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Nursing Science 3 > WEEK 5 - Endocrine Disorders > Flashcards

WEEK 5 - Endocrine Disorders Flashcards

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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
Q

Hyperfunction of the thyroid gland leads to?

A
  • Excessive thyroid hormone
  • Decreased TSH and TRH
  • High levels of T3 and 4
26
Q

Clinical manifestations of hyperthyroidism?

A
  • 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
Q

Treatment of hyperthyroidism?

A
  • Antithyroid drugs
  • Beta blockers for symptoms
  • Radioactive iodine ablation
  • Thyroidectomy
28
Q

Define hypothyroidism

A

Deficient production of thyroid hormone by the thyroid gland, more common in women than in men

29
Q

What are the causes of hypothyroidism?

A
  • 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
Q

Pathophysiology of primary hypothyroidism?

A
  • 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
Q

Pathophysiology of seconday hypothyroidism?

A
  • 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
Q

Clinical manifestations of hypothyroidism?

A
  • 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
Q

What is Cushing’s disease?

A

Excessive levels of cortisol secretion of excessive anterior pituitary secretion adrenocorticotrophic hormone (ACTH)

34
Q

Causes of Cushing’s disease?

A

Pituitary adenoma

Ectopic ACTH secreting tumours

35
Q

What is the pathophysiology of Cushing’s disease?

A
  • 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
Q

Clinical manifestations of Cushing’s disease?

A
  • 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
Q

Treatment of Cushing’s diseases?

A
  • Surgery
  • Radiotherapy
  • Bilateral adrenalectomy
  • Medications
38
Q

What is Addison’s disease?

A

Primary adrenal insufficiency, adrenal glands fail to produce sufficient cortisol

39
Q

What is the pathophysiology of Addison’s disease?

A
  • Destruction of the adrenal complex by autoantibodies
  • Decreased levels of cortisol
  • Increased levels of adrenocoticotrophic hormone due to loss of negative feedback
40
Q

Clinical manifestations of Addison’s disease?

A
  • 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
Q

Treatment of Addison’s disease?

A
  • Lifetime daily glucocorticoid replacement therapy e.g. fludrocortisone, hydrocortisone, prednisolone
  • Additional cortisol

Nursing Science 3 (21 decks)

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