CMS neurology form 2 question on fibromuscular dysplasia with paresis, occulomotor palsy

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.

CMS neurology form 2 question on headache, seizures, urinary incontinence, broad based gait

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.

NBME 7 question on intoxication

Disclaimer: This is an NBME form 7 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.

Fact of the day : Pinenes for refreshing your Airways

Hello

Did you know? One of the reasons your lungs feel refreshed ( increased mental focus and energy ) when you walk through the shades of beautiful pine forest is because of an anti - inflammatory compound called alpha -Pinene, that is found in conifers. It is used as a bronchodilator in the treatment of asthma and is abundantly present in marijuana.

- Jaskunwar Singh

Pill induced esophagitis mnemonic

Pill induced esophagitis is caused by a pill! :D

Causes of pill induced esophagitis mnemonic: A PILL.

Aspirin
Alendronate
Antibiotics like tetracycline, clindamycin

Potassium chloride
Iron
Less water
Lying down immediately

Interesting anatomy correlation:
The most common sites of injury are the proximal esophagus near the compression from the aortic arch and the distal esophagus in patients with left atrial enlargement.

The typical endoscopic appearance of pill-induced esophageal injury is a discrete ulcer with relatively normal surrounding mucosa.

That's all!
-IkaN

Motor nuclei in the brainstem : An overview

Hi everyone. Just thought of doing an overview of the various motor nuclei of cranial nerves in the brain stem.

So we can classify the motor nuclei into 3 groups -

1. Somatic motor efferent - 4
2. Branchial motor efferent - 4
3. Visceral motor efferent - 4

Now how are these classified ?

1. Somatic Motor Efferent

- In the embryological stage , there are certain precursors to muscle and skin segment groups called 'Somites'. These are processes of the paraxial mesoderm.
- Sach somite gives rise to a particular set of muscles called its myotome. 

- There 4 such important somite groups -->

A. Pre otic somites = 3.
So this is simple.
There are 3 pre otic somites giving rise to distinct groups of extraocular muscles supplied by their own cranial nerve.

Somite 1  =
Muscles -
All Extra ocular muscles except Lateral Rectus and Superior oblique.
Nerve -
Oculomotor nerve (III)
Nucleus -
Oculomotor nucleus in the Upper Midbrain.

Somite 2  =
Muscles -
Superior oblique.
Nerve -
Trochlear nerve (IV)
Nucleus -
Trochlear motor nucleus in the Lower Midbrain.

Somite 3  =
Muscles -
Lateral Rectus.
Nerve -
Abducent nerve (VI)
Nucleus -
Abducent motor nucleus in the Pons.

(I'm sure you remember the popular mnemonic - LR6 SO4)

B. Occipital somites

Muscles -
All muscles of the tongue except Palatoglossus
Nerve -
Hypoglossal I'm nerve (XII)
Nucleus -
Hypoglossal nucleus in the Medulla.

Since these nuclei represent the motor innervation to the derivatives of Somites , they're called Somatic Motor or General Somatic Efferent (GSE) Fibres. 

2. Branchial Motor Efferent - 

- In the embryological stage , there are various branchial or Pharyngeal arches that give rise to muscles , bones and cartilage supplied by a particular nerve of that arch.

- Each nucleus that supplies the muscles from such a Branchial arch is called Branchiomotor Efferent or Special Visceral Efferent. (SVE) 

- There are 4 such important arches - 

A. 1st Pharyngeal arch (mandibular arch)

Muscles -
All muscles of mastication + TT (Tensor tympani + Tensor veli Palatini) + Digastric anterior belly. ( And Meckel cartilage)
Nerve -
Mandibular branch of Trigeminal
Nucleus - 

Trigeminal motor nucleus in Pons 

B. 2nd Pharyngeal arch (hyoid arch) 

Muscles -
All muscles of facial expressions + Stapedius + Digastric posterior belly.  ( And Reichter cartilage)
Nerve -
Facial nerve (VII)
Nucleus - 

Facial motor nucleus in Pons 

C. 3rd Pharyngeal arch

Muscles -
Stylopharyngeus

(And the hyoid bone funnily.)
Nerve -
Glossopharyngeal nerve (IX)
Nucleus - 

Nucleus Ambiguus in Medulla

D. 4th and 6th Pharyngeal arches

Muscles -
- All muscles of  Soft palate ( except Tensor veli which is up in the 1st arch) by the 4th. + cricothyroid muscle of Larynx. 

- All muscles of Larynx by the 6th except cricothyroid which is by the 4th. 

(All laryngeal cartilage as well)
Nerve -
4th arch - Superior laryngeal nerve of the Vagus.(X)

6th arch - Recurrent laryngeal nerve of the Vagus (X)
Nucleus - 

Nucleus Ambiguus of Medulla 

Now there's another Motor nucleus - The Accessory nerve. It supplies Trapezius and Sternomastoid muscles but it's doubtful if it's Branchial or Somatic. 

3. Visceral Motor Efferent - General. 

- These nuclei are parasympathetic and stimulate a particular gland to secrete or a ganglion to function. 

- These are called Secretomotor or General Visceral Efferent Fibres 

Again , there are 4 of these. 

A. Ciliary ganglion 

Function mediated by - 
Sphincter pupillae - Constricts pupil 

(Mnemonic = Remember C and C - Cholinergic Constricts )
Nerve -
Oculomotor nerve
Nucleus - 

Edinger Westphal in Midbrain 

B. Pterygopalatine ganglion 

Function mediated by - 
Lacrimal glands, nasal mucosal, sinuses mucosal glands and pharynx mucosal - Secretomotor. 

Nerve -
Facial nerve  (Greater Petrosal)
Nucleus - 

Superior salivatory nucleus - Pons. 

C. Submandibular ganglion 

Function mediated by - 
Submandibular glands , sublingual glands - Secretomotor.

Nerve -
Facial nerve  (Chorda tympani)
Nucleus - 

Superior salivatory nucleus - Pons. 

D. Otic ganglion 

Function mediated by - 
Parotid gland

Nerve -
Glosspharyngeal nerve  (Lesser Petrosal)
Nucleus - 

Inferior salivatory nucleus - Pons. 

The Vagus nerve has the largest parasympathetic discharge and supplies a lot of visceral with this input in the guy as well.

Hope this helps you to re-orient yourself to neuroanatomy and grasp the roles of various brainstem structures ! 

Happy studying ! 

~ A.P.Burkholderia

Lacunar strokes : An Overview

      Hi everyone ! Here's a short post on Lacunar infarcts. Credits to IkaN without whom IKant have done this post. Haha ;;) here goes.

- A Lacunar infarct is an infarction occurring    in the deep penetrating branches supplying the deep subcortical structures - Mainly the Internal capsule and parts of thalamus. 

- These are some of the most common infarctions seen. 

- Causes of lacunar infarction include Hypertensive bleeds and Microthrombi. 

- So these infarcts can present as one of the following​ Syndromes --> 

1. Pure Motor 

2. Pure Sensory 

3. Combined Sensorimotor 

4. Ataxic 

5. Dysarthria- Clumsy hand syndrome. 

- The illustrations I've drawn below clearly depict the syndromes , their anatomical localization and the arteries commonly involved. 

- The commonest of the lot is the Pure Motor type of stroke that affects mainly the Internal capsule containing the motor corticospinal fibres. Since a multitude of Fibres is concentrated very judciously in the Internal capsule , the hemiplegia resulting from this type is a 'Dense' or total hemiplegia affecting both upper and lower limbs in equal measure. 

(click on the image to see them in better resolution ) 

- The management is much like the other strokes - 

1. Airway Breathing Circulation to be established. 

2. Check Blood sugar and BP.

3. Send for an emergency Non contrast CT scan to rule out hemorrhage. 

4. If within 3-4.5 hours and absence of hemorrhage = Thrombolyse. 

5. If hemorrhage - BP control and ICT management.

6. If beyond 4.5 hours = Symptomatic and Palliative care and treat risk factors.

- I hope all of these Syndromes are clear to you now !

 Let me know if you'll have any doubts. 

Happy Studying ! 

Stay awesome.

~ A.P.Burkholderia

Fact of the day: Marchiafava-Bignami disease

Marchiafava-Bignami disease is a rare disorder of demyelination or necrosis of the corpus callosum and adjacent subcortical white matter that occurs predominantly in malnourished alcoholics. Dementia, spasticity, dysarthria, and inability to walk may present as an acute, subacute or chronic condition.

Lesions appear as hypodense areas in portions of the corpus callosum on CT and as discrete or confluent areas of decreased T1 signal and increased T2 signal on MRI. Alcohol abusers without liver disease, amnesia, or cognitive dysfunction show thinning of the corpus callosum at autopsy and on MRI, suggesting that alcohol or malnutrition damages the corpus callosum commonly in the absence of the necrotic lesions of Marchiafava-Bignami disease.

Interesting, isn't it?
-IkaN

High ankle and low ankle sprain mnemonic

Hello!

High ankle and low ankle sprain

Atrial fibrillation begets Atrial fibrillation: Explanation

Hi ! Short post on pathophysiology of Atrial Fibrillation!

- Atrial Fibrillation is a fairly common disorder of rhythm, where the atria begin to beat at random , irregular and very high rates. Like 300-600 beats / min !
- Some of these MANY contractions get transmitted to the ventricles causing an Irregular , yet High , Ventricular rate - around 100-160 per minute or even higher.

Now how this occurs is a very interesting yet much-ignored mechanism.

- Due to some pre existing factors like Rheumatic heart disease , Myocardial ischemia or Thyroid abnormalities among many others, the atria get electrically irritated and begin to fire on their own.

- These ectopic foci are common along the opening of the pulmonary veins = called the pulmonary sleeve.
This area of hyperactivity and automaticity begins to fire from the left Atrium creating a wavefront of abnormal impulses.

- Say one of these myocytes becomes ectopic one day and produces an abnormal wavefront. This wavefront progresses across the atrium and in turn stimulates the other Atrial myocytes to inturn fire ectopically -- causing formation of multiple Daughter ectopic foci.

- These daughter ectopic foci produce daughter wavelets that then propagate through the atria , in turn producing more duaghter wavefronts.

- Eventually there are A LOT of Atrial foci causing multiple wavelets to produce multiple electrical wavefronts.

- Thus A-Fib causes multiple wavefronts which in turn cause more wavefronts eventually propogating A fib as a positive feedback mechanism​.

- In the long term, due to this constant irregular beating there is fibrosis and electrophysiological remodelling making the atrium more irritable and automatic.

Thus A-Fib begets A-Fib!

Hope you liked this !
Happy Studying !
Stay awesome.
~A.P.Burkholderia

Mitral Regurgitation Begets Mitral Regurgitation : Explanation

Hi everyone  ,just a short explanation of the famous phrase 'MR begets MR'.
Here goes.

- Mitral Regurgitation is a disease where the mitral valve is incompetent or insufficient and leaks or pukes when it should be shut. (Rather like a blithering idiot who keeps talking at the wrong time. =}. )

- So it allows the blood to puke back into the Left Atrium from the Ventricle during systole.

- So assume - 100 ml of blood would flow into LV from the LA normally which the LV would pump into the Aorta.

- Now because of the weird and incompetent valve , the LV can pump only like 70 ml into the Aorta and the rest of the 30 ml goes back into the LA.

- So now the LA volume is 30 ml + 100 ml
And it'll pour in 130 ml into the LV.

- So effectively, the LV has an overload of volume in it and over a period of time it would undergo Dilatational changes and increase in size.

- As the Ventricle increases in size , the mitral valve apparatus is stretched all the more.

-This is because the mitral valve is attached to the Ventricular myocardial tissue directly at the annulus as well as via the papillary muscles. Both of these are stretched. 

- The stretching causes further increase in MR. This causes further volume overload. Which causes further MR.

- Thus it is like a positive feedback response and a vicious cycle is formed.

This phenomenon is referred to as ' MR begets MR' which means MR basically causes Ventricular changes which stretch the heart and cause more MR which continues the cycle further.

Hope this helped !
Happy studying !
~ A.P. Burkholderia

Microbiology of Actinomyces vs Nocardia mnemonic

Hello! Let's go back to Microbiology today.

Nocardia typically appear as delicate filamentous gram-positive branching rods that appear similar to Actinomyces species.

Nocardia can usually be differentiated from Actinomyces by acid-fast staining, as Nocardia typically exhibit varying degrees of acid fastness due to the mycolic acid content of the cell wall.

Another useful clue is that Nocardia grow under aerobic conditions, whereas Actinomyces grow under anaerobic conditions.

How to remember this? Remember one mnemonic, the other one is the other one. Okay?

So let's start with nocardia.
nocarDIA. nocarDICA. ACID fast!
noCARDIA. Heart needs oxygen. Aerobic organism.

Therefore, the other one, Actinomyces is anaerobic, non acid fast.

Treatment mnemonic: PANT
Penicillin Actinomyces
Nocardia TMP-SMX

That's all!
-IkaN

Tay-Sachs disease notes and mnemonic

Hello!

Tay-Sachs disease is an autosomal recessive, neurodegenerative disease.

Plasma Proteins Mnemonic

Hello Everyone,
 Lets discuss plasma proteins.

1.How do we classify them?

• They are classified into Albumin, Globulin and Fibrinogen.
• Globulins are further classified into Alpha , Beta Globulins and Gamma Globulin.
• Alpha Globulin is further divided into Alpha 1 and Alpha 2 Globulins.

Memorising the examples of them is simple. 

Examples of Beta Globulins can be remembered as follows:

         B PTH

B-Beta Lipoproteins(LDL)

P-Plasminogen

T-Transferrin

H-Hemopexin

Interesting Fact:

Acute-phase proteins are a class of proteins whose plasma concentrations increase (positive acute-phase proteins) or decrease (negative acute-phase proteins) in response to inflammation. This response is called the acute-phase reaction.

• Positive acute-phase proteins increase in inflammation e.g., C-reactive protein, mannose-binding protein, complement factors, ferritin, ceruloplasmin, serum amyloid A and haptoglobin.
• Negative acute-phase proteins decrease in inflammation. Examples include albumin, transferrin, transthyretin, retinol-binding protein, antithrombin, transcortin. 

Thats all,

Thank you,

Chaitanya Inge

No cyanosis in cyanide poisoning. Why?

I was reading about cyanide poisoning today and saw "Cherry red skin" in the clinical manifestations. I know that carbon monoxide poisoning causes a cherry red color to blood. But why cyanide?

The curiosity lead to this post.

In normal cellular metabolism, most adenosine triphosphate (ATP) is generated from oxidative phosphorylation. .

Cyanide avidly binds to the ferric ion (Fe3+) of cytochrome oxidase a3, inhibiting this final enzyme in the mitochondrial cytochrome complex. When this enzyme's activity is blocked, oxidative phosphorylation ceases. The cell must then switch to anaerobic metabolism of glucose to generate ATP.

Anaerobic metabolism leads to the formation of lactic acid and the development of metabolic acidosis. Hydrogen ions produced by ATP hydrolysis are no longer consumed in aerobic ATP production, exacerbating this acidosis. Serum bicarbonate decreases as it buffers excess acid, leading to an increased anion gap.

Despite an ample oxygen supply, cells cannot utilize oxygen because of their poisoned electron transport chain. This functional (or "histotoxic”) hypoxia is particularly deleterious to the cardiovascular and central nervous systems (especially the basal ganglia).

Because of the decreased utilization of oxygen by tissues, the venous oxyhemoglobin concentration will be high, making venous blood appear bright red.

Therefore, despite hypotension, apnea, and/or bradycardia, the patient does not usually appear cyanotic in the setting of cyanide poisoning.

Clinical features:
Central nervous system toxicity is the most prominent in cyanide toxicity – Headache, anxiety, confusion, vertigo, coma, seizures.

Which should you suspect cyanide poisoning?
Victims of fires
Reported ingestions
Treatment with sodium nitroprusside

Antidote:
Hydroxocobalamin
Sodium thiosulfate
Nitrites (to induce methemoglobinemia)

That's all!
-IkaN

CT scans and role of Contrast enhancement

Contrast enhancement and it's role in CT scan
The concept of Contrast enhancement in radiology is not new and it has been in practice even before the Advent of CT scans.
CT scan as a modality of imaging was invented by a British engineer Godfrey Hounsfield in the year 1972.

Purpose of Contrast enhancement

Contrast enhancement is a method of exaggerating  the visible difference between adjacent structures on scan by administrating contrast agents.The term Contrast enhancement in CT scan includes usage of radio opaque substances for better visualization of the anatomic structures as well as better localization and characterization of the pathologies, better differentiation of the pathology from the normal surrounding structures.

Principle of Contrast enhancement

The diffusion of contrast agents from the blood stream to the body tissue is physiologically limited. In pathologies such as cancer, blood vessels grow (angioneogenesis) with increased leaking of contrast agents resulting in lesions much more visible on Contrast enhanced scans.
In CNS, contrast diffusion is limited by Blood brain barrier. Disruption of BBB lead to enhancement after administration of contrast agents.

Indications of Non Contrast CT (NCCT )
For detection of
1.Stones in kidney,ureter, cbd
2.Calcification
3. Fat in various tumors
4. Head injury
5. Acute hemorrhage
6. Stroke
7. SAH


CECT

The pathologic lesions show enhancement or attenuation depending upon the phase of contrast enhancement. So if you are looking for a particular pathology,it is important to know in which phase of CECT to look for.
For that purpose,I've enumerated the phase in which CT scan is done and can be recorded.

1. Non enhanced phase (NECT)
Uses are same as those of Ncct. Many a times this scan is done before administration of the dye to compare pre and post contrast enhancement study.
Calcification, fat in tumors, inflammation and infarction can be seen in this phase well.

2. Early arterial phase (15-20 secs post injection)
When contrast is still in the arteries, it has not enhanced the organs.
This phase is useful to look for vascular abnormalities such as aneurysms, vascular stenosis, etc

3. Late arterial phase (35-40 secs post injection)
Sometimes known as arterial phase.
All the structures that get their blood supply from arteries will show optimal enhancement in this phase.

4. Hepatic or late portal phase (70-80 secs post injection)
Liver parenchyma enhance trough blood supply by portal vein and some enhancement of hepatic veins.

5. Nephrogenic phase (100 secs post injection)
This is when all of the renal parenchyma including medulla enhances. Particularly helpful for small renal cell carcinoma which are otherwise missed.

6. Delayed phase (6-10 mins post injection) called as wash out phase or equilibrium phase
Washout of contrast in all abdominal structures except for fibrotic tissues which become relatively more dense in this phase.

Factors affecting CECT
The timings depend on
1. Organs to be scanned and focussed
2. Type of CT machine available, number of slice
3. Amount of contrast given depending upon the body weight of the patient
4. Injection rate of the contrast
5. Route by which contrast given. (Mainly IV but can be oral,rectal too)

Lesions / pathologies visualized on CECT
1. Liver tumors
Due to it's dual blood supply, 80% by portal vein and 20% by hepatic artery normal parenchymal enhancement maximally in hepatic phase . On the contrary, all all liver tumors are supplied 100% by hepatic artery. So hyper vascular tumors are best seen in late arterial phase. Hypovascular tumors on the other hand are better seen in hepatic phase.
2. Fibrotic lesions
Fibrotic lesions like cholangiocarcinoma and fibrotic mets hold contrast much longer than normal parenchyma hence best seen in delayed phase.
3. Pancreatic tumors most of them being hypovascular are seen best in late arterial phase. In cases of acute pancreatitis, late arterial phase best detects necrosis. Remember chronic pancreatitis can be very well appreciated on NCCT due to calcification.
4. Anastomosis leakage 
CECT done in post op patients to check anastomosis leakage. Oral contrast play a role here for check scans done in post op bowel anastomosis.

5. Pulmonary embolism - 
Good quality scans are required to delineate the emboli in the pulmonary vasculature.
6.CT angiography 
For vascular studies.

Dr. Shil Pill

Coccidioidomycosis mnemonic

Coccidioidomycosis is caused by Coccidioides immitis!

Diabetes insipidus and water deprivation test

In this video I talk about pyschogenic polydipsia, central diabetes insipidus, nephrogenic diabetes inspidius, water deprivation test :)

Theophylline toxicity mnemonic

Theophylline's effects arise from antagonism of adenosine receptors and indirect adrenergic activity.

It is used as a bronchodilator for patients with asthma or chronic obstructive pulmonary disease.

Chest x-ray - Left Lung.

Hello everybody!

Let's see the image correlations of the left lung today.

The left lung has an apical lobe ,lingula and a basal lobe.

Apical lobe has 2 segments: Anterior and posterior.
Lingula : The tongue like extension and the alleged counterpart of the middle lobe has 2 parts to it : Superior and Inferior.
Basal lobe has 4 segments namely : Superior, Posterior, Medial, Lateral.

Carefully observe how the identification of these segments differs while seeing an X-ray.

Apical lobe:

Basal Lobe:

So that's it with the interpretation of lung fields on X-rays!

Hope this is helpful!

-Medha.

“PILL” Esophagitis.

Hello!

Let's review a very common preventable condition of pill/drug induced esophagitis. 

It is occurs due to prolonged contact of the esophageal mucosa with a medication, which acts like the damaging agent.

Medications implicated in
“pill”esophagitis are :
Tetracycline
Potassium chloride
Ferrous sulfate
Nonsteroidal antiinflammatory drugs
Alendronate. 

Most often the offending tablet is ingested at bedtime with inadequate  water, this leads to prolonged contact  u of the drug with the esophageal mucosa leading to focal damage and esophagitis.

This causes acute discomfort followed  by progressive retrosternal pain,  odynophagia, and dysphagia.

Endoscopy reveals a focal lesion localized to one of the anatomic narrowed regions of the esophagus or an unsuspected pathologic narrowing. 

Treatment is supportive.
Antacids, topical anesthetics, bland or  liquid diets are often used.

Let's Learn Together!
-Medha.