Sunday, May 24, 2020

Tuesday, May 19, 2020

High-yield : Risk of stroke with cardioversion


Electrical/chemical cardioversion performed in a case of atrial fibrillation may carry a high-risk of stroke, especially if >48 hours of time has passed (thrombus formation takes about 48 hours).

Monday, May 18, 2020

Causes of holosystolic murmur mnemonic


Causes of holosystolic murmur: MTV reality shows
- Mitral regurgitation
- Tricuspid regurgitation
- Ventricular septal defect

- Jaskunwar Singh

Sunday, May 17, 2020

High-yield : Absence of tachycardia in cardiac tamponade (mnemonic)


Tachycardia is a characteristic feature of decreased systolic blood pressure in the patients of cardiac tamponade. However, there are exceptions to be taken care of during diagnosis and workup on the patients with following conditions (absence of tachycardia):

A Factor A Day Keeps Colon Cancer Away

Protective Factors For Colon Carcinoma

A - Aspirin,vitamin A 

B - Bisphosphonates
C - Calcium, Coffee, vitamin C
D - Dietary Fiber
E - vitamin E
F - Fruits
G - Green Vegetables

Clinical vignette: Chest pain in acute pericarditis


Acute myocardial infarction is one of the miscellaneous causes of acute pericarditis. Differentiating features of chest pain in these two cases are many, but the high-yield points to be noted are:-

Saturday, May 16, 2020

Friday, May 15, 2020

Pericardial knock v/s Pericardial rub


Pericardial knock:
- most common cause is constrictive pericarditis
- occurs during the healing phase of the disease (fibrocalcifications)
- during the early diastolic phase of cardiac cycle (after opening snap)
- On auscultation: high frequency sound

Pericardial rub:
- commonly seen in acute fibrinous or sero-fibrinous pericarditis
- sero-fibrinous exudate in between two layers of pericardium (disease process going on)
- may occur during ventricular systole, or ventricular early diastole (due to expansion) or late diastole (due to atrial contraction).
- on auscultation: rough scraping sound described as "leather rubbing against leather"

That's all
- Jaskunwar Singh

Thursday, May 14, 2020

Apraxia vs autotopagnosia

Hello Awesomites !

Here we will discuss two from many parietal lobe lesion.

Inability to carry out well organized voluntary movement correctly.
Despite motor, sensory & coordinated functions are not significantly impaired.

Ideomotor : It is a type of apraxia.
Patient performs the task but makes errors; there is a common tendency to substitute a body part for an object.
Abnormalities of perception of sensation despite normal sensory pathways.
Visual & body perception are impaired in parietal lobe lesions 

Agnosia of body scheme or autotopagnosia
Inability to locate, identify & orient one’s body parts.

Suppose while on rounds in neurology ward:- You see a patient brushing his knee early morning.(according to above discussion)

Apraxia -Patient has forgotten how to use toothbrush.Brushing knee as a toothbrush rather than pretending to hold one.
Autotopagnosia- the patient has forgotten the body part itself.

In either case localisation of lesion is PARIETAL LOBE.

Isn't the interpretation of one neurological sign seems interesting?
"Eyes see what mind knows"

Below is the link which is very descriptive and I came across it while reading more on this topic.
Happy studying !
-Upasana Y.

Beta 2 agonist and effect on muscles

Hello Awesomites !

I used to have a doubt why does Salbutamol cause uterine relaxation but causes contraction of skeletal muscle and cardiac muscle(tremors and tachycardia)?

Despite they have same receptors (Beta 2) how can be the action on muscle is so different.
Grossly it seems like one receptor Beta 2. This beta2 adrenergic receptor is a type of GPCR.
GPCR  are Gs, Gq ,Gi type.

Beta 2 receptor anywhere (Uterus -smooth muscle, heart- cardiac muscle, hands- skeletal muscle) is also same type of GPCR i.e Gs.

Still no difference.

Gs activates adenyl cyclase to form cAMP from ATP.
cAMP increases in all type of muscle on stimulation of Beta 2 receptor.
But it cause relaxation in smooth muscle (inhibit myosin light chain kinase)
And causes contraction of heart and skeletal muscle (activate cAMP dependent protein kinase A lead to activation of L-type calcium channel).

At one level we all may appear to be doing same thing yet at other level we are different and have our role.:)

 Happy studying !
-Upasana Y.

Wednesday, May 13, 2020

COVID-19 and Vasculopathy

Over the past few months, overwhelming evidence has accumulated suggesting the dysregulation of the coagulation pathways in COVID patients stemming from the altered immune and inflammatory response towards SARS-CoV2.

Observed coagulation abnormalities have multi-faceted pathogenesis. Most likely suspect is microvascular dysfunction secondary to cytokine storm like state, tipping the balance towards thrombosis. Direct vascular injury is also likely with evidence of endothelial viral inclusions in some cases.

-Pulmonary Intravascular Thrombosis

Evidence suggests that starking discrepancy exists between hypoxemia onset and respiratory failure in COVID patients, with former occurring fairly early in the disease course, pointing to the fact that it's not classic ARDS like pathology that is responsible for the marked deterioration in the pulmonary gas exchange process. It is appropriately explained by the diffuse thrombosis affecting the pulmonary vasculature. In fact, it's so prominent that a whole new entity called "Pulmonary Intravascular Thrombosis" has been proposed as the framework for explaining this phenomenon.

Pulmonary Intravascular Thrombosis could be considered as lying along the spectrum of classic DIC with few important dissimilarities. It is usually localized to the pulmonary vascular bed at least initially and doesn't feature hypofibrinogenemia, consistent with the acute phase response driving continued fibrinogen production. D-dimers levels, however, are significantly elevated suggesting the thrombus formation and ongoing hyperfibrinolysis.


ACE2 is expressed in huge numbers on the alveolar epithelial cells, especially type 2 cells and also pulmonary endothelial cells. Hence, in contrast to patchy involvement classically seen in bronchopneumonia, in COVID, extensive involvement of the alveolo-capillary network is seen. This, in turn, results in florid interstitial inflammation resulting in efflux and activation of macrophages in the alveoli. It is so rampant that it has been likened to Macrophage Activation Syndrome (MAS) or sHLH like state. Activated epithelial cells and macrophages then orchestrate the cytokine storm leading to microvascular dysfunction and widespread thrombosis in the juxtaposed capillary network. Enhanced tissue factor and thrombin expression, coupled simultaneously with the reduced levels of PAI-1 drives thrombosis. Hypoxemia due to V/Q mismatch further exacerbates this process.

Levels of ACE2 in alveoli initially decreases as the virus particles are internalized. ACE2, by virtue of it's ability to convert AngII to anti-inflammatory Ang1-7 peptide, keeps excessive inflammation in check. Hence, reduced ACE2 expression compounds the thrombotic propensity in the vascular bed. Direct involvement of endothelial cells by virus leading to endothelitis/vasculitis has also been suggested, although endothelial activation due to inflammatory cytokines seems more likely.

Reduced type 1 interferon signalling pathways is another intriguing possibility contributing to hyperinflammation. The role of positive pressure ventilation in forcing the viral particles and cytokines in vasculature also merits consideration.

- Skin manifestations

A variety of skin manifestations ranging from pseudo-chilblains to livedoid lesions have been described in COVID patients. While some of the lesions, like acral vesicles and pustules, confer to the pattern of viral exanthem, livedoid lesions suggest the possibility of vascular injury. These vasculopathic eruptions are known as "toevids", appearing as violaceous plaque-like eruptions over toes. Upon molecular testing, such patients often are negative, suggesting that they have probably cleared the infection and vascular injury is perhaps immune-mediated.
Interestingly, papular gloves and socks syndrome, occasionally seen in association with viral infections, especially Parvovirus, bears substantial similarity to certain COVID lesions, both clinically and histologically, with some reports even documenting evidence of leukocytoclastic vasculitis in former.

-Clinical Relevance

Significant elevations in pulmonary pressures due to diffuse thrombosis strains the right ventricle causing hemodynamic dysfunction. Elevated D-dimer, pro- BNP, and troponin levels have been proven to be poor prognostic markers consistently across various studies. Development of overt DIC like state certainly portends dismal prognosis.

Troponinemia in COVID can be attributed to severe right ventricular strain in the setting of pulmonary embolism and/or Pulmonary Intravascular Thrombosis. Some evidence also exists regarding the possibility of myocarditis, however, without classic lymphocytic infiltration characteristic of viral myocarditis.

To summarize, intricate interplay of diffuse pulmonary intravascular thrombosis and MAS like state drives the severe and often fatal pulmonary microvascular dysfunction in COVID.

SARS-CoV2 infection--> diffuse alveolar damage--> interstitial inflammation--> MAS like state--> massive activation of macrophages--> local inflammatory cytokine milieu--> Microvascular dysfunction--> Pulmonary  Intravascular Thrombosis

-Kirtan Patolia




Monday, May 4, 2020

Bugs causing bloody diarrhoea - mnemonic


Bugs that cause bloody diarrhoea : HE Is ClASSY

enteroHEmorragic E coli
enteroInvasive E coli

EntAmoeba histolytica
Salmonella (non-typh)
Y enterocolitica

Hope that helps
- Jaskunwar Singh