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Kaplan Qbank USMLE



Author7 Posts
  #1

Could somebody please explain the connection between calcium and tetany.

In Kaplan physiology book (pg 141) it says that tetany results from increasing the free intracellular calcium...but Goljan says in his endocrine lecture that decrease in free calcium causes tetany.

What am i missing here. Please explain

Thanks


  #2

HYPOCALCEMIA causes increase nerve excitability . in other word it decrease threshold of nerve action potential..

  #3

Tetany occurs during HYPOcalcemia... That means decreased Calcium extracellularly, and thus increased Calcium intracellularly.

so both Kaplan and Goljan are right. smiling face

___________________
Our greatest glory is not in never falling, but in rising every time we fall.

  #4

Also:
Calcium blocks Voltage gated Na Channels on the mucle cell at the NMJ.

In cases of Hypercalcemia - more Ca extracellularly, and block of voltage gated sodium channels, so decreases excitability.
In cases of Hypocalcemia - less calcium extracellularly, so less blockage of sodium channels, so sodium can enter the cell, so increased excitability and Tetany...

Edited by DrVirgo on 02/19/06 - 01:17 PM

___________________
Our greatest glory is not in never falling, but in rising every time we fall.

  #5

I agree with drVirgo. Just to add: when we say hypocalcemia we think of concentration of Ca in ECT (blood) not ICT

  #6

Right mildus... HYPO or HYPER-anything means the levels in the Extracellular Space.

Just a few more points about tetany while we are on the topic:
-Tetany can also be induced by multiple action potentials which will increase release of Ca from the SR thus causing more cycling of cross bridges.
-Complete Tetanus is obtained when enough Ca is avilable for continuous cycling of all available cross bridges.
-Can anyone explain the difference between complete and incomplete tetanus and how we incomplete tetanus?
Thanks.

___________________
Our greatest glory is not in never falling, but in rising every time we fall.

  #7

Tetany with carpopedal spasm * Pathophysiology o Abnormal Ca++ control of Na+ channels o Axonal hyperexcitability: Due to + Membrane depolarization + Reduced action potential threshold o Spontaneous repetitive discharges + Frequency: 5 to 15 Hz most common + Source: Arise in peripheral axons * Causes o Ion changes + Hypocalcemia + Hypoparathyroidism + Hypomagnesemia o Alkalosis: Respiratory o Normocalcemic tetany: Rare + Acquired: Associated with neoplasm + Hereditary: Dominant with epilepsy * Exacerbated by: Hyperventilation; Ischemia * EMG o Spontaneous axonal discharges at high rates: Up to 300 Hz o Repetitive discharges: Doublets or Multiplets o Intense spasm: Maximal interference pattern o Normal doublets occur at < 10 Hz * Diagnosis: Ischemic forearm test * Treatment: Calcium; Magnesium; Phenytoin







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