A&P 2 Exam 1 - Endocrine Glands, Functions, Regulation

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45 Terms

1
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Describe how the nervous system functions

  • Communicates through electrical impulses and neurotransmitters

  • Releases neurotransmitters at synapses at specific target cells

  • Effects are local, specific

  • Quickly responds to stimulus

  • Quickly stops response to stimulus

  • Quickly adapts to long-term stimulus

  • FAST

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Describe how the endocrine system functions

  • Communicates through hormones

  • Release hormones into bloodstream for distribution throughout body

  • Effects are general, widespread

  • Slowly responds to stimulus

  • Slowly stops response to stimulus

  • Slowly adapts to long-term stimulus

  • SLOW

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Describe the relationship between the nervous and endocrine system

  • Complementary function

  • Communicate chemically

  • Continually regulate each other

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Releasing hormones (RH)

  • Gland: hypothalamus

  • Type: peptide, water-soluble, membrane receptors

  • Target tissues: anterior pituitary

  • Effects: cause secretion of specific hormones

  • Stimulus: hormonal (regulated by levels of downstream hormones)

  • Regulation: negative feedback from the hormones they ultimately stimulate (thyroid hormone inhibits TRH/TSH release)

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Inhibiting hormones (IH)

  • Gland: hypothalamus

  • Type: peptides or amines, water-soluble, membrane receptors

  • Target tissues: anterior pituitary

  • Effects: inhibit secretion of specific hormones

  • Stimulus: hormonal/neuronal mix (regulated by circulating hormones or neural input like suckling)

  • Regulation: negative feedback (high GH → ↑ GHIH)

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Antidiuretic hormone (ADH)

  • Gland: posterior pituitary

  • Type: peptide, water-soluble, membrane receptor

  • Target tissues: kidneys

  • Effects: increase water content (decrease osmolality), increase blood volume/blood pressure, reduce urine volume/concentration

  • Stimulus: humoral stimulus. high electrolytes (salt), low water, low blood pressure

  • Regulation: negative feedback (enough water = stop releasing ADH = neg. feedback)

<ul><li><p>Gland: posterior pituitary</p></li><li><p>Type: peptide, water-soluble, membrane receptor</p></li><li><p>Target tissues: kidneys</p></li><li><p>Effects: increase water content (decrease osmolality), increase blood volume/blood pressure, <strong>reduce urine volume/concentration</strong></p></li><li><p>Stimulus: <strong>humoral stimulus.</strong> high electrolytes (salt), low water, low blood pressure</p></li><li><p>Regulation: <strong>negative feedback</strong> (enough water = stop releasing ADH = neg. feedback)</p></li></ul><p></p>
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Oxytocin

  • Gland: posterior pituitary

  • Type: peptide, water-soluble, membrane receptors

  • Target tissues: uterus, mammary glands

  • Effects: uterine contractions, milk ejection ("let-down”)

  • Stimulus: neuronal stimulus. uterine stretch, suckling

  • Regulation: positive feedback until event ends (birth, feeding)

<ul><li><p>Gland: posterior pituitary</p></li><li><p>Type: peptide, water-soluble, membrane receptors</p></li><li><p>Target tissues: uterus, mammary glands</p></li><li><p>Effects: uterine contractions, milk ejection ("let-down”)</p></li><li><p>Stimulus: <strong>neuronal stimulus.</strong> uterine stretch, suckling</p></li><li><p>Regulation: <strong>positive feedback</strong> until event ends (birth, feeding)</p></li></ul><p></p>
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Thyroid-stimulating hormone (TSH)

  • Gland: anterior pituitary

  • Type: peptide, water-soluble, membrane receptor

  • Target tissues: thyroid gland

  • Effects: secretion of thyroid hormone

  • Stimulus: hormonal. thyroid RH

  • Regulation: negative feedback (TRH from hypothalamus neg. fb from T3/T4)

<ul><li><p>Gland: anterior pituitary</p></li><li><p>Type: peptide, water-soluble, membrane receptor</p></li><li><p>Target tissues: thyroid gland</p></li><li><p>Effects: secretion of thyroid hormone</p></li><li><p>Stimulus: <strong>hormonal</strong>. thyroid RH</p></li><li><p>Regulation: <strong>negative feedback </strong>(TRH from hypothalamus <strong>→ </strong>neg. fb from T3/T4)</p></li></ul><p></p>
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Growth hormone

  • Gland: anterior pituitary

  • Type: peptide, water-soluble, membrane receptor

  • Target tissues: all tissues

  • Effects: increase protein synthesis, increase fat breakdown, increase glycogen (glucose storage), increases tissue, bone and cartilage growth

  • Stimulus: hormonal. GH-RH, stress, low blood glucose, sleep

  • Regulation: negative feedback (GHRH → negative feedback from IGF-1)

<ul><li><p>Gland: anterior pituitary</p></li><li><p>Type: peptide, water-soluble, membrane receptor</p></li><li><p>Target tissues: all tissues</p></li><li><p>Effects: increase protein synthesis, increase fat breakdown, increase glycogen (glucose storage), increases tissue, bone and cartilage growth</p></li><li><p>Stimulus: <strong>hormonal.</strong> GH-RH, stress, low blood glucose, sleep</p></li><li><p>Regulation: <strong>negative feedback (</strong>GHRH → negative feedback from IGF-1)</p></li></ul><p></p>
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Prolactin

  • Gland: anterior pituitary

  • Type: peptide, water-soluble, membrane receptor

  • Target tissues: mammary glands

  • Effects: increase milk production

  • Stimulus: hormonal. prolactin-releasing hormone (PRH). inhibited by prolactin-inhibiting hormones (PIH)

  • Regulation: negative feedback when milk production not needed

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Adrenocorticotropin hormone

  • Gland: anterior pituitary

  • Type: peptide, water-soluble, membrane receptor

  • Target tissues: adrenal cortex - zona fasciculata

  • Effects: secretion of glucocorticoids (cortisol)

  • Stimulus: hormonal. corticotropin RH

  • Regulation: negative feedback (CRH → negative feedback from cortisol)

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Melatonin

  • Gland: pineal gland

  • Type: amine, water-soluble, membrane receptor

  • Target tissues: brain, eye, cardiovascular system

  • Effects: sleep/wake cycles (promotes sleep)

  • Stimulus: neuronal. decrease in light

  • Regulation: Neural input from retina (light/dark) → negative feedback

<ul><li><p>Gland: pineal gland</p></li><li><p>Type: amine, water-soluble, membrane receptor</p></li><li><p>Target tissues: brain, eye, cardiovascular system</p></li><li><p>Effects: sleep/wake cycles (promotes sleep)</p></li><li><p>Stimulus: <strong>neuronal.</strong> decrease in light</p></li><li><p>Regulation: Neural input from retina (light/dark) → <strong>negative feedback</strong></p></li></ul><p></p>
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Thyroid hormone

  • Gland: thyroid gland - follicular cells

  • Type: amine, lipid-soluble, nuclear receptor

  • Target tissues: most cells

  • Effects: increases metabolism, increases body temperature

  • Stimulus: hormonal. TSH

  • Regulation: negative feedback by T3/T4 levels

<ul><li><p>Gland: thyroid gland - follicular cells</p></li><li><p>Type: amine, lipid-soluble, nuclear receptor</p></li><li><p>Target tissues: most cells</p></li><li><p>Effects: increases metabolism, increases body temperature</p></li><li><p>Stimulus: <strong>hormonal. </strong>TSH</p></li><li><p>Regulation: <strong>negative feedback by</strong> T3/T4 levels</p></li></ul><p></p>
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Calcitonin

  • Gland: thyroid gland - interstitial cells

  • Type: peptide, water-soluble, membrane receptor

  • Target tissues: bone

  • Effects: lowers blood calcium

  • Stimulus: humoral. high blood Ca2+

  • Regulation: negative feedback when blood calcium decreases

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Parathyroid hormone

  • Gland: parathyroid gland

  • Type: peptide, water-soluble, membrane receptor

  • Target tissues: bone, kidney, intestine

  • Effects: increases blood calcium, vitamin D

  • Stimulus: humoral. low blood Ca2+

  • Regulation: negative feedback when blood calcium normalizes

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Aldosterone (mineralocorticoids)

  • Gland: adrenal cortex - zona glomerulosa

  • Type: steroid, lipid-soluble, nuclear receptor

  • Target tissues: kidney

  • Effects: increases sodium reabsorption (reclaim sodium)

  • Stimulus: humoral. low salt, low water, low BP

  • Regulation: negative feedback when blood pressure & electrolyte levels normalize

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Cortisol (glucocoritcoid)

  • Gland: adrenal cortex - zona fasciculata

  • Type: steroid, lipid-soluble, nuclear receptor

  • Target tissues: most cells

  • Effects: increases fat and protein breakdown, increases blood glucose, decreases inflammation

  • Stimulus: hormonal. ACTH, low blood glucose, stress

  • Regulation: negative feedback by cortisol

<ul><li><p>Gland: adrenal cortex - zona fasciculata</p></li><li><p>Type: steroid, lipid-soluble, nuclear receptor</p></li><li><p>Target tissues: most cells</p></li><li><p>Effects: increases fat and protein breakdown, increases blood glucose, decreases inflammation</p></li><li><p>Stimulus: <strong>hormonal. </strong>ACTH, low blood glucose, stress</p></li><li><p>Regulation: <strong>negative feedback</strong> by cortisol</p></li></ul><p></p>
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Androgens

  • Gland: adrenal cortex - zona reticularis

  • Type: steroid, lipid-soluble, nuclear receptor

  • Target tissues: many tissues

  • Effects: stimulate cell growth and differentiation in target tissues, produce gender-related differences in skeleton and secondary sexual characteristics

  • Stimulus: hormonal. ACTH

  • Regulation: negative feedback by downstream sex hormones

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Epinephrine & norepinephrine

  • Gland: adrenal medulla

  • Type: amine, water-soluble, membrane receptor

  • Target tissues: heart, adipose, skeletal muscle, liver, blood vessels

  • Effects: increases blood glucose, increase fat breakdown, increase blood flow to heart and skeletal muscle, decrease blood flow to skin, urinary and digestive systems, increase blood pressure

  • Stimulus: neuronal (sympathetic nervous system). physical activity, low blood glucose

  • Regulation: short-term termination when stimulus removed

<ul><li><p>Gland: adrenal medulla</p></li><li><p>Type: amine, water-soluble, membrane receptor</p></li><li><p>Target tissues: heart, adipose, skeletal muscle, liver, blood vessels</p></li><li><p>Effects: increases blood glucose, increase fat breakdown, increase blood flow to heart and skeletal muscle, decrease blood flow to skin, urinary and digestive systems, increase blood pressure</p></li><li><p>Stimulus: <strong>neuronal </strong>(sympathetic nervous system). physical activity, low blood glucose</p></li><li><p>Regulation: <strong>short-term termination </strong>when stimulus removed</p></li></ul><p></p>
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Insulin

  • Gland: pancreatic β cells

  • Type: peptide, water-soluble, membrane receptor

  • Target tissues: most cells

  • Effects: lowers blood glucose (increasing glucose uptake), increase lipid and glycogen storage

  • Stimulus: humoral. high blood glucose

  • Regulation: negative feedback when blood glucose normalizes

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Glucagon

  • Gland: pancreatic α cells

  • Type: peptide, water-soluble, membrane receptor

  • Target tissues: liver, adipose, skeletal muscle

  • Effects: increase lipid metabolism, increase blood glucose

    • gluconeogenesis (glucose synthesis)

    • glycogen breakdown

  • Stimulus: humoral. low blood glucose

  • Regulation: negative feedback when blood glucose normalizes

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List the steps of thyroid hormone synthesis

  1. Iodide ions enter the follicle cell from the blood. This is controlled by a TSH-sensitive ion pump

  2. Thyroid peroxidase oxidizes iodide (I-) into iodine (I0)

  3. Iodine and thyroglobin enter colloid and iodine is bonded to tyrosines on thryoglobin

  4. Thyroglobin is endocytosed from colloid

  5. Thyroglobin is broken down in the lysosome. Other free amino acids are recycled

  6. Released thyroid hormones (T3 and T4) diffuse across membrane into blood

  7. Thyroid hormones bind to transport proteins

<ol><li><p>Iodide ions enter the follicle cell from the blood. This is controlled by a TSH-sensitive ion pump</p></li><li><p>Thyroid peroxidase oxidizes iodide (I<sup>-</sup>) into iodine (I<sup>0</sup>)</p></li><li><p>Iodine and thyroglobin enter colloid and iodine is bonded to tyrosines on thryoglobin</p></li><li><p>Thyroglobin is endocytosed from colloid</p></li><li><p>Thyroglobin is broken down in the lysosome. Other free amino acids are recycled</p></li><li><p>Released thyroid hormones (T<sub>3 </sub>and T<sub>4</sub>) diffuse across membrane into blood</p></li><li><p>Thyroid hormones bind to transport proteins</p></li></ol><p></p>
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Explain the importance of the hypothalamus/pituitary axis in regulating hormone homeostasis

  • Hypothalamus is the master control: regulates endocrine and neural activities. Regulates secretions of anterior and posterior pituitary gland, which release hormones that influence other endocrine glands and target tissues. Controls hormone homeostasis via releasing/inhibiting hormones

  • Ex:

    • stress response (HPA axis)

    • TRH → TSH → thyroid hormone → negative feedback

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What are the three types of endocrine reflexes?

Simple endocrine reflex, complex endocrine reflex, neuroendocrine reflexes

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Describe endocrine reflex

  • Involves only one hormone

  • Controls hormone secretion by the heart, pancreas, parathyroid gland, and digestive tract

  • Ex: ADH, insulin

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Describe complex endocrine reflex

  • One or more intermediary steps

  • Two or more hormones

  • Ex: TRH → TSH → TH

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Describe neuroendocrine reflexes

  • Pathways include both neural and endocrine components

  • Ex: sympathetic control of adrenal medulla

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Name the three ways two hormones may interact to influence physiological responses

Antagonistic effects, synergistic effects, permissive effects, integrative

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Describe antagonistic effects

  • Opposing hormones

  • Ex: (calcitonin, PTH) (hyperglycemic vs. hypoglycemic)

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Describe synergistic effects

  • Additive

  • Ex: hyperglycemic, GH, epinephrine, cortisol

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Describe permissive effects

  • One hormone is necessary for another to produce effect

  • Ex: estrogen up-regulates progesterone receptor in uterine lining. Progesterone comes later in cycle and promotes uterine growth and nourishment (glycogen storage)

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Describe integrative

Hormones produce different, but complementary results

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Describe the general stress response (general adaptation syndrome)

  • Stress response, how body responds to stress causing factors

  • Divided into three phases

    • Alarm phase (initial stress producer)

    • Resistance phase (maintain homeostasis)

    • Exhaustion phase (homeostasis broken down)

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Describe the alarm phase

  • Fight or flight; immediate

  • Sympathetic division of ANS system directs this response

  • Energy reserves are mobilized, mainly in the form of glucose

  • Body prepares to deal with the stress-causing factor by “fight or flight” responses (increase energy used)

  • Dominant hormone: epinephrine

<ul><li><p><strong>Fight or flight; immediate</strong></p></li><li><p>Sympathetic division of ANS system directs this response</p></li><li><p>Energy reserves are mobilized, mainly in the form of glucose</p></li><li><p>Body prepares to deal with the stress-causing factor by “fight or flight” responses (increase energy used)</p></li><li><p><strong>Dominant hormone: epinephrine</strong></p></li></ul><p></p>
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Describe the resistance phase

  • If a stress > few hours

  • Maintain for weeks - months

  • Dominant hormone: glucocorticoids (cortisol)

    • Epinephrine, GH, and thyroid hormones

  • Energy demands remain higher than normal

  • Neural tissue has a high demand for energy and requires a reliable supply of glucose

  • Hormones mobilize lipids and amino acids as energy sources to conserve glucose for use by neural tissue

<ul><li><p>If a stress &gt; few hours</p></li><li><p>Maintain for weeks - months</p></li><li><p><strong>Dominant hormone: glucocorticoids (cortisol)</strong></p><ul><li><p><strong>Epinephrine, GH, and thyroid hormones</strong></p></li></ul></li><li><p>Energy demands remain higher than normal</p></li><li><p>Neural tissue has a high demand for energy and requires a reliable supply of glucose</p></li><li><p>Hormones mobilize lipids and amino acids as energy sources to conserve glucose for use by neural tissue</p></li></ul><p></p>
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Describe the exhaustion phase

  • Homeostatic regulation breaks down

  • Unless corrective actions are taken immediately, the failure of one or more organ systems will provide fatal (too much K+ is used)

  • Chronic high aldosterone levels cause in a conservation of Na+ at the expensive of K+

  • As the body’s K+ content decreases, a variety of cells begin to malfunction

  • Underlying problem is the body’s inability to sustain the endocrine and metabolic adjustments of the resistance phase

<ul><li><p><strong>Homeostatic regulation breaks down</strong></p></li><li><p>Unless corrective actions are taken immediately, the failure of one or more organ systems will provide <strong>fatal</strong> (too much K<sup>+</sup> is used)</p></li><li><p><strong>Chronic high aldosterone levels cause in a conservation of Na<sup>+</sup> at the expensive of K<sup>+</sup></strong></p></li><li><p>As the body’s K<sup>+</sup> content decreases, a variety of cells begin to malfunction</p></li><li><p>Underlying problem is the<strong> body’s inability to sustain the endocrine and metabolic adjustments of the resistance phase</strong></p></li></ul><p></p>
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Show the control of blood nutrients during short-term exercise (<1 hour)

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Show the control of blood nutrients during long-term exercise (>1 hour)

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Diabetes insipidus

  • Disfunction: insufficient response to/secretion of ADH

    • Rare

    • Kidneys pass an abnormally large volume of fluid that is insipid (odorless, colorless)

  • Cause:

    • Central DI - ADH (vasopressin) not produced by posterior pituitary

    • Nephrogenic DI - kidneys do not respond to ADH (vasopressin)

  • Symptoms:

    • Constant thirst

    • Frequent urination

    • Normal blood glucose

<ul><li><p>Disfunction: insufficient response to/secretion of ADH</p><ul><li><p>Rare</p></li><li><p>Kidneys pass an abnormally large volume of fluid that is insipid (odorless, colorless)</p></li></ul></li><li><p>Cause:</p><ul><li><p>Central DI - ADH (vasopressin) not produced by posterior pituitary</p></li><li><p>Nephrogenic DI - kidneys do not respond to ADH (vasopressin)</p></li></ul></li><li><p>Symptoms:</p><ul><li><p>Constant thirst</p></li><li><p>Frequent urination</p></li><li><p>Normal blood glucose</p></li></ul></li></ul><p></p>
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Acromegaly

  • Disfunction: excessive GH

  • Cause: anterior pituitary tumor produces excess GH

  • Symptoms:

    • hands and feet larger and swollen

    • bone changes: brow and lower jaw jut out, bridge of nose bigger, space between teeth increases

    • skin becomes thick, coarse, oily

    • sweating and skin odor incrase

    • voice deeper

    • joint aches

    • vision problems

<ul><li><p>Disfunction: excessive GH </p></li><li><p>Cause: anterior pituitary tumor produces excess GH</p></li><li><p>Symptoms:</p><ul><li><p>hands and feet larger and swollen</p></li><li><p>bone changes: brow and lower jaw jut out, bridge of nose bigger, space between teeth increases</p></li><li><p>skin becomes thick, coarse, oily</p></li><li><p>sweating and skin odor incrase</p></li><li><p>voice deeper</p></li><li><p>joint aches</p></li><li><p>vision problems</p></li></ul></li></ul><p></p>
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Hyperthyroidism

  • Excessive TH

  • Grave’s disease: autoimmune disease caused antibody that mimics TSH, leading to overproduction of TH (most common)

  • Anterior pituitary adenoma (tumor): secerets excess TSH (rare)

  • Thyroid tumor/cancer: secretes excess TSH (rare)

  • Symptoms:

    • increased metabolic rate, high body temp

    • weight loss, increased appetite

    • weak skeletal muscles with tremors

    • diarrhea

    • protruding eyes (exophthalmos)

    • hyperactivity, insomnia

    • almost always a goiter

<ul><li><p>Excessive TH</p></li><li><p><strong>Grave’s disease: autoimmune disease caused antibody that mimics TSH, leading to overproduction of TH (most common)</strong></p></li><li><p>Anterior pituitary adenoma (tumor): secerets excess TSH (rare)</p></li><li><p>Thyroid tumor/cancer: secretes excess TSH (rare)</p></li><li><p>Symptoms:</p><ul><li><p>increased metabolic rate, high body temp</p></li><li><p>weight loss, increased appetite</p></li><li><p>weak skeletal muscles with tremors</p></li><li><p>diarrhea</p></li><li><p>protruding eyes (exophthalmos)</p></li><li><p>hyperactivity, insomnia</p></li><li><p>almost always a goiter</p></li></ul></li></ul><p></p>
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Hypothyroidism

  • Underproduction of thyroid hormone

  • Hashimoto’s thyroiditis: autoimmune disease caused by antibody that leads to destruction of thyroid gland (most common)

  • Iodine-deficiency: underproduction of thyroid hormone due to insufficient iodine intake

  • Symptoms:

    • decreased metabolic rate, low body temp

    • weight gain, reduced appetite

    • constipation

    • weak, untoned skeletal muscles

    • swelling of the face and body (myxedema)

    • possible goiter (enlargement of the thyroid gland)

<ul><li><p>Underproduction of thyroid hormone</p></li><li><p><strong>Hashimoto’s thyroiditis: autoimmune disease caused by antibody that leads to destruction of thyroid gland (most common)</strong></p></li><li><p>Iodine-deficiency: underproduction of thyroid hormone due to insufficient iodine intake</p></li><li><p>Symptoms:</p><ul><li><p>decreased metabolic rate, low body temp</p></li><li><p>weight gain, reduced appetite</p></li><li><p>constipation</p></li><li><p>weak, untoned skeletal muscles</p></li><li><p>swelling of the face and body (myxedema)</p></li><li><p>possible goiter (enlargement of the thyroid gland)</p></li></ul></li></ul><p></p>
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Adrenal insufficiency

  • Disfunction: adrenal glands fail to secrete enough cortisol and/or aldosterone

  • Primary: doesn’t produce aldosterone/cortisol

    • Addison’s disease: autoimmune disease destroys adrenal cortex outside to in, most common)

  • Secondary: impairment of anterior pituitary (decreased ACTH) (elsewhere)

  • Tertiary: impairment of the hypothalamus

  • Symptoms:

    • low blood levels of sodium and potassium

    • low blood pressure

    • depressed immune system

    • loss of appetite, nausea, vomiting

    • bronzing of skin due to increased pigmentation

<ul><li><p>Disfunction: adrenal glands fail to secrete enough cortisol and/or aldosterone</p></li><li><p>Primary: doesn’t produce aldosterone/cortisol</p><ul><li><p><strong>Addison’s disease: autoimmune disease destroys adrenal cortex outside to in, most common)</strong></p></li></ul></li><li><p>Secondary: impairment of anterior pituitary (decreased ACTH) (elsewhere)</p></li><li><p>Tertiary: impairment of the hypothalamus</p></li><li><p>Symptoms:</p><ul><li><p>low blood levels of sodium and potassium</p></li><li><p>low blood pressure</p></li><li><p>depressed immune system</p></li><li><p>loss of appetite, nausea, vomiting</p></li><li><p>bronzing of skin due to increased pigmentation</p></li></ul></li></ul><p></p>
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Cushing disease/syndrome

  • Disfunction: excessive amounts of cortisol and/or aldosterone

    • Syndrome: general characteristics of excessive cortisol/aldosterone

      • Exogenous: prolonged use of corticosteroid-like medication (prednisone)

    • Disease: anterior pituitary tumor causing excessive ACTH production

  • Symptoms:

    • high blood glucose levels, leads to diabetes mellitus

    • depressed immune system

    • muscle atrophy and weakness, osteoporosis

    • euphoria and depression

    • face looks swollen and puffy

<ul><li><p>Disfunction: excessive amounts of cortisol and/or aldosterone</p><ul><li><p>Syndrome: general characteristics of excessive cortisol/aldosterone</p><ul><li><p>Exogenous: prolonged use of corticosteroid-like medication (prednisone)</p></li></ul></li><li><p>Disease: anterior pituitary tumor causing excessive ACTH production</p></li></ul></li><li><p>Symptoms:</p><ul><li><p>high blood glucose levels, leads to diabetes mellitus</p></li><li><p>depressed immune system</p></li><li><p>muscle atrophy and weakness, osteoporosis</p></li><li><p>euphoria and depression</p></li><li><p>face looks swollen and puffy</p></li></ul></li></ul><p></p>
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Diabetes mellitus

  • Type 1 - 10% of cases - “juvenile”

    • Autoimmune disorder - antibodies produced that destroys β cells

    • Insulin dependent - injections are required

    • Symptoms:

      • increased thirst and hunger, frequent urination, yeast infections, headache, unexplained weight loss, fatigue and weakness

  • Type 2 - 90% of cases - “Adult”

    • Reduced ability of tissues to respond to insulin

    • Non-insulin dependent

    • Non-pharmaceutical treatments include diet, exercise, & weight loss

    • Symptoms: excessive thirst and hunger, frequent urination, unexplained weight loss, fatigue, genital yeast, headaches

<ul><li><p><strong>Type 1 - 10% of cases - “juvenile”</strong></p><ul><li><p>Autoimmune disorder - antibodies produced that destroys β cells</p></li><li><p>Insulin dependent - injections are required</p></li><li><p>Symptoms:</p><ul><li><p>increased thirst and hunger, frequent urination, yeast infections, headache, unexplained weight loss, fatigue and weakness</p></li></ul></li></ul></li><li><p><strong>Type 2 - 90% of cases - “Adult”</strong></p><ul><li><p>Reduced ability of tissues to respond to insulin</p></li><li><p>Non-insulin dependent</p></li><li><p>Non-pharmaceutical treatments include diet, exercise, &amp; weight loss</p></li><li><p>Symptoms: excessive thirst and hunger, frequent urination, unexplained weight loss, fatigue, genital yeast, headaches</p></li></ul></li></ul><p></p>