Hey Awesomites
The clinical features ( s/s ) that are presented by a patient with DNS are : NOSE MASH
NO - Nasal Obstruction
S - Septal cartilage and bone deformity
E - Epistaxis
M - Middle Ear infection
A - Anosmia
S - Sinusitis
H - Headache
- Jaskunwar Singh
Tuesday, April 25, 2017
C Peptide levels : An Overview
Hello everyone!So I ended up uttering 'C peptide' recently in my Medicine Viva and my professor screwed me over it.
(Clearly I didn't C it through :'D )
So I thought of doing a brief summary on it.
Here goes.
1. What is C peptide ?
- When pro- insulin is cleaved , it gives insulin and C peptide.
- C peptide in general has a longer half life than insulin and is easier to detect.
- The pathway is something like this :
Pre proinsulin produced in Rough Endoplasmic Reticulum of Pancreas --> Transported to the Golgi apparatus and cleaved to form Proinsulin --> Packed into secretory granules --> In these granules proinsulin is converted to : Insulin and C peptide.
- Traditionally it is said to have no intrinsic activity but recent studies say it might have anti oxidant and anti inflammatory properties.
2. What does it indicate ?
- So , its presence indicates presence of Insulin in the body in a proportionate amount.
- Hence in a case of Hypoglycemia if C peptide levels are high, it's likely to be due to increased endogenous Insulin levels.
3. C peptide levels increased in -
- Insulinoma
- Sulfonylurea induced Hypoglycemia ( As they are Insulin Secretagogues)
- Type 2 Diabetes Mellitus ( Hyperinsulinism due to resistance)
- Insulin Resistance states like Obesity , PCOS , Cushing's.
4. C peptide levels reduced in -
- Type 1 Diabetes as Insulin secretion is reduced
- Latent Autoimmune Diabetes of Adult (LADA )
- Factitious hypoglycemia - Due to excess exogenous Insulin administration.
- Hypoglycemia due IGF secreting tumors.
So if you get a patient with Hypoglycemia with elevated insulin levels , C peptide levels help you decide if due to exogenous Insulin , or Endogenous Insulin ( Sulfonylurea induced or Insulinoma).
Hope this helped !
Stay awesome.
Happy studying!
~ A.P Burkholderia.
Monday, April 24, 2017
The Basics : Middle Ear
Hey Awesomites
In this post, I will be talking about the middle ear structures and its relations with its neighbors ( just a summary ).
The Middle Ear is an air filled and bilaterally compressed/ concaved cavity lined by mucous membrane located in between the external and internal parts of ear. It is divided into:
- Epitympanum or the Attic ( 6mm ) - lies above pars tensa and medial to pars flaccida
- Mesotympanum ( 2mm ) - lies opposite to pars tensa
- Hypotympanum ( 4mm ) - lies below the level of pars tensa
BOUNDARIES of the middle ear ( homologous to structure of a cube ) :-
Roof : Tegmen tympani - a thin bony plate that is a part of petrous part of temporal bone, separates the middle ear cleft from middle cranial fossa.
- Infection in the middle ear may spread superiorly and lead to formation of abscess in the meninges ( especially Extradural abscess ), meningitis or if severe, it may even lead to abscess formation in the temporal lobe.
Floor : Jugular bulb - The middle ear cavity is separated from jugular bulb by a thin piece of bone that if deficient may lead to formation of a layer of fibrotic tissue and mucous membrane in between. The contents of jugular bulb are:
- Internal Jugular vein
- Glossopharyngeal nerve ( IX )
- Vagus ( X )
- Accessory nerve ( XI )
The tympanic branch of glossopharyngeal nerve enters the middle ear at the junction of the floor and medial wall to play an important role in formation of tympanic plexus.
Anterior wall : The upper part of the narrow anterior wall has two openings or tunnels for - ( mnemonic : TEA )
- Canal for Tensor tympani muscle
- Pharyngotympanic ( or Eustachian ) tube
The lower part of anterior wall is separated from the Internal Carotid Artery by a thin plate of bone. The ICA is surrounded by a plexus of sympathetic nerves that enter middle ear through openings in this bony plate to form tympanic plexus.
Posterior wall : Posteriorly, it is related to middle ear cleft ( Aditus, Antrum and mastoid air cells )
- Infection in this region may spread posteriorly into the sigmoid sinus ( in posterior cranial fossa ) and cause thrombophlebitis !!
Medial wall : Medially the middle ear cavity is related to the promontory, oval and round window
Lateral wall : Tympanic membrane separates the middle ear from the external ear.
A brief about the functions of middle ear:
On the incoming of sound waves, the tympanic membrane oscillates and these oscillations are sensed by the strongly attached and faithful middle ear ossicle, the Malleus. The sound energy is transmitted as such by the ossicles ( Malleus - Incus - Stapes ) to the internal ear for further processing.
The major function of these ossicles is amplification of sound waves - Tympanic membrane is 17 times larger than the oval window - So that means the sound energy is picked up by the larger area ( TM ) and impinged over a much smaller area ( oval window ) thus amplifying it 17 times.
In addition, the lever action of the ossicular chain is approx. 1.3 units. Thus the intensity ( force ) of sound waves/ vibrations changes ( increased by ~20 times ) and not the frequency !! If the sound waves are not amplified ( in case OC is removed ), the Air Conduction would be lost. So BC > AC and thus hearing would then be poor.
Thats all
Hope this helped :)
Stay Awesome!
- Jaskunwar Singh
In this post, I will be talking about the middle ear structures and its relations with its neighbors ( just a summary ).
The Middle Ear is an air filled and bilaterally compressed/ concaved cavity lined by mucous membrane located in between the external and internal parts of ear. It is divided into:
- Epitympanum or the Attic ( 6mm ) - lies above pars tensa and medial to pars flaccida
- Mesotympanum ( 2mm ) - lies opposite to pars tensa
- Hypotympanum ( 4mm ) - lies below the level of pars tensa
BOUNDARIES of the middle ear ( homologous to structure of a cube ) :-
Roof : Tegmen tympani - a thin bony plate that is a part of petrous part of temporal bone, separates the middle ear cleft from middle cranial fossa.
- Infection in the middle ear may spread superiorly and lead to formation of abscess in the meninges ( especially Extradural abscess ), meningitis or if severe, it may even lead to abscess formation in the temporal lobe.
Floor : Jugular bulb - The middle ear cavity is separated from jugular bulb by a thin piece of bone that if deficient may lead to formation of a layer of fibrotic tissue and mucous membrane in between. The contents of jugular bulb are:
- Internal Jugular vein
- Glossopharyngeal nerve ( IX )
- Vagus ( X )
- Accessory nerve ( XI )
The tympanic branch of glossopharyngeal nerve enters the middle ear at the junction of the floor and medial wall to play an important role in formation of tympanic plexus.
Anterior wall : The upper part of the narrow anterior wall has two openings or tunnels for - ( mnemonic : TEA )
- Canal for Tensor tympani muscle
- Pharyngotympanic ( or Eustachian ) tube
The lower part of anterior wall is separated from the Internal Carotid Artery by a thin plate of bone. The ICA is surrounded by a plexus of sympathetic nerves that enter middle ear through openings in this bony plate to form tympanic plexus.
Posterior wall : Posteriorly, it is related to middle ear cleft ( Aditus, Antrum and mastoid air cells )
- Infection in this region may spread posteriorly into the sigmoid sinus ( in posterior cranial fossa ) and cause thrombophlebitis !!
Medial wall : Medially the middle ear cavity is related to the promontory, oval and round window
Lateral wall : Tympanic membrane separates the middle ear from the external ear.
A brief about the functions of middle ear:
On the incoming of sound waves, the tympanic membrane oscillates and these oscillations are sensed by the strongly attached and faithful middle ear ossicle, the Malleus. The sound energy is transmitted as such by the ossicles ( Malleus - Incus - Stapes ) to the internal ear for further processing.
The major function of these ossicles is amplification of sound waves - Tympanic membrane is 17 times larger than the oval window - So that means the sound energy is picked up by the larger area ( TM ) and impinged over a much smaller area ( oval window ) thus amplifying it 17 times.
In addition, the lever action of the ossicular chain is approx. 1.3 units. Thus the intensity ( force ) of sound waves/ vibrations changes ( increased by ~20 times ) and not the frequency !! If the sound waves are not amplified ( in case OC is removed ), the Air Conduction would be lost. So BC > AC and thus hearing would then be poor.
Thats all
Hope this helped :)
Stay Awesome!
- Jaskunwar Singh
Craniopharyngioma mnemonic
The C's of Craniopharyngioma
Children
Calcification
Cholesterol crystals
Cyst formation
Central diabetes insipidus
Compresses chiasm, can't C (see, because butemporal hemianopia)
CR: CRAniopharyngioma RAthkes pouch remnant
Yup. That's all!
-IkaN
Sunday, April 23, 2017
'A' wave in JVP : Mnemonic and explanation
Hi everyone. So JVP is one of the most theoretical clinical signs I've ever studied. And though parts of it are logical , I find it tedious to memorize all causes for a particular finding.
So I've prepared a Mnemonic for prominent a waves.
Here goes.
The A wave is a positive wave of the JVP.
It represents the Right Atrial pressure during systole.
Causes of a prominent a wave
Remember :
CRePT's
C - Cor Pulmonale
R - Right heart Failure
P - Pulmonary stenosis
T - Tricuspid stenosis
S - The S tells you it's Stenosis for P and T.
The a wave essentially represents the pressure in the Right atrium during systole.
So any condition that causes this pressure to increase would cause a prominent A wave.
Cor Pulmonale and RVF are basically congestion in RV causing elevation of pressure in the RV.
This means the atrium needs to pump with greater force into the Ventricle for the venous return to enter the Ventricle. This increases the RA pressure causing prominent a wave.
Pulmonary Stenosis leads to accumulation of blood in the RV and this follows a similar fate as the above mentioned causes.
Tricuspid stenosis causes obstruction to the flow of blood from RA to RV. Thus accentuating the pressure in the RA.
That's the Prominent a wave for you !
~~~~~~~~~~~
Now there's something called the Cannon a wave.
These represents contraction of the RA against a closed Tricuspid valve.
The causes of this include -
A- V dissociation.
Heart blocks.
Ventricular arrhythmias - V tach , Ventricular premature complexes and Ventricular pacing.
~~~~~~~~~~~
The a wave would be absent in Atrial fibrillation as the atrium is functionally not pumping at all , and just vibrating.
These are the a wave findings for you !
Hope this helped
Stay awesome.
~ A.P. Burkholderia
Number needed to treat and number needed to harm mnemonic
Hello!
Number needed to treat = 1 / Absolute risk reduction
Mnemonic: TARR - Treat Absolute Risk Reduction
Number needed to harm = 1 / Attributable risk
Mnemonic: HARM - Harm Attributable Risk M
That's all
-IkaN
The Basics : Lateral wall of Nasal cavity
Hey Awesomites
In this post, I will be talking about the anatomical structures in the lateral wall of the nasal cavity.
Saturday, April 22, 2017
Clubbing : Why it occurs.
Hi everyone !
This is a short post on why clubbing happens.
So it's simple !
It's cause people like to go out and get drunk.
Just kidding. Here goes.
This is a short post on why clubbing happens.
So it's simple !
It's cause people like to go out and get drunk.
Just kidding. Here goes.
1. What is clubbing ?
- It's the bulbous enlargement of the terminal digits and the nail bed.
- It's the bulbous enlargement of the terminal digits and the nail bed.
2. What are its causes ?
- Symmetrical clubbing can occur due to a host of causes.
- To summarize :
A. Respiratory
: Lung cancer
: Suppurative lung conditions like
- Symmetrical clubbing can occur due to a host of causes.
- To summarize :
A. Respiratory
: Lung cancer
: Suppurative lung conditions like
Bronchiectasis , lung abscess and Chronic TB.
: Pulmonary Fibrosis
B. Cardiac
- Cyanotic heart disease
- Eisenmenger Syndrome
- Infective endocarditis
: Pulmonary Fibrosis
B. Cardiac
- Cyanotic heart disease
- Eisenmenger Syndrome
- Infective endocarditis
C. GIT
- Inflammatory bowel disease
- Cirrhosis - esp Biliary
D. Endocrine
- Thyroid Acropachy
- Acromegaly
- Inflammatory bowel disease
- Cirrhosis - esp Biliary
D. Endocrine
- Thyroid Acropachy
- Acromegaly
3. Why does it occur
So I've spent a lot of time researching theories on how clubbing occurs. And let me tell you in the start itself, they're not clear on why it occurs.
But what makes sense to me , I want to share with you'll! And it was an absolute pain to find something convincing enough. So just stick with me here ;;)
But what makes sense to me , I want to share with you'll! And it was an absolute pain to find something convincing enough. So just stick with me here ;;)
So the crux of clubbing lies in vasodilation of the digital vessels causing proliferation of the tissue there in.
The most widely accepted theory right now is the megakaryocyte theory.
The most widely accepted theory right now is the megakaryocyte theory.
So in the figure above , the left side in white shows the normal course of a megakaryocyte through the blood.
In altered cardiorespiratory conditions , these large platelets either bypass the Pulmonary circulation owing to the shunting produced due to Heart defects or the lung parenchyma itself proves to be less to purify the blood of the platelets.
This causes these giant platelets to go lodge into the digital circulation causing release of cytokines like Platelet derived growth factor (PDGF) and TGF beta amongst others. These GF's cause vasodilation and in return , nail bed proliferation and collagen deposition.
IBD - especially Crohn disease seen to have thrombocytosis eventually which may aggravate the PDGF.
In cirrhosis of liver , especially biliary , pulmonary arteriovenous shunting is observed. This could result in the megakaryocyte entrapment as explained.
Another theory suggests inflammation triggers a vagal response causing Vasodilator effects. ( Neurogenic).
Other theories -
Hypoxia induced
Reduced ferritin related
Neurogenic
Humoral - various PG's and other humoral molecules.
The most widely accepted theory is the Megakaryocyte theory.
Hope this satisfied you !
Thank you.
Stay awesome.
~A.P.Burkholderia
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