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3B week 2 - RAAS, electrolytes and acid-bases > calcium and potassium homeostasis > Flashcards

calcium and potassium homeostasis Flashcards

1
Q

where is the majority of calcium found in the body

A

in the bone

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2
Q

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

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

how does pH affect free Ca2+ levels

A

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

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4
Q

what form of calcium is not excreted by the kidneys

A

protein bound

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5
Q

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

A

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

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6
Q

where is calcium from food absorbed in the body

A

duodenum and jejunum

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7
Q

3 key regulators of calcium in the body

A
  1. PTH
  2. vit D
  3. calcitonin
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8
Q

5 key functions of calcium

A
  1. muscle contraction
  2. nerve impulse transmission
  3. wound healing
  4. cellular metabolism
  5. bone structure
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9
Q

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

A

calcitonin - increases
PTH- decreases

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10
Q

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

A
  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

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11
Q

why does hypocalcaemia occur in hyperventilation

A

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

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12
Q

2 signs of hypocalcaemia

A
  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
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13
Q

hypercalcaemia presentation

A

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

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14
Q

why are inhibitory symptoms seen in hypercalcaemia

A

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

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15
Q

what does hypercalcaemia + high PTH indicate

A

overactive PTH gland

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16
Q

hypercalcaemia mgx (7)

A
  1. fluids
  2. loop diuretics (Loop Looses calcium)
  3. bisphosphonates
  4. glucocorticoids (decrease gut absoroption of Ca2+)
  5. Cinacalcet
  6. calcitonin
  7. surgery (PTHectomy)
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17
Q

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

A

induces apoptosis

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18
Q

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

A
  1. Ca2+ pump
  2. Ca2+/Na+ exchanger
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19
Q

what is pesudohypercalcaemia

A

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

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20
Q

hypercalcaemia ECG

A
  1. tachycardia
  2. heart block
  3. short QT
  4. osborne waves
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21
Q

why might kidney failure result in hypocalcaemia

A

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

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22
Q

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

A

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

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23
Q

why does acute pancreatitis cause hypocalcaemia

A

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

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24
Q

why might blood transfusions lead to hypocalcaemia

A

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

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25
Q

hypocalcaemia presentaiton (5)

A

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

26
Q

what is the active form of vit D

A

calcitriol

27
Q

effect of vit D on intestines, bone, kidney

A

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

28
Q

3 regulators of K+ in the body

A
  1. insulin
  2. pH
  3. catecholamines
29
Q

where is the majority of intracellular K+ found

A

in muscle

30
Q

hyperkalemia mgx (7)

A

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)

31
Q

functions of potassium

A
  1. nerve conduction/AP generation
  2. water balance
  3. acid base balance
  4. muscle contractions
  5. regulates heart beat
  6. energy metabolism
32
Q

what is the internal potassium balance

A

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

33
Q

what channels maintain the intracellular K+ gradient

A
  1. Na+/K+ATPase
  2. inward K+ leak channels
34
Q

how is ingested K+ lost

A
  1. excreted in urine (majority)
  2. intestines (egestion)
  3. sweat
35
Q

why is hyperkalemia seen in T1DM

A

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

36
Q

why does (some) acidosis lead to hyperkalemia

A

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

and vice versa for alkalosis causing hypokalemia

37
Q

why do beta blockers cause hyperkalemia

A

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

38
Q

why do alpha agonists cause hyperkalemia

A

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

39
Q

how does hyperosmolarity result in hyperkalemia

A

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

40
Q

how does cell lysis result in hyperkalemia

A

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

41
Q

why can exercise result in hyperkalemia

A

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

42
Q

what can cause internal potassium balance shifts

A
  1. T1DM
  2. acidosis
  3. BBs
  4. alpha agonists
  5. hyperosmolarity
  6. cell lysis
  7. exercise
43
Q

where in the nephron is K+ reabsorbed

A
  1. PCT - 67%
  2. thick ascending limb - 20%
  3. distal tubule/collecting ducts (13%) - secretion and resorption can occur
44
Q

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

A

reabsorption - alpha-intercalated cells
secretion - principal cells

45
Q

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

A

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

46
Q

why does hypoaldosteronism result in hyperkalemia

A

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

vice versa for hyperaldosteronism

47
Q

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

A

block the action of aldosterone

48
Q

how does AKI lead to hyperkalemia

A
  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
49
Q

hyperkalemia ECG (4)

A
  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)
50
Q

hyperkalemia presentation (5)

A
  1. progressive ascending muscle weakness
  2. bradycardia
  3. heart block
  4. arrythmias
  5. cardiac arrest
51
Q

why does hyperkalemia cause muscle abnormalities

A

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

52
Q

why does AKI/CKD lead to hypocalcaemia

A

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

53
Q

how does hypercalcaemia lead to renal failure

A

may result in nephrocalcinosis -> reduced GFR

54
Q

hypokalemia presentation (9)

A
  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)
55
Q

hypokalemia ECG changes

A
  1. flattened T wave
  2. U wave (looks like double T wave)
  3. ST depression
56
Q

causes for hypokalemia

A
  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
57
Q

why does excess insulin cause hypokalaemia

A

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

58
Q

2 conditions that can cause hyperaldosteronism

A
  1. congenital heart failure
  2. cirrhosis

=> results in hypokalemia

59
Q

hypokalemia causes - external balance shift

A
  1. diahorrea
  2. vomiting -> results in metabolic alkalosis -> hypokalemia
  3. sweat
60
Q

hypokalemia mgx

A
  1. treat underlying causes
  2. replenish K+ stores -> oral if 3-3.5, if <3 then IV KCl (in fluid)
61
Q
A

3B week 2 - RAAS, electrolytes and acid-bases (5 decks)

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