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Medicine Phase 2a > Endocrine List 2 > Flashcards

Endocrine List 2 Flashcards

1
Q

Describe Graves disease

A

Hyperthyroidism due to pathological stimulation of TSH receptor
Autoimmune induced excess production of TH

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2
Q

Clinical presentation of Graves disease

A

Rapid Heart beat
Tremor
Diffuse palpable goiter with audible bruit
Eye problems: bulging outwards and lid retraction
Graves’ opthalmopathy
Graves dermopathy (rare)
Thyroid acropachy (clubbing, finger and toe swelling)

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3
Q

Pathophysiology of Graves disease

A

TSH receptor stimulating antibodies (TSHR-Ab) recognise and bind to the TSH receptors in thyroid

  • > stimulates thyroid hormone production 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
  • > as well as excess secretion of thyroid hormones, also results in hyperplasia of thyroid follicular cells resulting in hyperthyroidism and diffuse goitre
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4
Q

Aetiology/Risk factors of Graves disease

A

Some genetic element - association with HLA-B8, DR3 & DR2.
Smoking
Stress
High iodine intake
E.coli and other gram-NEGATIVE organisms contain TSH-binding sites so may initiate pathogenesis via ‘molecular mimicry’
Autoimmune disease.
Associated with other autoimmune diseases, such as Vitiligo (pale patches on skin), Addison’s, type 1 DM, pernicious anaemia and myasthenia gravis.

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5
Q

Epidemiology of Graves disease

A

Most common cause of hyperthyroidism (2/3 of cases)
More common in females
Typically presents at 40-60 years (appear earlier if maternal family history)

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6
Q

Diagnostic of Graves disease

A

High T3 and T4
Lower TSH than normal
Mild neutropenia
*TSH receptor stimulating antibodies (TSHR-Ab) raised

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7
Q

Treatment of Graves disease

A

Antithyroid drugs (Carbimazole or Propylthiouracil) with either dose titration or ‘block and replace’.
Thyroidectomy.
Radioactive iodine.
Beta blockers

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8
Q

Complications of Graves disease

A

Thyroid storm: treat with Propylthiouracil

Also similar to auto-antigen, can result in retro-orbital inflammation - graves opthalmopathy

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9
Q

Describe Hashimotos thyroiditis

A

Hypothyroidism due to aggressive destruction of thyroid cells
(autoimmune hypothyroidism)

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10
Q

Clinical Presentation of Hashimotos thyroiditis

A

Thyroid gland may enlarge rapidly, occasionally with dyspnoea or dysphagia from pressure on the neck
Hypothyroidism: Fatigue, cold intolerance, slowed movement, decreased sweating

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11
Q

Pathophysiology of Hashimotos 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.
Thyroid peroxidase is essential hormone for production and storage of thyroid hormone: Thyroid peroxidase antibodies (TPO-Ab) are present in high titres

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12
Q

Aetiology of Hashimotos thyroiditis

What are triggers?

A

Unknown.
Autoimmune.
Some genetic element.
Triggers; iodine, infection, smoking and possibly stress

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13
Q

Epidemiology of Hashimotos thyroiditis

A

12-20 times more frequent in women.

Most common cause of goitrous hypothyroidism.

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14
Q

Diagnostic tests of Hashimotos thyroiditis

A

TSH levels, usually raised in hypothyroidism.

Thyroid antibodies.

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15
Q

Treatment of Hashimotos thyroiditis

A 
Levothyroxine therapy (may shrink the goitre)
Thyroid hormone replacement 
Resection of obstructive goitre.
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16
Q

Complications of Hashimotos thyroiditis

A

Hyperlipidemia

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17
Q

Define Sequelae

A

condition which is the consequence of a previous disease or injury

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18
Q

Sequelae of Hashimotos Thyroiditis

A

Hashimotos encephalopathy

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19
Q

Describe hypothyroidism

A

Reduced action/levels of thyroid hormone

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20
Q

Types of hypothyroidism (briefly explain each)

A

Primary - disease associated with thyroid
Secondary - disease associated with pituitary or hypothalamus
Transient - disease associated with treatment withdrawal

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21
Q

Clinical presentation of Hypothyroidism

A

(same for all 3 types)
Insidious onset.
Tiredness, lethargy, intolerance of cold, goitre, slowing of intellectual activity, constipation, deep hoarse voice.
Puffy face, hands and feet.
Menorrhagia, weight gain, myalgia, dementia, myxoedema (accumulation of mucopolysaccharide in SC tissue)

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22
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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23
Q

Pathophysiology of Secondary Hypothyroidism

A

Reduced release or production of TSH by pituitary or hypothalamus (respectively)
-> reduced T3 and T4 release

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24
Q

Pathophysiology of Transient Hypothyroidism

A

The thyroid overcompensates until it can reestablish correct concentrations of Thyroid hormone

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25
Q

Aetiology of Primary Hypothyroidism

A

Autoimmune hypothyroidism (Hashimoto’s), iodine deficiency, congenital defects

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26
Q

Aetiology of Secondary Hypothyroidism

A

Isolated TSH deficiency, hypopituitarism (due to neoplasm, infection), hypothalamic disorders (neoplasms, trauma)

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27
Q

Aetiology of Transient Hypothyroidism

A

Withdrawal of thyroid suppressive therapy such as radioactive iodine

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28
Q

Epidemiology of Primary Hypothyroidism

A

More common in Japan

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29
Q

Diagnostic tests of Hypothyroidism

A

Thyroid Function Tests (TFTs)
Serum free T4 levels low
Thyroid antibodies may be present

Blood tests:
Raised serum aspartate transferase levels from muscle and/or liver
Increase serum creatinine kinase levels associated with myopathy
Hypercholesterolaemia
Hyponatraemia due to an increase in ADH and impaired free water clearance

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30
Q

Treatment of Primary Hypothyroidism

A

Thyroid hormone replacement (Levothyroxine) - dose is titrated until TSH normalises
Resection of obstructive goitre

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31
Q

Treatment of Secondary Hypothyroidism

A

Thyroid hormone replacement (Levothyroxine). Treat underlying cause

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32
Q

Treatment of Transient Hypothyroidism

A

Remits on its own

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33
Q

Complications of Hypothyroidism

A 
Myxoedema coma (20-50% mortality)
Reduced level of consciousness, seizures, cardiac failure, hypothermia and hypothyroidism

severe hypothyroidism/reduced T4

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34
Q

Types of thyroid cancer/malignancies

A

Papillary (named for papillae among its cells on microscopy)
Follicular
Anaplastic (one of most aggressive cancers in human)
Lymphoma
Medullary

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35
Q

What types of thyroid cancers fit this clinical presentation:
Usually asymptomatic thyroid nodule (usually hard and fixed). Possibly enlarged lymph nodes on examination.

A

Papillary
Follicular
Anaplastic

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36
Q

Clinical presentation of Lymphoma (thyroid malignancy)

A

Rapidly growing mass in the neck

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37
Q

Clinical presentation of Medullary cancer (thyroid malignancy)

A

Diarrhoea
Flushing episodes (similar to Carcinoid syndrome)
Itching

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38
Q

Pathophysiology of papillary thyroid cancer

A

Tends to spread locally in neck, compressing the trachea

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39
Q

Pathophysiology of follicular thyroid cancer

A

May infiltrate neck, but greater propensity to metastasise to lung and bones relative to papillary

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40
Q

Pathophysiology of anaplastic 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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41
Q

Pathophysiology of lymphoma thyroid cancer

A

Almost always non-hodgkins lymphoma

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42
Q

Pathophysiology of medullary thyroid cancer

A

Parafollicular calcitonin-producing C cells. Produce large amounts of peptide such as calcitonin

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43
Q

Aetiology of medullary thyroid cancer

A

Often familial

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44
Q

Epidemiology of papillary thyroid cancer

A

70% of thyroid cancer.
Young people.
Three times more common in women.

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45
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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46
Q

Epidemiology of anaplastic thyroid cancer

A

<5% of thyroid cancer

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47
Q

Epidemiology of lymphoma thyroid cancer

A

2% of thyroid cancer.

Often associated with Hashimoto’s thyroiditis.

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48
Q

Epidemiology of medullary thyroid cancer

A

5% of thyroid cancer.

More sporadic than hereditary.

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49
Q

Diagnostic tests of thyroid cancer

A

Fine needle aspiration.

Differences: Medullary; elevated serum calcitonin.

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50
Q

Treatment of medullary thyroid cancer

A

Total thyroidectomy and prophylactic central lymph node dissection

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51
Q

Which thyroid cancers would you treat via:

External radiotherapy to provide relief (largely palliative)

A

Anaplastic

Lymphoma

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52
Q

Treatment of Papillary thyroid cancer

A

Total thyroidectomy -> ablative radioactive iodine

same for follicular thyroid cancer

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53
Q

Treatment of Follicular thyroid cancer

A

Total thyroidectomy -> ablative radioactive iodine

same for papillary thyroid cancer

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54
Q

Describe Cushing’s syndrome

A

Persistently and inappropriately elevated circulating glucocorticoid (cortisol)
This is attributed to inappropriate ACTH secretion from the pituitary (due to tumour)

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55
Q

Clinical presentation of Cushing’s syndrome

A

(truncal) Obesity (fat distribution central, buffalo hump)
plethoric complexion
Rounded ‘moon face’, thin skin, bruising, striae, hypertension, pathological fractures
Acne

Cataracts, Ulcers, Skin striae, Hyperglycarmia/hypertension, Increased infection, Necrosis, Glucosuria/gonal dysfunction

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56
Q

Pathophysiology of Cushing’s syndrome

A

Excess cortisol can either result from excess ACTH which in turn stimulates excess cortisol release or from neoplasms in the adrenals which in turn stimulate the zona reticularis to release more cortisol.

Excess can also result from ingesting excess glucocorticoid itself e.g. PREDNISOLONE

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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57
Q

Aetiology of Cushing’s syndrome

A

ACTH (adrenocortiotropic hormone) dependent disease:
Cushings disease - Bilateral adrenal hyperplasia from an ACTH-secreting pituitary adenoma (benign).
Ectopic Cushings syndrome - paraneoplastic syndrome (tumour elsewhere in body producing ACTH - especially small cell lung cancer and carcinoid tumours)
ACTH treatment e.g. for asthma

ACTH independent:
Excess oral steroids! (iatrogenic)
Adrenal adenomas,
adrenal carcinomas, excess glucocorticoid administration (most common) e.g. Prednisolone

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58
Q

Epidemiology of Cushing’s syndrome

A

10/1,000,000.
Higher incidence in diabetes.
2/3 cases are Cushing’s disease.
Most common cause is oral steroids i.e. glucocorticoid therapy.
Spontaneous endogenous causes are rare, but 80% due to raised ACTH, with pituitary adenoma being the most common cause

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59
Q

Diagnostic tests of Cushing’s syndrome

A

Confirm raised cortisol: 48 hour low-dose dexamethasone: Fail to suppress cortisol is diagnostic of Cushings.
Urinary free cortisol over 24hrs (normal levels mean Cushings unlikely).
Late night salivary cortisol. Establishing cause: CT and MRI of renal and pituitary

NOT random plasma cortisol test as cortisol levels change through day (stress, illness, morning)

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60
Q

Treatment of Cushing’s syndrome

A

Stop steroids if iatrogenic
Transphenoidal removal of pituitary adenoma if Cushings disease
Adrenalectomy or Radiotherapy if Adrenal Adenoma
Ectopic ACTH: Surgical removal of tumour if location known

Cortisol synthesis inhibition: metyrapone, ketoconazole

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61
Q

Complications of Cushing’s syndrome

A

Hypertension, obesity, death

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62
Q

Describe Acromegaly

A

Overgrowth of all organ systems due to excess GH

Increased production of growth hormone occurring in adults after fusion of the epiphyseal plates

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63
Q

Clinical Presentation of Acromegaly

A

Slow onset (old photos). Larger hands/feet. Large tongue, prognathism, interdental separation, spade-like hands.

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64
Q

If (acromegaly) tumour arises before fusion of epiphyseal plates (children bones), what condition can result instead/like acromegaly

A

Gigantism

worse as don’t stop growing as bones not developed

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65
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.
Very slow insidious onset over many years

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66
Q

Aetiology of Acromegaly

A

Usually excessive GH secretion by a pituitary tumour. Other GH releasing tumours possible (hypothalamus, specific lung cancers).
Mainly pituitary adenoma

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67
Q

Epidemiology of Acromegaly

A

3 per million per year
Average 40 yrs.
Same in male and females

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68
Q

Diagnostic tests of Acromegaly

A

Glucose tolerance test: IGF-1 raised. GH raised.

MRI the pituitary fossa for adenomas

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69
Q

Treatment of Acromegaly

A 
Transsphenoidal resection surgery. 
Dopamine agonists (cabergoline), somatostatin analogues (octreotide) and GH receptor antagonists (pegvisomant)
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70
Q

Complications of Acromegaly

A

Hypertension, diabetes.
Untreated adenoma can impact the optic chiasm -> blindness
Colorectal cancer

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71
Q

Describe Conn’s syndrome

A

Primary hyperaldosteronism

High aldosterone levels independent of Renin-Angiotensin system

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72
Q

Clinical presentation of Conn’s syndrome

A 
Hypertension (possibly low urine output)
Hypokalemic:
-Constipation
-Weakness and cramps
-Paraesthesia
-Polyuria and polydipsia
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73
Q

What is secondary hyperaldosteronism

A

Hyperaldosteronism due to high renin levels

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74
Q

What is another name for Primary Hyperaldosteronism

A

Conn’s syndrome

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75
Q

Pathophysiology of Conn’s syndrome

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

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76
Q

Aetiology of Conn’s syndrome

A

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

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77
Q

Diagnostic tests of Conn’s syndrome

A

Plasma Aldosterone (increased) and Renin (decreased)
U and E
Adrenal CT
ECG

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78
Q

Treatment of Conn’s syndrome

A

Adenoma: Surgical removal (laparoscopic adrenalectomy)
Hyperplasia: aldosterone antagonist or potassium-sparing diuretic (spironolactone)

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79
Q

Describe Adrenal Insufficiency

A

Hypoadrenalism

due to destruction or reduced stimulation of adrenal cortex

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80
Q

What are types of Adrenal Insufficiency and describe the difference between the two

A

Primary insufficiency - Destruction of adrenal cortex

Secondary insufficiency - Reduction of adrenal cortex stimulation

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81
Q

What is another name for Primary Adrenal Insufficiency

A

Addison’s disease

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82
Q

What is key difference in clinical presentation between Primary and Secondary adrenal insufficiency

A

Primary - Hyperpigmentation

Secondary - no pigmentation

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83
Q

*Why does Primary Adrenal Insufficiency result in hyper pigmentation but Secondary AI does not?

A

Primary:
Destruction of adrenal cortex -> Less cortical products. Excess ACTH -> stimulates melanocytes -> hyper pigmentation
Secondary:
Reduction of adrenal cortex stimulation -> Less cortical products. Low ACTH -> less melanocytes stimulation -> no pigmentation

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84
Q

Clinical presentation of Addison’s disease (primary adrenal insufficiency)

A

Thin, tanned, tired and tearful.
HYPER-pigmentation.
Insidious. Non-specific symptoms; lethargy, depression, anorexia, weight loss, weakness and fatigue. Postural hypotension. GI: N+V, abdominal pain

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85
Q

Clinical presentation of Secondary Adrenal Insufficiency

A

Insidious. Non-specific symptoms; lethargy, depression, anorexia, weight loss, weakness and fatigue. Postural hypotension. Thin, tanned, tired and tearful.
NO pigmentation

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86
Q

Pathophysiology of Addison’s disease (primary adrenal insufficiency)

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.

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87
Q

Pathophysiology of Secondary Adrenal Insufficiency

A

Inadequate pituitary or hypothalamic stimulation of the adrenal glands. No pigmentation, since ACTH levels are low.

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88
Q

Aetiology of Addison’s disease (primary adrenal insufficiency)

A

Organ specific autoantibodies in 90% of cases. Rarely; adrenal gland tuberculosis, surgical removal or haemorrhage
Addisons is commonest cause in the UK of adrenal insufficiency, TB is most common cause WORLDWIDE

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89
Q

Aetiology of Secondary Adrenal Insufficiency

A

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

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90
Q

Epidemiology of Addison’s disease (primary adrenal insufficiency)

A

1/10,000

Addisons is commonest cause in the UK of adrenal insufficiency, TB is most common cause WORLDWIDE

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91
Q

Epidemiology of Secondary Adrenal Insufficiency

A

200/1,000,000

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92
Q

Diagnostic tests of Addison’s disease (primary adrenal insufficiency)

A

Sodium reduction, potassium elevation due to low aldosterone.

Short ACTH stimulation test (Give ACTH (synacthen), then measure cortisol level; in Addison, cortisol remains low after giving ACTH).

test for 21-hydroxylase adrenal autoabs (+ve in 80% Addisons)

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93
Q

Diagnostic tests of Secondary Adrenal Insufficiency

A

Long ACTH test (synacthen test) to distinguish from primary: ACTH raised in primary, lowered in secondary

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94
Q

Treatment of Addison’s disease (primary adrenal insufficiency)

A

Cortisol hormone replacement - glucocorticoid (hydrocotisone)
Aldosterone replacement via mineralocorticoid (fludrocortisone) - this also helps treat postural hypotension

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95
Q

Treatment of Secondary Adrenal Insufficiency

A

Hormone replacement (just hydrocortisone). If from steroid therapy; remove steroids very slowly

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96
Q

Complications of Addison’s

A 
Adrenal crisis (patients present with shock, severe hypotension, lost a lot of fluid via vomitting and reduced reabsorption of Na+ -> treat with fluid, hydrocortisone)
Reduced QOL
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97
Q

Describe Adrenal Hyperplasia

A

Defective enzymes mediating the production of adrenal cortex products.
Low cortisol, maybe low aldosterone, high androgen

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98
Q

Clinical presentation of Adrenal Hyperplasia

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.

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99
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

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100
Q

Aetiology of Adrenal Hyperplasia

A

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

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101
Q

Diagnostic tests of Adrenal Hyperplasia

A

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

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102
Q

Treatment of Adrenal Hyperplasia

A

Glucocorticoids: Hydrocortisone
Mineralocorticoids: Control electrolytes
If salt loss: Sodium chloride supplement

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103
Q

Describe Diabetes Insipidus

A

Hyposecretion or insensitivity to ADH

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104
Q

Types of Diabetes Insipidus and their difference

A

Cranial - Hyposecretion

Nephrogenic - Insensitivity

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105
Q

Clinical presentation of Diabetes Insipidus

A

Polyuria
Compensatory polydipsia
Dehydration

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106
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.

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107
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 response to ADH

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108
Q

Aetiology of Cranial Diabetes Insipidus

A

trauma, pituitary tumour

Neurosurgery,, infiltrative disease, idiopathic Genetic: Mutations in the ADH gene

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109
Q

Aetiology of Nephrogenic Diabetes Insipidus

A

Hypokalaemia, hypercalcaemia, drugs, renal tubular acidosis, sickle cell, prolonged polyuria, chronic kidney disease Genetic: Mutation in ADH receptor

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110
Q

Epidemiology of Diabetes Insipidus

A

1/25,000

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111
Q

Diagnostic tests of Diabetes Insipidus

A

Water deprivation test: Confirm DI
Restrict fluid, measure osmolarity (urine osmolarity low means DI)
Desmospressin (ADH analogues) to differentiate between cranial and nephrogenic

Urine volume: Confirm polyuria.
U&Es (urine and electrolytes): Confirm not a more common cause of polyuria
MRI of hypothalamus: Confirm CDI

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112
Q

Treatment of Cranial Diabetes Insipidus

A

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

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113
Q

Treatment of Nephrogenic Diabetes Insipidus

A

Bendroflumethizide (diuretics) -> cause more Na+ excretion
NSAIDs - reduce GFR

Treatment of the cause.

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114
Q

Describe syndrome of inappropriate ADH secretion

A

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

(opposite of DI)

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115
Q

Clinical presentation of syndrome of inappropriate ADH secretion

A

Nausea, anorexia, confusion
Concentrated urine

Irritability and headache with mild dilutional hyponatraemia.
Fits and coma with severe hyponatraemia.

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116
Q

Pathophysiology of syndrome of inappropriate ADH secretion

A

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

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117
Q

Aetiology 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

Drugs an CNS disorders also

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118
Q

Diagnostic tests of syndrome of inappropriate ADH secretion

A

(FBC)

Measure urine and plasma osmolarity

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119
Q

Treatment of syndrome of inappropriate ADH secretion

A

Route: IV
Treat underlying cause
Restrict fluid
Vasopressin receptor antagonists (vaptans)

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120
Q

Describe Hyperparathyroidism

A

Excessive secretion of PTH

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121
Q

Types of hyperparathyroidism (describe each briefly)

A

Primary - One parathyroid gland produces excess PTH
Secondary - Increased secretion of PTH to compensate hypocalcemia
Tertiary - Autonomous secretion of PTH due to CKD (chronic kidney disease)

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122
Q

Clinical presentation of primary hyperparathyroidism

A

70-80% asymptomatic. Bone pain, renal calculi, nausea, neuropsychiatric (Bones, stones, abdominal groans and psychic moans)
Bone resorption causes pain, fracture, osteoporosis. Leads to hypercalcaemia (weak, tired, depressed, thirsty, renal stones)
Hypertension

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123
Q

Clinical presentation of secondary hyperparathyroidism

A

Kidney disease, with skeletal or cardiovascular complications

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124
Q

Clinical presentation of tertiary hyperparathyroidism

A

Bone pain, renal calculi, nausea, neuropsychiatric (Bones, stones, abdominal groans and psychic moans)

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125
Q

Pathophysiology of primary hyperparathyroidism

A

Adenoma or hyperplasia provides additional secretive tissue to provide excess PTH

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126
Q

Pathophysiology of secondary hyperparathyroidism

A

Parathyroid gland becomes hyperplastic in response to chronic hypocalcemia

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127
Q

Pathophysiology of tertiary hyperparathyroidism

A

Glands become autonomous, producing excess of PTH even after the correction of calcium deficiency

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128
Q

Aetiology of primary hyperparathyroidism

A

Single parathyroid adenoma or hyperplasia
80% = solitary adenoma
20% = parathyroid hyperplasia
(parathyroid cancer rare)

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129
Q

Aetiology of secondary hyperparathyroidism

A

CKD (any condition with hypocalcaemia, such as vitamin D deficiency, GI disease such as Crohn’s preventing absorption of calcium)

130
Q

Aetiology of tertiary hyperparathyroidism

A

Develops from secondary hyperparathyroidism

131
Q

Epidemiology of primary hyperparathyroidism

A

Third most common endocrine disorder

132
Q

Diagnostic tests of primary hyperparathyroidism

A

Bloods: Hypercalcaemia
↑PTH, ↑Ca, ↓Phosphate
Increased 24hour urinary calcium excretion
DEXA bone scan for osteoporosis

133
Q

Diagnostic tests of secondary hyperparathyroidism

A

Bloods: low serum calcium
↑PTH, ↓Ca, ↑Phosphate
DEXA bone scan for osteoporosis

134
Q

Diagnostic tests of tertiary hyperparathyroidism

A

Bloods: Raised calcium, raised PTH
↑PTH, ↑Ca, ↑Phosphate
Increased 24hr urinary calcium excretion

135
Q

Treatment of primary hyperparathyroidism

A

Surgical removal of adenoma (treat underlying cause).

Fluids and bisphosphonates.

136
Q

Treatment of secondary hyperparathyroidism

A

Calcium correction. Treat underlying condition

137
Q

Treatment of tertiary hyperparathyroidism

A

Calcium mimetic (Cinacalcet), total or subtotal parathyroidectomy

138
Q

Complications of primary hyperparathyroidism

A

Hypercalcemia

139
Q

Complications of secondary hyperparathyroidism

A

Development into tertiary hyperparathyroidism

140
Q

Complications of tertiary hyperparathyroidism

A

Transient hypocalcaemia follows parathyroidectomy

141
Q

Describe hypoparathyroidism

A

Low levels of PTH
Also:
Hypocalcemia and Hyperphosphataemia

142
Q

Clinical Presentation of hypoparathyroidism

A

Increased excitability of muscles and nerves.
Numbness around the mouth/extremities, cramps, tetany, convulsions.
Chvostek and Trousseau signs.

143
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.

144
Q

Aetiology of hypoparathyroidism

A

May be transient.
Most commonly follows anterior neck surgery (secondary).
VD and/or Magnesium deficiency (Mg used in PTH production)
Genetic: Can be due to defects in PTH gene.
Can be autoimmune destruction of PT glands.

145
Q

Epidemiology of hypoparathyroidism

A

Rare

146
Q

Diagnostic tests of hypoparathyroidism

A

Bloods: Calcium and PTH low, phosphate high

Signs and symptoms of hypocalcaemia

147
Q

Treatment of hypoparathyroidism

A

Acute: IV calcium
Persistent: Vitamin D analogue (alfacalcidol)
Calcitriol (prevent low calcium levels)
Synthetic PTH

148
Q

Complications of hypoparathyroidism

A

Over-treatment with vitamin D -> hypercalcaemia

149
Q

Clinical Presentation of Hypercalcaemia

A

Can be asymptomatic.
More severe: malaise, bone pain, abdominal pain, nausea, constipation, psychiatric moans (affects NS - lethargy, fatigue, memory loss, depression)
Occasionally renal calculi and CKD.
Polyuria and polydipsia

150
Q

On PQRST of an ECG, what interval is affected by hypercalcaemia and what is the change

A

Shortening of QT interval

ventricular depolarisation (QRS) and re-polarisation (T)

151
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.

152
Q

Aetiology of Hypercalcaemia

A

> 90% of cases; primary hyperparathyroidism and malignancy. Primary hyperparathyroidism is caused by a single parathyroid gland adenoma, occasionally hyperplasia

153
Q

Epidemiology of Hypercalcaemia

A

30/100,000

154
Q

Diagnostic tests of Hypercalcaemia

A

Bloods: Raised calcium
CXR
Malignancy: raised calcium and phosphate in blood
ECG: tented T and short QT interval

155
Q

Treatment of Hypercalcaemia

A

Give saline drip (NaCl) which will help to dilute the levels of calcium in the blood if you bring the overall body fluids up (or can give Loop diuretic to return calcium to normal)

Bisphosphonate - encourage osteoclasts to undergo apoptosis so there is less bone breakdown

Primary hyperparathyroidism: surgical removal

156
Q

Clinical presentation of Hypocalcemia

A

Increased excitability of muscles and nerves. Numbness around the mouth/extremities, cramps, tetany, convulsions. Chvostek and Trousseau signs.

157
Q

On PQRST of an ECG, what interval is affected by hypocalcaemia and what is the change

A

QT prolongation (primarily by prolonging the ST segment/interval between depolarisation and repolarisation)

158
Q

Pathophysiology of Hypocalcemia

A

CKD -> Increased phosphate -> Microprecipitation of calcium phosphate in tissues -> Low serum level of calcium.
CKD -> Inadequate production of active vitamin D.

159
Q

Aetiology of Hypocalcemia

A

Increased serum phosphate:
Chronic kidney disease (most common) - poor calcium uptake, Phosphate therapy, Hypoparathyroidism (decreased phosphate excretion)
(Reduced PTH function: Post thyroidectomy and parathyroidectomy)
Low Phosphate:
Osteomalacia - soft bones due to low calcium and vitamin D deficiency, Acute pancreatitis, Vitamin D deficiency (reduced exposure to sunlight) - poor Ca uptake in GI tract and decreased kidney reabsorption

160
Q

Diagnostic tests of Hypocalcemia

A

History. eGFR to search for CKD. PTH, Vitamin D.

161
Q

Treatment of Hypocalcemia

A

Acute: IV calcium
Persistent: In vitamin D deficiency, vitamin D supplement. OR Calcium gluconate
(If hypoparathyroidism; alfacalcidol)

Mild - ADCAL

162
Q

Complication of Hypocalcemia

A

death possible

163
Q

Clinical presentation of Hyperkalemia

A

Few symptoms until it can cause MI.

Impaired neuromuscular transmission (muscle weakness and paralysis)

164
Q

On PQRST of an ECG, what interval is affected by hyperkalemia and what is the change

A

Tall tented T waves

165
Q

Pathophysiology of Hyperkalemia

A

Renal impairment can lead to retention of potassium in the nephron.
This is possible with potassium sparing diuretic.
Excessive K consumption at a fast rate -IV fluids

166
Q

Aetiology of Hyperkalemia

A 
Renal impairment (most common) and drug interference with potassium excretion. 
Elevated without either of these may be artifactual.
167
Q

Diagnostic tests of hyperkalemia

A

Bloods: Check potassium. Recheck unexpected result.
ECG: tall tented T waves, (prolonged PR), widened QRS and reduced P
QRS>0.12s

168
Q

Treatment of hyperkalemia

A

Dietary potassium restriction and loop diuretic.

Non urgent - Polystyrene sulphonate resin= Binds K+ in the gut decreasing uptake

Urgent - Calcium gluconate= decreases VF risk in the heart
Insulin= drives K+ into the cells

169
Q

Complication of hyperkalemia

A

Myocardial infarction -> Death

170
Q

Clinical presentation of Hypokalemia

A

Usually asymptomatic, possibly muscle weakness. Increased risk of cardiac arrhythmias. Polyuria.

171
Q

On PQRST of an ECG, what interval is affected by hypokalemia and what is the change

A

T wave inversion

possible prominent U wave

172
Q

Pathophysiology of hypokalemia

and how it leads to decreased mysocyte excitability

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

Low K+ in the serum (ECF) causes a water concentration gradient out of the cell (ICF)
Increased leakage from the ICF causing hyperpolarisation of the myocyte membrane decreasing myocyte excitability.

173
Q

Aetiology of hypokalemia

A

Diuretic treatment and hyperaldosteronism.
Possibly due to loss of GI fluids by constant vomiting/diarrhoea.
Fasting and anorexia

174
Q

Diagnostic tests of hypokalemia

A

Bloods: low magnesium and potassium
ECG: Flat T waves, ST depression, Long PR and prominent U waves
(U have no Pot (K+) & no Tea but a Long PR & a long QT. )
[K+] <3.5 mmol/L

175
Q

Treatment of hypokalemia

A

Treat underlying cause. Withdraw harmful medication. Normalise magnesium as well as potassium.
Mild hypokalaemia - oral K+
Severe hypokalaemia - IV K+

176
Q

Complication of hypokalemia

A

Cardiac arrhythmia and sudden death

177
Q

*Describe prolactinoma

A

Benign adenoma of the pituitary gland producing prolactin

178
Q

Types of Prolactinoma and which is more common

A

Micro (most common >90%)

Macro (>10mm)

179
Q

Clinical presentation of prolactinoma

A

Local effect of the tumour: headache, visual field defect (macroprolacinoma only).
Effects of prolactin (hyperprolactinaemia): menstrual irregularity, infertility, galactorrhoea, hypogonadism

180
Q

Pathophysiology of prolactinoma

A

Increased release of prolactin can cause galactorrhoea by stimulating milk production from mammary gland, as well as inhibit FSH and LH.
Additionally, it causes secondary hypogonadism, reduced libido and sexual dysfunction in men.
Dopamine has an inhibitory effect on prolactin.
Pituitary tumour is located near to the optic chiasm -> visual field disturbances.
Very rarely malignant.

181
Q

Aetiology of prolactinoma

A

Prolactinoma: Cause unknown. Some genetic association.
Other causes of Hyperprolactinaemia: Non functioning pituitary tumour; compress pituitary stalk -> no inhibition of prolactin release; Antidopaminergic drugs;
Head injury -> damage to the pituitary stalk

182
Q

Diagnostic tests of prolactinoma

A

Check prolactin

183
Q

Treatment of prolactinoma

A

Dopamine agonist (cabergoline). Transphenoidal pituitary resection.

184
Q

*Describe Pheochromocytoma

A

Catecholamine (adrenaline) secreting tumour

185
Q

Clinical presentation of Pheochromocytoma

A

Episodic.
Headaches, palpitations, sweating, tremor, anxiety, nausea and weight loss.
Hypertension, tachycardia and pallor.

186
Q

Types of Pheochromocytoma

A

Familial type: More noradrenaline

Sporadic: More adrenaline

187
Q

Pathophysiology of Pheochromocytoma

A

Catecholamine producing tumours of the chromafin cells of the medulla

188
Q

Aetiology of Pheochromocytoma

A

Inherited or spontaneous. Sometimes associated with multiple endocrine neoplasia.

189
Q

Epidemiology of Pheochromocytoma

A

10% malignant

190
Q

Diagnostic tests of Pheochromocytoma

A

24hr urine collection for urinary catecholamines and metabolites (metanephrines). Plasma catecholamines (not as sensitive)

191
Q

Treatment of Pheochromocytoma

A

Surgery (preceded by alpha and beta blocker to stagger adrenaline loss (alpha first, if beta at all))

192
Q

Complication of Pheochromocytoma

A

Can stroke out during surgery, due to the rapid effect of adrenaline on the BP

193
Q

*Describe carcinoid tumour

A

Serotonin secreting tumour.

Tend to express somatostatin receptors.

194
Q

Types of carcinoid tumours

A

Foregut
Midgut
Hindgut

195
Q

Clinical presentation of carcinoid tumour

A

Most clinically silent, can cause pain, weight loss or a palpable mass.
Carcinoid syndrome: Bronchospasm, diarrhoea, skin flushing and right sided heart lesions

196
Q

What is a common place of a carcinoid tumour of lung, bowel or stomach to metastasise to?

A

Liver

only symptomatic with liver metastasises

197
Q

Pathophysiology of carcinoid tumour

A

Derived from enterochromaffin cells. Can also be in the gallbladder, kidney, liver, pancreas and gonads.
They tend to secrete bioactive compounds, including serotonin and Kallikrein (lead to increase in bradykinin), which cause carcinoid syndrome.
GI carcinoid tumours only cause this if they metastasise to liver, where the products can drain into the heaptic vein.

198
Q

Diagnostic tests of carcinoid tumour

A

Urine: High volume of 5-hydroxyindoleacetic acid (breakdown product of serotonin).
Liver ultrasound: Confirm metastases
Octreoscan: Radiolabelled ocreotide (somatostatin analogue) hits the somatostatin receptors

199
Q

Treatment of carcinoid tumour

A 
Somatostatin analogue (octreotide). 
Surgical resection, to reduce tumour mass
200
Q

What conditions increase the incidence of carcinoid tumours?

A

MEN 1 (Multiple Endocrine Neoplasia)
MEN 2
Von-Hippel Lindau

201
Q

Why would a patient be more likely to first approach a dr in later stages of a carcinoid tumour

A

Only symptomatic with liver metastasises

202
Q

What cells do carcinoid tumours derive from?

A

Enterochromaffin cells

203
Q

Describe Graves’ Opthalmopathy

A

Presents in most Graves’ and some autoimmune hypothyroidism patients
Results in retro-orbital inflammation and swelling of the extrocular muscles
Eye discomfort, grittiness, increased tear production, photophobia, diplopia, reduced acuity
Exophthalmos - appearance of protruding eye and proptosis - eye protrudes beyond orbit
Conjunctival oedema
Corneal ulceration
Ophthalmoplegia - paralysis of eye muscles

204
Q

Describe treatment of Graves’ Opthalmopathy

A

Conservative treatment includes smoking cessation and sunglasses
Treated with IV METHYLPREDNISOLONE and surgical decompression or eyelid surgery

205
Q

How are eyes examined for Graves’ opthalmopathy (except seeing it for yourself)

A

CT or MRI of orbit

206
Q

Describe Graves’ dermopathy

A

Rare
Pretibial myxoedema
Thyroid acropachy

207
Q

*What is pretibial myxoedema

A

raised, purple-red symmetrical skin lesions over the anterolateral aspects of the shin

208
Q

What is thyroid acropachy

A

clubbing, swollen fingers and periosteal bone formation

209
Q

When would you see toxic multi nodular goitre?

A

Elderly - common older women
Iodine-deficient areas

(drug therapy rarely produces prolonged remission)

210
Q

*What is toxic multi nodular goitre?

A

nodules that secrete thyroid hormones

see mind maps hyperthyroidism

211
Q

What % of hyperthyroidism cases are solitary toxic adenoma/nodule

A

5%

212
Q

What is De Quervain’s Thyroiditis

A

Type of transient hyperthyroidism

Acute inflammation of the thyroid gland

213
Q

What causes De Quervains Thyroiditis

A

Acute inflammation of thyroid gland, generally due to viral infection

214
Q

Describe diagnosis of De Quervains Thyroiditis

A

Typical for there to be globally reduced uptake on technetium thyroidscan
Usually accompanied by fever, malaise and pain in the neck

215
Q

Treatment of De Quervains Thyroiditis

A

Aspirin

Prednisolone for severely symptomatic cases

216
Q

What drugs can cause hyperthyroidism?

A

AMIODARONE (anti-arrhythmic drug) - due to high iodine content
Iodine
Lithium

217
Q

Why can amiodarone also cause hypothyroidism

A

Inhibits conversion of T4 to T3

218
Q

Clinical presentation of hyperthyroidism specific to elderly

A

Atrial fibrillation

Tahcycardias and/or heart failure

219
Q

Clinical presentation of hyperthyroidism specific to young

A

Excessive height or excessive growth rate

Behavioural problems like hyperactivity

220
Q

Clinical presentation of Graves disease

A 
Palpitations
Diarrhoea
Weight loss and increased appetite
Oligomenorrhoea +/- infertility
Heat intolerance i.e. sweating a lot
Irritability/behavioural change
Tremor
Hyperkinesis
Warm (vasodilator peripheries)
Proximal myopathy and muscle wasting
Anxiety
Lymphadenopathy and Splenomegaly can occur
Diffuse goitre
Lid lag and stare
221
Q

What is oligomenorrhoea

A

infrequent periods

222
Q

What is hyperkinesis

A

muscle spasm

223
Q

Describe clinical presentation of hyperthyroidism in the hands

A

Palmar erythema
Warm moist skin
Fine tremor

224
Q

How does differential diagnosis of hyperthyroidism differ to mid anxiety

A

Eye signs e.g. lid lag & stare
Diffuse goitre
Proximal myopathy and wasting

225
Q

How could you differentiate Graves form toxic adenoma

A

Ultrasound of thyroid

226
Q

Diagnosis of hyperthyroidism

A 
Thyroid function tests (TFTs) (serum TSH is suppressed due to negative feedback, but T4 and T3 raised)
Thyroid peroxidase (TPO) and thyroglobulin antibodies (also presents tin 80% of Graves cases)
227
Q

Treatment of hyperthyroidism

A

Beta-Blockers e.g. propranolol for rapid control of symptoms
Anti-Thyroid drugs e.g. propylthiouracil or oral carbimazole
Radioactive iodine (131)
Surgery (thyroidectomy)

228
Q

What are 2 strategies for treatment of hyperthyroidism using anti-thyroid drugs

A

Titration e.g. ORAL CARBIMAZOLE for 4 wks then reduce doses according to thyroid function tests (TFTs; TSH, T3 & T4)
Block-replace therapy e.g. ORAL CARBIMAZOLE + THYROXINE (T4) which has less risk of developing hypothyroidism

229
Q

What is main side effect of anti-thyroid drugs like propylathiouracil or carbimazole

A

Agranulocytosis:
Results in leukopenia
If get sore throat, mouth ulcers and fevers then stop drug asap

230
Q

Side effects of anti-thyroid drugs

A 
Agranulocytosis
Rash
Arthralgia
Hepatitis
Vasculitis
231
Q

How does anti-thyroid drug Propylthiouracil work?

A

Stops the conversion of T4 to T3

232
Q

How does anti-thyroid drug Carbimazole (oral) work?

A

Blocks thyroid hormone biosynthesis and has immunosuppressive effects (which will affect Graves’ disease process)

233
Q

Radioactive I (131): contraindications and side effects

A

CI in pregnancy and breast feeding
SEs indue discomfort in the neck and hyperthyroidism initially
Can be given to all ages
Stop antithyroid drugs 4 days before giving iodine

234
Q

How does radioactive iodine (131) treatment work for hyperthyroidism

A

Iodine is essential for thyroid hormone production so is readily taken up by the thyroid gland
Here it accumulates and results in local irradiation and tissue damage with return to normal thyroid function over 4-12 weeks

235
Q

When would you undergo surgery for hyperthyroidism

A

Those with large goitre, poor response to drugs and have drug side-effects

236
Q

When would you undergo a subtotal and when a total thyroidectomy

A

Subtotal thyroidectomy only in those who have been rendered euthyroid (normal functioning thyroid gland)

Total thyroidectomy only in those with large goitre or suspicion of malignancy (toxic adenoma) in a nodule and also for Graves’

237
Q

Complications of surgery for hyperthyroidism

A

Hypothyroidism
Tracheal compression from postoperative bleeding
Laryngeal nerve palsy resulting in hoarse voice
Transient hypocalcaemia - due to removal of parathyroid gland too

238
Q

Complications of hyperthyroidism if untreated

A

Thyroid crisis or thyroid storm
Rare life threatening condition
Rapid deterioration of thyrotoxicosis (rapid T4 increase)

239
Q

Describe features of thyroid crisis or thyroid storm

A

hyperpyrexia, tachycardia, extreme restlessness
and eventually delirium, coma and death

Usually precipitated by stress, infection, surgery or radioactive iodine therapy in an unprepared patient

240
Q

Treatment of thyroid crisis or thyroid storm or untreated hyperthyroidism

A

Large doses of:

  • ORAL CARBIMAZOLE
  • ORAL PROPRANOLOL
  • ORAL POTASSIUM IODIDE (to block acutely the release of thyroid hormone from gland)
  • IV HYDROCORTISONE (to inhibits peripheral conversion of T4 to T3)
241
Q

Symptoms of hypothyroidism

A
  • Hoarse voice
  • Goitre
  • Constipation
  • Cold intolerant
  • Weight gain
  • Menorrhagia
  • Myalgia, weakness
  • Tired, low mood, dementia
  • Myxoedema - accumulation of mucopolysaccharide in SC tissue
242
Q

Signs of hypothyroidism

A 
BRADYCARDIC:
• Bradycardia
• Reflexes relax slowly
• Ataxia (cerebellar)
• Dry, thin hair/skin
• Yawning/drowsy/coma
• Cold hands +/- temperature drop 
• Ascites
• Round puffy face
• Defeated demeanour
• Immobile +/- Ileus (temporary arrest of intestinal peristalsis) 
• Congestive cardiac failure
243
Q

Primary cause of hypothyroidism

A

Disease of the thyroid gland

244
Q

Secondary cause of hypothyroidism

A

Hypothalamic or pituitary disease

leads to thyroid disease

245
Q

What % of the population is affected by hypothyroidism and what gender is more affected

A

0.1-0.2%

females

246
Q

Main cause of primary hypothyroidism

A

Iodine deficiency

247
Q

What genetic diseases associate with hypothyroidism

A

Turners*
Downs syndrome
Cystic fibrosis

Others:
Primary biliary cirrhosis
Ovarian hyper-stimulation

248
Q

In Hashimoto’s thyroiditis, describe thyroid gland appearance/feel

A

Gland is usually firm and rubbery but may range from soft to hard

249
Q

In Hashimoto’s thyroiditis, what causes goitre

A

Atrophic changes with regeneration result in GOITRE FORMATION due to lymphocytic and plasma cell infiltration

250
Q

What causes postpartum thyroiditis

A

Modifications to immune system necessary in pregnancy and histologically is a lymphocytes thyroiditis

251
Q

What can postpartum thyroiditis be misdiagnosed as?

A

Postpartum depression

therefore TFTs are essential to confirm diagnosis

252
Q

what is meant by iatrogenic?

A

caused by treatment or examination

253
Q

What iatrogenic factors can lead to hypothyroidism

A

Thyroidectomy (for treatment of hyperthyroidism or goitre)

Radioactive iodine treatment or external neck irradiation for head and neck cancer

254
Q

*What drugs can induce to hypothyroidism

A

Carbimazole
Lithium
Amiodarone (hyper or hypothyroidism)
Interferon

255
Q

Why can amiodarone cause hyper or hypothyroidism

A

Hyper - due to high iodine content

Hypo - as inhibits the conversion of T4 to T3

256
Q

What can result from dietary iodine deficiency?

A

Goitre

Patients have are euthyroid or hypothyroid, depending on the severity of iodine deficiency

257
Q

Where is iodine deficiency an issue in the world

A 
Netherlands
Western Pacific
India
SE Asia
Russia
some Africa
258
Q

*What is myxoedema?

A

Accumulation of mucopolysaccharide in SC tissue
Swelling of the skin and underlying tissues giving a waxy consistency, typical of patients with underactive thyroid glands

259
Q

Presentation of hypothyroidism in children

A

Slow growth velocity
Poor school performance
Sometime puberty arrest
may not show classic features

260
Q

Why is diagnosis of hypothyroidism in elderly difficult

A

Hard to differentiate clinical features from normal ageing

261
Q

Give example of lifelong thyroid hormone replacement drug

A

Oral Levothyroxine (T4)

262
Q

What would be seen in a blood test of hypothyroidism

A

Raised serum aspartate transferase levels from muscle and/or liver
Increase serum creatinine kinase levels associated with myopathy Hypercholesterolaemia
Hyponatraemia due to an increase in ADH and impaired free water clearance

263
Q

Complication of Hypothyroidism is Myxoedema coma, what is given in hospital to treat this?

A

IV/Oral T3

Glucose infusion

264
Q

In treating hypothyroidism with Levothyroxine, what important things must you bear in mind

A

Patients with IHD use with caution and start on lower dose

Don’t give too much as completely suppresses TSH as this carries risk of AF and osteoporosis

265
Q

What can occur from Levothyroxine overdose?

A

Can completely suppress TSH

Risk of AF and osteoporosis

266
Q

How can you monitor treatment of primary hypothyroidism?

A

Check T4 levels 6-8 weeks after dose adjustment

267
Q

How can you monitor treatment of secondary hypothyroidism?

A

TSH will always be low

T4 is monitored

268
Q

**General treatment of thyroid cancer

A

Radioactive iodine (will locally irradiate and destroy cancer - providing very little radiation damage to other surrounding structures)
Levothyroxine (T4) to keep TSH reduced as this is a risk factor
Chemotherapy helps reduce risk of spread and treats micro-metastases

269
Q

What is CRH

A

Corticotropin Releasing hormone

270
Q

Where is CRH released from

A

Hypothalamus

271
Q

CRH causes the release of what hormone

A

ACTH
Adrenocorticotrophic hormone
from anterior pituitary

272
Q

What is the function of ACTH

A

Stimulates cortisol and androgen production by the adrenal cortex

273
Q

Will aldosterone secretion be affected by disease of hypothalamus or pituitary?

A

No as aldosterone secretion responds to renin release by the juxtaglomerular cells of afferent arterioles kidney
Only pathology of kidney would

274
Q

Are the adrenal glands intra or retro-peritoneal

A

Retroperitoneal

275
Q

What are the 3 layers of adrenal cortex and what does each secrete

A

Zona glomerulosa - Mineralocorticoids e.g. aldosterone
Zona fasciculata - Glucocorticoids e.g. cortisol
Zona reticularis - Androgens (sex hormone)
(Makes Good Sex)

276
Q

What are all the layers of adrenal gland in order of most superficial to most deep

A 
Capsule
Zona glomerulosa 
Zona fasciculata
Zona reticularis
Adrenal medulla
277
Q

Androgens released by zone reticularis are converted to what peripherally

A

Testosterone

Dihydrotestosterone

278
Q

What does adrenal medulla secrete

A

Catecholamines e.g. Adrenaline or Noradrenaline

under sympathetic control

279
Q

Excess of what drug can mimic Cushings Disease?

A

Alcohol

280
Q

*What are the functions of cortisol

A
  • Increased carbohydrate and protein catabolism (breakdown)
  • Increased deposition of fat and glycogen
  • Na+ retention
  • Increased renal K+ loss
  • Diminished host response to infection
281
Q

Describe when corticotrophin and thus cortisol levels are highest and lowest

A

Released according to a Circadian Rhythm and stress
Highest levels in morning 7/9am
Lowest at midnight

282
Q

Give examples of things that can cause high-cortisol

A 
Alcohol pseudo-Cushings syndrome
Depression
Obesity
Pregnancy
(Stress also)
283
Q

Why do you get infections in Cushings syndrome more easily?

A

Anti-inflammatory effect of cortisol and poor healing

284
Q

Differential diagnosis of Cushings syndrome

A

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

285
Q

Diagnosis of Cushings

A

Drug history - oral steroids?
Random plasma cortisol
1st line test: Dexamethasone overnight suppression test (normally causes cortisol depression but this is not the case in cushings) or Urine free cortisol test over 24 hours

2nd line test:
if no suppression
48 hour

286
Q

Aetiology of hyperthyroidism

A

2/3 cases are Graves Disease
Toxic multi nodular goitre
Toxic thyroid adenoma
Iodine excess congenital (less common)

287
Q

Symptoms of hyperthyroidism

A 
(like how you feel before an exam)
Diarrhoea
Weight loss
Sweats
Heat intolerance 
Palpitations
Tremor
Anxiety
Menstrual disturbance
288
Q

Signs of hyperthyroidism

A 
Tachycardia
Thin hair
Lid lag
Lid retraction
Onycholysis
Exophthalmos
289
Q

Investigations of hyperthyoridism

A 
TFTs (thyroid function test)
Thyroid autoantibodies (Thyroid peroxidase, thyroglobulin, TSH receptor antibody)
Radioactive iodine isotope uptake scan
290
Q

What would a TFT show in primary hyperthyroidism

A

Low TSH

High T3/T4

291
Q

What would a TFT show in secondary hyperthyroidism

A

High TSH

High T3/T4

292
Q

Describe Graves Ophthalmology appearance

A

Extraocular muscle swelling
Eye discomfort
Lacrimation
Diplopia

293
Q

Define gigantism

A

Increased production of GH occurring in children

294
Q

Symptoms of acromegaly

A

Acroparaesthesia, Arthralgia, Sweating, Decreased libido, Headache

295
Q

Signs of acromegaly

A 
Massive growth of the hands, feet and jaw
Big tongue with widely spaced teeth
Puffy lips, eyelids and skin 
Darkening skin 
Obstructive sleep apnoea
Deep voice
296
Q

What is acroparaesthesia

A

pins and needles in extremities

297
Q

Why do you not do a growth hormone measurement to investigate if patient has acromegaly

A

GH is a pulsatile protein and levels vary throughout day

Do oral glucose tolerance test

298
Q

Describe ECG of Conns syndrome

A

Flat T
Long PR
Long QT
U waves

299
Q

What is pseudohypoparathyroidism

A

Decreased response to PTH
Bloodwork shows low Ca, high PTH
Treat as normal hypoparathyroid

300
Q

What hormone stimulates the secretion of potassium in the kidney?

A

Aldosterone

301
Q

Is hypokalaemia a result of high or low aldosterone

A

High aldosterone
More K excretion
Less K in body

302
Q

Hyperkalemia is a result of low aldosterone. What can therefore cause hyperkalemia

A

Low aldosterone - adrenal insufficiency
ACE inhibitors - block the binding of aldosterone to receptor
AKI - decreased fibrillation rate so more K+is maintained in the blood

303
Q

What is the role of K in the body

A

Charged and Helps maintain the resting potential of all muscles in the body

304
Q

Hypokalaemia - describe effects on muscles

A

Everything slows
Smooth - constipation
Skeletal - Weakness/cramps
Cardiac - Arrhythmias and palpitations

305
Q

Hyperkalaemia - describe effects on muscles

A 
Everything speeds up
Smooth - cramping
Skeletal - Weakness/ flaccid paralysis
Due to over contraction muscles become totally drained of energy  
Cardiac - Arrhythmias and arrest
306
Q

How does insulin affect potassium balance

A

Excess insulin -> Hypokalaemia
too much K+ follows insulin into cell

Insulin deficient -> Hyperkalemia
Not enough K+ follows into the cell

307
Q

**How does pH change with potassium balance

A

Alkalosis (high pH) -> H+ out of cell and K+ in -> hypokalaemia

Acidosis (low pH) -> H+ into cell and K+ out ->Hyperkalemia
(decrease K+ by replacing with H+)

308
Q

How do drugs acting on the Beta 2 receptor affect potassium balance

A

B2 agonists (SABA/LABA) -> increase B2 pumping of K+ into cell -> Hypokalaemia

Beta blocker -> inhibits pumping of K+ into cell -> Hyperkalemia

309
Q

How does cell lysis cause potassium balance issues

A

Intracellular contents released as get Hyperkalaemia

Severe burns or tumour lysis syndrome for example

310
Q

Symptoms of hypocalcaemia

A 
SPASM
Spasms
Peripheral paraesthesia
Anxious
Seizures
Muscle tone increase
311
Q

Signs of hypocalcaemia

A 
CATS
Convulsion
Arrhythmias
Tetany
Spasm and Stridor
312
Q

ECG of hypocalcaemia

A

Long QT interval

313
Q

What malignancies cause hypercalcaemia?

A

Myeloma

Non-hodgkin lymphoma

314
Q

What is difference between Cushings syndrome and disease?

A

Both involve:
Excess cortisol
Loss of hypothalamic pituitary axis feedback
Loss of circadian rhythm
C Disease also caused by pituitary adenoma

315
Q

How can an Adrenalectomy lead to Nelson’s syndrome

A

If you remove the adrenal glands then no cortisol will be produced in response to ACTH produced by the pituitary gland.
If no cortisol is produced then there is no negative feedback on ACTH levels which can cause ACTH to build up in the body tissues.
This can cause a bronze pigmentation of the skin, visual disturbances and headaches.

316
Q

a 16yr old female, presents to A&E with her mother after feeling vey weak and experiencing some palpitations. Her mother is concerned that her daughter is very skinny, you check her BMI and it is 16.What is the most likely cause of her condition?

Hypokalaemia
Hyperkalaemia
Hypocalcaemia
Hypercalcemia

A

Hypokalemia

anorexic BMI

317
Q

a 73 year old gentleman presents to his GP for some routine tests following a recent diagnosis of secondary hyperparathyroidism. All the results get mixed up in the pile which one is Jims?

A) Calcium high, Phosphate high, ALP high
B) Calcium low, phosphate low, ALP low
C) Calcium low, Phosphate high, ALP high
D) Calcium low, phosphate low, ALP high

A

A- tertiary
B Nothing
*C- secondary
D- primary

318
Q

A 29yo man presents with 4-week history of polyuria and extreme thirst. The urine is very dilute. The patient does not have any weight loss and maintains a good diet. No findings are found on urine dipstick. The most appropriate invevstigation is:

Serum osmolality
Fasting plasma glucose 
Urinary electrolytes 
MRI head 
Water deprivation test
A

*Water deprivation test = Diagnostic for DI

319
Q

The initial treatment for somebody having a thyrotoxic storm (hyperthyroid crisis) is:

IV 0.9% saline
Propanolol 
Salbutamol
Carbimazole
Omeprazole
A

Propanolol
(Carbimazole long term)

saline would probably be given but isn’t going to have much of an effect, salbutamol is for asthma / respiratory disease, carbimazole is an antithyroid treatment and would probably be given too but does not help immediately with symptoms, and omeprazole is a PPI. Therefore the best initial treatment is propanolol, a beta blocker

320
Q

Hypocalcaemia

A

Chvostek’s sign is the twitching of the facial muscles in response to tapping over the area of the facial nerve.
Trousseau’s sign is carpopedal spasm caused by inflating the blood-pressure cuff to a level above systolic pressure for 3 minutes.

Medicine Phase 2a (22 decks)

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