Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Board Qs Stef > Electrolytes > Flashcards

Electrolytes Flashcards

1
Q

How is Mg distributed within the body?

A

99% intracellular:
- 60% bone
- 20% skeletal muscle
- 19.5% heart, liver, other tissues
0.5% extracellular (serum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does Mg exist in serum?

A

63-66% ionized
30-31% protein bound
4-6% anion complexed (phosphate, HCO3, sulfate, citrate, lactate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How is cytosolic Mg maintained at constant cc despide EC Mg fluctuations?

A

3 mechanisms:
- IC protein binding
- influx and effluz across plasma memb of the cell
- sequestration within and transport out organelles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

The Ca sensing rec (CaSR) acts by which cell signalling pathway when activated by a low [Mg]?
A. Gs - activates adenyl cyclase - cAMP release
B. Gi - inhibits adenyl c and cAMP
C. Gq - phospholipase C activation - PIP2 cleaved to release DAG & IP3

A

A. Gs
CaSRs sense low extracell Mg levels- stimulates Gs prot - increase intracell cAMP, cause:
- Mg to be released from cell organelles
- excrete Mg through plasma memb via Na/Mg exchanger and basolat TRPM7 channel
- increase expression of TRPM6 channels on apical memb of some cells (GI, renal) allowing Mg to enter cell from lumen
TRPM= transient rec potential melastatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does norepinephrine disrupt Mg homeostasis?

A

Catecholamines decrease Mg due to a shift of Mg into cells as a result of stimulation of beta adrenergic receptors. High catecholamines may be one of the contributing factors for the hypoMg seen in congestive heart failure.
Beta rec stimulation stimulates Gs prot increasing cAMP (?)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Relating to the transient receptor potential melastatin (TRPM) channels, which is true?

A. Influx and efflux of Mg across cell memb is passive, with Mg moving down its concentration (from high to low conc)

B. Influx and efflux of Mg across cell memb is active (requiring ATP), with Mg moving from low to high conc

A

A. Influx and efflux of Mg across cell memb is passive, with Mg moving down its concentration (from high to low concentration)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the functions of Mg?

A

Mg:
- is required for many metabolic functions, most notably those involved in the production and use of ATP.
- is a coenzyme for the memb-bound Na/K ATPase pump and functions to maintain the Na/K gradient across all membs.
- is required for Ca ATPase and proton pumps.
- is essential for protein and nucleic acid synthesis,
regulation of vascular smooth muscle tone, cellular second messenger
systems, and signal transduction.
- exerts an important influence on lymphocyte activation, cytokine production, and systemic inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Why is Mg considered a Ca antagonist?

A

Mg competes with Ca for many of the divalent cation channels and receptor sites.
Extracell Mg considered to be a Ca antagonist via several mechanisms.
Clinical consequences:
Vascular smooth muscle relaxation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does Mg causes vasodilation?

A
  • Ca antagonism
  • cofactor for PGE1 and PGI2 (vasodilatory prostaglandins)
  • upregulates NO syntesis via eNOS activation
  • decreases catecholamine release from nerve endings (blocks mainly N-type Ca channels at nerve endings - inhibits norepi release).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the roles of Mg?

A
  • Skeletal and cardiac contractility
  • Regulation of other cations
  • Neurotransmission
  • Inflammation
  • Immune function
  • Coagulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is Mg reabsorbed in the GI tract? What is the major site of reabsorption?

A
  • Paracellular via tight junctions (e.g. claudin 16)
  • Passive
  • Ileum (25%), jejunum (10%),
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How much of Mg is reabsorbed in the colon? How?

A
  • Transcellular
  • 5%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Within the kidney, which segment of the nephron is responsible for the majority of magnesium reabsorption?

A

Loop of Henle (thick ascending limb), 70% of the filtered Mg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Mg is freely filtered through glomerulus.
> 95% filtered Mg reabsorbed.
Where? How?

A
  • 50-70% Mg2+ reabsorbed in thick ascending limb of Henle’s loop
  • Paracellular (via tight junctions)
  • Passive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How much of the filtered Mg is reabsorbed in the DCT? How?

A
  • 10%
  • transcellular mechanisms
  • Active
  • Activity of TRPM 6 regulated by intracell Mg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do CaSRs regulate Mg absorption & excretion?

A
  • low serum Mg: CaSR stimulates Gs = upregulation of apically located TRPM6 = facilitates absorption of Mg2+ from lumen into intracell space -
    Mg transported out of cell and into interstitium via TRMP7 and via Mg/Ca exchanger, both are located on basolateral memb of cell
  • high interstitial Mg:
    CaSR stimulates a Gi prot=
    Downregulation of TRPM 6= decreased absorption of Mg into cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which hormones can result in upregulation of TRPM 6 expression?

A

PTH
Calcitonin
Glucagon
ADH

Also:
vitamin D
aldosterone
PGE2 stimulate Mg2+ absorption via an unknown mechanism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How common is HypoMg in ICU patients?

A

Human ICU patients= Incidence varies from 9% to 65%
VetMed: 54% of critically ill pt (Martin L et al 1994)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

With what outcomes has hypoMg been associated?

A
  • Longer length of hospitalisation
  • 2.6 times more likely not to survive vs patients with normomagnesaemia (Martin L et al 1994)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What causes hypoMg in criticalli ill pts?

A

3 main categories: decreased intake (or absorption), increased
losses, and alterations in distribution.

  • GI losses (both upper and lower)
  • Proton pump inhibitor=
    Decreased affinity of TRPM6/7 channel for Mg
  • Renal disease= tubule dysfunction
  • cholestatic liver dz
  • metabolic acidosis
  • poor nutrition
  • hemodyalisis
  • peritoneal dyalisis
  • pancreatitis (sequestration - insolube soap)

Drugs:
- Na containing IVF= decreased Na reabsorption in PCT
- Diuretics
- Norepi/catecholamine excess (beta rec stimulation of lipolysis generates free fatty acids that chelate Mg)
- Insulin (IC shift)
- Dextrose (IC shift)
- bicarbonate (IC shift)
- amminoacids (IC shift)
- massive blood transfusion (citrate chelate Mg)
- Cyclosporine
- Aminoglycosides
- Cisplatin
= predispose to renal tubular injury and Mg loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

HypoMg is typically associated with what 2 electrolyte abnormalities. What are those? Why?

A
  • hypoK: Two mechanisms:
    Reduced Na-K-ATPase= net K loss
    Increased renal loss (ROMK channel in DCT)
  • hypoCa: HypoMg inhibits PTH release & response to PTH at target tissues (Woods’ paper 2021: 22% dogs with low iCa had low tMg. GI dz most common underlying condition causing low iCa & Mg.
    tMg concentration did not differ sig between ionised hypocalcaemia severity groups)
22
Q

What are the clinical manifestations of hypoMg?

A

Cardiovascular: Dysrhythmias, Poor contractility, Vasoconstriction, Hypertension,
coronary artery vasospasm, platelet aggregation

Neuromusc: Tetany,
Muscle spasms, Muscle weakness, Seizures

Resp: Bronchoconstriction

GI: in rodents fed hypoMg diet= increase intestinal vascular permeability & reduced intestinal function

23
Q

How does Mg affect the heart?

A

Magnesium regulates:
- Activity of cardiac cell ion channels, thereby affecting electrical properties of myocardium= Co factor for Na, K, Ca channels and Na-K-ATPase.
- Myocardial contractility and excitability by influencing intracell Ca mobility

24
Q

What ECG changes does hypoMg cause?

A

Subtle ECG changes may be seen before overt arrhythmia:
Prolongation of PR interval
Widening of QRS complex
ST segment depression
Peaking of T wave
= prolonged atrial depolarisation and ventricular repolarisation
(may be caused by concurrent lytes imbalances)

25
Q

What is the concern with QT prolongation (prolonged repolarisation)?

A

↑ likelihood for early after depolarisations due to activation L-type Ca channels?
Inability of cell to repolarise in late phase 2 & 3 - prolonged action potential duration - excessive Ca influx via ICaL current
Concurrent hypokalaemia?

  • may predispose to torsades de pointes
26
Q

What is the concern with digoxin administration in a patient with hypomagnesaemia?

A

Increased probability for digitalis toxicity
Toxicity: GI signs, cardiac arrhythmias
- Increased symapthetic tone= increased automaticity
- Slowed conduction and altered refractoriness may precipitate reentry
- Increased intracell [Ca] predispose to DADs

What other electrolyte abnormality predisposes to digoxin toxicity?
Hypokalaemia

27
Q

How does Mg work as an antiarrhythmic?

A
  • Co-factor Na-K-ATPase= maintain resting membrane potential
  • Decreased automaticity
  • Increased atrial and AV nodal conduction time
  • Increased atrial and AV nodal refractory period
  • Blocks conduction via accessory pathways
  • Decreases early/ delayed afterdepolarisations
  • Prolongs His-ventricular conduction time
28
Q

Why is Mg used as adjunctive tx for tetanus?

A

Role as a calcium antagonist= muscle relaxation
Also role in decreasing release of excitatory neurotransmitters (reduce catecholamine secretion from peripheral nerve endings & adrenal medulla)
(Associated with decrease urinary epinephrine excretion)

29
Q

Why is Mg used as adjunctive tx for pheochromocytoma?

A

Beneficial effects on life-threatening crisis including:
- Hypertension
- Hypertensive encephalopathy
- Catecholamine-induced cardiomyopathy

30
Q

Why could Mg help in the tx of TBI?

A

Mg deficiency common in human traumatic brain injury patients.
Incidence unknown in veterinary medicine.

2008 Cochrane systematic review found no beneficial role for Mg tx in acute TBI pts
2015 review found no sign improvement in mortality but did report a nonsign improvement in neurological scores with Mg tx

31
Q

What are the roles of Mg in sepsis?

A

Modulates immunological functions:
- Macrophage activation
- Leukocyte adherence
- Granulocyte oxidative burst
- Lymphocyte proliferation
- Endotoxin binding to monocytes
- ROS generation

Significant relationship between Mg & inflam cytokine production=
Mg deficiency can increase IL-1, TNF𝛼, IFN-𝛾, substance P.

MgSO4 has anti-inflammatory effects

32
Q

What is the dose of Mg to be administered?

A

Dose for life threatening ventricular arrhythmias:
0.15-0.3mEq/kg diluted over 5-15 minutes
Constant rate infusions:
Initial dosage of 0.5 to 1 mEq/kg q24h
Reduce to 0.25 to 0.5 mEq/kg q24h

Care with MgSO4 in hypocalcaemic patients

Reduce dose in azotemic pt, monitor ECG.

33
Q

How could Mg have analgesic properties?

A

Inhibits calcium ions from entering cells by blocking NMDA receptors.
Prevent central sensitisation (limited evidences).

34
Q

How could Mg prevent seizures?

A

Glutamate binds NMDA receptors= Blocks receptor

35
Q

What are the main causes of hyperMg?

A
  • Renal dysfunction
  • Endocrinopathies
    (exact mechanisms unclear)
    Includes: hypothyroidism, hypoadrenocorticism, hyperparathyroidism
  • Iatrogrenic (cathartics, laxatives, antacids)
36
Q

What are clinical signs of hyperMg?

A
  • Non specific: Lethargy, depression, weakness
  • Neuromuscular blockade
    Hyporeflexia
    Respiratory depression 2’ to respiratory muscle paralysis= hypoventilation
    Absent menace and palpebral reflex reported
  • ECG changes:
    Due to delayed AV and interventricular conductance, leading to:
    Bradycardia
    Prolongation of PR interval
    Widening of QRS complex;
    Complete heart block and asystole can occur.
    Hypotension
    Impaired platelet function= coagulopathy
37
Q

Which of these fluids contain Mg?
A. 0.9% NaCl
B. Normosol-R/Plasmalyte 148
C. Hartmanns/LRS

A

B. Normosol-R/Plasmalyte 148

38
Q

How do you treat hyperMg?

A
  • Stop exogenous supplementation
  • Increase Mg renal excretion (Furosemide,
    Saline diuresis)

For severe cases involving unresponsiveness, respiratory depression and any degree of haemodynamic instability=
Treat with Ca as antagonist of Mg=
Calcium gluconate 0.5 to 1.5ml/kg IV over 15-30 mins

  • Haemodialysis if due to severely impaired renal function
39
Q

What affects Mg excretion in the urine?

A

Load of Mg presented to the kidneys and prostaglandin E2 will increase excretion;
Mg deficiency, PTH, calcitonin, arginine
vasopressin, beta-adrenergic agonists, and epidermal growth factor, lactation will make kidneys conserve Mg.

40
Q

What are the ref ranges for Mg in dogs and cats?

A

iMg dogs: 0.43-0.6 mmol/L
iMg cats: 0.43-0.7 mmol/L

Tot Mg dogs: 1.89-2.51 mg/dl
Tot Mg cats: 1.75-2.99 mg/dl

41
Q

T/F Phosp is the major intracell anion

A

T

42
Q

What are the functions of Phosp?

A

Essential for production of:
- ATP
- Guanosine triphosphate
- Cyclic adenosine monophosphate (cAMP)
- Phosphocreatine
(= maintain cell memb integrity, energy stores, metabolic processes, and
biochemical messenger systems.)
- 2,3 di-phosphoglycerate (2,3 DPG)= regulation of tissue oxygenation (decrease affinity of O2 to Hb)
- Hydroxyapatite= maintain bone and teeth matrix

Structural role:Bone mineral, phospholipids of cell membrane,DNA and RNA

Regulatory role:Secondary messenger (IP3);
protein activity is turned on and off by phosphorylation and dephosphorylation

Metabolic role:
- Co-factor in O2 transport (as 2,3-DPG)
- Trapping glucose in cells (as glucose-6-phosphate)
- Synthesis of ATP (it’s the P in ATP)
- Acid-base regulation (urinaryand IC buffering)

43
Q

How is Phosp distributed throughout the body?

A
  • 80-85% bone and teeth as inorganic hydroxyapatite
    -14-15% soft tissues
    -<1% ECF= 85% unbounded free, 15% protein bounded

Organic phos is mostly IC VS inorganic is mostly EC.

2/3 of organic phos is in the form of phospholipids
(blood chemistry analyzers only measure the inorganic phos)

44
Q

T/F: Serum
Phosp remains relatively constant throughout the day.

A

F: transiently peaks 6 to 8 h after meals

45
Q

How much of ingested Phosp is reabsorbed in the small intestine?

A

60-70%.
Can be increased in case of hypoPhosp thanks to calcitriol= increase active transport of inorganic Phosp

46
Q

How much of the filtered Phosp is reabsorbed in the PCT?

A

60-90%

47
Q

What hormones increase tubular absorption of Phosp? And what substances increase its excretion?

A

Increase reabsorption: Growth hormone (hence why phosp high in puppies), insulin, insulin-like growth factor 1, and thyroxine
Increase excretion: PTH, phosphatonins (like FGF23), calcitonin,
atrial natriuretic peptide, supraphysiologic doses of vasopressin,
high doses of dexamethasone, adrenocorticotropic hormone

48
Q

What are the main causes of hypoPhosp?

A

3 main categories:
- decreased intestinal
absorption
- transcellular shifts (most commonly)
- increased urinary excretion; the
most common cause is transcellular shif

49
Q

What organs are involved in Phosp regulation?

A
  • bone
  • GI
  • kidneys
  • (parathyroids)
50
Q

How is Phosp reabsorbed in the GI tract?

A

Passive diffusion: primarily through paracell pathway
Active transport: mucosal phosp transport is a Na-dependent, saturable, carrier-mediated process
Influenced by calcitriol and dietary phosphate

Duodenum= diffusion and active transport
Jejunum + ileum= diffusion

Board Qs Stef (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions