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2nd Year > Urinary physiology > Flashcards

Urinary physiology Flashcards

1
Q

What are the 3 basic renal processes?

A

Filtration - formation at the glomerular capillaries of an essentially protein-free filtrate of plasma
Reabsorption - Substances that the body wants.
Secretion - Substances may be specifically removed from body in this way.

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2
Q

How much blood flow does the kidney receive?

A

1200mls/min - 20-25% of total cardiac output. Have almost the highest BF/g tissue of any tissue in the body.

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3
Q

Where is the blood filtered?

A

None of the red cells and only a fraction of the plasma is filtered into Bowman’s capsule.
Remainder passes via the efferent arterioles into the peritubular capillaries and then to renal vein.

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4
Q

How much of total BV does plasma account for? And what is the renal plasma flow?

A

55% of total

Renal plasma flow = 55% of 1200mls/min = 660mls/min.

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5
Q

What is Glomerular filtration?

What is its normal value?

A

First step in making urine - filter excess fluid and waste products out of blood and into urine collecting tubules.
Normally 125ml/min.
19% of renal plasma becomes glomerular filtrate.

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6
Q

What is Glomerular filtration dependent on?

A

Balance between hydrostatic forces favouring filtration and oncotic pressure forces favouring reabsorption.

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7
Q

What determines the permselectivity of glomerular barrier?

A

Molecular size
Electrical charge
Shape

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8
Q

Why is the Glomerular capillary pressure higher than in most of the capillaries in the body?

A

Afferent arteriole is short and wide so offers little resistance to flow. Blood arriving at glomerulus still has high hydrostatic pressure.
Unique arrangement of efferent arteriole (long and narrow) offers a high post-capillary resistance.

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9
Q

What is the golden rule of circulation?

A

If you have a high resistance, hydrostatic pressure upstream is increased, while pressure downstream is decreased.

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10
Q

What in terms of efferent and afferent contributes to very high Pgc.

A

Afferent and efferent arterioles contribute. At glomerular capillaries the hydrostatic P favouring filtration always exceeds the oncotic pressure.

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11
Q

What will be entering the glomerulus?

A

Fluid pressure created by fluid in bowman’s capsule.
Colloid osmotic pressure gradient due to proteins in plasma but not in Bowman;s capsule.
Osmotic effects driving fluids back into Bowman’s capsule.

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12
Q

What is leaving glomerulus?

A

Hydrostatic pressure (blood pressure).

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13
Q

What factors affect GFR?

A

PGC - dependent on afferent and efferent arteriolar diameter and the balance of resistance between them.

Extrinsic control:

  1. Sympathetic VC nerves - afferent and efferent constriction, (afferent greater sensitivity)
  2. Circulating catecholamines - constriction afferent.
  3. Angiotensin II - constriction of efferent [LOW], both afferent and efferent [HIGH]
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14
Q

What does renal vasculature have that helps it adjust it resistance in response to changes in arterial BP?

A

Well developed intrinsic ability.

Keeps BF and GFR essentially constant = auto regulation. (effective in range from 60-130mmHg)

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15
Q

When does auto regulation occur?

A

Independent of nerves or hormones, occurs in denervated and in isolated perfused kidneys.
* if mean arterial P increases, automatic increase in afferent arteriolar constriction, preventing a rise in glomerular PGC. (capillary pressure)

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16
Q

What can happen in situations where blood volume face serious compromise?

A

Interaction between intrinsic and extrinsic controls:
Activation of sympathetic VC nerves and ALL, can override auto regulation liberating blood for more immediate important organs.
800ml can thus be used to provide to perfuse other organs at expense of kidneys. Prolonged however can lead to damage.

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17
Q

How does filtration flow?

A
  1. Plasma volume entering afferent arteriole = 100%
  2. 20% of volume filters
  3. > 19% of fluid is reabsorbed
  4. > 99% of plasma entering kidney returns to systemic circulation
  5. <1% of volume is excreted to external environment
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18
Q

What are responsible for reabsorption?

A

Peritubular capillaries - unique efferent arterioles has important effects.
It offers resistance along its entire length, large P drop so hydrostatic pressure is very low.

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19
Q

Since the filtration fraction is 20% what does this mean for blood remaining in efferent arteriole?

A

Higher concentration of plasma proteins and therefore a higher ontotic pressure.
Favour reabsorption.
99% H2O, 100% glucose, 99.5% Na, 50% urea filtered at the glomerulus are reabsorbed within the tubule

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20
Q

How do you figure out the amount of solute excreted?

A

Amount filtered - amount reabsorbed + amount secreted.

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21
Q

Why is the Pressure in the peritubular capillaries very low?

A

Hydrostatic P overcoming frictional resistance in efferent arteriols.
Ontotic pressure is high compared to normal, loss of 20% plasma concentrates plasma protein.

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22
Q

What is the mechanisms of reabsorption?

A

Many substances are reabsorbed by carrier mediated transport systems e.g. glucose, amino acids, organic acids, sulphate and phosphate ions.

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23
Q

What is Tm?

A

Carriers have a maximum transport capacity which is due to saturation of the carriers.
If Tm is exceeded, then the excess substrate enters the urine.

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24
Q

What is the renal threshold?

A

Plasma threshold at which saturation occurs.

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25
Q

What is the most important substance to be considered?

A

Glucose - it is freely filtered, so whatever its [plasma] that will be filtered. Up to 10mmoles/l, all will be reabsorbed.

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26
Q

What happens when plasma glucose is over 10mmoles/l?

A

It appears in the urine due to renal plasma threshold for glucose.

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27
Q

What is glycosuria?

A

The appearance of glucose in the urine of diabetic patients - due to failure of insulin NOT the kidney.
ANY PATIENT WITH GLUCOSE IN THEIR URINE SHOULD BE FOLLOWED UP

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28
Q

What substances does the kidney regulate?

A

Sulphate and phosphate ions - by means of Tm mechanism.
Tm is set at a level whereby the normal [plasma] causes saturation.
Any increase in the normal level will be excreted, therefore achieving its plasma regulation

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29
Q

How are sodium ions reabsorbed?

A

99.5% is reabsorbed, 70% occurring in the proximal tubule. Reabsorbed by active transport, which establishes a gradient for sodium ions across the tubule wall.

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30
Q

How does sodium move passively into cells across the luminal membrane?

A

Active sodium pumps are located on the basolateral surfaces where there is high mitochondria - decreasing [Na] in epithelial cells - increasing gradient.

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31
Q

What is special about the brush birder of the proximal tubule?

A

Higher permeability for Na ions due to enormous SA offered by microvilli and large number of sodium ion channels.

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32
Q

Why is reabsorption of Na ions so important?

A

Key to the reabsorption of other components of the filtrate.

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33
Q

What happens when sodium and chlorine (down electrical) exit the tubule?

A

An osmotic force is created, drawing water out of the tubules. This then concentrates all substances left in tubule creating outgoing concentration gradients.

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34
Q

What does the rate of reabsorption of theses non-actively reabsorbed solutes depend on?

A
  1. amount of water removed, determines extent of concentration gradient
  2. The permeability of membrane to any particular solute.
    * Tubule membrane only moderately permeable to urea 50% reabsorbed.
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35
Q

Is active transport of sodium important for carrier mediated transport systems?

A

Yes, as substances such as glucose and amino acids share same carrier molecule.
High [Na} in tubule facilitates and low [Na] inhibits glucose transport.

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36
Q

Where are substances going if they are filtered?

A

From blood to lumen.

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37
Q

Where are substances going if they are reabsorbed?

A

From lumen to blood.

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38
Q

Where are substances going if they are secreted?

A

From blood to lumen.

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39
Q

Where are substances going if they are excreted?

A

From lumen to external environment.

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40
Q

What is tubular secretion?

A

Secretory mechanisms transport substances from peritubular capillaries into the tubule lumen and therefore provide a second route into the tubule.

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41
Q

Why is tubular secretion important?

A

For substances that are protein-bound, since filtration at glomerulus is very restricted.

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42
Q

Is there at threshold for carrier-mediated secretory mechanism?

A

Yes, Tm known for a large number of endogenous and exogenous substances such as dugs. e.g. penicillin.

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43
Q

What happens to K+ in the body?

A

K+ is filtered at the glomerulus and is reabsorbed, at proximal tubule.

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44
Q

What happens when there are changes to K+ excretion?

A

Due to changes in secretion in distal parts of tubule. Any increase in renal tubule cell [K] due to increased ingestion will increase K+ secretion, while a decrease in intracellular [K] will reduce secretion

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45
Q

How is K secretion regulated?

A

Adrenal cortical hormone aldosterone.
An increase in [K] in ECF bathing in aldosterone secreting cells stimulates aldosterone release - circulates to kidneys - stimulate increase in renal tubule cell K secretion.

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46
Q

What is hyperkalaemia?

A

Over 5.5mmoles/l of [K] - decrease in resting membrane potential of excitable cells and eventually ventricular fibrillation. Death.

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47
Q

What is hypokalaemia?

A

[K] <3.5 moles/l - increases resting membrane potential - hyper polarise muscles, cardiac cells - cardiac arrhythmias - death.

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48
Q

What is the function of the proximal tubule?

A

Major site of reabsorption, 65-75% of all NaCl and water all nutritionally important substances.

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49
Q

How are drugs and pollutants able to leave the body?

What is the role of the liver in this?

A

Removal of water in the proximal tubule establishes conc gradients for their reabsorption. Due to lipid solubility we would never get rid of them.
Liver metabolises them to polar compounds thus reducing their permeability and facilitating their excretion.

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50
Q

What is collecting duct a site of?

A

Site of water regulation under the control of ADH - vasopressin.

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51
Q

What happens at dilated tubule?

A

Ionic regulation

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52
Q

What happens in justamedullary nephron?

A

Loop of hence establishes hypotonic medullary gradient.

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53
Q

Where are the proximal and distal tubules of nephrons located?

A

In the cortex.

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54
Q

What is the special system attributed to loops of Henle
of juxtamedullary nephrons?
Why is it important?

A

Essential for water balance.
Important because through this the kidney is able to produce concentrated urine in times of water deficit. Max conc of urine = 1200-1400.

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55
Q

Why does the body require a minimum obligatory water loss of 500mls per day?
What happens if there is no water intake?

A

Urea, sulphate, phosphate and other products must be excreted each day.
No water - as long as the kidneys are functioning, this volume will be excreted.

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56
Q

How do loops of Henle act as counter-current multipliers?

A
  1. The ascending limb of the loop actively co-transports Na and Cl ions out of the tubule lumen into the interstitial. Ascending - impermeable to water.
  2. The descending limb is freely permeable to water but relatively impermeable to NaCl.
57
Q

What is the key step in counter-current multipliers?

A

Active removal of NaCl from ascending limb - Osmolarity in tubule decreases and the osmolarity in interstitial increases.
*If abolished - (diuretic frusemide) conc differences are lost and kidney can only produce isotonic urine.

58
Q

What happens to the water in the interstitium?

A

Reabsorbed by the high ontotic pressure and tissue pressure into the vasa recta.

59
Q

What happens to the concentration of the fluid as it moves?

A

Progressively concentrated as it moves down the descending limb and progressively diluted as is moves up the ascending limb.

60
Q

What doe the countercurrent multiplier achieve?

A
  1. Concentrates fluid on the way down and promptly re-dilutes it on the way back up, Not by adding water bu by removing NaCl.
  2. 15-20% of initial filtrate is removed from loop of hence
  3. Fluid which enters the distal tubule is more dilute than plasma.
    * *Creates an increasingly concentrated gradient in the medullary interstitium and delivers hypotonic fluid to the distal tubule.
61
Q

What is the vasa recta?

- hairpin loops.

A

Specialised arrangement of the peritubular capillaries of the juxtamedullary nephrons - acting as countercurrent exchanges.

62
Q

Functions of the case recta?

A
  1. Provide Oxygen for medulla
  2. Not disturb gradient
  3. Removes volume from interstitial, up to 36L/day.
    Flow rate through very low.
63
Q

How does starlings forces favour reabsorption?

A

Because of High ontotic pressure and high pressure in the tissues due to tight renal capsule which drives fluid into capillaries.

64
Q

What controls whether the dilute urine is delivered to the distal tubule or not?

A

Presence or absence of the posterior pituitary hormone ADH.

65
Q

How is secretion of ADh controlled?

A
  1. Primary control is plasma osmolarity (OP): when the effect OP of the plasma increases, the rate of discharge of ADH-secreting neurones in the supraoptic (SO) and Paraventricular (PVR) is increased - therefore increasing release of ADH from the posterior pituitary
  2. ECF volume: increase - decrease in [ADH]. Decrease - Decreases atrial receptor discharge - increases [ADH]
66
Q

What mediates discharge of neurones?

A

Osmoreceptors in ant. hypothalamus close to SO and PVR.

- Lateral hypothalamus mediate thirst.

67
Q

What happens when osmolarity in increased?

A
  • Water out of cell
  • Cell shrinks/stretch sensitive ion channel activated
  • Increase neural discharge
  • Increase in ADH secretion
68
Q

What happens when osmolarity is decreased?

A
  • Water enters cell
  • Cell swells
  • Decreased neural discharge
  • Decreased ADH secretion
69
Q

Why is plasma osmolarity regulated so precisely?

A

Small changes in either direction results in rapid changes in ADH. System has a very high gain , a 2.5% increase in osmolarity can produce 10x increase in ADH. Very high gain but very sensitive.

70
Q

Why “Effective” OP?

A

Increases in osmolarity that does not cause an increase in tonicity is ineffective in causing an increase in [ADH]

71
Q

What happens if you ingest hypertonic solutions? e.g. seawater

A

Increase solute load to be excreted and therefore increase urine flow - leading to dehydration, because more water is required to excrete the solute load than was ingested with it.

72
Q

What happens when vasopressin binds to membrane receptor?

A
  • Receptor activates cAMP second messenger system
  • Cell inserts AQP2 water pores into apical membrane
  • Water is absorbed by osmosis into the blood
  • Increases permeability of the collecting ducts to water, by incorporating water channels into luminal membrane.
73
Q

What happens in the collecting ducts when ADH is present?

A
  • Water able to leave collecting duct.
  • Corticol CD becomes equilibrated with cortical interstitium.
  • CD passes through hypertonic medullary interstitial gradient.
74
Q

If max ADH is present what happens in collecting ducts?

A

Contents equilibrates with that of the medullary interstituium via osmotic efflux of water and thus becomes highly concentrated at the tip of the medulla.

75
Q

What happens with urine when there is maximal [ADH]?

A

Produces a small volume of highly concentrated urine, contained relatively less of the filtered water than of solute.
- water is reabsorbed by oncotic P of vasa recta, even greater than usual in water deficit.

76
Q

What happens in collecting ducts in absence of ADH?

A

Collecting ducts impermeable to water, medullary interstitial gradient is ineffective in inducing water movement out of CD. Large volume of dilute urine excreted.

77
Q

What is the role of urea?

A

Production of concentrated urine. Presence of ADH - movement of water out, concentrates urea in ducts.
Permeable to medullary tips - enhanced by ADH.

78
Q

What happens in antidiuresis with high levels of ADH?

A

Urea reabsorbed from CD into interstitium, acts to reinforce interstitial gradient in region of thin ascending loops of henle.
*important that it is reabsorbed - if not reduces potential for rehydration.

79
Q

Where are low Pressure receptors located? What do they do?

A

L and R atria and great veins.

Monitor the return of blood to the heart and the fullness of circulation

80
Q

Where are high pressure receptors located?

A

Carotid and aortic arch baroreceptors.

81
Q

What stimuli affect ADH?

A

Increase: pain, emotion, stress, exercise, nicotine etc…
Decrease: Alcohol, surpasses ADH release.

82
Q

What is diabetes Insipidus?

A

ADH deficiency - hypothalamic regions synthesising ADH may become diseased or damaged. Collecting ducts insensitive to ADH = Peripheral DI - usually secondary to hypercalcaemia or hypokalaemia.

83
Q

Presentation of DI?

A

Passage of very large volumes of very dilute urine = polyuria.
Drink large volumes of water = polydipsia.
Central DI = treat by giving ADH.

84
Q

Define renal filtration

A

Mass movement of water and solutes from plasma to the renal tubule that occurs in renal capsule.

85
Q

Define renal reabsorption

A

Nephron removes water and solutes from tubular fluid and returns to circulating blood. Tubule - peritubular capillaries.

86
Q

Define renal secretion

A

Transfer of materials from peritubular capillaries to renal tubular lumen (Active transport) - opposite of reabsorption.

87
Q

What determines the distribution of TBW between cells and ECF?

A

The number of osmotically active particles in each compartment.

88
Q
  1. What are the major ECF osmoles?

2. What are the major ICF osmoses?

A
  1. Na and Cl.

2. K salts.

89
Q

Regulation of ECF volume =?

A

Regulation of body Na.

90
Q

If there are changes to sodium content of the ECF how will this affect volume and blood perfusion?

A

Changes ECF volume, affecting the volume of blood perfusing the tissues which affects effective circulating volume and BP.

91
Q

What is sodium regulation dependent on?

A

High and low Pressure baroreceptors.

92
Q

What is the renal response to a decrease in ECF volume? (hypovolaemia)

A

Increase salt and water loss (vommiting, sweating) - decreased PV - decreased venous P - decreased VR - decreased atrial pressure- decreased EDV - decreased SV - decreased CO - decreased BP - decreased carotid sinus baroreceptor inhibition of sympathetic discharge.
Therefore increase in sympathetic discharge to increase VC - increase TPR - increasing BP towards normal.

93
Q

What specific affect does decreased ECF volume have on the kidneys?

A

An increase in sympathetic discharge will lead to:
1. Increase in renal VC nerve activity - increasing arteriolar constriction and an increases in renin.

  1. increase in renin - increases angiotensin II - decreases peritubular capillary hydrostatic pressure - increasing na reabsorption from proximal tubule. (due to change of rate of uptake by peritubular capillaries)
94
Q

What regulates the distal tubule sodium reabsorption?

A

Aldosterone - adrenal cortical steroid hormone.

95
Q

How has the smooth muscle of the media of the afferent arteriole become specialised?

A

Contain large epithelial cells with plentiful granules called juxtaglomerular cells (JG). Closely related to macula densa (specialised loop at distal). Form juxtaglomerular apparatus.

96
Q

What do JG cells produce?

A

Hormone Renin - proteolytic enzyme which works on angiotensinogen - which becomes active angiotensin II.

97
Q

What does angiotensin stimulate?

A

Aldosterone - secreting cells in the bona glomerulosa of the adrenal cortex.

98
Q

What controls renin release?

A
  1. Increased renin when pressure in afferent arteriole at the level of JG cells decreases.
  2. Sympathetic nerve activity causes increase in renin release via beta 1 effect.
  3. Rate of renin secretion is inversely proportional to rate of delivery of NaCl at the macula densa. So decrease in NaCl delivery causes an increase in renin.
  4. Angiotensin II feeds back to inhibit renin
  5. ADH inhibit renin release (osmolarity control)
99
Q

What role does angiotensin II have in body’s response to hypovolaemia?

A
  1. It stimulates aldosterone and there NaCl and water retention.
  2. It is very potent biological vasoconstrictor
  3. It acts on the hypothalamus to stimulate ADH secretion - increasing water reabsorption from collecting duct
  4. It stimulates the thirst mechanism and the salt appetite.
100
Q

What happens when there is EVC compromise?

A

Volume considerations have primacy if EVC is compromised, so ADH will increase because of the baroreceptors. Volume becomes primary drive - save perfusion for the brain.

101
Q

Aldosterone promotes Na reabsorption and ANP promotes what?

A

ANP = Atrial Natriuretic peptide promotes Na excretion.

102
Q

If aldosterone is given what effects does it have on reabsorption and retention?

A
  • Increases Na reabsorption.
  • Increases K secretion
  • increases weight due to retention of water with increase Na
  • Volume expansion
  • Stimulation of release of ANP from atrial cells
  • loss of Na and water i.e. natriuresis
103
Q

Why does ANP override aldosterone?

A

Overrides its affects on Na reabsorption because of volume expansion = “aldosterone escape”

104
Q

What happens in uncontrolled diabetes mellitus - where the high plasma glucose exceeds the maximum reabsoptive capacity in the proximal tubule?

  1. Glucose
  2. Na reabsorption
  3. Descending limb of Loop of henle
  4. Ascending limb of loop of henle
  5. Distal tubule
A
  1. Glucose remains in the tubule and exerts an osmotic effect to retain water in the tubule.
  2. [Na] in the lumen is decreased because Na is present in a larger volume. Na reabsorption decreases and therefore the ability to reabsorb glucose as they share a symport.
  3. Descending limb of loop of henle, movement of water out of the tubule into the interstitial is reduced because glucose and excess Na exert an osmotic effect to retain water - therefore fluid in the descending limb is not so concentrated.
  4. Fluid delivered to ascending limb is less concentrated. NaCl pumps in limb are gradient limited. Considerable reduction in the volume of NaCl and water reabsorbed from loops of Henle. LARGE VOLUME OF NACL AND H20 IS DELIVERED TO DISTAL TUBULE AND INTERSTITIAL GRADIENT IS GRADUALLY ABOLISHED
  5. The macula densa will detect the high rate of delivery of NaCl so that renin secretion will be suppressed and Na reabsorption at the distal tubule will be decreased.
105
Q

Why is it useful to be able to measure GFR in clinical situations?

A
  1. Patients with renal disease - Progression of disease would be indicated by the reduction in GFR.
  2. Many drugs are removed from body by excretion by filtration - GFR falls, excretion falls so [drug] in plasma may rise causing toxicity - adjust dose appropriate to renal function.
106
Q

What is total GFR?

A

Sum of all filtration by functioning nephrons.

107
Q

What are used to measure renal function? (measure GFR)

A

Plasma clearance test:

measures the ability of kidney to clear the plasma of various substances.

108
Q

What is used for the clearance test?

A

51Cr-EDTA - suitable radioactive substance that doesn’t interfere with normal renal function. (too expensive)

109
Q

What is routinely used to estimate GFR? (eGFR)

A

Creatinine clearance: Endogenous, good agreement with inulin clearance.
GFR = CIN = CCR

110
Q

What factors affect serum Creatinine?

A

Muscle mass: athletes vs malnutrition
Dietary intake: creatine supplements vs vegetarians
Drugs: Some lead to spurious increases as does ketoacidosis.

111
Q

What is PAH (para-amino-hippuric acid) clearance a measure of?

A

All the plasma flowing through the kidneys in a given time = renal plasma flow.

112
Q

What is the 1. Internal urethral sphincter

2. External urethral spinster?

A
  1. NOT true sphincter - where smooth muscle at start of urethra acts as a sphincter when the smooth muscle is relaxed.
  2. TRUE sphincter, made up of skeletal muscle under voluntary control.
113
Q

What problems do

  1. urethral obstructions cause?
  2. Ureter obstruction?
A
  1. Bilateral renal problems

2. Unilateral renal problems

114
Q

What is the characteristic shape of the pressure-volume curve of the bladder?

A

Long flat-segment as initial increments of urine enter bladder and then sudden sharp rise as micturition reflex is triggered.

115
Q

Control of Micturition:

What motor innervation takes place?

A

Rich parasympathetic supply increases activity - increases contraction of detrusor muscle - increases pressure within bladder (S2-4)

116
Q

Control of Micturition:

What do somatic motorneurones do?

A

Innervate skeletal muscle that forms the external urethral sphincter, keeps sphincter closed, even against strong bladder contractions.

117
Q

What is main function of sparse sympathetic supply?

A

Prevent reflux of semen into bladder during ejaculation

118
Q

What sensory innervation is involved in control of peeing?

A

Stretch receptors afferent from bladder wall. As bladder fills - increased discharge in afferent nerves to spinal cord - via interneurones:

  1. excitation of parasympathetic flow
  2. Inhibition of sympathetic flow
  3. Inhibition of somatic motor neurones to external sphincter
  4. Pathway to sensory corrtex - sensation of fullness
119
Q

How do we get a delay of when we have a full bladder an then when we pee?

A

Descending pathways from many brain centres, including cortex and brainstem:
- inhibits parasympathetic
- stimulates somatic nerves to external sphincter - overriding input from bladder stretch receptors.
(voluntary initiation involves this)

120
Q

What are abnormalities of micturition?

A

3 major types due to neural lesions:
1. interruption of afferent nerves
2. interruption of both afferent and efferent nerves
3. Interruption of facilitatory and inhibitory descending pathways from the brain.
(urine left in the bladder)

121
Q

Where does the body get its sources of H ions?

A
  1. Respiratory Acid - not net contributor.
  2. Metabolic Acid (non-reap):
    via metabolism -
    a) Inorganic acids - e.g. S-containing amino acids
    b) Organic acids - fatty acids, lactic acid
122
Q

What is a major source of alkali?

A

Oxidation of organic anions such as citrate

123
Q
  1. What do buffers do?

2. What importance do extracellular buffers have?

A
  1. Minimise changes in pH when H ions are added or removed.

2. Most important in bicarbonate buffer.

124
Q

Why is the bicarbonate buffer system so crucial?

A

Increase in ECF - H ions drive the reaction to the right, removing additional H ions from solution - therefore reducing pH
( H ions + HCO3 H2CO3 H20 + CO2)

125
Q

How does the body eliminate H ions?

A

Kidneys and this excretion is coupled to the regulation of plasma [HCO3]
pH = renal regulation/Resp regulation

126
Q

What are intracellular buffers?

A

Proteins, organic and inorganic phosphates and haemoglobin.

127
Q

What do intracellular buffers do?

A

Cause changes in plasma electrolytes. Movement of H ions must be accompanied by Cl or exchanged for a cation, K.

128
Q

How does the kidney regular [HCO3]?

A
  1. reabsorbing filtered HCO3
  2. generating new HCO3
    - depend on active H ion secretion from tubule into lumen.
129
Q

What is the dial tubule a site of in terms of acid/base?

A

Formation of titratable acidity.

130
Q

When is ammonium excretion helpful?

A

Acid load - generates new HCO3 and excretes H ions.

131
Q

What is acidosis?

A

Decrease in pH

132
Q

What is alkalosis?

A

Increase in pH

133
Q
  1. What do Renal disorders affect?

2. What do respiratory disorders affect?

A
  1. [HCO3]

2. PCO2 - reduced ventilation and retention of CO2.

134
Q

Acid/Base disorders:
Resp acidosis:
what happens to H ions and pH?
Whats going wrong and what is compensated?

A

Increase in H ions
Decrease in pH
Primary disturbance in increase in PCO2
Compensation is increase in [HCO3]

135
Q

Acid/Base disorders:
Resp alkalosis:
what happens to H ions and pH?
Whats going wrong and what is compensated?

A

Decrease in H ions
Increase in pH
Primary disturbance is decreased PCO2
Compensation decreased [HCO3]

136
Q

Acid/Base disorders:
Metabolic acidosis:
What happens to H ions and pH?
Whats going wrong and what is compensated?

A

Increase H ions
Decreased pH
Primary disturbance decrease in [HCO3]
Compensation is decreased PCO2

137
Q

Acid/Base disorders:
Metabolic alkalosis:
What happens to H ions and pH?
Whats going wrong and what is compensated?

A 
decrease in H ions 
Increase pH 
Primary disturbance is increase [HCO3] 
Compensation is increase PCO2
*always look at pH
138
Q

Give NaCl, restore volume, alkalosis will be corrected

A

In vomiting and diarrhoea, lose acid and alkali - become alkalotic because decrease in ECF volume - increases aldosterone - “contraction alkalosis”

2nd Year (27 decks)

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