Owl’s eye appearance

 

Pulp Stones

This post is about age changes in the pulp. If the first thing that comes to your mind is pulp stone! That's correct! So, Let's dive into pulp and learn more about it :))

In Pulp cavity, age changes causes 

• Cellular changes
• Fibrosis of tissue
• Pulp stones or denticles
• Diffuse calcification

Cellular changes

There is a decrease in 

• Number of cells
• Size of cell 
• Number of Organelles

Fibrosis of tissue

• Accumulation of bundles of fibers
• In radicular pulp: longitudinal fiber bundle
• In coronal pulp: diffuse fibers

Therefore collagen fiber content increases in pulp organ. 

Pulp stone or denticle

• They are nodular or calcified masses
• They have calcium:phosphate ratio comparable to dentin
• They can be Single or multiple
• Present in functional and unerupted teeth
• It is present in both coronal and pulpal portion

Classification: According to structure 

True pulp stone

• Rare 
• Found in the apex region 
• The remnant of epithelial root sheath within pulp induce pulp cells to differentiate into odontoblast to form dentin masses

False pulp stone:  they appear as concentrically years of mineralized tissue

Classification: According to location

1. Free pulp stone is entirely surrounded by Dentin 
2. Attached pulpstone is partially fused with Dentin 
3. Embedded pulpstone is entirely surrounded by pulp 

This Post is written by Anisha Valli,

Types of Dentin

Hey friends,

Dentin is a very important question.

It comes as a question worth 4 points in my theory exam paper! I have tried my best to make it simpler for you all in this blog :))

I hope this will help you!

Primary Dentin

It is divided into Mantle and Circumpulpal Dentin 

A. Mantle Dentin 

• First formed dentin in the Crown
• Type III collagen
• It is less mineralized
• Matrix vesicles are present which help in Globular calcification

B. Circumpulpal Dentin

• It forms the bulk of the tooth
• Type one collagen
• It is more mineralized
• Matrix vesicles are present which help in Linear and globular calcification

Secondary Dentin

• It is formed after the root completion
• It contains dentinal tubules which are S-shaped
• The mineral ratio is similar to primary Dentin 
• Secondary Dentin is a narrow band of Dentin bordering the pulp
• As age increases, inorganic content increases
• Therefore the Dentin becomes sclerosed
• It means It protects the pulp from exposure in older teeth

Tertiary Dentin 

It is formed in response to stimuli

Attrition
Abrasion
Erosion
Cavity preparation

• It is deposited on the pulpal surface of Dentin only in the affected area
• The appearance of Dentin varies as it is formed by an odontoblast 
• Quality and quantity of tertiary Dentin depends on intensity and duration of stimuli

Reactionary Dentin 

Dentin is deposited by pre-existing odontoblasts

Reparative Dentin 

Dentin is deposited by newly differentiated odontoblast-like cells

Written by Anisha Valli :))))

MIL: Lichen Planus

Read more about Medicowesome Image Library (MIL) here.

Image: Plaques of Lichen Planus

Submitted by: Dr. Manasi Shirolikar

MIL: Impetigo

Read more about Medicowesome Image Library (MIL) here.

Image: Impetigo contagiosa

Submitted by: Sagar

MIL: Polar cataract

Read more about Medicowesome Image Library (MIL) here.

Image: Polar cataract

Submitted by:  Sushrut

MIL: Rhabdomyosarcoma of the Right Eye

Read more about Medicowesome Image Library (MIL) here.

Image: Rhabdomyosarcoma of the Right Eye

Submitted by: Does not wish to reveal identity

MIL: Psoriasis

Read more about Medicowesome Image Library (MIL) here.

Image: Plaques of psoriasis

Submitted by: Dr. Manasi Shirolikar

Introducing Medicowesome Image Library (MIL)

Hello everyone!

I wish to create a visual learning experience by adding images and videos along with what we write.

But since most images on Google have copyright issues, the Medicowesome authors can't use them :(

That is why, I'm asking medical students, residents and acquaintances to send me images of what they see to help create the Medicowesome Image Library (MIL).

It can be anything - a histology slide, a microbiology agar, a pathology specimen, a rash, an instrument, an x-ray - anything!

Myopathies series -Part 5

Hello! :)

8. APPEARNACE OF MUSCLE :-

- Hypertrophy of Calf muscles = Dytrophinopathies or Limb girdle muscular dystrophy.

-Pseudohypertrophy= Duchene's muscular dystrophy, infiltration by sarcoid granulomas,amyloid deposit, bacterial and parasitic infections.

-Atrophy of gastrocnemius muscles in medial aspect = Dysferlinooathies 

- Atrophy of humeral muscles= FSHD

9. REFLEXES PRESERVED

10. LAB INVESTIGATIONS:-

1. ENZYMES: - I have already discussed its role in metabolic myopathies.

- ALT, AST, LDH,aldolase :- Found in both skeletal muscle and liver.Elevated GGT help to establish its liver origin.

-CK (MM) help to evaluate myopathies.

2. ELECTRODIAGNOSTIC STUDIES: 

-EMG: - diagnose myopathy and help to choose right muscle for biopsy.

-NCS (nerve conduction studies):-Help to differentiate myopathies from neuropathy and NMJ disorders.

       

Diagnostic test for specific type of myopathies:-

1. FOREARM EXERCISE TEST:-

- Place an indwelling catheter in to an antecubital vein and obtain baseline blood sample for lactic acid and ammonia.

-The forearm muscles are exercised. Vigorously squeeze the sphygmomanometer bulb for 1 min.

-Blood is then obtained at the intervals of 1,2,4,6 and 10 min for comparison with baseline.

Normally, Both glucose and ammonia increases with exercise.

Interpretation:-

-Glycolytic defects: - Lactic acid rise is absent or below normal while rise in ammonia will reach the control values.

-Myoadenylate deaminase deficiency: - there occur a selective failure to increase ammonia.

2. DNA ANALYSIS: - Some muscle disorder are associated with gene defects like deletions and mutations. (In Duchene muscular dystrophy, we will see it.)

3. MUSCLE BIOPSY:-

-Safe diagnostic procedure in establishing the final diagnosis of suspected myopathy.

-Different techniques of microscopic evaluation: - Histology, immunohistochemistry with antibodies, electron microscopy.

-SITE: - muscle selected may have mild to moderate muscle weakness.

-NOT PERFORMED ON: - Muscle injured by previous trauma,injections and EMG needles 

-COMMON MUSCLES USED FOR BIOPSY:-

PROXIMAL: biceps, triceps, quadriceps

DISTAL: - Extensor carpi radialis, Anterior tibialis.

*Claps* 

We are done with the basic for myopathy.

Now I will go through individual myopathy. :D

I remember age and progression of myopathy part. :) I will discuss it in next part. 

Take care.

-Upasana Y. 

Steven-Johnson syndrome (SJS) / Toxic epidermal necrolysis (TEN) -Part 1

Hello! :)

TOXIC EPIDERMAL NECROLYSIS

-A severe form of adverse cutaneous drug reaction

-Idiosyncratic reaction

-Immunologically Mediated

- Fever and mucocutaneous lesions

-Epidermal sloughing

CLASSIFICATION

1. SJS= <10% BSA detachment

2. OVERLAPPING SJS/TEN= 10-30% detachment

3. TEN = >30% detachment

EPIDEMIOLOGY

-Both are rare but occur as a medical emergency.

-Incidence of SJS 1-7 Cases per million.

-SJS > TEN by 3: 1

-TEN tend to be older

-Worldwide distribution

-HIV positive cases have increased incidence.

ETIOLOGIES

-Drugs being the most common cause

-Infection (viral e.g. HSV, bacterial, fungi)

-Vaccination

-systemic disease (lupus)

-Physical agents (UV light, radiation)

-Idiopathic 25%

Drugs that result in this are:-

-Antibiotics = sulfonamides > penicillin > cephalosporin

-Anti-gout: allopurinol

-Anti-epileptics; carbamazepine, Dilantin

-Anti-psychotics

-Analgesic including NSAIDS

RISK FACTORS:

GENETIC SUSCEPTIBILITY:-

-HLA-B*1502 associated with greater risk with carbamazepine use in southeastern Asians.

-HLA-B*5801 confers risk with allopurinol associated reactions.

-HLA-B*44 Caucasians

HIV:-

-Slow acetylators so results in prolonged exposure to medications.

-Immune dysregulation

-Other infections

-40 Fold increased risk of SJS/TEN with cotrimoxazole (Remember! It is used as a prophylactic drug in HIV patients.)

CLINICAL PRESENTATION:-

-Drug exposure 1-3 weeks prior to onset of symptoms

-PRODROME=fever, flu-like, 1-3 days

-symmetrical lesion distribution

-starts on face and trunk before spreading

-skin blistering with sloughing for 2-3 days progressively then stabilizes

-Erythroderma

-Facial edema

-Skin pain- burning

-Palpable purpura

-Skin necrosis (Nikolsky sign)

-Blisters or epidermal detachment

-SJS tragetoid, TEN target lesions atypical

-Mucous membrane erosions or crusting

-tongue swelling

-conjuctival irritation

-Dysuria

-GI bleed

-Pulmonary bleed

LABORATORY FINDINGS

-Anemia

-Lymphopenia

-Neutropenia (poor prognosis)

-Elevated transaminases

-Cultures, If infected

-Skin biopsy-Rule out other conditions

-BUN/CR ratio

-Serum electrolytes

PATHOGENESIS

-not well understood

-Suspected immunologic

1. GRANULYSIN: Cytolytic protein from cytotoxic T-cell and NK - cells

(Highly expressed in SJS /TEN patients)

2. DEATH RECEPTOR CD95 (fas): Elevated fas ligand leading to apoptosis

3. Perforin, TNF-alpha and granzymes-B in higher concentration, associated with NON-APOPTOTIC death.

HISTOLOGY

-Early perivascular inflammation of T-lymphocytes, primarily CD8

-Monocytes infiltration

-Lymphocytes surrounding basal keratinocytes

-Subepidermal vesiculation

-Full thickness necrosis

-Increased adhesion molecules: VCAM, ICAM

EVALUATION AND DIAGNOSIS

-Clinical diagnosis on the basis on exclusion

-prior drug history or illness+fever+skin lesions with sloughing

DIFFERENTIAL DIAGNOSIS

-toxic shock syndrome (staphylococcus and streptococcus)

-Scalded skin syndrome (staphylococcus)

-Phototoxic eruptions (Sun exposure areas and known medications)

-Paraneoplastic pemphigus (Lymphoma)

-Erythematous drug eruptions (Lack mucosal involvement)

-Drug hypersensitivity syndrome /DRESS/DIHS (eosinophilia)

-Acute generalized exanthematous pustulosis (AGEP) (lack of pain and noted pustules)

-Toxic skin reaction (chemical irritant)

-Toxic erythema (Intoxication)

-Kawasaki's (diagnostic criteria)

EMM (ERYTHEMA MULTIFORME):

-targeted papules and plaques

-Acrally distributed

-Fever mild

-Significant skin detachment uncommon

-Histology: inflammation EMM>SJS

TREATMENT:-

-Immediate removal of possible triggers (especially drugs with longer half-life)

-SUPPORTIVE CARE

 - Wound care: burn unit with improved outcomes

 *avoid silver sulfadizine (Sulfonamide associated with SJS)

 -Fluid and electrolyte management (RL or NS)

 -Pain control (Local anesthetic cream)

 -Temperature regulation: caloric expenditure 

 -Monitor for infection: pseudomonas

 -Nutrition (High protein diet, Banana) (I will discuss it in next post)

 -Ocular care (Important)

 You can also refer this link 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3018455/

That's all for today.

I will discuss the case we have seen in the emergency ward on the same. And also the treatment aspect. 

-Upasana Y. :)

x

Soap bubble appearance on X ray:Differential diagnosis

Hello everyone!
I always find X rays quite confusing especially when they appear same.
It's a short post about differentiating bone tumors.

Soap bubble appearance on X ray is expansile, eccentric vaguely trabeculated space having thin sharp defined sclerotic margins.
Mostly seen in bone tumors and other bone lesions.
On X ray they all appear same, only way to differentiate them is to know their location and other associated factors.
Commonly seen in
1) Aneurysmal bone cysts-
  Location of ABC is Metaphysis.
It occurs in younger age group i.e less
than 20 years. So the X ray of such
patient will have non fused and 
immature bone.
Preferred sites are long bones of upper and lower limb, especially femur.

2) Giant cell tumor(osteoclastoma) -
Location of GCT is epiphysis
Here the prevalent age group is 20-40, which means an adult sketetal structure.
While the preferred sites are same like ABC.
So if one see epiphyseal lesion with soap bubble appearance in mature bone, it has to be Giant cell tumor.
GCT presents with other classical signs of Egg shell crackling on palpitations.
Giant cells on histology.
Which are NOT the tumor cells. So its one of the example of misnomers. They are meant to misguide you.

Thats it :)
Stay awesome

-Khushboo

Niemann-Pick disease notes and mnemonic

Hello!

Niemann-Pick disease (NPD; also called sphingomyelin-cholesterol lipidosis) is a group of autosomal recessive disorders associated with splenomegaly, variable neurologic deficits, and the storage of sphingomyelin.

Gap Junctions and Connexin Mutations

Let's start with a brief description of Gap Junctions. Take two empty cardboard boxes, assume they are cells. Bore a hole in each one of them and then enter a small straw in it. Then arrange the two boxes(cells) in such a way that the two straws are aligned perfectly with each other and that their cavities form a continuous column, so that if you pour water in one box it should completely go into the other one without even a single drop falling in between them.

Cronkhite Canada syndrome

Cronkhite Canada syndrome

Dr. Thinker: USMLE STEP 1

USMLE STEP 1

Ideal Duration: 6 months (But, remember it varies from individual to individual)

Resources: Kaplan notes, Kaplan Videos, First Aid, Uworld

 Alternative resources:  If  you are aiming for high scores    

I am finding first year MBBS extremely difficult and tough

"Sis.. I just joined medical college. Finding it extremely tough to study. None of the subjects seem familiar. I'm losing all my positivism and feeling helpless."

Firstly, take a moment to congratulate yourself. You've made it to medical school! New subjects is going to be so much fun!

"I feel left behind. I'm not able to answer. What is taught in lecture is very minimalistic compared to text book."

Thyroid carcinoma mnemonic

Hello! 
I made a real easy way of remembering thyroid tumors :)

Papillary carcinoma mnemonic:
Popular (Most common thyroid cancer)
Palpable lymph nodes (Lymphatic metastasis is common)
Positive I (131) uptake
Post radiation in head and neck (One of the causes)
Pops out of the capsule (Usually encapsulated but invades capsule)
Pops everywhere in the gland (Multifocal)
Positive, pleasing, perfect, parexcellence, peerless prognosis
(Excellent prognosis because it's slow growing)
[Another mnemonic is PG - Papillary, Good prognosis =D ]
Histology:
Popping eyes (Clear nuclei, Orphan Annie Eyes)
Papillary pattern
Psammoma bodies
Pseudoinclusions (Intranuclear cytoplasmatic inclusions)

Study group discussion: Extra books for USMLE

Could someone suggest books to use for mle step 1? Everyday someone new tells me that the kaplan book is not good for a particular subject.

Haha

BRS + Kaplan for physiology
Road map to gross anatomy
Biochemistry Kaplan (Pretty good)
Goljan for pathology
Microbiology Kaplan (more than enough)
Pharmacology Kaplan
Behavioral Kaplan + BRS + a lot of resources online and it's never enough

What about the other subsections of anatomy?

Umm which subsections? Embryology and Histology isn't high yield.

Oh alright. Neuroanatomy?

That's a pain! There are these anki flashcards I found on neuro.. I'll send you guys the link when I'm home. Thanks!

Do all brain stem sections for step 1. Any image on neuro and you need to identify the tracts/structures!

Ah. Why don't you try clinical neuroanatomy made ridiculously simple? I have heard its a recommended book for USMLE Step 1.

Ridiculously simple series is good!

Neuroanatomy one is really short and nice.

I've read the neuroanatomy book too. It's good.

Related post:
Preparing for the USMLE Step 1 exam
I have no idea about USMLE Step 1
USMLE for Indian medical students

Pathology brain tumors mnemonic

Hello, my favorite brainy people of the internet!
We'll be talking about some brain tumors today.
All of the mnemonics might not work for you, so take only what you need :)