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BIOL 2292 Notes
BIOL 2292 Notes
BIOL 2292 Notes
Types of Edema
Subcutaneous edema
Cerebral edema
Pulmonary edema
Dependent edema – depends on gravity
Periorbital edema
Anasarca
- Pitting is a common sign
Consequences of Edema
Cerebral Edema
Dangerous because brain is confined in cranium that is not flexible increase pressure in the brain
3 kinds of edema
o Vasogenic – increased permeability of vasculature
Fluid accumulates in extracellular spaces
E.g., neoplasms, infections, toxins, hemorrhage
o Cytotoxic edema – neurons swell with fluid
Fluid accumulates within brain cells
E.g., ischemia
o Interstitial edema – fluid accumulates in ventricles
Problem with cerebral spinal fluid (CSF) flow (hydrocephalus)
E.g., congenital, neoplasms, infections
Characteristics of brain with edema
o Flattened gyri and narrow sulci
o Affected persons experience nausea, vomiting, disorientation, and seizures
Intracranial pressure can force the brainstem downward, through the foramen magnum (not a condom
brand)
o This is fatal because the brain stem controls our basic functions that let’s us live laugh love (i.e.,
resp, heart rate, consciousness, BP and sleep) so if it gets squished or gets moved, these functions
can be altered and may cause fatal complications
Heart, lungs and abdominal organs are surrounded by serous membranes – i.e., pericardium, pleura, and
peritoneum
o Serous membranes line the internal cavities
Accumulation of fluids in the serous membranes leads to impaired organ function
Pleural effusion: fluid accumulation in pleural space
o Can be caused by; CHF, liver cirrhosis, kidney disease
o Can lead to lung compression and collapse
o Patient experience dyspnea, painful cough
Pericardial effusion: fluid accumulation in the pericardium
o Can be caused by; neoplasms, infection, autoimmune
o Hemopericardium: accumulation of blood in the pericardium due to hemorrhage
The blood leaks into the pericardium space (blood from the chambers)
o Can cause cardiac tamponade (compression of cardiac chambers)
Because the fluid in the pericardium squishes the heart and prevents it from pumping
Ascites: fluid accumulation in the peritoneal cavity
o Caused by; neoplasms, liver cirrhosis, inflammation, CHF
o Abdomen can become extremely distended
o Patients show loss of appetite, vomiting, shortness of breath
o Chylous ascites: accumulation of lipid-rich lymph fluid in peritoneal cavity if thoracic duct is
blocked
Hyperemia
Hemorrhage
Consequences of Hemorrhage
o A person could lose 20% of blood volume without major impact (even more if the loss is slower)
Greater loss leads to hemorrhagic (hypovolemic) shock
o Site of hemorrhage also important
Even small accumulations in closed spaces of skull can be deadly
o Chronic blood loss can lead to anemia
E.g., small gastrointestinal bleeds
Endothelial Cells
Platelets
Coagulation Cascade
Thrombosis
Arterial Thrombi
Venous Thrombi
Fate of Thrombus
Treatment/Prevention of Thrombosis
Embolism
Embolus: anything that can travel through the circulation, get stuck, and obstruct blood flow
Blockage leads to ischemia which leads rapidly to necrosis (infarction)
Thromboemboli are the most common
o Origin is thrombus
o Emboli can also be fat, nitrogen, bacteria, tumour fragments, bone marrow
Pulmonary Embolism
Infarction
Occur in solid organs with end-arterial circulation – only supplied by a single vessel
o Blockage occurs in the only artery that feeds the tissue
o Tissues is dense and does not have much space for blood to accumulate
E.g., heart, kidney, spleen
Brain infarction
Blood Pressure
BP = CO x SVR
o SVR – system vascular resistance
o CO – cardiac output
HR x SV
Shock
Pathophysiology of shock
Failure of myocardial pump (idk why she just doesn’t say heart), decrease in blood volume or systemic
dilation hypoperfusion hypoxia
Hypoxia leads to formation of free radicals (remember what Father Paul taught you)
Endothelial cell damage
o Increases vascular permeability, further decreasing volume
Impaired function of multiple systems
o Acidosis, hypercoagulability
Acidosis occurs because cells acid is a by product of glycolysis which cells use to make
ATP since there is no more oxygen
Multiple organ dysfunction morbidity and DIE
Non-progressive stage
o Body’s compensatory mechanisms work to maintain adequate perfusion
o Falling BP triggers compensatory mechanisms
Capillary BHP drops less fluid being pushed out of vessels
Hormones (e.g., ADH, RAA pathway) act on kidneys to increase blood volume
By reabsorption of sodium
Auto-regulation in brain and heart to dilate blood vessels to maintain perfusion
Baroreceptors detect reduction in pressure and signal cardiovascular center in medulla
oblongata via sympathetic NS
Increase heart rate and contractility
Vasoconstriction (V/c) in peripheral blood vessels, directing blood to heart and
brain
Progressive stage
o Compensatory mechanisms begin to fail
o Situation is still reversible, but worsening
o In the lungs
Tachypnea and dyspnea as lungs try to compensate for hypoxia
Gradual onset of pulmonary edema
o In the kidneys
Extensive vasoconstriction (to reduce urine production) reduced GFR oliguria
(reduced urine output)
o As lungs and kidneys fail, acidosis develops
You should know why acidosis develops
o Acidosis interferes with normal vasomotor response – vasoconstriction and vasodilation
Small blood vessels dilate and blood begins accumulating
Further decrease in cardiac output
Accumulating blood becomes hypoxic
Endothelial cell injury sets in
Disruption to normal coagulation pathways DIC
o Acidosis may also effect mental function, leading to confusion
o Tissues become hypoperfused
o Circulatory and metabolic problems get worse
Irreversible stage
o Game over for the girlies
o Widespread cell death
Lysosomal contents leak out, causing further damage
Ability of heart muscles to contract gets worse
Necrosis in large intestine may allow bacteria into circulation, increasing risk of septic
shock
Tubular necrosis in kidneys leads to kidney failure
o DIC leads to infarctions in organs
o Death is inevitable
Treating Shock
Severity and outcome depends on immune status, presence of co-morbidities, pattern of pathogenesis,
extent and virulence of infection
Management can include:
o Antibiotics, fluids, epinephrine
o Securing airway, blood transfusions
Goal of treatment is to increase urine output (shows that we are back to perfusing organs, also helps to
restore body’s pH) and blood pressure
Prognosis
o Survival is ~90% in young, healthy peeps
o Poor outcome for cardiogenic and septic shock