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The Endocrine System Flashcards

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1
Q

Endocrine System

A

communication system where cells release messenger substances into blood stream that have actions on specific target tissues

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2
Q

Messagers of the Endocrine System

A

Hormones
Neurohormones
Prostaglandins(Arachadonic Acid Cascade)

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3
Q

Classes of Hormones

A
  1. Protein(peptide) hormones
  2. Amines (neurohormones + thyroxine)
  3. Steroid hormones
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4
Q

Peptide + Amine Hormone Action

cAMP Mechanism

A
  1. Peptide/Amine hormone binds to membrane receptor
  2. activates G protein
  3. activates adenylate cyclase
  4. activates cAMP
  5. activates cAMP dependent Protein Kinases
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5
Q

Peptide + Amine Hormone Action

IP3/DAG Mechanism

A
  1. membrane receptor recieves signalfrom Peptide/Amine hormone
  2. G protein activation
  3. Phospholipase C cleaves PIP2 into IP3 and DAG
  4. Calcium release
  5. cell membrane ion channel alteration
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6
Q

Peptide + Amine Hormone Action

A
  1. cAMP Mechnanism
  2. IP3/DAG Mechanism
  3. Direct membrane Calcium Channel activation
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7
Q

Steroid Hormone action

A

activates cycoplasmic and nucleus receptors, activates genes (transcription, translation), triggers protein synthesis

can activate membrane receptors

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8
Q

Pituitary Gland

Anterior

A

synthesis of releasing factors and growth factors

derived from Rathke’s Pouch(mouth lining), contains blood portal system

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9
Q

Pituitary Gland

Posterior

A

secretes hormones that are stored in the posterior pituitary(ADH, Oxytocin)

derived from brain tissue

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10
Q

ADH

A

anti diuretic hormone,

small peptide (9AA)

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11
Q

ADH Modes of Action

A
  1. water reabsorbtion by DCT, collecting duct of nephron, and action on sweat glands and GI tract
  2. binding to receptors on smooth muscle, stimulating calcium entry and contraction, vasocontriction
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12
Q

Causes for ADH Release

A
  1. Changes is body osmolality (osmoreceptors shrinking-low bp)
  2. Drop in plasma volume (hemorrhage) detects 7-15% change
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13
Q

Diabetes Insipidis

A

not sugar diabetes, large amount of dilute urine produced,

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14
Q

Diabetes Insipidis

Neurogenic cause

A

no ADH release

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15
Q

Diabetes Insipidis

Nephrogenic cause

A

failure of tubules to respond to ADH,

similar to results when consuming alcohol

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16
Q

Oxytocin in Females

A

stimulates uterine contraction, released by milk ejection by mammary glands

does not induce labor naturally, but will trigger contractions if administered

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17
Q

Oxytocin

Function in Males

A

uncertain, but oxytocin levels are high in people who have longtime partners

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18
Q

Anterior Pituitary Cells

A

true endocrine cells, each cell produces their own hormones,

each cell can produce more that one hormone

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19
Q

Anterior Pituitary Regulation

A

Anterior Pituitary hormone release is regulated by hypothalmus regulatory hormones

CRH, GnRH

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20
Q

Anterior Pituitary Hormone

FSH, LH

A

stimulate gonads, Tropic Hormone

Follicle Stimulating hormone and Luteinizing hormone

Tropic Hormone - stimulates other glands

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21
Q

Anterior Pituitary Hormone

TSH

A

stimulates thyroid, Tropic Hormone

Thyroid Stimulating hormone

Tropic Hormone - stimulates other glands

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22
Q

Anterior Pituitary Hormone

ACTH

A

stimulates adrenal cortex, Tropic Hormone

Adrenocorticotropic Hormone

Tropic Hormone - stimulates other glands

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23
Q

Growth Hormone

A

growth of body tissues, shifts body metabolism to anabolic paths, main target is liver,

triggers somatomedin(IGF-1, IGF-2) release from liver

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24
Q

Prolactin

A

induces milk production in mature mammary glands

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25
# Growth Hormone Insulin-like Actions
Muscle: increase AA uptake, protein synthesis (increases muscle mass) Liver: increase protein synthesis ## Footnote storage, increased protein synthesis
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# Growth Homrone Anti-insulin Actions
Muscle: decrease glucose uptake Liver: increase gluconeogenisis Adipose: increase lipolysis, decrease glucose uptake ## Footnote increases plasma glucose
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Bone Somatomedins
increase protein and collagen synthesis, increase cell proliferation ## Footnote linear increase (growth)
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Tissue Somatomedins
increase cell proliferation, increase DNA, RNA, and protein synthesis
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Acromegaly
too much growth hormone
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Growth Hormone System
Hypothalamus 1. increase GHRH 2. Decrease Somatostatin Anterior Pituitary 3. GH release Liver 4. GH stimulates somatomedins 5. inhibit Anterior Pituitary GH release 6. Stimulates somatostatin release by hypothalmus 7. further inhibits GH release
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MSH
no function in humans, secreted by the Intermediate Lobe of Pituitary | melanocyte stimulating hormone ## Footnote oversecretion causes skin bronzing
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Thyroid Gland
metabolic rate regulator, calcium homeostasis, bilobed gland, below larynx, linked at center by isthmus
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Thyroxine
growth, development, and metabolism regulator, causes increased oxygen consumption, ## Footnote causes brown fat thermogenesis
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Glycogenolysis
glycogen breakdown
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Gluconeogenesis
glucose synthesis from fat
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Lypolysis
mobilizes free fatty acids ## Footnote mobilizes stored energy
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Follicular Cells
control the release of Thryoxine Hormone (TH)
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Colloid
Thyroglobulin, protein storage complex for Iodine, T3, T4 synthesis
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Parafollicular Cells
synthesizes Calcitonin, lowers plasma Ca++
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Parathyroid Gland
synthesizes Parathyroid Hormone, increases plasma Ca++, essential for life ## Footnote 4 pea sized glands on the Thyroid surface
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Hormonal Regulation Process
1. TRH from hypothalamus stimlates TSH from ant. pit. 2. active transport of Iodine into follicular cells 3. thyroglobulin synthesis 4. increased production of Thyroxine by colloid 5. increased pinocytosis of T3, T4 6. increased release of T3, T4 by follicular cell into blood ## Footnote is a loop somehow
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# * TH assembly
T4 = DIT + DIT T3 = MIT + DIT | tyrosine iodination
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DIT
diiodotyrosine
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MIT
monoiodotyrosine
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T4
4 iodines, high production, high plamsa concentration, prehormone ## Footnote deiodinated to form T3
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T3
3 iodines, low plasma concentration, biologically active, ## Footnote product of deiodination of T4
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RT3
biologically inactive, product of deiodination
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T3 and T4 in Plasma
they are bound to carrier proteins, inactive when bound ## Footnote Thyroxine Bindng Globulin and Albumin, unbound is active, but there is less unbound so there is always a large reserve for a contant supply if needed
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Hypothyroidism
underactive thyroid state ## Footnote In children: Cretinism In adults: Myxedema
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# Hypothyroidism Causes
1. Iodine Deficiency 2. Hypothalamus problem (decrease TRH) 3. Ant. Pit. problem (decrease in TSH or no response to TRH) 4. Hashimoto's Disease
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Hashimoto's Disease
autoimmune disease, antibodies attack thyroid gland and diminish its output
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# Hypothyroidism Symptoms
1. decreased metabolsm (weight and water gain) 2. decreased HR, SV, CO 3. cold, clammy, lethargic, decreased mental capability 4. depressed nail, bone, and hear growth 5. raspy voice (mucopolysaccharide accumilation in larynx)
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# Hyperthyroidism Symptoms
1. increased metabolism (weight loss, water loss) 2. increased HR, SV, CO 3. increased temp 4. exopthalmos
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# Hyperthyroidism Graves Disease
autoimmune disease whos antibodies resemble TSH and stimulate the thyroid ## Footnote basically no TRH, but high T3 and T4 levels
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# Hyperthyroidism Exopthalmos
swelling of eye muscles and fat, protruding eyes, autoimmune attack ## Footnote common in Graves disease
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# Hyperthyroidism Treatment
drugs that block iodine uptake by follicular cells, drugs that block iodination, destruction of the thyroid gland
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Destruction of the Thyroid Gland
done using surgery or radiation, treatment for hyperthyroidism ## Footnote TH replacement is required after Thyroid removal
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Goiters
enlarged thyroid glands, caused by hyperthyroidism(overstimulation), and hypothyroidism
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Hypothyroid Goiters
due to iodine deficiency, little T3, T4 for inhibition, high TSH stimulates glands
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Where is Calcium located?
99% of body calcium is found in bones(calcium hydroxyapatite), 1% is in plasma
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Plasma Calcium
narrow range of 10mg/dl, 45% is bound to albumin, 10% in phosphate/citrate complexes, 45% free and subject to hormonal control
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Osteoblasts
Calcium deposition on bone(calcitonin)
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Osteoclasts
bone reabsorbtion (Ca++ uptake)(PTH)
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Major Regulators of Body Ca++
1. Parathyroid Homrone (PTH) 2. Calcitonin (calcium regulating) 3. Vitamin D3 (allows calcium to be absorbed in diet)
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Parathyroid Hormone (PTH)
release caused by low plasma Ca++, increases bone reabsorbtion, increased plasma Ca++, increases Ca++ reabsorbtion in PCT, stimulates Vit D3 production
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Body Without PTH
1. low plasma Ca++ increases Na+ permeability 2. causes hyperexcitable nerves 3. leads to hypocalcemic tetany, Trousseau's sign
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Trousseau's Sign
praying mantis arms, thumbs under pointer and middle fingers
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# PTH Estrogen Effects
1. Estrogen decreases PTH release 2. Menopause decreases estrogen and therefore increases PTH 3. Bone reabsorbtion increases 4. Osteoporosis can result ## Footnote treatable with estrogen replacement therapy
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Calcitonin
from Parafollicular "C" cells of thyroid, decreases plasma Ca++, decreases bone reabsorbtion, decreases kidney reabsorbion of Ca++
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Vitamin D
allows Ca++ uptake by intestines, stimulate Ca++ reabsorbtion in kidneys, shuts down PTH release | 1,25 dihydroxycholecalciferol
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Vitamin D3 Synthesis
1. Synthesized with sunlight from dehydrocholesterol 2. in the liver, Vit D converted to 25 hydroxycholecalciferol 3. in the kidney, converted to 1,25 dihydroxycholecalciferol
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Body without Vitamin D3
poor intestinal Ca++ reabsorbtion, rickets or osteomalacia
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Osteomalacia
softening of bones due to lack of vitmain D
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Islets of Langerhans
endocrine Pancreas cells, A, B, D, F cells
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# Islets of Langerhans Alpha cells
glucagon, increases plasma glucose, catabolic ## Footnote body tissue breakdown
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# Islets of Langerhans Beta cells
insulin, decrease in plasma glucose, anabolic ## Footnote body tissue buildup
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# Islets of Langerhans Delta cells
somatostatin, inhibits A, B, and F cells
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F cell
amylin, slows gastric emptying, slows nutrient absorbtion, slows post-prandial glucose spike ## Footnote promotes satiety in concert with insulin
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# Liver Endocrine Functions
stores glucose, generates glucose through action of glucose 6 phosphate
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Insulin structure
produced by B cells, short arm of chromosome 11, 5 minute half life, broken down by insulin protease in liver or kidney ## Footnote proinsulin C chain is used to assay B cell funciton when exogenous insulin is administered
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Insulin Function
1. increased transport of glucose, AA, and K+ into insulin sensitive tissues, 2. synthesis of glycogen synthase 3. stimulation of protein synthesis 4. increases lipogenic enzymes 5. inhibits protein breakdown 6. inhibits gluconeogenic enzymes
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Insulin Sensitive Tissues
muscle, fat, liver
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Insulin Modes of Action
1. Tyrosine Kinase Receptor signal pathway 2. Adds GLUT transporters to cell membrane
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GLUT receptors
7 different types, allow for glucose to enter a cell
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GLUT 4
most important for insulin action, found in muscle, heart and adipose tissue
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GLUT 1, 3
found in brain, not insulin dependent
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GLUT 2
found in liver, not insulin dependent
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Diabetes Mellitus
sweet urine, lack of or inneffective use of insulin, | "sugar diabetes"
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Diabetes Mellitus Symptoms
Polyurea Polydipsea Polyphagia
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Experimental Causes of Diabetes Mellitus
1. Pancreatectomy (removal of part of or entire pancreas) 2. Streptozocin (B cell toxin, kills B cells)
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Normal Blood Glucose
resting at 80 mg/dl peak between 150-180 mg/dl
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Diabetic Blood Glucose
resting above 120 mg/dl peak above 200 mg/dl
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Type 1 Diabetes
body does not produce insulin, observed in young ages, no strong genetic link, 10% of diabetics, caused by antibodies destroying B cells, triggered by viral infections ## Footnote treated with insulin
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Untreated Type 1 Diabetes
high BG, body burns fats and proteins, ketoacidosis, ## Footnote acid + dehydration leads to coma and death
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Hyperglycemic Coma
acid + dehydration leading to coma, caused by high BG
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Insulin Shock
patient administed insulin without eating, results in Hypoglycemic Coma, glucose cures
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Type 2 Diabetes
usually ages 35+, obesity component, genetic component, peripheral tissues (muscle, liver, fat) becomes insulin resistant, reduced insulin output by B cells
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Type 2 Diabetes Treatment
low cal + low fat diet, exercise, Sulfonylurea drugs
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Sulfonylurea Drugs
1. depolarize B cells, 2. elevate intracellular Ca++, 3. enhance insulin release by B cells
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HbA1C or A1C test
tests for glycated hemoglobin, long term average for blood sugar levels ## Footnote Normal Person - 5% Diabetic Target - 7% Diabetic Uncontrolled - 25%
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Metformins
enhances insulin sensitivity in peripheral tissues(muscles, liver, fat), suppresses gluconeogenesis by liver
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GLP-1 | Glucagon Like Peptide
enhances insulin output by Beta cells when used with sulfonylurea drugs, suppresses glucagon release and slows gastric emptying
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GLP -1 + GIP
enhance insulin secretion, reduce glucagon levels, delay gastic emptying, decrease food intake, discourages alchohol use | gives a greater feeling of satiety ## Footnote marketed as a weight loss drug
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SLGT2 Inhibitors
blocks glucose reabsorbion in the PCT, excretes more glucose in urine ## Footnote lowers HbA1C, can lead to UTIs, Type 2 Diabetics Only
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Insulin Pumps
deliver various forms of insulin with a computer programmable pump ## Footnote pump can change insulin levels with regards to diet, exercise, and time of day
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Artificial Pancreas
pump delivery of insulin and glucagon, manages blood glucose in real time
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Stem Cell Treatments for Diabetes
pancreatic stem cells injected or transplanted to make a new pancreas ## Footnote not approved in the US
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BMI Formula's
mass in Kg/height in m squared 703 x weight in lbs/height in inches squared
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Potentially Underweight BMI
18-19
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Healthy BMI
20-24
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Overweight BMI
25-29 | 55% of Americans ## Footnote increased risk of diabetes, stroke, heart disease, and cancer when over 27
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Clinically Obese BMI
30+ ## Footnote even greater risk for medical conditions
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Orexins
compounds released by Hypothalmus in response to low BG, increases appetite
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Adrenal Gland
made of the cortex and medulla
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Adrenal Gland Cortex
produces mineralocorticoids, glucocortoroids, and sex steroid hormones
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Adrenal Gland Medulla
extension of sympathetic nervous system ## Footnote epinephrine and norepinephrine production/release
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Regulation and Secretory Control of Adrenal Cortex
1. CRH release from hypothalmus 2. stimulates ACTH release from pituitary 3. stimulates secretion of hormones from adrenal cortex (cortisols and androgens) 4. adrenal hormones provide negative feedback to hypothalmus and anterior pituitary to shut down ACTH production
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3 Zones of the Adrenal Cortex
1. Zona Glomerulosa 2. Zona Fasiculata 3. Zona Reticularis
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# Adrenal Cortex Zona Glomerulosa
produces aldosterone, a mineralocorticoid ## Footnote causes body to retain water
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# Adrenal Cortex Zona Fasiculata
produces glucocorticoids and cortisol compounds
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cortisol effects
1. immune system inhibition 2. decrease in muscle, bone, and connective tissue mass 3. glycogenolysis, gluconeogenesis, FFA release 4. increase BP 5. increase GFR ## Footnote useful as anti-inflammatory and anti-rejection drugs
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Zona Reticularis
produces androgens and sex hormone precursors
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Cushing's Syndrome
Excessive Cortisol Production leading to: 1. muscle atrophy 2. osteoporosis 3. thin skin w/visible blood vessels 4. accumulation of fat in the abdomen 5. capillary rupture and striae
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Addisons Disease
Lack of Adrenocortical Function leading to: 1. anorexia, fatigue, hypoglycemia 2. poor stress tolerance 3. lack of negative feedback from adrenal hormones on pituitary 4. 3 causes hypersecretion of ACTH 5. 4 stimulates melanocytes causes localized dark pigmentation on the body
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Conn's Syndrome | Primary Hyperaldosteronism
adrenal tumor or hypersecretion of aldosterone from Zona Glomerulosa results in elevated BP and K+ depletion and muscle weakness
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Androgenital Syndrome
excessive output of androgens causes masulization of the female body, can cause ambiguous genital development in infants
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