unit 8 Flashcards
(35 cards)
Endocrine Overview
Endocrine Disorders Can Arise When:
- Hormone is secreted to excess
- Hormone deficiency is present
- Target cells for the hormone are dysfunctional
- Hereditary or congenital defects affect endocrine secretions
- Blood supply to and endocrine tissue is affected
- Endocrine tissue has undergone hyperplasia
- Endocrine disorders are most commonly
Endocrine disorders are most commonly caused by tumour in the endocrine tissue:
- Usually begin
- Can be functional (–> oversecretion disorder)
- Can damage endocrine tissues (–> hormone deficiency)
Signs and Symtpoms of an Endocrine Disorder Reflect:
- Physiologic actions of the hormone
- Effects of tumour (if tumour is etiologic agent)
Describe Goitre
- Old french ‘goitron’ (gullet) or latin ‘guttur’ (throat)
- Enlargement of the thyroid gland that may be visible as a swelling in the throat area
- Clinical sign of thyroid gland dysfunction
- Goitre can occur from hypo or hyper thyroidism
Describe Hyposecretion (endemic) Goitre
- Low endemic iodine levels in soil and food
- Cannot have normal T3 and T4 production
Describe Hypersecretion (toxic) Goitre
- Iodine levels are not limited
- Thyroid gland is over stimulated therefore, excessive T3 and T4 production produces toxic effects
- May be due to excessive TSH stimulation ex: by substances as goitrogens
Describe Goitrogens and Goitre
Goitrogens are substances that block T3 and T4 secretion:
–> TSH levels rise –> TSH Causes thyroid hyperplasia (goitre)
Food goitrogens prmote goitre when ingested in large amounts (these act directly on the pituitary and stimulate TSH)
-Cabbage and turnips
Some minerals may also act as goitrogens
-lithium and fluoride
Describe Hyperthyroidism: Graves Disease
RECALL THYROID HAS EVERYTHING TO DO WITH METABOLISM
Often associated with autoimmune pathophysiology:
-autoantibodies stimulates TSH receptors on thyroid gland
Signs and Symptoms associated with Excess T3 and T4:
- Hypermetabolism causes heat intolerance and weight loss in despite increased appetite
- Increased sympathetic activity such as, heart palpitation, tachycardia and hypertension
Grave’s Dx: Exophthalmos
Protruding eyes:
-build up of tissues in orbit pushes eyes outward
Staring, unblinking eyes:
-sympathetic stimulation of eyelid muscle
May cause vision loss
Describe Hyperthyroidism: Thyrotoxicosis
- Also called thyroid storm
- Sudden onset of acute hyperthyroidism
- Usually precipitated by acute adrenalin episode: may be triggered by surgery or infection (ex: stress_
- Life threatening because of acute symptoms such as, hyperthermia, tachycardia, hypertension and heart failure
- Requires immediate tx to prevent death from arrhythmias
Describe Hypothyroidism
- Mild hypothyroidism is common and easily treated
- Signs and symptoms are generally opposite to hyperthyroidism and reflect hypo metabolism and decreased sympathetic activity
- Can result in a small or large thyroid
- Severe hypothyroidism has several manifestations that include hashimoto’s thyroiditis, myxedema and cretinism
Hypothyroidism: Hashimoto’s Thyroiditis
- Autoimmune destruction of thyroid tissue
- Insidious onset (months or years to detection): slow progression to hypothyroidism
- Affects between 0.1% and 5% of all adults in western countries and is most commonly seen in middle aged women
Hypothyroidism: Myxedema
Severe hypothyroidism in older children or adults
Hypothyroidism: Cretinism
- Severe hypothyroidism during infant or young child development
- Characterized by deficient brain development: T3 and T4 essential for neuronal development
- Formerly common in areas with low endemic iodine (himalayan, inland China, Africa, mountains)
- Other developmental retardation is also evident (T4 and T3 is essential in all cell and tissue metabolism), this can result in decreased feeding (decreased metabolic rate), stunted growth (decreased cellular metabolism), delayed tooth eruption and malocclusion
Adrenal Medulla: Pheochromocytoma
- Located at top of kidneys and is an excessive producion of adrenalin and noradrenalin by adrenal medulla
- Major cause of secondary hypertension
- S/S similar to intense sympathetic stimulation such as hypertension, heart palpitations and diaphoresis
Adrenal Cortex: Cushing’s Syndrome
Excessive glucocorticoid secretion
May be caused by multiple pathologies:
- Adrenal adenoma
- Pituitary adenoma (master/controlling gland of everything, may also release ACTH making excess amounts of cortizol)
- Paraneoplastic syndrome (tumours somewhere else in the body that is secreting abnormal hormones
- Iatrogenic
Paraneoplasti:c Cushing’s
Tumour is another tissue (ex:lungs) that secretes ACTH
Iatrogenic: Cushing’s
Long term chronic glucocorticoid administration:
- Feedback inhibition of ACTH secretion causes adrenal cortex atrophy
- Problematic in times of stress (increased cortisol need)
Cushing Signs and Symptoms
Glucocorticoids have multiple physiological effects
S/S are related to the effects of excessive glucocorticoids (cortisol secretion)
Effects on fat metabolism: redistribution of body fat causes moon face or buffalo hump
Effects on carbohydrates metabolism:
- Diabetes syndrome due to elevated blood glucose levels
- Results from glucose sparing effects of cortisol: gluconeogenesis
Effects of accelerated catabolism (breaking down):
- Fragile skin (due to skin collagen catabolism)
- Stretch marks (from purple striae)
- Osteoporosis ( from bone matrix catabolism)
- Muscle wasting (due to protein catabolism)
- Overall cortisol has catabolic effects
- Adrenal Cortical hormone ‘mimicry’:
- Hypertension (it mimics mineralocorticoid effects causing hypertension)
- Hirsutism (mimics androgenic effects and causes hirsutism)
- Acne (mimics androgenic affects and causes acne)
Other Effects include infection (immune suppression) and reduced stress response
Describe Addison’s Disease and its Etiology
Characterized by hyposecretion of all adrenal cortex hormones:
- Glucocorticoids (cortisol)
- Mineralocorticoids (alderstone)
- Androgens (testosterone)
Etiology:
- Commonly autoimmune reaction
- Infection
- Destructive Tumours
Addison’s Dx: Signs and Symptoms
Reflect glucocorticoids (cortisol) insufficiency:
- Hypoglycaemia (decreased glucose mobilization)
- Poor response to stress (GAS)
- Fatigue, weight loss, infection (decreased glucose mobilization
Reflect Mineralocorticoid (aldosterone) Insufficiency:
- Hypertension (loss of Na+ –> loss of H2O –> Low BV)
- Hypoatremia (reduced blood in Na+)
- Hyperkalemia (increased blood K+)
- Cardiac arrhythmias and failure
- Hyponatremia and hyperkalemia are bad because they lead to cardiac arrhythmias and failure
Reflect Androgen Insufficiency:
-Decreased body hair
Reflect Feedback Increase in ACTH Secretion:
-Hyperpigmentation (elevated ACTH precursor stimulates melanocytes) of the skin an mucosal surface (buccal mucosa)
Describe Diabetes Mellitues
Diabetes mellitus occurs asa result of insulin deficit
- Absolute deficit: loss of insulin production (autoimmune condition that is acting on and preventing the production insulin)
- Relative deficit: impairment of cellular response to insulin
*Increase glucose in the blood
Insulin is an anabolic hormone that
- Promotes formation of glycogen, protein and lipid
- Promotes glucose entry into cells except for the brain and excreting muscles
- Promotes GI absorption of amino acids
- Promotes glucose utilization by cells (including ATP generation)
Diabetes in on the rise in NA, except further increase in as incidence of obesity rises
Two Forms: type 1 and type 2
Type 1 Diabetes
Formerly called insulin dependent diabetes mellitus (IDDM) or juvenile diabetes, it is more common in children and adolescents
More severe form
Most likely to cause serious acute complication
Fundamental abnormality in Type 1 diabetes is autoimmune disorder (T-cell mediated), destruction insulin secreting pancreatic Beta Ce;;s (islets of langerhans) and creates an absolute insulin deficit (not enough insulin)
Clinically managed by insulin replacement therapy
Type 2 Diabetes
Originally called non-insulin dependent diabetes mellitus (NIDDM) or adult onset diabetes. It is usually a disease of over weight adults (although incidence in younger adults is rising)
Fundamental abnormality in Type 2 diabetes in an increased cellular resistance to effects on insulin and creates a relative insulin deficit (insulin present, but cannot act on cells)
Associated abnormalities are decreased insulin production (milk beta cell damage) and increased glucose production by the liver
Clinical management depends upon adjusting insulin need:
- Diet to reduce glucose intake
- Exercise promotes more effective glucose utilization
- Drugs stimulate beta cells to make more insulin
Type 2 is clinically less severe than Type 1, however, both types are associated with long-term complication of diabetes, which are the major causes of morbidity and death from diabetes
Diabetes: Diagnostic Tests
- Fasting blood glucose level
- Glucose tolerance test
- Glycosylated hemoglobin test (best test), it tests clinical and subclinical diabetes, monitors glucose levels over several months. A1C test (gold standard) is sometimes called the hemoglobin A1c, HbA1c, or glycohemoglobin test
Diabetes: Early Pathophysiology
Insulin deficit –> decreased glucose utilization
Hyperglycaemia (to much glucose in the blood):
-Non-utilized glucose accumulates
Glucosuria (glucose in urine):
-Filtered load in kidney exceeds capactiy of renal tubules to reabsorb
Polyuria (including nocturia is an increase in urination at night):
- Urinary glucose causes osmotic diuresis
- Diuresis causes electrolyte loss
Dehydration:
-Renal water loss and osmotic transfer of water from cells to blood
Polydipsia:
-Water loss increases thirst
Polyphagia:
-Cellular starvation increases appetite
