Renal Phys Flashcards
Describe renin. What produces it and what is its function?
produced by: juxtaglomerular cells of the kidney
function: converts angiotensinogen into angiotensin I
- rate limiting step of angiotensin II formation
angiotensin II function
- constricts vessels = increased BP
- stimulates adrenal glands to release aldosterone = increase Na + H2O resorption
Describe erythropoietin. What is it released by and what is its function?
secreted by: peritubular interstitial cells of the kidney
function: stimulates erythropoiesis in the bone marrow
- can be reduced in chronic kidney failure: can lead to anemia
Describe vasopressin/ADH. What produces it and what are its effects?
produced by: hypothalamus
released by: posterior pituitary
function:
- stimulates V1 receptors: increases smooth muscle contraction in vessels = increased kidney perfusion
- increases free water reabsorption in the collecting duct
- increase urea resorption: concentrates urine
Describe parathyroid hormone. What secretes it and what are its functions?
secretion: parathyroid gland
- stimulated by decreased Ca, vitamin D3, or increased PO4 in plasma
function - stimulates proximal convoluted tubule to:
- increase Ca absorption
- increase vitamin D3 synthesis
- decrease OI4 reabsorption
Describe the fluid compartments and their distribution.
Males - 60% fluid
2/3 intracellular fluid
1/3 extracellular fluid
~ 80% interstitial fluid (outside vessels)
~ 20% plasma (within vessels)
What are the portions of the renal corpuscle?
Bowman capsule + glomerulus
forms the filtration membrane
glomerulus:
- fenestrated epithelium
- glomerular basement membrane
bowman capsule: podocytes
Describe the proximal convoluted tubule. What kind of cells does it have?
site of most reabsorption: Na (67%), K, Cl, Mg
- glucose, bicarbonate, urea
contains brush border cells
- apical surface towards the tubular lumen contains microvilli to increase solute/H2O reabsorption
Describe the movement of ions in regards to the following channels on the proximal convoluted tubule:
Na-Glucose
Na-H
Na-K-ATPase
Na-HCO3
Na-glucose: apical cotransporter to get glucose into brush border cell
- glucose passively diffuses thru GLUT back to circulation
Na-H: Na in, H out on apical portion of brush border cell into filtrate
- H can become H2CO3
Na-K-ATPase: basolateral surface
- Na into interstitium: maintains low Na for concentration gradient
- K into brush border
Na-HCO3: basolateral surface cotransporter
- 85% of HCO3 reabsorbed into blood
What are the substances secreted by the proximal convoluted tubule? What is broken down to make them?
glutamine broken down into:
- NH4: goes into tubular fluid
- HCO3- gets reabsorbed into blood
organic acids + meds diffuse out of the peritubular capillary via transport proteinsD
Describe how the proximal convoluted tubule uses H to help with bicarbonate reabsorption
Na-H anti porters on apical surface
- pumps H out of brush border cell
- in tubular lumen, forms carbonic acid
carbonic anhydrase 4: cleaves H2CO3 into H2O + CO2 = easily diffuse across apical membrane
carbonic anhydrase 2: reforms H2CO3 in brush border cell
- dissolved into HCO3-
Na-HCO3- cotransporter on basolateral surface diffuses HCO3-
- allows for 85% of HCO3- reabsorption
What would you expect to see in someone with acidosis? How could you tell it were respiratory or metabolic?
< 7.35
respiratory acidosis: decreased PCO2
metabolic acidosis: decrease HCO3
what would you expect to see in someone with alkalosis? How could you tell if it were respiratory or metabolic?
> 7.45
respiratory alkalosis: decreased PCO2
metabolic alkalosis: increased HCO3-
What is the anion gap? What is normal?
metabolic acidosis
serum [Na] - [Cl] - [HCO3-]
normal 6-12
FUSEDCARS
fistula
uretogastric conduit
saline administration
endocrine - addisons
diarrhea
carbonic anhydrase inhibitors
ammonium chloride
rental tubular acidosis
spironolactone
What is an increased ion gap and its causes?
metabolic acidosis
serum [Na] - [Cl] - [HCO3-]
> 12
MUDPILES
methanol
uremia
diabetic ketoacidosis
paraldehyde
iron or isoniazid overdose
lactic acid
ethylene glycol
salicylate
What are some metabolic causes for metabolic alkalosis?
Chloride responsive
- hypovolemia
- renal losses
- cystic fibrosis
- dietary chloride deficiency
chloride resistant
- severe magnesium deficiency
- extreme hypercalcemia
- extreme hypokalemia
- high alkali load
- loop/thiazide diuretics
