Unit 2: Endocrinology Flashcards

1
Q

Calcium Importance

A
  • Building bones
  • Blood clotting
  • Muscle contraction
  • Heart function

Is typically poorly absorbed by the intestinal tract, unlike phosphate.

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2
Q

Vitamin D Effect on Gastrointestinal Tract

A
  • increases absorption
  • important to bone deposition and reabsorption; must be converted to 1,25-hydroxycholecalciferol in the kidney to be effective
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3
Q

PTH and Vitamin D

A
  • PTH is needed to prouduce 1,25-hydroxycholecalciferol formation
  • in high plasma calcium, formation is down regulated
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4
Q

1,25-hydroxycholecalciferol

A
  • increases calcium absorption in intestines; increasing calcium binding protein, a Ca/ATPase pump in the intestinal epithelial cells
  • transports calcium into the cell cytoplasm from the intestine, moves through the basolateral membrane of the cell by facilitated diffusion to be taken up by the blood
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5
Q

Plasma Calcium Regulation

A
  • regulated within a narrow range
  • 1.0mM combines with the plasma proteins and does not diffuse through the capillary
  • 0.2mM is diffusible, non-ionized calcium
  • 1.2mM is ionized and diffusible
  • increasing or decreasing calcium has significant effects on the body, associated with hormone levels
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6
Q

Hypocalcemia

A
  • results in spontaneous action potentials in peripheral nerves to muscles because of neuronal membrane permeability to sodium ions increases, allowing easy initiation of action potentials
  • low extracellular calcium allows influx of sodium ions through challenge, depolarizing the cell causing muscle twitch
  • at twitching 50% of normal, tetany will develop
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7
Q

Hypercalcemia

A
  • results in a depressed nervous system causing slow reflexes and heart rate, eventually the heart will stop in the contraction phase
  • heart slowing is due to the prolongation of the plateau phase of the action potential, delayed repolarization so the heart cannot maintain normal rhythm
  • high calcium levels in the brain also prevent repolarization, similar to the heart
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8
Q

Effects of Calcium Regulation Hormones

A
  1. PTH: calcium reabsorption and inhibiting phosphate reabsorption in the kidneys, bone resorption to the blood
  2. Vitamin D: Absorption of calcium and phosphate in the intestine, calcium and phosphate reabsorption in the kidney, bone resorption to the blood
  3. Calcitonin: inhibits calcium and phosphate reabsorption in the kidneys, bone deposition from the blood
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9
Q

PTH

A
  • absorption of calcium from the bones to increase plasma calcium concentration
  • decreases plasma phosphate levels, by reabsorption of phosphate from the bones and promote phosphate excretion from the kidneys
  • action is slow, promoting the production of osteoclasts by the bone marrow; maintain homeostasis with osteoblasts
  • may cause OSTEOLYSIS; rapid bone removal destroying the bone
  • increases rate of reabsorption of magnesium and hydrogen ions and decreases reabsorption of sodium, potassium, and amino acids by inhibiting transport mechanisms
  • increases 1,25-hydroxycholecalciferol; which also increases bone resorption by increasing calcium transport through cellular membranes
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10
Q

Control of PTH

A
  • decrease in extracellular calcium stimulates parathyroid gland to increase hormone secretion
  • if there is a deficiency of calcium, the gland will undergo hypertrophy
  • excess extracellular calcium is due to excess calcium or vitamin D3 in the diet or by bone reabsorption, decreases parathyroid secretion; hypertrophy in glands
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11
Q

Calcitonin

A
  • opposite effects of PTH
  • decreases absorptive activity of osteoclasts; favors osteoblasts reducing plasma calcium concentration
  • not as important as PTH in calcium regulation; removal of the hormone has little effect
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12
Q

Control of Calcitonin

A
  • release is stimulated by increasing in plasma calcium; working more rapidly than PTH
  • calcium feedback mechanism acts mostly in short term, is not activated by elevated calcium levels after a milk meal
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13
Q

Hypoparathyroidism

A
  • parathyroid glands do not secrets sufficient PTH, decreasing calcium reabsorption from the bones and plasma calcium concentration
  • does not decrease bone strength, if not treated could result in tetany
  • parathyroid replacement therapy is usually not practical because of cost, and the production of antibodies
  • large doses of vitamin D and calcium intake maintain healthy calcium range
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14
Q

Hyperparathyroidism

A
  • the parathyroid glands produce an excess of hormone increasing calcium levels, typically caused by a tumor
  • in mild cases, bone can be deposited rapidly enough to compensate for the increases osteoclastic activity
  • common to lead to kidney stones due to excess calcium and phosphate levels
  • severe cases, osteoclastic activity overpowers osteoblastic activity, weakening bones leading to breaks
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15
Q

Rickets

A
  • due to a calcium or phosphate deficiency based on lack of vitamin F in the diet; slightly depressing plasma calcium levels as PTH prevents calcium levels from falling by promoting bone absorption
  • phosphate levels are greatly depressed, without regulatory system for prevention
  • primarily in children
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16
Q

Adult Rickets

A
  • deficiency of vitamin D and calcium occurs as a failure to absorb fat
  • vitamin D is fat soluble and calcium tends to form insoluble soaps with fat, both are lost in feces
  • can be caused by excess intake of castor oil or a laxative favorited by some of the elderly
  • “renal rickets” results from prolonged kidney damages, fails to produce the active form of vitamin D, 1,25-hydroxycholecalciferol
17
Q

Osteoporosis

A
  • diminished organic bone matrix rather than abnormal bone calcification; osteoblastic activity is less than normal, depressing bone deposition rate
  • typical causes; lack of physical stress on bones, malnutrition so insufficient protein for matrix, lacking vitamin C needed for intercellular secretion, post menopausal lack of estrogen secretion (osteoblast stimulating activity), old age growth factors feminism decreasing protein anabolic function, cushing’s disease where large amounts of glucocorticoids cause decreased deposition of protein throughout the body, increases protein catabolism, decrease osteoblastic activity
18
Q

Adrenal Cortex Hormones

A
  • secretes corticosteroids; synthesized from cholesterol
  • mineralocorticoids (aldosterone); regulate sodium and potassium balanced, produced by the zona glomerulosa
  • glucocorticoids (cortisol); regulate glucose metabolism, produces by the zona fasciculata
  • androgens; weak androgens like DHEA that supplement sex steroids produced by the gonads, produced by the zona reticularis
19
Q

Aldosterone

A
  • promotes sodium absorption and potassium secretion in the nephron
  • potassium is regulated in narrow limits; ion is freely filtered at the glomerulus and is basically all reabsorbed
20
Q

Control of Aldosterone

A
  • increase in potassium concentration of extracellular fluid; small change causes large response
  • renin-angiotensin system; activated by reduction in blood flow to the kidney from reduced BV, angiotensin II stimulates aldosterone release increase king sodium and water absorption
  • decrease in sodium ion concentration in extracellular fluid; weak result
  • adrenocorticotropic hormone; effect is small, absence can greatly reduce aldosterone secretion
21
Q

Adrenal Medulla Hormones

A
  • secrete catecholamines adrenaline and noradrenaline
  • stimulate the sympathetic nervous system with longer effects; increase CO and HR, filet blood vessels, increase mental alertness, elevate metabolism, increase blood glucose and glucose release from the liver increasing glycolysis in liver and muscle
  • supplied by preganglionic sympathetic axons and secretes hormone whenever the sympathetic nervous system is activated
22
Q

Pancreas Hormones

A
  • pancreas consists of the endocrine and exocrine pancreas
  • endocrine secretes hormones to bloodstream; contains alpha cells secreting glucagon, beta cells secreting insulin, and delta cells that secrete somatostatin close to the islets of langerhans
  • exocrine secretes products through a duct to the outside of an epithelial membrane to the external environment; secretes pancreatic juices
  • insulin is the only hormone that effectively lowers blood glucose; glucagon raises blood glucose and somatostatin depressing insulin and glucagon secretion
23
Q

Insulin

A
  • rise in blood glucose after a meal trigger release; causing rapid uptake, storage and use of glucose by tissues except muscles, liver, and adipose tissue
  • binds to receptor on target cell; four subunits, two alpha outside the membrane and two beta in the membrane
  • bind to alpha phosphorylates beta subunits activating synthesis of protein carriers for glucose facilitated diffusion
  • resting muscle fibre is slightly permeable to glucose except in presence of insulin
  • low insulin allows muscles to use fatty acids for gluconeogenesis and energy production
  • in exercise, muscle glucose uptake increases after a large meal from high insulin levels, glucose over fatty acids because flow of fatty acids from adipose tissue is inhibited by insulin
24
Q

Glycogen

A
  • after a meal, if there is no exercise glucose is stored as glycogen for later use as energy in anaerobic exercise; breaks into lactic acid
  • insulin in the liver causes most of absorbed glucose to be stored as glycogen
  • between means, blood glucose falls and liver glycogen is converted to glucose in the blood
  • liver glucose storage is dependent on inhibition of glycogen phosphorylase (splits glycogen to glucose)
  • insulin enhances glucose uptake by the liver by increasing glucokinase (phosphorylates glucose to trap inside liver cells)
  • insulin increase phosphofructokinase and glycogen synthase
25
Q

Movement and Storage of Glucose

A
  • less insulin is produced as blood glucose levels fall and glucagon levels rise; activates glycogen phosphorylase, activated glucose phosphate so glucose can free into the blood stream
  • exceeding amounts of glucose in the liver prompt insulin to promote conversion of excess into fatty acids; where they are packaged as triglycerides in low density lipoproteins to be transported to the adipose tissue
  • insulin stimulates glucose uptake by adipose tissue, to provide the glycerol for deposition of fat
  • brain cells do not require insulin for glucose transport; rely on glucose for energy
26
Q

Insulin Effects of Fat Metabolism

A
  • insulin enhances fat storage in adipose tissues; store fat be increasing glucose usages in more tissue
  • promotes fatty acid synthesis in the liver, fatty acids are released to adipose tissue where insulin inhibits lipase
27
Q

Insulin Effects on Protein Metabolism

A
  • increase active transport of amino acids into cells and initiates ribosomal machinery for mRNA translation
  • increase rate of transcription and protein synthesis
  • in liver, depressed rate of gluconeogenesis by decreasing its enzymes; plasma amino acids are substrates for glucose synthesis but insulin conserves amino acids
  • in deficiencies, protein storage halts increasing protein catabolism and stopping protein synthesis; raises plasma amino acid levels and excess are used for energy or in gluconeogenesis increasing urea in the urine, muscle weakness, and derange organ function
28
Q

Control of Insulin

A
  • blood glucose, blood amino acids, gastrointestinal hormones, glucagon, GH, cortisol and progesterone and estrogen and nerve stimulation to the pancreas will release insulin
  • blood glucose, rapid feedback regulating release
  • increasing blood amino acids with increasing blood glucose stimulate release; Arg and Lys rise with glucose doubles secretion
  • gastrointestinal hormones release before meal is absorbed, small insulin release and regulation of glucose absorbed
  • glucagon, GH and cortisol are important in large amounts; can exhaust islets of langerhans causing diabetes mellitus
  • insulin promotes carbohydrate usage for energy, depressing fat utilization
29
Q

Type I Diabetes, Diabetes Mellitus

A
  • insulin deficiency; autoimmune disease incorporating the lack of insulin produced by the pancreas beta cells
  • associated with heredity, cell damage, abnormal secretion of other hormones
  • elevated blood glucose and glucose in urine; overshooting the max that can be absorbed by the kidney
  • glucose in grind has osmotic effect and water is carried out; causes polyuria and polydipsia, dehydration, blood volume reduction, circulatory shock, loss of body weight, lack of energy, loss of proteins and lack of glucose usage
  • increase acid production, lowering pH to acidosis; acid pulls out sodium ions in kidney excretion, increases respiratory rate and bicarbonate usage to buffer replacement H+
  • could lead to atherosclerosis, infection, diabetic retinopathy, cataracts, hypertension, chronic renal disease
30
Q

Type II Diabetes

A
  • insulin levels are near normal but insulin’s target cells do not respond to insulin
  • may be due to insufficient insulin receptors on target cells or intracellular process after receptor activation; from obesity or overeasting
  • insulin hyporesponsiveness secondary to overeating, can usually be completely reversed if the person reduces their intake
  • exercise increases the number of insulin receptors
31
Q

Hyperinsulinism

A
  • excess insulin can cause blood glucose to fall too low causing insulin shock
  • can result from tumor or overdose of insulin
  • blood sugar falls, increases neuronal activity causing nervousness, trembling, sweating, hallucinations
  • extremely low blood glucose can lead to a coma
  • diabetic coma will have acetone breath and deep breathing
  • insulin shock come will not exhibit those symptoms
32
Q

Glucagon

A
  • secretes by alpha cells of the islets of langerhans when blood glucose falls
  • stimulates gluconeogenesis activating enzyme cascade; in the liver, increases extraction of amino acids from the blood by liver cells making them available for conversion to glucose
  • secreted in hypoglycemia to increase blood glucose
  • secretion increases after a high protein meal and functions like insulin in exhaustive exercise
33
Q

Somatostatin

A
  • secretes by delta cells of the islets of langerhans
  • release stimulates by increase of blood glucose, amino acids, fatty acids, and gastrointestinal hormones (food ingestion)
  • acts locally to depress insulin and glucagon secretion
  • decreases motility of the stomach, duodenum and gallbladder
  • decreases secretion and absorption in the gastrointestinal tract
  • prolongs the availability of ingested nutrients
  • same compound as GHIH
34
Q

Cortisol

A
  • stimulates rate of gluconeogenesis in the liver
  • acts on liver nuclei to activate DNA transcription forming mRNA that leads to the formation of enzymes for gluconeogenesis and mobilized amino acids from muscle to be used
  • moderately decreases rate of glucose usage; high blood glucose
  • reduces protein stores in all cells except liver due to increase catabolism of protein and decreased protein synthesis; low amino transport and RNA formation in muscle and lymphoid tissue
  • in excess, muscles and immunity become weak
  • liver and blood plasma protein are increased
  • increase mobilization of fatty acids from adipose tissue, to use fats as energy; reduced transport of glucose into cells as a-glycerophosphate is limited, and cannot maintain triglycerides in cells
  • shifts metabolism in starvation or prolonged stress
  • increase fatty acid oxidation
  • excess results in excess fat deposition of the chest
35
Q

Control of Cortisol

A
  • all types of stress trigger release
  • almost entirely controlled by ACTH secretes from anterior pituitary; ADH increases ACTH production
  • hypothalamus release corticotropin releasing factors and ADH, enter portal system and carry to anterior pituitary
  • ACTH activated add to cyclades in the cell membrane of andre ivory ical cells; inducted cAMP formation activating cortisol production
  • has direct negative feedback to hypothalamus to decrease CRF and on the anterior pituitary to decrease ACTH
36
Q

Anti-inflammatory Effects of Cortisol

A
  • effective as an anti-inflammatory drug, blocks early stages of inflammation causing rapid resolution of inflammation increasing healing due to:
  • stabilizing lysosomal membranes preventing release of proteolytic enzymes from damaged cells
  • decrease capillary permeability causes by proteolytic enzymes or histamine, preventing leaking of plasma
  • decrease migration of WBC and phagocytosis
  • suppress immune system reducing T-lymphocytes; lessens tissue reaction
  • lowers fever be reducing interleukin-1 from leukocytes, lower body temp reduces vasodilation
  • does not correct the basic disease condition and may be deleterious
37
Q

Cortisol Effects on Allergy

A
  • does not affect basic allergic reaction between antigen and antibody; blocks potentially lethal inflammatory response
  • stops shock or death from anaphylaxis
  • in asthma stops the release of histamine by mast cells
38
Q

Melatonin

A
  • secretes by pineal gland on third ventricle of the brain
  • Regulates the wake-sleep cycle
  • secretion is affected by circadian rhythm, light inhibits secretion
  • helping to time the births of seasonally breeding animals; stimulates pituitary gland axis in short day breeders and inhibits axis in long day breeders
  • excessive production is associated with delayed onset puberty