calcium channels

NCLEX Pharmacology Medical Suffixes

  • -amil = calcium channel blockers
  • -caine = local anesthetics
  • -dine = anti-ulcer agents (H2 histamine blockers)
  • -done = opioid analgesics
  • -ide = oral hypoglycemics
  • -lam = anti-anxiety agents
  • -oxacin = broad spectrum antibiotics
  • -micin = antibiotics
  • -mide = diuretics
  • -mycin = antibiotics
  • -nuim = neuromuscular blockers
  • -olol = beta blockers
  • -pam = anti-anxiety agents
  • -pine = calcium channel blockers
  • -pril = ace inhibitors
  • -sone = steroids
  • -statin =antihyperlipidemics
  • -vir = anti-virais
  • -zide = diuretics

To remember about SVT, all you need to remember is the cause and you know the symptoms and treatment!

SVT occurs due to accessory conduction pathway through the AV node.

A - ABCD

Adenosine

Beta blockers

Calcium channel blockers

Digoxin

V - Vagal maneuvers

Valsalva

Ice immersion

Carotid massage

SVT: Start Vagal Treatment - - > If fails, use pharmacotherapy (ABCD drugs)

The P in Pvst reminds us that it presents with Palpitations in a hemodynamically stable patient (HR: 160-180/min)

*PVST: Paroxysmal supraventricular tachycardia

Interesting fact: In an asthmatic patient with SVT, you can’t give adenosine or beta blockers. The drug of choice in an asthmatic patient is therefore, diltiazem (A calcium channel blocker)

That’s all!

-IkaN

  • action potential: *activates voltage-gated ion channels*
  • voltage-gated calcium channels: *open*
  • calcium ions: *enter the cell*
  • synaptic vessicles: *fuse with the cell membrane and release neurotransmitter molecules into the synaptic cleft*
  • neurotransmitter molecules: *bind to postsynaptic receptors and create an excitatory or inhibitory postsynaptic potential*
Internship diaries: Calcium channel blockers and peripheral edema mnemonic

As you all know, I am doing internship or housejob and it’s really tiring but a good learning experience. Lemme share what I learnt / revised today!

In my medicine OPD, we start most newly diagnosed hypertensive patients on amlodipine, a calcium channel blocker. Many of the patients, after a few weeks of therapy, come back complaining of lower extremity edema. You check their electrolytes, LFT’s and RFT’s and they are all normal.

Then it dawns on you - Edema is a side effect of calcium channel antagonists like amlodipine!

You explain to them that it is a side effect of the medication, change the medication if it is really severe, otherwise you keep them on the same regimen.

It’s nice to learn a fact from the book and then see it in practice :)

Oh and I made a small mnemonic for this - Dipines make your legs dip in watery edema! :D

That’s all!

-IkaN

Diseases and their twins.

There a few diseases which quite resemble an other disease in presentation and sometimes pathology.Here’s a list I made-

1. Wolf-Parkinson-White and
   Lown-Ganong-Levine syndrome-

   -What’s similar?
    The tachycardia, short PR    
     interval, pre- excitation

  -What’s different?
    While in WPW syndrome,the
    culprit is a naughty extra pathway,
    the bundle of Kent, in LGL the AV
    node itself is naughty.(The
    hypothesized bundle of James  
    hasn’t been discovered yet)
    Conduction through the AV node
    occurs rapidly.
   
    ECG findings- WPW syndrome has
    a short PR interval and a Delta
    wave on the QRS complex. No
    Delta waves occur in the LGL
    syndrome.
   
    Also, the risk of sudden death
    remains lower in LGL syndrome.


2. Myasthenia Gravis and Lambert
   Eaton syndrome.

   -What’s similar?
    The muscle weakness.

  -What’s different?
   Oh almost everything. In MG,
   autoantibodies are formed against
   the nicotinic receptors whilst in
   LEMS(Lambert Eaton myasthenic  
   syndrome), the antibodies are  
   against ‘pre synaptic voltage  
   gated Calcium channels’.
   
    LEMS is mostly associated with
    underlying malignancies,
    making it a paraneoplastic
    syndrome.

     In contrast to MG, where
     distal musculature is affected
     the most, proximal musculature
     gets involved in LEMS. Arm
     muscles are frequently involved
     while MG prefers muscles of the
     leg.
     
     The autonomic nervous system
     also may be affected in LEMS.

    The most significant difference
    is that the strength actually
    improves on exertion in LEMS,
    known as ’Lambert’s sign’,  
    whereas in MG, weakness  
    prevails on repeated activity.


3. Multiple sclerosis and Devic’s
  disease
   
    -What’s similar?
    The demyelination and
    associated CNS symptoms.

    -What’s different?
     Many things. The optic nerve
     and spinal cord are affected more
     commonly in Devic’s. MS affects
     the CNS as a whole.

     Devic’s runs a more serious
     course than MS, the morbidity
     after an attack is more severe
     compared to it.

    MS is a T cell mediated
    autoimmune disease while IgG
    antibodies mediate Devic’s, more
    specifically the
    NMO(neuromyelitis optica)IgG.
    Oligoclonal bands are rare in
    Devic’s, and disappear after
    an attack.

    Uhthoff’s phenomenon, where
    symptoms worsen after exposure
    to higher temperatures,and the
    Lhermitte’s sign, where sudden,
    shock like sensation travelling
    through the spinal cord is felt,
    occur more commonly in MS.

4.Plague and Tularemia.
   
    -What’s similar?
      Those large, pus filled lymph
       nodes.
   
    -What’s different?
      Everything.Francisella
      tularensis is the causative agent,
      ticks and arthropods are the
      vectors, rabbits are the source,
      so on and so forth!