LV aneurysm: Difference between true LV aneurysm and LV pseudoaneurysm

LV aneurysms are most commonly caused by myocardial infarction. What's the difference between true aneurysm and pseudoaneurysm?

Types of pulmonary hypertension mnemonic

Here are my notes and a video on types of pulmonary hypertension - WHO classification! It comes with a mnemonic :)

Cardiac valves anatomy and mnemonics

Check out the YouTube video here!

-IkaN 

ECG axis mnemonic (short version)

Video here:

 

Notes below:

Abdominal aortic aneurysm notes

Here are my notes for the ABIM. Old post https://www.medicowesome.com/2016/11/step-2-ck-abdominal-aortic-aneurysm.html

-IkaN 

Colonoscopy screening intervals and management of polyps for ABIM boards

Here is the video

-IkaN

Colonoscopy screening intervals and management of polyps notes

Celiac Disease (Spectrum of Manifestations)

 Hello friends! I hope all of you are doing well. Today I wanted to share with you the many faces of Celiac Disease. Although considered as the disease which chiefly causes gastrointestinal symptoms, the entire spectrum of possible manifestations it can cause is quite broad.

Some significant associations are as follows:

1.) GI- Enteropathy associated T-cell lymphoma (EATL), Microscopic colitis

2.) Liver- NASH

3.) Spleen- Functional Asplenia (SLE & Amyloidosis being other notable causes)

4.) CNS- Seizures with posterior cerebral calcification, Neuro-psychiatric symptoms, Ataxia

5.) Hematology- Evans syndrome

6.) Pulmonary- Diffuse alveolar hemorrhage

Here is the full spectrum. Hope you like it.

-Kirtan Patolia

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! 🩺🫀

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 

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 :)

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...

Internal Medicine residency program Excel sheet (2020)

Hi guys,

I am sharing an excel sheet containing 200+ Internal Medicine residency programs. Feel free to download it and edit the information and programs according to your profile and needs. There may be a few IMG friendly programs that are missing, so do your homework and don't apply blindly. Use this as a template sheet to work on!

Kindly note, the comments are subjective, and none of the authors endorse them as proven facts. Some information may be incorrect as a lot of manual labor went into making this sheet.

Hope this helps in making the ERAS application process easier!

https://docs.google.com/spreadsheets/d/1l2Vra6wDcZX5_FMLOFcetZua64wwNsdXKDKB0saGykg/edit?usp=sharing

HERPANGINA vs HERPETIC GINGIVOSTOMATITIS

	HERPANGINA (Hand-Foot-Mouth Disease)	HERPETIC GINGIVOSTOMATITIS
CAUSATIVE VIRUS	Coxsackie A virus	Herpes Simplex type 1 virus (HSV-1)
AGE	3-10 years	6 months-5 years
CLINICAL                             PRESENTATION	Grayish Vesicles on                Posterior Oropharynx      (soft palate, tonsils, tonsillar pillars, Uvula)	Clusters of vesicles on       Anterior Oropharynx (Lips, buccal mucosa, tongue, gingiva, hard palate)
TREATMENT	Supportive management with oral hydration and analgesics	Oral Acyclovir

Glomerulonephritis associated with infectious diseases mnemonic

Hepatitis B: Membranous glomerulonephritis

Hepatitis C: Membranoproliferative glomerulonephritis

HIV: Focal segmental glomerulosclerosis

By IkaN

Creatinine clearance in elderly - basic notes

 Hi!

Elderly people have a decrease in creatinine clearance (CrCl), which means an increase in serum Cr. It is observed that annual rate of this decrease in CrCl is approximately 1 ml/min. after the age of 50 years.

Therefore, it is important to calculate the dose and dosing intervals of nephrotoxic drugs (eg., aminoglycosides) in these patients in order to prevent the precipitation of ARF.

In general,

CrCl <100 ml/min is abnormal.

However, CrCl <10 ml/min signifies the onset and worsening of acute renal failure.

Note -

• GFR is directly proportional to CrCl.

• GFR decreases by age, but not always accompanied by rise in Cr.

• Cockcroft-Gault formula is commonly referred to for calculating CrCl.

CrCl = (Ucr × V)/Pcr (~GFR)

• Double the Cr = Half the GFR.

Note that those patients with signs of worsening diabetes and resulting glomerulopathies, an increase in both GFR and CrCl is seen, which thus causes hyper filtration injury. 

That's all

- Jaskunwar Singh

Menkes disease and Wilson's disease - DDx

 Hi!

Okay so maybe they are the two of the options for a patient's clinical scenario question and you have a blurred memory for which is which in context to copper metabolism?

Let's clear the basic facts here...