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4th Year Medicine 2 > Endocrine (thyroid and diabetes) > Flashcards

Endocrine (thyroid and diabetes) Flashcards

1
Q

What is hyperthyroidism?

A
  • Overactivity of the thyroid
  • Nearly all cases are intrinsic thyroid disease
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2
Q

Causes of hyperthyroidism?

A
  • Graves disease is the most common cause and is an auto-immune process – TRAB antibodies bind to TSH receptors in the thyroid and stimulate thyroid hormone production
  • Solitary toxic adenomas
  • Toxic multinodular goitre
  • De Quervains thyroiditis
  • Amiodarone induced
  • Note: generally in younger people think Graves and in older people think toxic multinodular goitre
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3
Q

Clinical features of hyperthyroidism?

A

For any cause:
* Lid lag and stare in eyes
* Tremor
* Hyperkinesis
* Anxiety
* Tachycardia, AF, hypertension, heart failure and palpitations
* Weight loss
* Sweating
* Diarrhea
* Oligomenorrhoea/ amenorrhoea
* Heat intolerance
* Loss of libido

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4
Q

Clinical features specific to graves disease?

A

Only in Graves disease:
* Exophthalmos (anterior bulging of the eye)
* Ophthalmoplegia (paralysis of the extraocular muscles)
* Pretibial myxedema (thickened skin and might get plaques and nodules)
* Thyroid acropachy (this is rarely seen but you get soft tissue swelling of the hands and feet, clubbing and periosteal new bone formation)

The eye and skin manifestations in Graves is due to a specific immune response which causes retroorbital inflammation. There is swelling and oedema of the extraocular muscles which leads to the limitation in movement and proptosis.

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5
Q

Investigations for hyperthyroidism?

A
  • In primary thyroid disease (basically all forms of hyperthyroid) there is a low TSH and a high fT4/T3
  • If someone is hyperthyroid can then check for TRAb (thyroid stimulating hormone receptor antibody) antibodies which will be present in Grave’s disease
  • If there are no TRAb antibodies can do a radionuclide thyroid uptake scan (basically it will show if there is a nodule that has higher uptake or is it diffuse, can also see lower uptake too- pictures below)
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6
Q

Management of hyperthyroidism?

A

1st line drug = carbimazole
2nd line drug = propylthiouracil
symptomatic relief whilst waiting for drugs to work with beta blocker - propranolol
radio-iodine if this is unsuccessful or have TMG
surgery if radio-iodine not suitable

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7
Q

Risks of thyroid surgery?

A

will be left hypothyroid
may take out parathyroids and be left hypoparathyroid
vocal cord paralysis due to damage of recurrent laryngeal nerve

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8
Q

Disadvantages of radioactive iodine?

A

strict regulations
no contact with anyone for 3 days
no contact with children or pregnant people for 3 weeks
need to wait at least 6 months to become pregnant afterwards

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9
Q

Describe thyroid storm and treatment?

A
  • Rapid deterioration of hyperthyroidism with hyperpyrexia, severe tachycardia, extreme restlessness, cardiac failure and liver dysfunction
  • Urgent treatment is required: propranolol, potassium iodide, antithyroid drugs (propylthiouracil), corticosteroids and supportive measures (patient may require ventilation)
  • High dose iodine stuns the thyroid as too much availability – remains like this for 10 days – then need to have a plan in place e.g. thyroidectomy
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10
Q

What is the most common and second most common type of thyroid cancer? Name two rarer cancers?

A

most common = papillary
second most common = follicular
rarer = anaplastic (very aggressive) and medullary (neuroendocrine of C cells)

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11
Q

Presentation of thyroid cancer?

A
  • Large majority of these cancers are non-functioning so will not present with symptoms of hyperthyroidism
  • Majority of cancers present with palpable nodules
  • If the cancer is compressing structures they may present with unexplained hoarse voice, sore throat, pain in neck, dysphagia and difficulty breathing
  • Nice guidelines for suspected cancer suggest 2 week cancer suspicion referral in anyone with an unexplained thyroid lump
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12
Q

Describe papillary thyroid cancer?

A
  • Papillary thyroid cancer is the most common
  • These spread most commonly via the lymphatics
  • Histologically you see Orphan Annie Nuclei and Psammoma bodies
  • Associated with radiation exposure
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13
Q

Orphan Annie nuclei and psammoma bodies?

A

papillary thyroid cancer

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14
Q

Describe follicular thyroid cancer?

A
  • Second most common cancer
  • These spread most commonly via the blood particularly to the bones and lungs
  • Associated with low dietary iodine
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15
Q

Investigations for thyroid cancer?

A
  • Ultrasound first
  • Then usually offer FNA of the lesion, the patient may also need to go on for a lymph node biopsy
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16
Q

Management of thyroid cancer?

A

Surgery
* Surgery is treatment of choice
* AMES score is calculated (age, metastases, extent, size)
* Lobectomy with isthmusectomy is done for low risk groups
* Subtotal or total thyroidectomy is done for high risk groups
* Post op care should involve checking calcium (incase removed parathyroids) and discharging the patient on thyroid hormone replacement therapy (levothyroxine)

Radioactive Iodine Therapy
* This is used in patients who have undergone subtotal or total thyroidectomy
* Radioiodine is administered and 2 days later patients are brought back for a scan, if there is uptake in parts where the thyroid gland was then the patient has remnant ablation done
* Patient is given a massive dose of radioiodine therapy and then has to wait in a lead room until they are no longer radioactive!
* Normally after treatment the patients stay on T4, the replacement regimen is different than those with hypothyroid because the aim is to suppress TSH as a high TSH increase the risk of cancer recurrence
* In follow ups thyroglobulin can be used as a tumour marker as it is only produced by the thyroid (which the patient doesn’t have) or by thyroid cancer cells
* Risk of recurrence diminishes with time (after 2 years the patient is effectively cured)
* There are no long term effects of this therapy except a small increase in the incidence of acute myeloid leukaemia but this tends to be in patients who have undergone multiple treatments (the majority only undergo one)

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17
Q

Prognosis of thyroid cancer?

A
  • Differentiated thyroid cancer (papillary and follicular) has the best prognosis of all cancers except non-melanoma skin cancer
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18
Q

Causes of hypothyroidism?

A
  • Hashimoto’s Thyroiditis is the most common cause of hypothyroidism, it is an autoimmune conditions where antibodies attack the thyroid
  • Postpartum thyroiditis – condition after birth where the woman becomes transiently hyperthyroid followed by hypothyroidism 3-4 months post-partum, most women recover spontaneously and don’t need treatment but it should be noted that the hypothyroid phase is associated with postnatal depression
  • Iodine deficiency (common cause in the developing world)
  • Drug induced (amiodarone or lithium)
  • Surgery
  • Secondary- any disease of the hypothalamus or pituitary gland
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19
Q

Clinical features of hypothyroidism?

A
  • Cold skin and cold intolerance
  • Bradycardia
  • Dry skin, coarse and sparse hair
  • Decreased appetite but weight gain
  • Constipation
  • Macroglossia and a deep voice
  • Slow reflexes
  • Menorrhagia
  • Fluid retention and oedema
  • Loss of libido
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20
Q

Investigations for hypothyroidism?

A
  • In primary hypothyroidism there is an increased TSH and a decreased fT4/T3
  • In secondary hypothyroidism there is a decreased TSH and a decreased fT4/T3
  • Thyroid peroxidase antibodies (TPO) will be present in Hashimoto’s thyroiditis
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21
Q

Management of hypothyroidism?

A
  • If there is a fixable underlying cause e.g. iodine deficiency or drug that can be stopped or secondary cause with pituitary or hypothalamus that can be fixed – do so
  • Those with Hashimotos etc are given replacement therapy with levothyroxine (T4) for life
  • Starting dose depends on severity, age and fitness of the patient, 100ug daily for young and fit patients is given and for older patients they are started on 50ug and increased gradually to 100ug
  • The aim of therapy is to restore T4 and TSH to normal range
  • Those with Hashimoto’s thyroiditis are at higher risk of developing other auto-immune diseases
  • Should also be noted that women require higher thyroid hormone replacement during pregnancy
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22
Q

Who usually gets myxoedema coma? Presentation?

A
  • Affected people are typically older and have previously undiagnosed hypothyroidism or are poorly compliant with thyroid hormone medication. The precipitant is usually onset of another condition such as heart failure, sepsis, or stroke
  • Presents with hypothermia, severe cardiac failure (bradycardia, heart block, T wave inversion, prolonged QT), hypoventilation, hypoglycaemia and hyponaetremia
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23
Q

Management of myxoedema coma?

A
  • These patients need intensive care – they should get thyroid hormone replacement and glucocorticoid therapy
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24
Q

What is type 1 diabetes?

A
  • Absolute insulin deficiency
  • Auto-immune attack of beta cells which produce insulin in the pancreas
25
Q

Who gets type 1 diabetes?

A
  • Tends to present in first 5 decades
  • Big peak at school age
  • There is genetic susceptibility and HLA types
  • Associated with other organ specific auto-immune diseases such as thyroid, coeliacs, Addison’s and pernicious anaemia
26
Q

Presentation of type 1 diabetes?

A
  • Usually acute onset of symptoms and can present as DKA
  • Weight loss
  • Severe polyuria and polydipsia
  • Polyphagia
  • Fatigue
  • Weakness
  • Doesn’t usually present with diabetic complications as presentation is so acute
27
Q

Investigations for type 1 diabetes?

A
  • Can be diagnosed on clinical grounds if random plasma glucose is more than 11mmol/L
  • Type 1 antibodies test – have 95% sensitivity when combined – GAD, IA-2, ZnT8
  • Measure C peptide, not useful for diagnosis as it takes time to decrease but can be useful to confirm type 1 diagnosis later on (C peptide is a byproduct of insulin and will be reduced in type 1 as you produce no insulin)
28
Q

Management of type 1 diabetes?

A
  • If type 1 diabetes is suspected you need to refer the adult or child to same day diabetes care team in hospital to confirm diagnosis and provide immediate care
  • insulin therapy
29
Q

3 ways to evaluate metabolic control in diabetes?

A
  • Finger prick – glucose capillary – only provides a snapshot so doesn’t always give full picture
  • Glycated haemoglobin – HbA1c – measures blood glucose control over a long time
  • Flash glucose monitoring and continuous glucose monitoring – device worn that measures interstitial glucose
30
Q

Signs and symptoms of hypoglycaemia?

A
  • Sweating
  • Feeling tired
  • Dizziness
  • Feeling hungry
  • Tingling lips
  • Feeling shaky or trembling
  • A fast or pounding heartbeat (palpitations)
  • Becoming easily irritated, tearful, anxious or moody
  • Turning pale

Late symptoms:
* Weakness
* Blurred vision
* Confusion or difficulty concentrating
* Unusual behaviour, slurred speech or clumsiness (like being drunk)
* Feeling sleepy
* Seizures or fits
* Collapsing or passing out

31
Q

Management of hypoglycaemia?

A
  • Glucose below 4 = hypoglycaemia
  • Initially 10-20g of glucose by mouth, or 2 teaspoons of sugar, non diet sugary drinks
  • Hypoglycaemia that is not responding should be treated with 10% glucose infusion (100mls)
  • If it is causing unconsciousness this is an emergency – 20% IV glucose through large gauge needle, alternatively glucagon IM if in community
32
Q

What is type 2 diabetes?

A
  • Relative insulin deficiency
  • Predominantly insulin resistance
33
Q

Risk factors for type 2 diabetes?

A
  • Obesity
  • Genetic susceptibility
  • South-east Asia have higher rates in slimmer adults
  • Family history
  • Associated with hypertension, hyperlipidaemia, hyperglycaemia and PCOS (so must check for these)
34
Q

Presentation of type 2 diabetes?

A
  • May present asymptomatic from screening or incidental finding in hospital
  • Usually doesn’t present acutely and there are often signs of microvascular complications already
  • Symptoms include polydipsia, polyuria, thrush, weakness, fatigue, blurred vision, infections, complications e.g. neuropathy and retinopathy
35
Q

Define persistent hyperglycaemia?

A

Looking for persistent hyperglycaemia which can be defined as:
* HbA1c of 48 mm/mol or above
* Fasting plasma glucose of 7.0mm/L or above
* Random plasma glucose of 11.1mmol/L or above
* OGTT of 11.1mmol/L or above

36
Q

Management of type 2 diabetes?

A

Management
Lifestyle changes – diet, increase physical activity, stop smoking

Drug Treatments
* Metformin is first line (however it is contraindicated in renal impairment)
* Sulfonylureas (e.g. gliclazide, glipizide) are first line in those who are intolerant to metformin or have contraindications, can also be considered as an add on treatment
* In those with cardiovascular disease offer an SGLT-2 inhibitors (e.g. canagliflozin, dapagliflozin and empagliflozin) as these are proven to have cardiovascular benefit in addition to metformin
* If metformin is ineffective consider dual therapies with DPP-4 inhibitors (e.g. sitagliptin, saxagliptin) or sulfonylureas (e.g. gliclazide)
* GLP agonists for those with a BMI > 30 in combination as 3rd or 4th line therapy, these can facilitate weight loss (injectable drug) (e.g. liraglitide, semaglutide)
* Insulin is last line in type 2 diabetes when control cannot be achieved any other way

37
Q

HBA1c targets for type 2 diabetes?

A
  • 48mmol/mol is target for those on no drug therapy or those on drug therapy that doesn’t cause hypos
  • 53mmol/mol is target for those on drug therapies that cause hypoglycaemia (e.g. sulfonylureas)
38
Q

Macrovascular complications of diabetes?

A

stroke, MI, peripheral vascular disease, atherosclerosis risk all increased

39
Q

Diabetic eye disease?

A
  • Retinopathy
  • Macular oedema
  • Cataracts
  • Glaucoma
  • Visual blurriness in acute hyperglycaemia
40
Q

Diabetic nephropathy?

A
  • Earliest evidence is microalbuminuria, need special dipsticks or radio-immunoassay to detect
  • Progression to intermittent albuminuria then persistent proteinuria
  • All patients with diabetes should have urinary albumin concentration and serum creatinine measured at diagnosis and at regular intervals, usually annually
  • ACE (or ARBs if intolerant) are 1st line for nephropathy
41
Q

Diabetic neuropathy?

A
  • Peripheral neuropathy in glove and stocking distribution
  • Proximal neuropathy – rarer
  • Autonomic neuropathy – often affects the gut and can get gastroparesis
42
Q

Explain DKA?

A

Metabolic emergency occurring in T1DM characterized by:
1. Acidosis- blood pH below 7.3 or plasma bicarbonate below 15mmol/litre and
2. Ketonaemia- blood ketones above 3mmol/litre
3. Blood glucose levels are generally high above 11mmol/litre although children with known T1DM can develop it with normal glucose levels

  • Can be life threatening and the 3 complications which account for the majority of deaths in these children are – cerebral oedema, hypokalaemia and aspiration pneumonia
  • Essentially because you cannot utilize your glucose there is break down of adipose tissue resulting in rising levels of acidic ketone bodies – this causes metabolic acidosis
  • The hyperglycaemia and glycosuria results in osmotic diuresis and patient becomes polyuric resulting in dehydration
43
Q

Who gets DKA?

A
  • May be a first presentation of diabetes
  • May be due to non-compliance with insulin or changing insulin requirements e.g. in puberty
  • May be due to intercurrent illness – cortisol raises blood glucose
  • May be due to increased ingestion of glucose
44
Q

Clinical features of DKA?

A
  • General malaise and lethargy
  • Nausea and vomiting
  • Abdominal pain
  • If no current diagnosis of DM – weight loss, polyuria and polydipsia may be preceding symptoms
45
Q

Examination of DKA?

A
  • Kussmaul breathing (rapid deep breathing), tachypnoea, subcostal and intercostal recession
  • Shock - tachycardia, hypotension, increased cap refill and cool peripheries
  • Dehydration – dry mucous membranes, reduced skin turogor, sunken eyes/ fontanelle
  • Abdominal pain which may mimic a surgical acute abdomen
  • Potential signs of neurological compromise e.g. papilloedema if cerebral oedema, reduced consciousness etc.
  • Fruity ketotic breath
46
Q

Investigations for DKA?

A
  • Bedside blood glucose and ketones, urinary ketones can also be used
  • Blood gas – venous or capillary
  • Laboratory samples for blood glucose, U and Es, FBC and creatinine
  • 12 lead ECG – cardiac monitoring for signs of hyper or hypokalaemia
47
Q

Management of DKA?

A

Fluids to rehydrate - will need several litres of 0.9% saline
continuous variable infusion insulin - 0.1 unit/ kg/hr
should continue normal long acting insulin but stop short acting
once blood glucose < 14 mmol/l add 10% glucose to regime
monitor for hypokalaemia

48
Q

Explain hyperosmolar hyperglycaemic state?

A
  • This occurs in those with type 2 diabetes
  • This is characterised by severe hyperglycaemia with marked serum hyperosmolarity without evidence of significant ketosis
  • Hyperglycaemia causes an osmotic diuresis with hyperosmolarity leading to an osmotic shift of water into the intravascular compartment resulting in severe intracellular dehydration
  • Ketosis does not occur due to the presence of basal insulin secretion sufficient to prevent ketogenesis but insufficient to reduce blood glucose
49
Q

Presentation of HHS?

A
  • Dehydration
  • Focal or global neurological dysfunction
  • Generalised weakness
  • Leg cramps
  • Visual impairment
  • Nausea and vomiting – but less so compared to DKA
  • Seizures can occur
  • Tachycardia
  • Hypotension
50
Q

Investigations for HHS?

A
  • Urinalysis shows marked glycosuria with normal or only slightly elevated ketones
  • Capillary glucose is often over 30
  • Serum osmolarity is usually > 320
  • U and Es, FBC, CRP
  • ABG
  • ECG and CXR
51
Q

Management for HHS?

A
  • Use IV 0.9% sodium chloride solution
  • Only low dose IV insulin if the blood glucose stops falling with IV fluids alone
52
Q

What can cause euglycaemic DKA?

A

SGLT2 inhibitors

53
Q

Difference between dequervains and graves presentation?

A

de quervains causes a painful goitre
graves is not a painful goitre

54
Q

Explain what dequervains thyroiditis is?

A

granulomatous inflammation and destruction of thyroid following viral infection, hyper phase then hypo, it is self resolving

55
Q

PPIs can cause?

A

hyponatraemia

56
Q

IN acute mx of DKA insulin…..

A

should be fixed rate whilst continuing regular injected long acting insulin but stopping short acting injected insulin

57
Q

If metformin is not tolerated due to GI side effects?

A

try a modified release formulation before switching to a second line agent

58
Q

Describe the course of postpartum thyroiditis and the management?

A

hyper phase - propanolol for symptom relief, not typically given antithyroid drugs as the thyroid is not over active
hypo phase - treated with thyroxine
most recover to normal thyroid function but there is a high risk of recurrence in future pregnancies

59
Q

Antibodies in postpartum thyroiditis?

A

TPO antibodies are found in 90% of patients

4th Year Medicine 2 (14 decks)

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