Study group discussion: Drugs used in the treatment of Alzheimers disease

Can anyone help me with pharmacological classification of anti Alzheimer's agents?

For Alzheimers, cholinesterase inhibitors.. And a drug called memantine.

NMDA receptor antagonists.

Drugs: Tacrine (tetrahydroaminoacridine), donepezil, rivastigmine and galantamine.
Mechanism: Inhibition of cholinesterase, with a resulting increase in cerebral levels of acetylcholine.

Antioxidants, selegiline, tocopherol (vitamin E), estrogen replacement in females, Ginkgo Biloba extracts are other drugs which may benefit in Alzheimers disease.

Study group discussion: Eponymous terms in hernia and mnemonics

Here's a list of eponymous hernia terms I was sent. I added a few mnemonics to where I could. Others you'll have to memorize!

Gibbon's hernia- Hernia with hydrocoele

Berger's hernia - Hernia in Pouch of Douglas
Mnemonic: Burgers are made of dough.

Grynfelt's hernia - Upper lumbar triangle hernia.

Petit's hernia - Lower lumbar triangle hernia

Cloquet's hernia- Hernia through pectineal fascia
Mnemonic: The hernia is cloaked, peccantly.

Narath's hernia - Behind femoral artery

Hesselbach's hernia - Lateral to femoral artery
Mnemonic: hesseLBAch - Lateral to big artery.

Serofini's hernia - Behind femoral vessels
Mnemonic: SeroFini - Supported by femoral vessels.

Laugier's hernia - Through lacunar ligament
L for Laugier's, L for Lacunar

Tealse's hernia - In front of femoral vessels

Richter's hernia - Part of circumference of bowel wall is gangrenous
Mnemonic: Richie rich has a large circumference pocket of money.
Alternatively, riChter Circumference.

Littre's hernia - Hernia with Meckels's Diverticulum
Mnemonic: Meckels is a congenital defect, found in Little babies.

Sliding hernia - Posterior wall of sac is formed by colon or bladder

Maydl's hernia - 'w' hernia
Mnemonic: M upside down is W.
Phantom hernia - Localised muscle buldge following muscular paralysis
Mnemonic: Phantom for Phantom, P for Paralysis

Spigelian hernia - Through spegelian fascia

Obturator hernia - Through obturator foramen

Femoral hernia - Hernia medial to femoral vein

Beclard's hernia - Femoral hernia through saphenous opening

Study group discussion: Biliverdin

Why biliverdin is reduced to bilirubin? It isn't toxic, it is water soluble.. Then why convert it to bilirubin?

According to some, biliverdin works just fine. Mammals have evolved the energetically expensive, potentially harmful and apparently unnecessary capacity to reduce biliverdin.

According to others, the conversion is not a wasteful process. Bilirubin is a cytoprotectant and that's why biliverdin is converted into bilirubin. It's also a physiological anti oxidant!

Source: http://m.pnas.org/content/99/25/16093.full

About me!

Hello there awesomites! Feels great to write this for Medicowesome :-)

Where to start? Well, I am a total  astrophysics geek. Anything -spacetime,dark energy, black holes, wormholes catches my fancy.That type of guy who loves staring at the starry sky. Just finds amazing how the tiny word 'universe' encompasses the massive expanse lying out there. Loves going to the point where physics meets philosophy.

Likes looking into nothing, thinking and imagining.

House MD fan. Sherlocked.
Christopher Nolan worshipper. Interstellar fanatic.

I have a thing for rare, fancy medical syndromes! Dreams include running a diagnostics department like House. :-p

Talking of music,a Linkin Park fan, like the regular Bollywood music too.

Proud of India and its rich heritage.

Hobbies include driving cars, riding bikes and even bicycling. Gaming included.

Finally, an animal lover,dreamer and a bit of foodie..

-Sushrut



Posted via Blogaway

Heme synthesis mnemonic

Hey everyone! Long time no see!

Today we'll be learning about heme synthesis.

The biosynthesis of heme mnemonic 

Study group discussion: Temporal arteritis

A 60 year old male presents with headache, scalp tenderness, painful temples, pain on chewing & visual disturbances.. Diagnosis?

Answer: Temporal arteritis

What tests you would do to confirm the diagnosis?

Answer: Raised ESR, temporal artery biopsy

Treatment?

Answer: High dose steroids like prednisolone!

Temporal artery branch of?

Answer: ECA, the external carotid artery!

Study group discussion: Causes of edema

Today, we'll be talking about causes of edema.

Causes of Edema can be inflammatory and noninflammatory!

Noninflammatory causes:
1) Increased hydrostatic pressure
2) Hypoproteinaema
3) Lymphatic obstruction
4) Sodium retention

Inflammatory causes:
1) Acute inflammation
2) Chronic inflammation
3) Angiogenesis

Here is a mnemonic shared by an awesomite: HILARI IS SAVE (Hilary)
Heart failure
Iatrogenic
Liver causes
Aldosterone increased/ ADH increased
Renal cause
Inadequate protein in blood (hypoalbuminaemia)

Causes for the inadequate protein in blood are:
Intake Inadequate (Kwashiorkor)
Secretion fro pancreas decreased (pancreatitis)
Synthesis decreased (liver failure)
Absorption decreased (Crohn's disease)
Vomit (pyloric stenosis)
Excretion increased (nephrotic)

I remember this in Conrad Fischer's tone, "Cirrhotic, Nephrotic and CHF. Cirrhotic, Nephrotic and CHF!" though.

That's all!

-IkaN

Study group discussion: Drugs contraindicated in myasthenia gravis

Hey everyone!

Today's topic is about drugs that are contraindicated in myasthenia.

Can you guess them all?

Drug a. Myasthenic woman with eclampsia develops ptosis

Drug b. Patient with hepatitis C develops respiratory depression

Drug c. Filmstar drug

Drug d. Wilson's disease

Answers:
a. MgSO4
b. Interferon
c. Botox
d. Penicillamine

Random fact:
The actor, Amitabh Bachchan has interferon induced myasthenia gravis which was used to cure his hepatitis C infection. And because of that he can't use botox.. Hence, his skin looks so wrinkled compared to other film stars of his age. Hence, two important drugs causing myasthenia and who worsen it are interferon and botox.

More information on study group

Here is some more information, since people have been asking!

How do I join?

Click here!

Can I view the group discussions without being on the group?

Yes! View the Study group index. All topics discussed may or may not be posted on the blog, do to time limitation, of course.

Study group discussion: Evening rise of temperature in tuberculosis and malaria

Why is there an evening rise of body temperature in tuberculosis?

Answer: Because endogenous corticosteroid have their levels low in the evening. Cortisol bursts are least frequent in the evening. And steroids are anti-inflammatory!

Why not in all infections? What's special about tuberculosis?
We don't know the answer to this question. If you do, please tell us!

This answer was submitted to us by an awesomite: Increased Cortisol Cortisone Ratio in Acute Pulmonary Tuberculosis: Recent research works regarding TB has revealed that there is increased cortisol level in TB.
Cortisol & IL-1 interaction: At high level cortisol has negative feedback effect on IL-1.
Conclusion: In TB, cytokines, specifically, IL-1 level is markedly increase that leads to fever, but as cortisol level is also high than normal it counteract the action of IL-1 & as a result fever remains low grade.
Due to exaggerated diurnal variation,cortisol effect is very high in late night while very less in evening onwards that leads to evening rise of temperature & night sweating. Normal diurnal variation of body temperature also play a role to make this change more prominent.
Source: http://www.doctorshangout.com/m/blogpost?id=2002836%3ABlogPost%3A423964

Even malarial paroxysms occur in the evening, don't they?

Answer: Yep. Malarial paroxysms have a different reasons. Steroids ain't responsible.

What's the reason for malarial paroxysms then?

Answer: It depends when the entire cycle of trophozoites burst from RBC's.

Here's from one of the members personal experience:
I have had malaria.. I had paroxysms at late night.

Study group discussion: Smoking and hernia

I have a doubt .. Today in surgery ward, my professor asked me how does smoking directly cause hernia! :/

I know the indirect cause! Coughing!

By weakening collagen?

Does smoking affect collagen synthesis or metabolism? At which step does smoking affect collagen?

It causes less production!
The synthesis of subcutaneous collagen in smokers is specifically impeded, indicating an impaired wound-healing process. Because mature collagen is the main determinator of strength of an operative wound, the results support the view that patients should be advised to stop smoking before an operation.
Source: http://www.ncbi.nlm.nih.gov/pubmed/9551072

In conclusion, smoking is an important risk factor for recurrence of groin hernia, presumably due to an abnormal connective tissue metabolism in smokers.
Source: http://www.ncbi.nlm.nih.gov/pubmed/11910469

Oh....ok. Thanks!

Autonomic system drugs mnemonic

Please give some tips on remembering cholinergic and adrenergic drugs.

- ine are beta agonists
(Terbutaline, ritrodine)

Drugs ending in

-sin are alpha antagonists 

(Prazosin, terazosin)

- olol are beta blockers

(Propanolol, metoprolol)

- alol are alpha + beta blockers (Labetalol)

- stigmine are cholinergic drugs
(Neostigmine, physiostigmine)

Alice in Wonderland syndrome

Came across this interesting syndrome a few days back. Described by Dr. John Todd 1955, it is also known as Todd's syndrome or lilliputian syndrome. The causative factors involved are usually migraines, tumors or hallucinogens. Epstein Barr virus is also thought to be associated with it.

Study group discussion: Structures that pass through the diaphragm mnemonic

When we go to thorax or abdomen... It's hard to remember their relation... Are there any tips?

What sort of relation? The relation of structures that pass through the diaphragm?

Yep.

Ok I know one mnemonic for that.

I ate (8) ten eggs at twelve.

I: Inferior vena cava
aTe: T8!
Eggs: Esophagus (Vagus rhymes with it!)
Ten: T10
AT: Azygous vein, Thoracic duct! Twelve: T12

So to summarize:
IVC - T8
Esophagus, vagus - T10
Azygous, thoracic duct - T12

Hope this helps!

Study group discussion: Purtscher's retinopathy

Does anyone know the name of retinopathy occurring in pancreatitis?

Purtscher's retinopathy!

What are it's characteristics?

Signs visible on fundoscopic examination include
pathognomonic Purtscher flecken and cotton-wool spots around the optic nerve n intraretinal h'age

Yes. The macula is affected too. Granulocyte deposition occurs in the posterior retinal artery.

Study group discussion: Chloroquine and Behcets disease

Antimalarial that causes irreversible retinal toxicity??

Chloroquine?

Yes. It's hydroxychloroquine..!!

Also used in...??

DLE, rheumatoid arthritis!

Lepra reactions too!

Also in extra intestinal amoebiasis!

Skin lesions in dermatomyositis!

Okay, so what pathology in the eye does hydroxychloroquine cause..??

It accumulates there because of high volume of distribution?

It causes Bull's eye maculopathy..!!

And the pathogenesis?

It is said that the drug binds to melanin in the RPE, which could explain the persistent toxicity even if after discontinuation of the medication!!!

I remember the use of hydroxychloroquine (Plaquenil) in Behcet's Disease. Follow up with eye exam every 2-3 months.

What's Behcets disease?

Behcets syndrome is inflammatory, multi system disease of small vessels resulting in frequent aneurysms and rupture..!! Eyes, genitals and mucous membranes are involved.

It takes many months to treat genital ulcers!

What is that test to confirm behcets..??

Pathergy test

Pricking the skin with a needle = pathergy test. After one or two days, people with Behçet's can develop a lump or nodule where the needle broke the skin.

Correct!

I had a patient with several mouth ulcer's looking like Aphthous ulcer. No other symptoms, just episodic mouth ulcers!

Okay.. Could be due to stress and vitamin deficiency..

And it turned out to be Behçet's disease.

They have a lot Behçet's disease clinic's in Turkey! Must be genetic which is why it is so common.

The exact cause of the disease remains unclear. But Behçet's disease is thought to involve an autoimmune response. This means the body's defense mechanism begins to attack its own tissues. Something in the environment may trigger this abnormal immune response in susceptible individuals. Genetic factors may also play a role.

It is common in young men in Mediterranean area..

Our patient was a woman.

Oh nice to know, thanks!

Study group experience #14

Cutaneous signs of insulin resistance and lipoproteinemia

Diabetes 

Electrolyte abnormalities that cause constipation 

Biceps femoris reflex

Scissoring posture 

Aspirin 
Cycloserine 
Morphine and atropine 
Drug for neurological manifestations of Wilson's disease 

ACE in lung diseases 
Central trachea in pleural effusion 
Walking pneumonia 

Aortic regurgitation 
Pressure and volume reservoir in the human body 
HOCM 
Cardiac embryology and fetal heart sounds 
Atrial septal defects - Why do they present late? 

Gallstone ileus
Hepatic encephalopathy 
Kartageners syndrome 
Haemosiderosis and haemochromatosis

Thyroid surgery practicals viva questions 
Venous ulcer 

Pre-eclampsia and HELLP syndrome 
Differentials of discharge in a pregnant woman 

Glycogen storage diseases mnemonic
Cytochrome c 
Agranular cytoplasmic reticulum
Colorful amino acids and pH

Difference between antibody and anti-toxin 

Lymph nodes in various diseases 

Chionablepsia and Anisakiasis

It's been a crazy busy week, especially with group 3 and all, I stay on my toes!

-IkaN

Study group discussion: Haemosiderosis and haemochromatosis

Differences between haemosiderosis and haemochromatosis?

Haemochromatosis is iron overload primary and secondary, iron overload is within cells and interstitium, causes tissue damage. Hemochromatosis is primarily genetic!

Where as haemosiderosis  is a form of secondary hemochromatosis due to repeated blood transfusions, deposition of haemosiderin in the cells, with reversible accumulation of iron in RES. I hope its clear!

So heamochromatosis is irreversible?
The tissue damage, I agree, will have consequences. But you can chelate the excess iron?

Yes! But reversible if in the form of secondary- haemosiderosis

Blood letting! Pts encouraged to donate blood it seems, and iron chelating agents would help.

Those untreated develop HCC
Even cardiomegaly
And endocrine issues.. Especially, pituitary and the adrenals

Yeah I think they continuously need to get their iron chelated

So it can be counted as reversible then?

Not reversible..But manageable.

Yes that's a good term actually

Controllable I would say!

Heart failure cells are macrophages laden with haemosiderin in LVF OR pulmonary odema.

Was an episode in house MD. The girl was suspected to have it cause her skin tone had changed several tones darker.

There was this one more episode where they diagnosed Wilson's disease based on the colour change of nailbed on rubbing it with nail remover! I so want to try that.

Really ?

The blood copper level wasn't raised.. No kf rings in cornea.
The lady was a mean woman.. She couldn't feel emotions.. Was manipulative. And the change in personality happened when she was a teenager.

Interesting!

They applied nail remover and behold.. The  nail turned blue.
I had a suspected case of Wilson's disease in my college.. She took discharge before I could experiment this.

There is even one more episode on Wilson's in season 1. They diagnose it by observing KF ring over the cornea.
Also, an another episode on Hemochromatosis with a mean chess playing lad.

Yup.. I remember both the episodes! The alcoholic mom with schizophrenia had Wilson's. And the jerk xD

Yeah! Actually, she did not have schizophrenia. They were the manifestations of Wilson's itself.

It was pretty cool how House figures that self sacrifice isn't a symptom of Schizophrenia

Yeah! I love the way House has epiphanies leading to diagnoses.

Study group discussion: Haemosiderosis and haemochromatosis

Differences between haemosiderosis and haemochromatosis?

Haemochromatosis is iron overload primary and secondary, iron overload is within cells and interstitium, causes tissue damage. Hemochromatosis is primarily genetic!

Where as haemosiderosis  is a form of secondary hemochromatosis due to repeated blood transfusions, deposition of haemosiderin in the cells, with reversible accumulation of iron in RES. I hope its clear!

So heamochromatosis is irreversible?
The tissue damage, I agree, will have consequences. But you can chelate the excess iron?

Yes! But reversible if in the form of secondary- haemosiderosis

Blood letting! Pts encouraged to donate blood it seems, and iron chelating agents would help.

Those untreated develop HCC
Even cardiomegaly
And endocrine issues.. Especially, pituitary and the adrenals

Yeah I think they continuously need to get their iron chelated

So it can be counted as reversible then?

Not reversible..But manageable.

Yes that's a good term actually

Controllable I would say!

Heart failure cells are macrophages laden with haemosiderin in LVF OR pulmonary odema.

Was an episode in house MD. The girl was suspected to have it cause her skin tone had changed several tones darker.

There was this one more episode where they diagnosed Wilson's disease based on the colour change of nailbed on rubbing it with nail remover! I so want to try that.

Really ?

The blood copper level wasn't raised.. No kf rings in cornea.
The lady was a mean woman.. She couldn't feel emotions.. Was manipulative. And the change in personality happened when she was a teenager.

Interesting!

They applied nail remover and behold.. The  nail turned blue.
I had a suspected case of Wilson's disease in my college.. She took discharge before I could experiment this.

There is even one more episode on Wilson's in season 1. They diagnose it by observing KF ring over the cornea.
Also, an another episode on Hemochromatosis with a mean chess playing lad.

Yup.. I remember both the episodes! The alcoholic mom with schizophrenia had Wilson's. And the jerk xD

Yeah! Actually, she did not have schizophrenia. They were the manifestations of Wilson's itself.

It was pretty cool how House figures that self sacrifice isn't a symptom of Schizophrenia

Yeah! I love the way House has epiphanies leading to diagnoses.

Study group discussion: Haemosiderosis and haemochromatosis

Differences between haemosiderosis and haemochromatosis?

Haemochromatosis is iron overload primary and secondary, iron overload is within cells and interstitium, causes tissue damage. Hemochromatosis is primarily genetic!

Where as haemosiderosis  is a form of secondary hemochromatosis due to repeated blood transfusions, deposition of haemosiderin in the cells, with reversible accumulation of iron in RES. I hope its clear!

So heamochromatosis is irreversible?
The tissue damage, I agree, will have consequences. But you can chelate the excess iron?

Yes! But reversible if in the form of secondary- haemosiderosis

Blood letting! Pts encouraged to donate blood it seems, and iron chelating agents would help.

Those untreated develop HCC
Even cardiomegaly
And endocrine issues.. Especially, pituitary and the adrenals

Yeah I think they continuously need to get their iron chelated

So it can be counted as reversible then?

Not reversible..But manageable.

Yes that's a good term actually

Controllable I would say!

Heart failure cells are macrophages laden with haemosiderin in LVF OR pulmonary odema.

Was an episode in house MD. The girl was suspected to have it cause her skin tone had changed several tones darker.

There was this one more episode where they diagnosed Wilson's disease based on the colour change of nailbed on rubbing it with nail remover! I so want to try that.

Really ?

The blood copper level wasn't raised.. No kf rings in cornea.
The lady was a mean woman.. She couldn't feel emotions.. Was manipulative. And the change in personality happened when she was a teenager.

Interesting!

They applied nail remover and behold.. The  nail turned blue.
I had a suspected case of Wilson's disease in my college.. She took discharge before I could experiment this.

There is even one more episode on Wilson's in season 1. They diagnose it by observing KF ring over the cornea.
Also, an another episode on Hemochromatosis with a mean chess playing lad.

Yup.. I remember both the episodes! The alcoholic mom with schizophrenia had Wilson's. And the jerk xD

Yeah! Actually, she did not have schizophrenia. They were the manifestations of Wilson's itself.

It was pretty cool how House figures that self sacrifice isn't a symptom of Schizophrenia

Yeah! I love the way House has epiphanies leading to diagnoses.

Study group discussion: Hepatic encephalopathy

In liver failure, what is the cause of hepatic encephalopathy?

They are not sure yet but they think it's ammonia.

Yes, NH3 and other substances.

They act as pseudotransmitters.

But how do ammonia levels rise?

Liver detoxifies ammonia by forming urea.. Failure to convert ammonia into urea.

Since liver is damaged.. Ammonia rises.

Does it occur on inhaling ammonia?

You mean, inhaling ammonia when liver is damaged or in normal people? Ammonia is an irritant to the 5th nerve, if I am not wrong. Why would anyone inhale it for a long time?

If by an accident?

Umm. I haven't heard of a situation like that

We inhale ammonia everytime we pass an unclean public toilet! :P

Argh.

Hahaha!

Study group discussion: Walking pneumonia

What is walking pneumonia?

Walking pneumonia is generally atypical pneumonia. It's called walking because even though you feel sick, you are not sick enough and you're walking around unlike the usual can't-get-out-of-bed pneumonia patients.

These patients have an interstitial inflammation that does not cause a consolidation like that of typical pneumonia.

Common causes include Mycoplasma pneumoniae and Chlamydia pneumoniae. 

Study group discussion: Venous ulcer

*a picture of an ulcer was posted on which this discussion took place in the group*

Which side is the lesion on? Medial or lateral?

If it is medial, it can be venous ulceration too! Mass obstructing the venous outflow.

Yup could be as it is superficial.. And also it could be venous ulcer because it looks like the ulcer is in gaiters area..above the medial malleolus..

What is gaiters area?

Gaiters area is where venous ulcers are usually seen. Above medial malleolus!

Where there is highest preasure in vein due to gravitational pull! And incompetent valve also in varicose vein

What's the name of the perforator in that area?

They are cockett boyd dodd and hunter from below upwards.

I have a mnemonic for the perforators

Do share!

http://medicowesome.blogspot.ae/2014/09/types-of-perforators-of-lower-limb.html

Study group discussion: Kartageners syndrome

What is Kartagener syndrome?

Immotile cilia syndrome

May result in Situs inversus
Bronchiectasis
Sinusitis

Glue ear too!

Infertiliy? Sperm motility is also affected i guess

Sperm motility is affected.
The protein involved is 'dynein'.

I've seen a case of Kartageners in my hospital. The auscultation and looking at radiographs was fascinating!

Study group discussion: Gallstone ileus

*a picture of gall stone ileus was posted in the group as guess the diagnosis after which this discussion took place*

Commonest position of obstruction by gallstone in ileum

Ileocaecal junction?

Not ileocaecal valve. The position in books have been mentioned terminal ileum. A little proximal to the ileocaecal valve.

Most commonly, obstruction occurs at the distal ileum.

I didn't know gallstone ileus could be this big. I imagined them to be tiny!

Me too!

I've heard there has to be a fistula for the stone to be that big to obstruct the ileum. Something that connects the gall bladder to the intestine.. Because a stone this big wouldn't pass the common bile duct

I agree with IkaN

Yup I'm sure the patient suffered from a fistula too..

It enters the intestine through cholecystoduodenal fistula commonly..

I've heard my resident mention fistula once

Yep.. And the predisposed patients are those with Crohn's disease! Thanks, just wanted to confirm it :D

Large stones, >2.5 cm in diameter, are thought to predispose to fistula formation by gradual erosion through the gallbladder fundus...

Ohh that makes sense! The huge stone itself causes fistula formation which is why they are common!

"A fistula develops between a gangrenous gallbladder and the duodenum or other parts of the gastrointestinal tract, allowing passage of the stone. Occasionally the stone may enter the intestine through a fistulous communication between the bile duct and the gastrointestinal tract."

Study group discussion: Colorful amino acids and pH

Colorful aminoacids?

Donno. Maybe tyrosine because they add pigment?

Trytophan phenylalanine tyrosine. Tryptophan is major!

They add color to us! Makes sense. At first, I have to admit, I was imagining colors of the rainbow xD

Yeah and remaining are colorless!

At physiological pH what is the charge of amino group and Carboxyl group?

Positive amino negative carboxyl
PANCard

That's a good mnemonic! Will never forget this!

I just remember histidine is the one who is neutral at physiological pH.

Name the positively charged amino acids!

Basic are positively charged I guess. Histidine lysine arginine.

Mnemonic! http://medicowesome.blogspot.ae/2013/11/amino-acids-with-electrically-charged.html

IkaN mnemonic wow <3
Lady gaga is always negative hahaha!

Study group discussion: Cytochrome c

What is moonlight effect of cytochrome c?

Sounds interesting!

Cytochrome c in cytosol cause cell death by apoptosis. Cytochrome c in mitochondria helps in electron transport. This dual function!

Ooo.. Yes, the life maintainer and the killer! Why moonlight though?

Moon light means a job on the side, one that you wouldn't wanna disclose.
I have a question, what is the differences between cytochrome c1 and cytochrome c?

I think cyt c is mobile and the other is not.

Yep.

Study group discussion: Agranular cytoplasmic reticulum

What are the functions of agranular cytoplasmic reticulum?

Synthesise lipids, transportation of proteins,enzymes for detoxification of drugs,enzymes of glycolysis.

Study group discussion: Atrial septal defects - Why do they present late?

Why do ASD present later in life?

You mean atrial septal defects?

Yup.

The left atria is stronger than the right, so it's a left to right shunt, initially (Oxygenated blood getting more oxygenated kind of shunt.)
This is why, ASD is acyanotic at birth. It won't present till there is pulmonary hypertension (The lungs get fed up of the excess blood!)
This will cause a reversal of shunt - turning it into right to left. (Now, the deoxygenated blood is getting thrown into circulation!)
This reversal is also known as Eisenmenger's syndrome.
This is why, ASDs present late in life.

Okay.. So I think the compensatory mechanisms make up for the disturbances in circulation in early years but fail later hence the features appear later..

Also the atria contribute very little as compared to the ventricles.

Atrial defects are usually very small thus, less complications in infancy. And also murmurs heard in ASD are not very loud, so its difficult for a physician to detect it.
I think, it becomes complicated due to development of Eisenmenger syndrome in later years.

Yes.. And the patient hardly survive 5-6 yrs after development of Eisenmenger syndrome..

Sometimes, ASDs never get severe enough to present as a heart disease. A paradoxical embolus is the initial presentation of an ASD in some cases!

Study group discussion: Cardiac embryology and fetal heart sounds

Cardiac Embryology review question! Which blood vessel does the 6th arch artery give rise to?

Pulmonary arteries!

Common carotid artery derived from..??

3rd arch

Right!

Here's a mnemonic on the derivatives of arch arteries http://medicowesome.blogspot.ae/2013/11/aortic-arch-derivatives-mnemonic-images.html

The coronary arteries develop from which structure?

From aortic sinuses of valsalva..??

Endothelial tissue grows out of the aortic wall and connects with the subepicardial vessel plexus while the heart is developing to form coronary arteries.. Is that right??

Ya.. At first the cells are derived from venous sinus  then they transform to become arteries.

When does heart start pumping ?

I am guessing its 4wks?

First heart beat by 4 weeks!

When does the fetal heart beat for the first time in utero? And when is the heartbeat detected by ultrasound? I know 4 weeks is when the heart starts pumping but is it the same time we detect through USG?

I think there are 2 different terms!!
Fetal heart motion around 5-6 weeks
Fetal heart sounds can be heard around 8-10 weeks

Ohh.

Fetoplacental unit establishes around 21-22 days following fertilization.
Fetal heart motion: 9 weeks by doppler USG.
Fetal heart sounds 18-20 weeks by stethoscope.

When does the  fetal movements start?

18-20 weeks?

That's probably right. I know mothers start noticing moviments from 20th week on. a bit later if it is their first child and they don't how to recognise the sensation.

Yep. Multigravidas appreciate fetal movements earlier than primis

In 16 to 18 wks - That's for multigravida.

But fetal movements start at 8-9 weeks. They are perceived late I guess!

In what case foetal heart fails to mature enough such that we can't detect sounds even at 8w?

One case would be hydatidiform mole. No heart sounds heard.

I don't know what is a hydatidiform mole.

Hydatidiform mole isn't a fetus. It's a edematous condition of the Placental villi. You'll learn this is second year, Pathology!
There is no fetus or fetal parts. Not compatible with life... You'll have to read it up from books.

Here are some study links!
Embryology and gestational trophoblastic disease 

Difference between complete and partial mole mnemonic

Hydatidiform mole (Complete vesicular mole) mnemonic

Why is such a gap between starting of heart beats and its detection by US ??

I mean heart starts beating at around 4w and heart beats are detected at around 8w .. why so ?

That's a very interesting question.. But I have no idea regarding that!

Theories:
Maybe because motion is there but structurally heart is immature so no sound is there (av valve)

I think we don't have equipment to detect faint sounds. We could detect heart sounds along with the motion if we had the technology!
Maybe you guys will invent a fetoscope that detects it earlier in the future! :D

Study group discussion: HOCM

A young, apparently healthy athlete, while playing collapses to the ground and dies.. Diagnosis?

Hypertrophic obstructive cardiomyopathy.

Right, as always!

Will probably also have family history!

Oh oh review question - what is the site of obstruction in HOCM?

Ventricular septal wall?

Interventricular septum.

Left ventricular outflow is obstructed.

Yup. Basically below the outflow tract of the aorta.

What will happen to the intensity of the murmur in HOCM during Valsalva maneuver?

It will increase. HOCM and MVP are the only two conditions in which a decrease in blood volume to the heart increases the intensity of the murmur.

What's Brugada syndrome??

In Brugada syndrome there's risk of sudden cardiac death.. And it's also genetic..

Oh.. Didn't know. What is the defect in brugada syndrome? In HOCM it is beta myosin I guess.

Some defect in sodium or calcium channels I guess.. Not sure.

Ohh okay. Thanks!

Study group discussion: Differentials of discharge in a pregnant woman

Differentials of 28 week primi presenting with white discharge?

You wanna see for pooling of fluid in the fornices and check for pH.
It could be premature rupture of membranes. It could be stress incontinence. It could also be a normal excessive discharge.

Could it be infection?

Yep, it could be.

Depends on the quantity of discharge.

Um okay..

I had a case on this in my final year university exam
The entire viva went on it!

Mine was normal physiological discharge with oligohydramnios.

Study group discussion: Aortic regurgitation

What are the characteristic physical findings in aortic regurgitation?

You mean the characteristics signs from head to toe?

No, some special findings are present.

Collapsing pulse.

Yes, the water hammer pulse!

It was my viva question. I was asked to demonstrate it!

What else?

Like signs? Like pulsations at nail bed!

Yeah what's that called?

Pulsations at nail bed?

Quinckes sign!

Yes, exactly Quincke.

Hills sign.

The hills sign is the most significant.

What is hill sign?

Low BP in the upper limbs.

Upper limb bp is higher than lower limb.. Or vice versa.

Yup..right.. Cuz there's a difference of >10mmhg in upper and lower limbs..

And obviously, wide pulse pressure.

Plus, there is this austin flint murmur characteristic of severe AR.

Mullers sign - Pulsations of the uvula

Corrigans sign - Carotid pulsation visible

Landlof's sign

Oh landolf's sign is alternate dilatation and constriction of pupil with each heart beat.

I know Mussetts - the head bobbing

Traubes, I think, is shotty femoral pulse!

Lighthouse sign!

Lighthouse sign is blanching and flushing of forehead with each heart beat..

Duroziez - murmur over femoral artery

Locomotor brachii.

What's that?

Oh yes.. Locomotor brachii is the Thickened, tortuous brachial artery on Inspection.. You can see the twitchings clearly especially on the medial side of arm.. It basically indicates hypertension but commonly associated with AR.. I've seen it in patient with AR..

Which is the most diagnostic sign? Which is the most important of all the signs of aortic regurgitation?

The diastolic murmur is diagnostic of all!

Even mitral stenosis has a diastolic murmur! It should be Hills!

In MS, we also have the opening snap.. You need practice to be quick in identifying the psa and opening snap. Where as hills can be diagnosed with a BP cuff!

And there is difference in the sounds too.

Theoretically, we read that.. Frankly, I find it a great achievement if I can only say with confidence whether it's diastolic or a systolic murmur.

True!

Haha that's the truth actually!!

Aortic regurgitation -Soft blowing early diastolic decrescendo murmur.
Heard best at the left 2nd ICS without radiation.
May also hear systolic flow murmur and diastolic rumble (Austin Flint)

Mitral stenosis -Low frequency rumbling mid-diastolic murmur, with presystolic component possible.
Heard best at apex.
Accentuated in left lateral decubitus position.

What's the amount of blood regurgitated in aortic regurgitation?

Its 25% of ejection fraction

In mild AR?

Ya

What about moderate and severe types?

Maybe increases, I have to check.

It does. But since you were specific to say 25% There has to be specific values of the other two classes as well.

In severe, its more than 50%  I think, correct me if I'm wrong.

Will check out my books.

I had an aortic regurgitation case in my finals too.
I thought I was reading the blood pressure wrong but... The diastolic was 20mm Hg.
It can go so low.. The diastolic can even go till zero is what my professor said!

Study group discussion: Diabetes

I've noticed one thing with my "swedish" medical book.... It always give glucose values in ( mmmol/l ) and not ( mg/dl )

fP-Glucose > 7,0 mmol/l
How much mg/dl is that ?

The conversion factor is   mg/dl= 18 x mmol/l
So 7mmol/l is 126mg/dl
I'm actually majoring in pharmacology :) we had a lot of those ^^

HbA1c < 52 mmol/l = 6 %
For diabetes type 1
Hemoglobin A1c level should be held at 6%
I'm reading about diabetes type 1 treatment
And it's written here HbA1c level should be held < 52 mmol/mol
equals to 6%

*a conversion table was posted on the group by someone which sorted this dilemma*

That might be possible but for the diagnosis it is >6.5

You don't use A1c for diagnosis. It is used only for evaluating control over the last few months!

But now if it's >6.5 he is diagnosed diabetic.

Umm but.. Why would you use such a test when there are better screening tests?

Ummm its part of one of the criteria for diagnosis!! Though getting fasting samples and all are easy but you have to make the patient fast right!! In this one benefit would be take the samples anytime!

Oh yep.. Makes sense!

A diabetic patient is undergoing contrast angiography for some reason. He was asked to stop his oral hypoglycemic, metformin before the procedure. Why?

Lactic acidosis.
Renal failure will worsen it.
Contrast leads to renal damage.

Correct! You are concerned about lactic acidosis. Even slight renal failure due to the dye will precipitate lactic acidosis!

A diabetic patient controlled on Insulin develops fainting episodes. On investigations, he was found to have an elevated creatinine. What is the mechanism for the hypoglycemia?

Insulin excreted renally?

Yes, the half life of insulin is increased in renal failure!

A nurse presents with hypoglycemia. Her insulin levels are up but C peptide levels are low. Diagnosis?

Taking exogenous insulin.

Alright. You confront the patient and goes into counselling.

Now the same patient comes with hypoglycemia but this time her insulin and C peptide levels, both are elevated!
What happened this time?

Using sulphonylureas
Oral diabetic drugs - Glipizide, glimipiride, glyburide

Correct! How will you prove it?

proInsulin levels? Just guessing don't know that!!

U/A

What's u/a?

U/A is shortening for urine analysis

Correct! Urine for Sulfonylureas

If the urine test came negative, what could it be?

Insulinoma

And he scores again!

Wonderful questions!!

That'll be all for today!

Thank you for the great questions IkaN.

Never thought questions would be this much fun!

*After which someone else asked us a few review questions based on what he had studied! *

Which antidiabetic drug can lead to SIADH?

Chlorpropamide

I would take that!! All sulphonylureas lead to SIADH.

Ok one more!! How would you access severity of diabetic ketoacidosis?

*since no one could guess, we were given hints!*

Let me put in this way.. Which electrolyte would you Check in serum to access severity of DKA?

If you had to check just 1.

Bicarbonate.

Yes!!!

Why bicarbonate?

Because it is acidosis

Yes, you are right!!

Low bicarbonate would lead to what? This one entity is very important in DKA management!  If this is corrected patient is well and good!! Some difference in the cations and anions!! What's that called?

Anion gap

Yes, it is!! Finally!!

This anion gap is very important.

What the normal value?

10 to 15

Does this gap increase or decrease?

Increases.

ABG would tell is about acid base imbalance.

How does neuropathy occur in diabetes? What's the mechanism?

Occlusion of small venules?

Damage to autonomic NS..?

Microvascular occlusion?

Yes, nerves themselves have a supply of blood vessels. Diabetes damages these small blood vessels, thus decreases supply to nerves!!

You all were correct!!

I've read somewhere that sorbitol deposits also damage nerves?

Lens! It causes cataract.

Alright guys!! That's it!! I can't remember any more!!

Any mnemonics?

Here are all the study links!

http://medicowesome.blogspot.ae/2015/01/oral-hypoglycemic-drugs-and-weight.html

http://medicowesome.blogspot.com/2015/02/study-group-discussion-pharmacological_15.html

http://medicowesome.blogspot.ae/2015/02/study-group-discussion-metformin-and.html

http://medicowesome.blogspot.ae/2015/02/study-group-discussion-cardiac.html

http://medicowesome.blogspot.ae/2015/02/study-group-discussion-type-3-diabetes.html

Study group discussion: Pre-eclampsia and HELLP syndrome

Anybody up for discussion on eclampsia? :D

What is cause of right upper quadrant Pain in HELLP syndrome?

Stretching of the liver capsule.

What's the earliest sign of pre-eclampsia?

It's excess weight gain.

Why?

Due to retention of water.

Study group discussion: Electrolyte abnormalities that cause constipation

Q) Which electrolyte abnormalities can lead to constipation?

My friend says calcium.

Yes, hypercalcemia.

He screamed in my ear because he got excited :L

Hahaha

Hypercalcemia
Hypermagnesemia
Hypokalemia
Hypophophatemia

How does hypercalcemia lead to constipation??

Hypercalcemia increases the action potential threshold and hence decreased contraction n peristalsis.

Sounds good!! Thanks!!

Study group discussion: Chionablepsia and Anisakiasis

Learnt some new words today!
Chionablepsia - its inflammation of eyes due to UV rays!

What a word. I can't even pronounce it!

And this word has no -itis😃

They should've come up with uv-eye-itis instead! :P

Hehe

One more!

Anisakiasis !

A parasitic infection by anisakid (nematodes)

What does this parasite infect?

Stomach walls!

Caused by ingestion of larvae...say, by consuming infected squid or fish

Since it affects the stomach walls, wouldn't bleeding or abdominal pain be most prominent symptoms?

Nothing special ....abdominal pain, nausea, vomiting, diarrhea.

Oh alright!

Deceptive appearances.

A few medical conditions have presentations that are more or less the same to a layman but in reality, are polar opposites of each other. There are though, a few subtle clues which help in differentiating these conditions. Some of them are as follows-

1. The Somogyi effect and the dawn     phenomenon.
These are the conditions which occur in diabetic patients which are undergoing treatment.

In the Somogyi effect, there is a rebound hyperglycemia (in the mornings) following hypoglycemia(during the night) due to the release of counter regulatory hormones.

On the other hand,the dawn phenomenon is characterized by morning hyperglycemia due to inadequate insulin dosage. It may be a possibility that the raised blood sugar is due to nocturnal GH release or increased insulin clearance in the mornings.

So, what does the patient think? That the treatment is not working, is inadequate, but the reality may be starkly different.

To pinpoint, the patient may be asked whether he feels excessive hunger during the night, experiences persistent nightmares or any other symptom during night pertaining to hypoglycemia.

3am and morning blood samples reveal hypo and hyperglycemia in the case of Somogyi effect, while hyperglycemia both the times with dawn phenomenon.

Hence, the modification in Somogyi effect is actually to decrease the insulin dose and increasing it if the patient has dawn phenomenon.

2. Anorexia and Bulimia nervosa.
Both these conditions are characterised by the patient having weight concerns and multiple episodes of self induced vomiting ,laxative abuse or extreme exercise and fasting.One might get confused as to what exactly is the underlying condition.

The primary difference between the two according to me is the patient's attitude and the quantity of food consumed.

Anorexics are primarily worried about their weight(they tend to be ballet dancers or actresses) and hence consume very less amount of food to begin with and vomit out or use laxatives to get rid of whatever is consumed. The patient tends to be almost emaciated, they have a distortion of the bodily image and beliefs that they are still overweight.

Bulimia patients too, engage in similar kinds of behaviours to lose calories but these are more driven out of guilt rather than extreme weight concerns,they usually have a normal weight.The patients have a sense of achievement that they can eat whatever they want and in any quantity until they are losing calories through vomiting, excessive exercise or laxative abuse. Contrary to anorexia, patients have episodes of binge eating then compensatory behaviours followed by hunger and then again binge eating.

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Study group discussion: Difference between antibody and anti-toxin

What is the difference between an antibody and an antitoxin? Wikipedia says that antitoxin is also an antibody. But what's the difference between the two?

And if we take a vaccine, what is formed-an antibody or an antitoxin?

My understanding is a toxin cam be an antigen. An antigen is not necessarily a toxin. So an antitoxin can be an antibody, but not all antibodies are antitoxins.

Anti-toxin is something that neutralizes the toxins released by bacteria. Ex: Tetanospasmin released by Cl. tetani.
These conditions are life threatening acutely.. So you give pre-formed anti-toxin from horse serum or from multiple plasma donors.

Anti-toxin are antibodies. But you need to remember it is especially for neutralizing toxins released by bacteria.
Whereas, antibody is a very vast term. They can be formed against the cellwall of bacteria as well as one's own antigens (autoimmunity).

Multiple plasma donour means from many organisms?

When people donate blood, the antibodies from several of these people's blood is collected and given

Good explanation, Sakkan!

Study group discussion: Aspirin

Which is the classical triad of aspirin poisoning?

Idk the triad though... I just know some symptoms.

What are the symptoms?
Dehydration
Petechiae
Fever

The triad is hyperpyrexia, confusion and later death.

Death? :O

A very rare case.

Death is due to Respiratory collapse.

Fever? A drug used for pyrexia causes fever :D

Haha ironic, yes.

Pyrexia because of uncoupling of oxidative phosphorylation.

Yep. The energy in ATP gets disseminated in the form heat.

What is the treatment of aspirin overdose?

No specific antidote.
Symptomatic.. Cooling.
Vit k - For petechiae.

Increasing urine pH.

Right on! Aspirin is a weak acid.. Hence you increase its ionization to reduce absorption.. By giving sodium bicarbonate!

Yes!! Alkaline diuresis it's called!

Aspirin you just manage patient. Give iv fluid, increase urine pH, dialysis.

Dose of aspirin for prevention of MI?
Dose of aspirin in ongoing MI?

For prevention it is 81-160
For ongoing.. It is 160-325
Moving on

Why salicylates are contraindicated in children?

Reyes syndrome. They result in increase in liver transaminases plus encephalopathy.

Especially, when used for kids with viral fever.

Study group discussion: Cycloserine

I just came to know that One of the important side effects Cycloserine is suicidal tendencies!

And Cycloserine is used in MDR TB.

Exactly.

Does it have any other uses? Apart from TB?

Mental retardation... I searched online.

Hmm.

The person with MDR TB...Dies of suicide more often.

Now we know why!

No other infections?

Certain UTIs. It's antimicrobial action is due to inhibition of bacterial cell wall.

I see.

Study group discussion: Lymph nodes in various diseases

Characteristic lymph nodes in diseases:

Matted- Tuberculosis, LGV

Rubbery- Hodgkin's lymphoma.

Shotty- Syphilis.

Hard, fixed - Malignancy.

Do you know any more? Let us know in the comments section below!

Study group discussion: Biceps femoris reflex

Does anyone know what biceps femoris reflex is?

Biceps femoris reflex is a highly sensitive and reliable clinical tool for evaluation of the S1 spinal reflex pathway in radiculopathy.

It's the contraction of biceps femoris muscle when it is tapped on the lower part of its head just above its attachment on the head of fibula, with the limb slightly flexed at hip and knee.

Hope this helps :)

Thanks!

Study group discussion: ACE in lung diseases

Can anyone please explain why Serum ACE is elevated in Sarcoidosis?

ACE activity is increased in sarcoidosis, a systemic granulomatous disease that commonly affects the lungs. In sarcoidosis, ACE is thought to be produced by epithelioid cells and macrophages of the granuloma.

Serum ACE also appears to reflect the activity of the disease so we can estimate the severity or response to treatment..

You mean : Higher the ACE level , more the disease severity?

Yes.. Higher the level more the severity.

Got it . Thank yoh!

Both TB and sarcoidosis has increased levels of Adenosine Deaminase but Sarcoidosis can be distinguished from tuberculosis by serum ACE levels (In tuberculosis, decreased levels of serum ACE.)

Woah.

Study group discussion: Drug for neurological manifestations of Wilson's disease

Review question-
Which drug is used for neurological manifestations of Wilson's disease?

Penicillamine (cuprimine and depen) and trientine (syprine and trientine dihydrochloride).
Both of these drugs act by chelation of binding of copper, causing it's increased urinary excretion.

Yes, but any specific drug for neurological involvement?

It's Ammonium tetrathiomolybdate.

Glycogen storage diseases mnemonic

Hey everyone! Long time no see!

I was requested mnemonics for glycogen storage diseases recently so I thought I'd write about it -

Glycogen storage diseases from 1-6 are:
von Gierke's disease
Pompe's disease.
Cori's disease
Anderson’s disease
McArdles disease
Hers disease

The memory aid for remembering this one is actually a dirty mnemonic, I found it on tumblr (Can't remember where I read it!)

Anyway the mnemonic is -

Viagra
Pills
Cause
A
Massive
Hardon

Also, heart pumps (Pomps) blood. So that's how you can remember that the heart is affected in Pompe's disease!

And for the enzymes -

Glycogen storage disease type 1 mnemonic:
Geirke - Glucose 6 phosphatase. Both have a G!

Glycogen storage disease type 2 mnemonic:
The Pompe's disease mnemonic is a drag but for whoever this helps.. Do you guys know about the volcanic eruption in Pompeii?
The fires of Pompeii makes me think of acid (burns-fire-acid?) and how it killed children.
So acid alpha-glucosidase and affects children!

Glycogen storage disease type 3 and 4 mnemonic:
Mnemonic for Anderson’s and Cori’s is, "ABCD"
A-B(ranching)
Anderson’s - Branching enzyme.
C-D(ebranching)
Cori’s - Debranching enzyme.

Glycogen storage disease type 5 mnemonic:
Muscle phosphorylase for McArdles. Both have a M in the name!

Glycogen storage disease type 6 mnemonic:
LivHER. So Liver phosphorylase is affected in Hers disease.

That's all!

Hope you're having a wonderful time  and see you in the next post xo

-IkaN

Study group discussion: Thyroid surgery practicals viva questions

Anyway, speaking of triangles of the neck.. Do you guys know they are super important for surgery vivas?

I have surgery viva coming up !!

Omg. If you have a thyroid case, they are bound to ask you this!

I have thyroid - surgery review questions :D

Who is father of thyroid surgery?

Answer: Kocher

Which artery is ligated in thyroid surgery?

Answer: Superior  thyroid artery

Why don't you ligate two?

Answer: Superior thyroid artery is only ligated. The inferior one is left. If you ligate the inferior thyroid artery, the two inferior parathyroids will necrose. Hence the current dictum is not to ligate the ITA.

What about which artery to be ligated near the gland and which one far?

Answer: You ligate STA as near to the gland as possible to avoid injury to the nerve which runs along with it.

Differential diagnosis of midline neck swelling?

Thyroglossal cyst and thyroid are the common ones.

Thyroglossal cyst is embryological remanant of?

Thyroglossal duct.

Most early cause of respiratory difficulty postoperatively?

It's tracheomalacia. Immediately as soon as you withdraw the ET tube.. The trachea collpases. 

Reason?

Tracheomalacia is an inherent condition of weakness of the tracheal cartilage. The thyroid keeps it patent. After thyroidectomy, it might collapse. 

Interesting.. Didn't know this!

Which thyroid cancer can form renal stones?

Medullary. Due to calcitonin. 

At abnormally high levels, it increases urinary excretion of calcium causing renal stones. Medullary carcinoma can also present with hypocalcemia. 

In thyroid surgery, why are we ligating middle thyroid vein first?

To prevent metastasis or to prevent formation of seedling in case of cancer.

Can anyone please elaborate why hyperthyroidism causes oligomenorrhea and hypothyroidism causes menorrhagia?

Hypothyroidism increases TRH.
TRH increases prolactin.
Prolactin decreases GnRH.
GnRH decreases LH and FSH.

What are the complications of multinodular goitre?

Complications of MNG - Due to obstruction - Dyspnea, dysphagia.
Malignant change, calcification are also complications.

Thanks :) 

Study group discussion: Pressure and volume reservoir in the human body

Why arteries are labelled as pressure resevoir?

All artery..especially, arterioles are the main site of pressure regulation.
Veins on the other hand are called capacitance. They store at a time 60% of the total blood volume.
Therefore arterioles regulate the pressure.  On the other, hand..Veins monitor the volume of blood reaching the heart

I think that is true.
And vein also called main blood resevoir.

I found out a good explanation on - Why arteries are known as pressure reservoirs?

Arteries also contain an elastic layer in their walls. Elastin is a protein fiber that has elastic qualities. During systole, large arteries distend with blood as their elastic walls stretch. During diastole, the walls rebound, thus pushing blood along. In this way the arteries act as a pressure reservoir that maintains a constant flow of blood through the capillaries despite pressure fluctuation during the cardiac cycle.

Veins on the other hand, are known as blood reservoirs.

Veins are larger and more compliant (stretchable) than arteries, thus they can hold more blood. In fact, the veins act somewhat like a blood reservoir, containing 60% of the total blood volume at rest.

Study group discussion: Morphine and atropine

* Our discussion started with this: Acute LVF management
LMNOP:
Lasex (frusemide)
Morphine (diamorphine)
Nitrates
Oxygen (sit patient up)
Pulmonary ventilation (if doing badly)*

Morphine used even in the absence of infarction?

To treat severe pain.. Morphine is powerful analgesic.

Yes, but in which cases other than MI, pain is a significant symptom?

Post surgical pain, Cancer pain.

Morphine is indicated in only acute stabbing visceral pain. Except in abdominal emergency's.
Abdominal emergencies if due to biliary spasm. Give nitrous oxide. Or else pethidine.

Even for abdominal pain, if it's severe once after the examination of abdomen.

No, we don't use morphine in abdominal emergencies.

I think we do apart from biliary conditions.

Posting this again, since it's relevant. Opioids, morphine mnemonic http://medicowesome.blogspot.ae/2014/04/opioids-and-other-analgesics-mnemonic.html

Biliary spasm is due to contraction of sphincter of Oddi. Right?

Yep.

Is morphine used alone in biliary spasm??

No, no. It's specifically contraindicated in acute abdominal pain. Because it cause biliary spasm.

Yes, but if used along side of some particular drug it releives spasm.. What drug is it??

I think it's atropine.. Is that right?

Yes!

Atropine is used with morphine for treatment of renal and biliary colic.. Morphine alone may aggravate pain by causing spasm of sphincter of oddi.. Atropine relaxes the smooth muscle of gallbladder and increases the intrabiliary capacity and counteracts the spasmogenic effect of morphine..

I was asked this in a viva, why is atropine given before procedures like drainage of pleural effusion aka pleural tap?

Ummm don't know!!

Okay, I'll give you a hint.. What will happen when you push the needle into the patient

Bleeding?!

And?

Bleeding is minor, think of other things!

Atelectesis?!!

Think Neurologic.

Shock?

Yep. Vasovagal shock. That's why atropine is administered half an hour before the procedure.

Oooh.

Wow! Didn't know that!!

This should apply to all procedures then!

Yes, all procedures. But I was asked this specially because my case in finals was pleural effusion.

Thanks IkaN!

Study group discussion: Central trachea in pleural effusion

In which pleural effusions the trachea is central??

Bilateral ??

Okay.. But in which unilateral conditions?

Due to bronchogenic ca?
When there is pull + push of trachea, nullifying it?

Umm.. It's because of mesothelioma

Why?? I mean why specifically I'm mesothelioma?

If pleural effusion is because of mesothelioma then the negative pressure created by it doesn't effect that much... Sorry.. Don't know exactly.. I'll let you know..

In absorption collapse such as in bronchiogenic ca or foreign body impaction,
Bronchus is obstructed, intrapleural pressure remains negative and trachea is shifted to the same side.

In cases of compression collapse due to pleural effusion, pneumothorax or hydropneumothorax,
Bronchus is patent, intrapleural pressure is positive n so trachea is pushed to the opposite side.

So, if there is bronchogenic ca with pleural effusion, both mechanisms take place,
If pulling effect by bronchogenic ca plays more, trachea remains on the same side of effusion.
If both plays equally, trachea remains in central

Ah.. Push and pull which I mentioned earlier. Thanks a ton!