Study group discussion: REM Sleep Behavior Disorder and Parkinson's disease

I just studied that fatal familial insomnia is a prion disease.

We had a discussion on fatal familial insomnia before!

Fatal familial insomnia, harmful effects of working at night and sleeping during the day  http://medicowesome.blogspot.com/2015/02/study-group-discussion-fatal-familial.html

Oh, I shall have a look over that discussion!

So basically it's thalamus that is missing :)

What is the centre for REM sleep in particular that is affected in idiopathic Parkinson's? I can't remember that center! It's important because in idiopathic Parkinson's disease, earliest symptom REM sleep behavior disorder.

Umm.. I can't remember that! Is it the one which regulates the circadian rhythm?

I found an interesting read on Parkinson's, rem in Harrison. I'll post it here!

REM Sleep Behavior Disorder RBD is a rare condition that is distinct from other parasomnias in that it occurs during REM sleep. It primarily afflicts men of middle age or older, many of whom have a history of prior neurologic disease.

Infact, over one-third of patients will go on to develop Parkinson's disease within 10 to 20 years.

Presenting symptoms consist of agitated or violent behavior during sleep, reported by a bedpartner. In contrast to typical somnambulism, injury to patient or bed partner is not uncommon, and, upon awakening, the patient reports vivid, often unpleasant, dream imagery.

The principal differential diagnosis is that of nocturnal seizures, which can be excluded with polysomnography. In RBD, seizure activity is absent on the EEG, and disinhibition of the usual motor atonia is observed in the EMG during REM sleep, at times associated with complex motor behaviors.

The Pathogenesis is unclear, but damage to brainstem areas mediating descending motor inhibition during REM sleep may be responsible. In support of this hypothesis are the remarkable similarities between RBD and the sleep of animals with bilateral lesions of the pontine tegmentum in areas controlling REM sleep motor inhibition.

Treatment with clonazepam (0.5 to 1.0 mgqhs) provides sustained improvement in almost all reported cases.

So it's the brainstem! :D

Yep!

Study group discussion: How to determine which hemisphere is dominant

Why do we ask about handedness in CNS case?

Dominant hemisphere and handedness http://medicowesome.blogspot.in/2014/12/dominant-hemisphere-and-handedness.html

Yup but in both LEFT is only dominant.. Then why bother asking?

There are exceptions where right hemisphere is dominant. Only 85% population has left dominant. 15% has right dominant.

I had seen a case in which the right hemisphere was dominant, in a right handed person!

How did you know she was right dominant?

We asked her to write, comb hair, thread needle -  She was right handed.

She was right handed I agree ...
But how to know her right side is dominant?

She was right handed through history and examination.
Had UMN type of hemiparesis on the left side, clinically (Right hemisphere affected)
She also had difficulty in comprehension and speech, clinically (Brocas area affected)
So Brocas is usually on the left side, the dominant, that is.
But in this case, since the right hemisphere was affected, her Brocas was on the right side.

Our professors said shift of hemisphere can occur in childhood injury. Which could be a reason.. But there was no history suggestive of such insult in our case.

If broca is not affected.. We cant comment on right or left dominance?

I guess. No idea.

Study group discussion: Alcoholic liver disease, hepatic encephalopathy and stigmata

What is fetor hepaticus?

The characteristic odor in hepatic encephalopathy.

Mechanism?

Caused by volatile aromatic substances that accumulate in the blood and urine due to defective hepatic metabolism Also called as "liver breath"

Study group discussion: Fluoride bulb and glycolysis

Best agent to be added into blood sample that has to be transported for glucose estimation?

Fluoride!

It prevents glycolysis.

How does it prevents glycolysis?

Inhibits the enzyme enolase

Yeah, correct!

Why do we use fluoride bulb for glucose estimation?
Fluoride inhibits glycolysis. So the glucose in RBCs don't get metabolized and you won't get a false lower value of glucose (:

This is the note I took on fluoride! Apparently when coupled with Mg it ihhibits enolase.. So it stops glycolysis.

Study group discussion: Physics in Medicine

*I was announcing the pre med group when this discussion took place*

We just created a premeds group for physics, chemistry and biology discussions. Message me if you wanna join in!

Yup. Cause those physics laws always get applied in case of resistance in vessels and especially in lung volume and pressure curves.

They do! I remember studying vectors for understanding ECG in first year!

Speaking of physics, can anyone name the mechanics behind the law applicable in Aortic aneurysms that lead to rupture?

:O

Physics never leaves us!

Okay, I dint know this! :(

It says as the diameter increases, tension on the vessel wall increases. The aneurysm keeps expanding, leading to rupture of the aneurysm.

Laplace law.

Yep.

Laplace's law states that tension on the wall of a container is directly proportional to the pressure inside it and also to the radius of the container. It's inversely proportional to wall thickness. Which explains the more bigger the aneurysm, the more susceptibility to rupture.

It's the same concept in Surfactant!

Really?

If the surface tension is not kept low when the alveoli become smaller during expiration, they collapse in accordance with the law of Laplace. In spherical structures like the alveoli, the distending pressure equals two times the tension divided by the radius (P = 2T/r); if T is not reduced as r is reduced, the tension overcomes the distending pressure.

What is Pouiselle's law?

Pouiselle's law states about the relationship between velocity of fluids, viscosity and the pressure in a capillary.

So physics is really important in Medicine!!! I haven't seen anything of physics yet!

It's just a matter of time! :D

I am waiting anxiously!

Study group discussion: Polymyalgia rheumatica and polymyositis

Question: Which inflammatory condition is associated with temporal arteritis?

Answer: Polymyalgia rheumatica!

Question: A patient comes with pain and weakness in the proximal muscles with not much of stiffness! What would it be? Polymyositis or PR?

Answer: Polymyositis.

Stiffness is a present in both but more of a feature of PR.

Pain in proximal muscles along with stiffness is PR, there will be no weakness of muscles in PR.

On the other hand, in case of Polymyositis, there is weakness of the muscles that is the main difference!

There might be little tenderness in this case.. But whether weakness is present or not that differentiates the two!

Rest we can further elaborate based on the enzymes!

So to summarize:
Muscle weakness is more of feature of polymyositis.
Stiffness, pain goes with Polymyalgia rheumatica.

Question: Which enzymes will be raised in PM?

Answer:
Creatine kinase.
Aldolase.

Question: What would be elevated in PR?

Answer: ESR.

Question: How does one differentiate between PM and DM?

Answer: In dermatomyositis, you will be see above symptoms plus skin manifestations - Gottron papules, Heliotrope rash, Shawl sign.

Question: What is the most common serious complication of PM/DM?

Answer: Malignancy!

Which malignancy?

Ovaries are most common. Others are cervix, breast, lungs, pancreas.
Testing for malignancy which CA is helpful?

CA-125 - That's for ovarian cancer.
19-9 for pancreas!

Study group discussion: Oxytocin

Question: Why does oxytocin cause volume overload?

Answer: It is similar to vasopressin in structure.

Vasopressin and oxytocin are similar in structure. So vasopressin is ADH. It retains water. Which will cause Intravascular volume expansion

There are a lot of compounds which have a similar structure and interesting clinical effects. Here are a few http://medicowesome.blogspot.in/2014/11/hormones-that-have-similar-structure.html

Doubt: Several pharmacology books said that oxytocin may cause hypertension. But Williams obstetrics says that it will cause serious hypotension if given as undiluted iv bolus. I'm confused.

Answer:
Bolus causes hypotension.
Normal infusion causes fluid retention.
Although unlike ergonovine, oxytocin does not produce hypertension.

So don't give bolus is the moral of the story. It can cause Placental hypoperfusion.

Question: How does it cause Placental hypoperfusion?

Answer: If your blood pressure drops, blood supply to all organs will be compromised. Comprehende?
Think of placenta as an organ. So Placental hypoperfusion!

Doubt: Does anyone know why iv bolus of oxytoxin will have adverse effect of hypotension and tachycardia?

Answer: In high doses... Oxytocin has vasodilator action which produces hypotension and reflex tachycardia.

From what I read, oxytocin decreases venous return and systemic vascular resistance. So that'll cause a compensatory tachycardia.

Source: http://www.ncbi.nlm.nih.gov/pubmed/18513945

Study group discussion: Hutchinson's in medicine

Hutchinson's triad:
Seen in congenital syphilis. Includes -
1) Interstitial keratitis
2) Hutchinson's teeth (which are notched incisors)
3) Vestibular deafness

Hutchinson's Sign: Seen in Herpes Zoster Ophthalmicus.. Which says if the nose is involved, then the eyes have to be involved too.. Since they both are supplied by the Nasocilliary nerve.

Hutchinson's Pupil:
Seen in concussion injuries to brain (usually associated with the subdural hemorrhage).
The ipsilateral pupil is initially miotic... Then it becomes myriadtic due to raised IOP... Then as the IOP further  increases, the contralateral pupil also dilates... So we have bilateral dilated pupils not reacting to light. This is an indication for immediate cerebral decompression.

Hutchinson's mask:
A sensation often associated with tabes dorsalis in which the face feels as if it is covered with a mask or cobwebs.

Hutchinson's facies:
The peculiar facial expression produced by the
drooping eyelids and motionless eyes in external
ophthalmoplegia.

Study group discussion: Facies in medicine

Mitral facies - Malar erythema.

Hippocratic facies - Acute peritonitis.

Typhoid facies - Severe malaria.

Adenoid facies - Adenoids.

Chipmunk facies - Malar prominence, in Thalassemia.

Hepatic facies - liver failure.

Leonine facies - coarse features, leprosy.

Facies leprosa - Falling of teeth and nasal bridge depression in leprosy.

Mask face - Parkinsonism.

Cushing's face - Moon like round.

Hutchinson's facies - The peculiar facial expression produced by the
drooping eyelids and motionless eyes in external ophthalmoplegia.

Study group discussion: Anti-epileptic drugs

Carbemazepine is contraindicated in which type of seizure?

During pregnancy, eclampsia and absence seizures.

Which anti eplielptic drug is contraindicated in pregnancy?

All of them.

Which antiepileptics can be used in pregnancy?

Sodium valproate, lamotrigine and lavatriacetram are safe in pregnancy.

Pregnant lady with epilepsy well controlled on sodium valproate wants to get pregnant. What will you do?

You do not switch the drug. Valproate has a dose dependent side effect on the fetus. You will try tapering down the dose. The main word is well controlled.

If while tapering the dose, she starts having seizures you switch to a safer drug.

Study group discussion: MAC deficiency in Waterhouse Friedreichson syndrome

Waterhouse Friedrichson syndrome has which immune component deficient?

MAC
C5-C9

And infections with what organisms are the especially susceptible to?

Gonorrhoea also?

No, just meningococcal

And just neisseria? Ideally, shouldn't there be increased susceptibility to all gram -ve organisms?

It is caused due to haemorrhage in adrenal gland. Waterhouse is not just a primarily immune complex deficient state. It is a manifestation of systemic infection due to meningococcal meningitis

Umm. My book says that patients with meningococcemia who develop Waterhouse..... Are generally MAC deficient.

There isn't susceptibility to other gram negatives because membrane attack complex is a defense against bacteria which can survive intracellularly.
So basically, extracellular lysis by MAC is effective in killing only Neisseria species.

You're susceptible to N. meningitis only because Neisseria gonorrhea has an outer membrane protein. MAC interacts with it and fails to insert in the bacterial membrane.

And then E. Coli and Salmonella have long polysaccharide chains in cell wall and these side chains prevent the insertion of MAC into bacterial membrane.

So MAC is good at killing only one thing - N. meningitidis and the deficiency will predispose you to this one infection only!

If you're talking about an infection that hemorrhages into the adrenals - it has to get really out of control to do that. And MAC deficient patients can't control their Neisseria infections leading to Water House Friedreichson syndrome. So the book is fair in saying those who develop WHFS due to meningococcal infections are usually MAC deficient.

Study group discussion: Artery of Percheron

*a picture of artery of Percheron was posted in the group on which this discussion took place *

That's vertebral arteries combining to form basilar. And again dividing to posterior cerebral arteries.

This is an anatomical variant.. Any odd thing in the picture?

The supply from the right branch of posterior cerebral artery. That seems odd! If it was normal.. It should have a bilateral supply.

Exactly.
It's called artery of Percheron.

What is special about it?

A rare anatomical variant where the thalamic perforator branch supplies both sides of the midline.

Any occlusion and you'll have bilateral paramedian thalamic infarction.

Ohh.. What would be the symptoms?

Yup.. How would unilateral infarction differ from bilateral?

I can't figure out which structure the artery is supplying!
They're thalamic peduncles. Unilateral you'll have sparing on one side. In Bilateral, the structures below the thalamus will be totally cut off from the structures above.

And symptomatically we are talking depending on which relay centre is affected? Or is there a very specific pure motor, pure sensory stroke we get?

Bilateral paramedian thalamic strokes are typically characterized by a triad of altered mental status, vertical gaze palsy, and memory impairment.

Altered mental status can present anywhere on the spectrum from drowsiness or confusion to hypersomnolence or coma...most probably due to damage to the reticular formation.

Vertical gaze palsy suggests mesencephalic involvement.

Memory deficits mostly are due to damage to the papez circuit. ..Anterior nucleus of thalamus is a part of the Papez circuit.
And also the thalamus acts as a 'search engine' for memories.

I looked up a few parts on the net...

That's awesome!

This is what I found in Harrison - Occlusion of the artery of Percheron produces paresis of upward gaze and drowsiness, and often abulia.

I liked the search engine bit. Nice info!

By the way, a similar sounding condition, 'Purtscher's retinopathy' is associated with acute pancreatitis.

How to remember lobular carcinoma spreads to contralateral breast

Hello! A short sweet post for today :D

Mnemonic: LOBUlar
Located in
Other
Breast
Usually

That's all!

-IkaN

Intravenous dreams

You know you have done too many blood collections when you say stuff like, "Dreams are collapsible, like a vein. So make sure you put needle in a good one."

Study group discussion: Dua's membrane

Cool fact: A new layer of cornea is discovered. It's called the Dua's membrane.

The Dua's Layer lies between the stroma and the descmets.

It's said to be acellular.

It was discovered last year by an Indian opthalmologist, Dr. Harminder Singh Dua.

Related post: Layers of the cornea mnemonic

Study group discussion: Pleural tap

Which muscles are pierced in midaxillary line during pleural tap?
Answer:
- Serratus anterior
- External intercostals
- Internal intercostals
- Intercostalis muscle

What are the boundaries of the safety area that we chose for pleural tap?

Answer:
Anterior - Lateral border of pectoralis major
Lateral - Lateral border of trapezius
Inferior - 5th intercostal space
Superior - Base of axilla

It's also called safe triangle.

Related post: Why is atropine given before procedures like drainage of pleural effusion aka pleural tap?

Staghorn calculus mnemonic

Staghorn calculus mnemonic

I remember the word, "MAPS"

M: Magnesium Ammonium Phosphate Struvite stones

A: Alkaline pH (AlkAline has 2 A's, Acid has just 1 A.)

P: Proteus

S: Splitting organisms (Urea splitting, urease producing organisms)

Staghorn calculus

Study group discussion: Vitamins and renal stones

Question: Which vitamin is indicated in treatment of calcium stones?

Answer: Pyridoxine

And which vitamin is avoided in a patient with history of calcium stones?

Answer: Vitamin C, it will worsen calcium stones.

Why?

Answer: Vitamin C increases oxalate in body. Pyridoxine decreases oxalate level in body.

Extra: Vitamin A deficiency too causes stones. The desquamated epithelium in tubules acts as a nidus for stone formation.

Study group discussion: Signs in acute appendicitis

Most commonly asked appendicitis signs

Aaron’s sign: A referred pain or feeling of distress in the epigastrium or precordial region, on continuous firm pressure over McBurney’s point, in acute appendicitis.

Dieulafoy’s triad: Tenderness, muscular contraction and skin hyperaesthesia at McBurney’s point in appendicitis.

Obturator sign: It refers to presence of hypogastric pain on stretching the obturator internus due to its irritation in the pelvis. This test is performed by passive internal rotation of the flexed rightthigh with the patient supine.

Bastedo’s sign : Pain and tenderness in the right iliac fossa on inflation of the colon with air, in cases of chronic appendicitis.

Psoas sign  : It is positive in retrocecal appendicitis. In this, irritation of the of the psoas muscle gives rise to pain when the patient’s right thigh is extended from the flexed position.

Rovsing’s sign  : Pain at McBurney’s point induced in cases of appendicitis, by pressure exerted over the descending colon

That's a good summary. Thanks!

Study link! Clinical features of acute appendicitis mnemonic
http://medicowesome.blogspot.ae/2014/11/clinical-features-of-acute-appendicitis.html

Study group discussion: Vitamin K overdose and deficiency

What's the adverse effect of excess dose of vitamin K, if given in new born?

Answer: Neonates - In infants (particularly premature babies), excessive doses of vitamin K analogs during the first few days of life may cause severe hemolytic anemia; this in turn may result in  hyperbilirubinemia, kernicterus, leading to brain damage or even death.

Study group discussion: Serial interval and communicable period

What is the difference bw serial interval and communicable period?

Communicable period is the one in which the disease is transmitted from one case to another. (Also known as infectivity.)
The patient might have the disease but may not be infectious because of latent phase.

Serial interval is the time period in which the disease manifests from one case to another.

It's different from communicable period because the disease doesn't manifest immediately, so the case might present to you late.

Serial interval = Latent period + communicable period (Roughly)