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116 Cards in this Set
- Front
- Back
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Vasopressin (ADH)
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ADH is released when the body is dehydrated and causes the kidneys to conserve water, thus concentrating the urine and reducing urine volume. Produce by the posterior pituitary. In high concentrations, it also raises blood pressure by inducing moderate vasoconstriction. Released in response to Angiotensin II also.
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ACTH
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Secreted by anterior pituitary; causes prodcution and release of glucocorticoids in adrenal cortex
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TSH
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Secreted by anterior pituitary; causes secretion thyroid hormones; largely made up of IODINE. Negative feedback to keep more TRH and TSH from being synthesized when high levels.
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FSH
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Secreted by anterior pituitary; regulates the development, growth, pubertal maturation, and reproductive processes of the body. FSH and Luteinizing hormone (LH) act synergistically in reproduction
Inhibited by sex steroids (estrogen/progestin) |
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LH
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Secreted by anterior pituitary; In females, an acute rise of LH called the LH surge triggers ovulation and development of the corpus luteum. In males, where LH had also been called interstitial cell-stimulating hormone (ICSH), it stimulates Leydig cell production of testosterone; acts synergistically with FSH.
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GH
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Secreted by anterior pituitary; promotes growth; lipid and carbohydrate metabolism; targets adipose tissue and liver; stimulated by hypothalamic GHRH
DIABETOGENIC effect - decreases amt glucose that can enter cells Causes GIGANTISM during puberty and ACROMEGALY (long limbs) after puberty Sent to liver to produce IGH-1 (insulin-like growth hormone) to stimulate hypothalamus to release more SOMATOSTATIN - negative feedback that decreases GH secretion and inc GHRH secretion |
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PRL
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Secreted by anterior pituitary; secretion of estrogens/progesterone; milk production; targets ovaries & mammary glands
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Oxytocin
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Secreted by posterior pituitary; targets uterus & mammary glands to promote uterine contractions; lactation
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Zona glomerulosa
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OUTERMOST layer of the adrenal cortex; mineralcorticoid production = ALDOSTERONE ("salt" of "salt, sugar, sex")
Recall aldosterone acts on the late DCT to increase H2O resorption for increased blood volume = increased BP |
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Zona fasciculata
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MIDDLE layer of the adrenal cortex; glucocorticoid prodcution = CORTISOL ("sugar' of "salt, sugar, sex")
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Zona reticularis
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INNERMOST layer of adrenal cortex; produces ANDROGENS (DHEA and testosterone-precursor) - "sex" of "salt, sugar, sex"
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Epinephrine / Norepinephrine
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Produce by chromaffin cells of the adrenal MEDULLA; recall derived from tyrosine
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Aldosterone
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Mineralcorticoid produced by adrenal cortex zona glomerulosa;acts mainly on the distal tubules and collecting ducts of the nephron to cause the conservation of sodium, secretion of potassium, increased water retention, and increased blood pressure.
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Calcitonin
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Produced by parafollicular cells of the thyroid; reduces blood Ca2+ and re-constructs bone (inhibits osteoclast activity); opposes PTH action
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PTH
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Produced by chief cells of the parathyroid gland; increases blood Ca2+; indirectly stimulates osteoclast activity and osteoblast activity = bone resorption; opposes calcitonin action
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A1-receptor mechanism
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GPCR that stimulates IP3 (and DAG) production from PIP2 via PLC - leads to INCREASED intracellular Ca2+. Results in SM contraction
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A2-receptor mechanism
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GPCR that inhibits adenylyl cyclase-mediated production of cAMP and also inhibits Ca2+ increase - these inhibitory actions result in SM contraction and inhibition of neurotransmitter release, respectively
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B-1 and B-2 receptor mechanism
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Stimulate adenylyl cyclase to increase cAMP production - heart muscle contraction, SM relaxation and glycogenolysis, etc
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"2 eyes, 2 lungs, 1 heart"
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Mostly B-2 receptors exist in the eyes and lungs, and mostly B-1 receptors exist in the heart
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Nicotinic and muscarinic receptor MOA's
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Nicotinic: opens Na+ and K+ channels = depolarization (this is a UNIQUE MOA! Other receptors manipulate either cAMP or Ca2+)
Muscarinic - increase [IP3] to increase [Ca2+] (note this is the same MOA as alpha-1 receptors!) Nicotinic receptors are ionotropic and muscarinic receptors are metabotropic (use second messengers) |
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Definition of osmolality
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Concentration of total solute in moles/L of water.
A solution with higher osmolality has a higher osmotic pressure and H20 moves by osmosis to the solution w/ higher osmolality |
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Gap junctions are notably absent from ____?
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Skeletal muscle cells
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Tyrosine kinase receptor MOA
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Binding of ligand results in cross-linking of tyrosine kinases and phosphorylation of tyrosine residues (intrinsic phosphorylation) which phosphorylates another receptor w/o this intrinsic phosphorylation
E.g. INSULIN receptor |
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Ca2+ action inside the cell is terminated by 2 processes...
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(1) Dephosphorylation IP3
(2) Pumping Ca2+ out of cell or back into ER/SER using ATP |
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Mechanism of lung inspiration
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1. Diaphragm contracts, lowers, flattens = inc thoracic volume
2. Parasternal and EXTERNAL INTERCOSTAL muscles contract = lateral increase of thoracic volume 3. SCALENES lift the rib cage 4. Inc of thoracic volume decreases pulmonary pressure = air flows into lungs |
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Definition of osmolality
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Concentration of total solute in moles/L of water.
A solution with higher osmolality has a higher osmotic pressure and H20 moves by osmosis to the solution w/ higher osmolality |
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Gap junctions are notably absent from ____?
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Skeletal muscle cells
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Tyrosine kinase receptor MOA
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Binding of ligand results in cross-linking of tyrosine kinases and phosphorylation of tyrosine residues (intrinsic phosphorylation) which phosphorylates another receptor w/o this intrinsic phosphorylation
E.g. INSULIN receptor |
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Ca2+ action inside the cell is terminated by 2 processes...
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(1) Dephosphorylation IP3
(2) Pumping Ca2+ out of cell or back into ER/SER using ATP |
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Mechanism of lung inspiration
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1. Diaphragm contracts, lowers, flattens = inc thoracic volume
2. Parasternal and EXTERNAL INTERCOSTAL muscles contract = lateral increase of thoracic volume 3. SCALENES lift the rib cage 4. Inc of thoracic volume decreases pulmonary pressure = air flows into lungs 4. STERNOCLEIDOMASTOIDS are accessory inspiration muscles |
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Mechanism of lung expiration
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1. This is a passive process - recoil after contraction during inspiration
2. Diaphragm relaxes 4. Decreased lung volume increases pressure in alveoli to higher than atmospheric pressure = air leaves lungs 5. FORCED EXPIRATION involves the INTERNAL INTERCOSTAL and ABDOMINAL muscles |
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Direct lung volume measurements:
(1) Tidal volume (2) Inspiratory reserve volume (3) Expiratory reserve volume (4) Inspiratory capacity (5) Vital capacity |
(1) TV = normal air vol expired OR inspired with each breath
(2) IRV = maximum vol inspiration possible after a TV inspiration (3) ERV = maximum vol of expiration that can be pushed out after TV (4)IC = vol air inhaled during a maximal inspiration; begins at the end of a normal tidal expiration and is approx 3L (5) VC = total lung capacity that can be expired after a maximum inspiration; approx 4.5L; VC is the combo of TV, IRV and ERV! |
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Forced expiratory volume over 1 second (FEV1)
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-How much air can be forced out over 1 sec
-Used medically to determine if lung disease is restrictive or obstructive, compared to the total forced vital capacity (FVC) -Restrictive disease (e.g. TB, sarcoid, histo) shows an ELEVATED (or normal) FEV1/FVC ratio (can force out a lot in 1 sec compared to total capacity since lung expansion is inhibited!) -Obstructive disease (e.g. COPD, emphysema) shows a reduced FEV1/FVC ratio (can't force out enough air after an inspiration due to inelasticity) |
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Lung blood flow is highest at the (base or apex?)
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Base!
Means that gas exchange is highest at the base also |
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The majority of O2/CO2 are in what forms within the body?
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O2 - bound to hemoglobin (98%)
CO2 - bicarbonate (90%) |
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1.The partial pressure of O2 in the environment is (< or >) the partial pressure of CO2 in environment.
2.The partial pressure of O2 is (dec/inc) as it moves through the lungs and the partial pressure of CO2 is (dec/inc) as it moves though the lungs. |
1. PO2 > PCO2 in the environment (PO2 ~160mm Hg or 21% of environment's 760mm Hg; PCO2 is essentially zero)
2. PO2 decreases while PCO2 increases when moving into the body |
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The O2 dissociation curve is sigmoidal in shape b/c....
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O2-binding to hemoglobin is COOPERATIVE - binding of one molecule facilitates binding of others
*Shift of curve to left = Hg more readily binds O2 at a given partial pressure *Shift of curve to right = Hg less readily binds O2 *Factors that shift the curve to the right are: decreased pH, increased temp, increased CO2 levels |
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Carotid body
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The carotid body (carotid glomus or glomus caroticum) is a small cluster of chemoreceptors and supporting cells located near the fork (bifurcation) of the carotid artery (which runs along both sides of the throat).
The carotid body detects changes in the composition of arterial blood flowing through it, mainly the partial PRESSURE OF OXYGEN, but also of carbon dioxide. Furthermore, it is also sensitive to changes in pH and temperature. |
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Aortic body
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In the human heart, the aortic body ("glomus aorticum") is one of several small clusters of chemoreceptors, baroreceptors, and supporting cells located along the aortic arch. It measures changes in blood pressure and the composition of arterial blood flowing past it, including the partial pressures of oxygen and carbon dioxide and pH - SENSITIVE TO H+! The chemoreceptors responsible for sensing changes in blood gases are called glomus cells.
It gives feedback to the medulla oblongata via the afferent branches of the vagus nerve (X). The medulla, in turn, regulates breathing and blood pressure. |
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Respiratory acidosis is caused by (hyper-/hypo-) ventilation and respiratory alkalosis is caused by (hyper-/hypo-) ventilation.
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Acidosis = HYPOventilation (inc dissolved CO2 and plasma H+)
Alkalosis = HYPERventilation (decreased dissolved CO2) |
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1.The partial pressure of O2 in the environment is (< or >) the partial pressure of CO2 in environment.
2.The partial pressure of O2 is (dec/inc) as it moves through the lungs and the partial pressure of CO2 is (dec/inc) as it moves though the lungs. |
1. PO2 > PCO2 in the environment (PO2 ~160mm Hg or 21% of environment's 760mm Hg; PCO2 is essentially zero)
2. PO2 decreases while PCO2 increases when moving into the body |
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The O2 dissociation curve is sigmoidal in shape b/c....
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O2-binding to hemoglobin is COOPERATIVE - binding of one molecule facilitates binding of others
*Shift of curve to left = Hg more readily binds O2 at a given partial pressure *Shift of curve to right = Hg less readily binds O2 *Factors that shift the curve to the right are: decreased pH, increased temp, increased CO2 levels |
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Carotid body
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The carotid body (carotid glomus or glomus caroticum) is a small cluster of chemoreceptors and supporting cells located near the fork (bifurcation) of the carotid artery (which runs along both sides of the throat).
The carotid body detects changes in the composition of arterial blood flowing through it, mainly the partial PRESSURE OF OXYGEN, but also of carbon dioxide. Furthermore, it is also sensitive to changes in pH and temperature. |
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Aortic body
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In the human heart, the aortic body ("glomus aorticum") is one of several small clusters of chemoreceptors, baroreceptors, and supporting cells located along the aortic arch. It measures changes in blood pressure and the composition of arterial blood flowing past it, including the partial pressures of oxygen and carbon dioxide and pH - SENSITIVE TO H+! The chemoreceptors responsible for sensing changes in blood gases are called glomus cells.
It gives feedback to the medulla oblongata via the afferent branches of the vagus nerve (X). The medulla, in turn, regulates breathing and blood pressure. |
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Respiratory acidosis is caused by (hyper-/hypo-) ventilation and respiratory alkalosis is caused by (hyper-/hypo-) ventilation.
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Acidosis = HYPOventilation (inc dissolved CO2 and plasma H+ since CO2 is not being expired-off)
*The kidneys will often compensate for an imbalance - e.g. alkalosis = increased urinary loss of HCO3- Alkalosis = HYPERventilation (decreased dissolved CO2) |
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Blood flow through the heart
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1. Vena cava --> R atrium
2. R atrium-->(tricuspid)---> R ventricle 3. R ventricle -->(pulm artery)-->lungs 4. Lungs-->(pulmonary veins)--> L atrium 5. L atrium --> (mitral valve) --> L ventricle 6. L ventricle --> (aortic valve) --> aorta |
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During systole, the mitral and tricuspid valves (open/close)
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CLOSE
systole = contraction VENTRICLES = QT on EKC this is the first heart sound ("lub") |
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During diastole, the aortic and pulmonary valves (open/close)
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CLOSE
diastole = relaxation ventricles & contraction atria = TR on EKC this is the second heart sound ("dub") |
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Abnormal heart sounds
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S3 = rapid filling of ventricles, as in CHF
S4 = high atrial pressure/stiff ventricles, as in hypertrophic ventricles |
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The (SA/AV) node is the pacemaker of the heart.
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SA
since it self-generates action potentials, unlike the AV (dependent on SA) |
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Ventricular (fast) action potential
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Phase 0: rapid influx Na+ after opening of voltage-gates channels
Phase 1: brief repolarization with opening voltage-gated K+ (quick) and voltage-gated Ca2+ (slow) = K+ eflux and Ca2+ influx Phase 2: Ca2+ and K+ balance when more Ca2+ released from ER causes a plateau Phase 3: Closure all ion channels leads to rapid repolarization Phase 4: resting potential set by K+ current |
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Pacemaker (slow) action potential
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*No phases 1 or 2 in SA or AV nodes
Phase 0: opening of T-type voltage gated Ca2+ channels gives slow conduction velocity used by AV node to prolong transmission to allow for ventricular filling |
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Starling equation
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-Determines fluid mvt across capillary wall
- Basically oncotic pressure difference btwn inside and outside wall MINUS hydrostatic pressure difference |
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Ejection fraction, end-diastolic volume, end-systolic volume, stroke volume, cardiac output
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EF = blood pumped out of a ventricle w/ each beat
EDV = blood w/in ventricle before it contracts ESV = blood left in ventricle after it contracts SV = (EDV - ESV) / EDV *SV is basically the percent of blood that's pumped out of the ventricles *A normal SV is 50% or more - less than this means heart damage due to CHF or MI CO = amount blood ejected from heart per unit time *CO = SV x HR |
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Angiotensin II
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Released when [Cl-] is low (indicates body is not absorbing enough H20)
Most potent vasoconstrictor in the body Increases ADH from post pituitary and aldosterone from adrenal cortex Increases Na+ resorption in DCT and H20 resorption in collecting duct |
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Renin-aldosterone-angiontensin system
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1. Decreased blood flow to kidneys, decrease in blood volume, and increase in [K+] cause juxtaglomerular cells to release renin
2. Converts angiotensinogen to angiotensin 1 3. ACE converts angiotensin 1 to angiotensin 2 4. Angiotensin 2 causes release of aldosterone from adrenals 5. Aldosterone works on kidneys to inc salt and H2O retention = inc blood volume |
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Proximal convoluted tubule
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-"Workhorse" of nephron
- Glucose, amino acids, most HCO3- are absorbed and put back into circulation -Na+/K+ ATPase pump creates gradient where Na+ flows out of nephron; cotransport of Cl-, AA's, glucose -Na+/H+ countertransporter pumps H+ into nephron to make bicarbonate, which is then resorbed -ACETAZOLAMIDE and other CAI's act on the PCT to inhibit resorption of Na+/H20 and bicarbonate |
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Loop of Henle
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-Purpose is to concentrate the urine (set up gradient such that outside loop is hypertonic compared to inside)
-Descending loop highly impermeable to NaCl - ONLY H2O leaves here! -Ascending loop highly permeable to NaCl and actively pumps ions into interstitium, and H2O is NOT ABLE TO FOLLOW -This creates very high ionic concentration at bottom of loop which deters H2O resorption from descending loop (?) -K+ passively follows Na+ as it's pumped out -FUROSEMIDE acts on ascending loop to inhibit Na+/2Cl-/K+ cotransporter and can cause a state of HYPOKALEMIA |
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Distal convoluted tubule
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-Impermeable to water!
-Na+, Cl-, Ca2+ all leave filtrate here -THIAZIDE DIURETICS work on the early DCT to inhibit Na+/Cl- pump -ALDOSTERONE and K-SPARING DIURETICS work on the late DCT |
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Aldosterone's effect on DCT
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-Anti-diuresis
-Secreted from adrenals in response to low blood vol -Allows H2O and Na+ resorption, which causes K+ and H+ concentration in the urine -Causes hypokalemia |
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Collecting duct
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-Receives 8-10 DCT's
-Na/K pump on interstitial side creates gradient for resorption Na (similar to other kidney areas) -Unlike other areas, lumen side has separate channels for Na, K, H2O -K channel favors secretion K into lumen and an H+ channel also favors secretion H+ into lumen --> these are concentrated in the urine |
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Kidneys and RBC's
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-Low PO2 is detected by the kidney
-Kidneys produce erythropoietin! -Kidney damage = anemia possible |
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GnRH
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Gonadotropin-releasing hormone - stim synthesis gonadotropins (FSH and LH)
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Somatostatin
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Inhibitory hypothalamus hormone. Inhibits release of GH.
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Prolactin inhibiting factor
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Inhibitory hypothalams hormone - inhibits release of PRL; opposing action to TRH
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TRH
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Thyroid releasing hormone - from hypothalamus, stimulates release TSH and PRL; opposing action to prolactin-inhibiting factor
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Corticotropic releasing hormone (CRH)
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Hypothalamus hormone that stimulates release ACTH from anterior pituitary.
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During follicular phase of menstrual cycle ____ is high. Mid-cycle, ____ rises and stimulates surge of ____. Ovulation occurs and the luteal phase begins. Follicles develop into corpus luteum, which secretes ____ and ____. Menustration occurs when corpus luteum disintegrates and production of these last 2 hormones stops.
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FSH
Estrogen LH Estrogen, progesterone |
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Progesterone
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Released during luteal phase and inhibits uterine endometrial growth but promotes maintenance. CHORIONIC GONADOTROPIN secreted by an embryo maintains endometrium if fertillization occurs.
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PRL is inhibited by ___ and ___
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Prolactin inhibiting hormone and DOPAMINE
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T/F: ADH is produced by the anterior pituitary
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F
Produced by the hypothalamus and stored in Herring bodies in the POSTERIOR pituitary |
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________ is due to ADH deficiency. Sx include increased urination, thirst, HA, possible coma.
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Diabetes insipidus.
Can also occur if kidneys are insensitive to ADH/vasopressin. Main ADH function is VOLUME REGULATION! |
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T/F: Plasma Ca2+ and PO4- levels are directly related to bone density/turnover.
T/F: Most intracellular Ca2+ stored in ER, mitochondria, plasma membrane. Most intracellular PO4- is in the form of high-energy compounds like ATP |
T! Fall in blood Ca2+ or PO4- will induce a fall in bone density
T |
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Which of the following stimulate/inhibit bone formation?
GH, insulin, estrogen, androgen, Vit D, calcitonin, PTH, cortisol |
Stimulate:
GH, insulin, estrogen, androgen, Vit D, calcitonin Inhibit: PTH and cortisol NOTE that VitD stimulates both resorption and formation! |
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______ promote bone formation by synthesizing collagen.
______ are mature bone cells that transport Ca2+ and PO4- from inside to outside bone and vice versa. ______ are large cells that attach to bone surface to be remodeled/reabsorbed. |
Osteoblasts
Osteocytes Osteoclasts |
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Vit D role in bone density
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Stimulates interstitial Ca2+ and PO4- absorption and bone re-absorption
Stimulate osteoid (bone matrix) formation to increase bone density Allows SER uptake of Ca2+ |
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Which two hormones regulate osteoclast activity?
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PTH stimulates osteoclast activity
Calcitonin inhibits osteoclast activity |
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Islet of Langerhans cells and their function?
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1. Alpha cells - secrete glucagon when BSL is low
2. Beta cells - secrete insulin when BSL is high 3. Delta cells - secrete somatostatin which inhibits GH, TSH, and gastrointestinal hormones |
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Why do Type 1 diabetics who don't take their insulin suffer diabetic ketoacidosis?
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Insulin INHIBITS ketone body formation.
Ketone bodies are byproducts produced when fatty acids are broken down for energy in the liver and kidney. Acetone, acetoacetic acid, and beta-hydroxybutyrate. Accumulation of too many ketone bodies leads to drop in blood pH and acidosis. |
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Type 1 DM leads to hyperglycemia, glucosuria, and hyper-____.
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Hyperlipidemia
Due to decreased storage of free fatty acids and triglycerides since they're broken down for energy. Also increased lipolysis and transport of free fatty acids to the mitochondria. |
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Pancreatic release of somatostatin results in ?? (3 functions)
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1. Inhibition intestinal glucose and TG absorption
2. Dec rate of digestion of nutrients from GI 3. Inhibition of insulin and glucagon secretions |
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Which of the following sarcomere bands shorten during muscle contraction?
A, H, I, Z |
H, I, Z
1. ACh activation of nicotinic receptor = Na+/K+ pump activation 2. Na+ influx causes depol muscle fibers (AP travels along T-tubules) 3. Ca2+ channels open --> more Ca2+ released from SER 4. Ca2+ binds troponin C on thin actin myofilaments 5. Tropomyosin is allosterically modified so myosin binding site is exposed 6. Myosin binding hydrolyzes it's ATP to produce energy for sarcomere shortening (Z bands pulled towards each other) 7. Re-binding ATP "re-cocks" tropomyosin apparatus |
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T/F: skeletal muscle spindle fibers participate in muscle contraction
Golgi tendon organs signal the _____ on a muscle. T/F: Smooth muscle is organized in sarcomeres w/ troponin |
F
Muscle spindles are too weak to contribute to contraction - have sensory and motor axons and determine muscle LENGTH and RATE OF CHANGE on muscle length Force - Golgi tendons have stretch receptors sensed by nerve fibers; activated by stretch or contraction F |
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Smooth muscle contraction mechanism?
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Action potential generated by ligand-gated Ca2+ channels - Ca2+ binds CALMODULIN to activate myosin light chain kinase (MLCK), which interacts w/ G-actin to allow cross-bridge formation that allows muscle fibers to slide across one another
*Note that if MLCK can't be phosphorylated by calmodulin, can still bind to actin via LATCH-BRIDGE formation that requires no energy and still allows for muscle tension |
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T/F: CN2, 5, and 7, and 8 all participate in eyelid blinking or closure
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T
CN2 participates in REFLEX blinking due to bright light or an approaching object CN5 participates in REFLEX blinking due to touch, CN 7 carries out the blink CN 8 participates in REFLEX blinking due to loud noise Spontaneous blinking is due to contraction of orbicularis oculi (palpebral portion) Forced blinking is due to contraction of both orbicularis oculi (palpebral AND ocular portions) |
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Eyedrops are usually (strong/weak) bases. This helps in absorption since...
The pH of tears becomes more (basic/acidic) at night. Osmolarity of the aqueous layer of tear film?? |
Eyedrops are weak bases. The neutral pH of the tear film (7.45) keeps eyedrops in their non-ionized form, aiding in absorption by the hydrophobic corneal epithelium
acidic due to anaerobic respiration byproducts ~315Osm/kg ---> want AT's for dry eye to be LESS than this since a hypotonic solution is desirable in dry eye to counteract the hyperosmolarity of the tears! |
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Reflex and emotional tearing is produced by the (lacrimal/accessory) gland(s) and maintenance/normal tearing is produced by the (lacrimal/accessory) gland(s).
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Lacrimal
Accessory |
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Pursuits are controlled by (contralateral/ipsilateral) brain while saccades are controlled by (contralateral/ipsilateral) brain
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Ipsilateral parietal lobe
Contralateral FEF |
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Glucose concentration in the aqueous humour is (> / <) glucose in the tears
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[Glucoese] is highest in the aqueous humor! Very low in tears - eye is supplied w/ glucose by the aqueous humour
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Maintenance of corneal hydration:
Na/K pump on basal epithelium moves K+ into the (epith/stroma) and Na+ into the (epith/stroma). Na+ gradient created which is utilized by Na+/Cl-/K+ cotransporter to move Cl- and K+ (into/out of) the epithelium. |
-K+ to epihelium and Na+ out epithelium into stroma
-Cl- and K+ movement into epithelium **Cl- and K+ then move via their own channels into the tears and aq humour, respectively **Movement K+ into aqueous stimulates release of Cl- into tears - H2O moves with it to hydrate the cornea **So it's Cl- movement that hydrates the cornea! |
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Contact lenses should maintain partial pressures of O2 above ____.
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10-20mmHg
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T/F: The corneal stroma will not replace itself if damaged.
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F
The stroma replaces itself w/ disorganized, larger collagen that presents as a scar. |
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T/F: Descemet's and the corneal endothelium contain no nerves.
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T
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Refractive indices:
Vitreous Lens nucleus Aqueous Outer corneal surface |
1.336
1.50 1.336 1.37 |
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Glutathione, catalase, and Vitamin C protect the lens from _____.
Lens metabolism is mostly (aerobic/anaerobic). 90% of lens proteins are water-soluble _______ (type of protein). |
Oxidative damage
Anaerobic Crystallins. *Note that Alpha-crystallin helps prevent degradation of other crystallins. *Note that the lens has the highest % protein in the body |
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Vitreous is 99% water. Also contain collagen fibrils and _____ (which GAG?) that give vitreous its consistency.
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Hyaluronic acid
*Note that volume of the eye is 5mL, 4mL of which are vitreous |
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Vitreous transmits >90% visible light but blocks out most of which wavelength?
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UV range 300-350
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The perfusion pressure of the eye is approximately _ _____.
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50mmHg
Arterial pressure entering ~65 Episcleral pressure leaving ~15 |
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T/F: The optic nerve, retina, and choroid are able to maintain constant rate of blood flow despite moderate variations in mean arterial pressure and IOP
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F
all of this is true except the choroid DOES NOT show autoregulation |
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Rod and cone pigments are composed of 2 parts:
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(1) Opsin - rhodopsin in rods
(2) Chromophore - 11-cis retinal in both |
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Rod outer segments are shed in the (AM/PM) and cone outer segments are shed in the (AM/PM)
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Rods - AM
Cones - PM |
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Light absorption causes transformation of 11-cis retinAL to _____. This is moved to the RPE, which converts it to ______ and then oxidizes it to ______ before transporting back to the PR's.
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11-cis retinAl --> all-TRANS retinal ---> 11-cis retinOl ---> 11-cis retinAl
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Dark current
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Refers to flow of Na+ and other cations into/out of retinal while in the dark
Na/K pump uses ATP to pump Na out of inner segments Na flows into outer segments Retina is -50mV in the dark |
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Phototransduction
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1. Light absorbed by rhodopsin
2. Rhodopsin dissociation triggers transducin activation (G-protein) 3. Cascade leading to decrease in cGMP 4. cGMP is responsible for maintaining Na channels OPEN in the outer segment, allowing for dark-current depolarization -Closing of Na+ channels during phototransduction gives HYPERPOLARIZATION in the light (to ~-65mV) -Hyperpolarization results in a decrease in GLUTAMATE release to bipolar cells |
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Amacrine and horizontal cells release these inhibitory NT's
PR's, bipolar cells, and most GC's release this excitatory NT |
Inhibitory NT's: GABA & glycine
Excitatory NT: glutamate |
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(Bipolar/amacrine) cells have center-surround receptive fields and respond to graded potentials.
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BIPOLAR
Amacrine cells also have center-surround receptive fields respond to action potentials Horizontal cells do not have center-surround receptive fields and respond to graded action potentials Ganglion cells have center/surround receptive fields and produce action potentials. |
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CT vs MRI indications
PET indications |
CT is : faster, better for bone/calcification; denser tissues appear whiter
MRI is: slower, detailed pathology/anatomy of soft structures *General rule of thumb is that diseased tissue has MORE H2O PET analyzes metabolic activity of tissue by comparing glucose uptake - e.g. in identifying cancer |
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The first location along visual pathway to combine monocular info into binocular info?
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V1 (visual cortex)
LGN's are MONOCULAR and each layer contains contralateral nasal info and ipsilateral temporal info (this allows info from each eye about the same visual field to lie next to one another!) |
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Arden ratio
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EOG measurement of RPE health
EOG measures diff in electrical potential between the front and back of the eye Patients perform eye mvts during light and dark adaptation and these measurements are compared Arden ratio = light rise/dark trough Arden ratio of less than 1.50 is abnormal! |
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T/F: ERG includes GC activity
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F
ERG only measures activity of the outer retinal layers (PR's, bipolars) A-wave: PR's B-wave: Bipolars, Mueller's C-wave: RPE cells *In dark adaptation, the B-wave should show 75%/25% ratio rod/cone contribution |
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VEP mechanism
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Detects striate corticex LATENCY of activity in response to visual stimuli
Stimuli w/ abrupt pattern difference (e.g. checkerboard) should evoke response w/in 100msecs VEP can detect abnormality between the fovea and VI but CAN NOT localize it |
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Pupil constriction in response to light mediated from ______ nucleus to EW, while pupil constriction in response to near target mediated from _____ to EW
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Light response - pretectal nucleus
Near response - FEF |
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Why miosis during sleep/anesthesia?
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Sympathetic nervous system actively suppresses EW nucleus
When uninhibited, EW fires constantly to pupils (unique!) |
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NCT and GAT MOA's
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NCT: puff of air of known F directed at cornea, and time it takes for air be to maximally detected by a photocell is converted to mmHg
GAT: prism of known weight and diameter used to applanate the cornea and F necessary to flatten is measured; assumes one corneal thickness so underestimation/overestimation is possible w/ non-average corneal thickness |
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Uveoscleral outflow is (dependent on/independent of) IOP.
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INDEPENDENT
*Corneoscleral outflow is IOP-dependent - higher IOP = more outflow up to the point where Schelmm's collapses on itself due to high IOP NOTE that total aqueous humor is replaced every 100min and that total aqueous humour in the eye is 250uL |
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"Active secretion" and aqueous humor
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ATP-dependent transport of larger water-sol substances or ionic substances across nonpigmented ciliary epithelium accounts for 80-90% aqueous formation
Thus alterations in BP have little effect on aq humor formation Active secretion creates gradient in which aqueous is hypertonic to the blood by 5mOsm Utilizes ATP and two enzymes to move Na+ and HCO3- into the posterior chamber for aq production NOTE that aq humor has MUCH LESS PROTEIN (minimize light scattering) and MUCH MORE VITAMIN C (antioxidation) than plasma (but know that lens has highest Vitamin C AND protein) LACTATE is also found in higher conc in aqueous due to glycolysis of the lens and cornea |
