Flashcards in Renal Physiology EC Deck (44):
Fluid compartments and percent of body weight
60%= Total body water (TBW)
1/3TBW Extracellular (EC)
1/4 EC Plasma
3/4 EC Interstitial
What are the components of the glomerular filtration barrier? Loss of barrier leads to what syndrome?
Fenestrated capillary endothelium (size barrier)
Fused basement membrane w/ heparan sulfate (-charge barrier)
Epithelial layer w/ podocyte foot processes
Loss of barrier leads to nephrotic syndrome
What is the equation for renal clearance?
Clearance= ([Urine]*Volume) /[Plasma]
How do you calculate GFR? What substance is used? What is a normal value?
GFR=Clearance of inulin or creatinine (freely filtered and not absorbed or secreted - creatinine used clinically but overestimates GFR)
How do you calculate RPF (renal plasma flow)?
RPF= Clearance of PAH
How do you calculate RBF (renal blood flow)?
RBF= RPF / (1-hematocrit)
How do you calculate FF (filtration fraction)?
How do you calculate Filtered Load?
FL= GFR * [Plasma]
How do NSAIDs affect RPF, GFR, and FF?
NSAIDs decrease RPF and GFR by blocking production of prostaglandins that usually dilate afferent arteriole
FF does not change because RPF and GFR both decrease
How do ACE inhibitors affect RPF, GFR, and FF?
Constrict efferent arteriole
so Increase FF (GFR/RPF)
Where is glucose reabsorbed? At what plasma level does glucosuria begin? At what plasma level are transporters saturated?
Reabsorbed in proximal tubule by Na/glucose cotransport
Glycosuria begins at 160mg/dL
Saturation begins at 250mg/dL
How are amino acids reabsorbed?
Reabsorbed via Na-dependent transporters in proximal tubule
Deficiency in neutral amino acid transporter
Tryptophan deficiency leads to pellagra (diarrhea, dermatitis, dementia)
Early Proximal tubule: What is reabsorbed? What is secreted? What hormones act on?
Glucose, AA's, bicarb, Na, Cl, PO4, H2O via isotonic absorption
H+, Ammonia (acts as buffer for H+)
PTH: Inhibits phosphate reabsorption
AT II: Increases Na, H2O, and Bicarb reabsorption
Thin descending loop of Henle
Passively reabsorbs water via medullary hypertonicity
Thick ascending loop of Henle: What is reabsorbed? What is it's function? What diuretics act here/what affect do they have on body Ca?
Na/K/2Cl actively, parallel reabsorption of Mg and Ca (driven by K leak-back into tubule)
Loop diuretics act here
LOOPS LOSE CALCIUM (cause hypocalcemia)
Early distal tubule: What is reabsorbed? What is it's function? What hormones act here? What diuretics act here/what affect do they have on body Ca?
PTH increases Ca reabsorption
Thiazide diuretics act here (cause hypercalcemia)
Aldosterone - causes Na reabsorption and K/H secretion
ADH- causes water reabsorption (Aq channel insertion)
What is the function of the juxtaglomerular apparatus?
JG cells = secrete renin in response to decreased BP
Macula densa= NaCl sensor that increases sympathetic tone in response to decrease (Beta-1 receptors)
*Beta blockers decrease BP by blocking receptors on JGA*
Released by interstitial cells in the peritubular capillary bed in response to hypoxia
1,25-(OH)2 vit. D
Proximal tubule cells convert to active form via 1-alpha-hydroxylase
Secreted by JG cells in response to decreased renal BP and increased renal sympathetic discharge
Paracrine regulation of renal blood flow via dilation of afferent arteriole
(NSAIDs can cause acute renal failure by inhibiting)
ANP (atrial natriuretic peptide) action on kidney
Secreted in response to INCREASED RA pressure
Causes increased GFR and Na filtration with no compensatory Na reabsorption (Na and volume loss)
PTH (parathyroid hormone) action on kidney
Secreted in response to decreased plasma Ca, increased PO4, or decreased vit D
Causes Ca reabsorption (DCT), PO4 dumping (PCT), 1-OH-D production
Angiotensin II action on kindey
efferent arteriole constriction (increase GFR) w/ compensatory Na reabsorption
Preservation of renal function in low volume state w/ Na reabsorption
Aldosterone action on kidney
Secreted in response to decreased blood volume
Causes increased Na reabsorption, K and H secretion in collecting duct
ADH action on kidney
Secreted in response to increased plasma osmolarity
Increases number of aquaporin channels (increase water reabsorption)
What shifts K out of the cell?
"pt's w/ hyperkalemia? DO INSULIN LAB"
Lysis of cells
Na effects of low and high serum concentration
Nausea, malaise, stupor, coma
Irritability, stupor, coma
K effects of low and high serum concentration
U waves, flattened T waves on ECG, muscle weakness
Wide QRS, peaked T waves on ECG, muscle weakness
Ca effects of low and high serum concentration
Tetany (ie Chovek's sign), Seizures
"Stones (renal), Bones (pain), Groans (abdominal pain), Psychiatric overtones"
Mg effects of low and high serum concentration
Decreased DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia
PO4 effects of low and high serum concentration
Renal stones, metastatic calcifications/hypocalcemia (drives Ca into cells)
pH < 7.4 with a PCO2 of 50 (what is this and what are the causes)
Respiratory acidosis (no compensation)
Caused by hypoventilation
pH of 7.38 w/ a PCO2 of 35 (what is this and what are the causes)
Metabolic acidosis with respiratory compensation
Check ion gap for causes (see other card)
Causes of metabolic acidosis with an increased ion gap (>12)
Methanol (formic acid)
Iron tablets or Isoniazid
Ethylene glycol (oxalic acid)
Causes of metabolic acidosis with normal ion gap (8-12)
Renal tubular acidosis
Renal tubular acidosis type 1
Defect in collecting tubules ability to excrete H+
Present w/ low plasma pH, hypokalemia, and calcium phosphate stones
Renal tubular acidosis type 2
Defect in proximal tubule bicarb reabsorption (may be seen with Fanconi syndrome)
Presents with low plasma pH, hypokalemia, and hypophosphatemic rickets
Renal tubular acidosis type 3
Hypoaldosteronism (or lack of response to aldosterone)
Hyperkalemia impairs ammoniagenesis in proximal tubule leading to decreased buffering capacity and decreased urine pH
Case study: A woman has a history of weakness, weight loss, orthostatic hypotension, increased pulse rate, and increased skin pigmentation. She has decreased serum [Na], decreased serum osmolarity, increase serum [K], and arterial blood gases consistent with metabolic acidosis.
Lack of aldosterone (Na dumping, K saving, H+ saving) resulting in ECF VOLUME CONTRACTION, HYPERKALEMIA, and METABOLIC ACIDOSIS
ECF contraction leads to ADH which leads to fluid retention which worsens hyponatremia
Case study: A man is admitted to the hospital for evaluation of severe epigastric pain. He has had persistent nausea and vomiting for 4 days. Upper GI endoscopy shows pyloric ulcer with partial gastric outlet obstruction. He has orthostatic hypotension, decreased serum [K] and [Cl] with blood gases consistent with metabolic alkalosis and decreased ventilation rate.
Loss of H+ and Cl causes metabolic alkalosis and ECF contraction
Decreased ventilation as respiratory compensation
ECF contraction leads to decreased RBF and aldosterone causes increase bicarb reabsorption WORSENING METABOLIC ALKALOSIS (aka contraction alkalosis)
Also causes K secretion