📚 NEET MDS Lecture Notes
Adult Respiratory Distress Syndrome
General PathologyAdult Respiratory Distress Syndrome
A constellation of pathologic and clinical findings initiated by diffuse injury to alveolar capillaries. This syndrome is associated with a multitude of clinical conditions which primarily damage the lung or secondarily as part of a systemic disorder.
Pathogenesis
There are many types of injuries which lead to the ultimate, common pathway, i.e., damage to the alveolar capillary unit. The initial injury most frequently affects the endothelium, less frequently the alveolar epithelium. Injury produces increased vascular permeability, edema, fibrin-exudation (hyaline membranes). Leukocytes (primarily neutrophils) plays a key role in endothelial damage.
Pathology
Heavy, red lungs showing congestion and edema. The alveoli contain fluid and are lined by hyaline membranes.
Pathophysiology
Severe respiratory insufficiency with dyspnea, cyanosis and hypoxemia refractory to oxygen therapy.
Mylohyoid Muscle
AnatomyMylohyoid Muscle
- Origin: Mylohyoid line of the mandible.
- Insertion: Median raphe and body of the hyoid bone.
- Nerve Supply: Nerve to mylohyoid (branch of the trigeminal nerve, CN V3).
- Arterial Supply: Sublingual branch of the lingual artery and submental branch of the facial artery.
- Action: Elevates the hyoid bone, base of the tongue, and floor of the mouth; depresses the mandible.
Cell, or Plasma, membrane
PhysiologyCell, or Plasma, membrane
- Structure - 2 primary building blocks include
protein (about 60% of the membrane) and lipid, or
fat (about 40% of the membrane).
The primary lipid is called phospholipids, and molecules of phospholipid form a 'phospholipid bilayer' (two layers of phospholipid molecules). This bilayer forms because the two 'ends' of phospholipid molecules have very different characteristics: one end is polar (or hydrophilic) and one (the hydrocarbon tails below) is non-polar (or hydrophobic):
- Functions include:
- supporting and retaining the cytoplasm
- being a selective barrier .
- transport
- communication (via receptors)
THROMBOSIS
General PathologyTHROMBOSIS
Pathogenesis (called Virchow's triad):
1. Endothelial* Injury ( Heart, Arteries)
2. Stasis
3. Blood Hypercoagulability
- Endothelial cells are special type of cells that cover the inside surface of blood vessels and heart.
CONTRIBUTION OF ENDOTHELIAL CELLS TO COAGULATION
Intact endothelial cells maintain liquid blood flow by:
1- inhibiting platelet adherence
2- preventing coagulation factor activation
3- lysing blood clots that may form.
Endothelial cells can be stimulated by direct injury or by various cytokines that are produced during inflammation.
Endothelial injury results in:
1- expression of procoagulant proteins (tissue factor and vWF)→ local thrombus formation.
2- exposure of underlying vWF and basement membrane collagen → platelet aggregation and thrombus formation.
RESPONSE OF VASCULAR WALL CELLS TO INJURY( PATHOLOGIC EFFECT OF VASCULAR HEALING)
Injury to the vessel wall results in a healing response, involving:
- Intimal expansion (proliferating SMCs and newly synthesized ECM). This involves signals from ECs, platelets, and macrophages; and mediators derived from coagulation and complement cascades.
- luminal stenosis & blockage of vascular flow
Causes of Endothelial injury
1. Valvulitis
2. MI
3. Atherosclerosis
4. Traumatic or inflammatory conditions
5. Increased Blood Pressure
6. Endotoxins
7. Hypercholesterolemia
8. Radiation
9. Smoking
Stasis
- Stasis is a major factor in venous thrombi
- Normal blood flow is laminar (platelets flow centrally in the vessel lumen, separated from the endothelium by a slower moving clear zone of
plasma)
- Stasis and turbulence cause the followings:
Disuption of normal blood flow
prevent dilution of activated clotting factor
retard inflow of clotting factor inhibitor
promote endothelial cell injury
Causes of Stasis
1. Atherosclerosis
2. Aneurysms
3. Myocardial Infarction ( Non-cotractile fibers)
4. Mitral valve stenosis (atrial dilation)
5. Hyper viscosity syndromes (PCV and Sickle Cell anemia)
Hypercoagulability
A. Genetic (primary):
- mutations in the factor V gene and the prothrombin gene are the most common
B. Acquired (secondary):
- multifactorial and more complicated
- causes include: Immobilization, MI, AF, surgery, fracture, burns, Cancer, Prosthetic cardiac valves
MORPHOLOGY OF THROMBI
Can develop anywhere in the CVS (e.g., in cardiac chambers, valves, arteries, veins, or capillaries).
Arterial or cardiac thrombi→ begin at sites of endothelial injury; and are usually superimposed on an atherosclerotic plaque.
Venous thrombi → occur at sites of stasis. Most commonly the veins of the lower extremities (90%)
Thrombi are focally attached to the underlying vascular surface; arterial and venous thrombi both tend to propagate toward the heart.
→ The propagating portion of a thrombus is poorly attached → fragmentation and embolus formation
LINES OF ZAHN
Thrombi can have grossly (and microscopically) apparent laminations called lines of Zahn; these represent pale platelet and fibrin layers alternating with darker erythrocyte-rich layers.
Such lines are significant in that they represent thrombosis of flowing blood.
Mural thrombi = Thrombi occurring in heart chambers or in the aortic lumen.
Causes: -Abnormal myocardial contraction (e.g. arrhythmias, dilated cardiomyopathy, or MI) -endomyocardial injury (e.g. myocarditis, catheter trauma)
Vegetations ->Thrombi on heart valves
1- Bacterial or fungal blood-borne infections - (infective endocarditis,).
2- Non-bacterial thrombotic endocarditis occur on sterile valves.
Fate of thrombi
1. Propagation → Thrombi accumulate additional platelets and fibrin, eventually causing vessel obstruction
2. Embolization → Thrombi dislodge or fragment and are transported elsewhere in the vasculature
3. Dissolution → Thrombi are removed by fibrinolytic activity (Usually in recent thrombi)
4. Organization and recanalization → Thrombi induce inflammation and fibrosis. - recanalization (re-establishing some degree of flow) - Organization = ingrowth of endothelial cells, smooth cells and fibroblasts into the fibrin rich thrombus.
5. Superimposed infection (Mycotic aneurysm)
Venous thrombi → most common in veins of the legs
a. Superficial: e.g. Saphenous veins. - can cause local congestion, swelling, pain, and tenderness along the course of the involved vein, but they rarely embolize
a. Deep: e.g. Popliteal, Femoral and iliac vein. - more serious because they may embolize - can occur with stasis or hypercoagulable states