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Year 5 Core Conditions > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is the other term for primary adrenal insufficiency?

A

Addison’s disease

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2
Q

What does Addison’s disease cause?

A

Reduced production of glucocorticosteroids e.g. cortisol and mineralocorticoids e.g. aldosterone, and adrenal androgens
The absence of cortisol leads to increased production of adrenocorticotrophic hormone (ACTH) because negative feedback to the pituitary gland is reduced.

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3
Q

In the UK what is the most common cause of Addisons disease?

A

Autoimmune disease - 70-90% of cases - in 60% of these cases it is a multi-organ autoimmune polyendocrine syndrome

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4
Q

Worldwide, what is the most common cause of Addisons disease?

A

Infection - tuberculosis

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5
Q

Which two other autoimmune conditions are associated with Addisons disease (in about 50% of people)?

A
  1. Type 1 diabetes

2. Hypothyroidism

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6
Q

What is polyglandular autoimmune syndrome type 1 a triad of?

A
  1. Addisons disease
  2. Hypoparathyroidism
  3. Chronic candidiasis (fungal infections)
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7
Q

What is polyglandular autoimmune syndrome type 2?

A

This is more common than type 1, and is a complex genetic trait with links to HLA major histocompatibility - HLA DR3 and DR4
- Usually involves Addisons disease, thyroid disease and T1DM
(can also be associated with vitiligo, vitamin B12 deficiency, coeliac disease and hypoparathyroidism)

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8
Q

What is the most serious complication of Addisons disease?

A

Adrenal crisis - when the adrenal glands can’t supply the extra corticosteroids needed to cope with physical stress and life-threatening symptoms develop - severe dehydration, hypotension, hypovolaemic shock, altered consciousness, seizures, stroke or cardiac arrest

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9
Q

What are the typical features of Addison’s disease? (6)

A
  1. Anorexia, weight loss
  2. Dizzy, syncope
  3. Postural hypotension
  4. Bronze skin and pigmented palmar crease
  5. Fatigue, depression
  6. Nausea, vomiting, abdominal pain, diarrhoea or constipation
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10
Q

What are the three key features of DKA?

A
  1. Hyperglycaemia >11mmol/L (often >30)
  2. Positive ketones on dipstick or fingerprick
  3. Metabolic acidosis pH <7.3
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11
Q

What is the clinical presentation for DKA? (7)

A
  1. Polyuria
  2. Polydipsia
  3. N&V
  4. Weight loss
  5. Confusion and drowsiness
  6. Kussmaul breathing (deep hyperventilation)
  7. Vague abdominal pain
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12
Q

What investigations are carried out for DKA?

A
  1. Urine dipstick +++ ketones ++ glucose
  2. Blood glucose
  3. Capillary ketones >3mmol
  4. ABG - metabolic acidosis
  5. Bloods - FBC, U&Es, LFTs
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13
Q

What is the management for DKA? (4)

A

A-E assessment

  1. Fluid regimen
  2. Insulin - 50 units of act rapid with 50ml saline - fixed rate 0.1 units/kg/hour
  3. Once glucose <14, start 10% glucose
  4. K+ sulphate (must never give >10mmol K+ over 1 hour)
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14
Q

What does HONK AKA HHS refer to?

A

Hyperglycaemic hyperosmolar non-ketotic state

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15
Q

What is HHS?

A

A severe uncorrected hyperglycaemia in the presence of residual insulin production (T2DM) leading to dehydration but not ketoacidosis

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16
Q

What is the concern/risk with HHS?

A

High risk of thrombosis

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17
Q

What are the precipitants for HHS? (8)

A
  1. Infection
  2. MI
  3. CVA
  4. GI bleed
  5. Poor med compliance
  6. High sugar diet
  7. Neglect
  8. Diuretics/BBs/Antihistamines
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18
Q

How can HHS present? (5)

A
  1. Unknown history of diabetes
  2. Insidious onset of polyuria and polydipsia
  3. Severe dehydration
  4. Weakness, leg cramps and visual disturbances
  5. Reduced consciousness - related to plasma osmolality (>440 = coma)
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19
Q

What is the management for HHS?

A
  1. A-E assessment
  2. Fluid replacement - half the rate of DKA e.g. 1 litre of saline over 30 minutes, then 1 litre + potassium every 2-4 hours
  3. Treat causes e.g. infection
  4. Thromboprophylaxis e.g. LMWH
    only if ketonuria - then insulin infusion
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20
Q

What happens in the body with Addisons disease, as a result of low aldosterone?

A
  1. Hyperkalaemia
  2. Hyponatraemia
  3. Hypovolaemia
  4. Metabolic acidosis
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21
Q

How does hypoglycaemia tend to present? (7)

A
  1. Sweating
  2. Pallor
  3. Tachycardia/palpitations/anxiety
  4. Confusion
  5. Slurred speech/blurred vision
  6. Seizures
  7. Coma
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22
Q

What is the management for hypoglycaemia?

A
  1. ABCDE
  2. Blood guclose - before glucose administration!
  3. GCS 15 and safe swallow = fast acting glucose 10-20g orally in frequent and small doses, recheck blood glucose 10-15 mins after and repeat if not >4mmol
  4. When patient can eat give carbohydrate rich snack
  5. If alcoholic - consider pabrinex
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23
Q

What happens if the patient with hypoglycaemia cannot take oral glucose e.g. if GCS <15?

A

Give IV 100mls of 20% glucose or 50ml of 50%. If IV access is unattainable then give IM glucagon 1mg.

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24
Q

What are the two main types of diabetes insulin treatment regimen?

A
  1. Premix

2. Basal-bolus

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25
Q

What are the names of the premix drugs?

A
  1. Humalog mix 25
  2. Humalog mix 50
  3. Humalog M3
  4. Novomix 30
    the numbers refer to the % of short-acting insulin in each mix
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26
Q

In general, how many grams of carbohydrate are recommended for 1 unit of insulin?

A

10 grams

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27
Q

In general, what can the correction be for 1 unit of insulin, in terms of capillary blood glucose?

A

1 unit of insulin can equate to for example 3mmol/L of capillary blood glucose

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28
Q

How is type 1 diabetes investigated, what is the test?

A

Oral glucose tolerance test - 75g of glucose is given to a fasting patient, the baseline fasting glucose is measured and then 2 hours post glucose load.

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29
Q

What is the expected fasting blood glucose for a person without diabetes and with diabetes?

A

Without - <6

With - >6

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30
Q

What is the expected 2h post-glucose load for someone with and someone without diabetes?

A

Without - <7.8

With - >11.1

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31
Q

What are the macrovascular complications of diabetes?

A

CVA, MI, peripheral vascular disease

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32
Q

What are the microvascular complications of diabetes?

A

Retinopathy, nephropathy and neuropathy

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33
Q

What causes type 1 diabetes?

A

It is an autoimmune destruction of beta cells in the islets of langerhans, leading to absolute insulin deficiency.

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34
Q

There is a strong association with which HLA types and T1DM?

A

HLA-DR3 and DR4

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35
Q

What is the peak age of onset for T1DM?

A

Age 12

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36
Q

What are the classic symptoms associated with T1DM? (4)

A
  1. Polyuria
  2. Polydipsia
  3. Weight loss
  4. sometimes DKA is the presenting feature
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37
Q

What investigations are important to request/perform when someone presents with the symptoms indicative of T1DM? (4)

A

Bloods - FBC, U&Es, glucose, antibodies
Immunology - anti-islet cell Ab, anti-GAD Ab
Urine - ketones
ABG

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38
Q

Which annual reviews need to be performed in someone with diabetes? (9)

A
  1. Weight + BMI
  2. Creatinine
  3. Urinary ACR
  4. Cholesterol
  5. HbA1c (biannual)
  6. BP (aim <140/90)
  7. Smoking status
  8. Fundoscopy
  9. Feet examination
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39
Q

In addition to the annual reviews, what else needs to be checked more regularly in people with T1DM? (4)

A
  1. Injection sites
  2. BP monitoring
  3. Renal function
  4. Thyroid function
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40
Q

What are the complications of DKA? (5)

A
  1. Cerebral oedema
  2. Hypoglycaemia
  3. Hypokalaemia
  4. Hyperkalaemia
  5. Pulmonary oedema
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41
Q

What are the 4 different classes of drugs used in the treatment of T2DM?

A
  1. Biguanides (metformin)
  2. Sulphonylureas (gliclazide, glimepiride)
  3. Thiazolidinediones (rosiglitazone)
  4. alpha-Glucosidase inhibitors (acarbose)
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42
Q

What is the mechanism of action of metformin (biguanides)?

A

Improves the body’s sensitivity to insulin

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43
Q

What is the mechanism of action of sulphonylureas?

A

Stimulates the pancreatic insulin release

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44
Q

What is the mortality rate as a % for people who experience HONK/hyperosmolar non-ketotic coma/HHS?

A

20-40%

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45
Q

What are the triggers for hypoglycaemia?

A
  1. Sulphonylureas
  2. Alcohol/Addison’s
  3. Insulinomas/insulin/infection
  4. Liver failure
    SAIL
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46
Q

What are the signs/symptoms that can indicate hypoglycaemia? (8)

A
  1. Cold sweat
  2. Fatigue
  3. Irritability
  4. Confusion
  5. Loss of consciousness
  6. Collapse
  7. Tachycardia
  8. Seizures
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47
Q

Which hormones do the posterior pituitary gland produce? (2)

A
  1. ADH

2. Oxytocin

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48
Q

Which hormones are produced by the anterior pituitary gland? (6)

A
  1. ACTH - adrenocorticothrophic hormone
  2. TSH
  3. LH
  4. FSH
  5. GH
  6. Prolactin
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49
Q

Why does insulin resistance in T2DM lead to heart disease and stroke?

A

Insulin resistance has pro-thrombotic effects leading to a higher risk of emboli in coronary arteries

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50
Q

In addition to insulin resistance, what are the other two components than contribute to diabetic heart disease?

A
  1. Coronary atherosclerosis - due to smoking, poor diets, hypertension and damage to vessels from glucose
  2. Metabolic syndrome - large waistline, triglycerides
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51
Q

How is the risk of diabetic heart disease managed? (3)

A
  1. Lifestyle changes - smoking cessation, diet and exercise advice
  2. Statins
  3. Anti-hypertensives
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52
Q

If someone is on metformin but their HbA1c is still greater than 58mmol/mol (7.5%), what is the next step in treatment?

A

Add a gliptin or sulphonylurea

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53
Q

What treatment can be used to protect the kidneys in someone at risk of diabetic nephropathy?

A

Either an ACE inhibitor or losartan - even if BP is normal, as they inhibit RAAS

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54
Q

What is the primary cause of adrenal insufficiency?

A

Addison’s disease - autoimmune destruction of the adrenal gland. (typically 30-50 year old females)

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55
Q

Destruction of the adrenal cortex results in which adrenal hormones not being produced? (3)

A
  1. Mineralcorticosteroids (aldosterone)
  2. Glucocorticosteroids (cortisol)
  3. Androgens (mildly testosterone - mainly produced in the testes)
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56
Q

What are the two main categories of diabetic foot problems?

A
  1. Neuropathy

2. Ischaemia

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57
Q

What is the condition that can occur in foot neuropathy?

A

Charcot foot/joint

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58
Q

What is Charcot foot AKA Charcot arthropathy?

A

Charcot arthopathy is a serious condition, more common if people lose feeling in their feet. The bones in the foot can become weak and lead to dislocations, fractures and changes in the shape of the foot or ankle. It can develop in diabetes, and if it is not treated quickly, ulcers or other sores can develop.

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59
Q

What are the symptoms of Charcot arthropathy?

A

Foot feeling hot, painful and looking swollen or red. Additionally they will lose function, the arch may collapse and neuropathy may occur

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60
Q

What is the management of suspected Charcot arthropathy?

A

Referral to an MDT foot service within 1 working day, do not put any weight on that foot until the appointment and normally the person will receive X-rays/MRI scans. Treatment includes having a plaster cast fitted.

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61
Q

What are the typical features of Addison’sdisease?

A

It is often diagnosed late due to the vague symptoms that can present.
Lead + tired: anorexia, weight loss, dizzy, syncope, postural hypotension
Tanned: bronze skin, pigmented palmar crease + buccal mucosa
Tearful + wear: fatigue, depression, low self-esteem, psychosis
GI: nausea, vomiting, abdominal pain, diarrhoea or constipation

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62
Q

What are in the kidneys that act as receptors to ADH?

A

Aquaporins

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63
Q

Drinking water does has what effect on plasma osmolality?

A

Decreases plasma osmolality (diluting blood with water)

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64
Q

What happens when there is decrease in plasma osmolality due to an increase in water intake?

A

The hypothalamus tells the pituitary gland to not produce as much ADH, so that more water can be excreted in the urine (dilute urine)

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65
Q

What happens if ADH continues not to be released, even if the plasma osmolality has returned to normal?

A

The body recognises that the blood is getting dilute with water as it takes up more space in vessels, and causes aldosterone to stop being released. Less aldosterone floating around in the blood causes sodium to be released into urine. Concentration gradients cause water to follow the sodium, which normalises the water volume in the blood.

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66
Q

What is the problem with our body regulating water through aldosterone and sodium output?

A

The sodium is released into the urine from the blood, yet the sodium was already low in the blood to begin with. This means plasma sodium osmolality is dropping significantly. This is SIADH.

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67
Q

There are four patterns of SIADH, what are the 4 types?

A

Type A - erratic, independent of plasma osmolality. ADH levels tend to be very high, so the maximum amount fluid is retained, causing urine osmolality to be very high too.

Type B - constant release of moderate amount of ADH

Type C - this is when the baseline plasma concentration of sodium level is set lower than normal. This type is unique as the plasma sodium concentration is stable, but low.

Type D - ADH secretion is normal yet urine osmolality is still high

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68
Q

What are the symptoms of SIADH caused by?

A

Low sodium levels

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69
Q

What are the symptoms of SIADH? (5)

A
  1. Headache
  2. Nausea and vomiting
  3. Muscle cramps
  4. Tremors
  5. Cerebral oedema - hallucinations, mood swings, confusion
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70
Q

If SIADH symptoms are missed, what are the potential serious complications? (3)

A
  1. Seizure
  2. Coma
  3. Death
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71
Q

What would indicate SIADH using blood test results?

A
  1. Low blood sodium
  2. Low plasma osmolality
  3. High urine osmolality
  4. High urine sodium
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72
Q

What are the causes of SIADH?

A

Anything that disrupts the secretion of ADH.

  1. Stroke, haemorrhage, trauma to the brain
  2. Drugs - mood stabilisers or anti-epileptics
  3. Surgery
  4. Ectopic ADH release by tumours - small cell carcinoma
  5. Family history
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73
Q

What is the treatment for SIADH?

A

Treat the underlying cause, but also restricting fluid and increasing salt and protein in the diet.
Drugs that can inhibit ADH secretion can also work.

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74
Q

What the other term used to describe a hyperthyroid crisis?

A

A thyrotoxic storm

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75
Q

What are the symptoms of a thyrotoxic storm?

A
  1. Tachycardia
  2. Raised temperature
  3. Hypotension
  4. Confusion
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76
Q

What is the treatment for a thyrotoxic storm?

A
  1. Beta blockers
  2. Propylthiouracil (an anti-thyroid treatment to help reduce the effect of raised serum thyroid hormones)
  3. Hydrocortisone - treat any underlying adrenal insufficiency which is more common in patients suffering form hyperthyroidism and can also help reduced the serum thyroid hormone levels
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77
Q

6% of people with acromegaly have what inherited syndrome - characterised by the occurrence of tumours in the parathyroid, pituitary and adrenal glands?

A

MEN-1

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78
Q

What are the features of acromegaly? (5)

A
  1. Coarse facial appearance
  2. Spade-like hands
  3. Increase in shoe size
  4. Large tongue
  5. Excessive sweating and oily skin
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79
Q

What are the complications of acromegaly? (4)

A
  1. Hypertension
  2. Diabetes (>10%)
  3. Cardiomyopathy
  4. Colorectal cancer
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80
Q

What is the first line antihypertensive drug for all people with diabetes?

A

ACE inhibitors

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81
Q

What is the most likely diagnosis for an older female patient with polydipsia, polyuria, inappropriately normal or raised parathyroid hormone level and a raised calcium?

A

Primary hyperparathyroidism - 80% solitary adenoma

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82
Q

What are the symptoms of raised calcium? (6)

A

Bones, stones, abdominal groans and psychic moans

  1. Polydipsia, polyuria
  2. Peptic ulceration/constipation/pancreatitis
  3. Bone pain/fracture
  4. Renal stones
  5. Depression
  6. Hypertension
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83
Q

What might be found on investigation for hyperparathyroidism?

A
  1. Raised calcium, low phosphate
  2. PTH may be raised or normal
  3. Pepperpot skull is characteristic X-ray finding of hyperparathyroidism
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84
Q

What is the name for the appearance of lytic lesions in the brain associated with multiple myeloma?

A

Raindrop skull

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85
Q

What % of primary hyperparathyroidism are caused by parathyroid adenoma?

A

80%

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86
Q

What is the mechanism of action of empagliflozin - an SGLT-2 inhibitor?

A

It increases urinary glucose excretion - which causes the following side effects: increased urine output, weight loss and risk of UTIs

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87
Q

What is the recommended amount of carbohydrate to treat a hypoglycaemic state?

A

10-20grams

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88
Q

What can be given to someone in a hypoglycaemic state?

A
  • If they have a safe swallow and normal GCS, Lucozade, glucose gel or tabs to chew.
  • If reduced GCS - IV access is preferred to give 20% glucose approx. 50-100ml (don’t give 50% as it damages veins)
  • Last resort is IM glucagon (high chance of inducing sickness so not recommended unless vital)
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89
Q

What are the signs of a hypoglycaemic state? (8)

A
  1. Palpitations
  2. Shaking
  3. Hunger
  4. Irritability
  5. Headache
  6. Sweating
  7. Dizziness
  8. Unconscious
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90
Q

What is hyperparathyroidism?

A

When there is excessive sections of parathyroid hormone from the parathyroid glands located in the neck.

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91
Q

What are the parathyroid hormone do?

A

Regulates serum calcium and phosphate levels and also plays a part in bone metabolism

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92
Q

What are the different types of parathyroidism?

A
  1. Primary - one parathyroid gland (or more) produces excess PTH. This may be asymptomatic
  2. Secondary - there is increased secretion of PTH in response to low calcium because of kidney, liver or bowel disease
  3. Tertiary - there is autonomous secretion of PTH, usually because of CKD
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93
Q

What does the parathyroid gland do?

A
  1. Increases the release of calcium from the bone matrix
  2. Increases calcium reabsorption by the kidneys
  3. Increases renal production of 1,25-dihydroxyvitamin D3, which increases intestinal absorption of calcium
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94
Q

Where is calcium homeostasis regulated? (3)

A
  1. Intestinal tract
  2. Kidneys
  3. Bone
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95
Q

What is 1,25-dihydroxyvitain D3 also known as?

A

Calcitriol

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96
Q

Calcitonin can also affect calcium homeostasis. What is it produced by and where from?

A

Produced by C cells of the thyroid gland

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97
Q

What does calcitonin do?

A

Inhibits osteoclast activity and reduces the release of calcium and phosphate from bone

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98
Q

Primary hyperparathyroidism is the third most common endocrine disorder. Who does it most commonly affect?

A

Postmenopausal women

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99
Q

What causes primary hyperparathyroidism?

A
  1. A single parathyroid gland adenoma (85%)
  2. 4-gland hyperplasia (10-15%)
  3. Double adenomas (3-5%)
  4. Parathyroid carcinoma (<1%)
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100
Q

Familial cases of hyperparathyroidism can occur, what endocrine syndromes are known to be related? (3)

A
  1. Multiple endocrine syndromes e.g. MEN-1 or MEN-2a
  2. Hyperparathyroid-jaw tumour (HPT-JT)
  3. Familial isolated hyperparathyroidism (FIHPT)
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101
Q

How can hyperparathyroidism present?

A

In those who are symptomatic (20-30%) it is the features of hypercalcaemia ‘bones, stones, abdominal groans and psychic moans’

  1. Muscle weakness, proximal myopathy
  2. Abdominal pain, peptic ulcer disease
  3. Renal colic, haematuria
  4. Neuropsychiatric manifestations - depression, confusion, dementia
  5. Hypertension
  6. Bone pain from osteoporosis
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102
Q

Why do people with hyperparathyroidism get osteoporosis and osteopenia?

A

Due to the excessive calcium resorption from the bone it leads to osteoporosis and causes the bone pain and pathological fractures

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103
Q

What is osteitis fibrous cystica?

A

It occurs in severe cases of hyperparathyroidism. It presents with subperiosteal resorption of the distal phalanges, tapering of distal clavicles, salt and pepper appearances of the skull and brown tumours of the long bones.

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104
Q

What does excessive renal calcium excretion lead to?

A

Renal calculi

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105
Q

Why can hyperparathyroidism lead to peptic ulcer disease?

A

Hypercalcaemia can increase gastric acid secretion leading to ulcers

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106
Q

What are the differentials for hyperparathyroidism? (6)

A
  1. Lithium-induced hypercalcaemia
  2. Malignancy
  3. Thyrotoxicosis
  4. Sarcoidosis
  5. Paget’s disease of the bone
  6. Addison’s disease
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107
Q

What investigations can be carried out if someone presents with hypercalcaemia?

A
  1. Look for obvious drug causes e.g. lithium, thiazide diuretics
  2. Repeat plasma albumin-adjusted calcium levels
  3. Ensure renal function is normal
  4. Measure PTH, with will be raised in primary HPT.
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108
Q

What will phosphate levels be like in primary hyperparathyroidism?

A

Low - hypophosphataemia

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109
Q

What is the treatment for mild, asymptomatic hyperparathyroidism? (6)

A
  1. Surveillance can be used in patients with mildly elevated calcium levels and close to normal renal and bone status
  2. Check serum creatinine level and calcium levels every 6 months
  3. 3 site DEXA study every 1-2 years
  4. Avoid dehydration
  5. Avoid thiazide like diuretics
  6. There is no recommendation to limit calcium intake
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110
Q

What is the only potential cure for hyperparathyroidism?

A

Surgery - parathyroid surgery to remove abnormal parathyroid gland(s) is suggested in most sympathetic patients.

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111
Q

What are the guidelines for the surgical management of PHPT?

A
  1. Age under 50
  2. Serum albumin-adjusted calcium is more than 0.25mmol/L above the upper limit of normal
  3. Creatnine clearance <60ml/minute
  4. Renal calculi
  5. DEXA -2.5
  6. Vertebral fractures
  7. Patient request
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112
Q

What do they do during surgery to determine if the abnormal gland has been removed?

A

Intraoperative PTH is measured, PTH levels drop by 50% within 10-15 minutes of the hyper-functioning parathyroid tissue being removed

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113
Q

If people don’t meet the criteria for surgical treatment of PHPT, or they don’t want surgery, what is the medical management? (3)

A

Treatment is aimed at improving bone density and achieving calcium homeostasis.

  1. HRT and raloxifene may be used in postmenopausal women. They have been shown to reduced calcium levels as well as improve bone density.
  2. Bisphosphonates (particularly alendronate)
  3. Cinacalcet reduces both serum calcium and PTH levels and raises serum phosphate. Cinacalcet does not, however, reduced bone turnover or improve bone mineral density
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114
Q

What are the complications of PHPT surgery? (3)

A
  1. Hypocalcaemia due to ‘hungry bone syndrome’ - until the normal parathyroid glands regain sensitivity, there will be a hypoparathyroidism. Calcium and vitamin D supplements may be required.
  2. Recurrent laryngeal nerve injury - if a patient develops new hoarseness postoperatively. Immediate laryngoscopy is required.
  3. Haematoma formation - if this occurs in the pre-tracheal space, urgent evacuation is required before airway obstruction occurs.
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115
Q

What are the causes of secondary hyperparathyroidism?

A

CKD - the parathyroid gland becomes hyper plastic after long-term stimulation in response to chronic hypocalcaemia

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116
Q

Who is most likely to develop SHPT?

A

People with stage 5 CKD - those on dialysis (almost all patients on dialysis have SHPT)

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117
Q

In addition to people with CKD, who else can develop SHPT?

A

Potentially anyone with chronic hypocalcaemia - e.g. vitamin D deficiency or malabsorption

118
Q

What are the findings for someone with SHPT?

A
  1. Low/normal calcium
  2. Raised PTH
  3. Phosphate levels depend on aetiology - high in renal disease, low in vitamin D deficiency
119
Q

What is the treatment for SHPT?

A

Medical management is the mainstay of treatment and treating the underlying condition for example correcting vitamin D deficiency.
Treatments include:
1. Calcium supplementation
2. Correction of vitamin D
3. Phosphate restriction or phosphate binders
4. Vitamin D analogues
5. Calcimimetics e.g. cinacalcet (though NICE only recommends the use of this in people who have end-stage kidney disease)

120
Q

What causes tertiary HPT?

A

Prolonged SHPT - the glands become autonomous, producing excessive PTH even after the cause of hypocalcaemia has been corrected, resulting in hypercalcaemia. CKD is the most common cause.

121
Q

What are the findings on investigations of THPT?

A
  1. Raised calcium
  2. Raised PTH
  3. Raised phosphate
122
Q

What is the recommended treatment for THPT?

A

Total or subtotal parathyroidectomy

123
Q

What does hyperlipidaemia refer to?

A

It is a term used to denote raised serum levels of one or more of total cholesterol, low-density lipoprotein cholesterol, and/or triglycerides.

124
Q

Hyperlipidaemia is one of the three modifiable risk factors for CVD, what are the other two?

A
  1. Smoking

2. Hypertension

125
Q

Approximately what % of the UK population has a serum cholesterol level greater than 5.2mmol/L?

126
Q

What are the inherited disorders that cause hyperlipidaemia/hypercholesterolaemia?

A
  1. Familial dyslipidaemias
  2. Familial hypercholesterolaeima
  3. Familial combined hyperlipidaemia
  4. Apoprotein disorders
127
Q

What are the secondary causes of hyperlipidaemia? (5)

A
  1. Medical conditions e.g. hypothyroidism, obstructive jaundice, Cushing’s syndrome, anorexia, nephrotic syndrome, diabetes and CKD
  2. Drugs e.g. thiazide-like diuretics, ciclosporin, beta-blockers, COCP
  3. Pregnancy
  4. Obesity
  5. Alcohol abuse
128
Q

What two measurements can be done to achieve the best estimate for CVD risk?

A
  1. Total cholesterol

2. HDL-C

129
Q

Before starting someone on lipid modification therapy for primary prevention of CVD, what lipid samples need to be take first?

A
  1. T-chol
  2. HDL-C
  3. non-HDL-C
  4. TG concentrations
130
Q

When should the possibility of familial hypercholesterolaemia be considered in someone with raised cholesterol?

A

If total cholesterol is more than 7.5mmol/L and there is family history of premature CHD

131
Q

What pattern of inheritance is familial hypercholesterolaemia?

A

Autosomal dominant

132
Q

How many people in the UK have familial hypercholesterolaemia?

A

Between 1 in 250 and 1 in 500 - so approximately 130,000-260,000-

133
Q

What % risk coronary heart disease is there for men and women respectively with heterozygous familial hypercholesterolaemia?

A

50% in men by age 50 and 30% in women by age 60

134
Q

At what total cholesterol level should specialist assessment be arranged?

A

TChol >9.0mmol/L or a non-HDL-C concentration of >7.5mmol/L (even in the absence of a first degree relative with premature CHD)

135
Q

Although the diagnosis for familial hypercholesterolaemia is primarily biochemical, what two physical signs may be evident in patients?

A
  1. Premature arcus senilis - a white or gray opaque ring in the corneal margin
  2. Tendon xanthomata - hard, non-tender nodular enlargement of tendons. They are most commonly found on the knuckles and the Achilles tendon.
136
Q

What criteria is used to diagnose familial hypercholesterolaemia?

A

Simon Broom diagnostic criteria

137
Q

What is included in the Simon Broom criteria?

A
  1. A TChol level in an adult of >7.5mmol/L
    AND
  2. Tendon xanthomata or evidence of these signs in a first degree/second degree relative
    OR
  3. DNA evidence of an LDL receptor mutation, familial defective apo-B-100 or PCSK9 mutation
138
Q

What is the most common genetic dyslipidaemia, occurring in how many people?

A

Familial combined hyperlipidaemia occurring in 1 in 100 people

139
Q

When is familial combined hyerplipidaemia suspected? (2)

A
  1. There is a family history of hyperlipidaemia or premature CHD not due to familial hypercholesterolaemia
  2. Moderate-to-severe mixed hyperlipidaemia (typically TChol 6.5-8.0 mmol/L and TG 2.3-5.0 mmol/L)
140
Q

What investigations need to be carried out in suspected familial mixed hyperlipidaemia? (5)

A
  1. Lipid profile
  2. Fasting blood glucose (to exclude hyperlipidaemia secondary to diabetes)
  3. Renal function (to exclude CKD)
  4. LFTs - transaminases to rule out liver disease in the event of a statin having to be initiated - though a statin can still be initiated unless the levels are greater than three times the upper limit of normal
  5. TSH - to exclude myxoedema
141
Q

How is hypercalcaemia diagnosed?

A

If the serum calcium concentration is higher than 2.6mmol/L on two occasions following adjustment (correction) for the serum albumin concentrations.

142
Q

What are the causes of hypercalcaemia? (8)

A
  1. Hyperparathyroidism
  2. Malignancy
  3. Drugs
  4. Granulomatous diseases
  5. Renal
  6. Familial hypocalciuric hypercalcaemia
  7. Non-parathyroid endocrine diseases
  8. Immobility
143
Q

What are the mechanisms of hypercalcaemia in malignancy? (2)

A
  1. In 80% the mechanism is secretion of parathyroid hormone-related protein and other circulating factors by the tumour (a paraneoplastic syndrome)
  2. In 20% bone metastases cause osteolysis and release skeletal calcium, for example in breast cancer and multiple myeloma
144
Q

What are the drugs that can cause hypercalcaemia? (4)

A
  1. Thiazide diuretics - caused by reduced urinary excretion
  2. Lithium - lithium may directly stimulate PTH secretion and increase renal calcium reabsorption
  3. Vitamin D
  4. Vitamin A
145
Q

What are the granulomatous diseases that can lead to hypercalcaemia?

A
  1. Sarcoidosis
  2. TB
  3. Leprosy
  4. Candidiasis
  5. and tons other random ones
    - mechanism is thought to be ectopic production of calcitriol by cells in the lungs and lymph nodes
146
Q

What is the renal disease cause of hypercalcaemia?

A

In CKD, low calcium levels cause parathyroid gland hypertrophy

147
Q

What are the non-parathyroid endocrine disease?

A
  1. Thyrotoxicosis
  2. Addison’s disease
  3. Phaeochromocytoma
  4. Vasoactive intestinal polypeptide hormone-producing tumour
148
Q

What are the skeletal symptoms/signs related to hypercalcaemia? (4)

A
  1. Bone pain
  2. Skeletal deformities
  3. Osteoporosis
  4. Fractures
149
Q

What are the neuropsychiatric signs/symptoms of hypercalcaemia? (4)

A
  1. Drowsiness, delirium, coma
  2. Fatigue, lethargy, muscle weakness, insomnia
  3. Impaired concentration and memory loss
  4. Depression, anxiety, irritability, psychosis
150
Q

What are the gastrointestinal signs/symptoms of hypercalcaemia? (3)

A
  1. Nausea, vomiting, anorexia, weight loss
  2. Constipation, abdominal pain
  3. Peptic ulcer, pancreatitis
151
Q

What are the renal signs/symptoms of hypercalcaemia? (3)

A
  1. Renal colic due to renal stones
  2. Thirst, polyuria, polydipsia, nocturia and dehydration
  3. Renal impairment due to obstructive uropathy
152
Q

What are the cardiovascular sign/symptoms of hypercalcaemia? (3)

A
  1. Hypertension
  2. Shortened QT interval, prolonged PR interval
  3. Cardiac arrhythmias such as VF
153
Q

What is the management of someone who is found to have severe hypercalcaemia or severe symptoms?

A

Arrange emergency hospital admission

154
Q

What is a phaeochromocytoma?

A

It is a rare tumour that secretes catecholamines. It is derived from chromaffin cells, usually in the adrenal medulla, however occasionally extra-adrenal phaeochromocytomas or paraglangliomas occur.

155
Q

What is the other name for a phaeochromocytoma if it is located not in the adrenal medulla?

A

A paraganglioma

156
Q

What can the excessive production of catecholamines from the phaeochromocytoma cause? (2)

A
  1. Life-threatening hypertension

2. Cardiac arrhythmias

157
Q

What are the gene mutations known to be associated with phaeochromocytomas 1/3 of the time? (4)

A

They are from germline mutations in:

  1. MEN 2
  2. Von Hippel-Lindau disease
  3. Neurofibromatosis type 1
  4. Paraganglioma syndromes type 1, 3 and 4
158
Q

What does phaeochromocytoma mean?

A

Greek Phios means dusky, chroma means colour and cytoma means tumour. It refers to the colour of the tumour cells when stained with chromium salts.

159
Q

What are phaeochromocytomas known to produce? (3)

A
  1. Noradrenaline
  2. Adrenaline
  3. Dopamine
160
Q

What do the familial phaeochromocytomas (PHOCC) produce more often?

A

Noradrenaline

161
Q

What do the sporadic phaeochromo’s produce most often?

A

Adrenaline

162
Q

What % of phaeochromo’s are malignant?

163
Q

What % of phaeochromo’s are familial?

164
Q

Which familial syndromes can phaeochromos present in? (3)

A
  1. MEN syndrome
  2. Neurofibromatosis
  3. Von Hippel-Lindau disease
165
Q

In which syndrome can phaeochromos occur bilaterally?

A

70% of them in people with MEN syndromes

166
Q

Why can symptoms of phaeochromo’s vary in duration and severity?

A

Because they may secrete constantly or intermittently

167
Q

What are the symptoms associated with phaeochromo’s? (12 - the first 4 are most common)

A
  1. Headache
  2. Profuse sweating
  3. Palpitations
  4. Tremor
  5. Nausea
  6. Weakness
  7. Anxiety
  8. Sense of doom
  9. Epigastric pain
  10. Flank pain
  11. Constipation
  12. Weight loss
168
Q

If a person with a phaeochromo also has neurofibromas, what may be seen on examination?

A

Cafe au lait patches

169
Q

What may be found on blood tests when suspecting phaeochromo’s?

A
  1. Blood glucose is often raised
  2. Calcium may be elevated
  3. Haemoglobin is elevated due to haemoconcentration from reduction in circulating volume
  4. Plasma catecholamines and plasma metanephrines have both been used in diagnosis.
170
Q

Which blood test is the first line for diagnosing phaeochromo’s?

A

Plasma free metanephrines

171
Q

Which drugs may interfere when testing for phaeochromos and why? (6)

A

Drugs that elevate metanephrines e.g.

  1. Tricyclic antidepressants
  2. Alcohol
  3. Levadopa
  4. Labetalol
  5. Sotalol
  6. Benzodiazepines
172
Q

Where as the common locations for extra-adrenal phaeochromo’s? (5)

A
  1. Close to the origin of the inferior mesenteric artery
  2. Bladder wall
  3. Heart
  4. Mediastinum
  5. Carotid and glomus jugulare tumours
173
Q

Which imaging technique is gold standard for diagnosing phaeochromo?

174
Q

What are the risk factors for precipitating a hypertensive crisis in someone with a phaeochromo? (6)

A
  1. Induction of anaesthesia
  2. Opiates
  3. Dopamine antagonists
  4. Decongestants such as pseudoephedrine
  5. X-ray contrast media
  6. Childbirth
175
Q

What is the management of phaeochromocytomas?

A

Surgical resection

176
Q

What medical management needs to be done before surgical resection of phaeochromo’s?

A

Alpha and beta blockers given to control blood pressure and prevent intra-operative hypertensive crisis

  1. Alpha blockers are started at least 7 days before the operation to allow for expansion of blood volume
  2. Beta blockers are then started only after alpha blockers have been started
  3. CCBs are also useful
177
Q

What is tested after surgical resection of phaeochromo’s to confirm the surgery has worked?

A

2 weeks after surgery a 24-hour urine collection for total catecholamines, metanephrines and VMA is done and is results are normal, the prognosis is excellent.

178
Q

When is a phaeochromo most likely to be malignant?

A

If it has arisen in childhood

179
Q

What is Cushing’s syndrome and what is it caused by?

A

It is caused by prolonged exposure to elevated levels of either endogenous or exogenous glucocorticoids AKA the body is producing too much cortisol

180
Q

What are the two groups Cushing’s syndrome can be divided into? (2)

A
  1. ACTH-dependent disease; excessive ACTH from the pituitary (Cushing’s disease), ectopic ACTH-producing tumours
  2. Non-ACTH-dependent; adrenal adenomas, adrenal carcinomas, excess glucocorticoid administration
181
Q

Who is more likely to get Cushing’s syndrome? (4)

A

People with:

  1. Diabetes
  2. Obesity
  3. Hypertension
  4. Osteoporosis
182
Q

What is the most common cause of Cushing’s syndrome?

A

Exogenous glucocorticoids

183
Q

For the endogenous causes of Cushing’s syndrome, which one isomer common - corticotropin-dependent or corticotropin-independent?

A

Corticotropin-dependent - accounting for 80-85% of cases

184
Q

What % of corticotropin-dependent causes are due to Cushing’s disease?

185
Q

If cushing’s disease accounts for 80% of corticotrophin-dependent causes of Cushing’s syndrome, what causes the remaining 20%?

A

Ectopic corticotropin syndrome - usually due to small-cell lung carcinoma and bronchial carcinoid tumours (though others including phaeochromocytoma, pancreatic neuroendocrine tumours, medullary thyroid cancers etc. can also be a cause)

186
Q

What are the causes of corticotropin-independent Cushing’s syndrome?

A

Often due to unilateral tumours - adrenal adenoma (60%) or adrenal carcinoma (40%). There are other rarer causes for example McCune-Albright syndrome.

187
Q

What are the clinical features of Cushing’s syndrome/how can it present? (14) …fun

A
  1. Truncal obesity
  2. Facial fullness/moon face/facial plethora
  3. Proximal muscle wasting/weakness
  4. Diabetes/impaired glucose tolerance
  5. Reduced libido
  6. Hypertension
  7. Nephrolithiasis
  8. Skin atrophy, hirsutism, acne
  9. Depression, cognitive dysfunction
  10. Osteoporosis
  11. Oedema
  12. Thirst, polydipsia, polyuria
  13. Impaired immune function - increase infections
  14. Growth restriction in children
188
Q

What are the differential diagnoses for Cushing’s syndrome? (5)

A
  1. Chronic severe anxiety/depression
  2. Obesity
  3. Chronic excess alcohol consumption - Cushingoid appearance
  4. Poorly controlled diabetes
  5. HIV infection
189
Q

What are the recommended diagnostic tests for the presence of Cushing’s syndrome? (3)

A
  1. 24-hour urinary free cortisol
  2. 1mg overnight dexamethasone suppression test
  3. Late-night salivary cortisol
190
Q

What is involved in the 24-hour urinary free cortisol collection for diagnosis of Cushing’s syndrome? (3)

A
  1. Ideally three collections, measuring creatinine excretion at the same time
  2. Cushing’s syndrome can be confidently diagnosed if two or more collections measure cortisol excretion as ore than three times the upper limit for normal
  3. The test needs to be repeated if creatinine excretion varies by more than 10% between collections
191
Q

When may false positives occur when doing the 24-hour urinary free cortisol collection? (6)

A
  1. Anorexia
  2. Pregnancy
  3. Exercise
  4. Psychoses
  5. Alcohol/withdrawal
  6. Illness
192
Q

What is the definitive management of endogenous Cushing’s syndrome?

A

Tumour resection

193
Q

If surgical resection is not possible, what is the medical management of endogenous Cushing’s syndrome?

A
  1. Metyrapone
  2. Ketoconazole
  3. Mitotane
    (first two short acting, third one is long-acting)
194
Q

What are the complications of Cushing’s syndrome? (9)

A
  1. Metabolic syndrome
  2. Hypertension
  3. Impaired glucose tolerance and diabetes
  4. Obesity
  5. Hyperlipidaemia - raised LDL
  6. Coagulopathy - thrombophilia
  7. Osteoporosis
  8. Impaired immunity
  9. Nelson’s syndrome
195
Q

What are the causes of premature death in untreated Cushing’s syndrome? (3)

A
  1. Vascular disease - MI/stroke
  2. Uncontrolled diabetes/complications of diabetes
  3. Infections
196
Q

How does cortisol regulate the action of insulin?

A

Cortisol makes fat and muscle cells resistant to the action of insulin, and enhances the production of glucose by the liver.

197
Q

What is Cushing’s disease?

A

It is when you have a pituitary adenoma or other problem in the pituitary gland leading to Cushing’s syndrome

198
Q

Which HLA types are associated with type 1 diabetes?

A

DR3 and DR4

199
Q

Which antibody is associated with type 1 diabetes?

A

Islet cell

200
Q

What are the risk factors for T2DM? (9)

A
  1. Obesity (especially central)
  2. Lack of physical activity
  3. Ethnicity
  4. History of gestational diabetes
  5. Impaired glucose tolerance
  6. Impaired fasting glucose
  7. Drug therapy - thiazide diuretic with a beta blocker
  8. Low fibre, high-glycemic index diet
  9. Metabolic syndrome
201
Q

What programme is offered to patients recently diagnosed with diabetes?

A

DESMOND - diabetes education and self management for ongoing and newly diagnosed

202
Q

If metformin is not adequate, or is contraindicated, what are the other options to treat type 2 diabetes?

A
  1. DPP-4 inhibitor e.g. sitagliptin
  2. Pioglitazone
  3. Sulfonylurea
203
Q

What would be the expected TFTs for a person with thyrotoxicosis e.g. Graves’ disease?

A

TSH: low
T4: high

204
Q

What would be the expected TFTs for someone with primary hypothyroidism?

A

TSH: high
T4: low

205
Q

What would be the expected TFTs for someone with secondary hypothyroidism?

A

TSH: low
T4: low

206
Q

What would be the expected TFTs for someone with subclinical hypothyroidism?

A

TSH: high
T4: normal

207
Q

What would be the expected TFTs for someone with poor compliance with thyroxine?

A

TSH: high
T4: normal

208
Q

What is the expected TFTs for someone on steroid therapy?

A

TSH: low
T4: normal

209
Q

In sick euthyroid syndrome, which TFT is particularly low?

210
Q

What is hypoparathyroidism characterised by?

A
  1. Hypocalcaemia
  2. Hyperphosphataemia
  3. Low or inappropriately normal levels of parathyroid hormone (PTH)
211
Q

Why does hypoparathyroidism lead to high phosphate levels?

A

Because phosphate reabsorption from the kidney is reduced by the parathyroid hormone. If the PTH levels are low, serum phosphate will rise (more will be reabsorbed)

212
Q

What is the most common cause of hypoparathyroidism?

A

Iatrogenic - following anterior neck surgery

213
Q

What is transient hypoparathyroidism in neonates?

A

In healthy term neonates, a reduction in serum calcium levels happen by 24-48 hours of age. If neonates are high risk for example infants of mothers with diabetes or hyperparathyroidism, or preterm, they may develop hypocalcaemia, requiring at least 72 hours of calcium supplementation.

214
Q

Which congenital/genetically inherited syndrome is associated with a defect parathyroid gland?

A

DiGeorge syndrome - abnormal development of the parathyroid glands.

215
Q

What are the two autoimmune conditions that hypoparathyroidism can present in?

A
  1. Autoimmune polyglandular syndrome type 1 (APS-1): features include hypoparathyroidism, adrenal insufficiency and chronic candidiasis
  2. Autoimmune polyglandular syndrome type 2 (APS-2): adrenal insufficiency, insulin-dependent diabetes and thyroid disease.
216
Q

What are the two genetic syndromes (other than DiGeorge) that include hypoparathyroidism?

A
  1. Hypoparathyroidism, deafness and renal dysplasia (HDR) syndrome
  2. Hypoparathyroidism, retardation and dysmorphism (HRD) syndrome
217
Q

What are the causes of acquired hypoparathyroidism? (5) good luck with them

A
  1. Neck surgery (thyroid, parathyroid, laryngeal etc)
  2. Radiation or drugs
  3. Infiltration of the parathyroid glands - destruction due to iron deposition or copper deposition e.g. Wilson’s disease
  4. Magnesium deficiency - which can occur in chronic alcoholism, burns and hereditary renal or intestinal hypomagnesaemia.
  5. Magnesium excess (when it is used to treat preterm labour/pre-eclampsia)
218
Q

How can hypoparathyroidism present? …what are the symptoms of hypocalcaemia? (15…..15 of them!)

A
  1. Muscle pains
  2. Bone pain
  3. Abdominal pain
  4. Paraesthesiae
  5. Facial twitching
  6. Stridor
  7. Convulsions - usually grand mal
  8. Syncope
  9. Memory impairment
  10. Lethargy
  11. Anxiety and depression
  12. Confusion
  13. Headaches
  14. Brittle nails, dry hair and skin
  15. Painful menstruation
219
Q

If considering hypoparathyroidism as a differential, what important points should be elicited in the history? (2)

A
  1. History of previous neck surgery

2. Family history of any hypoparathyroid disorders

220
Q

What is Chvostek’s sign?

A

Tapping of the fifth facial nerve in front of the ear with the patients mouth slightly open causes contraction of the facial muscles

221
Q

What is Trousseau’s sign?

A

Occlude the arterial circulation of the forearm using a blood pressure cuff inflated to the systolic blood pressure for three minutes. Carpopedal spasm is induced.

222
Q

What investigations - bloods - need to be done when suspecting hypoparathyroidism?

A
  1. Calcium (low)
  2. Phosphate (high)
  3. PTH (low)
  4. Alkaline phosphatase (normal)
223
Q

If there is pseudohypoparathyroidism , what would the blood picture show?

A

Low calcium but high or normal PTH

224
Q

What is the management/treatment for hypoparathyroidism?

A
  1. If severe hypocalcaemia - IV calcium
  2. A diet rich in diary products containing calcium and vitamin D is recommended
  3. Basis of treatment = calcium and vitamin D
225
Q

What is the most common malignancy of the endocrine system?

A

Thyroid cancer

226
Q

Which types of thyroid cancer are highly treatable and usually curable?

A

The differentiated tumours - papillary or follicular

227
Q

Which are the undifferentiated thyroid tumours?

A

Medullary and anaplastic - they are less common of the thyroid cancers but are aggressive and metastasise early

228
Q

What is the most common form of thyroid cancer, accounting for 70% of cases?

A

Papillary thyroid carcinoma

229
Q

What is the peak age range of onset of papillary thyroid cancer and which sex is it more common in?

A

Age 35-40 years and three times more common in women

230
Q

What is the second most common form of thyroid cancer, accounting for 10% of them?

A

Follicular thyroid cancer

231
Q

At what age range do follicular thyroid cancers tend to present and what is it associated with?

A

30-60 years of age, and tend to occur in areas of low iodine (it has a greater propensity to metastasise to the lung and bones than papillary carcinoma)

232
Q

Where do medullary thyroid cancers arise from?

A

Parafollicular calcitonin-producing C cells of the thyroid - accounting for 5-8% of all thyroid malignancies

233
Q

Which type of thyroid/blood cancer is associated with Hasimoto’s thyroiditis?

A

Thyroid lymphomas (almost always non-Hodgkin’s)

234
Q

What are the risk factors for thyroid cancer? (5)

A
  1. Exposure to ionising radiation (increased incidence of thyroid cancer in children and adolescents in areas close to the Chernobyl incident)
  2. History of goitre, thyroid nodules or thyroiditis, +ve FHx, female gender and asian race
  3. Genetics
  4. Familial adenomatous polyposis
  5. Obesity
235
Q

What are the red flag features associated with thyroid cancer? (7)

A
  1. A family history of thyroid cancer
  2. History of previous irradiation
  3. A child with a thyroid nodule
  4. Unexplained hoarseness or stridor with a goitre
  5. A painless thyroid mass enlarging rapidly
  6. Palpable cervical lymphadenopathy
  7. Insidious or persistent pain lasting for several weeks
236
Q

Apart from clinical features, how else can you differentiate between type 1 and type 2 diabetes?

A

Presence of autoantibodies - islet cell antibodies (ICA) and anti-glutamic acid decarboxylase (GAD) antibodies

237
Q

For treatment of type 2 diabetes, what are people normally started on first?

238
Q

What does metformin do, and what are its side effects?

A

It increases insulin sensitivity in the body and helps with weight loss.
It’s side effects include nausea, diarrhoea and abdominal pain.

239
Q

Why should metformin be avoided if someone has an eGFR are <36?

A

They are at risk of lactic acidosis (must also be stopped if tissue hypoxia e.g. sepsis or MI)

240
Q

When should another treatment be added after metformin for people with type 2 diabetes?

A

If their HbA1c >53mmol/L 16 weeks after starting metformin

241
Q

What is step 2 in the treatment for type 2 diabetes (after metformin)

A

Sulfonylurea e.g. gliclazide 40mg/d

242
Q

For someone with diabetic retinopathy - background (stage 1), what is seen? (2)

A
  1. Dot and blot (micro aneurysms and haemorrhages)

2. Hard exudates

243
Q

What is seen in pre-proliferative retinopathy?

A
  1. Cotton-wool spots

2. Haemorrhages

244
Q

What is seen in proliferative retinopathy?

A

Neovascularisation

245
Q

What is seen in maculopathy?

A

Suspect if decreased visual acuity

246
Q

Which electrolyte disturbance is most commonly associated with diabetes insipidus?

A

Hypernatraemia

247
Q

What are the causes of hypernatraemia? (3)

A
  1. Diabetes insipidus
  2. Dehydration
  3. Hyperosmolar non-ketotic diabetic coma (HHS)
248
Q

What are the causes of hyponatraemia? (10)

A
  1. SIADH
  2. Thiazides
  3. Addisons
  4. Vomiting
  5. Heart failure
  6. Hypothyroidism
  7. Burns
  8. Diarrhoea
  9. Liver cirrhosis
  10. Psychogenic polydipsia
249
Q

Which hormone is secreted in carcinoid sydnrome?

250
Q

Carcinoid syndrome typically occurs when there are metastases where?

A

Liver metastasis

251
Q

What are the features of carcinoid syndrome? (7)

A
  1. Flushing
  2. Diarrhoea
  3. Bronchospasm
  4. Hypotension
  5. Right heart valvular stenosis
  6. Production of ACTH and GHRH - resulting in Cushing’s syndrome
  7. Pellagra
252
Q

What are the investigations for carcinoid syndrome? (2)

A
  1. Urinary 5-HIAA

2. Plasma chromogranin A y

253
Q

What is diabetes insipidus (DI)?

A

It is a condition caused by hyposecretion of, or insensitivity to the effects of, ADH (AKA arginine vasopressin AVP). Its deficiency or failure to act, causes an inability concentrate urine in the distal renal tubules, leading to the passage of copious volumes of dilute urine.

254
Q

How much urine does a person with diabetes insipidus pass in 24 hours?

A

> 3 litres per 24 hours of low osmolality urine

255
Q

What are the two major forms of DI?

A
  1. Cranial DI

2. Nephrogenic DI

256
Q

What happens in cranial DI?

A

There is decreased secretion of ADH. This reduces the ability to concentrate urine so causes polyuria and polydipsia.

257
Q

What happens in nephrogenic DI?

A

Decreased ability to concentrate urine because of resistance to ADH in the kidneys

258
Q

In addition to the two main forms of DI, what are the two rarer forms?

A
  1. Gestational DI

2. Primary polydipsia - caused by primary defect in osmoregulation of thirst

259
Q

Nephrogenic DI occurs most commonly as a result of what?

A

Adverse effect of lithium - occurs in up to 40% of patients taking lithium

260
Q

What is the most common cause of cranial DI?

A

This is usually due to disease of the hypothalamus or surrounding tissues. Posterior pituitary disease tends not to cause DI, as secretion continues in the hypothalamus, unless a pituitary tumour extends above into the sella, putting pressure on the hypothalamus,

261
Q

What are the causes of acquired cranial DI? - as in what causes disease of the hypothalamus or surrounding tissues? (8)

A
  1. Idiopathic
  2. Tumours - craniopharyngioma, germinoma
  3. Intracranial surgery
  4. Head injury
  5. Granulomata
  6. Infections - encephalitis, meningitis, cerebral abscess
  7. Vascular disorders - haemorrhage/thrombosis
  8. Post-radiotherapy
262
Q

What are the inherited causes of cranial DI? (2)

A
  1. Autosomal recessive compilation of DI, diabetes, optic atrophy, deafness (DIDMOAD) - known as Wolfram’s syndrome
  2. Autosomal dominant mutations of vasopressin gene
263
Q

What are the acquired causes of nephrogenic DI? (7)

A
  1. Idiopathic
  2. Hypokalaemia
  3. Hypercalcaemia
  4. CKD
  5. Drugs - lithium, orlistat
  6. Renal tubular disease - sickle cell, pyelonephritis
  7. Pregnancy
264
Q

What are the congenital causes of nephrogenic DI? (2) (good luck with that)

A
  1. X-linked mutation in V2 ADH-receptor gene

2. Autosomal recessive defect in aquaporin 2

265
Q

What are the symptoms of diabetes insipidus and how can they present? (4)

A

The onset of symptoms can be vague and insidious.

  1. Marked polyuria (>3 litres a day)
  2. Polydipsia and chronic thirst
  3. Nocturia (children may develop nocturnal enuresis where they have previously been continent)
  4. Infants present with irritability, failure to thrive, protracted crying, fever, anorexia
266
Q

What are the signs of DI?

A
  1. Dehydration
  2. Bladder grossly enlarged
  3. 24-hour urinary collection will show volume >3 litres
267
Q

What are the differentials for DI?

A
  1. Diabetes
  2. Psychogenic or primary polydipsia
  3. Cushing’s syndrome
  4. Hyperkalaemia
268
Q

What investigations are done for someone with suspected DI? (5)

A
  1. Biochemistry - plasma glucose, U&Es, urine specific gravity
  2. 24-hour urine collection
  3. Fluid deprivation test with response to desmopressin
  4. MRI of the pituitary, hypothalamus and surrounding tissues
  5. Renal tract USS may be used to assess for obstructive complications caused by the high urinary back-pressure
269
Q

How does the fluid deprivation test work for investigating DI?

A

The patient is deprived of fluids for up to 8 hours or 5% loss of body weight, following which desmopressin 2mcg IM is given.

270
Q

What would you expect to see after doing the fluid restriction and desmopressin test in someone with cranial DI?

A

The urine would be even more concentrated as the desmopressin acts in a similar way to ADH if it was released, and would retain fluid in the body

271
Q

What would you expect to see after doing the fluid restriction and desmopressin test in someone with nephrogenic DI?

A

The urine would remain less concentrated - all fluid would still be lost as the problem is in the kidneys, not how much ADH or desmopressin is given.

272
Q

The fluid restriction and desmopressin test is based on urine osmolality before and after the desmopressin. It is about how concentrated the urine is. What would be expected with a primary/psychogenic polydipsia?

A

Very concentrated urine after fluid restriction and desmopressin - as there is no cranial or nephrogenic reason as to why the ADH and desmopressin would not work

273
Q

What is the management for cranial DI?

A
  1. As the primary problem is a hormone deficiency - physiological replacement with desmopressin is usually effective. This ca be given orally, intranasally or parenterally.
  2. Mild cases of DI (urine output 3-4 litres in 24 hours) can be managed by ingestion of water to quench thirst
  3. It is essential to avoid chronic overdosage of desmopressin
274
Q

Why is it essential to avoid chronic overdosage with desmopressin?

A

It will cause hyponatraemia

275
Q

What is sometimes recommended to try and avoid the development of hyponatraemia in people taking desmopressin for cranial DI?

A

Miss one desmopressin treatment each week

276
Q

What is the treatment for nephrogenic DI?

A
  1. If daily urine volume is <4litres/24 hours and the patient does not have severe dehydration, then definitive therapy is not always necessary. It is important for patients to have access to drinking water and enough to satiate their thirst
  2. Stop any drugs that are causing the problem
  3. Dietary advice to eat less protein and salt
  4. Patients with severe nephrogenic DI, may be prescribed a combination of thiazide like diuretics and NSAIDs
277
Q

What are the side effects of desmopressin? (5)

A
  1. Headache
  2. Stomach pain
  3. Feeling sick
  4. Blocked or runny nose
  5. Nosebleeds
278
Q

What are the symptoms of hyponatraemia? (3)

A
  1. Severe or prolonged headache
  2. Confusion
  3. Nausea and vomiting
279
Q

Which two drugs are commonly known to cause nephrogenic DI? (2)

A
  1. Lithium

2. Tetracycline

280
Q

Why are thiazide like diuretics and NSAIDs prescribed in nephrogenic DI?

A

Thiazide diuretics can reduce the rate the kidneys filter the blood, which reduces the amount of urine passed from the body over time, and NSAIDs help reduce urine volume further.

281
Q

What do they mean by high plasma osmolality and low urine osmolality in DI?

A

High plasma osmolality means high levels of salt in the plasma and low urine osmolality means low levels of salt

282
Q

What is the test for Wilsons disease called?

A

Caeruloplasmin

283
Q

If someone has hereditary haemochromatosis, what type of DI are they are risk of developing?

284
Q

So for DI to be diagnosed, what must the urine osmolality be? (high or low)?

285
Q

Why does the action of thiazides releasing sodium into the urine help break the polyuria-polydipsia cycle?

A

Because DI leads to hypernatraemia so people drink lots of water, but if you lose the salt, you won’t drink as much water . sorted.

286
Q

What is Wolfram’s syndrome?

A 
DIDMOAD
DI
DM
Optic atrophy
Deafness
287
Q

What are carcinoid tumours?

A

Carcinoid tumours are rare, slow-growing tumours that originate in cells of the diffuse neuroendocrine system. They occur most frequently in tissues derived from the embryonic gut.

288
Q

How can the carcinoid tumours be classified in terms of locations?

A

As they are derived from the embryonic gut - they are divided into the:

  • Foregut (25%)
  • Midgut (50%)
  • Hindgut (15%)
289
Q

What do carcinoid tumours secrete?

A

Various bioactive compounds including:
1. Serotonin
2. Bradykinin
…leading to carcinoid syndrome

290
Q

What are the features of carcinoid syndrome?

A
  1. Bronchospasm
  2. Diarrhoea
  3. Skin flushing
  4. Right-sided valvular heart lesions (tricuspid and pulmonary valve stuff)
291
Q

Which carcinoid tumours are most likely to cause carcinoid syndrome?

A

Carcinoid tumours in the ileum and jejunum - especially if they are larger than 1cm

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