Sunday, July 23, 2017

Triad of Retinitis pigmentosa mnemonic

The mnemonic for remembering the Triad of retinitis pigmentosa (RP) is BAD

1. B- jet Black spots which are perivascular.
2. A- Attenuation of arterioles.
3. D- Disc palor.

Thanks for reading.

Madhuri Reddy

Myopathies series -Part 3


Hello! :)

In previous post, I discussed about metabolic myopathies.
Today we see the general classification of myopathies.

Myopathies are classified as

-CONGENITAL
-ACQUIRED

I. CONGENITAL:-

1. Denervation atrophy;-
-spinal muscular atrophy (infantile motor neuron disease)

2. Muscular dystrophies

a) Autosomal recessive Muscular dystrophy 
-Limb-girdle form

b) Autosomal dominant muscular dystrophy
-Facioscapulohumeral
-Occular

c) Sex linked muscular dystrophy
-Duchene 
-Becker
-Emery Dreifuss

3. Myotonic dystrophy

4. Ion channel myopathies

5. Congenital myopathies

6. Myopathies associated with inborn errors of metabolism (This we have already studied in previous posts.)

II.ACQUIRED MYOPATHIES

1. Inflammatory myopathies

-Infectious
-non-Infectious
-systemic inflammatory disease (involves other organs also)

2. Toxic myopathies

-Thyrotoxic myopathy (There is an awesome post By Ojas )
http://www.medicowesome.com/2017/03/pathophysiology-of-myopathy-caused.html

-Ethanol myopathy
-Drug induced myopathy

So this means, we have long way to go: D


 "MOTOR ACTIVITY” is a broad term. It includes 
1) Voluntary movements 
2) Reflex movements
3) Rhythmic motor patterns

The pathway of any motor activity includes:

1. Cortical level
2. Brainstem and associated structures 
-Brainstem centers 
-Basal ganglia
-cerebellum

3. Spinal cord
4. Lower motor neurons
5. Neuromuscular junction 
6. Muscle 

 Myopathy means we are discussing problem in MUSCLES.
So how do we know the correct site of lesion?

To diagnose any myopathy, we need to know its site and cause of lesion. The following helps in the diagnosis.
1. History
2. Examination
3. Investigations 

Take care.
-Upasana Y. :)

Brain Abscess - Important facts

Hello guys! Here are some important facts about Brain Abscess.

Most Common site: Frontal lobe

Sequence of involvement: Frontal lobe > Temporal lobe > Parietal Lobe > Occipital lobe.

Most Common site of Brain Abscess in Tetralogy of Fallot: Parietal Lobe.

Most Common site of Brain Abscess in CSOM: Temporal lobe (Mastoiditis).

Most Common organisms involved are Anaerobic bacteria > Staphylococcus aureus > Streptococcus pyogenes.

Empirical therapy: Vancomycin + Ceftriaxone + Metronidazole for 4 to 8 weeks.

I hope that it's helpful to you.
Thank you!

MD Mobarak Hussain (Maahii)

Granulomas and hematolymphoid malignancies

Granulomas are rare findings in a bone marrow of hematolymphoid malignancies. They are commoner with Hodgkin lymphoma and rarer with acute leukemias. They are most commonly non caesating epitheloid granulomas and may stain negative for tuberculosis and fungi! So, what are they really? They are believed to be a immune response to tumour antigens or to immune complexes when the patient is on treatment...
All granulomas need not be tubercular!

Saturday, July 22, 2017

Branches of subclavian artery mnemonic

Hello friends,

Today let's memorise the branches of subclavian artery.

The mnemonic is  VITamin 'C ' and 'D'

Here VIT corresponds to branches arising from first part. 

'C' from second part. 

'D' from third part  of subclavian artery.

So from first part:

V - Vertebral

 I - Internal thoracic artery

T - Thyrocervical trunk or Thyroscapulocervical trunk( this makes our task easy to memorize branches of this trunk)

Thyroscapulocervical - Gives  rise to 3 arteries:

Thyro -- Inferior thyroid artery

Scapul-- suprascapular artery

Cervical - superficial cervical artery.

From second part:

C - Costocervical trunk which gives rise to superior intercostal artery and deep cervical artery.

From third part:

D - Dorsal scapular artery.

Sometimes, instead of superficial cervical and dorsal scapular arteries arising as 2 separate arteries, there is a single branch which arises from 1 st part of subclavian artery that is Transverse cervical artery.

This artery divides into superficial ascending branch and deep descending branch as shown in the flow chart below.

Thanks for reading and do correct me if there is anything wrong.

Madhuri Reddy (Madhu)

Rash involving hands and feet mnemonic

This is the association I use to remember the organisms causing rash that includes hands and feet - You drive CARS with your hands and feet. 

CA- Coxsackie A virus
R- Rickettsia rickettsii 
S- Syphilis (secondary)
S - Staphylococcus (TSS) 

We often forget Toxic Shock Syndrome in our differential. Keep it in mind! 

That's all! 
-IkaN 

Hypervitaminosis A mnemonic

Hello!

Here's a mnemonic to remember the features of Hypervitaminosis A.

The mnemonic is, "H.A.R.D. Puzzle."
H - Hepatosplenomegaly, Hair sparse, Hyperostosis
A - Anemia, Anorexia
R - Really painful bones
D - Dry skin
Puzzle - Pseudotumor cerebri

Thank you.

MD Mobarak Hussain (Maahii)

Necrotizing Enterocolitis - Important points

Here are some high yield points about Necrotizing Enterocolitis.

1. It is the most common life threatening emergency of gastrointestinal tract in neonates.

2. Triad of - Intestinal ischemia, enteral nutrition and bacterial translocation.

3. Distal part of Ileum and proximal segment of colon are most frequently involved.

4. Coagulation necrosis is the characteristic histological finding in the intestinal specimens in Necrotizing Enterocolitis.

5. Pneumatosis intestinalis (air in the bowel) is diagnostic on X-ray.

6. Portal venous gas shadow is a sign of severe Necrotizing Enterocolitis on X-ray.

7. Most important risk factor is Prematurity.

8. Pneumoperitoneum is a sign of advanced NEC with perforation.

These points should help you in quick revision.

Thank you!

MD Mobarak Hussain (Maahii)

Lung Cancer Subtypes

Subtypes of lung cancer:-
1. Squamous cell cancer-
Most common variant in India.
Smoking is a risk factor.
Central in location.
Local growth is surgically resectable.
Cavity formation is seen.

2. Adenocarcinoma-
Most common variant of lung cancer overall.
Most common lung cancer among non smokers.
Peripheral in location.
Transbronchial spread i.e. it arises at one lobe and spreads to the another lobe.

3. Small cell carcinoma/Oat cell carcinoma-
Most aggressive variant.
Smoking is a risk factor.
Central  in location.
It exhibits micrometastasis.
It has worst prognosis.

4. Large cell carcinoma-
Observed in Non smokers.
Peripheral in location.
This is associated with Estrogen production which manifests as Gynecomastia.

I hope this will help you to distinguish between the various subtypes.

Thank you
-Md Mobarak Hussain (Maahii)

Friday, July 21, 2017

Oxalate stones in Crohn's Disease


A tricky Concept based question often asked in Medicine/Pathology MBBS Professional Exam-
Why Crohn's Disease patient often develop Kidney/Renal STONES, particularly OXALATE stones?
Well...I would like to explain few Concepts separately Step by step...so at the end, you could CONNECT all THE hidden DOTS.
1.Crohn's Disease commonly affects ILEUM & terminal Small intestine
2.Disease affected Ileum in Crohn's Disease leads to REDUCED Bile salt absorption                                              
3.Reduced Bile salt absorption leads to subsequent FAT MALABSORPTION .
4.As Fat is not getting absorbed , Free Fatty Acids then start to bind with Calcium.
5.As more calcium is getting binding with Free Fatty Acids , it LEAVES MORE OXALATE to be absorbed in the intestine.
6.As more & more OXALATE gets absorbed, it leads to Hyperoxaluria & leads to renal OXALATE Stone formation....that's the complete explanation.

I hope you it helps.
Thank you

-Md Mobarak Hussain (Maahii)

Tachyarrhythmias

Here are some high yielding MCQ points on arrhythmia

Most common arrhythmia mechanism is re-entry.
Most common sustained arrhythmia is atrial fibrillation.
Most common benign rhythm identified is atrial premature contraction.
Most common arrhythmia in COPD patient is multifocal atrial tachycardia.
Post operative atrial fibrillation is managed with landiolol hydrochloride.
Atrial fibrillation getting converted to ventricular fibrillation is seen with accessory pathway conducting antegradely like Bundle of Kent in WPW syndrome.
VT storm or electrical storm is  3 or more separate episodes of VT within 24 hours.
Most commonly identified arrhythmia in cardiac arrest patient is ventricular fibrillation.
Most common cause of Sudden death in HCM is polymorphic VT/Ventricular fibrillation VF.

Thank you

-Md Mobarak Hussain (Maahii)

ERAS token, AAMC account, Letter of Recommendation

My juniors and colleagues requested that I guide them through this, so ta-da, another "How to" post.

I am attaching screenshots of the process - step by step. Sorry for all the scribbling. I was too bored to Photoshop.

Thursday, July 20, 2017

Viral Exanthems - Mnemonic

Mnemonic to remember the Viral Exanthems of childhood

ME gave ROSE to my BELLA after eating CHICKEN at 5 PM.

ME =MEasles
ROSE= ROSEola
BELLA = ruBELLA
CHICKEN = CHICKEN Pox
5 P= 5th disease (Parvovirus)

Thank you!
-Md Mobarak Hussain (Maahii)

Megaloblastic Anemia


1. Why do we get " Megaloblasts" in Megaloblastic anaemia?
2. Why we get anaemia in Megaloblastic anaemia?
Megaloblastic anaemia is called so due to presence of " Megaloblasts" in bone marrow.
What are " Megaloblasts" They're gigantic, abnormally BIG RBC-precursors seen in bone marrow. WHY do we see them ?
It needs some conceptual understanding.                           
Normally, RBC-precursors are big cells which divide rapidly as they mature & become progressively smaller as they divide while maturing towards mature-form of RBCs.  Now, the problem begins in Megaloblastic anaemia that this cell-division is impaired due to lack of nutrients ( Folate & Vitamin B12).  Vit B12 & Folate are critical for normal DNA synthesis & cell maturation.                                                             It's also described by a complex -term called " Nuclear-Cytoplasmic Asynchrony".
As DNA-synthesis is impaired, nuclear maturation of RBC-precursors get slowed up & could not match with the pace of cytoplasmic maturity/development. This DEFECTIVE NUCLEAR MATURATION halts cell-division & those big "MEGA" RBC-precursors remain as Big, MEGA, gigantic " Megaloblasts" in bone marrow giving the name as " Megaloblastic anaemia". Moreover, these " Megaloblasts" do NOT mature enough to get released into the peripheral blood & most RBC-precursors undergo " apoptosis " or apoptotic-death in bone marrow ..this  causes anaemia in Megaloblastic anaemia.

Hope this helps some of you to understand the basic concepts.

-Md Mobarak Hussain (Maahii)

Step 2 CK: Which Pneumococcal Vaccine to administer & when?



Monday, July 17, 2017

Brain to gut: Lets talk

Hey Awesomites

The brain and gut chat and share neurohumoral and immunologic messages with each other most of the times. That is why our emotions affect our stomach and intestines and vice versa. This healthy communication is disturbed when we are stressed out, anxious, or depressed.



Stress (more of psychological type) influences the type of bacteria inhabiting the gut, making a loss of our bowel flora diversification and increasing the concentration of harmful pathogens in the gut, thus leading to certain inflammatory and infectious processes.

Chronic flare - ups of inflammatory bowel disease result in deviation of the mood towards negative side by upto 60 percent by a process of rewiring the neuronal circuitary, called neuroplasticity. This inturn worsens the condition of gut on long-term basis.
Recent studies suggest that talk therapy - particularly cognitive behavioral therapy, and anti- depressants may be supportive in such cases to reduce the flaring up of inflammatory bowel syndrome.

In case of irritable bowel syndrome, that is a functional disorder ( without any actual organic cause ), the CBT and use of anti- depressants improve the symptoms in upto 60 percent patients. But which patients are likely to benefit still needs further research. Till then, we know that a referral for talk therapy in the patients of IBS is a must.


Thats all
- Jaskunwar Singh

Sunday, July 16, 2017

Favorites of brain cells: The game of genetics

Hey Awesomites

Many cells in the brain express two copies of a gene - maternal and paternal. But some express only one. If the single copy that is expressed carries a genetic mutation, it may result in cellular dysfunction and thus there are consequences.

Research on newborn mouse suggests that in about 85 percent of genes in the dorsal raphe nucleus, known for secreting serotonin, differentially activate their maternal and paternal gene copies. Ten days later in the juvenile brain, both copies are activated equally for all but 10 percent of genes.

The disparity also occurs in humans and in other systems like liver and muscles.

Like for example, in humans, a gene called DEAF1 that is implicated in autism and intellectual disability, shows a preferential expression of one copy of genes in multiple areas of brain. This is true for genes in other mental and neurologic disorders like Huntington's disease, schizophrenia, ADHD, and bipolar disorder.
Source )


Thats all
- Jaskunwar Singh

Novel Monoclonal Antibodies: Emicizumab and Caplacizumab


Emicizumab:

Patients with Haemophilia A need regular infusions of Factor VIII, and a majority of patients develop antibodies against this exogenous factor VIII rendering the therapy less effective.

Emicizumab is here to solve this problem. It mimics the physiological function of factor VIII, that is to enhance the interaction between activated factor IX and factor X to facilitate the activation of factor X. Emicizumab binds both factor IXa and factor X and increases the interaction between them.

Caplacizumab:

Patients with Thrombotic Thrombocytopenic Purpura(TTP) has antibodies against ADAMTS13. Reduction of ADAMTS13 levels leads to formation of vWF multimers that enhance platelet aggregation and consequent thrombus formation in all major systemic blood vessels. The current therapy protocol consists of Plasma exchange and Immunosuppressants.

Caplacizumab binds to vWF and prevents its interaction with GP1b receptor on platelets, thereby inhibiting platelet aggregation.




-VM

Fact of the day: Liquid biopsy for cancer detection

Hey Awesomites

We have known since long that surgical biopsies done routinely in cancer patients to diagnose and detect progression of the disease may increase the risk of carcinogenic changes in the cells in future, due to the changes that had prompted the biopsies.

A non - invasive and painless diagnostic tool that replaces the cutting is "liquid biopsy" that finds the hidden cancer cells anywhere in the body. The liquid biopsy is taken from a simple blood test to look for microscopic pieces of DNA circulating in the blood that contains genetic mutations causing tumors to spread, among billions of other DNA that were in the blood.
A year ago, a circulating tumor DNA test was approved by FDA that spots these mutations.


Thats all
- Jaskunwar Singh

Saturday, July 15, 2017

Poikilocytosis

Red blood cells

Also known as erythrocytes, is the most common type of blood cell and the principal means of oxygen transport in the body.

The normal biconcave shape is the essential feature of its biological function.
Through various stages of development and maturation, RBC loses its nucleus and most organelles in order to accommodate maximum space for haemoglobin.
This feature of RBC is critically affected by genetic and acquired pathological conditions.

Poikilocytosis is the term used to denote the variation in the shape of red blood cells.
Let's look at the major abnormalities in the shape of RBCs and the conditions in which they are seen:

1. Spherocyte - hereditary spherocytosis, autoimmune haemolytic anaemia, ABO haemolytic disease of the new born

2. Schistocyte - thalassemia, hereditary elliptocytosis, megaloblastic anaemia, iron deficiency anaemia and severe burns

3. Irregular contracted red cells - drug and chemical induced haemolytic anaemia, unstable haemoglobinopathies

4. Target cell (a type of leptocytosis)- iron deficiency anaemia, thalassemia, chronic liver disease and after splenectomy

5. Sickle cell (drepanocyte)- sickle cell anaemia

6. Tear drop cell - myelofibrosis, underlying marrow infiltrate

7. Crenated red cell - in blood films due to alkaline pH, presence of traces of fatty sustances on the slides or film allowed to stand over night

8. Acanthocyte - post splenectomy, chronic liver disease, Abetalipoproteinemia, McLeod blood group phenotype

9. Burr cell - uremia, liver disease, artifact

10. Stomatocyte - hereditary stomatocytosis, chronic alcoholism

11. Ovalocyte - hereditary ovalocytosis, hereditary elliptocytosis, severe iron deficiency anaemia

The diagram given represents the corresponding cells





Credits to: Shivani Mangalgi.

Myopathies series- Part 2


METABOLIC MYOPATHIES





In previous post, I gave an introduction of metabolic myopathies.

Today we cover:-

I.Diagnostic role of creatine kinase in metabolic myopathies.

II.Metabolic myopathies and its types.


Diagnostic role of enzyme in myopathies.

The following diagram shows the enzymes related to myopathies and their associated metabolic reactions.( Note:- The metabolic pathway is not only for skeletal muscle .It is in general . My main aim is to show enzymes of liver and muscle along with the pathways.Remember urea cycle occurs in liver )


Creatine kinase: - This enzyme will help us to evaluate different METABOLIC myopathies.

  1. ELEVATED CK: - In Glycogen storage disease associated myopathies.
     (In some GSD there will be mild elevated CK)
  2. MILD ELEVATED CK:- In Fatty acid oxidation disorder.
  3. NORMAL CK: - In Mitochondrial myopathies.Also in some fatty acid oxidation disorder.

    Metabolic myopathies types:-
I.                    DISORDER OF GLYCOGEN METABOLISM (MUSCLE GYCOGENOSES)
II.                  DISORDER OF FATTY ACID OXIDATION
III.                MITOCHONDRIAL MYOPATHIES








CLINICAL FINDINGS :-

1.
Second wind phenomenon: - suggestive of GSD V / McArdle’s
2. Out-of-wind phenomenon: - suggestive of GSD VII/ Tarui
3. Myoglobinuria (Burgundy colored urine):- GSD V, GSD IX
                                                                         LDH, PGM or PGK enzyme deficiency
                                                                         CPTII Deficiency
4. Proximal weakness: - GSD II / Pompe.
5. Exercise intolerance,ataxia,multisystem involvement:- Mitochondrial disorder, Coenzyme Q10 Deficiency.
LAB TESTS:-
1. Serum CK levels.
2. Lactate 
3.Serum electrolytes.
4. ammonia
5.AST,ALT,GGT 
6. Urinalysis
7.Forearm exercise test.
8.EMG
9.Routine muscle biopsy
SPECIFIC TESTS:- 
1. Urine organic acids
2. Plasma acylcarnitine profile
CONFIRMATORY BUT COSTLY :-
1. Enzyme analysis
2. DNA Analysis on leukocytes, fibroblasts and liver.

Click on the below given link to read on how to differentiate between McArdle, CPT II deficieny and mitochondrial myopathy. (this link helped me with the notes) 
*If you are running short of time, then Read only Case 1 and Case 2
I hope it helped. 
-Upasana Y. :)

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