Test: Hemodynamics- 1 - NEET PG MCQ

The extrinsic pathway is triggered when plasma comes into contact with surfaces that carry a negative charge.

However, when plasma interacts with negatively charged surfaces, it actually activates the intrinsic pathway rather than the extrinsic one.

The attachment of clotting factors II, VII, IX, and X to calcium is reliant on the γ carboxylation of glutamic acid residues present in these proteins. This process necessitates the presence of vitamin K as a cofactor.

Na⁺ and water retention is currently the primary factor contributing to oedema in nephrotic syndrome. For further information, please refer to the chapter on the kidney. It is essential to differentiate receptor Na⁺ and water retention from option (a), which involves Na⁺ and water restriction.

The complex eliminates thrombin and simultaneously activates protein C, which then inactivates the activated factors V and VIII.

All endothelial cells, with the exception of those in the cerebral microcirculation, generate thrombomodulin, a protein associated with thrombin, and display it on their surface.

• Protein C and protein S are anticlotting proteins that depend on vitamin K (notably, factors II, VII, IX, and X are also vitamin K-dependent clotting factors).
• These proteins function by inactivating factors Va and VIIIa.

Thromboxane A₂ (TXA₂) is produced and released by activated platelets (not white blood cells). TXA₂ acts as a potent vasoconstrictor and bronchoconstrictor. Low-dose aspirin (50-325 mg) serves as an antiplatelet medication because it irreversibly inhibits COX, thereby reducing the production of TXA₂ by platelets.

VWF (von Willebrand Factor) is generated by endothelial cells and is essential for the binding of platelets to collagen and various other substances.

Consequently, it functions as a procoagulant factor.

The individual described in the question stem is likely suffering from liver cirrhosis as a result of chronic alcohol consumption. Key aspects of this condition include:

• A decrease in hepatic albumin synthesis, which is the primary factor influencing plasma oncotic pressure.
• Ascites, which occurs due to heightened sodium and water retention, a consequence of the activation of the renin-angiotensin-aldosterone system (RAAS).
• A lesser contribution from hydrostatic forces, stemming from intra-hepatic scarring and partial blockage of portal venous return, leading to fluid transudation and enhanced hepatic lymph secretion.

Examples of tissue macrophages include:

• Kupffer cells (found in the liver)
• alveolar macrophages (located in the lung)
• osteoclasts (present in bone)
• Langerhans cells (located in the skin)
• microglial cells (found in the central nervous system)

In the lungs, alveolar macrophages have the ability to phagocytose red blood cells that gather in the alveoli of individuals experiencing congestive heart failure. These macrophages contain hemosiderin and are known as “heart failure cells.”

• Hodgkin’s disease (option B) leads to the formation of large splenic nodules, containing Reed-Sternberg cells surrounded by mature lymphocytes, eosinophils, and neutrophils.
• Rheumatoid arthritis (option C) and various other chronic inflammatory conditions cause reactive hyperplasia of the spleen, resulting in numerous large germinal centres within the splenic follicles.
• Sickle cell anaemia (option D) causes multiple small infarctions in the spleen, which are often triangular in shape.

• Antibodies are formed against the phospholipid beta–2-glycoprotein 1 complex.
• These antibodies also attach to the cardiolipin antigen, causing false positive results in syphilis tests.
• Additionally, they disrupt in vitro clotting times, which is why they are termed lupus anticoagulants.

The lungs possess a dual blood supply, which results in the occurrence of red infarcts. These infarcts can be classified as either red (haemorrhagic) or white (anaemic) and may also be either septic or bland.

• All infarcts typically exhibit a wedge shape, with the occluded vessel located at the apex and the periphery of the organ constituting the base.
• Microscopically, the infarct displays characteristics of ischaemic coagulative necrosis.

The elements that increase the risk of venous thrombosis were first outlined by Virchow in 1856 and are referred to as Virchow’s triad. These factors consist of:

• Stasis
• Vascular damage
• Hypercoagulability

A mutation in the factor V gene occurs due to the replacement of glutamine for the typical arginine residue at position 506. This alteration is referred to as the Leiden mutation, which is the most prevalent inherited reason for hypercoagulability.

Note: The Lisbon mutation is linked to a mutation in the thyroid peroxidase gene.

Hemorrhagic infarction can occur in:

• Hypercoagulable conditions (such as the use of OCPs, pregnancy, polycythemia vera, malignancies, etc.)
• Embolism - The infarct results from the breakdown of a clot, which exposes the infarcted tissue and its permeable capillary network to circulating blood.
• Venous thrombosis.

Hyperviscosity is observed in:

• Multiple myeloma
• Lymphoplasmacytic lymphoma (Waldenström’s macroglobulinemia)
• Cryoglobulinaemia
• Myeloproliferative disorders
• MGUS (Monoclonal Gammopathy of Uncertain Significance)

In the case of MGUS:

• The M Protein can be detected in the serum of 1% of healthy individuals over 50 years old.
• This percentage increases to 3% in those older than 70 years.
• It represents the most prevalent type of monoclonal gammopathy.
• In MGUS, there is less than 3 g/dL of monoclonal protein in the serum and no presence of Bence Jones proteinuria.

The normal viscosity of blood is 1.8.