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Phase 2a > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Describe the mechanism of action of water soluble hormones, giving some examples of them.

A
  • They are synthesised + then stored in vesicles to be released when they’re required.
  • They enter cells by binding to cell surface receptors.
  • Peptide hormones like TRH, LH + FSH
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2
Q

Describe the mechanism of action of fat soluble hormones, giving some examples of them.

A
  • They are synthesised + released on demand.
  • Cell receptors are located in the cytoplasm.
  • Steroid hormones like cortisol.
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3
Q

Describe the synthesis pathway of amine hormones and how they are broken down.

A

Phenylalanine > L-tyrosine > L-dopa > Dopamine > NAd + Ad.

  • Broken down into normetadrenaline + metadrenaline by the enzymes MAO + COMT.
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4
Q

Give examples of hormones that act on nuclear cell receptors.

A

Thyroid, vitamin A + D and oestrogen.

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5
Q

What part of the trilaminar disc is the anterior pituitary gland derived from?

A

The ectoderm (Rathke’s pouch).

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6
Q

How do hormones travel from the hypothalamus to the anterior pituitary gland?

A

The hypothalamo-hypophyseal portal vessels.

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7
Q

Name the 6 hormones produced by the hypothalamus.

A
  • Thyrotropin-releasing hormone (TRH).
  • Corticotropin-releasing hormone (CRH).
  • Gonadotropin-releasing hormone (GnRH).
  • Growth hormone releasing hormone (GHRH).
  • Somatostatin (inhibitor).
  • Dopamine (inhibitor).
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8
Q

Name the 6 hormones produced by the anterior pituitary gland.

A

FLATPIG…

  • Follicle stimulating hormone (FSH).
  • Luteinising hormone (LH).
  • Adrenocorticotropic hormone (ACTH).
  • Thyroid stimulating hormone (TSH).
  • Prolactin.
  • Growth hormone (GH).
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9
Q

Describe the thyroid axis.

A

Hypothalamus > TRH > TSH > Thyroid > T3+4

  • T3/4 have a -ve feedback effect on the hypothalamus + anterior pituitary gland.
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10
Q

Which has a longer half-life, triiodothyronine (T3) or thyroxine (T4) and so which is more metabolically active?

A
  • T4 has a half-life of 5-7 days.
  • T3 has a half-life of 1 day.
  • T4 has the longer half-life + so T3 is more metabolically active.
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11
Q

What happens to T4 peripherally?

A
  • It’s converted into T3, the more metabolically active form.
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12
Q

What is the function of T3/4 in the body?

A
  • Food metabolism.
  • Protein synthesis.
  • Heat production.
  • Increased sympathetic action like CO + HR.
  • Needed for growth + development.
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13
Q

Describe the adrenal cortex axis.

A

Hypothalamus > CRH > ACTH > Adrenal cortex (zona fasciculata) > glucocorticoid synthesis e.g. cortisol.

  • Cortisol has a -ve feedback effect on the hypothalamus + anterior pituitary gland.
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14
Q

What are the three zones of the adrenal cortex and what do they produce?

A
  • All produce different types of steroids called corticosteroids, where cholesterol is the precursor.
  • Zona glomerulosa, produces mineralocorticoids like aldosterone.
  • Zona fasiculata, produces glucocorticoids like cortisol (+ small amounts of androgens).
  • Zona reticularis, produces androgens (+ small amounts of cortisol).
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15
Q

What are the functions of cortisol in response to stress?

A
  • Mobilises energy sources via lipolysis, gluconeogenesis + protein breakdown as it inhibits insulin + activates glucagon.
  • Vasoconstriction.
  • Suppresses inflammatory + immune responses.
  • Inhibits non-essential functions like growth + reproduction.
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16
Q

Describe the gonadal axis.

A

Hypothalamus > GnRH > FSH/LH > ovaries/testes.

  • FSH/LH has a -ve feedback effect on the hypothalamus + anterior pituitary gland.
  • Inhibin + activin also acts on the anterior pituitary gland to regulate FSH levels.
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17
Q

What is the function of FSH/LH in females?

A
  • FSH acts on granulosa cells to produce oestrogen from androgens using the aromatase enzyme.
  • LH acts on theca cells to produce androgens that diffuse into granulosa cells to be converted into oestrogen.
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18
Q

What is the function of FSH/LH in males?

A
  • FSH acts on sertoli cells to stimulate spermatogenesis + also produces Mullerian inhibition factor (MIF), inhibin + activin.
  • LH acts on Leydig cells to produce testosterone.
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19
Q

Describe the GH/IGF-1 axis.

A

Hypothalamus > GHRH (+) or somatostatin (-) > GH > Liver > IGF-1.

  • IGF-1 + GH has a -ve feedback effect on the hypothalamus + anterior pituitary gland.
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20
Q

What is the function of IGF-1?

A

Induces cell division, cartilage + skeletal growth + protein synthesis.

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21
Q

What can inhibit GH production?

A
  • High glucose levels.
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22
Q

Describe the prolactin axis.

A

Hypothalamus > dopamine (-) > inhibited prolactin.

Prolactin has a -ve feedback effect on the hypothalamus + anterior pituitary gland.

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23
Q

What does prolactin do?

A

Acts on the mammary glands to produce milk.

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24
Q

Where is the posterior pituitary gland derived from embryologically?

A
  • The floor of the ventricles.
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25
Q

What are the two hormones synthesised in the posterior pituitary gland + where are they synthesised?

A
  • Oxytocin = para-ventricular nucleus.

- Vasopressin/ADH = supra-optic nucleus.

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26
Q

What is the function of oxytocin?

A

Acts by stimulating milk secretion + uterine contractions.

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27
Q

What is the function of vasopressin/ADH?

A

Acts on the collecting ducts of the nephron + increases the insertion of aquaporin 2 channels to cause water retention.

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28
Q

TYPE 1 DIABETES MELLITUS

What is the pathophysiology of T1DM and the effect of this?

A
  • Autoimmune destruction of the pancreatic beta cells.
  • Causes severe insulin deficiency meaning that glycogenolysis/gluconeogenesis/lipolysis are NOT suppressed + there is reduced peripheral glucose uptake leading to hyperglycaemia + glycosuria.
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29
Q

TYPE 1 DIABETES MELLITUS

What genetics are associated in T1DM?

A
  • HLA-DR3 + HLA-DR4 but triggered by one or more environmental antigens.
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30
Q

TYPE 1 DIABETES MELLITUS

What is the aetiology of T1DM?

A

Insulin deficiency from autoimmune destruction of the insulin-secreting pancreatic beta cells as they express HLA antigens.

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31
Q

TYPE 1 DIABETES MELLITUS

What is the clinical presentation of T1DM?

A
  • Typically presents in childhood, before puberty + patients often slim.
  • Polydipsia (fluid + electrolyte loss).
  • Polyuria (osmotic diuresis).
  • Weight loss.
  • Ketosis.
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32
Q

TYPE 1 DIABETES MELLITUS

What is the diagnostic criteria for T1DM?

A

Signs of hyperglycaemia + one or more of…

  • Ketosis.
  • Rapid weight loss.
  • Age of onset <5 y/o.
  • BMI < 25kg/m^2.
  • FHx of autoimmune disease.
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33
Q

TYPE 1 DIABETES MELLITUS

What are the 2 main complications with T1DM?

A
  • Diabetic ketoacidosis (DKA).

- Hypoglycaemia.

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34
Q

TYPE 1 DIABETES MELLITUS

What happens in DKA?

A
  • Occurs due to the absence of insulin, there is uncontrollable lipolysis which causes an increased production of free fatty acids.
  • These free fatty acids are oxidised in the liver to form ketone bodies causing ketoacidosis to occur.
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35
Q

TYPE 1 DIABETES MELLITUS

Give some examples of ketone bodies.

A
  • Acetoacetate.
  • Acetone.
  • Beta-hydroxybutyrate.
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36
Q

TYPE 1 DIABETES MELLITUS

What are the signs of DKA?

A
  • HYPOtension.
  • TACHYcardia.
  • Kussmaul’s breathing (deep + laboured).
  • Ketotic breath (fruity).
  • Dehydration.
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37
Q

TYPE 1 DIABETES MELLITUS

How does hypoglycaemia present?

A
  • Sweating.
  • Palpitations.
  • Confusion.
  • Drowsiness.
  • Seizures.
  • Potentially comas.
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38
Q

TYPE 1 DIABETES MELLITUS

What is the most common cause of hypoglycaemia in patients with T1DM?

A
  • Insulin therapy.
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39
Q

TYPE 1 DIABETES MELLITUS

How is hypoglycaemia diagnosed + managed?

A
  • Plasma glucose ≤ 3mmol/L.

- Managed with glucose (food/IV infusion based on consciousness), glucagon + medication review.

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40
Q

TYPE 1 DIABETES MELLITUS

What is the general treatment for T1DM?

A

Education + lifestyle advice.

- Ensure patient understands benefits of exercise, eating healthily (less sat fats, sugars + more carbohydrates).

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41
Q

TYPE 1 DIABETES MELLITUS

What is the pharmacological treatment for T1DM and how is it administered?

A

Insulin.

  • Usually administered by subcutaneous injection.
  • Sometimes administered by insulin pump (continuous SC injection) when attempts to reach HbA1c goal with multiple daily injections hasn’t worked or caused disabling hypoglycaemia.
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42
Q

TYPE 1 DIABETES MELLITUS

What are the complications with insulin therapy?

A
  • HYPOGLYCAEMIA.
  • Lipohypertrophy at injection site (cycle injection sites).
  • Insulin resistance.
  • Weight gain.
  • Lifestyle interference.
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43
Q

TYPE 2 DIABETES MELLITUS

What is the pathophysiology in T2DM?

A
  • Beta cell mass is reduced to 50% of the normal mass resulting in an inappropriately low insulin secretion + peripheral insulin resistance causing impaired glucose tolerance.
  • Impaired insulin secretion is thought to be as a result of lipid deposition in the pancreatic islets.
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44
Q

TYPE 2 DIABETES MELLITUS

What is the aetiology of T2DM?

A
  • Genetic predisposition + environmental factors.

- NO HLA LINK.

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45
Q

TYPE 2 DIABETES MELLITUS

What are the risk factors for T2DM?

A
  • Obesity.
  • Physical inactivity.
  • FHx.
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46
Q

TYPE 2 DIABETES MELLITUS

What is the clinical presentation of T2DM?

A
  • Typically presents in Asians, men + has an older presentation.
  • Often asymptomatic.
  • Can present with signs of hyperglycaemia like polyuria + polydipsia if v severe.
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47
Q

TYPE 2 DIABETES MELLITUS
Impaired glucose tolerance can be an indicator of pre-diabetes and so insulin resistance. What would the Oral Glucose Tolerance Test (OGTT) show in someone with pre-diabetes?

A

7.8mmol/L ≤ 2-hour value < 11.1mmol/L.

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48
Q

TYPE 2 DIABETES MELLITUS
Impaired fasting glucose can be an indicator of pre-diabetes and so insulin resistance. What would the fasting plasma glucose (FPG) be in someone with pre-diabetes?

A

6.1mmol/L ≤ FPG < 7.0mmol/L.

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49
Q

TYPE 2 DIABETES MELLITUS

What 3 diagnostic criteria are needed to make a diagnosis of T2DM?

A
  • Symptomatic + 1 abnormal glucose result.
  • Asymptomatic + 2 separate abnormal glucose results.
  • Abnormal HbA1c.
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50
Q

TYPE 2 DIABETES MELLITUS

When is a HbA1c test contraindicated for diagnosing T2DM?

A
  • Pregnancy.
  • T1DM.
  • Children.
  • Haemoglobinopathies.
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51
Q

TYPE 2 DIABETES MELLITUS

What are the symptoms of hyperglycaemia + so T2DM?

A
  • Polyuria.
  • Polydipsia.
  • Unexplained weight loss.
  • Lethargy, visual blurring.
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52
Q 
TYPE 2 DIABETES MELLITUS
What are the diagnostic values in T2DM for...
i) Fasting plasma glucose.
ii) Random plasma glucose.
iii) OGTT 2-hour value.
(iv) HbA1c
A

i) Fasting ≥7mmol/L
ii) Random ≥11.1mmol/L.
iii) OGTT 2-hour value ≥11.1mmol/L.
iv) HbA1c ≥48mmol/mol.

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53
Q

TYPE 2 DIABETES MELLITUS

What are the main complications associated with T2DM?

A
  • Hyperglycaemia hyperosmolar state.

- Hypoglycaemia.

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54
Q

TYPE 2 DIABETES MELLITUS

Why is ketoacidosis not a feature of T2DM?

A
  • Despite the impaired insulin secretion there are still some low levels of plasma insulin which is enough to prevent muscle catabolism + ketogenesis.
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55
Q

TYPE 2 DIABETES MELLITUS

What is hyperglycaemic hyperosmolar state caused by and how do patients present?

A
  • Caused by insufficient oral hypoglycaemia agents.
  • Presents with polydipsia, polyuria, nausea + dry skin.
  • Plasma glucose can be ≥40mmol/L.
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56
Q

TYPE 2 DIABETES MELLITUS

What are the potential complications in the hyperglycaemic hyperosmolar state and how are these managed?

A
  • Causes hyperviscosity of the blood + so a risk of stroke/MI.
  • Managed with low molecular weight heparin prophylaxis, fluids + insulin if v severe.
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57
Q

TYPE 2 DIABETES MELLITUS

How does hypoglycaemia present and what is the most common cause of it in T2DM?

A
  • Presents as sweating, palpitations, confusion, drowsiness, seizures + potentially comas.
  • Most common cause in T2DM is sulfonylurea treatment.
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58
Q

TYPE 2 DIABETES MELLITUS

How is hypoglycaemia diagnosed + managed?

A
  • Plasma glucose ≤ 3mmol/L.

- Managed with glucose (food/IV infusion based on consciousness), glucagon + medication review.

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59
Q

TYPE 2 DIABETES MELLITUS

What is the first-line treatment for pre-diabetes and T2DM?

A

Lifestyle modification advice + risk factor reduction.

- Control diet, weight + exercise more.

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60
Q

TYPE 2 DIABETES MELLITUS

What drug is used first for monotherapy in T2DM?

A
  • Metformin.
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61
Q

TYPE 2 DIABETES MELLITUS

What drugs other than Metformin are used to treat T2DM?

A
  • Sitagliptin.
  • Glitazone.
  • Gliclazide.
  • Empagliflozin.
  • Insulin (last resort).
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62
Q

TYPE 2 DIABETES MELLITUS

Describe the pharmacology of Metformin.

A
  • Biguanide.
  • Increases insulin sensitivity, reduces gluconeogenesis in the liver + helps weight.
  • SIde effects can include nausea, diarrhoea + abdominal pain.
  • Does NOT cause hypoglycaemia.
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63
Q

TYPE 2 DIABETES MELLITUS

Describe the pharmacology of Sitagliptin.

A
  • DPP4-inhibitor/gliptin.
  • Inhibits DPP4 + increases the effect of incretins which stimulate insulin secretion.
  • Does NOT affect weight.
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64
Q

TYPE 2 DIABETES MELLITUS

Describe the pharmacology of Glitazone.

A
  • Pioglitazone.
  • Enhances uptake of fatty acids + glucose.
  • Side effects can include HYPOGLYCAEMIA, WEIGHT GAIN + fluid retention.
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65
Q

TYPE 2 DIABETES MELLITUS

Describe the pharmacology of Gliclazide.

A
  • Sulfonylurea.
  • Stimulates beta cells to secrete insulin.
  • Side effects can include HYPOGLYCAEMIA + WEIGHT GAIN.
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66
Q

TYPE 2 DIABETES MELLITUS

Describe the pharmacology of Empagliflozin.

A
  • Selective sodium-glucose co-transporter-2 inhibitor (SGLT-2i).
  • Blocks the reabsorption of glucose in the kidneys + promotes excretion of excess glucose in the urine.
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67
Q

DIABETES MELLITUS

What is the main risk factor for diabetic complications?

A

Poor glycaemic control.

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68
Q

DIABETES MELLITUS

What can acute and chronic hyperglycaemia cause?

A
  • Acute = DKA + hyperosmolar coma.

- Chronic = micro/macrovascular tissue complications.

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69
Q

DIABETES MELLITUS

Give 3 examples of microvascular diabetic complications.

A
  • Diabetic retinopathy.
  • Diabetic nephropathy.
  • Diabetic peripheral neuropathy.
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70
Q

DIABETES MELLITUS

What is the pathophysiology of diabetic retinopathy?

A

Micro-aneurysms lead to pericyte loss + protein leakage resulting in occlusion + subsequent ischaemia.

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71
Q

DIABETES MELLITUS

What are the types of diabetic retinopathy?

A
  • R1 grade = non-proliferative/background retinopathy.
  • R2 grade = pre-proliferative.
  • R3 grade = proliferative.
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72
Q

DIABETES MELLITUS

What is seen in R1 grade retinopathy?

A
  • Micro-aneurysms (dots).
  • Haemorrhages (blots).
  • Hard exudates (lipid deposits).
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73
Q

DIABETES MELLITUS

What is seen in R2 grade retinopathy?

A

Signs of ischaemia…

  • Cotton-wool spots (e.g. infarcts).
  • Haemorrhages.
  • Venous beading.
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74
Q

DIABETES MELLITUS

What is seen in R3 grade retinopathy?

A

New vessel formation.

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75
Q

DIABETES MELLITUS

What are the risk factors for diabetic retinopathy?

A
  • Poor glycaemia control + long-term DM.
  • HTN.
  • High HbA1c.
  • Insulin therapy.
  • Pregnancy.
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76
Q

DIABETES MELLITUS

What is the treatment for diabetic retinopathy?

A
  • Offered annual screening to assess visual acuity.

- Laser therapy used to treat neovascularisation.

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77
Q

DIABETES MELLITUS

What is the hallmark of diabetic nephropathy?

A
  • Development of proteinuria + progressive decline in renal function.
  • Microscopically, there is thickening of the glomerular basement membrane as a result of hyperglycaemia.
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78
Q

DIABETES MELLITUS

What are the differences in presentation with diabetic nephropathy?

A
  • T1DM = microalbuminuria develops 5-10 years AFTER diagnosis.
  • T2DM = microalbuminuria PRESENT AT diagnosis.
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79
Q

DIABETES MELLITUS

What is the treatment for diabetic nephropathy?

A
  • Glycaemic + BP control.
  • Inhibition of RAAS system with an ACEi or ARB even when normotensive will protect kidney.
  • Spironolactone (K-sparring diuretic) may help.
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80
Q

DIABETES MELLITUS

What is the commonest form of diabetic peripheral neuropathy?

A

Distal symmetrical polyneuropathy.

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81
Q

DIABETES MELLITUS

What are the clinical consequences of diabetic peripheral neuropathy?

A

Pain…
- Described as burning, paraesthesia w/ nocturnal exacerbation.
Autonomic neuropathy…
- Loss of cerebrovascular autoregulation for functions like BP, HR, bowel/bladder emptying.
Insensitivity…
- Can lead to foot ulceration causing infection w/ ?amputation.

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82
Q

DIABETES MELLITUS

What are the signs of autonomic neuropathy in diabetic peripheral neuropathy?

A
  • HYPOtension.
  • HR affected.
  • Diarrhoea or constipation.
  • Incontinence.
  • Erectile dysfunction.
  • Dry skin.
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83
Q

DIABETES MELLITUS

What is the pattern of insensitivity in diabetic peripheral neuropathy?

A
  • Starts in the toes + moves proximally.

- Glove + Stocking distribution, symmetrically.

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84
Q

DIABETES MELLITUS

What are the risk factors for diabetic peripheral neuropathy?

A
  • Poor glycaemic control + long-term DM.
  • HTN.
  • Smoking.
  • High HbA1c.
  • Being overweight.
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85
Q

DIABETES MELLITUS

What are the treatments for diabetic peripheral neuropathy?

A
  • Improve glycaemic control.
  • Tricyclic anti-depressants (amitriptyline).
  • Pain relief (paracetamol).
    Podiatrist.
  • MDT foot clinics.
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86
Q

DIABETES MELLITUS

Give examples of macrovascular complications of DM.

A
  • Cardiovascular disease + stroke.
  • Vascular disease is the chief cause of death.
  • MI more likely to be silent + women are at high risk as DM removes the vascular advantage of females.
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87
Q

DIABETES MELLITUS

What are the signs of acute ischaemia in macrovascular DM complications?

A
  • Pulseless.
  • Pale.
  • Perishing cold.
  • Pain.
  • Paralysis.
  • Paraesthesia.
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88
Q

DIABETES MELLITUS

What are the treatments of macrovascular DM complications?

A
  • Address other risk factors like diet, smoking + HTN.
  • ?Statins (atorvastatin).
  • Prophylactic aspirin 75mg (secondary prevention).
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89
Q

THYROTOXICOSIS

What is the pathophysiology of thyrotoxicosis and what are the mechanisms involved?

A

Clinical effect of excess thyroid hormone, usually from gland hyperfunction.

3 mechanisms…

  • Overproduction of thyroid hormone.
  • Leakage of pre-formed hormone from thyroid.
  • Ingestion of excess thyroid hormone.
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90
Q

THYROTOXICOSIS

What is the epidemiology of thyrotoxicosis?

A
  • Females&raquo_space; males.

- Presentation mainly 20-40 y/o.

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91
Q

THYROTOXICOSIS

What is the aetiology of thyrotoxicosis?

A
  • 2/3 cases = Graves’ disease.
  • Toxic multinodular goitre.
  • Toxic adenoma.
  • Exogenous iodine excess.
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92
Q 
THYROTOXICOSIS
Explain how the following cause thyrotoxicosis...
i) Toxic multinodular goitre.
ii) Toxic adenoma.
iii) Exogenous iodine excess
A

i) Nodules secrete excess thyroid hormones.
ii) Solitary nodule produces T3/4.
iii) Food contamination or drugs like lithium + amiodarone.

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93
Q

THYROTOXICOSIS

What are the symptoms of thyrotoxicosis?

A

Body goes on overdrive…

  • Diarrhoea.
  • Weight loss.
  • Increased appetite.
  • Irritability + insomnia.
  • Sweats + heat intolerance.
  • Palpitations, tremor.
  • Amenorrhoea.
94
Q

THYROTOXICOSIS

What are the signs of thyrotoxicosis?

A
  • Tachycardia/irregular pulse (can be atrial fibrillation or supraventricular tachycardia).
  • Lid lag + retraction.
  • Thin hair.
  • Warm, moist skin.
95
Q

THYROTOXICOSIS

What are the investigations used for someone with suspected thyrotoxicosis?

A 
Thyroid function tests...
- Primary = low TSH (as suppressed), high T3/4.
- Secondary = both high.
Thyroid autoantibodies.
Isotope scan.
96
Q

THYROTOXICOSIS

What are the treatments for thyrotoxicosis?

A

Beta-blockers…
- Rapid symptom control during thyroid storm.
Anti-thyroid medication…
- Carbimazole.
Radioiodine therapy…
- In active thyroxicosis risk of thyroid storm.
Thyroidectomy.

97
Q

THYROTOXICOSIS

How can anti-thyroid medication like Carbimazole be started?

A
  • Titration (find the right value for the patient by slowly increasing doses).
  • Block + replace (remove all T3/4 and make patient go hypo and then replace the T3/4, keeping it under control).
98
Q

THYROTOXICOSIS

What are the negatives with a thyroidectomy?

A
  • Risk to recurrent laryngeal nerve (hoarse voice).

- Hypothyroidism + so patients will need thyroid replacement.

99
Q

GRAVES’ DISEASE

What is the pathophysiology of Graves’ disease?

A
  • Autoimmune induced excess production of thyroid hormone.
  • Increased levels of TSH receptor stimulation antibody (TRAb, IgG) which causes excess thyroid hormone secretion from the thyroid as it binds to TSH receptors.
100
Q

GRAVES’ DISEASE

What is the aetiology of Graves’ disease?

A
  • Autoimmune so unknown.

- Can be triggered by stress, infection + genetics.

101
Q

GRAVES’ DISEASE

What are the symptoms of Graves’ disease?

A

Body goes on overdrive…

  • Diarrhoea.
  • Weight loss.
  • Increased appetite.
  • Sweats + heat intolerance.
  • Palpitations, tremor.
  • Amenorrhoea.
102
Q

GRAVES’ DISEASE

What are the unique symptoms of Graves’ disease?

A 
Graves' ophthalmology...
- Diplopia.
- Ophthalmoplegia.
- Increased tear production.
Thyroid acropachy...
- Painful finger.
- Toe swelling.
103
Q

GRAVES’ DISEASE

What are the unique signs of Graves’ disease?

A 
Graves' ophthalmology...
- Exophthalmos.
- Papilloedema.
Thyroid acropachy...
- Clubbing.
- Swelling of soft tissues.
Pretibial myxoedema (localised skin lesion, esp. on skin in front of tibia due to increased glycosaminoglycans).
Diffuse goitre.
104
Q

GRAVES’ DISEASE

What are the investigations used for someone with suspected Graves’ disease

A 
Thyroid function tests...
- Primary = low TSH (as suppressed), high T3/4.
- Secondary = both high.
Thyroid autoantibodies.
- Focus on TRAb.
Isotope scan.
105
Q

GRAVES’ DISEASE

What are the treatments for Graves’ disease?

A

Beta-blockers…
- Rapid symptom control during thyroid storm.
Anti-thyroid medication…
- Carbimazole.
Radioiodine therapy…
- In active thyroxicosis risk of thyroid storm.
Thyroidectomy.

106
Q

HYPOTHYROIDISM

What is the pathophysiology of hypothyroidism?

A

The clinical effect of lack of thyroid hormone.

107
Q

HYPOTHYROIDISM

What is the epidemiology of hypothyroidism?

A
  • Common (4/1000 per year).

- Females&raquo_space; males.

108
Q

HYPOTHYROIDISM

What is the aetiology of autoimmune hypothyroidism?

A
  • Primary atrophic hypothyroidism.

- Hashimoto’s thyroiditis.

109
Q

HYPOTHYROIDISM
Explain how the following cause hypothyroidism…
i) Primary atrophic hypothyroidism.
ii) Hashimoto’s thyroiditis.

A

i) Diffuse lymphocytic infiltration of the thyroid, leading to atrophy + so NO goitre.
ii) Autoimmune destruction of the thyroid, goitre due to lymphocytic + plasma cell infiltration, more common in women aged 60-70 y/o.

110
Q

HYPOTHYROIDISM

What are the non-autoimmune aetiologies of hypothyroidism?

A
  • Iodine deficiency.
  • Post-thyroidectomy/radioiodine Tx.
  • Drug-induced such as from anti-thyroid medication.
111
Q

HYPOTHYROIDISM
What is the most common cause of hypothyroidism…
i) in the UK.
ii) worldwide.

A

i) Hashimoto’s thyroiditis.

ii) Iodine deficiency.

112
Q

HYPOTHYROIDISM

What are the symptoms of hypothyroidism?

A

Body goes down low…

  • Constipation.
  • Weight gain.
  • Cold intolerance.
  • Tiredness/sleepy/lethargic.
  • Increased menstruation.
113
Q

HYPOTHYROIDISM

What are the signs of hypothyroidism?

A

BRADYCARDIC…

  • Bradycardia.
  • Reflexes relax slowly.
  • Ataxia.
  • Dry thin hair/skin.
  • Yawning.
  • Cold hands.
  • Ascites.
  • Round puffy face.
  • Defeated demeanour.
  • Immobile.
  • Congestive heart failure.
114
Q

HYPOTHYROIDISM

What are the investigations used in someone with suspected hypothyroidism?

A

Thyroid function tests…
- Serum TSH high (confirm primary hypothyroidism).
- Serum free T4 low.
Thyroid antibodies…
- Thyroid peroxidase antibody (TPO-Ab) in Hashimoto’s thyroiditis.

115
Q

HYPOTHYROIDISM

What is the treatment for hypothyroidism?

A

Lifelong thyroid hormone replacement…

  • Levothyroxine (T4).
  • Start normally in healthy + young.
  • Gradually increase dose steadily in elderly + patient’s with ischaemic heart disease (can cause angina/MI).
  • Repeat TSH test after 4 weeks
116
Q

THYROID CARCINOMA

What is the pathophysiology of thyroid carcinomas?

A
  • Minimally active hormonally.
  • Over 90% secrete thyroglobulin which can be used as a tumour marker after thyroid ablation.
  • Radiation is a risk factor.
117
Q

THYROID CARCINOMA

What is radioiodine ablation used for?

A

Used as the thyroid will readily take up radiactive iodine which in turn will locally irradiate + destroy cancer, providing very little radiation damage to other surrounding structures.

118
Q

THYROID CARCINOMA

What are the symptoms of thyroid carcinomas?

A

Often obstructive…

  • Dysphagia (oesophagus).
  • Hoarse voice (recurrent laryngeal nerve).
119
Q

THYROID CARCINOMA

What are the signs of thyroid carcinomas?

A
  • 90% present as thyroid nodules.

- Can present with cervical lymphadenopathy.

120
Q

THYROID CARCINOMA

What are the 5 types of thyroid carcinomas?

A
  • Papillary (60%).
  • Follicular (≤25%).
  • Medullary (5%).
  • Lymphoma (5%).
  • Anaplastic (rare).
121
Q

THYROID CARCINOMA

Give an overview and explain the treatment options for a papillary thyroid carcinoma.

A

Overview…
- Well differentiated, often in younger patients + local spread to lymph nodes + lung.
- Better prognosis if young + female.
Tx…
- Total thyroidectomy to remove non-obvious tumour (±node excision or radioiodine ablation).
- Levothyroxine to suppress TSH (growth factor for cancer).

122
Q

THYROID CARCINOMA

Give an overview and explain the treatment options for a follicular thyroid carcinoma.

A 
Overview...
- Middle-age, spreads early via blood to lung/bone.
- Well differentiated.
Tx...
- Total thyroidectomy.
- T4 suppression.
Radioiodine ablation.
123
Q

THYROID CARCINOMA

Give an overview and explain the treatment options for a medullary thyroid carcinoma.

A 
Overview...
- 80% sporadic.
- May produce calcitonin (can be used as tumour marker).
Tx...
- Total thyroidectomy.
- Lymph node clearance.
124
Q

THYROID CARCINOMA

Give an overview and explain the treatment options for a lymphoma thyroid carcinoma.

A 
Overview...
- Female >> male (3:1).
- May present with stridor or dysphagia.
Tx...
- Chemoradiotherapy helps reduce risk of spread + treats undetectable micro-metastases.
125
Q

THYROID CARCINOMA

Give an overview and explain the treatment options for an anaplastic thyroid carcinoma.

A 
Overview...
- Female >> male (3:1).
- Common in elderly, undifferentiated.
Tx...
- Poor response to any.
- External radiotherapy can provide brief respite.
- Mainly palliative.
126
Q

CUSHING’S SYNDROME

What is the pathophysiology of Cushing’s syndrome?

A

The clinical state caused by chronic glucocorticoid excess + loss of normal feedback mechanisms in the hypothalamo-pituitary-adrenal axis + loss of circadian rhythm of cortisol secretion.

127
Q

CUSHING’S SYNDROME

What is Cushing’s disease?

A

Bilateral adrenal hyperplasia causing Cushing’s syndrome as a result of an ACTH-secreting pituitary adenoma.

128
Q

CUSHING’S SYNDROME

What are the ACTH-dependent aetiologies of Cushing’s syndrome?

A
  • Cushing’s disease = ACTH-secreting pituitary adenoma causing bilateral adrenal hyperplasia.
  • Ectopic ACTH production = ACTH producing tumour located elsewhere in the body (e.g. small cell lunger cancer).
129
Q

CUSHING’S SYNDROME

What are the ACTH-independent aetiologies of Cushing’s syndrome?

A
  • Adrenal adenoma.

- Iatrogenic (pharmacological doses of steroids).

130
Q

CUSHING’S SYNDROME

What are the symptoms or Cushing’s syndrome?

A
  • Increased weight.
  • Mood change – depression, lethargy, irritability.
  • Gonadal dysfunction – erectile dysfunction/irregular menses.
131
Q

CUSHING’S SYNDROME

What are the signs of Cushing’s syndrome?

A
  • Central obesity.
  • Moon face.
  • Buffalo hump.
  • Purple abdominal striae.
  • HTN.
132
Q

CUSHING’S SYNDROME

What is the gold standard investigation for Cushing’s syndrome?

A

Overnight dexamethasone suppression test.

- Dexamethasone usually suppresses cortisol levels + so failure to suppress over a 24-hour period is diagnostic.

133
Q

CUSHING’S SYNDROME

What other investigation could you do to rule out Cushing’s syndrome and why may it be misleading?

A

Random plasma cortisol tests

  • 24-hour urinary free cortisol measurement can exclude Cushing’s syndrome if results are normal.
  • May be misleading as cortisol levels are dependent on many factors.
134
Q

CUSHING’S SYNDROME

What are the treatment options for Cushing’s syndrome?

A
  • Cushing’s disease – trans-sphenoidal removal of pituitary adenoma.
  • Ectopic ACTH – surgery if tumour is located + hasn’t spread.
  • Adrenal adenoma – adrenalectomy.
  • Iatrogenic – stop steroid medications if possible.
135
Q

ACROMEGALY
Define…
i) Acromegaly.
ii) Gigantism.

A

i) Acromegaly is the increased secretion of GH occurring in adults AFTER the fusion of the epiphyseal plates.
ii) Gigantism is the increased secretion of GH occurring in children BEFORE the fusion of the epiphyseal plates.

136
Q

ACROMEGALY

What is the pathophysiology of Acromegaly?

A
  • Increased levels of GH secretion causes increased secretion of insulin-like growth factor-1 leading to bone + soft tissue growth.
  • Very slow insidious onset across many years.
137
Q

ACROMEGALY

Describe the epidemiology of Acromegaly.

A
  • Incidence = 3 million/year.
  • M=F.
  • Mean age of diagnosis about 40 y/o.
138
Q

ACROMEGALY

What is the aetiology of Acromegaly?

A

99% = benign pituitary adenoma.

139
Q

ACROMEGALY

What are the symptoms of Acromegaly?

A
  • Acroparaesthesia.
  • Decreased libido.
  • Amenorrhoea.
  • Excessive sweating.
  • Headache.
140
Q

ACROMEGALY

What are the signs of Acromegaly?

A
  • Macroglossia w/ widely spaced teeth.
  • Darkening of skin.
  • Bitemporal hemianopia.
  • Increased growth of hands (spade-like), jaw + feet.
  • Obstructive sleep apnoea.
141
Q

ACROMEGALY

What investigation is used to exclude a diagnosis of Acromegaly?

A

Plasma GH levels.

- Not diagnostic as GH is a pulsatile protein + many factors affect its secretion.

142
Q

ACROMEGALY

What other investigations can be used to diagnose Acromegaly?

A

Oral glucose tolerance test (OGTT).
- Normally, rise in blood glucose will suppress GH levels, in acromegaly GH release fails to suppress.
Serum IGF-1 levels raised.
MRI scan of pituitary fossa.

143
Q

ACROMEGALY

What is the treatment for Acromegaly?

A

Trans-sphenoidal surgery = first line.
Medical therapy and/or radiotherapy.
- Use a somatostatin analogue (SSA) like Octreotide – preferred over radiotherapy.
GH antagonist like Pegvisomant.

144
Q

HYPERALDOSTERONISM

What is the pathophysiology of hyperaldosteronism?

A

Primary hyperaldosteronism meaning the excess production of aldosterone, independent of the RAAS, causing increased Na+, H20 retention, K+ excretion + decreased renin release.

145
Q

HYPERALDOSTERONISM

What are the aetiologies of hyperaldosteronism?

A
  • 2/3 is Conn’s syndrome = solitary aldosterone-producing adenoma (linked to mutations in K+ channels).
  • 1/3 = bilateral adrenocortical hyperplasia.
146
Q

HYPERALDOSTERONISM

What are the symptoms for hyperaldosteronism?

A

General hypokalaemic symptoms…

  • Muscle weakness + cramps.
  • Paraesthesia.
  • Polyuria + polydipsia.
147
Q

HYPERALDOSTERONISM

What are the signs of hyperaldosteronism?

A
  • HTN – due to increased blood volume.
  • Hypokalaemia.
  • Na+ tends to be mildly raised or normal.
148
Q

HYPERALDOSTERONISM

What investigations would you do on someone with suspected hyperaldosteronism and what would they show?

A 
Blood tests.
- U+E = low K+
- Low renin.
- High aldosterone.
ECG(hypokalaemia) – U have no Pot + no T but a long PR + a depressed ST.
- Prominent U waves.
- Small/inverted T waves.
- Increased PR interval.
- Depressed ST segments.
149
Q

HYPERALDOSTERONISM

What is the treatment for hyperaldosteronism?

A
  • Conn’s syndrome = laparoscopic adrenalectomy.

- Bilateral adrenocortical hyperplasia = aldosterone antagonist like sprionolactone.

150
Q

ADDISON’S DISEASE

What is the pathophysiology of Addison’s disease?

A

Primary adrenal insufficiency caused by the autoimmune destruction of the entirety of the adrenal cortex leading to glucocorticoid + mineralocorticoid deficiency.

151
Q

ADDISON’S DISEASE

What are the aetiologies of Addison’s disease?

A
  • 80% due to autoimmunity.
  • TB.
  • Adrenal metastases.
  • Adrenal haemorrhage.
152
Q

ADDISON’S DISEASE

What is the most common cause of Addison’s disease worldwide?

153
Q

ADDISON’S DISEASE

What is the clinical presentation of Addison’s disease?

A
  • Insidious with non-specific symptoms = late diagnosis.
  • Thin, tanned, tired + tearful.
  • Hyperpigmentation (decrease in cortical products cause excess ACTH which stimulates melanocytes).
  • Nausea, abdominal pain.
  • Postural hypotension.
154
Q

ADDISON’S DISEASE

What are the investigations for someone with suspected Addison’s disease?

A

Bloods – FBC, U+E.
- Na+ decrease, K+ increase due to decreased mineralocorticoid.
ACTH stimulation test (synacthen test).
- Patient with Addison’s disease will NOT respond.
Serum glucose decreased due to decreased cortisol.
Take serum cortisol at multiple time points.

155
Q

ADDISON’S DISEASE

What is the main complication with Addison’s disease, how does it present and how is it treated?

A

Addisonian crisis –

  • Shock (increased HR, vasoconstriction, postural hypotension, comatose), ? infection.
  • Ensure electrolytes stable, hydrocortisone, IV fluid bolus, monitor blood glucose.
156
Q

SECONDARY ADRENAL INSUFFICIENCY

What is the pathophysiology of secondary adrenal insufficiency?

A

Inadequate pituitary or hypothalamic stimulation of the adrenal glands causing decreased ACTH and so decreased adrenal products.

157
Q

SECONDARY ADRENAL INSUFFICIENCY

What are the aetiologies of secondary adrenal insufficiency?

A
  • Iatrogenic due to long-term steroid therapy causing suppression of the pituitary-adrenal axis, only apparent after steroid withdrawal.
  • Rare cause includes hypothalamic-pituitary disease causing decreased ACTH production.
158
Q

SECONDARY ADRENAL INSUFFICIENCY

What is the clinical presentation of secondary adrenal insufficiency?

A
  • Insidious with non-specific symptoms = late diagnosis.
  • Thin, tanned, tired + tearful.
  • Nausea, abdominal pain.
  • NO hyperpigmentation as ACTH is LOW.
159
Q

SECONDARY ADRENAL INSUFFICIENCY

What investigations would you do on someone with suspected secondary adrenal insufficiency?

A

Bloods – FBC, U+E.
- Na+ decrease, K+ increase due to decreased mineralocorticoid.
Long ACTH stimulation test (synacthen test), distinguishes as response after prolonged exposure.
Serum glucose decreased due to decreased cortisol.

160
Q

SECONDARY ADRENAL INSUFFICIENCY

What does the synacthen test do?

A
  • Acts like ACTH to stimulate the adrenal glands.

- If this doesn’t cause appropriate increased amounts of cortisol this is diagnostic for adrenal insufficiency.

161
Q

SECONDARY ADRENAL INSUFFICIENCY

What is the treatment for secondary adrenal insufficiency?

A
  • Steroid hormone replacement with hydrocortisone (glucocorticoid replacement).
  • If iatrogenic, remove steroids v slowly.
162
Q

SECONDARY ADRENAL INSUFFICIENCY

What is the main complication with secondary adrenal insufficiency, how does it present and how is it treated?

A

Addisonian crisis –

  • Shock (increased HR, vasoconstriction, postural hypotension, comatose), ? infection.
  • Ensure electrolytes stable, hydrocortisone, IV fluid bolus, monitor blood glucose.
163
Q

HYPERKALAEMIA

What is the pathophysiology of hyperkalaemia?

A
  • Defined by a plasma K+ > 5.5mmol/L.
  • Increased serum K+ resulting in the threshold for an AP being significantly decreased, leading to arrhythmias which can lead to VFib + cardiac arrest.
164
Q

HYPERKALAEMIA

What are the aetiologies for hyperkalaemia?

A
  • AKI (decreased filtration rate + so more K+ in blood).
  • Metabolic acidosis.
  • Addison’s disease.
  • K+ sparing diuretics.
165
Q

HYPERKALAEMIA

What are the symptoms of hyperkalaemia?

A
  • Fast irregular pulse.
  • Weakness, light headedness.
  • Palpitations, chest pain.
166
Q

HYPERKALAEMIA

What investigations would you do for someone with hyperkalaemia?

A 
Bloods.
- U+E show K+ > 5.5mmol/L.
- URGENT hyperkalaemia is K+ >6.5mmol/L.
ECG.
- Tall tented T waves.
- Small P waves.
- Wide QRS.
167
Q

HYPERKALAEMIA

What is the treatment for non-urgent hyperkalaemia?

A

Treat the underlying cause.

- Polystyrene sulfonate resin (binds to K+ in gut, decreasing uptake).

168
Q

HYPERKALAEMIA

What is the treatment for urgent hyperkalaemia?

A
  • Calcium gluconate (decreases VFib risk as it reduces excitability of cardiomyocytes).
  • Insulin can drive K+ into cells.
169
Q

HYPOKALAEMIA

What is the pathophysiology of hypokalaemia?

A
  • Defined by plasma K+ < 3.5mmol/L.
  • Low K+ in the serum (ECF) causes a [water] gradient OUT of the cell (ICF).
  • Increased leakage from the ICF causes hyperpolarisation of the myocyte membrane + this decreases myocyte excitability.
170
Q

HYPOKALAEMIA

What are the aetiologies of hypokalaemia?

A
  • Diuretics.
  • Diarrhoea + vomiting.
  • Conn’s syndrome.
  • Cushing’s syndrome/steroids.
171
Q

HYPOKALAEMIA

What are the symptoms of hypokalaemia?

A
  • Palpitations + arrhythmias.
  • Muscle weakness.
  • Tetany.
  • Hypotonia + hyporeflexia.
172
Q

HYPOKALAEMIA

What investigation would you do for someone with suspected hypokalaemia and what would it show?

A

ECG – U have no Pot + no T but a long PR + a depressed ST.

  • Prominent U waves.
  • Small/inverted T waves.
  • Increased PR interval.
  • Depressed ST segments.
173
Q

HYPOKALAEMIA

What is the treatment for hypokalaemia?

A 
Identify + treat underlying cause.
Mild/asymptomatic.
- Oral K+
Severe/symptomatic
- K+ < 2.5mmol/L requires URGENT treatment via IV K+.
174
Q

SiADH

What is the pathophysiology of the Syndrome of inappropriate Secretion of ADH (SiADH)?

A
  • Continued secretion of ADH despite the plasma being V dilute leading to water retention (v concentrated urine), hypervolaemia + so hyponatraemia.
175
Q

SiADH

What are the aetiologies of SiADH?

A 
Malignancy.
- E.g. small cell lung cancer, lymphoma.
CNS disorders.
- Stroke.
- Subarachnoid/subdural haemorrhage.
Chest disease.
- TB, pneumonia.
Iatrogenic.
- Psychotropics, selective serotonin re-uptake inhibitors (SSRIs).
176
Q

SiADH

What are the symptoms of SiADH?

A
  • Anorexia.
  • Nausea.
  • Headache/irritability/confusion.
177
Q

SiADH

What are the signs of SiADH?

A
  • Decreased GCS/seizures.

- Concentrated urine.

178
Q

SiADH

What investigations would you do for someone suspected to have SiADH?

A
  • Concentrated urine in the presence of hyponatraemia.

- Low plasma osmolality in the absence of hypovolaemia, oedema or diuretics.

179
Q

SiADH

What are the treatments for SiADH?

A
  • Treat underlying cause.
  • Restrict fluid intake to 500–1000mL.
  • Hypertonic saline ± loop diuretic if severe.
  • ADH receptor antagonists (vaptans) like tolvaptan.
180
Q

DIABETES INSIPIDUS

What is the pathophysiology of Diabetes Insipidus? What are the 2 types and how do you differentiate?

A
  • The passage of large volumes (>3L/day) of dilute urine due to impaired water reabsorption by the kidney.
  • Cranial DI as a result of reduced ADH secretions from the posterior pituitary gland.
  • Nephrogenic DI as a result of impaired response of the kidney to ADH.
181
Q

DIABETES INSIPIDUS

What are the aetiologies of Diabetes Insipidus?

A 
Cranial.
- Idiopathic (50%).
- Congenital defects in ADH gene.
- Pituitary tumour.
Nephrogenic.
- Inherited mutation of ADH receptor.
- Metabolic (hypokalaemia, hypercalcaemia).
- Chronic renal disease.
182
Q

DIABETES INSIPIDUS

What are the symptoms of Diabetes Insipidus?

A
  • Polyuria + polydipsia.
  • Dehydration.
  • Symptoms of hypernatraemia like lethargy, irritability + confusion.
183
Q

DIABETES INSIPIDUS

What are the signs of Diabetes Insipidus?

A
  • Excessive urine production (>3L/day).
  • Very dilute urine.
  • Hypernatraemia.
184
Q

DIABETES INSIPIDUS

What are the differential diagnoses with Diabetes Insipidus?

A

Other causes of polyuria + polydipsia…

  • Diabetes mellitus.
  • Hypokalaemia.
  • Hypercalcaemia.
185
Q

DIABETES INSIPIDUS

What investigations would you do with someone suspected of having Diabetes Insipidus?

A

Water deprivation test.
- Restrict fluid intake.
- Measure the urine osmolality (+ve for DI if urine osmolality is low).
- Desmopressin (ADH analogue) helps differentiate between cranial + nephrogenic.
If suspect cranial then head MRI, check pituitary gland.

186
Q

DIABETES INSIPIDUS

How does desmopressin help to differentiate between cranial and nephrogenic diabetes insipidus?

A

Cranial – urine osmolality INCREASES after desmopressin.

Nephrogenic – urine osmolality DOESN’T INCREASE after desmopressin.

187
Q

DIABETES INSIPIDUS

What is the treatment for diabetes insipidus?

A 
Cranial = desmopressin.
Nephrogenic = treat the underlying cause, Bendroflumethiazide or NSAIDs.
188
Q

HYPERCALCAEMIA

What are the aetiologies of hypercalcaemia?

A
  • Hyperparathyroidism.
  • Hypercalcaemia of malignancy (bone metastases, myeloma).
  • Vitamin D toxicity.
189
Q

HYPERCALCAEMIA

What is the typical clinical presentation for someone with hypercalcaemia?

A

Bones, stones, groans + psychic moans.

  • Bone pain.
  • Renal stones.
  • Abdominal groans (abdominal pain, vomiting, constipation).
  • Psychic groans (confusion, depression).
190
Q

HYPERCALCAEMIA

What investigations would you do for someone with suspected hypercalcaemia?

A

Find the cause by…
- Checking electrolytes like calcium + phosphate.
- Checking parathyroid hormone.
ECG shows short QT interval.

191
Q

HYPERCALCAEMIA

How can blood tests show you what’s causing the hypercalcaemia and is the action of PTH appropriate or not?

A
  • Primary hyperparathyroidism = High PTH (inapp), high calc, low phos.
  • Tertiary hyperparathyroidism = all high (inapp).
  • Hypercalcaemia of malignancy = low PTH (app), high calc.
192
Q

HYPERCALCAEMIA

What is the treatment for hypercalcaemia?

A
  • Correct the dehydration (IV 0.9% saline).
  • Bisphosphonates.
  • Treat underlying cause.
193
Q

HYPERPARATHYROIDISM

What is the pathophysiology of primary hyperparathyroidism?

A

Excess PTH production + so hypercalcaemia.

194
Q

HYPERPARATHYROIDISM

What is the pathophysiology of secondary hyperparathyroidism?

A

Physiological compensatory hypertrophy of ALL parathyroid lands resulting in excess PTH due to hypocalcaemia.

195
Q

HYPERPARATHYROIDISM

What is the pathophysiology of tertiary hyperparathyroidism?

A

Occurs after prolonged secondary hyperparathyroidism, causing glands to act autonomously having undergone hyperplastic + adenomatous change resulting in excess PTH secretion that is unlimited by feedback control.

196
Q

HYPERPARATHYROIDISM

What is the pathophysiology of malignant hyperparathyroidism?

A

Production of parathyroid-related protein (PTHrP) which acts in the same way as PTH, having the same effects.

197
Q

HYPERPARATHYROIDISM

What are the aetiologies for the different types of hyperparathyroidism?

A

Primary…
- 80% solitary adenoma, 20% hyperplasia of all glands.
- Rarely parathyroid cancer.
Secondary…
- Decreased vitamin D intake.
- Chronic renal failure (can’t activate vit D).
Tertiary…
- Long term chronic renal failure.
Malignant…
- Some squamous cell lung cancers, breast + renal cell carcinomas.

198
Q

HYPERPARATHYROIDISM

What is the typical clinical presentation of someone with hyperparathyroidism?

A

Bones, stones, groans + psychic moans.
- Bone pain.
- Renal stones.
- Abdominal groans (abdominal pain, vomiting, constipation).
- Psychic groans (confusion, depression).
Secondary hyperparathyroidism = fractures + osteopenia due to hypocalcaemia.
Also HTN.

199
Q

HYPERPARATHYROIDISM
What are the different blood test results for the different types of hyperparathyroidism and is the action of PTH appropriate or not? What other investigation would you do?

A
  • Primary hyperparathyroidism = High PTH (inapp), high calc, low phos.
  • Secondary hyperparathyroidism = high PTH (app), low calc, low phos.
  • Tertiary hyperparathyroidism = all high (inapp).
  • Malignant = low PTH (app), high calc.
  • DEXA bone scan for osteoporosis.
200
Q

HYPERPARATHYROIDISM

What is the treatment for the different types of hyperparathyroidism?

A 
Primary...
- Surgical removal of solitary adenoma or parathyroidectomy (all 4 glands).
Secondary + tertiary...
- Treat underlying causes.
Malignant...
- Chemotherapy might help.
Overall...
- High fluid intake, low calcium diet to prevent renal stones.
201
Q

HYPERCALCAEMIA OF MALIGNANCY

What is the pathophysiology of hypercalcaemia of malignancy?

A
  • PTH-related hormone is produced by the tumour causing local osteolysis leading to increased Ca2+.
  • Osteoclast stimulation increases osteolysis + inhibition of osteoblast precursors.
  • Poor prognostic sign.
  • Most common in multiple myeloma + bone metastases.
202
Q

HYPERCALCAEMIA OF MALIGNANCY

What is the clinical presentation of hypercalcaemia of malignancy?

A
  • Weight loss.
  • Anorexia.
  • Nausea.
  • Polydipsia + polyuria.
  • Dehydration.
203
Q

HYPERCALCAEMIA OF MALIGNANCY

What investigations would you do for someone suspected to have hypercalcaemia of malignancy and what would they show?

A

Bloods…
- Low PTH (app), high Ca2+.
ECG…
- Short QT interval.

204
Q

HYPERCALCAEMIA OF MALIGNANCY

What is the treatment for hypercalcaemia of malignancy?

A 
Short term...
- Aggressive rehydration.
- Bisphosphonates.
Long term...
- Control of underlying malignancy.
205
Q

HYPOCALCAEMIA

What are the aetiologies of hypocalcaemia?

A

HAVOC…
- Hypoparathyroidism.
- Acute pancreatitis.
- Vitamin D deficiency.
- Osteomalacia.
- Chronic kidney disease (inadequate production of active vitamin D).
Hypoparathyroidism + CKD are with HIGH phosphate, others are with low.

206
Q

HYPOCALCAEMIA

What is the clinical presentation for hypocalcaemia?

A

SPASM…

  • Spasms (Trousseau’s sign = carpopedal spasm where inflating BP cuff causes wrist + fingers to flex + draw together), (Chvostek’s sign = tap over facial nerve to get facial muscle spasm).
  • Peripheral paraesthesia.
  • Anxious.
  • Seizures.
  • Muscle tone increase in smooth muscle (wheeze, dysphagia).
207
Q

HYPOCALCAEMIA

What are the ECG changes for someone who is hypocalcaemic?

A
  • Long QT interval.
208
Q

HYPOCALCAEMIA

What is the treatment for hypocalcaemia?

A
  • Mild = alfacalcidol (AdCal).

- Severe = calcium gluconate.

209
Q

HYPOPARATHYROIDISM

What is the pathophysiology + aetiology of primary hypoparathyroidism?

A
  • Autoimmune destruction of the parathyroid glands = gland failure.
  • Autoimmune DiGeorge syndrome is a congenital familial condition in which the parathyroid glands fail to develop.
  • Can be idiopathic.
210
Q

HYPOPARATHYROIDISM

What is the pathophysiology + aetiology of secondary hypoparathyroidism?

A
  • Radiation or parathyroidectomy affecting amount of PTH produced.
  • Hypomagnesaemia as Mg2+ required for PTH secretion.
  • Most common.
211
Q

HYPOPARATHYROIDISM

What is the pathophysiology + aetiology of pseudohypoparathyroidism?

A
  • Failure of target cell response to PTH.

- Genetic.

212
Q

HYPOPARATHYROIDISM

What is the pathophysiology + aetiology of pseudopseudohypoparathyroidism?

A
  • Feature of pseudohypoparathyroidism but with normal biochemistry.
  • Genetic.
213
Q

HYPOPARATHYROIDISM

What is the clinical presentation of hypoparathyroidism?

A

SPASM…

  • Spasms (Trousseau’s sign = carpopedal spasm where inflating BP cuff causes wrist + fingers to flex + draw together), (Chvostek’s sign = tap over facial nerve to get facial muscle spasm).
  • Peripheral paraesthesia.
  • Anxious.
  • Seizures.
  • Muscle tone increase in smooth muscle (wheeze, dysphagia).
214
Q

HYPOPARATHYROIDISM
What are the different blood test results for the different types of hypoparathyroidism and is the action of PTH appropriate or not?

A 
Hypoparathyroidism...
- Low PTH (inapp), low calc, high phos.
Pseudo...
- High PTH (app), low calc, high phos.
Pseudopseudo...
- Normal biochemistry.
215
Q

HYPOPARATHYROIDISM

What is the treatment for hypoparathyroidism?

A
  • Calcium supplements.

- Calcitriol.

216
Q

PROLACTINOMA

What is the pathophysiology of prolactinoma?

A
  • Benign adenoma of the pituitary gland producing prolactin, can be micro (>90%), or macro (>10mm).
  • There is increased release of prolactin which can cause galactorrhoea by stimulating milk production from the mammary gland, as well as inhibit FSH + LH.
217
Q

PROLACTINOMA

What are the aetiologies of prolactinoma?

A
  • Benign pituitary adenoma.

- Anti-dopaminergic drugs.

218
Q

PROLACTINOMA

What is the clinical presentation of prolactinoma due to local effects of the tumour?

A
  • Pressure on local structures like optic chiasm = bitemporal hemianopia (macroprolactinoma).
  • Headache.
219
Q

PROLACTINOMA

What is the clinical presentation of prolactinoma due to hyperprolactinaemia.

A
  • Decreased libido.
  • Increased weight.
  • Galactorrhoea.
  • F = amenorrhoea or oligomenorrhoea.
  • M = erectile dysfunction.
220
Q

PROLACTINOMA

What investigations would you do for someone suspected of having a prolactinoma?

A
  • Measure serum prolactin.

- MRI pituitary.

221
Q

PROLACTINOMA

What is the treatment for prolactinoma?

A
  • Dopamine agonists like cabergoline are first line treatment.
222
Q

PHEOCHROMOCYTOMA

What is the pathophysiology of pheochromocytoma?

A
  • Arise from sympathetic paraganglia cells (phaeochrome bodies), which are collections of chromaffin cells usually found in the adrenal medulla.
  • Catecholamine producing tumours…
    => Alpha receptors in veins (vasodilation) + GI tract (decrease muscle motility).
    => Beta receptors in bronchioles (smooth muscle relaxation), heart (increased HR).
223
Q

PHEOCHROMOCYTOMA

What is the 10% rule in pheochromocytoma?

A
  • 10% = malignant.
  • 10% = extra-adrenal.
  • 10% = bilateral.
  • 10% = familial.
224
Q

PHEOCHROMOCYTOMA

What are the aetiologies of pheochromocytoma?

A
  • 90% sporadic (more noradrenaline).

- 10% part of hereditary cancer syndromes (more adrenaline).

225
Q

PHEOCHROMOCYTOMA

What is the clinical presentation of pheochromocytoma?

A

Classic triad…

  • Episodic headache.
  • Sweating (w/ palpitations, anxiety, nausea).
  • Tachycardia (±hyper/hypo/normotension).
226
Q

PHEOCHROMOCYTOMA

What investigations would you do in someone suspected of having pheochromocytoma?

A
  • 24hr urine collection of urinary catecholamines + metabolites (metanephrines/normetaneprhines).
  • Plasma catecholamines (not as sensitive).
227
Q

PHEOCHROMOCYTOMA

What is the treatment for pheochromocytoma? What is the main complication of this?

A
  • Surgery w/ alpha-blocker (phenoxybenzamine) pre-op to be used before beta-blocker (propranolol) to stagger adrenaline loss + avoid hypertensive crisis.
  • Can stroke out during surgery due to the rapid effect of adrenaline on BP.
228
Q

CARCINOID TUMOUR

What is the pathophysiology of carcinoid tumours?

A
  • Diverse group of tumours of enterochromaffin cell (neural crest) origin that are capable of producing bioactive compounds like serotonin, bradykinin, ACTH that can lead to carcinoid syndrome.
  • Can also be present in the gallbladder, kidney, liver, pancreas + gonads.
229
Q

CARCINOID TUMOUR

What is the clinical presentation of carcinoid tumours?

A
  • Most clinically silent, can cause Cushing’s syndrome, pain or palpable mass.
  • Only symptomatic when GI tumours metastasise to the liver, where the products can drain into the hepatic vein causing carcinoid syndrome.
230
Q

CARCINOID TUMOUR

What is carcinoid syndrome?

A
  • Bronchoconstriction.
  • Diarrhoea.
  • Paroxysmal flushing.
231
Q

CARCINOID TUMOUR

What are the investigations for someone suspected of having a carcinoid tumour?

A
  • 24hr urine shows a high volume of 5-HIAA (serotonin metabolite).
  • Liver ultrasound (confirm metastases).
  • Octreoscan (radiolabelled octreotide, somatostatin anaogue, hits the somatostatin receptors).
232
Q

CARCINOID TUMOUR

What are the treatment for carcinoid tumours?

A
  • Somatostatin analogue (octreotide).

- Surgical resection to reduce tumour mass.

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