Endo Flashcards
What is T1DM?
Type 1 diabetes is a condition in which the pancreas stops producing adequate insulin. Without insulin, the body’s cells cannot absorb glucose from the blood and use it as fuel. The glucose level in the blood keeps rising, resulting in hyperglycaemia.
Type 1 diabetes is an autoimmune condition.
Risk Factors for T1DM?
Specific genes and a positive family history increase the risk. Viruses (e.g., Coxsackievirus B) may be implicated in triggering the condition.
Patients with type 1 diabetes are more likely to develop:
Autoimmune thyroid disease
Coeliac disease
Primary adrenal insufficiency (Addison’s disease)
Vitiligo
Pernicious anaemia
Presentation of T1DM
About 25 – 50% of new type 1 diabetic children present in diabetic ketoacidosis (DKA).
The remaining paediatric patients present with the classic triad of symptoms of hyperglycaemia:
Polyuria (excessive urine)
Polydipsia (excessive thirst)
Weight loss (through dehydration)
Less typical presentations include secondary enuresis (bedwetting in a previously dry child) and recurrent infections.
Key features of DKA
Hyperglycaemia
Ketoacidosis (metabolic acidosis with raised ketones and low bicarbonate)
Dehydration
Potassium imbalance
Patients with diabetic ketoacidosis may present with:
Polyuria (high urine output)
Polydipsia (excessive thirst)
Nausea and vomiting
Acetone smell to the breath
Dehydration
Weight loss
Hypotension (low blood pressure)
Altered consciousness
They may have signs and symptoms of an underlying trigger, such as an infection.
Dx of DKA
A diagnosis requires all three of:
Hyperglycaemia (e.g., blood glucose above 11 mmol/L)
Ketosis (e.g., blood ketones above 3 mmol/L)
Acidosis (e.g., pH below 7.3)
Children with DKA are at high risk of developing ______ when they start treatment.
cerebral oedema
How does cerebral oedema occur in DKA?
Dehydration and the high blood glucose concentration cause water to move from the intracellular space in the brain to the extracellular space. This causes the brain cells to shrink and become dehydrated.
Correction of dehydration and hyperglycaemia (with fluids and insulin) causes a fall in the extracellular osmolarity and a shift in water from the extracellular space to the intracellular space in the brain cells. This causes the brain to swell and become oedematous, which can lead to brain cell destruction and death.
Neurological observations are monitored very closely (e.g., hourly).
Signs of cerebral oedema during treatment for DKA include:
Headaches
Altered behaviour
Bradycardia
Changes in consciousness
Falling serum sodium level
Managment of cerebral oedema
Management options for cerebral oedema are slowing IV fluids, IV mannitol and IV hypertonic saline. These will be guided by an experienced paediatrician.
Initial management of DKA
IV fluids using 0.9% sodium chloride with added potassium is the initial priority. IV fluids address the dehydration and dilute the glucose and ketones.
Management for dehydrated DKA
Dehydrated patients are given an initial fluid bolus of 10 ml/kg over 30 minutes (without added potassium). The remainder of their fluid deficit is corrected over 48 hours. Giving fluids more rapidly increases the risk of cerebral oedema.
Other management options for DKA
A fixed-rate insulin infusion (typically 0.05-0.1 units/kg/hour) is started 1-2 hours after starting the IV fluids. Insulin allows cells to start using glucose again and switches off the production of ketones.
Other important principles:
Treat underlying triggers (e.g., antibiotics for bacterial infections)
Prevent hypoglycaemia with IV glucose once the blood glucose falls below 14mmol/l
Include potassium in IV fluids (40 mmol/litre) and monitor serum potassium closely
Monitor for signs of cerebral oedema
Monitor glucose, ketones and pH to assess progress and determine when to switch to subcutaneous insulin
Severely unwell DKA child may need….
Nasogastric tube (reduced consciousness and vomiting)
Airway protection (reduced consciousness)
Additional fluid boluses (under expert guidance)
Inotropes (shock)
Key complications of DKA during treatment
Hypoglycaemia (low blood glucose)
Hypokalaemia (low potassium)
Cerebral oedema
Pulmonary oedema
Long term management of T1DM
Monitoring and treatment are relatively complex. Type 1 diabetes is life-long and requires the patient and parents to understand and engage fully. It involves the following components:
Subcutaneous insulin
Monitoring dietary carbohydrate intake
Monitoring blood glucose levels upon waking, at each meal and before bed
Monitoring for and managing short-term and long-term complications
A basal-bolus regime of insulin involves a combination of:
Background long-acting insulin injected once a day
Short-acting insulin injected 30 minutes before consuming carbohydrates (e.g., at meals)
Repeated injections in the same area causes what?
Injecting into the same spot can cause lipodystrophy, where the subcutaneous fat hardens. Areas of lipodystrophy do not absorb insulin properly from further injections. For this reason, patients should cycle their injection sites. If a patient is not responding to insulin as expected, ask where they inject and check for lipodystrophy.
What are Insulin Pumps?
Insulin pumps are small devices that continuously infuse insulin at different rates to control blood sugar levels. They are an alternative to basal-bolus regimes. The pump pushes insulin through a small plastic tube (cannula) inserted under the skin. The cannula is replaced every 2-3 days, and the insertion sites are rotated to prevent lipodystrophy and absorption issues.
What are the advanatges of an Insulin Pump?
The advantages of an insulin pump are better blood glucose control, more eating flexibility, and fewer injections.
What are the disadvantages of an Insulin Pump?
Difficulties learning to use the pump
Having it attached at all times
Blockages in the infusion set
A small risk of infection
Different types of insulin pumps
Tethered pumps are devices with replaceable infusion sets and insulin. They are usually attached to the patient’s belt or around the waist with a tube connecting the pump to the insertion site. The controls for the infusion are on the pump itself.
Patch pumps sit directly on the skin without any visible tubes. When they run out of insulin, the entire patch pump is disposed of, and a new pump is attached. A separate remote usually controls patch pumps.
What is monitored in the long term management of T1DM?
HbA1c measures glycated haemoglobin, which is how much glucose is attached to the haemoglobin molecule. This reflects the average glucose level over the previous 2-3 months (red blood cells have a lifespan of about 4 months).
Capillary blood glucose (finger-prick test) can be measured using a blood glucose monitor, giving an immediate result. Patients use this for self-monitoring their glucose levels.
Continuous glucose monitors use a sensor on the skin that measures the glucose level of the interstitial fluid in the subcutaneous tissue. The sensor records the glucose readings at short intervals and sends these readings to the patient’s phone, giving an excellent record of the glucose levels over time. Sensors need replacing regularly (e.g., every 2 weeks). There are two options:
Continuous glucose monitors send the readings wirelessly
Flash glucose monitors require the patient to swipe their phone across the sensor to collect the readings
Short-term complications relate to immediate insulin and blood glucose management:
Hypoglycaemia (low glucose level)
Hyperglycaemia (and diabetic ketoacidosis)
Hypoglycaemia may be caused by:
Too much insulin
Inadequate carbohydrates for the insulin administered
Not processing the carbohydrates correctly (e.g., in malabsorption, diarrhoea or vomiting)
Symptoms of hypoglycaemia
hunger, tremor, sweating, irritability, dizziness and pallor. More severe hypoglycaemia will lead to reduced consciousness, coma and death unless treated.
Tx of hypoglycaemia
Hypoglycaemia needs to be treated initially with rapid-acting glucose (e.g., a high-sugar-content drink). Once the blood glucose improves, they consume slower-acting carbohydrates (e.g., biscuits or toast) to prevent it from dropping again. Options for treating severe hypoglycaemia are IV dextrose and intramuscular glucagon.
Long term complications of T1DM
Type 1 diabetes can impair growth during childhood.
Chronic hyperglycaemia damages the endothelial cells of blood vessels, leading to leaky, malfunctioning vessels that cannot regenerate. Over time, microvascular and macrovascular complications can develop. Hyperglycaemia causes immune system dysfunction and creates an optimal environment for infectious organisms.
Infection-related complications include:
Urinary tract infections
Pneumonia
Skin and soft tissue infections, particularly in the feet
Fungal infections, particularly oral and vaginal candidiasis
Microvascular T1DM complications
Retinopathy
Kidney disease, particularly glomerulosclerosis
Periodontitis (gum disease)
Peripheral neuropathy
Gastroparesis (delayed gastric emptying)
Macrovascular T1DM complications
Coronary artery disease (a significant cause of death in people with diabetes)
Peripheral ischaemia, causing poor skin healing and diabetic foot ulcers
Stroke
Hypertension
What is T2DM?
Type 2 diabetes is a condition where a combination of insulin resistance and reduced insulin production cause persistently high blood sugar levels.
Risk Factors for T2DM
Non-modifiable risk factors:
Older age
Ethnicity (Black African or Caribbean and South Asian)
Family history
Modifiable risk factors:
Obesity
Sedentary lifestyle
High carbohydrate (particularly sugar) diet
Presentation of T2DM
Tiredness
Polyuria and polydipsia (frequent urination and excessive thirst)
Unintentional weight loss
Opportunistic infections (e.g., oral thrush)
Slow wound healing
Glucose in urine (on a dipstick)
Acanthosis nigricans is characterised by the thickening and darkening of the skin (giving a “velvety” appearance), often at the neck, axilla and groin. It is often associated with insulin resistance.
What is Pre-Diabetes
Pre-diabetes is an indication that the patient is heading towards diabetes. They do not fit the full diagnostic criteria but should be educated about the risk of diabetes and lifestyle changes.
An HbA1c of 42 – 47 mmol/mol indicates pre-diabetes.
The HbA1c is a blood test that reflects the average glucose level over the previous 2-3 months.
Dx of T2DM
An HbA1c of 48 mmol/mol or above indicates type 2 diabetes.
The sample is typically repeated after 1 month to confirm the diagnosis (unless there are symptoms or signs of complications).
Management fof T2DM
The NICE guidelines (updated 2022) recommendations on managing type 2 diabetes include:
A structured education program
Low-glycaemic-index, high-fibre diet
Exercise
Weight loss (if overweight)
Antidiabetic drugs
Monitoring and managing complications
Treatment targets for T2DM
The NICE guidelines (updated 2022) recommend the following HbA1c treatment targets:
48 mmol/mol for new type 2 diabetics
53 mmol/mol for patients requiring more than one antidiabetic medication
The HbA1c is measured every 3 to 6 months until under control and stable.
First line tx for T2DM
First-line is metformin.
Once settled on metformin, add an SGLT-2 inhibitor (e.g., dapagliflozin) if the patient has existing cardiovascular disease or heart failure. NICE suggest considering an SGLT-2 inhibitor in patients with a QRISK score above 10%.
Second line tx for T2DM
Second-line is to add a sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor.
Third line tx for T2DM
Triple therapy with metformin and two of the second-line drugs
Insulin therapy (initiated by the specialist diabetic nurses)
When third line options fail, what is next for T2DM?
Where triple therapy fails, and the patient’s BMI is above 35 kg/m2, there is the option of switching one of the drugs to a GLP-1 mimetic (e.g., liraglutide).
MoA of Metformin
Metformin increases insulin sensitivity and decreases glucose production by the liver. It is a biguanide (the class of medication). It does not cause weight gain (and may cause some weight loss). It does not cause hypoglycaemia.
SE of Metformin
Gastrointestinal symptoms, including pain, nausea and diarrhoea (depending on the dose)
Lactic acidosis (e.g., secondary to acute kidney injury)
Patients with gastrointestinal side effects with standard-release metformin can try modified-release metformin.
Examples of SGLT-2 inhibitors
SGLT-2 inhibitors end with the suffix -gliflozin. Examples are empagliflozin, canagliflozin, dapagliflozin and ertugliflozin.
MoA of SGLT-2 Inhibitors
The sodium-glucose co-transporter 2 protein is found in the proximal tubules of the kidneys. It acts to reabsorb glucose from the urine back into the blood. SGLT-2 inhibitors block the action of this protein, causing more glucose to be excreted in the urine. Loss of glucose in the urine lowers the HbA1c, reduces the blood pressure, leads to weight loss and improves heart failure. They can cause hypoglycaemia when used with insulin or sulfonylureas.
SGLT-2 inhibitors reduce the risk of cardiovascular disease. Empagliflozin and dapagliflozin are also licensed for heart failure. Dapagliflozin is also licensed for chronic kidney disease.
SE of SGLT-2 Inhibitors
Glycosuria (glucose in the urine)
Increased urine output and frequency
Genital and urinary tract infections (e.g., thrush)
Weight loss
Diabetic ketoacidosis, notably with only moderately raised glucose
Lower-limb amputation may be more common in patients on canagliflozin (unclear if this applies to the others)
Fournier’s gangrene (rare but severe infection of the genitals or perineum)
MoA of Pioglitazone
Pioglitazone is a thiazolidinedione. It increases insulin sensitivity and decreases liver production of glucose. It does not typically cause hypoglycaemia.
SE of Pioglitazone
Weight gain
Heart failure
Increased risk of bone fractures
A small increase in the risk of bladder cancer
Example of a Sulfonylurea
Glicazide
MoA of Sulfonylureas
Sulfonylureas stimulate insulin release from the pancreas.
SE of Sulfonylureas
Weight gain
Hypoglycaemia
What are incretins?
Incretins are hormones produced by the gastrointestinal tract. They are secreted in response to large meals and act to reduce blood sugar by:
Increasing insulin secretion
Inhibiting glucagon production
Slowing absorption by the gastrointestinal tract
What is the main incretin + what are they inhibited by?
The main incretin is glucagon-like peptide-1 (GLP-1). Incretins are inhibited by an enzyme called dipeptidyl peptidase-4 (DPP-4).
MoA of DPP-4 inhibitors
DPP-4 inhibitors block the action of DPP-4, allowing increased incretin activity
Examples of DPP-4 inhibitors
sitagliptin and alogliptin
SE of DPP-2 inhibitors
do not cause hypoglycaemia.
Notable side effects of DPP-4 inhibitors:
Headaches
Low risk of acute pancreatitis
What are GLP-1 mimetics?
GLP-1 mimetics imitate the action of GLP-1. They are given as subcutaneous injections. Liraglutide can also be used for weight loss in non-diabetic obese patients.
Examples of GLP-1 mimetics?
Examples are exenatide and liraglutide.
SE of GLP-1 mimetics
Reduced appetite
Weight loss
Gastrointestinal symptoms, including discomfort, nausea and diarrhoea
How long does it take for Rapid-Acting Insulins to work and last? (give an example too)
Rapid-acting insulins (e.g., NovoRapid) start working after around 10 minutes and last about 4 hours.
How long does it take for Short-Acting Insulins to work and last? (give an example too)
Short-acting insulins (e.g., Actrapid) start working in around 30 minutes and last about 8 hours.
How long does it take for Intermediate-Acting Insulins to work and last? (give an example too)
Intermediate-acting insulins (e.g., Humulin I) start working in around 1 hour and last about 16 hours.
How long does it take for Long-Acting Insulins to work and last? (give an example too)
Long-acting insulins (e.g., Levemir and Lantus) start working in around 1 hour and last about 24 hours or longer.
What are combination insulins?
Combinations insulins contain a rapid-acting and intermediate-acting insulin. In brackets is the ratio of rapid-acting to intermediate-acting insulin:
Humalog 25 (25:75)
Humalog 50 (50:50)
Novomix 30 (30:70)
Key complications of type 2 diabetes are:
Infections (e.g., periodontitis, thrush and infected ulcers)
Diabetic retinopathy
Peripheral neuropathy
Autonomic neuropathy
Chronic kidney disease
Diabetic foot
Gastroparesis (slow emptying of the stomach)
Hyperosmolar hyperglycemic state
What is HHS?
Hyperosmolar hyperglycemic state (HHS) is a rare but potentially fatal complication of type 2 diabetes. It is characterised by hyperosmolality (water loss leads to very concentrated blood), high sugar levels (hyperglycaemia) and the absence of ketones, distinguishing it from ketoacidosis.
It presents with polyuria, polydipsia, weight loss, dehydration, tachycardia, hypotension and confusion.
It is a medical emergency with high mortality. Involve experienced seniors early. Treatment is with IV fluids and careful monitoring.
What is hypothyroidism ?
Hypothyroidism refers to insufficient thyroid hormones, triiodothyronine (T3) and thyroxine (T4).
What is Primary hypothyroidism?
Primary hypothyroidism is where the thyroid behaves abnormally and produces inadequate thyroid hormones. Negative feedback is absent, resulting in increased production of TSH. TSH is raised, and T3 and T4 are low.
What is Secondary hypothyroidism?
Secondary hypothyroidism, also called central hypothyroidism, is where the pituitary behaves abnormally and produces inadequate TSH, resulting in under-stimulation of the thyroid gland and insufficient thyroid hormones. TSH, T3 and T4 will all be low.
Causes of Primary hypothyroidism
Hashimoto’s thyroiditis is the most common cause of hypothyroidism in the developed world. It is an autoimmune condition causing inflammation of the thyroid gland. It is associated with anti-thyroid peroxidase (anti-TPO) antibodies and anti-thyroglobulin (anti-Tg) antibodies.
Iodine deficiency is the most common cause of hypothyroidism in the developing world. In the UK, iodine is particularly found in dairy products and may be added to non-dairy milk alternatives (e.g., soya milk).
Which medications (used to treat hyperthyroidism) can cause hypothyroidism?
Carbimazole
Propylthiouracil
Radioactive iodine
Thyroid surgery
What is Lithium and how does it impact hypothyroidism?
Lithium inhibits the production of thyroid hormones in the thyroid gland and can cause a goitre and hypothyroidism.
What is Amiodarone and how does it impact hypothyroidism?
Amiodarone interferes with thyroid hormone production and metabolism, usually causing hypothyroidism but can also cause thyrotoxicosis.
Cause of Secondary hypothyroidism?
Secondary hypothyroidism is often associated with a lack of other pituitary hormones, such as ACTH, referred to as hypopituitarism. This is rarer than primary hypothyroidism, and may be caused by:
Tumours (e.g., pituitary adenomas)
Surgery to the pituitary
Radiotherapy
Sheehan’s syndrome (where major post-partum haemorrhage causes avascular necrosis of the pituitary gland)
Trauma
Presentation of hypothyroidism
Weight gain
Fatigue
Dry skin
Coarse hair and hair loss
Fluid retention (including oedema, pleural effusions and ascites)
Heavy or irregular periods
Constipation
Which conditions cause a goitre in hypothyroidism?
Iodine deficiency causes a goitre.
Hashimoto’s thyroiditis can initially cause a goitre, after which there is atrophy (wasting) of the thyroid gland.
Management of hypothyroidism
Oral levothyroxine is the mainstay of treatment of hypothyroidism. Levothyroxine is a synthetic version of T4 and metabolises to T3 in the body.
The dose is titrated based on the TSH level, initially every 4 weeks. Liothyronine sodium is a synthetic version of T3 and is very rarely used under specialist care where levothyroxine is not tolerated.
Most common cause of hypothyroidism in developed countries?
Hashimoto’s thyroiditis
Complications of hypothyroidism
Myxoedema coma: altered mental state, hypothermia, bradycardia, hypoventilation; treated with thyroid replacement, glucocorticoids, supportive measures.
Cardiac complications: heart disease (coronary artery disease, heart failure, atherosclerosis) due to elevated serum cholesterol.
Reproductive complications: sub-fertility, increased risk of miscarriage, stillbirth, pre-eclampsia, postpartum haemorrhage.
What is the most common cause of hypothyroidism worldwide/ developing world?
Iodine deficiency.
What is the most common cause of hypothyroidism in UK?
Hashimotos
Autoantibody testing in hypothyroidism
Testing for autoantibodies such as anti-thyroid peroxidase (anti-TPO) can aid the identification of autoimmune thyroid conditions. TPO antibodies are found in 90% of people with Hashimoto’s thyroiditis. However, they may also be present in Grave’s thyrotoxicosis.
What is Hyperthyroidism ?
Hyperthyroidism is where there is over-production of the thyroid hormones, triiodothyronine (T3) and thyroxine (T4), by the thyroid gland.
What is thyrotoxicosis?
Thyrotoxicosis refers to the effects of an abnormal and excessive quantity of thyroid hormones in the body.
What is primary Hyperthyroidism ?
Primary hyperthyroidism is due to thyroid pathology. The thyroid is behaving abnormally and producing excessive thyroid hormone.
What is secondary Hyperthyroidism ?
Secondary hyperthyroidism is due to pathology in the hypothalamus or pituitary. The pituitary gland produces too much thyroid-stimulating hormone, stimulating the thyroid gland to produce excessive thyroid hormones.
What is subclinical Hyperthyroidism ?
Subclinical hyperthyroidism is where the thyroid hormones (T3 and T4) are normal and thyroid-stimulating hormone (TSH) is suppressed (low). There may be absent or mild symptoms.
What is Grave’s disease?
Graves’ disease is an autoimmune condition where TSH receptor antibodies cause primary hyperthyroidism. These TSH receptor antibodies, produced by the immune system, stimulate TSH receptors on the thyroid. This is the most common cause of hyperthyroidism.
What is a toxic multinodular goitre?
Toxic multinodular goitre (also known as Plummer’s disease) is a condition where nodules develop on the thyroid gland, which are unregulated by the thyroid axis and continuously produce excessive thyroid hormones. It is most common in patients over 50 years.
What is exophthalmos?
Exophthalmos (also known as proptosis) describes the bulging of the eyes caused by Graves’ disease. Inflammation, swelling and hypertrophy of the tissue behind the eyeballs force them forward, causing them to bulge out of the sockets.
What is pretibial myxoedema?
Pretibial myxoedema is a skin condition caused by deposits of glycosaminoglycans under the skin on the anterior aspect of the leg (the pre-tibial area). It gives the skin a discoloured, waxy, oedematous appearance over this area. It is specific to Grave’s disease and is a reaction to TSH receptor antibodies.
Causes of Hyperthyroidism
G – Graves’ disease
I – Inflammation (thyroiditis)
S – Solitary toxic thyroid nodule
T – Toxic multinodular goitre
Causes of thyroiditis?
Thyroiditis (thyroid gland inflammation) often causes an initial period of hyperthyroidism, followed by under-activity of the thyroid gland (hypothyroidism). The causes of thyroiditis include:
De Quervain’s thyroiditis
Hashimoto’s thyroiditis
Postpartum thyroiditis
Drug-induced thyroiditis
Presentation of Hyperthyroidism
Anxiety and irritability
Sweating and heat intolerance
Tachycardia
Weight loss
Fatigue
Insomnia
Frequent loose stools
Sexual dysfunction
Brisk reflexes on examination
Specific features of Grave’s disease
Diffuse goitre (without nodules)
Graves’ eye disease, including exophthalmos
Pretibial myxoedema
Thyroid acropachy (hand swelling and finger clubbing)
What is a solitary toxic thyroid nodule?
A solitary toxic thyroid nodule is where a single abnormal thyroid nodule acts alone to release excessive thyroid hormone. The nodules are usually benign adenomas. Treatment involves surgical removal of the nodule.
What is De Quervain’s Thyroiditis?
De Quervain’s thyroiditis, also known as subacute thyroiditis, is a condition causing temporary inflammation of the thyroid gland.
3 phases of De Quervain’s Thyroiditis
Thyrotoxicosis
Hypothyroidism
Return to normal
Initial thyrotoxic phase of De Quervain’s Thyroiditis
Excessive thyroid hormones
Thyroid swelling and tenderness
Flu-like illness (fever, aches and fatigue)
Raised inflammatory markers (CRP and ESR)
Tx for De Quervain’s Thyroiditis
It is a self-limiting condition, and supportive treatment is usually all that is necessary. This may involve:
NSAIDs for symptoms of pain and inflammation
Beta blockers for the symptoms of hyperthyroidism
Levothyroxine for the symptoms of hypothyroidism
Prognosis of De Quervain’s Thyroiditis
A small number (under 10%) remain hypothyroid long-term.
Thyroid storm
Thyroid storm is a rare presentation of hyperthyroidism. It is also known as thyrotoxic crisis. It is a rare and more severe presentation of hyperthyroidism with fever, tachycardia and delirium. It can be life-threatening and requires admission for monitoring. It is treated the same way as any other presentation of thyrotoxicosis, although they may need additional supportive care with fluid resuscitation, anti-arrhythmic medication and beta blockers.
Management of hyperthyroidism
Carbimazole
Propylthiouracil
Radioactive iodine
Beta blockers
Carbimazole : how long is it taken for? + what after?
usually taken for 12 to 18 months. Once the patient has normal thyroid hormone levels (usually within 4-8 weeks), usually taken for 12 to 18 months. Once the patient has normal thyroid hormone levels (usually within 4-8 weeks), they continue on maintenance carbimazole and either:
The carbimazole dose is titrated to maintain normal levels (known as titration-block)
A higher dose blocks all production, and levothyroxine is added and titrated to effect (known as block and replace)
Risk associated with Carbimazole
acute pancreatitis
2nd line tx for hyperthyroidism
Propylthiouracil is the second-line anti-thyroid drug. It is used in a similar way to carbimazole.
Risks associated with Propylthiouracil
There is a small risk of severe liver reactions, including death, which is why carbimazole is preferred.
Both carbimazole and propylthiouracil can cause ___
Both carbimazole and propylthiouracil can cause agranulocytosis, with a dangerously low white blood cell counts. Agranulocytosis makes patients vulnerable to severe infections. A sore throat is a key presenting feature of agranulocytosis. In your exams, if you see a patient with a sore throat on carbimazole or propylthiouracil, the cause is likely agranulocytosis. They need an urgent full blood count and aggressive treatment of any infections.
Radioactive iodine use
Radioactive iodine treatment involves drinking a single dose of radioactive iodine. The thyroid gland takes this up, and the emitted radiation destroys a proportion of the thyroid cells. The reduction in the number of cells results in a decrease in thyroid hormone production. Remission can take 6 months, after which the thyroid is often underactive, requiring long-term levothyroxine.
Strict rules for tx with radioactive iodine
Women must not be pregnant or breastfeeding and must not get pregnant within 6 months of treatment
Men must not father children within 4 months of treatment
Limit contact with people after the dose, particularly children and pregnant women
Beta blockers for hyperthyroidism
Beta blockers are used to block the adrenalin-related symptoms of hyperthyroidism. Propranolol is the usual choice, as it non-selectively blocks adrenergic activity (as opposed to something like bisoprolol, which is more selective). Beta blockers do not treat the underlying problem but control the symptoms, while definitive treatment takes time. They are particularly useful in patients with thyroid storm.
Definitive tx for hyperthyroidism
Surgery is a definitive option. Removing the whole thyroid gland (thyroidectomy), or the toxic nodules, effectively stops the excess thyroid hormone production. Patients will be hypothyroid after a thyroidectomy, requiring life-long levothyroxine.
