What is Virchow's triad for thrombosis? Explain please.
Virchow's triad... If there is stasis (Blood ain't flowing to wash out the collected coagulation factors), hypercoagulability (More coagulation factors) or endothelial injury (Stuff that activates coagulation factors) there'll be a predisposition to thrombosis.
In Virchow's triad 2 things are missing:
1. Role of platelets
2. Coagulation system
Which is the most common site of intraperitoneal abscess?
It's pelvic.
The reason being gravity, common sites are subphrenic, paracolic, pelvic and right iliac fossa.
Pelvic is most common due to pelvic position of appendix and fallopian tubes, and due to leakages from colorectal surgeries.
I had a MCQ asking me to choose between paracolic, subphrenic and pelvic and stuff as options for the most common site.
So in that case, what would be the answer?
Pelvic would be the most common site, according to my teachers.
What is the best way to get to a pelvic abscess sample?
Through rectum? They usually burst into rectum and resolve.
In women, from the umm what do you call it..
Pouch of Douglas!
Nice Ikan :)
I tried so hard to recall the name. Almost blanked out for a moment there!
In women vaginal drainage is done.. Through posterior fornix vaginl drainage in women.
And if the abscess is pointing in rectum, rectal drainage is done.
In males, you would pass a needle through the rectum
Laparotomy is almost never necessary and rectal drainage is preferred over suprapubic which risks exposing the general peritoneal cavity to infection.
What's Heparin induced thrombocytopenia??
Antibodies are formed in the blood platelets due to heparin in certain individuals. This causes widespread petechia.
You discontinue heparin and give something else in HIT.
Lepirudin
Bivalrudin
Argatroban
And now the cool part :D
The drug Lepirudin is derived from the salivary glands of LEECH!
I know!!!
Haha ain't this cool?
Leech.. Didn't know that!
In school, they used to say if a leech bites you, you die. I never found out the truth though.
Maybe cause it releases these substances in your system..And you are not able to clot inside?
My 12th standard books also mentioned about leech having anticoagulant properties....Now I find out that it's used to prepare drugs!
HIRUDIN is the substance that is secreted by the salivary glands of leech!
I just Googled can a leech bite kill you :D
I don't think they can kill you, they don't take enough blood in a fast amount of time unless you put a few 100,000 on your body and left them there for a while.
100, 000...That's a lot of leech!
Lol I think it was a hyperbole!
I don't remember exactly....but I had heard of alopecia being treated with leech.
How? :O
The leech would suck blood... So keeping them for just the right amount of time they would increase the blood supply... I'm not sure though.
Leech therapy is known to increase blood circulation, therefore when therapy is applied to thinning or bald areas, the increase of blood circulation helps enhance the concentration and delivery of nutrients that assist in making hair follicles strong, thereby assisting in the promotion of hair growth. People suffering alopecia caused by fungal infections or dandruff can also benefit through the antibacterial component in the leeches saliva, which helps combat fungal infections.
It's also used in arthritis :O
The FDA approved the use of leeches in the USA in 2004. In October 2005 the first American hospital 'Beth Israel Medical Center New York' offered Leech Therapy to treat Osteoarthritis of the knee.
Arthritis?! Woah.
Tell me little bit about what do you know about AV Block?
They occur when atrial depolarizations fail to reach the ventricles or when atrial depolarization is conducted with a delay. There are 3 degrees which we can recognize.
First degree consists of prolongation of the PR interval on the ECG (>200 msec in adults and >160 msec in young children).
In second degree, we can find atrial impulses that fail to conduct to the ventricles. And variations like mobitz I and II.
And finally, third degree, where we get multiple P waves that don't conduct at all.
Tell me differences in type 1 and 2 mobitz?
Well, in type I there is a prolongation of the PR interval until it drops and doesnt conduct
And in type 2, there is a constant PR interval and then it drops (:
Poem:
If your R is far from P, then you have a 1st degree.
Longer, longer, longer, drop...Then you have a Wenckebach.
If your PS don't go through, then you have a Mobitz 2.
If your PS don't agree, then you have a 3rd degree.
What's the treatment? For all of them?
First and second degree (mobitz I) only require treatment if they are symptomatic.
Mobitz II and 3rd degree usually require temporary and/or permanent cardiac pacing.
This was fun, thanks for the drawings!
*the drawings of medcomic were shared on the group, you should check them out*
Review question:
Which of the following is not a feature of complete heart block on the ECG:
a) Constant RR interval
b) Constant PP interval
c) Constant PR interval
d) PP interval shorter than RR interval
Answer: C
First, you need to get the concepts right. Speed read and get a big picture, then understand the little details.
I dived into minute things I didn’t understand right away.. Now that I look back, I think I should’ve been patient.
Anyway, lil doubts made great blog posts!
Example: Why is lidocaine preferred in patients with arrhythmias following myocardial infarction?
It’ll take time to get a hang of the names of various drugs.. If mnemonics work for you, you should try making em! Try to put mechanism in the mnemonic to make it simpler (That’s what I do!)
Here are some recent examples of how I make my pharmacology mnemonics -
Antifungal drugs with mechanisms
Antiparkinsonism drugs with mechanisms
There are certain drugs which are unique and that is why remembering mechanism of action or their pharmacological property becomes very difficult :/
I talk about how to remember them in this post --> http://medicowesome.blogspot.ae/2014/06/pharmacology-study-tip.html
I requested my study group awesomites to contribute their tips so that I can share them. Here are the suggestions, tips, tricks, life hacks they told us! :D
One awesome way is to make a self constructed table. Side by side drugs.. Uses. Side effects and specific points. Helps a lot.
- Great tip by Sakkan.
I had small classification charts put up all over my cupboard and wall! I Would revise them at night....Since I found classifications a bit volatile.
- The repetitive memorization trick was submitted by Priyanka. (I made flash cards for the same!)
One useful tip is whenever you see a sachet of drug.. Just read the contents and dosages.
- Awesome tip by Sakkan. (Wish I did that earlier!)
And try explaining uncles and aunties taking them what's going on :D
- I like how Sakkan said, "Try" explaining. (She says she gets a lot off oooo, aaa and even a couple of blank faces too!)
I always discussed pharmacology with my friends, and mostly, taught juniors. You get good karma + revision.
- Manisha (Good karma always helps!)
It is very volatile but this subject manages appear everywhere.. All subjects. Everywhere there are therapeutic drugs mentioned. Makes it really difficult to grab the essence if you don't do pharmacology.
- Sakkan's way of telling us take pharmacology seriously.
I drew small cartoons...Of concepts I found difficult to remember.
- Priyanka (Send us your cartoons soon, girl!)
Book recommendations by awesomites:
A very good book for pharmacology is Colored Atlas pharmacology. For retaining most of it. By thieme. A page of drug and a page of illustration. Very helpful.
And there's at a glance series. Exists for all subjects. Comprises cool diagrams, flowcharts and accompanied with a page of description. Pretty standard text in her very easy format.
Motsbys pharmacology memory note cards. If you like cartoons this little book is great. (It's very adorable.) I have to admit there are drawings which I dont really get. Thats why doing your own drawings also comes in handy :)
I wonder if all international students refer Katzung or whether they have local authors too.
I think Lippincott is the standard, internationally.
Lippincott is simple to understand- standard and interesting book to read.
A book very commonly referred to in India is KD Tripathi.
We have Farrukh Jabbar, here, in Pakistan.
That's all!
I'll keep updating the post, adding new tips and tricks, till then, stay awesome!
-IkaN
*We were discussing lepra reactions when we diverted to hypersensitivity reactions the other day*
I can't remember the types.
Here's a life saver for your soul - http://medicowesome.blogspot.ae/2012/03/hypersensitivity-types-mnemonic.html
Apparently there is type 5 and type 6 hypersensitivity reactions too.
5? What's type 6? Oh my god.
I had received a long fan mail on it a few days back:
We had a test about 4 days ago on hypersensitivity reaction type 5 and a lot of people left it blank because they thought it was a typo. Well, I later found out that it is the same as type 2 non cytotoxic (In fact, there is a type 6. Can you believe it? ). In situations like this, I always imagine there is a bored researcher sitting in a corner of his office, maybe eating a donut and taking a sip of milk from a beaker or conical flask, who thinks the best pass time activity is to screw around with the heads of medical students. So he gets his iPad, types a whole new ( and sometimes unnecessary) classification, sends it to a journal thus forcing medical students to add one more thing to that cramped up space called the head.
Hahahahha. The fanmail is hilarious. Made my day! :D
Myasthenia gravis? Which type of hypersensitivity reaction?
Myasthenia is type 2. So is Grave's.
Nope. It's Type 5.
Why?
Type 5 is an extension of 2.
It is because of it's blocking antibody, right? Or because it doesn't incite any inflammation?
In that case what would Graves be that antibody is stimulating?
Graves and gravis are caused due to effect of cellular functions. Graves - Increase in cellular functions. Gravis decrease in cellular functions.
"Instead of binding to cell surface components, the antibodies recognise and bind to the cell surface receptors, which either prevents the intended ligand binding with the receptor or mimics the effects of the ligand, thus impairing cell signaling.
Some clinical examples:
Graves' disease
Myasthenia gravis
The use of Type 5 is rare. These conditions are more frequently classified as Type 2, though sometimes they are specifically segregated into their own subcategory of Type 2."
- Source: Wikipedia
So type 5 includes autoimmunity, right?
Yes.
I didn't know they had classified it under autoimmunity now. Got it!
Type 6 is Antibody Dependent Cell Mediated Cytotoxicity.. The NK cell stuff.
They kill viruses laden cells and tumors.
Basically, any antibody that causes a effect besides inflammation due to binding to cell receptors is type 5.
Immunology comics on ADCC :D http://immense-immunology-insight.blogspot.ae/2013/10/functions-of-antibodies-simplified.html
Okay, review questions!
Name type of hypersensitivity!
Poison ivy reaction after 48 hours in a camping trip.
Type 4.
Correct!
A person who was given horse serum for something.
Type 3. Type 1 if he presents early!
Good job!
Person underwent a screening test for tuberculosis.
Type 4.
Excellent!
Person develops hemolysis after receiving penicillin.
Type 2.
Oh kid gets a bee sting.
Type 1.
Person with leprosy develops new lesions after starting drug therapy.
Type 3.
Awesome!
Hypersensitivity pneumonitis?
It is both type 3 as well as type 4.
Even atropine high dose causes hyperthermia. But I don't know, the mechanism to it.
Atropine is because it inhibits sweating.
Children are especially susceptible.
Oh.
Review question time B)
Name the oral anti-diabetic drugs which increase release of insulin?
Sulphonyl urea.
One more!
Meglitinides such as repaglinide and nateglinide are prandial insulin releasers that stimulate rapid insulin secretion.
So which oral diabetic drugs will you give in a thin person and a overweight one? And why?
Overweight - Metformin
Thin - Sulphonylurea
Metformin decreases gluconeogenesis.
Sulfonylurea have weight gain as a side effect. Metformin have anorexia and weight loss as a side effect.
Which of the oral drugs class is cardiotoxic? Because of which many have been with drawn from the market.
Rosaglitazone.
Correct!
Name the sulfonylureas you know.
Chlorpropamide
Tolbutamide
Glipizide
Glimipiride
Gliclazide
Glyburide
Which of these is most likely to cause hypoglycemia?
All of them?
They all do. Right.. But one of them is most likely to do so.
Glibenclamide. It is the most potent.
Nice to meet glibenclamide :P
Which type of insulin do you give in ketoacidosis?
Intravenous.
Not which route, which type?
Regular.
Correct.
The lente rapid acting type is given.
Which is given in pregnancy?
Regular insulin? The same?
Correct.
Which of these oral drugs have nausea as the main side effect?
Nausea - Umm the alpha glycosidase inhibitor?
They cause hepatitis and flatulence. So they are generally not preferred so much is what I read.
Nope. It's incretin mimetics. 40-50% patients taking incretin mimetics have nausea
Oh. I didn't know that.
An easy question - Which oral hypoglycemic drug causes lactic acidosis?
Metformin
Correct!
Which drug will you not use in renal failure? Why?
Metformin not used in renal. Same reason.
A patient has an attack of hypoglycemia while on a oral diabetic drug..He eats a spoonful of sugar. But even then he collapses and worsens. What went wrong?
Sugar needs to be metabolized @_@
^Random guesses!
Haha. No.
Must have taken complex carbohydrate. Need to use simpler ones like candy and all.
Yup. Sugar contains sucrose.
Hey I said the same thing.. Needs to be metabolized! T_T
I didn't use complex words :P
Haha! Not a convincing enough answer. But you on the right path.
Awww.
Examiner is strict!
It's okay. One point to R!
Hahaha.
Yay!
The sugar he ain't couldn't be broken down to simple sugars. Why?
He used an alpha glucosidase inhibitor! Acarbose!
Oooo that's interesting.
Correct.
Bang on!
Yaay!
He had to take glucose. Since he took sucrose (table sugar) it didn't help him.
Oh I lost the point now! :O
Nice question!
Haha we're equal now, R :P
Acarbose stops conversion to monosaccharides! So if he is on acarbose and takes a complex carbohydrate for increasing glucose levels, he won't be able to break it. Acarbose is a glucosidase that acts upon 1, 4 - alpha bonds which breaks down starch and disaccharides to glucose.
Sucrose is a disaccharide (table sugar) so yeah.
Easy question - what is the effect of insulin on potassium?
Hypokalemia.
Why is it clinically relevant in a patient with diabetic keto acidosis?
Need potassium supplementation along with insulin. Otherwise hypokalemia occurs. Causing cardiac and other emergency conditions.
Causes insulin causes the uptake of potassium by cells. Therefore, in hyperkalemia, the main line of management is giving insulin along with glucose.
Correct!
Why isn't bicarbonate preferred in patients with DKA?
Good question. I wonder about that answer too.
Tell us?
It causes cerebral edema.
Oh. If given in large doses?
Nope. Not dose related. Only in children though.
Can you explain?
Needed a research paper to back me up -
Adverse effects of bicarbonate therapy in DKA: In essence, possible mechanisms include initial cerebral vasoconstriction and reduced cerebral blood flow from acidosis and hypocapnia, cytotoxic edema, and cerebral injury, followed by cerebral hyperemia, reperfusion injury, and vasogenic edema, coupled with increased blood brain barrier permeability, during the rehydration phase of DKA. Several reports of sudden death following irreversible coma in children and young adults with DKA were published in the 1960s, including development of diabetes insipidus in some, with postmortem findings of CE and neuronal degeneration.
I'll send you the link.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3224469/
Read: Clinical impact of bicarbonate therapy in DKA
The paper is huge, read that specific part.
Thanks!
