Monday, February 9, 2015
Study group discussion: Why adrenaline is NOT given by the intravenous route?
Study group discussion: Calorie test and true coma
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
Electrolyte abnormalities
WPW syndrome
Tricyclic antidepressants
Study group experience #6
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
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
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*
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.