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112 Cards in this Set

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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"immunoflorescence
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 reabsorption of urea
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"
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
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
-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
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
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
-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
-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
-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
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
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
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
-also caused by hyperphosphatemia(component of renal failure)
Perct. of filtered Phosphate reabsorbed in the proximal tubule via Na-phosphate cotransport
-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)
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)