physio final

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physio final
2013-05-20 15:19:07
physio final

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  1. Explain how the kidneys regulate blood volume. P591
    The kidneys produce urine by filtering blood plasma into a system of tubules. The more filtrate that becomes urine and is excreted from the body, the less blood volume a person will have. While the volume of filtrate produced is very large, most of the filtered volume returns to the circulatory system by a process known as reabsorption. The percent of the filtrate reabsorbed can be adjusted by means of hormones that act on the kidneys, and in this way the kidneys can adjust the blood volume according to the needs of the body. When blood vol is low due to water loss, the hypothalamus directs the posterior pituitary to secrete ADH which stimulates the kidneys to reabsorb water from the filtrate, so that a lower volume of more highly concentrated urine is excreted. Low blood vol causes low BP and kidney secretes rennin in response.  Renin causes and increase in Angiotensin II which stimulates the adrenal cortex to produce aldosterone. Aldosterone causes the kidney to reabsorb more Na+ from the filtrate, Cl and water follow, increasing blood volume and pressure.  High blood volume will cause ADH to decrease. More water will pass out in urine and BV will decrease.
  2. A person who is dehydrated drinks more and urinates less. Explain the mechanisms involved.
    Dehydration stimulates osmoreceptors in the hypothalamus, which make a person thirsty and drink more. These osmoreceptors stimulate other neurons in the hypothalamus which cause the posterior pituitary to secrete ADH. ADH stimulates the kidneys to reabsorb water from the filtrate, so that a lower volume of more highly concentrated urine is excreted.
  3. Describe the intrinsic and extrinsic control mechanisms of the glomerular filtration rate (5)
    Renal Autoregulation of GFR = 125ml /min 

    • Intrinsic              
    • a. myogenic --incr BP--> aff art vasoconstriction--> decr GFR   decr BP--> vasodilation              
    • b. tubulo-glomerular: decr GFR or decreased osmolarity of filtrate--    macula densa?> endothelin? factors causing    vasodilation of affa art--> incr rate              

    • Extrinsic              
    • a. decr BP-=-> baroreceptor reflex-->SNS--> vasconstriction--> incr BP              
    • b. decr BV--JG cells--> renin--> AT-->Ald-->incr reab Na--> water follows-->BP               incr GFR
  4. Describe the process of tubular Reabsorption in the kidney. Name specific molecules and mechanisms.              p580-p602
    • Active tubular reabs: Na+ ATP powered in basolateral  membrane of tubular cells                           Glucose, AA cotransported with Na+ at luminal membrane.  passive fac diff in apical membrane              
    • Na is actively absorbed in the ascending limb of the loop of Henle with K+.                    
    • In the PCT water and Cl follow Na+  by osmosis. In the DCT and CD water is controlled by ADH.              
    • HCO3- is actively absorbed at basolateral membrane of PCT and DCT.
  5. Describe the process of tubular secretion in the kidney. Name specific molecules and mechanisms.               p580-p602
    • Tubular secretion to remove poisons/wastes XS H+ or K+ still in blood.              
    • occurs in PCT and DCT.
    • Active transport of H+ and K+ thru apical surface into filtrate              
    • wastes move by diffusion
    • e.g.  urea              
    • K+ is usually actively secreted into the filtrate in exchange for Na+ absorption.
  6. Explain why the filtrate becomes increasingly hypertonic in the deep medulla increasingly hypotonic in the cortex.
    Filtrate becomes hypotonic at top of loop of Henle because Na and Cl are pumped out by ascending limb but water cannot pass into ECF.  Therefore filtrate becomes more dilute.  Filtrate at bottom of loop is hypertonic to blood because water passes out of descending filtrate osmotically by attraction to the salt extruded from the ascending loop.  (+ feedback) Salt is not allowed to pass out of the desceding loop so filtrate becomes hypertonic.
  7. Describe the pathway for the micturition reflex.
    Micturition reflex:  stretch of bladder walls--> receptors--> splanchnic nerves-->sp cord-->splanchnic nerves-->relaxation of int urethral sphincter--> urine into urethra-->ext urethral sphincter--> controlled and released at will.
  8. Explain how some Diuretics work
    A diuretic can be a substance not reabsorbed from the filtrate Exerting  an osmotic effect by holding water in the  filtrate..  Some loop diuretics increase dilute urine output by inhibiting the Na/K/Cl symporter in the ascending limb of the loop of Henle.  More salt stays in the filtrate and water follows, resulting in more water lost from the body.  Alcohol acts as a diuretic since it inhibits the release of ADH from the post Pituitary. ADH normally causes water reabsorption at the collecting ducts.
  9. Explain how glomerular filtrate is produced and why it has a low protein concentration.
    Glomerular ultrafiltrate is produced from plasma that passes through the pores in the glomerular capillaries, the basement membrane, and the slit-pores in the glomerular capsule to enter the interior of the capsule. Fluid enters the capsule because the hydrostatic pressure of the blood is greater than the sum of opposing forces (the hydrostatic pressure of the filtrate and the colloid osmotic pressure of the plasma). Proteins are excluded partially because of their large size and partially because of their negative charge, which is repelled by the negatively charged glycoproteins in the basement membrane.
  10. Explain how the countercurrent multiplier system works, and describe its functional significance. p586
    The ascending limb actively extrudes salt into the interstitial fluid of the renal medulla, but this segment of the tubule does not allow water to follow. As a result, the renal medulla becomes hypertonic. The descending limb is passively permeable to water, and but not to salt, so that water leaves as a result of the osmotic effect of  salt being extruded from the ascending limb. In this way, the fluid that arrives at the ascending limb is made more concentrated  This a positive feedback mechanism that acts to greatly increase the hypertonicity of the medulla. The significance of this hypertonicity is that it acts as the driving force for the reabsorption of water from the collecting ducts, which is a process subject to regulation by ADH according to the needs of the body.
  11. 11. Explain how countercurrent exchange occurs in the vasa recta, and describe its functional significance
    Since salt is more concentrated in the surrounding tissue fluid than in the descending limb of the vasa recta, salt diffuses into this vessel. The descending limb is close to the ascending limb, however, so that much of this salt will next diffuse from the fluid in the ascending limb into the less concentrated descending limb. Salt is therefore recycled and trapped in the medulla. Water, conversely, is drawn out of the descending limb and into the ascending limb, and so is carried away by the blood. This countercurrent exchange in the vasa recta acts to maintain the hypertonicity of the renal medulla which was created by countercurrent multiplication by the loop of Henle.
  12. 12. Describe how the Na+ and K+ content of blood is regulated by the kidney.p602
    a. Aldosterone Modifies urine by increasing reabs of Na+ in DCT. In exchange for K+.  Therefore lowers urine Na+ and increases urine K+. Water and Cl follows Na+ osmotically to decrease urine volume and conserve water.

    b. decr  blood Na+—macula densa --> renin--> ATI and ATII-->Aldosterone from adrenal cortex-->incr reab Na+-->incr blood Na+

    c. increased blood Na+ --> less renin--> less ATI and II --> less aldosterone --> less Na+ reabsorbed --> lower blood Na+.
  13. Describe the regulation of gastric secretion
    1. During the cephalic phase, the  sight and smell of food stimulates parasympathetic fibers from the vagus nerve to stimulate gastric secretion and contraction. Chief cells are stimulated to release pepsinogen, while parietal cells are stimulated through ACh binding to muscarinic receptors to secrete HCl. The major mechanism for HCl secretion is indirect, through the vagus nerve stimulation of ECL cells and subsequent secretion of histamine, which in turn stimulates parietal cells to secrete HCl. 

    2. Food in the stomach: During the gastric phase, secretion of acid and pepsin is stimulated in response to two factors: (1) distension of the stomach by the volume of chyme; and (2) the chemical nature of the chyme.  The presence of partially digested protein in the stomach lumen stimulates the chief cells to secrete pepsinogen and the G cells to secrete the hormone, gastrin. Gastrin, then is recirculated back to stimulate more pepsinogen and more HCl secretion (indirectly) creating a positive feedback loop.  Fat inhibits acid secretion and glucose has no effect. As the pH of gastric juice drops, so does the secretion of gastrin and HCl release (perhaps mediated by the release of somatostatin from D cells). 3. During the intestinal phase, food is in the small intestine. Both neural reflexes from the duodenum in response to stretch and osmolality and a chemical hormone (enterogastrone, such as GIP, CCK and scretin) secreted by the duodenum appear involved in the inhibition of gastric secretion following a meal. This is to allow more time for the the small intestine to digest and absorb food in the chyme.
  14. Describe how pancreatic enzymes are activated in the lumen of the small intestine and why they are secreted in an inactive form..
    Most of the enzymes of pancreatic juice are released into the duodenum in inactive forms (zymogens). The brush border enzyme called enterokinase converts the inactive trypsinogen in pancreatic juice to active trypsin. Trypsin is a proteolytic enzyme that cleaves off parts of other inactive enzymes, thus activating the other enzymes of pancreatic juice. Since the pancreatic enzymes are generally inactive within the acini of the pancreas, there is less danger of these enzymes promoting self-digestion of the pancreas.
  15. Explain the consquences of gallstones and abnormal liver function on bilirubin metabolism
    (a) Gallstones block the excretion of conjugated bilirubin in the bile, thus resulting in the accumulation of this conjugated bilirubin in the blood.

    (b) A high rate of red blood cell destruction results in excessive conversion of heme to free bilirubin. This free bilirubin accumulates in the blood and tissues, causing jaundice.

    (c) Liver disease also results in the presence of high concentrations of free bilirubin, because the diseased liver cannot conjugate the bilirubin and excrete it in the bile. Since phototherapy converts free bilirubin to a water-soluble form that can be excreted in the bile, it would be an effective treatment of jaundice for cases (b) and (c). A person with gallstones, however, cannot excrete the bilirubin, so the jaundice caused by gallstones could not be treated effectively with phototherapy.
  16. Describe the digestion and absorption of fats in the small intestine.
    Before fat can be digested, it must be emulsified so that the surface area is increased. Fat digestion occurs at the surface of the droplets by pancreatic lipase, colipase, and phospholipase A. These enzymes hydrolyze the lipids to liberate free fatty acids and monoglycerides. The free fatty acids, monoglycerides, and lysolecithin products of digestion form “mixed micelles” then move into the intestinal epithelial cells and are synthesized into triglycerides and phospholipids. Triglycerides and phospholipids form particles called chylomicrons, which are secreted into the lymphatic capillaries of the intestinal villi. Absorbed lipids then pass through the lymphatic system, eventually entering the venous blood by way of the thoracic duct.
  17. Explain the function of MHC Antibodies in the body.
    All cells in the body except red blood cells make class-1 MHC molecules. Class-2 MHC molecules are produced only by macrophages, dendritic cells, and B-lymphocytes as antigen presenting cells to help promote the interactions between helper T cells and B-cell immune response.
  18. Describe the process of T and B cell activation.
    T cell activation: T helper cell (Th)  binds to APC (macrophage or dendritic cell). CD4 receptor binds to CD4 protein on cell surface.  Th recognizes MHCII Ag on macrophage.=  Costimulation.. APC secretes IL-1 stimulates T cell proliferation into clones.

    B cell activation: B cell has antibodies on surface that act as receptors for free Ag.  B cell shuffles genes for these receptors until it finds a match to a specific Ag.   The B cell then forms clones of plasma cells which produce huge quantities of specific Ab and B memory cells  for immune surveillance. This protects us against future attacks of the same Ag.  B cells can also be activated by binding to a Th cell or in response to interleukins released by Th, or APC cells.
  19. Explain how vaccinations work in active immunity
    Vaccinations confer active immunity (secondary response protection) because the person is injected with antigens (killed or attenuated pathogens or their toxins). The person is deliberately exposed to Ag and makes their own specific Ab.  Each lymphocyte is genetically able to produce one type of antibody, or (for T cells) attack one type of antigen by other means. The antigen that is involved can bind to a receptor protein on the surface of that lymphocyte in a specific manner. Following a vaccination, when such binding occurs, the lymphocyte is stimulated to proliferate and develop a clone of memory cells competent to attack that antigen. So, upon subsequent exposure to the same antigen, the person has many more competent lymphocytes and is able to combat the infection much more effectively than was possible upon the primary exposure.
  20. Explain how antibodies help destroy invading bacterial cells. P496-->
    Antibodies bind to antigens on the bacterial surface and in the process stimulate the cascade leading to complement fixation. This punctures the bacterial cell membrane and destroys the bacteria. Also, free complement fragments attract phagocytic cells and increase their activity, leading to phagocytosis of the bacteria.(opsonization). Ab also coat microbes to make them more attractive to phagocytes. Ab can also form completxes with Ag to neurtralize them or agglutinate microbial cells together.  Ab/Ag complexes can precepitate out harmful toxins.
  21. Explain how T lymphocytes interact with macrophages and the infected cells in fighting viral infections
    Macrophages partially digest the virus particles and present viral antigens together with class-2 MHC antigens to the helper T cells. The activated helper T cells proliferate and secrete interleukin-2, which stimulates the proliferation of specific cytotoxic T cells. The cytotoxic T cells have a receptor for the viral antigens and for class-l MHC antigens which are presented by the infected cells. When the cytotoxic T cells interact in this way with the infected cells they secrete Iymphokines which act to destroy the infected cells.
  22. Explain the possible roles of helper and suppressor T lymphocytes in (a) defense against infections and (b) tolerance to self-antigens.
    When stimulated by foreign antigens, both helper and suppressor cells proliferate. Helper cells proliferate faster, so that the infection is fought, but eventually the immune response is controlled by the delayed action of suppressor T cells. It is believed that suppressor cells may normally inhibit the production of autoantibodies and thus prevent the development of an immune response to self-antigens. In this way tolerance to self-antigens may be produced.
  23. Describe the clonal selection theory, and use this theory to explain how active immunity is produced.
    Each lymphocyte is genetically able to produce one type of antibody, or (for T cells) attack one type of antigen by other means. The antigen that is involved can bind to a receptor protein on the surface of that lymphocyte in a specific manner. When such binding occurs, the lymphocyte is stimulated to proliferate and develop a clone of cells competent to attack that antigen. So, upon subsequent exposure to the same antigen, the person has many more competent lymphocytes and is able to combat the infection much more effectively than was possible upon the primary exposure.
  24. Describe the role of the Sertoli cells in spermatogenesis, and describe the hormonal control of spermatogenesis. p706 -->
    Sertoli cells engulf the cytoplasm of the spermatids as they are changed to spermatozoa. The Sertoli cells aid the developing sperm cells metabolically by secreting Androgen Binding protein in response to FHS. This allows the developing sperm to respond to testosterone.  In the mature adult, testosterone maintains spermatogenesis.
  25. Explain the hormonal interactions that control ovulation and make it occur at the proper time. p716 -->
    The follicles develop under stimulation by FSH. This development entails the maturation of the ovum as the follicle gets larger. As the follicle increases in size there are more granulosa cells, and so estrogen (estradiol) secretion by the granulosa cells increases. The blood levels of estradiol thus increase. At some point near ovulation estrogen positively feeds back on the hypothalamus GnRH to suddenly increase LH.  The surge in LH mid cycle triggers ovulation.  After ovulation estrogen falls rapidly until the corpus luteum develops fully.

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