Pathophysiology(Renal)*

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Congenital Renal abnormality resulting in oligohydramios: Bilateral Reanl Agenesis
Renal congenital abnormality resulting in polyhydramnios: Duodenal atresia or tracheoesophageal fistula
Glomerular Dse. characterized by massive proteinuria(>4gms/day), hypoalbuminemia,generalized edema, hyperlipidemia & hypercholesterolemia: Nephrotic Synd.
Glomerular dse. found often in children; prototype of nephrotic synd.; characterized by lipid-laden cortices & disappearance or fusing of epithelial foot processes: Minimal Change Dse(lipoid nephrosis)
Glomerular dse. w/c is a major cause of nephrotic synd. in teenagers charact. by thickened capillary walls, nephrotic synd w/ azotemia & "spike & dome" appearance: Membranous Glomerulonephritis
-assoc. w/ SLE,HBV,syphlis,malaria & may cause renal vein thrombosis
Nephrotic dse. charact. by inc. mesangial matrix resulting in diffuse glomerulosclerosis & nodular glomerulosclerosis(Kimmelstiel-Wilson nodules): Diabetic Nephropathy
-demonstrates thickening of vascular basement memb.
Nephrotic Dse assoc. w/ chronic inflammatory dse.(rheumatoid arthritis) & Plasma Cell disorders (multiple myeloma);charact. by subendothelial & mesangial amyloid deposits: Renal Amyloidosis
Nephrotic dse. classified into 5 renal patterns:Type I,Type II(mesangial form),TypeIII(focal proliferative form),Type IV(diffuse proliferative form,Type V(membranous form): Lupus Nephropathy
Most severe renal pattern in lupus nephropathy assoc. w/ both nephrotic & nephritic synd. charact. by "wire loop abnormality",endothelial cell proliferation & subendothelial immune complex deposition: Type IV(Diffuse Proliferative Form)
Renal dse. charact. by inflammatory rupture of the glomerular capillaries resulting leakage of red cells into the bowman space forming red cell casts or granular casts: Nephritic Synd.
-assoc. w/ oliguria,azotemia, hypertension,hematuria & "smoky brown urine"
Nephritic synd. assoc. w/ grp.A B-hemolytic strep. post infection charact. by an infl. rxn. of all glomeruli in both kidneys resulting in punctate hemorrhages,electron-dense "humps",enlarge bloodless glomeruli & "lumpy-bumpy"immun: Poststreptococcal Glomerulonephritis (Acute Proliferative Glomerulonephritis)
Nephritic synd. charact. into 3 classes:Immune Complex(poststrep. etiology-50%),Antiglomerular Basement Memb. Antibodies(Goodpasture synd-10%), Antineutrophil Cytoplasmic Antibodies(Wegner Granulomatosis): Rapidly Progressive(crescentic) Glomerulonephritis(RPGN)
-progresses to renal failure w/ in weeks & charact. by deposition of fibrin & proliferation of parietal epithelial cells in the bowman space & capsule
Renal dse. often in males in mid-20's charact. by nephritic synd,pneumonitis w/ hemoptysis,RPGN crescentic morph. & demonstrates linear immunoflourescence: Goodpasture synd.(antiglomerular basement memb. antibodies)
-caused by antibodies against antigens in the glomerular & pulmonary alveolar basement memb.
An immune complex dse. assoc. w/ various disorders(SLE,subacute bact. endocarditis,polyarteritis nodosa, Goodpasture synd,Wegner Granulomatosis, IgA nephropathy): Focal Glomerulonephritis
-differs from focal segmental glomerulosclerosis in w/c there is sclerotic rather than infl. & proliferative changes
Hereditary nephritis assoc. w/ nerve deafness & ocular disorders(lens dislocation,cataracts);often progres to end-stage renal dse. by age 30: Alports Synd.
-caused by mutation in the gene for alpha-5 chain of type IV collagen
Characterized by benign recurrent hematuria in children following an infect. w/ deposition of IgA in the mesangium: Berger Dse(IgA nephropathy)
-assoc. w/ Henoch-Schonlein Dse. & focal glomerulonephritis
Characterized by slow progression to chronic renal dse. w/c occurs in 2 forms:TypeI(Immune Complex Nephritis) & TypeII(Dense Deposit Dse.): Membranoproliferative Glomerulonephritis
-has "Tram-track appearance" on silver stain
Findings in Acute Pyelonephritis(acute infect. of renal parenchyma): Fever,leukocytosis,flank tenderness, urinary white cells,white cell casts in urine;common in women during pregnancy
Acute interstitial renal infl. caused by penicillin derivatives(methicillin),NSAID,diuretics;resolves upon cessation of the inciting drug: Acute drug-induced Interstitial nephritis
-may present eosinophilia & eosinophiluria
Assoc. w/ DM,long term abuse of Phenacetin w/ aspirin & other analgesics w/c may lead to Chronic Analgesic Nephritis: Renal Papillary Necrosis(necrotizing papillitis)
-may be a catastrophic consequence of Acute Pyelonephritis
Most common reversable cause of Acute Renal Failure precipitated by renal ischemia,crush injury w/ myoglobinuria & injury to proximal tubules due to ingestion of toxic subst(Mercuric Chloride,Gentamycin,antifreeze): Acute Tubular Necrosis
-may lead to cardiac standstill due to hyperkalemia during the initial oliguric phase
Dysfunction of the proximal tubules manifesting in Glycosuria, hyperphosphaturia,hypophosphatemia, aminoaciduria & systemic acidosis: Fanconi Synd.
-characterized my impared absorption of glucose,A.A,phosphate,bicarbonate
Impaired reabsorption of Tryptophan leading to Pellagra like manifestation: Hartnup Dse.
Renal tubular disorder charact. by coarse,asymmetric corticomedullary scarring,interstitial fibrosis & tubular atrophy resulting in eosinophilic proteinaceous casts(Thyroidization of the kidney): Chronic Pyelonephritis
-result from chronic urinary tract obstruction;leads to hypertension & end-stage renal dse.
An acute generalized ischemic infarction of the cortices of both kidneys assoc. w/ obstetric catastrophies(abruptio placentae, eclampsia) & septic shock: Difffuse Cortical Necrosis
-caused by end-organ spasm & DIC
Four types of stone in urolithiasis: Calcium stones(80-85%),Ammonium Magnesium Phosphate stones(2nd most common),Uric Acid stone(hyperuricemia),Cystine stone
Most common inherited autosomal dominant kidney disorder w/c manifests from ages 15-30 w/ hypertension,hematuria,palpable renal masses & progression to renal failure: Adult Polycystic Kidney Dse.
-assoc. w/ berry aneurysm of the Circle of Willis & cystic dse. of the liver & other organs
An autosomal recessive kidney disorder manifested by multiple cysts evident at birth resulting in death shortly after birth: Infantile Polycystic Kidney Dse.
An acute or chronic renal disorder resulting from glomerular or tubulointerstitial pathology assoc. w/ azotemia of renal origin & results in uremia: Renal failure
Major clinical characteristics of Uremia(denotes the biochemical & clinical synd. characteristic of symptomatic renal dse.: Azotemia,Acidosis(inc. sulfate,phosphate,organic acid),Hyperkalemia,abnormalcontrol of fluid vol.(inability to concentrate urine in early phase,inability to dilute urine in later phase),Hypocalcemia(inability to synthesize Vit.D~lead to renal osteodystrophy),Anemia(dec. erythropoeitin),Hypertension(hyperproduction of renin)
Clinical characteristics of uremia: Anorexia,nausea,vomitting,neurologic disorders(diminished mental fxn.,convulsions,coma),bleeding(platelet disfunction),accumilation of urochrome in the skin,fibrinous pericarditis
Type of azotemia resulting from dec. renal bld. flow;characterized by inc. tubular reabsorption of Na+ & H2O resulting in oliguria, concentrated urine, dec. urinary sodium excretion; BUN:Crea ratio >15 due to dec. GFR & inc. tubular reabsorpti: Prerenal Azotemia
2 types of benign tumors of the kidney: 1)Adenoma(asymptomatic,derived from renal tubules,precursor to renal carcinoma) 2)Angiomyolipoma(assoc. w/ Tuberous Sclerosis Synd.,consist of fat smooth muscle, bld. vessels)
Most common renal malignancy, often in men(50-70yrs)who cigarette smoke, w/c originate from the renal tubules~invades renal veins~extend up the vena cava resulting in early hematogenous dissimemination & characterized by "Polygonal Clear Cells&q: Renal Cell Carcinoma
-triad of flank pain,palpable mass,hematuria(most common);fever,Secondary Polycythemia(erythropoietin production),ectopic prod. of hormones(ACTH,prolactin,renin,gonadotropin)
Most common renal malignancy in children(2-4yrs) presenting most often w/ palpable flank mass;assoc w/ WAGR complex(Wilms tumor,Aniridia, Genitourinary malformation,mental-motor Retardation),Denys-Drash Synd,Beckwith-Wiedmann Synd.: Wilms Tumor(nephroblastoma)
-assoc w/ deletions of the short arm of chromosome 11
Synd. assoc. w/ Wilms Tumor characterized by hemihypertrophy, macroglossia,organomegaly,neonatal hypoglycemia & various embryonal tumors: Beckwith-Weidemann Synd
-assoc w/ deletion of WT-2 gene
Synd. assoc. w/ Wilms Tumor characterized by abnormalities of the WT-1gene,intersexual disorders, nephropathy: Denys-Drash Synd
Most common tumor of the collecting system assoc. w/ toxic exposure(benzidine or B-naphthylamine,an aniline dye,cigerette smoking,cylophosphamide,phenacetin); presenting often w/ hematuria: Transitional Cell Carcinoma
-multifocal in origin,recur after removal,spread by local extension
Carcinoma of the kidney w/c often results from chronic infl. processes such as chronic bact. infxn.(Schistosoma haematobium infxn): Squamous Cell Carcinoma
-comprises small % of urinary tract malignancies
Clinical manifestations of UTI: Urinary frequency,dysuria,Pyuria,Hematuria,Bacteriuria
2 types of manifestations that presents w/ "Oliguria of Shock", one of w/c is present in Prerenal Azotemia: 1)Oliguria caused by dec. renal bld. flow~dec. GFR~inc. reabsorption of Na+~dec. urinary soudium 2)Oliguria in Acute Tubular Necrosis~impaired tubular reabsorption of Na+~inc. urinary Na+
Body fluid w/c measures 60% of body weight, highest in new borns & adult males,lowest in females & people w/ large % of adipose fat: Total Body Water(TBW)
-separated into compartments(ICF-2/3 of TBW,ECF-1/3 of TBW)
What is the "60-40-20 rule"?: TBW-60% of body weight, ICF-40% of body weight, ECF-20% of body weight
Markers used to measure volume in the TBW,ECF,Plasma,Interstitial,ICF: TBW(tritiated H2O & D2O),ECF(sulfate,inulin,manitol),Plasma(radioiodinated serum albumin-RISA & Evans blue),Interstitial(ECF vol.-plasma vol.),ICF(TBW-ECF)
Equation for finding the vol. of distribution in a specific compartment: Volume=Amount/Conc.(substance measured in plasma)
Type of change in vol. & osmolarity of body fuid in Diarrhea: Isosmotic vol. contraction
-dec. ECF vol.,no change in ICF vol., no change in ECF osmolarity,inc. Hct, no change in Na+
Type of change in vol. & osmolarity of bofy fluids in high NaCl intake: Hyperosmotic Vol. expansion
-inc. ECF vol.,dec. ICF vol.,inc. ECF osmolarity,dec. Hct, inc. Na+
Type of change in vol. & osmolarity in sweating, fever, diabetes inspidus: Hyperosmotic vol. contraction
-dec. ECF vol.,dec. ICF vol.,inc. ECF osmolarity,no change in hematocrit, inc. Na+
Type of change in vol. & osmolarity of body fluids in SIADH: Hyposmotic Vol. expansion
-inc. ECF vol.,inc. ICF vol.,dec. ECF osmolarity,no change in Hct,dec. Na+
Type of change in vol. & osmolarity of body fluids in adrenal insufficiency: Hyposmotic Vol. contraction
-dec. ECF vol.,inc. ICF vol.,dec. ECF osmolarity,inc. Hct,dec. Na+
Equation w/c indicates the vol. of plasma cleared of a substance per unit time: Clearance equation
-clearnce(ml/min or ml/24hr)=[urine conc.(mg/ml)][urine vol./time(ml/min)]all devided by plasma concent.(mg/ml)
Circulation in the renal system w/c is 25% of cardiac output,proportional to the pressure diff. betw. the renal art. & vein,inversely proportional to the resistance in the renal vasculature: Renal Blood Flow(RBF)
2 types of autoregulation of RBF: 1)Myogenic mechanism:renal artioles contract in response to inc. art. pressure~inc. resistance to maitain costant bld flow 2)Tubuloglomerular feedback:inc. renal art. press.~incr. flow to macula densa~macula densa causes constriction of afferent arteriole
Used to measure renal plasma flow(RPF): Clearance of para-aminohippuric acid(PAH)
-RPF=clearnce of PAH=[urine conc. of PAH(mg/ml)][urine flow rate(ml/min or ml/24hr)] all devided by plasma conc. of PAH(mg/ml); filtered & secreted
Equation for the measurement of RBF: RBF=RPF/1-Hct
Substance used to measure GFR: Clearance of Inulin
-not reabsorbed or secreted in the renal tubules; GFR=[(urine conc. of inulin)(urine flow)]/plasma conc. of inulin
Equation used to measure the fraction of RPF filtered across the glomeular capillaries: Filtration Fraction=GFR/RPF
-normally 20% of RPF;remaining 80% leaves the glomerular capillaries via efferent arterioles
Changes in starling forces on GFR, RPF, & filtration fraction in constriction of afferent arteriole: Dec. GFR(due to dec. capillary hydrostatic pressure),dec. RPF, no change in filtration fraction
Changes in starling forces on GFR, RPF, & filtration fraction in inc. plasma(protein): Dec. GFR(due to inc. glomerular oncotic pressure),no change in RPF, dec. filtration fraction(dec.GFR/unchanged RPF)
Changes in starling forces on GFR, RPF, & filtration fraction in Uretral stone: Dec. GFR(due toinc. hydrostatic pressure in the bowman space),no change in RPF, dec. filtration fraction(dec.GFR/unchange RPF)
Changes in starling forces on GFR, RPF, & filtration fraction in constriction of efferent arteriole: Inc. GFR(due to inc. glomerular hydrostatic pressure),dec. RPF,inc. filtration fraction(inc.GFR/dec.RPF)
Equation for computing for Filtered load & Excretion rate: Filtered load=GFR[plasma conc.(mg/dl)]
Excretion rate=[urine flow(ml/min)][urine conc.(mg/dl)]
Plasma glucoe conc. at w/c Na-glucose cotransport in the proximal tubule for reabsorption are fully saturated: 350mg/dl(Tm)
-inc. of plasma glucose >350mg does not result in inc. rates of reabsorption
Plasma glucose concentration at w/c glucose first appears on the urine: Threshold(250mg/dl)
Ratio w/c gives the fraction of filtered load remaining at any point along the nephron: [TF/P]x/[TF/P]inulin ratio
-corrects the TF/P x ratio for water reabsorption
Used as a marker for H2O reabsorption along the nephron; inc. as water is reabsorbed: (TF/P)inulin
Used to compare the conc. of a substance in tubular fluid along the nephron w/ the conc. in plasma: (TF/P)x ratio
Equation used to calc. the fraction of filtered H20 that has been reabsorbed: Fraction of filtered H2O reabsorbed=1- [1/(TF/P)inulin]
Mechanism & perct. of Na+ reabsorbed in the proximal tubule: 67% isosmotic reabsorption of Na+ & H2O via cotransport w/ glucose,A.A, phosphate,lactate w/c acccount for all filtered glucose & A.A; via countertransport(Na-H exchange) w/c is linked to reabsorption of HCO3; Carbonic anhydrase inhibitors(acetazolamide) act on proximal tubule by inhibiting HCO3 reabsorption
Mechanism & perct. of Na+ reabsorbed in the thick ascending limb of the loop of Henle: 25% reabsorption of filtered Na+ via Na-K-2Cl cotransport;site of action of loop diuretics(Furesemide,ethacrynic acid) w/c inhibit Na-K-2Cl cotransport; impermeable to water
Mech. & perct. of Na+ reabsorbed in the distal tubule & the collecting duct: 8% reabsorption of filtered Na via Na-Cl cotransport;site of action of thiazide diuretics;impermeable to water
2 cell types found in the late distal tubule & collecting ducts: 1)Principal cells:reabsorb Na & H2O, secrete K 2)Alpha-Intercalated cells:secrete H, reabsorb K
Action of aldosterone,ADH, & K-sparing diuretics on the late distal tubule & collecting ducts: 1)Aldosterone inc. Na reabsorption & K+ secretion in the principal cells; inc. H+ secretion in alpha-intercalated cells 2)ADH inc. H2O permeability in the principal cells, w/o w/c the principal cells would be impermeable to water 3)K-sparing diuretics decrease K+ secretion in the principal cells
Factors w/c causes shift of K+ out of the cell(hyperkalemia): Insulin def.,Adrenergic antagonist, acidosis,hyperosmolarity(H2O flows out of the cell bringing K+ w/ it), inhibitors of Na-K pump(digitalis), exercise,cell lysis
Mech. & perct. of K+ reabsorb in the proximal tubule & loop of Henle: 67% reabsorption in the proximal tubule; 20% reabsorption in the loop of Henle via Na-K-2Cl cotransport
Mech. & perct. of K+ reabsorbed in the distal tubule & collecting duct: % of reabsorption is determined by dietary intake of K+; via H,K-ATPase in the alpha-intercalated cells
Mech. of w/c K+ is secreted from the kidney: K+ is actively transported through basolateral memb. via Na-K pump~inc. in K+ conc. in the cell provides a driving force of K+ passively secreting through the luminal memb. into the tubules
Factors w/c affect K+ secretion in the distal tubule: 1)Dietary intake:inc. diet inc. secretion & vice/versa 2)Aldosterone: stimulate K+ secretion by inc. Na-K pump 3)Acid-base:due to H-K exchange across the basolateral memb.;acidosis dec. secretion,alkalosis inc. secretion 4)Thiazide & loop diuretics: inc. K secretion 5)K-sparing diuretics: dec.K+ secretion 6)Luminal anions:inc. anions inc.secretion
Perct. of filtered urea reabsorbed passively in the proximal tubule: 50%
-ADH inc. reabsorption in inner medullary collecting ducts w/c contribute to urea recycling in the inner medulla & development of corticopapillary osmotic gradient
Perct. of filtered Ca+ reabsorbed accross the proximal tuble & thick ascending limb via passive process coupled to Na+ reabsorption: 90%
-PTH inc. reabsorption via adenylate cyclase in the dital tubule;Thiazide diuretics inc. reabsorption(tx. hypercalciuria); Loop diuretics inc. excretion by inhibiting Na+ reabsorption(tx.hypercalcemia)
Substance w/c compete w/ magnesium in the loop of henle for reabsorption: Calcium
-hypercalcemia inc. Mg excretion; hypermagnesemia inc. Ca+ excretion
Response to water deprivation: Deprived water~inc. plasma osmolarity~ stimulation of osmoreceptor(ant. hypothalamus~inc. secretion of ADH(post. pituitary)~inc. H2O permeability of late distal tubule & collecting duct~inc. H2O reabsorption~ inc. urine osmolarity & dec. urine vol.~dec. plasma osmolarity toward normal
Response to water intake: Drink H2O~dec. plasma osmolarity~ inhib. osmoreceptors in ant. hypothalamus~dec. secretion of ADH(post.pituitary)~dec.H2O permeability of late distal tubule & collecting duct~dec. H2O reabsorption~dec. urine osmolarity & inc. urine vol.~inc. plasma osmolarity toward normal
Used to estimate the ability to concentrate or dilute the urine: Free-water clearance=urine flow rate(ml/min)-osmolar clearance[(Urine osmolarity)(urine flow)/plasma osmolarity](ml/min)
Effect of primary polydipsia on serum ADH,serum osmolarity/serum Na,urine osmolarity,urine flow rate,free water clearance: Dec. serum ADH & serum osmolarity/ serum Na,hyposmotic urine osmolarity, high urine flow rate,positive free water clearance
Effects of Central diabetes insipidus on serum ADH,serum osmolarity/serum Na, urine osmolarity,urine flow rate, free water clearance: Dec. ADH,Inc. serum osmolarity/serum Na(due to excretion of too much H2O), hyposmotic urine,high urine flow rate, positive free H2O clearance
Effect of Nephrogenic diabetes insipidus on serum ADH,serum osmolarity/serum Na, urine osmolarity,urine flow rate, free water clearance: Inc. serum ADH(due to inc. plasma osmolarity),inc. serum osmolarity/ serum Na(due to excretion of to much H2O),hyposmotic urine,high urine flow rate,positive free water clearance
Effect of water deprivation on serum ADH,serum osmolarity/serum Na, urine osmolarity,urine flow rate, free water clearance: Inc. serum ADH,high-normal serum osmolarity/serum Na,hyperosmotic urine, low urine flow rate,neg. free water clearance
Effects of SIADH on serum ADH,serum osmolarity/serum Na, urine osmolarity,urine flow rate, free water clearance: Inc. ADH,dec. serum osmolarity/serum Na(due to inc. reabsorption of H2O), hyperosmotic urine,low urine flow rate, neg. free water clearance
Second most common renal calculi assoc. w/ ammonia producing organisms(Proteus Vulgaris,Staphylococcus); forms "Staghorn(struvite)calculi": Ammonium Magnesium Phosphate stones
Caused by hypercalcemia(hyperthyroidism,Milk-alkali synd) w/c results in deposition of calcium in the kidney parenchyma leading to renal failure: Nephrocalcinosis
-also caused by hyperphosphatemia(component of renal failure)
Perct. of filtered Phosphate reabsorbed in the proximal tubule via Na-phosphate cotransport: 85%
-PTH inhibits phosphate in the proximal tubule causing phosphaturia & inc. urinary cAMP; PO4 is a buffer for H+~excreted as H2PO4(titratable acid)
Arrange in order of highest clearance of substances to lowest clearance (Inulin,K+,glucose,urea,Na+,PAH,HCO3-, A.A): PAH>K+>inulin>urea>Na+>glucose,A.A,HCO3
In the rxn: CO2+H2O--H2CO3--(H+)+HCO3, what enzyme catalyzes the reversible rxn. betw. CO2 & H2O?: Carbonic Anhydrase
The mech. of action & effect on the kidney by PTH: Mech.(Basolateral receptor,cAMP-urine); Effect on kidney(dec. phosphate reabsorption in the proximal tubule,inc. Ca reabsorption in distal tubule,stimulate 1alpha-hydroxylase in the proximal tubule)
Mech. of action & effect on the kidney of ADH: Mech.(Basolateral V2 receptor,cAMP); Effect on kidney(inc. H2O permeability in late distal tubule & collecting duct principal cells)
Mech. of action & effect on the kidney of aldosterone: Mech.(new protein synthesis); Effect on kidney(inc. Na reabsorption in distal tubule principal cells, inc. K+ secretion in distal tubule alpha intercalated cells)
Stimulus for secretion, mech. of action, & effect on the kidney by ANF(atrial natriuretic factor): Stimulus(inc. atrial pressure); Mech. of action(Guanylate cyclase); Effect in the kidney(inc. GFR,dec. Na reabsorption)
Effect of Angiotensin II on the kidney: Inc. Na-H exchange & HCO3 reabsorption in the proximal tubule
Mech. in the reabsorption of filtered HCO3 w/c results in net reabsorption of filtered HCO3: In proximal tubule(H2O+CO2--H2CO3--H+ HCO3)~H+ is transported via H-Na exchange into the lumen & HCO3 is reabsorbed~in the lumen(H+ & filtered HCO3--H2CO3--CO2+H20)~both CO2 & H2O is reabsorbed to start the cycle again
Hormone w/c stimulates H-Na exchange in the proximal tubule cells increasing reabsorption of HCO3: Angiotensin II
-contributes to contraction alkalosis w/c occurs 2nd to ECF vol. contraction
Mech. in w/c H+ are excreted through the kidneys as titratable acid(H2PO4): H(secreted)+ HPO4(filtered)=H2PO4 (excreted)
-net secretion of H & net reabsorption of HCO3;dec. urinary pH;amount of H+ excreted is determined by amount of urinary buffer & pK of the buffer
Mech. in the excretion of H+ as NH4: NH3(produced from glutamine,diffused thru luminal memb.)+(H+)secreted=NH4(excreted)
-determined by the amount of NH3 synthesized & urine pH;the lower the pH, the greater the excretion of H+ as NH4
Represents unmeasured anions(phosphate,citrate,sulfate,protein, lactate,B-hydroxy butyrate,formate) in serum w/c inc. in metabloic acidosis to replace depleted HCO3: Serum anion gap=[Na+]-[Cl+HCO3]
-if serum inc.,unmeasured anions have inc. to replace depleted HCO3;if serum is normal(8-16mEq/L),Cl is inc. to replace HCO3(hyperchloremic metabolic acidosis)
Vomitting,hyperaldosteronism,loop & thiazide diuretics are causes of this acid-base disorder: Metabolic Alkalosis
-due to loss of gastric H+,inc. H+ secretion by tubules,volume contraction alkalosis
Opiates,sedatives,anesthesia,airway obstruction,ARDS,COPD are causes of this acid-base disorder: Resp. Acidosis
-due to inhibition of medullary resp. center,weakening of resp. muscle & dec. CO2 exchange
Pneumonia,pulmonary embolus,high altitude,salicylate intoxication can cause this type of acid-base disorder: Resp. Alkalosis
-due to hypoxemia causing inc. ventilation,stimulation of medullary resp. center
Ketoacidosis,salicylate intoxication, diarrhea,type 4 RTA are causes of this acid-base disorder: Metabolic Acidosis
-due to accumulation of B-OH-butyric acid & acetacetic acid,inc. anion gap, GI loss of HCO3,hypoaldosteronism
Site of action,mech. & effect of Carbonic Anhydrase inhibitors on the kidney: Site(proximal tubule); Mech.(inhibit carbonic anhydrase), effect(inc. HCO3 excretion)
Major effect of loop diuretic on the kidney: Inc. NaCl,K+,Ca+ excretion; dec. ability to conc. urine(due to dec. corticopapilary gradient); dec. ability to dilute urine(due to inhib. of diluting segment)
Site of action,mech. & effect of thiazide diuretics on the kidney: Site(early distal tubule); Mech.(inhibit NaCl reabsorption); Effect(inc. NaCl & K+ exretion,dec. Ca+ excretion & ability to dilute urine); no effect on ability to conc. urine
Site of action,mech. & effect of potassium sparing diuretics: Site(late dital tubule & collecting ducts); Mech.(inhibit Na reabsorption & K+ secretion); Effect(inc. Na excretion,dec. K+ & H+ secretion)

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