WEEK 5 - Endocrine Disorders Flashcards

1
Q

What is the endocrine system?

A

Consists of groups of cells (glands) that make hormones and release them directly into the bloodstream (ductless)

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2
Q

Principles of hormones?

A
  • They are chemical messengers
  • They control the activity of the cells they bind to
  • Hormones will only bind to cells that have their receptors on their surface
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3
Q

What are the principal endocrine glands?

A
Hypothalamus
Pineal
Pituitary
Parathyroid
Thyroid
Thymus
Adrenal (cortex and medulla) 
Pancreas (islets of Langerhan) 
Ovaries (female)
Testes (male)
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4
Q

Functions of the endocrine system?

A
  • Maintain homeostasis
  • Control reproduction
  • Promote smooth, sequential growth and development
  • Regulate RBC production
  • Digestion and absorption
  • Stress response - fight or flight
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5
Q

What is the hypothalamic-pituitary axis?

A

The control of the hypothalamus over the release of hormones of the anterior and posterior pituitary glands

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6
Q

How does the hypothalamus communicate with the anterior pituitary?

A

Via a vascular pathway, the anterior pituitary releases its hormones straight into the bloodstream when stimulated via hormones of the hypothalamus

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7
Q

How does the hypothalamus communicate with the posterior pituitary?

A

Via a neural pathway, neurosecretory cells connect the two glands, have their cell bodies in the hypothalamus and secrete hormones when stimulated via APs

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8
Q

What hormones does the anterior pituitary secrete?

A
  • Growth hormones
  • Gonadotrophic hormones
  • Adrenocorticotrophic hormones

Trophic - regulate the secretion of hormones of another gland

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9
Q

What hormones does the posterior pituitary secrete?

A

Vasopressin and oxytocin

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10
Q

How does the endocrine system regulate homeostasis?

A

Via negative feedback systems

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11
Q

Principles of endocrine dysfunction?

A
  • HYPOsecretion - not enough hormone, may be due a problem with the gland (primary) or with the hormone itself (secondary)
  • HYPERsecretion - too much hormone, may be due to tumours (primary) or with the hormone itself (secondary)
  • Target cell hyporesponsiveness - decreased number of receptors or impaired function, does not allow the target cell to respond adequately to hormones (eg. insulin resistance)
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12
Q

What is syndrome of antidiuretic hormone secretion?

A

High levels of ADH despite normal circulating blood volume and serum osmolality - causes fluid acculumation

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13
Q

Syndrome of antidiuretic hormone secretion is caused by?

A
  • Cancers
  • Trauma
  • Infection of the CNS
  • Drugs
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14
Q

Clinical manifestations of syndrome of antidiuretic hormone secretion?

A
Serum hyposomolarity and hyponatraemia (Na<135mmol/L)
Thirst
Nausea
Fatigue
Headache
Vomiting
Lethargy
Dyspnea
Seizures, loss of consciousness (cerebral oedema), respiratory arrest (Na+<115mmol/L)
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15
Q

Treatment of syndrome of antidiuretic hormone secretion?

A
  • Correction of underlying problem
  • Emergency correction of severe hyponatraemia - GIVE SALT SLOWLY, otherwise can cause seizures and cerebral oedema, rise in ICP
  • Diuretics to aid fluid removal
  • Fluid restriction and daily weighs
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16
Q

What are the two types of diabetes insipidus and their causes?

A

Neurogenic:
Caused by insufficient amounts of ADH despite low plasma volumes and high serum osmolality

Nephrogenic:
Caused by an inadequate response by the renal collecting tubules to ADH

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17
Q

Neurogenic diabetes insipidus is caused by?

A
  • Brain tumours
  • Neurosurgery
  • Increased ICP
  • CNS infections
18
Q

Nephrogenic diabetes insipidus is caused by?

A
  • Genetic abnormalities

- Disorders and drugs that damage renal tubules

19
Q

Clinical manifestations of diabetes insipidus?

A
  • Serum osmolarity
  • Polyuria
  • Nocturia
  • Extreme thirst and polydipsia
  • Hypovolaemia/hypotension
  • Poor skin turgor, dry mucous membranes
  • Confusion, irritability
20
Q

Treatment of diabetes insipidus?

A
  • ADH replacement with desmopression aceteate/vasopression

- Fluids - oral or IV

21
Q

What is hyperthyroidism?

A

Increased levels of T3 and T4 (thyroid hormones)

22
Q

What is primary hyperthyroidism and what is it caused by?

A

Primary = excess thyroid hormone made and secreted by the thyroid gland.
Caused by Graves disease, goiters, follicular adenoma, thyroid medications in excess

23
Q

What is secondary hyperthyroidism and what is it caused by?

A

Excessive thyroid stimulating hormone production (TSH)

Caused by TSH-secreting pituitary adenomas

24
Q

Describe the pathophysiology of graves disease?

A

Autoimmune disease
T cells stimulate B cells to produce IgG ABs specific to TSH receptors
ABs bind to TSH receptors in the thyroid = stimulate synthesis and secretion of thyroid hormone

25
Hyperfunction of the thyroid gland leads to?
- Excessive thyroid hormone - Decreased TSH and TRH - High levels of T3 and 4
26
Clinical manifestations of hyperthyroidism?
- Bulging eyes - Goitre - Weight loss and diarrhoea - Increased appetite - Tachycardia and palpitations - Sweating, flushing - Hair loss - Menstrual changes/fertility issues - Lability and insomnia - Dsypnoea
27
Treatment of hyperthyroidism?
- Antithyroid drugs - Beta blockers for symptoms - Radioactive iodine ablation - Thyroidectomy
28
Define hypothyroidism
Deficient production of thyroid hormone by the thyroid gland, more common in women than in men
29
What are the causes of hypothyroidism?
- Failure of the thyroid gland to produce thyroid hormone (primary); caused by iodine deficiency, Hashimoto's disease, loss of thyroid tissue - Deficiency of TRH/TSH/both (secondary); caused by pituitary or hypothalamic failure, failure to stimulate thyroid function
30
Pathophysiology of primary hypothyroidism?
- Loss of functional thyroid tissue - Decreased production of thyroid hormone - Lack of negative feedback to T3/4 = increase in TRH and TSH secretion - Leads to low levels of TH and high levels of TRH and TSH - TSH = goitre
31
Pathophysiology of seconday hypothyroidism?
- Injury to the pituitary gland = decreased TSH - Leads to low levels of Th and TSH and elevated TRH Or - Injury to the hypothalamus - Decreased production of TRH - Leads to low levels of TH, TSH and TRH = thyroid shrinks
32
Clinical manifestations of hypothyroidism?
- Lethargy/fatigue - Weight gain and fluid retention - Normal or small thyroid - Goitre - Bradycardia - Breathlessness - Cold intolerance - Constipation - Muscle pain and weakness - Depression - Thinning of hair - Low libido/decreased fertility
33
What is Cushing's disease?
Excessive levels of cortisol secretion of excessive anterior pituitary secretion adrenocorticotrophic hormone (ACTH)
34
Causes of Cushing's disease?
Pituitary adenoma | Ectopic ACTH secreting tumours
35
What is the pathophysiology of Cushing's disease?
- Pituitary adenoma secretes ACTH - Increased secretion of ACTH results in increased production of cortisol by adrenal cortex - Some normal feedback inhibition by cortisol - Hypercortisolism
36
Clinical manifestations of Cushing's disease?
- Weight gain - High BGLs or diabetes - Acne - Increased body and facial hair - Facial flushing - Purple striae - Easy bruising - Thin extremities - Osteoporosis - HTN - Increased susceptibility to infections - Irritability and depression
37
Treatment of Cushing's diseases?
- Surgery - Radiotherapy - Bilateral adrenalectomy - Medications
38
What is Addison's disease?
Primary adrenal insufficiency, adrenal glands fail to produce sufficient cortisol
39
What is the pathophysiology of Addison's disease?
- Destruction of the adrenal complex by autoantibodies - Decreased levels of cortisol - Increased levels of adrenocoticotrophic hormone due to loss of negative feedback
40
Clinical manifestations of Addison's disease?
- Weakness and fatigue - Anorexia - Weight loss - Nausea - Diarrhea - Hypoglycaemia - Hyponatraemia, hyperkalaemia - Orthostatic hypotension - Hyperpigmentation - Addisonian crisis = severe hypotension and vascular collapse as a result of combined effects of hypocortisolism, hypoaldosteronism, extracellular volume depletion and some precipitating stressor
41
Treatment of Addison's disease?
- Lifetime daily glucocorticoid replacement therapy e.g. fludrocortisone, hydrocortisone, prednisolone - Additional cortisol