Resources: CDC, UpToDate, WHO website.
Video by Drashtant Prajapati, MBBS.
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
Wednesday, February 26, 2020
Congestive hepatopathy
Short post!
In congestive heart failure, the elevated pressure is transmitted from the right heart chambers (right ventricle and atrium) to the hepatic veins and sinusoids leading to intrahepatic edema, decreased perfusion and oxygen diffusion as well as hemorrhagic injury and modification on the hepatocyte architecture and atrophy with associated collagen deposition, and fibrosis to the hepatic veins and sinusoids.
In congestive heart failure, the elevated pressure is transmitted from the right heart chambers (right ventricle and atrium) to the hepatic veins and sinusoids leading to intrahepatic edema, decreased perfusion and oxygen diffusion as well as hemorrhagic injury and modification on the hepatocyte architecture and atrophy with associated collagen deposition, and fibrosis to the hepatic veins and sinusoids.
Sunday, February 23, 2020
Schroeder's Vs Bandl's ring
Schroeder's Vs Bandl's ring
Bandl's ring:-
1) It is seen in obstructed labour
2) It is a pathological ring
3) It is a retraction ring
4) It moves up with uterine contractions
5) It can be palpable per-abdominally but not pervaginally
(Remember- Bandl has A after B which stands for per-abdominally)
6) Management: Like obstructed labour, C-section and antibiotics.
Schroeder's ring:-
1) Seen when oxytocin is used injudiciously.
2) It is a physiological ring.
3) It is a constriction ring.
4) It is fixed ring, does not move with uterine contractions
5) It can be palpable pervaginally but not per-abdominally.
6) Management: It dissolves on it's own.
If not, then management in first stage of labour includes C-section.
Management in second stage includes forceps or c section.
That's it!
Demotional bloke
Friday, February 21, 2020
Post Partum Hemorrhage - Updates
Following bleeding scenarios amount to PPH under the latest WHO document
- Blood loss >500 mL in c/o Vaginal delivery
- Blood loss > 1 L in c/o C Section + in c/o twins
- Blood loss > 1.5 L in c/o Hysterectomy
- Blood loss on any case more than what is expected over a period of 24 hours
Following bleeding scenarios amount to PPH as per the latest ACOG recommendations
- Blood loss equal to or more than 1 L irrespective of mode of delivery
- Bleeding with signs and symptoms of hypovolemia
Updates in Management of PPH
- Uterine massage is added along with uterotonics
- PGE1 if given Per Rectally (not recommended), 1000 micrograms is advised
- Inj Tranexamic Acid is recommended in all bleeding diasthesis - 1 gram slow IV (over 20 minutes)
- Mechanical Devices allowed
- Sengstaken Blakemore Catheter
- Bakri Balloon Catheter
Tuesday, February 18, 2020
Actions of Intrinsic laryngeal muscles of Vocal cord mnemonic video
Hello!
This is video is on Actions of Intrinsic laryngeal muscles.
This is video is on Actions of Intrinsic laryngeal muscles.
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