calcium channel

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
3

Migraine stats:

• Migraine is the 3rd most prevalent illness in the world.

• Nearly 1 in 4 U.S. households includes someone with migraine.

• 12% of the population – including children – suffers from migraine.

• 18% of American women, 6% of men, and 10% of children experience migraines.

• Migraine is most common between the ages of 25 and 55.

• Migraine tends to run in families.

• About 90% of migraine sufferers have a family history of migraine.

Mechanism of migraine:

Dilation and inflammation of cephalic arteries and intracranial extra cerebral arteries cause the migraine headache. The migraine-associated symptoms result from the activation of the sympathetic nervous system caused by the pain. The migraine aura is caused by the neurophysiological phenomenon of spreading excitation/depression. The various mechanisms are tied together in the so-called “parallel theory” of the pathogenesis of the migraine attack

Common symptoms:

  • Throbbing, pulsating pain – 85 percent
  • Light sensitivity  – 80 percent
  • Sound sensitivity – 76 percent
  • Nausea – 73 percent
  • Pain on one side – 59 percent
  • Vision changes, blurred vision – 44 percent
  • Aura – 36 percent
  • Vomiting – 29 percent


Uncommon symptoms:

• Limb numbness/ limb tingling

• Hypersensitivity to touch - allodynia

• Slurred speech

• Auditory hallucinations

• Hiccups

• Metamorphosis - distortion of body image and perspective

• Olfactory hallucinations - smelling odors that aren’t real

• Excessive Yawning

• Monocular Blindness

• Sever Anxiety

• Fever

• Hives

• Diarrhea - constipation

• Fatigue

• Swollen eyelid

• Food cravings

• Vertigo - feeling as if you or objects around you are moving while they’re not

Action of antimigraine medications:

The abortive antimigraine medications act by constricting the dilated arteries through stimulation of the serotonin 1B receptor. The preventive antimigraine medications act by increasing the tone of the extacranial arteries, inhibiting the mechanism of neurogenic inflammation, or inhibiting pain transmission within the central nervous system.

Drugs used to stop migraines:

• acetaminophen (Tylenol)

• non-steroidal ani-inflammatory drugs ( aspirin, ibuprofen, naproxen)

Excedrin

• triptans - serotonin receptors agonists (ImitrexZomig)

• ergotamine derivatives (Cafergot)

The preventive antimigraine medications:

• anticonvulsants ( Topiramate)

• antidepressants

• antihistamine (Cyproheptadine)

• beta-blockers (Propranolol)

• calcium channel blockers (Verapamil)

currently crying at a bus stop because i just got out of an appointment with a new cardiologist, because my last one was having issues billing medicaid and i am still having a couple of issues while on the new meds

and the new cardiologist thinks i’m faking it/hysterical/whatever.

he kept telling me that he “disagrees” with diagnoses like IST because it “creates a self-fulfilling prophecy of people thinking they’re disabled.” he says he “disagrees” with me being prescribed calcium-channel blockers for it. he kept cutting me off when i tried to talk about what issues i was having. he kept asking me “but how do you know your heart rate is going up when you do x.” he said he would review my records again and “think about” scheduling a stress test

so apparently i get to choose between paying $95 per appointment, and sometimes having to deal with $800 bills because they accidentally fucked something up when trying to bill medicaid

or not having a doctor who takes me seriously

¯\_(ツ)_/¯

anonymous asked:

Are there any spells/other things like that, to let spirits (ghosts) know they are welcome in a household?

Yes there are! While I don’t have any spells off the top of my head, I’ll give you some ingredients and advice that might be helpful when crafting your own spell 🖤

🌙 The waxing moon phases are useful in spells geared towards building relationships, so this would be a good phase to preform a spell for building relationships with the spirits around you

🌧 The elements air and water focus on psychic abilities, emotions, and the soul, and may be useful in spirit focused spell work.

🌿 Chives- Protection against evil spirits

🍃 Golden Rod- To help you find what you’re looking for

🌿 Hazel- Spirit contact and manifestation

🍃 Holly- Death and rebirth, used to contact spirits

🌿 Onions- To enhance the lunar energies used in the spell

🍃 Poppies- Conjuring, meditation, psychic abilities

🔮 Bonded crystals such as aura quartz can be associated with building friendships and peacemaking. Keep in mind they may also carry the properties of which metal they were bonded to and the type of crystal used as well

🖤 Aragonite -Psychic energy and meditation

🔮 Bismuth- Channeling and astral travel

🖤 Bone/Calcium- Channeling and astral travel

🔮 Glass- A good combination of the elements, but specifically water

🖤 Kyanite- A link between people and the spirits of plants and animals

🔮 Opalite- Communication with entities

Here’s a good list of ingredients to get you started, of course you don’t have to use all of these but this list is to help you come up with a spell of your own.

I’ve also heard of people building spirit homes, like little gardens or small houses that spirits are invited to take up residence in. Similar things are used in contacting fae as well.

You might also consider a form of divination such as ouija boards or tarot cards 🔮

I hope this was helpful!! 🖤

*Disclaimer, I am not a spirit worker and my knowledge of spirit work is minimal at best

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

D&D Homebrew Poisons

So, im working on a mini series for badassdanddpics and was wondering if you guys had any ideas. im calling the mini series “Bewildering Botany and Perilous Poisons” that will basically showcase magical plant homebrew that will aid adventures and villains alike. for the poison section of it, i put together some basic information from D&D about the rules as well as how they are applied and used against others as well as common symptoms from plants in the real world.

different poisons are applied to victims by

  • contact
  • ingested
  • inhaled
  • injury
  • smoke from being burned

common rules (for 5th edition D&D regarding poison)

  • A weapon coated with poison will dry out in one minute.
  • When you are poisoned, you will usually suffer from the poisoned condition.
  • Poison can be bought or crafted using the downtime rules and a poisoner’s kit.
  • Cures for poison include low level spells or anti-toxin.
  • Truth Serum is listed under poisons, and is something I think could be useful in your campaign in many different ways.
  • Poisoned: A poisoned creature has disadvantage on attack rolls and ability checks.
  • each round until you make a saving throw.

Common symptoms of poisoning include nausea, vomiting, convulsions, liver failure, disables nerves, lowers blood pressure, and can stop the heart, muscle twitches, and sometimes paralysis, irritation of skin throat and mouth, swelling, burning pain, breathing difficulties and stomach upset. dilated pupils, sensitivity to light, blurred vision, tachycardia, loss of balance, staggering, headache, rash, flushing, dry mouth and throat, slurred speech, urinary retention, constipation, confusion, hallucinations, delirium, convulsions and photo-toxicity

underneath the “keep reading” i have included some actual plants that could help with creating realistic homebrew.

Keep reading

Quick fact. Ready?
Magnesium is one of the most abundant minerals in our body, 35% of it being stored in our bones.

A deficiency in Magnesium can lead to an increase in blood pressure, impaired glucose intolerance, or an excitation of neurons.

Often times, Magnesium makes one feel tired or relaxed due to the affect that it has on calcium channels in the brain.

The best sources of Magnesium are green leafy vegetables like spinach or kale, not only because of their high content, but because of their higher absorption rates.

anonymous asked:

hi aunty!! what would dying of takotsubo cardiomyopathy look like/feel like? i have a character whose son dies and then he's supposed to die shortly after of a "broken heart" but nothing will tell me what that's supposed to look like ;;. thanks in advance and thank you for running this blog!!

Hey there nonny! 

Dying of heart failure – really, any kind of heart failure – sucks pretty heart. 

Takotsubo cardiomyopathy – TCM for the remainder of this post – basically looks like a heart attack. The character will present with pain in their chest, possibly radiating down the left arm or into the jaw. They might also present with fainting or shortness of breath. 

On an EKG, they would have a finding called ST-segment elevation (ST elevation for short), which is indicative of a heart attack. 

On bloodwork, they would be positive for a kind of cardiac enzyme called troponins, which are released during a heart attack (and the only way to be sure, by the way, that a character is having a heart attack). Doctors might call this “positive troponins” or “elevated troponins”. 

But here’s where the diagnosis of TCM (or SCM, stress cardiomyopathy) starts to veer apart from the diagnosis of myocardial infarction (heart attack). The definitive treatment for an MI is usually to get the character into the cardiac cath lab, which will allow doctors to thread a wire into the coronary vasculature and find the blocked artery, so that the blockage can be cleared and blood flow restored. 

A patient with TCM will get a coronary cath, which will find…. nothing. Absolutely nothing. No blockage of any kind. (This is actually part of the diagnostic criteria for Takotsubo’s.) 

Also, the heart typically has abnormal wall motion, evident on ultrasound or CT. (CT is performed during the cardiac cath, because these procedures require fluoroscopy; that is, being able to see an X-ray or CT in real-time.) 

Now. You asked specifically about dying of TCM. This is going to look like most other kinds of heart failure following MI. 

The character may get chest pain and have their heart simply fail on them. This can happen quickly or fairly slowly. 

Chest pain and worsening shortness of breath are both very likely, as is difficulty walking, fatigue, and other nonspecific cardiac symptoms. The character may wind up with fluid in his lungs (since, if the left ventricle fails, blood basically backs up into the pulmonary system), he may be pale and sweaty, he may feel as though he’s about to die – this is an actual symptom of heart failure (and most kinds of shock). 

If the pulmonary edema (fluid backup in the lungs) gets bad enough, he may have some pink, frothy spittle, and he might feel like he’s drowning, because he is – in his own blood. 

However, there’s something important to know about TCM. Takotsubo cardiomyopathy is usually not a lethal condition. Mortality is only 1-3%, and most patients make a full recovery in 4-8 weeks. 

Treatment, by the way, is usually supportive: beta blockers or calcium channel blockers are used to reduce stress levels (since the physiological manifestation of stress is high adrenaline levels), and worse comes to worst the character might get put on a balloon pump (which basically inflates a balloon in the aorta to support the heart and reduce workload). 

So I hope that gives you what you need to know about Takotsubo cardiomyopathy!! 

Thanks for your ask and write a kick-ass story! 

xoxo, Aunt Scripty

[disclaimer]

Patreon: a magical land where the ask box never closes. Care to visit?  

Ebook for Free! 10 BS “Medical” Tropes that Need to Die TODAY!

GPCRs/7-transmembrane receptors (7TM receptors)

G-protein-coupled receptors (GPCRs) are the largest and most diverse group of membrane receptors in eukaryotes. 

Structure

  • single polypeptide chain comprising of seven transmembrane α-helices
  • extracellular N-terminal domain of varying length, 
  • intracellular C-terminal domain.
  • length of the extracellular N terminus and the location of the agonist binding domain determines family.
  • The long, third cytoplasmic loop couples to the G-protein 
  • Usually particular receptor subtypes couple selectively with particular G-proteins
  • For small molecules, such as noradrenaline, the ligand-binding domain of class A receptors is buried in the cleft between the α-helical segments within the membrane. Peptide ligands bind more superficially to the extracellular loops

G protein system

GPCRs interact with G proteins in the plasma membrane when an external signaling molecule binds to a GPCR, causes a conformational change in the GPCR.  G-proteins comprise a family of membrane-resident proteins
whose function is to recognise activated GPCRs and
pass on the message to the effector systems that generate
a cellular response. 

  • G proteins are specialized proteins with the ability to bind the nucleotides guanosine triphosphate (GTP) and guanosine diphosphate (GDP). 
  • The G proteins that associate with GPCRs are heterotrimeric, (alpha beta and gamma subunits)
  •  alpha and gamma are attached to the plasma membrane by lipid anchors 
  • Trimer in resting state 
  • activated alpha monomer and beta/gamma dimer

Guanine nucleotides bind to the α subunit, which has enzymic activity, catalysing the conversion of GTP to GDP. The β and γ subunits remain together as a βγ complex. All three subunits are anchored to the membrane through a fatty acid chain, coupled to the G-protein through a reaction known as prenylation.

  • G-proteins are freely diffusible so a single pool of G-protein in a cell can interact with several different receptors and effectors 
  • When GPCR is activated by an agonist, a conformational change causes it to acquire high affinity for αβγ (G protein)
  • bound GDP dissociates and is replaced with GTP, which in turn causes dissociation of the G-protein trimer, releasing α-GTP and βγ subunits - the ‘active’ forms of the G-protein
  • which diffuse in the membrane and can associate with various enzymes and ion channels
  • Signalling is terminated on hydrolysis of GTP to GDP through the GTPase activity of the α subunit.
  • resulting α–GDP dissociates from the effector, and reunites with βγ
  • Attachment of the α subunit to an effector molecule increases its GTPase activity
  • GTP hydrolysis is termination –> activation of the effector tends to be self-limiting

Second messenger targets for G proteins

Main targets:

  • Adenylyl cyclase (responsible for cAMP formation)
  • Phospholipase C (inositol phosphate and diacylglycerol (DAG) formation)
  • Ion channels, particularly calcium and potassium channels
  • Rho A/Rho kinase (system controlling the activity of many signalling pathways for cell growth and proliferation, smooth muscle contraction, etc.)
  • Mitogen-activated protein kinase (MAP kinase) system controlling cell functions eg division.

(notes on these coming soon)

anonymous asked:

hey, just so you know, that post about thigmonasty and thigmotropism in plants isn't factually sound. plant consciousness is fringe science and widely disputed because it's like a plant biologist's wishful dreaming with essentially no evidence. aquaporins and calcium channels get damaged with overuse; auxins, gradients, and calcium levels increase or decrease as an automatic plant response to stimuli, it goes on and on. there's far more concrete evidence against "thinking" plants than for it!

people are still very interested in tropisms and nastic movements, & there’s a lot more new stuff to learn. the effects and levels of plant hormones, newly discovered molecules, & ions are rapidly being made known to the plant bio community. all of the things i mentioned play a role in these responses to stimuli, how rapidly&frequently they can happen, or whether they can even happen at all in some circumstances! plus without a cns plants cannot experience cognition in any way animals do, period

This is all very good stuff! Thanks for writing it out.

I gotta be honest, I don’t even think that the article mentioned plants experiencing cognition like animals. I agree that would be ludicrous. I just thought the experiment itself was really cool in terms of how the responses to stimuli changed!

I understand that fringe science isn’t something to be pounced on and taken lightly and believed at first sight. But to be honest there’s nothing wrong with taking a healthy, skeptical interest in various theories without getting tangled up in tinfoil hat stuff.  

Personally for me, in the linguistics side which takes my interest the most (development of language in humans) this is probably something akin to the claim that “whales have a language!”. The parameters we use to measure specific concepts like “language” and “consciousness” are guarded by constraints that scientists put on them to make them easier to identify. However, that doesn’t mean that either one is a binary THERE or NOT type of deal. 

Correct me if I’m wrong but… Cognition is a flowing scale. Language and communication is a flowing scale. Human language and human cognition are specifically defined terms that cannot be over-applied. Animal communication and animal cognition, while not the same as human language and human cognition, nonetheless exist on the spectrum of our understanding of the parameters outside of our own experience. Why can’t we also consider this, theoretically, to be at some point connecting to non-animal organisms? Despite their existence being incredibly far-off from that of the consciousness that we know, it’s still cool to theorize about how they experience their world. 

Sorry, I know that this type of stuff is actually going CLOSER to fringe science, and I know that it’s also ridiculous. :D It’s just cool in theory. Doesn’t mean I think plants can experience their world the same way as animals.  

anonymous asked:

I start pharmacology in 2 weeks. I'm hoping to get a bit ahead, so I've been reading the medication sections in my Saunders NCLEX prep book. My question is, how the hell do you study all of this and organize it?? It's SO much information! I'll be taking that AND foundations of nursing together and I'm pretty nervous for both!

Hi!! (This turned out longer than I expected, but I hope it’s helpful!)

Reading the medication sections in the Saunders book is definitely a great place to get a general idea of the most important drugs/drug types in nursing! I relied on this type of book to review in preparation for exams throughout the semester.

I don’t know how your course is going to be set up, but mine was split into 5 units, and each of those contained several “categories” of medications.  For example, Unit 2 contained neuropharmacology, mental health pharmacology, opioid analgesics/antagonists, and drugs used for the treatment of Parkinson’s, Alzheimer’s, and seizures.  

For each category, my professor provided a powerpoint and assigned readings in the textbook.  The powerpoints detailed the systems on which those drug categories would be working, how those drugs would affect those systems, and then pointed out the most important medications to know.  

So, for example, in mental health pharmacology, the slides were organized by mental disorder (schizophrenia, depression, anxiety, bipolar, etc.), and the different classes of drugs/specific drugs that are used to treat those illnesses were explained.  


As far as studying and organizing all of the material goes, I would keep drugs within their classes (you will find that many drugs within medication classes function in similar ways), and keep these drug classes associated with the system on which they work.  

I found this method of organization necessary throughout the whole course, but it was especially helpful when tackling larger categories of drugs, such as in neuropharmacology and cardiology.  

***Also, you will see that certain classes of medications can be identified by common prefixes or suffixes: ACE inhibitors end in “-pril” (lisinopril, captopril), cephalosporins (an antibiotic class) usually begin with “cef-” (ceftriaxone, cefaclor)***


For example: 

Within cardiology there are numerous possible diseases/symptoms of diseases that may need to be treated (such as: hypertension, heart failure, edema, high cholesterol, angina, clotting), and each of these diseases has a different set of drug classes associated with it.  After identifying the classes of drugs used to treat different pathologies, you can memorize which specific drugs are within classes.

  • Hypertension, heart failure, and edema can be treated with different combinations of the following drug classes: diuretics (there are many classes of diuretics), drugs that target the RAAS system (ACE inhibitors and ARBs, etc.), calcium channel blockers, vasodilators, inotropic agents, and antidysrhythmics
  • High cholesterol can be treated with statins, nicotinic acid, bile sequestrants, fibric acids
  • Angina is usually treated with nitroglycerine
  • Clots/high risk for clotting can be treated with antiplatelets, anticoagulants, direct thrombin inhibitors, thrombolytic agents, and factor Xa inhibitors

My professor was also kind enough to provide a list of the most important drugs from each unit before exams, and I would go through this list memorizing key information about each drug.  I would make flashcards for each one of these drugs with the drug name on one side, and the most important information about the drug on the other.

For each drug it is usually important to know:

  • pharmaceutical class
  • indication (purpose for medication: what it treats)
  • pharmacodynamics (what the drug does)
  • pharmacokinetics (how drug goes through body: admin route, half life, location of metabolism and excretion)
  • nursing assessments (that should be done when patient is on this drug)
  • lab considerations (drugs like lithium require specific levels in the body)
  • age-related considerations
  • precautions/contraindications
  • possible drug-drug interactions
  • patient teaching if necessary (ex: patients must sit or stand upright for 30 minutes after taking a bisphosphonate because they have the potential to damage the esophagus)
  • any weird and unique side effects


I’m going to lie, there is a TON of information that needs to be studied in Pharmacology but it is totally doable!  Organization is crucial, and you will find the form of organization and studying that works best for you, and fits best with the teaching style and expectations of your professor.  When you get the course syllabus I suggest reading through it and taking note of when the exams will be, and the order in which drug categories will be presented.

Foundations of nursing (at least at my college) was heavily based in A&P so I didn’t find it too difficult, but I did take it the semester before Pharm.  I took Pharm and Med Surg 1 together, and while it was a lot of information, I was able to stay organized and do well in both courses! So don’t be nervous, and if you have any more questions feel free to ask!

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

  • 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*

anonymous asked:

Have you ever made a med error and if so how did you handle it?

Yes. I promise, if you have been a nurse for longer than a week, you have made a med error.

If someone tells you they haven’t made a med error they are either 1. Lying or 2. Too dumb to realize it, which is really scary.

Here’s what I do: Don’t freak out, tell the doc, and go from there. I have been lucky, not to make a significant error that caused the patient harm.

Other med errors are scarier, just know that the sooner you come clean, the safer it is for the patient. One time, a new nurse was on orientation on my unit. There’s calcium channel blocker med we give to SAH patient to prevent vasospasm. The patient was intubated, so this med need to down the patient’s dobb hoff tube. The pill was a liquid capsule. So, what we would do was, insert a needle  with a 10 cc syringe into the capsule, draw out the liquid in a syringe and then give the med via the dobb hoff tube. This new nurse does that, then sees this 10cc syringe of liquid in her hand and it feels natural to give that IV, right? So she did. It was 60 mg of a calcium channel blocker given IV. So, what do you think happened? The patient’s ECG began to have dysrhythmias, he went into v-tach. The doc was called and ACLS was started. Around this time the new nurse realized her error. She told her preceptor off to the side and the preceptor told the doc. They began pushing calcium chloride and the patient improved, NSR was restored after a lot of calcium. The new nurse was written up. But the process was also changed. Pharmacy began supplying us with that medication already in the liquid form, so no more drawing up liquid out of a capsule pill. That was unsafe practice, so the system improved.

It’s not fun owning to a mistake, but it’s necessary.

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!