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Physiology > Kidney > Flashcards

Kidney Flashcards

1
Q

Autoregulation of renal circulation

A

Independent of the systemic circulation. Blood flow of the kidney consistently adapts to the demand of the excretion => achieve its excretory function

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2
Q

Filtration

A
  • CFC (capillary filtration coefficient): ultrafiltration in renal glomerulus is 100X higher than in any other capillary, due to the (-) charge of its lamina densa which strongly reflects the proteins.
  • EFP (effective filtration pressure): extent of ultrafiltration depends on pressure gradient, components: Phydrostatic of glomerulus, Bowman’s sheath P, colloid-osmotic P of plasma
    EFP = GP - (CP + GCP)
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3
Q

Reabsorptin

A

Extremly large filtration rate => fatal loss of fluid.

2 main pathways: paracellular, transcellular

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4
Q

Secretion

A

From plasma leaving the glomerulus (eff arteriole). Some after filtration + reabsorption, some directly. Transcellular + paracellular

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5
Q

Excretion

A

Filtration, reabsorption, secretion => secondary filtrate of urine
Rate= urine / selected material excreted. 2-3 mL/min/100 kg bwt urine

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6
Q

Glomerular filtration rate

A

Amount of filtrate produced/t. Material which is ONLY filtrated and its load + rate has to be equal to the amount appearing in urine/t (eg.insulin = 120mL/min/100 kg bwt)
Autoregulation of GFR: constant (myogenic mechanism, tubulo-glomerular feedback)

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7
Q

Extraction

A

Elimination of a substance.
[substance] in renal a -> kidney -> same/reduced amount leaves through the v
Max: when substance doesn’t appear at all on the venous side (E=1)
Min: entire amount appears on the venous side + nothing un urine (E=0).
E = Pa - Pv / Pa

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8
Q

Clearance

A

Remove a substance from the plasma + forward it to the urine.
- Exclusively filtered (neither absorbed nor secreted) => clearance = GFR
- Entirely secreted (eg.p-aminohippuric acid)- clearance => RPF
▪️PAH: const in low [], in higher clearance decreases
▪️insulin: its [] does not influence its clearance
▪️urea: freely filtered, unlimited capacity of filtration
▪️glucose: freely filtered, normal plasma [] => clearance = 0. In diabetes glucose appears in the urine (no reabsorption)

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9
Q

Renal plasma flow

A 
Amount of plasma flowing around the kidney
Flick principle (law of conservation of matter): amount of substance entering the kidney (arterial side) must = amount leaving (venous side + urine)
RPF = U X V / (Pa - Pv)
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10
Q

Loop of Henle and distal tubule

A

30% of Na is reabsorbed here.
- Thick descending limb: NO active transport, high permeability, electrical potential gradient bw the lumen + interstitium
- Thick ascending limb: 25% of the filtered amount is reabsorbed here
Na/K-ATPase pump: Na- cell -> interstitium + K- interstitium -> cell
Na can be reabsorbed in the luminal side + excess K via K channels leave
Na/K/2Cl symporter (luminal side) => electroneutral transport (inhibitor: furosemide) -> water + salt loss => diuresis
TAL impermeable to water => lumen = hypoosmotic
- Distal convoluted tubule: Na/Cl symport absorbs further 5% of the filtered Na (inhibitor: thiazide derives => diuresis)
Cl carried by K/Cl cotransported
Ca transport directed by the calcium saving effect of PTH.

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11
Q

Hormonal + Pharmacological effects

A
  • Distal convoluted tubule: PTH: Ca reabsorption, calcitonin: Ca excretion, both: P excretion
  • Proximal + Distal convoluted tubules + collecting ducts: carbonic anhydrase inhibitors
  • Thick ascending limb: furosamide
  • Distal convoluted tubule: thiazide
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12
Q

Transport in the distal connective tubule + collecting tubule

A

Formation of the hormonally regulated final urine:

  1. CNT, CCT = mineralocorticoid Na dependent reasorption
  2. CCT = ADH-dependent water reabsorption
  3. MCT = ADH-dependent water + urea reabsorption
  4. ANP-dependent Na excretion

▪️Mineralocorticoid dependent Na/K transport: Na/K pump (basolateral side), Na and K channels (luminal side). Aldosterone dependent. Transport of K is passive in both directions + determined by aldosterone []. If K in excess => more aldosterone => more channels
▪️Active water transport: water flow is directed by osmotic forces. In CCT + CNT / MCT sections: water transport is hormonally regulated: aquaporin-2.
▪️Acid-base balance: CCT + CNT. K secretion + hydrocarbonate reabsorption. Alkalosis: independent hydrocarbonate prod + secr
- Defense against acidosis: H (water) -> lumen by ATPase, the carbonic anhydrase unites CO2 + OH => HCO3, which is transported to the blood by Cl/HCO3 antiporter.
- Defense against alkalosis: dissociation of water => H -> interstitium by H/K ATPase pump. HCO3 -> lumen via HCO3/Cl antiporter.
▪️K transport: [K] is regulated by the organism, as its [] change affects all irritable tissues. CCT principal cells: reabsorption of Na + mineralocorticoid dependent secretion of K, CCT intercalary cells: reabsorption with H/K exchange.

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13
Q

Transport- proximal tubule

A

70% of the filtrate is reabsorbed here.
Actively -> interstitium
Passively -> peritubular capillaries
- Na: Na -> interstitium, K -> cell (Na/K-ATPase pump)
- H: Na => H secretion. Inhibited by amiloride
- Bicarbonate: cell is impermeable to it. CO2 diffused -> cell, H with the help of carbonic anhydrase => HCO3 (indirect)
- Cl: prerequisite: lower pH in lumen than in cell. Cl-acidic anion antiporter: Cl -> cell + acidic anion -> lumen. Cl binds H => free acid (diffuses back) then dissociates
- Water: increased peritubular oncotic P => water migrates from lumen -> interstitium. Aquaporin-1
- Glucose, aa: 100% withdrawn from prox tubule. They have their own specific carriers + inhibitors
- Urea: half = passively reabsorbed, the rest stays in the interstitium => special osmotic layering in the kidney
- Proteins: some -> lumen, majority -> back to the tubular cells by pinocytosis

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14
Q

Osmoregulation

A

Maintain osmotic homeostasis, because a shift may destroy important physiological processes.
Salt deficiency/ excess, shortage/ excess of water => feedback.
Fast restoration is carried out on the expense of a shift of the isovolaemia.

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15
Q

Hyperosmosis

A

Due to mannit + glucose, Na. EC + IC are getting osmotic equalized => hyperosmotic isovolaemia.

  • Hypothalamic osmoreceptor activity + ADH level: increase
  • Expression of AQP-2: increases, water clearance: decreases
  • > direction of isosmotic hypovolemia
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16
Q

Hypoosmosis

A

[osmotic] of EC decreased, due to reduced salt intake/salt loss => inhibition of ADH, water clearance increases => hypovolemic isoosmosis

17
Q

ADH-mechanism

A

Maintain isoosmosis. At the connecting point of dist.tubule + collecting duct.

  1. Kidney => hypoosmotic urine due to lack of endocrine mechanisms => ADH readjusts isosmosis
  2. Damage to hypothalamic ADH => hypoosmotic urine
  3. Increased diuresis can be blocked by ADH
  4. Hydropenia => immediate blood => ADH increases
18
Q

The countercurrent system

A

The maintenance of isoosmosis + isovolemia requires that urine V + urine osmolarity change in a wide range. This is achieved by the osmotic layering of the kidney and countercurrent multiplier + countercurrent exchanger are responsible for its creation

19
Q

Osmotic gradient of kidney

A

Osmolarity increases from cortex -> papilla (300-1200mosmol/L). The cells lying deeper in the medullary portion work under hyperosmotic circumstances by providing an osmolarity within the cell to that lf the environment.
Factors creating it:
- Reabsorption of Na/K/Cl of thick asc limb
- The rising interstitial [osmotic] attracts water from the desc limb.
- Process: from top -> bottom.
- The countercurrent flow of the 2 tubes
Countercurrent multiplier- vasa recta system: runs parallel to the Henle loop, it can keep the hyperosmosis because of its anatomical position
Affects quantity + composition of urine

20
Q

Clearance of free water

A

Osmotic clearance: amount of plasma cleared of all osmotically active particles/t. It’s a virtual no => how much water does the kidney ADD (diluting kidney) or REMOVE (concentrating kidney) from the isosmotic urine.
- Clearance value (knowing the minute of urine V):
Cosm = Uosm / Posm X V
Free water clearance value: CH2O = V - Cosm => = V X 1 - (Uosm / Posm), if 0 = equilibrium, if >1 = - [], if <1 = + dilution

21
Q

V regulation

A
  • Physiological: NaCl uptake + excretion are balanced
  • Extra salt intake => hyperosmosis => sensation of thirst -> drink => isosmosis, but extra salt + water stay in EC => hypervolaemia
  • Elimination: gradually
    Extra V of water => increase vlood V + arterial P, peripheric vasodilation, decrease of oncotic P
22
Q

RAS (Renin Angiotensin System)

A
  • Renin: no direct effect
  • Angiotensin I: no direct, precursor
  • Angiotensin II: pressor effect, RBF/GFR decrease, increased peripheral resistance, most important stimulator of aldosterone -> salt retention. In nervous system: arterial P is increased, increases thirst, increased peripheral catecholamine synthesis, ADH stimulation.
  • Angiotensin III: 50% lower pressor effect than II
23
Q

ANP (atrial natriuretic peptide)

A

Primary stimulus: atrial stretch -> pre-pro ANP -> ANP
salt load -> ANP, fluid load -> ANP
ANP: Na excretion increases => cGMP increases: Na/H exchange decreases. Direct inhibition of aldosteron, ADH + renin secretion

24
Q

Aldosterone

A

Most important member of mineralocorticoids. A steroid hormone, produced by the zona glomerulosa of adrenal cortex.
Key enzyme: 18-aldolase
Na reabsorption + K excretion, essential in the retention of Na + water
Primary stimulus: increase of [K], defense against hyperkalemia
ADH: setting pasma osmolality, main side of aldosterone effect = dist tubule and cortical section of connecting + collecting ducts.

25
Q

Urination process

A
  • Rhythmical contractions of calyx => urine -> renal oekvis
  • Peristalsis of urine forwards the urine, speed = 2-3 cm/s
  • Bladder wall: smooth muscle elements + elastic fibers which react to stretch by relaxation. Filling phase: tension increases (mechanoreceptors are slightly stimulated), filling at a certain point: increased activity of mechanoreceptors => urination
26
Q

Regulation of urination

A

Emptying of the bladder is controlled by the urinary center in the pons.
Execution: lumbal (S), sacral (PS), somatic (abd.mm, perineum, outer sphincter)
1. Saturational: filling phase: PS -> contraction of the wall of the bladder, S (beta2-receptor): releases the detrusor mm + contracts via alpha1-receptors
2. Urination: increased mechanoreceptor activity => affects the center in the pons => increases PS + inhibits S and somatic activity => bladder wall contracts, sphincters relax, urination.

Physiology (6 decks)

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