Computer generated transcript

Warning!
The following transcript was generated automatically from the content and has not been checked or corrected manually.

Kidney Physiology 2439957l@student.gla.ac.ukKidney anatomy  Retroperitoneal  Left kidney = T12 – L3  Right kidney = L1 – L4 → Sits lower due to relationship with the liver  Adrenal glands sit superiorly separated in envelope of renal fascia  Lymph drainage = para- aortic nodesKidney anatomyKidney anatomy - microvasculature Segmental Interlobar Arcuate Interlobular Afferent arterioles  InterlobAR = around renal pyramid  InterlobULAR = arise at 90 angleKidney anatomy Kidney physiology A.W.E.T.B.E.D A = acid-base balance W = Water balance E = electrolyte balance T = Toxin removal B = Blood pressure control E = Erythropoietin production D = Metabolism of vitamin DKidney physiology – The nephronBowman’s capsule – ultrafiltration Filtration barrier 3 layers:  Endothelial cells of glomerular capillaries (parietal)  Fenestrae preventing filtration of RBCs  Glycocalyx coating luminal surface consisting of negatively charged glycosaminoglycans which hinder diffusion of negatively charged molecules (such as albumin) but allows positive substances such as Na+  Glomerular basement membrane  Type IV collagen  Podocytes (epithelial cells of Bowman’s capsule)(visceral)  Forms filtration slits containing pores preventing large molecules such as proteins from crossing  Works with mesangial cells to support structure and functionBowman’s capsule – Juxtaglomerular apparatus Macula Densa  Monitors NaCl in distal tubule  Controls secretion of:  Adenosine  Renin – Secreted from juxtaglomerular (granular) cellsAdenosine Increased NaCl Constriction detection by Release of of afferent Reduction in macula adenosine arteriole eGFR densa Renin Decreased Preferential NaCl Release of Activation constriction Increase in detection renin from of RAAS of efferent eGFR by macula arterioles arteriole densaBowman’s capsule – Juxtaglomerular apparatus Macula Densa  Monitors NaCl in distal tubule  Controls secretion of:  Adenosine  Renin – Secreted from juxtaglomerular (granular) cells Adenosine Renin  Increased NaCl  Decreased NaCl Ne densatiot e Feacula densation ack Loopa  Release of adenosi arterioles renin from  Constrictic Ver afferent occurs arteriole  Activation of RAAS  Reduction in eGFR  Preferential constriction of efferent arteriole  Increase in eGFR Bowman’s capsule – Juxtaglomerular apparatus Extraglomerular mesangial cells  These cells have a contractile property similar to vascular smooth muscles and thus play a role in “regulating GFR” by altering the vessel diameter.  Removes protein debris from basement membrane  Also contains reninKidney physiology - PCT Absorption  H20 and Na = 66%  Glucose and amino acids = 100%  Potassium = 65%  Urea = 50%  Phosphate = 80%  Citrate = 70-90%Kidney Physiology – PCT Sodium  3Na/2K ATPase channel on apical membrane drives absorption process  Decreases sodium conc in endothelial cell  Na/H antiporter moves sodium in Glucose  SGLT – 2 transporter (symporter)  Sodium dependant  Simple diffusion across apical membrane Proteins (amino acids)  Absorbed via symporter with sodium Symporter – Transport protein that moves 2 different on diagram)ral membrane (not seen molecules in the same direction Antiporter – Transport protein involved in secondary active transport that moves 2 different molecules in opposite directionsKidney Physiology – PCT Urea  Paracellular fluid reabsorption causes reabsorption of urea via solvent drag Water  Mostly moves via paracellular route via osmosis  Can also move via transcellular routeKidney physiology – Loop of Henle Loop Rules  Thick ascending limb is impermeable to water, but actively transports sodium, potassium and chloride  Thick ascending limb provides the concentration gradient to promote water reabsorption from the thin DLH  Thin descending limb is freely permeable to salt and water  Vasa recta doesn’t wash away the gradient by using countercurrent exchangeKidney physiology – Loop of Henle Thick ascending limb  Impermeable to water due to lack of aquaporins  Na+/K+ ATPase channel drives reabsorption on basolateral membrane  3Na+ actively pumped out of tubule cell and 2K+ in  This decreases sodium concentration and makes cell negatively charged creating electrochemical gradient  Sodium then moves into cell from tubule through NKCC2 channel where a K+ ion and 2 x Cl- ions are absorbed  Potassium ions are transported back into the tubule by renal outer medullary potassium (ROMK) channels on the apical membrane to prevent toxic build up within the cell  Magnesium and calcium are absorbed paracellularlyKidney physiology – Loop of HenleKidney physiology – Loop of Henle Counter-Current multiplication  Thick ascending limb is impermeable to water  Interstitium has ↑osmolarity due to ↑ion concentration  Water reabsorbed from descending limb into an area of high osmolarity (interstitium) This system is known as counter- the kidneys to reabsorb and it allows around 99% of filtered waterKidney physiology – Loop of Henle Thin descending limb  Highly permeable to water  Water travels via osmosis through aquaporins  Small amounts of urea and sodium are absorpbed Vasa Recta • Carries away water and solutes • Helps maintain concentration gradient • Allows continuous reabsorption of fluids and electrolytesKidney physiology – DCT and collecting duct Early distal convulated tubule  Impermeable to water  Absorption of sodium, chloride and calcium  Contains macula densa  Na+/K+ ATPase drives reabsorption on basolateral membrane (Na in/K out)  Sodium diffuses in via NCC (symporter) which also draws in Ca2+. (target site of thiazide diuretic  Ca2+ leaves via NCX channel on basolateral membrane drawing more calcium in via uniporter in apical membraneKidney physiology – DCT Late distal convulated tubule and collecting duct  Principle cells → H2O & Na+ reabsorption and secrete K+  Intercalated cells → Acid-base balance (H+ secretion, HCO3- synthesis) Principle cells  Process driven by Na+/K+ ATPase channel  Sodium diffuses into cell via ENaC (epithelial Na+ channel)  Increase in cell electrical gradient and K+ concentration form Na+/K+ channel drives K+ diffusion out of apical membrane into the lumen, hence K+ secretionKidney physiology – DCT Intercalated cells – Type A  Hydrogen-ATPase and H+/K+ ATPase secrete H+ into lumen  HCO3- absorbed  HCO3- also synthesised in cell by carbonic anhydrase from CO2 and H2O  Secreted H+ can go on to react with NH3 or HPO4(2-)  K+/Cl- symporter on basolateral membrane allows transport of ions into interstitium preventing toxic accumulation Intercalated cells – Type B  The opposite is true, so transporters are on opposite sides of the cell  Allows acid-base compensationKidney physiology – Collecting duct  Main role is water reabsorption via anti-diuretic hormone (ADH) and aquaporins Anti-diuretic hormone  Synthesised in hypothalamus and stored and secreted by posterior pituitary  When secreted ADH binds to V2 receptors on the tubule cells  Adenylyl cyclase activated which leads to an increase in cyclic AMP  Vesicles containing aquaporin channels fuse to apical membrane thus inserting the water permeable channels allowing more water to be absorbed Urea is also absorbed in the collecting duct Histology!!!!!! – Bowman’s capsule  AA/A = afferent arteriole  MD = macule densa  L = extraglomerular mesangial cells  J = Juxtaglomerular cells  GBM = Glomerular basement membrane  C = capillaries  M = mesangium (containing mesangial cell)s  E = endothelial cells  S = epithelium cellsHistology!!!!!! – PCT vs DCT  PCT has abundant dark-pink cytoplasm (mitochondria)  PCT has prominent brush border (increases surface area  DCT has smaller cells with less cytoplasm which gives an impression of more nuclei in a cross sectionHistology!!!!!!  CD = Collecting Duct  T = Thin Descending Dimb  A = Thick Ascending Dimb  V = Vasa RectaMCQs!!!!!! What type of collagen is the glomerular basement membrane made up of? 1. Type I 2. Type II 3. Type III 4. Type IVMCQs!!!!!! What type of collagen is the glomerular basement membrane made up of? 1. Type I 2. Type II 3. Type III 4. Type IVMCQs!!!!!! What is the function of podocytes in the glomerulus? 1. Prevents negatively charged molecules entering the tubule 2. Prevents filtration of red blood cells 3. Prevents large molecules from passing into the tubules 4. Removes debris from the basement membraneMCQs!!!!!! What is the function of podocytes in the glomerulus? 1. Prevents negatively charged molecules entering the tubule 2. Prevents filtration of red blood cells 3. Prevents large molecules from passing into the tubules 4. Removes debris from the basement membraneMCQs!!!!!! Which of the following is true regarding the action of adenosine in the kidney? 1. Dilation of afferent arteriole 2. Constriction of afferent arteriole 3. Dilation of efferent arteriole 4. Constriction of efferent arterioleMCQs!!!!!! Which of the following is true regarding the action of adenosine in the kidney? 1. Dilation of afferent arteriole 2. Constriction of afferent arteriole 3. Dilation of efferent arteriole 4. Constriction of efferent arterioleMCQs!!!!!! On which part of the nephron would this transporter be found? 1. Proximal convoluted tubule 2. Descending loop of henle 3. Ascending loop of henle 4. Distal convoluted tubuleMCQs!!!!!! On which part of the nephron would this transporter be found? 1. Proximal convoluted tubule 2. Descending loop of henle 3. Ascending loop of henle 4. Distal convoluted tubuleMCQs!!!!!! Which receptor does ADH bind to on the collecting duct? 1. V1 2. V2 3. V3 4. V4MCQs!!!!!! Which receptor does ADH bind to on the collecting duct? 1. V1 2. V2 3. V3 4. V4MCQs!!!!!! In this histology slide what is X? 1. Afferent arteriole 2. Distal convoluted tubule 3. Proximal convolutes arteriole 4. CapillaryMCQs!!!!!! In this histology slide what is X? 1. Afferent arteriole 2. Distal convoluted tubule 3. Proximal convolutes arteriole 4. CapillaryThank you! Any Questions? 2439957l@student.gla.ac.ukAcid – Base BalanceWhy is balance important?  At normal physiological pH metabolic pathway precursors are ionised  Phosphate  Ammonium  Carboxylic acid groups  This traps them inside cells/organelles  Deviation from normal pH (acidity) impairs tis process and therefore metabolic function  Proteins (particular enzymes) tertiary (3D) structure can be influences by pH changes leading to denaturing due to disruption of hydrogen bonds, impairing their function.Balance, Buffering and Compensation  Balancing – The concept of managing any additions or losses of acids and bases over time.  Buffering – Manages instantaneous variations in pH (H+ concentration) and aims to limit its effect  Compensation – The response from renal and respiratory systems to perturbation of H+Balance Manages threats to homeostasis:  Generation of CO2 from aerobic respiration  Metabolism of food generating acid or alkali  Metabolism of amino acids can create and acid load (lysine, arginine, methionine) or alkali load (glutamate, aspartate)  Protein rich “western diet” is an acid-load  Anaerobic respiration  Keto-acids, lactic acid  Loss of alkali in still or loss of acid in vomitingAcid or Base  Acid = proton (H+) donor  Base = Proton (H+) receiver CO2 = ? HCO3- = ? H+ = ?Acid or Base  Acid = proton (H+) donor  Base = Proton (H+) receiver CO2 = Acid HCO3- = ? H+ = ?Acid or Base  Acid = proton (H+) donor  Base = Proton (H+) receiver CO2 = Acid HCO3- = Base H+ = ?Acid or Base  Acid = proton (H+) donor  Base = Proton (H+) receiver CO2 = Acid HCO3- = Base H+ = Measure of acidity/alkalinity (technically an acid as well)Volatile vs fixed acid  CO is2a volatile acid– meaning it can be eliminated from the body as a gas  Dietary acids and acid produced by anaerobic respiration are “fixed” – they cannot be “converted “ to CO 2  Buffering a fixed acid consumes HCO , but 3lthough CO will be 2en+ilated, this will be at expense of lowered [HCO ] –3to remove the H effectively more HCO mus3 be generated  Regulation of [HCO ] i3 the job of the kidneys – where excretion of H and + regeneration ofHCO are 3inked.What is pH and how is it calculatedBuffering  Buffers are weak acids partial dissociated in solution – which means there is an equilibrium between the acid and the base (unlike strong acids)  CO - 2CO syst3m is the principle physiological buffer + CO +2H O2↔ H CO 2 HCO3+H 3The 2 main buffering systemsBuffering  CO - HCO system is the principle physiological buffer 2 3 CO 2 H O2↔ H CO 2 HC3 +H 3 +  CO2 is highly diffusible and is regulated and controlled by respiration CO2 so is the substance the body aims to maintain constant  Excess H+  Excess H+ consumes HCO3  The equilibrium shifts to the right (makes more chemical that are on the right of the equation)  More CO2 and H20 is generated  Excess CO2 is exhaled and homeostasis is once again reachedBuffering  CO - HCO system is the principle physiological buffer 2 3 CO +2H O2↔ H CO 2 HCO3+H 3 +  CO2 is highly diffusible and is regulated and controlled by respiration CO2 so is the substance the body aims to maintain constant  Loss of H+  If there is loss of H+ the body wants to make more of it  CO2 and H20 react together and the equilibrium shifts to the right (Makes more chemicals on the left)  CO2 and H20 decreases as they have been used up  More H+ is made and homeostasis reaches  HCO3- levels also increase and it is a by-product of H+ formationCompensationCompensationOther buffers  Haemoglobin – Buffers CO2 in blood  Proteins – Important intracellular buffer  Bone – Long term buffer  PO4 – intracellular and urinary bufferReabsorbing HCO3-  Largely PCT with contribution from TALH and DCT  This contributes to a major mechanism of H+ entering the tubule  Na/H antiporter drives this process  For each HCO3- reabsorbed 1 Na ion is also reabsorbed  Very active process consuming lots of energy  Not net loss of H+ or gain of HCO3-  Inability to reabsorb filtered HCO3- is a cause of metabolic acidosisExcretion of acid  Tubular cells generate a new HCO3- which is absorbed, along with a H+ that is titrated (binds to) a base other than HCO3-, thus reducing acidity  Excretion of fixed acid involves either:  Titration of filtered PO4-  Secretion of NH4 into urine  Failure to be able to secrete H+ is another cause of acidosisSecreting H+ mechanism 1 – Titration of phosphate (HPO4)  This is dependent on delivery of filtered buffer and is relatively fixed thus not regulated  Major non-HCO3 buffer in urine  Accounts for excretion of 40mmol H+/day Secreting H+ mechanism 2 – Excretion of ammonium PCT↓↓  Glutamine is metabolised in the PCT to form NH4+ and HCO3  glutamine transport and oxidationetabolic demands as acidosis stimulates  Accounts for 50-100 mmol H+/dayAcid-base disorders  In all types of acid-base disorder there is a primary disturbance which tends to make H+ abnormal  The acute change will be buffered and there will be a compensatory response – So H+ remains in or close to normal range but at the expense of abnormal HCO3 or CO2  This compensatory response may not always be complete either due to insufficient time for the renal response to complete or limitations of the respiratory response (there is a limit to how hard patients can drive ventilation without tiring.Interpreting ABGs Step 1 – What is the pH?  ↑ pH = ?  ↓ pH = ?  ↑ H+ = ?  ↓ H+ = ?Interpreting ABGs Step 1 – What is the pH?  ↑ pH = Alkalotic  ↓ pH = ?  ↑ H+ = ?  ↓ H+ = ?Interpreting ABGs Step 1 – What is the pH?  ↑ pH = Alkalotic  ↓ pH = Acidic  ↑ H+ = ?  ↓ H+ = ?Interpreting ABGs Step 1 – What is the pH?  ↑ pH = Alkalotic  ↓ pH = Acidic  ↑ H+ = Acidic  ↓ H+ = ?Interpreting ABGs Step 1 – What is the pH?  ↑ pH = Alkalotic  ↓ pH = Acidic  ↑ H+ = Acidic  ↓ H+ = Alkalotic pH is a measure of H+ ions on a logarithmic scale. This means a low pH = lots of H+ ions (and vice versa)Interpreting ABGs Normal pH Step 1 – What is the pH? 7.35-7.45  ↑ pH = Alkalotic  ↓ pH = Acidic  ↑ H+ = Acidic  ↓ H+ = Alkalotic pH is a measure of H+ ions on a logarithmic scale. This means a low pH = lots of H+ ions (and vice versa) Check if ABG is showing pH or H+!!!!!!!Interpreting ABGs Step 2 – What is causing the pH disturbance?  Check the CO2 and HCO3- levels  ↑ CO2 = ?  ↓ CO2 = ?  ↑ HCO3- = ?  ↓ HCO3- = ?Interpreting ABGs Step 2 – What is causing the pH disturbance?  Check the CO2 and HCO3- levels  ↑ CO2 = Acidotic  ↓ CO2 = ?  ↑ HCO3- = ?  ↓ HCO3- = ?Interpreting ABGs Step 2 – What is causing the pH disturbance?  Check the CO2 and HCO3- levels  ↑ CO2 = Acidotic  ↓ CO2 = Alkalotic  ↑ HCO3- = ?  ↓ HCO3- = ?Interpreting ABGs Step 2 – What is causing the pH disturbance?  Check the CO2 and HCO3- levels  ↑ CO2 = Acidotic  ↓ CO2 = Alkalotic  ↑ HCO3- = Alkalotic  ↓ HCO3- = ?Interpreting ABGs Step 2 – What is causing the pH disturbance?  Check the CO2 and HCO3- levels  ↑ CO2 = Acidotic  ↓ CO2 = Alkalotic  ↑ HCO3- = Alkalotic  ↓ HCO3- = AcidoticInterpreting ABGs Step 2 – What is causing the pH disturbance?  Check the CO2 and HCO3- levels  CO2 = respiratory  HCO3- = Alkalosis  ↑ CO2 = Respiratory Acidosis  ↓ CO2 = Respiratory Alkalosis  ↑ HCO3- = Metabolic Alkalosis  ↓ HCO3- = Metabolic Acidosis  ↑ pH = ↑ HCO3- or ↓ H+  ↓ pH = ↓ HCO3- or ↑ H+Interpreting ABGs Step 2 – What is causing the pH disturbance? ACID BASE pH PaCO2 HCO3 Normal 7.35 – 7.45 4.5-6 22-26 RESPIRATORY ↓ ↑ ↔ ACIDOSIS RESPIRATORY ↑ ↓ ↔ ALKALOSIS METABOLIC ↓ ↔ ↓ ACIDOSIS METABOLIC ↑ ↔ ↑ ALKALOSISInterpreting ABGs Step 2 – What is causing the pH disturbance?  Sometimes there can be BOTH a metabolic and respiratory cause for a acid-base imbalance  This seen with both CO2 and HCO3- being seen in amounts outside of their normal range  Both of these changes will both being causing one of: acidosis or alkalosis  Mixed acidosis = ↑ CO2and ↓HCO3-  Mixed alkalosis = ↓ COand ↑HCO3-Interpreting ABGs Step 3 – Is there any compensation occuring?  Have either CO2 or HCO3- changed to compensate for the original acid- base disruption? For example:  If the CO2 has increased (causing acidosis) has the HCO3- increased, balancing out the acidosis with the presence of an alkali?  If the HCO3- has increased (causing alkalosis) has the CO2 increased, balancing out the alkalosis with the presence of an acid?  Is the pH back within normal range?  If the pH is back within normal range then the acid-base disruption has been fully compensated  If the pH is not back within normal ranges then the acid-base disruption has been partially compensatedInterpreting ABGs Step 3 – Is there any compensation occuring? ACID BASE pH PaCO2 HCO3 Normal 7.35 – 7.45 4.5-6 22-26 Respiratory ↓ ↑ ↑ ACIDOSIS with partial metabolic compensation Metabolic ↑ ↓ ↓ ACIDOSIS with partial respiratory compensation Mixed acidosis ↓ ↑ ↓ Mixed alkalosis ↑ ↓ ↑ Lets practice!!  What is the pH?  What is causing the pH disturbance?  Is there any compensation?  Is the compensation complete? Lets practice!!  What is the pH? = 7.15 – It is acidic  What is causing the pH disturbance?  Is there any compensation?  Is the compensation complete? Lets practice!!  What is the pH? = 7.15 – It is acidic  What is causing the pH disturbance? – The HCO3- is low = metabolic acidosis  Is there any compensation?  Is the compensation complete? Lets practice!!  What is the pH? = 7.15 – It is acidic  What is causing the pH disturbance? = The HCO3- is low = metabolic acidosis  Is there any compensation? = The CO2 is low as well so compensation is occurring  Is the compensation complete? Lets practice!!  What is the pH? = 7.15 – It is acidic  What is causing the pH disturbance? = The HCO3- is low = metabolic acidosis  Is there any compensation? = The CO2 is low as well so compensation is occuring  Is the compensation complete? = The pH is still outside normal range so its is partialLets practice!! Metabolic acidosis with partial respiratory compensation Lets practice!!  What is the pH?  What is causing the pH disturbance?  Is there any compensation?  Is the compensation complete? Lets practice!!  What is the pH? = 7.35 – It is within normal ranges but it is on the acidotic side  What is causing the pH disturbance?  Is there any compensation?  Is the compensation complete? Lets practice!!  What is the pH? = 7.35 – It is within normal ranges but it is on the acidotic side  What is causing the pH disturbance? = The CO2 is raised which means it is a respiratory acidosis  Is there any compensation?  Is the compensation complete? Lets practice!!  What is the pH? = 7.35 – It is within normal ranges but it is on the acidotic side  What is causing the pH disturbance? = The CO2 is raised which means it is a respiratory acidosis  Is there any compensation? = The HCO3- is raised showing metabolic compensation  Is the compensation complete? Lets practice!!  What is the pH? = 7.35 – It is within normal ranges but it is on the acidotic side  What is causing the pH disturbance? = The CO2 is raised which means it is a respiratory acidosis  Is there any compensation? = The HCO3- is raised showing metabolic compensation  Is the compensation complete? = The pH is within normal ranges so there is complete compensationLets practice!! Respiratory acidosis with complete metabolic compensationCauses of acid-bace disturbances Anion Gap – Metabolic acidosis  The anion gap is an artificial concept that may indicate the cause of a metabolic acidosis  It represents the disparity between the major measured plasma cations (sodium) and the anions (chloride and bicarbonate)  The anion gap represents the minor unmeasured anions such as organic acids (lactic acid, ketoacids, formic acid (from methanol)) (Na) – (Cl + HCO3) = anion gap  Normal anion gap = 8 – 16 mmol/L -  Must remain electroneutral – so if HCO ↓ a3 additional anion must be present – if this is Cl then anion gap unchanged; if this is not Cl then anion gap will riseCauses of acid-bace disturbances Anion Gap – Metabolic acidosis  Metabolic acidosis can be classified into increased anion gap and normal anion gap.  Essentially a high anion gap is due to the presence of an organic acid mainly lactate or ketones  A normal anion gap means a loss of bicarbonates or their precursors or decreased renal acid excretion Raised anion gap – new acid added to the body M.U.D.P.I.L.E.S M = Methanol U = Uraemia D = DKA P = Paracetamol and propylene glycol I = Iron/isoniazid L = Lactate E = Ethylene Glycol S = SalicyclatesCauses of acid-bace disturbances Anion Gap – Metabolic acidosis Normal anion gap causes: - Loss of bicarbonate or bicarbonate precursors  Diarrhoea or other intestinal losses  Type 2 renal tubular acidosis  Carbonic anhydrase inhibitors Causes of acid-base disruptions Acidosis Alkalosis Respiratory Hypoventilation in: Hyperventilation in: • Lung disease (COPD, severe asthma • Anxiety attack, pulmonary oedema • Hypoxia • CNS depression • Acute pulmonary insult (PE, • Mechanical lung dysfunction (obesity, pneumonia, asthma attack, Guillain barre, myasthenia gravis) pulmonary oedema Metabolic Increased anion gap Acid loss in: M.U.D.P.I.L.E.S • Chloride responsive: vomiting, diuretics, corticosteroids Normal anion gap • Chloride resistant: any Retaining H+ (RTA) or loosing HCO3- hyperaldosterone state (cushing’s (diarrhoea) hypokalaemia) MCQs!!!!! Normal values: pH = 7.35 – 7.45 CO2 = 35 – 45 mmHg HCO3- = 22-26 mEq/L What acid-base disturbance is seen here? 1. Respiratory acidosis with full metabolic compensation 2. Metabolic acidosis with full respiratory acidosis 3. Respiratory acidosis with partial metabolic compensation 4. Mixed acisosis MCQs!!!!! Normal values: pH = 7.35 – 7.45 CO2 = 35 – 45 mmHg HCO3- = 22-26 mEq/L What acid-base disturbance is seen here? 1. Respiratory acidosis with full metabolic compensation 2. Metabolic acidosis with full respiratory acidosis 3. Respiratory acidosis with partial metabolic compensation 4. Mixed acisosis MCQs!!!!! What acid-base disorder does this patient have? 1. Respiratory alkalosis with partial metabolic compensation 2. Metabolic alkalosis with partial respiratory compensation 3. Uncompensated metabolic alkalosis 4. Mixed alkalosis MCQs!!!!! What acid-base disorder does this patient have? 1. Respiratory alkalosis with partial metabolic compensation 2. Metabolic alkalosis with partial respiratory compensation 3. Uncompensated metabolic alkalosis 4. Mixed alkalosis MCQs!!!!! What acid-base disorder does this patient have? 1. Metabolic alkalosis with partial respiratory compensation 2. Respiratory alkalosis with partial metabolic compensation 3. Metabolic acidosis with partial respiratory compensation 4. Respiratory acidosis with partial respiratory compensation MCQs!!!!! What acid-base disorder does this patient have? 1. Metabolic alkalosis with partial respiratory compensation 2. Respiratory alkalosis with partial metabolic compensation 3. Metabolic acidosis with partial respiratory compensation 4. Respiratory acidosis with partial respiratory compensationMCQs!!!!! ABG results Reference range • pH = 7.27 • pH = 7.35 – 7.45 • pCO2 = 5.2 • pCO2 = 4.5 – 6.0 • HCO3- = 15 • HCO3- = 22 - 28 • Na+ = 142 • Na+ = 135 - 145 • Cl- = 101 • Cl- = 96 - 106 Which of the following is a potential cause of this person’s acid-base disorder? 1. Severe asthma attack 2. Paracetamol overdose 3. Renal tubular acidosis 4. Profound vomitingMCQs!!!!! ABG results Reference range • pH = 7.27 • pH = 7.35 – 7.45 • pCO2 = 5.2 • pCO2 = 4.5 – 6.0 • HCO3- = 15 • HCO3- = 22 - 28 • Na+ = 142 • Na+ = 135 - 145 • Cl- = 101 • Cl- = 96 - 106 Which of the following is a potential cause of this person’s acid-base disorder? 1. Severe asthma attack – Respiratory acidosis 2. Paracetamol overdose 3. Renal tubular acidosis – non anion gap metabolic acidosis 4. Profound vomiting – Metabolic alkalosisThank you! Any Questions? 2439957l@student.gla.ac.uk