Tuesday, March 3, 2015

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.


Monday, March 2, 2015

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!

Study group discussion: Scissoring posture

1 and a half year old child when suspended by the axillae, his legs maintain scissoring posture. What can you think of?

Cerebral palsy!
Or UMN lesion!

Which type?

Spastic diplegia

What is the reason for such kinda posture?

Scissoring is a sign of hypertonia.

Patient tone is increased!!

Yes

Everything related to UMN lesion

Spasticity, hyper reflexia, upgoing plantar.. You will see in this patient!

What can be the possible treatment?

Baclofen + physiotherapy.
A pillow or ball between the legs while sleeping!

Yeah, baclofen will relieve the spasticity.

Study group discussion: Cutaneous signs of insulin resistance and lipoproteinemia

These are skin tags. What do you think of when these are present?

Aren't these harmless with no associated risk?

Nope. They represent something! Ok! These are signs of insulin resistance!

What are other cutaneous signs of insulin resistance?

Acanthosis nigricans

Yes!!

One more.. Although that one is associated with hyperlipidemia too.

Xanthelasma?

Yes!!! Xanthelesma.

Since we are on hyperlipidemia http://medicowesome.blogspot.ae/2013/08/how-to-remember-lipoprotein-disorders.html

So cutaneous signs of insulin resistance include:
Skin tags
Acanthosis Nigricans and
Xanthelesma

Mnemonic: SAX!

In which condition do you see orange tonsils?

Rifampicin intake?

Haha nope. It's related to the topic.. A high cholesterol condition!

Lol no idea then!

Tangier disease.. It's due to lack of cholesterol transporter gene. The disease is characterized by atherosclerosis, hepatosplenomegaly, polyneuropathy and orange tonsils.

Ohh!!!

Another review question.. Why is type 1 lipoproteinemia associated with pancreatitis?

Short of knowledge on this topic maybe someone else would answer it?

It's because chylomicrons obstruct the pancreatic duct.

Sunday, March 1, 2015

Study group experience #13

Ligamentum venosum and ligamentum arteriosum

Shift to left 

Uncouplers of oxidative phosphorylation 

What does emulsification mean in fat digestion 

Chagas disease 

Parasites that cause carcinoma of the gall bladder 

Lemierre's syndrome

Acute lymphangitis

Chain messages 

Alcohol and sex

How and when do children understand the concept of death

Abnormal breath sounds: Crackles, Wheeze, Rhonchi and Stridor 

Mechanism of tet spells 

CHARGE syndrome and related case 

Pfeiffer disease and Pfeiffer syndrome

Heyde's syndrome 

Fontanelles and thyroid hormone

Fixed specific gravity 

Neurological emergencies and isoniazid overdose 

Medial medullary syndrome and crossed paralysis

Locked in syndrome and total locked in syndrome

Cool fact about optic nerve

Marcus gunn jaw winking syndrome and Ptosis

Relative afferent pupillary defect (Marcus Gunn pupil) vs Optic nerve lesion

Water intoxication syndrome

Hernia

Varicocele

Leriche syndrome

45 centimetres in length and tubes

To vaccinate or not to vaccinate

Non contraceptive uses of condom

Hyperuricemia

Drug causing hypertrophic pyloric stenosis

Beta blockers

Drug therapy for asthma

Low molecular weight heparin vs unfractionated heparin

Thiazides

Fluoroquinolones

Cool fact about GLP 1 agonists

Phew! That was a lot, was it not? So much more to come! I could create a separate blog for these xD

We also reached 100 awesomites in group 2! Yaay!

Which also means new comers will have to wait till there are enough awesomites to form group 3. Sorry for the delay!

How sign up for the study group

Study group discussion: Relative afferent pupillary defect (Marcus Gunn pupil) vs Optic nerve lesion

*A picture was posted on the group on which this discussion took place.

Description of the picture for the readers convenience:
In the first picture, we see normal pupils.
In the second picture, light is shone in the left eye. Right and left pupil constrict.
In the third picture, light is shone in the right eye. Right and left pupils do not constrict.
In the fourth picture, light is again shone on the left eye and again, both pupils constrict*

RAPD?
Also know as Marcus Gunn eye!
Aka prostitute's pupil :P

Nope. Optic nerve is affected on the left side. As there are absolutely no afferents from left eye, indirect is absent.

Yes.. The 3rd nerve efferent is intact and optic nerve is affected.

There is crossing of the afferent fibres of each eye. That's why when you stimulate one eye the other eye also dilates via the efferent fibres. That's how the other eye also constricts (indirect). In this picture, there is complete afferent defect. The optic nerve is completely transected.

Why not RAPD?

In RAPD, when light is shone to the diseased eye, direct absent.. Therefore, doesn't constrict.
Mnemonic: Direct Diminishes in a Diseased eye, indirect present.

RAPD is diagnosed by swinging light test. When you alternate the flashlight.. The affected pupil ( less number of afferent fibres ) has a release phenomenon and dilates instead of constricts. The affected pupil initially constricts..But when you swing the flashlight repeatedly it dilates. The pic hasn't shown frequent swinging. And the pupil remains dilated in the first go when the light is shown. So there is no relative afferent defect.

I haven't heard of the release phenomenon, I've thought it's because relative to the normal eye, the disease eye appears to dilate. It always constricts but because you compare it with the normal eye, it seems to dilate.

But why do we call it relative? The direct being present and the indirect being absent?

I dont think we call it relative cause efferent is intact. We call it relative cause, relative to the normal eye..The affected eye has reduced optic nerve fibres. This is done to detect early loss of fibres in optic neuritis.

I'm such type of patient. I mean my left optic nerve is affected.

Really? How were you diagnosed and when?

I met with an accident. It was a severe injury on left  eye. 3rd nerve got damaged at first. Doctors said it's severe. It will heal with time. But doctors were not sure it will heal completely or not.

Oh I'm so sorry!
Can you see?

After 1 yr, I again went for checkup.. Doc said 3rd nerve is alright now but optic nerve is affected due to increased stress. Now, I have only partial vision left eye. It's 6/24 (Normal is 6/6)
And it'll not heal completely for whole life.

Optic field shows that the person can't see through different angles with the defective eye. That's why, it's called Partial Vision.
Because of damage to optic nerve.. Healing depends upon the degree of damage. Meconerv Forte is the medicine for that.. But chances of complete healing are rare..

Difficulties make us more strong! Just keep going no matter what.

Yeah, of course. Thanks!

Saturday, February 28, 2015

Study group discussion: Marcus gunn jaw winking syndrome and Ptosis

Interesting one - congenital ptosis associated with winking motion of the affected eyelid on the movement of the jaw. Known as Marcus gunn jaw winking syndrome.

On opening, side ward movements of jaw, increase of palpebral aperture!

Usually jaw movement to opposite side! Jaw winking.

What are the causes of Ptosis?

Neurologic causes of Ptosis include Horner's syndrome, in which the pupil is constricted, and third nerve palsy, in which there are abnormalities of eye movements and the pupil may be dilated. Local causes include congenital and acquired disorders of the levator muscle complex and tumors and infections of the eyelid. Myasthenia should always be considered.

Study group discussion: Medial medullary syndrome and crossed paralysis

Which of the following are clinical features of medial medullary syndrome?

A. Ipsilateral numbness of arm and trunk
B. Horners syndrome
C. Ipsilateral 12th cranial nerve palsy
D. Contralateral pyramidal tract sign