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Renal Physiology-Nursing 2024-25.pdf

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Renal & Acid Base Physiology (For Nursing) 4 lectures Dr. Ahmed Badar ([email protected]) Dr. Maiadah Nasser Alfares ([email protected]) Lectures 1 & 2 Overview of kidney function Filtration, Reabsorption, Secretion Functions of the Kidney...

Renal & Acid Base Physiology (For Nursing) 4 lectures Dr. Ahmed Badar ([email protected]) Dr. Maiadah Nasser Alfares ([email protected]) Lectures 1 & 2 Overview of kidney function Filtration, Reabsorption, Secretion Functions of the Kidney A. Regulation of Extracellular Fluid (HOMEOSTASIS): H2O, Electrolytes (Na, K, Ca, Cl, HCO3) pH (acid base balance) & osmolarity (concentration of solutes) Functions of the Kidney B. Excretion of metabolic wastes urea ,uric acid creatinine foreign compounds drugs, food additives Functions of the Kidney C. Endocrine secreting Erythropoietin (Red blood cell production) secreting Renin (fluid, electrolyte and BP regulation) converting Vitamin D3 into active form (Calcium metabolism) D. Gluconeogenesis: converting amino acids to glucose Functional unit of the kidney is Nephron Each kidney has one million nephrons Functions of Nephron 1:Filtration 2: Reabsorption 3: Secretion Glomerular Filtration 1. Glomerular Filtration Plasma is filtered through a very thin membrane - the Barr called the glomerular membrane (see figure) The filtered material is called ultrafiltrate because it contains all the constituents of plasma except the proteins. > the reason - thatallesma to transfer is the It is the first step in urine formation star atcher Entirely a passive process (non-selective membrane process) of Process by which filtrate is formed “Ultrafiltration” Glomerular membrane/ Capillary Podocytes Filtration surface endothelium is 2 cell layers Inner cells of Bowman’s capsule 100 times more permeable than any other capillaries Basement membrane between 2 layers is formed of 1- Collagen for support 2- Glycoprotein negatively charged That way the protin Characteristics of glomerular Highly permeable capillaries Particles Less than 4nm freely pass More than 8nm cannot pass Between 4-8 nm depends on charges (negatively charged particles can not cross because basement membrane is also negatively Charged. Plasma proteins are negatively charged) Glomerular filtrate is exactly same as the plasma minus its plasma proteins Glomerular Filtration rate (GFR) = 125 ml/min So about 180 liters is filtered daily (125mlx 24 hours x 60 min = 180L) Tubular functions Reabsorption Secretion Tubular Reabsorption Reabsorption Transfer of substances from the tube to blood (through peritubular capillaries) water water don't allowing pass pass 2. Tubular reabsorption It is the process to return materials needed by the body from the filtrate back to the plasma. A highly selective process Out of the 180 liters of plasma filtered each day 99% or 178.5 L are reabsorbed. (The remaining 1.5 L eliminated as urine.) The reabsorbed substances include 99% of the filtered amounts of water and electrolytes All the filtered amounts of nutritional substances are reabsorbed Tubular reabsorption is through passive or active transport ↳ Recods Energy Active & Passive Reabsorption The nutritional substances (glucose, amino acids, vitamin) and cations (Na+, K+, Ca2+, Mg2+) = are reabsorbed actively. > Water and anions (Cl-, HCO3, NO3, PO4, SO4) and urea are reabsorbed passively 19 Sodium Reabsorption (example of active transport ) i36 Er %. 9 3 2. 99.5 % of Na+ is reabsorbed throughout the tubule Na+ is reabsorbed throughout the tubule to varying extents in different regions % of Na Controlling Tubules reabsorbed mechanism Only 8% reabsorbed from the Distal tubules is “controllable” Proximal 67 % Obligatory/ tubules uncontrolled Loop of Henle 25% Obligatory/ uncontrolled Distal tubules 8% Controlled by hormone ALDOSTERONE Proximal Play a key role in reabsorption of Convoluted many substances; Glucose, amino acids (actively Tubules reabsorption) Water, urea, & chloride (passively reabsorbed) Importance of Na Loop of Henle Critical for kidneys ability to reabsorption dilute and concentrate urine Distal convoluted Important to regulate ECF tubules volume, (hormonally regulated by ALDOSTERONE). The hormone Aldosterone induces Sodium (Na+) Reabsorption in the distal tubules This leads to Na+ retention (directly) and water retention (indirectly) Water reabsorption Water is passively reabsorbed by osmosis along the length of the tubule (99% reabsorbed ). Most of the water follows Na+ by osmosis Tubules % of Water Controlling reabsorbed mechanism Only 20% reabsorption (distal tubules) is Proximal tubules 65% Passive/ Obligatory “controllable” Osmotic following active Na reabsorption Loop of Henle 15% Passive/ Obligatory Osmotic following active Na reabsorption Distal tubules 20% Passive controlled by hormone ADH The hormone ADH (antidiuretic hormone) (Also called vasopressin) Promotes: Passive water reabsorption (only) in the distal tubules Tubular/Transport maximum (Tm) In dibet's Is the maximum amount of a substance that the tubular cells can the pucose actively transport within a given time period. It puts a limit to the reabsorption. it's headed +O carryer Tubular maximum for glucose 7 Tmo G Is the maximum amount of glucose that can be reabsorbed by all nephrons of both kidneys in a minute Glucosuria When glucose starts appearing in urine? If the filtered load for glucose is higher than Tm for glucose, (Glucose in then glucose appears in the urine, because the glucose carriers are saturated at that time, and the excess glucose Urine) that fails to be reabsorbed will appear in the urine. This condition is called GLUCOSURIA (Example Diabetes Mellitus). 27 3. Tubular Secretion Secretion Transfer of substances from blood (peritubular capillaries) directly to the tube. Tubular Secretion Hydrogen Ions L = PH PCT: Proximal convoluted tubule ( PCT, DCT, CD ) DCT: Distal convoluted tubule CD: Collecting duct Potassium Ions Secretion - ( DCT , CD ) Endogenous: Creatinine, Uric Acid, urea Organic Compounds ( PCT ) Exogenous: Drugs H+ secretion (Important for pH maintenance) -Active, Primary & Secondary transport mechanisms -All parts of tubules secrete H+(except Loop of Henle) - H+ secretion is directly proportional to plasma H+ concentration -red veryimportant as Fluid Balance ECF: Extracellular Fluid ICF: Intracellular Fluid Fluid balance is maintained by regulating regulating ECF volume ECF osmolarity ⑧O essential for essential for maintenance of maintenance of blood pressure - cell size - reation by sea Fluid balance is maintained by regulating regulating ECF volume ECF osmolarity = requires requires t ↓ salt balance water balance - accomplished by Aldosterone (hormone) 20 accomplished by ADH (hormone) Control of ECF volume A reduction in ECF volume causes fall in arterial blood pressure  ECF volume  plasma volume  arterial blood pressure Na+ load and ECF volume  Na+ low  Na+ increase decrease will will hold more water - hold less water due to osmotic due to  osmotic gi - activity activity ji 23  ECF  ECF volume volume Therefore regulation of ECF volume depends primarily on controlling salt balance Na+ reabsorption is mainly controlled through the renin-angiotensin-aldosterone system  NaCl  ECF volume  BP  Na+ & H2O reabsorption Helps correct tope Helps correct the on Granular Adrenal of Distal & cells in kidney cortex the collecting Kidny Renin ACE (Angiotensin Converting Enzyme) Angiotensinogen Angiotensin I Angiotensin II Aldosterone Circulation want is the that do or things healp Vaso- constriction Thirst Vasopressin - Renin- Angiotensin-Aldosterone  Fluid  H2O System intake reabsorption Renin- Angiotensin- Aldosterone function S system E 's increas Control of ECF Osmolarity important to Call's said Control of ECF osmolarity prevents changes in ICF volume Fluid hypertonicity Fluid hypotonicity (water deficit) (water excess) Cell Cell loses water gains water and shrinks in and swells size up Brain Brain cells adversely affected cells adversely affected mental confusion, delirium lethargy, headache, vomiting and coma and dizziness Shruken RBCs get destroyed Swollen RBCs burst up Control of fluid balance Water output Water intake (Urine) (thirst) controlled by ADH (also called vasopressin)  ECF osmolarity is sensed by osmoreceptors  ECF osmolarity  ECF osmolarity is water Shrinkage of  Conservation of H2O > - very less osmoreceptors without influencing salt - will Stimulation of posterior  water reabsorption detectors pituitary S  permeability to water acts on distal and - Release of vasopressin (ADH) collecting tubules Consequences of Osmolarity changes Hypertonicity Hypotonicity Cell shrinkage Cell swell Consequences of Volume changes T Dehydration - S 19 Hydration (overhydration) feels - Lowers ABP - (Arterial Blood Pressure) Raises ABP - Lecture 3 (Formation & Passing of urine) depend on Patient d Kidneys have ability to excrete urine of different osmolarity (concentration) > - high 100 – 1200 mosmol/L Y very light Formation of Dilute and Concentrated Urine Secretion Y dehaldrated urine less volume Kidney regulates the water output by regulating the urine volume Antidiuretic hormone or vasopressin (ADH- released by the posterior pituitary gland) plays a key role in regulating concentration of urine. If there is Maximum ADH secretion: concentrated urine (hypertonic urine) will be produced. If there is Minimum ADH secretion: diluted urine (hypotonic urine) will be produced. IF the body is in: Kidneys change 1- fluid balance Urine osmolarity = isotonic = 300 mosm/l urine 2- overhydration, concentration Urine osmolarity= hypotonic=100 mosm/l from 100 – 1200 3- dehydration (water deficit) mosm/l Urine osmolarity= hypertonic =1200 mosm/l DESCENDING LOOP: 1- Highly permeable to water TRANSPORT AND 2- Impermeable to Na PERMEABILITY CHARACTERISTICS OF LOOP OF HENLE ASCENDING LOOP: I 1- Impermeable to water 2- Permeable to Na U Shep In Water Deficit dehadrated hormone ADAD Vasopressin secretion is stimulated Maximum vasopressin secretion causes maximum permeability of distal and collecting tubules to H2O Osmolarity of fluid in collecting duct will progressively increase, reaching maximum 1200 mosm/l Excreted urine will be 1200mosm/l Inhibition of vasopressin secretion Distal & collecting tubules are impermeable to In Water water Excreted fluid will be diluted (hypotonic) Excess Because fluid leaving loop of Henle is diluted (100mosm/l). Diuresis Urine Volume Causes of Diuresis more fuld Water Diuresis Vasopressin 65- - Pathological Physiological ↳ Diabetes Insipidus Drinking Large volume of water 35 Causes of Diuresis Osmotic Diuresis Excess of unabsorbed solute high level org Glucose X Salts Diuretic Drugs Diabetes Mellitus MICTURITION (Passing of urine) Micturition Micturition/Urination is the process of bladder emptying. Micturition is controlled by 2 Mechanisms. Micturition Reflex Voluntary Control ~ (Voluntary control is not developed in infants; It is learned during toilet training in early childhood) Nervous control of Micturition x b Pelric Y Skeletal neuve muste going to allows the contraction of opining Nervous control of Micturition allove the eyet.Nervous supply to urinary bladder and internal urethral sphincter is via parasympathetic system, which when stimulated would lead to contraction of bladder and relaxation of internal sphincter. The external urethral sphincter is skeletal muscle supplied by somatic nerves and is under voluntary control. The neural control of bladder emptying Spinal reflex initiated by stretch receptors in the bladder and mediated in the sacral spinal segments (micturition center) of spinal cord. Higher CNS regulation helps to achieve micturition at appropriate time and suitable place F Reflex and Voluntary control Of Micturition Micturition reflex A spinal reflex facilitated and inhibited by higher brain centers and subject to voluntary & facilitation and inhibition. Urinary bladder serves to store the urine and evacuate when filled. It has smooth muscle (detrusor) and guarded by sphincters. signal Micturition reflex Is Spinal reflex Filling of bladder (250 – 400 ml) stimulates stretch Activated Contraction of receptors → send micturition center bladder wall and afferent impulses sends relaxation of to efferent impulses internal urethral micturition center through pelvic nerve sphincter located in Sacral causes part of spinal cord (S2,3,4) Inhibitory impulses sent to motor neurons that supply external urethral sphincter (EUS)→ EUS opens→ urina on Acid-Base Balance (Lecture 4) Objectives 1 2 3 Understand the Understand the role Name the four acid importance of PH of the 3 systems base imbalances regulation involved in and their causes maintaining acid- base balance Normal range Venous blood Arterial blood 35 Average Acidosis : Alkalosis 6.8 6.9 7.0 7.1 7.2 En 7.3 7.4 7.5 7.6 7.7 7.8 7.9 8.0 pH range compatible with life Death Death Acidic Plasma pH range under normal, acidosis and alkalosis conditions Normal ACID – BASE Status The relevant arterial blood gas components in evaluating acid – base status are : & Normal range  pH (7.35 to 7.45)  PCO2 (35 to 45 mmHg) importiet very  HCO3 - (22 to 26 mEq/L ) pH has to be kept normal for normal life Normal arterial blood pH Average : 7.4 Range : 7.35 – 7.45 Enzyme Activity in the body is pH dependent Low pH (acidosis) depress neuronal excitability high pH (alkalosis) increase neuronal excitability active over Acidosis Alkalosis Acidosis & A decrease in pH An increase in pH Alkalosis pH Less than () maximum normal that is 7.35 normal pH that is 7.45 Systems cast system maintaining ciecal acid-base 1. Buffers (react immediately; in fraction of a balance second) 2. Respiratory system (acts within minutes) 3. Renal system acts slowly (within hours or days) Prevents marked changes in pH when either an& - acid or base is added to the solution. - Chemical Chemical buffer systems& + - do not eliminate H added but bind ↑ Buffer them until they are removed. detatchment  Carbonic acid / Bicarbonate buffer ( H2CO3 / NaHCO3 ) Systems - Important Buffer in ECF (Extracellular Fluid) -  Protein buffer Important buffer in ICF (Intracellular Fluid)  Hemoglobin buffer Important buffer in RBCs. (Red Blood Cells)  Phosphate buffer Important buffer in renal tubular cells ( urinary buffer ) HCO3- : H2CO3 Main ECF buffer Each component is closely regulated ( open system) + deviled to ↑ CO2 + H2O H2CO3 carbonic by HCO3- + H+ acidity Add Lung Kidney ~ control py -> First Line of Defence Buffer Action Action Starts Immediately (within seconds) not free In Acidosis: Buffers binds H+ and this Normalizes pH free In Alkalosis: Buffers liberate H+ and this Normalizes pH Respiratory System Regulates pH by regulating rate of ventilation Rate of Co2 wash out of Act within minutes ( fast) : 2nd line of defense Effectiveness is 50-75% = Acidosis high level Role of  H+ of hydrogen Respiratory System + Normalize Chemoreceptors  ventilation increase  PCO2 decreas Alkalosis level Role of  H+ Oxygen Respiratory System - Normalize Chemoreceptors  ventilation  PCO2 Regulation of pH by Kidneys (Renal System) most important In Acidosis most effect ↑ A & More Secretion of H+ & More Reabsorption of HCO3- In Alkalosis to H No secretion of H+ & > more Excretion of HCO3- Act within days ( slow) : 3rd line of defense BUT * the most powerful system 5 Respiratory Acidosis O Primary abnormality more increases C Increased arterial pCO2 ( > 45 mmHg ) CO2 + H2O H2CO3 HCO3- + H+ - Causes of Respiratory Acidosis Hypoventilation : Respiratory center depression Respiratory system abnormalities: 1. Airway obstruction 2. Respiratory muscle weakness 3. Holding breath Respiratory Alkalosis Primary abnormality earer than Decreased arterial PCO2 (< 35 mmHg) Y Respiratory Alkalosis & washing Causes Hyperventilation : > - out - all th Co2  Respiratory center stimulation: ex. Fever, anxiety, aspirin poisoning, high altitude orgen level Metabolic Acidosis Primary abnormality Decreased plasma [HCO3- ] < 22 mEq / L => Causes of Metabolic Acidosis 1. Accumulation of fixed ( nonvolatile ) acids in the blood : Ketoacids Lactic Acid Renal failure 2. Loss of HCO3- from body fluid: Diarrhea Metabolic Alkalosis Mrs 5 Primary abnormality more than 26 Increased plasma [HCO3- ] > 26 mEq / L ataeft Metabolic Alkalosis Causes 1. Loss of acids: Vomiting 2. Gain of alkali: Massive blood transfusion Please note that all the figures and tables in this presentation are included in the syllabus for exam Reminder Thank You

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