J de Zoysa: Renal Physiology; Potassium and Magnesium Flashcards Preview

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Flashcards in J de Zoysa: Renal Physiology; Potassium and Magnesium Deck (37)
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1
Q

Key roles of the the Kidneys

A
  1. ) Elimination of waste products
  2. ) Control of fluid balance

3.) Control of minerals: K+ and Mg2+

  1. ) Regulate acid-base balance
  2. ) Produce hormones
2
Q

What is Magnesium and how much? distribution?

A
  • Is an essential cation vital for numerous physiological functions.​
  • The total magnesium content of the human body is ~20 mmol/kg of fat-free tissue.
    • ​​~1000mmol in average man
  • Highly soluble
    • 99% of Mg is found in bone, muscle and soft tissue.
    • helps form the structure of the bone, hard to get at
  • Decreases with age
  • Intracellular Mg concentrations range from 5 to 20 mmol/L
  • Extracellular Mg accounts for 1% (0.7-1mmol/L)
    • some protein bound, some ionised, important for enzyme function
3
Q

Physiological purpose of Magnesium?

A
  • Bone formation
  • Co-factor in > 300 enzymatic reactions.
  • ATP metabolism, (key enzyme)
  • Muscle contraction and relaxation,
  • Normal neurological function
  • Release of neurotransmitters
  • Regulation of vascular tone
  • Cardiac rhythm
  • Platelet-activated thrombosis
4
Q

Magnesium is highly soluble, what does that mean?

A

It binds a large amount of water molecules very easily, which increase its diameter and makes it hard to move through intracellular channels. Needs to be actively stripped from water molecules to move through IC

5
Q

Describe magnesium homeostasis.

A
  • Mostly sourced from diet
    • 300mg from diet needed, some of this is from water (low amounts in NZ)
    • cereals, nuts, green leafy veges great sources
  • Absorbed in the GI tract
  • Kidney has a key role in regulation responding to loads or depletion
6
Q

How are the kidneys important to Magnesium?

A
  • Serum Mg is controlled by its excretion in the urine.
  • ~2400 mg of Mg is filtered by the glomeruli.
  • ~95% is immediately reabsorbed
    • 10-20% PCT
    • 60-70% Thick ascending limb
    • 10% DCT
  • ~100 mg (5%) is excreted in the urine
7
Q

Proximal convoluted tubule Magnesium reabsorbtion ?

A
  • Mechanism unsure (10-20% reabsorbed)
  • speculated that the Na/K ATPase could drag it through when pulling water across
8
Q

Thick ascending limb reabsorption of Magnesium?

A

The primary place of reabsorption

  • Lots of water is reabsorbed in the descending limb, which concentrates the electrolyte concentration, so K+ and Mg2+ is high by the time it reaches the ascending limb
  • Most important are the paracellular channels (formed by claudine 16 and Claudin 19) which are vital for magnesium reabsorb
    • those with mutations in this paracellular channel develop hypomagnesia with a low conc of magnesium in the blood, and can develop issues with this
  • Other channels: Na/K transport channels, K channels that impact Mg reabsorption
    • arters syndrome; hypermagnesemia
9
Q

Reabsorption of Mg in the DCT?

A
  • transient receptor potential channels important
  • Mutations can occur here → hyper magnesic → secondary hyper calcaemic → chance of developing kidney stones
  • abnormalities of Mg and Ca in children can present in these cases and lead top kidney failure
10
Q

How do we assess Mg?

A
  • Serum Mg: most common, tightly regulated (0.7-1), sometimes not a good measure of bone stores
  • Red cell Mg: if low they may need Mg
  • 24 hour excretion: will tell us if there’s renal loss occuring (happens more over night)
  • Mg retention test : give them an oral load, if it doesn’t rise then there’s an absorbtion issue
  • Isotope analysis: to see distribution of Mg - NOT typically done
11
Q

Causes of Hypomagnesamia

A
  1. Decreased dietary intake (water, meats, nuts)
  2. GI malabsorption and loss
  3. Endocrine – hyperaldosteronism, DM, SIADH, “hungry bone” syndrome
  4. Renal loss
    • Congenital
    • Acquired: eg; Drug-induced
12
Q

Drugs that can cause acquired Hypomagnesia?

A

• Aminoglycosides

• Amphotericin B

  • CNI
  • Cisplatin
  • Cetuximab

• Omeprazole: Protein pump inhibitor, now more commonly used

  • Pentamidine
  • Foscarnet
13
Q

Symptoms of Hypomagnesaemia are?

A
  • Weakness and fatigue

In severe cases:

  • Fasciculations /cramps
  • Tetany/carpopedal spasm
  • Numbness paresthesiae
  • Seizures
  • Arrhythmias

although it’s uncommon in the community this is common in the hospital setting due to diet, drugs

14
Q

How do you treat hypomagnesemia

A
  • IV magnesium (MgS) - acute cases in hospital
  • Oral is used in most cases
15
Q

When does hypermagnesaemia occur?

A

Usually very rare!

• In advanced CKD the compensatory mechanisms start to become inadequate and hypermagnesaemia may develop. (but usually these patient have problems with anorexia so this doesn’t occur often)

• Excessive oral administration of magnesium salts or magnesium-containing drugs: lots of reflux medication.

• Typically = Iatrogenic: resp depression, seizures, arrhythmias

16
Q

What is Potassium? our levels? Homeostasis?

A
  • Potassium is the most abundant cation in the intracellular fluid.
  • Maintaining the proper distribution of potassium across the cell membrane is critical for normal cell function.
  • Adult contains ~3500mmol K+
    • 300mmol in skeleton,
    • 80mmol in ECF,
    • Majority 90% in cells (IC) (2700mmol in muscle cells)
  • Daily oral intake 1560-5850mg/day (pregnant/lactating women need more)
  • At healthy steady state: 90 – 95% excreted in urine
  • 5 – 10% excreted in faeces
17
Q

Internal balance of Potassium is maintained by? How?

A
  • The kidney is primarily responsible for maintaining total body K.
  • Initial changes in extracellular K are initially buffered by movement of K into or out of skeletal muscle regulated by insulin and catecholamines.

Short term: buffered by K+ moving in/out of cells

Long term: buffered by the kidneys

18
Q

Tonicity and pH can affect K+ how?

A

Tonicity: Hyperglycaemia will lead to K efflux from the cell. Patients who present with TKA will often have a high initial K

pH:

  • Acidosis can also drive K efflux. (to balance unbound H+)
  • Alkalosis will leave to K influx. (to balance bound H+)
19
Q

Whats the overview of K+ reabsorption

A
  • Freely filtered at the glomerulus
  • 60-70% at PCT
  • 30% at Thick ascending limb
  • DCT and collecting ducts have a huge amount of control
20
Q

K+ reabsorption in the PCT

A
  • paracellular mechanism driving reabsorbtion
  • Na/K+ ATP ase drives K+ intracellularly, which causes paracellular movement of K+ into the blood from the lumen
21
Q

K+ reabsorption in the Thick ascending limb

A
  • Active reabsorption of K+ via a Na/K/ClCl channel and the ROMK channel, and the Na/K ATPase pump
22
Q

But lots of regulation occurs at the DCT via hormones such as : Aldosterone (and angiotensin)

How

A
  • If there’s a reduction in the EC vol or a reduction in salt, this will drive renin → angiotensin and AT II → aldosterone production
23
Q

What affects Serum K+ levels?

A
  • K+ intake (diet)
  • K+ losses
  • K redistributed from ECF in/out of cells
24
Q

Hypokaelaemia is defined as? What are the symptoms

A
  • Serum K < 3.5mmol/L -5mmol/L
  • Symptoms:
  • Muscle Weakness
  • Paralysis (severe cases)
  • Cardiac Conduction Abnormalities - dizzy, light-headed
  • Cramps
  • Constipation
25
Q

What is Hyperkalaemic Periodic Paralysis

A

• Autosomal dominant (rare) or thyrotoxic

• Abnormal K+ channels on cell membrane

  • Trigger is often high carb meal ( as this produces insulin) or SNS activation (b-agonist) eg. Anxiety or exercise
  • Excessive movement of K+ into cells
  • leads to extreme weakness
26
Q

Where can you get K+ losses via Renal routes which cause Hypokalaemia

A

• RENAL

  • Hyperaldosteronism: adrenal aldosterone-secreting tumor (Conns Syndrome) which overrides the usual regulation.
    • present with hypokalemia and hypertension
  • Licorice produces an enzyme that has an aldosterone-like effect an cause K+ stimulation
  • Diuretics affects both Na and K+ excretion. Drugs acting on the PCT the most common cause - PCT- mannitol/acetozalamide, LOH-frusemide, DCT-metolozone
  • Renal Tubular Acidosis
27
Q

Where can you get K+ losses via Gut routes which cause Hypokalaemia?

A
  • • K losses from Faeces or Vomit
    • Ileostomy: hypokalaemia
    • Diarrhoea
    • Bowel Fistulae
    • Vomiting
    • NG Tube Losses
28
Q

Treatment of hypokalaemia?

A
  • Treat the underlying problem (reason for loss)
  • For mild hypokalaemia (oral supplementation)
  • For severe use IV replacement
29
Q

Hyperkalaemia is? What are the symptoms?

A
  • Defined by a K > 5.0mmol/L (5.8 is where symptoms start)

Symptoms:

  • Fatigue or weakness: end stage renal disease
  • Paraesthesia
  • Nausea or vomiting
  • Dyspnoea
  • Palpitations - and then promotion of arrythmias
30
Q

How do you get Pseudo-hyperkalaemia

A
  • When lab tests are left sitting, the blood cells haemolyse and the K is released from its high conc intracellular storage
    • ask them if they have symptoms of hyperkalaemia (fatigue/weakness), if not do a fast repeat test
  • Can do an ECG just to be sure that there is no major isssues with hyperkalaemia if the lab does show high on the first test
31
Q

Cause of Hyperkalaemia

A
  • Increased Intake: usually only an issue with those with CKD (stage 4-5) then they are unable to manage the load. Usually normal people are fine
  • Disruption of cell intake:
    • Beta blockers (block β agonist effect)
    • Acidosis: H+ high moving IC and Pushing K out
    • Rhabdomyolysis: large breakdown of cells that cause K+ release
  • Decreased Excretion:
    • Renal Failure
    • Hypoaldosteronism
    • ACEi/ARB: drugs that cause this
  • Other Drugs:
32
Q

What is Addisons disease? opposite of conns

A
  • Deficient secretion of aldosterone, cortisol adrenal gland not functioning
  • Characteristic hyperpigmented/tanned: appearance due to excessive ACTH excretion
  • stimulating melanocytes
  • Symptoms: lethargy, weakness,
  • weight loss, low BP (excrete salt and water)

Lab tests: for hyperkalaemia and hyponatraemia
Diagnosis: Short synacthen test
Scans
Treatment: Dexamethasone, fludrocortisone

33
Q

Why should we be worried about hyperkalaemia. How do we treat it?

A

Because it can be an emergency.

K+ is a huge regulator of cardiac contractility, so can get a widening of the AP, leading to eventual VF

Treatment of this:

  • Short term: Stabilise AP
    • Using Intravenous Calcium → Push K into cells
    • This normalises membrane excitatbility for 30min
  • Med-long term: Reduce K absorbtion:
    • ‘Calcium Resonim: gets into GI tract, bings to K in gut (increasing faecal elimination) swapping it for calcium. Can be given orally or rectally, takes 4-6hrs.
34
Q

How do B-agonists treat Hyperkalaemia

A
  • Ventolin nebulisers
  • 5mg salbutamol
  • can do hourly
  • reduces K by 0.9-1.5mmol/L
  • Takes ~1/2 to 1 hour to acts, lasts 4-6 hours
35
Q

Insulin as a treatment of hyperkalaemia

A
  • Insulin (SA, 10 units) + Dextrose (50ml 50%)
    • done w dex. as insulin alone will drop glucose!!
  • Works in 10-20mins, peaks at 30-60mins
  • Duration 4-6ht
36
Q

Metabolic acidosis can also cause hyperkalaemia. How do we treat the MA?

A
  • Oral Bicarbonate tablets 840mg 2-3 bd/tds
  • In emergency; IV Bicarb 8.4% 50mL over 2 hours and repeat
37
Q

We can increase elimination and reduce absorption?

A

Increase elimination

  • K losing diuretic -frusemide
  • Dialysis

Reduce absorption:

  • Cation exchange products bind in the gut
  • Calcium resonium can be given orally or rectally