Monday, August 21, 2017
Introducing Medicollabowesome
Hello everyone!
We, the Medicowesome authors, decided to do something new this month and bring to you - Medicollabowesome.
The idea originated from wanting to see how different people present information uniquely on the same topic.
The Medicowesome authors decided that most of us will (try) to write on one particular topic every month.
Hopefully, we will learn so much together :D
The topic for the month of August: HIV & AIDS.
We've already begun writing (:
I invite readers to participate in Medicollabowesome too by emailing your article to us!
Email the title, post and author name to medicowesome@gmail.com with "Medicollabowesome" in the subject line.
This is so exciting!
-IkaN
Sunday, August 20, 2017
Saturday, August 19, 2017
Friday, August 18, 2017
Drug of choice : Dermatology
Hello everyone!
Here's a collection of Drugs of choice (DOC) for some Dermatology conditions. These are some of the most commonly asked questions in Post Graduation entrance exams.
1. DOC for severe erythrodermic psoriasis?
Cyclosporin
2. DOC for erythrodermic psoriasis?Methotrexate
3. DOC for pustular psoriasis?
Acitretin
4. 2nd choice for pustular psoriasis?Methotrexate
5. DOC for arthritis mutilans?
Etanercept
6. DOC for impetigo herpetiformis?
Systemic steroids
7. DOC for psoriatic arthritis?
Methotrexate
8. DOC for psoriatic erythroderma in pregnancy?
Systemic steroid
-Md Mobarak Hussain (Maahii)
Thursday, August 17, 2017
Clubbing
CLUBBING:
Bulbous enlargement of the distal portion of the digits due to increased subungual soft tissue.
It is also known as the "Hippocratic fingers", as it is believed that perhaps Hippocrates was the first to document clubbing as a sign of disease.
Grades of clubbing-
Grade I- presence of fluctuation test °
Grade II- obliteration of Lovibond angle*
Grade III- parrot beak or drumstick appearance
Grade IV- hypertrophic osteoarthropathy (HOA)
*Refer the diagram
°Refer the video clipping
Theories of clubbing-
1. Neurogenic theory- vagal stimulation via neural reflexes can lead to proliferation of connective tissue at the distal extremities resulting in clubbing.
2.Humoral theory- Normally lungs throws out all the soluble substances by inactivation. But in case of lung problems, these systems reach the systemic circulation in active state and stimulate the changes seen in HOA (growth hormone, PTH, bradikynin, prostaglandin, ferritin)
3.Hypoxic theory- Hypoxia is suggested to be a stimulus for HOA. It leads to opening of deep arteriovenous shunts and fistulae which increase blood flow to the extremities and leads to hypertrophy.
4.Platelets derived growth factor- Normally megakaryocytes and large platelets get destroyed in the lungs. But in lung pathology they escape the lung and reach the distal extremities. Here they interact with the endothelial cells and release platelet derives growth factor (PDGF) post activation. PDGF and other mediators then activate the fibroblasts and transforming growth factor beta which lead to collagen production and connective tissue laying down ultimately giving rise to clubbing and HOA.
This is the latest accepted theory.
Causes of clubbing-
'CLUBBING'
C - cyanotic heart diseases, chron's disease
L - lung causes (lung abscess, emphysema, interstitial lung disease, bronchogenic carcinoma, tuberculosis)
U - ulcerative colitis
B - biliary cirrhosis
B - benign mesothelioma
I - infective endocarditis, idiopathic, inherited
N - neurogenic tumors
G - graves disease
Shivani Mangalgi
Medicowesome 2017
Bulbous enlargement of the distal portion of the digits due to increased subungual soft tissue.
It is also known as the "Hippocratic fingers", as it is believed that perhaps Hippocrates was the first to document clubbing as a sign of disease.
Grades of clubbing-
Grade I- presence of fluctuation test °
Grade II- obliteration of Lovibond angle*
Grade III- parrot beak or drumstick appearance
Grade IV- hypertrophic osteoarthropathy (HOA)
*Refer the diagram
°Refer the video clipping
Theories of clubbing-
1. Neurogenic theory- vagal stimulation via neural reflexes can lead to proliferation of connective tissue at the distal extremities resulting in clubbing.
2.Humoral theory- Normally lungs throws out all the soluble substances by inactivation. But in case of lung problems, these systems reach the systemic circulation in active state and stimulate the changes seen in HOA (growth hormone, PTH, bradikynin, prostaglandin, ferritin)
3.Hypoxic theory- Hypoxia is suggested to be a stimulus for HOA. It leads to opening of deep arteriovenous shunts and fistulae which increase blood flow to the extremities and leads to hypertrophy.
4.Platelets derived growth factor- Normally megakaryocytes and large platelets get destroyed in the lungs. But in lung pathology they escape the lung and reach the distal extremities. Here they interact with the endothelial cells and release platelet derives growth factor (PDGF) post activation. PDGF and other mediators then activate the fibroblasts and transforming growth factor beta which lead to collagen production and connective tissue laying down ultimately giving rise to clubbing and HOA.
This is the latest accepted theory.
Causes of clubbing-
'CLUBBING'
C - cyanotic heart diseases, chron's disease
L - lung causes (lung abscess, emphysema, interstitial lung disease, bronchogenic carcinoma, tuberculosis)
U - ulcerative colitis
B - biliary cirrhosis
B - benign mesothelioma
I - infective endocarditis, idiopathic, inherited
N - neurogenic tumors
G - graves disease
Shivani Mangalgi
Medicowesome 2017
Courtesy YouTube
Hypergraphia - An intriguing brain anomaly
HYPERGRAPHIA
It is a condition in which an individual feels the driving compulsion to write; the overwhelming urge to write.
Hypergraphia has also been called 'midnight disease'.
Well based on how we perceive it, the "disease" could either be all about writing or writer's block.
Neurologically-
This unstoppable drive to write can be triggered by temporal lobe epilepsy(hippocampus and Wernicke's area in specific), intolerant mood disorders or dopamine.
What is very fascinating about this condition is that there are NO other vicious symptoms (other than a little irritability-which is quiet expected) and the fact that the patient can go on writing on anything from toilet papers to wall to even roads.
And what is more fascinating to know is that many famous authors and poets like Sylvia Plath, Stephen King and Leo Tolstoy (that's how the world got "War and Peace") suffered from hypergraphia.
Ingenious result from a brain defect.
Now a question might arise..if the quality of writing in these patients is any good?
To answer this, it is important to know that patient with hypergraphia exhibit wide variety of writing style and content. To elucidate this statement, let's go through few accounts:
1. Alice Flaherty (Harvard Medical school neurologist) gets episodes of hypergraphia following any grief incidences that have grave affect on her brain.
She has started her 4th book and is doing research to help explain how the muse comes and goes.
2. Mendez- He felt the unreasonable compulsion to write poetry even though the patient had no previous history of being a poet.
3. Patient who wrote everything backwards!
4. Patients writing same word over and over again but with differing calligraphy.
5. Patients' writing consists of sheer scribbling and frantic random thoughts.
Therefore on a lighter note, if you have the wrong brain defect but fall under the right category...then voilà ...YOU shall be famous!
Shivani Mangalgi
Medicowesome 2017
It is a condition in which an individual feels the driving compulsion to write; the overwhelming urge to write.
Hypergraphia has also been called 'midnight disease'.
Well based on how we perceive it, the "disease" could either be all about writing or writer's block.
Neurologically-
This unstoppable drive to write can be triggered by temporal lobe epilepsy(hippocampus and Wernicke's area in specific), intolerant mood disorders or dopamine.
What is very fascinating about this condition is that there are NO other vicious symptoms (other than a little irritability-which is quiet expected) and the fact that the patient can go on writing on anything from toilet papers to wall to even roads.
And what is more fascinating to know is that many famous authors and poets like Sylvia Plath, Stephen King and Leo Tolstoy (that's how the world got "War and Peace") suffered from hypergraphia.
Ingenious result from a brain defect.
Now a question might arise..if the quality of writing in these patients is any good?
To answer this, it is important to know that patient with hypergraphia exhibit wide variety of writing style and content. To elucidate this statement, let's go through few accounts:
1. Alice Flaherty (Harvard Medical school neurologist) gets episodes of hypergraphia following any grief incidences that have grave affect on her brain.
She has started her 4th book and is doing research to help explain how the muse comes and goes.
2. Mendez- He felt the unreasonable compulsion to write poetry even though the patient had no previous history of being a poet.
3. Patient who wrote everything backwards!
4. Patients writing same word over and over again but with differing calligraphy.
5. Patients' writing consists of sheer scribbling and frantic random thoughts.
Therefore on a lighter note, if you have the wrong brain defect but fall under the right category...then voilà ...YOU shall be famous!
Shivani Mangalgi
Medicowesome 2017
Leucocoria
Leucocoria:
Also known as the white pupillary reflex, is an abnormal white reflection from the retina of the eye.
Pathologically it's the absence of the red reflex.
Clinically the pupils appear white rather than the usual black color.
Mnemonic for causes of leukocoria-
'CREAM PIGMENT'
C - Coats disease/ Coloboma/ Cataract
R - Retinoblastoma/ Retinal dysplasia/ ROP/ Retinal fold
E - Endophthalmitis
A - Astrocytic hamartoma/ Anisometropia
M - Myelinated retinal nerve fiber layer
P - Persistent fetal vasculature/ PHPV
I - Incontinentia pigmenti/ Inflammation (uveitis)
G - Granuloma
M - Melanoma/ Medulloepithelioma
E - Familial exudative vitreoretinopathy (FEVR)
N - Norrie
T - Trauma/ Toxocariasis
Go ahead and add more causes to make your own list!
Shivani Mangalgi
Medicowesome 2017
Also known as the white pupillary reflex, is an abnormal white reflection from the retina of the eye.
Pathologically it's the absence of the red reflex.
Clinically the pupils appear white rather than the usual black color.
Mnemonic for causes of leukocoria-
'CREAM PIGMENT'
C - Coats disease/ Coloboma/ Cataract
R - Retinoblastoma/ Retinal dysplasia/ ROP/ Retinal fold
E - Endophthalmitis
A - Astrocytic hamartoma/ Anisometropia
M - Myelinated retinal nerve fiber layer
P - Persistent fetal vasculature/ PHPV
I - Incontinentia pigmenti/ Inflammation (uveitis)
G - Granuloma
M - Melanoma/ Medulloepithelioma
E - Familial exudative vitreoretinopathy (FEVR)
N - Norrie
T - Trauma/ Toxocariasis
Go ahead and add more causes to make your own list!
Shivani Mangalgi
Medicowesome 2017
Post operative ileus ( mechanical obstruction vs paralytic )
Hey Awesomites
Under normal circumstances, bowel movements usually do not appear till 72 hours after a certain abdominal or non - abdominal surgery, with a characteristic pattern of initiation of small bowel movements within 24 hours, stomach within 48 and colonic ( proximal to distal ) within 72 hours after surgery.
The assessment of gastrointestinal recovery is done with consideration to certain factors like the time taken to ingestion of first solid food, and time to either bowel movements or the first flatus passed, whichever occurs later.
Prolonged post operative paralytic ileus means:
- No return of bowel movements ( on auscultation ) after 72 hours
- Absence of flatus or stool on day 6 after surgery
- Feeling of discomfort, nausea or vomiting on oral intake, thus requiring i.v. support, NG tube placement by PO day 5.
- Partial return of bowel movements after PO day 5.
- No return of bowel movements ( on auscultation ) after 72 hours
- Absence of flatus or stool on day 6 after surgery
- Feeling of discomfort, nausea or vomiting on oral intake, thus requiring i.v. support, NG tube placement by PO day 5.
- Partial return of bowel movements after PO day 5.
On the other hand, post operative ileus due to mechanical obstruction, inspite of sharing many signs and symptoms, is an important differential to exclude. Most of the patients with PO mechanical obstruction in the bowel ( due to herniation, adhesions, stomas, masses, etc. ) have an initial return of bowel function that may be partial/ complete, and oral intake, after a physiological period of 72 hours post operatively.
It is then followed by intermittent episodes of nausea, feculent vomiting abdominal intense cramping pain and distension, that is often paroxysmal and rapidly progressing..
Also, patient with mechanical bowel obstruction after surgery may have other signs suggestive of ischemia of bowel loop distal to the obstruction, such as localised tenderness, fever, tachycardia, and peritoneal signs, which would mean immediate surgical intervention so as to prevent further complications !!
( Refer to UpToDate)
( Refer to UpToDate)
Thats all
Hope this helps :)
Hope this helps :)
- Jaskunwar Singh
Wednesday, August 16, 2017
Causative microbes in acute osteomyelitis
Hello Awesomites!
Let's discuss some facts about Common microbes involved in Acute Osteomyelitis.
Staphylococcus aureus is the most common infecting organism found in older children and adults with osteomyelitis.
Gram negative bacteria - vertebral body infections in adults.
Pseudomonas - intravenous drug abusers.
Fungal osteomyelitis - chronically ill patients receiving long-term intravenous therapy or parenteral nutrition.
Salmonella osteomyelitis - Sickle cell hemoglobinopathies - tends to be diaphyseal.
Infants -S. aureus (most common),group B streptococcus & gram-negative coliforms .
Group B streptococcus - otherwise healthy infants 2 to 4 weeks of age.
Animal Bite - Pasteurella
Human Bite - Eikinella
That's all!
Thank you.
MD Mobarak Hussain (Maahii)
Tuesday, August 15, 2017
Paramedian pontine reticular formation and MLF
Hello :)
-Upasana Y. :)
PPRF = Paramedian pontine reticular formation
MLF = Medial longitudinal fasciculus
-Upasana Y. :)
Third nerve palsy
Hello :)
Before starting with the III nerve, Let us understand the term.
According to TABER'S medical dictionary, We need to understand 3 main type of palsy here.
1.NUCLEAR palsy :- Paralysis caused by lesion of the nuclei in CNS.
2.OCULAR palsy :- Paralysis of extraocular nd intraocular muscles.
3.MUSCULAR palsy :- Loss of the capacity of muscle to contract. It may be due to structural or functional disorders
-in the muscle at the myoneural junction,
-in efferent nerve fibres,
-in the cell bodies of nuclei of origin of the brain or of the gray matter of the spinal cord,
-in conducting pathways of the brain or spinal cord,
-in motor centres of the brain.
Third cranial nerve supplies
1. EXTRAOCULAR MUSCLES
-Superior rectus
-Inferior oblique
-Medial rectus
-Inferior rectus
2.INTRAOCULAR MUSCLES
-Levator palpebral superioris
-Ciliary body
-Iris sphincter msucle
THE LOCALIZATION OF THIRD NERVE LESION
-Supranuclear
-Nuclear
-Fascicular
-Basilar
-Intra-Cavernous sinus
-Superior orbital fissure
-Intra Orbital part
CLINICAL FEATURES OF THIRD NERVE PALSY:-
1. Ptosis - paralysis of LPS muscle.
2. Deviation – out, down and intorted (unopposed action of LR and SO).
3. Ocular movements:
• Adduction – MR
• Elevation – SR and IO
• Depression – IR
• Extorsion – IR and IO
4. Pupil is fixed and dilated – paralysis of sphincter pupillae muscle.
5. Accommodation is completely lost – paralysis of ciliary muscle.
6. Crossed diplopia – paralytic divergent squint.
7. Head posture – If the pupillary area is uncovered, head takes a posture consistent with the directions of actions of the paralysed muscles, i.e., head is turned on the opposite side, tilted towards the same side and chin is slightly raised. (Pathways between vestibular nuclei and oculomotor nuclei. These are Intranuclear pathway.)
FEATURES AND CAUSES OF THIRD NERVE LESIONS AT VARIOUS LEVELS
1. Supranuclear lesions
• Lesions of the cerebral cortex and supranuclear pathway produce conjugate paresis which affect both eyes equally.
• In supranuclear lesions although position and movements of the eyes are abnormal, they maintain their relative co-ordination and produce no diplopia.
2. Nuclear lesions
• Lesions involving purely the third nerve nucleus are relatively uncommon.
• Common causes include ; vascular diseases, demyelination, primary tumors and metastasis
• Lesions involving entire nucleus cause
-an ipsilateral third nerve palsy with ipsilateral sparing and
-contralateral weakness of elevation.
• Lesions involving paired medial rectus subnuclei (ventromedial nucleus) cause a wall-eyed bilateral internuclear ophthalmoplegia ( WEBINO ) characterised by defective convergence and adduction.
Before starting with the III nerve, Let us understand the term.
According to TABER'S medical dictionary, We need to understand 3 main type of palsy here.
1.NUCLEAR palsy :- Paralysis caused by lesion of the nuclei in CNS.
2.OCULAR palsy :- Paralysis of extraocular nd intraocular muscles.
3.MUSCULAR palsy :- Loss of the capacity of muscle to contract. It may be due to structural or functional disorders
-in the muscle at the myoneural junction,
-in efferent nerve fibres,
-in the cell bodies of nuclei of origin of the brain or of the gray matter of the spinal cord,
-in conducting pathways of the brain or spinal cord,
-in motor centres of the brain.
Third cranial nerve supplies
1. EXTRAOCULAR MUSCLES
-Superior rectus
-Inferior oblique
-Medial rectus
-Inferior rectus
2.INTRAOCULAR MUSCLES
-Levator palpebral superioris
-Ciliary body
-Iris sphincter msucle
THE LOCALIZATION OF THIRD NERVE LESION
-Supranuclear
-Nuclear
-Fascicular
-Basilar
-Intra-Cavernous sinus
-Superior orbital fissure
-Intra Orbital part
CLINICAL FEATURES OF THIRD NERVE PALSY:-
1. Ptosis - paralysis of LPS muscle.
2. Deviation – out, down and intorted (unopposed action of LR and SO).
3. Ocular movements:
• Adduction – MR
• Elevation – SR and IO
• Depression – IR
• Extorsion – IR and IO
4. Pupil is fixed and dilated – paralysis of sphincter pupillae muscle.
5. Accommodation is completely lost – paralysis of ciliary muscle.
6. Crossed diplopia – paralytic divergent squint.
7. Head posture – If the pupillary area is uncovered, head takes a posture consistent with the directions of actions of the paralysed muscles, i.e., head is turned on the opposite side, tilted towards the same side and chin is slightly raised. (Pathways between vestibular nuclei and oculomotor nuclei. These are Intranuclear pathway.)
FEATURES AND CAUSES OF THIRD NERVE LESIONS AT VARIOUS LEVELS
1. Supranuclear lesions
• Lesions of the cerebral cortex and supranuclear pathway produce conjugate paresis which affect both eyes equally.
• In supranuclear lesions although position and movements of the eyes are abnormal, they maintain their relative co-ordination and produce no diplopia.
2. Nuclear lesions
• Lesions involving purely the third nerve nucleus are relatively uncommon.
• Common causes include ; vascular diseases, demyelination, primary tumors and metastasis
• Lesions involving entire nucleus cause
-an ipsilateral third nerve palsy with ipsilateral sparing and
-contralateral weakness of elevation.
• Lesions involving paired medial rectus subnuclei (ventromedial nucleus) cause a wall-eyed bilateral internuclear ophthalmoplegia ( WEBINO ) characterised by defective convergence and adduction.
3. Fascicular lesions
• Causes are similar to nuclear lesions.
-Benedikt syndrome involves the fasciculus as it passes through the red nucleus and is characterised by ipsilateral 3rd nerve palsy and contralateral extrapyramidal signs such as hemitremor.
-Weber syndrome involves the fasciculus as it passes through the cerebral peduncle and is characterised by ipsilateral 3rd nerve palsy and contralateral hemiparesis.
-Nothangel syndrome involves the fasciculus and the superior cerebellar peduncle and is characterised by ipsilateral 3rd nerve palsy and cerebellar ataxia.
-Claude syndrome is a combination of Benedikt and Nothangel syndromes.
4. Lesions involving basilar part of the nerve
• As the nerve runs in the subarachnoid space at the base of skull unaccompanied by any other cranial nerve, isolated third nerve palsies are frequently basilar.
• Causes :
1. Aneurysms at the posterior communicating artery cause isolated third nerve palsy with involvement of pupil.
2. Extradural hematomas which may cause tentorial pressure cone with downward herniation of the temporal lobe. This compresses the third nerve as it passes over the tentorial edge. Initially there occurs fixed, dilated pupil, which is followed by a total third nerve palsy.
3. Diabetes causes isolated 3rd nerve palsy with sparing of the pupillary reflexes.
5. Lesions involving intracavernous part of the nerve
• Because of its close proximity to other cranial nerves, intracavernous 3rd nerve palsies are usually associated with involvement of the 4th and 6th nerves, and the 1st division of trigeminal nerve.
-PULSATILE EXOPHTHALMOS can also be seen.
-PULSATILE EXOPHTHALMOS can also be seen.
• In intracavernous 3rd nerve palsy, pupil is spared. Sometimes, pupil may be constricted owing to inv of sympathetics.
• Causes :
• Causes :
1. Diabetes may cause vascular palsy.
2. Pituitary apoplexy – may cause a third nerve palsy as a result of hemorrhagic infarction of a pituitary adenoma (after child birth), with lateral extension into cavernous sinus.
3. Intracavernous lesions – aneurysms, meningiomas, carotid-cavernous fistulae and Tolosa-Hunt syndrome (granulomatous inflammation).
6. Lesions of the intraorbital part of the nerve
• May cause isolated extraocular muscle palsies or may involve either superior division or inferior division or both.
• Causes : orbital tumors, pseudotumors, trauma and vascular diseases.
7. Lesions of pupillomotor fibres
• B/w the brainstem and the cavernous sinus, pupillomotor fibres are located superficially in the superior median quadrant of the nerve.
• They derive the blood supply from the pial blood vessels whereas the main trunk of the 3rd nerve is supplied by vasa nervorum.
I want to thank my teacher for such a beautiful explanation.
I hope it helped.
Do read about the following . (though I will write on this topic also)
1.Injury of Paramedian pontine reticular formation
2. Ptosis in Horner's syndrome and oculomotor nerve palsy.
-Upasana Y. :)I want to thank my teacher for such a beautiful explanation.
I hope it helped.
Do read about the following . (though I will write on this topic also)
1.Injury of Paramedian pontine reticular formation
2. Ptosis in Horner's syndrome and oculomotor nerve palsy.
Drugs that can cause TOXIC MYOPATHIES
Hello :)
1. TYPE- Inflammatory
-Cimetidine
-D- Penicillamine
-Procainamide
-L-tryptophan
-Levodopa
2.TYPE- Non-Inflammatory necrotizing or vacuolar
-Alcohol
-Cholestrol lowering agents
-Chloroquine
-Colchicine
-Cyclosporine and tacrolimus
-Emetine
-Isoretinoic acid
-Vincristine
-Labetalol
3.TYPE -Rhabdomyolysis and myoglobinuria
-Alcohol
-Amphetamine
-Cocaine
-Heroin
-Phencyclidine
-Meperidine
4.TYPE -myosin loss
-Non depolarizing neuromuscular blocking agent
-steroid
That's all.
-Upasana Y. :)
1. TYPE- Inflammatory
-Cimetidine
-D- Penicillamine
-Procainamide
-L-tryptophan
-Levodopa
2.TYPE- Non-Inflammatory necrotizing or vacuolar
-Alcohol
-Cholestrol lowering agents
-Chloroquine
-Colchicine
-Cyclosporine and tacrolimus
-Emetine
-Isoretinoic acid
-Vincristine
-Labetalol
3.TYPE -Rhabdomyolysis and myoglobinuria
-Alcohol
-Amphetamine
-Cocaine
-Heroin
-Phencyclidine
-Meperidine
4.TYPE -myosin loss
-Non depolarizing neuromuscular blocking agent
-steroid
That's all.
-Upasana Y. :)
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