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60 Cards in this Set

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ICF vs ECF
vs Interstitial and intracellular
fluid compartments
TBW = 60% bw
ICF = 2/3 tbw = 40%
EFF = 1/3 tbw = 20%
*Interstitial = 3/4
*plasma= 1/4
Measuring ECF
Mannitol
too large to enter ICF
sulfate, inulin
Measuring Plasma
Evans Blue
binds to serum albumin
RISA - radioidinated serum albumin
RBF and autoregulation
renal blood flow is 25% of CO
Mechanisms are there to attempt to keep RBF constant
1. Myogenic reg - renal arterioles contract in response to stretch
2. Tubuloglomerular fdbk: macula densa senses incr fluid delivery constricts the afferent arteriole.
measuring RPF
measured by PAH which is fully filtered and secreted.
Cl of PAH measures effective RPF and underestimates true RPF by 10%
measuring RBF
RBF = RPF/(1-HCT)
Inulin
for measuring GFR because it is filtered but not secr or reabsorbed.
Filtration fraction
FF = GFR/RPF
nl is 20%
Rest of RPF leaves via efferent arteriole and becomes the peritubular circ
Glomerular Barrier
Capillary Endothelium
Basement membrane
Foot of podocytes
Anionic glycoproteins line filtration barrier to keep proteins from filtering out.
Glomerular capillary oncotic press
Increases along the length of the glom cap because of the incr in protein as water filters out.
Filtered load
Excretion rate
GFR x Plama []
V(ml/min) x [urine]
Glucose reabsorption
Na-Glucose cotransport in PCT
up to 250mg/dl all reabsorbed (threshold)
over 350mg/dl transporters are all saturated = Tm
Splay: region between threshold and Tm - due to heterogeneity of nephrons.
Secreted PAH Tm
Secr of PAH occurs from peritubular cap blood into tubular fluid via Carriers in Proximal tube.
AT LOW CONC of PAH secr increases with plasma conc.
Until Tm. After that the curve flattens and matches filtration curve.
PAH Cl approximates RPF at conc lower than Tm
[TF/P]inulin
Inulin freely filtered and not secr or reabsorbed
increases as water is being reabsorbed.
Frax of filtered water that has been reabsorbed = 1-1/[Tf/P]inulin
[Tf/P]x / [Tf/P]inulin
frax of filtered load remaining at any point along the nephron.
PCT - absorptions
Na, H20, Cl, HCO3, lactate, AA, phosphate, urea
Na-H+ countertransport
Na-Cl- cotransport
66% of filtered Na and H2O - glomerulotubular balance-starling forces
ISOOSMOTIC
Thick ascending loop of henle
Na-K-2Cl cotransport
25% of Na reabsorption
Imperm to H2O thus diluting segment.
Loop diuresis- ethacrynic acid, bumetanide, furosemide
Distal tubule and collecting duct
8% of Na reabsorption
Cortical diluting segment
Na-Cl cotransport
Thiazide diuresis
Imperm to H20
Principle cells
Alpha intercalated cells
Late distal tubule collecting duct
Principle-Cells: reabsorb Na and H2O and secrete K+.
Passive K+ secr depends on luminal []
Aldosterone: incr Na reabsorb and to secr K+
ADH: incr H2O perm
Alpha Intercalated Cells:
Secr H+ via an H+-ATPase
reabsorb K+ via H-K-ATPase (only occurs on low K+)
Aldosterone: incr H+ secr by stim H+ ATPase
Causes of hyperkalemia
K+ shift out of cells
insulin deficiency
beta antagonist
acidosis (extracell H+ for intracell K+)
Hyperosmolarity (K+ flows out with H2O)
Digitalis
Exercise
Cell lysis
Causes of hypokalemia
K+ shift into cells
insulin
hypoosmolarity
beta agonist
alkalosis (exchange of intracell H+ for extracell K+)
Secretion of K+
acidosis vs alkalosis
prinicple cells:
depends on gradient:
Dietary K+, aldo, acid-base status, urine flow rate.
Passive secr into lumen based on electrical chemical gradient
Aldo works by stim Na/K ATPase leading to incr K+ in cell-> incr secr gradient
Acidosis - decr K+ secr
Alkalosis - incr K+ secr
Urea
50% reabsorbed in PCT
only the inner medullary collecting ducts are permeable via ADH
Leads to urea recycling creating the CORTICOPAPILLARY OSMOSTIC GRADIENT
Phosphate
85% reabsorbed in PCT
PTH: inhibits reabsorption via inhibiting Na-phos cotransport and incr cAMP. causes phosphaturia and urinary cAMP
PTH
PTH inhibits reabsorption of phosphate at PCT via inhibiting Na-phos cotransport and incr cAMP by stim adenyl cyclase
Stimulates 1alpha-hydroxylase in PCT
causes phosphaturia and urinary cAMP
Incr Ca reabsorption by activating adenyl cyclase in distal tubule.
Calcium
60% filtered
90% reabsorbed in PCT and ascending limb coupled to Na.
Loop Diuretics: Ca excretion
Thiazides: incr Ca excretion
Mg
In thick ascending limb competes with Ca++ for reabsorption
Hypercalcemia causes incr Mg excretion and vice versa
Free water clearance
ClH2O = V- [ Uosm x V / Posm ]
Free water Cl = 0 : loop diuresis
Free water Cl = + : diabetes inispidus
Free water Cl = - : incr ADH
Bicarb reabsorption
ECF volume
AT-II
At PCT lumenal HCO3 combines with H+ (from Na-H+ exchange). CA enzyme -> CO2 and H2O absorbed. CA in cell -> bicarb absorbed into blood, H+ goes to exchange again. Controlled by CO2 levels.
Net Bicarb resorption
No Net H+ absorption
ECF volume: incr leads to decr bicarb resorption
decr ECF more bicarb resorption = CONTRACTION ALKALOSIS
AT-II: stim Na-H+ exchange -> contraction alkalosis
NH3 and pH
NH3 is produced in renal cells from glutamine.
and excreted after it combines with luminal H+ (diffusion trapping)
In acidosis NH3 production is increased leading to more New Bicarb to be made.
Serum Anion Gap
Na - (Cl+HCO3)
nl gap is 8-16.
Incr gap acidosis: bicarb is replaced by something like phosphate, lactate, or betahydroxybutyrate
Nl gap acidosis: bicarb is replaced by Cl-. (hyperchloremic acidosis)
Calcium and respiratory alkalosis
hypocalcemia because H+ and Ca++ compete for binding sites on albumin. Thus incr binding by Ca++ and decr free serum Ca++
Hypoaldosteronism
Decr Na resoprtion - ECF vol contraction -> incr ADH -> hyponatremia
Decr K+ secr - hyperkalemia
Decr H+ secr - metabolic acidosis
Contraction Alkalosis
Decr renal perfusion from hypovolemia -> incr renin->incr ATII -> incr bicarb resorption in PCT
Vomiting
Metabolic Alkalosis + vol contraction
Decr vent
decr renal perfusion -> incr renin
Contraction Alkalosis (AT II resportion of bicarb)
incr Aldo -> hypokalemia, distal H+ secr
Incr excretion of fixed H+
Tx - saline + K+
Stimulus for ADH rls
incr plasma osmolarity
decr in ECF
Macula Densa
where is it?
At the border btw the thick ascending limb and the dital convoluted tubule.
Filtration frax
with PGE and ATII
GFR/RPF
PGE: dilate afferent arteriole - incr GFR and incr RPF - FF unchanged
ATII: constricts efferent arteriole
incr GFR, decr RPF -> incr filtration frax
Plasma protein concentration and FF
Incr Plasma prot:
unchanged RPF, decr GFR, decr FF
Decr PP:
unchanged RPF, incr GFR, incr FF
Stimulus of JGA
WIll rls renin when stimulated by...
decr renal BP
decr Na delivery to distal tubule (macula densa)
incr sympathetic tone
Henderson Hasselbach for Renal Acid Base
pH=pka + log [HCO3-] / 0.03(PCO2)
Metabolic gap acidosis
Gap = Na -[Cl + HCO3]

Methanol
Uremia
Diabetic ketoacidosis
Paraldehyd, phenformin
Iron, INH
Lactic acidosis
Ethylene glycol
Salicylates.
Causes of metabolic alkalosis
Vomiting
antacid use
Diuretics
Hyperaldosteronism
causes of normal anion gap metabolic acidosis
diarrhea
Glue sniffing
RTA
hyperchloremia
Metabolic acidosis vs metabolic alkalosis eqn
Metabolic acidosis:
PCO2 = 1.5(bicarb) +8 +/- 2
Metabolic alkalosis
PCO2 incr 0.7 for every 1 meq/L incr of bicarb
Resp acidosis vs alkalosis eqqn
Resp Acidosis
Acute: bicarb incr 1 for every 10mmHg incr of PCO2
Chronic: bicarb incr 3.5 for every 10mmHg incr of PCO2
Resp alkalosis:
Acute: bicarb decr 2 for every 10mmHg decr of PCO2
Chronic: bicarb decr 5 for every 10 mmHg decr of PCO2
Struvite Stones
Magnesium ammonium
2nd most common
Infection stones from PROTEUS, STAPH, KLEBSIELLA splitting urea to form ammonia
Renal Cell Carcinoma
causes
pathology
ass syndromes
route of spread
Incr with smoking, obesity, vHL (Cr 3)
Polycythemia
Paraneoplastic syndromes: EPO, ACTH, PTH, PRL
spreads to IVC
WAGR complex
Wilms tumor - Cr11
Aniridia
Genitourinary malformation
Retardation
TRansitional Cell Carcinoma
Painless hematuria
Renal calyces, Renal pelvis, ureter, bladder
Ass with
Phenacetin
Smoking
Aniline dyes
Cyclophosphamide
Diffuse Cortical Necrosis
acute generalized infarction of cortex of both kids
Vasospasm + DIC
ass with placental abruption and septic shock
ATN
most common cause of acute renal failure, death without tx
caused by: ischemia(shock), trauma(myoglobinuria), toxins
Renal Papillary Necrosis
1. DM
2. Acute pyelonephritis
3. Phenacetin Use
Types of acute Renal failure
Acute decline in fx with:
incr Cr, incr BUN over several days
1. Prerenal Azotemia: decr RBF
2. Renal: ATN, ischemia/toxins
Patchy necrosis leads to obstructive debris in tubule and fluid backflow across necrotic tubule -> decr GFR, urine epith/granular casts
3. Post renal (bilateral obstruction)
Consequences of renal failure
(8)
Failure to make urine and excrete Nitrogenous waste
Uremia: incr BUN + Cr
Acute: hypoxia
Chroni: DM, HTN
1. Anemia
2. Renal Osteodystrophy (def prod of vit D)
3. Metabolic Acidosis
4. Hyperkalemia
5. Na and H20 excess -> CHF
6. Uremic Encephalopathy
7. Chronic Pyelonephritis
8. HTN
K+
high vs low
Low: U waves, flattened T waves, arrhythmias, paralysis
High: Peaked T waves, arrhythmias
Ca++
low vs high
Low: tetany, neuromuscular irritability
High: delerium, renal stones, abdominal pain
Bladder instability
freq and urgency
oxybutnin
antispasmodic, inhibits muscarinics
Urinary retention
tx
bethanecol
stimulates musc receptors tx
helps you pee
Embryo
Development of thekids
Metanephros:
Uteric bud (collecting duct, renal calyces, renal pelvis, ureter) penetrate the ->
Metanephric mesoderm:
forms metanephric vesicles (blastema) ->primitive renal tubules forming most of kids.
Fetal Metanephros ascends and rotates 90 degrees medially.