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AANIYA PATH > Aani CP: Sodium/Potassium/Calcium > Flashcards

Aani CP: Sodium/Potassium/Calcium Flashcards

1
Q

What is the normal range of serum sodium?

A

135-145 mmol/l

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2
Q

What is the osmolar gap?

A

Difference between osmolality and osmolarity

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3
Q

Why is an osmolar gap caused? Why is it useful?

A

Increased solutes in the plasma.

Helps differentiate the cause of HAGMA (high anion gap metabolic acidosis)

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4
Q

How to calculate osmolality ?

A

Anions (Na + K+ ) + Cations (Cl- + HCO3-) + Urea + Glucose

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5
Q

What should serum osmolality be normally?

A

285

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6
Q

How to calculate osmolarity?

A

2 (Na+K) + Urea + Glucose

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7
Q

What is the normal range for osmolar gap?

A

Normal <10

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8
Q

Symptoms of hyponatraemia? (4) with Na values!

A

Nausea/vom <135
Confusion <131
Seizures <125
Coma/death <117

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9
Q

What happens when you correct sodium levels too quickly?

A

Central pontine demyelinosis i.e. osmotic demyelination quadriplegia/seizures/death

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10
Q

Where is ADH made? Where is it secreted?

A

Made in: Hypothalamus

Secreted from: Posterior pituitary

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11
Q

What does ADH do?

A

Acts on V2 receptor at Renal collecting ducts. Inserts aquaporin 2 channels into renal collecting ducts to retain water

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12
Q

What is the underlying cause of hyponatraemia?

A

Increased extracellular fluid (caused by increased ADH)

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13
Q

Which 2 situations cause appropriate release of ADH?

A
  1. Increased osmolality (i.e. increased Na conc.) Mediated by osmoreceptors. You want to retain water to correct this.
  2. Low blood pressure – detected by baroreceptors in carotids/atria.
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14
Q

What is the effect of ADH on serum sodium?

A

Lowers it –> Hyponatraemia

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15
Q

Signs of hypovoleamia?

A 
Reduced skin turgor
Dry mucous membranes
Tachycardia
Low blood pressure
Low urine output
KEY: LOW URINE SODIUM (<20) because kidneys want to hold on to water and so they don’t excrete Na and water follows – reliable!
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16
Q

Signs of hypervolaemia?

A

Peripheral oedema
Raised JVP
Bibasal crepitations

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17
Q

Causes of hyponatraemia in hypovolaemic pts?

A

Diarrhoea
Diuretics
Vomitting
Salt-losing nephropathy

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18
Q

Causes of hyponatraemia in hypervolaemic pts?

A

Cardiac failure
Liver failure
Nephrotic syndrome

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19
Q

What is the role of albumin?

A

Move water back into vessels
Maintains oncotic pressure for distribution of body fluids. Albumin prevents fluid from being forced into interstitial space from vessels. Low ambumin causes extravascular fluid oedema.

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20
Q

What are the causes of euvolaemic hyponatraemia?

A
  1. Hypothyroidism (Low C.O Low BP Baroreceptors detect it = More ADH)
  2. Adrenal insufficiency = low cortisol (cortisol needed to maintain BP) low BP increased ADH
  3. SIADH
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21
Q

Causes of SIADH?

A
  1. Tumours/pathology of the brain/lung
  2. Drugs e.g. SSRIs, PPIs, TCAs, opiates
  3. Surgery (due to pain more ADH)
  4. Ectopic secretion from other tumours e.g. pancreas/prostate
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22
Q

What will the plasma osmolality be in SIADH?

A

Low because lots of water retention so hyponatraemic (osmolality is basically sodium conc)

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23
Q

What will the urine osmolality be in SIADH?

A

High because water is being reabsorbed so only little water with lots of sodium is excreted. Urine sodium will be >100.

In SIADH, Urine osmolality is high, Plasma osmolality is low

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24
Q

Which tests will you order in a Pt with euvolaemic hyponatraemia?

A
  • TFTs cos hypothyroidism can cause hyponatraemia.
  • Short SynthACTHen test to check for adrenal insufficiency (low cortisol causes hyponatraemia)
  • Plasma and urine osmolality to check for SIADH (to confirm – plasma osmolality low, urine osmolality high)
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25
Q

How would you manage hypovolaemic hyponatraemia?

A

Stop cause e.g. diuretics
Give fluid replacement with 0.9% (normal) saline.
N.B. Never give saline to pts with SIADH - it will make it worse

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26
Q

How would you manage hypervolaemic/euvolaemic hyponatraemia?

A

Fluid restriction and treat underlying cause

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27
Q

Management of severe hyponatraemia? Give details

A

Correct sodium levels with hypertonic saline (3%)

Do not correct more than 10 mmol/l for 24 hours

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28
Q

If fluid restriction is not working for SIADH which drugs can you give?

A

Domeclocycline (reduced collecting duct responsiveness to ADH)- but risk of nephrotoxicity
Tolvaptan (V2 receptor antagonist)

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29
Q

What is more common hypo or hypernatraemia?

A

What is more common hypo or hypernatraemia?

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30
Q

Symptoms of hypernatraemia?

A
  • Lethargy
  • Thirst
  • Irritability
  • Fits
  • Coma
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31
Q

What is the underlying cause of hypernatraemia?

A

Water loss

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32
Q

Causes of hypernatraemia?

A
  • Water loss via GI tract (if this is corrected by drinking water it can cause hyponatraemia)
  • Inadequate ADH release (cranial) or action (nephrogenic) i.e. Diabetes insipidus
  • Poor water intake e.g. child/elderly
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33
Q

Causes for cranial DI?

A

Trauma
Surgery
Tumour

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34
Q

Cause for nephrogenic DI?

A
  • Renal failure/CKD
  • Lithium
  • Inherited resistance
  • High Ca or Low K can cause resistance to ADH nephrogenic DI.
    Treat by giving K or reducing Ca
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35
Q

What would the plasma and urine osmolality be in hypernatraemia?

A

Plasma: high (less water in plasma)
Urine: low (water lost so low sodium either via ADH resistance or by body trying to retain water via retaining sodium)

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36
Q

Diagnosing Diabetes Insipidus?

A

Water deprivation test:
Normal person’s urine would concentrate to reduce water loss
Craniogenic: would concentrate after ADH given
Nephrogenic: would not concentrate

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37
Q

How do you correct hypernatraemia?

A

Rehydration with dextrose

Hypernatraemia is water LOSS so do NOT give normal saline. Give water i.e. 5% dextrose.

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38
Q

If hypernatraemic pt is also volume depleted e.g. low BP, what do you do?

A

Correct fluid depletion with normal saline. Give 0.9% saline.
Check Serum Na every 4-6 hours.

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39
Q

What test do you do for suspected DI?

A

K and Ca to see if it’s caused by Low K and high Ca
Look at drugs (lithium?)
Glucose to exclude DM
Plasma and urine osmolality (plasma would be high, urine would be low)
Water deprivation test

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40
Q

When can D&V cause hyponatraemia vs hypernatraemia?

A

Hypernatraemia if you don’t drink e.g. child/elderly or DI

Hyponatraemia if you correct with drinking

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41
Q

What is the normal range of K+ in the blood?

A

3.5-5.5mmol/l

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42
Q

Is K+ predominantly intracellular or extra?

A

Intracellular

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43
Q

Where is Renin secreted from?

A

Juxtaglomerullar Apparatus

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44
Q

What does Renin do?

A

Stimulates angiotensin release by converting Angiotensinogen to angiotensin

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45
Q

Where is angiotensinogen released from?

46
Q

Where is ACE found (3)?

A

Lung capillaries
Epithelial cells
Kidney epithelial cells

47
Q

Role of ACE?

A

Angiotensin 1 to angiotensin 2 converter

48
Q

What stimulates aldosterone release?

A

Potassium and Angiotensin 2

49
Q

What does aldosterone do?

A

It acts on the principle cells of the cortical collecting tubule.
Water retention via sodium retention and potassium loss
This is done by reducing NED4 degredation which increases Na/K pump activity

50
Q

Where do loop diurectics work?

A

Thick ascending limb of loop of henle

51
Q

How do loop diuretics work>?

A

Block Na/K/Cl channel in ascending loop of henle

So LESS Na, Cl and K is reabsorbed and less water is reabsorbed.

52
Q

How do loop diuretics affect K+?

A

Potassium is LOST.
So at the Na/K/Cl co-transporter, none of these 3 are reabsorbed anymore. And so already some K is lost. And THEN, because less Na is reabsorbed into blood at the TAL, more Na travels to the distal convoluted tubule. Here the tubule tries to correct the Na loss by reabsorbing lots of Na+ and excreting lots of K+ via the K+/Na+ channel. So lots of K+ is lost.

The water loss caused by Na+ loss can also trigger the RAS Renin release K+ loss.

53
Q

What is the effect of low K+ on the blood pH?

A

K+ is acidotic so loss of K+ Increased PH Metabolic alkalosis

54
Q

Apart from loop diuretics, what else affects the Na/K/Cl co-transporter?

A

Bartter Syndrome
Gitelman Syndrome
Liddle syndrome

55
Q

What are the endocrine causes of K+ loss?

A

Hyperaldosteronism (Conn’s) or adrenal adenoma

Cushing’s (excess cortisol acts on Na/K, acts like aldosterone)

56
Q

What are the causes of HYPOkalaemia?

A
  1. Renal loss e.g. Diuretics/Syndromes/Endocrine causes/RTA (can’t secrete H+ so secrete K+ instead)
  2. Insufficient intake
  3. Loss via skin/GI
  4. Redistribution into cells (alkalosis, insulin, B agonists)
  5. DKA (because 1. Dehydrated so the RA system kicks in and excretes K. 2. Because when you correct it and give insulin the insulin moves K into cells)
57
Q

What are the clinical features of hypokalaemia?

A

Arrhythmias
Muscle weakness
Polyuria and polydipsia (because low K causes nephrogenic DI)

58
Q

What are the ECG changes ass. w/ high K?

A

Tall tented T waves

59
Q

What does hypokalaemia cause polyuria/polydipsia?

A

low K causes nephrogenic DI

60
Q

If a pt has high aldosterone, what would you expect their Renin to be?

A

Low

Aldosterone: Renin ratio will be HIGH.

61
Q

How do you treat low K?

A

Correct underlying cause
If <3.5mmol/l give oral KCL (2 sandok tablets)
If <3.0mmol/l give IV KCL (max 10mmol/hr)

62
Q

At what level does hyperkalaemia become lifethreatening?

63
Q

Causes of hyperkalaemia (>4.5mmol/l)?

A
  • Redistribution into cell; acidosis
  • Cell damage (released from cells)
  • Low insulin. insulin usually moves K+ into cells so it would move out
  • Reduced excretion: K+ sparing diuretics (aldost antag), ACE inhibs, ARBS, NSAIDs lower Renin release so low aldosterone less K+ excreted
  • Adrenal insufficiency (cos low aldosterone)
  • Excessive intake: parenteral nutrition, blood transfusion, K+ supplements
  • CKD = low GFR less K+ excreted
    Type 4 renal tubular acidosis (diabetic nephropathy) = Less Renin released
64
Q

Clincial features of hyperkalaemia?

A

Arrhythmias
Weakness
Tingling
Tall tented T waves

65
Q

Which molecule is involved in degrading sodium-potassium ATPase channels?

66
Q

Management of hyperkalaemia?

A
  • INSULIN: 50 mls of 50% dextrose w/ 10 units of insulin (to increase cellular K+ uptake and reduce hypoglycaemia)
  • B AGONISTS: Nebulised salbutamol (activation of Beta receptors stimulates uptake of K+ into cells)
  • Calcium gluconate 10%
  • Correct underlying cause
67
Q

What is the name of the gene that encodes the Na/K-ATPase channel?

A

sgk-1

So sgk-1 codes for NED4

68
Q

Normal plasma calcium range?

A

2.2-2.6 mmol/l

69
Q

Where does PTH get calcium from?

A

Gut via Vit D
Bones - acts directly on osteoblasts to act on osteoclasts
Kidney via Vit D activation and also resorption of Ca and pO4 loss

70
Q

What is the first molecule in Vit D synthesis?

A

7 dehydrocholesterol

71
Q

What is 7 dehydrocholesterol activated by? Where?

A

Skin by the sun (UVB)

72
Q

What does 7 dehydrocholesterol become?

A

Cholecalciferol (D3)

73
Q

What happens to D3?

A

25 hydroxylated by 25 hydroxylase enzyme in the liver

74
Q

What does D3 become?

A

25 hydroxycholecalciferol

75
Q

What does 25 OH D3 become? How?

A

It becomes dihydroxycholecalciferol (i.e. CALCITRIOL- active Vit D) by being hydroxylated again by 1 alpha hydroxylase, secreted by the kidney (And ectopic sarcoid lung cells)

76
Q

What stops too much Vit D from being activated?

A

PTH regulates it by regulating secretion of 1 alpha hydroxylase

77
Q

How does PTH affect the bones?

A

PTH binds to osteoblasts which then expresses RANK ligand which binds to RANK causes osteoclast precursors to differentiate and survive. Osteoclasts bind to bone and initiate bone resorption. Calcium is released.

78
Q

How many amino acids in PTH?

79
Q

Which cells secrete PTH?

A

Chief cells in Parathyroid gland

80
Q

How does PTH affect the kidneys?

A

Promotes reabsorption of calcium and excretion of phosphate. Phosphates bind to free calcium so this indirectly also increases serum calcium.
It also causes more released of 1 alpha hydroxylase.

81
Q

How does PTH get calcium from the gut?

A

1,25 dihydroxycholecalciferol (activated Vit D) stimulates intestinal absorption of calcium. Vit D can only be activated by 1 alpha hydroxylase. 1 alpha hydroxylase release is stimulated by PTH.

82
Q

Where do we get cholecalciferol from?

A
  1. Made by UVB in skin from 7-dehydrocholesterol

2. Eaten from diet (animals)

83
Q

When PTH is high, what is the alk phos (ALP)?

A

HIGH. PTH causes bone resportion osteoclast activity. When bone is breaking down, ALP is high.

84
Q

What happens in Paget’s?

A

Normal everything except high ALP because it directly stimulates osteoclasts

85
Q

Describe the osteoclasts in Paget’s?

A

VERY BIG with >100 nuclei

86
Q

Treatment of Paget’s?

A

Bisphosphonates

for pain esp PAMIDRONATE

87
Q

Describe the biochem of osteoporosis?

88
Q

What is the biochemical abnormality in Paget’s?

89
Q

What happens to serum Calcium in Vit D deficiency?

90
Q

What is Rickets?

A

Disorder of bone mineralization caused by low Vit D Low Calcium weak bones
Condition caused by Vit D deficiency

91
Q

What are Looser zones a sign of?

A

Vit D deficiency

92
Q

Causes of Vit D deficiency?

A 
Low sun exposure
Low dietary intake/absorption (coeliac)
Renal failure (cannot activate it)
Liver failure (cannot activate it)
Phytic acid (in chapattis)
93
Q

Symptoms of Rickets?

A 
Bowed legs (tibias)
Beading of ribs - Rachitic Rosary 
Pigeon chest
Wide epiphyses (wrists)
Paralysis 
Myalgia
94
Q

Symptoms of Osteomalacia?

A

Myalgia
Fractures
Pseudofractures (looser zones)

95
Q

Why can rickets present as paralysis?

A

Low Vit D –> low Calcium –> Poor neurotransmission

96
Q

Causes of primary hyperparathyroidism?

A 
Parathyroid adenoma (non-cancerous) 
MEN 1 - chief cell hyperplasia
97
Q

Symptoms of hypercalcaemia

A 
Can be asymptomatic
Renal Stones 
Bone pain 
Thrones (constipation, bowel slows down)
Abdo pain, can get pancreatitis
Psych symptoms (depression)
Polyuria (calcium is an osmotic diuretic)
98
Q

What will calcium renal stones look like on Xray?

A

Radio opaque

99
Q

If your Ca is high and your PTH is high, what do you have?

A

Primary hyperparathyroidism

OR familial hypocalcuric hypercalcemia

100
Q

If your Ca is high and your PTH is normal, what do you have?

A

Normal parathyroid gland but excess Ca from elsewhere e.g. cancer (bone mets) or sarcoidosis (increased 1 alpha hydroxylase so higher Vit D activation) or sunbeds

101
Q

Causes of hypercalcaemia?

A 
CHIMPS D
Cancer
Hyperthyroidism/hypoadrenalism (addison's - less Ca removed by kidney)
Iatrogenic (lithium/thiazides)
Milk Alkali/MEN2 (Men 2 = parahyperthyroidism)
Parathyroid hyperplasia/adenoma
Sarcoidosis 
Vit D excess (sunbeds/intake etc)
102
Q

How does sarcoidosis cause hypercalcaemia?

A

Ectopic 1 alpha hydroxylase from lungs activates Vit D

103
Q

Which drug should you avoid in hyperparathyroidism?

A

Thiazides (rises Ca and PTH! Masks biochem abnormalities, makes it harder to differentiate tings)

104
Q

What can advanced hyperparathyroidism give rise to (rare condition)?

A

Osteitis Fibrosa Cystic (OFC):
Van recklinghausen’s disease of the bone.
Salt & pepper skull
Brown Tumour

105
Q

Treatment of hypercalcaemia?

A
  • FLUIDS – IV normal saline 4L in 24hrs (frusemide to promote calciuresis and make space for fluids)
  • Bisphosphonates (helps prevent cancer invasion into bone)
  • Correct cause of hypercalcaemia
  • Surgery to correct a cancer
106
Q

2 signs seen in Hypocalcaemia?

A 
Trousseaus  = Take BP, cannot extend flexed hand
Chvostek's = Tapping of face  Twitching
107
Q

Other symptoms of Hypocalcaemia

A 
CATS
Convulsions
Arrhythmias
Tetany
Spasms (laryngeal spasm can be fatal)
108
Q

Causes of hypocalcaemia with high PTH?

A

CKD (cannot make alpha 1 hydroxylase)
Vit D deficiency
Pseudohypoparathyroidism i.e. PTH resistance - so calcium doesnt actual respond to high PTH levels so PTH keeps getting higher - phosphates will also be high

109
Q

Causes of hypocalcaemia with low PTH?

A 
Primary hypoparathyroidism (autoimmune/surgery/trauma)
Congenital absence of parathyroid (DiGeorge syndrome)
110
Q

Treatment of hypocalcaemia?

A

Depends on cause.
Renal failure Give synthetic 1 alpha hydroxylase
Give calcium in mild hypocalcaemia
Severe? Give 10% calcium gluconate IV

AANIYA PATH (31 decks)

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