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23 Cards in this Set
- Front
- Back
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Describe the forces at work in filtration and reabsorption in the arterioles, venules. What changes from arterioles to veins?
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Arterioles: general filtration of 8mmHg from:
hydrostatic pressure = 35mmHg oncotic pressure = 27mmHg Veins: general absorption of 7mmHg from: hydrostatic pressure = 20mmHg oncotic pressure = 27 mmHg There is a drop in the hydrostatic pressure from arterioles to veins due the resistance created by the capillaries. |
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What is edema?
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Excessive fluid in the interstitium caused by the lymphatic system being overwhelmed. This can occur with increased hydrostatic pressure, decreased plasma oncotic pressure, increased capillary permeability, or lymphatic blockage.
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Describe in detail the mechanism behind weight gain from eating salty foods?
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When you eat salty foods, you become thirsty and drink fluids. The resulting increase in circulating blood volume is sensed by low pressure baroreceptors in the subendocardium of the atria (and in large vessels of the lung) which relay this information to the medulla via vagal afferents. The vasomotor center in the medulla responds by diminishing impulse traffic over sympathetic nerves to arterioles, which then dilate. This allows a greater amount of the pressure generated by the left ventricle to be transmitted to the capillaries. This increase in hydrostatic capillary pressure results into more fluid being filtered into the interstitium. This results in weight gain, and if excessive, edema.
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Describe in detail how an increase in venous pressure can result in edema. When does this occur?
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The venous end of capillaries is not protected by sphincters like the arterial end, so that an increase in CVP is automatically transmitted down the capillaries, resulting in edema. This is frequently seen in patients with Right Heart Failure. Blood is normally moved through the veins via being squeezed through valves by skeletal muscle. If a person stands still, or if valves are incompetent (varicose veins), venous pressure rises.
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How can plasma oncotic pressure affect the development of edema?
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The plasma oncotic pressure normally draws fluid back into the capillaries with a force of about 27mmHg. A decrease in the [plasma protein]-- either through Kwashiorkor, nephrotic syndrome (lost in urine), protein-losing gastro-enteropathy (lost in stool), or liver disease (decreased synthesis) can reduce plasma oncotic pressure, reducing reabsorption of water and creating edema.
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How do inflammation, burns, toxins, and allergens affect capillary filtration?
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When capillary permeability to protein is increased (by inflammation, burns, toxins, and allergic reactions), proteins diffuse into the interstitial space. This reduces the plasma oncotic pressure and causes edema. It can be localized (e.g. histamine causing hives) or systemic (anaphylactic shock).
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How can edema be localized to a certain part of the body?
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If the lymphatic drainage of a part of the body (e.g. an arm) is interrupted-- e.g. by lymph node resection due to breast-cancer, or filariasis blocking a lymph vessel-- then edema can develop locally.
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How do tissues autoregulate their own blood flow?
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1) myogenic hypothesis
-sudden stretching of arteriolar smooth muscle automatically causes the muscle to contract-- e.g. in glomeruli of kidney. 2) metabolic hypothesis -vasodilator substances released by cell's metabolism cause relaxation of vascular smooth muscle in precapillary sphincters, metarterioles, and arterioles. Different metabolites are more pertinent in different systems: e.g. CO2 is the major autoregulator inthe brain, and adenosine is of primary importance in the coronary circulation. |
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What is active hyperemia?
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The increase in blood flow to tissues (e.g. muscle) due to an increase in the build-up of metabolites from the tissue (e.g. during exercise).
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What is reactive hyperemia?
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The increase in blood flow to tissues whose blood flow was previously occluded (e.g. brachial artery/BP cuff). Vasodilatory substances accumulate in higher concentrations, and when the obstruction is relieved, a large amount of blood flows through to repay the oxygen debt of the tissues.
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What is Reynaud's phenomenon? Why does the observed phenomenon occur?
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A condition in which vascular smooth muscle in the fingers and toes go into spasm when exposed to cold/in response to emotional stress. The fingers first turn white. As venodilators build up, the spasms in venules are first overcome and the fingers turn blue as deoxy blood moves back into the capillaries. As the arterioles relax, the capillaries are then flooded with oxygenated blood and the fingers turn red and throb painfully.
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Describe neural regulation of circulation. How does it work in the case of hemorrhage?
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During certain occasions (e.g. hemorrhage), the medulla and pons act to redistribute a diminished cardiac output appropriately. Impulses from the Vasomotor Center travel along preganglionic SNS neurons to sympathetic chain ganglia (ACh) and from there impulses travel along postganglionic SNS to vascular smooth muscle to cause arteriolar constriction (NE --> alpha-1 receptors). This sympathetic outflow overrides autoregulation in the kidneys, gut, muscle, and skin, and thus diverts this blood to the coronaries and to the brain.
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List different elements that affect the reflex regulation of blood pressure.
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1) Pain
2) Volume-receptors 3) Chemo-receptors 4) Baroreceptors 5) Ischemic-receptors 6) Emotions |
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Describe vasovagal syncope and how it occurs.
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Severe embarrassment may cause emotional fainting or vasovagal syncope. This occurs when there is an increase in vagal impulse traffic to the heart, and activation of sympathetic vasodilator fibers to muscle. The decrease in TPR and CO causes a sudden fall in mean systemic arterial pressure (MSAP = TPR x CO) which results in diminished cerebral perfusion and loss of consciousness.
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Describe the physiological response to hemorrhage
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Hemorrhage decreases centricular filling and left ventricular stroke volume. This decreases the stretch of sensors in the carotid sinus and aortic arch, which send signals to the VMC. PSNS impulses to SA node are decreased, and SNS impulses to adrenal cortex are increased. This results in increased HR, myocardial contractility, constriction of arterioles to skin, gut, kidneys, muscles, and contraction of venous blood reservoirs.
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Describe how the circulation adjusts to a person standing up
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Gravity causes pooling of blood in the limbs and a decreased VR/CO, which leads to a fall in blood pressure (BP = CO*TPR) and decreased stretch of baroreceptors in the carotid sinus. Fewer impulses are sent via IX to the VMC in the upper medulla/lower pons. This decreases inhibitory vagal impulses to SA node, causing tachycardia. Simultaneously, the VMC increases SNS outflow which first tenses venous capacitance vessels and constricts arterioles to gut, kidney, muscle, skin. This increases TPR, maintaining CO.
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Describe how the body reacts to a loss of plasma volume
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Hypovolemia causes the stretch receptors in the carotid sinus and the atria to fire fewer impulses along IX and X to the medulla. Neurotransmitter depolarizes vasopressin secretory granules causing the release of VP into bloodstream. At initial lower concentrations VP has an antidiuretic effect by acting on V2 receptors in the kidney. If Pa continues to drop, much greater amounts of VP are secreted which act on v1-receptors of smooth muscle, increasing their intracellular calcium ion concentrations.
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What role does vasopressin play in osmoregulation?
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Vasopressin in also released form the post. pit. during dehydration, when plasma becomes more concentrated and the increase in plasma osmolality is sensed by osmoreceptors in the HT. Increased [VP] act on the kidneys (V2 receptors) so more water is reabsorbed, and less is excreted. Thus the urine osmolality is high, and the volume is low (more concentrated urine).
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What is the mechanism of action of vasopressin?
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The apical sides of the cells of the renal papillary collecting duct are impermeable to water and urea, whereas the basolateral side (towards the blood) is freely permeable to water and urea with or without ADH present. Protein pores are stored in vesicles that are delivered to the apical side in the presence of ADH via 1) V2-receptor 2) stimulatory G-protein 3) a membrane-bound adenylate cyclase emzyme (cAMP ^^)
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Describe the renin-AT-aldosterone pathway
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A decrease in blood volume and cardiac output are sensed by stretch receptors in the atria, carotid sinuses, and afferent arterioles of the kidneys. SNS nerves, [Epi], and decreased renal perfusion trigger JGA --> renin. Renin converts AT into ATI in liver. ATI -> ATII via ACE in lungs. ATII acts on adrenal cortex to release Aldosterone. Aldosterone increases Na+ reabsorption via protein synthesis, insertion of more Na,K channels in apical membrane and Na/K pumps in basolateral membrane. This restores blood volume/cardiac output.
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Describe the synthesis, release, and metabolism of NE, Epi.
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Epi is synthesized from tyrosine via L-DOPA, dopamine, and NE in chromaffin cells of the adrenal medulla. The AM is innervated by preganglionic SNS neurons, so whenever the SNS is activated, Epi is released into the circulation. This Epi reaches the same target cells/receptors which are served by SNS nerves which use NE as a transmitter (alpha-1, beta-1). In addition, Epi acts on beta-2 --> relaxation of vascular and bronchial smooth muscle. Epi, NE are degraded by Monamine Oxidase (MAO), leaving metanephrine and vanillylmandelic acid in the urine.
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Pheochromocytoma: description, effects on hemodynamics
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Chromaffin cell tumor of the adrenal medulla that results in a large amount of NE, Epi being released in bursts into the circulation. The hypertension can be sporadic, e.g. following abdominal palpation, or upon urination. Suspect with patients with paroxysmal hypertension associated with headaches, profuse sweating, and tachycardia. Diagnose with elevated metanephrine in urine, plus radiology.
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What are some physiological approaches to hypertensive therapy as applies to: 1) Renin cascade 2) Vasomotor Center 3) Kidney 4) Arterioles
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HTN must be treated because of myocardial hypertrophy, CAD, MI, strokes, renal failure. 1) Renin cascade: ACE inhibitors prevent ATI -> ATII conversion.
2) VMC: VMC inhibited by alpha-2 agonist. Synaptic transmission of impulses slowed at sympathetic ganglia by ACh blockers (not used). 3) Kidneys: Renin release from JGA blocked by beta-antagonist. Diuretics enhance Na/H2O excretion, decreasing CO/VR. 4) Arterioles: Alpha-1 antagonists block NE contriction of arterioles. Type-L Ca2+ channel blockers prevent Ca2+ entry. NO forming compounds induce smooth muscle relaxation. |
