Lecture 6: Disturbances of potassium homeostasis in poisoning Flashcards

1
Q

What is homeostasis

A

maintenance of metabolic equilibrium

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2
Q

What regulates the total body K+ levels

A

Kidneys

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3
Q

What controls distribution of K+ between ICF and ECF

A

non-renal mechanisms

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4
Q

What transporter is responsible for active uptake of K+

A

Na+/K+ ATPase

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5
Q

What is the normal intracellular concentration of K+

A

~140 mmol/L

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6
Q

How is K+ passively lost through cells

A

Through K+ channels

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7
Q

How does disturbing K+ balance affect cells

A

disrupts stability of excitable cells as they need rapid changes in membrane potential to function

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8
Q

What is the normal range for [K+]

A

3.3 - 5.1 mmol/L

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9
Q

What are the two non-renal mechanisms resonsible for [K+] disturbances in poisoning

A
  • Na+/K+ ATPase
  • K+ channels
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10
Q

What is hypokalaemia and what potassium concentration would you find

A

Low potassium levels
[K+] < 3.3 mmol/L

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11
Q

Name 3 mechanisms for hypokalaemia

A
  • Increased Na+/K+ ATPase activity
  • Competitive blockade of K+ channels
  • Gastrointestinal losses of potassium
  • Renal losses of potassium
  • Systemic alkalosis leading to shift in K+ from ECF to ICF
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12
Q

How does increased Na+/K+ ATPase activity lead to hypokalaemia

A
  • greater cAMP production
  • increased affinity for intracellular Na+
  • increased affinity for Na by Na+/K+ ATPase
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13
Q

Clinical features of hypokalaemia

A
  • weakness of limbs in skeletal muscle
  • paralytic ileus (no movement of gut muscle)
  • cardiac muscle impairment leading to arrythmia and ECG changes
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14
Q

What ECG changes would you see in someone with hypokalaemia

A
  • Flat or inverted R waves
  • Extra abnormal U wave
  • ST segment depression
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15
Q

How does Salbutamol increase hypokalaemia

A
  • Salbutamol is a beta2 receptor agonist
  • Beta2 receptors are coupled to adenylyl cyclase
  • stimulation of beta2 receptors increases intracellular cAMP
  • increase Na+/K+ ATPase activity
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16
Q

How does the dose of Salbutamol affect hypokalaemia

A

More salbutamol = more ATPase upregulation = more hypokalaemia

17
Q

Are soluble barium salts toxic if ingested

A

Yes

18
Q

Are insoluble barium salts toxic if ingested and why

A

No- they are not absorbed

19
Q

How does Barium cause hypokalaemia

A
  • Vomiting and diarrhea add to K+ loss
  • Barium reversibly blocks K+ channels
  • Passive K+ loss reduced, Na+/K+ ATPase continues to pump into cell
  • ICF [K+] rises and ECF [K+] falls
  • As ECF [K+] falls, Na+/K+ ATPase declines steeply reducing cellular K+ uptake
20
Q

Management of hypokalaemia

A
  • reduce/ remove exposure
  • respiratory support
  • IV potassium
21
Q

Name 3 indirect mechanisms of hyperkalaemia

A
  • Inhibition of Na+/K+ ATPase activity
  • Depletion of cellular inhibition of cytochrome oxidases
  • Activation of Ca2+ dependent K+ channels
  • Ingestion of K+ salt
  • systemic alkalosis shifting K+ from ICF to ECF
  • rhabdomyolysis
22
Q

Direct mechanisms of hyperkalaemia (3)

A
  • Unconsciousness (muscle hypoxia due to lack of blood supply)
  • Seizure (vigorous muscle activity)
  • Acute renal failure (impaired excretion of potassium)
23
Q

Clinical features of hyperkalaemia

A
  • pain in smooth and skeletal muscle (not paralysis)
  • arrhythmia
  • ECG changes
24
Q

What ECG changes are seen in hyperkalaemia

A
  • Tall, peaked T waves
  • ST segment depression
  • Prolonged PR interval
  • Widening of QRS wave
25
Q

T wave difference in hypokalaemia and hyperkalaemia

A

Hypo = low K+ = low/ upside down T waves
Hyper = high K+ = high T waves

26
Q

Management of Hyperkalaemia

A
  • Digoxin-specific antibody fragments
  • Antidotes for cyanide
  • Insulin and dextrose
27
Q

Why are insulin and dextrose given together in treatment for hyperkalaemia

A
  • insulin shuts down Na+/K+ ATPase, reducing K+ conc
  • needs to give sugar as well otherwise patient will develop hypoglycemia