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86 Cards in this Set
- Front
- Back
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pH
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negative logarythm of the concentration of H+ ions in 1 mol H2O
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pH of body fluids
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-gastric : 1.2-3.0
-vaginal : 3.5-4.0 -pancreas: 7.1-8.2 -semen: 7.2-7.6 - blood: 7.35-7.45 -CSF: 7.4 -bile: 7.6-8.6 -constant pH vital, most close to 7.4 (basic) |
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acids
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dissociate in a solution to yield protons and the corresponding base
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bases
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in solution, accept proton, thereby forming the corresponding undissociated acid
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strong acid
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-ionizes almost completely in soln
-conjugate base weak meaning a high proton concentration is required to accept a proton and form an undissociated acid |
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weak acid
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-ionizes only partially in soln
-conjugate base is strong meaning the binding force to H is high, thus acception protons is already at low proton concentrations |
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buffer system
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-consists of weak acid plus its strong base
-reduces the changes in pH when acids or bases added -free H ions can combine with a buffer base to form a weak undissociated acid -reaction depends on pH |
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H and buffer system
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-increase of H concentration forces the reaction more to the right and more H ions are bound to the buffer
-decrease of H concentration shifts the reactions more to the left and more H ions are released from the buffer |
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decomposition of aa's and organic salts
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-methionine, cysteine, arginine, lysine
eg cys --> glc + urea + sulfate and 2H eg Naglutamate --> glc + urea + Na + OH |
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pKa
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-pH at which individual acid or base is dissociated to 50%
-resulting concentrations of acid and base are equal -->max buffering - Henderson-Hasselbach: pH= pK +log (A-/HA) - |
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buffer capacity
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-how much acid or base can be added to change the pH for a certain value
-determined by two factors: 1. pK 2. concentration of the buffer |
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3 buffer systems
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1. lactic acid-lactate: pH 1.9- 5.9
2. phosphate buffer: covers biological pH's from 4.8- 8.8 3. ammonium: 9.4 |
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phosphate buffer
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-advantage: pK=6.8, close to physiological pH values
- blood: very low []in blood plasma and the ECF it has almost no importance -intracellular: IC [] much higher, except erythrocytes, and is important buffer |
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protein buffer
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- important IC buffer in all cells b/c high protein concentration
- pK of many close to 7.4 - IC: buffers metabolic pH changes - EC: buffers, H diffuses through cell membrane - hemoglobin in erythrocutes buffers respiratory pH changes |
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bicarbonate buffer
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-maintains constant blood pH
-amounts of reactants varies due to changes in metabolism and excretion =open buffer system -flexibility, high capacity -extra CO2 quickly expired by lung or slowly, but more powerfully excreted by the kidney - H2CO3: formed by gas= volatile acid |
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bicarbonate buffer capacity
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-pK of carbonic acid= 6.1, but buffering capacity is high because:
1. high concentration: 25.2 mM 2. constant plasma [CO2] 3. continuous metabolic formation and continuous excretion via respiration and urine |
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effectiveness of bicarbonate buffer
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Henderson Hasselbach: at pH 7.4 there is 20 times more base than acid and therefore the buffering is better against excess acid than excess base
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regulation of acids and bases
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-despite metabolic acids from endogenous protein and carbonic acid from respiration,
-pH in blood and ECF maintained by: 1. buffers 2. respiration 3. renal excretion -regulation of [H] - kidneys play role in excretion of H+ ions |
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acidosis
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-condition in which arterial blood pH <7.36
-respiratory compensates for metabolic alkalosis - metabolic compensate for respiratory alkalosis |
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alkalosis
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-condition in which arterial blood pH >7.44
- respiratory compensates for metabolic acidosis - metabolic compensates for respiratory acidosis |
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respiratory acidosis
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PCO2 > 40mmHg
HCO3- >24 mEq/L -metabolic compensation |
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metabolic acidosis
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-respiratory compensation
PCO2 < 40mmHg HCO3- <24 mEq/L |
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respiratory alkalosis
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PCO2 < 40mmHg
HCO3- <24 mEq/L -metabolic compensation |
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metabolic acidosis
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-respiratory compensation
PCO2 > 40mmHg HCO3- >24 mEq/L |
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acid-base nomogram
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-shows arterial blood pH, arterial plasma HCO3-, and PCO2 values
-shaded areas show approximate limits for normal compensation cause by simple respiratory and metabolic disorders |
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buffers and H+ changes
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-1st line of defense against H+ changes because of their immediate reaction to the acid-base disturbance
- capacity limited as a given amount of buffer becomes saturated |
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respiratory system and H+ changes
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- second line of defense in H changes when buffer systems have reached saturation
- compensation via increasing or decreasing CO2 elimination -limits the disturbance but rarely returns pH back to normal |
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renal system and H+ changes
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-within hours after disturbance, kidneys are recruited as 3rd line of defense
- compensate via changing excretion of H+ and bicarbonate - activity develops gradually and takes days to become fully activated |
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respiratory acidosis examples
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-alveolar PCO2 increased by:
1. lung disease 2. weakness of respiratory muscles 3. CNS disease 4. drug overdose (hypnotics, anaesthetics) |
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respiratory alkalosis examples
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-alveolar PCO2 decreased:
1. voluntary overbreathing 2. artificial ventilation 3. drug overdose: salicylate poisoning causes stimulation of the respiratory centers causes increased expiration of CO2 |
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metabolic acidosis: H+ production exceeds excretory capacity
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-disorder of metabolism: starvation, ketosis, diabetis ketoacidosis, lactic acidosis
- ingestion of substances that give rise to H+: eg methanol, paraldehyde, salicylate poisoning |
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metabolic acidosis: H+ excretion failure (rate too low)
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-inadequate production of NH3 by kidney: chronic renal failure
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metabolic acidosis: loss of HCO3- from the body
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-from GI tract: severe diarrhea
- urine: carbonic anhydrase inhibitors, proximal renal tubular acidosis |
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metabolic alkalosis: loss of H from the body
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-vomiting
-diuretics: eg thiacides -glucocorticoid excess, mineralcorticoid excretion - severe K depletion |
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treatment of acidosis
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1. orally: sodium bicarbonate
2. IV: sodium lactate, sodium gluconate |
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treatment of alkalosis
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1. orally: ammonium chloride
2. IV: lysine hydrochloride |
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buffer base in acid-base disorders
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-buffer base (BB)=sum of all conjugate bases in 1L of arterial whole blood
-normals: 1. bicarb: 24 mEq 2. protein: 15 mEq 3. HHb/HbO2: 9/48 mEq |
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Base excess in acid-base status
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= observed [BB]- normal [BB]
(-): base deficit, acidosis (+) base excess, alkalosis -can use this to estimate treatment, eg. -10mEq treated with equal amount to neutralize excess H+ |
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anion gap and acid-base status
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=([Na] + [K])-([HCO3]+[Cl])= 17mEq
-not 0 because not all anions routinely measured -increased in metabolic acidosis, decreased in most cases of metabolic alkalosis |
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lab parameters
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1. GFR
2. renal clearance 3. excretion, resorption and secretion rates 4. renal blood flow 5. clearance ratio 6. clinical screening |
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GFR
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-V filtered from capillary blood into Bowman's per min
-(ml/min) determined by: 1. Pf: mean net filtration P across the glomerular membrane 2. Kf: filtration coefficient (ml/min/mmHg): how many ml of primary urine is filtered per min and per mmHg from the blood into Bowman's -GFR= Pf x Kf |
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Renal clearance meaning
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-water soluble metabolic wastes are mainly eliminated in urine
-RC gives us an idea of the rate at which the blood plasma is cleaned or cleared of a certain substance |
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renal clearance general
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1. how much substance is excreted or how many ml/min of the plasma is completely cleared of the substance?
2. which parameters are accesible |
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renal clearance variables
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-Vu: urine flow rate (ml/min)
-Ps: plasma concentration of substance - Us: urine concentration of the substance |
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Renal clearance equation
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Cs= Vu x (Us/Ps)
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Cs x Ps
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if you suppose:
1.Cs is the plasma volume cleared of the substance -and- 2. Ps is the plasma concentration -then- Cs x Ps is the amount of substance removed from the plasma per unit time |
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Vu x Us
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this amount is removed from blood and added to the urine
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Cs x Ps = Vu x Us
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the amount removed from plasma = amount added to urine
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inulin
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-clearance used to determine GFR
- just flows through the kidney and into urine |
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creatinine general
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~ used as inulin for fast screening of GFR
- not as accurate as inulin because creatinine produced in the body |
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PAH general
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clearance used to determine the renal plasma flow/ renal blood flow
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glucose general
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clearance is zero
- blood is not cleared of glucose because normally all filtered glucose is resorbed |
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basic processes of the nephron
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1. glomerular filtration: initial filtered load of a solute
2. tubular resorption: reduces excretion of a solute 3. tubular secretion: increases excretion of a solute |
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excretion rate
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= Us x Vu
-how much excreted per minute - Us= mg/ml of urine - Vu= ml/min - |
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resorption rate
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=(GFR x Ps) - (Us x Vu)
-GFR x Ps = absolute amount filtered per minute - Us- Vu= amount ending up in urine per minute |
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secretion rate
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=(Us x Vu) - (GFR x Ps)
= excretion rate - absolute amount filtered per minute - additional amount was therefore secreted from the blood into the tubular fluid |
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GFR and inulin
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GFR= (U inulin x Vu)/ Pinulin
-inulin freely filtered like water, not reabsorbed or secreted by the tubular system |
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PAH and effective renal plasma flow
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=CPAH= (UPAHx Vu)/ PPAH
-PAH is an exogenous marker that is about 90% cleared from the plamsa by filtration and secretion - good approximation of renal plasma flow |
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PAH and renal plasma flow
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= ERPF/ 0.9
-correct ERPF knowing the extracting rate of 90% for PAH |
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Renal blood flow and Hct
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= RPF/ (1- Hct)
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clearance ratio = 1
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= Cs/ Cinulin
=1: clearance of the substance is the same as inulin, therefore only filtered, not reabsorbed or secreted |
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clearance ratio < 1
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= Cs/ Cinulin
substance is partly reabsorbed by the tubular system |
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clearance ratio > 1
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= Cs/ Cinulin
in addition to filtration in the glomerulus, the substance is also secreted by the tubular system |
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clinical screening with Creatinine and BUN
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-Creatinine widely used endogenous marker of GFR
-more convienient than inulin, etc. - wastes secreted by kidney produced and excreted at a constant rate -plasma concentration fairly constant -kidney disease decreases excretion then plasma [] increases |
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GFR and plasma creatinine concentration
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-GFR decreases in kidney disorder causing production to exceed excretion and increased plasma level
- eg 50% GFR, plasma creatinine 2x normal -eg 25% GFR, plasma creatinine 4x normal |
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BUN testing
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=blood urea nitrogen
- can be quickly measured with test strips that change color with addition of blood product - often require further testing as levels vary depending on age, muscle volume and exercise |
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creatinine testing
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-reagent incubation with color change
- chemistry analyzers - often require further testing as levels vary depending on age, muscle volume and exercise |
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normal micturition
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=urine
-full bladder--> stretch receptors --> spine --> PS activated and S inhibited --> motor neurons of ext sphincter are inhibited --> center in pons (interconnected with uppermedulla, hypothalamus, and cerebrum) starts voluntary flow--> increase in bladder P assures complete emptying |
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diuretics general
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-increase the excretion of solutes and water
- goals: 1. lower BP 2. rid body of excess interstitial fluid eg edema -classified by their mechanism and site of action |
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diuretics: osmotically active agents
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-freely filtered into Bowman's
- not reabsorbed from tubules - more osmotically active particles remain in tubular fluid = more water bound and not resorbed -both water and diuretic excreted, increasing urine volume |
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diuretics: transport inhibitors
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-transport systems like Na/K pump, NaCl symport or Na/K/2Cl symport inhibited
=their solutes and related volume of water are excreted -increases the urine volume |
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diuretics: carbonic anhydrase inhibitors
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-diffusion coefficient of CO2 is higher than bicarbonate
-inhibiting formation of CO2 in the tubular fluid causes more carbonic acid to remain in the tubules = excreted with related water, increasing urine volume |
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diuretics: site of action in proximal tubule
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1. osmotic
2. carbonic anhydrase inhibitors |
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diuretics: site of action in early distal tubule
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thiacide diuretics
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diuretics: site of action in cortical collecting duct
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K+ sparing diuretics
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osmotic diuretics fx
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-filtered into but not reabsorbed by tubular system
- NaCl excretion increases - onset of diuresis: 1-3 hours -duration: 3-6 hours |
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osmotic diuretics indications
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-drug classes: mannitol, glycerol
-indications: 1. treatment or prevention of acute renal failure 2. accelerated excretion of toxins -contraindication: edema caused by cardiac failure |
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site actions of loop diuretics
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thick ascending loop of Henle
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carbonic anhydrase inhibitors fx
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-decreased resorption of bicarb
-mild diuresis effect -danger of acidosis: excretion of base - Na and K excretion increases as less K available for antiport - duration: ceases after 2-3 days due to low blood levels of bicarb |
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carbonic anhydrase inhibitors indications
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-drug classes: acetalamide, dichlorphenamide, metazolamide
-indications: 1. reduction of intraocular P in glaucoma 2. mountain sickness (decrease in bicarb) |
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loop diuretics fx
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-block Na/K/Cl symport in L o Henle
- Na, K, Cl and H2O excretion increases: K wasting effect -very potent diuresis effect: high ceiling diuretics, excretion of up to 30% of glomerular filtrate - onset: after 5min IV and 20-60min oral -duration: 2-8 hours |
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loop diuretics indications
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-drug classes: furosemide, bumetanide, torsemide
- indications: 1. hypertension 2. congestive heart failure 3. ascites 4. acute and chronic renal failure 5. acute pulmonary edema |
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thiacide diuretics fx
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-block Na/Cl symport in early distal tubule
- Na and K excretion increases - medium effect - wide therapeutic range: toxic dose= 100-1000x therapeutic dose -onset: 1 hours oral -duration: 6-48 hours - |
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thiacide diuretics indications
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-drug classes: chlorothiazide, hydrochlorothiazide
- indications: 1. hypertension 2. edema resulting from congestive heart failure |
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K sparing diuretics fx
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-spirolactone: competitively blocks Na resorption and K secretion caused by aldosterone
- triamterene and amiloroide: blocks Na/K pump in distal tubule and collecting duct - Na excretion increases, K decreases (danger of intoxication) - medium effect - onset: after 1 hour - duration: 6-48 hours |
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K sparig diuretics indications
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-drug classes: spironolactone, triamterene, amiloroide
- indications: 1. chronic liver disease combined with ascites 2. congestive heart failure= counteracting K loss of other diuretics |
