditis –> Painful Swollen tender goitre post viral infection (with symptoms of hyperthyroidism) - treated with Aspirin. (Goitre- lump at the front of neck due to swollen thyroid) -
SYMPTOMS
- Heat intolerance
- Weight loss
- Diarrhoea
- Increased appetite - Hyperphagia
- Anxiety
- Gynaecomastia
- Tachycardia
- Insomnia
- Amenorrhea
Signs: Graves is a triad of
- Thyroid eye disease (exophthalmos) -> bulging eyeball
- Pretibial myxodema (dermopathy) - thick scaly skin on anterior inferior legs
- Acropachy - thickening of extremities - Digital clubbing, soft tissue swelling
- Shiny skin
- Diffuse goitre
INVESTIGATIONS
First line - Thyroid function test
- Primary hyperparathyroidism - High T3,T4, low TSH (GRAVES - abnormality of thyroid gland)
- Secondary hyperparathyroidism - High T3,T4, high TSH (abnormality of pituitary gland)
GS - TSH receptor antibodies
Treatment
1st line- Carbimazole (Side effect of sore throat due to AGRANULOCYTOSIS) - decreases uptake of T3,T4 into cells
CONTRAINDICATED IN PREGNANCY
Give PROPYL THIOURACIL instead
(Thionamide) - decreases production of T3,T4 into cells.
- Radioactive iodine
- Last resort - surgery
Complication of hyperthyroidism
Thyroid storm - Thyrotoxic crisis
Result of untreated/under treated hyperthyroidism
Can also be due to infection, stress, surgery
Symptoms of: hypertension, delirium, pyrexia, confusion, shock
Treat with propylthiouracil and potassium iodide
(Tachyarrhythmia is cause of death)
Complication of hypothyroidism
Myxoedema coma - often due to infection
Hypothermia/low temperature, hypotension, unresponsive
Hypothyroidism
RF
Pathology
Symptoms
Investigations
Treatment
Inadequate output of thyroid hormone by thyroid gland
RF - Female, family history of autoimmune thyroiditis, iodine deficiency, traumatic brain injury
PATHOLOGY
Causes
1) Primary - Hashimoto’s thyroiditis (main cause in developed world) - Autoimmune inflammation of the thyroid gland involving anti thyroid peroxidase antibodies and anti thyroglobulin antibodies
2) Iodine deficiency (main cause in developing world + world wide)
3) Postpartum thyroiditis - inflammation of thyroid after giving birth - associated with anti TPO antibodies
4) Secondary hypothyroidism - Hypopituitarism
SYMPTOMS
- Cold intolerance
- Constipation
- Weight gain
- Bradycardia
- Goitre
- Hair loss
- Joint pain
- Difficulty concentrating
- Menorrhagia
INVESTIGATIONS
1st line - Thyroid function test
Hashimoto’s - Low T3,T4, High TSH
Secondary - Low T3,T4 and TSH.
GS - Anti TPO antibodies - elevated
TREATMENT
1st line - Levothyroxine (synthetic T4) - T4 levels must be monitored as often can cause iatrogenic hyperthyroidism
Thyroid cancer
What are the common types of thyroid cancer?
Pathology
Symptoms
Investigations
Treatment
1) 70-80% Papillary
2) 10-20% follicular
3) Anaplastic - Worst prognosis –> metastasises the most
Symptoms
- Thyroid nodules
- Dysphagia
- Enlarged, hard and irregular nodule
(May have hoarse voice)
INVESTIGATIONS
- Fine needle aspiration biopsy – helps determine if mass is benign or malignant
- Thyroid ultrasound
- TFTs
TREATMENT
- Papillary/follicular –> Total thyroidectomy
- Anaplastic
- Mostly palliative care
(Systemic therapy - surgery + chemotherapy)w
Where can Thyroid cancer metastasise to?
Lungs (50%), Bone (30%), Liver (10%), Brain (5%)
