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Sharon's Phase 2a Medicine Revision > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Briefly describe what type 1 diabetes mellitus is

A

An autoimmune disease that causes the destruction of beta cells in the islets of Langerhans in the pancreas. This leads to chronic hyperglycemia due to insulin dysfunction.

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2
Q

What is the epidermology of type 1 diabetes mellitus?

A
  • Usually presents ages 5-15
  • 10% of diabetes = T1DM
  • Lean
  • Mostly north European ancestry
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3
Q

What is the aetiology of type 1 diabetes?

A
  • Mutations occur in HLA (human leukocyte antigen) -DR3/4 gene in >90% cases
  • It may be triggered by the Coxsackie B virus and enterovirus
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4
Q

Describe the pathophysiology of type 1 diabetes

A

Autoantibodies attack beta cells in the Islets of Langerhans leading to Insulin deficiency = chronic hyperglycaemia

As the body cannot use glucose as fuel, cells think the body is starved. So continuous breakdown of glycogen from liver (gluconeogenesis) > glycosuria (glucose in urine)

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5
Q

What are the risk factors for type 1 diabetes?

A
  • Northern European ancestry
  • Genetic suspeciability
  • Certain viral infections (e.g. coxsackie B virus or enterovirus)
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6
Q

How would a patient with type 1 diabetes present in clinic?

A

They would complain of

  • Polydipsia (abnormally thirsty)
  • Polyuria
  • Rapid weight loss (BMI <25)

The patient will be young (<30), and may note personal or family history of autoimmune diseases

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7
Q

What tests are used to diagnose type 1 diabetes?

A

Random plasma glucose >11.1 mmol/L (along with symptoms, this alone is enough for a diagnosis)

Fasting plasma glucose >7 mmol/L

HbA1c (glycated haemoglobin) > 6.5% / 48mmol/mol.

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8
Q

What is the management plan (treatment) for type 1 diabetes?

A

Glycaemic control through diet (low sugar, low saturated and trans fat, high starch) and basal-bolus insulin

  • Basal = Long-acting (12 -14 hours) once daily
  • Bolus = Short-acting (4 -6 hours) twice daily with meals

Exercise encouraged.

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9
Q

Define hypoglycaemia

A

Hypoglycaemia is a low blood sugar level (below 4mmol/L)

In diabetes, this is caused by too much insulin, insufficient carbohydrates or not processing the carbohydrates properly, for example, in malabsorption, diarrhoea, vomiting and sepsis.

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10
Q

What early symptoms of a low blood sugar level might a patient with T1DM experience?

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

Please note that some patients might be unaware of their symptoms until they are severely hypoglycaemic

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11
Q

What symptoms might a patient with T1DM experience if they were experiencing a more serious hypoglycaemic episode?

A
  • Confusion or difficulty concentrating
  • Unusual behaviour, slurred speech or clumsiness (like being drunk)
  • Feeling sleepy
  • Collapsing or passing out
  • Seizure
  • Coma
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12
Q

How is hypoglycaemia treated?

A

Hypoglycaemia is usually treated with rapid-acting glucose e.g., Lucozade and slower-acting carbohydrates, such as biscuits and toast.

For severe hypoglycaemia where the patient is unconscious, having seizures or in a coma and oral glucose would not be safe, treatment is IV dextrose and intramuscular glucagon.

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13
Q

How are patients with type 1 diabetes monitored?

A
  • HbA1c tests - 3 to 6 monthly
  • Capillary blood glucose (finger prick) - immediate glucose reading, for self monitoring in T1DM and T2DM
  • Flash glucose monitoring (e.g. Freestyle Libre) - sensor placed in patient’s arm allows reader to measure glucose levels of interstitial fluid. Reading lags 5 mins behind blood glucose levels. Need to change every 2 weeks.
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14
Q

What are the complications of uncontrolled T1DM/T2DM?

A
  • Diabetic ketoacidosis

Microvascular

  • Diabetic neuropathy leads to lack of sensation in feet > occult foot ulcers
  • Diabetic retinopathy
  • Diabetic nephropathy

Macrovascular:

  • Strokes
  • Renovascular disease
  • Limb ischaemia
  • Heart disease
  • Hyperosmolar hyperglycaemic nonketotic coma (mostly in type 2s)
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15
Q

Briefly describe what type 2 diabetes mellitus is

A

A disease characterised by abnormally low insulin secretions and peripheral insulin resistance, which leads to chronic hyperglycemia due to insulin dysfunction

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16
Q

What is the epidemiology of T2DM?

A
  • Onset older (>30 years)
  • Usually overweight
  • More common in certain ethnic groups (Black African, Afro-Caribbean, Chinese, South Asian)
  • 90% of diabetes = T2DM
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17
Q

What is the aetiology of T2DM?

A

Genetic susceptibility, but no HLA gene link like in T1DM

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18
Q

What are the risk factors for T2DM?

A

Non-Modifiable:

  • Older age
  • Ethnicity (Black, Chinese, South Asian)
  • Family history

Modifiable:

  • Obesity
  • Sedentary lifestyles
  • High carbohydrate (particularly refined carbohydrate) diet
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19
Q

How would a patient with T2DM typically present in clinics? What signs and symptoms are present?

A

Consider T2DM in any patients with risk factors.

Additional symptoms:

  • Fatigue
  • Polydipsia and polyuria (thirsty and urinating a lot)
  • Unintentional weight loss

Signs

  • Opportunistic infections
  • Slow healing
  • Glucose in urine (on dipstick)
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20
Q

What tests are used to diagnose T2DM?

A
  • Fasting plasma glucose (≥7.0 mmol/L)
  • HbA1c (≥48 mmol/mol (≥ 6.5%)

Oral glucose tolerance test:

  • Takes baseline fasting plasma glucose before breakfast
  • Give 75g glucose drink
  • Measure glucose 2 hours after - ≥ 11.1 mmol/L
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21
Q

What is pre-diabetes?

A

Pre-diabetes is an indication that the patient is heading towards developing T2DM. They do not fully fit the diagnostic criteria for T2DM but should be educated on diabetes and lifestyle changes

Not recommended to start treatment

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22
Q

What tests are used to diagnose pre-diabetes?

A
  • HbA1c test – 42-47 mmol/mol
  • Impaired fasting glucose – fasting glucose 6.1 – 6.9 mmol/l
  • Oral glucose tolerance test:

Impaired glucose tolerance – plasma glucose at 2 hours 7.8 – 11.0 mmol/l on an OGTT

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23
Q

What is the management plan for T2DM?

A

Two-pronged approach:

Lifestyle:

  • Dietary change (veg, oily fish, low GI, high fibre foods)
  • Exercise
  • Stop smoking
  • Weight loss

Target HbA1c = 48mmol/mol (6.5%), if above, start metformin

Medical

  • First line: metformin
  • Second line: metformin + SGLT-2 inhibitor/ GLP-1 receptor agonist
  • Third line: triple therapy with metformin and two of the second line drugs combined, or metformin plus insulin
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24
Q

What is the mechanism of action of metformin?

A

Metformin is a biguanide, and it lowers blood glucose by increasing the response (sensitivity) to insulin.

It suppresses hepatic glucose production (gluconeogenesis), increases glucose uptake and utilisation by skeletal muscle and suppresses intestinal glucose absorption.

Does not stimulate pancreatic insulin secretion and so does not cause hypoglycemia

Can stimulate weight loss

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25
Q

What are the side effects of metformin?

A

Common: Abdominal pain; appetite decreased; diarrhoea; gastrointestinal disorder; nausea; taste altered; vitamin B12 deficiency; vomiting

Rare or very rare: hepatitis; lactic acidosis (discontinue); skin reactions

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26
Q

How is metformin excreted from the body? How does this affect how it is prescribed?

A

Excreted unaltered by the kidneys

Therefore contraindicated in patients with severe renal impairment.

Dose reduction needed in patients with moderate renal impairment

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27
Q

Sodium-glucose co-transporter-2 (SGLT2) inhibitors (e.g. Dapagliflozin)

1) Use
2) MOA
3) Side effects

A

1) Type 2 diabetes mellitus

2) SGLT2 inhibitors reduce the amount of glucose being reabsorbed in the kidneys so that it is passed out in the urine

3) UTI

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28
Q

GLP-1 receptor agonists (glucagon-like receptor agonists) e.g. semaglutide

1) Use
2) MOA
3) Side effects

A

1) Type 2 diabetes mellitus

2) GLP-1 receptor agonists stimulate the release of insulin and suppress glucagon secretion only when blood glucose concentrations are elevated; thus, the risk of hypoglycaemia is low

3) GI: decreased appetite, N + V, headache, renal impairment

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29
Q

How are patients with T2DM monitored?

A

Same as T1DM

  • HbA1c tests - 3 to 6 monthly
  • Capillary blood glucose (finger prick) - immediate glucose reading. Patients with T1DM and T2DM use these to self-monitor
  • Flash glucose monitoring (e.g. Freestyle Libre) - sensor placed in patient’s arm allows reader to measure glucose levels of interstitial fluid. Reading lags 5 mins behind blood glucose levels. Need to change every 2 weeks.
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30
Q

What is diabetic ketoacidosis?

A

In type 1 DM, cells cannot use glucose as fuel and think they are starving. They undergo ketogenesis so that they have usable fuel.

  • Over time the patient gets higher and higher glucose and ketones levels.
  • Initially, the kidneys produce bicarbonate to counteract the ketone acids in the blood and maintain a normal pH.
  • Over time the ketone acids use up the bicarbonate and the blood becomes acidic > metabolic acidosis (pH < 7.3). This is called ketoacidosis.
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31
Q

How would a patient with diabetic ketoacidosis present?

A

Symptoms

  • Polyuria
  • Polydipsia
  • Nausea and vomiting

Signs

  • Acetone smell to their breath
  • Dehydration and subsequent hypotension
  • Altered Consciousness
  • They may have symptoms of an underlying trigger (i.e. sepsis)
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32
Q

What can diabetic ketoacidosis lead to?

A

DEATH! The most dangerous aspects are dehydration, potassium imbalance and acidosis which can kill the patient

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33
Q

How is diabetic ketoacidosis diagnosed?

A

Hyperglycaemia (i.e. blood glucose > 11 mmol/l)
Ketosis (i.e. blood ketones > 3 mmol/l)
Acidosis (i.e. pH < 7.3)

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34
Q

How is diabetic ketoacidosis treated?

A

FIG-PICK - follow local protocols carefully

  • F – Fluids – IV saline
  • I – Insulin – IV insulin
  • G – Glucose – monitor and add a dextrose infusion if too low (e.g. 14 mmol/l)
  • P – Potassium – Closely monitor serum potassium (e.g. 4 hourly) and correct as required
  • I – Infection – Treat underlying triggers such as infection
  • C – Chart fluid balance
  • K – Ketones – Monitor blood ketones/bicarbonate

Establish the patient’s normal subcutaneous insulin regime before stopping the insulin and fluid infusion.

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35
Q

Briefly describe diabetic ketoacidosis and its aetiology

A

DKA is a complete lack of insulin that results in high ketone production

Medical emergency!

Results from untreated T1DM or infections/illness

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36
Q

Briefly describe hyperosmolar hyperglycaemic state (HHS) and its aetiology

A

A disease characterised by marked hyperglycemia, hyperosmolality and mild/no ketosis

Results from untreated T2DM usually

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37
Q

What is the pathophysiology of HHS?

A

Low blood insulin means cells think the body is starving, increased gluconeogenesis which leads to hyperglycaemia, but enough insulin to inhibit ketogenesis

Hyperglycemia -> osmotic diuresis (presence of increased glucose leads to increased urination) -> dehydration

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38
Q

What are the signs and symptoms of HHS?

A

Extreme diabetes symptoms and:
- Confusion and reduced mental state
- Lethargy
- Severe dehydration

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39
Q

What is the treatment for HHS?

A

Replace fluid - 0.9% saline IV
Insulin - at low rate of infusion!
Restore electrolytes - e.g. K+
Low-moecular weight heparin (anti-coagulant)

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40
Q

Briefly describe hyperthyroidism

A

Hyperthyroidism is a disease characterised by the over-production of thyroid hormones T3 and T4 by the thyroid gland.

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41
Q

What is the aetiology of hyperthyroidism?

A
  • Graves disease - 65-75%, Autoimmune
  • Toxic multi-nodular goitre
  • Toxic adenoma
  • Metastatic follicular thyroid cancer
  • Iodine excess (e.g. IV contrast)
  • Secondary causes - TSH secreting pituitary tumour
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42
Q

What is Graves disease?

A

An autoimmune condition where TSH receptor antibodies cause a primary hyperthyroidism (thyroid dysfunction)

These TSH receptor antibodies are abnormal antibodies that mimic TSH and stimulate the TSH receptors on the thyroid.

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43
Q

What is the epidemiology of hyperthyroidism?

A

Mainly young women 20 - 40
Ratio F to M 9:1

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44
Q

What are the risk factors for hyperthyroidism?

A
  • Smoking
  • Stress
  • HLA-DR3 (susceptibility gene)
  • Other autoimmune diseases e.g. T1DM, Addisons, Vitiligo
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45
Q

What is the pathophysiology of hyperthyroidism?

A

Excess blood levels of T3 increases metabolic rate, cardiac output, bone resorption and stimulates the sympathetic nervous system

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46
Q

What signs and symptoms might a patient with hyperthyroidism present with?

A

Everything goes faster than it should :(

Symptoms:

  • Hot + sweaty
  • Diarrhoea
  • Hyperphagia (excessive eating)
  • Weight loss
  • Palpitations
  • Tremor
  • Irritability
  • Anxiety/restlessness

Signs

  • Oligomenorrhoea (infrequent mensuration)
  • Goitre
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47
Q

What is the treatment for hyperthyroidism?

A
  • Beta-blockers - rapid relief from adrenaline related symptoms
  • 1st line Carbimazole - bocks synthesis of T4 (TETRAOGENIC!)
  • 2nd line Propylthiouracil - prevents T4->T3 conversion
  • Radioactive iodine is first-line definitive treatment in more-than-mild Graves’ - destroys part of thyroid
  • Thyroidectomy - hemi or total
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48
Q

What is De Quervain’s thyroiditis?

A

Swelling of the thyroid glands due to viral infection, patient will present with fever, neck pain and tenderness, dysphagia and features of hyperthyroidism.

Hyperthyroid phase followed by a hypothyroid phase as the TSH level falls due to negative feedback.

  • Self-limiting condition
  • Treat with NSAIDs for pain and inflammation
  • Beta-blockers for symptom relief of hyperthyroidism
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49
Q

Which 2 drugs can cause hypothyroidism?

A
  • Lithium (mood stabiliser)
  • Amiodarone (cardiac arrhythmia)
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50
Q

What is post-partum thyroiditis?

A

Post-partum women (around 8%) can develop lymphocytic thyroiditis, which causes transient primary hypothyroidism

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51
Q

What are symptoms specific to Graves disease?

A
  • Hyperthyroidism symptoms plus:
  • Thyroid eye disease (25-50%)
  • Eyelid retraction
  • Periorbital swelling (swollen eyes)
  • Proptosis/Exophthalmos (bulging eyes)
  • Pretibial myxoedema (skin disorder associated with Graves disease)
  • Thyroid acropachy (signs associated with autoimmune thyroid disease)
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52
Q

What are some complications that can arise from hyperthyroidism?

A

Cardiovascular: heart failure, atrial fibrillation

Musculoskeletal: osteoporosis

Thyrotoxic crisis (thyroid storm):

  • Life-threatening, more severe form of hyperthyroidism, medical emergency!
  • Often occurs secondary to infection or trauma in patients with known hyperthyroidism
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53
Q

What is the treatment for a thyroid storm?

A
  • Admission for monitoring
  • Supportive care with:
  • Fluid resuscitation
  • Antithyroid drugs: propylthiouracil
  • Corticosteroid: IV hydrocortisone
  • Beta-blockers: propanolol
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54
Q

Briefly describe hypothyroidism

A

Hypothyroidism is a pathological state reflecting a reduction in circulating T3 and T4.

  • Primary - abnormal decreased thyroid function resulting in failure to produce thyroid hormones
  • Secondary - abnormal decreased TSH production by the pituitary gland
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55
Q

What is the pathophysiology of hypothyroidism?

A

Aggressive destruction of thyroid cells by various cell and antibody mediated immune processes. Antibodies bind and block TSH receptors -> inadequate thyroid hormone production and secretion

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56
Q

What is the epidemiology of hypothyroidism?

A

4/1,000 per year
Mainly >40 years old
Ratio of affected female: male - 6:1

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57
Q

What is the main cause of hypothyroidism?

A
  • Hashimoto’s (inflammation and goitre)
  • Autoimmune disease where immune system attacks thyroid cells
  • More common in females 60-70 years old
    Primary atrophic hypothyroidism (atrophy -> no goitre)
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58
Q

What are symptoms (experienced by patient) might a patient with hypothyroidism present with?

A

Everything goes slower than it should!

Fatigue
Weight gain
Loss of appetite
Cold
Lethargy
Constipation
Low mood/depression
Menorrhagia (heavy periods)
Goitre

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59
Q

What are SIGNS (found through examination or investigation) might a patient with hypothyroidism present with?

A
  • Bradycardia
  • Reduced Reflexes (deep tendon)
  • Dermatological: hair loss, loss of lateral eyebrows, dry and cold skin, coarse hair
  • Goitre
  • Carpal tunnel syndrome
  • Hoarse voice: rare
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60
Q

What are the investigations/tests used to diagnose hypERthyroidism?

A

1st line: thyroid function tests - increased T4/T3, but:

Primary hyperthyroidism (e.g. Graves): lower TSH than normal

Secondary hyperthyroidism: higher TSH than normal

Thyroid autoantibodies (anti-TSH receptor)

Ultrasound and CT of the head (if serology cannot confirm_

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61
Q

What are the investigations/tests used to diagnose hypOthyroidism?

A

TFTs - ↓T4 ↓T3

Primary: ↑TSH

Secondary ↓TSH

TPO (thyroid peroxidase) antibodies - associated with Hashimoto’s

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62
Q

What is the treatment for hypothyroidism?

A

Levothyroxine (T4 analogue)

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63
Q

Briefly describe Cushing’s syndrome

A

The clinical manifestation of pathological hypercortisolism from any cause

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64
Q

What is the aetiology of Cushing’s syndrome?

A

Adrenocorticotropic hormone (ACTH) dependent:

  • Cushing’s Disease - ACTH secreting from pituitary adenoma
  • Ectopic ACTH production from small-cell lung cancer

ACTH independent:

  • Iatrogenic- steroid use (most common)
  • Adrenal adenoma
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65
Q

What signs and symptoms may a patient with Cushing’s syndrome present with?

A
  • Moon face
  • Central obesity
  • Buffalo hump
  • Acne
  • Hypertension
  • Abdominal striae (stretch marks)
  • Hirsutism (excessive hair growth in women)
  • weight gain
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66
Q

What are the risk factors for Cushing’s syndrome?

A
  • Exogenous corticosteroid use (e.g. steroids)
  • Pituitary adenoma
  • Adrenal adenoma
  • Adrenal adenocarcinoma
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67
Q

What are the investigations/tests used to diagnose Cushing’s syndrome?

A
  • Random plasma cortisol- raised
  • Overnight dexamethasone suppression test- most sensitive
  • Low-dose dexamethasone suppression (1mg), normal/high cortisol with high-dose (8mg) dexamethasone - low cortisol > Cushing’s syndrome
  • Urinary free cortisol (24 hr) (most commonly performed) - elevated
  • Plasma ACTH
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68
Q

Hypercortisolism: what is a raised plasma ACTH suggestive of?

A

An ACTH-dependent cause > high dose dexamethasone suppression test (8mg)

If high-dose dexamethasone suppresses cortisol levels, then the diagnosis is Cushing’s disease.

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69
Q

Hypercortisolism: what is a low plasma ACTH suggestive of?

A

Suggests an ACTH-independent cause and warrants CT adrenals to look for adrenal pathology

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70
Q

What is a high-dose dexamethasone suppression test?

A

Given at night (10pm), measured in the morning (9am)

8mg dexamethasone administered to patient, suppression of cortisol occurs in Cushing’s disease (pituitary adenoma), but not in an ectopic ACTH source

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71
Q

What is the differential diagnosis (DDx) for Cushing’s syndrome?

A

Pseudo-Cushing’s syndrome - caused by excess alcohol, resolves after 1-3 weeks of alcohol abstinence

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72
Q

What is the management plan/treatment for Cushing’s syndrome?

A

Depending on the underlying cause:

ACTH-dependent causes:

  • Cushing’s disease (pituitary adenoma): 1st line treatment is with trans-sphenoidal resection of the pituitary tumour.
  • Medical therapy (e.g. glucocorticoid antagonists) or radiotherapy if surgery fails
  • Ectopic ACTH source: treatment of underlying cancer

ACTH-independent causes:

  • Iatrogenic: review the need for medication and try weaning if possible
  • Adrenal tumour: tumour resection or adrenalectomy
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73
Q

Briefly describe acromelogy

A

Release of excess growth hormone(GH)causing overgrowth of all systems

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74
Q

What is the epidemiology of acromelogy?

A
  • Rare (3 per million/year)
  • Equal prevalence between males and females
  • Incidence is highest in people 40 +
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75
Q

What is the aetiology of acromelogy?

A
  • Most commonly caused by benign GH-producing pituitary tumours
  • Rare case caused by cancers that secrete ectopic GH release
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76
Q

What are the risk factors for acromology?

A

5% are associated with the inherited disorder MEN-1 (multiple endocrine neoplasia-1)

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77
Q

What are the signs and symptoms of acromology?

A
  • Prominent forehead and brow
  • Increased jaw size
  • Large hands, nose, tongue, feet
  • Visual field defect (bitemporal hemianopia)
  • Polyuria and polydipsia: due to T2DM
  • Profuse sweating
  • Lower pitch of voice
  • Obstructive sleep apnoea
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78
Q

What is the pathophysiology of acromlogy?

A
  • Increased GH either secreted by pituitary tumour or ectopic carcinoid tumour travels to tissues such as the liver and results in an increase in insulin-like Growth Factor-1
  • This stimulates skeletal and soft tissue growth giving rise to ‘giant-like’ appearance and symptoms
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79
Q

What are the investigations/tests for diagnosing acromlogy?

A

1st line: Insulin-like Growth Factor 1 test = raised

Gold standard: Oral glucose tolerance test while measuring GH levels (high glucose suppresses GH)

80
Q

What are the treatments for acromology?

A
  • 1st line: Transsphenoidal resection surgery (if cause is adenoma)
  • 2nd line: Somatostatin analogue eg. Octreotide
81
Q

Briefly describe prolactinoma

A

Benign adenoma of anterior pituitary gland producing excess prolactin.

82
Q

What is the epidemiology of prolactinoma?

A
  • Most common hormonal disturbance of the pituitary
  • More common in females than males
  • Presents earlier in women ( with menstrual disturbance) but later in men (with erectile dysfunction)
83
Q

What is the aetiology of prolactinoma?

A
  • Micro tumour (less than 10mm diameter on MRI - 90%)
  • Macro tumour (more than 10mm diameter on MRI- 10%)
  • Non-functional tumour that compresses the pituitary gland, inhibiting dopamine release > disinhibition of prolactin release
  • Antidopaminergic drugs
84
Q

What is the pathophysiology of prolactinoma?

A

Increased release of prolactin from the benign tumour in anterior pituitary gland can cause galactorrhoea (breast milk production not associated with pregnancy or breast-feeding) by stimulating milk production from the mammary gland and inhibiting FSH (follicle-stimulating hormone) and LH (luteinizing hormone)

85
Q

What signs and symptoms may a patient with prolactinoma present with?

A
  • Visual field defect
  • Headache
  • Menstrual irregularity
  • Infertility
  • Galactorrhoea (milky discharge from nipples)
86
Q

What investigations/tests are used to diagnose prolactinoma?

A

The baseline level of prolactin is measured and will be very high

87
Q

What is the treatment for prolactinoma?

A

Gold standard

  • Transsphenoidal resection surgery of pituitary gland

1st line

  • Dopamine agonists: Bromocriptine/cabergoline (Dopamine has an inhibitory effect on prolactin)
88
Q

Briefly describe Conn’s syndrome

A

Primary hyperaldosteronism due to an aldosterone producing adrenal adenoma

89
Q

What are the risk factors for Conn’s syndrome?

A

Hypertension in patients:

  • Under 35 yrs with no family history of hypertension
  • With accelerated (malignant) hypertension
  • With hypokalaemia before diuretic therapy (helps rid the body of sodium and water)
  • Resistant to conventional antihypertensive therapy e.g. more than 3 drugs
  • With unusual symptoms e.g. sweating attacks or weakness
90
Q

What is the pathophysiology of Conn’s syndrome?

A

Excess production of aldosterone from the adrenal cortex, independent of the renin-angiotensin system leads to:

  • High Sodium and water retention
  • Increased potassium excretion in kidneys
  • Low renin release
91
Q

What signs and symptoms may a patient with Conn’s syndrome present with?

A

Symptoms:

  • Lethargy
  • Mood disturbance
  • Paresthesia and muscle cramps (due to hypokalemia)

Signs:

  • Hypokalaemia (< 3.5mmol/l)
  • Refractory hypertension
92
Q

What investigations/tests are used to diagnose Conn’s syndrome?

A

1) 1st line screening test:

  • Plasma aldosterone: renin ratio (ARR) > increased aldosterone, low renin > CT

High-resolution CT abdomen: useful to exclude carcinoma

93
Q

What is the treatment for Conn’s syndrome?

A

1st line:

  • Spironolactone - a potassium sparing diuretic for pre-op controls of BP and K+ levels

Gold standard:

  • Laparoscopic Adrenalectomy

The aim is to lower BP, decrease aldosterone levels and resolve electrolyte imbalance

94
Q

Briefly describe Addison’s disease

A

Primary adrenal insufficency

95
Q

What is the epidemiology of Addison’s disease?

A
  • Very rare - 0.8 per 100,000
  • Can be fatal
  • Marked female preponderance
96
Q

What is the aetiology of Addison’s disease?

A
  • Autoimmune adrenalitis - most common 80% of cases in the UK
  • TB (most common cause worldwide)
  • Adrenal metastases
97
Q

What is the pathophysiology of Addison’s disease?

A

Destruction of the entire adrenal cortex resulting in mineralocorticoid (aldosterone, zona glomerulosa), glucocorticoid (cortisol, zona fasciculata) and androgens (precursors of sex hormones, zona reticularis) deficiency.

Corticosteroids (glucocorticoids and mineralocorticoids) are involved in renal excretion of potassium and acid as well as sodium reabsorption. Hence, adrenal insufficiency results in a metabolic acidosis coupled with hyperkalaemia and hyponatraemia.

98
Q

What are some risk factors for Addison’s disease?

A

Autoimmune adrenalitis is associated with other autoimmune diseases including DMT1, pernicious anaemia and hypothyroidism

If the patient has one of the above and present with symptoms of Addison’s, it is worth considering

99
Q

What signs and symptoms might a patient with Addison’s disease present with?

A
  • Tanned skin
  • Lean
  • Fatigue
  • Pigmentation especially of palmar creases (increased ACTH cross-reacts with melanin receptors)
  • Postural Hypotension
  • Vomiting and nausea
100
Q

What investigations/tests are used to diagnose Addison’s disease?

A

1st line:

  • Morning serum cortisol (8 - 9am sample as peak cortisol levels) - abnormally low at <100 nanomols/L
  • 100 - 500nmol/L = refer to ACTH stimulation test
  • > 500nmol/L = normal

Gold standard:

  • ACTH stimulation test:
  • Measure plasma cortisol before and 30 mins after IM TETRACOSACTIDE (Synacthen - ACTH analogue)
  • Addison’s is excluded if 30 min cortisol > 550nmol/L (diagnostic if below 550nmol/L)

8am plasma adrenocorticotrophic hormone (ACTH): increased due to loss of negative feedback from cortisol

Serum electrolytes: hyponatraemia & hyperkalaemia due to a decrease in aldosterone

101
Q

What are some DDx for Addison’s disease?

A
  • Adrenal suppression due to the use of glucocorticoid
  • Central (secondary or tertiary) adrenal insufficiency (pituitary or hypothalamic lesions)
102
Q

What is the treatment/management plan for Addison’s disease?

A

Replace steroids depending on signs, and symptoms:

  • Hydrocortisone (glucocorticoid) - replaces cortisol
  • Fludrocortisone (mineralocorticoid) - replaces aldosterone
  • Treat the underlying cause and warn against abruptly stopping steroids
  • Double hydrocortisone dose if intercurrent illness
103
Q

What is an adrenal crisis?

A

Adrenal crisis or Addisonian crisis, is a state of acute insufficiency of adrenocortical hormones.

Most often occurs in patients with established Addison’s disease due to poor medication compliance, infection, trauma, surgery, or myocardial infarction.

104
Q

What signs and symptoms might a patient with an adrenal crisis present with?

A

Symptoms

  • Nausea and vomiting
  • Abdominal pain
  • Trigger e.g. infection or MI

Signs

  • Hypotension
  • Hypovolemic shock
  • Reduced GCS
105
Q

What is the management plan for an adrenal crisis?

A
  • Corticosteroid: hydrocortisone 100 mg IV STAT!
  • IV saline and dextrose if hypoglycemic
106
Q

Briefly describe SIADH

A

Syndrome of inappropriate ADH: abnormally increased ADH secretion from the posterior pituitary or an ectopic source, causing water retention and hypernatremia

107
Q

What is the aetiology of SIADH?

A
  • Tumours (SCLC, prostate, pancreatic)
  • Post-operative from major surgery
  • Infection (TB and pneumonia which causes lung abscess)
  • Head injury
  • Medications (thiazide diuretics) are the most common cause
108
Q

What is the pathophysiology of SIADH?

A

Excess release of ADH will result in the increased aquaporin 2 channels in the collecting duct

Excess water retention > dilute plasma > hyponatraemia < 135 mmol/L (more water so lower concentration of sodium)

There is a loss of an effective feedback mechanism > continuous ADH production irrespective of serum osmolality > a low serum sodium and relatively high urinary sodium with concentrated urine.

109
Q

What signs and symptoms might a patient with SIADH present with?

A

Symptoms are a result of hyponatraemia:

  • Headache
  • Nausea
  • Fatigue
  • Muscle cramps
  • Confusion

If severe > seizures and coma

Fluid status:

  • Euvolaemic: no features of hypervolaemia or hypovolaemia as water reabsorbed is distributed evenly across the extra and intravascular compartment
110
Q

What investigations/tests are used to diagnose SIADH?

A

SIADH is a diagnosis of exclusion as we do not have a reliable test to measure ADH activity directly.

Clinical examination will show

  • Euvolaemia.
  • U+Es will show hyponatraemia (< 135mmol/L)
  • Urine sodium and osmolality will be high.

Other causes of hyponatraemia need to be excluded:

  • Negative short synacthen (ACTH analogue) test to exclude adrenal insufficiency
  • No history of diuretic use
  • No diarrhoea, vomiting, burns, fistula or excessive sweating
  • No excessive water intake
  • No chronic kidney disease or acute kidney injury
111
Q

What is the management plan for SIADH?

A
  • Stop causative medication
  • Fluid restriction to 500mls – 1litre. This may be enough to correct hyponatraemia without medications.
  • Tolvaptan. “Vaptans” are ADH receptor blockers. Causes a rapid increase in sodium. So initiated by a specialist endocrinologist and require close monitoring.
112
Q

Briefly describe arginine vasopressin deficiency (previously diabetes insipidus - includes pathophysiology)

A

2 types: cranial and nephrogenic

The passage of large volumes (>3L/day) of dilute urine due to impaired water reabsorption in the kidney either because of:

  • Reduced ADH secretion from the posterior pituitary - cranial AVD/DI
  • Impaired response of the kidney to ADH - nephrogenic AVD/DI
113
Q

What is the aetiology of cranial AVD/DI?

A
  • Idiopathic (unknown cause)
  • Congenital
  • Tumour
  • Trauma
  • Infection
114
Q

What is the aetiology of nephrogenic DI?

A
  • Inherited
  • Metabolic (low potassium, high calcium)
  • Drugs (lithium)
  • Chronic renal disease
115
Q

What signs and symptoms might a patient with AVD/DI present with?

A

Symptoms
Polyuria (excessive urine production)
Polydipsia (excessive thirst)

Signs
Dehydration
Postural hypotension
Hypernatraemia

116
Q

What are some DDx for DI?

A

Polyuria and polydipsia can also be indicative of diabetes mellitus

117
Q

What investigations/tests are used to diagnose DI?

A

GOLD STANDARD!

Water deprivation test to determine if it is DI and desmopressin stimulation test to determine if cranial or nephrogenic

  • Patient goes without fluids for 8 hours
  • Urine osmolarity measured

If cranial - urine osmolarity:

  • After water deprivation - low (still dilute)
  • After ADH analogue - high (back to normal) as kidneys can still respond to ADH

If nephrogenic - urine osmolarity:

  • After water deprivation - low (still dilute)
  • After ADH analogue - low (still dilute) as kidneys cannot respond to ADH
118
Q

What is the management plan/treatment for DI?

A
  • Treat underlying cause. Mild cases can be managed conservatively without any intervention.
  • Desmopressin (synthetic ADH) can be used in:
  • Cranial diabetes insipidus to replace ADH
  • Nephrogenic diabetes insipidus in higher doses under close monitoring
119
Q

What is the risk factor AVD/DI?

A

Family history

120
Q

Briefly describe hyperparathyroidism (primary, secondary and tertiary)

A

Parathyroid hormone (PTH) elicits several functions that increase plasma Ca2+ levels

Hyperparathyroidism is the excessive secretion of PTH and can be primary, secondary or tertiary

Primary hyperparathyroidism - excessive PTH secretion from the parathyroid glands

Secondary hyperparathyroidism - hypertrophy of parathyroid glands to compensate for hypocalcemia

Tertiary hyperparathyroidism - autonomous secretion of PTH from parathyroid glands due to hyperplasia.

121
Q

What is the aetiology of primary, secondary and tertiary hyperparathyroidism?

A

Primary hyperparathyroidism - tumour of the parathyroid glands causing excessive secretion of PTH

Secondary hyperparathyroidism - chronic kidney disease, and vitamin D deficiency due to diet or GI diseases (e.g. Crohn’s) > hypocalcaemia

Tertiary hyperparathyroidism - occurs after persistent parathyroid hyperplasia (as in secondary HPT) after correction of underlying cause, often seen in chronic renal failure

122
Q

What are the risk factors for developing hyperparathyroidism?

A
  • Female sex: 3:1 female to male ratio in primary hyperparathyroidism
  • Radiation therapy to the neck
  • Severe vitamin D or calcium deficiencies
  • Familial rare conditions: MEN1 and 2A
123
Q

What is the pathophysiology of hyperparathyroidism?

A

Primary hyperparathyroidism - caused by uncontrolled parathyroid hormone produced by a parathyroid tumour which leads to hypercalcemia.

  • Serum calcium = high, PTH = high

Secondary hyperparathyroidism - insufficient vitamin D or chronic renal failure leads to low calcium absorption from the intestines, kidneys and bones > hypocalcemia

Parathyroid glands respond by releasing more PTH, and this leads to hyperplasia over time.

  • Serum calcium = low/normal, PTH = high

Tertiary hyperparathyroidism is as a result of secondary hyperparathyroidism > hyperplasia of parathyroid gland > baseline PTH level inappropriately high even after the cause of SHP treated > high absorption of calcium in the intestines, reabsorption from kidneys and release from bones > hypercalcaemia.

  • serum calcium = high, PTH = high
124
Q

What signs and symptoms might a patient with hyperparathyroidism present?

A

Stones, bones, groans and moans!

Renal stones
Painful bones
Abdominal groans - constipation, nausea and vomiting
Psychiatric moans - fatigue, depression and psychosis

125
Q

What investigations/tests are used to diagnose hyperparathyroidism?

A

Measuring serum calcium and PTH levels

Primary: serum calcium = high, PTH = high

Secondary: serum calcium = low/normal, PTH = high

Tertiary: serum calcium = high, PTH = high

126
Q

What are the treatments for hyperparathyroidism?

A

Primary: surgical removal of the causative tumour

Secondary: correcting the vitamin D deficiency or performing a renal transplant to treat renal failure.

Tertiary: surgical removal of part of the parathyroid tissue to return the parathyroid hormone to an appropriate level or removal of whole gland

127
Q

Briefly describe hypoparathyroidism (includes aetiology)

A

Primary hypoparathyroidism: low PTH due to parathyroid gland failure, autoimmune destruction or congenital DiGeorge syndrome (22q11 del)

Secondary hypoparathyroidism: low PTH after parathyroidectomy or thyroidectomy surgery. This is the most common form of hypoparathyroidism

128
Q

What is the pathophysiology of hypoparathyroidism?

A

Low PTH results in:

  • Hypocalcaemia
  • Hyperphosphatemia (as PTH usually inhibits phosphate resorption at the kidneys)
129
Q

What signs and symptoms might a patient with hypoparathyroidism present with?

A

It causes increased excitability of muscles and nerves so many symptoms are a result of this:

Symptoms (experienced by patient): CATS Go Numb

  • Convulsions
  • Arrhythmia
  • Tetany (intermittent muscle spasms)
  • Spasm
  • Numbness

Signs (found through examination/investigation):

Chvostek’s sign - tapping on the facial nerve in the parotid gland (salivary gland below ears) causes ipsilateral twitching of facial muscles

Trousseau’s sign - spasm of the wrist/hand caused by inflating the blood pressure cuff at the brachial artery above systolic pressure. Causes wrist flexion and fingers to pull together

130
Q

What are some risk factors for hypoparathyroidism?

A
  • Thyroid surgery
  • Parathyroid surgery
  • Hyper- and hypomagnesaemia (magnesium needed for PTH production, but high levels can suppress process)
  • Moderate and chronic maternal hypercalcaemia (neonatal hypocalcaemia)
131
Q

What are the investigations/tests used to diagnose hypoparathyroidism?

A

Bloods - Bone profile

  • Decreased Ca2+
  • Decreased PTH
  • Increased/normal phosphate
  • Vitamin D - confirm/exclude deficiency as a cause for hypoparathyroidism

ECG

  • Prolonged QT interval (time taken for ventricular depolarisation and repolarisation)
132
Q

What are some DDx for hypoparathyroidism?

A
  • Vitamin D deficiency
  • Hypomagnesaemia (low serum magnesium)
  • Hypoalbuminemia (low serum albumin)
133
Q

What is the management plan/treatment for hypoparathyroidism?

A
  • Severe symptomatic hypocalcemia: IV calcium
  • Vitamin D deficiency: calcitriol
  • Hypoparathyroidism: oral calcium + calcitriol
  • Synthetic PTH if required
134
Q

Briefly describe phaeochromocytoma

A

Adrenaline is a catecholamine produced by the “chromaffin cells” in the adrenal medulla of the adrenal glands.

A phaeochromocytoma is a tumour of the chromaffin cells that secrete unregulated and excessive amounts of adrenaline.

135
Q

What is the epidemiology of phaeochromocytoma?

A

Rare condition
Annual incidence: ~0.6 per 100,000 person-years

136
Q

What is the aetiology of phaeochromocytoma?

A
  • Most sporadic
  • 25% familial and associated with multiple endocrine neoplasia type 2 (MEN 2) syndrome.

There is a 10% rule to describe the patterns of tumours:

  • 10% bilateral
  • 10% cancerous
  • 10% outside the adrenal gland
137
Q

What is the pathophysiology of phaeochromocytoma?

A

Usually, adrenaline stimulates the sympathetic nervous system and is responsible for the “fight or flight” response.

In patients with pheochromocytoma, the adrenaline is secreted in bursts giving periods of worse symptoms followed by more settled periods.

138
Q

What signs and symptoms might a patient with phaeochromocytoma present with?

A

Signs and symptoms tend to fluctuate with periods when the tumour is secreting adrenaline:

  • Anxiety
  • Sweating
  • Headache
  • Hypertension
  • Palpitations, tachycardia and paroxysmal atrial fibrillation (irregular heartbeat that returns to normal within 7 days)
139
Q

What investigations/tests are used to diagnose phaeochromocytoma?

A

1) 1st line:

  • 24 hr urinary metanephrine (a breakdown product of catecholamines) collection
  • Plasma-free metanephrines: first-line along with urine metanephrines

Results = elevated

2) CT abdomen and pelvis: if there is biochemical evidence of a phaeochromocytoma, then CT imaging can be performed to look at the adrenals

140
Q

What is the management plan/treatment for phaeochromocytoma?

A

Alpha blockers (i.e. phenoxybenzamine) - to lower blood pressure

Beta blockers once established on alpha blockers - to slow down the heart

Adrenalectomy to remove tumour is the definitive management

Patients should have symptoms controlled medically before surgery to reduce the risk of the anaesthetic and surgery.

141
Q

Briefly describe hypercalcaemia

A

Abnormally high serum calcium

Normal serum calcium range is 2.13 to 2.63mmo/l and ionised calcium range is 1.15 to 1.27mmol/l

Hypercalcemia = 2 standard deviations above normal range

142
Q

What is the epidemiology of hypercalcaemia?

A
  • Mild asymptomatic hypercalcaemia occurs in 1 in 1000 of the population
  • Occurs especially in elderly women
  • Hypercalcaemia occurs in 20% to 30% of patients with cancer.
143
Q

What is the aetiology of hypercalcaemia?

A
  • Primary hyperparathyroidism and malignancy are the most common causes and account for 90% of cases
  • Secondary hyperparathyroidism
  • Tertiary hyperparathyroidism
144
Q

What is the pathophysiology of hypercalcaemia?

A

Pathophysiology of primary, secondary and tertiary hyperparathyroidism is covered in the “hyperparathyroidism” flashcards

Malignancies cause hypercalcaemia by:

  • Bony involvement by the tumour: may lead to massive osteoclastic activity (osteolytic lesions)

Common malignancies leading to hypercalcaemia include multiple myeloma, leukaemia, lung cancer, and breast cancer.

When malignancies cause hypercalcaemia, the tumour = advanced.

145
Q

What signs and symptoms might a patient with hypercalcemia present with?

A

Hyperparathyroidism

Stones, bones, groans and moans!

  • Renal stones
  • Painful bones
  • Abdominal groans - constipation, nausea and vomiting
  • Psychiatric moans - fatigue, depression and psychosis

Malignancy

Hypercalcemia usually occurs in advanced cancers

146
Q

What are the risk factors for hypercalcaemia of malignancy?

A
  • Familial Multiple endocrine neoplasia (MEN) type 1 and MEN type 2a (Sipple) or isolated familial hyperparathyroidism.
  • There is an association of primary hyperparathyroidism with neurofibromatosis (syndrome where multiple tumours affect brain and spinal cord) and von Hippel-Lindau disease (condition that causes tumous to grow in parts of the body).
147
Q

What are the investigations/tests used to diagnose hypercalcaemia of malignancy?

A

PTH/bone profile:

  • Low/undetectable PTH since tumour may be secreting parathyroid-like protein > hypercalcaemia but PTH levels will not increase
  • Low albumin (some serum calcium is bound to albumin)
  • Increased alkaline phosphatase
  • Protein electrophoresis to look for myeloma - B2-microglobulin will be present
148
Q

What is management plan/treatment for hypercalcaemia of malignancy?

A

Mild hypercalcaemia or asymptotic: treatment of underlying malignancy + supportive measures + monitoring

Moderate/severe hypercalcaemia or symptom without advanced kidney disease: IV saline and IV biphosphonate/denosumab (prevents cancer related bone fractures and problems)

Moderate/severe hypercalcaemia or symptom with advanced kidney disease: renal dialysis +- denosumab

149
Q

What is the monitoring strategy for hypercalcaemia of malignancy?

A

Serum calcium will fall to its lowest within 7 days following bisphosphonate administration. Responses last 1 to 4 weeks, so constant calcium monitoring calcium is important.

150
Q

What are the complications of hypercalcaemia caused by malignancy?

A
  • Acute kidney injury
  • Coma
151
Q

Briefly describe hypocalcaemia

A

Hypocalcaemia is a state of electrolyte imbalance in which the circulating serum calcium level is low (please note that hypocalcaemia usually has an underlying cause which should be investigated)

152
Q

What is the aetiology of hypocalcaemia?

A

Chronic kidney disease is the most common cause of hypocalcaemia

Severe vitamin D deficiency from:

  • Reduced UV exposure
  • Malabsorption
  • Anti-epileptic drugs - induce enzymes that increase vitamin D metabolism

Primary or secondary hypoparathyroidism (see hypoparathyroidism flashcards)

153
Q

What signs and symptoms might a patient with hypocalcaemia present with?

A

It causes increased excitability of muscles and nerves because the threshold needed for neuron activation is decreased. Symptoms related to this.

Symptoms (experienced by patient): CATS Go Numb

Convulsions
Arrhythmia
Tetany
Spasm
Numbness

Signs (found through examination/investigation):

Chvostek’s sign - tapping on the facial nerve in the parotid gland causes ipsilateral twitching of facial muscles

Trousseau’s sign - Carpopedal spasm caused by inflating BP cuff above systolic BP, causes wrist flexion and fingers to pull together

154
Q

What investigations/tests are used to diagnose hypocalcaemia?

A
  • ECG: prolongation of QT intervals (hypocalcaemia)
  • Decreased calcium and increased phosphate levels
  • LFTs: Alkaline phosphate raised in vitamin D deficiency and bone metastases
  • PTH
  • Vitamin D
  • U&Es: chronic kidney disease
155
Q

What is the treatment/management plan for hypocalcaemia?

A
  • Aggressive IV fluids
  • Consider IV bisphosphonates if no response to fluids
  • Treat the underlying cause
156
Q

What is the normal range of serum potassium levels?

A

3.5 – 5.3mmol/l

157
Q

Briefly describe hyperkalaemia

A

Hyperkalaemia is high serum potassium >5.5mmol/L
Serum K+ > 6.5mmol/L = MEDICAL EMERGENCY!

158
Q

What is the aetiology of hyperkalaemia?

A

Conditions:

  • Acute kidney injury (common)
  • Chronic kidney disease
  • Rhabdomyolysis (muscle cell (myocyte) lysis)
  • Adrenal insufficiency
  • Tumour lysis syndrome

Medications:

  • Aldosterone antagonists aka potassium sparing diuretics) (spironolactone and eplerenone) (common)
  • ACE inhibitors (common)
  • Angiotensin II receptor blockers
  • NSAIDs (common)
  • Potassium supplements
159
Q

What is the pathophysiology of hyperkalaemia?

A

The amount K+ in the blood determines the excitability of nerve and muscle cells, including the heart muscle or myocardium

  • Raised K+ levels in the blood reduces the difference in electrical potential between cardiac myocytes and outside of the cells
  • Threshold for action potential is significantly decreased
  • Increased abnormal action potentials
  • Thus abnormal heart rhythms that can result in ventricular fibrillation and cardiac arrest
160
Q

What signs and symptoms might a patient with hyperkalaemia present with?

A

Symptoms:
- Muscle weakness

  • Muscle cramps
  • Paresthesia
  • Palpitations

Signs:

  • Tachycardia associated with arrhythmias (Potential cardiac arrest)
161
Q

What investigations/tests are used to diagnose hyperkalaemia?

A
  • ECG
  • Bloods - full blood count & U and E (diagnostic)
  • Urine osmolality and electrolytes

ECG:

  • Go - absent P wave
  • Go long - Prolonged PR interval (conduction through AV node >200ms))
  • Go tall - Tall tented T waves
  • Go under - wide QRS interval (>120ms)

Abnormal creatinine, urea and eGFR = hyperkalemia caused by acute or chronic renal failure

162
Q

What is the treatment for hyperkalaemia?

A

Medical emergency: >= 6.5mmol/L - IV 10ml 10% calcium gluconate - stabilises the cardiac muscle cells and reduces the risk of arrhythmias

≥ 6 mmol/L and ECG changes need urgent treatment

≤ 6 mmol/L with stable renal function = a change in diet and medications (i.e. stopping their spironolactone or ACE inhibitor).

If non-urgent, then insulin and dextrose infusion. Insulin and dextrose drives carbohydrates into cells and takes potassium with it, reducing the blood potassium.

163
Q

Briefly describe hypokalaemia

A

Low serum potassium of <3.5mmol/L

Serum K+ < 2.5 mmol/L = MEDICAL EMERGENCY!

164
Q

What is the aetiology of hypokalaemia?

A

1) Increased secretion

  • Most common cause = diuretic treatment: thiazide diuretics e.g. bendroflumethiazide, loop diuretics e.g. furosemide
  • Renal disease
  • Conn’s syndrome (excess aldosterone)

2) Decreased intake:

  • Dietary deficiency or fasting

3) Redistribution to intracellular:

  • Metabolic alkalosis
  • Drug effect (Insulin, B2 agonists)

4) GI losses:

  • Vomiting, severe diarrhoea and laxative abuse
165
Q

What signs and symptoms might a patient with hypokalaemia present with?

A

Symptoms:

  • Usually asymptomatic
  • Fatigue and light-headedness
  • Weakness
  • Cramps
  • Palpitations
  • Constipation

Signs:

  • Arrhythmias (especially AF)
  • Hypotonia
  • Hyporeflexia
166
Q

What investigations/tests are used to diagnose hypokalaemia?

A
  • Serum K+ < 3.5mmol/L = hypokalaemia
  • Serum K+ < 2.5mmol/L = URGENT TREATMENT!

ECG:

  • Small or inverted T waves
  • Depressed ST segments
  • Prominent U waves (after T waves)
  • Long PR interval
167
Q

What is the treatment for hypokalaemia?

A
  • K+ replacement (oral or IV)
  • Aldosterone antagonist (K+ sparing diuretics)
  • Identify and treat the underlying cause
  • Acute can resolve on own, majority just need withdrawal from diuretics or laxatives
168
Q

What is thyroid cancer?

A

Cancer of the thyroid glands:

4 types account for 98% of cases:

  • Papillary
  • Follicular
  • Anaplastic (worst prognosis :( )
  • Medullary

Papillary most common ~80% of cases

169
Q

What signs and symptoms might a patient with thyroid cancer present with?

A

Symptoms

Asymptomatic neck lump - most common presentation

Hoarseness - suggests local invasion and recurrent laryngeal nerve involvement

Signs:
Dyspnoea: due to pressure on the trachea

Cervical lymphadenopathy (abnormal enlargement of lymph nodes in head and neck - indicates lymphatic metastasis.

Tracheal deviation: due to pressure effect

170
Q

What investigations/tests are used to diagnose thyroid cancer?

A

Thyroid function tests: usually normal - most cancers do not affect thyroid function

Neck ultrasound: first-line imaging to visualise the thyroid and can be highly specific for certain subtypes e.g. papillary

Fine needle biopsy: key procedure to confirm/exclude malignancy and performed under ultrasound guidance

171
Q

What is the management plan for thyroid cancer?

A

Papillary, follicular and medullary:

  • Total thyroidectomy
  • Radioiodine ablation (I-131) - papillary and follicular subtypes
  • Lifelong levothyroxine (synthetic thyroxine T4)
  • Tyrosine kinase inhibitors in aggressive/metastatic disease

Anaplastic:

  • Resection (if possible)
  • Palliative: isthmusectomy and radiotherapy
172
Q

What are the most common metastatic sites for anaplastic thyroid cancer?

A
  • Lung (50%)
  • Bone (30%)
  • Liver (10%)
  • Brain (5%)
173
Q

Define hypernatremia

A

Serum sodium concentration > 145 mmol/L

Normal range is 135 - 145 mmol/l

174
Q

Define hyponatremia

A

Serum sodium concentration < 135 mmol/L

175
Q

Define carcinoid syndrome

A

Carcinoid syndrome occurs due to release of serotonin (5-hydroxytryptamine) and other vasoactive peptides into the systemic circulation from a carcinoid tumour (type of neuroendocrine tumour that grows from neuroendocrine cells - cells in the body that release hormones).

176
Q

What are the most common sites for carcinoid syndrome to occur?

A

Most commonly arise from GI tract followed by lungs, liver, ovaries thymus

  • Small intestine malignancy (Most common)
  • Appendix most common GI tract site
  • Liver most common site for metastasis from ileal tumours
177
Q

What is the pathophysiology of carcinoid syndrome?

A
  • Neuroendocrine tumours normally secrete serotonin into the circulation.
  • With GI tract tumours, hormones secreted> enters enterohepatic circulation> liver inactivates hormones> No symptoms.
  • However, when liver metastases are present (liver tumour) > hormone secretion> released into circulation + liver dysfunction> symptoms.
178
Q

What signs and symptoms might a patient with carcinoid syndrome present with?

A

Symptoms

  • Flushing of the skin (particularly face),
  • Diarrhoea
  • Abdominal cramps
  • Breathlessness and wheezing
  • Palpitations

Signs

Fibrosis (heart valve dysfunction)

179
Q

What investigations are used to diagnose carcinoid syndrome?

A

1st line: Urinary 5-hydroxyindoleacetic acid test - elevated levels

Chest X-ray + Chest/pelvic MRI/CT- helps locate primary tumours

180
Q

What is the treatment/management plan for carcinoid syndrome?

A
  • Surgery- Resection of tumour is the only cure for carcinoid tumours
  • Somatostatin analogues- Octreotide, blocks release of tumour mediators and counters peripheral effects
  • Debulking, embolization, or radiofrequency ablation for hepatic masses/metastases can decrease symptoms
181
Q

DDx for carcinoid syndrome

A
  • IBS
  • Crohn’s
  • Menopause
182
Q

DDx for diabetes mellitus type 2

A
  • Non-diabetic hyperglycaemia (pre-diabetes)
  • Diabtes mellitus type 1
  • Gestational diabetes
183
Q

What is Maturity-onset diabetes of the young (MODY)

A

MODY describes a group of conditions characterised by an autosomal dominant mutation in a single gene, which leads to impaired beta-cell function. This is in contrast to T1DM and T2DM, which are polygenetic conditions.

MODY does not involve autoimmune pathology or insulin resistance. Rather, the mutations involved lead to impaired glucose sensing and insulin secretion.

184
Q

What type of MODY is most common?

A

Type 3 (50-65%)

Due to mutations in Hepatocyte nuclear factor-1-alpha

Very responsive to Sulfonylurea (80% response)

185
Q

What are the typical features of MODY?

A
  • Presentation < 25 years of age
  • Strong family history
  • Normal BMI
  • Lack autoantibodies
  • No ketosis
  • Insulin not usually required
186
Q

What is MODY often misdiagnosed as and what tests can help?

A

Often misdiagnosed as DM type 1 or young onset type 2.

So genetic testing may be indicated in the following situations:

  • Young patient
  • Autosomal dominant mode of inheritance
  • Non-acute presentation
  • Lack of evidence of autoimmunity, e.g. autoantibody negative
  • Lack of evidence of insulin resistance, e.g. normal BMI
187
Q

DDx for Graves disease (hyperthyroid)

A
  • Toxic nodular goitre
  • Painless, postnatal thyroiditis
188
Q

DDx for Hashimoto’s thyroiditis (hypothyroid)

A
  • Painless thyroiditis - variant presentation of Hashimoto’s thyroiditis
  • Graves disease
189
Q

DDx for pituitary adenoma

A
  • Prolactinoma
  • Acromegaly
  • Cushing’s syndrome
190
Q

DDx for Cushing’s syndrome

A
  • Obesity
  • Metabolic syndrome
191
Q

DDx Conn’s

A

Essential hypertension

192
Q

DDx SIADH

A
  • Hypovolaemia
  • Pseudohyponatraemia
193
Q

DDx primary hyperparathyroidism

A
  • Secondary hyperparathyroidism (DDx for this is primary hyperparathyroidism)
  • Hypercalacaemia of malignancy
194
Q

DDx for hypocalcaemia

A
  • Iatrogenic post-surgery hypoparathyroidism
  • Vitamin D deficiency
195
Q

DDx diabetes insipidus

A

Diabetes mellitus

196
Q

DDx hyperkalaemia

A
  • CKD
  • Diabetic ketoacidosis/hyperosmolar hyperglycaemic state (potassium shifts from the intracellular to the extracellular space due to a lack of insulin, resulting in hyperkalemia.)

Sharon's Phase 2a Medicine Revision (10 decks)

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