calcium and potassium homeostasis

Question 1

where is the majority of calcium found in the body

Answer 1

in the bone

Question 2

how does calcium exist in the serum (what forms - 3)

Answer 2

1. 40% protein bound
2. 10% anion complex
3. 50% ionised

Question 3

how does pH affect free Ca2+ levels

Answer 3

H+ binds to albumin, displacing Ca2+ from it => acidic pH leads to increased Ca2+ levels in the serum (hypercalcaemia)

Question 4

what form of calcium is not excreted by the kidneys

Answer 4

protein bound

Question 5

what must total serum calcium be corrected for and what is the equation for this

Answer 5

corrected for serum albumin conc
corrected calcium = Ca measured (mmol/L) + 0.02(40-albumin)

Question 6

where is calcium from food absorbed in the body

Answer 6

duodenum and jejunum

Question 7

3 key regulators of calcium in the body

Answer 7

1. PTH
2. vit D
3. calcitonin

Question 8

5 key functions of calcium

Answer 8

1. muscle contraction
2. nerve impulse transmission
3. wound healing
4. cellular metabolism
5. bone structure

Question 9

what happens to PTH and calcitonin levels as [Ca2+] increases

Answer 9

calcitonin - increases
PTH- decreases

Question 10

what is the action of PTH at the intestines, kidneys and bones

Answer 10

1. intestines - increases Ca2+ absorption, driven by vit D
2. kidneys - increases Ca2+ reabsoprtion in the distal tubule
3. bones - increases osteoclast activity => increased bone reabsorption and increased Ca2+ release

i.e. increase in serum Ca2+ levels, calcitonin does the opposite

Question 11

why does hypocalcaemia occur in hyperventilation

Answer 11

leads to respiratory alkalosis -> ionised Ca2+ binds to albumin in alkaline conditions

Question 12

2 signs of hypocalcaemia

Answer 12

1. chvostek’s sign - ipsilateral twitching of the facial muscles occurs when repeatedly tapping the cheek
2. trousseau’s sign - sign of latent tentany, when a BP cuff is inflated above their systolic BP a spasam (flexion at wrist, fingers and thumb) is induced

Question 13

hypercalcaemia presentation

Answer 13

inhibitory effects
1. neuro - decreased reflexes, lethargy, coma, seizures
2. cardio - depressed activity, dysarrythmia, cardiac arret
3. GI - decreased GI motility, N/V, constipation
4. genitourinary - kidney stones, flank pain
5. MSK - muscle fatigue, hypotonia, bone pain, osteoporosis, fractures

moans, bones, groans, thrones, stones

Question 14

why are inhibitory symptoms seen in hypercalcaemia

Answer 14

Ca2+ increase inhibits Na+/K+ATPase => depol/repol of cells in effected -> inhibitory effectsw

Question 15

what does hypercalcaemia + high PTH indicate

Answer 15

overactive PTH gland

Question 16

hypercalcaemia mgx (7)

Answer 16

1. fluids
2. loop diuretics (Loop Looses calcium)
3. bisphosphonates
4. glucocorticoids (decrease gut absoroption of Ca2+)
5. Cinacalcet
6. calcitonin
7. surgery (PTHectomy)

Question 17

what happens to a cell if intracellular Ca2+ levels are high

Answer 17

induces apoptosis

Question 18

what are the main 2 channels responsible for the removal of Ca2+ from inside cells

Answer 18

1. Ca2+ pump
2. Ca2+/Na+ exchanger

Question 19

what is pesudohypercalcaemia

Answer 19

when there is hyperalbuminaemia leading to high levels of bound Ca -> bloods may show elevated Ca levels but this needs to be corrected for albumin

seen in dehydration

Question 20

hypercalcaemia ECG

Answer 20

1. tachycardia
2. heart block
3. short QT
4. osborne waves

Question 21

why might kidney failure result in hypocalcaemia

Answer 21

the nephron doesn’t effectively reabsorb calcium, which allows it to get excreted into the urine

Question 22

why does tissue injury (e.g. rhabdo, tumor lysis, burns) lead to hypocalcaemia

Answer 22

large numbers of cells die releasing intracellular phosphate into the blood. The phosphate binds to the ionized calcium and forms calcium phosphate, making it insoluble and effectively decreasing the total amount in blood

Question 23

why does acute pancreatitis cause hypocalcaemia

Answer 23

free fatty acids end up binding to ionized calcium, which is also insoluble and precipitates out as a soap-like substance

Question 24

why might blood transfusions lead to hypocalcaemia

Answer 24

additives in the blood like citrate and EDTA can chelate or bind to calcium, forming complexed calcium, which is an inactive molecule

Question 25

hypocalcaemia presentaiton (5)

Answer 25

excitatory symptoms 1. neuro - tingling, convulsions, hyperreflexia 2. pulmonary - larynogospasm, bronchospasm 3. cardio - dysarrythmias, cardiac arrest, bruising, bleeding 4. GI - increased peristalsis, N&V, diahorrea 5. MSK - osteoporosis-> fractures, abnormal deposits of calcium in body tissues, muscle spasam, tetany

Question 26

what is the active form of vit D

Answer 26

calcitriol

Question 27

effect of vit D on intestines, bone, kidney

Answer 27

intestine - increased CaHPO4 absorption bone - (w PTH) CaHPO4 release kidney - decreased Ca2+ and phosphate excretion

Question 28

3 regulators of K+ in the body

Answer 28

1. insulin 2. pH 3. catecholamines

Question 29

where is the majority of intracellular K+ found

Answer 29

in muscle

Question 30

hyperkalemia mgx (7)

Answer 30

first priority is to save cardiac muscle 1. calcium gluconate -> stabilises myocardial membrane 2. salbutomol 3. insulin (+ dextrose to control glucose level) 4. glucose 5. sodium bicarbonate 6. potassium wasting diuretics 7. dialysis (extreme)

Question 31

functions of potassium

Answer 31

1. nerve conduction/AP generation 2. water balance 3. acid base balance 4. muscle contractions 5. regulates heart beat 6. energy metabolism

Question 32

what is the internal potassium balance

Answer 32

the overall electrochemical gradient across the cell membrane due to the much higher levels of K+ inside the cells than out -> Acid-base disturbances cause potassium to shift into and out of cells

Question 33

what channels maintain the intracellular K+ gradient

Answer 33

1. Na+/K+ATPase 2. inward K+ leak channels

Question 34

how is ingested K+ lost

Answer 34

1. excreted in urine (majority) 2. intestines (egestion) 3. sweat

Question 35

why is hyperkalemia seen in T1DM

Answer 35

Insulin also increases the activity of the sodium/potassium pump, which pulls potassium into cells -> lack of insulin productino in T1DM leads to K+ sitting intot he interstitium as it is not being pulled into the cells by the action of insulin

Question 36

why does (some) acidosis lead to hyperkalemia

Answer 36

in order to compensate for acidosis K+ leaves the cell (goes into serum) and H+ enters instead and vice versa for alkalosis causing hypokalemia

Question 37

why do beta blockers cause hyperkalemia

Answer 37

When activated, beta-2-adrenergic receptors stimulate the sodium-potassium pump, which pulls potassium from the blood into cells -> blocking this results in K+ build up vice versa for hypokalaemia

Question 38

why do alpha agonists cause hyperkalemia

Answer 38

alpha-adrenergic receptors cause a shift of potassium out of cells via calcium-dependent potassium channels -> agonism of this channel leads to increased K+ out of the cell

Question 39

how does hyperosmolarity result in hyperkalemia

Answer 39

increases osmotic gradient pulls water out of cells and into the extracellular space -> Less water in the cells increases the intracellular potassium concentration, which increases potassium’s concentration gradient, and pushes more of it out of the cell and into the interstitium and blood

Question 40

how does cell lysis result in hyperkalemia

Answer 40

so much K+ kept in the blood -> when cells die/lyse this is released into the interstitium

Question 41

why can exercise result in hyperkalemia

Answer 41

depletion of ATP triggers potassium channels on the membrane of muscle cells to open up, which allows potassium to moves down its electrochemical gradient and out of the cell -> usually only noticable if taking BBs or kidney issues

Question 42

what can cause internal potassium balance shifts

Answer 42

1. T1DM 2. acidosis 3. BBs 4. alpha agonists 5. hyperosmolarity 6. cell lysis 7. exercise

Question 43

where in the nephron is K+ reabsorbed

Answer 43

1. PCT - 67% 2. thick ascending limb - 20% 3. distal tubule/collecting ducts (13%) - secretion and resorption can occur

Question 44

what cells control reabsorption and secretion of K+ in the distal tubule

Answer 44

reabsorption - alpha-intercalated cells secretion - principal cells

Question 45

what hormone helps to regulate K+ resorption/secretion in the distal tubule and how (4)

Answer 45

aldosterone 1. increases the number of Na+ channels and the number of K+ channels on the lumen side of the principal cell as well as Na+/K+ pumps on the basolateral side of the principal cells 2. allows sodium to move from the tubule into the cell, and then to get pumped into the blood by the Na+/K+ pumps 3. more potassium gets pumped into the cell (via Na+/K+ pumps), which raises the intracellular potassium concentration 4. intracellular potassium and also having more potassium channels promotes potassium secretion

Question 46

why does hypoaldosteronism result in hyperkalemia

Answer 46

there’s less potassium secretion by the principal cells, and therefore more potassium is retained, leading to hyperkalemia vice versa for hyperaldosteronism

Question 47

why can ACEi/ARBs/ K+ sparing diuretics result in hyperkalemia

Answer 47

block the action of aldosterone

Question 48

how does AKI lead to hyperkalemia

Answer 48

1. the nephron tries to hold on to salt and water, so by the time filtrate has moved into the distal tubule, there’s very little of both sodium and water 2. little water in the lumen, creates a relatively high potassium concentration in the lumen 3. because less sodium is in the distal tubule, less of it moves through the luminal sodium channel into the principal cell and gets pumped over to the other side by the basolateral sodium-potassium pump => less K+ into the principal cell so builds up in the blood

Question 49

hyperkalemia ECG (4)

Answer 49

1. tall peaked T waves with a narrow base in V1-6 2. short QT 3. depressed ST (4. severe -> PR interval, a diminished or absent P wave, and a widened QRS complex)

Question 50

hyperkalemia presentation (5)

Answer 50

1. progressive ascending muscle weakness 2. bradycardia 3. heart block 4. arrythmias 5. cardiac arrest

Question 51

why does hyperkalemia cause muscle abnormalities

Answer 51

the resting potential of the membrane becomes higher than the threshold potential => once the muscle depolarizes and contracts, it can’t repolarise to allow another contraction

Question 52

why does AKI/CKD lead to hypocalcaemia

Answer 52

damaged kidneys -> cant produce 1,25OH vit D -> vit D deficency driven

Question 53

how does hypercalcaemia lead to renal failure

Answer 53

may result in nephrocalcinosis -> reduced GFR

Question 54

hypokalemia presentation (9)

Answer 54

1. flaccid paralysis/ muscle weakness (hyperpolarisation of membrane potential as more K+ inside, APs not fired) 2. fatigue 3. cramps 4. constipation 5. polyuria 6. polydipsea 7. arrhythmias 8. hypertension 9. metabolic alkalosis (increased acid excretion)

Question 55

hypokalemia ECG changes

Answer 55

1. flattened T wave 2. U wave (looks like double T wave) 3. ST depression

Question 56

causes for hypokalemia

Answer 56

1. decreased K+ intake/reduced absorption 2. increased entry into cells - elevated beta-adrenergic activity or increased availability of insulin will act to drive potassium into cells 3. increased gastrointestinal loss -prolonged diarrhoea can cause significant hypokalaemia 4. increased urinary loss e.g. due to diuretics, renal tubular acidosis

Question 57

why does excess insulin cause hypokalaemia

Answer 57

Insulin increases the activity of the sodium/potassium pump, which pulls potassium into cells -> watch for insulin overdose in T1DM

Question 58

2 conditions that can cause hyperaldosteronism

Answer 58

1. congenital heart failure 2. cirrhosis => results in hypokalemia

Question 59

hypokalemia causes - external balance shift

Answer 59

1. diahorrea 2. vomiting -> results in metabolic alkalosis -> hypokalemia 3. sweat

Question 60

hypokalemia mgx

Answer 60

1. treat underlying causes 2. replenish K+ stores -> oral if 3-3.5, if <3 then IV KCl (in fluid)