Tuesday, June 1, 2021

Cluster Headache

 Is the cluster headache giving you a headache?

Here's an easy way to remember it.

C-Conjunctival congestion

L-Lacrimation

U-Unilateral

S-same time, periodicity

T-Tearing of conjunctiva

E-Excess autonomic activity

R-Rhinorrhoea

These clinical features help us to differentiate cluster headache from other types of unilateral headaches.

Treatment includes

1. 100% Oxygen at 10-12L/min for 15-20 mins

2.Sumitriptan 6mg S/c

3. Sumitriptan 20mg and Zolmitriptan 5mg nasal spray

Remember ORAL SUMITRIPTAN DOES NOT WORK!!

That's it folks!

Happy studying!

Dr. ShilPill

Saturday, May 29, 2021

The Happy face

 Hi everyone!

Lets talk about a 2 year old girl with a h/o seizure disorder who presents to your clinic for the first time for routine care. Past medical records shows that the patient is on anti-seizure medication since the last year. There is no family history of seizures. Parents report poor feeding and sleep disturbances. The girl appears to be very happy, laughing all the time for no reason. On examination, her head circumference is in the 10th percentile and is noted to have hand flapping behavior. She has not met the expected milestones for her age. What is the diagnosis?

???

ANGELMAN SYNDROME 























Fun fact: Angelman Syndrome was previously known as "Happy Puppet Syndrome"πŸ˜„


- Padma Sri Katikaneni

Psychogenic non epileptic seizure (PNES)

 PNES  characteristics : 

  • No loss of consciousness or postictal period

Comorbidities  
  • Psychiatric conditions (depression, anxiety)
  • Physical/sexual abuse
  • Epilepsy

Mnemonic = “WALT” - means Unsteady! 


Thank you! πŸ©ΊπŸ«€


Friday, May 28, 2021

Red blood cell transfusion thresholds mnemonic

 Hello everyone! Just look here.. 

What does it mean ? SHOAN …? 
the name Shoan is of Hebrew origin and means "Gift of Salvation". 
That’s all!
Thank you! πŸ©ΊπŸ«€


Subarachnoid haemorrhage

Clinically important steps required for SAH management ( from its onset ) 


  • Most commonly due to ruptured saccular (berry) aneurysm
  • Severe & sudden onset of headache different from previous headache pattern or described as "worst headache of my life"
  • Nausea, vomiting, brief loss of consciousness, focal neurologic deficits, or meningismus
  • Noncontrast head CT >90% sensitive within 2-6 hr of SAH onset
  • Lumbar puncture required to exclude SAH definitively in patients with negative CT scan of the head
  • Xanthochromia confirms diagnosis (usually >6 hr from SAH onset)
  • Cerebral angiography to identify bleeding source

Happy studying! 
Thanks folks! 🩺

A cardiologist and infectious disease specialist discuss their favorite statin

Cardiologist: What's your favorite statin? Atorvastatin? Rosuvastatin? 
Infectious disease specialist: Cilastatin! 

I onced misspelled it as cilastin and this joke was inspired. Idea credits to Randy Bornmann! 

Biophysical Profile Mnemonic

 

Biophysical Profile 
Just add an extra “V” 
See the management here .. 

“ The value of experience is not in seeing much, but in seeing wisely”.  - William Osler  

Thank you! 🩺

Thursday, May 27, 2021

Immunofluorescence patterns in glomerular diseases notes and mnemonics

Immunopathologic patterns of immunoglobulins (Igs) and/or complement components deposited in glomerular diseases notes and mnemonics

Linear deposition:
Anti-GBM disease (mainly IgG)
unspecifically IgG in diabetes mellitus

Granular deposition: 
membranoproliferative GN
post-infectious GN
membranous GN
IgA, IgM, C1q, C3

Pauci immune deposition:
Granulomatosis with polyangiitis (Wegener) PR3-ANCA/c-ANCA
Eosinophilic granulomatosis with polyangiitis (Churg-Strauss)
Microscopic polyangiitis MPO-ANCA/p-ANCA

Love,
IkaN 

Treatment options for latent tuberculosis mnemonic

Treatment options for latent tuberculosis 

6 or 9 months of isoniazid 

3 months of isoniazid plus rifapentine, given once weekly

4 months of rifampin, given daily

3 months of isoniazid plus rifampin, given daily


That's all!
IkaN 

Fact of the day - hypercalcemia in sarcoidosis

 Hi!


Hypercalcemia and hypervitaminosis-D is seen in patients with sarcoidosis and other granulomatous inflammatory conditions. This is because the granulomatous macrophages have high 1-alpha hydroxylase activity --> high levels of 1,25-OH2 vitamin D (calcitriol), produced in addition to this enzyme's normal activity in the kidneys.


That's all

- Jaskunwar Singh

Tuesday, May 25, 2021

Salter-Harris classification of fractures


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

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


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

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

Hope this helps!
-Padma Sri Katikaneni







 

Basal Ganglia Circuit

Hello everyone!  Confusing loop has now simplified look! πŸ‘€ 

First of all, Basal ganglia receives cortical input, provides negative feedback to cortex to modulate movement.

3 things must be remembered. 

  • SNc (Substantia nigra) input to the striatum via the nigrostriatal dopaminergic pathway releases GABA.
  • Dopamine binds to D1 , stimulating the excitatory pathway, and to D2 , inhibiting the inhibitory pathway. 
  • Pathways from Thalamus to Motor cortex & from Motor cortex to Basal ganglia - “Stimulatory” 

That’s why this circuit is important in voluntary movements and adjusting posture. 

Here is my attempt to simplify this circuit through a drawing. By understanding that you’ll never forget it! 



  • I-N-hibitory pathway goes through Gp-I & N-ucleus(Subthalamic)!
  • If BG output = +, then increased motor activity
  • If BG output = -, then decreased motor activity 

In PARKINSON’S DISEASE, SNc degenerates = lose dopaminergic input to BG
Less stimulation of direct pathway (⬇️gas) and less Inhibition of Indirect pathway (⬆️ brake) = overall indirect wins =less motor activity. This explains bradykinesia and rigidity of PD but not tremor. 

STN and GPi are targets of Deep Brain Stimulation in PD. 
Deep brain Stimulation INHIBITS activity in these structures—inhibiting either would lead to decreased inhibitory output of BG = increased motor activity-> improve PD symptoms. 

Lesion of STN -HEMIBALLISMUS= uncontrolled erratic large amplitude movements on one side.  Why INCREASED movement with STN lesion? 
By decreasing STN excitation of GPi we essentially ‘remove’ indirect pathway from equation, and direct pathway becomes unchecked -> ⬆️ movement      

Thank you! 🩺

Sunday, May 23, 2021

Ehler-Danlos Syndrome (EDS) - High yield only

Hi! So let's learn EDS together. I've tabled a list of high-yield points of all the types of EDS. It requires little bit of revision but once you get a pictorial familiarity you should be able to recall them all. 

Have fun!

So, how to remember?

Step 1. Divide the table into 2 halves. Sl no. 1,2,3 have in common a lot of features:
  • They are all Autosomal Dominant. 
  • They have common Clinical features - skin HYPERelasticity, joint HYPERmobility and HYPER (easy) bruising. 
  • Go serially, Classical has the first 2, Type I and II and HYPERmobile is III and lastly Vascular is type I
  • Vascular type has additionally - arterial & uterine rupture.
Step 2. Now the second section Sl no. 4,5,6
  • EDS types with enzyme defects are Autosomal Recessive. So, 4 and 6 are AR. 
  • Kyphoscoliotic EDS is Type VI (K rearranged is a V and I)
  • For the last 2, mnemonic is ABCDπŸ˜› Arthrochalasia VII a, b and VII c is Dermatosparaxis.
  • KyphoSCOLIOTIC EDS - defective lysyl hydroxylase (=> abnormal cross linking of collagen or KOLLAGEN => think of bones 🦴 => congenital SCOLIOSIS)
  • ARTHROchalasia is COL IA (1st letter is A) and hence presents with severe JOINT hyper mobility.
  • DERMATospARaxis is AR and a defective Procollagen-N-peptidase and presents with CUTIS laxa. (Cuties are Pros ;)

Step 2. For the Gene types, come down in descending order: 5 4 3 2 1


Step 3. Remember Type V - DOEST NOT EXIST. 

Step 4. Revise again πŸ˜‰

That's it! Stay safe 🌸
- Anagha :)