1. EMBOLISM
1.1. Displacement of embolic material from one anatomic vascular location to another and lodging in pumonary or systemic circulation
1.2. Types of embolic material
1.2.1. SOLID
1.2.1.1. thrombus - sterile or infected
1.2.1.2. atheroclerotic plaque
1.2.1.3. neoplastic cells
1.2.2. LIQUIDIC
1.2.2.1. fat
1.2.2.2. amniotic fluid
1.2.3. GASEOUS
1.2.3.1. air
1.2.3.2. nitrogen
1.2.3.2.1. decompression sickness
2. SHOCK
2.1. LIFE-THREATENING CONDITION OF CIRCULATORY FAILURE
2.2. generalized ⇩ tissue perfusion (CO & SVR) with microcirulatory stasis and failure -> ⇩oxygenation -> tissue hypoxia with cellular and molecular changes
2.2.1. Derangements at cellular level progress to systemic level
2.2.1.1. Inciting event->systemic circulatory abnormality (manifested as refractory HYPOTENSION)-> irreversible end-organ damage and death
2.3. The initial effects of shock are reversible but rapidly become irrevesible resulting in multiorgan failure & death 1. COMPENSATED 2. REVERSIBLE DECOMPENSATED 3. IRREVESIBLE DECOMPENSATED
2.3.1. DYSREGULATED HOST RESPONSE https://image.slideserve.com/255951/slide30-l.jpg
2.3.2. SIRS – systemic inflammatory response syndrome is a common feature of many types of advanced shock
2.4. TYPES
2.4.1. HYPOVOLEMIC
2.4.1.1. Loss of Na+ containing fluid resulting in decreased intravascular volume
2.4.1.1.1. bleeding
2.4.1.1.2. excessive diarrhea, vomiting
2.4.1.1.3. severe burns
2.4.2. CARDIOGENIC
2.4.2.1. diseases of myocardium, valves, pericardium and extracardiac (pulmonary embolism & cardiac tamponade - OBSTRUCTIVE SHOCK )
2.4.3. DISTRIBUTIVE
2.4.3.1. Sepsis
2.4.3.1.1. Septic shock is the most common among ICU patients
2.4.3.2. Anaphylaxis
2.4.3.3. Neurogenic
2.4.4. OBSTRUCTIVE
2.4.5. COMBINED
2.5. PATHOLOGY
2.5.1. PATHOLOGY
3. INFARCTION
3.1. Process of infarct formation
3.2. INFARCT: localized necrosis caused by markedly decrease tissue perfusion (ischemia/hypoxemia/impaired drainage)
3.2.1. thrombotic/embolic occlusion
3.2.2. cmpression/torsion
3.2.3. vasospasm
3.2.4. low flow states
3.3. MORPHOLOGY: Necrosis +- haemorrhagic lesions
3.4. TYPES
3.4.1. Pale
3.4.1.1. critical ischaemia leading to severe hypoxia
3.4.1.1.1. critical narrowing/blockage of end-circulation artery
3.4.1.1.2. low perfusion pressure
3.4.1.2. hypoxemia nad anemia may contribute
3.4.2. Red
3.4.2.1. blockage of artery
3.4.2.1.1. dual blood supply
3.4.2.1.2. arterio-arterial arcades
3.4.2.2. blockage of vein
3.4.2.2.1. impaired drainage
3.4.2.3. necrosis superimposed on hyperemia and hemorrhagic changes
4. HYPEREMIA
4.1. Localized ⇧ in blood volume in capillaries and small vessels
4.2. MORPHOLOGY: dilated vascular spaces + associated lesions
4.2.1. Associated lesions:
4.2.1.1. edema
4.2.1.2. inflammatory infiltrate
4.2.1.3. hypoxic degeneration
4.2.1.4. necrosis and fibrosis
4.2.1.5. haemorrhage/hemosiderosis
4.3. TYPES
4.3.1. Active
4.3.2. Passive (Congestion)
5. EDEMA
5.1. ⇧ fluid in the interstitial space, body cavities and transcellular ECF compartments
5.2. Mechanisms
5.2.1. ⇧HYDROSTATIC PRESSURE ~ ⇩ONCOTIC PRESSURE
5.2.1.1. ⇧HP
5.2.1.1.1. edema in congestive heart failure/CHF
5.2.1.2. ⇩OP
5.2.1.3. ⇧HP +⇩OP
5.2.1.3.1. ascites in cirrhosis /Cirr
5.2.1.3.2. edema in nephrotic syndrome/NS
5.2.1.4. SYSTEMIC EDEMATOUS STATES (CHF, NS, CirrLiv)
5.2.1.4.1. associated with persistent RENAL SALT RETENTION (NaCl)
5.2.2. ⇧ PERMEABILITY
5.2.3. ⇩ LYMPHATIC DRAINAGE
5.3. TYPES
5.3.1. COMPOSITION
5.3.1.1. Transudate
5.3.1.1.1. protein poor, cell poor
5.3.1.1.2. MECHANISM:alterations in Starling forces
5.3.1.1.3. Clinically: pitting edema, effusions (fluid in serous spaces)
5.3.1.2. Exudate
5.3.1.2.1. protein rich, cell rich
5.3.1.2.2. MECHANISM: increased vascular permeability
5.3.1.2.3. Clinically: tissue swelling, effusions
5.3.1.3. lymphedema
5.3.1.3.1. protein rich
5.3.1.3.2. tissue swelling
5.3.1.4. myxedema
5.3.1.4.1. GAGs deposition
5.3.2. LOCATION
5.3.2.1. Pleural effusion
5.3.2.1.1. Exudate, Pyo- Hydro-, Hemo-, Chylothorax
5.3.2.2. Pericardial effusion
5.3.2.2.1. Exudate, Pyo- Hydro-, Hemo-, Chylopericardium
5.3.2.3. Ascites - excessive serous fluid in peritoneal cavity
5.3.2.4. Anasarca - severe generalized edema
5.3.3. EXTENT
5.3.3.1. Generalized
5.3.3.2. Organ specific
5.3.3.3. Localized
6. THROMBOSIS
6.1. Thrombus formation
6.2. THROMBUS: Intravascular mass/conglomerate of fibrin, platelets and morphotic blood elements as a result of intravascular activation of coagulation: Macroscopically: gray-red, friable.
6.2.1. BLOOD CLOT:Conglomerate that forms intravascularly after death (postmortem blood clot) or extravascularly after hemorrhage (fibrin clot) Macroscopically : "currant jelly" or "chicken fat", soft glistering.
6.3. Pathogenesis
6.4. MORPHOLOGY: Depends on the site of formation. Adherent to the blood vessel wall
6.4.1. PALE: platelets and fibrin - (VALVULAR VEGETATIONS
6.4.2. MIXED: platelet&fibrin intervening with RBCs, WBCs&fibrin (ARTERIAL)
6.4.2.1. lines of Zahn/LAMINATION
6.4.2.1.1. arterial thrombus
6.4.3. RED: fibrin network + large amount of RBS & small number of WBCs (VENOUS)
6.4.3.1. layering not so promient, resembels blood clot
6.5. Fate of thrombus
6.5.1. Resolution
6.5.2. Organisation
6.5.2.1. Recanalisation
6.5.3. Detachment/Fragmentation - Embolism
6.6. TYPES
6.6.1. Venous
6.6.1.1. Deep veins in the lower extremities (less freq hepatic vein, dural sinuses, organ draining)
6.6.1.1.1. clinically pain,swelling discoloration
6.6.1.1.2. COMPLICATIONS
6.6.2. Arterial
6.6.2.1. Elastic & muscular arteries with atherosclerotic plaques
6.6.2.2. Heart
6.6.2.3. Aortic aneurysms
6.6.2.3.1. Turbulent flow
6.6.2.4. COMPLICATIONS
6.6.2.4.1. ISCHAEMIA OR INFARCTION
6.6.2.4.2. SYSTEMIC EMBOLISM
7. HAEMORRHAGE
7.1. Escape of blood outside the vascular system as a result of blood vessel or heart destruction
7.2. TYPES
7.2.1. to the surrounding tissues
7.2.1.1. hematoma
7.2.1.2. hemorrhagic focus
7.2.2. to the body cavities
7.2.2.1. hemothorax
7.2.2.2. hemopericardium
7.2.2.3. hemoperitoneum
7.2.3. to the lumen of hollow organ or directly outside
7.2.4. to the skin,serous or mucous membranes
7.2.4.1. petechiae
7.2.4.1.1. petechiae
7.2.4.2. PURPURA/PURPURIC RASH
7.2.4.2.1. Red-purple confluent lesions that result from the extravasation of blood into the skin or mucous membranes , do not blanch when pressed
7.2.4.2.2. classification
7.2.4.2.3. etiology
7.2.5. Abnormal uterine bleeding
7.2.5.1. Irregular bleeding
7.2.5.1.1. METRORRHAGIA -irregular non-menstrual
7.2.5.1.2. MENOMETRORRHAGIA- irregular and excessive/prolonged menstrual
7.2.5.2. MENORRHAGIA- excessive &/or prolonged menstrual (>80ml or >7 days)
7.2.5.3. OLIGOMENORRHEA - >38 days of menstrual cycles
7.2.5.4. POSTMENOPAUSAL
7.2.6. VENOUS/ARTERIAL/CAPILLARY