Medicowesome

Wednesday, July 26, 2017

Acute Pancreatitis - Mnemonic

Hello Awesomites!
Here's a Mnemonic on the causes of Acute Pancreatitis.
The mnemonic is- GET SMASHED

G- Gall Stones
E- Ethanol (Alcohol consumption)
T- Trauma
S- Steroids
M- Mumps
A- Autoimmune
S- Scorpion stings
H- Hyperlipidemia /Hypercalcemia
E- ERCP (Iatrogenic)
D- Drugs

I hope that this is useful for you guys.
Thank you.

MD Mobarak Hussain (Maahii)

Spine abnormalities in neurofibromatosis

Neurofibromatosis is an autosomal dominant disease.There are 3 types of neurofibromatosis. Type 1 is more common among all and is characterized by tumors that develop along nervous system.

This post deals with spinal abnormalities that occur in type 1 neurofibromatosis.

Due to presence of multiple neurofibromas of spinal nerves, there is increased CSF pressure, this causes protrusion of duramater, this ballooned sac containing cerebrospinal fluid is known as dural ectasia.

This condition may result in pain in the back and limbs, bladder control problems, and numbness in severe cases.
Neurofibromatosis may cause tumors around the spinal cord. Scoliosis, an irregular side curvature of the spine from left to right, and kyphosis, or a rounded or forward angulated back, occur together or separately in about one in five people with neurofibromatosis type 1.

Children with neurofibromatosis type I develop one of two forms of scoliosis, dystrophic or non- dystrophic scoliosis. Non-dystrophic type is similar to ' typical ' scoliosis called as adult idiopathic scoliosis.

Dystrophic scoliosis, on the other hand, is a form of scoliosis that occurs due to bony changes related to neurofibromas affecting the spine. Dystrophic scoliosis is identified by looking for specific features on X-rays of the spine. For patients and their families, dystrophic scoliosis is known as a more severe form of scoliosis. It may also occur with abnormally thin ribs, weakened vertebral bones, and severe spinal curvatures including kyphosis and rotational deformities and is often associated with dural ectasia.

Treatment for scoliosis due to neurofibromatosis is challenging, particularly when dystrophic scoliosis is present. Effective treatment requires the knowledge and skill of an experienced orthopedic surgeon who specializes in scoliosis treatment.

Thanks for reading.

Madhuri Reddy

Tuesday, July 25, 2017

Image based question on gallstone

Hello awesomites!

Yesterday, we posted an Image based MCQ on Facebook, Instagram, Tumblr and Twitter - And as promised, here is the answer!

Q. What type of stone is this?
Hint - This is the most common stone worldwide.

Options:
A. Cholesterol
B. Mixed
C. Black
D. Brown

The correct answer is B. Mixed gallstone.

The given pathological specimen shows a Gall Bladder removed after cholecystectomy and multiple faceted stones found inside it.

Stones are multiple in number, the cut section shows the central brown core which is pigmented surrounded by whitish/pale layer of cholesterol making it a mixed stone.

Hope you enjoyed this question and we will be back with another one soon!

-MD Mobarak Hussain (Maahii)

Fact of the day : Reduced white matter due to depression

Hey Awesomites

People ( or patients ) suffering from depression have reduced integrity of white matter substance. This means the neuronal circuit loses its connections with other parts of brain due to miscommunication between the brain cells.

A recent study mapped the internal structures of brain using diffusion tensor imaging ( DTI ) technology, that is a specialised MRI scan that creates a 3D map as it follows the diffusion of water in brain tissue.
( Source )

- Jaskunwar Singh

Steven-Johnson syndrome (SJS) / Toxic epidermal necrolysis (TEN) -Part 2

Hello :)

Have you heard of SCORTEN SCORE?

It is a score used to assess the severity of illness in TEN.

Go to the link below:-

https://image.slidesharecdn.com/delayedtypedrughypersensitivityinterhospitalconference-100803104905-phpapp01/95/delayed-type-drug-hypersensitivity-35-728.jpg?cb=1280833217

-We can assess the nutritional status by the body weight.

-Body is in the condition of hyper metabolism which will lead to excessive proteolysis.

-For the above thing, check albumin levels.

-Due to excessive fluid loss body will undergo dehydration and hypotension.

-Temperature should be noted. As each degree increase in temperature over normal, increases metabolism by 5-8%.

-Ocular examination is important part.

-Check for LFT and RFT.

-Late ophthalmic complications are mainly due to functional alteration of the conjunctival epithelium with dryness and abnormal lacrimal film. This leads to chronic inflammation, fibrosis, entropion, trichiasis, and symblepharon. Long-term irritation and deficiency of stem cells in the limbus may result in metaplasia of corneal epithelium with painful ulcerations, scarring, and altered vision.

- Esophageal, intestinal, urethral, and anal strictures may also develop in rare cases.

Nutrition: -

Consist 2 parts

1) parentral

2) Entral

Parentral nutrition consist of dextrose.

Entral is important for this patient.

-Protein powder.

-Dal.

-Fruits e.g. Banana

-We use various feeding devices like nasogastric tube or ryles tube.

Treatment:-

-Stop all the drugs

-airway breathing circulation fluids

-Symptomatic treatment

MEDICATIONS

Antibiotic to treat and prevent infections.

Used to treat and prevent severe skin inflammation.

Ranitidine reduces the acidity.

BETADINE MOUTH GARGLE: Oral antiseptic for relief of painful infections and inflammatory conditions of mouth and pharynx

Anti-inflammatory, Anti-pruritic, and Vaso-constructive properties. To cure mouth ulcers.

-Burns guideline (but lesser fluids)

That's all for today .

-Upasana Y. :)

Genetics in Alzheimer's disease mnemonic

__________ gene is associated with early onset Alzheimer's disease (AD).

__________ gene is associated with late onset Alzheimer's disease.

Answers:
Early onset - APP gene
Late onset - Apo E4 gene

Awesomite: I need a mnemonic for this.

Mnemonic:
apO E4 in Old Elderly
aPP in Pediatric Patients

-IkaN

Monday, July 24, 2017

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. :)

Myopathies series - Part 4

Hello! :)

In previous post, I left you with a question

How do we identify the site and cause of lesion?

Important points in history and neurological examination that is suggestive of myopathy are:-

1. MUSCLE WEAKNESS

According to Taber's medical dictionary, Lacking physical strength or vigor; infirm especially as compared with what would be the normal or usual for that individual.

Most muscle diseases produces symmetrical weakness of the large muscles of the girdles and trunk.

A) HIP GIRDLE (MOST COMMONLY AFFECTED)

- Difficulty in getting up from squatting position or from low chair,

-Inability to climb stairs,

-Waddling gait.

B) UPPER GIRDLE WEAKNESS

- Difficulty in hanging clothes on a cloth line

-Difficulty in taking down item from high shelves.

C) TRUNK WEAKNESS

-Difficulty in turning in bed and getting up from recumbent position.

D) NECK MUSCLE WEAKNESS

-Inability to control neck while in a vehicle as it rapidly accelerates and decelerates.

-neck pain and stiffness.

E) CRANIAL MUSCULATURE WEAKNESS

1. FACIAL WEAKNESS:-

-Inability to close eyes fully.

-Difficulty in drinking with a straw.

2. OCCULAR WEAKNESS:- (I will explain this below in bit detail )

-ptosis

-extraoccular movement weakness are seen.

F) DISTAL MUSCULATURE WEAKNESS

-Difficulty in opening lids of jar

-turning keys in keyholes

-tend to trip on uneven ground with repeated falls.

2. GAIT

3. FATIGUE

According to Taber's medical dictionary, the condition of an organ or tissue in which its response to stimulation is reduced or lost as a result of over activity.

Abnormal fatigability after exercise can result from certain metabolic and mitochondrial myopathies.

And as I have already discussed the importance of duration and intensity of exercise that provokes fatigue. It helps to distinguish metabolic myopathies.

4. MYALGIA

-Episodic= metabolic myopathies

-Constant=inflammatory muscle disorders

5. OCULOBULBAR WEAKNESS

6. SENSORY SYSTEM = NORMAL

7. MYOGLOBINURIA

- Why? As caused by the excessive release of myoglobin from muscles during periods of rapid muscles destruction (rhabdomyolysis)

-Results in renal failure in severe cases.

-Patient complains of exercise induced myalgia then ask about "Cola colored" or "red colored” urine during this episodes.

That's all for today.

I hope it helped.

In next post I will continue with the relation of age and progression to diagnose myopathy.

-Upasana Y. :)

Emphysematous Cholecystitis

Hello guys! Here's a brief description about Emphysematous Cholecystitis.

What are the risk factors for Emphysematous Cholecystitis?

1. Diabetes Mellitus (Most Important)
2. Immunosuppresion
3. Vascular compromise (Obstruction & stenosis of Cystic artery).

Emphysematous Cholecystitis is a life-threatening form of Acute cholecystitis & caused due to infection of the gall bladder wall with Gas forming bacteria like: Clostridium welchi.
Gas forms in gall bladder wall with occasional detection of crepitation (that's why called Emphysematous).

Development of gangrene & perforation is common.

It is managed by Emergency cholecystectomy with broad spectrum antibiotics.

Thank you

MD Mobarak Hussain (Maahii)

How to study for USMLE Step 2 CK

If you are short of time, don't read this. Seriously, if you have 2-3 months to prepare - Just do UW, assessments and give the exam. You will do great!

If you have a good 6-12 months, you are just starting your prep and need honest advice, here is mine.

I haven't got my score yet, but the post has been requested before I even gave my exam. So here it is =) I wonder if my credibility changes after my result. Oh well, guess I'll never know.