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Mechanisms of Disease Exam II

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creatinine clearance
(U x V)/ P then divide by minutes in day (1400)
a. normal urine output
b. oliguria
c. anuria
d. polyuria
a. 750-2000 mL/day
b. <500
c. <100
d. >2500
fractional excretion of urea
(Una x Pcre)/ (Pna x Ucre) then x 100
prerenal azotemia
anything that creates inadequate blood flow to kidneys
-secretion of ADH = ocnc urine
Una <10meq/L, 350-400 mOsm
renal azotemia
nephrons don't do work, Na lost to urine
Una>40meq/L, <350 Osm
causes renal azotemia
glomerulonephritis
acute tubular necrosis
pyelonephritis
diff b/t uremia and azotemia
azotemia- increased plasma creatinine and BUN with NO symptoms
uremia- increased WITH symptoms (many)
prerenal ARF caused by:
1. hypotension (sepsis, dehydration, hemorrhage)
2.edematous states (CHF, cirrhosis, nephrotic syndrome)
nephrotic syndrome leaks...
nephritic syndrome leaks...
>3g protein/day
<3g protein/day (post-infectious glomerulonephritis)
intrinsic RF caused by:
-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)
post RF/ obstructive RF caused by:
commonly nephrolithiasis/urethrolithiasis, usually uric acid stones --> gout or CHEMO
-also tumors, BPH
universal early sn that kidney function is compromised by whatever cause
increased BUN and Pcre
GFR in chronic renal failure
goes to 10 mL/min and below
NL Pcre
<1.3 mg/dl
Total urinary creatinine per day
1-2 g
BUN
8-20 mg/dl
NL BUN/Pcre ratio
10-15
BUN/Pcre in prerenal azotemia
>/= 20
FEna
NL <1-5%
prerenal azotemia <1%
contrast agent prerenal azo <1%
renal azotemia >1%
postrenal azotemia >1% (>4%)
Prerenal azotemia values
Una <10 mEq/L
Uosm >450 mOsm/kg
FEna <1%
BUN/Pcre >20
Renal azotemia values
Una >40 mEq/L
Uosm <450
FEna >1%
BUN/Pcre <20
Postrenal azotemia FEna
FEna >4%
hypokalemia
<3.5 mEq/L
hyperkalemia
>5.5 mEq/L
NL total urinary protein per day
150 mg
minimal proteinuria
<0.5 g/day
moderate proteinuria (nephritic syndrome)
.5-3.5 g/day
marked proteinuria (nephrotic syndrome)
>3.5 g/day
NL urinary protein/ creatinine on "spot" urine
<0.2
NL urine osmolality on "spot" urine after 12 hr fluid restriction
>800 mOsm/kg
<400 = renal impairment
spot urine for myoglobin- + indicates:
crush injury
polymyositis
recent surgery
rhabdomyolysis
electrical burn
hematuria
>5 cells per hpf
pyuria (WBC's)
>5 cells per hpf
dysmorphic RBCs or RBC casts (even one) in urine is
PATHGNOMONIC for:
glomerulonephritis
WBC casts in urine indicate
pyelonephritis
epithelial casts in urine indicate
acute tubular necrosis
fatty casts (oval fat bodies) in urine indicate
nephrotic syndrome
waxy casts indicate
chronic renal failure
urine dip should be negative for:
-protein
-glucose
-ketones
-RBC's
-bilirubin
-nitrite
-leukocyte esterase
on microscopic analysis, urine should be negative for:
-bacteria
-casts: RBC, WBC, waxy or fatty
NL to see these in urine under microscope:
an occasional hyaline or epithelial cell cast
urine dip = + for blood but no cells on microscopic analysis?
Hb or Mb in urine
kidneys regulate blood flow by 3 different mechanisms:
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
parts of juxtaglomerular apparatus
1. macula densa
2. granular cells
3. extraglomerular mesangial cells (secrete chem. junk)
4. sympathetic nerves (no para in kidney!)
macula densa detects:
increase in flow rate-->sends signal to granular cells-->causes afferent arteriole to constrict-->decrease GFR
release of NE by sympathetic nerves on alpha-1 receptors causes:
vasoconstriction
-receptors found on renal arterioles
release of NE by sympathetic nerves on beta-1 receptors causes:
release of renin
-receptors found on granule cells in JGA
release of NE by sympathetic nerves in renin tubule causes:
increase in Na reabsorption
CO2 causes
arteriole vasodilation (more blood can flow to exercising muscles)
2 mechs that regulate BP long term:
1. angiotensin II induced vasoconstriction
2. aldosterone and ADH mediated regulation of circulatory fluid volume
3 detectors to control renin secretion:
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
besides vasocontriction, angiotensin II ALSO CAUSES:
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
% Na reclaimed by kidneys and H2O equivalent
2% reclaimed by aldosterone
= 3.6 extra L fluid
treatment for CHF:
(to fight kidney's cycle of vasoconsriction and increased fluid vol.)
1. diurectics
2. Ca channel blockers, ACE inhibs, ARB's
glucose in urine if... (=renal clearance of glucose)
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)
glucose cotransported with:
-Na
-amino acids (Bence Jones proteins cause max to be exceeded, released in urine)
a.) if you dilate AFFERENT arteriole, GFR will _____
b.) if you constrict afferent arteriole, GFR will ____
increase, decrease
crush efferent arteriole, GFR will______
pressure will back up, GFR increases
ACE inhibs dilate the ______ arteriole
EFFERENT
H2CO3 is a ______ acid. these are eliminated by the ____
volatile, lungs
(emphysema= CO2 builds up, pH drops)
nonvolatile acids
H2SO4 (result of metab), H3PO4
kidney response if plasma/body pH decrease
inc. H= secretion/excretion, increase reabsorb of bicarbonate, increase creation of new bicarb.
Na/H antiporters where?
proximal tubule
-secrete H into tubular fluid, reabsorb Na
intercalated cells where?
collecting duct of nephrons
-proton pumps pump H out interstitium into tubular fluid a/g gradient
buffers in tubular fluid
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
primary glomerulopathies
PIGN (nephritic), IgA nephropathy (berger's disease, nephritic), Goodpasture's (antiGBM GN, nephritic), minimal change disease (nephrotic)
secondary glomerulopathies
DM, SLE, amyloidosis
-larger systemic disease that usually causes glomerulopathy, usually nephritic
nonglomerular diseases
1. tubulo interstitial nephritis (drug rxns)
2. infectious tubulointerstitial nephritis = pyelonephritis
3. tubular injuries...acute tubular necrosis from drugs, ischemia, heavy metals
proximal renal tubular acidosis symp:
glucosuria, aa uria, uricosuria
distal renal tubular acidosis
salt wasting, hypercholemia, hyponitremia
medullary area injured
polyuria- inability to concentrate urine
anemia differential dx:
Chronic fatigue
COPD
Congestive Heart Failure
Hypothyroidism
Anemia
Lupus
Infectious mononucleosis
Depression
COPD symptoms:
-history of smoking, chronic SOB
-abnormal chest diameter
-faint breath & heart sounds (hyperinflated lungs)
-exhaling >6 sec.
-percussion hyperresonant
CHF:
-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)
hypothyroidism:
-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
Lupus
-fever, anorexia, weight loss
-raynaud's
-malar rash
-joint pain
-RF, generic ANA's, anti-dsDNA Ab's, anti-smith ab's
Mono
-fever, sore throat, anorexia, myalgia
-pharynx may look like strep
-possible rash
-lymphadenopathy
-enlarged tender spleen
-positive monospot
-lymphocitosis w/ atypical (large) lymphocytes
female anemia hematocrit, Hb
<37%, <12 g/dl
male anemia H + H
<41%, <13.5 g/dl
used to describe and detect anemia:
RBC count, HCT, Hb <--calc from these are:
MCV, MCH, MCHC, RDW, blood smear
normal blood values:
RBC- 4.2-6.1 X 10^6 microliters
MCV- 80-100 fL
blood smear- normocytic, normochromic, no unusual shapes
used to detect response to infection, allergy, cancer (normal values):
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
H + H =
total red cell MASS - indirect measure of RBC count
Decreased RBC production(decreased Hb synth anemias):
-Fe-deficiency
-thalassemia
-anemia of chronic disease
-B12 deficiency
-folate def
-alcohol
intrinsic hemolysis:
-hereditary spherocytosis = membrane
-sickle cell = Hb defect
-G6PD deficiency = oxidation
extrinsic hemolysis:
-autoimmune
-microangiopathic = mech. cardiac valve
-hypersplenism = spleen eats
if MCV is normal:
normocytic anemia
if MCV is increased:
macrocytic anemia/ megaloblastic
if MCV decreased:
microcytic anemia
microcytics
Fe def
thalassemia
chronic disease
hereditary spherocytosis
hypersplenism
macrocytics
alcohol
B12 (mega)
folate (mega)
serum ferritin below ____ means absent Fe stores
30 microliters
TIBC (total iron binding capacity)
-measure of how much iron can be added and bound by various proteins
-increased with 70% Fe def patients = further proof of deficiency
4 main kidney functions
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 _____
25 (OH)Vit D, 1.25(OH) Vit. D (active form)
ADH
released from post pit in response to dehydration
-increased H2O reabsorp in collecting duct
dehydration value
plasma osmolality too high - above about 290 millimoles/liter
what monitors plasma osmolality?
preoptic/periventricular nuclei of hypothalamus
mesangial cells
-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)
triple layer of glomerulus
-glomerular capillary endothelial cells
-basement membrane
-visceral epithelial cells (podocytes)
what composes most of the plasma's negative charge?
albumin
average GFR
125 mL/min
effective renal plasma flow
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
renal flow thru kidney:
afferent arteriole -> glomerular capillaries -> Bowman's capsule -> proximal convoluted tubule -> descending loop -> loop of Henle -> ascending loop -> distal convoluted tubule -> collecting duct
blood flow in glomerulus:
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)
amt excreted =
amt filtered + amt secreted - amt reabsorbed
H2O is passively reabsorbed in thin ______ loop of Henle, Na+ is passively reabsorbed in thin _____ loop of Henle
descending, ascending (traps Na+ at bottom loop of Henle interstitium
counter-current multiplier of Henle's loop creates ____osm fluid
1200
in the ascending limb ___ is pumped out, ___ passively follows it
Cl-, Na+
plasma creatinine value
should be 1.2 mg/mL - higher than that indicates poor renal function
renal clearance
(Udrug x V)/ Pdrug

how many individual mL of blood are cleared of the solute they are carrying
= mL/min not mg/min
nephron
anatomic unit of kidney - each human has ~ 1 mil.
glomerulus
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
mesangium
space b/t cap's in glomerulus- extension of basement membrane
-intrinsic glomerular cells and tissue macrophages - both respond to cytokines
podocytes
epithelial cells on glom basement membrane
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
medullary oxygen consumption
redistribute blood from cortex to medulla
-constriction of some vascular beds, dilation of others
loss of nephrons
compensatory glomerular hyperfiltration and renal hypertrophy -->progression to chronic renal failure begins
causes of renal artery stenosis:
-atherosclerosis in renal arteries (usually 45+ y.o.)
-fibromuscular dysplasia
things to look for in dx of renal artery stenosis:
-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
primary hydronephrosis
blockage occurs at uteropelvic junction
secondary hydronephrosis
blackage anywhere lower in urinary tract
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
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
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