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 .. 

https://www.medicowesome.com/2016/09/biophysical-profile-mnemonic-and-step-2.html

See the video here https://www.medicowesome.com/2018/03/nonstress-test-and-biophysical-profile_6.html 

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

Thank you! 🩺

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

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! 👀 

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! 🩺

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 IV 
• 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 ABCD😛 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 0 

Step 3. Remember Type V - DOEST NOT EXIST. 

Step 4. Revise again 😉

That's it! Stay safe 🌸

- Anagha :)

Types of COVID-19 antibody tests

Hi everyone! 

In this post, I will go over in very short the different types of  COVID-19 antibody tests.

Cancer Screening - US Preventive Services Task Force (USPSTF) guidelines

     As the saying goes - "Awareness is Power in a world where information is everywhere", lets quickly learn the USPSTF recommended guidelines for Cancer screening

CANCER	SCREENING MODALITY	AGE GROUP
Breast Cancer	Biennial Mammography	Women aged 50 to 74 yrs
Cervical Cancer	Cervical cytology every 3yrs   Cervical cytology every 3 yrs  or High risk HPV(hrHPV) testing every 5 yrs or hrHPV testing in combination with cytology every 5yrs (cotesting)	Women aged 21 to 29 yrs  Women aged 30 to 65 yrs
Lung Cancer	Annual Low dose CT chest (who have a 20 pack-year smoking history and currently smoke/quit within past 15 yrs)	Adults aged 50 to 80 yrs
Colorectal Cancer	Colonoscopy screening every 10 yrs Flexible sigmoidoscopy every 5 yrs Computed tomography colonography every 5 yrs High-sensitivity guaiac fecal occult blood test (HSgFOBT) or fecal immunochemical test (FIT) every yr Stool DNA-FIT every 1 to 3 yrs	Adults aged 45 to 75 yrs

P.S. - USPSTF now recommends screening for Colorectal cancer in adults aged 45 to 75 years

- Padma Sri Katikaneni                                                                                                                       

                  

Human herpes viruses (HHV) types mnemonic

Human herpes viruses mnemonic... In case you get them mixed up...

Fact of the day - Athlete's heart

Hi!

Athlete's heart - physiologic eccenteric hypertrophy (cardiac remodeling) - changes include resting bradycardia, higher cardiac output with exercise, dilatation of LV cavity size with hypertrophy of myocytes compared to normal heart.

vs pathologic hypertrophy in case of systolic heart failure, aortic/mitral regurgitation, dilated cardiomyopathy(DCM) (volume overload conditions).

LV systolic ejection fraction is normal - low-normal in athletes.

(vs HCM- high, DCM- low)

HCM is a common cause of death in athletes, especially those with family history.

That's all

- Jaskunwar Singh