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137 Cards in this Set
- Front
- Back
creatinine clearance
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(U x V)/ P then divide by minutes in day (1400)
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a. normal urine output
b. oliguria c. anuria d. polyuria |
a. 750-2000 mL/day
b. <500 c. <100 d. >2500 |
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fractional excretion of urea
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(Una x Pcre)/ (Pna x Ucre) then x 100
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prerenal azotemia
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anything that creates inadequate blood flow to kidneys
-secretion of ADH = ocnc urine Una <10meq/L, 350-400 mOsm |
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renal azotemia
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nephrons don't do work, Na lost to urine
Una>40meq/L, <350 Osm |
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causes renal azotemia
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glomerulonephritis
acute tubular necrosis pyelonephritis |
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diff b/t uremia and azotemia
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azotemia- increased plasma creatinine and BUN with NO symptoms
uremia- increased WITH symptoms (many) |
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prerenal ARF caused by:
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1. hypotension (sepsis, dehydration, hemorrhage)
2.edematous states (CHF, cirrhosis, nephrotic syndrome) |
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nephrotic syndrome leaks...
nephritic syndrome leaks... |
>3g protein/day
<3g protein/day (post-infectious glomerulonephritis) |
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intrinsic RF caused by:
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-acute tubular necrosis = ischemia= tubules sick
-nephrotoxic drugs (aminoglycosides, radiocontrast) -heavy metals =injure tubules, necrosis -glomerulonephritis interstitial nephritis (drugs) -infectious int. neph (usually E.Coli) -vasculitis (vessels disrupted by IC deposition) |
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post RF/ obstructive RF caused by:
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commonly nephrolithiasis/urethrolithiasis, usually uric acid stones --> gout or CHEMO
-also tumors, BPH |
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universal early sn that kidney function is compromised by whatever cause
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increased BUN and Pcre
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NL GFR and creatinine clearance
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both @ 125 mL/min
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GFR in chronic renal failure
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goes to 10 mL/min and below
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NL Pcre
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<1.3 mg/dl
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Total urinary creatinine per day
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1-2 g
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BUN
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8-20 mg/dl
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NL BUN/Pcre ratio
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10-15
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BUN/Pcre in prerenal azotemia
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>/= 20
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FEna
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NL <1-5%
prerenal azotemia <1% contrast agent prerenal azo <1% renal azotemia >1% postrenal azotemia >1% (>4%) |
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Prerenal azotemia values
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Una <10 mEq/L
Uosm >450 mOsm/kg FEna <1% BUN/Pcre >20 |
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Renal azotemia values
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Una >40 mEq/L
Uosm <450 FEna >1% BUN/Pcre <20 |
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Postrenal azotemia FEna
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FEna >4%
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hypokalemia
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<3.5 mEq/L
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hyperkalemia
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>5.5 mEq/L
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NL total urinary protein per day
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150 mg
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minimal proteinuria
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<0.5 g/day
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moderate proteinuria (nephritic syndrome)
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.5-3.5 g/day
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marked proteinuria (nephrotic syndrome)
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>3.5 g/day
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NL urinary protein/ creatinine on "spot" urine
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<0.2
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NL urine osmolality on "spot" urine after 12 hr fluid restriction
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>800 mOsm/kg
<400 = renal impairment |
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spot urine for myoglobin- + indicates:
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crush injury
polymyositis recent surgery rhabdomyolysis electrical burn |
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hematuria
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>5 cells per hpf
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pyuria (WBC's)
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>5 cells per hpf
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dysmorphic RBCs or RBC casts (even one) in urine is
PATHGNOMONIC for: |
glomerulonephritis
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WBC casts in urine indicate
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pyelonephritis
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epithelial casts in urine indicate
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acute tubular necrosis
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fatty casts (oval fat bodies) in urine indicate
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nephrotic syndrome
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waxy casts indicate
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chronic renal failure
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urine dip should be negative for:
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-protein
-glucose -ketones -RBC's -bilirubin -nitrite -leukocyte esterase |
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on microscopic analysis, urine should be negative for:
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-bacteria
-casts: RBC, WBC, waxy or fatty |
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NL to see these in urine under microscope:
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an occasional hyaline or epithelial cell cast
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urine dip = + for blood but no cells on microscopic analysis?
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Hb or Mb in urine
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kidneys regulate blood flow by 3 different mechanisms:
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1. myogenic mech- main way, so partially responsible for GFR maint. too = afferent arteriole constricts
2. tubuloglomerulo feedback- JGA regulates GFR against momentary changes in BP 3. glomerulotubular balance - keep amt. filtered solute (NaCl) constant during time that GFR might be increased by change in BP-maintains constant fraction being filtered |
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parts of juxtaglomerular apparatus
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1. macula densa
2. granular cells 3. extraglomerular mesangial cells (secrete chem. junk) 4. sympathetic nerves (no para in kidney!) |
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macula densa detects:
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increase in flow rate-->sends signal to granular cells-->causes afferent arteriole to constrict-->decrease GFR
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release of NE by sympathetic nerves on alpha-1 receptors causes:
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vasoconstriction
-receptors found on renal arterioles |
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release of NE by sympathetic nerves on beta-1 receptors causes:
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release of renin
-receptors found on granule cells in JGA |
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release of NE by sympathetic nerves in renin tubule causes:
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increase in Na reabsorption
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CO2 causes
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arteriole vasodilation (more blood can flow to exercising muscles)
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2 mechs that regulate BP long term:
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1. angiotensin II induced vasoconstriction
2. aldosterone and ADH mediated regulation of circulatory fluid volume |
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3 detectors to control renin secretion:
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1. hi pressure baroreceptors in carotid sinus/aortic arch- detect decrease, increase symp activity, triggers granular cells to release renin...
2. intrarenal baroreceptors (granular receptors= stretch receptors) 3. macula densa cells - decrease release of chem junk that inhibits renin from being released by gran cells |
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besides vasocontriction, angiotensin II ALSO CAUSES:
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1. aldosterone secretion by zona glomerulosa of adrenal glands-->increased renal Na absorption-->increased fluid volume-->increased BP
2. release of ADH from posterior pituitary -->increased water reabsorption in collecting duct |
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% Na reclaimed by kidneys and H2O equivalent
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2% reclaimed by aldosterone
= 3.6 extra L fluid |
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treatment for CHF:
(to fight kidney's cycle of vasoconsriction and increased fluid vol.) |
1. diurectics
2. Ca channel blockers, ACE inhibs, ARB's |
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glucose in urine if... (=renal clearance of glucose)
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plasma load causes filtered load to exceed Tm (amount filtered in is more than the 375 mg/min max can reabsorb back into bloodstream- whatever is over 375 goes into urine)
|
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glucose cotransported with:
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-Na
-amino acids (Bence Jones proteins cause max to be exceeded, released in urine) |
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a.) if you dilate AFFERENT arteriole, GFR will _____
b.) if you constrict afferent arteriole, GFR will ____ |
increase, decrease
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crush efferent arteriole, GFR will______
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pressure will back up, GFR increases
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ACE inhibs dilate the ______ arteriole
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EFFERENT
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H2CO3 is a ______ acid. these are eliminated by the ____
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volatile, lungs
(emphysema= CO2 builds up, pH drops) |
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nonvolatile acids
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H2SO4 (result of metab), H3PO4
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kidney response if plasma/body pH decrease
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inc. H= secretion/excretion, increase reabsorb of bicarbonate, increase creation of new bicarb.
|
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Na/H antiporters where?
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proximal tubule
-secrete H into tubular fluid, reabsorb Na |
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intercalated cells where?
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collecting duct of nephrons
-proton pumps pump H out interstitium into tubular fluid a/g gradient |
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buffers in tubular fluid
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NH3- H+ goes with NH3 to form NH4 which can bind to Na
HPO4 2- --> takes on 2 H+ ions and remove from tub fluid |
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primary glomerulopathies
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PIGN (nephritic), IgA nephropathy (berger's disease, nephritic), Goodpasture's (antiGBM GN, nephritic), minimal change disease (nephrotic)
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secondary glomerulopathies
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DM, SLE, amyloidosis
-larger systemic disease that usually causes glomerulopathy, usually nephritic |
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nonglomerular diseases
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1. tubulo interstitial nephritis (drug rxns)
2. infectious tubulointerstitial nephritis = pyelonephritis 3. tubular injuries...acute tubular necrosis from drugs, ischemia, heavy metals |
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proximal renal tubular acidosis symp:
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glucosuria, aa uria, uricosuria
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distal renal tubular acidosis
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salt wasting, hypercholemia, hyponitremia
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medullary area injured
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polyuria- inability to concentrate urine
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anemia differential dx:
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Chronic fatigue
COPD Congestive Heart Failure Hypothyroidism Anemia Lupus Infectious mononucleosis Depression |
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COPD symptoms:
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-history of smoking, chronic SOB
-abnormal chest diameter -faint breath & heart sounds (hyperinflated lungs) -exhaling >6 sec. -percussion hyperresonant |
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CHF:
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-smoking, HTN, MI, CAD, valve/myocarditis
-SOB/DOE -JVD -chest heave over R/L ventricle -PMI enlarged, displaced -heart murmur -hepatosplenomegaly/ascites -HJR -rales in LVF, pedal edema in RVF -cardiomegaly on CXR -azotemia due to renal failure -**inc plasma BNP (brain natriuretic peptide) |
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hypothyroidism:
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-h/o cold intol, const, absence sweating, menorrhagia
-hoarseness, dry puffy skin, hard pitting edema -possible goiter -slow speech, delayed DTR's -blood TSH inc. in primary, dec. in secondary -T4 usually low |
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Lupus
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-fever, anorexia, weight loss
-raynaud's -malar rash -joint pain -RF, generic ANA's, anti-dsDNA Ab's, anti-smith ab's |
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Mono
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-fever, sore throat, anorexia, myalgia
-pharynx may look like strep -possible rash -lymphadenopathy -enlarged tender spleen -positive monospot -lymphocitosis w/ atypical (large) lymphocytes |
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female anemia hematocrit, Hb
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<37%, <12 g/dl
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male anemia H + H
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<41%, <13.5 g/dl
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used to describe and detect anemia:
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RBC count, HCT, Hb <--calc from these are:
MCV, MCH, MCHC, RDW, blood smear |
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normal blood values:
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RBC- 4.2-6.1 X 10^6 microliters
MCV- 80-100 fL blood smear- normocytic, normochromic, no unusual shapes |
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used to detect response to infection, allergy, cancer (normal values):
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WBC- 4.5-11 x 10^3/ microliter
and differential: neutrophils - bands (immature), segs (mature) 54-62% lymphocytes, monocytes, eosinophils, basophils platelets - 150-450 x 10^3 |
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H + H =
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total red cell MASS - indirect measure of RBC count
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Decreased RBC production(decreased Hb synth anemias):
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-Fe-deficiency
-thalassemia -anemia of chronic disease -B12 deficiency -folate def -alcohol |
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intrinsic hemolysis:
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-hereditary spherocytosis = membrane
-sickle cell = Hb defect -G6PD deficiency = oxidation |
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extrinsic hemolysis:
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-autoimmune
-microangiopathic = mech. cardiac valve -hypersplenism = spleen eats |
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if MCV is normal:
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normocytic anemia
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if MCV is increased:
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macrocytic anemia/ megaloblastic
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if MCV decreased:
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microcytic anemia
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microcytics
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Fe def
thalassemia chronic disease hereditary spherocytosis hypersplenism |
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macrocytics
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alcohol
B12 (mega) folate (mega) |
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serum ferritin below ____ means absent Fe stores
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30 microliters
|
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TIBC (total iron binding capacity)
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-measure of how much iron can be added and bound by various proteins
-increased with 70% Fe def patients = further proof of deficiency |
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4 main kidney functions
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1. reabsorb filtered nutrients (proximal tubule)
2. secretion 3. eliminate/conserve H2O - adjust urine osmolality 4. adjust pH of plasma- secrete H+ ions and make/conserve bicarbonate ions |
|
kidney converts ______ to _____
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25 (OH)Vit D, 1.25(OH) Vit. D (active form)
|
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ADH
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released from post pit in response to dehydration
-increased H2O reabsorp in collecting duct |
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dehydration value
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plasma osmolality too high - above about 290 millimoles/liter
|
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what monitors plasma osmolality?
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preoptic/periventricular nuclei of hypothalamus
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mesangial cells
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-contractile
-phagocytic -respond to complement cascade by secreting chemical junk (this can affect rest of cells + decrease function) -also secret mesagial matrix (supports glomerular tuft) |
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triple layer of glomerulus
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-glomerular capillary endothelial cells
-basement membrane -visceral epithelial cells (podocytes) |
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what composes most of the plasma's negative charge?
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albumin
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average GFR
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125 mL/min
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effective renal plasma flow
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total amount plasma going to kidneys and thru glomeruli
-all plasma flow in ALL afferent arterioles over 1 minute -not all blood filtered thru each pass thru glom- some escapes thru efferent artery but might be filtered on next pass |
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renal flow thru kidney:
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afferent arteriole -> glomerular capillaries -> Bowman's capsule -> proximal convoluted tubule -> descending loop -> loop of Henle -> ascending loop -> distal convoluted tubule -> collecting duct
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blood flow in glomerulus:
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capillaries -> fenstrae (holes permit leakage) -> basement membrane -> foot processes of visceral podocytes -> fluid falls into Bowman's Space (or other blood exits glom cap's via efferent arterioles which branch into peritubular cap's)
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amt excreted =
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amt filtered + amt secreted - amt reabsorbed
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H2O is passively reabsorbed in thin ______ loop of Henle, Na+ is passively reabsorbed in thin _____ loop of Henle
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descending, ascending (traps Na+ at bottom loop of Henle interstitium
|
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counter-current multiplier of Henle's loop creates ____osm fluid
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1200
|
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in the ascending limb ___ is pumped out, ___ passively follows it
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Cl-, Na+
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plasma creatinine value
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should be 1.2 mg/mL - higher than that indicates poor renal function
|
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renal clearance
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(Udrug x V)/ Pdrug
how many individual mL of blood are cleared of the solute they are carrying = mL/min not mg/min |
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nephron
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anatomic unit of kidney - each human has ~ 1 mil.
|
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glomerulus
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tuft of cap's
-lined by endothelial cells -covered by epithelial cells (podocytes) -glomerular basement membrane in the middle -continuous layer with those of bowman's capsule |
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mesangium
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space b/t cap's in glomerulus- extension of basement membrane
-intrinsic glomerular cells and tissue macrophages - both respond to cytokines |
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podocytes
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epithelial cells on glom basement membrane
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tubuloglomerular feedback
|
if inc. in Na+, sensed by macula densa-->afferent arteriole vasoconstriction- this dec. GFR so smaller. amt solute per unit time-->Na+ more efficiently reclaimed
|
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medullary oxygen consumption
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redistribute blood from cortex to medulla
-constriction of some vascular beds, dilation of others |
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loss of nephrons
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compensatory glomerular hyperfiltration and renal hypertrophy -->progression to chronic renal failure begins
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causes of renal artery stenosis:
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-atherosclerosis in renal arteries (usually 45+ y.o.)
-fibromuscular dysplasia |
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things to look for in dx of renal artery stenosis:
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-refractory HTN (BP uncontrolled even w/ 3meds)
-new onset of HTN -ARF upon starting ACE inhib -bruit |
|
fibromuscular dysplasia
|
women 25-45
unexplained HTN fibromuscular struc crowds lumen of arteriole *beads on a string* in renovascular system angioplasty/stint |
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primary hydronephrosis
|
blockage occurs at uteropelvic junction
|
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secondary hydronephrosis
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blackage anywhere lower in urinary tract
|
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polycystic kidney disease
|
genetic autosomal- chr 16
cysts take over polycystin present (to fight or the cause?) enlarged kidneys approx 40 y.o. hematuria, HTN increased UTI cysts in liver dialysis, transplant |
|
general symptoms of chronic renal failure:
|
-inc. BUN and creatinine due to inc. GFR
-N/V, fatigue, anorexia, disrupted sleep all due to toxin buildup -dec seizure threshold, peripheral neuropathy (restless legs) -HTN, pericarditis from uremia-->cardiac tamponade -bone pain, patholog fx, soft tissue calc. -GI bleeding |
|
causes of CRF:
|
-diabetes (10+ yrs)
-HTN (nephrosclerosis) -glomerulonephritis (primary or secondary) -interstitial nephritis (drugs, heavy metals) -polycystic kidney disease -injury to any part |
|
consequences of RF:
|
1. dec ability to secrete or excrete Na+
2. dec. ability to handle water (hyponatremia or hypernatremia) 3. become hyperkalemic- heart dysrhythmias 4. acidemia (increased H+, bicarb not being formed, not enough ammonia) 5. no conversion to active form vit. D -->hypocalcemia 6. drug doses larger b/c not clearing as fast |
|
which tubules handles potassium?
|
distal tubule
|
|
what fits in glomeruli:
|
things <2.5 nm (glucose, water, urea)
things >4 nm won't fit -albumin is 3.6 = borderline, but - charge repels |
|
components of protein in urine
|
40% albumin
40% Tamm-Hursfall proteins (from thick ascending limb) rest = IgG, IgA, light chains |
|
causes of minimal proteinuria (<.5 g/day)
|
exercise, fever, postural, HTN, UTI, polycystic kidney disease, renal tub dysfunction
|
|
cause of moderate (.5-3 g/day)
|
glomerulonephritis, preeclampsia, CHF, mild diabetec nephropathy, multiple myeloma (bence jones)
|
|
marked proteinuria causes:
|
glomerulonephritis, severe diabetic nephropathy, lupus, amaloidosis
|
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orthostatic proteinuria
|
</= 2g day, normal at night
tenns/ young adults at night, lying down= BP dec, goes away |
|
functional proteinuria
|
high fever, cold exposure, strenuous exercise
|
|
mech of pathologic proteinuria
|
1. loss charge = albuminuria (MCD)
2. loss size barrier (RA, SLE, diabetes, amaloidosis) 3. overload proteinuria (multiple myeloma, hemolysis in vascular spaces) 4. proximal tubule dysfunction |