Ductus Arteriosus : Review of Key Points

Hi everyone ! Just a short review on Ductus Arteriosus.

- Ductus Arteriosus is basically a communication between the Pulmonary trunk and the Systemic Aorta.
- This communication is between pulmonary trunk and the end of Arch of aorta. Just after the Brachiocephalic trunk , and Left Common carotid and Subclavian have branched off.
- In embryonic life this communication helps transport blood from RV- Pulmonary artery to the Systemic circulation.

So ,
Remember :
Prostaglandins Persist

-Prostaglandins, especially PGE1 , act on the Ductal muscle tissue and keep it Open.
-So the Ductus arteriosus stays open.

-This is important in certain Duct dependent lesions
- Duct dependent heart lesions are those which need the presence of an Open ductus to receive blood in systemic / Pulmonary circulation.

- For example -->
✓ Duct dependent lesions for Systemic Circulation are those that cause obstruction to the Left side heart to pump blood into the aorta. These include :

- Coarctation of Aorta ( especially pre Ductal ) : Here there is a constriction of the aorta just before the ductus Arteriosus. So , a persistent Ductus would transport blood from pulmonary circulation into the systemic. 
If ductus gets closed , there would be minimal blood flow to the Lower limbs and abdomen.

- Critical Aortic stenosis.
- Left side Hypoplastic heart.

~~~~~~~~~~~~~~~~~~~~~~~~~

✓ Duct dependent lesions for pulmonary circulation
-These are lesions where pulmonary blood flow would be severely reduced due to some RV- Outflow tract Abnormality and the only source to the lungs would be through the ductus shunting some blood from aorta into the pulmonary vein.

- These include : 

- Critical Pulmonary Stenosis
- Hypoplastic Right heart syndrome
- Tetrology of Fallot
- Tricuspid Atresia
- Ebstein Anomaly

Another important disease is Transposition of the great vessels where this sort of corrects the defect.
~~~~~~~~~~~~~~~~~~~~~~~~~

So. We've seen in what conditions we'd like to keep the Ductus Arteriosus open / persistent.
Normally this Ductus closes functionally within 24 hours of birth. And anatomically between 10 and 14 days post natally.

If this persists on its own for a long time it causes a Congenital Heart Disease called Patent Ductus Arteriosus.
This defect is characterised by shunting of blood into the pulmonary trunk constantly during systole and diastole causing a Continuous murmur.

To close this ductus , we could try using Indomethacin / Ibuprofen especially in preterm children.
These drugs inhibit Prostaglandin synthesis , thus causing Ductus Smooth muscle to constrict and eventually close.

So that's all about the ductus !

Happy studying !
And Stay Awesome !

~ A.P.Burkholderia

Jaundice Syndromes : Mnemonic

Hey everyone. Just a short post on how to remember the Jaundice Syndromes.

So.

Remember :
CGI
(As in the CGI special effects in movies.)

C - Criggler Najjar Syndrome
G - Gilbert Syndrome
I  - Indirect Jaundice ( Unconjugated Bilirubin).

So this would make Dublin Johnson and Rotor Syndromes Direct Jaundice.

Another useful fact :
All are inherited as Autosomal recessive trait except Gilbert and Criggler Najjar 1.

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

Lowe syndrome mnemonic

Lowe Syndrome (Oculocerebrorenal dystrophy) mnemonic

Think of Lowe = Love and it'll make sense.

Lowe makes you blind (cataracts, glaucoma)

Lowe makes you HAPpy (High Alkaline Phosphatase along with normal calcium, low phosphate)

Lowe messes with your head (intellectual disability)

LoveR - Renal defects (proximal tubular acidosis, aminoaciduria, and low-molecular-weight proteinuria)

Lowes syndrome is a cause of Fanconi syndrome.

That's all!

-IkaN

Renal Cell Carcinoma Etiology : Summary

Hi everyone. Here's a short summary of the causes for Renal cell carcinoma !

Renal Cell Carcinoma ( or RCC) is a common tumor of the kidneys and is essentially an Adenocarcinoma.
It's quite often called as the 'great mimic' as it is relatively hard to diagnose.

Here's the list of causes of this tumor.

Remember :
CCCC or C4

C = Cigarette smoking and Tobacco usage.
C = Chronic Kidney Disease / Cystic (Acquired) Disease of kidneys.
C = Cadmium, Asbestos and other occupational Exposures.
C = Cancer Syndromes.
Important Cancer Syndromes =

- Von Hippel Lindau Syndrome :
3p mutation in VHL Gene which is a tumor suppressor --> Tumors seen include Cerebellar and Retinal Hemangioblastomas , Pheochromocytoma, RCC (Clear type) and various other Cystic tumors.

- Tuberous Sclerosis

- Birt Hogg Dube Syndrome : Associated with various weird skin changes and chromophobe type RCC.
Skin changes include --> Tumors of Hair disc (Tricho-discoma) , Tumors of Hair follicle - Fibrofolliculoma and Acrochordons ( skin tags).

- Hereditary Papillary Cancer : Associated with MET Gene mutations

- Hereditary Leiomyomatosis with RCC : Associated with multiple Fibroids in the uterus.

That's​ all for today!
Hope this helped.
Happy Studying !
And, as always , Stay awesome !

~ A.P.Burkholderia

Step 2 CK: Differentiating ileus from SBO

Hello! Short post.

SBO: Small bowel obstruction.

Both: Nausea, vomiting, abdominal distension

Ileus: Hypoactive bowel sounds
Dull and constant pain
Dilated bowel but no air fluid levels

SBO: Initially hyperactive, later hypoactive
Colicky abdominal pain
Air fluid levels seen

That's all!
Back to studying.
-IkaN

Neuroblastoma mnemonic

Hello!

The term neuroblastoma is commonly used to refer to a spectrum of neuroblastic tumors (including neuroblastomas, ganglioneuroblastomas, and ganglioneuromas) that arise from primitive sympathetic ganglion cells and, like paragangliomas and pheochromocytomas, have the capacity to synthesize and secrete catecholamines.

Remember the N myc mnemonic for neuroblastoma :

N - Neuroblastoma, N myc gene
M - Crosses midline (differentiates from Wilms)
MY - MYoclonus (Opoclonus myoclonus)
C - Calcifications in tumor present
C - Catecholamine secretion

You can also remember "High BP" for additional findings seen in neuroblastoma:

Horner syndrome
Heterochromia iridis (different colors of the iris or portions of the iris)
Hypertension
Homovanillic acid and vanillylmandelic acid elevated in urine
Bombesin positive
Back pain
Bone pain
Beckwith-wiedemann syndrome association
Posterior mediastinum or retroPeritoneal mass
Pseudorosette
Purple skin lesions
Proptosis
Periorbital ecchymoses

That's all!
-IkaN

Doyne's macular degeneration

So, the other day the head of my department asked us about Doyne's maculopathy. Couldn't find rest until I searched it up on Google. Here what it is in short-

1. Accumulation of material between
the Bruch's membrane and the retinal pigment epithelium.

2. This results into the formation of a drusen, which is a radially localised
white, large one which spreads over
time.

3. The cause is a mutation in the
EFEMP1 gene,on chromosome
2p16, inherited as an autosomal
dominant trait which results in the
formation of a misfolded protein
which is poorly secreted as well.

4. All this results into a gradual loss of
vision.

5. Photodynamic therapy forms the
mode of treatment for subfoveal nets which may also occur in the disease.

It is also known as 'Honeycomb retinopathy'

That's all!

-Sushrut Dongargaonkar

The Romberg's Test.

Hello,
Today's review is on Rombergs test.

Romberg/Brauch-Romberg sign:
In cases where the proprioception is disturbed, patient may be able to stand with eyes open but sways or falls with eyes closed.

Romberg described this test, in patients with tabes dorsalis where the Dorsal Columns are damaged.
Well he did not state that the feet should be placed together; it was added later.. Nor did he comment on where the arms were to be positioned.

It is just a common practice to have the patient hold the arms outstretched in front, in order to check simultaneously for pronator drift or to perform finger-to-nose testing; it is not what the original test was.

The Romberg sign is often misunderstood and misinterpreted. 

The essential finding is a difference between standing balance with eyes open and closed. To test this function, the patient must have a stable stance, eyes open and then demonstrate a decrease in balance with eyes closed, when visual input is eliminated.
This is the time patient must rely on proprioception to maintain balance.

The Romberg sign is used primarily as a test of proprioceptive, not cerebellar, function, patients with cerebellar disease, particularly disorders of the vestibulocerebellum or spinocerebellum, may have some increase in instability with eyes closed, but not usually to the degree seen with impaired proprioception.

A patient with an acute unilateral vestibulopathy may fall toward the side of the lesion when standing with eyes closed.

Additional Manuevers for this Sign.

1) Ropper's Refined Rombergs Test :
Turning the head side to side eliminates vestibular clues and increases the reliance on proprioception.

2) The Sharpened Romberg Test :
It is done by having the patient stand in tandem position with eyes open and closed; the limits of normality for this variation are conjectural.

Hope this was helpful!

Let's Learn Together!
-Medha.

MCQ Pointers - Pityriasis Versicolor.

Hello!

If you see some of the below "pointer" words in MCQs the ans would most likely be pointing towards Pityriasis Versicolor.

-Acquired lesions.
-Hypopigmented small macules coalescing to form Patches classically on the chest (m/c),back,face.
-Perifollicular (around hair follicles) distribution.
-Fine scaling on lesions which becomes prominent on scratching - Scratch sign+.
-Pale yellow fluorescence of the lesions on Wood's lamp examination.

Finally the classic - Indicating the causative organism : Malasessia.
Spaghetti and meat balls appearance or Banana and Grapes appearance on KOH mount.

Lemme know more of pointers you know about.
Let's Learn Together!
-Medha.

Step 2 CK: Psychiatry tip for possible depression questions

Hello! 

Whenever I come across a possible major depression question, I write SIGECAPS (full form at the end of the post) down and strike out the alphabets as and when I come across the symptoms.

For example, weight loss - strike out A for appetite change, fatigue because staying up at night - strike out S for sleep change, E for loss of energy.

Then re-read the stem and see for symptoms I missed out due to twisted wording (she stopped singing a month ago - strike out I for loss of interest)

It REALLY helps in figuring out 5/9 SIGECAPS for diagnosis of MDD because if you are not actively looking for the symptoms in the question stem, you'll miss them out. Also, if you are not counting, you might wrongly over diagnose MDD.

Writing it down also saves time because you don't have to keep re-reading the stem over and over.

It also helps getting the count right because if you have already striked out an alphabet, you can't strike it out again. So you won't get the count wrong for possible rephrasing of the same symptom in the question stem. (patient says she has lost appetite, there is weight loss - it is one alphabet in SIGECAPS, so you can't strike A out again - you will get the symptom count right!)

That's all!

I've read so many comments by students in forums where people get MDD wrong just because they didn't see the obvious 5/9 SIGECAPS. Don't miss it out guys, it's very easy to diagnose with this trick! :)
Hope that helps!

-IkaN

For those who don't know what SIGECAPS stands for :

S: Sleep changes: Increase during day or decreased sleep at night

I: Interest (loss): of interest in activities that used to interest them

G: Guilt (worthless): Devalue themselves, feel guilty

E: Energy (lack): common presenting symptom (fatigue) 

C: Cognition / Concentration: Reduced cognition &/or difficulty concentrating

A: Appetite (weight loss): Usually declined, occasionally increased

P: Psychomotor: Agitation (anxiety) or retardations (lethargic)

S: Suicide / preoccupation with death

Originally when a physician would write a prescription, the abbreviation “SIG” would be written which was to mean directions. The "E" CAPS was to remind the prescriber to write “Energy” capsules for depression (antidepressants).

Hence:  SIG:  E. CAPS

Therapist near me, BetterHelp

GLP-1 analogues mnemonics

Hello!

Mechanism of action of GLP 1 analogues
- Increase glucose dependent insulin release
- Decrease glucagon release

Motor Neurone Disease : Why and How to rule it out.

Hi everyone ! Here's a short post on How and why to rule out Motor Neuron diseases.

Motor Neurone Disease includes a group of conditions where the Motor Neurons of your body begin to degenerate.
If these neurons are located above the level of the Alpha motor neuron of spinal cord , the result is UMN lesions , like Primary Lateral Sclerosis.
If the degeneration occurs in the Alpha motor neurons themselves , the result is LMN type paralysis, like Spinal Muscular Atrophy..
A combination of the two - UMN + LMN features as seen in - Amyotrophic Lateral Sclerosis.

Now a few set of conditions are used as a way to exclude to MND.
MND itself isn't very common , and carries an extremely poor prognosis. Treatment options are extremely limited. So it's important to rule it out whenever you come across a Paraplegia , Quadriplegia, Bulbar or Pseudobulbar palsy patient .

An MND has No COBS.
C - No Cognitive changes
O - No Ocular motility involvement till late.
B - No Bladder bowel involvement till late.
S - No Sensory involvement.

There are a few exceptions to this -
Cognitive changes can be present if it's associated with Fronto temporal dementia. A lot of the familial cases are associated with this.

Behavorial changes can also be seen in a Pseudobulbar palsy patient. (More on that some other day !)

Sensory involvement may be seen in Hereditary spastic paraplegia - a variant of MND.

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

~ A.P.Burkholderia.

Clonus - A review.

Hello everybody!
Let's review Clonus breifly today.

So what is it?
It is a series of rhythmic involuntary muscular contractions induced by the sudden passive stretching of a muscle or tendon.

Clonus occurs most frequently at the ankle, knee, and wrist, occasionally elsewhere.

The important Clonus that we all frequently examine is the Ankle Clonus so let's see that in detail here.

Ankle clonus is a series of rhythmic alternating flexions and extensions of the ankle.

How to do it?
The leg and foot should be well relaxed, the knee and ankle in moderate flexion, and the foot slightly everted.
The examiner supports the leg, with one hand under the knee or the calf, grasps the foot from below with the other hand, and quickly dorsiflexes the foot while maintaining slight pressure on the sole at the end of the movement.
A single tap on the tendon to elicit the ankle jerk may occasionally provoke clonus.

Unsustained clonus fades away after a few beats; sustained clonus persists as long as the examiner continues to hold slight dorsiflexion pressure on the foot.

Unsustained (transient) symmetric ankle clonus may occur in normal individuals with physiologically fast Deep Tendon Reflexes. Nonorganic clonus occurs rarely. False clonus (pseudoclonus) in psychogenic disorders is poorly sustained and irregular in rate, rhythm, and excursion.

Sustained clonus is never normal. In severe spasticity, clonus may occur spontaneously or with the slightest stimulus. At the ankle, true clonus can usually be stopped by sharp passive plantar flexion  of the foot or the great toe; false clonus is not altered by such a maneuver

Mechanism:
Part one - For ankle clonus, the sudden stretch of the gastrosoleus muscle elicits a contraction essentially analogous to a stretch reflex that causes a contraction with resultant plantar flexion of the foot. The foot goes down. 
Part two - This contraction increases tension in the Golgi tendon organs in the gastrosoleus tendon, sending a volley of impulses via the Ib fibers that then inhibit the contraction of the gastrosoleus and facilitate contraction of its antagonist, the tibialis anterior muscle.  The foot goes up. 
This in turn passively stretches the gastrosoleus, and the cycle is repeated.

A simpler explanation is alternating stretch reflexes.

A few other Clonus' seen are :

1) Patellar clonus :
It consists of a series of rhythmic up-and-down movements of the patella. It may be elicited if the examiner grasps the patella between index finger and thumb and executes a sudden, sharp, downward thrust, holding downward pressure at the end of the movement. 

The leg should be extended and relaxed. Patellar clonus may appear when eliciting the patellar or suprapatellar reflex.

2) Wrist Clonus :
It is produced by a sudden passive extension of the wrist or fingers.

3) Jaw Clonus occurs occasionally.

So that's all about clonus.
Hope it was helpful!

Let's learn Together!
-Medha!

Alternate methods of Eliciting Toe Dorsiflexion in Corticospinal tract lesions.

Hello!

Let's review few minor signs of eliciting toe dorsiflexion when we are suspecting  a Corticospinal tract lesion.

Gordon’s sign :
Squeezing of calf muscles.

Schaefer’s sign :
Deep pressure on Achilles tendon.

Bing’s sign :
Pricking dorsum of foot with a pin.

Moniz’ sign :
Forceful passive plantar flexion at ankle.

Throckmorton’s sign :
Percussing over dorsal aspect of metatarsophalangeal joint of great toe just medial to Extensor Hallucis Longus tendon.

Marie Foix sign :
Squeezing the toes or strongly plantar   flexing toes or foot.

Gonda (Allen) :
Forceful downward stretching or snapping of second, third, or fourth toe; if response is difficult to obtain, flex toe slowly, press on nail, twist the toe, and hold it for a few seconds.

Stransky :
Small toe forcibly abducted, then released.

Allen and Cleckley :
Sharp upward flick of second toe or pressure applied to ball of toe.

Strümpell’s  phenomenon :
Forceful pressure over anterior tibial region.

Cornell response :
Scratching dorsum of foot along inner side of Extensor Hallucis Longus tendon.

All the above signs may not be always seen and sometimes these may be the Only signs present and hence it is necessary for us as students to screen as many patients as we can and increase our understanding and clinical acumen, cause the eyes can't see what the brain doesn't know.

Let's learn Together!
-Medha.

Tetralogy of fallot mnemonic

Hello!

Here is a short note on tetralogy of fallot. Tetralogy of fallot is a congenital disorder of heart. It shows four signs, as indicated in it's name (tetra).

Mnemonic for it is - PRVO virus ( parvo virus )

1. Pulmonary stenosis
2. Right ventricular hypertrophy
3. Ventricular septal defect
4. Overriding of aorta.

That's all :)

H@Mid.

Ano-Rectal anatomy: Above and below pectinate line

Here's an illustration I made :)

It shows the embryology, pathology, innervation, blood supply, venous drainage and lymphatic drainage on the rectum above and below pectinate line.

Examination of Subtle Hemiparesis - Barré's Sign.

Hello everybody!

So today let's learn about examination of subtle hemiparesis, a very important inspectory finding.

Sometimes patients with mild CST (Corticospinal Tract) lesions may have normal strength to routine testing, but the deficit may be brought out using ancillary maneuvers like the examination for pronator drift (Barré’s sign).

With the patient’s upper extremities outstretched to front, palms up and with the eyes closed, we have to observe the position of hands.
Normally patient should hold this position for at least 20 to 30 seconds and the palms will remain straight with the elbows straight, and the limbs horizontal.

Any deviation from this position should be similar on the two sides.

(One exception to the usual symmetry is that the dominant hand occasionally may pronate slightly more than the nondominant, perhaps because the nondominant extremities tend to be more flexible than the dominant extremities, making it more difficult to stretch the dominant hand to a horizontal position.)

However, greater pronation of the nondominant arm is sometimes an indication of subtle hemiparesis.

Three types of drifts may occur when the patient attempts to hold the arms outstretched with eyes closed: pyramidal drift, parietal drift, and cerebellar drift. In pronator drift (Barré’s sign) due to a pyramidal lesion, the arm sinks downward and there is accompanying pronation of the forearm.

In parietal drift, the arm usually rises and strays outward (updrift).  

With cerebellar drift, the arm drifts mainly outward, either at the same level, rising, or less often sinking.

The patient with a mild CST deficit may demonstrate “pronator drift” to varying degrees.

Mild drift : there is slight pronation of the hand and slight flexion of the elbow on the abnormal side. 

Severe drift : there is more prominent pronation and obvious flexion of the elbow, and there may be downward drift of the entire arm.

Mechanism: Because of the innervation pattern of the CST, the minimally weak CST innervated muscles are overcome by the non-CST muscles.

With a mild CST lesion, the minimally weak muscles in the upper extremity are the extensors, supinators, and abductors.  These are overcome by the uninvolved and therefore stronger muscles: the pronators, biceps, and internal rotators of the shoulder. As these overcome the slightly weakened CST innervated muscles, the hand pronates, the elbow  flexes, and the arm drifts downward.

The tendency to pronation and flexion in mild hemiparesis has also been attributed to subtle hypertonicity in the pronator and flexor muscle groups.

Imagine what would occur if this motion continued to the extreme: the hand would become hyperpronated, the elbow fully exed, and the shoulder internally rotated, that is, the position of spastic hemiparesis.

The abnormal upper limb positions in minimal pronator drift and in severe spastic hemiparesis are due to the same underlying phenomenon: strong non-CST muscles overcome variably weak CST muscles involved by the disease process.

The examination for pronator drift is a very important part of the neurologic examination. If only one motor test could be done on a patient, the best single test to use would probably be examining for drift.

Hope this was informative!
Let's learn Together!
-Medha.

Glargine insulin mnemonic

Mini post!

Pathophysiology of anorexia in chronic kidney disease

Normal appetite regulation: Appetite regulation involves the gastrointestinal tract (ghrelin as an appetite stimulant, and cholecystokinin, glucagon-like peptide-1, and neuropeptide YY as appetite inhibitors); the adipose tissue with leptin, a potent appetite inhibitor; the vagal system; and the brain, which integrates the stimuli in the hypothalamus area. Satiety relies on the melanocortin receptors with serotonin as the main neurotransmitter and is challenged with hunger peptides, namely, neuropeptide Y and agouti-related peptide.

What happens in CKD?

Pharmacotherapy for PTSD in pregnancy mnemonic

The two FDA approved drugs for PTSD are: Paroxetine and Sertaline.

Fact of the day: Valbenazine for treatment of tardive dyskinesia

Here's a cool fact: Valbenazine is a highly selective vesicular monoamine transporter 2 (VMAT2) inhibitor. It modulates dopamine release during nerve communication.