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60 Cards in this Set
- Front
- Back
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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 |
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Measuring ECF
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Mannitol
too large to enter ICF sulfate, inulin |
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Measuring Plasma
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Evans Blue
binds to serum albumin RISA - radioidinated serum albumin |
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RBF and autoregulation
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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. |
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measuring RPF
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measured by PAH which is fully filtered and secreted.
Cl of PAH measures effective RPF and underestimates true RPF by 10% |
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measuring RBF
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RBF = RPF/(1-HCT)
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Inulin
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for measuring GFR because it is filtered but not secr or reabsorbed.
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Filtration fraction
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FF = GFR/RPF
nl is 20% Rest of RPF leaves via efferent arteriole and becomes the peritubular circ |
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Glomerular Barrier
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Capillary Endothelium
Basement membrane Foot of podocytes Anionic glycoproteins line filtration barrier to keep proteins from filtering out. |
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Glomerular capillary oncotic press
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Increases along the length of the glom cap because of the incr in protein as water filters out.
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Filtered load
Excretion rate |
GFR x Plama []
V(ml/min) x [urine] |
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Glucose reabsorption
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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. |
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Secreted PAH Tm
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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 |
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[TF/P]inulin
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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 |
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[Tf/P]x / [Tf/P]inulin
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frax of filtered load remaining at any point along the nephron.
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PCT - absorptions
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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 |
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Thick ascending loop of henle
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Na-K-2Cl cotransport
25% of Na reabsorption Imperm to H2O thus diluting segment. Loop diuresis- ethacrynic acid, bumetanide, furosemide |
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Distal tubule and collecting duct
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8% of Na reabsorption
Cortical diluting segment Na-Cl cotransport Thiazide diuresis Imperm to H20 |
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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 |
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Causes of hyperkalemia
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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 |
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Causes of hypokalemia
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K+ shift into cells
insulin hypoosmolarity beta agonist alkalosis (exchange of intracell H+ for extracell K+) |
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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 |
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Urea
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50% reabsorbed in PCT
only the inner medullary collecting ducts are permeable via ADH Leads to urea recycling creating the CORTICOPAPILLARY OSMOSTIC GRADIENT |
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Phosphate
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85% reabsorbed in PCT
PTH: inhibits reabsorption via inhibiting Na-phos cotransport and incr cAMP. causes phosphaturia and urinary cAMP |
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PTH
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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. |
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Calcium
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60% filtered
90% reabsorbed in PCT and ascending limb coupled to Na. Loop Diuretics: Ca excretion Thiazides: incr Ca excretion |
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Mg
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In thick ascending limb competes with Ca++ for reabsorption
Hypercalcemia causes incr Mg excretion and vice versa |
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Free water clearance
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ClH2O = V- [ Uosm x V / Posm ]
Free water Cl = 0 : loop diuresis Free water Cl = + : diabetes inispidus Free water Cl = - : incr ADH |
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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 |
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NH3 and pH
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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. |
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Serum Anion Gap
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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) |
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Calcium and respiratory alkalosis
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hypocalcemia because H+ and Ca++ compete for binding sites on albumin. Thus incr binding by Ca++ and decr free serum Ca++
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Hypoaldosteronism
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Decr Na resoprtion - ECF vol contraction -> incr ADH -> hyponatremia
Decr K+ secr - hyperkalemia Decr H+ secr - metabolic acidosis |
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Contraction Alkalosis
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Decr renal perfusion from hypovolemia -> incr renin->incr ATII -> incr bicarb resorption in PCT
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Vomiting
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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+ |
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Stimulus for ADH rls
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incr plasma osmolarity
decr in ECF |
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Macula Densa
where is it? |
At the border btw the thick ascending limb and the dital convoluted tubule.
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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 |
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Plasma protein concentration and FF
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Incr Plasma prot:
unchanged RPF, decr GFR, decr FF Decr PP: unchanged RPF, incr GFR, incr FF |
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Stimulus of JGA
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WIll rls renin when stimulated by...
decr renal BP decr Na delivery to distal tubule (macula densa) incr sympathetic tone |
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Henderson Hasselbach for Renal Acid Base
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pH=pka + log [HCO3-] / 0.03(PCO2)
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Metabolic gap acidosis
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Gap = Na -[Cl + HCO3]
Methanol Uremia Diabetic ketoacidosis Paraldehyd, phenformin Iron, INH Lactic acidosis Ethylene glycol Salicylates. |
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Causes of metabolic alkalosis
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Vomiting
antacid use Diuretics Hyperaldosteronism |
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causes of normal anion gap metabolic acidosis
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diarrhea
Glue sniffing RTA hyperchloremia |
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Metabolic acidosis vs metabolic alkalosis eqn
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Metabolic acidosis:
PCO2 = 1.5(bicarb) +8 +/- 2 Metabolic alkalosis PCO2 incr 0.7 for every 1 meq/L incr of bicarb |
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Resp acidosis vs alkalosis eqqn
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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 |
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Struvite Stones
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Magnesium ammonium
2nd most common Infection stones from PROTEUS, STAPH, KLEBSIELLA splitting urea to form ammonia |
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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 |
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WAGR complex
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Wilms tumor - Cr11
Aniridia Genitourinary malformation Retardation |
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TRansitional Cell Carcinoma
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Painless hematuria
Renal calyces, Renal pelvis, ureter, bladder Ass with Phenacetin Smoking Aniline dyes Cyclophosphamide |
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Diffuse Cortical Necrosis
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acute generalized infarction of cortex of both kids
Vasospasm + DIC ass with placental abruption and septic shock |
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ATN
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most common cause of acute renal failure, death without tx
caused by: ischemia(shock), trauma(myoglobinuria), toxins |
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Renal Papillary Necrosis
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1. DM
2. Acute pyelonephritis 3. Phenacetin Use |
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Types of acute Renal failure
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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) |
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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 |
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K+
high vs low |
Low: U waves, flattened T waves, arrhythmias, paralysis
High: Peaked T waves, arrhythmias |
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Ca++
low vs high |
Low: tetany, neuromuscular irritability
High: delerium, renal stones, abdominal pain |
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Bladder instability
freq and urgency |
oxybutnin
antispasmodic, inhibits muscarinics |
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Urinary retention
tx |
bethanecol
stimulates musc receptors tx helps you pee |
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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. |
