Conditions of the Endocrine System Flashcards

1
Q

Describe the condition of hypertcortisolism

A

Definition:

  • umbrella term for a range of conditions characterized by excessive circulating cortisol levels
  • Cushing’s disease: caused by increased ACTH secretion from anterior pituitary
  • Cushing’s syndrome: occurs independently of ACTH secretion

Aetiology:

  • Cushing’s Disease: usually caused by a pituitary microadenoma (benign hormone secreting tumour in anterior pituitary)
  • Cushing’s Syndrome: usually iatrogenic (glucocorticoid hormone therapy)
  • other: tumour of adrenal cortex, neuroendocrine tumours of the lung (SCLC) that produce ACTH

SSX (caused by increased glucocorticoid activity)

  • tunical obesity
  • abdo striations
  • buffalo hump
  • ‘moon face’ with flushed red cheks
  • muscle atrophy
  • myalgia, arthralgia
  • osteoperosis and bone fractures
  • insulin resistance
  • poor wound healing and skin infections
  • if zona reticularis involved, SSX of hyperandrogenism (hirsuitism, menstrual irregularity)

Management:

  • if untreated 50% fatality rate within 5 years
  • pituitary / adrenal / neuroendocrine tumours: surgery, radio and/or chemotherapy
  • iatrogenic: discontinue glucocorticoid therapy
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2
Q

Which types of tumours can cause hypercortisolism?

A
  1. pituitary microadenoma
    - 70% of cases
    - benign hormone secreting tumour of anterior pituitary gland
  2. tumour of adrenal cortex
  3. neuroendocrine tumours of the lung (SCLC / small cell lung carcinoma)
    - secrete hormones including ACTH
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3
Q

Describe the condition of adrenal cortical hypofunction

A

Definition:
- inability of adrenal cortex to produce sufficient cortical hormones

Classifications:

  1. Primary adrenocortical insufficiency
    - high ACTH levels, decreased cortisol
    - called Addison’s disease
    - caused by intrinsic dysfunction of adrenal cortex (usually autoimmune attack)
  2. Secondary adrenocortical insufficiency
    - low ACTH and cortisol levels
    - caused by pituitary or hypothalamic dysfunction or after glucocorticoid therapy

SSX:

  • decreased mineralocorticoid activity (dehydration, hypotension, hyperkalaemia)
  • decreased glucocorticoid activity (hypoglycaemia, postural hypotension)
  • systemic (severe fatigue, weakness, weight loss, GI disturbance)
  • skin changes (hyperpigmentation caused by excess ACTH secretion, vitiligo)

Management:
- hormone supplementation (cortisol for glucocorticoids, fludocortisone for mineralcorticoids)

Acute adrenaocortical insufficiency /Addisonial crisis / adrenal crisis:

  • medical emergency
  • IV fluids and cortisol
  • life threatening emergency associated with severe hypotension, hyperkalaemia, hypoglycaemia
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4
Q

What is Addison’s disease?

A
  • another term for primary adrenocortical insufficiency (adrenal cortical hypofunction)
  • caused by intrinsic dysfunction of adrenal cortex
  • 80% of cases caused by autoimmune attack
  • characterized by normal ACTH and low cortisol levels
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5
Q

What is ACTH and how is it implicated in the conditions hypercortisolism and adrenal cortical dysfunction?

A

ACTH:

  • adreno corticotrophic hormone
  • produced by anterior pituitary gland
  • stimulates release of cortisol and androgens

In hypercortisolism (Cushing’s Disease):

  • increased ACTH secretion from anterior pituitary
  • causes excessive amounts of circulating cortisol

In primary adrenocortical insufficiency (Addison’s)
- ACTH levels are normal, but cortisol levels are high because of adrenal cortex dysfunction

In secondary adrenocortical insufficiency:

  • ACTH levels are low, causing low cortisol levels
  • caused by pituitary or hypothalamic dysfunction
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6
Q

What are the symptoms of abnormally high cortisol levels (hypercortisolism) and abnormally low cortisol levels (adrenal cortex hypofunction)

A

High:

  • tunical obesity, moon face, buffalo hump
  • muscle atrophy, osteoperosis
  • myalgia, arthralgia
  • insulin resistance
  • HTN
  • poor wound healing and skin infections

Low:

  • severe fatigue
  • weight loss
  • GI disturbances
  • hyperpigmentation
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7
Q

Describe the condition of phaeochromocytoma

A

Definition:
- adrenal tumour arising from chromaffin cells of adrenal medulla

Pathophysiology:
- most common cause of excess catecholamine production (epinephrine, norepinephrine)

SSX:

  • CVD (HTN, AMI, stroke, AAA, heart failure, palpitations)
  • systemic (pallor, sweating, weight loss)
  • GI (abdo pain, vomiting, constipation)
  • other (severe HA, anxiety, tremours)

Management:

  • can cause death by catastrophic hypertensive crisis or fatal cardiac arrythmias
  • surgical resection
  • long term adrenergic blockade
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8
Q

Which group of hormones is affected by phaeochromocytomas?

A

Phaeochromocytomas:

  • adrenal tumour arising from chromaffin cells
  • cause increased catecholamine production (epinephrine, norepinephrine)
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9
Q

Describe the condition of simple / non-toxic goitres

A

Definition:

  • enlarged thyroid gland
  • thyroid function maintained

Classifications:

  • simple diffuse (uniform enlargement) - most common in young women, pregnant women
  • simple multinodular (enlargement with nodule formation)

Aetiology:

  1. iodine deficiency
    - most common cause
    - higher levels of TSH are secreted to maintain normal levels of T3 and T4
    - causes hyperplasia of follicular cells in thyroid and resulting enlargement
  2. Other:
    - ingestion of goitrogens (lithium, tobacco)
    - pregnancy, OCP
    - early stage Hashimoto’s thyroiditis

SSX:

  1. simple diffuse
    - soft and symmetrical goitre
    - neck tightness with swallowing
    - non tender
    - no bruit
  2. simple multinodular
    - can become very large
    - if haemorrhaged into a nodule: pain and oedema
    - if compressing mediastinal structures: cough, dysphagia, stridor, oedema

Management:

  • asymptomatic simple: observation
  • iodoine supplementation (helps childhood goiotres, doesn’t impact adulthood goitres)
  • if compressive SSX: partial thyroidectomy (high risk of recurrence)
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10
Q

What are dietary sources of iodine, and how is iodine implicated in goitres?

A

Dietary sources:
- dairy, eggs, seafood

Iodine:

  • synthesizes production of T3 and T4 from thyroglobulin in thyroid glands
  • if insufficient iodine: T3 and T4 levels drop, so anterior pituitary secretes more TSH (thyroid stimulating hormone)
  • elevated TSH causes hyperplasia of follicular cells
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11
Q

Describe the condition of hypothyroidism

A

Definition:
- deficiency of T3 and T4 thyroid hormones

Classifications:

  1. Primary:
    - caused by thyroid gland failure
    - most common cause: Hashimoto’s thyroiditis (autoimmune)
    - other causes: iatrogenic, congenital, iodine deficiency
  2. Secondary:
    - caused by TSH deficiency
    - caused by pituitary adenoma, pituitary surgery
  3. Tertiary:
    - caused by TRH deficiency
    - caused by hypothalamic dysfunction

SSX:

  • puffiness and pallor = sterotypical features
  • myxedema (non-pitting oedema) especially in hands, feet and eyelids (periorbital oedema) - caused by GAG / glycosaminoglycan accumulationo in various body tissues
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12
Q

Describe the condition of Hashimoto’s thyroiditis

A

Definition:
- autoimmune disease of thyroid gland causing hypothyroidism

Incidence:

  • most common type of primary hypothyroidism in Aus
  • 10 x more common in females
  • typically onset in middle age

Precipitating factors:

  • high iodine supplementation
  • lithium amiodarone drugs

Pathophysiology:

  • autoimmune disorder
  • lymphocyte mediated inflammation and fibrosis of thyroid
  • secretion of IgG antibodies against thyroglobulin and thyroid peroxidase
  • causes goitre (early stage)
  • causes thyroid atrophy (late stage)
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13
Q

Describe the condition of thyrotoxicosis

A

Definition:
- clinical state caused by an excess of thyroid hormones

Classifications:

  1. toxic diffuse goitre (Grave’s)
  2. toxic multinodular goitre
  3. toxic solitary nodule

Aetiology:

  • usually caused by hyperthyroidism
  • can also be caused by levothyroxine ingestion

SSX:

  1. goitre
    - diffuse enlargement
    - audible bruit
  2. ocular changes (GAG accumulation)
    - lid retraction and bulging eyes
    - corneal ulceration and conjunctivitis
    - excessive lacrimation
    - diplopia
    - decreased visual acuity
  3. increased metabolic rate
    - heat intolerance
    - weight loss
    - sweating
  4. GIT
    - increased appetite and thirst
    - hyperdefecation, diarrhea
  5. CVS / Respiratory
    - palpitations and atrial fibrillation
    - exacerbated asthma
  6. neuro
    - nervousness, emotional lability, psychosis
    - hyper-reflexia, tremor
    - muscle atrophy
  7. reproductive
    - menstrual irregularities
    - loss of libido
  8. skin
    - GAG accumulation in skin of legs causes pretibial skin myxedema and thicke
    Management:
    - anti-thyroid drugs, beta-blockers, radioactive iodine
    - surgery: sub-total thyroidectomy (risk for hypothyroidism, damage to laryngeal nerves or parathyroid gland)
    - good prognosis with management, risk for hypothyroidism
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14
Q

Describe Grave’s disease

A

Definition:

  • toxic diffuse goitre
  • autoimmune disease
  • most common cause of thyrotoxicosis (excess of thyroid hormones)

Incidence:
- 8 x more common in females

Risk factors:
- familyl history, high dose iodine supplementation, major stressors causing an autoimmune response

Pathophysiology:

  • autoantibodies present in 50% of cases are directed against thyroid stimulating hormone receptors
  • causes goitre production and elevated T3 and T4 levels
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15
Q

Describe the condition of thyroid cancer

A

Incidence:

  • 7th most common cancer in women
  • much more common in women

Risk factors:

  • family history
  • benign thyroid disease
  • exposure to ionizing radiation (20 years latency)

Classifications:

  • papillary carcinoma (80%, begins as a solitary nodule and spreads through gland)
  • follicular, medullary and anaplastic carcinomas

SSX:

  • rapid onset nodule enlargement (firm and non-tender)
  • large tumours can cause discomfort, dysphagia, Horner’s syndrome
  • metastatic spread: Cx lymphadenopathy

Management:

  • excellent prognosis: if tumour under 2cm, patient under 50 and no spread, no change to life expectancy
  • surgical resection
  • hemi or total thyroidectomy
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16
Q

Describe the condition of hyperparathyroidism

A

Definition:
- increased PTH (parathyroid hormone) secretion

Classifications:

  1. Primary
    - adenoma of a single PT gland (most common)
    - causes increased PTH secretion and increased serum calcium levels
  2. Secondary:
    - secondary to a pathology causing low serum calcium levels (rickets, malabsorption)
    - PTH levels increase as a response to low serum calcium levels

SSX: (bones, stones, abdo groans, psychic moans and fatigue overtones)

  • 50% asymptomatic, SSX usually mild
  • SSX caused by hypercalcaemia
  1. Bones
    - reduction in bone density (osteoclastic bone resorption and fibrous replacement)
    - bone pain
    - fracture
    - arthralgia
  2. stones
    - nephrolithiasis
  3. abdo groans
    - anorexia
    - nausea
    - constipation
    - polydipsia
    - polyuria
  4. psychic moans
    - HA
    - insomnia
    - irritability
    - depression
    - paraesthesia
    - poor concentration / memory loss
  5. fatigue overtones
    - maliase
    - muscle cramps
    - weakness
    - hyporeflexia
  6. cardiac changes
    - hypercalcaemia increases cardiac contractility and excitability
    - arrythmias and HTN

Management:

  • monitor if asymptomatic
  • symptomatic or pregnant: surgical excision
17
Q

Describe the condition of hypoparathyroidism

A

Definition:

  • insufficiency of PTH
  • causes hypocalcaemia

Aetiology:

  • removal of parathyroid adenoma causing suppression of other parathyroid glands
  • thyroid surgery
  • autoimmune disease, infection

SSX:
(hypocalcaemia increases excitability of sensory and motoor nerves)

  1. muscular:
    - increased tone
    - hyperreflexia
    - Chvostek sign and Troussea phenomenon
  2. neuro
    - paraesthesia
    - irritabiity
    - confusion
    - premature cataracts
  3. cardiac changes
    - decreased cardiac contractility and excitability

Life threatening SSX: tetany of laryngeal muscles

Management:

  • no effective PTH replacements
  • calcium supplementation
18
Q

Which conditions are involved in pathological changes to serum calcium levels?

A
  1. Hypercalcaemia:
    - caused by primary hyperparathyroidism (adenoma of a parathyroid gland)
    - causes increased PTH secretions and increased serum calcium levels
  2. Hypocalcaemia
    - caused by hypoparathyroidism (decreased PTH secretion causes decreased serum calcium levels)
    - also present in secondary hyperparathyroidism (pathology causing low serum calcium levels already present, causes increased PTH secretions to try to raise calcium)
19
Q

What are the SSX of hypercalcaemia and hypocalcaemia?

A

Hypercalcaemia (primary hyperparathyroidism):

  • causes increased cardiac muscle contractility and excitability
  • bones, stones, abdo groans, psychic moans, fatigue overtones

Hypocalcaemia (hypoparathyroidism, secondary hyperparathyroidism:

  • causes decreased cardiac muscle contractility and excitability
  • increases muscle and nervous excitability
20
Q

Which conditions cause hypercortisolism, and which cause hypocortisolism?

A

Hypercortisolism:

  • Cushing’s Disease (caused by increased ACTH secretion) - usually caused by a pituitary microadenoma
  • Cushing’s Syndrome (independent of ACTH secretion)
  • tumour of adrenal cortex, neuroendocrine tumour of lungs

Hypocortisolism:

  • primary adrenocortical insufficiency (Grave’s disease) caused by adrenal cortex dysfunction
  • secondary adrenocortical insufficiency - caused by pituitary or hypothalamic dysfunction
21
Q

What are the symptoms of hypercortisolism and hypocortisolism?

A

Hypercortisolism

  • caused by Cushings, or pituitary or neuroendocrine tumour
  • tunical obesity, buffalo hump, moon face
  • myalgia, arthralgia
  • muscle atrophy, osteoperosis
  • insulin resistance
  • HTN
  • poor wound healing and skin infections

Hypocortisolism:

  • caused by primary adrenocortical insufficiency (Addison’s) or secondary adrenocortical insufficiency
  • severe fatigue, weakness, weight loss
  • GI disturbance
  • hyperpigmentation
  • acute adrenal crisis: medical emergency (can be fatal)
22
Q

Which endocrine pathology affects catecholamine production?

A

Phaeochromocytoma:

  • tumour of adrenal medulla (from chromaffin cells)
  • causes excessive catecholamine production
23
Q

Which endocrine pathologies affect levels of thyroid hormones?

A

Hypothyroidism:

  • primary (most common: Hashimoto’s thyroiditis)
  • secondary (caused by pituitary adenoma or pituitiary surgery)
  • tertiary (caused by hypothalamic dysfunction

Hyperthyroidism / Thyrotoxicosis:

  • toxic diffuse goitre (Grave’s)
  • toxic multinodular goitre
  • toxic solitary nodule
24
Q

What are the symptoms of hyperthyroidism and hypothyroidism?

A

Hypothyroidism:

  • puffiness and pallor
  • GAG accumulation causes non-pitting oedema (myxedema)

Hyperthyroidism:

  • goitre
  • ocular changes (bulging eyes, diplopia, conjunctivitis, lacrimation)
  • increased BMR
  • increased appetite and thirst, hyperdefecation / diarrhea
  • CVS/resp: palpitations, atrial fibrillation, exacerbates asthma
  • neuro: nervousness, psychosis, tremor, hyper-reflexia, muscle atrophy
  • reproductive: menstrual irregularities, loss of libido
  • GAG accumulation in skin of legs: pretibilal skin myxedema and thickening
25
Q

What are GAGs and how are they involved in pathologies of the thyroid gland?

A

GAGs:

  • glycosaminoglycans
  • proteoglycans normally found in ECM of connective tissue

Hypothyroidism:

  • GAGs accumulate in body tissues due to reduced rate of protein breakdown
  • causes myxedema of hands, feet and eyelids

Hyperthyroidism:

  • GAGs accumulate in skin of legs
  • causes pretibial myxedema