Renal System Physiology 3 - Teel Flashcards
Isosmotic urine:
Hypoosmotic urine:
Hyperosmotic urine:
U/P osmolarity of 1
U/P osmolarity < 1 (less solutes in urine) (lighter) (positive free water clearance)
U/P osmolarity > 1 (more solutes in urine) (darker) (negative free water clearance)
U/P = Urine / Plasma osmolarity
Countercurrent multiplication concept
Conditions in descending limb affect conditions in ascending limb
Why does osmolarity not change during secretion in proximal tubule?
Equal amount of solute and water secrete, so osmolarity does not change.
Thin descending limb
Permeable to water but not solute
Thin ascending limb
Permeable to solute. Salt leaves
Thick ascending limb
Salt leaves. becomes hypoosmotic
Distal tubule
Water and salt reabsorbed
Cortical / medullary collecting ducts
water nacl urea can be reabsorbed into medullary interstitium
Maximum medullary concentration gradient
1200 mosm/L. This is about 4x osmolarity of plasma (300)
Vasa recta definition
Peritubular capillaries that follow loop of henle
countercurrent exchange
Vasa Recta facts
Freely permeable, unlike ascending/descending limb
Osmolarity of blood in vasa recta = medullary interstitium
Vasa recta stabilizes medullary concentration gradient.
AVP (Arginine vasopressin) mechanism
Stimulates insertion of AQP2 (aquaporins) water channels into apical membranes of tubular principal cells in cortical / medullary collecting ducts
Also stimulates transport of urea from medullary collecting ducts into medullary interstitium.
Might be on Quiz:
Where’s most of our body water?
Intracellular fluid: 28 L
Extracellular Fluid: 14 L -> Interstitial fluid 10.5 L (between cells), Plasma 3.5 L
Answer: Intra
How to maintain osmolarity of extracellular fluid if its too high?
AVP.
1.) high plasma osmolarity (too much solute in plasma)-> shrinkage of osmoreceptors -> hypothalamus secretes AVP.
ADH vs. AVP
ADH is a characteristic of AVP. AVP has an antidiuretic effect.
ADH is just an effective AVP.
Point is its going to affect permeability of nephron / collecting duct which will influence urine output.
Factors that stimulate hypothalamic neurons and secretion of AVP:
increased plasma osmolarity
decreased blood volume
decreased blood pressure
nausea
morphine/nicotine/cyclophosphamide
What happens when you increase your excretion load of salt?
This can decrease ECF volume (increase osmolarity of ECF)
What monitors salt in filtrate
Important quiz question
Macula Densa Cells in distal convoluted tubules monitor salt in tubular fluid.
Granular Cells (juxtaglomerular cells) in afferent arterioles sense osmolarity of blood.
JG cells secrete ____ in response to ____.
JG cells secrete renin in response to lower renal perfusion pressure or lower salt load delivered to the macula densa.
Renin-angiotensin-aldosterone system
lower MAP -> lower renal perfusion pressure -> renin (from kidney)
Renin makes angiotensinogen (from liver) to angiotensin I
ACE (from lung) converts angiotensin I -> 2
Angiotensin II signals release of Aldosterone (from adrenal gland) and vasoconstriction
Aldosterone -> increase Na+ reabsorption, increase blood volume -> increase MAP
Vasoconstriction -> increase TPR -> increase MAP
All of this is a whole negative feedback loop.
Volume contraction
Isosmotic contraction:
Hypoosmotic contraction:
Hyperosmotic contraction:
Isosmotic contraction: water and solutes are lost equally. Maintain normal ECF
Hypoosmotic contraction: solutes are lost and not replaced in ECF-> hyponatremia
Hyperosmotic contraction: loss of more water than solutes -> hypernatremia
Volume Expansion
Isosmotic expansion:
Hypoosmotic expansion:
Hyperosmotic expansion:
Isosmotic expansion: occurs with excess intake of 0.85% saline (same conc. as plasma)
Hypoosmotic expansion: occurs with intake/retention of pure water.
Hyperosmotic expansion: occurs with drinking / IV infusion of hypertonic solutions. Water moves into ECF
extra: Difference between osmolarity and tonicity
tonicity: effect of concentration on osmolarity
When does edema occur?
When filtration forces exceed reabsorption (increase CHP, increase TOP, decrease POP)
increased permeability of systemic capillaries too.
Review: Hydrostatic pressure makes it go away from start point. Oncotic pressure makes it bring towards it.
Capillary hydrostatic pressure = goes out of capillaries
tissue oncotic pressure = goes out of capillaries
plasma oncotic pressure = goes out of tissue
tissue hydrostatic pressure = goes out of tissue
Congestive heart failure (CHF)
Hearts not pumping efficiently. Tend to retain fluids, leading to increase of blood volume in capacitance vessels (veins). body misinterprets this thinking its hypovolemia, so it increases AVP and RAA.
Nephrotic syndrome
Results in more plasma proteins being filtered out than it should be, thus decreasing POP, increases RAA activity -> retention of salt/water
Cirrhosis
Renal retention of NaCl and water -> increased intravascular volume -> increased CHP. Decrease synthesis of albumin -> decrease POP.
What diseases cause edema?
caused b y altered starling forces.
CHF
Nephrotic syndrome
Cirrhosis of the liver
Cyclic Edema (female menstrual cycle)
NSAIDS
Hypernatremia
Hyponatremia
Hyperkalemia
Hypokalemia
Hypernatremia: excess intake of salt
Hyponatremia: Not enough salt
Hyperkalemia: excess potassium
Hypokalemia: not enough potassium
Volatile problem for ventilation:
How to handle it?
Retain CO2, you’re going to create acid condition in blood. get rid of too much, you create alkaline problem.
Handle by breathing
Non volatile problem in kidneys:
How to manage this?
metabolic reactions can create nonvolatile acids like h2so4, h3po4, urea, etc.
Handle by reclaiming filtered bicarbonate.
In bowman’s capsule: we filter tons of things like bicarbonate. Bicarbonate has an alkaline effect, so if you lose it, it impacts pH of blood, so u don’t normally want to lose it. So you reabsorb it.
Mechanism of reabsorption of HCO3-
80% in proximal tubules, 10% distal tubular a-intercalated cells.
In Tubule lumen, bicarbonate is broken into CO2 and Water, where it can pass through basolateral membrane. It converts back to bicarbonate in the tubule cell, then exits through apical membrane to interstitial space. It is thus reabsorbed.
Tubular cell MUST secrete a H+ ion to convert OH- to H2O in lumen so H2O can thus go into tubular cell.
Titratable acid
H+ that is secreted into lumen can acidify HPO4 2- to H2PO4 -. Makes it less basic and more acidic in lumen.
Ammonium excretion
Tubule cells can metabolize glutamine. When they do this, they can generate 2NH4+., 2 H+, 2 NH3.
NH3 secreted into tubular fluid, combines with secreted H+ and makes NH4+ in lumen. When this happens, a new HCO3- is formed.
How is NH4+ recycled / reabsorbed?
NH4+ in tubular fluid is reabsorbed into medullary interstitium from TAL. It recycles by reentering thin regions of ascending/descending limbs and medullary collecting ducts.
Purpose of upregulating glutamine metabolism?
Helps get rid of acid. Helps reclaiming filtered bicarbonate, and generating hydrogen ions in exchange for bicarbonate.
