Brainscape's Knowledge GenomeTM

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


See full index

Progress test study > Electrolyte imbalances > Flashcards

Electrolyte imbalances Flashcards

1
Q

Signs of hyperkalaemia. Actual values?

A

malaise + muscle weakness/flaccid paralysis. Often asymptomatic till cardiac toxicity; eg arrhythmias,cardiac arrest, peaked T waves etc

K >6mmol/L

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

Signs of hypokalaemia. Actual values

A

lethargy + muscle weakness/hypotonia + muscle cramps + impaired cognition + cardiac arrhythmias

K <2.5mmol/L

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

Signs of hypernatraemia? Actual values

A

Early symptoms may include a strong feeling of thirst, weakness, nausea, and loss of appetite

Due to brain cell shrinkage:

  • Oliguria
  • confusion
  • muscle twitching and cramps
  • Orthostatic hypotension
  • seizures/coma

Na >145mmol/L

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

Low volume Hypernatraemia is attributed to?

A
  • Sweating
  • Vomiting
  • Watery Diarrhoea
  • Osmotic Diuretics mannitol
  • Glycosuria
  • Kidney Disease
  • Inadequate water intake with whole body Na depletion, usually in those who are mentally impaired with a defective thirst mechanism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Normal Volume Hypernatraemia is attributed to?

A

Diabetes insipidus

Fever

Inappropriately decreased thirst

Prolonged increased breath rate

Lithium

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

High Volume Hypernatraemia is attributed to?

A
  • Hyperaldosteronism
  • Excessive administration of IV 3% normal saline or Sodium bicarbonate: (hypertonic solution with minimal fluid intake)
  • Excessive salt intake: seawater ingestion or soy sauce
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Treatment of acute (<48hr) hypernatraemia

A

5% Dextrose in water

at 3-6mL/kg/Hour

*patients with diabetes insipidus will also require Desmopressin

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

What is Diabetes Insipidus (briefly)

A

Either impaired production of ADH or impaired kidney response to ADH. This leads to an excessive excretion of water from the kidneys

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

What is the danger of rapidly correctly Hypernatraemia?

A

The body (in particular the brain) adapts to the higher sodium concentration. Rapidly lowering the sodium concentration with free water, creates an osmotic gradient that causes water to flow into brain cells and causes them to swell.

This can lead to cerebral edema, potentially resulting in seizures, permanent brain damage, or death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How to correct chronic (>48hr) hypernatraemia

A

5% dextrose in water

70mL/hour for 50kg

100mL/hour for 70kg

OR water through NG tube

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

When will you get dextrose induced hyperglycaemia

A

Hyperglycemia may develop with rapid infusions of 5 percent dextrose; at a rate to fast for bodily response (eg; epinephrine release) and for the bodies ability to metabolise glucose.

A slower rate of infusion (<3-4mL/kg) or a change to 2.5 percent dextrose in water may be required after several hours.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the definition of Hypercalaemia?

A

A calcium level of >2.6mmol/L

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

Where is calcium distributed in the body and why is this tightly regulated?

A
  • 99% in bones as Calcium Phosphate
  • 0.99% is extracellular in blood and interstitium
  • 0.01% is Intracellular

An increase in the intracellular calcium levels → cell apoptosis

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

How does calcium get in and out of cells?

A

In:

  • Voltage gated channels
  • Ligand gated channels

Out

  • ATP-dependent calcium channels
  • Na/Ca exchangers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the distribution of extracellar calcium in the body?

A

it’s 50:50 diffusible and non-diffusible

Diffusible: can get across CM

  • Free Ionised:
    • For muscle contraction, hormone regulation, blood coagulation and neuron AP
  • Comlexed:
    • ​eg; calcium oxilate, electrically neutral

Non-Diffusible:

  • Ca2+- albumin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does extracellular calcium vary?

A

With Blood-pH

  • Low pH: lots of H+ → increasingly positively charged albumins that repel positively charged Ca2+ → more free ionised Ca2+ in the EC → hypercalcaemia
  • High pH: less H+ → free ionised albumin that attracts more Ca2+ → less free ionised in the EC → Hypocalcaemia
17
Q

how does albumin levels cause Pseudohypercalcaemia?

when can this occur?

A

As albumin increase it binds more calcium → increased conc. of portein-bound non-diffusible calcium

BUT free-ionised calcium concentrations stay the same

leads to pseudohypercalcaemia. This can occur when people get severe/acute dehydrated and their serum albumin levels increase.

18
Q

What is the hormone regulator of calcium?

A

Parathyroid Hormone (PTH) which is released by the four-sectioned parathyroid glands, located in your neck at the edge of the thyroid gland

19
Q

How does the parathyroid glands respond to low EC calcium levels

A

They increase the release of PTH which…

  1. Increases calcium release from bone (by incr. osteoclast resorption)
  2. Increases calcium reabsorbtion in the kidneys
  3. Stimulates kidneys to synthesize calcitriol → increased GI absorbtion of calcium
    • via conversion of 25-hydroxy vitamin D into 1,25-dihydroxy vitamin D (calcitriol)
20
Q

How do you get true hypercalcaemia

A
  • Osteoclast bone resorption → lytic bone lesions
    • 1<span>o </span>Hyperparathyroidism
    • PTHrP malignancy
    • Lithium use
    • Hyperthyroidism
    • Multiple myeloma
    • Prolonged immobilization
    • Paget’s disease
    • Vitamin A intoxication
  • increased GI absorbtion
    • Vitamin-D intoxication
    • Sarcoidosis and TB causing elevated calcitriol
  • increased Distal tubule reabsorbtion
    • Thiazide diuretics
21
Q

How does increased calcium impact the neuron?

A

a neurons sodium-channels resting state is stabilised by Ca2+

Therefore inc. calcium → less likely to depolarise → less excitable

Therefore there are slower/absent reflexes!

22
Q

What are the symptoms of hypercalcaemia?

(keep in mind many are due to calciums relationship with neuronal depol!!!)

A

“Stones, Bones, Groans, Thrones and Psychiatric Overtones”

  • Kidney stones
  • Bone pain
  • Abdominal pain and nausea
  • Polyuria and constipation
  • Hallucinations, confusion, stupor

ALSO: muscle weakness, slowed/absent reflexes, cardiac arrhythmias

23
Q

What would you see on ECG with hypercalcaemia?

A

Brady cardia

?AV block

<qt>

<p>Osborn wave</p>
</qt>

24
Q

What is the treatment of hypercalcaemia?

A
  • Volume expansion with isotonic saline
  • Administration of salmon calcitonin
    • ​blocks bone resorption and also increases urinary calcium excretion by inhibiting calcium reabsorption by the kidney
  • The concurrent administration of zoledronic acid or pamidronate
    • bisphosphonates are pyrophosphate analogues with high affinity for bone, especially areas of high bone-turnover, that inhibit osteoclast resorbtion
25
Q

Is frusemide recommended for hypercalcaemia treatment?

A

Not currently.

After rehydration, a loop diuretic such as furosemide can be given to permit continued large volume intravenous salt and water replacement while minimizing the risk of blood volume overload and pulmonary oedema. In addition, loop diuretics tend to depress calcium reabsorption by the kidney thereby helping to lower blood calcium levels.

BUTit is not reccomended for its potential complications

26
Q

How do you get pseudohypocalcaemia?

A

Low levels of albumin leads to less protein bound calcium, so although free ionised stays the same you get pseudocalcaemia

27
Q

List how you can get true Hypocalcaemia?

A

Less Calcium entering the blood

  • Hypoparathyroidism
    • surgical removal
    • AI destruction
    • Congenital; digeorge syndrome
    • Mg deficiency (needed for PTH prod.)
  • Low Vit D
    • Malabsorbtion
    • cirrhosis
    • decreased sunlight
    • chronic RF

Too much excretion

  • Kidney Failure
  • tissue injury, tumor lysis syndrome

Acute pancreatitis: FFAs bind to calcium and are excreted as soap like substance

28
Q

What are the symptoms of hypocalcaemia and why?

A
  • Tetany
  • Chvosleks sign: ipsilateral masseter twitch when tapping the facial nerve
  • Trousseuous sign: occlude brachial plexus, >> flexion of the wrist
  • Muscle cramps
  • abdominal pain
  • perioral tingling
  • Seizures

This is because low Ca gives the neurons the ability to depolarise at a lower threshold

29
Q

what would you see on ECG with hypocalcaemia

A

Prolonged QT

Prolonged ST

arrhythmias: torsade de pointes or AF

30
Q

Treatment of hypocalcaemia

A
  • Calcium glutamate
  • Vitamin D supplementation if appropriate
31
Q
A

Progress test study (31 decks)

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