Test: Hemodynamics- 2 - NEET PG MCQ

As mentioned, the majority of pulmonary emboli (between 60% and 80%) remain clinically undetected as they tend to be small in size. Over time, these emboli become organised and are integrated into the vascular wall.

• Obstruction of medium-sized arteries by emboli can lead to pulmonary haemorrhage.
• However, it typically does not result in pulmonary infarction, due to the dual blood supply to the region provided by the bronchial circulation.

Hyperhomocystenemia^Q is a mixed condition (both inherited and acquired) that can lead to thrombosis in both venous and arterial systems.

Hemostasis consists of five distinct phases:

• Vessel spasm.
• Formation of the platelet plug.
• Blood coagulation or the creation of an insoluble fibrin clot.
• Clot retraction.
• Clot dissolution.

Glycoprotein IIb/IIIa inhibitors (tirofiban, eptifibatide, and abciximab) inhibit the function of the specific platelet surface receptor glycoprotein complex, which is essential for the creation of fibrinogen connections between neighbouring platelets (platelet aggregation).

The patient experiences extended immobilisation of the limb, leading to venous stasis that contributes to both superficial and deep venous thrombosis. The most concerning complication of the venous thrombi is the risk of embolisation to the lungs.

Gangrene can develop as a result of arterial obstruction rather than venous obstruction.

Hematomas typically manifest immediately following trauma and are expected to decrease in size after 12 days, as indicated in the question stem.

Fat embolism occurs following fractures, with symptoms emerging 1-3 days post-trauma.

The differential diagnosis for recurrent spontaneous abortions in women encompasses:

• Deficiencies in protein C and protein S
• The existence of the lupus anticoagulant, which is associated with the anti-phospholipid syndrome

An embolus is a mass that has detached from a blood vessel and is transported by the bloodstream to a location different from its origin. Most emboli are derived from thrombi (thrombotic emboli); however, they can also arise from substances that are not thrombi (non-thrombotic emboli). Examples of non-thrombotic emboli include:

• Fat emboli
• Air emboli
• Amniotic fluid emboli

Fat emboli, which occur as a result of severe injuries and fractures of long bones, will exhibit a positive reaction to oil red O stain or Sudan black stain. These can be life-threatening, as they may harm the endothelial cells and pneumocytes in the lungs.

Lab tests in DIC show the following:

• Reduced platelet count
• Extended aPTT/PT/TT
• Lowered fibrinogen levels
• Increased fibrin degradation products (D-dimers)

• Peripheral vasodilation and blood pooling
• Activation or injury of the endothelium
• Damage caused by leukocytes
• Disseminated intravascular coagulation
• Activation of cytokine cascades

• Thrombosis
• Increased vascular permeability
• Vasodilation

D-dimer is a product of fibrin degradation, consisting of a small protein fragment found in the bloodstream following the breakdown of a blood clot via fibrinolysis. It is termed D-dimer because it comprises two crosslinked D fragments from the fibrinogen protein. The concentration of D-dimer can be measured through a blood test, which assists in diagnosing thrombosis.

• D-dimer testing is clinically relevant when there is a suspicion of deep venous thrombosis (DVT) or pulmonary embolism (PE).
• In cases where disseminated intravascular coagulation (DIC) is suspected, D-dimers can help in the diagnostic process.

Shock lung is commonly referred to as acute respiratory distress syndrome, diffuse alveolar damage, acute alveolar injury, and acute lung injury.

Shock is defined by the dysfunction of several organ systems as a result of systemic hypoperfusion, which occurs due to either a decrease in cardiac output or a reduction in effective circulating blood volume.

• Liver → Fatty changes accompanied by central necrosis with bleeding.
• Kidneys → Significant tubular ischemic injury (Acute tubular necrosis).
• Lungs → Pulmonary congestion along with widespread alveolar damage.
• Adrenal → Lipid depletion in cortical cells.
• Brain → Ischemic encephalopathy.
• Heart → Coagulative necrosis or contraction band necrosis.
• GIT → Hemorrhagic enteropathy.

Respiratory distress occurs immediately after amniotic fluid embolism, as the emboli, which comprise squamous cells, lanugo, and mucus, accumulate in the pulmonary microcirculation, leading to multiple small pulmonary infarcts.

• The severe respiratory distress may also indicate the effects of prostaglandins and other bioactive substances that are found in high levels in the amniotic fluid embolus.
• Placental abruption (option a) does not result from an amniotic fluid embolism.
• Renal failure (option b) is most likely triggered during the peri-partum period by factors such as eclampsia, hypovolemic shock, and ascending infections.
• Amniotic fluid embolism can also lead to shock and renal failure.
• Splinter haemorrhages (option d) are small bleeding spots observed on the fingers and toes due to micro emboli originating in the arterial circulation.

Amniotic fluid emboli develop in the veins and then migrate to the lungs.

Dysfibrinogenemia produces hypercoagulable state and leads to thrombus formation in some patients. Other causes have already been discussed.