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ESA 3 > Urinary 6 > Flashcards

Urinary 6 Flashcards

1
Q

What is the normal range of plasma pH?

A

7.38 - 7.42

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2
Q

What are the major clinical effects of Alkalaemia?

A

Lowers free Ca2+ in serum:

Increases excitability of nerves

If greater than 7.45:

Parasthesia (tingling)

Tetany (Involuntary muscle contraction, danger to breathing)

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3
Q

What are the mortality rates of Alkalaemia at pH 7.55 and 7.65?

A

45% at 7.55

80% at 7.65

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4
Q

What are the major clinical effects of Acidaemia?

A

Increase plasma potassium

Affects enzymes:

Reduced cardiac and skeletal muscle contractility

Reduced glycolysis in many tissues

Reduced hepatic function

Effects sever below 7.1 and life threatening below 7.0

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5
Q

How is plasma pH determined? What systems are involved?

A

Dependent on pCO2 to [HCO3-] ratio

pCO2 determined by respiration

[HCO3-] determined by kidney

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6
Q

What causes respiratory acidaemia and alkalaemia?

A

Resipiratory Acidaemia:

Hypoventilation leads to hypercapnia, causing plasma pH to fall

Repiratory Akalaemia:

Hyperventilation leads to hypocapnia causing plasma pH to rise

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7
Q

Explain briefly the role of chemoreceptors in pH balance

A

Central:

Keeps pCO2 within tight limits

Corrects disturbances in pH with respiratory changes

Peripheral:

Enable changes in respiaration driven by changes in plasma pH

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8
Q

Explain the role of the kidneys in correcting respiratory driven pH changes

A

Kindey control [HCO3-] and hence can conpensate for change in pCO2 with change in [HCO3-]

Respiratory acidaemia can be compensated by increase in [HCO3-] (Compensated respiratory acidaemia)

Respiratory alkalaemia can be compensated by decrease in [HCO3-] (Compensated respiratory alkalaemia)

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9
Q

Describe metabolic acidaemia and it’s compensation

A

Metabolic acidaemia:

Tissues produce acid (E.g. H+) that reacts with HCO3-

This leads to a fall in plasma pH

Also produces an anion which can replace HCO3-

Compensation via change in ventilation:

Peripheral chemoreceptors

Increased ventilation lowers pCO2

Restores normal pH (ideally)

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10
Q

Describe metabolic alkalaemia and its compensation

A

Metabolic alkalaemia:

Plasma [HCO3-] rises (E.g. post-vomiting)

Leads to rise in plasma pH

Compensation via ventilation change:

Decrease in ventilation can only partially compensate

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11
Q

Briefly describe renal control of [HCO3-]

A

Large quantities filtered per day (4500mmol)

Should be able to lose HCO3- very easily

To increase [HCO3-] must both recover all filtered and make new

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12
Q

How does the kidney produce HCO3-?

A

Normal metabolic activity:

CO2 + H2O = HCO3- + H+

HCO3- enters plasma

H+ excreted in urine

Additionally:

HCO3- can be produced from amino acids, this produces NH4- to enter urine

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13
Q

From where in the kidney tubule is HCO3- recovered?

A

80-90% in PCT

Rest in Tal of LoH

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14
Q

Describe the reabsorption of HCO3- from the kindey lumen

A

Basolateral Na+/K+ ATPase produces Na+ gradient across luminal membrane

Gradient allows Na+/H+ exchanger to pump H+ out of cell and Na+ in

H+ reacts with HCO3- in the lumen

HCO3- + H+ = H2O + CO2

H20 and CO2 are reabsorbed and react

H20 + CO2 = HCO3- + H+

HCO3- is reabsorped through basolateral membrane

H+ is recycled

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15
Q

How is HCO3- produced via the mechanism specific to the proximal tubule?

A

Glutamine is broken down to produce Alpha-Ketoglutarate and NH4-

Alpha-Ketoglutarate makes 2 HCO3-

HCO3- into ECF

NH4- into lumen

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16
Q

How does the kidney produce HCO3- via a mechanism specific to the DCT?

A

Intercalated cells:

Metabolic CO2 reacts with H20 to produce HCO3- and H+

HCO3- secreted into ECF

Na+ gradient insufficient to drive H+ secretion into lumen

Active secretion of H+ used instead

H+ in lumen buffered by filtered phosphate and excreted ammonia

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17
Q

What is the total acid excretion per day in the kidneys?

In what form is H+ found in the urine?

A

50-100mmol of H+

Some H+ buffered by phosphate, the rest attached to ammonia

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18
Q

How is H+ excretion controlled?

A

Probably by changes in tubular cell’s intracellular pH

This pH change is the concequence of changing rates of [HCO3-] export

Therefore control of H+ is acheived through control of [HCO3-]

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19
Q

How might respiratory function lead to a change in H+ excretion?

A

Respiratory acidaemia/alkalaemia will affect intercellular pH in the renal tubule due to changes in CO2 diffusing in as pCO2 is altered

This will produce an increase/decrease in HCO3- export to plasma and hence increase/decrease H+ excretion

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20
Q

How does [K+] affect pH of plasma?

A

[K+] affects HCO3- reabsorption and ammonia excretion

E.g. [K+] rise leads to decreased capacity of the kidney to reabsorb and create HCO3-

Hypokalaemia can therefore lead to metabolic alkalosis

Hyperkalaemia can lead to metabolic acidosis

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21
Q

Outline the renal cellular responses to acidosis

A

Enhanced H+/Na+ exchange (Fully recover filtered HCO3-)

Increase NH4- production in PCT

Increased H+ ATPase in DCT

All lead to an increased capacity for the renal cells to produce and export HCO3- and correct acidosis

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22
Q

Explain the Anion Gap

A

Difference between ([Na+] + [K+]) and ([Cl-] + [HCO3-])

Indicates whether HCO3- has been replaced with something other than Cl- (ie. unaccounted ions)

Normally 10-15mmol.l-1

Increased if anions from metabolic acids have replaced plasma HCO3-

Sometimes renal problems can reduce [HCO3-] and not increase the anion gap as the HCO3- has been replaced with Cl-

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23
Q

Describe the kidney response to metabolic alkalosis

When might problems arise with correction?

A

[HCO3-] increases after persistent vomitting

HCO3- infusions can be corrected extremely rapidly as rise in intracellula pH in the renal tubule leads to decreased H+ secretion and hence HCO3- recovery

But:

If there is also volume depletion, Na+ conservation is prioritised

High rates of Na+ reabsorption raise H+ excretion, favouring HCO3- recovery

This limits our ability to excrete HCO3-

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24
Q

Describe the kidney’s response to respiratory alkalosis

A

Rise in tubular pH due to lower pCO2 induce less HCO3- export by reducing H+ secretion into lumen (hence reduing HCO3- recovery from lumen)

HCO3- is therefore excreted and [HCO3-] falls to correct the [HCO3-]/pCO2 ratio

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25
Q

Give the reference ranges for:

pH

pCO2

[HCO3-]

pO2

A

pH = 7.38 - 7.42/7.46

pCO2 = 4.2 - 6.0 kPa

[HCO3-] = 22 - 29 mmol.l-1

pO2 = 9.8 - 14.0 kPa

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26
Q

What are the would you expect an increase or decrease in the values given below in uncompensated metabolic acidosis?

pH

pCO2

[HCO3-]

pO2

A

Decrease

Normal

Decrease

Normal

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27
Q

What are the would you expect an increase or decrease in the values given below in compensated metabolic acidosis?

pH

pCO2

[HCO3-]

pO2

A

Normal or Low

Low

Low

Normal

28
Q

What are the would you expect the values given below to be low, high or normal in uncompensated metabolic alkalosis?

pH

pCO2

[HCO3-]

pO2

A

High

Normal

High

Normal

29
Q

What are the would you expect the values given below to be low, high or normal in compensated metabolic alkalosis?

pH

pCO2

[HCO3-]

pO2

A

High/Normal

High

High

Low

30
Q

What are the would you expect the values given below to be low, high or normal in uncompensated respiratory acidosis?

pH

pCO2

[HCO3-]

pO2

A

Low

High

Normal

Low

31
Q

What are the would you expect the values given below to be low, high or normal in compensated respiratory acidosis?

pH

pCO2

[HCO3-]

pO2

A

Low/Normal

High

High

Low

32
Q

What are the would you expect the values given below to be low, high or normal in uncompensated respiratory alkalosis?

pH

pCO2

[HCO3-]

pO2

A

High

Low

Normal

Normal/High

33
Q

What are the would you expect the values given below to be low, high or normal in compensated respiratory alkalosis?

pH

pCO2

[HCO3-]

pO2

A

High/Normal

Low

Low

High/Normal

34
Q

What is the total body K+?

How is it distributed?

A

Total:

3500mmol

ICF

98%

120-150mmol/l

Mainly in skeletal muscle cells, liver, RBCs and bone

ECF:

2%

3.5-5mmol/l

35
Q

What maintains the difference between ICF and ECF [K+]?

A

Na+/K+ ATPase

36
Q

Why is tight regulation of [K+] critical?

A

High ICF and low ECF [K+] contributes to the resting membrane potential and allows for action potentials

An increase in ECF [K+] would depolarise cells

A decrease in ECF [K+] would hyperpolarise cells

These changes would have profound effects on excitability of cardiac and nuromuscular tissues:

Problems with cardiac conduction and pacemaker automaticity

Alter neuronal function, skeletal and smooth muscle function

Arrhhythmias, cardiac arrest, muscle paralysis

37
Q

What events follow a meal containing K+?

A

Intestine and colon absorb K+

Substatial amounts of K+ therefore enter the ECF (Danger!)

Kidney’s cannot excrete this K+ fast enough

4/5 of ingested K+ moves into ICF/cells within minutes

After a slight delay K+ is released from ICF slowly as Kidney’s begin to excrete K+

Excretion takes 6-12h

38
Q

What 2 processes are responsible for K+ homeostasis?

A

External balance:

Adjustment of renal K+ to match intake

Responsible for longer term control of total K+

Internal balance:

Moves K+ between ICF and ECF to correct ECF levels of K+ should they rise or fall

Effect is immediate (within minutes of imbalance)

Responsible for moment to moment control

39
Q

Internal K+ balance is a result of 2 processes, what are they?

A

Movement of K+ into ICF via Na+/K+ ATPase

Movement of K+ out of ICF into ECF via K+ channels (E.g. ROMK)

40
Q

What are the factors promoting uptake of K+ into ICF?

A

Hormones (acting on Na+/K+ ATPase):

Insulin
Aldosterone
Catecholamines

Increased [K+] in ECF

Alkalosis:

Low ECF [H+] causes H+ to move out of cells and correct imbalance causing a reciprocal shift of K+ into cells (maintains electrochemical balance)

41
Q

Why is insulin used as an emergency therapy for hyerkalaemia?

A

K+ in plasma stimulates insulin release under normal physiological conditions

This leads to increased K+ uptake by muscle and liver via an increase in Na+/K+ ATPase channels

Administration of insulin boosts this process and lowers ECF [K+]

42
Q

How is Aldosterone involved in K+ homeostasis?

A

K+ in serum stimulates aldosterone secretion

Which in turn stimulates uptake of K+ via Na+/K+ ATPase

43
Q

How are Catecholamines involved in K+ homeostasis?

A

Acts via B2 adrenoceptors which in turn stimulate Na+/K+ ATPase

This increases the cells uptake of K+

44
Q

What are the factors promoting K+ shift into ECF

A

Low ECF [K+]

Exercise

Cell lysis (K+ leaks through ruptured membrane)

Increase in ECF osmolarity

Acidosis (Increase in ECF [H+]:

Shift of H+ into cells and reciprocal K+ shift out (to preserve electrochemical gradient)

45
Q

How does exercise affect K+ homeostasis?

A

Skeletal muscle contraction leads to a net loss in K+ during recovery phase of action potential

Damage to muscle also releases K+

Increases are proportional to intensity of exercise

Uptake of K+ into non-contracting cells + Exercise stimulation of catecholamines prevents dangerous rise

Cessation of exercise leads to rapid fall in ECF [K+] (often <3mmol/l)

46
Q

How is cell lysis involved in K+ homeostasis?

Give examples where this effect is significant

A

K+ leaks through ruptured membranes

Rhabdomyolysis:

Trauma to skeletal muscle resulting in muscle cell necrosis

Intravascular haemolysis:

Breakdown of RBC in vascular system

E.g. Incompatible blood transfusion

Cancer chemotherapy

47
Q

How can a rise in plasma/ECF tonicity lead to K+ movement into the ECF?

A

Water moves out of cells into ECF to correct osmolarity

Increase in [K+] in ICF

Net movement of K+ into ECF via concentration gradient (despite action of Na+/K+ ATPase)

48
Q

How do [K+] balance disturbances affect ECF pH?

A

K+ movement in and out of a cell causes H+ to move in opposite direction

Significant K+ movement (Hypo/hyperkalaemia) can therefore lead to acidosis or alkalosis

49
Q

Describe renal handling of K+ under physiological conditions

A

K+ freely filtered at glomerulus

PCT:

Uptake via paracellular diffusion

67% of filtered load reabsorbed

Thick al of LoH:

Uptake is active (Driven by basolateral Na+/K+ ATPase and Na+/K+/2Cl- transporter in apical membrane

20% reabsorbed

Principal cells of DCT and Cortical CD:

Substantial secretion of K+ in a normal or high K+ diet

Little secretion in a low K+ diet

Intercalated cells of DCT and CD:

Reabsorb 10-12%

50
Q

Outline the mechanism of K+ secretion from principal cells in the DCT and Cortical CD

A

Na+/K+ activity on BLM

High intracellular K+ creates chemical gradient across luminal membrane

Luminal ENaC allows Na+ to move down chemical gradient, producing an electrical gradient

Favourable electrochemical gradient allows K+ secretion via K+ luminal channels

51
Q

What factors influence the K+ secretion from principal cells of the DCT and Cortical CD?

A

ECF [K+]:

Stimulates Na+/K+ ATPase

Increases permeability of apical K+ channels

Stimulates aldosterone secretion

Aldosterone:

Increases transcription of Na+/K+ ATPase, K+ channels and ENaC

Acid/Base:

Acidosis decreases K+ channel permeability, inhibits Na+/K+ ATPase (hence decreasing K+ secretion)

Alkalosis increases K+ secretion through stimulation of Na+/K+ ATPase and K+ channels

Luminal factors:

Distal tubular flow rate washes away luminal K+ hence increasing K+ secretion

Increased Na+ in DCT, more Na+ absorbed hence more K+ loss

52
Q

What is the mechanism of K+ absorption via Intercalated cells in the DCT and CD:

A

Active process

Uptake via H+/K+ ATPase

53
Q

Define hyperkalaemia

A

[K+] = >5.0mmol/l

54
Q

What problems with internal K+ balance might cause hyperkalaemia?

A

Problems with external balance

Increased intake:

Only causes problem when there’s renal impairment

Unless there has been an inappropriate dose given IV

Inadequate renal excretion

55
Q

What might be the causes for inadequate renal excretion of K+?

A

AKI

Chronic kidney injury

Reduced aldosterone (with normal kidneys):

Adrenal insufficiency

Aldosterone blockers (secretion or action)

K+ sparing diuretics

ACE Inhibitors

56
Q

What might be the cause of hpyerkalaemia due to problems with internal K+ balance?

A

Diabetic ketoacidosis:

No insulin reduces K+ intake into ICF

Plasma hypertonicity (Causes shift of K+ into ECF)

Metabolic acidosis causes reciprocal shift of K+ into ECF as H+ moves into ICF

Other causes of metabolic acidosis

Cell lysis

Exercise

57
Q

What is the effect hyperkalaemia on the resting membrane potential?

What is the direct concequence of this to cardiac tissue?

A

Raises the resting membrane potential (depolarisation)

Cardiac:

More Fast Na+ channels remain inactive and the heart is less excitable

58
Q

What are the clinical features of hyperkalaemia?

A

Heart:

Altered excitability - Arrhythmias, heart block

GI:

Neuromuscular dysfunction - Paralytic ileus

Acidosis

59
Q

Outline the ECG changes that occur as hyperkalaemia progressively worsens

A

Symptoms worsen as [K+] rises as demonstrated by incresing numbers below

  1. High T wave
  2. As above + Prolonged PR interval and depressed ST segment
  3. P wave absent and intraventricular block
  4. VFib
60
Q

What is the emergency treatment method for hyperkalaemia?

A

Reduce K+ effect on heart:

IV calcium gluconate

Shift K+ into ICF:

Glucose + IV insulin

Nebulised B agonists (salbutamol)

Remove excess K+:

Dialysis

61
Q

What are the long term treatment steps for Hyperkalaemia?

A

Treat cause

Reduce intake

Measures to remove excess K+:

Dialysis

Oral K+ binding resins to bind K+ in gut

62
Q

Define Hypokalaemia

A

[K+] = <3.5mmol/l

63
Q

What might cause hypokalaemia?

A

Problems of external balance:

Excess GI loss (bulimia/vomiting)

Excess renal loss (Diuretics, Osmotic diuresis - Diabetes, High Aldosterone)

Problems with internal balance:

Shift of K+ into ICF (Metabolic alkalosis)

64
Q

What is the effect of hypokalaemia on the resting membrane potential?

What is the direct concequence of this in cardiac muscle?

A

Hyperpolarisation

More fast Na+ channels active in cardiac muscle

Cardiac muscle is more excitable

65
Q

What are the clinical feature of hypokalaemia?

A

Heart:

Altered excitability - Arrhythmias

GI:

Neuromuscular dysfunction - Paralytic Ileus

Skeletal muscle:

Neuromuscular dysfunction - Muscle weakeness

Renal:

Dysfunction of CD cells - Unresponsive to ADH causing nephrogenic diabetes insipidus

66
Q

outline the ECG changes that occur with worsening hypokalaemia

A

Worsening degree of hypokalaemia indicated by numbers below:

  1. Low T wave
  2. As above + High U wave
  3. As above + Low ST segment
67
Q

Outline treatment of hypokalaemia

A

Treat cause

Potassium replacement (IV/Oral)

If due to increase mineralocorticoid activity:

Potassium sparing diuretics which block action of aldosterone on principal cells

ESA 3 (54 decks)

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