http://www.brooksidepress.org/Products/OperationalMedicine/DATA/operationalmed/Procedures/TreataSuckingChestWound.htm
I was looking at a statement talking about sucking chest wound.
The statement as shows: First aid for sucking chest wound is with occlusive dressing that allows air out (taped on three sides) but not in.
I didn't quite get it. Just imagine one day, you are walking in an American street and you witnessed a gun fight. Someone got shot on the chest. In such scenario, let's just test how much knowledge you know for this scenario ya? By the way, the above statement was from Kaplan Surgery CK 2008-2009. For the pictures, just go and visit the html at the top of the post.
A sucking chest wound is identified by the sucking or hissing sound made during breathing by the casualty.
With this type of wound, the chest cavity is no longer sealed, allowing air to rush through the wound and into the chest during inhalation. This causes the lung to collapse. This is a life-threatening condition and requires immediate treatment.
Start by uncovering the wound. If the clothing is stuck to the wound or in a chemical environment, then clothing should not be removed. Don't attempt to clean the wound. That will be done later.
Use the casualty's hand to cover the wound while you quickly prepare an occlusive patch. The plastic wrapper of a battle dressing works very well, although any air-tight material can be substituted, such as:
Cellophane
Aluminum foil
Duct Tape
Vaseline Gauze
The patch should be large enough to extend 2 inches beyond the edge of the wound. Smaller patches tend to get pulled back into the wound.
Secure the patch to the wound with adhesive tape. Three sides should be taped, while the 4th side is left untaped. Whenever the casualty breaths out (exhales), air is expelled from the chest cavity and escapes from underneath the open edge of the patch. Whenever the casualty breaths in (inhales), the patch sticks to the skin and keeps air from returning into the chest cavity. This helps to re-inflate the collapsed lung.
Place a small battle dressing over the patch, but don't make it so tight that the casualty can't breath.
Sometimes, you won't have any adhesive tape, or the tape won't stick (blood, water, mud, or perspiration may keep it from sticking). In that case, it is still very helpful to use the patch, held in place by a battle dressing or triangular bandage.
Finally, roll the patient onto the injured side while awaiting transportation.
Some medical bags include pre-packaged chest seals. These are easy to use and fast.
· Use the enclosed gauze pad to wipe the skin dry around the wound.
· Peel off the paper backing and place the sticky side of the seal over the wound and surrounding skin
· The one-way flutter valve will allow air to be expelled from the chest, but will keep the outside air from returning.
Wednesday, November 25, 2009
Sunday, October 18, 2009
Catheter ablation & Heart Surgery
http://www.revolutionhealth.com/articles/catheter-ablation-for-atrial-fibrillation/hw159948
http://www.texasheartinstitute.org/hic/topics/proced/
http://www.texasheartinstitute.org/hic/topics/proced/mazes.cfm
Basically this is an extension on the previous topic. Related but is a different thing altogether. It's about atrial fibrillation. Basically these procedures are done when conventional medical treatment fails to treat the condition.
Catheter Ablation
Indication: Refractory atrial fibrillation (not responding to medication)
Method: Thin, flexible wires are inserted into a vein in the groin and threaded up through the vein and into the heart. There is an electrode at the tip of the wires. The electrode sends out radio waves that create heat. This heat destroys the heart tissue that causes atrial fibrillation or the heart tissue that keeps it happening.
1) Focal ablation
2) Circumferential ablation
3) Pulmonary vein ablation
4) Nodal ablation (attempt to control symptoms)
http://www.revolutionhealth.com/articles/av-node-ablation/zm6205
Of note of this procedure is that a permanent pacemaker would be inserted (note that this procedure actually destroys an AVN. So definitely you need to reimburse something right?)
Maze Surgery
Indication: Chronic Atrial Fibrillation
Method: Refer to Day of Surgery
http://www.texasheartinstitute.org/hic/topics/proced/
http://www.texasheartinstitute.org/hic/topics/proced/mazes.cfm
Basically this is an extension on the previous topic. Related but is a different thing altogether. It's about atrial fibrillation. Basically these procedures are done when conventional medical treatment fails to treat the condition.
Catheter Ablation
Indication: Refractory atrial fibrillation (not responding to medication)
Method: Thin, flexible wires are inserted into a vein in the groin and threaded up through the vein and into the heart. There is an electrode at the tip of the wires. The electrode sends out radio waves that create heat. This heat destroys the heart tissue that causes atrial fibrillation or the heart tissue that keeps it happening.
1) Focal ablation
2) Circumferential ablation
3) Pulmonary vein ablation
4) Nodal ablation (attempt to control symptoms)
http://www.revolutionhealth.com/articles/av-node-ablation/zm6205
Of note of this procedure is that a permanent pacemaker would be inserted (note that this procedure actually destroys an AVN. So definitely you need to reimburse something right?)
Maze Surgery
Indication: Chronic Atrial Fibrillation
Method: Refer to Day of Surgery
Check out this website
http://www.hrsonline.org/Education/SelfStudy/
Okay, so I come across this website. I was looking on a trial--AFFIRM trial just to take a look on the efficacy of antiarrhythmic drugs. For further information about the trial, http://www.hrsonline.org/Education/SelfStudy/ClinicalTrials/AF/AFFIRM.cfm, check out the website I put out.
One word about the AFFIRM study. It's basically comparing the efficacy of using rate-limiting method and rhythm-limiting method to control atrial fibrillation. Result is that no statistical difference observed in both treatment. Rhythm-limiting method is referred usage of sodium channel blockers whilst rate-limiting method is referred to usage of beta-blockers, ccb etc. methods to control atrial fib.
Currently I can't think of any good subject to write on. But what I can do is just look out for good websites where they can provide a certain good information that we could appreciate as a medical student who hungers for nothing but knowledge.
Okay, so I come across this website. I was looking on a trial--AFFIRM trial just to take a look on the efficacy of antiarrhythmic drugs. For further information about the trial, http://www.hrsonline.org/Education/SelfStudy/ClinicalTrials/AF/AFFIRM.cfm, check out the website I put out.
One word about the AFFIRM study. It's basically comparing the efficacy of using rate-limiting method and rhythm-limiting method to control atrial fibrillation. Result is that no statistical difference observed in both treatment. Rhythm-limiting method is referred usage of sodium channel blockers whilst rate-limiting method is referred to usage of beta-blockers, ccb etc. methods to control atrial fib.
Currently I can't think of any good subject to write on. But what I can do is just look out for good websites where they can provide a certain good information that we could appreciate as a medical student who hungers for nothing but knowledge.
Thursday, September 17, 2009
Doppelgänger
I spent some of time waiting for the result playing some games and studying, of course. I recently finished my Silent Hill 2. Quite nice a game with interesting storyline, a bit boring as I need to minimize my window to see the walkthrough. The reason I brought this up because of the fact of the two characters inside the story, namely Mary and Maria. I know why they put the names so close, at least I makes James thinks that Maria can be Mary, but it's not. At first, the story can be confusing but if you tie up everything together, i.e. summarizing the plot of the story from the beginning to the end, everything make sense.
Okay, back to the doppel thing. Mary and Maria are in fact Doppelgänger, according to wikipedia. All the characters depicted meant something. It is not there for nothing. Maria is actually what James depict of from Mary. The other thing is don't treat Silent Hill as some non-sensical illogical horror story. In fact everything happened in the event is just a hallucination, or if strictly speaking, the very inside fear or horror of James (the protagonist) himself.
Just think that this story is on psychology and you will understand and appreciate it. I'd love psychology but I don't like to be in the psychiatrist. That's me^^ Something interesting doesn't mean that you should pursue it forever. You do it when you have the moment to do so.
Anyways, the main thing I want to point out from this game is this phenomenon. Doppelgänger. You bet it, it's a German word. If you like long articles: http://en.wikipedia.org/wiki/Doppelgänger#Left_temporoparietal_junction and
http://paranormal.about.com/library/weekly/aa111102a.htm
Basically it's a phenomenon, more or less pointing towards the fact of one felt another part of oneself away from the body, better known as Out-of-Body Experience (OBE). Below is an interesting article touching a little bit about neurology.
http://www.telefonica.net/web2/lupelandia/piramidescerebro/BLANKE05.pdf
The reason I checked this out because I want to see a real published article about this experiment of out-of-body experience thingy. I bet a lot of people create or listen to hell lots of stories about OBE thingy. Since I am in the field of science, I'd better put up at least a prove to really tell people that hey, this is in fact true and it's written.
Basically it's about the temporoparietal junction playing all these things up. Temporal lobe dysfunction can be a cause of epilepsy of some patients. That's what I know of. Hearing can be affected. In short, it's relative. It depends on which exact nerve got hit. There are lots of myths about this Doppelgänger thingy. But as a fellow human being, like the Confucius said, we have to take care outselves first before thinking about ghost thingy. If you can't be a perfect human being, what's there to talk about ghost? Right? Well, it's just another moral of the story...
Life just not about medicine, ya know?
Okay, back to the doppel thing. Mary and Maria are in fact Doppelgänger, according to wikipedia. All the characters depicted meant something. It is not there for nothing. Maria is actually what James depict of from Mary. The other thing is don't treat Silent Hill as some non-sensical illogical horror story. In fact everything happened in the event is just a hallucination, or if strictly speaking, the very inside fear or horror of James (the protagonist) himself.
Just think that this story is on psychology and you will understand and appreciate it. I'd love psychology but I don't like to be in the psychiatrist. That's me^^ Something interesting doesn't mean that you should pursue it forever. You do it when you have the moment to do so.
Anyways, the main thing I want to point out from this game is this phenomenon. Doppelgänger. You bet it, it's a German word. If you like long articles: http://en.wikipedia.org/wiki/Doppelgänger#Left_temporoparietal_junction and
http://paranormal.about.com/library/weekly/aa111102a.htm
Basically it's a phenomenon, more or less pointing towards the fact of one felt another part of oneself away from the body, better known as Out-of-Body Experience (OBE). Below is an interesting article touching a little bit about neurology.
http://www.telefonica.net/web2/lupelandia/piramidescerebro/BLANKE05.pdf
The reason I checked this out because I want to see a real published article about this experiment of out-of-body experience thingy. I bet a lot of people create or listen to hell lots of stories about OBE thingy. Since I am in the field of science, I'd better put up at least a prove to really tell people that hey, this is in fact true and it's written.
Basically it's about the temporoparietal junction playing all these things up. Temporal lobe dysfunction can be a cause of epilepsy of some patients. That's what I know of. Hearing can be affected. In short, it's relative. It depends on which exact nerve got hit. There are lots of myths about this Doppelgänger thingy. But as a fellow human being, like the Confucius said, we have to take care outselves first before thinking about ghost thingy. If you can't be a perfect human being, what's there to talk about ghost? Right? Well, it's just another moral of the story...
Life just not about medicine, ya know?
Thursday, September 10, 2009
mecA? WTF?
http://gateway.nlm.nih.gov/MeetingAbstracts/ma?f=102244956.html
Quantification of mecA mRNA in Methicillin-Resistant Staphylococcus aureus (MRSA) Strains by Competitive Reverse Transcription-PCR with an Internal cRNA Standard.
Article from: http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T30-4B4VPRF-1&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=1006926609&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=17e63154dff694c0158e73ee4745a762#toc10
Real-time PCR assays were developed for the quantifiable detection of the antibiotic-resistance genes vanA of enterococci, ampC of Enterobacteriaceae, and mecA of staphylococci in different municipal wastewater samples.
Now, say you love genetics. You'd better!! Actually then name itself makes a lot of sense.
P/S: Taken my Step One. I would like to thank also to lots of people, including the person who uploaded Goljan's audio. (Thank you to learnerstv for saving my ass also on neuroanatomy and thank you everyone who supported me throughout)
Quantification of mecA mRNA in Methicillin-Resistant Staphylococcus aureus (MRSA) Strains by Competitive Reverse Transcription-PCR with an Internal cRNA Standard.
Article from: http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T30-4B4VPRF-1&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=1006926609&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=17e63154dff694c0158e73ee4745a762#toc10
Real-time PCR assays were developed for the quantifiable detection of the antibiotic-resistance genes vanA of enterococci, ampC of Enterobacteriaceae, and mecA of staphylococci in different municipal wastewater samples.
Now, say you love genetics. You'd better!! Actually then name itself makes a lot of sense.
P/S: Taken my Step One. I would like to thank also to lots of people, including the person who uploaded Goljan's audio. (Thank you to learnerstv for saving my ass also on neuroanatomy and thank you everyone who supported me throughout)
Monday, September 7, 2009
Opioid induced histamine release
First we look at what exactly is opioid mechanism: http://www.opioids.com/receptors/index.html
Well, I come across this cute question about opioid. When an opioid compound, especially a µ-receptor agonist (such as morphine), is administered in response to chronic pain, this causes the release of histamine in neurons. This leads to the activation of histamine H2 receptors, which play a role in the relief of pain.
Well, take a look at this: http://www.rch.org.au/pharmacy/drugs/index.cfm?doc_id=2113
It seems that it's really opioid fault for inducing histamine release. I find it quite strange as activating histamine can cause pain, doesn't it? How come it is the histamine, especially H2 receptor involved in relieving the pain? Article: Enhanced antinociceptive effects of morphine in histamine H2 receptor gene knockout mice
I shall leave the question mark here. One thing of interest is if in the exam, the other 4 options seem illogical, pick something which you think is logical, though you may or may not know the thing you are going to pick.
Well, I come across this cute question about opioid. When an opioid compound, especially a µ-receptor agonist (such as morphine), is administered in response to chronic pain, this causes the release of histamine in neurons. This leads to the activation of histamine H2 receptors, which play a role in the relief of pain.
Well, take a look at this: http://www.rch.org.au/pharmacy/drugs/index.cfm?doc_id=2113
It seems that it's really opioid fault for inducing histamine release. I find it quite strange as activating histamine can cause pain, doesn't it? How come it is the histamine, especially H2 receptor involved in relieving the pain? Article: Enhanced antinociceptive effects of morphine in histamine H2 receptor gene knockout mice
I shall leave the question mark here. One thing of interest is if in the exam, the other 4 options seem illogical, pick something which you think is logical, though you may or may not know the thing you are going to pick.
Glaucoma
http://www.aafp.org/afp/20030501/1937.html
Cool website with fascinating pictures.
Current treatment: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1705630
Cool website with fascinating pictures.
Current treatment: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1705630
Sunday, September 6, 2009
Osteomalacia
From: http://www.scielo.br/scielo.php?pid=S1807-59322009000200015&script=sci_arttext
In case you are wondering osteomalacia, a condition due to lack of Vitamin D, can cause a deficit in mineralization of osteoid matrix which leads to decrease osteoid altogether. The former is correct but not the latter, i.e. it causes accumulation of osteoid tissue (Relative excess of osteoid) instead of its lost. Great, get it wrong again...
In case you are wondering osteomalacia, a condition due to lack of Vitamin D, can cause a deficit in mineralization of osteoid matrix which leads to decrease osteoid altogether. The former is correct but not the latter, i.e. it causes accumulation of osteoid tissue (Relative excess of osteoid) instead of its lost. Great, get it wrong again...
Purpose of Fructose in Glycogenosis disease
Quote from article: http://www.freepatentsonline.com/4024250.html
Fructose is used to alleviate physiologically-induced stress in the human body. Rationale that comes to from me dad is that fructose stress the liver to break down the glycogen to glucose. In cases like glycogen storage disease, we take von Gierke’s disease (type I) for example, since it's a glucose-6-phosphatase defecient thingy, it can't break down glycogen, which explains it's inability to produce glucose upon the stress from fructose administration.
Cool critical clinical thinking?
Fructose is used to alleviate physiologically-induced stress in the human body. Rationale that comes to from me dad is that fructose stress the liver to break down the glycogen to glucose. In cases like glycogen storage disease, we take von Gierke’s disease (type I) for example, since it's a glucose-6-phosphatase defecient thingy, it can't break down glycogen, which explains it's inability to produce glucose upon the stress from fructose administration.
Cool critical clinical thinking?
Metachromatic granules
I just know this stuff. I was very surprised myself. You might think this is the metachromatic leukodystrophy(ML) (why? coz it's metachromatic). Wrong. It's a totally different thing altogether.
In ML, it's an accumulation of metachromatic lipid which is gives brownish color upon staining of toluidine blue.
However, when they say about this metachromatic granules, they are bascially Alder-Reilly bodies. Well, what the hell is that? It's actually an accumulation of glycosaminoglycans within leukocytes. It's seen in mucopolysaccharidoses aka the famous Hurler's and Hunter's syndrome which I believe USMLE Step 1 love to ask. You can observe large purple cytoplasmic granules, which is the metachromatic granules, of course (source from :http://www.learnerstv.com/onlinetest/medicine/ in Pathology Q11 and Pathology Concise) I can't find a good picture in any books, what I can find is this: http://images.google.com.my/images?hl=en&source=hp&q=Metachromatic+granules&um=1&ie=UTF-8&ei=IcKjSunTNIyBkQXPxo33Dw&sa=X&oi=image_result_group&ct=title&resnum=4
Ah, just google yourself. Till then...
In ML, it's an accumulation of metachromatic lipid which is gives brownish color upon staining of toluidine blue.
However, when they say about this metachromatic granules, they are bascially Alder-Reilly bodies. Well, what the hell is that? It's actually an accumulation of glycosaminoglycans within leukocytes. It's seen in mucopolysaccharidoses aka the famous Hurler's and Hunter's syndrome which I believe USMLE Step 1 love to ask. You can observe large purple cytoplasmic granules, which is the metachromatic granules, of course (source from :http://www.learnerstv.com/onlinetest/medicine/ in Pathology Q11 and Pathology Concise) I can't find a good picture in any books, what I can find is this: http://images.google.com.my/images?hl=en&source=hp&q=Metachromatic+granules&um=1&ie=UTF-8&ei=IcKjSunTNIyBkQXPxo33Dw&sa=X&oi=image_result_group&ct=title&resnum=4
Ah, just google yourself. Till then...
Cool Physiology Website
If you like cracking your head with physiology, try this: http://www2.kumc.edu/ki/physiology/course/outline.htm
If you are studying for your exam and that the exam is about next week, do give yourself a break ya? Phys is hard
Notice something from here: http://www2.kumc.edu/ki/physiology/course/six/6_1.htm
1. A Na-H antiport is present in the apical membrane (Fig 6-2). This electrically neutral 1:1 transporter is driven primarily by the chemical gradient for Na across the membrane. This is a major mechanism for Na entry.
Get it?
If you are studying for your exam and that the exam is about next week, do give yourself a break ya? Phys is hard
Notice something from here: http://www2.kumc.edu/ki/physiology/course/six/6_1.htm
1. A Na-H antiport is present in the apical membrane (Fig 6-2). This electrically neutral 1:1 transporter is driven primarily by the chemical gradient for Na across the membrane. This is a major mechanism for Na entry.
Get it?
Saturday, September 5, 2009
Ventilation Perfusion Defect
This is from: http://www.ccmtutorials.com/rs/oxygen/page09.htm
A word about this thing. It causes hypoxemia, which leads to stimulation of peripheral chemoreceptor in which causing hyperventilation thus lowering arterial carbon dioxide pressure. Cool?
A word about this thing. It causes hypoxemia, which leads to stimulation of peripheral chemoreceptor in which causing hyperventilation thus lowering arterial carbon dioxide pressure. Cool?
Friday, September 4, 2009
Serotonin Syndrome vs NMS
Article from: http://uuhsc.utah.edu/poison/healthpros/utox/Vol4_No4.pdf
This article quotes some interesting facts about serotonin syndrome. As you know, NMS (I forgot the whole name, but it's written there and is caused by dopamine antagonist effect) can have certain common features in terms of the clinical presentation. Therefore I would like to bring a certain attention over this matter.
Feature: Serotonin Syndrome
Mechanism: Serotonin excess
Onset of Symptoms: Minutes to hours
Resolution of symptoms: Less than 24 hours
Neuromuscular: Myoclonus, hyperreflexia
Rhabdomyolysis: Rare
Metabolic acidosis: Rare
Elevated transaminases: Rare
Feature: Neuroleptic Malignant Syndrome
Mechanism: Dopamine antagonism
Onset of Symptoms: Days to weeks
Resolution of symptoms: 5-14 days
Neuromuscular: “lead pipe” rigidity
Rhabdomyolysis: Common
Metabolic acidosis: Common
Elevated transaminases: Common
Anyways, this is from table 3 in the article. I finally found the answer to this mystery to me^^
This article quotes some interesting facts about serotonin syndrome. As you know, NMS (I forgot the whole name, but it's written there and is caused by dopamine antagonist effect) can have certain common features in terms of the clinical presentation. Therefore I would like to bring a certain attention over this matter.
Feature: Serotonin Syndrome
Mechanism: Serotonin excess
Onset of Symptoms: Minutes to hours
Resolution of symptoms: Less than 24 hours
Neuromuscular: Myoclonus, hyperreflexia
Rhabdomyolysis: Rare
Metabolic acidosis: Rare
Elevated transaminases: Rare
Feature: Neuroleptic Malignant Syndrome
Mechanism: Dopamine antagonism
Onset of Symptoms: Days to weeks
Resolution of symptoms: 5-14 days
Neuromuscular: “lead pipe” rigidity
Rhabdomyolysis: Common
Metabolic acidosis: Common
Elevated transaminases: Common
Anyways, this is from table 3 in the article. I finally found the answer to this mystery to me^^
Some USMLE Prep
I come across this website: http://en.wikibooks.org/wiki/USMLE_Step_1_Review
Okay, it listed out some website I think it is useful to those students who are preparing for the boards exam.
1) http://www.learnerstv.com
2) http://www.stepprep.com
3) http://www.clinicalreview.com/welcome/
I have doubts on the third site, but the top two sites, I think, are quite good. Since it's free, why not just give a try? I seriously don't have much time to waste. Next Thursday will be my exam. Hope everything goes well and hope that all the questions which appear during the exam are all of which I had done them before or know the answer, somehow. Pray hard...
Okay, it listed out some website I think it is useful to those students who are preparing for the boards exam.
1) http://www.learnerstv.com
2) http://www.stepprep.com
3) http://www.clinicalreview.com/welcome/
I have doubts on the third site, but the top two sites, I think, are quite good. Since it's free, why not just give a try? I seriously don't have much time to waste. Next Thursday will be my exam. Hope everything goes well and hope that all the questions which appear during the exam are all of which I had done them before or know the answer, somehow. Pray hard...
Friday, August 28, 2009
4 random names of syndromes
1. Gradenigo syndrome
Triad: abducens nerve palsy, pain in distribution of trigeminal nerve, otitis media.
The syndrome must be suspected in patients with suppurative otitis media presents with orbital or retro-orbital pain and or cranial nerve palsy. This syndrome normally presents as a complication of another disease, i.e. acute suppurative otitis media. It takes time to develop before it really cause serious major complication. Treatment has to be started immediately.
2. Vernet syndrome
Paresis of 9th–11th (with or without 12th) cranial nerves together.
Also known as jugular foramen syndrome. Make sense. If you love long articles, like me, do read this. Read this also: http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T06-4SF9CFC-1&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=993765207&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=9e52d751ce6f397a23719b0a362ac454.
3. Villaret syndrome
This syndrome is characterized by an ipsilateral paralysis of cranial nerves numbers IX ,X, XI, XII, and sometimes cranial nerve number VII, and it can also involve the cervical ganglia of the sympathetic trunk. Paralysis is caused by a lesion in the posterior retroparotid space, e.g. glomus tumors (most frequently).
P/S: Looks like the V syndromes concern more on the jugular foramen nerve thingy...
4. Foix-Jefferson syndrome ( also known as Also known as: Godtfredsen's disease, Foix’ syndrome II)
Syndrome of trigeminal neuralgia, oculomotor paralysis, XIIth nerve paralysis and ophthalmoplegia, due to invasion of nasopharyngeal tumours into the base of the skull and adjacent structures, and compression of the hypoglossal nerve by enlarged retropharyngeal lymph nodes. Generally similar to the Jacod’s syndrome (retrosphenoidal syndrome). From http://www.whonamedit.com/synd.cfm/1525.html
Foix-Jefferson syndrome: Formation of a blood clot composed of platelets and fibrin in the CAVERNOUS SINUS of the brain. Infections of the paranasal sinuses and adjacent structures, CRANIOCEREBRAL TRAUMA, and THROMBOPHILIA are associated conditions. Clinical manifestations include dysfunction of cranial nerves III, IV, V, and VI, marked periorbital swelling, chemosis, fever, and visual loss. (From Adams et al., Principles of Neurology, 6th ed, p711)
Sounds like: cavernous sinus thrombosis? http://www.wrongdiagnosis.com/medical/foix_jefferson_syndrome.htm
So that's all for the weirdo names. One thing interesting are that they concern on neurology. Though some names can be quite confusing.
Triad: abducens nerve palsy, pain in distribution of trigeminal nerve, otitis media.
The syndrome must be suspected in patients with suppurative otitis media presents with orbital or retro-orbital pain and or cranial nerve palsy. This syndrome normally presents as a complication of another disease, i.e. acute suppurative otitis media. It takes time to develop before it really cause serious major complication. Treatment has to be started immediately.
2. Vernet syndrome
Paresis of 9th–11th (with or without 12th) cranial nerves together.
Also known as jugular foramen syndrome. Make sense. If you love long articles, like me, do read this. Read this also: http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T06-4SF9CFC-1&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=993765207&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=9e52d751ce6f397a23719b0a362ac454.
3. Villaret syndrome
This syndrome is characterized by an ipsilateral paralysis of cranial nerves numbers IX ,X, XI, XII, and sometimes cranial nerve number VII, and it can also involve the cervical ganglia of the sympathetic trunk. Paralysis is caused by a lesion in the posterior retroparotid space, e.g. glomus tumors (most frequently).
P/S: Looks like the V syndromes concern more on the jugular foramen nerve thingy...
4. Foix-Jefferson syndrome ( also known as Also known as: Godtfredsen's disease, Foix’ syndrome II)
Syndrome of trigeminal neuralgia, oculomotor paralysis, XIIth nerve paralysis and ophthalmoplegia, due to invasion of nasopharyngeal tumours into the base of the skull and adjacent structures, and compression of the hypoglossal nerve by enlarged retropharyngeal lymph nodes. Generally similar to the Jacod’s syndrome (retrosphenoidal syndrome). From http://www.whonamedit.com/synd.cfm/1525.html
Foix-Jefferson syndrome: Formation of a blood clot composed of platelets and fibrin in the CAVERNOUS SINUS of the brain. Infections of the paranasal sinuses and adjacent structures, CRANIOCEREBRAL TRAUMA, and THROMBOPHILIA are associated conditions. Clinical manifestations include dysfunction of cranial nerves III, IV, V, and VI, marked periorbital swelling, chemosis, fever, and visual loss. (From Adams et al., Principles of Neurology, 6th ed, p711)
Sounds like: cavernous sinus thrombosis? http://www.wrongdiagnosis.com/medical/foix_jefferson_syndrome.htm
So that's all for the weirdo names. One thing interesting are that they concern on neurology. Though some names can be quite confusing.
Atrioventricular Septal Defect
Two types, namely partial and complete. Important point here is that this condition is most related to Down syndrome.
Partial: Primum atrial septal defect combined with cleft mitral valve. I can't find any good source related to this, but I do find this.
http://www.med.yale.edu/intmed/cardio/chd/e_cleft_mv/index.html
Well, I can't differentiate which is what. (where the hell is the cleft mitral valve? ==) I found this from: http://www.mayoclinic.org/atrial-septal-defect/types.html
A mitral valve cleft is a slit-like or elongated hole in one of the leaflets (anterior leaflet) that form the mitral valve.
Check out some cool pictures from there ya?
Complete: Common atrioventricular canal. How about this in http://en.wikipedia.org/wiki/Atrioventricular_septal_defect Look at the picture there. I think it's self explanatory.
Partial: Primum atrial septal defect combined with cleft mitral valve. I can't find any good source related to this, but I do find this.
http://www.med.yale.edu/intmed/cardio/chd/e_cleft_mv/index.html
Well, I can't differentiate which is what. (where the hell is the cleft mitral valve? ==) I found this from: http://www.mayoclinic.org/atrial-septal-defect/types.html
A mitral valve cleft is a slit-like or elongated hole in one of the leaflets (anterior leaflet) that form the mitral valve.
Check out some cool pictures from there ya?
Complete: Common atrioventricular canal. How about this in http://en.wikipedia.org/wiki/Atrioventricular_septal_defect Look at the picture there. I think it's self explanatory.
Thursday, August 27, 2009
Short cases for MRCP
http://www.mrcophth.com/commonshortcases/commonshortcasesindex1.html
I was looking at this part of the case: http://www.mrcophth.com/ptosis/ptosiscommoncases.html#mgjw
Maybe I didn't tell everything. Lolz. I was checking out the "down-and-out" phenomenon of the CN III palsy. http://www.mrcophth.com/ptosis/thirdnerveplasy.html
Play odds. What is the cause of CN III palsy? Uncal herniation...(lolz, play odds)
I was looking at this part of the case: http://www.mrcophth.com/ptosis/ptosiscommoncases.html#mgjw
Maybe I didn't tell everything. Lolz. I was checking out the "down-and-out" phenomenon of the CN III palsy. http://www.mrcophth.com/ptosis/thirdnerveplasy.html
Play odds. What is the cause of CN III palsy? Uncal herniation...(lolz, play odds)
Saturday, August 22, 2009
Adjustment Disorders
Source from: http://www.athealth.com/consumer/disorders/adjustment.html
Adjustment disorder
According to DSM-IV-TR subtypes, are divided into:
1) With depressed mood
2) With anxiety
3) With mixed anxiety and depressed mood
4) With disturbance of conduct
5) With mixed disturbance of emotion and conduct
Listed below are some of the characteristics associated with adjustment disorders:
A person with an adjustment disorder with depressed mood may have mostly a depressed mood, hopeless feelings, and crying spells.
A person with an adjustment disorder with anxiety would experience anxious feelings, nervousness, and worry.
Someone with an adjustment disorder with mixed anxiety and depressed mood would, obviously, have a mixture of anxious and depressed feelings.
An individual with an adjustment disorder with disturbance of conduct may act out inappropriately. This person may act out against society, skip school, or begin to have trouble with the police.
A person with an adjustment disorder with mixed disturbance of emotions and conduct would have a mixture of emotional and conduct problems.
Hope that's helpful. Anyways it's a problem of anxiety, depressed mood and disturbance of conduct. 3 stuffs. Despite the word anxiety, it's not categorized as an anxiety disorder, rather it's put in other psychiatric disorder. Just a small comment by me, correction anyone? And oh yeah, it can bring impact to one's social life. So it does have an impact on psychological well being of the person.
Adjustment disorder
According to DSM-IV-TR subtypes, are divided into:
1) With depressed mood
2) With anxiety
3) With mixed anxiety and depressed mood
4) With disturbance of conduct
5) With mixed disturbance of emotion and conduct
Listed below are some of the characteristics associated with adjustment disorders:
A person with an adjustment disorder with depressed mood may have mostly a depressed mood, hopeless feelings, and crying spells.
A person with an adjustment disorder with anxiety would experience anxious feelings, nervousness, and worry.
Someone with an adjustment disorder with mixed anxiety and depressed mood would, obviously, have a mixture of anxious and depressed feelings.
An individual with an adjustment disorder with disturbance of conduct may act out inappropriately. This person may act out against society, skip school, or begin to have trouble with the police.
A person with an adjustment disorder with mixed disturbance of emotions and conduct would have a mixture of emotional and conduct problems.
Hope that's helpful. Anyways it's a problem of anxiety, depressed mood and disturbance of conduct. 3 stuffs. Despite the word anxiety, it's not categorized as an anxiety disorder, rather it's put in other psychiatric disorder. Just a small comment by me, correction anyone? And oh yeah, it can bring impact to one's social life. So it does have an impact on psychological well being of the person.
Friday, August 14, 2009
HMO vs PPO
http://healthinsurance.about.com/od/jobbasedcoverage/a/hmovsppo.htm
In case, you come across this stuff. You know, the highly debated American health care system. No, it's just a difference between HMO and PPO. You don't know what it is? Go wiki it. I know it's kinda long winded, but it gives you at least some idea on the health care insurance type.
Quote from my friend: these stuffs are extremely low yield. No need to spend too much time on this stuffs? Sounds rational to me...
In case, you come across this stuff. You know, the highly debated American health care system. No, it's just a difference between HMO and PPO. You don't know what it is? Go wiki it. I know it's kinda long winded, but it gives you at least some idea on the health care insurance type.
Quote from my friend: these stuffs are extremely low yield. No need to spend too much time on this stuffs? Sounds rational to me...
Contaminant on culture dish?
http://faculty.mc3.edu/jearl/ML/ml-9.htm
Well, just a picture about contaminants found on culture dish.
Well, just a picture about contaminants found on culture dish.
Monday, August 3, 2009
Brainstem Anatomy
http://www.medicalgeek.com/mnemonics/21971-brainstem-anatomy-mnemonics.html
Well I found it hard to understand this stuff. But erm, just go and check out this cool mnemonics, ya?
Well I found it hard to understand this stuff. But erm, just go and check out this cool mnemonics, ya?
Thursday, July 30, 2009
Dermatology
http://www.medscape.com/features/slideshow/mole-melanoma
A good slideshow displaying a series of dermatological pictures and description. Excellent start for IMU students like us in Phase 1 who haven't studied a little on dermatological problems.
A good slideshow displaying a series of dermatological pictures and description. Excellent start for IMU students like us in Phase 1 who haven't studied a little on dermatological problems.
Wednesday, July 29, 2009
Spiders
Okay, just listened to Dr. Goljan audio lectures. Stunned to me is that he mentioned spiders. I never thought spiders can even come out as question itself in any exam. Well, guess a little information won't ruin you right? But the overwhelming information does. So, this is what I found out about spiders:
There are 2 types of feared spiders we need to know in States, i.e. Latrodectus mactans, otherwise known as the (southern) Black widow spider and the brown recluse spider, Loxosceles reclusa. The first one was well known of an interesting fact, which is male cannibalism (meaning the spider will "eat" up the male after mating. That's why they are widows!) Take note that not all black widow spider does this, this is only special on the above mentioned species. The venom of brown recluse spider is a more fearsome one compared to Latrodectus mactans.
Lactrodectus mactans
(Check out: http://www.emedicinehealth.com/black_widow_spider_bite/article_em.htm & http://en.wikipedia.org/wiki/Latrodectus_mactans)
Basically this is the one which secretes neurotoxic venom. Something like painful muscle contraction those kind of stuff. Latrodectism (http://en.wikipedia.org/wiki/Latrodectism), main thing here is the group of muscle pain presented in the clinic with particular interest on abdominal cramps. One may even ended up a surgery to see what's inside, only to find that everything's normal.
Loxosceles reclusa
(Check out http://en.wikipedia.org/wiki/Brown_recluse_spider)
Symptoms otherwise known as loxoscelism. This is a much more deadlier, a more potent venom, even deadlier than cobras? Come out during the night. Can cause much more severe symptoms than latrodectism, includes DIC, hemolysis etc.
Treatment tends to skew towards giving anti-venom, because it's obvious to give anti-something treatment. Of course there are other treatment as well. Main thing here is if you don't disturb them, they don't disturb you. Please do check out how to prevent this pests from hurting you. No need for arachno-phobia, just be yourself and take all necessary precautions. That's all.
There are 2 types of feared spiders we need to know in States, i.e. Latrodectus mactans, otherwise known as the (southern) Black widow spider and the brown recluse spider, Loxosceles reclusa. The first one was well known of an interesting fact, which is male cannibalism (meaning the spider will "eat" up the male after mating. That's why they are widows!) Take note that not all black widow spider does this, this is only special on the above mentioned species. The venom of brown recluse spider is a more fearsome one compared to Latrodectus mactans.
Lactrodectus mactans
(Check out: http://www.emedicinehealth.com/black_widow_spider_bite/article_em.htm & http://en.wikipedia.org/wiki/Latrodectus_mactans)
Basically this is the one which secretes neurotoxic venom. Something like painful muscle contraction those kind of stuff. Latrodectism (http://en.wikipedia.org/wiki/Latrodectism), main thing here is the group of muscle pain presented in the clinic with particular interest on abdominal cramps. One may even ended up a surgery to see what's inside, only to find that everything's normal.
Loxosceles reclusa
(Check out http://en.wikipedia.org/wiki/Brown_recluse_spider)
Symptoms otherwise known as loxoscelism. This is a much more deadlier, a more potent venom, even deadlier than cobras? Come out during the night. Can cause much more severe symptoms than latrodectism, includes DIC, hemolysis etc.
Treatment tends to skew towards giving anti-venom, because it's obvious to give anti-something treatment. Of course there are other treatment as well. Main thing here is if you don't disturb them, they don't disturb you. Please do check out how to prevent this pests from hurting you. No need for arachno-phobia, just be yourself and take all necessary precautions. That's all.
Tuesday, July 28, 2009
ECG Quiz
http://ecg.bidmc.harvard.edu/maven/mavenmain.asp
Yes, I found a good website. A harvard website apparently, talking about ECG. Challenge yourself with the 404 ECG questions posted there.
Yes, I found a good website. A harvard website apparently, talking about ECG. Challenge yourself with the 404 ECG questions posted there.
Friday, July 24, 2009
Histology
Go check out this histology site I found. Challenge yourself by identifying all the structures or organelles, to be accurate, in a simple cell.
http://www.bu.edu/histology/m/t_electr.htm
P/S: If there is no label for the EM graphs, I wouldn't have known what I am seeing, seriously...
http://www.bu.edu/histology/m/t_electr.htm
P/S: If there is no label for the EM graphs, I wouldn't have known what I am seeing, seriously...
Sunday, July 19, 2009
Protein Synthesis
This is a good site for biochemistry learning in terms of protein synthesis: http://www.biostudio.com/d_%20Protein%20Synthesis%20Prokaryotic.htm
It so happen that I was doing my USMLE question bank and I was shocked that there is a certain stuff which is not known to me until recently after I surf the net. Okay, it's just a sequence in the mRNA which is named Shine-Dalgarno sequence. It is the initiator of the protein synthesis in prokaryotes. Homologous to this in eukaryotes is Kozak sequence. I am not sure whether this is tested as I seldom see this in my books. There are also lots of factors playing around in the process of protein synthesis. Main thing we are concern of in clinical practice is the diphtheria toxin which inhibits protein synthesis via ADP ribosylation of EF-2. EF-2 is essential in eukaryotes in peptide elongation (translation process), as the same function as it is being named after. If it's the case of prokaryotes, then it is EF-Tu, something like that. Of course these are not just the only factors involved in the protein synthesis.
It so happen that I was doing my USMLE question bank and I was shocked that there is a certain stuff which is not known to me until recently after I surf the net. Okay, it's just a sequence in the mRNA which is named Shine-Dalgarno sequence. It is the initiator of the protein synthesis in prokaryotes. Homologous to this in eukaryotes is Kozak sequence. I am not sure whether this is tested as I seldom see this in my books. There are also lots of factors playing around in the process of protein synthesis. Main thing we are concern of in clinical practice is the diphtheria toxin which inhibits protein synthesis via ADP ribosylation of EF-2. EF-2 is essential in eukaryotes in peptide elongation (translation process), as the same function as it is being named after. If it's the case of prokaryotes, then it is EF-Tu, something like that. Of course these are not just the only factors involved in the protein synthesis.
Thursday, July 16, 2009
An Abnormal Fetal Ultrasound
This is from the website: http://cme.medscape.com/viewarticle/705813?src=emed_case_nl_0
Just wanted to put it in a way that I could understand the stuff.
A 30-year-old gravida 3, para 2 patient who is 23 weeks pregnant presents to the maternal-fetal medicine department. She was referred to the maternal-fetal medicine department at the request of her primary obstetrician following an obstetric ultrasound that demonstrated complete placenta previa. The patient has a history of 2 prior pregnancies complicated by complete placenta previa. Both prior pregnancies were delivered by low transverse cesarean sections (LTCS). The patient has no other previous surgical history or significant past medical history. She has no known allergies and is not currently taking medications. She does not report any vaginal bleeding. She has no abdominal pain, cramps, or contractions. Quickening was first noted at 19 weeks and she continues to feel regular fetal movement. She denies having any vaginal discharge or leakage of fluid. She has no other complaints.
The patient is well-appearing on physical examination. Her blood pressure is 90/60 mm Hg and her heart rate is 90 bpm. She has normal respirations at a rate of 12 breaths/min, with an oxygen saturation of 96% while breathing room air and a tympanically obtained temperature of 99°F (37.2°C). She weighs 165 lb (74.8 kg) and has a body mass index (BMI) of 28.3. The cardiovascular and respiratory examinations are unremarkable. The abdomen is gravid, with a fundal height of 24 cm. She has positive bowel sounds in 4 quadrants and no tenderness to palpation. No peripheral edema or rash is present.
The patient is blood type A-positive, with a negative antibody screen. Additionally, the rapid plasma reagent (RPR) examination is nonreactive for syphilis, and the hepatitis B surface antigen test is negative. A diabetes screen is normal at 23.4 weeks (however, this is typically done at 26-28 weeks). Her antibody screen is negative. Her complete blood cell count (CBC) demonstrates a hemoglobin of 14 g/dL (140 g/L; normal range, 12.0-15.0 g/dL) and a platelet count of 290 × 103/µL (290 × 109/L; normal range, 100-450 × 103/µL). The urine analysis demonstrates no evidence of hematuria or proteinuria. A follow-up ultrasound is performed (see Figures 1 and 2), followed by magnetic resonance imaging (MRI) (see Figure 3).
ANSWER:
The ultrasound demonstrated complete placenta previa (see Figure 1). Additionally, at the site of previous cesarean section, there was significant thinning of the uterus with loss of the placental-uterine interface (see Figure 2). It was also difficult to visualize a plane between the bladder and the uterus and, because of this, placenta accreta or percreta was suspected. Additional Doppler imaging did not demonstrate serosal extension of the placental vascularity. The subsequent MRI scan (see Figure 3) also demonstrated focal loss of the uterine-placental interface (best visualized on the T2-weighted sequences) within the lower uterine segment at the site of previous cesarean section (Figure 4), which is consistent with at least placenta accreta. No placental invasion was visualized, but the fat plane between the bladder and the uterus was not clearly identified to rule out bladder invasion.
Placenta accreta was at one time a quite rare condition, but it is becoming increasingly more common. The etiology is thought to be the rising cesarean delivery rate, which reached an all-time high of 29.1% in the United States in 2004.[1] Other risk factors for placenta accreta include multiparity, increasing maternal age, endometrial defects, scarring of the uterus (Asherman syndrome), and most significantly, placenta previa. Placenta previa is implantation of the placenta in the immediate vicinity of the cervical canal. In complete placenta previa, the placenta covers the entire opening of the internal cervical os. In partial placenta previa, the placenta partially covers the internal cervical os. Marginal placenta previa and low lying placenta are also described; these occur when the placenta extends to the edge of the internal cervical os or within 2.0 cm of the internal cervical os, respectively. An important point is that most cases of complete previa early in the second trimester will resolve during the pregnancy.[1]
Placenta accreta is one of 3 different types of abnormal placentation. Placenta accreta, accounting for 75% of all the cases, is the most common presenting type. Placenta accreta occurs when the placental villi adheres directly to the myometrium but does not penetrate the muscular layer, with the complete or partial absence of the decidua basalis. Placenta increta accounts for 15% of all cases and is characterized by the adherence of placental villi directly to the myometrium and demonstrates penetration within the myometrium. Placenta percreta, the least common of the 3, is the penetration of the placental villi into the serosal layer of the uterus. There may also be direct attachment to adjacent organs. Although all 3 types are characteristically different, the literature many times collectively refers to abnormal placentation together as placenta accreta. The clinical history in this particular case is extremely important since a patient with a placenta previa and a history of 2 previous cesarean sections carries a risk of approximately 40% for placenta accreta. Imaging can help raise or lower the concern for accreta in high-risk patients, but it is not usually definitive, which limits its ability to change management in these patients.
Transabdominal and transvaginal ultrasonography remain the imaging modalities of choice in detecting placenta accreta. In women with a previous history of cesarean section, second trimester sonographic evaluation may be helpful. The location of the previous cesarean section should be closely examined because the placenta has a tendency to adhere to this area. MRI is commonly used when ultrasonography remains uncertain (please see below). Although the use of ultrasonography and MRI provide a high degree of suspicion of placenta accreta, there is no imaging study that can diagnose placenta accreta with absolute accuracy. This has been demonstrated in a number of recent studies that compared the imaging findings of placenta accreta to the pathologic evaluation. Sonographic findings that give a high index of suspicion of placenta accreta include, but are not limited to, loss of the hypoechoic retroplacental myometrial zone, thinned hyperechoic uterine-bladder interface, presence of placental lacunae, and focal exophytic masses within the bladder. Color Doppler imaging also aids in the evaluation of placenta accreta. The use of color-Doppler has improved the sensitivity of grayscale ultrasonography because it depicts the local vascular anatomy within the uterus and related organs.[2]
MRI has come to the forefront in the evaluation of placenta accreta. MRI findings that are suggestive of placenta accreta include uterine bulging, heterogeneous signal intensity within the placenta, and the presence of dark intraplacental bands on T2-weighted imaging.[3] There have been a limited number of studies that have compared the accuracy of MRI and ultrasonography in the diagnosis of placenta accreta. A recent study found that ultrasonography had a sensitivity of 77% and a specificity of 96%. In comparison, MRI had a sensitivity of 88% and a specificity of 100%. The superiority of MRI over ultrasonography, however, was not statistically significant.[1] In this study, all patients with ultrasonographic examinations suggestive of placenta accreta underwent MRI scanning. If the appearance of placenta accreta was suspected, the patient also underwent a dynamic gadolinium-enhanced MRI series. This confirmed the presence of deep invasion. Palacios et al studied 300 patients with suspected placenta accreta using gadolinium contrast in an attempt to classify the depth levels and topographic areas in relation to the posterior bladder wall.[4] The MRI scans where then compared to the pathologic findings. The results of this study, however, were not used to further define the screening characteristics of placenta accreta, but rather to establish a modified surgical technique. The aim was to reduce complications at the time of surgery. Because gadolinium crosses the placenta, and the half-life and safety profile in pregnancy has not been established, the American College of Radiology recommends its usage only if the benefits outweigh the potential risks. Kim et al defined the appearance of the placental myometrial interface using the half-Fourier acquisition single-shot turbo spin-echo (HASTE) sequence: it has 3 layers, including the inner low signal-intensity layer, middle high signal-intensity layer, and an outer low signal-intensity layer.[8] In placenta accreta, there was focal nonvisualization of the inner layer. The limitations of this study were that only 5 patients were included, all of whom had prior cesarean deliveries, and no comparative studies could be made. Since there is only a limited amount of literature describing the normal anatomy of this area with the use of fast sequences, MRI remains only an adjuvant to inconclusive ultrasonography findings, or it can be used to evaluate accreta when adherence occurs in the posterior or fundal portions of the uterus.[1,2,3]
Placenta accreta is potentially life-threatening to both mother and fetus. The immediate clinical consequence of placenta accreta is massive hemorrhage at the time of placental removal, and it is the most common indication for emergency intra- or postpartum hysterectomy.[1] Since it is known that placenta previa is a risk factor for placental accreta, it is common for a patient to present with third trimester painless vaginal bleeding. Complications such as hematuria may occur if placenta percreta is present, resulting from direct penetration into the bladder. Because of this, a urine analysis is sometimes performed. In a patient with imaging findings highly suggestive of placenta accreta, management must begin in the prenatal period. In this period, it is essential that a multidisciplinary approach be used to fully inform the patient and family of the potential outcomes and management options. The risks and benefits of extirpative versus conservative management should be adequately discussed with the patient. Extirpative management, with a scheduled cesarean section and hysterectomy at 35-37 weeks of gestation, may be performed. If the patient opts for uterine conservation to allow for subsequent pregnancy, there are measures that can be implemented. Commonly, cesarean section alone can be successful, since most cases of accreta are focal. Methotrexate administration and uterine artery embolization have been reported, and the literature has either demonstrated various results (with methotrexate) or has suggested no benefit (uterine artery embolization).[7] Whether extirpative or uterine-conserving management is chosen, it is important that the delivery be performed in a center with staff trained for complicated surgeries potentially involving the bowel or bladder, and appropriate equipment and resources should be available to handle the many significant complications that may be encountered at the time of the procedure. A blood bank capable of providing large volumes of blood in emergency situations is particularly important.[1,7]
Given the patient's findings on ultrasonography and MRI, a cesarean delivery was scheduled, with a high probability of hysterectomy. At the time of the cesarean delivery, the patient was 36 weeks and 5 days intrauterine gestation by ultrasonographic dating. As a result of the close approximation of the ureters and the increased risk of trauma during this procedure, the patient underwent bilateral ureteral stent placement for direct visualization of the ureters. After delivery of the fetus, a portion of the placenta remained tightly adherent to the uterus. The decision was made to proceed with a cesarean supracervical hysterectomy. The patient tolerated the procedure well. No complications were noted, and the patient was taken to the recovery room in stable condition. The pathologic findings were an area of thinning consistent with previous low-transverse incision, with scar formation on the anterior surface of the uterus. This scarred area was focally and markedly thinned to 2 mm in thickness. The placenta was adherent to this area. Examination of the surgical specimen displayed a uterus with focal changes of placenta accreta. The patient was discharged to home from the hospital 4 days after her surgery.
Figure 1
Figure 2
Figure 3
Figure 4
Just wanted to put it in a way that I could understand the stuff.
A 30-year-old gravida 3, para 2 patient who is 23 weeks pregnant presents to the maternal-fetal medicine department. She was referred to the maternal-fetal medicine department at the request of her primary obstetrician following an obstetric ultrasound that demonstrated complete placenta previa. The patient has a history of 2 prior pregnancies complicated by complete placenta previa. Both prior pregnancies were delivered by low transverse cesarean sections (LTCS). The patient has no other previous surgical history or significant past medical history. She has no known allergies and is not currently taking medications. She does not report any vaginal bleeding. She has no abdominal pain, cramps, or contractions. Quickening was first noted at 19 weeks and she continues to feel regular fetal movement. She denies having any vaginal discharge or leakage of fluid. She has no other complaints.
The patient is well-appearing on physical examination. Her blood pressure is 90/60 mm Hg and her heart rate is 90 bpm. She has normal respirations at a rate of 12 breaths/min, with an oxygen saturation of 96% while breathing room air and a tympanically obtained temperature of 99°F (37.2°C). She weighs 165 lb (74.8 kg) and has a body mass index (BMI) of 28.3. The cardiovascular and respiratory examinations are unremarkable. The abdomen is gravid, with a fundal height of 24 cm. She has positive bowel sounds in 4 quadrants and no tenderness to palpation. No peripheral edema or rash is present.
The patient is blood type A-positive, with a negative antibody screen. Additionally, the rapid plasma reagent (RPR) examination is nonreactive for syphilis, and the hepatitis B surface antigen test is negative. A diabetes screen is normal at 23.4 weeks (however, this is typically done at 26-28 weeks). Her antibody screen is negative. Her complete blood cell count (CBC) demonstrates a hemoglobin of 14 g/dL (140 g/L; normal range, 12.0-15.0 g/dL) and a platelet count of 290 × 103/µL (290 × 109/L; normal range, 100-450 × 103/µL). The urine analysis demonstrates no evidence of hematuria or proteinuria. A follow-up ultrasound is performed (see Figures 1 and 2), followed by magnetic resonance imaging (MRI) (see Figure 3).
ANSWER:
The ultrasound demonstrated complete placenta previa (see Figure 1). Additionally, at the site of previous cesarean section, there was significant thinning of the uterus with loss of the placental-uterine interface (see Figure 2). It was also difficult to visualize a plane between the bladder and the uterus and, because of this, placenta accreta or percreta was suspected. Additional Doppler imaging did not demonstrate serosal extension of the placental vascularity. The subsequent MRI scan (see Figure 3) also demonstrated focal loss of the uterine-placental interface (best visualized on the T2-weighted sequences) within the lower uterine segment at the site of previous cesarean section (Figure 4), which is consistent with at least placenta accreta. No placental invasion was visualized, but the fat plane between the bladder and the uterus was not clearly identified to rule out bladder invasion.
Placenta accreta was at one time a quite rare condition, but it is becoming increasingly more common. The etiology is thought to be the rising cesarean delivery rate, which reached an all-time high of 29.1% in the United States in 2004.[1] Other risk factors for placenta accreta include multiparity, increasing maternal age, endometrial defects, scarring of the uterus (Asherman syndrome), and most significantly, placenta previa. Placenta previa is implantation of the placenta in the immediate vicinity of the cervical canal. In complete placenta previa, the placenta covers the entire opening of the internal cervical os. In partial placenta previa, the placenta partially covers the internal cervical os. Marginal placenta previa and low lying placenta are also described; these occur when the placenta extends to the edge of the internal cervical os or within 2.0 cm of the internal cervical os, respectively. An important point is that most cases of complete previa early in the second trimester will resolve during the pregnancy.[1]
Placenta accreta is one of 3 different types of abnormal placentation. Placenta accreta, accounting for 75% of all the cases, is the most common presenting type. Placenta accreta occurs when the placental villi adheres directly to the myometrium but does not penetrate the muscular layer, with the complete or partial absence of the decidua basalis. Placenta increta accounts for 15% of all cases and is characterized by the adherence of placental villi directly to the myometrium and demonstrates penetration within the myometrium. Placenta percreta, the least common of the 3, is the penetration of the placental villi into the serosal layer of the uterus. There may also be direct attachment to adjacent organs. Although all 3 types are characteristically different, the literature many times collectively refers to abnormal placentation together as placenta accreta. The clinical history in this particular case is extremely important since a patient with a placenta previa and a history of 2 previous cesarean sections carries a risk of approximately 40% for placenta accreta. Imaging can help raise or lower the concern for accreta in high-risk patients, but it is not usually definitive, which limits its ability to change management in these patients.
Transabdominal and transvaginal ultrasonography remain the imaging modalities of choice in detecting placenta accreta. In women with a previous history of cesarean section, second trimester sonographic evaluation may be helpful. The location of the previous cesarean section should be closely examined because the placenta has a tendency to adhere to this area. MRI is commonly used when ultrasonography remains uncertain (please see below). Although the use of ultrasonography and MRI provide a high degree of suspicion of placenta accreta, there is no imaging study that can diagnose placenta accreta with absolute accuracy. This has been demonstrated in a number of recent studies that compared the imaging findings of placenta accreta to the pathologic evaluation. Sonographic findings that give a high index of suspicion of placenta accreta include, but are not limited to, loss of the hypoechoic retroplacental myometrial zone, thinned hyperechoic uterine-bladder interface, presence of placental lacunae, and focal exophytic masses within the bladder. Color Doppler imaging also aids in the evaluation of placenta accreta. The use of color-Doppler has improved the sensitivity of grayscale ultrasonography because it depicts the local vascular anatomy within the uterus and related organs.[2]
MRI has come to the forefront in the evaluation of placenta accreta. MRI findings that are suggestive of placenta accreta include uterine bulging, heterogeneous signal intensity within the placenta, and the presence of dark intraplacental bands on T2-weighted imaging.[3] There have been a limited number of studies that have compared the accuracy of MRI and ultrasonography in the diagnosis of placenta accreta. A recent study found that ultrasonography had a sensitivity of 77% and a specificity of 96%. In comparison, MRI had a sensitivity of 88% and a specificity of 100%. The superiority of MRI over ultrasonography, however, was not statistically significant.[1] In this study, all patients with ultrasonographic examinations suggestive of placenta accreta underwent MRI scanning. If the appearance of placenta accreta was suspected, the patient also underwent a dynamic gadolinium-enhanced MRI series. This confirmed the presence of deep invasion. Palacios et al studied 300 patients with suspected placenta accreta using gadolinium contrast in an attempt to classify the depth levels and topographic areas in relation to the posterior bladder wall.[4] The MRI scans where then compared to the pathologic findings. The results of this study, however, were not used to further define the screening characteristics of placenta accreta, but rather to establish a modified surgical technique. The aim was to reduce complications at the time of surgery. Because gadolinium crosses the placenta, and the half-life and safety profile in pregnancy has not been established, the American College of Radiology recommends its usage only if the benefits outweigh the potential risks. Kim et al defined the appearance of the placental myometrial interface using the half-Fourier acquisition single-shot turbo spin-echo (HASTE) sequence: it has 3 layers, including the inner low signal-intensity layer, middle high signal-intensity layer, and an outer low signal-intensity layer.[8] In placenta accreta, there was focal nonvisualization of the inner layer. The limitations of this study were that only 5 patients were included, all of whom had prior cesarean deliveries, and no comparative studies could be made. Since there is only a limited amount of literature describing the normal anatomy of this area with the use of fast sequences, MRI remains only an adjuvant to inconclusive ultrasonography findings, or it can be used to evaluate accreta when adherence occurs in the posterior or fundal portions of the uterus.[1,2,3]
Placenta accreta is potentially life-threatening to both mother and fetus. The immediate clinical consequence of placenta accreta is massive hemorrhage at the time of placental removal, and it is the most common indication for emergency intra- or postpartum hysterectomy.[1] Since it is known that placenta previa is a risk factor for placental accreta, it is common for a patient to present with third trimester painless vaginal bleeding. Complications such as hematuria may occur if placenta percreta is present, resulting from direct penetration into the bladder. Because of this, a urine analysis is sometimes performed. In a patient with imaging findings highly suggestive of placenta accreta, management must begin in the prenatal period. In this period, it is essential that a multidisciplinary approach be used to fully inform the patient and family of the potential outcomes and management options. The risks and benefits of extirpative versus conservative management should be adequately discussed with the patient. Extirpative management, with a scheduled cesarean section and hysterectomy at 35-37 weeks of gestation, may be performed. If the patient opts for uterine conservation to allow for subsequent pregnancy, there are measures that can be implemented. Commonly, cesarean section alone can be successful, since most cases of accreta are focal. Methotrexate administration and uterine artery embolization have been reported, and the literature has either demonstrated various results (with methotrexate) or has suggested no benefit (uterine artery embolization).[7] Whether extirpative or uterine-conserving management is chosen, it is important that the delivery be performed in a center with staff trained for complicated surgeries potentially involving the bowel or bladder, and appropriate equipment and resources should be available to handle the many significant complications that may be encountered at the time of the procedure. A blood bank capable of providing large volumes of blood in emergency situations is particularly important.[1,7]
Given the patient's findings on ultrasonography and MRI, a cesarean delivery was scheduled, with a high probability of hysterectomy. At the time of the cesarean delivery, the patient was 36 weeks and 5 days intrauterine gestation by ultrasonographic dating. As a result of the close approximation of the ureters and the increased risk of trauma during this procedure, the patient underwent bilateral ureteral stent placement for direct visualization of the ureters. After delivery of the fetus, a portion of the placenta remained tightly adherent to the uterus. The decision was made to proceed with a cesarean supracervical hysterectomy. The patient tolerated the procedure well. No complications were noted, and the patient was taken to the recovery room in stable condition. The pathologic findings were an area of thinning consistent with previous low-transverse incision, with scar formation on the anterior surface of the uterus. This scarred area was focally and markedly thinned to 2 mm in thickness. The placenta was adherent to this area. Examination of the surgical specimen displayed a uterus with focal changes of placenta accreta. The patient was discharged to home from the hospital 4 days after her surgery.
Figure 1
Figure 2
Figure 3
Figure 4
Friday, June 26, 2009
Stevens-Johnson syndrome -- AIDS
Since I am looking for information on regards of Stevens-Johnson syndrome. I come across this good atlas. It's about AIDS. A lot of good pictures you shouldn't have missed them.
http://www.aids-images.ch/index.php?what=images&id=1756&t=22&print=true
A little bit about the disease
From: http://emedicine.medscape.com/article/756523-overview
First described in 1922, Stevens-Johnson syndrome (SJS) is an immune-complex–mediated hypersensitivity complex that is a severe expression of erythema multiforme. It is known by some as erythema multiforme major, but disagreement exists in the literature. Most authors and experts consider Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) different manifestations of the same disease. For that reason, many refer to the entity as SJS/TEN. SJS typically involves the skin and the mucous membranes. While minor presentations may occur, significant involvement of oral, nasal, eye, vaginal, urethral, GI, and lower respiratory tract mucous membranes may develop in the course of the illness. GI and respiratory involvement may progress to necrosis. SJS is a serious systemic disorder with the potential for severe morbidity and even death. Missed diagnosis is common.
Although several classification schemes have been reported, the simplest breaks the disease down as follows:
Stevens-Johnson syndrome
A "minor form of TEN," with less than 10% body surface area (BSA) detachment
Overlapping Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN)
Detachment of 10-30% BSA
Toxic epidermal necrolysis
Detachment of more than 30% BSA
Pathophysiology
Stevens-Johnson syndrome is an immune-complex–mediated hypersensitivity disorder that may be caused by many drugs, viral infections, and malignancies. Cocaine recently has been added to the list of drugs capable of producing the syndrome. In up to half of cases, no specific etiology has been identified. Pathologically, cell death results causing separation of the epidermis from the dermis. The death receptor, Fas, and its ligand, FasL, have been linked to the process. Some have also linked inflammatory cytokines to the pathogenesis.
Mortality/Morbidity
Mortality is determined primarily by the extent of skin sloughing. When BSA sloughing is less than 10%, the mortality rate is approximately 1-5%. However, when more than 30% BSA sloughing is present, the mortality rate is between 25% and 35%.
Lesions may continue to erupt in crops for as long as 2-3 weeks. Mucosal pseudomembrane formation may lead to mucosal scarring and loss of function of the involved organ system. Esophageal strictures may occur when extensive involvement of the esophagus exists. Mucosal shedding in the tracheobronchial tree may lead to respiratory failure.
Ocular sequelae may include corneal ulceration and anterior uveitis. Blindness may develop secondary to severe keratitis or panophthalmitis in 3-10% of patients. Vaginal stenosis and penile scarring have been reported. Renal complications are rare.
In the USMLERx, they give a case of a young patient treated for seizure disorder but eventually landed up with rashes on skin and mucous membrane and rashes starting as macular then developing into bullae and rupture. Patient eventually dies. The culprit is the drug being used to treat the disease. (What drug is it? You got to find out)
http://www.aids-images.ch/index.php?what=images&id=1756&t=22&print=true
A little bit about the disease
From: http://emedicine.medscape.com/article/756523-overview
First described in 1922, Stevens-Johnson syndrome (SJS) is an immune-complex–mediated hypersensitivity complex that is a severe expression of erythema multiforme. It is known by some as erythema multiforme major, but disagreement exists in the literature. Most authors and experts consider Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) different manifestations of the same disease. For that reason, many refer to the entity as SJS/TEN. SJS typically involves the skin and the mucous membranes. While minor presentations may occur, significant involvement of oral, nasal, eye, vaginal, urethral, GI, and lower respiratory tract mucous membranes may develop in the course of the illness. GI and respiratory involvement may progress to necrosis. SJS is a serious systemic disorder with the potential for severe morbidity and even death. Missed diagnosis is common.
Although several classification schemes have been reported, the simplest breaks the disease down as follows:
Stevens-Johnson syndrome
A "minor form of TEN," with less than 10% body surface area (BSA) detachment
Overlapping Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN)
Detachment of 10-30% BSA
Toxic epidermal necrolysis
Detachment of more than 30% BSA
Pathophysiology
Stevens-Johnson syndrome is an immune-complex–mediated hypersensitivity disorder that may be caused by many drugs, viral infections, and malignancies. Cocaine recently has been added to the list of drugs capable of producing the syndrome. In up to half of cases, no specific etiology has been identified. Pathologically, cell death results causing separation of the epidermis from the dermis. The death receptor, Fas, and its ligand, FasL, have been linked to the process. Some have also linked inflammatory cytokines to the pathogenesis.
Mortality/Morbidity
Mortality is determined primarily by the extent of skin sloughing. When BSA sloughing is less than 10%, the mortality rate is approximately 1-5%. However, when more than 30% BSA sloughing is present, the mortality rate is between 25% and 35%.
Lesions may continue to erupt in crops for as long as 2-3 weeks. Mucosal pseudomembrane formation may lead to mucosal scarring and loss of function of the involved organ system. Esophageal strictures may occur when extensive involvement of the esophagus exists. Mucosal shedding in the tracheobronchial tree may lead to respiratory failure.
Ocular sequelae may include corneal ulceration and anterior uveitis. Blindness may develop secondary to severe keratitis or panophthalmitis in 3-10% of patients. Vaginal stenosis and penile scarring have been reported. Renal complications are rare.
In the USMLERx, they give a case of a young patient treated for seizure disorder but eventually landed up with rashes on skin and mucous membrane and rashes starting as macular then developing into bullae and rupture. Patient eventually dies. The culprit is the drug being used to treat the disease. (What drug is it? You got to find out)
Wednesday, June 10, 2009
Neurofibromatosis type I
One thing I wanted to share with everyone. This is a website from University of Malaysia Sarawak. http://www.sarawakeyecare.com/caseoftheweek/case14.htm
Okay, the above mentioned case is on neurofibromatosis type I. Quite nice a case study. Go and check this out.
Okay, the above mentioned case is on neurofibromatosis type I. Quite nice a case study. Go and check this out.
Wednesday, May 27, 2009
Collagen
This is from the NBME question bank. Each of the question stirs up my interest in looking for the answer. This time, I shall talk about the wonderful world of collagen.
Case as follows:
A 2-year-old boy has brittle depigmented hair, cerebral atrophy, delayed myelination, motor delay, and mental retardation. Lysyl oxidase activity is decreased. The function of which of the following substances is most likely to be defective in this patient?
A) Albumin
B) Ceruloplasmin
C) Chondroitin sulfate
D) Collagen
Obviously the answer has to be collagen isn't it? One will ask so what's the diagnosis? Possible answer is Menkes Disease, which is an X-linked neurodegenerative disease of impaired copper transport. (obtained from http://emedicine.medscape.com/article/1180460-overview) It is also known as the kinky hair disease. The disease speaks for itself, kinky hair. Everything links to the defect of the collagen synthesis itself as well as the copper metabolism.
As an IMU student, we might think that copper metabolism? Isn't that something to do with Wilson's disease, better known as hepatolenticular degeneration in which there is autosomal recessive genetic disorder in which copper metabolism is affected and that copper builds up in the body. The most well known symptom is the Kayser-Fleischer rings which we always say when during our OSCE practice. We haven't seen one before so we don't know how it looks like. Other symptoms include neuropsychaitric symptoms, RTA, cardiomyopathy etc. One important thing about copper is that copper is an important component of several metabolic enzymes, including lysyl oxidase, cytochrome c oxidase, superoxide dismutase, and dopamine beta-hydroxylase. The main enzyme we are going to talk now is lysyl oxidase.
So what's so great about this enzyme? Lysyl? Something to do about collagen? Yes, absolutely. Collagen occurs in all multicellular animals and is the most abundant protein of vertebrates. It is a extracellular protein that is organised into insoluble fibers of great tensile strength. This suits collagens role as components of connective tissues such as bone, teeth, cartilage, tendon etc.(from Vishna' lecture note)
Mammals have at least 17 genetically distinct polypeptide chains (called chains) comprising 10 collagen variants as listed below:
Type Distribution
I Skin, bone, tendon, blood vessels andcornea
II Cartilage
III Blood vessels, foetal skin
IV Basement membrane
Collagen has a distinctive amino acid composition-nearly one third of its residues are Gly, another 15-30% are Proline, 4-hydroxyproline,and hydroxylysine. The hydroxylated residues appear only after collagen polypeptides are synthesised. The enzyme that converts Proline to Hydroxyproline is prolyl hydroxylase. Hyroxyproline is important as it confers stability upon collagen (intramolecular hydrogen bonds that may involve bridging water molecules). However, prolyl hydroxylase requires ascorbic acid (Vit C) to maintain its enzymatic activity. Thus for people with scurvy: skin lesions, blood vessels fragility, results because collagen cannot form fibres properly. This explains the importance of Vit C not only as an antioxidant itself but also a cofactor for prolyl hydroxylase in healthy growth of collagen in mammals. Reaction is as follows for prolyl hydroxylase:
Proline + α-ketoglutarate + O2 + Fe2+ → 4-hydroxyproline + Fe4+ + CO2 + succinate
One point which I want to point out in the case mentioned is the enzyme lysyl oxidase. A brief introduction of the enzyme by wikipedia:
Lysyl oxidase also known as protein-lysine 6-oxidase is a protein which in humans is encoded by the LOX gene. Its inhibition can cause lathyrism, but at the same time, its upregulation by tumor cells may promote metastasis of the existing tumor, causing it to become malignant and cancerous. Lysyl oxidase is an extracellular copper enzyme that catalyzes formation of aldehydes from lysine residues in collagen and elastin precursors.
This enzyme requires copper, therefore in any form of disease which impairs the synthesis of copper, it will result in this enzyme difficiency and the disease which can be resulted involves the as mentioned in the italic statement as well as the symptoms occuring in Menkes disease.The Menkes gene is located on the long arm of the X chromosome at Xq13.3, and the gene product (ATP7A) is a 1500–amino acid P-type adenosine triphosphatase (ATPase) that has 17 domains—6 copper binding, 8 transmembrane, a phosphatase, a phosphorylation, and an ATP binding.(from: http://emedicine.medscape.com/article/1180460-overview) This is the syndrome the boy is suffering from.
Another collagen disease is Ehlers-Danlos Syndrome. The famous one in which everyone see the clinical picture and say the condition is the Type I and II which have hypermobility of joint, skin hyperextensibility and wide atrophic scars. (from : http://emedicine.medscape.com/article/943567-overview) Type IV is the vascular one in which it is important to take note of and diagnose it as it will have disastrous consequences.
Type IV is the vascular/ecchymotic form. Patients with type IV Ehlers-Danlos syndrome have prominent venous markings, which are readily visible through the skin. Diagnostically, this type is most important because patients are subject to spontaneous rupture of the bowel, medium-sized arteries, or both. Often, rupture leads to early death. Median life expectancy in these patients is 45-50 years.
So that's about collagen for the while. I shall end this topic with collagen and aging.
Collagen and Aging
The sixth theory of aging is the Collagen Theory of Aging, This theory says that as we age, our collagen in our bodies gets older. When that happens the old collagen gets stiff and does not act as flexibly, causing problems, e.g., causes hypertension by not expanding to accomodate the flow of blood through the vessels, stiff collagen causes organs to malfunction as they seem to be "crispy" and hinder metabolic reactions.
Case as follows:
A 2-year-old boy has brittle depigmented hair, cerebral atrophy, delayed myelination, motor delay, and mental retardation. Lysyl oxidase activity is decreased. The function of which of the following substances is most likely to be defective in this patient?
A) Albumin
B) Ceruloplasmin
C) Chondroitin sulfate
D) Collagen
Obviously the answer has to be collagen isn't it? One will ask so what's the diagnosis? Possible answer is Menkes Disease, which is an X-linked neurodegenerative disease of impaired copper transport. (obtained from http://emedicine.medscape.com/article/1180460-overview) It is also known as the kinky hair disease. The disease speaks for itself, kinky hair. Everything links to the defect of the collagen synthesis itself as well as the copper metabolism.
As an IMU student, we might think that copper metabolism? Isn't that something to do with Wilson's disease, better known as hepatolenticular degeneration in which there is autosomal recessive genetic disorder in which copper metabolism is affected and that copper builds up in the body. The most well known symptom is the Kayser-Fleischer rings which we always say when during our OSCE practice. We haven't seen one before so we don't know how it looks like. Other symptoms include neuropsychaitric symptoms, RTA, cardiomyopathy etc. One important thing about copper is that copper is an important component of several metabolic enzymes, including lysyl oxidase, cytochrome c oxidase, superoxide dismutase, and dopamine beta-hydroxylase. The main enzyme we are going to talk now is lysyl oxidase.
So what's so great about this enzyme? Lysyl? Something to do about collagen? Yes, absolutely. Collagen occurs in all multicellular animals and is the most abundant protein of vertebrates. It is a extracellular protein that is organised into insoluble fibers of great tensile strength. This suits collagens role as components of connective tissues such as bone, teeth, cartilage, tendon etc.(from Vishna' lecture note)
Mammals have at least 17 genetically distinct polypeptide chains (called chains) comprising 10 collagen variants as listed below:
Type Distribution
I Skin, bone, tendon, blood vessels andcornea
II Cartilage
III Blood vessels, foetal skin
IV Basement membrane
Collagen has a distinctive amino acid composition-nearly one third of its residues are Gly, another 15-30% are Proline, 4-hydroxyproline,and hydroxylysine. The hydroxylated residues appear only after collagen polypeptides are synthesised. The enzyme that converts Proline to Hydroxyproline is prolyl hydroxylase. Hyroxyproline is important as it confers stability upon collagen (intramolecular hydrogen bonds that may involve bridging water molecules). However, prolyl hydroxylase requires ascorbic acid (Vit C) to maintain its enzymatic activity. Thus for people with scurvy: skin lesions, blood vessels fragility, results because collagen cannot form fibres properly. This explains the importance of Vit C not only as an antioxidant itself but also a cofactor for prolyl hydroxylase in healthy growth of collagen in mammals. Reaction is as follows for prolyl hydroxylase:
Proline + α-ketoglutarate + O2 + Fe2+ → 4-hydroxyproline + Fe4+ + CO2 + succinate
One point which I want to point out in the case mentioned is the enzyme lysyl oxidase. A brief introduction of the enzyme by wikipedia:
Lysyl oxidase also known as protein-lysine 6-oxidase is a protein which in humans is encoded by the LOX gene. Its inhibition can cause lathyrism, but at the same time, its upregulation by tumor cells may promote metastasis of the existing tumor, causing it to become malignant and cancerous. Lysyl oxidase is an extracellular copper enzyme that catalyzes formation of aldehydes from lysine residues in collagen and elastin precursors.
This enzyme requires copper, therefore in any form of disease which impairs the synthesis of copper, it will result in this enzyme difficiency and the disease which can be resulted involves the as mentioned in the italic statement as well as the symptoms occuring in Menkes disease.The Menkes gene is located on the long arm of the X chromosome at Xq13.3, and the gene product (ATP7A) is a 1500–amino acid P-type adenosine triphosphatase (ATPase) that has 17 domains—6 copper binding, 8 transmembrane, a phosphatase, a phosphorylation, and an ATP binding.(from: http://emedicine.medscape.com/article/1180460-overview) This is the syndrome the boy is suffering from.
Another collagen disease is Ehlers-Danlos Syndrome. The famous one in which everyone see the clinical picture and say the condition is the Type I and II which have hypermobility of joint, skin hyperextensibility and wide atrophic scars. (from : http://emedicine.medscape.com/article/943567-overview) Type IV is the vascular one in which it is important to take note of and diagnose it as it will have disastrous consequences.
Type IV is the vascular/ecchymotic form. Patients with type IV Ehlers-Danlos syndrome have prominent venous markings, which are readily visible through the skin. Diagnostically, this type is most important because patients are subject to spontaneous rupture of the bowel, medium-sized arteries, or both. Often, rupture leads to early death. Median life expectancy in these patients is 45-50 years.
So that's about collagen for the while. I shall end this topic with collagen and aging.
Collagen and Aging
The sixth theory of aging is the Collagen Theory of Aging, This theory says that as we age, our collagen in our bodies gets older. When that happens the old collagen gets stiff and does not act as flexibly, causing problems, e.g., causes hypertension by not expanding to accomodate the flow of blood through the vessels, stiff collagen causes organs to malfunction as they seem to be "crispy" and hinder metabolic reactions.
Tuesday, February 17, 2009
Rehabilitation of a Colles Fracture – Physiotherapy
Author: Jonathan Blood-smythColles' fractures, named after Abraham Colles who first described in 1814 the common fracture of the last inch of the radius and ulna near the wrist, is a very common consequence of a fall on the outstretched hand (FOOSH). Typical treatment is immobilisation in a plaster of Paris or similar material for five to six weeks to allow bony union, followed by a rehabilitation period of a month or more, a short period of which might involve a wrist brace for comfort during activity. Due to the functional importance of the hand, the period of immobilisation is kept to a minimum to prevent dysfunction of the hand and wrist.
Physiotherapy examination starts once the hand has been released from the Plaster of Paris, manually feeling the fracture site which should not be more than minimally uncomfortable, signifying the fracture is well on the way to healing. Hand colour should be normal, the hand should not be swollen much nor have severe muscle wasting. Wrist movements are often restricted in one or two planes but all the movements should not normally be reduced or not significantly. Pain may be present but again should not be severe or occur on all hand movements.
Two hourly range of motion exercises are the first treatment taught to the patient by the physiotherapist and in many cases the wrist movements improve sufficiently for this alone to be required. Elbow and shoulder movement should be reviewed to rule out restrictions before moving on to the rotatory forearm movements of pronation and supination which are important for normal hand use. Further movements assessed are flexion and extension of the wrist, fingers and thumb, along with thumb adduction and abduction. Wrist extension and forearm supination are the most commonly affected movements.
After the plaster comes off the wrist often feels vulnerable, partly because the plaster is seldom left on until the bone is entirely healed to prevent the onset of complications due to immobilisation. Physiotherapists may give the patient a futura type brace, a fabric brace with Velcro straps and a metal piece for the underside of the wrist to stiffen it. This is not meant to keep the wrist immobilised further but to support the wrist while the patient is performing functional activities and then to be removed for light activities and regular exercise performance.
If the ranges of motion do not improve as they should then the physiotherapist will consider using joint mobilisations to ease the movements. Accessory movements can be performed to the inferior radio-ulnar joint to help pronation and supination, and to the radiocarpal (wrist) and midcarpal joints, with the physiotherapist fixing one side of the joint as he or she moves the other side of the joint passively. This can be done gently or more vigorously at the end of range to push against the restrictions within the joint. Mobilisations can also be performed with the joint at the end of its available movement to give it the sliding and gliding movements it requires.
Strengthening the wrist occurs with a gradual increase in functional activities but joining a hand class can instruct the patient in practicing the large variety of small movements that the hand can perform and needs to strengthen for optimum hand function. Repetitive work at pieces of apparatus can strengthen and harden the hand to turning, twisting, pulling, grasping and fine work with the thumb and index finger. This can move on to work with weights or functional activities if the person needs to return to manual labour or another job requiring upper limb strength.
Urgent treatment is indicated if the hand is extremely painful, tightly swollen and has poor movements, before a pain syndrome develops. At this stage medical review is important to make sure there are no complications with the fracture such as poor healing or lack of healing. Analgesia and contrast baths can help with the pain, desensitisation with the hypersensitive areas which can develop and massage and exercise with the swelling. Patient education is vital so they know they have to work hard and through the pain to rehabilitate their hand.
Jonathan Blood Smyth is a Superintendent of Physiotherapy at an NHS hospital in the South-West of the UK. He specialises in orthopaedic conditions and looking after joint replacements as well as managing chronic pain. Visit the website he edits if you are looking for physiotherapists in Birmingham.
Article Source: http://www.articlesbase.com/health-articles/rehabilitation-of-a-colles-fracture-physiotherapy-727809.html
Friday, January 23, 2009
Thursday, January 22, 2009
Pathophysiology and Aging of Bone
Sources: http://www.springerlink.com/content/x208624555xgu576/
This is an article in regards to pathophysiology and aging of bone by Peitschmann et al.
I will list out the points of interest in this article.
Bone loss due to aging:
1) overall decline in protein synthesis and protein turnover and accumulation of damaged molecules
2) number of adhesion colony forming cells significantly lower in marrow cells
3) requirement of higher concentration of growth factors and hormones
==> Impaired growth of human endosteal bone cells from men aged over 50 years
4) lower production of osteocalcin after stimulation with 1,25-(OH)2D3
Age related osteopenia may result from inversely related changes in pool size of hematopoietic osteoclast precursor cells and osteogenic stromal cells; reduced production of osteoprotegerin and enhanced RANKL expression would additionally promote the formation of osteoclasts.
Currently available markers of bone formation are:
total and bone-specific alkaline phosphatase activity, osteocalcin and type I collagen terminal extension peptides.
Bone resorption is assessed by
urinary excretion or serum levels of bone type I collagen degradation products eg. pyridinium crosslink and N- and C-telopeptide of collagen crosslinks.
Factors affecting invidividual bone mass include:
A) Peak bone mass (the amount of bone mass achieved at skeletal maturity)
B) Subsequent rate of bone loss
What is bone quality, one may ask. According to Mary Bouxsein: "the totality of features and characteristics that influence a bone's ability to resist fractures". Nevertheless, compromised trabecular architecture portrays as an independent causal factor in the pathogenesis of vertebral fractures.
It is well established that estrogen deficiency is a major determinant of the accelerated bone loss in postmenopausal women. This leads to the most infamous term called "osteoporosis" which everyone in the world knows and aware about it. One of the major worry which medical personnals are concerned of is the fracture of the neck of the femur in osteoporotic patients. Of course there are other fractures that could happen in osteoporotic bone in this case, eg. Colles fracture and crush fractures of thoracic and lumbar verterbra. For short, osteoporosis contributes in the increment of fragility (low energy) fractures and severity of traumatic (high energy) fractures.
HORMONAL INFLUENCES IN BONE LOSS
Androgen deficiency can impale high-turnover osteopenia in males (be it rats or males). Unfortunately, there isn't a clear distinction in this statement as some studies quoted positive correlation between free androgen index and femoral neck bone mineral density. It is interesting to note that in the study conducted by Kelly and coworkers (1990) reported that radial bone mineral density could be predicted by an index of free testosterone and weight. However, the fact that bioavailable estrogen was most strongly associated with bone mineral density, and thus, bioavailable of estrodiol rather than testosteonr is used as the most consistent predictors of bone turnoever and bone loss. There is another possible role of using dehydroepiandrosterone (DHEA) and DHEA sulfate to correlate bone density in healthy women.
OTHER INFLUENCE
We know that growth hormones stimulate growth. Nevertheless it stimulates the growth of bones. It is not surprising to note that growth hormone secretion declines as we age. Role of growth hormone/insulin-like growth factor is clearly shown in cases with growth hormone deficiency, leading to dwarfism and acromegaly in cases of excess growth hormones. 1,25-dihydroxyvitamin D3 acts as a central regulator of calcium and phosphorus homeostasis. It is interesting to note that there exists an association between bone mineral density and vitamin D receptor allele. As shown in literatures, vitamin D receptor polymorphisms appear to influence bone mineral density in primary as well as secondary osteoporosis.
To summarize, estrogen deficiency acts as the major determinant of bone loss in women and men whilst Vit D3 portray as a factor of bone turnover in elderly.
RIGGS, KHOSLA AND MELTON UNITARY MODEL OF INVOLUTIONAL OSTEOPOROSIS
Involutional osteoporosis is defined as the common form of osteoporosis that begins in middle life and becomes increasingly more frequent with age and there are two tyesp: type I ("postmenopausal") and type II ("senile").
Type I osteoporosis presents during the first 15-20 years after menopause and is characterized by excessive loss of trabecular bone, which causes the fractures typical of postmenopausal osteoporosis such as vertebral fractures and Colles' fracures. Type II is characterized by loss of trabecular and cortical bone, and the most frquent fractures involve the proximal femur and vertebra.
One point of interesting note is that cigarette smoking has been identified as risk factor for low bone mineral density. It is shown that 25-OH vitamin D and osteocalcin levels are low in smokers. Impairment of intestinal calcium absorption may contribute to the bone loss as well.
To conclude, humans will get old, we can get old. Nevertheless, with the understanding of these conditions, it is possible that one can prevent osteoporosis by doing the right activities to minimize of one's risk of getting osteoporosis. So start a healthy diet, do exercise and stop smoking!!!
This is an article in regards to pathophysiology and aging of bone by Peitschmann et al.
I will list out the points of interest in this article.
Bone loss due to aging:
1) overall decline in protein synthesis and protein turnover and accumulation of damaged molecules
2) number of adhesion colony forming cells significantly lower in marrow cells
3) requirement of higher concentration of growth factors and hormones
==> Impaired growth of human endosteal bone cells from men aged over 50 years
4) lower production of osteocalcin after stimulation with 1,25-(OH)2D3
Age related osteopenia may result from inversely related changes in pool size of hematopoietic osteoclast precursor cells and osteogenic stromal cells; reduced production of osteoprotegerin and enhanced RANKL expression would additionally promote the formation of osteoclasts.
Currently available markers of bone formation are:
total and bone-specific alkaline phosphatase activity, osteocalcin and type I collagen terminal extension peptides.
Bone resorption is assessed by
urinary excretion or serum levels of bone type I collagen degradation products eg. pyridinium crosslink and N- and C-telopeptide of collagen crosslinks.
Factors affecting invidividual bone mass include:
A) Peak bone mass (the amount of bone mass achieved at skeletal maturity)
B) Subsequent rate of bone loss
What is bone quality, one may ask. According to Mary Bouxsein: "the totality of features and characteristics that influence a bone's ability to resist fractures". Nevertheless, compromised trabecular architecture portrays as an independent causal factor in the pathogenesis of vertebral fractures.
It is well established that estrogen deficiency is a major determinant of the accelerated bone loss in postmenopausal women. This leads to the most infamous term called "osteoporosis" which everyone in the world knows and aware about it. One of the major worry which medical personnals are concerned of is the fracture of the neck of the femur in osteoporotic patients. Of course there are other fractures that could happen in osteoporotic bone in this case, eg. Colles fracture and crush fractures of thoracic and lumbar verterbra. For short, osteoporosis contributes in the increment of fragility (low energy) fractures and severity of traumatic (high energy) fractures.
HORMONAL INFLUENCES IN BONE LOSS
Androgen deficiency can impale high-turnover osteopenia in males (be it rats or males). Unfortunately, there isn't a clear distinction in this statement as some studies quoted positive correlation between free androgen index and femoral neck bone mineral density. It is interesting to note that in the study conducted by Kelly and coworkers (1990) reported that radial bone mineral density could be predicted by an index of free testosterone and weight. However, the fact that bioavailable estrogen was most strongly associated with bone mineral density, and thus, bioavailable of estrodiol rather than testosteonr is used as the most consistent predictors of bone turnoever and bone loss. There is another possible role of using dehydroepiandrosterone (DHEA) and DHEA sulfate to correlate bone density in healthy women.
OTHER INFLUENCE
We know that growth hormones stimulate growth. Nevertheless it stimulates the growth of bones. It is not surprising to note that growth hormone secretion declines as we age. Role of growth hormone/insulin-like growth factor is clearly shown in cases with growth hormone deficiency, leading to dwarfism and acromegaly in cases of excess growth hormones. 1,25-dihydroxyvitamin D3 acts as a central regulator of calcium and phosphorus homeostasis. It is interesting to note that there exists an association between bone mineral density and vitamin D receptor allele. As shown in literatures, vitamin D receptor polymorphisms appear to influence bone mineral density in primary as well as secondary osteoporosis.
To summarize, estrogen deficiency acts as the major determinant of bone loss in women and men whilst Vit D3 portray as a factor of bone turnover in elderly.
RIGGS, KHOSLA AND MELTON UNITARY MODEL OF INVOLUTIONAL OSTEOPOROSIS
Involutional osteoporosis is defined as the common form of osteoporosis that begins in middle life and becomes increasingly more frequent with age and there are two tyesp: type I ("postmenopausal") and type II ("senile").
Type I osteoporosis presents during the first 15-20 years after menopause and is characterized by excessive loss of trabecular bone, which causes the fractures typical of postmenopausal osteoporosis such as vertebral fractures and Colles' fracures. Type II is characterized by loss of trabecular and cortical bone, and the most frquent fractures involve the proximal femur and vertebra.
One point of interesting note is that cigarette smoking has been identified as risk factor for low bone mineral density. It is shown that 25-OH vitamin D and osteocalcin levels are low in smokers. Impairment of intestinal calcium absorption may contribute to the bone loss as well.
To conclude, humans will get old, we can get old. Nevertheless, with the understanding of these conditions, it is possible that one can prevent osteoporosis by doing the right activities to minimize of one's risk of getting osteoporosis. So start a healthy diet, do exercise and stop smoking!!!
Tuesday, January 20, 2009
Obs & Gyn
This is from: http://ob-ultrasound.net/
Written here are the 4 lengths discussed during my lecture dated 21st Jan 2009. Though it is MSK week, there are couple of things the lecturer wants us to know.
Determination of gestational age and assessment of fetal size.
Fetal body measurements reflect the gestational age of the fetus. This is particularly true in early gestation. In patients with uncertain last menstrual periods, such measurements must be made as early as possible in pregnancy to arrive at a correct for the patient. In the latter part of pregnancy measuring body parameters will allow assessment of the size and growth of the fetus and will greatly assist in the diagnosis and management ofintrauterine growth retardation (IUGR).
The following measurements are usually made:
a) The Crown-rump length (CRL)
This measurement can be made between 7 to 13 weeks and gives very accurate estimation of the gestational age. Dating with the CRL can be within 3-4 days of the last menstrual period. An important point to note is that when the due date has been set by an accurately measured CRL, it should not be changed by a subsequent scan. For example, if another scan done 6 or 8 weeks later says that one should have a new due date which is further away, one should not normally change the date but should rather interpret the finding as that the baby is not growing at the expected rate.
b) Biparietal diameter(BPD)
The diameter between the 2 sides of the head. This is measured after 13 weeks. It increases from about 2.4 cm at 13 weeks to about 9.5 cm at term. Different babies of the same weight can have different head size, therefore dating in the later part of pregnancy is generally considered unreliable. Dating using the BPD should be done as early as is feasible.
c) The Femur length (FL)
Measures the longest bone in the body and reflects the longitudinal growth of the fetus. Its usefulness is similar to the BPD. It increases from about 1.5 cm at 14 weeks to about 7.8 cm at term. Similar to the BPD, dating using the FL should be done as early as is feasible.
d) The Abdominal circumference (AC)
The single most important measurement to make in late pregnancy. It reflects more of fetal size and weight rather than age. Serial measurements are useful in monitoring of the fetus. AC measurements should not be used for dating a fetus.
The weight of the fetus at any gestation can also be estimated with great accuracy using polynomial equations containing the BPD, FL, and AC. computer softwares and lookup charts are readily available. For example, a BPD of 9.0 cm and an AC of 30.0 cm will give a weight estimate of 2.85 kg.
Written here are the 4 lengths discussed during my lecture dated 21st Jan 2009. Though it is MSK week, there are couple of things the lecturer wants us to know.
Determination of gestational age and assessment of fetal size.
Fetal body measurements reflect the gestational age of the fetus. This is particularly true in early gestation. In patients with uncertain last menstrual periods, such measurements must be made as early as possible in pregnancy to arrive at a correct for the patient. In the latter part of pregnancy measuring body parameters will allow assessment of the size and growth of the fetus and will greatly assist in the diagnosis and management ofintrauterine growth retardation (IUGR).
The following measurements are usually made:
a) The Crown-rump length (CRL)
This measurement can be made between 7 to 13 weeks and gives very accurate estimation of the gestational age. Dating with the CRL can be within 3-4 days of the last menstrual period. An important point to note is that when the due date has been set by an accurately measured CRL, it should not be changed by a subsequent scan. For example, if another scan done 6 or 8 weeks later says that one should have a new due date which is further away, one should not normally change the date but should rather interpret the finding as that the baby is not growing at the expected rate.
b) Biparietal diameter(BPD)
The diameter between the 2 sides of the head. This is measured after 13 weeks. It increases from about 2.4 cm at 13 weeks to about 9.5 cm at term. Different babies of the same weight can have different head size, therefore dating in the later part of pregnancy is generally considered unreliable. Dating using the BPD should be done as early as is feasible.
c) The Femur length (FL)
Measures the longest bone in the body and reflects the longitudinal growth of the fetus. Its usefulness is similar to the BPD. It increases from about 1.5 cm at 14 weeks to about 7.8 cm at term. Similar to the BPD, dating using the FL should be done as early as is feasible.
d) The Abdominal circumference (AC)
The single most important measurement to make in late pregnancy. It reflects more of fetal size and weight rather than age. Serial measurements are useful in monitoring of the fetus. AC measurements should not be used for dating a fetus.
The weight of the fetus at any gestation can also be estimated with great accuracy using polynomial equations containing the BPD, FL, and AC. computer softwares and lookup charts are readily available. For example, a BPD of 9.0 cm and an AC of 30.0 cm will give a weight estimate of 2.85 kg.
Tuesday, January 6, 2009
Clinical Trigger for CME Clinical Anatomy at 10th Jan 2009
Session 1 9.45 AM Anterior Abdominal Wall
Facilitator: AP Joachim Perera
Clinical Trigger I (30 minutes)
A 25-year-old man presents to a surgical clinic with a dull, ‘dragging’ pain in his left groin, which has persisted for some months. A lump is felt at the medial end of his left groin extending to the scrotum. The lump increases in size when he stands up and when coughing. The doctor diagnoses of him having an indirect inguinal hernia.
Areas of discussion:
§ Anatomy of the inguinal canal and scrotum
§ Inguinal mechanisms in preventing hernias
§ Anatomical basis of direct and indirect inguinal hernias
§ Anatomical basis of differentiating between inguinal and femoral hernias
Questions of interest:
How much of the inguinal canal is traversed by an indirect inguinal hernia?
Which structure lies immediately medial to the deep inguinal ring?
Which layer covering the spermatic cord corresponds to the Internal Oblique muscle of the anterior abdominal wall?
How would you identify the Vas Deferens clinically in the living subject?
Which anatomical structure causes femoral hernia to get strangulated very often?
Facilitator: AP Joachim Perera
Clinical Trigger I (30 minutes)
A 25-year-old man presents to a surgical clinic with a dull, ‘dragging’ pain in his left groin, which has persisted for some months. A lump is felt at the medial end of his left groin extending to the scrotum. The lump increases in size when he stands up and when coughing. The doctor diagnoses of him having an indirect inguinal hernia.
Areas of discussion:
§ Anatomy of the inguinal canal and scrotum
§ Inguinal mechanisms in preventing hernias
§ Anatomical basis of direct and indirect inguinal hernias
§ Anatomical basis of differentiating between inguinal and femoral hernias
Questions of interest:
How much of the inguinal canal is traversed by an indirect inguinal hernia?
Which structure lies immediately medial to the deep inguinal ring?
Which layer covering the spermatic cord corresponds to the Internal Oblique muscle of the anterior abdominal wall?
How would you identify the Vas Deferens clinically in the living subject?
Which anatomical structure causes femoral hernia to get strangulated very often?
Clinical trigger II (10 minutes)
Given below is a picture of a small tense and tender mass in the right groin of a 70-year-old woman.
She presented with clinical features intestinal obstruction.
Diagnose the condition. Explain anatomical reasons for the diagnosis.
Clinical trigger III (30 minutes)
A 50 years old man presented with generalized abdominal pain of one day’s duration. He has a history of constant upper abdominal pain and heartburn for last 2 years, which was often relieved by over-the-counter antacids.
An erect X ray of the abdomen was done which showed gas shadow under the right dome of the diaphragam.
What is the most proble diagnosis?
Given below is a picture of a small tense and tender mass in the right groin of a 70-year-old woman.
She presented with clinical features intestinal obstruction.
Diagnose the condition. Explain anatomical reasons for the diagnosis.
Clinical trigger III (30 minutes)
A 50 years old man presented with generalized abdominal pain of one day’s duration. He has a history of constant upper abdominal pain and heartburn for last 2 years, which was often relieved by over-the-counter antacids.
An erect X ray of the abdomen was done which showed gas shadow under the right dome of the diaphragam.
What is the most proble diagnosis?
Areas of discussion:
Based on the picture given below, discuss lesser sac, greater omentum and greater sac
Structure and blood vessels of stomach
Based on the picture given below, discuss lesser sac, greater omentum and greater sac
Structure and blood vessels of stomach
Questions of interest:
A surgical incision through fundus of stomach will require clamping of which artery?
Which artery is lying in close relation to lesser sac and is well visible because of tortuous nature?
Why ulcers are more common over lesser curvature of the stomach?
Session 2 11.00 AM Head Injuries
Facilitator: Dr Nilesh Kumar
Clinical Trigger IV (30 minutes)
A 15-year-old baseball player was hit by a baseball over the right temple area. He lost consciousness briefly but woke up after about 45 seconds and had no neurological deficits. He was taken to the emergency room and seemed to be in good condition.
Four hours later, while being observed, he complained of an increasing headache and had a seizure. On examination, the patient’s right pupil appeared dilated and reacted sluggishly to light. The neurosurgeon was concerned about the increased intracranial pressure.
What is the most likely diagnosis?
Areas of discussion:
· Anatomical explanation of the causative condition causing increased intracranial pressure.
· Arrangement of the meningeal layers in the cranial cavity
· Dural folds and intracranial venous sinuses (Related structures of importance)
· Vascular supply to the meninges
· Anatomical explanation of the causative condition causing increased intracranial pressure.
· Arrangement of the meningeal layers in the cranial cavity
· Dural folds and intracranial venous sinuses (Related structures of importance)
· Vascular supply to the meninges
Questions of interest:
What are the vessels, which carry infections from the scalp to the venous sinuses?
What is the danger area of the face? Why is it called so?
How can a scalp injury produce a black eye?
Clinical trigger V (30 minutes)
One morning, while shaving, a 65-year-old industrial worker noticed in the mirror that he was unable to elevate his left upper eyelid. The doctor found the left eyelid to be drooped (ptosis). He also told the doctor that left side of his face was flushed and felt warm but there was no sweating even in the intense heat of the factory. The doctor observed that the left side pupil was constricted and the other eye was unaffected.
The man’s medical record showed that he was a heavy smoker. The doctor advised a chest radiograph, which revealed a shadow at the apex of the left lung indicative of a cancer.
Explain the anatomical basis of the patient’s presenting symptoms.
What are the vessels, which carry infections from the scalp to the venous sinuses?
What is the danger area of the face? Why is it called so?
How can a scalp injury produce a black eye?
Clinical trigger V (30 minutes)
One morning, while shaving, a 65-year-old industrial worker noticed in the mirror that he was unable to elevate his left upper eyelid. The doctor found the left eyelid to be drooped (ptosis). He also told the doctor that left side of his face was flushed and felt warm but there was no sweating even in the intense heat of the factory. The doctor observed that the left side pupil was constricted and the other eye was unaffected.
The man’s medical record showed that he was a heavy smoker. The doctor advised a chest radiograph, which revealed a shadow at the apex of the left lung indicative of a cancer.
Explain the anatomical basis of the patient’s presenting symptoms.
Areas of discussion:
· Discussion about the structures of the head and neck affected to produce the symptoms
· Pathway of direct and consensual light reflex
· Nervous mechanism of sweating
Session 3 1.00 PM Neck Lymph nodes, Deep cervical fascia
Facilitator: Dr Daw Khin Win
Clinical Trigger VI (30 minutes)
A 50 years old farmer came to the OPD with a lump in the left side of the neck. He noticed the lump about 2 weeks ago. It was not tender nor had any discharge. He also noticed he had been salivating a lot and had a sore on the side of his tongue. He has a habit of chewing tobacco since he was 30 years old and he also used to smoke 3 to5 cigarettes daily.
On examination, the patient’s jugulo-digastric nodes were found to be enlarged. They were mobile, not fixed to the surrounding tissue, not tender but stony hard. The examining doctor also found an ulcer on the left side of the anterior two third of the tongue.
Areas of discussion:
Extrinsic and intrinsic muscles of the tongue
Nerve supply of the tongue - sensory, motor
Lymphatic drainage of the tongue
Superficial and deep lymph nodes of head and neck
MSKCC (Head and Neck Service at Memorial Sloan-Kettering Centre) method of describing nodal groups of level I to level V
Clinical trigger VII (30 minutes)
A 45-year-old labourer presented with a lump in his right axilla. It was small at first but increased in size slowly during the past one month. Now pus was coming out from a small sinus from the lump and it had become tender. He said he felt hot and sweaty in the evenings.
On taking past medical history, it was found that he had been losing weight and had sever pain in his neck when he moved his neck. He said he was under antiTB treatment regime for a swelling of neck lymph glands about 5 years ago and stopped the treatment about 3 years back.
He was admitted to drain the abscess and for further investigations.
Explain the anatomical basis for the patient’s presenting symptoms
· Discussion about the structures of the head and neck affected to produce the symptoms
· Pathway of direct and consensual light reflex
· Nervous mechanism of sweating
Session 3 1.00 PM Neck Lymph nodes, Deep cervical fascia
Facilitator: Dr Daw Khin Win
Clinical Trigger VI (30 minutes)
A 50 years old farmer came to the OPD with a lump in the left side of the neck. He noticed the lump about 2 weeks ago. It was not tender nor had any discharge. He also noticed he had been salivating a lot and had a sore on the side of his tongue. He has a habit of chewing tobacco since he was 30 years old and he also used to smoke 3 to5 cigarettes daily.
On examination, the patient’s jugulo-digastric nodes were found to be enlarged. They were mobile, not fixed to the surrounding tissue, not tender but stony hard. The examining doctor also found an ulcer on the left side of the anterior two third of the tongue.
Areas of discussion:
Extrinsic and intrinsic muscles of the tongue
Nerve supply of the tongue - sensory, motor
Lymphatic drainage of the tongue
Superficial and deep lymph nodes of head and neck
MSKCC (Head and Neck Service at Memorial Sloan-Kettering Centre) method of describing nodal groups of level I to level V
Clinical trigger VII (30 minutes)
A 45-year-old labourer presented with a lump in his right axilla. It was small at first but increased in size slowly during the past one month. Now pus was coming out from a small sinus from the lump and it had become tender. He said he felt hot and sweaty in the evenings.
On taking past medical history, it was found that he had been losing weight and had sever pain in his neck when he moved his neck. He said he was under antiTB treatment regime for a swelling of neck lymph glands about 5 years ago and stopped the treatment about 3 years back.
He was admitted to drain the abscess and for further investigations.
Explain the anatomical basis for the patient’s presenting symptoms
Areas of discussion:
Prevertebral and post vertebral muscles
Superficial cervical fascia — nerves and vessels
Arrangement of deep fascia of the neck
Investing layer of deep cervical fascia
Pretracheal layer and its importance
Fascial compartments of the neck
Prevertebral space
Prevertebral and post vertebral muscles
Superficial cervical fascia — nerves and vessels
Arrangement of deep fascia of the neck
Investing layer of deep cervical fascia
Pretracheal layer and its importance
Fascial compartments of the neck
Prevertebral space
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