Pathophysiology and Radiologic patterns of Atelectasis

Hey guys!

This post will be on the classification of Atelectasis based on its pathophysiology and a brief overview of its radiology patterns. 

Let us deal with the radiology aspects first:

1. Opacification of airless lobe and displacement of fissures,

2. displacement of hilar and cardiomediastinal structures toward the side of collapse,

3. narrowing of the ipsilateral intercostal spaces,

4. elevation of the ipsilateral hemidiaphragm,

5. compensatory hyperinflation and hyperlucency of the remaining aerated lung and

6. obscuration or desilhouetting of the structures adjacent to the collapsed lung (eg, diaphragm and heart borders).

Google the Chest X ray scans for atelectasis to consolidate the above points.

Now the lengthy part, The Pathophysiology. Let us start with active or obstructive atelectasis. 

1. Active/Obstructive Atelectasis.

Obstructive atelectasis is a consequence of blockage of an airway. Air retained in the alveoli distal to the occlusion is absorbed into the pulmonary capillary blood since the pressure of gases in the blood plasma (PvO2) is lower than that in the alveoli. For this reason, it is also called absorptive atelectasis. This causes the affected regions to become totally gasless and then collapse. 

Obstruction of a segmental bronchus is less likely to result in segmental atelectasis than obstruction of a lobar bronchus is to produce lobar atelectasis. This difference is because of collateral ventilation between bronchopulmonary segments within a lobe. 

Collateral ventilation occurs via the age-old physiologic adaptive process of recruitment and distension of neighbouring bronchioles. But three are three other players here, or brothers as I like to call them. A small anecdote to remember these three brothers:

Once there was a priest named Kohn who decided to help out a fellow bronchopulmonary segment in aeration. Brother Kohn being eldest and hence weak could only manage to dig a pore. His work was carried on by Brother Boren who bored (as his name suggests) and made this pore into a fenestration. There was still some work left. And for that Brother Boren asked the help of the engineer Brother Lambert. Brother Lambert, after much hard work was eventually able to dig up a canal all the way upto the neighbouring segment so that they can share the aeration bestowed upon them by Lord Almighty!

So we have three distinct collateral connections: 1. Pores of Kohn, 2. Fenestrations of Boren and 3. Canals of Lambert.

So you need to defeat these three if you want to cause obstructive atelectasis.

Let's dig a bit deeper into Fenestrations of Boren. These collateral channels are extensively prominent in an emphysematous lung. Now take a case of a 60 year old male smoker with emphysema who has now developed small cell carcinoma. Suppose there is a tumor mass obstructing the right bronchus, this patient will take a lot of time to develop obstructive atelectasis in the right lung because of the presence of extensive network of fenestrations of Boren. Hence, this patient will become symptomatic late and thereby will be diagnosed late. Blessing or Curse!

One more thing, it has been observed that atelectasis occurs more rapidly in patients on oxygen therapy. Why? There is a simple reason behind this. Oxygen is more soluble than nitrogen in water, when you give inhalational O2 with a FiO2 take 50%, you are altering the partial pressures of gases in the alveoli, Nitrogen which was 79% will fall down to below 50% and O2 which was 20% will rise upto 50%. Hence overall solubility rises, this elevates the tendency and spontaneity of gases diffusing into the blood plasma.

Honestly speaking, rest of the causes are nowhere as important as the one mentioned above so let us try to ace them quickly. 

2. Nonobstructive Atelectasis

A. Relaxation (ie, passive) atelectasis ensues when contact between the parietal and visceral pleurae is eliminated. While this is usually due to a pleural effusion or pneumothorax, a large emphysematous bulla can have a similar effect. In this case, the residual physiologic elastic recoil of normal lung parenchyma allows the normal lung to collapse away from the chest wall with consequent loss of volume.

The middle and lower lobes may shrink more than the upper lobe in the presence of a pleural effusion, while the upper lobe may be affected more by a pneumothorax.

B. Adhesive atelectasis is a consequence of alveolar instability due, in part, to surfactant deficiency or dysfunction. As its name suggests, the alveoli walls will collapse into the alveolar space sticking with each other. In the normal lung, surfactant reduces the surface tension of alveoli and decreases the tendency of alveoli to collapse. Decreased production or inactivation of surfactant leads to alveolar instability and collapse. Adhesive atelectasis is a major problem in respiratory distress syndrome of premature infants(IRDS), acute respiratory distress syndrome (ARDS) in adults, acute radiation pneumonia, and posttraumatic lung contusion.

C. Cicatrization (ie, cicatricial atelectasis) results from diminution of lung volume due to severe parenchymal scarring. Common underlying etiologies include granulomatous disease (eg, sarcoidosis), necrotizing pneumonia, and radiation pneumonia.

D. Acceleration Atelectasis- This type of atelectasis has been described in pilots subjected to very high, vertical accelerative forces between 5G and 9G: at 5G, up to 50 percent of pulmonary airways are distorted and closed due to gravitational forces. The atelectasis is exacerbated by breathing a high fractional concentration of oxygen. Decreases in vital capacity are a reflection of this type of atelectasis in pilots. Acceleration atelectasis can cause symptoms like chest pain, coughing, and dyspnea.

E. Rounded atelectasis (also called folded lung, Blesovsky’s syndrome, or atelectatic pseudotumor) is a distinct form of atelectasis associated with pleural disease, particularly following asbestos exposure and in India following pleural tuberculosis. Asbestosis is associated with pleural plaques and diffuse pleural thickening while pleural TB will have pleural thickening alongwith pleural effusion which eventually resolves with or without organization and pleural septations(Harbingers of Fibrothorax). 

In this condition, there is a subpleural mass mainly in the middle or lower lobes from which bronchi and blood vessels arise and they form a structure like a comet tail which traverses through the underlying atelectatic lung parenchyma to join at the hilum. Some un-astronomical sources compare this to a Vacuum Cleaner, with the dirt box as the subpleural mass and the hose as the comet tail. 

P.S. Blesovsky's Syndrome is not the only syndrome connected to pneumoconiosis, there is also Caplan's syndrome(Rheumatoid pneumoconiosis); which has a well-known mnemonic CAPlaN;

C- Coal workers' pneumoconiosis

A- Rheumatoid Arthritis

PlaN- Pulmonary nodule

That's all! 

-VM

Pills of knowledge in Ophthalm- Nodal cataract

The condition where 'day blindness' is present is a cataract at the nodal point. Nodal point of the eye is where the rays of light pass through the lens without any refraction, usually at the centre of the lens. Thus, during the day, especially when out in the sun, the pupil contracts and the light has to pass through the cataractous area, causing diminution of vision.

Immunotherapy for Prostate cancer

Hey Awesomites

Immunotherapy is now an emerging and much promising intervention in the treatment of prostate cancer, apart from the traditional cancer treatments - chemotherapy, radiation and surgery.

Research Update - The Multitasking Brain.

Hello there!

So you must be probably Studying (I assume and if not,you better be!)with your Cellphone besides you,
And you hear the Pinggg!!!
Aha.. GOTHAM needs you!! You shift your focus from the task of studying to the task of on your cellphone,and simultaneously thinking about how good you are at multitasking!

 Well don't pat your Backs yettt.

Although “multitasking” is a popular buzzword, research shows that only 2% of the population actually multitasks efficiently.

Most of us just shift back and forth between different tasks, a process that requires our brains to refocus time and time again — and reduces overall productivity by a whopping 40%.

 Told ya! No need to pat your backs,for decreasing your efficiency. So the next time your Read ,you only Read.

New Tel Aviv University research identifies a brain mechanism that enables more efficient multitasking. 

The key to this is “reactivating the learned memory,” a process that allows a person to more efficiently learn or engage in two tasks in close conjunction.

How does this work???

Starts with - Training the brain.

“When we learn a new task, we have great 

difficulty performing it and learning something else at the same time.

This is due to interference between the two tasks, which compete for the same brain resources.

The research demonstrates that - By pairing the brief reactivation of the original memory with the exposure to a new memory, long-term immunity to future interference was created.

For example- researchers first taught student volunteers to perform a sequence of motor finger movements with Right hand. 

After acquiring this learned motor memory, the memory was reactivated on a different day, during which the participants were required to briefly do some task with their Left hand — with an addition of brief exposure to the same learned motor task being performed by the Right hand.

By utilizing the memory reactivation paradigm, the subjects were able to perform the two tasks without interference.

So well we now have an overview of how the brains circuits are intimately connected and how they can still constantly evolve.

Hope this was helpful.

With this I finish the blog and my cup of tea!!

So much for Multitasking! 

Let's Learn Together.

-Medha 😊

Hematuria: A clinical pearl

Hey Awesomites

Hematuria (blood in urine) may be microscopic or macroscopic/ gross.

The American Urological Association (AUA) defines microscopic hematuria as 3 red blood cells/ high - power field on microscopic examination of the centrifuged urine specimen in two of the three freshly voided, clean- catch, midstream urine samples.

Gross/ visible hematuria can result from as little as 1mL of blood in 1L of urine, and therefore, the color of urine does not necessarily reflect the degree of blood loss.

Now lets have a brief review of the clinical presentation of hematuria on the basis of its source -

- A glomerular source of bleeding (nephronal/ glomerular hematuria) usually results in persistent microscopic hematuria that may be with/ without intermittent periods of gross hematuria.

- Total hematuria (present throughout the void) indicates bleeding of bladder/ upper tract origin.

- If renal sources of hematuria are present, the blood is equally dispersed throughout the urine stream  and does not clot.

In cases of clotting, its localisation is a must to evaluate the underlying cause:

- Hematuria/ clots at the beginning of the urine stream ( initial hematuria ) is a symptom of a urethral cause.

Terminal hematuria occurring at the end of stream may be caused due to either prostatic, bladder, or trigonal source of bleeding.


Thats all
- Jaskunwar Singh

Grossing the thyroid and differentials to be considered

Thyroidectomy is often received for lesions found suspicious on FNA or in cases where goitrous enlargement causes clinical symptoms of obstruction. Hemi includes the lobe and the isthmus, lobectomy only the lobe, while near total includes almost the entire thyroid except a small part of the thyroid left behind.
The following key factors should be described of the received specimen:

1. Type of the specimen
2. Dimensions of all the lobes
3. Size- If enlargement seen, is it diffuse or focal
4. Colour- Brown ( Normal); yellowish white/ beefy red/ mahogany brown
5. Consistency of the lesion - cystic ( single or multiple; bilateral or unilateral lobe involvement); solid; solid- cystic
6. Relation of the lesion to the adjacent thyroid
7. Surface of the thyroid - Smooth/ infiltrated - hemorrhagic irregular areas
8. Whether received intact or in pieces due to extensive extrathyroidal adhesions ( Reidel thyroiditis)

Serotonin receptor agonist and antagonist notes

1. 5-HT 1A receptor :- 

Partial agonists of this receptor are BusPIRONE,

IsaPIRONE, GePIRONE.

These are useful as anti-anxiety drugs.

2. 5-HT 1B/1D receptor :-

Agonists at this receptors are sumaTRIPTAN, NataTRIPTAN.

These are useful for the treatment of acute migraine attacks.

3. 5-HT 2A/2C receptor :-

Antagonists are clozapine and risperidone.

These are used as atypical antipsychotic agents.

4. 5-HT 3 receptor :-

Antagonists are ondanSETRON, graniSETRON, tropiSETRON.

These agents are used in chemotherapy induced vomiting.

5. 5-HT 4 receptor :-

Agonists on this receptors are cisaPRIDE, 

mosaPRIDE.

These are useful in the treatment of GERD.

-Upasana Y. :)

mPFC activation in depression: The Associations

Hey Awesomites

I had talked about how people with neuroticism also have an advantage of being creative in a previous post.
Lets now know the basis of this in brief -

Sinus of Morgagni- Contents

There occurs a gap in the pharyngeal wall between the base of the skull and superior constrictor muscle called as Sinus of Morgagni. This space is closed by the pharyngeobasilar fascia.

Contents- (mnemonic PLATE)

1. Palatine branch of ascending pharyngeal artery
2. Levator palati muscle
3. Ascending palatine artery
4. Tensor vetli palatini
5. Eustatian tube

In nasopharyngeal carcinoma, the tumor may extend laterally and involve this sinus involving the mandibular nerve. This produces a triad of symptoms known as Trotter's Triad. 

These symptoms are:

1) Conductive deafness 

2) Ipsilateral immobility of the soft palate

3) Trigeminal Neuralgia

Hope that helped!

Ashita Kohli

Zenker's Diverticulum

Zenker's Diverticulum is a posterior pulsion diverticulum which occurs through the Killian's Dehiscence.

Killian's Dehiscence is a potential gap between the oblique and transverse fibres of the inferior constrictor muscle. It is also known as the gateway of tears as it is a potential site of perforation during oesophagoscopy. 

Zenker's diverticulum occurs due to the outpouching of the pharyngeal mucosa at the site of Killian's dehiscence.
There is incoordination between the descending peristaltic wave and the cricopharyngeus muscle at the upper oesophageal spincter which leades to high intra luminal pressure and the mucosal herniation through the weak area of Killian's Dehiscence.

It is not a true diverticulum as it has just the herniation of the pharyngeal mucosa. ( A true diverticulum has all the layers of the oesophageal wall)

It is usually seen in elderly above the age of 60.

Symptoms-

1. The most common symptom is Dysphagia, which is intermittent initially and later becomes progressive.
2. Halitosis ( ie. bad breath, well ofcourse because food can get trapped in this pouch)
3. Regurgitation of food and cough.
4. There maybe regurgling sounds in the neck, gurgling sensation on palpation is known as Boyce sign.

Malignancies may develop in 0.5-1% cases.

Diagnosis- Barium Swallow and videofluoroscopy

Treatment-
1. Endoscopic stapling of the diverticulo esophageal sphincter.
2. In patients not fit for major surgeries, Dohlman's surgery may be done.

Hope that helped!
Ashita Kohli

Waldeyer's Ring

Waldeyer's Ring is an aggregation of lymphoid tissue seen in the subepithelial lining of pharynx guarding the nasopharynx and oropharynx in the form of a ring.

The ring is bounded by-

1. Palatine Tonsils ( also called as Faucial Tonsil)- Situated in between the anterior and posterior pillars on each side of oropharynx
2. Adenoids (aka Lushka's Tonsil)- Lies at the junction of roof and posterior wall of nasopharynx
3. Tubal Tonsils ( aka Gerlach's Tonsil)- Lies in the fossa of rosenmuller behind the eustatian tube opening
4. Lateral Pharyngeal Band and Nodules

Hope that helped!
Ashita Kohli

Rhinolalia Aperta

Rhinolalia Aperta is a speech disorder which involves hypernasality in voice.
The defect is seen in the failure of the nasopharynx to cut off from oropharynx.

Some fibres of palatopharyngeus muscle make the posterior pillar, go posteriorly in the posterior wall of nasopharynx and along with the lower fibres of the superior constrictor muscle forms a ridge known as the Passavant's Ridge. 

During swallowing and speaking the passavant's ridge closes the nasopharyngeal isthmus.
When this doesn't happen (eg- cleft lip, paralysis of palate) it leads to nasal regurgitation of food and nasal tone in speech known as Rhinolalia Aperta.

Treatment-

1. In children with cleft palate, special exercises can help in strengthening the muscles so as to reduce the nasality in voice.

2. Surgery- Posterior Pharyngeal Flap
                   Sphincter Pharyngeoplasty


Hope this helps!
Ashita Kohli 

Differentials of lower limb ulceration: Venous, arterial or neuropathic?

Hello!

Q. Today, in our OPD, a 45 year old diabetic Male, farmer by profession presented with an ulcer on left lateral malleolus.

He had a history of edema in lower limb associated with an itching 2 years ago. Since 6 months he got a non-healing ulcer on left lateral malleolus.

On examination:-

Pigmentation of skin, eczema lipodermatosclerosis, atrophied Blanche are present and dilated veins on the medial aspect of left lower limb.

My question is how to differentiate whether the ulcer is due to neuropathy, venous stasis or obliteration of artery.

Why do the above doubt arise?

Because venous ulcer are commonly found at the lower third of the leg usually on the medial side and even on the foot.

Ans.

(I) to rule out neuropathy,

1. Ask whether he feel the ground and pebble while walking barefoot

2. Test for the pain sensation, whether it is intact or not.

(II) Venous ulcer have characteristic findings. History is utmost important. They are shallow and flat. The edge is sloping and purple blue color.

The floor: - appears pink due to presence of granulation tissue. If it is a chronic ulcer there is more white fibrous tissue. Most important is A FAINT BLUE RIM of advancing epithelium may be seen at the margin.

(III) To check for arterial obliteration

1. Feel the dorsal pedis pulsation.

2. Ask for claudication also.

Conclusion: - It was venous ulcer.

Then why did it appear on the lateral side? Remember! On inspection dilated veins were found on the medial side.

Before answering the above question. Let us ask why is it most common on medial side?

There are more perforating veins on the medial side means more pressure in that area. But that doesn't mean lateral side is spared .There is some rise in pressure on lateral side also. The only thing that precipitated this was “Trauma”. Due to more itching on lateral side, he traumatised that area .It was initially small in size, non-healing ulcer which is gradually increasing in the size.

Found this great article on the lower limb ulcers.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1127371/

Take care:)

-Upasana Y.

Authors diary: Tip for solving multiple choice questions

So this random tip comes from a fun conversation that I was having with my study partner today.

Baclofen for treatment of alcohol dependence

Hello!

Recent evidence suggest that the gamma-aminobutyric acid-B receptor agonist baclofen is a promising agent for the treatment of alcoholism.

Yep!

Baclofen produces an effortless decrease or suppression of alcohol craving. It decreases alcohol consumption including in those with poor motivation. The drug causes few side effects and does not add to the intoxication effect of alcohol.

It benefits patients with alcohol dependence (even those who are still in precontemplation stage of motivation!)

Research has shown that baclofen reduces withdrawal symptoms of alcohol and is safe in those with liver impairment.

Although further studies that compare long-term alcohol-related outcome of baclofen with established drugs such as naltrexone and disulfiram are needed.

Interesting, isn't it?

-IkaN

More than what you know about vitamins!

Hello! :)

These were the questions asked during my pharmacology vivas. And I found it fascinating after studying. I have never studied these points about vitamins before! 

Q. Which vitamin deficiency is related with lowering of seizure threshold?

Ans. Pyridoxine Vitamin B6. 

Why? As it is associated with synthesis of neurotransmitter GABA. Therefore, it is indicated during isoniazid induced convulsions. :)

Q. Why laropiprant (20mg) + Niacin (1g) is used in combination?

Ans. Nicotinic acid (a derivative) results in flushing of face.

Why? Vasodilation of cutaneous vessels.

Therefore, we combine it with specific anti-flushing drug called laropiprant.

Q. In hyperemesis gravidarum, what do you give for associated Wernicke's encephalopathy following hyperemesis? 

Ans. I thought of anti-emetics at first but the answer is vitamin B1. (Wernicke's encephalopathy doesn't always result from alcohol :P )

That's for today.
Take care. :)
-Upasana Y.

Lacunar infarction notes + mnemonic

Lacunar infarcts are small (0.2 to 15 mm in diameter) noncortical infarcts caused by occlusion of a single penetrating branch of a large cerebral artery.

Pathophysiology:
Lipohyalinosis of the penetrating arteries. (Mnemonic: L for Lipohyalinosis, L for Lacunar)
Microatheroma of the origin of the penetrating arteries.
Lacunar stroke is usually related to a chronic vasculopathy associated with systemic hypertension.

Clinical features:
Penetrating artery occlusions usually cause symptoms that develop over a short period of time, typically minutes to hours. However, a stuttering course may ensue, as with large artery thrombosis, and symptoms sometimes evolve over several days.

As a general rule, lacunar syndromes lack findings such as aphasia, agnosia, neglect, apraxia, or hemianopsia (so-called "cortical" signs). Monoplegia, stupor, coma, loss of consciousness, and seizures also are typically absent.

These syndromes are common :
● Pure motor hemiparesis
● Pure sensory stroke
● Ataxic hemiparesis
● Sensorimotor stroke
● Dysarthria-clumsy hand syndrome

Pure motor hemiparesis: Characterized by weakness involving the face, arm, and leg on one side of the body in the absence of "cortical" signs (aphasia, agnosia, neglect, apraxia, or hemianopsia) or sensory deficit.

Artery / structure involved: Posterior limb of the internal capsule.

Mnemonic: PM - Pure Motor, Posterior limb of internal capsule.

Pure sensory stroke: Numbness of the face, arm, and leg on one side of the body in the absence of motor deficit or "cortical" signs.

Artery / structure involved: Thalamogeniculate branches of the posterior cerebral artery (Ventral posterolateral and ventral posteromedial nuclei)

Mnemonic: MIST
Motor - Internal capsule
Sensory - Thalamus

Ataxic hemiparesis: Ipsilateral weakness and limb ataxia that is out of proportion to the motor deficit. Some patients may exhibit dysarthria, nystagmus, and gait deviation towards the affected side. As with other lacunar syndromes, the above-mentioned "cortical" signs are absent.

Artery / structure involved:  Fibres of the fronto-ponto-cerebellar system in the internal capsule / corona radiata.

Sensorimotor stroke: Characterized by weakness and numbness of the face, arm, and leg on one side of the body in the absence of the aforementioned "cortical" signs.

Artery / structure involved: Sensorimotor strokes arise from infarcts involving the posterolateral thalamus and posterior limb of the internal capsule. The exact vascular anatomy is debated. 

Dysarthria-clumsy hand syndrome: Facial weakness, dysarthria, dysphagia, and slight weakness and clumsiness of one hand are characteristic. There are no sensory deficits or "cortical" signs.

Artery / structure involved: Lacunar infarctions of the anterior limb of the internal capsule, genu of the internal capsule, or corona radiata.

Treatment:
Intravenous alteplase (recombinant tissue-type plasminogen activator or rt-PA) improves outcomes for patients with ischemic stroke in general if administered within 4.5 hours of symptom onset. The available evidence suggests that intravenous thrombolysis is beneficial for patients with lacunar stroke. Most patients with acute ischemic stroke who are not eligible for thrombolytic therapy should be treated with aspirin.

That's all!
-IkaN

Changes in glomerular dynamics mnemonic

Hello everyone!

If you forgot the afferent - efferent stuff from step 1, I have a mnemonic.

Remember ACE ID, PDA ANC.

Step 2 CK: Management of thromboembolic stroke

Here are my notes. The most simplified version you'll get. 

That's all!

-IkaN

So I've been questioned the most about the last point, regarding heparin. Here's the source and reading material:

There are additional situations of high thrombotic risk after ischemic stroke where anticoagulation may be beneficial but for which there are little or no data. These include mechanical heart valves, carotid artery dissection, and large artery atherosclerotic stenosis.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4031793/

Drugs used to lower BP acutely in severe preeclampsia mnemonic

Drugs used to lower blood pressure acutely in severe preeclampsia (Maternal hypertensive crisis) mnemonic

"Lower Hypertension Now"

Labetalol iv preferred (Avoid in bradycardia)

Hydralazine iv

Nifedipine oral

That's all!
-IkaN

Micturition and Neurological diseases

Here, presenting you a detailed description of Pathologies of Bladder in Neurology. I believe this is the best resource on this topic available online for free. :)

Diaphragmatic hernia : Mnemonic and Review

Here's a short post on the key points about Congenital Diaphragmatic Hernia.

So there's deficiency in the diaphragm during development causing abdominal contents to budge into the Thorax.

There are 2 main types -->

1. Bochdalek.

2. Morgagni.

Now out of these 2, Bochdalek is commoner.
(It's hard to remember the word Bochdalek. I struggle with it every day. )

You can memorize it by realising that it rhymes with ' Scotch da Lake '
(Which means a lake of scotch in Punjabi)

Key points about Bochdalek -
BBBB

- Back  - Located posteriorly
- Big - Bigger than the Morgagni form
- Bad - Poor prognosis
- Bag and Mask Contra indicated. 

Also realise - Bochdalek
So it's got an L in it. L = Left. So it's more common on the left side. These hernia classically cause a scaphoid abdomen and Mediastinal shift to the opposite side.

Morgagni can be remembered by the opposite of the BBB
So it's
- Not on the back - Anteriorly
- Not Big - Small sized.
- Not as Bad - Prognosis is alright.

Also realise - Morgagni
It's got an R in it = Right. So it's more common on the right side. And it contains the Transverse colon generally.

So that's all !
Happy studying! 
Stay awesome !

~ A.P.Burkholderia 

Croup : Review of key points

Here's a short Mnemonic/Review of Important facts about Croup - Acute Tracheobronchitis !

Remember :
CROUPS

C - Common respiratory disease
R - Respiratory viruses like Parainfluenza
O - Oxygen Treatment (Humidified)
U - Ugly Cough - Barking / Seal like cough
P - Prodrome of illness followed by Inspiratory Stridor
S - Steeple sign on X Ray

It's helpful to remember Acute EPIGLOTTITIS as the complete opposite of CROUPS using similar ideas.

- Not as common.
- Caused by Bacteria generally (Strep , Hib)
- Oxygen Therapy + AntiBiotics
- Ugly - Sniffing dog like position + Drooling
- Prodrome not particularly, but Stormy acute onset.
- Shows Thumb print appearance on X Ray.

Hope this helped !
Happy Studying !
Stay awesome.

~ A.P.Burkholderia

CMS neurology form 2: Question on numbness, tingling and decreased grip strength

Disclaimer: This is an CMS neurology form 2 question for step 2 CK. If you are planning to take USMLE step 2 CK in the future, I would recommend that you DO NOT read this post because it will bias your assessments.

Differentiating C8 radiculopathy from ulnar neuropathy

Hello. This is a very short post (because I am super busy studying)

It's on differentiating C8 radiculopathy from Ulnar neuropathy based on a question I solved the other day. How would you differentiate the two in clinical practice?

C8 radiculopathy:
- Thumb abduction weakness: abductor pollicis brevis (C8, T1)

- Triceps affected (C6, C7, C8)

- Radiculopathies are often painful.

Ulnar neuropathy:
- Hand intrinsics (C8, T1) affected:
Palmar and dorsal interossei
Lumbricals III & IV
Abductor/opponens/flexor digiti minimi

- Basically, all hand intrinsics except for the median-supplied "LOAF" muscles (lumbricals I & II, opponens/ abductor/flexor pollicis brevis)

- Triceps not affected.

- Focal neuropathies aren't painful.

Conclusion: The ulnar nerve innervates all intrinsic hand muscles, except the abductor and flexor pollicis brevis, opponens pollicis, and lateral two lumbricals, which are innervated by C8 and T1 via the median nerve which helps differentiating the ulnar neuropathy from C8 radiculopathy.

That's all!
-IkaN

Pills of knowledge in Ophthalm- Anterior ciliary artery

The point where the anterior ciliary artery pierces the sclera is often marked by a pigment. This is of particular importance while cauterization as in a bid to make everything look neat and shiny, the pigmented part shouldn't be cauterized as it will cause necrosis of the structures supplied by the artery. 

Effects of Angiotensin-II on GFR

So this is a highly confusing topic. No matter how many times you read it, some amount of doubt is always there in your mind. So an advice to the readers, bookmark this post because you will be needing to read it more than once to get the drift.

First of all, let us review the effects of Angiotensin II on Glomerulus.

It constricts both the afferent and efferent arterioles but preferentially increases efferent resistance. Why? 3 reasons:

1. Efferent arterioles have a smaller diameter in their basal state.

2. Ang II stimulates the release of vasodilator NO from the afferent arteriole.

3. Ang II minimizes vasoconstriction at the afferent arteriole via the stimulation of Ang II type 2 (AT-2) receptors, which result in vasodilatation through a CYP450 dependent pathway.

The net effect of preferential rise in efferent arteriolar resistance is that the glomerular pressure is increased or stabilized(in hypoperfusion states), which helps to maintain or increase GFR. But in the long run, lots of fluid have been filtered out leaving behind the proteins which raise the colloid osmotic pressure, eventually enough to overrule the hydrostatic pressure and hence it leads to decrease in GFR.

Ang II also reduces GFR by causing constriction of the mesangial cells which reduces the effective surface area for filtration. 


-VM

Pills of knowledge in Ophthalmology- Squint and refractive errors

1.A refractive error should be thoroughly assessed prior to surgical squint correction or the squint may recur.

2. Divergent squint occurs in myopes as the divergent system of muscles is more active during far vision. So, the far vision in myopes being hampered, the eyes try to diverge more.

3. Same goes for hypermetropes. They end up with a convergent squint if left uncorrected.

-That's all!

Sushrut Dongargaonkar

Differentiating peroneal neuropathy, sciatic nerve injury and L5 radiculopathy

This post is on differentiating weak dorsiflexion of foot - I made a little algorithm on it. (I'll add images later)

If there's weakness in foot dorsiflexion, check plantar flexion and inversion.

If plantar flexion and inversion is normal: Peroneal neuropathy.

If plantar flexion and inversion is weak: Check hip movements.

If weakness at hip joint: S5 radiculopathy.

If no weakness at hip joint: Sciatic nerve compression.

You can differentiate based on sensory levels and reflexes too but this is easier.

Conclusion:
Peroneal nerve supplies the dorsiflexors and evertors of the foot. There will be no weakness in plantar flexion and inversion in peroneal nerve injury.

Hip abduction is an action of Gluteus medius and minimus muscles. These are Superior gluteal nerve innervated muscles. This nerve arises from L4, L5 and S1 roots . If there is hip abduction deficit with foot drop, it means pathology at the radicular ( root) level. 

Here's the reading material.

Common peroneal neuropathy presentation:
- Acute foot drop (difficulty dorsiflexing the foot against resistance or gravity).
- Patients describe the foot as limp; there is a tendency to trip over it unless they compensate by flexing the hip higher when walking, producing what is called a "steppage" gait.
- Patients may also complain of paresthesias and/or sensory loss over the dorsum of the foot and lateral shin.
- Examination typically reveals weakness in foot dorsiflexion and foot eversion (deep and superficial peroneal nerve-innervated, respectively), with normal inversion and plantar flexion (posterior tibial nerve).
- Sensory disturbance is confined to the dorsum of the foot, including the web space between digits 1 and 2 and the lateral shin.
- Reflexes are normal.

Sciatic nerve injury presentation:
- Weakness affecting most of the lower leg musculature, including the hamstrings.
- Hip flexion, extension, abduction and adduction, and knee extension are normal.
- Sensory loss involves the entire peroneal, tibial, and sural territories.
- In the lower leg, however, the medial calf and arch of the foot may be spared secondary to innervation by the preserved saphenous nerve (a branch of the femoral nerve). Sensation is also spared above the knee both anteriorly and posteriorly.
- The knee jerk is normal, but the ankle jerk is unobtainable.

L5 radiculopathy presentation:
- Back pain that radiates down the lateral aspect of the leg into the foot.
- On examination, strength can be reduced in foot dorsiflexion, toe extension, foot inversion, and foot eversion.
- Mild weakness in leg abduction may also be evident in severe cases due to involvement of gluteus minimus and medius. Atrophy may be subtle; it is most readily observed in extensor digitorum brevis.
- Sensory loss is confined to the lateral shin and dorsum of the foot.
- Reflexes are generally normal.

That's all!
-IkaN

Alvarado Score Parameters Mnemonic ; For Appendicitis

Alvarado score is one of the most famous scores to clinically diagnose Appendicitis. Without further adieu let us delve into it.

            Anorexia or ketones in urine           - 1 
            Leukocytosis >10,000                      -2  
            Vomiting/Nausea                             -1
     migrAtory pain to right iliac fossa            -1
           Rebound tenderness                         -1
 temperAture above 37.3 celsius                 -1
      tenDerness in right iliac fossa              -2
   neutrOphilia >70%                                 -1

Of these the second parameter from above and second parameter from below have 2 points credited for each. Every other parameter is credited with 1 point each.

The overall aggregate comes out of 10, which the highest possible score for Alvarado score.

If, the aggregate is,

<3 - Low risk for appendicitis
4-6 - Mid risk for appedicitis
>=7 - High risk for appendicitis

In some hospitals where a differential count is difficult to find, use a modified score with 9.

That's all guys, if you find any mistake let me know.

With love,
Jay~

P.S. - yayyy.....missed me much awesomites? I was away from the blog for the last 6 months from posting, because I had very disastrous scores for surgery in my university and I didn't feel worthy enough to write for you guys. (So my activity was largely concentrated in the Whatsapp Medicowesome groups, and the Author's page.) Anyways, I had to take a remedial exam for Surgery 2 weeks ago. And BAAM!!!!.....the results were released today, and yayyyyy.....I passed surgery! :)

I must thank all my Medicowesome admin/author collegues for tolerating my rants and, help me to push through the hellish scary time together. Thanks everyone. Finally I'm through it, and I'm back to writing for you all guys. So thought to start the first post after returning, with a General Surgery Diagnosing score with the help of Schwartz Textbook of Surgery.

See ya soon peepz! :)