Mini mnemonic for the day!
OsGood SchaTTer: Oh God. Traction shattered my Tibial Tuberosity.
-IkaN
Mini mnemonic for the day!
OsGood SchaTTer: Oh God. Traction shattered my Tibial Tuberosity.
-IkaN
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!
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
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!
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.
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.
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!
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.
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
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!
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.
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.
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.
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)
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.