Mini mnemonic for the day!
OsGood SchaTTer: Oh God. Traction shattered my Tibial Tuberosity.
-IkaN
Monday, February 9, 2015
Study group discussion: Why NSAIDs are avoided in MI, why aspirin is an exception
Why NSAIDs are not given in acute Myocardial Infarction?
I think it's because they're not strong enough and don't act fast enough. The pain relief lowers the stress on the heart.
NSAIDs hamper the process of scar formation after MI, there is chance of wall rupture.
Steroids too.
Yes.
Isn't aspirin an NSAID? We give that in MI.
Yes, aspirin should be an NSAID. It's not a steroid, and it's anti-inflammatory. So I don't see any reason why it wouldn't be one.
Edit, I just looked it up on the internet, and it's listed as one of the most common NSAIDs (along with ibuprofen and naproxen).
You give aspirin in antiagregation range. In order to help dissolve the cloth and prevent new ones.
Well, I asked in reference to the comment on why NSAIDs should not be given in MI. But I read and found out that Aspirin is permitted as an exception.
None other NSAID should be given.
Aspirin is essential in the management of patients with suspected STEMI and is effective across the entire spectrum of acute coronary syndromes. Rapid inhibition of cyclooxygenase-1 in platelets followed by a reduction of thromboxane A2 levels is achieved by buccal absorption of a chewed 160–325-mg tablet in the Emergency Department. This measure should be followed by daily oral administration of aspirin in a dose of 75–162 mg.
Glucocorticoids and nonsteroidal anti-inflammatory agents, with the exception of aspirin, should be avoided in patients with STEMI. They can impair infarct healing and increase the risk of myocardial rupture, and their use may result in a larger infarct scar. In addition, they can increase coronary vascular resistance, thereby potentially reducing flow to ischemic myocardium.
Source: Harrison.
I think aspirin has a different mechanism to other NSAIDs. Aspirin, can worsen a bleed, for example, but is unlikely to be the direct cause of gi bleeding. I'm assuming it works differently with regards to myocardial repair too.
Non-selective NSAIDs enter the channels in both (cox1 and 2) enzymes and, except for aspirin, block them by binding with hydrogen bonds to an arginine halfway down. This reversibly inhibits the enzymes by preventing the access of arachidonic acid. Aspirin is unique in that it acetylates the enzymes (at serine 530) and is therefore irreversible.
I was taught that aspirin is the only NSAID you give in myocardial Infarction.
You have to give it as soon as possible because the latter you give, the benefit decreases.
That is why the first step in management of a patient with MI is aspirin (Not O2, not nitroglycerin, not beta blockers, not morphine) because aspirin has a time dependent mortality benefit.
Aspirin and clopidogrel!
Study group discussion: Management of enuresis
What's the guidance for action in case of enuresis of the child?
You test for urinary tract infections and look for stressors. First try non pharmacological methods like alarms, avoiding water intake at night etc. Then you use drugs.
If there's no infection and the non pharmacological methods don't work, what's the treatement?
Desmopressin then Imipramine.
Study link!
Uses of tricyclic antidepressants mnemonic http://medicowesome.blogspot.com/2015/02/uses-of-tricyclic-antidepressants.html
Study group discussion: Why adrenaline is NOT given by the intravenous route?
Why is adrenaline / epinephrine not given intravenously in anaphylactic shock? Why intramuscular injection?
Study group discussion: Calorie test and true coma
How will you find out whether the prisoner is faking a coma or not?
Cold caloric oculovestibular reflex - A highly sensitive and specific test.
That's one of the test I had read used to pronounce the person brain dead. You push cold water in the person's ear, it stimulates a reflex. Rapid movement towards opposite side is normal.
Mnemonic is COWS.
Cold: Opposite side
Warm: Same side
Sunday, February 8, 2015
Study group discussion: Mechanism of action of Digoxin
Oubain and digoxin got a connection. Both are cardiac glycosides.
Well, last I studied Digoxin used to block the NaKAtpase and thus stopping the secondary active transport of Ca leading to increased cardiac contractility. Look what I found. According to a new research its not the actual mechanism. Digoxin here, goes into the cardiac myocyte and act on Rynodine receptors instead. http://www.ncbi.nlm.nih.gov/m/pubmed/21642827/
Can somebody comment on the reliability of such articles?
Well, I had read about its action on rynodine recepters in my text book...What I know is that it acts on rynodine recepters (there is a specific name RY something which I don't remember), it increases Ca inside the sarcoplasmic reticulum of myocytes with each contraction... Meaning it sends some Ca which comes in from outside into the SR... So that the subsequent contraction is more forceful as the Ca now available from the SR is more than the prev contraction...
It's RyR2!
RyR2, yes!
Study group discussion: Why does ingestion of salt cause high blood pressure?
Why does salt increase blood pressure? I Googled it but there is no biochemical info.
Salt in the blood takes water out from cells into veins and here we got blood pressure.
Excessive NaCl ingestion or NaCl retention by the kidneys and the consequent tendency toward plasma volume expansion lead to hypertension. Nevertheless, the precise mechanisms linking salt to high blood pressure are unresolved. The discovery of endogenous ouabain, an adrenocortical hormone, provided an important clue. Ouabain, a selective Na+ pump inhibitor, has cardiotonic and vasotonic effects. Plasma endogenous ouabain levels are significantly elevated in approximately 40% of patients with essential hypertension and in animals with several forms of salt-dependent hypertension.
Source: http://www.ncbi.nlm.nih.gov/pubmed/16467498
I was reading about it and people on the internet believe that salt causing hypertension is a myth :/
It was also given on wikipedia, I donno how you missed it..
When too much salt is ingested, it is dissolved in the blood as two separate ions - Na+ and Cl-. The water potential in blood will decrease due to the increase solutes, and blood osmotic pressure will increase. While the kidney reacts to excrete excess sodium and chloride in the body, water retention causes blood pressure to increase inside blood vessel walls.
Study group discussion: Cardiac shunts and snowman sign
Congenital heart diseases
-> Right to left shunts:
Truncus arteriosus
Transposition of the heart arteries
Tricuspid atresia
Tetralogy of falloy
Total anomalous pulmonary venous return TAPVR
-> Left to right shunts:
VSD
ASD
PDA
Eisenmenger
The right to left shunts all start with T. It's a good memory aid!
Snowman sign X ray feature of?
Snow man is a type of the cardiac silhoutte, right?
Another name figure of 8 sign.
Study group discussion: Eisenmenger's syndrome
I think Eisenmenger (shunt reversal) is actually R to L shunt.
It is observed in case of L to R shunt, with time right ventricle get hypertrophied and can overcome left ventricle.
It's due to pulmonary hypertension. Reversal shunt that is. Right ventricular hypertrophy is just a consequence of PH.
And why does Pulmonary hypertension arise in that case?
Too much blood going to the lungs causes edema and hypertrophy of the pulmonary vasculature.
Increased flow of blood through pulmonary vasculature in cases of left to right shunt.
Normally, the pulmonary system is a low pressure system 25 / 8 mm of hg in compared to the normal 120/80 mm hg of systemic vessels
The pressure increases in hope to reduce blood flow through the lungs..through the shunt.
But instead of being a protective response.. It ends up making the whole situation much more severe.
Plethoric lungs, basically.
Or it Is it due to hypoxia which causes pulmonary vasocontriction which leads to pulmonary hypertension?
Yes, that's a contributory factor too
Why too much blood going to lungs.. Is it due to compensatory effort by Increasing HR?
The left ventricle is stronger than the right. So more blood goes to the right ventricle. Hence, more blood to the lungs.
It's the shunt..Left side of heart has a higher pressure compared to the right side of heart..Hence in cases of ASD and VSD.
Due to free communication.. Blood flows from high pressure to low pressure system.
In case of right to left shunts..There is obstruction which doesnt let blood enter the lungs (eg tetralogy of fellot where there is pulmonary trunk stenosis)
So a right to left shunt.
Thanks for explaining it to me, you guys!
Study group discussion: Short PR interval causes
Review question c: What are 3 causes of a short PR interval?
Wolff Parkinson White syndrome is one.
Yeah, but in general? What physiological alterations can cause that?
The re-entrant pathway.
As in... WPW causes it because it works as an accessory AV pathway.
1. Accelerated AV conduction
2. Tachycardia
3. Accessory AV pathway
Other cause is rheumatic fever.
It's one of the minor criteria for diagnosis in the Jones criteria.
Oops.. Rheumatic fever is a cause for increased PR interval.. My bad.
Study group discussion: Wolff-Parkinson-White (WPW) and increased QRS interval
Causes of increased QRS interval?
BBBs (Bundle branch block)
Electrolyte abnormalities
WPW syndrome
Electrolyte abnormalities
WPW syndrome
Medications like:
Procainamide
Tricyclic antidepressants
Tricyclic antidepressants
Study group experience #6
Here's what we discussed:
Our first group reached 100 awesomites today. So happy!
Here are a few messages from the group:
A century of awesomeness.
WOOTS PARTY AND LOTS OF MESSAGES HAHHAA.
Proud to be a part.
Proud to be a silent contributer to the 100. Been reading all your messages like a creep this entire time. Congrats!
I think I don't have enough knowledge to answer most questions here, but I do like reading yours!
Yup me too a silent one! But I really love this group. Boosts me to learn more.
Cheers to all 100 <3
WOOTS PARTY AND LOTS OF MESSAGES HAHHAA.
Proud to be a part.
Proud to be a silent contributer to the 100. Been reading all your messages like a creep this entire time. Congrats!
I think I don't have enough knowledge to answer most questions here, but I do like reading yours!
Yup me too a silent one! But I really love this group. Boosts me to learn more.
Cheers to all 100 <3
To all the new coming awesomites, since the first group is full, I'll make your group in a week irrespective of the number.
How to sign up for the group: Medicowesome study group on Whatsapp - The Official invitation
Uses of tricyclic antidepressants mnemonic
Amitryptyline for neuropathic pain.
When you say “Aah” in pain, remember Amitryptyline!
Clomipramine for obsessive compulsive disorder.
Clomi when you feel Compulsion ;)
Imipramine for nocturnal enuresis.
Eemi Eee.. will not let you pee in bed ^__^
Lame but helps :D
Saturday, February 7, 2015
Hematology and chemical pathology mnemonics
An awesomite requested for Pathology hematology bottles mnemonics. I asked him (or her) to send notes and attempted to make lame mnemonics on the same.
Uploading the notes + mnemonics for reference:
THE PURPLE ONE (aka “Lavender”)
These bottles are generally used for haematology tests where whole blood is required for analysis.
These bottles are generally used for haematology tests where whole blood is required for analysis.
ADDITIVE: EDTA (ethylenediaminetetraacetic acid)
COMMON TESTS:
Full blood count (FBC)
Erythrocyte sedimentation rate (ESR)
Blood film for abnormal cells or malaria parasites
Reticulocyte
Red cell folate
Monospot test for EBV
HbA1C for diabetic control
Parathyroid hormone (PTH)*
less commonly used for: ciclosporin/tacrolimus levels, some viral PCR tests, G6PD, ACTH level*, porphyria screen*, plasma metanephrines*, fasting gut hormone screen*
Mnemonic: PurplE
P: Parasite, PTH, PCR, Porphyria
E: EDTA
P: Parasite, PTH, PCR, Porphyria
E: EDTA
Friday, February 6, 2015
Study group discussion: Safflower, Butter and Cholesterol.
Out of butter and safflower oil.. Which of it contains cholesterol? And which doesn't, and why?
This has to be tricky.
It wouldn't be fun if it wasnt! :D
Well, defying logic, butter doesn't and safflower does?
Haha. Wrong!
Oh man. I hate vivas.
What's the reason?
Butter does because it comes from animals. Plant products never contain cholesterol, only animal products do.
Correct!
Study group discussion: Weight loss in malignancy
What's the cause of weight loss in malignancy?
Malignancy is cachexia.. Due to increased TNF and IL - 1.
Malignancy: Due to decreased appetite.
The TNF and IL - 1 decrease appetite as well as increase protein catabolism.
Study group discussion: Sweet syndrome
Has anyone out here heard of sweet syndrome?
And I checked it's not related to diabetes. -__-
Acute febrile neutrophilic dermatitis.
It is caused due to?
Acute febrile neutrophilic dermatosis (Sweet syndrome) is a reactive process (a hypersensitivity reaction) that occurs in response to systemic factors, such as hematologic disease, infection, inflammation, vaccination, or drug exposure.
Named after Rober Sweet.
Study group discussion: Necrobiosis lipoidica
What is necrobiosis lipoidica?
Which condition causes it?
Papule on Lowerlimb seen in DM.
What's DM?
Diabetes mellitus.
It's not simply a papule. It's necrosis of the skin.
Study group discussion: Cushing's syndrome
What is Cushing Reflex?
It's related to cushing syndrome or disease?
Nah. It consist of signs of Raised I.C.T: Hypertension, bradycardia, dilatation of pupil and pyramidal tract sign.
It is caused due to raised ICT?
There is more entity..Cushing's ulcer and curling ulcer. One of them is caused due to raised ICT I think. The other being a stress ulcer. Both in the stomach.
Curling ulcer is due to burns.
They both are confusing terms.
Cushing ulcer is caused when there's brain injury. With ICT as mention above
Agree.
Does anyone know the mechanism?
Cushing ulcer and Curling ulcer are peptic ulcers caused by CNS injury and burns respectively.
One possible explanation for the development of Cushing ulcers is the stimulation of vagal nuclei due to the increased intracranial pressure which leads to increased secretion of gastric acid.
Curling ulcers may be explained by a reduced plasma volume, which leads to sloughing of the gastric mucosa or secretion of burn toxins (necrotic and carbonaceous materials released from burned cells) by the stomach.
There is the cushing sign too
Must you know the difference between Cushing's disease and Cushing syndrome then?
Cushing disease is the disease caused due to a tumor of the pituitary..With increased secretion of ACTH.
The other is the syndrome caused due to excess cortisol in the blood.. Exogenous commonly. I am not sure whether adrenal tumors are also included in Cushing syndrome or not.
Cushing sign occurs as a result of Cushing reflex.
Here are study links on Cushing's!
Cushing's ulcer mnemonic: http://medicowesome.blogspot.ae/2014/03/ulcers-of-stomach-mnemonic.html
Cushing syndrome notes: http://medicowesome.blogspot.ae/2014/12/how-to-make-concise-medical-notes.html (View image)
Study group discussion: Smallest, largest and longest muscle
Which is the smallest muscle in the body?
Stapedeus.
Nope, stapedius ain't the answer.
Then?
Erector pili muscle. The one responsible for goose bumps.
Oh yes! I forget it's a muscle cause it is so small and seems insignificant.
Haha me too!
Awesome.
Largest muscle?
Gluteus maximus!
The longest muscle?
Sartorius. Originates from ASIS to Pes anserinus.
Updated on 22nd February, 2015:
I read the previous posts, errector pili -smallest smooth musle, smallest skeletal muscle -stapedius!
Smooth muscle not in our control , innervated by sympathetic system,triggering agents - cold, fear.
Which is the strongest muscle in the body?
Ahh makes sense.
Strongest would be the one in the thigh?
Gluteus maximus!
Nope.
Masseter.
True! Well done!
Shouldn't it be the quadriceps? I don't see the masseter kicking foot balls and running with the weight of the body :P
Yes, based on its weight, with all muscles working together it can close the teeth with a force of 25 kgs on the incisors.
Ooh.
Or 90 kgs on molars!
I got a good link on that!
There are lots of ways to measure strength. One is brute force, in which case biggest is best. All skeletal muscles are bundles of many individual fibers that contain small force generating structures called sarcomeres. “Generally speaking, more muscle tissue means a larger total number of sarcomeres, which means greater maximum force generation,” Tasko says. That means the largest muscles—the quadriceps on the front of your thighs and the gluteus maximus on your rear—produce the most force.
I thought the strongest was the tongue!
I was told that it was the muscle that can do the most amount of damage - the tongue (Obviously, not physical damage, you know what I mean, right?)
Oh oh most hard working muscle in the body?
Heart <3
Why not diaphragm?
Umm I donno.. Because you can have a paralyzed diaphragm and live but you can't have a paralyzed heart?
I personally think that heart is made popular for no reason :P
Study group discussion: Babinski sign
What is pyramidal tract sign?
Did you mean Babinski sign ?
There are a specific set of clinical signs for pyramidal tract disease..I haventy heard of just one particular one.. But yes, out of the many..Babinski is the most specific for pyramidal tract disease.
A few days after UMN syndrome, motor signs appear
These include spasticity, hyperactive reflexes, extensor plantar responses.
That's because the CSF will press on the cortical neurons.. And cause a upper motor neuron type of lesion.
UMN lesion is due to lesion in corticospinal tract between cerebral cortex and SC.
Well, not all pyramidal signs are called Babinski. Babinski is the extensor response to plantar reflex when the lateral surface of the feet is striken/scratched.
Achcha what are the components of the positive babinski reflex? - review question.
Extension of great toe, fanning of other toes, contraction of tensor fascia lata.
Plus, dorsiflexion of ankle and knee joint.
Yeah, that.
Other ways to elicit a babinski ?
Plus the equivalent of babinski in the upper limbs?
It's plantar reflex. It can be elicited different ways, one's babinski, others are Oppenheim and Chaddock.
Schaeffer too.
Yep.
And do you elicit Babinski with sharp end or blunt end of the hammer? (Viva question)
In Babinski, you have to produce pain and pressure both at same time so I guess blunt end if the hammer is used.
To support my answer - I have also seen many doctors using their keys (blunt end) for eliciting Babinski.
The tip of a pen can also be used to elicit Babinski.
Yeah, they taught us that we could use keys if we didn't have a hammer handy.
Always red, it looks better on a patient's foot.
In paediatrics.. We used our own nails to elicit Babinski!
I was doubtful that it would work.. But it did.. Especially, children aged below 3-5 years.
Study group discussion: Monospot test for EBV infection
Anyone explain Monospot test please!
Heterophile antibodies in the blood?
I was just reading this. The test works with the agglutination of horse's RBC when in contact with heterophile antibodies.
Yes.. Used in detection of these antibodies in infectious mononucleosis.
When you have infectious mononucleosis you produce antibodies anti-epstein barr virus and other unspecific antibodies which are called heterophile antibodies.
Aren't anti sheep antibodies produced in monospot test ?
I mean Heterophile anti sheep red cell antibodies?
That would be Paul Bunnel test.
But infected B cells secrete anti sheep red cell antibodies that are diagnosed for mononucleosis. .
I think the only difference between monospot and paul bunnel test is the origin of the RBC. In monospot they come from horses and on Paul Bunnell, from sheeps.
Study group discussion: Sarcoidosis and calcium regulation
I have a review question for sarcoidosis.
What is the characteristic appearance of sarcoidosis radiological imaging?
Lambda sign?
Panda sign?
No. Hint..That's also what tuberculosis shows positive.
BL hilar lymphadenopathy.
Tree in the bud sign.
You then differentiate it from TB ..Based on whether the lymph nodes are showing necrosis or not.
Can you elaborate on the tree in bud sign?
It's an appearance on chest CT. I read it is specific for TB and sarcoidosis.
Oh so if there is necrosis, it's Tb? If not, it's sarcoidosis?
Yup. That too can be differentiated on CT.. By looking at the lymph nodes.
I have a review question. Which cells will you see in sputum examination of a patient with sarcoidosis?
Elevated CD4/CD8 ratio.
Why is that?
I don't know exactly but CD 4 + inflammation is specific to sarcoidosis. Helps differentiate it from other non granulomatous interstitial lung diseases.
*A parallel discussion on calcium was going on, since they both are related to each other, I'm posting the calcium discussion here as well*
Percentage of dietary calcium absorbed is inversely related to intake. How is this possible?
If you take more calcium, it absorbs less? I don't know how that is possible.
The body has to maintain a homeostasis for calcium.. If reduced intake..There will be paradoxical increased receptors via Vitamin D. To maintain a constant absorption.
If increased intake..The body reduces the absorption. The mechanism..PTH is stimulated via low serum calcium.. And PTH is the one responsible to make the final active form of vitamin D.
So if calcium in the blood stabilizes, there will be reduced impulses by PTH..conversely less vitD and less absorption.
It means that if your body's need/absorption of calcium equals x.
If your intake equals x, you'd be absorbing 100% of it.
If your intake equals 2x , you'd be absorbing 50% of it.
If it equals 4x you'd be absorbing 25% of it, and so on.
At a normal steady state of absorption, the more the intake is, the less the absorption percentage of it.
Excellente.
Can anyone associate calcium and sarcoidosis?
Hypercalemia.
Why?
Because of increase in Vitamin D by granulomas.
PTH decreases then.
Which enzyme?
And which cell is involved?
It's the interstitial alveolar macrophages that secrete alpha hydroxylase that activates vitamin D.
Is sarcoidosis a cause for dystrophic calcification then?
No, metastatic.
Bravo!
Medicowesome study group on Whatsapp: The Official invitation
It started as a small experiment and turned out to be one word - AWESOME.
What's the study group for?
A bunch of medical students from all over the world, discussing study related concepts!
You may share your experiences, what you studied today, ask interesting questions to help other people learn or simply revise, ask doubts about things you don't understand, answer other people or just tell a fact you learnt that fascinates you.
We learn something new on a daily basis <3
How do I sign up for the group?
All you've got to do is message me your number. You can email me at medicowesome@gmail.com with "Whatsapp study group" in the subject.
Important: Make sure you include your proper country code when you email me your number. (Otherwise your number won't be displayed in my Whatsapp list and I might miss you out!)
After you have emailed me your number, you'll receive instructions from us.
The group is for medical students only. We do not add pharmacy / nursing / pre med students.
"I want to join but.. I'm hesitant because I'll be sharing my number to a lot of people."
It's risky, I know, but we have solutions - Block users. So I don't think you should hold back on your awesomeness. I have added over 800 people so far and they are loving it.
We have had a few spammers, flirts and inappropriate members, but we removed them. We highly encourage awesomites to report such people to the admins (We have more than 5 admins) and necessary action will be taken.
Your number will be shared with at least 100 other medical students who are strangers - So if you aren't comfortable, don't join.
-IkaN
Related post: More information on study group
What's the study group for?
A bunch of medical students from all over the world, discussing study related concepts!
You may share your experiences, what you studied today, ask interesting questions to help other people learn or simply revise, ask doubts about things you don't understand, answer other people or just tell a fact you learnt that fascinates you.
We learn something new on a daily basis <3
How do I sign up for the group?
All you've got to do is message me your number. You can email me at medicowesome@gmail.com with "Whatsapp study group" in the subject.
Important: Make sure you include your proper country code when you email me your number. (Otherwise your number won't be displayed in my Whatsapp list and I might miss you out!)
After you have emailed me your number, you'll receive instructions from us.
The group is for medical students only. We do not add pharmacy / nursing / pre med students.
"I want to join but.. I'm hesitant because I'll be sharing my number to a lot of people."
It's risky, I know, but we have solutions - Block users. So I don't think you should hold back on your awesomeness. I have added over 800 people so far and they are loving it.
We have had a few spammers, flirts and inappropriate members, but we removed them. We highly encourage awesomites to report such people to the admins (We have more than 5 admins) and necessary action will be taken.
Your number will be shared with at least 100 other medical students who are strangers - So if you aren't comfortable, don't join.
-IkaN
Related post: More information on study group
Study group experience #5
Here's what we discussed!
I particularly like how when one person answers correctly in the group, even if it's to a simple question, someone says a positive word like, "Excellent!", "Well done" or "Bravo!"
If you answer incorrectly, we'll tell you, "We are here to make mistakes so that we can avoid them in real life."
Oh and the science discussions! They make me lose my sense of time.. I feel completely enraptured. We end up in deep thought, amazed by the wonders of nature when those insightful discussions happen.
Oh and the science discussions! They make me lose my sense of time.. I feel completely enraptured. We end up in deep thought, amazed by the wonders of nature when those insightful discussions happen.
It's this kind of positive reinforcement that makes it not just a study group but a vast, open, refreshing and fascinating learning group to me.
Thank you, good hearted awesomites, to make this such a beautiful experience.
To all the future awesomites, hope you continue the legacy.
-IkaN
Thursday, February 5, 2015
The illusion of ST segment elevation in transmural myocardial infarction
To, understand the WHY of it all, we need to understand
what is the electrical vector?
1.Before the incoming of any impulse, the heart
muscle is polarized- meaning the outside of heart muscles is more positive in
compared to the inside of the heart muscle. This means that the ECF all over
the heart has a positive charge
2. With the incoming of the impulse from the S.A node, the heart muscle depolarizes..means positive ions are going inside. Which means the overlying ECF is becoming negative in compare to the surrounding area
3. This change in electrical charge, generates a current in the ECF ..this current flows from negative to positive and thus generates what is called the electrical vector
4. The electrical vector changes in size and direction as the wave of depolarization spread
5. Also, our body is a volume conductor..which means when the electrical energy flows..there is an electrical field generated around it. And different points on the field have a potential, based on their location from the electrical vector
6. When we connect two potential in this field, and measure the potential difference between them, we get the electrocardiogram (ECG)
Next important point to be understood is
how the strength of the vector is measured, whether the wave will be negative,
or positive..and what will be its strength?
The axis of the electrical field is determined from negative
to positive
Suppose there is a vector AB, what we do to measure the value of this
vector is project the same vector on this electrical field.
Hence, the strength of the voltage is +4 mv, and since the
value is positive we get a positive wave
On the other hand, this vector has a value of -3mv, and it
will be a negative wave
Whenever, there is an infarction in the myocardial
tissue..the cell looses its polarity, meaning it becomes depolarized.
So even when the whole heart is in the resting stage..there
is some amount of current flow from the infarcted tissue ( this is called funny
currents-If)
Also remember, the ST segment is an isoelectic line, meaning
there is no flow of charge in the heart muscle during this time..that is either
the heart is completely polarized ( resting stage- all over positivity outside) or the
heart is completely depolarized (all over negativity outside)
So now when you take an ecg of this heart..example with an infarction
in the anterior wall, on the V1 lead, the overall voltage of the heart is
reduced, this is because the constant flow of funny currents from anterior to
posterior. This modifies the electrical vector ( with change in its direction
and size)
But now as the wave of depolarization is completed (the QRS
complex), the funny currents are abolished..cause they too are in the
depolarized state (negativity outside). Hence, no flow of funny currents.
This makes the st segment isoelectric (that is 0mv)
When we see this graph, it seems the st segment has
elevated, but in reality it is just an illusion, cause the st segment is right
where it was supposed to be, what has changed is the voltage of the rest of the
ECG
Study group discussion: Wernicke Korsakoff syndrome
Review question:
What triad is present in Wernicke's encephalopathy?
What triad is present in Wernicke's encephalopathy?
Opthalmoplegia, ataxia and confusion.
Excellent!
What is the treatment?
Thiamine.
Route?
Intravenous or parenteral route is used.
Do we give glucose before the thiamine or after the thiamine?
Study group discussion: Somatostatin
What is the function of the hormone somatostatin? In relation to the regulation of blood sugar level?
Somatostatin is the hormone which keeps the blood glucose level smooth... Prevents fluctuation.
It inhibits both insulin as well as glucagon release, plus decreases the overall transit time of food in your GIT
Somatostatin is the reason why you need only three meals a day... It doesn't allow all the glucose to enter your body at once and maintains a continuous supply.
There is something a professor always says, "Somatostatin never met a hormone it didn't like to inhibit."
coOl.
True. I haven't come across one thing it stimulates ^_^"
Study group discussion: O negative blood group
Review question time!
Which is the universal donor?
And why?
O negative. No antigens.
But it still has anti-A and and anti-B antibody... Won't they react to the RBC present in the recipient?
Confused at the O negative thing. Will read it.
The things is when you give blood to the recipient.. The plasma in the O- blood is rapidly mixed with the 5 litres of the recipients plasma.
So the antibodies are diluted..they are not effective in causing agglutination of the recipients RBC
Why doesn't this happen with any other mis matched blood groups?
Cause in those cases the RBC's are having antigens... So they are rapidly agglutinated.
Mismatched blood transfusions are due to agglutination of donors RBC, never the recipients RBC.
Oohh yes... Cool.
Study group discussion: von Willebrand factor and disease
Drug of choice for Von Willebrand factor deficiency?
I know this! Vasopressin!
Route? :D
I think.. Nasal spray?
Yes! The drug can't be used chronically but cause it just causes release of preformed vWF factors.
vWF is for platelet adhesion.. Right? In normal haemostasis?
Yes, vWF sticks platelets to the blood vessel wall. Gp 1b helps in platelet adhesion.
It's present in Weibel Palade bodies.
What are these bodies?
Weibel–Palade bodies store and release von Willebrand factor and P-selectin. Mnemonic: http://medicowesome.blogspot.ae/2014/01/cell-mnemonic.html
And can any one name another disease related to Von Willebrand's factor? (Indirectly related)
Bernard
Sullivan syndrome.
Umm woah I didn't know so many diseases with vWF.
I was thinking of thrombotic thrombocytopenic purpura.
ADAM TS 13 is defective, which is involved in the degradation of vWF
I didn't find any Sullivan syndrome!
I think he meant Bernard - Soulier syndrome.
Bernard Soulier, you mean?
Yeah. Still spelt it wrongly.
Haha it's okay! I was spelling "Wobble palade" bodies myself. I Googled before typing it though.
Study link! http://medicowesome.blogspot.ae/2013/12/anti-platelet-drugs-receptor-and-their.html
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