Physio 4.7 H2O & Electrolytes Regulation, Micturition Reflex & Urinalysis_Jerez

August 2, 2018 | Author: lovelots1234 | Category: Urination, Angiotensin, Urinary Bladder, Physiology, Organ (Anatomy)
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Physiology 4.7

H2O & Electrolytes Regulation, Micturition Reflex & Urinalysis

Nov 23, 2011 Dr. Carolina C. Jerez

OUTLINE WATER AND ELECTROLYTE REGULATION I. Effects of sodium reabsorption II. Blood pressure regulation III. Potassium regulation IV. Factors maintaining the tonicity of the medullary interstitium V. Plasma osmolarity regulation MICTURITION REFLEX I. Micturition contraction II. Control of brain in micturition URINALYSIS I. Macroscopic examination

II.

Microscopic examination Add’ Add’l info from Berne and Levy in Times New Roman (bold)

WATER AND ELECTROLYTE REGULATION I. EFFECTS OF SODIUM REABSORPTION     

Creates an osmolarity favoring the reabsorption of water Helps prevent excessive water loss in the stool Nutrients, phosphates, sulfates are also reabsorbed Achieves hydrogen ion secretion Chloride reabsorption – excessive chloride secretion can cause diarrhea

Figure 1. Role of Renin

Table 1. Different Effcets of Angiotensin II

II. BLOOD PRESSURE REGULATION  

  

One function of the kidney Set Point: value of BP at any give n time (depending on the individual’s activity) Detectors – to determine the changes in BP Signals generated in response with each changes Effectors – supposed to bring back BP to normal Ex. Compensatory mechanism

RESPONSES TO CHANGES IN BP 





Short term: Baroreceptor term:  Baroreceptor reflexes (detect changes in the amount of blood in the body passing through the specific area) Intermediate: o Renin  Secreted when there is low BP and BP and detected by the granular cells (which also secretes renin)  Needed in the conversion of angiotensinogen which co mes from the liver to become Angiotensin I  Angiotensin II in the lungs in the presence angiotensin converting enzyme which is the ACE (Fig 1)  Renin-angtiotensin is an intermediate compensatory mechanism for changes in blood pressure  Regulator of Na+ and K+ balance o Macula Densa cells will detect the amount of fluid and sodium chloride flowing chloride flowing through the juxtamedullary apparatus What will be the main effect o f angiotensin II? o It is a vasoconstrictor agent and thus changes total peripheral resistance  increase blood pressure o Stimulates the release of aldosterone and antidiuretic hormone (ADH)  long term response to changes in blood pressure (Figure 2) Figure 2. Effects of Angiotensin II

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Long term: term: Renal regulation of water and NaCl o ALDOSTERONE from adrenal glands  Stimuli for the release of aldosterone: Presence of ACTH (Adrenocorticotrophic Hormone), Angiotensin II, and an increase of plasma Potassium  Effects : Increase sodium and fluid retention (increase reabsorption of sodium in the distal collecting tubule, CT and ducts) o ADH (Antidiuretic Hormone) from the Posterior Pituitary Gland  Ways of releasing ADH  – stimulating either the baroreceptor and the osmoreceptor   Effects of ADH: Increase water permeability in areas in whic h it is not permeable (DT but primarily in the cortical and outer medullary areas of the CT and ducts). ADH is also a powerful antidiuretic, increasing water reabsorption and reducing urine excretion.  The mechanism by which ADH is able to increase water reabsorption will be the increase of water channels (Aquaporin II). So with an increase of water and sodium reabsorption able to maintain a normal blood volume and a new set point for blood pressure. Atrial Natriuretic Hormone/Factor (ANH/ANF) o  Released from Atrium when there is an i ncrease volume in atria (inc blood volume)  Effect is inc in naturesis inc sodium excretion

   

+

+

High K  diet (avocado and baby carrots)  inc K  secretion + + Low K  diet  dec K  secretion + + K  - sparing diuretic  dec K  secretion During diuretic therapy: + o K   gets out of the cell and into the lumen   excreted in the urine  can cause hypokelemia + o K -sparing diuretics are use to prevent hypokalemia

IV. FACTORS MAINTAINING TONICITY IN THE MEDULLARY INSTERSTITIUM A.COUNTERCURRENT MULTIPLIER SYSTEM

Figure 5. Countercurrent Multiplier System  



Figure 3 . Summary of the Regulation of Sodium and Water by aldosterone,  ADH, and ANH

III. POTASSIUM REGULATION

Critical for concentrating a person’s urine Repetitive reabsorption of NaCl by the thick ascending loop of Henle and continued inflow of new NaCl from the proximal tubule into the loop of Henle NaCl reabsorption at the ascending limb  establishes a concentration gradient between the interstitium and ascending limb of the loop of Henle of 200 mili-osmole o The descending limb and the interstitium will have the same osmolarity but a 200 mili osmol difference for the ascending and descending limb  Why? Because of the slow blood flow in the medullary area  not all sodium which gets o ut of the interstitium can be reabsorbed right away  NaCl will stay in the interstitium  maintaining the osmolarity in the medulla  No medulla  no reabsorption of water (passive reabsorption of water) In the presence of ADH o  more water reabsorption in the collecting tubules and more concentrated urine  more NaCl reabsorption in the ascending limb

B. VASA RECTA 

Peritubular capillaries that go down with the loop of Henle in the medullary area, supplying blood and nutrients to the renal medulla. Also highly-permeable highly-permeable to solute and water via AQP1 and works at the same time to move excess solute and water out

Figure 4 . Potassium handling Group 5 | Ballero, Baluyot, Bamba, Bañas

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Descending limb of vasa recta: IN since fluid inside the vasa recta is less tonic than o Solute goes IN since outside OUT since the intertitium has a higher osmolarity o Water moves OUT since Ascending limb Ascending limb of vasa recta OUT since fluid inside the vasa recta has higher o Solute goes OUT since osmolarity IN in response to the increased osmolarity from o Water moves IN in the descending limb Therefore this is an EXCHANGER so that the osmolarity will not vary so much  maintaining the tonicity of the medullary area

MICTURITION REFLEX  









Also known as urination, voiding or peeing. Micturition center is in the the rostral pons, specifically specifically the Barrington’s Barrington’s Center It is the process of disposing uri ne from the urinary bladder via the urethra Full bladder felt at 200-300 mL Trips mechanoreceptors that are eventually triggered by the pressure, resulting in discharge Normally under voluntary control but may occur involuntarily especially in infants, elderly and those with neurologic injuries Involves coordination of the central, autonomic and somatic nervous systems I. MICTURITION CONTRACTION







Product of stretch reflex from the sensory stretch receptors found in the bladder wall Receptors in the posterior urethra also have an influence in the production of contractions Signals from stretch receptors →sacral segments of the spinal cord via pelvic nerves→ ba ck to the bladder via parasympathetic nerve fibers

Figure 6. Countercurrent Exchange in the Vasa recta

C. UREA  







product of protein metabolism is really filtrable, 50% of urea will be reabsorbed in the PCT; 50% in the tubular lumen the distal tubule, cortical collecting ducts and the outer medullary collecting ducts are IMPERMEABLE to urea; thus no urea is reabsorbed in these segments ADHinc urea permeability of the inner medullary collecting ducts into the insterstitial fluid contributes to urea recycling Urea secretion varies with urine flow rate (UFR) o High water reabsorption (low UFR)  greater urea reabsorption and dec urea excretion o Low water reabsorption (high UFR)  less urea reabsorption and inc urea excretion

Figure 7. Urinary Bladder Fullness Sensation Note: The detrussor muscle contracts while the urethra and pelvic floor relaxes at the emptying phase to phase  to initiate micturition 

Bladder only partially filled. Contractions usually relax spontaneously o Contraction of detrussor muscle ceases o Results to pressure going back to baseline Bladder gradually fills up o Micturition reflex becomes more frequent o Detrussor muscle produces greater contractions o Pressure in the urinary bladder is l ow during filling (5 to 10 cm H2O), but it increases abruptly when micturition begins Important: Micturition reflex is self regenerative o Initial contraction of bladder activates stretch receptors→production of greater impulses to the bladder and posterior urethra o This then results to further increase in the reflex contraction of the bladder o Becomes a cycle until bladder reaches a str ong enough degree of contraction After a few seconds to more than a minute, the reflex fatigues and the cycle ceases →bladder relaxes  Thus the reflex is a single complete cycle of: o

V. REGULATION OF PLASMA OSMOLARITY 

Accomplished by varying the amount of water excreted relative to the amount of solute excreted ( i. e., by varying the urine osmolarity.



A. RESPONSE TO WATER DEPRIVATION 

water deprivation  inc plasma osmolarity  stimulates osmoreceptors  inc secretion of ADH  inc water permeability of late distal tubule and collecting duct  inc water reabsorption  INC urine osmolarity and DEC urine volume  DEC plasma osmolarity toward normal



B. RESPONSE TO INTAKE 

water intake  dec plasma osmolarity  inhibits osmoreceptors  dec secretion of ADH  dec water permeability of late distal tubule and collecting duct  dec water reabsorption  DEC urine osmolarity and INC urine volume  INC plasma osmolarity toward normal

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Progressive and rapid increase in pressure A period of sustained pressure Return of pressure to the basal tone basal tone of the bladder If a reflex occurs but is not followed by successful bladder micturition, the nervous components of the refle x remain inhibited for a few minutes to one hour or more prior to occurrence of another reflex As the bladder continues to fill up with urine, the reflex occurs more frequently and more powerfully o If it is powerful enough, it causes another reflex  Reflex passes through the pudendal nerves nerves to the external sphincter to inhibit it  If inhibition is more potent in the brain than voluntary control, urination will occur o If this is not so, the bla dder will continue to fill up with urine until the reflex becomes powerful enough to cause urination. II. ROLE OF BRAIN IN MICTURITION









Micturition is a completely autonomic spinal cord reflex  but can be inhibited or facilitated by brain centers Brain centers include: o Brain stem mainly in the pons (facilitate and inhibitory centers) o bladder afferent fibers excite neurons that project to the brainstem and activate the micturition center in the rostral pons (Barrington's center) o Cerebral cortex (mainly inhibitory but some excitatory) Reflex is the basic cause of micturition but higher centers exert final control o These higher centers keep the reflex partially inhibited except when micturition is desired o Higher centers can also prevent micturition even if the reflex occurs  This is via the continual tonic contraction of the external bladder sphincter until a convenient time is available When the time is right, cortical centers facilitate sacral micturition centers initiating the reflex at the same time producing inhibition of the external urinary sphincter

o

o

Micturition reflex excited with simultaneous inhibition of external urethral sphincter Urination

I. 

 

URINALYSIS MACROSCOPIC EXAMINATION

Most Ideal sample: early morning urine (since it is the most concentrated); get midstream urine Normal urine is typically light yellow and clear without cloudiness An important and routine tool for detecting disease

A.PHYSICAL CHARACTERISTICS 









Volume : Volume : 600-2000 ml /day (She ( She explicitly said she would go with 500-2000 ml/day ) o Oliguria : decrease in the normal volume of urine o Polyuria : increased in normal urine volume Color : Color : colorless –black o Pale yellow, straw, light yellow, dark yellow, amber o If your taking medicines, there will be changes in the urinehighly colored Appearance refers Appearance refers to clarity of the urine o Freshly voided urine is clear o Cloudiness due to amorphous phosphates and carbonates  may be due to the pres ence also of: WBC, RBC,  may o Turbidity  Epithelial Cells, Bacteria Specific gravity: gravity: determines how dilute or concentrated the urine o Density of a substance compared with a similar volume of distilled water at a similar temperature o Can be determined using dipstick or urinometer o Normal Value = 1.010 to 1.025 (higher value = more concentrated) Odor: Odor: faintly aromatic  usually due to the breakdown of urea

B.CHEMICAL ANALYSIS Urine chemical dipstick analysis - narrow plastic strip with squares of different color attached to it. Strip is dipped into the sample and the color changes will take place and be interpreted accordingly (think pH paper) pH: pH: 4.5-8 o Acidic Urine: due to high meat or high protein and cranberry  juice (Uric acid will precipitate in acidic urine) o Alkaline Urine: Vegetarian diets (Phosphates will precipitate in alkaline urine) Protein in Protein in the urine is most indicative of renal problem (signifies that high molecular weight substances have passed through t he glomerular filtration barrier; more sensitive to albumin than other globulins). Higher than trace amounts of protein is usually indicative of disease. o N.V.: 10 mg/dl or 100 mgs /24 hours o Microalbuminuria: proteinuria that cannot be detected by reagent strips (Significant if 30-300 mgs/24 hrs.) o Orthostatic Proteinuria:  Caused by High fever, Exposure to cold, Strenuous exercise, Dehydration, Acute phase of severe illness Blood in the Urine: o Hematuria: RBC in urine  Causes: Renal calculi (renal stones), glomerulonephritis, pyelonephritis, tumors, trauma, exposure to toxic chemicals, strenuous exercise Glucose: indicates that filtered load of glucose exceeds the maximal tubular capacity for glucose. In diabetes mellitus, urine 



Figure8. Brain Control in Micturition center , periaqueductal Note: Brain centers include the pontine micturition center, gray and gray and cerebral cortex. cortex. 

VOLUNTARY URINATION Pressure in the bladder contracts abdominal muscles o Pressure in the bladder increases; extra urine enters bladder neck and posterior urethra o Walls of the bladder and posterior urethra stretch o Stretch receptors stimulated o

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testing for glucose is often substituted for blood glucose monitoring Ketones: detects acetoacetic acid only. In ketoacidosis (insulin deficiency or deprivation), it can be present in large amounts in urine before elevated in plasma Nitrite: Positive in bactenuria caused by gram negative bacteria which produce nitrate reductase enzyme Bilirubin: indicates presence of liver disease or biliary obstruction. Very low levels of bilirubin can be detected in urine even when serum levels are below clinical detection of jaundice. Urobilinogen : Urobilinogen : increased in any condition t hat causes an increase in production or retention of bilirubin

II. MICROSCOPIC EXAMINATION 

In a centrifuge urine sample, look for o Formed elements (RBC, WBC, Epithelial Cells) o Bacteria o Crystals Casts: formed in the lumen of the Distal Convoluted Tubules o Casts: (DCT) and Convoluted Tubules (CT)  TYPES: Hyaline, Red cells, WBC casts, Bacteria, Epithelial cell, Granular

Table2. Normal Urine Constituents Excreted (in g/24 hrs) Urea 25-30 Sodium 1-5 (NaCl-15.0) Uric Acid 0.6-0.7 Potassium 2-4 Creatinine 1.0-1.2 Calcium 0.2-0.3 Hippuric Acid 0.7 Magnesium 0.1 Ammonia 0.7 Chloride 7 Amino Acids 3 Phosphate/Sulfate 1.7/1.8-2.5

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