PART 1
edema
altered endothelial function
raised vascular hydrostatic pressure
plasma protein content decreased
life-threatening hypoxia
edema with fluid filled alveoli
hemostasis
-process of blood clotting -prevent excessive bleeding after blood vessels damaged
Inadequate hemostasis leads to
hypotension
shock
death
Inappropriate clotting leads to
-thrombosis
-embolism -causing ischemia death
(infarction) thromboembolism leads to
myocardial infarction
pulmonary embolism
cerebrovascular accident (Stroke)
hyperemia and congestion
-raised blood volume within a tissue
hyperemia VS congestion
active VS passive process
Acute Pulmonary congestion
blood-engorged alveoli
variability in alveolar septal edema
intra alveolar haemorrhage
chronic pulmonary congestion
thickened and fibrotic septa
alveolar space with macrophage (laden with hemosiderin- heart failure-cells/phagocytosed red blood cells)
acute hepatic congestion
distended central vein and sinusoids
necrosis of centrally located hepatocytes
less severe hypoxia at the periportal hepatocytes due to proximity to the hepatic arterioles, they will develop reversible fatty change.
chronic passive congestion of the liver
red brown central region of the hepatic lobules, depressed (cell loss)
surrounded by uncongested tan, fatty liver (nutmeg)
centrilobular necrosis, hemorrhage , hemosiderin laden macrophage
edema
accumulation of body fluid in the interstitial spaces
effusion
extravascular fluid accumulate in body cavities
Examples of effusions
pleural effusion (hydrothorax)
pericardial effusion (hydropericardium)
peritoneal cavity (hydroperitoneum, ascites)
anasarca
severe / massive generalised edema
profound swellings of the subcutaneous tissue
accumulate in body cavities
Factor affecting fluid movement
vascular hydrostatic pressure
colloid osmotic pressure (induced by plasma protein)
net outflow fluid
drain by lymphatic vessels
edema fluid accumulation aetiology
increased vascular hydrostatic pressure ( due to impaired venous return, arteriolar dilation)
decreased osmotic colloid pressure
inflammation- increased vascular permeability
lymphatic obstruction
Na+ retention
transudate caused by imbalanced of pressure (protein poor)
exudate caused by injury or inflammation (protein rich due to increased vascular permeability)
elevated hydrostatic pressure aetiology
impaired venous return
DVT (distal leg)
congestive heart failure (raised venous hydrostatic pressure due to decrease cardiac output leading to systemic venous congestion)
cardiac/ renal / hepatic failure
decreased osmotic pressure
due to albumin loss 1. nephrotic syndrome
2. leaky glomerular capillaries
3. liver cirrhosis (decreased albumin synthesis)
increased water and sodium retention by the kidney do not correct the plasma volume deficit, in contrary in exacerbate edema
lymphatic obstruction
compromised resorption of fluid from the interstitial spaces
elephantiasis: parasitic infection filariasis (massive edema of the lower extremity, external genitalia) with inguinal lymph node and lymphatic fibrosis
decreased plasma albumin aetiology
malnutrition, hepatic synthesis, nephrotic syndrome
decreased renal blood flow leads to
activation of RAAS
vicious cycle
does not solve the underlying problems while exacerbate edema
excessive salt and water retention due to
post-streptococcal glomerulonephritis
acute renal failure
most common location of edema
lungs
subcutaneous tissues
brain
recumbent -lying down
dependent edema
edema most pronounced in leg when standing edema most pronounced in sacrum when lying down
edema due to renal dysfunction/ nephrotic syndrome
initial manifestation in loose CT
eg: eyelids, periorbital edema
blood-tinged- blood streak
brain edema
sulci narrow
gyri swell
subcutaneous edema
potential underlying cardiac/ renal diseases (eg: left ventricular failure, renal failure, respiratory distress syndrome, lung infection and inflammation- interfering the normal ventilatory function which leads to death)
significant edema can impair wound healing and infection clearance
may lead to brain herniation through the foramen magnum
increased intracranial pressure leads to brain stem vascular supply compressions. This in turn leads to medullary center ischemic injury compromising respiration and other important functions
Hemorrhage is extravasation of blood
Hemorrhage main etiology
damage to the blood vessels
defective clot formation
Chronic congested tissue leads to capillary bleeding
Hemorrhage in specific etiology
trauma
atherosclerosis
inflammation
neoplastic erosion of vessel wall
Hemorrhagic Diatheses
A collective term for risk of hemorrhage
Inherited or acquired defects
Defects in blood vessels walls, platelets, coagulation factors.
Hematoma
hemorrhage accumulate within a tissue range from trivial injury (bruise) to fatal (massive retroperitoneal hematoma from ruptured Dissecting Aortic Aneurysm)
jaundice after massive hemorrhage due to massive breakdown of rbc and hemoglobin
Petechiae
1-2mm diameter -hemorrhage into the skin, mucous membranes or serosal surfaces
causes of petechiae
thrombocytopenia
defective platelet functions
loss of vascular wall support
vitamin c deficiency
purpura
larger (3-5mm)
causes of purpura
could be same as petechiae
trauma
vasculitis
increased vascular fragility
ecchymoses
larger (1-2cm)
bruises (subcutaneous hematoma)
color changes of bruises
hemoglobin (red-blue) to bilirubin (blue-green)
hemosiderin (golden brown)
little impact if there is
rapid blood loss up to 20% blood volume slow blood loss of greater than 20% blood volume
massive blood loss leads to
hypovolemic shock
chronic/ recurrent external blood loss leads to iron deficiency anemia (loss of iron in hemoglobin) due to
peptic ulcer OR
menstrual bleeding
hematoma
internal bleeding does not result in iron deficiency as a result of recycling of phagocytosed red blood cells.
Part 2
Hemostasis & Thrombosis
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