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(SG) condensed phase 2a > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Define diabetes mellitus

A

Chronic hyperglycaemia due to insulin dysfunction.

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2
Q

Types of diabetes mellitus

A

Type 1.

Type 2.

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3
Q

Clinical presentation of diabetes mellitus

A

Young: 2-6w history of thirst, polyuria and weight loss. Ketoacidosis if not picked up earlier (fruity breath).

Older: Similar, but over longer period.

Also lack of energy and eye problems (blurred vision).

Neuropathy, eventually (glove and stockings).

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4
Q

Diabetes mellitus - note

A

In practice, both types exist as a spectrum.

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5
Q

Pathophysiology of type 1 diabetes mellitus

A

Autoimmune destruction of the pancreatic beta cells.

Associated with HLA genetics, but triggered by 1+ environmental antigens.

Autoantibodies directed against insulin and islet cell antigens predate onset by several years.

Polyuria: Blood glucose exceeds renal tubular reabsorptive capacity (renal threshold) -> Osmotic diuresis

Weight loss: fluid depletion,

Insulin deficiency -> Muscle and fat breakdown.

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6
Q

Pathophysiology of type 2 diabetes mellitus

A

Polygenic.

Env factors (central obesity) trigger onset in genetically susceptible.

Beta cell mass reduced to 50% of normal.

Inappropriately low insulin secretion and peripheral insulin resistance.

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7
Q

Cause of type 1 diabetes mellitus

A

HLA-DR3/4 affected in >90%.

Autoimmune disease targeting islet cells.

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8
Q

Cause of type 2 diabetes mellitus

A

Genetic susceptibility, but no HLA link.

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9
Q

Epidemiology of type 1 diabetes mellitus

A

Onset younger (<30 years).

Usually lean.

More north European ancestry.

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10
Q

Epidemiology of type 2 diabetes mellitus

A

Onset older (>30 years).

Usually overweight.

More common in African/Asian.

More common in general.

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11
Q

Diagnostic test for diabetes mellitus

A

Fasting >7 (or random >11.1) plasma glucose (mmol/L).

HbA1c: 6.5% / 48mmol/mol.

C peptide goes down in type 1 but persists in type 2.

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12
Q

Treatments for type 1 diabetes mellitus

A

Glycaemic control through diet (low sugar, low fat, high starch)

and insulin (twice daily and with meals).

Exercise encouraged.

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13
Q

Treatments for type 2 diabetes mellitus

A

Diet and exercise changes.

If no change;

  • > Biguanide (Metformin)
  • >
    • sulfonylurea (gliclazide) / DPP4I (sitagliptin)
  • >
    • insulin
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14
Q

Complications of diabetes mellitus

A

ketoacidosis/
nephropathy
/neuropathy (-> lack of sensation in feet -> occult foot ulcers)
/diabetic retinopathy,

Hyperosmolar hyperglycaemic nonketotic coma (mostly in type 2s).

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15
Q

Define Graves disease

A

Hyperthyroidism due to pathological stimulation of TSH receptor.

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16
Q

Define Hashimoto’s thyroiditis

A

Hypothyroidism due to aggressive destruction of thyroid cells.

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17
Q

How does Graves disease clinically present?

A

Rapid heart beat, tremor, diffuse palpable goiter with audible bruit.

Eye problems: bulging outwards and lid retraction.

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18
Q

How does Hashimoto’s thyroiditis clinically present?

A

Insidious onset.

Tiredness, lethargy, intolerance of cold, goitre, slowing of intellectual activity, constipation, deep hoarse voice.

Puffy face, hands and feet.

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19
Q

Pathophysiology of Graves disease

A

Thyroid stimulating immunoglobulins recognise and bind to the TSH receptor which stimulates T4 and T3

  • > thyroxine (T4) receptors in the pituitary gland are activated by excess hormone
  • > reduced release of TSH in a negative feedback look
  • > Very high levels of circulating thyroid hormones, with a low TSH
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20
Q

Pathophysiology of Hashimoto’s thyroiditis

A

Aggressive destruction of thyroid cells by various cell and antibody mediated immune processes.

Antibodies bind and block TSH receptors

-> inadequate thyroid hormone production and secretion.

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21
Q

Cause of Graves disease

A

Unclear - some genetic element.

Autoimmune disease.

Associated with other autoimmune diseases, such as pernicious anaemia and myasthenia gravis

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22
Q

Cause of Hashimoto’s thyroiditis

A

Unknown. Autoimmune.

Some genetic element.

Triggers; iodine, infection, smoking and possibly stress

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23
Q

Epidemiology of Graves disease

A

Most common cause of hyperthyroidism.

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24
Q

Epidemiology of Hashimoto’s thyroiditis

A

More common in Japan

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25
Q

Diagnostic test for Graves disease

A

High T3+T4,

Lower TSH than normal.

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26
Q

Diagnostic test for Hashimoto’s thyroiditis

A

TSH levels, usually raised in hypothyroidism.

Thyroid antibodies.

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27
Q

Treatment for Graves disease

A

Antithyroid drugs (carbimazole or propylthiouracil) with either dose titration

or ‘block and replace’.

Thyroidectomy.

Radioactive iodine.

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28
Q

Treatment for Hashimoto’s thyroiditis

A

Thyroid hormone replacement (Levothyroxine).

Resection of obstructive goitre.

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29
Q

Complications of Graves disease

A

Thyroid storm: treat with propylthiouracil.

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30
Q

Complications of Hashimoto’s thyroiditis

A

Hyperlipidaemia and consequences.

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31
Q

Sequelae of Hashimoto’s thyroiditis

A

Hashimoto’s encephalopathy.

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32
Q

Define hypothyroidism

A

Reduced action of thyroid hormone.

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33
Q

Types of hypothyroidism

A

Primary

Secondary

Transient

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34
Q

How does hypothyroidism clinically present?

A

Thyroid gland may enlarge rapidly, occasionally with dyspnoea/dysphagia from pressure on the neck.

Hypothyroidism: Fatigue, cold intolerance, slowed movement, decreased sweating.

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35
Q

What is primary hypothyroidism a disease associated with?

A

the thyroid.

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36
Q

What is secondary hypothyroidism a disease associated with?

A

Pituitary or hypothalamus.

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37
Q

What is transient hypothyroidism associated with?

A

Treatment withdrawal.

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38
Q

Pathophysiology of primary hypothyroidism

A

Aggressive destruction of thyroid cells by various cell and antibody mediated immune processes.

Antibodies bind and block TSH receptors

-> inadequate thyroid hormone production and secretion

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39
Q

Pathophysiology of secondary hypothyroidism

A

Reduced release or production of TSH

-> reduced T3 and T4 release.

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40
Q

Pathophysiology of transient hypothyroidism

A

The thyroid overcompensates until it can re-establish correct concentrations of Thyroid hormone.

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41
Q

Cause of primary hypothyroidism

A

Autoimmune hypothyroidism (Hashimoto’s),

iodine deficiency,

congenital defects.

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42
Q

Cause of secondary hypothyroidism

A

Isolated TSH deficiency,

hypopituitarism (due to neoplasm, infection),

hypothalamic disorders (neoplasms, trauma).

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43
Q

Cause of transient hypothyroidism

A

Withdrawal of thyroid suppressive therapy such as radioactive iodine.

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44
Q

Epidemiology of primary hypothyroidism

A

12-20 times more frequent in women.

Most common cause of goitrous hypothyroidism.

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45
Q

Diagnostic test for hypothyroidism

A

Serum free T4 levels low,

thyroid antibodies may be present.

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46
Q

Treatment for primary hypothyroidism

A

Thyroid hormone replacement (Levothyroxine).

Resection of obstructive goitre.

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47
Q

Treatment for secondary hypothyroidism

A

Thyroid hormone replacement (Levothyroxine).

Treat underlying cause.

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48
Q

Treatment of transient hypothyroidism

A

Remits on its own.

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49
Q

Complications of thyroidism

A

Myxoedema coma: 20-50% mortality.

Reduced level of consciousness, seizures, hypothermia and hypothyroidism.

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50
Q

Define thyroid cancer

A

Cancer of the thyroid tissue.

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51
Q

Types of thyroid cancer

A

Papillary

Follicular

Anaplastic

Lymphoma

Medullary

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52
Q

How does papillary, follicular and anaplastic thyroid cancer clinically present?

A

Usually asymptomatic thyroid nodule (usually hard and fixed).

Possibly enlarged lymph nodes on examination.

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53
Q

How does lymphoma - thyroid cancer - clinically present?

A

Rapidly growing mass in the neck.

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54
Q

How does medullary thyroid cancer clinically present?

A

Diarrhoea,

flushing episodes (very similar to carcinoid syndrome)

and itching.

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55
Q

Papillary thyroid cancer - note

A

Named for the papillae among its cells on microscopy.

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56
Q

Anaplastic thyroid cancer - note

A

‘One of the most aggressive cancers in humans’.

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57
Q

Pathophysiology of papillary thyroid cancer

A

Tends to spread locally in the neck, compressing the trachea.

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58
Q

Pathophysiology of follicular thyroid cancer

A

Follicular cells of the thyroid,

but does not retain original cell features like iodine uptake or synthesis of thyroglobulin.

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59
Q

Pathophysiology of anaplastic thyroid cancer

A

May infiltrate neck,

but greater propensity to metastasise to lung and bones relative to papillary.

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60
Q

Pathophysiology of lymphoma - thyroid cancer

A

Almost always non-hodgkins lymphoma.

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61
Q

Pathophysiology of medullary thyroid cancer

A

Parafollicular calcitonin-producing C cells.

Produce large amounts of peptide such as calcitonin.

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62
Q

Epidemiology of papillary thyroid cancer

A

70% of thyroid cancer.

Young people.

Three times more common in women.

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63
Q

Epidemiology of follicular thyroid cancer

A

20% of thyroid cancer.

Middle age.

Tends to be in areas of low iodine.

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64
Q

Epidemiology of anaplastic thyroid cancer

A

<5% of thyroid cancer.

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65
Q

Epidemiology of lymphoma - thyroid cancer

A

2% of thyroid cancer.

Often associated with Hashimoto’s thyroiditis.

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66
Q

Epidemiology of medullary thyroid cancer

A

5% of thyroid cancer.

More sporadic than hereditary.

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67
Q

Cause of medullary thyroid cancer

A

Often familial.

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68
Q

Diagnostic tests for thyroid cancer

A

Fine needle aspiration.

Differences: Medullary; elevated serum calcitonin.

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69
Q

Treatment of papillary and follicular thyroid cancer

A

Total thyroidectomy

-> ablative radioactive iodine.

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70
Q

Treatment of anaplastic and lymphoma - thyroid cancer

A

External radiotherapy to provide relief (largely palliative).

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71
Q

Treatment of medullary thyroid cancer

A

Total thyroidectomy

and prophylactic central lymph node dissection.

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72
Q

Define Cushing’s syndrome (Hypercortisolism)

A

Persistently and inappropriately elevated circulating glucocorticoid (cortisol).

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73
Q

Define Acromegaly

A

Overgrowth of all organ systems due to excess GH

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74
Q

Define Conn’s syndrome (primary hyperaldosteronism)

A

High aldosterone levels independent of renin-angiotensin system.

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75
Q

How does Cushing’s syndrome (Hypercortisolism) clinically present?

A

Obesity (fat distribution central, buffalo hump),

plethoric complexion,

rounded ‘moon face’,

thin skin, bruising, striae, hypertension, pathological fractures.

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76
Q

How does Acromegaly clinically present?

A

Slow onset (old photos).

Larger hands/feet.

Large tongue, prognathism, interdental separation, spade-like hands.

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77
Q

How does Conn’s syndrome (primary hyperaldosteronism) clinically present?

A

Hypertension (possibly low urine output),

hypokalaemic.

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78
Q

Cushing’s syndrome (Hypercortisolism) - note

A

Cushing’s disease:

When elevated glucocorticoid is attributed to inappropriate ACTH secretion from the pituitary.

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79
Q

Acromegaly - note

A

If before fusion of epiphyseal plates (children); gigantism.

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80
Q

Conn’s syndrome (primary hyperaldosteronism)

A

Hyperaldosteronism due to high renin levels is called Secondary hyperaldosteronism.

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81
Q

Pathophysiology of Cushing’s syndrome (Hypercortisolism)

A

Many features due to protein-catabolic effects of cortisol; thin skin, easy bruising, striae.

Excessive alcohol consumption can mimic the clinical and biochemical signs (Pseudo-Cushings’s), but resolves on alcohol recession.

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82
Q

Pathophysiology of Acromegaly

A

GH acts directly on tissues such as liver, muscle bone or fat,

as well as indirectly through induction of insulin like growth factor.

Excess causes uncontrolled growth of organ systems.

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83
Q

Pathophysiology of Conn’s syndrome (primary hyperaldosteronism)

A

Aldosterone causes an exchange of transport of sodium and potassium in the distal renal tubule.

Therefore, hyperaldosteronism causes increased reabsorption of sodium (and water) and excretion of potassium

84
Q

Cause of Cushing’s syndrome (Hypercortisolism)

A

ACTH (adrenocortiotropic hormone) dependent disease:

excessive ACTH from pituitary,

ACTH producing tumour or excess ACTH administration

Non-ACTH dependent: adrenal adenomas, adrenal carcinomas, excess glucocorticoid administration (most common)

85
Q

Cause of Acromegaly

A

Usually excessive GH secretion by a pituitary tumour.

Other GH releasing tumours possible (hypothalamus, specific lung cancers).

86
Q

Cause of Conn’s syndrome (primary hyperaldosteronism)

A

Adrenal adenoma secreting aldosterone in Conn’s syndrome (or possibly bilateral adrenal hyperplasia).

87
Q

Epidemiology of Cushing’s syndrome (Hypercortisolism)

A

10/1,000,000.

Higher incidence in diabetes.

2/3 cases are Cushing’s disease.

88
Q

Epidemiology of Acromegaly

A

1/200,000.

Average 40 yrs.

89
Q

Diagnostic tests for Cushing’s syndrome (Hypercortisolism)

A

Confirm raised cortisol: 48 hour low-dose dexamethasone: Fail to suppress cortisol.

Urinary free cortisol over 24hrs.

Late night salivary cortisol.

Establishing cause: CT and MRI of renal and pituitary.

90
Q

Diagnostic test for Acromegaly

A

Glucose tolerance test: IGF-1 raised.

GH raised.

91
Q

Diagnostic test for Conn’s syndrome (primary hyperaldosteronism)

A

Plasma aldosterone and renin.

92
Q

Treatment of Cushing’s syndrome (Hypercortisolism)

A

Tumours: Surgical removal

Cortisol synthesis inhibition: metyrapone, ketoconazole.

93
Q

Treatment of Acromegaly

A

Transsphenoidal resection surgery.

Dopamine agonists (cabergoline), somatostatin analogues (octreotide)

and GH receptor antagonists (pegvisomant).

94
Q

Treatment of Conn’s syndrome (primary hyperaldosteronism)

A

Adenoma: Surgical removal

Hyperplasia: aldosterone antagonist (spironolactone).

95
Q

Complications of Cushing’s syndrome (Hypercortisolism)

A

Hypertension,

obesity,

death.

96
Q

Complications of Acromegaly

A

Hypertension,

diabetes.

Untreated adenoma can impact the optic chiasm -> blindness,

colorectal cancer.

97
Q

Sequelae of Cushing’s syndrome (Hypercortisolism)

A

Rare remission.

98
Q

Define Adrenal insufficiency (hypoadrenalism).

A

Destruction of the adrenal cortex

-> reduction in adrenal hormones

99
Q

Define Adrenal hyperplasia.

A

Defective enzymes mediating the production of adrenal cortex products.

100
Q

Types of Adrenal insufficiency (hypoadrenalism)

A

Primary insufficiency (Addison’s disease).

Secondary.

101
Q

How does primary adrenal insufficiency (Addison’s disease) clinically present?

A

Insidious.

Non-specific symptoms; lethargy, depression, anorexia, weight loss, weakness and fatigue.

Postural hypotension.

Thin, tanned, tired and tearful.

Hyperpigmentation.

102
Q

How does secondary adrenal insufficiency clinically present?

A

Insidious.

Non-specific symptoms; lethargy, depression, anorexia, weight loss, weakness and fatigue.

Postural hypotension.

Thin, tired and tearful.

103
Q

How does adrenal hyperplasia clinically present?

A

In severe forms; salt loss.

Female: Ambiguous genitalia with common urogenital sinus.

Male: no signs at birth, bar subtle hyperpigmentation and possible penile enlargement.

104
Q

Primary adrenal insufficiency (Addison’s disease) - note

A

Destruction of adrenal cortex

-> Less cortical products.

Excess ACTH

  • > stimulates melanocytes
  • > hyper pigmentation.
105
Q

Secondary adrenal insufficiency - note

A

Reduction of adrenal cortex stimulation

-> Less cortical products.

Low ACTH

  • > less melanocytes stimulation
  • > no pigmentation.
106
Q

Adrenal hyperplasia - note

A

Low cortisol,

maybe low aldosterone,

high androgen.

107
Q

Pathophysiology of Primary adrenal insufficiency (Addison’s disease)

A

Autoimmune destruction of the entirety adrenal cortex.

Associated with other autoimmune conditions.

Loss of cortex -> reduction in ability to produce cortisol and/or aldosterone.

Excess ACTH stimulates melanocytes -> pigmentation.

108
Q

Pathophysiology of Secondary adrenal insufficiency

A

Inadequate pituitary or hypothalamic stimulation of the adrenal glands.

No pigmentation, since ACTH levels are low.

109
Q

Pathophysiology of Adrenal hyperplasia

A

Defective 21-hydroxylase -> disruption of cortisol biosynthesis.

This causes cortisol deficiency, with or without aldosterone deficiency and androgen excess.

In severe forms, aldosterone deficiency -> salt loss.

110
Q

Causes of Primary adrenal insufficiency (Addison’s disease)

A

Organ specific autoantibodies in 90% of cases.

Rarely; adrenal gland tuberculosis,

surgical removal or haemorrhage.

111
Q

Causes of Secondary adrenal insufficiency

A

Hypothalamic-pituitary disease

or from long term steroid therapy leading to hypothalamic-pituitary-adrenal suppression.

112
Q

Cause of Adrenal hyperplasia

A

Genetic

21-hydroxylase deficiency is the cause of about 95% of cases.

113
Q

Epidemiology of Primary adrenal insufficiency (Addison’s disease)

A

1/10,000

114
Q

Epidemiology of Secondary adrenal insufficiency

A

200/1,000,000.

115
Q

Diagnostic tests for Primary adrenal insufficiency (Addison’s disease)

A

Sodium reduction, potassium elevation.

Cortisol taken across multiple time points.

116
Q

Diagnostic test for Secondary adrenal insufficiency

A

Long ACTH test (synacthen test) to distinguish from primary:

ACTH raised in primary, lowered in secondary.

117
Q

Diagnostic test for Adrenal hyperplasia

A

Serum 17-hydroxyprogesterone (precursor to cortisol) levels: high.

118
Q

Treatment of Primary adrenal insufficiency (Addison’s disease)

A

Hormone replacement (glucocorticoid (hydrocortisone)

and mineralocorticoid (fludrocortisone).

119
Q

Treatment of Secondary adrenal insufficiency

A

Hormone replacement (just hydrocortisone).

If from steroid therapy; remove steroids very slowly.

120
Q

Treatment of Adrenal hyperplasia

A

Glucocorticoids: Hydrocortisone Mineralocorticoids:

Control electrolytes

If salt loss: Sodium chloride supplement.

121
Q

Complications of Primary adrenal insufficiency (Addison’s disease)

A

Adrenal crisis, reduced QOL.

122
Q

Define diabetes insipidus

A

Hyposecretion or insensitivity to ADH.

123
Q

Types of diabetes insipidus

A

Cranial.

Nephrogenic.

124
Q

How does diabetes insipidus clinically present?

A

Polyuria,

compensatory polydipsia.

125
Q

Cranial diabetes insipidus - note

A

Hyposecretion.

126
Q

Nephrogenic diabetes insipidus - note

A

Insensitivity.

127
Q

Pathophysiology of cranial diabetes insipidus

A

Disease of the hypothalamus, where ADH is produced -> Insufficient ADH production.

Interestingly, damage to the Posterior Pituitary gland, does not lead to ADH deficiency, as it can still ‘leak’ out.

128
Q

Pathophysiology of nephrogenic diabetes insipidus

A

Depends on the aetiology.

Can be due to disruption of the channels,

damage to the kidney

-> Lack of appropriate response to ADH.

129
Q

Causes of cranial diabetes insipidus

A

Neurosurgery, trauma, tumour, infiltrative disease, idiopathic

Genetic: Mutations in the ADH gene

130
Q

Cause of nephrogenic diabetes insipidus

A

Hypokalaemia, hypercalcaemia, drugs, renal tubular acidosis, sickle cell, prolonged polyuria, chronic kidney disease.

Genetic: Mutation in ADH receptor.

131
Q

Epidemiology of diabetes insipidus

A

1/25,000.

132
Q

Diagnostic tests for diabetes insipidus

A

Urine volume: Confirm polyuria.

Water deprivation: Confirm DI.

U&Es: Confirm not a more common cause of polyuria

MRI of hypothalamus: Confirm CDI

133
Q

Treatment of cranial diabetes insipidus

A

Mild cases: thiazide diuretics, carbamazepine and chlorpropramide to sensitise the renal tubules to endogenous vasopressin.

Desmopressin.

134
Q

Treatment of nephrogenic diabetes insipidus

A

Treatment of the cause.

135
Q

Define Syndrome of inappropriate ADH secretion

A

Continued ADH secretion in spite of plasma hypotonicity and normal plasma volume.

136
Q

How does Syndrome of inappropriate ADH secretion clinically present?

A

Nausea, irritability and headache with mild dilutional hyponatraemia.

Fits and coma with severe hyponatraemia.

137
Q

Pathophysiology of Syndrome of inappropriate ADH secretion

A

Ectopic production increases the amount of ADH produced, beyond mechanisms of control.

138
Q

Causes of Syndrome of inappropriate ADH secretion

A

Disordered hypothalamic-pituitary secretion, or ectopic production of ADH.
Neurological: Tumour, trauma, infection

Pulmonary: Lung small cell cancer (common), mesothelioma, cystic fibrosis.

139
Q

Diagnostic test for Syndrome of inappropriate ADH secretion

A

FBC.

Diagnose by serum concentrations.

140
Q

Treatment of Syndrome of inappropriate ADH secretion

A

Underlying cause.

Water restriction.

Demeoclocycline; inhibition of ADH.

141
Q

Define Hyperparathyroidism

A

Excessive secretion of PTH

142
Q

Define Hypoparathyroidism

A

Low levels of PTH

143
Q

Types of hyperparathyroidism

A

Primary

Secondary

Tertiary

144
Q

How does primary hyperparathyroidism clinically present?

A

70-80% asymptomatic.

Bone pain, renal calculi, nausea, neuropsychiatric.

(Bones, stones, abdominal groans and psychic moans)

145
Q

How does secondary hyperparathyroidism clinically present?

A

Kidney disease,

with skeletal or cardiovascular complications.

146
Q

How does tertiary hyperparathyroidism clinically present?

A

Bone pain, renal calculi, nausea, neuropsychiatric.

(Bones, stones, abdominal groans and psychic moans).

147
Q

How does hypoparathyroidism clinically present?

A

Increased excitability of muscles and nerves.

Numbness around the mouth/extremities, cramps, tetany, convulsions.

Chvostek and Trousseau signs.

148
Q

Primary hyperparathyroidism - note

A

One parathyroid gland produces excess PTH.

149
Q

Secondary hyperparathyroidism - note

A

Increased secretion of PTH to compensate hypocalcaemia.

150
Q

Tertiary hyperparathyroidism - note

A

Autonomous secretion of PTH,

due to CKD.

151
Q

Hypoparathyroidism - note

A

Hypocalcaemia

and hyperphosphataemia.

152
Q

Pathophysiology of Primary hyperparathyroidism

A

Adenoma or hyperplasia provides additional secretive tissue to provide excess PTH.

153
Q

Pathophysiology of Secondary hyperparathyroidism

A

Parathyroid gland becomes hyperplastic in response to chronic hypocalcaemia.

154
Q

Pathophysiology of Tertiary hyperparathyroidism

A

Glands become autonomous,

producing excess of PTH even after the correction of calcium deficiency.

155
Q

Pathophysiology of Hypoparathyroidism

A

PTH stimulates the activation of vitamin D,

which facilitates intestinal calcium absorption,

renal reabsorption of calcium as well as calcium release from bone.

Phosphate reabsorption is inhibited by PTH.

In disease, these processes do not occur.

156
Q

Causes of Primary hyperparathyroidism

A

Single parathyroid adenoma

or hyperplasia.

157
Q

Causes of Secondary hyperparathyroidism

A

CKD (any condition with hypocalcaemia, such as vitamin D deficiency).

158
Q

Cause of Tertiary hyperparathyroidism

A

Develops from secondary hyperparathyroidism.

159
Q

Cause of Hypoparathyroidism

A

May be transient.

Most commonly follows anterior neck surgery.

Genetic: Can be due to defects in PTH gene.

Can be autoimmune.

160
Q

Epidemiology of Primary hyperparathyroidism

A

Third most common endocrine disorder.

161
Q

Epidemiology of Hypoparathyroidism

A

Rare.

162
Q

Diagnostic test for Primary hyperparathyroidism

A

Bloods: Hypercalcaemia.

163
Q

Diagnostic test for Secondary hyperparathyroidism

A

Bloods: low serum calcium.

164
Q

Diagnostic test for Tertiary hyperparathyroidism

A

Bloods: Raised calcium, raised PTH.

165
Q

Diagnostic test for Hypoparathyroidism

A

Bloods: Calcium and PTH low, phosphate high.

166
Q

Treatment of Primary hyperparathyroidism

A

Surgical removal of adenoma.

Potentially bisphosphonates.

167
Q

Treatment of Secondary hyperparathyroidism

A

Calcium correction.

Treat underlying condition.

168
Q

Treatment of Tertiary hyperparathyroidism

A

Calcium mimetic (Cinacalcet),

total or subtotal parathyroidectomy.

169
Q

Treatment of Hypoparathyroidism

A

Acute: IV calcium

Persistent: Vitamin D analogue (alfacalcidol).

170
Q

Complication of Primary hyperparathyroidism

A

Hypercalcaemia

171
Q

Complication of Secondary hyperparathyroidism

A

Development into tertiary hyperparathyroidism.

172
Q

Complication of Tertiary hyperparathyroidism

A

Transient hypocalcaemia follows parathyroidectomy.

173
Q

Complication of Hypoparathyroidism

A

Overtreatment with vitamin D

-> hypercalcaemia.

174
Q

Define Hypercalcaemia

A

Excess of calcium

175
Q

Define Hypocalcaemia

A

Deficiency of calcium

176
Q

How does Hypercalcaemia clinically present?

A

Can be asymptomatic.

More severe: malaise, depression, bone pain, abdominal pain, nausea, constipation.

Occasionally renal calculi and CKD.

Polyuria and polydipsia.

177
Q

How does Hypocalcaemia clinically present?

A

Increased excitability of muscles and nerves.

Numbness around the mouth/extremities, cramps, tetany, convulsions.

Chvostek and Trousseau signs.

178
Q

Hypercalcaemia - note

A

Shortening of the QT interval.

179
Q

Hypocalcaemia - note

A

QT prolongation (primarily by prolonging the ST segment).

180
Q

Pathophysiology of Hypercalcaemia

A

Ectopic secretion of PTH is very rare.

Tumour related hypercalcaemia tends to work by a secretion of a peptide with PTH-like activity,

direct invasion of bone and production of local factors for calcium mobilisation.

181
Q

Pathophysiology of Hypocalcaemia

A

CKD

  • > Increased phosphate
  • > Microprecipitation of calcium phosphate in tissues
  • > Low serum level of calcium.

CKD

-> Inadequate production of active vitamin D.

182
Q

Cause of Hypercalcaemia

A

> 90% of cases; primary hyperparathyroidism and malignancy.

Primary hyperparathyroidism is caused by a single parathyroid gland adenoma, occasionally hyperplasia.

183
Q

Cause of Hypocalcaemia

A

Increased serum phosphate: Chronic kidney disease (most common), Phosphate therapy

Reduced PTH function: Post thyroidectomy and parathyroidectomy

Vitamin D deficiency: Reduced exposure to sunlight

184
Q

Epidemiology of Hypercalcaemia

A

30/100,000

185
Q

Diagnostic test for Hypercalcaemia

A

Bloods: Raised calcium

186
Q

Diagnostic test for Hypocalcaemia

A

History.

eGFR to search for CKD.

PTH,

Vitamin D.

187
Q

Treatment of hypercalcaemia

A

Loop diuretic to return calcium to normal.

Primary hyperparathyroidism: surgical removal.

188
Q

Treatment of hypocalcaemia

A

Acute: IV calcium

Persistent: In vitamin D deficiency, vitamin D supplement.

If hypoparathyroidism; alfacalcidol.

189
Q

Complication of hypocalcaemia

A

Death.

190
Q

Define hyperkalaemia

A

Excess of potassium.

191
Q

Define hypokalaemia

A

Deficiency of potassium.

192
Q

How does hyperkalaemia clinically present?

A

Few symptoms until it can cause MI.

Impaired neuromuscular transmission (muscle weakness and paralysis).

193
Q

How does hypokalaemia clinically present?

A

Usually asymptomatic, possibly muscle weakness.

Increased risk of cardiac arrhythmias.

Polyuria.

194
Q

Hyperkalaemia - note

A

Tall tented T waves

195
Q

Hypokalaemia - note

A

T wave inversion, prominent U wave(?)

196
Q

Pathophysiology of Hyperkalaemia

A

Renal impairment can lead to retention of potassium in the nephron.

This is possible with potassium sparing diuretic.

197
Q

Pathophysiology of Hypokalaemia

A

Excessive loss of potassium through the kidneys in response to aldosterone or diuretic therapy.

GI fluid loss

  • > less chloride
  • > increase in aldosterone
  • > Decreased potassium reabsorption
198
Q

Cause of Hyperkalaemia

A

Renal impairment (most common) and drug interference with potassium excretion.

Elevated without either of these may be artefactural.

199
Q

Cause of Hypokalaemia

A

Diuretic treatment and hyperaldosteronism.

Possibly due to loss of GI fluids by constant vomiting/diarrhoea.

200
Q

Diagnostic test for Hyperkalaemia

A

Bloods: Check potassium.

Recheck unexpected result.

ECG: peaked T waves, prolonged PR, widened QRS and reduced P

201
Q

Diagnostic test for Hypokalaemia

A

Bloods: low magnesium and potassium

ECG: Flat T waves, ST depression, prominent U waves.

202
Q

Treatment of Hyperkalaemia

A

Dietary potassium restriction

and loop diuretic.

203
Q

Treatment of Hypokalaemia

A

Treat underlying cause.

Withdraw harmful medication.

Normalise magnesium as well as potassium.

204
Q

Complications of Hyperkalaemia

A

Myocardial infarction

-> Death

205
Q

Complications of Hypokalaemia

A

Cardiac arrhythmia

and sudden death.

(SG) condensed phase 2a (9 decks)

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