general notions Flashcards
CONGESTION
• Definition
• Morphology
• Evolution:
• Definition:
– Congestion is the hyperemia which occurs through an arterial, active mechanism.
• Morphology
– Macroscopically:the aspect of the organ is:
• larger
• heavier
• blood-red
• warmer
• pulsatile
• painful
• Microscopically:
– enlarged capillaries, filled with blood
• Evolution:
– The pattern may return to normal when the causative factors dissapear
– Complications that may occur: edema and micro-hemorrhages
- Stasis: definition, causes, macroscopy, microscopy, types of stasis
What is STASIS
• Definition:
– Stasis is the hyperemia produced by a venous, passive mechanism.
• Pathogenesis:
– the presence of an obstacle in the lumen of a vein: thrombus, embolus
– the narrowing of the lumen secondary to a venous wall thickening: inflammation (phlebites)
- compression on a vein: neoplasia
Macroscopically:the aspect of the organ:
• Larger
• Heavier
• Colder
• cyanotic
• Microscopically: enlarged veins, filled with blood
• Types of stasis:
– local stasis
– regional stasis
– generalized stasis
Local stasis:
• stasis occurring in an organ with an obstacle at the level of its main draining venous system
• it may be acute described above or chronic.
Generalized stasis
• Definition:
– the stasis extended or generalized to all the organs of the body
• Pathogenesis:
– heart failure, due to a gradual decrease in the contractile force of the left ventricle
- Ischemia: definition, causes, macroscopy, microscopy, evolution
What is ISCHEMIA?
• Definition:
– the decrease of the arterial blood flow into a tissue or organ
• Pathogenesis: arterial obliteration due to:
– a. causes related to the arterial lumen:
• thrombi
• emboli
– b. causes related to the arterial wall:
• arteritis (inflammation of the arterial wall and narrowing of the lumen)
• atherosclerosis (inflamatory and metabolic disease with subendothelial deposition of lipids and inflammatory cells resulting in atheromas)
• accumulation of different substances (calcium, hyalin, amyloid, etc.)
• spastic contractions (under the action of various vasoconstrictive factors)
– c. causes related to external compressions:
• adenopathy (enlarged lymph nodes)
• tumors
• medical procedures: external ligature/compression
• Macroscopy:
– initially the organ is pale, then progressively it develops one of these two posibilities: necrosis or sclerous atrophy
• Microscopy:
– narrowing or disappearance of the arterial lumen
• Evolution:
I. The evolution depends on:
• the type of ischemia: total or partial
• the way of its installation: sudden or slowly progressive
– total and sudden ischemia leads to infarction (necrosis of the tissue caused by lack of oxigen, that is anoxic conditions)
– partial and slow ischemia leads to sclerous atrophy (sclerous = hardening of the tissuees due to replacement of the parenchima with fibrous tissue; atrophy = the decrease in the size of an organ)
II. Evolution is influenced by:
– 1. The resistance of the tissues to hypoxia:
• the Central Nervous System (neurons) resist 3-5 minutes
• the myocardial fibers resist 20-30 minutes
• the kidney resists for about 1 hour
• the skeletal muscle resist 8-10 hours
– 2. The type of vascularization:
• An existing double or collateral circulation (e.g. double circuit in the liver and lung, rich anastomotic network in the intestinal wall) reduces the consequences of the ischemia
• the terminal type circulation (heart, kidney, spleen and brain) has a very poor ability to compensate ischemia and the consequences are severe.
– 3. The speed with which the hypoxia is installed:
• Slowly- allows adaptation by opening or developing collateral branches
• Rapidly- intrerrupts suddenly the oxigen and energy supply to the tissue, without enough time to compensate the loss
- Hemorrhage: definition, mechanisms of production
• Definition: – the exit of blood outside the blood vessels in a living organism • Pathogenesis: 3 basic mechanisms: • rupture • erosion • erythrodiapedesis 1.rupture • the breaches in the vessel walls or in the heart can be produced by: – trauma: lesions produced by cutting, bone fractures 2.erosion The erosion of the vessels may be: • Chemical b. Traumatic c. Inflammatory d. Neoplasic Erythrodiapedesis represents the exit of the red cells outside the vascular wall, and is produced by: – at the capillaries level – in a passive way – when there are large parietal lesions which cause increase in permeability, in cases like: • prolonged hyperemia • Scurvy (vitamin C deficiency) • microbial toxins - drugs • DIC capillary fragility can appear because of vitamin C deficiency
- Hemorrhage: classification after the site of appearing of blood
• Regarding their site, hemorrhage may be classified in:
– external
– exteriorized
– internal
• 1. External hemorrhages regarding the type of the affected vessels at the outer surface of the body may be:
– arterial, with a rapid, pulsatile flow of bright red blood
– venous, with a slow, continuous flow of dark red blood
– capillary, with a dotted pattern or as a diffuse, whole organ bleeding
– cardiac, with a strong spurt of the blood from the heart
• 2. The exteriorized hemorrhages are produced in cavitary organs and exteriorized through natural channels, their origins giving their specific name :
– epistaxis (from the nasal cavities)
– otorrhagia (auditory channel)
– gingivorrhagia (from the gums)
– stomatorrhagia (from the oral mucosa) - Internal hemorrhages are produced inside the body:
• a. in serous cavities
• b. in tissues (in extravascular spaces):
- on surfaces (skin, serous membranes) as purpura (small red spots of 1-2mm), petechiae (red spots of 2-3mm) or ecchymoses (bruises) of different sizes- a ” permanent” red spot can be distinguished from a simple congestion by compression with a glass slide- in various tissues or organs as hematomas
- Hematoma: definition, macroscopy, microscopy, evolution
– A hematoma is a well delineated collection of blood, which appears in different organs (e.g. frequently in the brain, skeletal muscle, but also in other organs)
• Macroscopy of hematoma:
– nodular or oval, pushing the normal tissue
– With a slow change in color (gradually, from red to purple, then green and yellow, following the normal bilirubin breakdown) until its disappearance
Microscopy of hematoma:
erythrocytes extravasate into the interstitium and release hemoglobin. Under the action of inflammatory proteases, hemoglobin is gradually transformed into hemosiderin (brown color), then incorporated in macrophages (siderophages), which together with the lymph remove the hematoma
• Evolution of hematoma:
– Complete resorbtion, in the case of small hematomas
– Enclosure, in the case of large hematomas. They cannot be totally resorbed, but may be slowly surrounded and encased in connective tissue. A yellowish serous component remains usually in the center and hemosiderin and calcium may finally precipitate in the connective tissue which surrounds the old hematomas
– Infection of the hematoma, if an infection develops in the proximity of the hematoma
– Fibrosis of the entire hematoma – resulting in a small scar which, in some cases it may involve depositions of hemosiderin and calcium
- Embolism: definition, consequences
What is EMBOLISM?
• Definition:
– embolism is the mobilization and migration through the bloodstream of a structure named embolus, structure other than blood or aqueous solutions\ hydrosoluble fluids
• Major consequences of embolism:
– arterial emboli can cause ischemia and infarction in different organs
– infectios emboli can spread infections
– tumoral emboli can disseminate the tumor leading to metastasis
– pulmonary thrombembolism is still a frequent cause of death
- Thrombosis: definition, macroscopy, microscopy, evolution
What is THROMBOSIS?
• Definition:
– Thrombosis is the coagulation of blood inside blood vessels and the heart in a living organism.
• Predisposing factors for the formation of thrombus (the Virchow triad)
– Quallity of the vessel vall (endothelial lesions)
– Nature of the blood flow (disorders of the circulation like stasis or turbulent flow)
– Composition of the blood (factors causing hyper coagulation)
1. The lesions of the vascular wall may have a crucial role in the thrombus formation, and may particularly appear in the following circumstances:
– in the arteries: atherosclerosis, HT, artheritis, action of chemical factors (nicotine)
– in the veins: sclerosing substances, hypoxia, neoplastic invasion
– in the capillaries: extreme temperatures (cold, warm)
2. Disorder of the circulation:
a. Stasis (decrease in the speed of the bloodstream)
• appears in:
– heart failure, bed-ridden patients, phenomena of local stasis
• effects:
– the contact between thrombocytes and endothelial cells, the local accumulation of activated factors of coagulation produced by endothelial cells (which are normally washed by the rapid bloodstream), and the hypoxia of the stasis affects the endothelial cells.
b. The turbulent flow makes the blood elements to impact against the vascular wall which may cause endothelial lesions:
• aneurysms, hidrostatic varices
• at the site of vessel branching
• preexisting lesions that traumatize the vascular wall (atheroma, mural thrombi)
• vegetations or valvular verucae
3. The hypercoagulation of blood can occur in:
– some genetic diseases or
– under the action of some factors acquired during lifetime.
• Macroscopy of thrombus:
A. Differences between thrombus and postmortem clot:
– The thrombus is:
• adherent
• frail
• undeformable
• dull
– The clot is:
• non-adherent
• elastic
• deformable
• glossy
Evolution of thrombus:
1. Autolysis (of small thrombi)
– the activation of fibrinolysis
2. The organization in connective tissue (of larger thrombi): thrombus->granulation tissue->connective tissue scar
-PMN penetrate into the thrombus and slowly remove the fibrin using hidrolytic enzymes
- macrophages engulf the remaining fibrin and blood cells
- myofibroblasts enter from the base of the thrombus and multiply inside the thrombus
- from vasa vasorum, the endothelial cells multiply and enter the thrombus forming small capillaries, initially without basement membrane (it is formed later)
-the mixture of myofibroblasts, macrophages, neutrophils, other inflammatory cells and the numerous new formed capillaries, form the granulation tissue- the first step in connective tissue scarring
- myofibroblasts produce collagen fibers that have contractile properties (the contraction of the thrombus)
- the capillaries lose their lumen and slowly disappear
- finally, the thrombus transforms in a connective tissue scar
– advantage: it fixes the thrombus to the wall (prevent thrombembolism)
– disadvantage: stays attached permanently, like a mass that deforms and obstructs the vessel
3. The recanalization of the thrombus (partial reestablishment of the blood flow):
– partial lysis of the thrombus
– contraction of the myofibroblasts generates a space between the thrombus and the vascular wall
– the newly formed capillaries in the thrombus (angiogenesis) grow along the vascular axis, crossing the thrombus
4. The noninfectious (sterile) degradation of the thrombus:
– In large thrombi, that have a small connection with the walls of the veins, neutrophils enter and, with the help of their enzymes, melt the thrombus, liquefying its central core
5. The infective degeneration of the thrombus:
– Is encountered in thrombi colonized by bacteria, derived from an infectious source
– Infected thrombi can generate emboli, further spreading the infection
6. The calcification of the thrombus:
– calcium deposits may form inside venous thrombi (phlebolites) or on endocardial vegetations
7. The mobilization of thrombus:
– By partial desintergation of the thrombus and its dislodging, the fragments may enter the bloodstream
- Infarction: definition, causes, evolution
What is INFARCTION?
• Definition:
– necrosis of a limited area of tissue through an ischemic mechanism
– necrosis = the death of cells in a living organism
• Pathogenesis:
– the same causes as those of ischemia (thrombosis, embolism, atherosclerosis, vascular spasms, external pressure)
Evolution:
• death, if the infarction appears in a vital area for the organism (the brain stem, the His bundle), or if the infarction is extensive
• connective organization, (if the organism survives the infaction): a process of organization in connective tissue scar of the infarcted area
• The infection of the affected area
- Edema: definition, glottic edema
What is EDEMA?
• Definition:
– the increase of fluids in the interstitial compartment
• Pathogenesis:
– Increase of hydrostatic pressure: hyperemia
– Decrease of the oncotic pressure: hypoproteinemia
– The retention of Na ions
– Disorders of lymphatic circulation: lymphedema
Glotic edema:
• Definition:
– the accumulation of liquid in the glotic mucosa
• Etiopathology:
– - acute respiratory infections
– - immune reactions: angioedema (the Quincke edema)
• Evolution:
– death caused by asphixiation (suffocation) unless an emergency tracheostomy is performed
