Chemosis is known as oedema of conjunctiva.
Reason:due to exudation from the abnormal capillaries.This retained exudate gives a swollen and gelatinous appearance.
Regions: loosely attached areas of the bulbar conjunctiva and fornices.
Causes: ABC
A: Acute inflammations like gonococcal conjunctivitis, panophthalmitis, dacryocystitis, periostitis, orbital cellulitis.
B: Blood conditions (abnormal) like anaemia, urticaria, angioneurotic oedema, lymphocytic infiltration.
C: Circulatory obstruction in conditions like pulsating exophthalmos or due to pressure of an orbital tumour which may interfere with the lymph and blood drainage.
Thanks for reading.
Madhuri
Hello Awesomites!
Here's a Blog on Tay Sachs Disease and some common questions related to it.
Tay-Sachs disease
It is a genetic disorder that results in the destruction of nerve cells in the brain and spinal cord. Tay–Sachs disease is caused by a genetic mutation in the HEXA genes on chromosome 15. It is inherited from a person's parents in an autosomal recessive manner. The mutation results in problems with an enzyme called beta-hexosamidase A ,located on lysosomes,which results in the build up of the toxin GM2 ganglioside within cells. The most common type, known as infantile Tay–Sachs disease, becomes apparent around three to six months of age with the baby losing the ability to turn over, sit, or crawl. This is then followed by seizures, hearing loss, and inability to move. An eye abnormality called a cherry-red spot, which can be identified with an eye examination, is characteristic of this disorder. Death usually occurs in early childhood. Less commonly the disease may occur in later childhood or adulthood. These forms are generally milder in nature.Diagnosis is by measuring the blood hexosaminidase A level or genetic testing.
Frequently asked questions -
The substance which accumulates in Tay Sach’s disease is Ganglioside.
Deficiency of enzyme Hexosaminidase-A causes Tay Sach’s disease.
Cherry red spot at macula may be seen in Tay Sach’s disease.
That's all!
Thank you.
MD Mobarak Hussain (Maahii)
Hey Awesomites
Stimulation of trigeminal nerve in the face, vagus nerve, or carotid sinus in the neck may cause a reflex drop in heart rate, dilatation of peripheral blood vessels, and constriction of cerebral blood vessels, which leads to a sudden loss of brain perfusion and unconsciousness. This type of knockout is called "neurovascular knockout".
Blow to the eyesocket, as during boxing may cause a similar knockout, called the oculocardiac reflex due to stimulation of trigeminal nerve ( ophthalmic branch ) and vagus nerve.
- Jaskunwar Singh
Let us suppose that a patient has the classic signs & symptoms of Asthma and with that she has eosinophilia ( Absolute eosinophil count above 500/mm3).
The next step should be to look at the serum IgE levels.
If it is also elevated-
1. Do a stool examination and serological testing for strongyloidiasis.
2. Do Aspergillus-skin testing and check for aspergillus specific IgE.
If you have got a positive result for one of the above two, you have your diagnosis.
But what if both of the above results come out to be negative.
Then consider Churg Strauss syndrome or Eosinophilic granulomatosis with polyangiitis.
That's it!
-VM
Hey guys!
I saw a patient today, a 37 year old female patient with chief complaints of cough and shortness of breath. She has a history of allergic rhinitis and migraine. She is also obese with an BMI of 31.
As you must have guessed already she was diagnosed with Bronchial asthma. On the spirometry report done 4 months back, there was an obstructive pattern and after giving bronchodilators her FEV1 increased by 22% (>12%) and FEV1 vol increased by 300ml (>200ml). These findings also strongly support the diagnosis of asthma.
She was started on Albuterol as needed and Salmeterol-fluticasone MDI. She didn't show good response in the first 4 weeks, so she was also started on Montelukast and Tiotropium inhaler.
Now after 4 months, she still had cough and shortness of breath. She had bilateral polyphonic wheezes. A chest X Ray was done which came out to be normal. On pulse oximetry, SaO2 was 97% while breathing ambient air. On chest CT we found two attributes:
Subpleural opacities and Ground glass opacities.
So based on the CT scan findings, differential diagnosis:
Subpleural opacities:
1. Eosinophilic granulomatosis with polyangiitis( previously called Churg Strauss).
2. Organizing pneumonia
3. Pulmonary embolism with resultant subpleural pulmonary infarction
4. Allergic bronchopulmonary aspergillosis ( well, not really, actually in this case, there is peripheral air space opacification which looks identical to subpleural opacities)
Now Ground glass opacities:
1. Atypical pneumonia
2. Hypersensitivity pneumonia
3. Several ILDs
4. Sarcoidosis
5. Pulm Edema
6. Pulm Haemorrhage
That's all!
-VM
Hello awesomites!
Here's a collection of Cutaneous infections/diseases caused by Streptococcus pyogenes
Direct infections of skin or subcutaneous tissue-
1. Cellulitis
2. Impetigo
3.Ecthyma,Erysipelas
4. Vulvovaginitis
5. Perianal infection
6. Streptococcal ulcers
7. Blistering distal dactylitis
8. Necrotizing fasciitis
Secondary infection-
Eczema, infestations, ulcers, etc.
Tissue damage from circulating toxins-
1. Scarlet fever
2. Toxic‐shock‐like syndrome
3. Recurrent toxin‐mediated perineal erythema
Skin lesions due to allergic hypersensitivity to Streptococcal antigens
1. Erythema nodosum
2. Vasculitis
Skin disease provoked or influenced by Streptococcal infection (mechanism uncertain)-
1. Psoriasis, especially guttate forms.
2. Kawasaki disease.
That's all!
MD Mobarak Hussain (Maahii)
The optic disc margins start to blur in the following order in papilledema-
1. Superior
2. Inferior
3. Nasal
4. Temporal
Blurring first occurs where the nerve fibre density is the highest.The optic disc being ovoid in shape, with taperings superiorly and inferiorly, the nerve fibre density is higher there. Hence such a sequence.
That's all!
-Sushrut Dongargaonkar
