endocrine Flashcards
aging and the endocrine system
Ageing negatively affects hormone secretion by the glands of the endocrine system, – older people more prone to insomnia, fractures, diabetes and cognitive changes
Levels of most hormones decrease – such as estrogen (women), testosterone (men), growth hormone, melatonin, aldosterone, calcitonin, renin
Levels of some hormones do not change – such as cortisol, epinephrine, insulin, thyroid hormones T3 and T4
Levels of some hormones increase – such as follicle-stimulating hormone, luteinizing hormone, norepinephrine, parathyroid hormone
Some hormone receptors less receptive – decline in endocrine function
Production rates of some hormones may decrease
Pituitary gland becomes smaller
Thyroid gland becomes more lumpy or nodular; beginning around age 20, metabolism gradually declines
Hormones that usually decrease with age include aldosterone, renin, calcitonin, and growth hormone; specific hormones decrease in older women (estrogen and prolactin) and older men (testosterone).
Hormones that may increase with age include follicle-stimulating hormone (FSH), luteinizing hormone (LH), norepinephrine, and antidiuretic hormone (ADH).
Hormones that remain unchanged or are only slightly decreased with age include thyroid hormones (T3 and T4), cortisol, insulin, epinephrine, parathyroid hormone, and 25-hydroxyvitamin D.
Blood glucose levels rise with age
Insulin levels remain unchanged with age, decreased glucose tolerance may occur due to changes in the cell receptor sites: the older adult experiences hypoglycemia more quickly than a younger person and may progress to dangerously low levels of blood glucose before signs and symptoms are obvious. This decreased glucose tolerance because of cell receptor change can place the older adult at risk for hyperglycemia and the onset of type 2 diabetes.
Thyroid hormone levels may decrease with aging, the body makes up for it by decreasing the rate at which thyroid hormone is broken down; therefore resting levels of thyroid hormone are usually normal in the elderly. Thyroid disorders are, however, twice as common in the older adult. Hypothyroidism is the most common thyroid disorder, especially in older women.
The amount of hormones secreted by the older adult changes, decreasing the individual’s ability to adapt to stress and respond to environmental changes.
principal endocrine glands
Hypothalamus Pituitary Pineal Thyroid Parathyroid Thymus Adrenals Pancreas Ovaries Testes
hormones
Releasing hormones –produced by hypothalamus to trigger the pituitary to release stimulating hormones
Stimulating hormones – stimulate target organs to secrete their hormones
Negative feedback – prevents over-secretion of any hormone; “turns off” the system when the “right point” has been reached
patterns of hormone secretion
Rhythms
Diurnal: day-night/sleep-wake
Prolactin, growth hormone, testosterone secretion during sleep
Circadian: internal process recurring naturally on a 24-hour cycle
Cortisol
Pulsatile, Acute, Cyclic
Pulsatile: secretion of constant level of hormone over a long period
Acute: rapid increase in hormone level for a short time in response to a stimulus
Cyclic: hormone levels increase and decrease in a constant pattern
pathologies of endocrine system hyper states
Hyper-states: increased hormone secretion
Primary disorder: Target gland oversecretes due to pathology directly affecting it
Level of hormone secreted by gland high but the stimulating hormone [from pituitary] level low—due to increased negative feedback from hyperactive target gland secretion
Secondary disorder: Pituitary or hypothalamus over-stimulates a target gland
Target gland hormone and stimulating hormone levels will be high
Ectopic site of hormone production –secretion of hormone by some cancers
Target hormone receptors become hyperactive – genetic mutation
pathologies of the endocrine system hypo states
Hypo-states: decreased hormone secretion
Primary disorder: Target gland undersecretes due to a congenital or acquired problem
Target hormone levels low and stimulating hormone levels high—due to a loss of negative feedback from the hypo-active target gland
Secondary disorder: Pituitary does not secrete enough stimulating hormone
Decrease in target gland hormone and stimulating hormone levels
Tertiary disorder: Hypothalamus does not secrete enough releasing hormone
Defective hormone – high levels of hormone but the function that is supposed to be initiated by the hormone will not occur
Target organ receptor not responsive
High levels of stimulating hormone as the target gland tries to stimulate the target organ to respond
hypothalamus hormones
thyrotropin-releasing hormone (TRH) gonadotropin-releasing hormone somatostatin corticotropin-releasing hormone prolactin-inhibiting factor prolactin-releasing factor
anterior pituitary hormone
adrenocorticotropin hormone (ACTH) thyroid stimulating hormone (TSH) growth hormone prolactin luteinizing hormone (LH) follicle stimulating hormone (FSH)
posterior pituitary hormones
antidiuretic hormone (ADH) oxytocin
alterations of thyroid function
Thyroid hormone (TH) regulates the basal metabolic rate (BMR):
Regulates protein, carbohydrate and fat metabolism
Thyroid secretes two types of hormones:
TH – made up of
Thyroxine (T4) 90% – reservoir for T3
Triiodothyronine (T3) 10% – most active form
Calcitonin –responsive to hypercalcemia
Hyper or Hypo
Hyperthyroidism – hypermetabolism
Hypothyroidism – slowed metabolism
primary thyroid disorders
Pathology of the thyroid gland
Influences levels of thyroid hormone synthesized and secreted
secondary thyroid disorders
Pathology related to the pituitary gland or hypothalamus
Levels of Thyroid- stimulating hormone (TSH) influencing levels of thyroid hormones
risk factors for thyroid disease
Men: age ≥ 60 years
Women: age ≥ 50 years
personal history or strong family history of thyroid disease
diagnosis of other autoimmune diseases
past history of neck irradiation
previous thyroidectomy or radioactive iodine ablation
drug therapies such as lithium and amiodarone
dietary factors (iodine excess and iodine deficiency in patients from developing countries); or
certain chromosomal or genetic disorders (e.g., Turner syndrome,Down syndrome and mitochondrial disease)
hypothyroidism
thyroid hormone deficiency Prevalence 2/100 Canadians Mainly women – middle to older-aged Why? Underactive thyroid function Insufficient amount of thyroid hormone Causes Globally in iodine-deficient regions Iodine deficiency Most common cause in Canada Hashimoto’s thyroiditis
causes of hypothyroidism
Primary Hypothyroidism Hashimoto’s thyroiditis (autoimmune) Congenital Surgical removal of thyroid gland Ablation with radioactive iodine Radiotherapy Thyroid tumour Drug toxicity (lithium, interferon, amiodarone) Secondary Hypothyroidism Disorders of pituitary or hypothalamus
hypothyroidism pathophysiology
Primary: due to thyroid dysfunction
Thyroid hormone level is low and decreases negative feedback on the pituitary: TRH and TSH is high and TH low
related to destruction of thyroid tissue or problems with hormone synthesis
Secondary: due to pituitary dysfunction
Thyroid hormone level is low due to low secretion of TSH by pituitary: TH and TSH low, TRH high
Tertiary: due to hypothalamus dysfunction
Thyroid hormone level is low due to low secretion of TRH by hypothalamus leading to low secretion of TSH by pituitary: TH, TSH, TRH low
Transient: some cases of thyroiditis or on discontinuation of thyroid hormone therapy
clinical manifestations of hypothyroidism
Metabolic: Cold intolerance, modest weight gain hypothermia
Neurologic: Forgetfulness
Psychiatric: Personality changes, depression
Dermatologic: Facial puffiness; sparse, coarse and dry hair; coarse, dry, scaly and thick skin
Ocular: Periorbital swelling, droopy eyelids
Gastrointestinal: Constipation
Gynecologic: Menorrhagia or secondary amenorrhea
Cardiovascular: Slow heart rate
Other manifestations: hoarse voice, and slow speech
hypothyroidism assessment
Observe for early and subtle changes Ask patient about: weight gain and mental changes, fatigue, slowed and slurred speech, cold intolerance, skin dryness, constipation and dyspnea, muscular aches and pains, bradycardia, distended abdomen Patients with hypothyroidism are sensitive to narcotics like opioids (avoid dilaudid, morphine, fentanyl) and other sedatives (could lead to myxedema coma). Recommend use of alternatives for pain such as non-narcotics (Tylenol, Ibuprofen)
complications of hypothyroidism: myxedema coma
Medical Emergency: long history of hypothyroidism with uncontrolled low thyroid production
Precipitated by: illness, infection, trauma, meds that suppress CNS, exposure to cold
Clinical presentation:
Decreased mental status/LOC or coma
Hypoventilation
Hypothermia
Hypotension
Seizures
Shock
Myxedema – thickened, nonpitting edema of skin
hypothyroidism diagnostics/labs
History and physical examination
Serum TSH and free T4 levels
Serum T3 [not sensitive to hypothyroidism] and serum T4 levels
Thyrotropin-releasing hormone (TRH) stimulation test
Thyroid peroxidase (TPO) antibody (TPOAb) test
Thyroid ultrasound – nodules in enlarged gland
Thyroid biopsy – nodules
hyperthyroidism causes
Most common cause: Grave’s Disease (thyrotoxicosis)- 1 in 100
Autoimmune: autoantibody against thyroid receptor for TSH which stimulates synthesis and secretion of excess T4 and T3
Other common causes:
Multinodular goiter or Single, autonomous, hyperfunctioning “hot” nodule
Thyroiditis
Other causes: excess iodine ingestion, pituitary tumours, thyroid cancer
hyperthyroidism pathophysiology
Three mechanisms:
Increased synthesis and secretion of thyroid hormones by the thyroid gland [Primary]: Increased secretion of T3 and T4 and increased conversion of T4 to T3
Pituitary over-stimulates the thyroid to secrete thyroid hormones [Secondary]
Exogenous source of thyroid hormone
Increased levels of TH binding to receptors on mitochondria – increase metabolic rate, nutrient breakdown
Increase in metabolic rate leads to increased use of fat reserves
Increased levels of TH increase heart rate and BP; increase vasodilation to enhance blood flow to organs
Increased levels of TH increase neuromuscular activity: brisk reflexes, muscle weakness
hyperthyroidism assessment
Weight loss (burning calories increased) –increased appetite
Heat intolerance (feel extremely hot…sweaty)
Tachycardia (sympathetic system in overdrive)
Cardiac dysrhythmias: A-fib [heart failure in older adults]
Hypertension (sympathetic system in overdrive)
Diarrhea (GI system working harder and faster)
Skin smooth (from increased blood flow)
Fine, soft hair/ hair loss
Enlarged thyroid (warm on palpation)
Warm skin, sweaty palms
Brisk/Hyper reflexes
Fine tremor
Irregular menstruation/hypomenorrhea in women
Personality changes/Emotional instability: irritable, moody, insomnia, anxiety, fatigue
hyperthyroidism diagnostic evaluation
History
Physical Examination
Thyroid Function Tests
Increased T3 and T4
Decreased TSH in primary hyperthyroidism [increased TH increased negative feedback on the pituitary]
Increased TSH in secondary hyperthyroidism [over secretion by pituitary]
Radioactive iodine uptake test (sometimes)
thyroid gland assessment
Supply the person with a glass of water, and first inspect the neck as the person takes a sip and swallows. Posterior approach-palpation Anterior approach-palpation Auscultate the thyroid Auscultate for the presence of a bruit
graves disease
Caused by production of IgG antibodies against thyrotropin receptor on pituitary gland—bind and activate receptor leading to autonomous production of thyroid hormones Less common in children: usually occurs between 6 - 15 years more common in girls than boys Mothers with Graves’ can pass certain antibodies to babies –neonatal Familial association Autoimmune disorder Autoantibodies bind to TSH receptors in thyroid [act like TSH] and stimulate thyroid to release thyroid hormone Characteristic presentations: Ophthalmopathy Pretibial myxedema Goiter Graves' dermopathy (rarely) May have other autoimmune disorders most common cause of hyperthyroidism
goiter
Indicates a condition causing the thyroid gland to grow abnormally
Occurs with over or under production of thyroid hormones [hypo or hyper- thyroidism]
Results from excess TSH stimulation which causes thyroid gland to increase in size and produce more TH: such as when the amount of circulating TH is deficient, abnormal growth stimulating immunoglobulins, or substances that inhibit TH synthesis.
Toxic Multinodular Goiter
Gene mutations to TSH receptor causing continuous thyroid activation
Nodules in the thyroid gland cause thyroid enlargement – increased secretion of TH
thyroid storm (thyrotoxic crisis)
Acute, life-threatening
Occurs with poorly controlled hyperthyroidism
Precipitated by infection, surgery, radio-iodine therapy, withdrawal from an anti-thyroid medications
manipulation of the thyroid gland during surgery and the release of thyroid hormone into the bloodstream.
Clinical Manifestations:
Hyperthermia, tachycardia, heart failure, tremor, extreme agitation, delirium, nausea, vomiting, diarrhea, dehydration, coma
pathologies of the adrenal glands
Cushing’s Syndrome – Hypercorticolism
Addison – Hypocorticolism
Hyperaldosteronism
Hypoaldosteronism
cortisol
Secreted by Cortex of Adrenal Gland
Glucocorticoid Steroid hormone
Controls stress/stimuli response, blood glucose levels, inflammatory responses and blood pressure
When secreted in response to stress/stimuli:
Increases heart rate blood pressure, blood glucose, respiration , muscle tension
Temporarily shuts down digestion and reproduction
Facilitates control of blood sugar – acts on liver, muscle, adipose tissue, pancreas
Increased cortisol increases gluconeogenesis to increase production of glucose – body’s need for energy
Regulates metabolism
Facilitates reduction of inflammation
Supports memory formulation
Facilitates salt and water balance and BP control
Cortisol Secretion: Hypothalamic-Pituitary-Adrenal [HPA] axis
Cortisol secretion by the adrenal cortex is stimulated by adrenocorticotropic hormone (ACTH) produced by pituitary which is stimulated by corticotropin releasing hormone (CRH) by the hypothalamus
Negative feedback system – presence of cortisol inhibits production of corticotrophin-releasing hormone (CRH) by the hypothalamus and adrenocorticotrophic hormone (ACTH) by the pituitary
The HPA axis maintains an unstressed circadian rhythm of cortisol release: ACTH and cortisol [responsive to ACTH] are released just before awakening and decline through the day
Stressors/Stimuli stimulate hypothalamus to initiate the HPA axis – stimulating increase in cortisol levels during stress (i.e. surgery, burns, anxiety, fever, psychoses, hypoglycemia)
hypercortisolism
Cortisol affects: Arousal, cognition, mood, sleep, metabolism, maintenance of cardiac tone, growth and reproduction
Chronic stress leads to constant secretion of cortisol - Chronic dysregulation of the HPA axis – linked to obesity, infections, insomnia, irritability, depression, fat deposition, loss of bone and muscle
Cushing’s Syndrome: Pathological elevation of cortisol - Hypercortisolism
Causes:
Long-term treatment with steroids
Primary — over-secretion by adrenal glands
Over-stimulation of adrenal glands by an ACTH-secreting tumor in the pituitary – Cushing Disease
Over-stimulation of adrenal glands by an ectopic ACTH producing tumor – most commonly small cell lung cancer
cushing disease vs syndrome
Cushing Disease
Form of Cushing Syndrome
Excessive anterior pituitary secretion of adrenocorticotropic hormone (ACTH)
Cushing Syndrome
Disorder of high levels of cortisol
Excessive circulating free cortisol, regardless of cause
May be caused by excessive or prolonged steroid therapy
The condition is reversible once steroids are discontinued
Abrupt withdrawal of steroids may precipitate acute adrenal insufficiency
assessment for cushing syndrome
Weight gain (accumulation of adipose in trunk, face and cervical areas) ‘moon face’
Muscle wasting (from catabolic effects of cortisol on periphery)—leads to muscle weakness, osteoporosis
Loss of collagen, weakened integumentary
Purple striae on trunk
Brownish hyperpigmentation of skin, mucous membranes and hair from ++ACTH
Vascular sensitivity leads to hypertension and vasoconstriction
Alterations in mental status- irritability to depression and schizophrenia
cushing syndrome diagnostic tests
Late –Night Salivary Cortisol 24-hour urine free cortisol Low-dose Dexamethasone Suppression Test Adrenal CT for tumour Pituitary MRI for tumour Serum ACTH
Additional tests for complications can include:
Hyperglycemia
Glycosuria
Hypokalemia
Adrenal Insufficiency–Hypocortisolism
Primary (Addison’s Disease): Pathology of one or both adrenal glands
Cortisol and Aldosterone secretion affected
Secondary: Lack of ACTH stimulation from the pituitary
Cortisol secretion affected
Tertiary: lack of CRH from the hypothalamus
Cortisol secretion affected
addison’s disease
1-2 per 100,000
Affects men and women alike
Occurs in all age groups including children
Most are the result of idiopathic atrophy of adrenal cortex:
Autoimmune mechanisms that destroy adrenocortical cells
Remaining cases are the result of adrenal gland destruction by tumor, granuloma, hemorrhage, inflammatory necrosis, or medications
90% of adrenocortical tissue destroyed before signs
addison’s disease assessment
Early symptoms Weakness, severe fatigue Hyperpigmentation of skin Orthostatic hypotension Anorexia/decreased appetite Nausea vomiting and abdominal pain; diarrhea Salt cravings Vitiligo Muscle or joint pains Later stages Weight loss Hypotension Dehydration Hypoglycemia
addisonian crisis or adrenal crisis
Life-threatening — acute adrenal insufficiency – acute lack of glucocorticoids or mineralocorticoids
Precipitated by stress such as infection, trauma, surgery, MI, dehydration, exposure to cold/burns, overexertion, or abrupt withdrawal of exogenous corticosteroid use or adrenal or pituitary injury
Characterized by extreme weakness, severe pain in abdomen, lower back or legs, peripheral vascular collapse, renal shutdown
Fever or low body temperature
Shock
Include hyponatremia, hyperkalemia, hypoglycemia, and hypotension
addison’s disease diagnostic evaluation
Decreased serum and urine levels of cortisol
ACTH stimulation test to confirm Addison’s disease
Decreased aldosterone
Increased ACTH
Increased BUN
Serum glucose low
Adrenal antibodies test
Potassium increased
Abdominal CT – adrenal gland size
Pituitary MRI – secondary adrenal insufficiency
Diabetes: Microvascular Chronic Complications
Complications affecting small vessels
Characterized by thickening of capillary basement membrane leading to vessel dysfunction and alterations in tissue perfusion and impacting microcirculation of organ/system
Neuropathy – nerves
Retinopathy – eyes
Nephropathy – kidneys
Complications affecting the large vessels
Characterized by atherosclerosis of large vessels leading to:
Coronary artery disease – MIs
Transient ischemic attacks (TIAs) and Strokes
Peripheral arterial disease
diabetes complications: immune dysfunction
Hyperglycemic affect weakens cellular immunity
Increased susceptibility to bacterial and fungal infections
Compounded by neuropathy, reduced blood flow to extremities, slow healing, unawareness of injury
Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
Hypersecretion of ADH without “appropriate” stimuli
Stimulated by hypothalamus or from ectopic source
Causes:
Most common cause are ectopic production of ADH by tumors in the body
Pulmonary diseases such as Pneumonia, TB, asthma, CF, and respiratory failure
CNS disorders such as encephalitis, meningitis, intracranial hemorrhage, tumors within the brain, and trauma
Medications such as narcotics, general anesthetics, chemotherapeutic agents, NSAIDS, and synthetic ADH analogs and psychiatric illnesses treated with antidepressants or antipsychotics:
Medications can stimulate ADH release, potentiate effects of ADH, or by unclear mechanism
Other causes: Surgical procedure
pathophysiology of SIADH
Enhanced water reabsorption due to inappropriate secretion and action of ADH
ADH normally stimulates renal collecting ducts to increase permeability for water reabsorption
Characterized by euvolemic hyponatremia with decreased serum osmolality and elevated urine osmolality
Dilutional hyponatremia
Concentrated urine – increased urine sodium
SIADH clinical manifestations
Initial: Serum Na below 135 mmol/L Thirst Impaired taste Loss of appetite, N & V Anorexia Fatigue Low urine output No Edema High levels of ADH Serum Na below 125 mmol/L Confusion, aggression, irritability Drowsiness Lethargy Weakness Muscle cramps Convulsions, seizures Tachycardia Symptoms resolve with correction of hyponatremia
medical diagnosis SIADH
The Schwartz and Bartter Clinical Criterion
Serum sodium less then 135mEq/L
Serum osmolality less then 275 mOsm/kg
Urine sodium greater then 40 mEq/L (due to ADH-mediated free water absorption from renal collecting tubules)
Urine osmolality greater then 100 mOsm/kg
The absence of clinical evidence of volume depletion - normal skin turgor, blood pressure within the reference range
The absence of other causes of hyponatremia - adrenal insufficiency, hypothyroidism, cardiac failure, pituitary insufficiency, renal disease with salt wastage, hepatic disease, drugs that impair renal water excretion
nursing assessment SIADH
Frequent measurement of vitals signs Strict monitoring of Ins and Outs Measurement of urine specific gravity Daily weights Monitor LOC Monitor for signs of hyponatremia such as: Nausea and vomiting. Headache. Confusion. Loss of energy, drowsiness and fatigue. Restlessness and irritability. Muscle weakness, spasms or cramps. Seizures. Coma. Monitor of heart and lung sounds
diabetes insipidus
Decrease of ADH secretion or decrease of ADH’s action
Leads to dilute (hyponatremic) urine and concentrated (hypernatremic) serum
May be transient or chronic lifelong condition
There are three forms:
Neurogenic or Central - insufficient secretion of ADH
Nephrogenic - abnormal response of the renal tubules to ADH
Dipsogenic or primary polydipsia - excessive water intake due to defect in thirst mechanism in hypothalamus
[Gestational—only during pregnancy]
diabetes insipidus pathophysiology
Pathophysiology:
Characterized by passage of large volumes of dilute urine
Decreased ability to concentrate urine
Neurogenic DI – decreased secretion of ADH
Nephrogenic DI – ADH levels normal but kidneys resistant to ADH action
collecting ducts not responsive to ADH stimulation
Both lead to an inability of the kidney to increase permeability to water causing excretion of large volumes of dilute urine, leading to an increase in plasma osmolality (hypernatremia)
Thirst mechanism is stimulated leading to polydipsia
Excessive thirst
diabetes insipidus clinical manifestations
Urine output varies but can increase from normal 1-2 L/day to as much as 3-20 L/day
Urine specific gravity is low: 1.005 or less
Urine osmolality of < 100 mmol/kg with elevated serum osmolality > 295 mmol/kg
Excessive thirst and craving cold drinks
Weakness and nocturia
Most common – Central DI – following trauma or Sx to region of pituitary or hypothalamus – has three patterns: transient, permanent and triphasic
Triphasic pattern:
acute phase (abrupt onset of polyuria 4-5 days)
interphase (urine volume normalizes 5-6 days)
third phase (central DI is permanent)
Severe fluid volume deficit [dehydration] manifested by weight loss, constipation, poor tissue turgor, hypotension, low body temperature, fatigue, kidney damage, tachycardia and shock
CNS manifestations include irritability, and mental dullness to coma related to increasing serum osmolality and hypernatremia
diabetes insipidus nursing assessment
Frequent measurement of vitals signs Strict monitor of Intake and output Measurement of urine specific gravity Daily weights Monitor LOC Monitor for signs of hypernatremia Monitor of heart and lung sounds
