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Phase 2a Gold Standard > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What hormones are secreted by the anterior pituitary gland

A

Good Morning FLAT P
GMFLATP
- GH (growth hormone)
- MSH (Melanocyte-stimulating hormone)
- FSH (Follicle-stimulating hormone)
- LH (luteinising hormone)
- ACTH (Adrenocorticotrophic hormone)
- TSH (Thyroid stimulating hormone)
- Prolactin

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2
Q

What hormones are secreted by the posterior pituitary gland

A

A-O lets go
ADH
Oxytocin

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3
Q

Effects of insulin

A
  • Suppresses hepatic glucose output (less glycogenolysis and gluconeogenesis)
  • increases glucose uptake into insulin sensitive tissues (muscle, fat)
  • Suppresses lipolysis and breakdown of muscle
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4
Q

Effects of glucagon

A

Aids increase in blood glucose
- Increases hepatic glucose output (glycogenolysis, gluconeogenesis)
- Reduces peripheral glucose uptake
- Stimulates lipolysis and muscle glycogenolysis and breakdown

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5
Q

How does diabetes cause morbidity (3) and main cause of mortality

A
  • Acute hyperglycaemia leading to crises such as DKA or Hyperosmolar hyperglycaemic state
  • Chronic hyperglycaemia leading to tissue complications
  • Treatment side effects

CVD and stroke main cause of death

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6
Q

Complications of diabetes

A
  • Diabetic retinopathy
  • Diabetic nephropathy
  • Stroke
  • Cardiovascular disease
  • Diabetic neuropathy (foot ulcers lead to lower extremity amputation)
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7
Q

Investigations for Diabetes Mellitus

A

Random plasma glucose >11mmol/L
Fasting plasma glucose >7mmol/L
HbA1C (measures glycated haemoglobin) > 48mmol/L
Oral glucose tolerance test >11mmol/L 2 hours after a 75g oral glucose load (used in borderline/prediabetes cases)

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8
Q

What is the oral glucose tolerance test and what can it help identify?

A

Fast for 8 hours, take 75g glucose, then glucose measured at intervals. After 2 hours 7.9-11mmol/L indicates prediabetes/impaired glucose tolerance. >11mmol/L indicates diabetes

Helps identify prediabetes, insulin resistance, reactive hypoglycaemia, gestational diabetes

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9
Q

4 features suggestive of type 1 diabetes instead of type 2

A

Early age onset
Lean body/ weight loss
High levels of islet autoantibodies
Prone to ketoacidosis

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10
Q

4 features suggestive of type 2 diabetes instead of type 1

A

Over 30s
Gradual onset
Familial Hypercholestraemia often positive
Hyperglycaemia can be controlled by diet, exercise, oral medication

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11
Q

Symptoms of Diabetes Mellitus (8)

A

Polydipsia
Polyuria
Nocturia
Weight loss in type 1, Weight gain in type 2
Fatigue
Hunger
Pruritus vulvae (itching of the vulva)
Blurred vision

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12
Q

What do uncontrolled Type 1 and Type 2 Diabetes lead do

A

Type 1 - Diabetic ketoacidosis
Type 2 - Hyperosmolar hyperglycaemic state

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13
Q

Signs of Diabetes Mellitus

A

Acanthosis nigricans (T2DM)
Glycosuria
Ketonuria
Glove and stocking sensory loss
Diabetic retinopathy
Diabetic foot disease (reduced pulses, calluses, ulceration, charcot foot)

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14
Q

3 other types of Diabetes Mellitus

A

Maturity onset diabetes of youth (MODY or monogenic diaebtes) - rare genetic diabetes, c peptide present, no autoantibodies
Endocrine diabetes - in endocrine disease (acromegaly/cushings)
Pancreatic Diabetes

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15
Q

What is C peptide

A

A by product of insulin production. C peptide present usually means there is endogenous insulin production

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16
Q

Genes involved in DM type 1

A

HLA-DR3-DQ2 or HLA-DR4-DQ8

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17
Q

Treatment of type 1 diabetes

A

Basal bolus insulin
Basal - long acting, maintain stable levels throughout day and overnight (levemir)
Bolus - Fast acting, before each meal, spike insulin (Novorapid)

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18
Q

Complications/side effects of insulin therapy

A

Lipohypertrophy at site of injection
Hypoglycaemia [main one!]
Weight gain due to feeling more hungry
Insulin resistance

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19
Q

Risk factors for type 2 diabetes (7)

A

Increasing age
Obesity, hypertension
Sedentary lifestyle
Ethnicity - middle eastern, south asian, south east asian
Gestational diabetes
Family history
Dyslipidaemia

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20
Q

What is assessed at an annual diabetes review?

A

Retinopathy
Diabetic foot problems
CVD risk factors
Nepthropathy (eGFR, Albumin:Creatinine ratio)

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21
Q

What is a characteristic skin sign in T2DM that isnt in T1DM

A

Acanthosis Nigricans - Dark pigmentation at nape of neck and in axillae

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22
Q

Macrovascular and microvascular diabetes complications

A

Macrovascular
MI, Ischaemic stroke, PAD, Heart failure

Microvascular
Retinopathy, neuropathy, nephropathy

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23
Q

Treatment of Type 2 diabetes

A

1st - Metformin (class is biguanides)
2nd - SGLT2 inhibitor (empagliflozin) or DPP-4 inhibitor (linagliptin) or GLP1 analogue (liraglutide) Dual Therapy W/ metformin
3rd - Triple therapy
4 - + Basal insulin

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24
Q

MoA and side effects of metformin

A

Decreases gluconeogenesis, and increases peripheral utilisation of glucose (only acts in presence of insulin)

Side effects: nausea/vomiting, abdominal pain, diarrhoea, altered taste
VITAMIN B12 DEFICIENCY

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25
Q

Indication and example of SGLT-2 inhibitors

A

Indication: DMT2, second line treatment

Example: empagliflozin

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26
Q

MoA of SGLT-2i

A

Sodium-glucose co-transporter-2 inhibitors. Block reabsorption of glucose in kidney, increasing glucose excretion

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27
Q

Side effects of SGLT-2 inhibitor

A

Side effects: Dehydration, UTI, genital thrush

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28
Q

Indication and Example of DPP4 inhibitors

A

Indication: Second line dual therapy T2DM

Example: Linagliptin

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29
Q

MoA of DPP4i

A

Inhibits dipeptidylpeptidase-4 to increase insulin secretion and decrease glucagon secretion.

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30
Q

Side effects of DPP4 i

A

Stomach pain, nasopharyngitis,
upper resp tract infection, hypoglycaemia when taken with other medication

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31
Q

Indications, Example of GLP1 analogues

A

Indication: Second line dual therapy T2DM, especially to aid weight loss!

Example: Liraglutide

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32
Q

MoA of GLP1 analogues

A

MoA: Binds to and activate GLP-1 (glucagon like peptide 1) receptor, increases insulin secretion, suppresses glucagon secretion, slows gastric emptying

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33
Q

Side effects of GLP1 analogues

A

Side effects: Decreased appetite, headache, dizziness, dry mouth

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34
Q

Why doesn’t DKA occur in type 2 diabetes?

A

Insulin levels sufficient to suppress ketogenesis

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35
Q

When is insulin indicated in type 2 diabetes?

A

When hba1c levels don’t recover after triple therapy

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36
Q

Main side effect of insulin treatment

A

Hypoglycaemia

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37
Q

Give the classification of hypoglycaemia

A

Level 1: Plasma glucose<3.9mmol/L
Level 2: Plasma glucose<3mmol/L
Level 3/Severe: Impaired cognitive function sufficient to need extra help to recover

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38
Q

How often should Hba1c be checked in diabetes?

A

Every 3-6 months

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39
Q

Why doesn’t DKA occur in type 2 diabetes?

A

Insulin levels sufficient to suppress ketogenesis

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40
Q

Risk factors for severe hypoglycaemia

A

Daily insulin usage
Low HbA1c
Long duration of diabetes
Hypoglycaemia history
Physical activity

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41
Q

Signs/symptoms of hypoglycaemia

A

Autonomic: Trembling, palpitations, sweating, hunger

Neuroglycopenic: confusion, weakness, drowsiness, vision changes, nausea, headache

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42
Q

Treatment of hypoglycaemia

A

Treatment: 15g fast acting carbohydrates until blood glucose >4.0mmol/L

If recurrent, Continuous Glucose Monitoring (CGMS)

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43
Q

Hypoglycaemia complications

A

Brain: Blackouts, seizures, comas
Heart: MI risk, arrhythmia
Circulation: Inflammation, endothelial dysfunction, falls, accidents

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44
Q

Hypoglycaemia driving rule

A

More than 1 episode of hypoglycaemia whilst awake or 1 whilst driving = Tell DVLA immediately. License is revoked but can reapply after 3 months

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45
Q

How many GLUT (glucose transporter) channel proteins are there and what are their functions

A

GLUT-1: Non insulin stimulated glucose uptake
GLUT-2: Found in beta-cells of pancreas, enabling them to sense glucose levels. High affinity transporter; only allow glucose in when concentration is high, when insulin needs to be released. Also found in kidney and liver.
GLUT-3: Non insulin mediated glucose uptake into brain, neurons, placenta
GLUT-4: Mediates peripheral action of insulin, glucose taken up into muscle and adipose tissue after insulin stimulation

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46
Q

Diabetic ketoacidosis pathophysiology

A

Complication of Type 1 diabetes where complete absence of insulin means body is unable to store or use glucose, leading to it’s buildup in blood. Causes lipolysis of fat, which undergoes ketogenesis to use as energy source, causing buildup of ketones. Ketones are acidic, so you get:

Hyperglycaemia, acidosis and ketosis.

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47
Q

Signs/symptoms, and electrolyte change associated with diabetic ketoacidosis

A

Signs:
- fruity smell of acetone on breath
- Kussmaul breathing (rapid, deep - compensatory mechanism to blow off CO2, reduce acidity)
- Reduced tissue turgor
- Hypotension

Symptoms:
Diabetes symptoms + abdominal pain, nausea/vomiting, confusion, leg cramps
- Hyperkalaemia

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48
Q

What are the diagnostic criteria for diabetic ketoacidosis? What shows up in urine and what electrolyte dysfunction does it cause

A
  1. Ketonaemia >3mmol/L
  2. Hyperglycaemia >11mmol/L (RPG)
  3. Acidosis <7.3pH

Also find:
Ketonuria/ Glycosuria
Hyperkalaemia common, but hypokalaemia suggests severe DKA

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49
Q

Treatment of diabetic ketoacidosis

A
  1. ABCDE (emergency)
    IV fluids (0.9% saline)
  2. Insulin infusion
  3. Potassium monitoring, replacement may be needed.
  4. Anticoagulant
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50
Q

Precipitants of HHS

A

Undiagnosed diabetes
Poor medication compliance
Infection
stroke
Corticosteroid usage

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51
Q

Define hyperosmolar hyperglycaemic state with pathophysiology

A

Complication of type 2 diabetes usually triggered by precipitant. Hyperglycaemia leads to osmotic diuresis in kidneys, with loss of sodium and potassium, and severe dehydration.

This leads to hyperglycaemia, hyperosmolality (Thick blood) and hypovolaemia.

No ketosis as insulin sufficient to prevent it

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52
Q

Signs and symptoms of Hyperosmolar Hyperglycaemic State

A

Signs -
- Reduced consciousness/GCA
- Dehydration!
- Tachycardia
- Hypotension
- Reduced tissue turgor

Symptoms - Polyuria/polydipsia + confusion, cramps, visual disturbances, headache

(Slower onset than DKA)

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53
Q

Investigations and main findings in Hyperosmolar Hyperglycaemic State.

AND Treatment

A

Glucose, ABG, Blood ketone level, serum osmolality, U&E (monitor electrolyte levels)

Will show Hyperglycaemia, hyperosmolality and hypovolaemia.

NO Ketonuria or ketonaemia

Treatment:

1 - IV Fluid (0.9% saline)
2 - Insulin (potassium/glucose maybe too)
3 - LMWH may also be needed (as blood is thicker)
4 - Potassium replacement may also be needed

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54
Q

Hyperthyroidism vs thyrotoxicosis

A

Hyperthyroidism is an excess of thyroid hormone from an endogenous source (usually thyroid gland). Thyrotoxicosis is inappropriately high levels of t3/t4 from any source

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55
Q

What are the 3 mechanisms by which thyroid hormone can be high in blood

A
  1. Overproduction of thyroid hormone
  2. Leakage of preformed hormone from thyroid
  3. Ingestion of excess thyroid hormone
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56
Q

What are 5 primary causes of hyperthyroidism?

A

Graves disease (75-80% cases) (Autoimmune)
Toxic multinodular goitre
Toxic adenoma (thyroid adenoma)
Ectopic T3/T4 production
De quervains (post-viral - painful goitre!)

(drugs separate card)

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57
Q

Drug causes of hyperthyroidism (4)

A

Lithium
Iodine
Amiodarone (Anti-arrhythmic drug can cause hypo and hyper)
Levothyroxine (hypothyroid treatment causing iatrogenic hyperthyroidism)

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58
Q

Secondary causes of hyperthyroidism

A
  • Pituitary adenoma secreting TSH
  • Ectopic tumour secreting TSH
  • Hypothalamic tumour secreting TRH (thyrotropin releasing hormone)
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59
Q

What cause a diffuse or nodular goitre?

A

Diffuse:
- Graves, Hashimoto’s, De Quervains (Only PAINFUL goitre!!)

Nodular:
- multinodular goitre, Carcinoma, Adenoma (SOLITARY NODULE)

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60
Q

Definition of Graves’ with 5 risk factors

A

Autoimmune. TSH receptor antibodies bind to TSH receptors on thyroid gland causing excess T3/T4 release.

  • Female (especially post partum!)
  • Autoimmune disease
  • Family history (HLA-DR3)
  • Iodine intake
  • Radiation
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61
Q

Symptoms of hyperthyroidism (with pneumonic)

A

Everything speeds up!
THYROIDISM
Tremor
Heart rate increase (tachycardia)
Yawning
Restlessness
Oligomenorrhoea
Irritability
Diarrhoea
Intolerance to heat
Sweating
Muscle wasting (WEIGHT LOSS)

Key others include
Reduced libido
Weight loss
Palpitations

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62
Q

General Hyperthyroid signs (5)

A

Goitre
Lid lag
postural tremor
hyperreflexia
sinus tachycardia

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63
Q

5 Graves specific signs

A

Diffuse goitre
Thyroid bruit
Thyroid eye disease (Exophthalmos + Ophthalmoplegia (bulging eyes + paralysed eye muscles))
Pretibial myxoedema (lesions on shins)
Acropachy (thick extremities)

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64
Q

Investigations for hyperthyroid diseases

A

1st - Thyroid Function Test
- TSH low, T3/T4 high in Primary (e.g. Graves’)
- TSH high, T3/T4 high in Secondary
- If TSH high/low, T3/T4 normal, subclinical hypo/hyper

2nd - Antibodies
TSH receptor antibodies (TRAb) high in Graves’
Anti-TPO - both Graves and Hashimoto’s (which is HYPO)

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65
Q

Treatment of hyperthyroidism

A

1 - Carbimazole (class - thionamides) Decreases synthesis of new T4.
- Block and replace regimen with levothyroxine (T4) in Graves when EUTHYROID (normally functioning). (Propylthiouracil if contraindicated)

2 - Radioiodine (131I). Direct ionisation of thyroid cells.

3- Thyroidectomy (partial if possible/needed)

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66
Q

Side effects of Carbimazole and surgery for thyroidism

A

Carbimazole. (TERATOGENIC)
Common: Rash
Severe: Agranulocytosis (sore throat, fever, mouth ulcers

Surgery
Hypothyroidism, laryngeal nerve palsy

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67
Q

Side effects of radioiodine

A

Early: Necrosis of follicular cells, Vascular occlusion
Long term: Chronic inflammation, Atrophy/fibrosis, Hypothyroidism

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68
Q

Define Thyroid storm

A

Life threatening hyper-metabolic state induced by excess T3/T4, most commonly seen in Graves or toxic multinodular goitre.

Occurs secondary to factor such as trauma or infection, or suddenly stopping meds, in those with hyperthyroidism

Also known as Thyrotoxic crisis

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69
Q

Signs/symptoms of thyroid storm (6)

A

Acutely worsened:

  • Pyrexia
  • Tachycardia
  • Reduced GCS
  • Nausea/vomiting
  • Abdominal pain
  • Diarrhoea
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70
Q

Treatment of thyroid storm

A
  • IV Fluid, NG tube if vomiting
  • Propylthiouracil 1st
  • IV hydrocortisone
  • Propanolol also given
  • Oral iodine >1hour after propylthiouracil
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71
Q

Define Hashimoto’s thyroiditis

A

Hypothyroidism caused by Anti-TPO antibodies leading to autoimmune inflammation of thyroid glands.

(Thyroid peroxidase converts iodide into iodine, essential for thyroid hormone production)

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72
Q

Main causes of hypothyroidism

A
  • Hashimoto’s thyroiditis (most common developed nations)
  • Iodine deficiency (most common worldwide)
  • Post partum (self limiting, autoimmune, resolves in 12 months)
  • Drugs
  • Secondary to hyperthyroid treatment (Carbimazole, propylthiouracil, Radioiodine, surgery)
  • Secondary to pituitary failing to produce TSH (often associated deficiency e.g. ACTH.)
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73
Q

Drug causes of hypothyroidism

A

Lithium (inhibits thyroid hormone production)
Amiodarone (Anti-arrhythmic drug can cause hypo and hyper)

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74
Q

Signs/symptoms of hypothyroidism

A

Everything slows. (BRADYCARDIC)
Bradycardia
Reflexes reduced
Ataxia
Dry hair/skin (+queen annes sign + hair loss)
Yawning
Cold peripheries and constipation
Ascites and oedema (fluid retention)
Round face
Depression/lethargy/fatigue
Immobile
Congestive heart failure

Others:
Goitre
Carpal tunnel
Cold intolerance
Weight gain!!

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75
Q

Investigations for hypothyroidism

A

1 - TFT
- TSH high, T4 low = primary e.g. Hashimoto’s. Pathology affects thyroid gland
- TSH low, T4 low = secondary. Pathology usually affects pituitary

2 - antibodies
Anti-TPO (Hashimoto’s)
Anti-thyroglobulin (less sensitive)

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76
Q

Treatment of hypothyroidism

A

Synthetic Levothyroxine (T4) - Review after 8 weeks

(T4 is metabolised to T3 in body)

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77
Q

Causes of child hypothyroidism

A

Neonatal hypothyroidism
Resistance to thyroid hormone
Isolated TSH deficiency

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78
Q

Thyroid cancer types and features

A
  • Papillary (most common, spreads locally)
  • Follicular (low iodine/women, metastasises to lung and bone)
  • Medullary (other card)
  • Anaplastic (Worst prognosis, most aggressive)
  • Lymphoma (usually non Hodgkins. Hashimotos associated)
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79
Q

Features of medullary thyroid cancer (3)

A
  • Derived from calcitonin producing C cells; Can cause hypocalcaemia and diarrhoea as a result.
  • Associated with MEN 2A and 2B
  • Metastasises to lymph nodes
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80
Q

Signs and symptoms of thyroid cancer (other than typical cancer signs) (5) and metastases (5)

A
  • Hard, irregular, nodular thyroid.
  • Tracheal deviation
  • Hoarse voice
  • Dysphagia
  • Dyspnoea

Metastasis to LLLBB
Lymph nodes, Lung, Liver, Brain, Bone

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81
Q

Investigations of thyroid cancer

A

Fine needle aspiration and biopsy GOLD

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82
Q

Treatment of thyroid cancer

A

Treatment:
Lobectomy + radioiodine. T4 or TSH replacement may also be needed.
Anaplastic: Total thyroidectomy or palliative care

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83
Q

What cells secrete PTH and what is its function (4)

A

Secreted by chief cells in response to low calcium

  • Increases Ca2+ reabsorption and phosphate excretion in kidneys.
  • Increases calcium resorption by osteoclasts in bones
  • Increases calcium absorption in gut
  • Activates 1,25(OH)2 vitamin D (Ca2+ absorption in gut and kidney, increases osteoclast activity)
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84
Q

Equation to calculate corrected calcium in cases of hypoalbuminaemia

A

total serum calcium + 0.02*(40-serum albumin)

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85
Q

Primary vs secondary vs tertiary hyperparathyroidism

A

Primary hyperparathyroidism - Uncontrolled PTH due to tumour (parathyroid adenoma)
Secondary hyperparathyroidism - Response to low calcium caused by Insufficient vit D or CKD (Low absorption of calcium from intestines and kidneys.)
Tertiary - Continued hyperparathyroidism leading to hyperplasia of parathyroid glands.

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86
Q

Signs/symptoms of hyperparathyroidism

A

Hypercalcaemia symptoms

“Bones, stones, groans, moans.”
Bone pain
Renal/gallstones
Abdominal groans (constipation, nausea, vomiting)
Psychiatric moans (fatigue, depression, psychosis)

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87
Q

Investigations for hyperparathyroidism

A

Bloods for PTH, calcium, phosphate, vit D. ALP raised due to bone activity

Primary - high PTH and calcium, low phosphate
Secondary - High PTH, low/normal calcium, low phosphate
Tertiary - High PTH, calcium and phosphate

Others: ECG - short QT
XrayKUB - renal stones
DEXA - Bone density
Urinary calcium - Raised
U&E - assess kidney function

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88
Q

Hyperparathyroid treatments + main complications

A

1° - Removal of tumour/parathyroidectomy
2° - Treat underlying cause, correct vit D, use phosphate binders, renal transplant
3° - Surgical removal of parathyroid tissue

  • Acute severe hypercalcaemia - treat with IV fluids and bisphosphonates
  • Calcification of blood vessels due to high calcium and phosphate
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89
Q

Name causes of hypocalcaemia

A

With raised phosphate:
CKD
Pseudohypoparathyroidism and hypoparathyroidism
Acute rhabdomyolysis

Normal/low phosphate:
Vit D deficiency
Respiratory alkalosis
Pancreatitis

90
Q

Signs/symptoms of hypocalcaemia, and ECG change

A

SPASM(O)DICCC
Spasms
Paraesthesia
Anxiety, irritable, irrational
Seizures
Muscle tone increase (colic, wheeze, dysphagia)
-
Dermatitis
Impetigo herpetiformis (psoriasis in pregnancy)
Chvostek’s sign (facial muscle twitch)
Cataracts (chronic hypocalcaemia)
Confusion

ECG change shows long QT

91
Q

Two hypocalcaemia signs on examination, and a differential diagnosis for hypocalcaemia

A

Trousseau’s sign - blood pressure cuff inflated, occluding brachial artery. Puts enough pressure on nerve to cause firing of nerve, causing flexion of wrist and metacarpophalangeal joints.

Chvostek’s sign - Tap over facial nerve, causes twitching of facial muscles.

Differential is hypoalbuminaemia, low serum albumin. (Calcium bound to albumin, so low calcium may be due to low albumin. Low bound calcium but free ionised levels the same)

92
Q

Causes of hypercalcaemia

A

90% due to bone malignancy/myeloma or 1° hyperparathyroidism

Other causes are:
Acidosis
Sarcoidosis
Thiazide usage
Thyrotoxicosis
Addisons
Phaeochromocytoma

93
Q

Signs/symptoms and consequences of hypercalcaemia

A

Harder to open voltage gated sodium channels.

Thirst, polyuria
Nausea
Constipation
Muscle weakness
Confusion -> Coma

Consequences:
Renal stones, Short QT on ECG, ectopic calcification

94
Q

Treatment of hypercalcaemia

A

Depends on cause
Increase excretion: Rehydrate, loop diuretics (furosemide - inhibit calcium reabsorption in loop of Henle)

Decrease calcium absorption in GI tract: glucocorticoids

Prevent bone resorption:
Bisphosphonates/calcitonin

95
Q

Causes of hypoparathyroidism (Primary and secondary)

A
  • Hyperparathyroidism treatment
  • 1° - Di George syndrome (PTH glands dont develop), Autoimmune polyendocrine syndrome type 1 (APS-1)
  • 2° - Removal of parathyroid gland during surgery, hypomagnesium, haemochromatosis, wilson’s disease
96
Q

How do PTH, calcium and phosphate look in hypoparathyroidism?

A

PTH low
Calcium low
Phosphate high (opposite to PTH and calcium in parathyroidisms)

97
Q

How do PTH, calcium and phosphate look in pseudohypoparathyroidism?

A

PTH high
Calcium low
Phosphate high

98
Q

How do PTH, calcium and phosphate look in vit D deficiency?

A

PTH high
Calcium low
Phosphate low

99
Q

How do PTH, calcium and phosphate look in hypercalcaemia of malignancy?

A

PTH low
Calcium high

100
Q

What is the differential diagnosis for hypoparathyroidism and how do patients usually look?

A

Pseudohypoparathyroidism type 1A - kidneys and bones dont respone to PTH due to PTH receptor fault

Patients short, round face, calcified basal ganglia, low calcium high phosphate.

101
Q

What is the differential diagnosis for hypoparathyroidism and how do patients usually look?

A

Pseudohypoparathyroidism type 1A - kidneys and bones don’t respond to PTH due to PTH receptor fault

Patients short, round face, calcified basal ganglia, low calcium high phosphate.

102
Q

Hyperkalaemia causes

A

Decreased excretion
- AKI/CKD - low urine, less excretion
- Addison’s disease

Shift from intracellular to extracellular:
- Diabetic ketoacidosis - Insulin deficiency causes K+ to not be shifted inwards into cells.
- Metabolic acidosis - H+ pumped into blood, in exchange for K+
- Tumour lysis syndrome

103
Q

Drugs that can cause hyperkalaemia

A

Impaired excretion:
Potassium sparing diuretics (Spironolactone)
ACEi
NSAIDs

Extracellular shift
Beta blockers
Digoxin

104
Q

Pathophysiology of hyperkalaemia and effect in skeletal and smooth muscle

A

K+ determines excitability of nerve and muscle cell.
In hyper, resting membrane potential is less negative. This means cells depolarise faster, but are not able to fully repolarise (as resting potential is now too high). This causes decreased excitability of nerves and muscle, so contractions and reflexes are diminished

In cardiac myocytes, diminished contractions = arrhythmia/cardiac arrest

Smooth muscle - cramping, due to easy depolarisation
Skeletal muscle - flaccid paralysis, as resting potential too positive

105
Q

signs, symptoms and ECG of hyperkalaemia

A

Signs
Tachycardia
Fast irregular pulse

Symptoms
Muscle cramps, weakness, chest pain, arrhythmia

ECG (tall tented T wave, absent p wave, wide QRS, ST depression)

106
Q

Hyperkalaemia treatment

A

1st line: IV Calcium gluconate if ECG changes (repolarise cardiac membranes)
2nd line: Insulin/dextrose infusion
3rd: Salbutamol

107
Q

Consequences of hyperkalaemia (6)

A

MURDER
Muscle weakness/wasting
Urine: Oliguria (decreased filtration/eGFR)
Respiratory distress
Decreased cardiac contractility - decreased CO and BP
ECG changes
Reflexes reduced!

108
Q

What are the zones of the adrenal gland and what do they secrete

A

Zona glomerulosa - mineralocorticoids e.g. Aldosterone
Zona fasciculata - glucocorticoids e.g. Cortisol
Zona reticularis - gonadocorticoids e.g. Androgens
Adrenal medulla - NAd, Adr

109
Q

Causes of hypokalaemia

A

Renal
- Diuretics (loop, thiazide)
- Renal tubular acidosis
- Hypoaldosteronism and Cushings

Shift intracelluarly:
- Alkalosis, H+ moves out of cell, swaps for K+
- Insulin excess, Na+/K+ pump moves insulin into cell
- Activation of beta adrenergic receptors (e.g. Salbutamol)

  • Vomiting/diarrhoea
  • Inadequate intake
110
Q

Pathophysiology of hypokalaemia

A

Low K+ levels make resting potential more negative, greater stimulus needed to generate action potential. This causes reduced excitability except in heart, where it is increased.

Cardiac - arrhythmia/cardiac arrest
Smooth muscle - Constipation
Skeletal muscle - weakness, cramps, flaccid paralysis
Respiratory muscles - Respiratory depression

111
Q

Signs/symptoms of hypokalaemia

A

Hypotonia, hyporeflexia
Arrythmia
Constipation
Fatigue
Weakness
Palpitations

112
Q

What electrolyte dysfunction causes increased arrhythmia risk in hypokalaemia

A

Hypomagnesaemia

113
Q

Investigations for hypokalaemia

A

Plasma potassium
ECG - flat/inverted T waves, prominent U waves, ST depression, PR elongation

Check magnesium

114
Q

Hypokalaemia treatment

A

1st.
- K+ replacement
- Replace diuretic with potassium sparing (spironolactone)

2nd - severe
- IV 0.9% saline with potassium chloride
- Continuous cardiac monitoring
- Correct magnesium

115
Q

Define diabetes insipidus

A

Excess ADH = decreased renal water reabsorption, leading to excessive, hypotonic (dilute) urine. Osmoreceptors in hypothalamus and baroreceptors in brainstem (emergency) detect dehydration and make patient thirsty (polydipsia)

Cranial - Insufficient production/secretion of ADH
Nephrogenic - decreased response by kidneys to ADH

116
Q

Causes of diabetes insipidus

A

Cranial
- Brain malformations
- Brain tumour (e.g. craniopharyngioma)
- infection (TB, meningitis)
- Head trauma

Nephrogenic
- ADH resistance defect (X linked - AVPR2 gene, autosomal - aquaporin 2 defect)
- hypokalaemia/hypercalcaemia
- drugs (lithium)
- chronic renal impairment

117
Q

What does ADH do?

A

Increases aquaporin 2 insertion in the distal convoluted tubule and the collecting ducts, causing re-absorption of water

118
Q

What receptors does ADH bind to

A

Vasopressin receptors (G protein coupled transmembrane receptors)

V1a - vasculature - vasoconstriction
V1b - pituitary - ACTH
V2 - renal collecting tubules - controls reabsorption of water

119
Q

Signs/symptoms of diabetes insipidus

A

Polyuria, polydipsia, dehydration. Lethargy confusion when severe

Signs:
Hypernatraemia, postural hypotension

NO GLYCOSURIA

120
Q

Differential for polyuria/polydipsia, and the investigation that confirms this

A

Primary polydipsia (overdrinking)

If water deprivation test conducted, urine osmolality is normal after deprivation, and will increase after desmopressin given, as ADH works normally

121
Q

Investigations for diabetes insipidus

A

Urine volume - >3L a day
Urine/serum osmolality - high serum, low urine

1 - Water deprivation test;
- No fluid for 8 hours, urine osmolality measured, then desmopressin given, 8 hours later urine osmolality measured again. In cranial, urine osmolality will go from low->high. In nephrogenic, unable to respond to ADH, so osmolality will remain low.

U&E - check kidney function and hypernatraemia

May be worth doing serum glucose/HbA1c to exclude DM

122
Q

Treatments for Diabetes Insipidus

A

Correct underlying cause

Cranial - Desmopressin
Nephrogenic - Thiazide diuretic and Underlying cause
Scans such as MRI may be needed to check pituitary

123
Q

What are the symptoms of hyponatraemia

A

headache
vomiting
irritability
mental slowing (decreased GCS)
unstable gait
disorientation

(acute or chronic severe symptoms)
Stupor/coma, Convulsions, respiratory arrest, brainstem herniation

124
Q

Investigations and treatments in Hyponatraemia

A

Plasma/urine osmolality
Urinary Na+
Review drug chart
Cortisol

Treatments:

If hypovolaemic (dehydrated), saline replacement
If normo or hypervolaemic, fluid restriction

125
Q

What is the most common electrolyte disorder?

A

Hyponatraemia

126
Q

Definition of SIADH

A

Too much ADH causes excess water reabsorption and compensatory sodium excretion to maintain volume. Blood becomes hyponatraemic, hypotonic, eu/normovolaemic. Disease presents with hyponatraemia symptoms

127
Q

SIADH causes

A

S - Pancreas, Thymus, SCLC, lymphoma, prostate
I - infection (encephalitis, meningitis, pneumonia, TB)
A - brain Abscess
D - Drugs (carbamazepine, PPI, thiazides, SSRIs)
H - Head trauma, pneumothorax, severe asthma/emphysema

(causes either CNS disorders, drugs, resp disoders or tumours)

128
Q

In SIADH, what happens to:

Plasma (osmolality and sodium)
Urine (osmolality and sodium)
Circulating volume

A

Plasma osmolality and sodium decrease

Urine osmolality and sodium increase

Circulating volume stays the same

129
Q

Investigations for SIADH

A

Serum osmolality low
Serum sodium low
Urine osmolality high
Urine sodium high
Plasma volume NORMAL

U+E monitored daily in acute, less often in chronic

130
Q

What can rapid correction of sodium cause?

A

Osmotic demyelination syndrome - demyelination of descending axons.

Risk factors include:
Hypokalaemia, chronic excess alcohol. malnutrition. hyponatraemia, rapid soidum correction

131
Q

SIADH treatment

A

Check for causative drugs, treat underlying condition, ensure correct diagnosis

1st/Acute -
Fluid restriction + 3% Hypertonic saline to correct blood concentration and sodium

Pharmacological/chronic -
Tolvaptan (Selective V2 receptor antagonist), causes loss of water without electrolyte
Furosemide

132
Q

How can SIADH be differentiated from general Na+ depletion

A

By giving 0.9% saline

In SIADH this will fail to normalise

133
Q

Give possible causes of dehydrated hyponatraemia

A

Vomiting
Diarrhoea
Burns
Diuretics
Insufficient intake

134
Q

Effects of serotonin on GI tract, vasculature and connective tissue of heart

A

GI - Increased motility/peristalsis
Vasculature - platelets take up and cause vasoconstriction
Connective tissue - collagen deposition

135
Q

Complications of hyponatraemia

A

cerebral oedema, brain herniation, cardiac arrest, seizures

136
Q

Define Cushing’s disease/syndrome

A

Cushings refers to excess cortisol in the blood.

Cushings disease - Pituitary adenoma causing excess ACTH secretion

Cushings syndrome - hypercortisolaemia of any cause

137
Q

Functions of cortisol (5)

A

Increased renal K+ loss
Increased deposition of fat and glycogen
Carbohydrate and protein breakdown (muscle wasting)
Na+ retention
Diminished immune response

138
Q

Causes of Cushing’s syndrome (2 ACTH dependent and 2 ACTH independent)

A

ACTH Dependent
1 - Cushing’s disease - Pituitary adenoma secreting ACTH
2 - Ectopic ACTH production (SCLC)

ACTH independent
1 - Steroid usage (glucorticoid)
2 - Adrenal adenoma producing cortisol

139
Q

Signs/symptoms of Cushing’s

A

-Central (belly,chest,neck) fat deposition
-Moon face and plethoric complexion
-Purple abdominal striae
-Muscle wasting
-Easy bruising/infection
-Mood swings, gastric ulcers, osteoporosis

140
Q

Investigations for Cushing’s

Including other investigations

A

Check drug history (rule out steroids) and pregnancy.

1st - 12am cortisol (as normally lowest here)
2nd - Dexamethasone suppression test (low dose first if Cushings syndrome not diagnosed, then high dose)
3rd - 9am plasma ACTH to measure if cause is ACTH dependent or not.
- If low, adrenal imaging (cortisol producing tumour)
- If high, cause is ACTH dependent -> distinguish cause. If suppression at high dose DST then pituitary adenoma. CT chest, abdomen, pelvis, MRI neck and abdomen to check for ectopic ACTH production.

Other investigations include:
24 hour urinary free cortisol
MRI brain (pituitary adenoma)
Chest, abdomen CT (SCLC, adrenal adenoma)

141
Q

Explain the dexamethasone suppression test

A

Carried out overnight, dexamethasone given at 12am, measured at 8am, this normally shows cortisol suppression.
First carried out at low dose.

Low dose dexamethasone should suppress CRH from hypothalamus and ACTH from pituitary, reducing cortisol. If no/little cortisol suppression, Cushing’s syndrome.

High dose carried out to determine cause. Suppression at high dose suggests Cushing’s disease (pituitary adenoma), no suppression suggests ectopic cause or adrenal tumour producing cortisol

Summary:
Low dose result - suppression = normal, no suppression = Cushing’s SYNDROME.
High dose result - suppression = Cushing’s DISEASE, no suppression = ectopic ACTH or adrenal adenoma

142
Q

Treatment of Cushings syndrome

A

Depends on cause

  • Cushings disease: Transphenoidal removal of pituitary adenoma
  • Adrenal adenoma - Adrenalectomy and radiotherapy
  • Ectopic ACTH - surgical tumour removal
143
Q

Complications of Cushings, as well as big complication of treatment

A

Osteoporosis, Diabetes mellitus, immunosuppression

Complication of complete adrenalectomy: Nelson’s syndrome
- No adrenal gland = no cortisol = no negative feedback on pituitary so ACTH can build up in excess.
Causes bronze skin pigmentation, visual disturbances and headache

144
Q

When is cortisol highest and lowest in the blood?

A

Highest 7-9am morning

Lowest at midnight

145
Q

What is pseudo-cushings?

A

Chronic alcohol excess, severe depression, obesity or pregnancy can cause high cortisol and cushings-esque features but no HPA pathology. False positive DSA test, but can be differentiated using insulin stress test.

146
Q

What stimulate (2) and inhibit (3) growth hormone?

A

GHRH and ghrelin stimulate growth hormone

Somatostatin, glucose and dopamine inhibit growth hormone

147
Q

Define acromegaly with its main cause, and what is it also known as in children

A

Excess growth hormone causing characteristic excess growth of extremities. Main cause is pituitary adenoma

Known as gigantism before fusion of epiphyses of bones (children)

148
Q

Facial features in acromegaly (4)

A
  • Prominent jaw with lower jaw protrusion
  • Coarse facial appearance
  • Splaying of teeth
  • Large tongue
149
Q

Signs of acromegaly (6)

A
  • Bitemporal hemianopia (optic chiasm compression)
  • Spade like hands
  • Sweaty palms/oily skin
  • Carpal tunnel syndrome
  • Large hands/feet
  • Sleep apnoea
150
Q

Symptoms of acromegaly

A
  • Visual disturbances (bitemporal hemianopia)
  • Headaches
  • Obstructive sleep apnoea
  • Carpal tunnel syndrome

Hyperprolactinaemia also possible (galactorrhoea, hypogonadism, decreased libido, infertility)

151
Q

Investigations for Acromegaly

A

1st line
- IGF-1 - elevated in Acromegaly

Gold standard
- Oral glucose tolerance test: Glucose load should cause suppression of growth hormone. Failure of GH suppression 2 hours after 75g glucose load indicates Acromegaly.

Pituitary MRI and pituitary hormone screen (for prolactin) may also be needed. May be worth doing GHRH screen and CT chest abdomen and pelvis if cause is ectopic GHRH production

152
Q

Genetic risk factor for pituitary adenomas

A

MEN-1

153
Q

Other causes of acromegaly

A

Ectopic GH release
Ectopic GHRH release
Excess hypothalamic GHRH production

154
Q

By which two mechanisms does GH act

A

Directly on tissues such as liver, muscle, bone, fat.

Indirectly through induction of IGF-1, which is synthesised in liver and other tissues

155
Q

Treatment of Acromegaly

A

1st line
- Transphenoidal pituitary surgery

2nd
- Dopamine agonist (cabergoline)
- Somatostatin analogue (octreotide)
- Gh antagonist (pegvisomant)

If all else fails: Radiotherapy

156
Q

Complications and monitoring for acromegaly

A

Complications:
- Sleep apnoea
- Cardiomyopathy
- T2DM
- Carpal tunnel syndrome

Serum IGF-1 and GH will need lifelong monitoring

157
Q

Risk factors and aetiology of prolactinoma

A

MEN-2a/2b (multiple endocrine neoplasia) gene
Female (20-50 years)

Aetiology:
- usually adenoma of Lactotrophs in anterior pituitary causing excess prolactin release. Dopamine inhibits prolactin, so can also be caused by dopamine secretion/transport disturbance.

158
Q

Pathophysiology of prolactinoma

A

Lactotrophs in pituitary release prolactin causing lactation. Prolactin negatively feeds back onto Gonadotrophin releasing hormone causing decreased testosterone and oestrogen. Oestrogen usually inhibits osteoclasts, so risk of fracture is increased.

159
Q

Clinical effects of prolactinoma

A

Local tumour effect:
- Headache
- Bitemporal hemianopia
- CSF leak

Prolactin effects:
- Amenorrhoea
- Infertility
- Galactorrhoea (milky nipple discharge)
- Low libido/testosterone/oestrogen
- Vaginal dryness and brittle bones

160
Q

Treatment of prolactinoma

A

Usually medical rather than surgical

Dopamine agonist - cabergoline (dopamine inhibits prolactin)

Usually shrinks macroadenoma - sight saving. If microadenoma, patient will only need small doses a couple times a week.

161
Q

Investigations for prolactinoma

A

Serum prolactin
Thyrotropin releasing hormone
MRI to classify adenoma (>10mm is macroprolactinoma)

162
Q

Give monogenic causes of Diabetes

A

MODY (maturity onset diabetes of the young)
- Commonest, autosomal dominant, non-insulin dependant, diagnosed <25y. Usually mistaken for type 1

Permanent neonatal diabetes (De novo)
<6 months
- small babies, epilepsy, muscle weakness

163
Q

What might suggest MODY instead of type 1 diabetes?

A
  • One or both parents affected
  • Absence of islet autoantibodies
  • Sensitivity to sulphonylurea
  • Non insulin dependence (no ketosis, measurable C peptide, good control low insulin)
164
Q

Exocrine pancreas causes of diabetes

A

Acute inflammation
Chronic Pancreatitis (alcohol)
Pancreatic cancer
Cystic fibrosis

165
Q

Endocrine causes of diabetes

A

Acromegaly
Cushings
Phaeochromocytoma

166
Q

Drug induced causes of diabetes

A

Glucocorticoids increase insulin resistance
Thiazides
Protease inhibitors

167
Q

Explain the RAAS system

A
  • Juxtaglomerular cells in the afferent ateriole of the kidney sense low blood pressure and cleave prorenin into renin.
  • This converts liver secreted angiotensin into angiotensin I which is converted to angiotension II by ACE in the lungs.
  • Angiotensin II is a hormone with various effects, including causing aldosterone release by adrenal glands, which causes Na+/water reabsorption/retention and K+/H+ excretion, increasing blood pressure.
168
Q

Effects of angiotensin II

A
  • Systemic vasoconstriction
  • Thirst/water intake
  • Sodium/water retention
  • Reduced baroreflex to increased blood pressure
169
Q

Give primary causes of hyperaldosteronism

A
  • Bilateral adrenal hyperplasia (idiopathic, 2/3)
  • Adrenal adenoma (Conn’s syndrome, 1/3)
  • Familial hyperaldosteronism
170
Q

Define Conn’s syndrome

A

Excess aldosterone secretion (zona glomerulosa of adrenal) INDEPENDENT of RAAS system. Characterised by refractory high blood pressure, increased aldosterone, and low renin.

171
Q

Pathophysiology of Conn’s syndrome

A

Excess aldosterone causes excess Na+/water retention and K+/H+ excretion. Leads to refractory hypertension with low renin and high aldosterone.

Can also lead to alkalosis and hypokalaemia

172
Q

Signs and symptoms of Conn’s

A

Symptoms:
Muscle weakenss, paraesthesia, lethargy, muscle cramps. Polyuria/nocturia

Signs:
Refractory hypertension
Hypokalaemia
Metabolic alkalosis

173
Q

Investigations in Conn’s

A
  • Aldosterone:renin ratio:
    Decreased renin, increased aldosterone. This diagnoses primary aldosteronism
  • U&E: Hypokalaemia (could do ECG as well)
  • ABG: alkalosis
  • High resolution abdomen CT: determine unliteral or bilateral
174
Q

Management of Conn’s

A

1- Laparoscopic adrenalectomy
or Aldosterone antagonist (spironolactone) if bilateral, and before surgery

175
Q

Causes and pathophysiology of secondary hyperaldosteronism

(only ones different to primary highlighted)

A

Causes
- Renal artery stenosis
- Renal artery obstruction
- Heart failure

Pathophysiology:
Blood pressure of kidneys lower than rest of body, falsely causes excess renin secretion

176
Q

Investigations and management in secondary hyperaldosteronism

(only ones different to primary highlighted)

A

Investigations
- Aldosterone:renin ratio BOTH renin and aldosterone high

  • Doppler ultrasound or CT Angiogram: Check for renal artery stenosis

Management:
Treat underlying cause
- Surgical: Percutaneous renal artery angioplasty
- Aldosterone antagonist: spironolactone

177
Q

Carcinoid syndrome vs Carcinoid tumours

Where they normally occur and what they produce.

A

Carcinoid tumours - Largely asymptomatic tumour of enterochromaffin cells in GI tract, appendix, terminal ileum and pancreas.

Carcinoid syndrome - Usually occurs when tumour metastasises to liver, causing symptoms.

Tumours secrete 5-HT. Also causes increased histamine and bradykinin

178
Q

Why are carcinoid tumours only symptomatic once they metastasise to liver?

A

Liver is able to metabolise all the extra 5-HT/serotonin until liver is affected. It is then dumped into hepatic veins, circulating it.

179
Q

Symptoms, investigations and treatments of carcinoid syndrome

A

Diarrhoea, shortness of breath, itching, flushing, RUQ pain. Symptoms worsened by alcohol and stress.

Investigations: Urinary 5-Hydroxyindoleacetic acid (5-HIAA): increased
Liver ultrasound

Management: Surgical excision of tumour or octreotide (somatostatin analogue)

Can lead to carcinoid crisis

180
Q

What factors affect aldosterone release?

A

Angiotensin II
low sodium
high potassium

(aldosterone works to increase BP and volume, increase Na+ and decrease K+)

181
Q

Primary causes of adrenal insufficiency, and what is this disease called

A

Addisons - direct damage to adrenal gland

  • Autoimmune (MC in developed world) against 2,1-hydroxylase enzyme
  • TB infection (MC worldwide)
  • Metastatic cancer
  • Adrenal haemorrhage/infarction
182
Q

What hormones are deficient in adrenal insufficiency

A
  • Cortisol
  • Aldosterone
  • Androgens (these symptoms affect women more as men largely produce testosterone from their testes)
183
Q

General signs and symptoms of adrenal insufficiency

A

Signs: (tanned tired toned tearful)
Vitiligo
Postural hypotension
Hyperpigmentation (particularly in palmar creases, and only in addisons due to increased ACTH)
Hair loss (mostly women’s axillary and pubic hair, due to androgen deficiency)

Symptoms:
Nausea, vomiting, fatigue
Cramps
Reduced libido
Disorientation
Weight loss
Salt craving

184
Q

Generic blood / U+E results in adrenal insufficiency (5)

A

Hypovolaemia
Hypoglycaemia
Metabolic acidosis
Increased potassium
Decreased sodium

185
Q

Risk factors for adrenal insufficiency

A
  • Female
  • Autoimmune conditions
  • Recent TB infection
  • Coeliac
186
Q

What is waterhouse friedrichsen syndrome, with a big cause and complication

A

Adrenal insufficiency caused by rupturing of adrenal blood vessels caused by rapid BP change, leading to adrenal haemorrhage

Meningococcal meningitis can cause this!

Can lead to Addisonian crisis

187
Q

Investigations for adrenal insufficiency

A

1st - Morning serum cortisol (cortisol highest at 9am)

Gold - ACTH stimulation test (Synacthen) - cortisol measured before and 30 mins after giving synacthen. No cortisol rise = adrenal insufficiency.

Others:
- U+E (hyponatraemia, hyperkalaemia, hypoglycaemia)
- ABG (metabolic acidosis)
- CT adrenal
- Serum ACTH - if ACTH high, Addison’s. If low, ACTH is cause so adrenal insufficiency is secondary

188
Q

Causes for secondary adrenal insufficiency

A

Low ACTH causing secondary adrenal insufficiency

  • Most commonly glucocorticoid usage causing ACTH/CRH suppression, leading to reduced cortisol and aldosterone production. (importantly as no ACTH excess, no hyperpigmentation occurs)
  • Can also be due to pituitary resection
189
Q

Treatment of adrenal insufficiency

A

Hydrocortisone and fludrocortisone therapy

androgen replacement may be needed in women

190
Q

Complications of adrenal insufficiency

A
  • Secondary Cushings due to excess hormone replacment
  • Osteopenia
  • Addisonian crisis!!!!!
191
Q

Define Addisonian crisis with pathophysiology

A

Acute deficiency of adrenal hormones under stress such as;
- dehydration
- infection
- sepsis/surgery
- meningococcal infection (waterhouse-freiderichsen syndrome)

Supply cannot meet increased demand leading to severe hyperkalaemia, metabolic acidosis, hyponatraemia and dehydration

192
Q

What are the metabolic features of Addisonian crisis (4)

A
  • Hyperkalaemia
  • Hyponatraemia
  • Metabolic Acidosis
  • Hypoglycaemia
193
Q

Signs/symptoms of addisonian crisis

A

Hypovolaemic shock
Reduced GCS
Pyrexia
Abdominal, back or leg pain!!
Vomiting profusely

194
Q

Treatment of addisonian crisis

A

IV fluids and hydrocortisone

(no fludrocortisone)

195
Q

Define Phaeochromocytoma with its risk factors

A

Tumour of the chromaffin cells of the adrenal medulla, causing excess adrenaline and noradrenaline release

RF:
MEN 2a/2b genes (multiple endocrine neoplasia)
Von Hippel Lindau syndrome

196
Q

Phaeochromocytoma presentation and investigations

A

Classic triad:
Episodic headaches, palpitations/tachycardia (paroxysmal AF), sweating
Anxiety and HTN

Investigations:
- 24 hour urinary catecholamines
- Plasma free metanephrines

197
Q

In phaeochromocytoma, why are catecholamines measured over 24 hours?

Why are metanephrines also measured if the tumour is secreting catecholamines?

A
  • Serum catecholamines unreliable as they naturally fluctuate. Measuring 24 hour urine catecholamines gives an idea of how much adrenaline is being secreted by the tumour over the period
  • Adrenaline has a short half life in blood, but metanephrines (breakdown product of adrenaline) have a longer one, so wont fluctuate as much
198
Q

Treatment of phaeochromocytoma, and metastatic spread

A

Alpha blocker first (phenoxybenzamine)
Beta blocker (atenolol)
Adrenalectomy is definitive management

Metastasises to lymph nodes, liver, bones, lung

199
Q

Define breast cancer

A

Uncontrolled growth of epithelial cells in the breast

200
Q

Causes of breast cancer

A

Gene mutation:
BRCA1 - Chromosome 17
BRCA2 - Chromosome 13
Autosomal dominant and also predispose to ovarian, pancreatic and prostate cancer

HER2 receptor mutation too

201
Q

What is an important oncogene that is over expressed in breast cancer

A

HER2 receptor- enables cell growth, survival and proliferation

202
Q

5 risk factors for breast cancer

A

Oestrogen exposure
- Hormone replacement therapy
- Early menarche and late menopause
- Not breast feeding
- First pregnancy>30 years
- Nulliparity

203
Q

What are the classifications of breast cancer

A

In situ - non invasive/ dont penetrate basement membrane
Invasive - penetrate basement membrane

Can be Lobular - Grow within lobules, without invading the ducts
Can be Ductal - Grow from the ducts of the walls into the lumen. These in situ can go on to become invasive

204
Q

What occurs if a Ductal carcinoma in situ migrates?

A

Pagets disease of the nipple

DCIS migrates along lactiferous duct through the pore onto the skin over the nipple. Presents with scaly, red nipple and rash

205
Q

What is the most common invasive breast cancer

A

Invasive ductal carcinoma

206
Q

Skin, lump, nipple changes in breast cancer

A

Skin:
- Tethering
- Oedema
- Thickened and dimpled (peau d’orange)

Lump:
- Hard/firm and irregular

Nipple
- Inversion
- Discharge
- Dilated veins
- Pagets (itchiness, redness, crusting, discharge)

207
Q

Where does breast cancer metastasise

A
  • Bone
  • Liver
  • Lungs
  • Brain
208
Q

How is breast cancer screened for?

A

Mammogram scans from 50 to 71

209
Q

Other investigations for breast cancer

A

Ultrasound if under 40
Fine needle aspiration and core biopsy

Receptor status (checks for progesterone and oestrogen receptors (PR+ and ER+) These have proliferative effects and enables treatment options. Triple negative (HER2-, PR-, ER-) limits treatment options and has poor prognosis
TNM for staging

Assess axillary lymph nodes

210
Q

Pharmacological management of breast cancer

A
  • HER2 positive - Herceptin

ER/PR positive -
- Men and premenopausal women - Tamoxifen (oestrogen receptor blocker)
- Post menopausal women - Anastrozole (Aromatase inhibitor- prevents conversion of androgens to oestrogens)

211
Q

Medication to suppress ovarian function

A

GnRH analogue (goserelin)

212
Q

Surgical management of breast cancer

A

Breast conservation
Mastectomy

Sentinel lymph node biopsy to check metastases

213
Q

What diabetes treatment has the highest Hypo risk?

A

Sulfonylurea (gliclazide)

214
Q

What is used to treat diabetic neuropathy

A

Duloxetine or pregabalin or gabapentin

215
Q

Side effects of levothyroxine

A
  • Osteoporosis
  • Cardiac arrhythmia
216
Q

Consequences of hyperkalaemia (4)

A
  • Diminished heart contractions -> reduced cardiac output -> reduced BP
  • Constipation, followed by nausea/vomiting
  • Muscle weakness/wasting
  • Respiratory distress and difficulty breathing
217
Q

Why does hyperphosphataemia cause hypocalcaemia

A

Excess phosphate deposits as calcium phosphate in kidney tubules, depleting calcium and causing AKI

218
Q

What is klinefelter syndrome

A

47 XXY

Extra X chromosome causes hypogonadism, tall stature, gynaecomastia and delayed puberty

219
Q

What is Multiple endocrine neoplasia 1?

A

Increased risk of developing these endocrine tumours:

  • Parathyroid adenoma
  • Pituitary prolactinoma or acromegaly
  • Pancreatic endocrine tumours
220
Q

What is caused by multiple endocrine neoplasia II

A
  • Medullary thyroid cancer
  • Parathyroid hyperplasia
  • Phaeochromocytoma
221
Q

What differentiates MENIIb from MENIIa

A

No hyperparathyroid in b

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