Renal Physiology Lectures 33-45 PDF

RENAL PHYSIOLOGY -- LECTURES 33-45 ================================== **[Lecture 33 - Distribution and Measurement of Fluid Volumes]** - List the varying compartments of fluid distribution and accompanying spaces connecting them. - 60% of total body weight is water - 40% of...

RENAL PHYSIOLOGY -- LECTURES 33-45 ================================== **[Lecture 33 - Distribution and Measurement of Fluid Volumes]** - List the varying compartments of fluid distribution and accompanying spaces connecting them. - 60% of total body weight is water - 40% of total body weight is Intracellular Fluid - 20% of total body weight is Extracellular Fluid - 15% is Interstitial Fluid - 5% is Plasma - Intracellular Fluid Cell Membrane Interstitial Fluid Capillary Membrane Plasma - Understand the properties of substances that are used to measure extracellular fluid volume. - V = amount/concentration - 1ml of a 1,000 mg/ml solution and final concentration of 0.3mg/ml - V = (1ml\*1,000 mg/ml)/0.3mg/ml - V = 3,000 ml - Albumin is an anion that does not cross capillaries and should not be in the urine - Mannitol can cross capillaries - Determine how SIADH impacts body fluid distribution. - In SIADH, water is added to both the ECF and ICF, resulting in a decrease in osmolarity (keeps free water). - This is a hypoosmotic situation in which there is volume expansion (water is gained). **[Lecture 34 - Principles and Overview of Renal Function]** - List and compare the competing Starling forces that control fluid movement across a capillary wall. - Hydrostatic pressure is what primarily causes water and solutes to be pushed out of the plasma and into urine. - Dialysis is driven by a hydrostatic pressure gradient. - There is no capillary osmotic pressure in a healthy Bowman's capsule due to the lack of albumins - Determine how plasma volume impacts RAAS activity. - Renin secretion can be stimulated by decrease blood pressure, decreased sodium delivery in the Macula Densa, increased sympathetic tone - Low blood volume that results in low blood pressure will activate RAAS - Renin is released by the kidney and converts Angiotensinogen to Angiotensin I - ACE is released by the lungs and converts Angiotensin I to Angiotensin II - Activation of RAAS leads to - Kidney -- Constriction of the glomerular efferent arteriole and an increase in Na^+^/H^+^ exchanger activity - Posterior Pituitary -- ADH secretion (Reabsorption of free water and urea) - Vascular Smooth Muscle -- Hypotension - Hypothalamus -- Stimulates thirst - Adrenal Cortex -- Aldosterone secretion (Increase Na reabsorption) **[\ ]** **[Lecture 35 - Renal Blood Flow and Glomerular Filtration Rate I]** - List how constriction of the afferent arteriole effect glomerular hemodynamics. - Constriction of the Afferent Arteriole decreases both RPF and GFR. There is no change in the FF due to a drop in both RPF and GFR. - List how changes in glomerular capillary pressure impact GFR (Glomerular Filtration Rate), RBF (Renal Blow Flow) and FF (Filtration Fraction). - A list of medical terminology Description automatically generated with medium confidence - Recall Starling forces in the kidney and how they impact net filtration pressure. - Net Filtration Pressure = Glomerular Hydrostatic Pressure -- Bowman's Capsule Pressure (Hydrostatic) - Glomerular Oncotic Pressure - 10 mmHg = 60 mmHg -- 18 mmHg -- 32 mmHg - Glomerular Hydrostatic Pressure - Glomerular Oncotic Pressure - Bowman's Space Hydrostatic Pressure - Bowman's Space Oncotic Pressure **[Lecture 36 - Renal Blood Flow and Glomerular Filtration Rate II]** - Understand renal handling of creatinine. - GRF = (creatinine in urine x flow volume) / creatinine in blood - GFR = (125 mg/ml x 1ml/min) / 1mg/ml - GFR = 125 ml/min - Creatinine is higher in urine than the blood - Creatinine is endogenous - Predict the effects of change in tone of the afferent or efferent arteriole on GFR, RBF, and FF. -  - Determine the handling of a substance by comparing its clearance to that of inulin. - GRF = (Inulin in urine x flow volume) / inulin in blood - Inulin is the best way to determine GFR and is not endogenous - It is filtered at approximately 100% at the glomerulus **[\ ]** **[Lecture 37 - Reabsorption and Secretion I]** - List the primary substances that are reabsorbed in the proximal tubule. - Na^+^, Mg^2+^ - Na^+^ with Cl^-^, Ca^2+^, PO~4~^3-^ - 85-90% of bicarbonate (HCO~3~^-^) in the form of CO~2~ and water on the apical side - Amino acids, glucose (SGLT2 in early PCT, SGLT1 in late PCT) - Water and urea passively - List the transporters in the proximal tubule involved in the physiologic response to reduced extravascular volume. - Per Chat GPT - In the context of reduced extravascular volume, the kidney activates several mechanisms to conserve sodium, water, and other vital solutes: - Enhanced sodium reabsorption through NHE3, SGLT2, and NaPi transporters. - Increased water reabsorption via aquaporins (AQP1). - Modulation of acid-base balance via bicarbonate transporters (NBCe1, NHE3). - Optimized solute transport via Na+/K+ ATPase pumps to establish gradients for sodium reabsorption. - These transporters are critical in the proximal tubule\'s adaptive response to conserve sodium and water during volume depletion and contribute to the maintenance of extracellular fluid volume and blood pressure. - Understand that when plasma glucose is above the transport maximum (Tm) of the renal glucose transporters that excess glucose is not reabsorbed and is excreted into the urine. - Some nephrons may become saturated at 350 mg/min, while others may be able to keep up at levels of 400 mg/min. Average is considered 375 mg/min. **[Lecture 38 - Reabsorption and Secretion II]** - Recognize that albumin, immunoglobulins, and some medications are reabsorbed by endocytosis, a completely different mechanism than channels or transporters. - Proteins, such as albumin, and peptide hormones, such as insulin, are reabsorbed by endocytosis and later converted to free amino acids. - List renal transporters and determine what type of transport they provide. - Secondary - Cotransport with Na^+^. - Glucose, amino acid, phosphate, lactate, citrate. - Countertransport - Na^+^/H^+^ - Hydrogen into the lumen to combine with bicarbonate (HCO~3~^-^) to form of CO~2~ and water - Recognize splay and recall why it occurs. - Splay phenomenon is due to variability in saturation thresholds amongst different nephrons. - Some nephrons may become saturated at 350 mg/min, while others may be able to keep up at levels of 400 mg/min. **[\ ]** **[Lecture 39 - Sodium Balance I]** - List the segments of the nephron and how potassium is handled in each. - K^+^ - Reabsorption - 67% in the proximal convoluted tubule - 20% in the thick ascending limb - Na^+^/K^+^ (3/2) is used in the early PCT to reabsorb Na^+^. Potassium is transported into the cells. - NKCC (Na-K-2Cl) symporter is in the Thick Ascending Limb - Na^+^, excretion is about 100 mmol/day, reabsorption: - 67% in the proximal convoluted tubule - 25% in the thick ascending limb - 5% in the distal convoluted tubule - 3% in the inner medullary collecting duct - Determine which segment of the nephron does not require energy to reabsorb water. - Water Reabsorption is passive - 67% in the proximal convoluted tubule - 15% in the loop of Henle - 0% in the early distal convoluted tubule - 8-17% in the late distal tubule and collecting duct - List the physiological effects of mineralocorticoid blockade. - Aldosterone's major site of function is the late DCT and cortical collecting duct - Aldosterone increases K^+^ secretion and increases Na^+^ reabsorption. - Blocking aldosterone results in decreased K^+^ secretion and decreased Na^+^ reabsorption. - This results in natriuresis and hyperkalemia. - This results in decreased blood pressure and hypovolemia. **[Lecture 40 - Sodium Balance II]** - Understand that the Na/K ATPase creates an electrochemical gradient to allow for transport the epithelial cell. - Na^+^/K^+^ (3/2) is used in the early PCT to reabsorb Na^+^. Potassium is transported into the cells. - Name the terminal site of sodium reabsorption of the nephron. - 3% is reabsorbed in the inner medullary collecting duct - List the mechanisms of potassium-sparring diuretics. - Spironolactone, a steroid and aldosterone-antagonist, prevents aldosterone from entering the nucleus of the principal cells and therefore blocks the synthesis of mRNAs and new proteins. - Amiloride and triamterene bind to the luminal membrane Na+ channels and inhibit the aldosterone-induced increase in Na+ reabsorption. - The K+-sparing diuretics produce only mild diuresis because they inhibit such a small percentage of the total Na+ reabsorption. However, as the name suggests, their main use is in combination with other diuretics to inhibit K+ secretion by the principal cells, as discussed in the section on K+ handling. **[\ ]** **[Lecture 41 - Potassium, Phosphate and Calcium Balance ]** - List the effect that phosphate has on PTH secretion and the impact that PTH has on renal phosphate handling. - Parathyroid hormone (PTH) regulates the reabsorption of phosphate in the proximal tubule by inhibiting Na^+^-phosphate cotransport, thereby decreasing the Tm for phosphate reabsorption. When PTH inhibits phosphate reabsorption, it causes phosphaturia, or increased phosphate excretion. - Little to no reabsorption occurs beyond the proximal tubule. - Understand how excess parathyroid hormone will impact renal calcium and phosphorous. - PTH decreases phosphate reabsorption in the proximal tubule, leading to excretion. - PTH increases Ca^2+^ reabsorption in the distal tubule - Recall the physiologic effects of calcitriol. - Calcitriol is a hormone (Vitamin D3 hormone). - In the proximal tubule of the kidney, PTH creates the active form. - Calcitriol is one of the hormones that controls Ca^2+^. - Calcitriol leads to decreased Ca^2+^ and phosphate excretion in the kidney and increased Ca^2+^ and phosphate release in the bones. - AKA Calcitriol allows for calcium to be reabsorbed in the kidney **[Lecture 42 - Acid Base Chemistry]** - Describe the variables of the Henderson-Hasselbalch equation. *(Listed twice)* **Variable** **Definition** **Example in Physiology** -------------- ------------------------------------------------------- ------------------------------------------------- **pH** Measure of hydrogen ion concentration (acidity). Blood pH (\~7.4) **pKₐ** The pH at which a weak acid is 50% dissociated. pKₐ of carbonic acid is 6.1 in blood buffering. **\[A⁻\]** Concentration of the conjugate base (the anion form). Bicarbonate ions (HCO₃⁻) in blood. **\[HA\]** Concentration of the weak acid (proton donor). Carbonic acid (H₂CO₃) in blood. - Respiratory Alkalosis - Can be caused by hyperventilation - Increased pH due to decrease in CO~2~ - Respiratory Acidosis - Can be caused by shallow breathing - Decreased pH due to increase in CO~2~ - Metabolic Alkalosis - Increased pH due to increase in HCO~3~^-^ - Metabolic Acidosis - Decreased pH due to decrease in HCO~3~^-^ **[Lecture 43 - Water Balance]** - List serum and urine osmolality values expected in diabetes insipidus. - With diabetes insipidus, there is an inability to concentrate urine. - List how ADH is regulated by hyperosmolarity and hypotension. - ADH release is increased with increased osmoreceptor firing, which is due to elevated plasma osmolality. - ADH release is decreased with increased baroreceptor firing, which is due to low blood pressure. - Recall the renal site of action of anti-diuretic hormone. - ADH increases the permeability of the collecting ducts to water (increases urea reabsorption) **[\ ]** **[Lecture 44 - Acid-Base I ]** - Determine acid base status of blood and list causes of high anion gap acidosis. - The mnemonic \"MUDPILES\" is often used to remember the common causes of high anion gap acidosis: - M - Methanol poisoning - U - Uremia (renal failure) - D - Diabetic ketoacidosis (DKA) - P - Paraldehyde poisoning - I - Infection (sepsis) - L - Lactic acidosis - E - Ethylene glycol poisoning - S - Salicylate toxicity (e.g., aspirin overdose) - Recognize that high plasma glucose will lead to production of ketoacids, thereby causing an increased anion gap. - Diabetic Ketoacidosis - Define anion gap and determine how decreased tissue blood flow may cause increased anion gap acidosis. - Anion Gap = Na^+^ - (Cl^-^ + HCO~3~^-^) - Lactic acidosis is the most common cause of increased anion gap metabolic acidosis **[Lecture 45 - Acid-Base II ]** - Recognize that proteins can present as a cation, and that excess unmeasured cations also contribute to low anion gap acidosis. - Normal anion gap is 12 ± 2 - Examples of unmeasured cations include IgG, K^+^, Mg^2+^, and Ca^2+^ - Understand that unmeasured osmols, such as ethylene glycol can present early on with elevated osmolar gap. - Determine that chronic use of diuretics leads to the development of metabolic alkalosis and that the respiratory system compensates for this.