Showing posts with label Musculoskeletal system. Show all posts
Showing posts with label Musculoskeletal system. Show all posts

Tuesday, May 25, 2021

Salter-Harris classification of fractures

Salter Harris classification is used for fractures involving the physis ( growth plates) of long bones. These fractures are common in children as their skeletal growth is not fully complete.

Depending on the extent and the structures involved, there are 5 types as follows: 

Here is a mnemonic to remember the different types, which actually goes by the name of the classification itself!

S - Separation through growth plate or physis
A - Above the physis
L - Lower to physis
T - Through the physis, metaphysis, epiphysis
ER-ERasure of physis ( as it is a compression fracture of growth plate)

Hope this helps!
-Padma Sri Katikaneni


Saturday, May 1, 2021

Lyme's disease - a review


Lyme's disease/ Lyme borreliosis

A patient with a typical history of frequent visits to the woods with bull's eye rash, neurologic features, cardiac abnormalities, and musculoskeletal features.

Tuesday, March 10, 2020

Thursday, June 27, 2019

What Is Going On In Fibromyalgia?

Hi there! Let’s talk about pathophysiology of fibromyalgia; a chronic disorder where fatigue and widespread pain feature prominently.

Current hypothesis says, it’s caused by aberrant peripheral and central pain processing.
Two key features are allodynia, that is, pain in response to a non-painful stimulus and hyperaesthesia, which is, exaggerated perception of pain in response to mildly painful stimulus.

Modern research says, certain antidepressants- with both serotonergic and noradrenergic activity- such as TCAs and venlafaxine, can relieve pain and other symptoms; suggesting the pathway involvement.

Some evidence says, alternative therapies such as acupuncture and spa therapies alleviate pain, which have been postulated to act via similar spinal pain-modulatory pathways.

CSF studies show increased levels of substance P, with decreased levels of noradrenaline and serotonin metabolites. All three are neurotransmitters involved in descending pain-modulatory pathways in the spinal cord.

PET images show an abnormal central dopamine response to pain.

The critical question here is: what is cause and what is effect?

Small sample size and short periods of study, remain the most cumbersome challenge to our complete understanding of fibromyalgia.  

Thank you for reading.
- Ashish Singh.

Friday, September 29, 2017

Rotator Cuff muscles and their actions (mnemonic)

To remember the actions of Rotator Cuff muscles ( Supraspinatus, Infraspinatus, Teres Minor and Subscapularis), just remember the following:

1- The mnemonic for the muscles is: SITS
2- We will start with ABDuction and finish with ADDuction
3- The vowels in English can be remembered by AEEIou ( shout to remember better :P )
4- Now just match letters from the 2 mnemonics in the same order they are written in
 as you can see in the table:

So S goes with A...I goes with E...T goes with E and the last S goes with I.

Never forget the action of Rotator Cuff muscles again :)


Tuesday, August 15, 2017

Drugs that can cause TOXIC MYOPATHIES

Hello :)

1. TYPE- Inflammatory

-D- Penicillamine

2.TYPE- Non-Inflammatory necrotizing or vacuolar

-Cholestrol lowering agents
-Cyclosporine and tacrolimus
-Isoretinoic acid

3.TYPE -Rhabdomyolysis and myoglobinuria

4.TYPE -myosin loss

-Non depolarizing neuromuscular blocking agent

That's all.
-Upasana Y. :)

Tuesday, August 8, 2017

Myopathies series - Part 7

Hello :)

In previous post, We discussed about myopathy caused due to structural changes.
Today, I will explain it in detail. (SOURCE :- Harrison's Principle of internal medicine )

Two complex are important here :-

- Dystrophin-glycoprotein complex confer stability to the sarcolemma
- deficiency of dystrophin (Duchennes dystrophy) may lead to secondary loss of the sarcoglycans and dystroglycan
-Loss of a single sarcoglycan (LGMD) results in secondary loss of other sarcoglycans in the membrane without affecting dystrophin
-Disruption of the dystrophin-glycoprotein complexes weakens the sarcolemma, causing membrane tears and a cascade of events leading to muscle fiber necrosis.

Let us discuss dystrophinopathies first .

1.Duchene’s muscular dystrophy 
-Most common muscular dystrophy
- X-linked recessive disorder
- Onset before age 5

-Age : Present at birth ,Usually becomes apparent between ages 3 and 5
-Sex : Male

-XR (Deletion mutation of the gene that encodes dystrophin)

Laboratory Tests
• Serum CK
 – Elevated to between 20 and 100 times normal
 – Abnormal at birth but declines late in the disease because of inactivity and loss of muscle mass.

 Mutation analysis on peripheral blood leukocytes
• Identification of a specific mutation in dystrophin gene
– Allows for unequivocal diagnosis
– Makes possible accurate testing of potential carriers
 – Is useful for prenatal diagnosis

Diagnostic Procedures
• EMG -> Myopathic

Muscle biopsy
• Muscle fibers of varying size
• Small groups of necrotic and regenerating fibers
• Connective tissue and fat replace lost muscle fibers.
Definitive diagnosis is established on the basis of dystrophin deficiency.
• Diagnosis can also be made by Western blot analysis of muscle biopsy specimens.
– Abnormalities on the quantity and molecular weight of dystrophin protein

• Immunocytochemical staining of muscle with dystrophin antibodies
– Can be used to demonstrate absence or deficiency of dystrophin
 – localizing to the sarcolemmal membrane
– Possible mosaic pattern in carriers of the disease
 – Dystrophin analysis of muscle biopsy specimens for carrier detection not reliable

Prednisone 0.75 mg/kg per d
– Significantly slows progression for up to 3 years
– Some patients cannot tolerate glucocorticoid therapy
• Weight gain is significant
– Complications of long-term use often outweigh the benefits.

Exon skipping therapy
• Duchenne's disease may benefit from novel therapies that either replace the defective gene or missing protein or implement downstream corrections (e.g., skipping mutated exons or reading through mutations that introduce stop codons)

2. Becker’s Muscular dystrophy
-Less-severe form of XR muscular dystrophy
-allelic defects of same gene of Duchenne ( ~10 times less frequent than Duchenne)

 -Age : – Most between ages 5 and 15
Onset in the third or fourth decade or even later can occur 
- Sex : Male

Symptoms & Signs
• Onset of symptoms occurs between ages 5 and 15.

I.Muscular manifestations – Pattern of muscle wasting closely resembles Duchenne.
– Progressive weakness of girdle muscles, especially of lower extremities
 – Weakness becomes generalized as disease progresses.
 – Hypertrophy, particularly in calves, is an early and prominent finding.
By definition, patients walk beyond age 15 (whereas patients with Duchenne dystrophy are typically in a wheelchair by the age of 12). 
– Significant facial muscle weakness is not a feature.
– Respiratory failure may develop by fourth decade.

II. Extramuscular manifestations
– Cardiac, may result in heart failure
– Mental retardation may occur, not as common as in Duchenne
• Other less common presentations
 – Asymptomatic hyper-CK-emia
Myalgias without weakness 
– Myoglobinuria

Laboratory Tests
• Serum CK – Closely resembles findings in Duchenne dystrophy
• Mutation analysis on peripheral blood leukocytes
– Deletions or duplications of the dystrophin gene in 65% of patients (same as in Duchennes dystrophy)
– 95% of patients, the DNA deletion does not alter the translational reading frame of mRNA.
 These "in-frame" mutations allow for production of some dystrophin, which accounts for the presence of altered rather than absent dystrophin on Western blot analysis 
• EMG – Myopathic
• Muscle biopsy – Results closely resemble those in Duchenne dystrophy.
 – Diagnosis requires Western blot analysis of muscle biopsy samples demonstrating a reduced amount or abnormal size of dystrophin.

• Use of glucocorticoids has not been adequately studied
Endurance training may be helpful

That's all for today.
-Upasana Y. :)

Composition of Bone cement

Hello :)

Today I saw a case of Infected AMP implant. Following questions were asked to me regarding bone cement.
Q. Composition of bone cement.

A. Bone cement consist of :- Powder and liquid.

1. Polymer : Polymethylmethacrylate (PMMA)
2. Initiator : Benzoyl peroxide (BPO)
3. Radio-opacifier : Barium sulphate , Zirconia
4. Antibiotic :- Gentamicin (commonly)

1. Monomer : Methylmethacrylate (MMA)
2. Accelerator : N,N Dimethy Paratoluidine (DMPT)
3. Stabilizer : Hydroquinone

Q.Antibiotics used as additives for PMMA bone cement.
A. Antibiotics commonly used as additives for PMMA bone cement include:
- vancomycin, (MRSA)
-in addition to tobramycin.

Also, successful non-antibiotic bactericides that have been used as bone cement additives include:-
- Quaternary ammonium compounds (benzalkonium chloride and cetylpyridinium chloride)

That's all for today.
-Upasana Y. :)

Wednesday, August 2, 2017

Myopathies series - Part 6

Hello :)

Now we will discuss individual myopathies in detail.

We have discussed the association between metabolic disorder and myopathies.
Metabolic myopathies Intro
Metabolic myopathies (differential diagnosis)
In this part, we will discuss the association between structure of cell (myocytes) and myopathy. Look at the diagrams below :-


In the next post, I will explain the pictures in detail.
I hope it helped.
-Upasana Y. :)

Thursday, July 27, 2017

Myopathies series -Part 5

Hello! :)


- 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



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.

-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:-

- 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.

-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.)

-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 
PROXIMAL: biceps, triceps, quadriceps
DISTAL: - Extensor carpi radialis, Anterior tibialis.

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. 

Monday, July 24, 2017

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:-


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.

- Difficulty in getting up from squatting position or from low chair,
-Inability to climb stairs,
-Waddling gait.

- Difficulty in hanging clothes on a cloth line
-Difficulty in taking down item from high shelves.

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

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

-Inability to close eyes fully.
-Difficulty in drinking with a straw.

2. OCCULAR WEAKNESS:- (I will explain this below in bit detail )
-extraoccular movement weakness are seen.

-Difficulty in opening lids of jar
-turning keys in keyholes

-tend to trip on uneven ground with repeated falls.



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.

-Episodic= metabolic myopathies

-Constant=inflammatory muscle disorders




- 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. :)

Sunday, July 23, 2017

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



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

c) Sex linked muscular dystrophy
-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.)


1. Inflammatory myopathies

-systemic inflammatory disease (involves other organs also)

2. Toxic myopathies

-Thyrotoxic myopathy (There is an awesome post By Ojas )

-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

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. :)


Saturday, July 15, 2017

Myopathies series- Part 2


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:-


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.
1. Serum CK levels.
2. Lactate 
3.Serum electrolytes.
4. ammonia
6. Urinalysis
7.Forearm exercise test.
9.Routine muscle biopsy
1. Urine organic acids
2. Plasma acylcarnitine profile
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. :)

Thursday, July 13, 2017

Myopathies series - Part 1

Hello :)

Before starting with the series, I will post on the basics you need to know for myopathies.

Q. What do you mean by muscular dystrophy and myopathy?
A. I found that following definition from Harrison is simple.

Skeletal muscle disease myopathies, are disorder with structural changes or functional impairment of muscle.

Muscular dystrophy refers to a group of hereditary progressive diseases with unique phenotypic and genetic features.

Do you know glycogen storage diseases?
Yes! But why do you need to mention it here? Because, skeletal muscles are the store house of glycogen. It gets converted into glucose-6-phosphate (Note:- Never in glucose unlike liver. Why? Otherwise glucose will move out from the myocyte to blood. And myocytes will fail to utilize their own stored glycogen. That is why muscle lack an enzyme called glucose-6-phosphatase.)

There are some glycogen storage disease which will lead to myopathies.

For now remember that myopathies have different way of presentation. 
Muscle weakness is one of the clinical feature.
The muscle weakness can either be 1. Intermittent or 2. Persistent.
If there is energy deficiency in muscle, it will become weak.
Today, we are focusing mainly on skeletal muscle energy metabolism.

Glycogen storage disease are described in the Roman numerals. Not all glycogen storage disease lead to myopathies. Some glycogen storage disease lead to myopathies is mentioned in the diagram.

 More is coming up.:) 
-Upasana Y.  

Friday, May 12, 2017

Marfan syndrome - High Yield Information.

Hello everybody,
lets today briefly revise all the high yield points on Marfan syndrome.

Marfan syndrome is an example of structural protein disorder and with autosomal dominant inheritance, lets see what exactly goes wrong in this condition.


There is a missense mutation seen in the fibrillin-1 gene located on the chromosome no.15.
So to understand the condition better, lets understand a bit about fibrillin.

Fibrillin forms the glycoprotein component of cellular microfibrils and also provides a scaffold for the elastin deposition.
Abundant fibrillin is found in the connective tissues of the aorta,ligaments and the eye, these are the structures predominantly affected in the disorder too.

The defective fibrillin leads to defective microfibril assembly intracellularly and reduced elasticity in connective tissues.
 Defective fibrillin also leads to decreased TGF-beta(Transforming growth factor ) sequestration, and excess of TGF-B hampers normal vascular smooth muscle development and matrix production.

Morphological Features:

1) Skeletal changes:
    Tall stature with long extremities.
     Long tapering fingers and toes.(Arachnodactyly)
     Kyphosis ans scoliosis.
     Pectus excavatum or Pigeon breast deformity.

2) Cardiovascular changes:
     Aortic regurgitation: Due to aortic cystic medial degeneration leading to valvular ring dilatation & valvular incompetence. Most threatening valvular lesion.
     Mitral valve prolapse : Most common valvular lesion.
     Aortic Dissections are the most common cause of death in these patients.

3) Occular changes:
    Ectopia Lentis: bilateral superotemporal dislocation of lenses.
    Retinal Detachment : due to increased axial length of the globe.


Currently Revised Ghent Criteria is used for the diagnosis of Marfan syndrome.
It considers:
Family history,
Cardinal Clinical Signs in absence of family history,
Presence or absence of Fibrillin Mutation.

so that's all on marfans syndrome.

Fun Fact:
We all have been hearing about some famous personalities with Marfan syndrome like Abraham Lincon and Michael Phelps, but Tutankhamen the 11th pharoh of 18th Egyptian Dynasty was diagnosed to be suffering from Marfan's Syndrome by a series of CT scans and DNA tests carried out on his MUMMY!

Do post any other interesting facts you know about Marfan's Syndrome.

Let's Learn Together!

Thursday, March 16, 2017

Pathophysiology of myopathy caused during hypothyroidism and hyperthyroidism

Hello awesomites! Today's topic of discussion is - Myopathy in thyroid disease.
Interestingly, it is caused by both, hypothyroidism as well as hyperthyroidism.

What is myopathy?
It is a disease of muscle tissue where, ultimately, muscles get weak and are unable to perform work due to deficiency of ATP.

Why is there myopathy in hyperthyroidism?
The thyroid hormone is a catabolic hormone. Hyperthyroidism increases energy expenditure, glucose turnover, lipolysis, and protein breakdown (proteolysis). But here is the catch - Hyperthyroidism increases whole-body protein turnover and breakdown before any measurable changes in energy expenditure or glucose and fat metabolism, suggesting that amino acid and protein metabolism is an early and primary target for thyroid hormone action in humans. It was therefore concluded that the thyroid-hormone concentration may be an important factor in regulating muscle proteolysis. The altered protein metabolism causes myopathy.

Then, one may ask, why myopathy in hypothyroidism? Less thyroid hormone should lead to less protein breakdown, shouldn't it?

Well, this is a good question! Slightly complex and tricky to answer though. 

In hypothyroidism, there is abnormal glycogenolysis, defective mitochondrial oxidative metabolism and triglyceride storage.

Abnormal glycogenolysis and triglyceride storage: Less glucose is released and utilised because of this. The body starts using more proteins usually derived from muscles leading to myopathy.

Mitochondrial oxidative metabolism defect: Thyroid hormone is responsible for activation of bc1 complex also known as complex 3 & succinate dehydrogenase. Less activation of bc1 leads to less formation of ATP from glucose.... So again, the body switches to proteins from muscles as a source of energy!

That's all!
Stay cool :)

Wednesday, February 1, 2017

GABA A and GABA B receptor agonist antagonist mnemonic

Here's a super short post.

Flumazenil acts on the GABA-A receptor and baclofen acts on the GABA-B receptor.

How do you remember this?

Wednesday, December 14, 2016

A 7 year old with hyperextensible joints

A 7 year old boy is brought to you. He is intellectually disabled. On examination, you notice hyperextensible joints. Large hands, large feet, protruding ears, elongated face are also seen. The patients testes are large in size compared to his age. Diagnosis?

Marfans syndrome
Ehler Danlos syndrome
Fragile X syndrome
Friedreichs Ataxia

Answer below
It's Fragile X syndrome. Why isn't it's Marfans? Because Marfans has normal IQ.

Here are my notes + mnemonic for Fragile X syndrome.

Did you know?
Fragile X is the most common cause of inherited mental retardation.
It was the first trinucleotide repeat disorder to be recognized.

That's all!