Hey Awesome peeps :)
This post is about variation in the effects of epi- and norepinephrine depending on its dose.
Saturday, June 13, 2020
Monday, June 8, 2020
Topical Drug Absorption.
Hello everyone!
This is the brief mention about the extent of topical absorption of drugs.
In decreasing order-
Posterior auricular
Scrotal
Scalp
Dorsum of hand
Plantar area.
Absorption mainly depends on the thickness of the skin and is inversely proportional to it.
Hope this was helpful!
Let's learn Together!
Dr. Medha Vyas
Tympanogram.
Hello Everybody!
Let us quickly review the different curves of a tympanogram.
The following are the yypes of curves in you'll see on a tympanogram:
Type A – Normal pressure and normal compliance in normal ear.
Type As – Reduced compliance (‘s’ means stiffness leading to reduced compliance) and normal pressure.
- Seen in
- Otosclerosis or other ossicular fixation
- Tympanosclerosis
- Seen in
- Ossicular discontinuity
- Thin and lax TM
Type B – Flat or dome shaped graph i.e. reduced compliance.
Seen in case of:Serous otitis media.
Thick tympanic membrane.
Type C – Normal compliance but negative pressure due to eustachian tube obstruction.
- Seen in case of:
- Retracted tympanic membrane,
- Early stages before collection of fluid in middle ear.
Hope this was helpful.
Let's Learn Together!
Dr. Medha Vyas
Tuesday, June 2, 2020
Tuesday, May 26, 2020
Sunday, May 24, 2020
Two components of Sulfasalazine : Indications
Hello
Sulfasalazine has two components:
- 5-ASA
- Sulfapyridine (SP)
Sulfasalazine has two components:
- 5-ASA
- Sulfapyridine (SP)
Tuesday, May 19, 2020
High-yield : Risk of stroke with cardioversion
Hello
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).
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
Hello
Causes of holosystolic murmur: MTV reality shows
- Mitral regurgitation
- Tricuspid regurgitation
- Ventricular septal defect
- Jaskunwar Singh
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)
Hello
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):
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
A - Aspirin,vitamin A
B - Bisphosphonates
C - Calcium, Coffee, vitamin C
D - Dietary Fiber
E - vitamin E
F - Fruits
G - Green Vegetables
Chest pain in acute pericarditis vs myocardial infarction
Hello
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:-
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:-
Friday, May 15, 2020
Mnemonico diagnostico - murmur in mitral stenosis
Hello
Mitral stenosis murmur features:
(mnemonic: MITRAL STENOSIS)
Mitral stenosis murmur features:
(mnemonic: MITRAL STENOSIS)
Pericardial knock v/s Pericardial rub
Hello
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
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.
1.APRAXIA
Inability to carry out well organized voluntary movement correctly.
Despite motor, sensory & coordinated functions are not significantly impaired.
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.
2.AGNOSIA
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.
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.
Tuesday, May 12, 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. The 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 the 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 thrombus formation and ongoing hyperfibrinolysis.
-Pathogenesis
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 decrease as the virus particles are internalized. ACE2, by virtue of its 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 signaling pathways are 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 vasculopathy 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 the 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. The development of an overt DIC-like state certainly portends a 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, the 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
Reference:
1.) https://doi.org/10.1016/S2665-9913(20)30121-1
https://www.thelancet.com/journals/lanrhe/article/PIIS2665-9913(20)30121-1/fulltext
2.) https://doi.org/10.1111/bjd.19163
https://onlinelibrary.wiley.com/doi/abs/10.1111/bjd.19163
Observed coagulation abnormalities have multi-faceted pathogenesis. The 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 the 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 thrombus formation and ongoing hyperfibrinolysis.
-Pathogenesis
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 decrease as the virus particles are internalized. ACE2, by virtue of its 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 signaling pathways are 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 vasculopathy 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 the 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. The development of an overt DIC-like state certainly portends a 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, the 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
Reference:
1.) https://doi.org/10.1016/S2665-9913(20)30121-1
https://www.thelancet.com/journals/lanrhe/article/PIIS2665-9913(20)30121-1/fulltext
2.) https://doi.org/10.1111/bjd.19163
https://onlinelibrary.wiley.com/doi/abs/10.1111/bjd.19163
Monday, May 4, 2020
Bugs causing bloody diarrhoea - mnemonic
Hello
Bugs that cause bloody diarrhoea : HE Is ClASSY
enteroHEmorragic E coli
enteroInvasive E coli
Campylobacter
EntAmoeba histolytica
Salmonella (non-typh)
Shigella
Y enterocolitica
Hope that helps
- Jaskunwar Singh
Bugs that cause bloody diarrhoea : HE Is ClASSY
enteroHEmorragic E coli
enteroInvasive E coli
Campylobacter
EntAmoeba histolytica
Salmonella (non-typh)
Shigella
Y enterocolitica
Hope that helps
- Jaskunwar Singh
Sunday, May 3, 2020
Thursday, April 30, 2020
Metronidazole : spectrum of organisms covered mnemonic
Hello
Metronidazole has bactericidal activity against
Protozoa:
- Giardia
- Entamoeba
- Trichomonas
Bacteria: (anaerobic gram-negatives)
- Bacteroides
- Clostridium sp (doc in pseudomembranous colitis)
- GARDNerella
- H. pylori
mnemonic: GET BaC in the GARDEN, Hippo
- Jaskunwar Singh
Metronidazole has bactericidal activity against
Protozoa:
- Giardia
- Entamoeba
- Trichomonas
Bacteria: (anaerobic gram-negatives)
- Bacteroides
- Clostridium sp (doc in pseudomembranous colitis)
- GARDNerella
- H. pylori
mnemonic: GET BaC in the GARDEN, Hippo
- Jaskunwar Singh
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