Brainscape's Knowledge GenomeTM

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


See full index

Disease of Major Organs > Potassium > Flashcards

Potassium Flashcards

1
Q

Where does the majority of K reside?

A

In the intracellular fluid

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

How is the K conc retained?

A

Regulated using the sodium-potassium exchange pump. Where 3 sodium ions from the ICF are exchanged for 2 potassium ions using ATP hydrolysis to exchange the two. Working against the conc gradient.

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

Match term with appropriate serum conc of calcium

  1. Hyperkalaemia
  2. Hypokalaemia
  3. Physiological range

A. >2.5 mmol/L
B. 3.5-5.3mmol/L
C. >6.5mmol/L

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

When does potassium shift into the ICF?

A

Via the actions of insulin, beta agonists and during alkalosis (H+ enters the ICF and K+ enters ECF to maintain electron neutrality- DCT)

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

When does potassium shift into the ECF?

A

Whereas potassium will shift out of the ICF during cell lysis, exercise, hypertonicity, alpha-agonists and during acidosis.

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

What cells control the renal absorption of K?

A

principal cells

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

What hormone can regulate potassium reabsorption? and whats the purpose?

A

Aldosterone acts to increase tubular reabsororption of K to increase BP

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

Whats the role of the RAAS axis?

A

Important role in regulating blood volume and systemic vascular resistance, which together influence cardiac output and arterial pressure

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

Briefly describe RAAS actions

A

Liver releases angiotensinogen in response to blood pressure dropping. A decrease in renal perfusion causes kidney to release renin. Renin cleaves angiotensiogen to angiotenisn I.. Angiotensin I is then further cleaved by ACE to make angiotensin II. The angiotensin II has a range of effector functions, such as increasing sympathetic function, increase tubular reabsorption, arteriolar vasoconstriction (increase BP), or increase H2O reabsorption in the collecting duct.

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

What lab investigations are available to investigate the K homeostasis?

A

Investigation can be done by measuring sodium, urea & creatinine, magnesium, calcium and phosphate, glucose, bicarbonate, blood gases and urine potassium.

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

What systems are affected by decreased potassium?

A

Changes to cardiovascular, neuromuscular, neuropsychiatric, renal and Gi systems.

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

How does hypokalamaemia manifest in the ECG?

  1. Decreased QST segment
  2. Depressed ST
  3. Inverted T waves
  4. Depressed U waves
  5. Prominent U waves
A

2,3,5

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

Hypokalamaemia symptoms specific to renal

A

polyuria and sodium retention

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

What is the goal of managing hypokalaemia?

A

Ensuring the minimal 40mmol/day is accounted for

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

True or false. If the K is >2.5mmol/L then use IV K+ in normal saline, whilst <2.5mmol/L should use oral IV.

A

False. >2.5mmol/L use oral and if its <2.5mmol/L then use IV K+ in normal saline.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are some important treatment cautions? (hypokalaemia)

A

The replacement should occur slowly under 48/72 hr replacement, with regular K+ checks. Higher rates may be given in an ITU setting with cardiac monitoring

17
Q

What are some broad causes of hypokalaemia?

A

In vivo or In vitro redistribution or true deficit.

18
Q

What is the first step in investigating true deficit and what does it inidcate? hypokalaemia

A

Urine K+ measured
<10mmol/L means the cause is extra renal. Acid base balance needs to be assessed. There are some causes in normal acid:base and in metabolic acidosis.
If urine K>10mmol/L then its renal losses, e.g. metabolic acidois or alkalosis or variable acid base

19
Q

In hypokalameamia caused by renal loss due to metabolic alkalosis, what is the next step in investigation?

A

Urine chloride

20
Q

What are two syndrome associated with hypokalaemia?

A

Bartters and Gitelmans

21
Q

What causes Bartters and what does it result in?

A

Due to mutations in genes encoding proteins that transport ions across renal cells in the thick ascending limb of the nephron. This causes hyper-reninaemic hyper-aldosteronism. Presents with increased blood pH and normal to low BP. Polyuria and polydipsia is also common.

22
Q

What causes Gitelmans and what does it result in?

A

caused by inactivating mutations in the SLC12A3 gene resulting in a loss of function of the encoded thiazide-sensitive sodium chloride co-transporter (NCCT). This cell membrane protein participates in the control of ion homeostasis at the distal convoluted tubule portion of the nephron (reabsorbs one sodium for one chloride). Will present with high blood pH, low Cl,K,Mg, and decreased sodium excretion

23
Q

What are these conditions?

  1. Familial hypokalaemic periodic paralysis
  2. hypokalaemic periodic paralysis with thyrotoxicosis
A

These are autosomal dominant conditions affecting the muscles due to the redistribution of K+ from the ECF into the ICF
FHH is a mutation in skeletal muscle voltage-gated calcium channel. Both conditions manifest with flaccid paralysis of limbs and trunk. As well as cardiac arrythmias.

24
Q

What are some signs and symptoms of hyperkalaemia?

A

changes to cardiovascular, renal and neuromuscular systems

25
Q

Describe the ECG changes associated with hyperkalaemia

A

Tall T waves, prolonged PR intervals, flat P waves and the widening of QRS complex.

26
Q

Name 3 causes of hyperkalaemia

A

Redistribution, increased intake, decreased output and syndromes of hypoaldosteronims

27
Q

In investigating the cause of hyperkalaemia what is the first step?

A

To rule out pseudohyperkalamia, which can occur due to EDTA contamination (contaminate serum tube causing high K and undetectable Ca), IV contamination or in vitro redistribution

28
Q

What redistributions cause hyperkalaemia?

A

Due to acidosis, insulin deficiency with high glucose, drugs (beta blockers), acute tissue damage (hypoxia, tumour lysis) or hyperkalaemic periodic paralysis.

29
Q

How does hypoaldosteronims cause hyperkalaemia?

A

In simple aldosterone acts to excrete K+ into the DCT lumen. With decreased aldosterone we can retian more K+.

30
Q

What drugs can induce hyperkalaemia?

A

Drugs that reduce aldosterone secreiton (NSAID, ACEi), block aldosterone binding to receptor (spirolactone), inhibit activity of epithelial sodium (potassium sparing diuretics), alter transmembrane K+ movement (beta blockers)

31
Q

What lab investigations are done for hyperkalaemic cases?

A
  1. The spurious (pseduohyperkalaemic) cases need to be excluded by looking at time/date (delayed separation)/storage/WCC/platelets/Ca/ and EDTA contamination.
  2. The renal function can be assessed by calculating the eGFR.
  3. Assessment of acid-base status as well as glucose
  4. Consider the patients drug intake and cortisol levels
  5. Renin & aldosterone levels need to be checked
    a. With caution. High potassium will stimulate aldosterone but suppresses the renin (blocking the axis by negative feedback), note as eGFR falls the aldosterone increases and renin decreases.
32
Q

What is hyperkalaemic periodic paralysis?

A

This is an autosomal dominant disorder with a K+ of 8mmol/L. Caused by mutation occurs in skeletal muscle voltage-gated sodium channel X-subunit. It can be investigated using an ECG showing tall T waves, but cardiac arrhythmias are rare. This condition can be managed by salbutamol inhalers (a beta-adrenergic agonists) to induce rebalance.

33
Q

What is the first step to managing hyperkalaemia?

A

To protect the heart by stabilising the myocardium using clacium gluconate or chloride, and ECG.

34
Q

What rate should calcium gluconate or chloride be administered?

  1. 10ml of 10% over 10min intervals till ECG improves
  2. 10ml of 25% over 30min intervals till ECG improves
A

1.10ml of 10% over 10min intervals till ECG improves

35
Q

How is the redistribution in hyperkalaemia assessed/treated?

A

using salbutamol (10-20mg) or using insulin + glucose (10 units of insulin in 25g glucose). In insulin + glucose, if K+ remains high a continuous infusion of insulin and glucose may be required.

36
Q

How can clinicians increase K+ excretion

A

sing haemodialysis or using calcium resonium (mild/moderate). The calcium resonium should be given four times a day (15g), but in enema 30g in 100ml may be given to asymptomatic hyperkalaemia. May take a couple of days to take effect. HD is required in persistent hyperkalaemia (>7mmol/L), severe or worsening metabolic acidosis (pH<7.2).

37
Q

Reducing intake load can be achieved by….

A

discontinue prescriptions and stopping K+ supplements, ACEi, or K-sparing diuretics

Disease of Major Organs (14 decks)

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