Draw the Cranial Nuclei

Part 1: Understanding motor and sensory tracts in the brainstem and spinal cord

Part 2: Adding in the cranial nerve nuclei

Learning medicine through questions

FOR MORE QUESTIONS, COME VISIT OUR FACEBOOK PAGE. WE WILL BE REGULARLY UPLOADING NEW QUESTIONS THROUGHOUT THE WEEK.

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We’ve all heard the theories on different study methods and finding the right type for each of us. Some of us are auditory learners, some of us are visual. Recently I’ve experimented with learning through questions. After all, we need to recall the knowledge when prompted by the question.

I’ve made a few questions and answers for you guys to sample and see if it suits you.

Click for ANSWER

 

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Click for ANSWER: 

 

 

For more questions, come visit our Facebook page. WE WILL be regularly uploading new questions throughout the week.

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Fighting Cancer

This TED talk really got me excited, particularly now that we have finished our oncology block and starting microbiology. I love these radical approaches that could potentially revolutionise our current thinking and therapeutic approaches. Watch this short video and let us know what you think

HS

Tests in clotting disorders

The following are some tests ordered when assessing/diagnosing some clotting diseases.

Platelet tests:

A normal platelet count would yield ~ 150 – 400 x 10^9 /L platelets.

Bleeding time (BT) evaluates the platelet function up to the formation of the temporary platelet thrombus (primary hemostasis). A normal bleeding time is around 2 – 7 mins.

Platelet aggregation tests look at the aggregation response in response to regents such as ADP, adrenaline, collagen and ristocetin (induces platelet aggregation).

Tests for von Willebrand  factor (vWF) include ristocetin cofactor activity or vWF antigen assays. Ristocetin cofactor activity evaluates the function of vWF, where as the assays measures the quantity of vWF present in the serum.

Coagulation tests:

Prothrombin time (PT) assesses the extrinsic and common coagulation pathway. It involves factors VII, X, II and I. A normal PT is around 11 to 15 seconds. PT is commonly used to evaluate liver synthetic function, detect factor VII deficiency or monitor patients who are on warfarin.

The International normalized ratio (INR) is a value derived from PT, used as a standard to monitor patients on warfarin. While varying with the condition, a normal INR target for warfarin patients is between 2-3.

The activated Partial Thromboplastin Time (aPTT) evaluates the intrinsic and common pathway. The factors involved are XII, XI, IX, VIII, X,V,II,I. The normal reference interval would be 25-40 seconds. It is most commonly used to monitor heparin anticoagulation therapy. It’s also used to detect factor deficiencies in the intrinsic coagulation system.

Fibrinolytic sytem tests:

Fibrin(ogen) degradation products (FDP) are used to detect fragments associated with the plasmin degradation of fibrinogen or insoluble fibrin in the fibrin clots.

D-Dimer assays are specific tests that determine degradation of cross-linked fibrin monomers only. It does not detect fibrinogen degradation products as they do not form cross-links. It’s of particular clinical use when assessing deep vein thrombosis, pulmonary thromboembolisms and disseminated intravascular coagulation.

Reference:

Goljan Rapid review Pathology 4^th edition

Knowing your anti-coagulants and anti-platelets

I’ve noticed as a student that lots of people get them confused. It’s simple because they both thin the blood right?

Unfortunately, it’s not appropriate to mix up the two terms. Precision is key guys!

Want a quick two min crash course? Read on!

Anti-platelets

Affect primary hemostasis as they target platelet aggregation. Platelet aggregation involves linking to other platelets through fibrinogen through receptors called glycoprotein 2b3a (GP2b3a). This linking forms a platelet plug.

Aspirin – inactivates cyclo-oxygenase 1 (COX-1) there by reducing Thromboxane A2 (TXA2) which promotes aggregation. Clopidogrel – inhibit ADP dependent aggregation. This reduces the ability for the GP2b3a receptor to be expressed. GP2b3a antagonists (Abciximab) – prevents fibrinogen to bind to the receptor.

Anti-coagulants

Act on the coagulation cascade. The coagulation cascade occurs in secondary hemostasis with the primary goal to convert fibrinogen into fibrin. This would stabilize the platelet plug as fibrin a lot more stable than fibrinogen.

Warfarin – prevents the synthesis of Vit K dependent coag factors (2,7,9,10, C and S). Heparin – activates anti-thrombin 3 (AT3) and has an effect on thrombin and Xa. Low Molecular Weight Heparin – activate AT3 but only has an effect on Xa. Xa inhibitors – inhibit Xa. Direct thrombin inhibitors inhibits thrombin.

From this, I hope you can see why it’s very wrong to call warfarin an anti-platelet. Similarly, aspirin is not an anti-coagulant.

3 Conditions to Form Thrombus

Thrombus are the pathological formation of intravascular blood clots that are attached to the vessel wall (If it’s not attached, it could be an embolus!). This can either be in an artery or a vein, each leading to different complications. The most common type of thrombus is a Deep Vein Thrombus (DVT) in the leg below the knee.

Cause of a thrombus:

The causes closely relate to Virchow’s triad

1. Disruption of normal blood flow:

Normal blood flow is expected to be linear and non-turbulent. When blood stops flowing (stasis) or becomes turbulent, clots start to form.

For example:

• Stasis:
  • Due to immobilisation / prolonged bedrest
  • Left atrial dilatation due to mitral stenosis
• Turbulent flow:
  • Arterial stenosis (narrowing of the vessels)
  • Cardiac wall dysfunction
  • Atrial fibrillation

2. Endothelial damage:

Damage to the vessel walls expose the subendothelial collagen fibres and trigger platelet adhesion, aggregation and the clotting cascade to occur (listen to our haemostasis podcast).

Diseases that precipitate thrombi formation from vessel damage include:

• Atherosclerosis
• Vasculitis
• High levels of homocysteine (from B12 and Folate deficiency)
  • can lead to atherosclerosis
• Cigarette smoking

3. Where the blood is in a hypercoagulable state

A disease causes a hypercoagulable state in the blood by having either too much pro-coagulation factors or too little anti-coagulant proteins. Patients with these diseases will present with recurrent DVTs or at a very young age.

Disease include:

• Activation of coagulation system
  • Disseminated Intravascular Coagulation (DIC)
• Hereditary or acquired factor deficiencies
  • Hereditary antithrobin III deficiency
  • Oral Contraceptives (Estrogen)
• Antiphospholipid syndrome
  • Due to lupus anticoagulant
• Thrombocytosis: (Too many platelets)
  • Malignancy

References:

• Pathoma 2011
• Goljan Rapid Review of pathology 4th ed.

Head Transplant

I don’t know how I feel about this.  This is either science gone mad or huge progress in surgical advancement.  I’m not a believer in god but I can’t help but wonder if medical science has gotten so advance that we are beginning to play the role of god.

Also so many ethical issues to think about. It challenges the notion of our identify and self-hood. Imagine the impact this has on the family members of the transplant recipient and donor.

Very spooky medicine. Check out part of the talk:

HS

Tests and markers in hemolysis

Direct and Indirect Coombs test:

Their use is to detect antibodies that BIND to the surface of red blood cells (RBC).

Basic principle:

     Anti-Human Globulins (AHG) are mixed with the patient’s RBCs. If the RBC has the antibodies attached, the AHG will bind to those antibodies and bind RBCs together. This will lead to agglutination – a visible clumping of red blood cells.

Direct Coombs’ test:

Is used to detect antibodies already attached onto the red blood cell. This could be for cases such as immune mediated haemolytic anaemias.

Steps:

1. Add AHG to washed red cell
   • Washed = removing the patient’s own plasma
2. Wait and see if there is agglutination.

Indirect Coombs’ test:

This test is used to determine antibodies in patient’s serum that is unbound to their red blood cells. This is useful in cases such as crossmatching prior to transfusion, and also in pre-natal screening of pregnant women.

Steps:

1. Serum from the patient is cultured with RBCs of a known antigenicity from another patient.
2. This process allows binding of antibodies to RBCs in vitro
3. AHG then added to RBC
4. Wait and see if there is agglutination

          Still unclear? Watch a youtube video

Serum Haptoglobin:

An indication of serum haptoglobin is to determine if hemolysis is present.

Haptoglobin is a protein produced by the liver and is found in the blood. Haptoglobin binds to free hemoglobin released from red blood cells. The Haptoglobin-hemoglobin complex will then be removed by the reticulo-endothelial system.

Hemoglobin is released in large quantities into the blood during hemolysis. This will cause lots of serum haptoglobin to bind to hemoglobin and consequently be removed.

Thus, during hemolysis, it is reasonable to expect haptoglobin levels to decrease.

Lactate Dehydrogenase (LDH) levels

Is an enzyme found in almost all cells. There are many indications to test for LDH levels. During haemolytic anaemias, the lysis of red blood cells causes a release of LDH into the blood. Thus it is reasonable to expect LDH levels as a marker of hemolysis.

Another indication for observing LDH levels is when the patient experiences muscle trauma or injury as it can also indicate tissue damage.

References:

1. Kumar P, Clark M. Kumar & Clark Clinical Medicine. 5th ed. London: Elsevier limited; 2002.
2. Hoffbrand A, Moss P. Essential Haematology. 6th ed. Oxford: Wiley-Blackwell; 2011.

The FIVE white blood cells you must know.

White blood cells can be classified as either phagocytes or immunocytes. Of the phagocytes they can be further classified as granulocytes (Basophils, Eosinophils and Neutrophils) as well as monocytes. The immunocytes are the lymphocytes including B and T cells and Natural Killer Cells.

The following is a short blurb on what each does:

Basophils: Are the least common leucocyte, contributing to less than 1% of circulating leucocytes. They have a intensely basophilic (blue) granular appearance. Have IgE attachment sites that lead to histamine release for degranulation.  When migrated into the tissue, basophils mature into Mast Cells.

Eosinophils: Contribute towards 1% of circulating leucocytes. Stain red with eosin. Have a strong role in allergic responses and host defence against parasites. Their production is stimulated by IL-5. Release granules that contain basic proteins and also peroxides.

Neutrophils: Contribute 75% to the circulating leukocytes. Multi lobular nucleus with a granulated appearance. They usually maintain in the circulation. Only present in tissues in large numbers during acute inflammation, killing invading microorganisms via phagocytosis.

Monocytes: In the blood they are known as monocytes, once they migrate into the tissue they mature into macrophages (or histiocytes) . In different tissues they are known as different names.  You may know them by:

• Kidney: Intraglomerular mesangial cells
• Brain: Microglia
• Serosa: Macrophages
• Lung: Alveolar macrophages
• Liver: Küpffer cells
• Spleen: Sinus macrophages, Antigen Presenting Cells (APC)
• Bone Marrow: macrophages, APC
• Lymph nodes: macrophages, APC

Lymphocytes: Second most common circulating leukocytes making up nearly 25%. Appear round and have a densely stained nucleus. They include B cells, T cells and also NK cells.

Reference sources:

1. Young B, Lowe J, Stevens A, Heath J. Blood. Wheater’s Functional Histology. 5th ed. Philadelphia: Elsevier limited; 2006. p. 46–56.
2. Hoffbrand A, Moss P. White cells: Granulocytes and monocytes.Essential Haematology. 6th ed. Oxford: Wiley-Blackwell; 2011.