Aani CP: Sodium/Potassium/Calcium Flashcards
1
Q
What is the normal range of serum sodium?
A
135-145 mmol/l
2
Q
What is the osmolar gap?
A
Difference between osmolality and osmolarity
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)
4
Q
How to calculate osmolality ?
A
Anions (Na + K+ ) + Cations (Cl- + HCO3-) + Urea + Glucose
5
Q
What should serum osmolality be normally?
A
285
6
Q
How to calculate osmolarity?
A
2 (Na+K) + Urea + Glucose
7
Q
What is the normal range for osmolar gap?
A
Normal <10
8
Q
Symptoms of hyponatraemia? (4) with Na values!
A
Nausea/vom <135
Confusion <131
Seizures <125
Coma/death <117
9
Q
What happens when you correct sodium levels too quickly?
A
Central pontine demyelinosis i.e. osmotic demyelination quadriplegia/seizures/death
10
Q
Where is ADH made? Where is it secreted?
A
Made in: Hypothalamus
Secreted from: Posterior pituitary
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
12
Q
What is the underlying cause of hyponatraemia?
A
Increased extracellular fluid (caused by increased ADH)
13
Q
Which 2 situations cause appropriate release of ADH?
A
- Increased osmolality (i.e. increased Na conc.) Mediated by osmoreceptors. You want to retain water to correct this.
- Low blood pressure – detected by baroreceptors in carotids/atria.
14
Q
What is the effect of ADH on serum sodium?
A
Lowers it –> Hyponatraemia
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!
16
Q
Signs of hypervolaemia?
A
Peripheral oedema
Raised JVP
Bibasal crepitations
17
Q
Causes of hyponatraemia in hypovolaemic pts?
A
Diarrhoea
Diuretics
Vomitting
Salt-losing nephropathy
18
Q
Causes of hyponatraemia in hypervolaemic pts?
A
Cardiac failure
Liver failure
Nephrotic syndrome
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.
20
Q
What are the causes of euvolaemic hyponatraemia?
A
- Hypothyroidism (Low C.O Low BP Baroreceptors detect it = More ADH)
- Adrenal insufficiency = low cortisol (cortisol needed to maintain BP) low BP increased ADH
- SIADH
21
Q
Causes of SIADH?
A
- Tumours/pathology of the brain/lung
- Drugs e.g. SSRIs, PPIs, TCAs, opiates
- Surgery (due to pain more ADH)
- Ectopic secretion from other tumours e.g. pancreas/prostate
22
Q
What will the plasma osmolality be in SIADH?
A
Low because lots of water retention so hyponatraemic (osmolality is basically sodium conc)
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
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)
25
How would you manage hypovolaemic hyponatraemia?
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
26
How would you manage hypervolaemic/euvolaemic hyponatraemia?
Fluid restriction and treat underlying cause
27
Management of severe hyponatraemia? Give details
Correct sodium levels with hypertonic saline (3%)
| Do not correct more than 10 mmol/l for 24 hours
28
If fluid restriction is not working for SIADH which drugs can you give?
Domeclocycline (reduced collecting duct responsiveness to ADH)- but risk of nephrotoxicity
Tolvaptan (V2 receptor antagonist)
29
What is more common hypo or hypernatraemia?
What is more common hypo or hypernatraemia?
30
Symptoms of hypernatraemia?
- Lethargy
- Thirst
- Irritability
- Fits
- Coma
31
What is the underlying cause of hypernatraemia?
Water loss
32
Causes of hypernatraemia?
- 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
33
Causes for cranial DI?
Trauma
Surgery
Tumour
34
Cause for nephrogenic DI?
- 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
35
What would the plasma and urine osmolality be in hypernatraemia?
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)
36
Diagnosing Diabetes Insipidus?
Water deprivation test:
Normal person's urine would concentrate to reduce water loss
Craniogenic: would concentrate after ADH given
Nephrogenic: would not concentrate
37
How do you correct hypernatraemia?
Rehydration with dextrose
| Hypernatraemia is water LOSS so do NOT give normal saline. Give water i.e. 5% dextrose.
38
If hypernatraemic pt is also volume depleted e.g. low BP, what do you do?
Correct fluid depletion with normal saline. Give 0.9% saline.
Check Serum Na every 4-6 hours.
39
What test do you do for suspected DI?
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
40
When can D&V cause hyponatraemia vs hypernatraemia?
Hypernatraemia if you don't drink e.g. child/elderly or DI
| Hyponatraemia if you correct with drinking
41
What is the normal range of K+ in the blood?
3.5-5.5mmol/l
42
Is K+ predominantly intracellular or extra?
Intracellular
43
Where is Renin secreted from?
Juxtaglomerullar Apparatus
44
What does Renin do?
Stimulates angiotensin release by converting Angiotensinogen to angiotensin
45
Where is angiotensinogen released from?
Liver
46
Where is ACE found (3)?
Lung capillaries
Epithelial cells
Kidney epithelial cells
47
Role of ACE?
Angiotensin 1 to angiotensin 2 converter
48
What stimulates aldosterone release?
Potassium and Angiotensin 2
49
What does aldosterone do?
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
Where do loop diurectics work?
Thick ascending limb of loop of henle
51
How do loop diuretics work>?
Block Na/K/Cl channel in ascending loop of henle
| So LESS Na, Cl and K is reabsorbed and less water is reabsorbed.
52
How do loop diuretics affect K+?
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
What is the effect of low K+ on the blood pH?
K+ is acidotic so loss of K+ Increased PH Metabolic alkalosis
54
Apart from loop diuretics, what else affects the Na/K/Cl co-transporter?
Bartter Syndrome
Gitelman Syndrome
Liddle syndrome
55
What are the endocrine causes of K+ loss?
Hyperaldosteronism (Conn's) or adrenal adenoma
| Cushing’s (excess cortisol acts on Na/K, acts like aldosterone)
56
What are the causes of HYPOkalaemia?
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
What are the clinical features of hypokalaemia?
Arrhythmias
Muscle weakness
Polyuria and polydipsia (because low K causes nephrogenic DI)
58
What are the ECG changes ass. w/ high K?
Tall tented T waves
59
What does hypokalaemia cause polyuria/polydipsia?
low K causes nephrogenic DI
60
If a pt has high aldosterone, what would you expect their Renin to be?
Low
| Aldosterone: Renin ratio will be HIGH.
61
How do you treat low K?
Correct underlying cause
If <3.5mmol/l give oral KCL (2 sandok tablets)
If <3.0mmol/l give IV KCL (max 10mmol/hr)
62
At what level does hyperkalaemia become lifethreatening?
>6mmol/l
63
Causes of hyperkalaemia (>4.5mmol/l)?
- 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
Clincial features of hyperkalaemia?
Arrhythmias
Weakness
Tingling
Tall tented T waves
65
Which molecule is involved in degrading sodium-potassium ATPase channels?
NED4
66
Management of hyperkalaemia?
- 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
What is the name of the gene that encodes the Na/K-ATPase channel?
sgk-1
| So sgk-1 codes for NED4
68
Normal plasma calcium range?
2.2-2.6 mmol/l
69
Where does PTH get calcium from?
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
What is the first molecule in Vit D synthesis?
7 dehydrocholesterol
71
What is 7 dehydrocholesterol activated by? Where?
Skin by the sun (UVB)
72
What does 7 dehydrocholesterol become?
Cholecalciferol (D3)
73
What happens to D3?
25 hydroxylated by 25 hydroxylase enzyme in the liver
74
What does D3 become?
25 hydroxycholecalciferol
75
What does 25 OH D3 become? How?
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
What stops too much Vit D from being activated?
PTH regulates it by regulating secretion of 1 alpha hydroxylase
77
How does PTH affect the bones?
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
How many amino acids in PTH?
84
79
Which cells secrete PTH?
Chief cells in Parathyroid gland
80
How does PTH affect the kidneys?
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
How does PTH get calcium from the gut?
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
Where do we get cholecalciferol from?
1. Made by UVB in skin from 7-dehydrocholesterol
| 2. Eaten from diet (animals)
83
When PTH is high, what is the alk phos (ALP)?
HIGH. PTH causes bone resportion osteoclast activity. When bone is breaking down, ALP is high.
84
What happens in Paget’s?
Normal everything except high ALP because it directly stimulates osteoclasts
85
Describe the osteoclasts in Paget’s?
VERY BIG with >100 nuclei
86
Treatment of Paget’s?
Bisphosphonates
| for pain esp PAMIDRONATE
87
Describe the biochem of osteoporosis?
NORMAL
88
What is the biochemical abnormality in Paget’s?
High ALP
89
What happens to serum Calcium in Vit D deficiency?
Lowers
90
What is Rickets?
Disorder of bone mineralization caused by low Vit D Low Calcium weak bones
Condition caused by Vit D deficiency
91
What are Looser zones a sign of?
Vit D deficiency
92
Causes of Vit D deficiency?
```
Low sun exposure
Low dietary intake/absorption (coeliac)
Renal failure (cannot activate it)
Liver failure (cannot activate it)
Phytic acid (in chapattis)
```
93
Symptoms of Rickets?
```
Bowed legs (tibias)
Beading of ribs - Rachitic Rosary
Pigeon chest
Wide epiphyses (wrists)
Paralysis
Myalgia
```
94
Symptoms of Osteomalacia?
Myalgia
Fractures
Pseudofractures (looser zones)
95
Why can rickets present as paralysis?
Low Vit D --> low Calcium --> Poor neurotransmission
96
Causes of primary hyperparathyroidism?
```
Parathyroid adenoma (non-cancerous)
MEN 1 - chief cell hyperplasia
```
97
Symptoms of hypercalcaemia
```
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
What will calcium renal stones look like on Xray?
Radio opaque
99
If your Ca is high and your PTH is high, what do you have?
Primary hyperparathyroidism
| OR familial hypocalcuric hypercalcemia
100
If your Ca is high and your PTH is normal, what do you have?
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
Causes of hypercalcaemia?
```
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
How does sarcoidosis cause hypercalcaemia?
Ectopic 1 alpha hydroxylase from lungs activates Vit D
103
Which drug should you avoid in hyperparathyroidism?
Thiazides (rises Ca and PTH! Masks biochem abnormalities, makes it harder to differentiate tings)
104
What can advanced hyperparathyroidism give rise to (rare condition)?
Osteitis Fibrosa Cystic (OFC):
Van recklinghausen’s disease of the bone.
Salt & pepper skull
Brown Tumour
105
Treatment of hypercalcaemia?
- 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
2 signs seen in Hypocalcaemia?
```
Trousseaus = Take BP, cannot extend flexed hand
Chvostek's = Tapping of face Twitching
```
107
Other symptoms of Hypocalcaemia
```
CATS
Convulsions
Arrhythmias
Tetany
Spasms (laryngeal spasm can be fatal)
```
108
Causes of hypocalcaemia with high PTH?
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
Causes of hypocalcaemia with low PTH?
```
Primary hypoparathyroidism (autoimmune/surgery/trauma)
Congenital absence of parathyroid (DiGeorge syndrome)
```
110
Treatment of hypocalcaemia?
Depends on cause.
Renal failure Give synthetic 1 alpha hydroxylase
Give calcium in mild hypocalcaemia
Severe? Give 10% calcium gluconate IV
