small group - circulation I Flashcards
what does congestion of the liver look like?
centrilobular congestion/hyperemia
bright red spots
nutmeg liver - because of stripes and dark and light alternating
what’s the difference between a thrombus and a clot?
a thromus is a coagulum that forms inside the blood vessel that involves the blood
a clot is blood that has coagulated anywhere else except inside a blood vessel
what is edema?
presence of excessive fluid in a tissue or body cavity
what is the difference between transudate and exudate edema?
transudate - low protein content, low specific gravity, low cell content (blister) - usually due to increased hydrostatic pressure or reduced plasma protein
seen in patients with heart failure, hepatic failure, malnutrition
exudate - pus - high protein content and cell content - inflammatory - due to increased vascular permeability
what is dependent edema?
detectable increase in extracellular fluid volume localized in a dependent area such as a limb, characterized by swelling or pitting
influenced by gravity
greater in the lower part of the body than in the part above the heart
what is pitting edema?
fluid is mobile - pressure leaves a persistent depression in the tissues
what is ascites?
abnormal accumulation of fluid in the abdomen
what is anasarca?
extreme generalized edema with widespread subcutaneous tissue swelling
what are the mechanisms of edema formation?
1: increased intravascular hydrostatic pressure (heart failure, venous obstruction)
2: decreased serum oncotic pressure (low/absent protein synthesis, protein loss)
3: increased permeability of vessel walls (burns, inflammation, chemical injury)
4: lymphatic obstruction or destruction (neoplasia, post-surgery, parasites)
what are the causes of edema?
1: increased hydrostatic pressure
2: decreases oncotic pressure
3: increased permeability
4: lymphatic obstruction
what normal liquid movement in the arterial system?
fluid moves around the capillaries
most is taken up by venous system
what’s not taken up there is taken up into the lymphatic system
what does increased hydrostatic pressure do to create edema?
the increased venous hydrostatic pressure prevents the liquid from being resorbed into the veins
the lymphatic tissue can take up more liquid than normal, but can’t take up everything so get edema
how does decreased oncotic pressure lead to edema?
the increased oncotic pressure in the blood prevents the liquid in the interstitium from being reabsorbed so must go into lymphatics, but lymphatics can’t take it all up so get edema
how does increased vascular permeability lead to edema?
get additional leakage from the arterial side and leakage rather than reabsorption on the venous side
again, lymphatic system can’t keep up
how does lymphatic obstruction lead to edema?
lymphatic tissue can’t take fluid being excreted, and venous system can’t take up all of the liquid so get edema
what are some causes of increased hydrostatic pressure?
increased venous pressure
heart failure
what is an example of decreased oncotic pressure?
decreased serum albumin
what are examples of things that will cause increased permeability?
inflammation, histamine
what are examples of things that will cause lymphatic obstruction?
cancer, filariasis
what are the gross morphological changes due to edema?
organ or tissue swells
increased mass of the tissue due to influx of fluid
what does edema look like histologicallly?
separation of tissue elements by a pale pink (on H&E) material that is protein-containing fluid
no new cellular elements in the tissue
can be subtle histologically
what is hyperemia?
increased volume of blood within a specific vascular bed
what is the difference between active and passive hyperemia?
active = increased flow into the area passive = decreased outflow of blood
what would be the morphology of hyperemia?
organ or tissue can appear redder
blood remains within the blood vessels
vessels dilated, full of RBCs, but not damaged
edema is not a required part of the process
what is hemorrhage?
flow of blood from the vascular compartment
can be out of the body, into a tissue or organ, into a body cavity, or can create a space where there previously was none
what is the morphology of a hemorrhage?
blood - either in a solid mass or spread between tissue elements or as a free fluid
that is no longer contained in the normal chambers of the heart or within the lumen of a blood vessel
what are some local causes of hemorrhage?
trauma infection inflammation tumor iatrogenic vascular malformation focal tissue necrosis
what are some of the systemic causes of hemorrhage?
coagulopathy (naturally occurring or iatrogenic) vascular defects (vasculitis)
what are the factors determining the clinical significance of a hemorrhage?
volume of blood
rate of bleeding
site where hemorrhage occurs (including whether the blood leaves the body or accumulates as a hematoma)
what is petechiae? what are possible causes?
red or purple spots on the body - due to minor hemorrhage (broken capillary blood vessels)
asphyxia - on eyelids
septic emboli
often due to increased intravascular pressure, low platelet counts, or defective platelet function
what is purpura? what causes it?
red or purple discolorations on the skin that don’t blanch on applying pressure
small blood vessels join together or leak blood under the skin
can be due to increased intravascular pressure, low platelet counts, defective platelet function, trauma, vascular inflammation, increased vascular fragility
what are ecchymoses?
bruises - blood diffuses through the tissue
due to trauma
have degraded and phagocytized RBCs
what is hematoma?
localized collection of blood outside the blood vessels, usually in liquid form within the tissue
like blood under toenail
what is hemoptysis?
coughing up blood
what is hematemesis?
vomiting blood
what is melena?
black, tarry feces - associated with GI hemorrhage
what is ischemia?
reduction or loss of blood supply to a tissue or organ
major problem = reduction in O2 - but also reduction/loss of other blood constituents
what is hypoxia versus anoxia?
low O2 supply versus no O2 supply
what is infarction?
death of cells, a tissue, or an organ due to insufficient or absent blood supply - caused by occlusion of either arterial supply or venous drainage
nearly all due to thrombotic or embolic arterial occlusions
what are the factors affecting the development of ischemia and infarction?
1: supply of blood/O2 available
2: vascular pattern (single vs. complex arterial supply, collaterals)
3: rate of decrease of blood supply (sudden versus slowly over years - tissue can adapt over years)
4: tissue vulnerability (metabolic rate, ability to do anaerobic glycolysis)
what is the gross morphology of infarction? (bland versus hemorrhagic)
bland infarct - tissue is pale, anemic, white
hemorrhagic infarct - bleeding into dead tissue
infarcts are often wedge shaped
what does an infarct look like histologically?
coagulative necrosis
cells become eosinophilic, nuclei shrink, become hyperchromatic, less distint, then break up
neutrophils infiltrate to digest dead tissue
macrophages remove/digest debris
scarring forms except in the brain
what is backward heart failure?
failure to pump blood out of the veins
aka congestive failure
what is forward heart failure?
failure to pump blood into the arteries with sufficient pressure to perfuse the organs
can cause ischemia
what is global heart failure?
failure having elements of both backward and forward failure
usually a sign of diffusely diseased myocardium
what are the consequences of heart failure?
congestion in lungs and liver
edema in lungs and liver and dependent, pitting edema
pleural effusion, ascites, dyspena at rest
what are the consequences of congestive (right-sided) heart failure?
chronic congestion of the liver
increased venous pressure leading to dependent edema
what can be the causes of increased interstitial fluid?
increased capillary pressure
diminished colloid osmotic pressure
what causes increased hydrostatic pressure?
focal impairment in venous return
deep venous thrombosis in lower extremity
can have generalized increases => systemic, usually due to congestive heart failure (compromised right ventricular function => pooling of blood on venous side of circulation)
what causes reduced plasma oncotic pressure?
albumin not synthesized in adequate amounts or is lost from circulation
can be due to nephrotic syndrome - glomerular capillaries become leaky => generalized edema
severe liver disease or severe malnutrition => reduced albumin synthesis
both lead movement of fluid into tissues => plasma volume contraction
what is congestion? what does it look like?
passive process due to reduced outflow of blood from tissue
can be systemic (cardiac failure) or local (isolated venous obstruction
tissues have dusky reddish-blue color due to red cell stasis and accumulation of deoxygenated Hg
what is chronic passive congestion?
long-standing
edema due to increased volumes and pressures due to congestion
causes chronic hypoxia => ischemic tissue injury and scarring
can also get capillary rupture => small hemorrhagic foci => catabolism of RBCs => residual clusters of hemosiderin-laden macrophages
what does acute pulmonary congestion look like?
engorged alveolar capillaries with alveolar septal edema and focal intra-alveolar hemorrhage
what does chronic pulmonary congestion look like?
septa thickened and fibrotic
alveoli have hemosiderin-laden macrophages = heart failure cells
what happens in acute hepatic congestion?
central vein and sinusoids distended
centrilobular hepatocytes ischemic and periportal hepatocytes just develop fatty change
what does chronic passive hepatic congestion look like?
in cetrilobular regions = grossly red-brown and slightly depressed, surrounding zones = nutmeg liver
what are the potential locations of red infarcts?
1: due to venous occlusions
2: in loose tissues where blood can collect
3: in tissues with dual circulations
4: in tissues previously congested by sluggish venous outflow
5: when flow is reestablished to a site of previous arterial occlusion and necrosis
what are the potential locations of white infarcts?
1: with arterial occlusions in solid organs with end-arterial circulation
2: where tissue density limits the seepage of blood from adjoining capillary beds into the necrotic area
when do septic infarctions occur?
when infected cardiac valve vegetations embolize or when microbes seed necrotic tissue - infarct zone becomes abscess
when does CHF occur?
when heart is unable to pump blood at a rate sufficient to meet the metabolic demands of the tissues or can do so only at an elevated filling pressure
usually due to chronic work overload, such as in valve disease or hypertension, or ischemic heart disease (due to MI)
can suddenly appear due to acute hemodynamic stresses too = fluid overload, acute valvular dysfunction, large MI
what causes cardiac hypertrophy? what is different in hypertrophic cells?
increased mechanical work due to pressure or volume overload
trophic signals
dependent on increased protein synthesis => assembly of additional sarcomeres
also have increased mitochondria and enlarged nuclei
what are the consequences of hypertrophied heart?
heightened metabolic demands due to increases in wall tension, heart rate, and contractility => increased cardiac O2 consumption => makes heart vulnerable to decompensation which can evolve to cardiac failure
what are the most common causes of left-sided heart failure?
1: ischemic heart disease
2: hypertension
3: aortic and mitral valvular diseases
4: myocardial diseases
what changes would be seen in the heart due to left-sided heart failure?
grossly: MI, deformed, stenotic, regurgitant valve
left ventricle usually hypertrophied, often dilated
usually interstitial fibrosis
dilation of left atrium => increased the risk of atrial fibrillation => stasis
what changes would be seen in the lungs due to left-sided heart failure?
pulmonary congestion and edema - heavy, wet lungs
perivascular and interstitial edema, particularly in interlobular septa
progressive edematous widening of alveolar septa
accumulation of edema fluid in alveolar spaces
will be some RBCs in edema fluid - phagocytized and digested by macrophages - store iron from Hb as hemosiderin = heart failure cells
what’s the difference between systolic and diastolic left-sided heart failure?
systolic: defined by insufficient cardiac output - caused by disorders that damage or derange contractile function of the left ventricle
diastolic = cardiac output preserved at rest, left ventricle abnormally stiff or restricted in ability to relax during diastole => heart can’t increase output in response to increased metabolic demands
hypertension
what is right-sided heart failure usually caused by?
left-sided heart failure - any increase in pressure in pulmonary circulation incidental to left-sided failure inevitably burdens the right side of the heart
what is the morphology of right-sided heart failure in the heart?
varies with cause
can be structural defects like valvular abnormalities or endocardial fibrosis (rare)
what is the morphology of right-sided heart failure in the liver and portal system?
liver increased in size, weight due to passive congestion
congestion most prominent around central veins within hepatic lobules - have red-brown cetrilobular discoloration and paler, sometimes fatty peripheral regions (nutmeg liver)
can also be centrilobular necrosis
can get fibrosis in central areas = cardiac sclerosis/cirrhosis
also get enlargement of spleen due to portal hypertension
