Study Medicine 📖🩺

Perioperative Management of Patients Taking Direct Oral Anticoagulants

Paget-Schroetter Syndrome.


This condition should be considered for those patients who present with axillary-subclavian vein thrombosis that is associated with strenuous and repetitive activity of the upper extremities. 

Primary upper extremity deep vein thrombosis is defined as thrombosis of the deep veins that drain the upper extremity (axillary, subclavian) due to an underlying anatomic anomaly at the thoracic outlet causing compression or repetitive venous injury (ie, repetitive trauma to the endothelium of the subclavian vein).

It will often present in young individuals. It presents as a sudden and severe upper extremity pain and swelling following vigorous upper extremity activity.

Doppler ultrasound is the preferred initial test. Some consider performing CT venography or Contrast-enhanced MRI imaging.

An aggressive multimodal treatment strategy consisting of anticoagulation, catheter-directed thrombolysis, with or without early thoracic outlet decompression, is oftentimes needed.

Thoracic outlet decompression involves resection of the first rib, division of the scalenus muscles and the costoclavicular ligament.

Patients with an acutely symptomatic, primary upper extremity DVT should be given anticoagulation for at least 3 months. Patients who develop moderate-to-severe acute symptoms who are diagnosed with primary upper extremity deep vein thrombosis, should be considered for thrombolysis and anticoagulation over anticoagulation alone. Subsequently, patients with moderate-to-severe symptoms should be considered for thoracic outlet decompression. This approach decreases the risk for recurrent thrombosis and post-thrombotic syndrome.

Paget-Schroetter Syndrome.

Factor Deficiency

PHYSICIANS'
CANCER CHEMOTHERAPY
D R U G MANUAL

DDAVP Should be avoided in :
- Type II vWD (IIB)
- Type 1C
- Type III
- Hemophilia B
- Epidural anesthesia during pregnancy prior to delivery

Treatment of Suspected ITP

Cancer Associated Thrombosis + Thrombocytopenia

Majeed syndrome is a rare condition in which patients will have recurrent episodes of fever and inflammation in the bones and skin. One of the major features of Majeed syndrome is an inflammatory bone condition known as chronic recurrent multifocal osteomyelitis (CRMO). This condition causes recurrent episodes of pain and joint swelling beginning in infancy or early childhood. These symptoms persist into adulthood, although they may improve for short periods of time. CRMO can lead to complications such as slow growth and the development of joint deformities (contractures), which restricts the movement of certain joints.

Another feature of Majeed syndrome is the development of a blood disorder, Congenital dyserythropoietic anemia.

Most patients with Majeed syndrome also develop inflammatory disorders of the skin, most often a condition known as Sweet syndrome. The symptoms of Sweet syndrome include fever and the development of painful bumps or blisters on the face, neck, back and arms.

It is inherited in an autosomal recessive manner. Majeed syndrome results from mutations in the LPIN2 gene. This gene provides instructions for making a protein called lipin-2. This protein may play a role in the processing of fats, controlling inflammation and in cell division.

The treatment for this disease is uncertain. However, reports suggests that for severe disease, IL-1β blockade has been reported to be highly effective at controlling osseous and systemic inflammation. MTX and bisphosphonates have also shown to be beneficial

Genetic of Hereditary Hemochromatosis

Treatment of acute acquired methemoglobinemia:

➡️A offending agent should be removed and/or discontinued.

The most commonly implicated agents include dapsone, local (topical) anesthetic agents, aniline dyes, and high nitrate levels in water supplies.

➡️In asymptomatic patients, usually those with methemoglobin levels <20 percent, no therapy other than discontinuation of the offending agent.

➡️If the patient is symptomatic does not have(G6PD) deficiency, use IV Methylene blue. 
The usual dose in this setting is 1 to 2 mg/kg, given over five minutes. 

➡️If a patient has G6PD deficiency, should be offered Ascorbic acid.

..

Common antibodies used in flow cytometric immunophenotyping of acute leukemia include: 
Stem cell/hematopoietic precursors:
CD34 [Early precursor]
HLA-DR [Positive in most cases of AML, negative in APL]
Terminal deoxynucleotidyl transferase/TdT

Myeloid markers:
cMPO
CD13
CD33
CD117
CD15

Monocytic markers:
CD64, CD14, CD11b, CD11c, Lysozyme

Erythroid:
CD71, CD235a

Megakaryocytic:
CD41 [Platelet Glycoprotein IIb/IIIa complex]
CD61, CD36, CD42b

B lymphoid markers:
CD19, CD10, CD20, CD22, CD79a
Tdt (Moderate to Bright)

T lymphoid markers:
CD3, CD5, CD7, CD1a, CD2, CD4, CD8

Natural killer:
CD56

*Lymphomas: *
-t(8;14) = MYC-IgH = BL
-t(2;8) = IgK-MYC = BL
-t(8;22) = MYC-IgL = BL
-t(14;18) = IgH-BCL2 = FL
-t(2;18) = IgK-BCL2 = FL
-t(18;22) = BLC2-IgL = FL
-t(11;14) = CCND1-IgH = MCL

-t(11;18) = API2-MALT1 = MZL H. pylori-
-t(2;5) = NPM1-ALK = ALCL ALK+
-t(6;7) = DUSP22-FRAH7H = ALCL ALK-
-iso7q = HSTCL
-inv(14) = t(14;14) = MTCP1 = T-PLL
-t(X;14) = TCL1 = T-PLL
-del(11q) = ATM = CLL (intermediate)
-del(13q) = RB1 = CLL (good)
+12 = CLL (good)

*Myelomas*
-t(4;14) = FGFR3-IgH = Myeloma (intermediate risk with bortezomib)
-1q gain (4 or more) = Myeloma (high risk)
-t(14;16) = IgH-cMAF = Myeloma (high risk)
-t(14;20) = IgH-MAFB = Myeloma (high risk)
-del(17p) = TP53 = Myeloma (high risk)
-t(9;22) = BCR-ABL1 = CML/B-ALL/AML (rare)

*Leukemias*
-t(8;21) = RUNX1-RUNX1T1 = AML (good risk)
-inv(16) = t(16;16) = CBFB-MYH11 = AML with eos (good risk)
-t(15;17) = PML-RARA = APL
-t(11;17) = PLZF1-RARA = APL (rare+resistant to ATRA)
-t(5;17) = NPM1-RARA = APL (rare+sensitive to ATRA)
-t(11;17) = NuMA-RARA = APL (rare+sensitive to ATRA)
-t(17;17) = STAT5b=RARA = APL (rare+resistant to ATRA)
-t(9;11) = KMT2A-MLLT3 = AML (intermediate risk)
-t(6;9) = DEK-NUP214 = AML (poor risk)
-inv(3) = t(3;3) = MECOM/EVI1-GATA2 = AML (poor risk)
-t(1;22) = RBM15-MKL1 = Megakaryoblastic AML in children
-del(17p) = TP53 = AML (poor risk)
-5/-7 = alkylating induced t-MN
-11q23.3 translocations = KMT2A = topoisomerase II inhibitor induced t-MN
-t(12;21) = ETV6-RUNX1 = Childhood B-ALL (good risk)

chemotherapy extravasation management

Gaucher’s disease

Gaucher’s disease

How I treat thrombocytopenia in pregnancy 🤰

AML Treatment

Complications of Massive Blood Transfusion

⬆️PT/PTT = pRBC contain no coagulation factors
⬇️Platelet = pRBC contain no plt
⬇️Ca = Citrate in pRBC binds Ca
⬆️K = K leaks out of cells in stored RBCs
⬇️Temp (hypothermia) = RBC stored at 4°C
⬆️pH from metabolism of citrate to bicarb in pRBC.

Monitor:
PT/PTT, fibrinogen, ionized calcium, chemistries

Goals:
Temp >35 C
pH > 7.2
Lactate < 4
Plt > 50
INR < 1.5
Fibrinogen > 1 g/L

Great medicine tip sheet summarization

Hepatitis B - Serology

Encapsulated Bacteria 🦠

CD Antigens

https://youtu.be/_CWMUt8Xi_Y?si=6qluSTG81CaGpMxP

Iron absorption

Hematology Board Review

initial treatment of immune thrombotic thrombocytopenic purpura (TTP)

Porphyria

pseudo pelger huet neutrophils

Babesiosis

Majeed syndrome is a rare condition in which patients will have recurrent episodes of fever and inflammation in the bones and skin. One of the major features of Majeed syndrome is an inflammatory bone condition known as chronic recurrent multifocal osteomyelitis (CRMO). This condition causes recurrent episodes of pain and joint swelling beginning in infancy or early childhood. These symptoms persist into adulthood, although they may improve for short periods of time. CRMO can lead to complications such as slow growth and the development of joint deformities (contractures), which restricts the movement of certain joints.

Another feature of Majeed syndrome is the development of a blood disorder, Congenital dyserythropoietic anemia.

Most patients with Majeed syndrome also develop inflammatory disorders of the skin, most often a condition known as Sweet syndrome. The symptoms of Sweet syndrome include fever and the development of painful bumps or blisters on the face, neck, back and arms.

It is inherited in an autosomal recessive manner. Majeed syndrome results from mutations in the LPIN2 gene. This gene provides instructions for making a protein called lipin-2. This protein may play a role in the processing of fats, controlling inflammation and in cell division.

The treatment for this disease is uncertain. However, reports suggests that for severe disease, IL-1β blockade has been reported to be highly effective at controlling osseous and systemic inflammation. MTX and bisphosphonates have also shown to be beneficial.

Treatment of acute acquired methemoglobinemia:

➡️A offending agent should be removed and/or discontinued.

The most commonly implicated agents include dapsone, local (topical) anesthetic agents, aniline dyes, and high nitrate levels in water supplies.

➡️In asymptomatic patients, usually those with methemoglobin levels <20 percent, no therapy other than discontinuation of the offending agent.

➡️If the patient is symptomatic does not have(G6PD) deficiency, use IV Methylene blue. 
The usual dose in this setting is 1 to 2 mg/kg, given over five minutes. 

➡️If a patient has G6PD deficiency, should be offered Ascorbic acid.