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Flashcards in deck_1460742 Deck (47):
1

How much K+ is found in the body?

3500 mmol

2

How is the K+ distributed through the body?

98% in the intracellular fluid 2% in the extracellular fluid

3

How are the concentrations of K+ in different body compartments maintained?

Na-K-ATPase pump

4

Why is K+ regulation important?

1. K+ determine the resting membrane potential and any changes have significant effects on the excitability of cardiac and neuromuscular tissues, which will effect their functions. 2. Intracellular K+ levels are important for cell functione.g. Cell volume and growth, DNA/protein synthesis, enzyme function

5

What are the mechanisms for controlling K+ levels?

External balance adapts excretion to match the K+ intake and regulates the total potassium contentInternal balance regulates the [K+] in the ECF.

6

Describe the external balance of K+ and its characteristics

Kidneys adjust excretion to match intakeIs slower to act -- 6-12 hoursIs responsible of K+ levels in the long term

7

Describe the internal balance of K+ and its characteristics

Has an immediate effectResponsible for moment to moment controlShifts the K+ from the ICF to the ECF

8

Describe the events of K+ following a meal

Intestine and colon absorb K+ directlySubstantial amount of K+ enters the ECF80% of ingested K+ moves into the cellsKidneys begin to excrete K+ after a slight delay Excretion is complete in 6-12 hours

9

What channels control the internal balance of K+?

1. Movement of K+ from ECF into cells by Na-K-ATPase2. Movement of K+ out of cells to the ECF by K+ channels (determine K+ permeability of the cell membrane)

10

What three factors promote the uptake of K+ into cells?

HormonesAlkalosisIncreased [K+] in the ECF

11

What are the three hormones that promote the uptake of K+ into cells?

InsulinAldosteroneCatecholamines

12

Describe the effect of insulin on [K+] in the blood

K+ in the blood stimulates insulin secretionInsulin promotes the uptake of K+ into muscle and liver cells via Na-K-ATPase

13

Describe the effect of aldosterone on [K+] in the blood

K+ in the blood stimulates aldosterone secretion which in turn stimulate the excretion of K+ by Na-K-ATPase by increasing transcription of Na-K-ATPase

14

What factors promote the shift of K+ out of the cells and into the ECF?

1. Low ECF [K+]2. Exercise3. Cell lysis4. Increase in ECF osmolality/tonicity5. Acidosis and alkalosis

15

What affect does exercise have on the [K+]?

During skeletal muscle contraction, there is a net release of K+ in the recover period of APPlasma [K+] increases proportionally with the amount of exercise doneNon-contracting tissues take up excess K+ (prevents hyperkalaemia)Increase secretion of catecholamines increase K+ uptake in other cells

16

What can causes cell lysis?

Trauma to skeletal muscle, causing muscle cell necrosis (Rhabdomyolysis)Intravascular haemolysisCancer chemotherapy

17

How does plasma tonicity cause K+ to move out of cells?

Water moves into cells from ECFCauses an increase in [K+] in the ICFK+ leaves down its concentration gradient

18

What effects does acidosis have on the [K+]?

Causes H+ to move into cells which cause K+ to move out of the cell causing hyperkalaemia

19

What effects does alkalosis have on the [K+]?

Causes H+ to move out of cells, which causes K+ to move into the cells causing hypokalaemia

20

Where is K+ reabsorbed in the kidney?

PCTThick ascending limbIntercalated cells of DCTIntercalated cells of cortical collecting ductIntercalated cells of medullary collecting duct

21

Where is K+ secreted from in the kidney?How much K+ is secreted?

Principal cells of the DCT and the cortical collecting duct20%

22

How much reabsorption occurs at the different parts of the kidney?

Most at PCT -- 67%TAL -- 20%Others -- 10-12%

23

What can a very low K+ lead to?

Inability of kidney to form concentrated urineIncreased tendency to develop metabolic alkalosisEnhancement of renal ammonium excretion

24

What and an increase [K+] in the ECF do to the cell membrane?

Depolarises the cell membrane

25

What does a decreased [K+] in the ECF do to the cell membrane?

Hyperpolarises the cell membrane

26

Describe the characteristics of K+ secretion from principal cells

Is a passive process (driven by electrochemical gradient of K+ between principal cell and lumen)Na+ is reabsorbed through ENaC which drives K+ out of the cell through a separate K+ channelIs driven by Na-K-ATPase in the basolateral lumen

27

What factors affect K+ secretion?

Aldosterone levelsECF [K+]Acid base status of the bloodIncrease distal tubular flow rate causes an increase K+ lossIncrease Na delivery to distal tubule causes more K+ loss

28

Describe the absorption of K+ in the distal tubules and the collecting duct

K+ is absorbed by intercalated cellsIs an active processMediate by H+ K+ ATPase in the apical membrane

29

What is the result of poor perfusion of a kidney due to renal artery stenosis on K+ levels?

Causes hypokalaemia-- the poor perfusion activate the RAAS which increases the amount of aldosterone which will increase the amount of K+ excretion

30

Why can Cushing's Syndrome cause hypokalaemia?

Increased levels of glucocorticoids in the blood can bind to mineralocorticoid receptors and mimic their physiological actions

31

What can be given to patient in order to reduce plasma K+ levels?

Insulin promotes the uptake go K+ into cells

32

What is the main effect of changes to the [K+]?

Alters the cell membrane resting potentialAffects neuromuscular excitability- problems with cardiac conduction and pacemaker automaticity- affects neuronal function- alter skeletal and smooth muscle function

33

What are the main clinical effects of altered [K+]?

ArrhythmiasCardiac ArrestMuscle paralysis

34

What are some causes of Hyperkalaemia?

Increased intake of K+-- renal dysfunction or inappropriate K+ IV dosesInadequate renal excretionInternal shifts in [K+]

35

What are some things that could causes inadequate urinary excretion of K+?

Acute renal injuryChronic renal injuryReduced aldosterone

36

What are some things that could cause the internal [K+] to change?

DIabetic ketoacidosisMetabolic acidosisCell lysis

37

What are the main effects of hyperkalaemia?

Heart issues -- arrhytmias and heart blockGastro intestinal (paralytic ileus due to neuromuscular dysfunction)Acidosis

38

What effect does hyperkalaemia have on cardiac tissue?

It increases the resting membrane potential, therefore depolarising the cell-- Fast Na channels remain in the active forms the heart is less excitable

39

What are the ECG changes that you see in hyperkalaemia?

1. Tall T waves2. Prolonged PR interval Depresses ST segmentTall T waves3. Widening of QRS complex4. Ventricular fibrillation(get more of these as the serum K+ levels increase)

40

What is the emergency treatment for hyperkalaemia?

Reduce the effect the K+ is having on the heart-- IV calcium gluconateShift K+ into the intracellular fluid -- Glucose and insulin IV-- Nebulised beta agonists (salbutamol)Remove excess K+-- Dialysis

41

What are the longer term treatment for hyperkalaemia?

Treat causesReduce intakeTake measures to remove excess K+

42

What is the measure that defines hypokalaemia?

[K+]

43

What are some causes of hypokalaemia?

Excessive loss of K+-- diarrhoea, vomiting-- diuretic drugs, osmotic diuresis in diabetes, high aldosterone levelsShifts of K+ into the ICF-- metabolic alkalosis

44

What affect does hypokalaemia have on the resting cell membrane potential?

Cell membrane is more hyper polarised so there are more fast Na channels in an active form and the heart is more excitable

45

What are the clinical features of hypokalaemia?

ArrhythmiasParalytic ileusMuscle weaknessCD cells are unresponsive to ADH --> nephrogenic diabetes insipidus

46

What are the ECG changes that you will see in someone with hypokalaemia?

Low T waveHigh U waveLow ST segment

47

What is the treatment for hypokalaemia?

Treat the causePotassium replacement with IV or orallyPotassum sparing diuretic if it is due to an increased mineralocorticoid activity (blocks aldosterone action on principal cells)