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Urinary > Session 5 > Flashcards

Session 5 Flashcards

1
Q

What is the effect on low extracellular potassium on the membrane potential

A

More negative

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2
Q

How is extracellular potassium regulated short and long term?

A

Short term - internal balance between ICF and ECF

Long term - external balance (renal excretion - regulated K+ SECRETION in late DT and early CD)

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3
Q

What happens to potassium after a meal?

A

4/5ths moves into cells within minutes. After slight delay kidneys excrete the excess potassium.

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4
Q

What factors increase potassium uptake into cells? (Na/K ATPase)

A

Hormones (insulin, aldosterone, catecholamines)
Increased concentration of potassium in ECF
Alkolosis

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5
Q

What factors increase potassium shift out of cells? (K+ channel)

A 
Exercise
Cell lysis
Increase in ECF osmolality
Low concentration of potassium in ECF
Acidosis
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6
Q

What prevents hyperkalaemia during exercise?

A

There is potassium uptake by non contracting tissues and exercise produces catecholamines, which stimulate Na/K ATPase

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7
Q

How do acid-base disturbances affect the ECF concentration of potassium?

A

They act as if there is a reciprocal shift between K+ and H+

E.g. Acidosis -> hyperkalaemia and hypokalaemia -> alkalosis

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8
Q

What are the tubular factors that affect K+ secretion in principle cells of DT & CCD?

A

ECF [K+] - stimulates Na/K ATPase, increases permeability of apical K channels and stimulates aldosterone
Aldosterone - increases transcription of channels involved in K+ secretion
Acid base status - acidosis inhibits K+ secretion

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9
Q

What are the luminal factors that affect K+ secretion in principle cells of DT & CCD?

A

Increased DT flow rate washes away luminal K+, increasing loss

Increased Na delivery to DT increases Na reabsorption, increasing K+ loss

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10
Q

How is potassium absorbed by intercalated cells in the DT/CD?

A

Via H+/K+ ATPase (secreted acid)

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11
Q

What are the causes of hyperkalaemia? [k+]>5mmol/L

A 
Increased uptake (rare - only real Lin if inappropriate IV K+ dose given)
Decreased renal excretion- acute/chronic kidney injury, drugs blocking K+ secretion (ACEi, K+ sparing diuretics), low aldosterone state(addisons)
Internal shifts - diabetic ketoacidosis (no insulin & acidosis & plasma hyperosmolarity), cell lysis, metabolic acidosis, exercise
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12
Q

What are the clinical features of hyperkalaemia?

A

Arrhythmias/heart block - heart less excitable because more fast Na channels remain inactive
Paralytic ileum - GI muscular dysfunction
Acidosis

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13
Q

Describe the ECG changes seen in hyperkalaemia

A

Normal -> High T wave -> High T wave, prolonged PR, depressed ST -> Atrial standstill, IV block -> ventricular fibrillation

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14
Q

What is the emergency treatment for hyperkalaemia?

A

Reduce the K+ effect on the heart - IV calcium gluconate
Shift k+ into cells by giving glucose plus insulin or nebulised B agonists (salbutamol)
Remove excess K+ - dialysis

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15
Q

What is the longer term treatment for hyperkalaemia?

A

Treat cause - stop medication, treat DKA etc
Reduce intake
Remove excess K+ - dialysis, oral binding resins

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16
Q

What are the causes of hypokalaemia? [k+]<3.5mmol/L

A

External balance - excessive loss by vomiting, diarrhoea, high aldosterone
Internal balance - shift into cells e.g. Metabolic alkalosis

17
Q

What are the clinical features of hypokalaemia?

A

Cardiac arrhythmias - hyperpolarised RMP means more fast Na channels so heart more excitable
Paralytic ileum -> GI muscular dysfunction
Skeltetal muscle weakness
Kindness unresponsive to ADH

18
Q

Describe the ECG changes seen in hypokalaemia

A

Normal -> low T wave -> low T wave, high U wave -> low T wave, high U wave, depressed ST segment

19
Q

What is the treatment for hypokalaemia?

A

Treat cause
IV/oral K+ replacement
K+ soaring diuretics that block aldosterone if that is the cause

20
Q

Describe the effects of alkalaemia

A

Lowers free calcium by causing them to come out of solution. This increases neuronal excitability and can lead to paraesthesia and tetany. 80% mortality at pH >7.65

21
Q

Describe the effects of acidaemia

A

Increases plasma K+ and denatures proteins<7.0

22
Q

Describe the process leading up to respiratory acidaemia

A

Hypoventilation -> hypercapnia -> acidaemia

Opposite for respiratory alkaemia

23
Q

Where is pCO2 detected and controlled?

A

Central chemoreceptors which change ventilation rate accordingly. Peripheral chemoreceptors are quicker but produce a smaller overall effect.

24
Q

Where is [HCO3-] detected and controlled?

A

Peripheral chemoreceptors

25
Q

What can cause metabolic alkalosis and what is the main problem?

A

Repeated vomiting - can only be partially compensated by decreasing ventilation due to hypoxia

26
Q

What is the role of the kidneys in maintaining pH?

A

They compensate for respiratory changes on pCO2 and also correct metabolic pH disturbances by varying excretion of HCO3-, or by making more.

27
Q

How do the kidneys increase plasma pH?

A

They recover all filtered HCO3-, make new HCO3- and secrete acid.

28
Q

Describe how the kidneys make new HCO3-

A 
From CO2 (from metabolism) plus H2O in DCT. HCO3 enters the blood stream and H+ leaves in the urine via H+ ATPase.
From glutamine in the PCT, producing NH4+, which enters urine.
29
Q

Describe how the kidneys recover HCO3- in the PCT

A

H+ enters lumen via NHE and reacts with HCO3-. CO2 enters cell and reacts with water. HCO3- leaves across basolateral membrane via Na-3HCO3- cotransporter.
Carbonic anhydrase is present inside the cell and on apical membrane

30
Q

What factors does a decreased pH enhance in the kidney?

A

Activity of NHE in PCT (increasing HCO3 recovery)
Ammonium production in PCT (increasing synthesis of HCO3)
Activity of H+ ATPase in DCT (increasing synthesis of HCO3)
Capacity to export HCO3 into ECF

31
Q

What is the anion gap and when does it increase?

A

The difference between [Na+] + [K+] and [Cl-] + [HCO3-].

The gap increases if HCO3- is replaced by an anion other than Cl- (e.g. Lactate/ketone) in metabolic acidosis.

32
Q

Give an example of when metabolic acidosis does not produce an anion gap

A

Renal problems can cause decreased [HCO3-] and replace it with Cl-, hence no anion gap.

Urinary (12 decks)

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