Endocrinology Flashcards
What are the causes of primary hyperparathyroidism?
Causes of primary hyperparathyroidism:
80%: solitary adenoma
15%: hyperplasia
4%: multiple adenoma
1%: carcinoma
Symptoms of primary hyperparathyroidism?
“Stones, Bones, Abdominal groans, Thrones and Psychiatric moans”.
- polydipsia, polyuria
- peptic ulceration/constipation/pancreatitis
- bone pain/fracture
- renal stones
- depression
- hypertension
What are the lab results in primary hyperparathyroidism?
- Raised calcium
- Low phosphate
- PTH raised or normal (inappropriately, given the raised calcium)
pepperpot skull is a characteristic X-ray finding of hyperparathyroidism
What is the first line investigation for Acromegaly?
Serum insulin-like growth factor (IGF-1) levels are now the first-line test for acromegaly.
The OGTT test is recommended to confirm the diagnosis if IGF-1 levels are raised.
- in normal patients GH is suppressed to < 2 mu/L with hyperglycaemia
- in acromegaly there is no suppression of GH
- may also demonstrate impaired glucose tolerance which is associated with acromegaly
A pituitary MRI may demonstrate a pituitary tumour!
Low TSH, high free T4?
Thyrotoxicosis (e.g. Graves’ disease)
Low TSH, Low free T4?
Secondary hypothyroidism
- Replacement steroid therapy is required prior to thyroxine
High TSH, Low free T4?
Primary hypothyroidism (primary atrophic hypothyroidism)
High TSH, Normal free T4?
Subclinical hypothyroidism
OR
Poor compliance with thyroxine
What causes T1DM?
Autoimmune disorder where the insulin-producing beta cells of the islets of Langerhans in the pancreas are destroyed by the immune system.
This results in an absolute deficiency of insulin resulting in raised glucose levels.
Patients tend to develop T1DM in childhood/early adult life and typically present unwell, possibly in diabetic ketoacidosis.
Signs and symptoms of diabetes?
T1DM
- Weight loss
- Polydipsia
- Polyuria
- May present with diabetic ketoacidosis
- abdominal pain
- vomiting
- reduced consciousness level
T2DM
Often picked up incidentally on routine blood tests.
- Polydipsia
- Polyuria
Remember that the polyuria and polydipsia are due to water being ‘dragged’ out of the body due to the osmotic effects of excess blood glucose being excreted in the urine (glycosuria).
Microvascular and macrovascular complications of diabetes?
Micro:
-Retinopathy
- Neuropathy
- Nephropathy
Macro:
- Ischaemic heart disease
- Stroke
Which drugs are given to manage diabetic neuropathy?
Diabetes typically leads to sensory loss and not motor loss in peripheral neuropathy. Painful diabetic neuropathy is a common problem in clinical practice.
Diabetic neuropathy is now managed in the same way as other forms of neuropathic pain:
- First-line treatment: Amitriptyline, Duloxetine, Gabapentin or Pregabalin
- if the first-line drug treatment does not work try one of the other 3 drugs
- tramadol may be used as ‘rescue therapy’ for exacerbations of neuropathic pain
- topical capsaicin may be used for localised neuropathic pain (e.g. post-herpetic neuralgia)
- pain management clinics may be useful in patients with resistant problems
What are the features of Subacute (De Quervain’s) thyroiditis?
Subacute thyroiditis (also known as De Quervain’s thyroiditis) is thought to occur following viral infection and typically presents with hyperthyroidism.
There are typically 4 phases;
phase 1 (lasts 3-6 weeks): HYPERTHYROIDISM, PAINFUL GOITRE, RAISED ESR
phase 2 (1-3 weeks): euthyroid
phase 3 (weeks - months): HYPOTHYROIDISM
phase 4: thyroid structure and function goes back to normal
Ix: thyroid scintigraphy: globally reduced uptake of iodine-131
Mx: usually self-limiting - most patients do not require treatment. Thyroid pain may respond to aspirin or other NSAIDs. In more severe cases steroids are used, particularly if hypothyroidism develops
Dietary advice for T2DM?
Dietary advice:
- encourage high fibre, low glycaemic index sources of carbohydrates
- include low-fat dairy products and oily fish
- control the intake of foods containing saturated fats and trans fatty acids
- limited substitution of sucrose-containing foods for other carbohydrates is allowable, but care should be taken to avoid excess energy intake
- discourage use of foods marketed specifically at people with diabetes
- initial target weight loss in an overweight person is 5-10%
Drug treatment for T2DM?
Tolerates metformin:
Metformin is still first-line and should be offered if the HbA1c rises to 48 mmol/mol (6.5%)* on lifestyle interventions.
if the HbA1c has risen to 58 mmol/mol (7.5%) then a second drug should be added from the following list:
- sulfonylurea
- gliptin
- pioglitazone
- SGLT-2 inhibitor
if despite this the HbA1c rises to, or remains above 58 mmol/mol (7.5%) then triple therapy with one of the following combinations should be offered:
metformin + gliptin + sulfonylurea
metformin + pioglitazone + sulfonylurea
metformin + sulfonylurea + SGLT-2 inhibitor
metformin + pioglitazone + SGLT-2 inhibitor
OR insulin therapy should be considered
Criteria for glucagon-like peptide1 (GLP1) mimetic (e.g. exenatide):
- if triple therapy is not effective, not tolerated or contraindicated then NICE advise that we consider combination therapy with metformin, a sulfonylurea and a glucagonlike peptide1 (GLP1) mimetic if:
- BMI >= 35 kg/m² and specific psychological or other medical problems associated with obesity OR
- BMI < 35 kg/m² and for whom insulin therapy would have significant occupational implications OR
weight loss would benefit other significant obesity related comorbidities
- only continue if there is a reduction of at least 11 mmol/mol [1.0%] in HbA1c and a weight loss of at least 3% of initial body weight in 6 months
Starting insulin
- metformin should be continued. In terms of other drugs NICE advice: ‘Review the continued need for other blood glucose lowering therapies’
- NICE recommend starting with human NPH insulin (isophane, intermediate acting) taken at bed-time or twice daily according to need
EXAMPLES:
- you review an established type 2 diabetic on maximum dose metformin. Her HbA1c is 55 mmol/mol (7.2%). You do not add another drug as she has not reached the threshold of 58 mmol/mol (7.5%)
- a type 2 diabetic is found to have a HbA1c of 62 mmol/mol (7.8%) at annual review. They are currently on maximum dose metformin. You elect to add a sulfonylurea
Drug therapy for T2DM who are unable to tolerate metformin?
Cannot tolerate metformin or contraindicated:
if the HbA1c rises to 48 mmol/mol (6.5%)* on lifestyle interventions, consider one of the following:
- sulfonylurea
- gliptin
- pioglitazone
if the HbA1c has risen to 58 mmol/mol (7.5%) then a one of the following combinations should be used:
- gliptin + pioglitazone
- gliptin + sulfonylurea
- pioglitazone + sulfonylurea
if despite this the HbA1c rises to, or remains above 58 mmol/mol (7.5%) then consider insulin therapy
How is diabetes diagnosed?
The diagnosis of type 2 diabetes mellitus can be made by either a plasma glucose or a HbA1c sample. Diagnostic criteria vary according to whether the patient is symptomatic (polyuria, polydipsia etc) or not.
If the patient is symptomatic:
- fasting glucose greater than or equal to 7.0 mmol/l
- random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)
If the patient is asymptomatic the above criteria apply but must be demonstrated on TWO SEPARATE ocassions
In 2011 WHO released supplementary guidance on the use of HbA1c on the diagnosis of diabetes:
- a HbA1c of greater than or equal to 48 mmol/mol (6.5%) is diagnostic of diabetes mellitus!
- a HbAlc value of less than 48 mmol/mol (6.5%) does not exclude diabetes (i.e. it is not as sensitive as fasting samples for detecting diabetes)
- in patients without symptoms, the test must be repeated to confirm the diagnosis. it should be remembered that misleading HbA1c results can be caused by increased red cell turnover (haemoglobinopathies, CKD, IDA..)
Impaired fasting glucose and impaired glucose tolerance:
- A fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l implies impaired fasting glucose (IFG)
- Impaired glucose tolerance (IGT) is defined as fasting plasma glucose less than 7.0 mmol/l and OGTT 2-hour value greater than or equal to 7.8 mmol/l but less than 11.1 mmol/l
Diabetes UK suggests:
‘People with IFG should then be offered an oral glucose tolerance test to rule out a diagnosis of diabetes. A result below 11.1 mmol/l but above 7.8 mmol/l indicates that the person doesn’t have diabetes but does have IGT.’
Causes of diabetic foot disease?
It occurs secondary to two main factors:
- neuropathy: resulting in loss of protective sensation (e.g. not noticing a stone in the shoe), Charcot’s arthropathy, dry skin
- peripheral arterial disease: diabetes is a risk factor for both macro and microvascular ischaemia
Signs and symptoms of diabetic foot disease?
- Neuropathy: loss of sensation
- Ischaemia: absent foot pulses, reduced ankle-brachial pressure index (ABPI), intermittent claudication
- Complications: calluses, ulceration, Charcot’s arthropathy, cellulitis, osteomyelitis, gangrene
Signs and symptoms of diabetic foot disease? Screening?
- Neuropathy: loss of sensation
- Ischaemia: absent foot pulses, reduced ankle-brachial pressure index (ABPI), intermittent claudication
- Complications: calluses, ulceration, Charcot’s arthropathy, cellulitis, osteomyelitis, gangrene
All patients with diabetes should be screened for diabetic foot disease on at least an annual basis:
- screening for ischaemia: done by palpating for both the dorsalis pedis pulse and posterial tibial artery pulse
- screening for neuropathy: a 10 g monofilament is used on various parts of the sole of the foot
Management: All patients who are moderate or high risk (I.e. any problems other than simple calluses) should be followed up regularly by the local diabetic foot centre. See notes for low, moderate and high risk patients diabetic foot disease.
What is the antibody found in Hashimoto’s thyroiditis?
Anti-thyroid peroxidase (TPO) antibodies.
Hashimoto’s thyroiditis (chronic autoimmune thyroiditis) is an autoimmune disorder of the thyroid gland. It is typically associated with hypothyroidism although there may be a transient thyrotoxicosis in the acute phase. It is 10 times more common in women.
features of hypothyroidism:
- Goitre: firm, non-tender
- Anti-thyroid peroxidase (TPO) (not that specific, can be found in Grave’s disease as well as healthy individuals)
- also anti-thyroglobulin (Tg) antibodies
- Associated with other autoimmune conditions e.g. coeliac disease, type 1 diabetes mellitus, vitiligo.
Hashimoto’s thyroiditis is associated with the development of MALT lymphoma
Which kind of thyroid problems have goitre?
Goitre is a non-specific indicator of thyroid dysfunction, being found in hypothyroid, euthyroid and hyperthyroid conditions.
What is the commonest cause of thyrotoxicosis?
Graves’ disease is the most common cause of thyrotoxicosis. It is typically seen in women aged 30-50 years.
Features
- typical features of thyrotoxicosis
- specific signs limited to Grave’s
Features seen in Graves’ but not in other causes of thyrotoxicosis:
Eye signs (30% of patients)
- exophthalmos
- ophthalmoplegia
- Pretibial myxoedema
Thyroid acropachy, a triad of:
- digital clubbing
- soft tissue swelling of the hands and feet
- periosteal new bone formation
What is the autoantibody found in Grave’s disease?
Autoantibodies:
- TSH receptor stimulating antibodies (90%)
- Anti-thyroid peroxidase antibodies (75%)
What are the precipitating factors for DKA? What are the syptoms?
Diabetic ketoacidosis (DKA) may be a complication existing type 1 diabetes mellitus or be the first presentation, accounting for around 6% of cases. Rarely, under conditions of extreme stress, patients with type 2 diabetes mellitus may also develop DKA.
DKA is caused by uncontrolled lipolysis (not proteolysis) which results in an excess of free fatty acids that are ultimately converted to ketone bodies.
The most common precipitating factors of DKA are infection, missed insulin doses and myocardial infarction.
Features:
- abdominal pain
- polyuria, polydipsia, dehydration
- Kussmaul respiration (deep hyperventilation)
- Acetone-smelling breath (‘pear drops’ smell)
