Ampulla of the fallopian tube is the most common site for fertilization.
Fertilization
AMpulla
Ectopic
Inflexible
Stiff
THick
MUScularis
-IkaN
Hello everyone!
We are going to learn about Meckel Gruber syndrome today!
It's an autosomal recessive syndrome characterized by GRUBEP!
G: ambiguous Genitalia
R: Renal dysplasia
U: Ureteric hypoplasia
B: Bladder hypoplasia
E: Encephalocele
P: Polydactyly
Pancreatic dysplasia
That's all!
There is nothing free except the grace of God.
-IkaN
Today's discussion is about Carbamoyl Phosphate Synthetase!
What are differences between CPS 1 and CPS 2?
CPS 1 works in the urea cycle.
CPS 2 in pyramidine synthesis.
CPS 1 is mitochondrial.
CPS 2 is cytosolic.
(Medicowesome mnemonic: Two is cys-two-lic)
The source of nitrogen for CPS 1 is ammonia.
For CPS 2, it is the amide group of glutamine.
N acetyl glutamate is activator for CPS 1.
ATP is activator for CPS 2.
Woah that's a lot of points I didn't know about!
Which essential amino acid interferes with the conversion of which another essential amino acid into niacin?
Leucine.
In shorghum or jowar, high leucine content inhibits conversion of tryptophan into niacin active form.
Any one knows the mechanism?
Because it inhibits quinolinate phopshoribosyl transferase.
Lack of estrogen causes a decrease in osteoprotegerin.
Osteoprotegerin (OPG), also known as osteoclastogenesis inhibitory factor (OCIF), is a cytokine and a member of the tumor necrosis factor (TNF) receptor superfamily.
Osteoprotegerin inhibits the differentiation of macrophages into osteoclasts and also regulates the resorption of osteoclasts.
Mnemonic: Osteoprotegerin protects bone (By preventing macrophage differentiation into osteoclasts.)
Osteoprotegerin, a RANK homolog, works by binding to the RANK-ligand on Osteoblast/Stromal cells, thus blocking the RANK-RANK lingand interaction between Osteoblast/Stromal cells and Osteoclast precursors. This has the effect of inhibiting the differentiation of the Osteoclast Precursor into a mature Osteoclast.
Mnemonic: Osteoprotegerin ranks high in protecting bones.
So, estrogen kinda inhibits the osteoclasts which causes osteoporosis is the moral of the story?
Yep.
Extra: Recombinant human osteoprotegerin specifically acts on bone, increasing bone mineral density and bone volume. Osteoprotegerin has been used experimentally to decrease bone resorption in women with postmenopausal osteoporosis and in patients with lytic bone metastases.
That's all!
-IkaN
Here are some beautifully presented points on Chagas disease written by Jolhf Mathai Koshy.
I didn't know about Romanas sign and Chagomas.
The MEGA mnemonic for cardiomegaly, splenomegaly, megaeosophagus and megacolon is brilliant.
Now, my brain is swollen up with sweet information! Thanks a lot, Jolhf!
-IkaN
Related post: Study group discussion on Chagas disease
Review - How do KW lesions, disease and syndrome differ from each other?
KW lesions refer to nodular glomerulosclerosis - the KW nodules
KW syndrome is nephrotic syndrome developing due to the lesions.
KW disease refers to any other manifestations occurring due to the lesions.
Any other manifestations like?
Manifestations of glomerulonephropathy. I guess hematuria, anasarca, uremia and others.
20 year old girl with a TB contact history comes to OPD with complaint of hemoptysis. Her TST is 20mm and her smear & culture is positive for mycobacterium TB.
Now some questions related to pulmonary TB!
What is brocks syndrome?
When the enlarging hilar lymph node causes collapse of bronchi, leading to bronchiectasis is called Brocks syndrome. Specially right middle lobe.
What do you exactly mean by post primary tuberculosis?
Post primary refers to TB that occurs few weeks after primary TB when the immunity has developed.
Chemoprophylaxis with which drug should be prescribed if a patient is gonna undergo some immunity wrecking thing like eg, gonna take long term steroids and their CXR shows evidence of previous TB?
Isoniazid.
Hello!
So today, I forgot the types of breech.
And that's why, I made a illustration with eh mnemonic.
There are two types of full breech:
- Complete breech
- Frank breech
There are many types of incomplete breech:
- Footling
- Kneeling
That's all!
-IkaN
Question: Definition of Koch's contact!
Answers, comments posted on the group -
1. Should have:
Sputum positive pulmonary tuberculosis or sputum negative culture positive pulmonary TB
2. Person who is open case of Koch, person who just started AKT and person who completed AKT within 2 years.
Extras:
It was my pediatrics viva question. I didn't know the answer back then! Thanks!
The contact should be a member of the household or be frequenting regularly.
The first identified case in a household is called as index case.
What are causes of wasting of small hand muscles?
The approach is to start with the spinal cord and move towards the muscles.
Spinal cord
Syringomyelia
Cervical spondylitis with compression of c8 root segment
Tumour
Trauma
Anterior horn
Motor neuron disease
Polio
Spinal muscular atrophy
Root lesion
C8 compression
Lower trunk brachial plexus
Thoracic outlet syndrome
Trauma, radiation, infiltration, inflammation
Peripheral nerve
Median and ulnar nerve lesion
Peripheral motor neuropathy
Myopathy
Distal myopathy
Dystrophia myotonica
Trophic disorder
Arthripathies
Ischaemia including vasculitis
Shoulder hand syndrome
That's a long list!
You're right. The most important thing is to remember the categories and some of the more common things listed.
Yup I love the way you listed it out.
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Exergonic reaction - Thermodynamics |
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Endergonic reaction - Thermodynamics |
Hi everyone!
Now - a - days, monospot test is used to diagnose infectious mononucleosis rapidly.
But heterophile antibody test was used in the past and remembering it is high yield for exams.
Infectious mononucleosis is caused by EBV, which gives a heterophile positive antibody test.
In a minority of cases, infectious mononucleosis is caused by CMV, which gives a heterophile negative antibody test.
How do I remember this?
Mnemonic!
Ataxia + Ichthyosis + Retinitis pigmentosa + Don't drink milk.
Associated with which inherited autosomal recessive condition?
Refsums disease.
It's a rare AR disease.. The signs and symptoms of Refsum disease result from the abnormal buildup of a type of fatty acid called phytanic acid. This substance is obtained from the diet, particularly from beef and dairy products. It is normally broken down through a process called alpha-oxidation, which occurs in cell structures called peroxisomes.
Milk, cabbage etc. contain phytanic acid. That's why, they should be avoided.
Why does hypoxia in the brain cause liquefactive necrosis? And why does hypoxia cause coagulative necrosis in all other tissues?
Let's take it step by step!
What's the basis of coagulative necrosis in hypoxia? How does it appear?
The framework and architecture of the cells is maintained.
The reason is - In hypoxia, there is early reduction of ATP. Hence, there is a switch to anaerobic pathways. Increased lactic acid production causes a decrease in pH which results in the inactivation of even the proteolytic enzymes.
The organelles dissolve to some extent, but as the pH increases, enzymes are inactivated, leaving behind the framework.
So.. Why is there no coagulative necrosis in the brain?
There is no anaerobic metabolism in the brain. Hence, no lactic acid to stop the proteolytic enzymes.
Also, in brain there is no supporting matrix. It is all neurons and supporting cells.
In other words,there are no acellular substances. Whereas in other tissues, there is an acellular supporting matrix.
When hypoxia strikes, everything dies in brain.
Hence, liquefactive. In other tissues, the ECM maintains the structure a little bit.
Cool concept. Made me go woah.
Interesting fact: It has been established that casseous necrosis is not necrosis per say, but it is mass apoptosis of macrophages. Robbins mentions it as necroapoptosis.
Thanks for the tumblr fanmail (: |
So I'm just going to start with my paediatrics posting and I really really wanna be a paediatrician. Could anyone share any tips on how to be a good paediatrician?
Spend time in clinic/wards..
take histories. Try to make differential diagnosis yourself and discuss it with your teachers..
Yaah..and examine as many kids as you can.
Take a lot of toys / chocolates with you to keep the child busy when you examine.
I used to gift my patients toys and they'd smile so huge! One kid, even though seemed uneducated, told me a thank you! :D
The parents seem really tense, it's a sick child after all. You wanna be very gentle with them and talk cuddly. If you treat the kid more as a patient and less like a child, they are more likely to get pissed.
Good tips, IkaN!
Oh and when you present the case to the attending and the patient's parents are around, don't start with, "Patient, Jane Doe, 2m old female.."
Say, "Child, Jane Doe.."
No one would like their child to be addressed as a patient.
IkaN *thumbs up*
My peds HOD won't let us examine children, if we don't bring candies for them :)
My peads attending said to my friend after a viva, "What did you bring for the kid?"
My friend had not got anything so the ma'am said jokingly, "Nothing for the kid? Okay then, no marks for you!" :P
Awesome tips for peds, IkaN!
They'll be super helpful even during volunteering.
Omg. So you can give them chocolates?
I guess you can give chocolates.. Unless they are lactose intolerant / allergic.
Toys are better, I guess. They keep kids busy for hours!
Give them under parental supervision just to be safe xD
How do you get kids to let you auscultate them? They cry and then you can't hear anything
That's a two people job then, one of you has to distract the baby while the other one auscultates!
And try warming the diaphragm of your stetho a little, the kid probably also cries because it's cold.
Worst case, ask the mother to feed/play with the child.
Distract it, that normally does the trick. Carry a small torch and distract it with the light, it's a trick that usually works.
How to remember the atypical antipsychotic that causes cataract
If your lens shine,
you may have been taking quietapine.
Lens shining = Cataract
Related post: Side effects of atypical antipsychotics mnemonic
Discussion on drugs for Alzheimer's.
What is the basic pathology in Alzheimers disease?
Amyloid deposition in the Ach neurons. Hence, decrease acetylcholine in the brain.
Amyloid precusor proteins in the circulation are acted upon by two enzymes -
Alpha secretase: Which forms soluble proteins. These are good.
Beta gamma secretase: Which forms insoluble proteins. These are bad.
These insoluble proteins polymerise to form the plaque. So these insoluble plaque get preferentially deposited in Ach neurons and cause a foreign body reaction.. Leading to inflammation and death of neurons. Hence Alzheimers.
How alpha secretase is good?
Cause it cause soluble products.. These can be washed out by blood. The insoluble ones will precipitate.
There are 5 classes of drugs.. Guess their mechanism based on the pathology discussion!
First class: AchE inhibitors. How do they help?
They will inhibit break down of Ach.. Indirectly, increasing their levels.
Donepezil, Rivastigmine and Galantamine are examples.
They are lipid soluble and cross the blood brain barrier easily. They are also called centrally acting anticholinesterase.
Interesting fact: Nicotine acts both presynaptic and post synaptically to release Ach hence smoking is thought to be protective against AD. However, one of the hypothesis for AD is free radical damage, which can be caused by smoking.
Second class: A drug which will increase activity of alpha secretase.
The name for this drug is deprenyl.
Third class: A drug that inhibits beta secretase.
Beta- gamma secretase has got an inhibitor called tarenflurbil.
Fourth class: These are primary drugs. Inhibit polymerization.
Drug named Tramiprostate
Fifth class: This one removes the pre formed polymers.
Bapineuzumab is the drug.
I love the way you explain things. Starting right from basics!
Extras -
Glutamate antagonists - Memantine. How would antagonism of glutamate help?
Block glutamate excitotoxicity.
Can anyone mention something about infantile hernia?
The pathology or the physiological hernia that is normal?
Both!
Alright, there are a couple of hernias related to infants that I know about.
One of them is the physiological hernia, which is a thing that happens to all babies during fetal period. So it's normal.
The intestines herniate out of the body of the fetus and rotate 90 degrees at week 6 of development. Then at week 10 they rotate a further 180 degrees and come back into the body. This is the phenomenon that forms the spiral-like location of intestines.
Now there are two pathologies.
One is the Ompholocele, where the intestines fail to come back at week 10.
The other is Gastroschisis where the physiological hernia happens normally but the abdominal wall fails to close so the gastrointestinal system protrudes directly into the amniotic cavity.
Thanks for explaining! Here's a study link!
http://medicowesome.blogspot.ae/2014/09/gastroschisis-vs-omphalocele-mnemonic.html
Side effect of cyclophosphamide?
Bladder carcinoma is the commonest one!!
It can also lead to Haemorrhagic cystitis!
Maximum cyclophosphamide can be given for 18 months.. After that it has to be replaced with Methotrexate or azathioprine..
May cause infertility in male patients who received high doses as children.
Okay.. Didn't know that.. Thanks
Risk of potentially fatal and irreversible interstitial pulmonary fibrosis if given over prolonged periods.
Which nerves have a pseudoganglion?
Nerve to teres minor!
Correct.
Others are lateral terminal branch of deep peroneal nerve and posterior interosseous.
But why name pseudoganglion..??
Pseudo ganglion is only a nerve thickening resembling the presence of a ganglion.
Ohh.
What could be the possible cause of a sudden episode of nose bleeding in a patient who has a history of open heart surgery?
It could be because of anticoagulation. Hypertension is also a cause.
Since we are on this topic, any one would like to go over the differentials of epistaxis?
Excessive scratching of nasal area
Anticoagulation meds or any coagulation disorder
Traumatic
Leukemia
ITP
Problems in liver
Rhinosporidiosis
Polyps
Foreign bodies
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!
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.
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.
*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!
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!
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
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.
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.
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.
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.
*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.
Hello! A short sweet post for today :D
Mnemonic: LOBUlar
Located in
Other
Breast
Usually
That's all!
-IkaN
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."