Video by Drashtant
Monday, March 23, 2020
Saturday, March 21, 2020
Recent updates about treatment of COVID19
All things you need to know about COVID19
Recent Updates:
At present Best Option = HydroxyCQ +/- Azithromycin
HydroxyCQ for 10 day ( 200 mg TDS )
As ACE 2 enzyme is receptor for SARS-Cov-2 & these RAS inhibitors ⬆️ ACE2 enzyme. So hypothetically, there's an ⬆️ Risk of Covid19. But the guidelines recommend that ACEI / ARBs should not be discontinued.
Drugs under Clinical Trials:
Remdesivir (USA)
Ritonavir-Lopinavir
Tocilizumab (IL6)
Sarilumab (IL6)
Favipiravir+ Tocilizumab
Meplazumab (CD147)
Fingolimod
Darunavir + Cobicistat
Thank you..
- Drashtant
Sunday, March 15, 2020
Isatuximab (Novel monoclonal antibody)
Isatuximab (a novel monoclonal antibody that binds
selectively to CD38), which is widely expressed on the plasma
cells, and kills myeloma cells via multimodal mechanisms
including antibody-dependent cellular cytotoxicity,
antibody-dependent cellular phagocytosis, complement-
dependent cellular cytotoxicity, and immune cell
depletion or inhibition of immunosuppressive cells, as has been described with daratumumab.
Additionally, isatuximab, similar to other CD38 antibodies, modulates
the NADase enzymatic activity of CD38.
However, isatuximab differentiates itself from daratumumab in its
ability to induce direct apoptosis without cross-linking, and in its binding epitope.
Isatuximab is approved in combination with pomalidomide and dexamethasone for adult patients with multiple myeloma who have received at least two prior therapies including lenalidomide and a proteasome inhibitor.
A pretty amazing mechanism, right?
Kirtan
selectively to CD38), which is widely expressed on the plasma
cells, and kills myeloma cells via multimodal mechanisms
including antibody-dependent cellular cytotoxicity,
antibody-dependent cellular phagocytosis, complement-
dependent cellular cytotoxicity, and immune cell
depletion or inhibition of immunosuppressive cells, as has been described with daratumumab.
Additionally, isatuximab, similar to other CD38 antibodies, modulates
the NADase enzymatic activity of CD38.
However, isatuximab differentiates itself from daratumumab in its
ability to induce direct apoptosis without cross-linking, and in its binding epitope.
Isatuximab is approved in combination with pomalidomide and dexamethasone for adult patients with multiple myeloma who have received at least two prior therapies including lenalidomide and a proteasome inhibitor.
A pretty amazing mechanism, right?
Kirtan
Tuesday, March 10, 2020
Saturday, March 7, 2020
Layers Of The Abdomen
SUB - Skin
CUTANEOUS- Camper's Fascia
SYSTEM - Scarpa's Fascia
EXITS - External Oblique
INTESTINAL- Internal Oblique
TRANSPORTw/ - Trs Abdominis
FREE- Fascia Transversalis
EXIT- Extra Peritoneal C/T
PASS- Parietal peritoneum
Friday, March 6, 2020
Everything you need to know about coronavirus COVID-19
Resources: CDC, UpToDate, WHO website.
Video by Drashtant Prajapati, MBBS.
Everything you need to know about coronavirus COVID-19
Resources: CDC, UpToDate, WHO website.
Video by Drashtant Prajapati, MBBS.
Wednesday, March 4, 2020
Sunday, March 1, 2020
Acquired coagulopathy
Apart from congenital disorders, various clinical scenarios can give rise to altered hemostatic patterns leading to the state of so-called "acquired coagulopathy".
1.) Due to Factor inhibitors:
Classically it is seen in pregnant patients and those with lymphoproliferative disorders like CLL. However, it could be idiopathic.
Usually, it leads to the acquired factor Vlll and V deficiency.
Classically it is seen in pregnant patients and those with lymphoproliferative disorders like CLL. However, it could be idiopathic.
Usually, it leads to the acquired factor Vlll and V deficiency.
Mixing studies are employed to differentiate between acquired and congenital factor deficiency. Failure of correction of clotting assays after mixing studies suggests the presence of inhibitors.
2.) Amyloidosis
Sequestration of Factor X by amyloid fibrils leads to an acquired deficiency-like state. Amyloid vasculopathy along with factor X deficiency often leads to purpura and ecchymosis in these patients.
Sequestration of Factor X by amyloid fibrils leads to an acquired deficiency-like state. Amyloid vasculopathy along with factor X deficiency often leads to purpura and ecchymosis in these patients.
3.) Myeloproliferative neoplasms
Apart from acquired vWD due to loss of HMW vWF multimers, acquired factor V deficiency can also be seen. This has been attributed to adherence of Factor V to megakaryoblasts similar to the relation between factor X and amyloid fibrils. However, severe clinical manifestations might not necessarily reflect upon clotting assays or factor levels with the latter suggesting functional factor V deficiency.
Apart from acquired vWD due to loss of HMW vWF multimers, acquired factor V deficiency can also be seen. This has been attributed to adherence of Factor V to megakaryoblasts similar to the relation between factor X and amyloid fibrils. However, severe clinical manifestations might not necessarily reflect upon clotting assays or factor levels with the latter suggesting functional factor V deficiency.
3.) Thrombotic microangiopathies and DIC
Usually leads to both thrombotic and bleeding manifestations. The spectrum of TMA includes HUS, aHUS, TTP, HELLP syndrome, DIC, cAPLA, scleroderma renal crisis, malignant hypertension, and radiation or HSCT-induced vasculopathy.
Usually leads to both thrombotic and bleeding manifestations. The spectrum of TMA includes HUS, aHUS, TTP, HELLP syndrome, DIC, cAPLA, scleroderma renal crisis, malignant hypertension, and radiation or HSCT-induced vasculopathy.
4.) Coagulopathy of liver failure
Classically seen in the setting of fulminant liver injury which may be due to the infections, drugs, autoimmune hepatitis, ischemic hepatitis/shock liver, or rarely in Wilson's disease due to massive hepatocyte destruction.
One of the hallmark lab findings includes normal factor VIII levels. This is due to the fact that factor VIII, unlike other factors, is chiefly produced by endothelial cells rather than by hepatocytes. In fact, due to its reduced metabolism by hepatocytes in the state of liver failure, factor VIIl levels are often elevated.
Classically seen in the setting of fulminant liver injury which may be due to the infections, drugs, autoimmune hepatitis, ischemic hepatitis/shock liver, or rarely in Wilson's disease due to massive hepatocyte destruction.
One of the hallmark lab findings includes normal factor VIII levels. This is due to the fact that factor VIII, unlike other factors, is chiefly produced by endothelial cells rather than by hepatocytes. In fact, due to its reduced metabolism by hepatocytes in the state of liver failure, factor VIIl levels are often elevated.
Other miscellaneous causes include Acute fatty liver of pregnancy, fat embolism syndrome, amniotic fluid embolism, and other pregnancy-associated complications.
- Kirtan Patolia
Acquired Von willebrand disease
Von Willebrand disease is one of the most commonly encountered congenital bleeding disorders in clinical practice. Broadly speaking they are classified as type 1, 2A, 2B, 2M, 2N, and 3. Each one of them is distinct from the other in subtle ways.
However, it could be acquired in a number of ways.
a.) In patients with thrombocytosis > 1 million cells/ microliter, especially in essential thrombocythemia, loss of HMW vWD multimers leads to reduced vWF Ristocetin activity: vWF antigen ratio (<0.6) suggesting type 2 like pattern.
b.) In patients with aortic stenosis, due to extreme shear stress, vWF unfolds prematurely at the site of the valve revealing ADAMTS13 binding sites, ultimately resulting in its cleavage and loss of HMW multimers. So basically, it could be visualized as the pattern that is just opposite to TTP wherein defective ADAMTS13 activity results in excess of HMW vWF multimers.
It is often associated with either angiodysplasia or AVMs of the GI tract that further predisposes to bleeding. Although the exact pathogenesis of these lesions is not understood, one postulated mechanism suggests chronic colonic ischemia leading to sympathetic nervous system-induced vasodilation as a potential culprit.
In this context, it is also known as Heyde's syndrome.
c.) Sometimes in severe hypothyroidism, often the production of vWF by endothelial cells itself is markedly reduced.
d.) Rarely in the setting of multiple myeloma and various other neoplasms, tumor cells express the excess of Gpllb/llla leading to enhanced clearance of vWF from circulation.
One of the common lab findings in acquired vWD is reduced vWF Ristocetin activity: vWF antigen ratio pointing to the disproportionate decrease in activity compared to antigen levels.
It is due to the loss of HMW multimers.
- Kirtan Patolia
However, it could be acquired in a number of ways.
a.) In patients with thrombocytosis > 1 million cells/ microliter, especially in essential thrombocythemia, loss of HMW vWD multimers leads to reduced vWF Ristocetin activity: vWF antigen ratio (<0.6) suggesting type 2 like pattern.
b.) In patients with aortic stenosis, due to extreme shear stress, vWF unfolds prematurely at the site of the valve revealing ADAMTS13 binding sites, ultimately resulting in its cleavage and loss of HMW multimers. So basically, it could be visualized as the pattern that is just opposite to TTP wherein defective ADAMTS13 activity results in excess of HMW vWF multimers.
It is often associated with either angiodysplasia or AVMs of the GI tract that further predisposes to bleeding. Although the exact pathogenesis of these lesions is not understood, one postulated mechanism suggests chronic colonic ischemia leading to sympathetic nervous system-induced vasodilation as a potential culprit.
In this context, it is also known as Heyde's syndrome.
c.) Sometimes in severe hypothyroidism, often the production of vWF by endothelial cells itself is markedly reduced.
d.) Rarely in the setting of multiple myeloma and various other neoplasms, tumor cells express the excess of Gpllb/llla leading to enhanced clearance of vWF from circulation.
One of the common lab findings in acquired vWD is reduced vWF Ristocetin activity: vWF antigen ratio pointing to the disproportionate decrease in activity compared to antigen levels.
It is due to the loss of HMW multimers.
- Kirtan Patolia
Saturday, February 29, 2020
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