Lecture 14 Flashcards
Active hyperemia
inc blood volume due to arteriolar dilation and expansion of the perfused capillary bed
Passive congestion
a passive process in which inc blood volume within the vasculature of a tissue is due to impairment of venous outflow
In what circumstances does active hyperemia develop?(2)
inc blood flow to GIT after eating
inc blood flow to skeletal muscle during exercise
Why is active hyperemia a localized phenomenon
insufficient blood volume to permit generalized active hyperemia while maintaining adequate systemic blood pressure
In what circumstances does localized passive congestion develop(2)
luminal obstruction of a vein or external compression of a vein
intestinal strangulation due to torsion or volvulus->compression of mesenteric arteries
in what circumstances does generalized passive congestion develop?
Almost always congestive heart failure (left or right)
left-lungs
right-cranial and caudal vena cava
How to grossly distinguish between active/passive hyperemia in a live animal?
active- appear red, swollen, warm, turgid, bright red O2 blood
Passive/congestion- red-purple to blue-black, poorly O2 blood
Potential consequences of passive congestion of tissues(2)
venous hypertension (inc hydrostatic pressure within engorged veins)-> edema if it develops slowly->acquired PSS
Gross lesions during necropsy of animal that died of left sided congestive heart failure (2)
lungs are heavy, wet, rubbery. do not fully collapse
edema fluid pours from cut surface of lungs-stable foam
Gross lesions during necropsy of animal that died of right sided congestive heart failure and why (2)
liver is swollen, dark red purple, venous blood oozes from cut surfaces
Blood from right side heart backs up into liver
Edema
accumulation of excess body fluid
Ascites
non inflammatory edema fluid within the peritoneal cavity
hydothorax
non inflammatory edema fluid within the pleural cavity
Hydropericardium
non inflammatory edema fluid iwthin the pericardial sac
hydorcoele
non inflammatory edema fluid within cavity of tunica vaginalis of scrotum
anasarca
severe generalized edema
5 mechanisms that can lead to edema development
inc plasma hydrostatic pressure dec plasma colloid osmotic pressure lymphatic obstruction inc vascular permeability Na retention
What circumstances lead to inc plasma hydrostatic pressure in capillary bed?(2)
impaired venous return to heart-> activation of RAAS
local obstruction of venous outflow
Why is extracellular edema NOT expected with systemic hypertension
inc arterial BP causes reflex vasoconstriction of the pre capillary arteriole sphincter in order to protect the delicate capillary bed
2 assays to initially categorize the edema fluid samples
protein [ ]
total nucleated cell count
Transudate
cell poor, protein poor
modified transudate
cell poor, but addition of protein
exudate
cell rich and protein rich
Gross features of edematous tissue
excess watery, colorless pale yellow clear non viscous fluid within interstitial tissues and or body cavities
Potential consequences of edema(2)
impaired would healing
susceptible to secondary bacterial infection
Severe edema can prove fatal, why? (2)
cerebral- inc intracranial pressure, stretching, compression of cerebral blood vessels
pulmonary- prevents ventilation and gas exchange
Forces promoting fluid movement from plasma -> interstitum(2)
plasma hydrostatic pressure (inc)
interstitial colloid osmotic pressure
Forces promoting fluid movement from interstitum -> plasma(2)
plasma colloid osmotic pressure (inc)
interstitial hydrostatic pressure
Arteriole end has net
filtration pressure
venular end has net
absorptive pressure
