Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Path Quiz 1 > small group - circulation I > Flashcards

small group - circulation I Flashcards

1
Q

what does congestion of the liver look like?

A

centrilobular congestion/hyperemia
bright red spots
nutmeg liver - because of stripes and dark and light alternating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what’s the difference between a thrombus and a clot?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is edema?

A

presence of excessive fluid in a tissue or body cavity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is the difference between transudate and exudate edema?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is dependent edema?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is pitting edema?

A

fluid is mobile - pressure leaves a persistent depression in the tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is ascites?

A

abnormal accumulation of fluid in the abdomen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is anasarca?

A

extreme generalized edema with widespread subcutaneous tissue swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the mechanisms of edema formation?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the causes of edema?

A

1: increased hydrostatic pressure
2: decreases oncotic pressure
3: increased permeability
4: lymphatic obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what normal liquid movement in the arterial system?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what does increased hydrostatic pressure do to create edema?

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how does decreased oncotic pressure lead to edema?

A

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 well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how does increased vascular permeability lead to edema?

A

get additional leakage from the arterial side and leakage rather than reabsorption on the venous side
again, lymphatic system can’t keep up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how does lymphatic obstruction lead to edema?

A

lymphatic tissue can’t take fluid being excreted, and venous system can’t take up all of the liquid so get edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are some causes of increased hydrostatic pressure?

A

increased venous pressure

heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is an example of decreased oncotic pressure?

A

decreased serum albumin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are examples of things that will cause increased permeability?

A

inflammation, histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are examples of things that will cause lymphatic obstruction?

A

cancer, filariasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are the gross morphological changes due to edema?

A

organ or tissue swells

increased mass of the tissue due to influx of fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what does edema look like histologicallly?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is hyperemia?

A

increased volume of blood within a specific vascular bed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is the difference between active and passive hyperemia?

A 
active = increased flow into the area
passive = decreased outflow of blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what would be the morphology of hyperemia?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
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
26
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
27
what are some local causes of hemorrhage?
``` trauma infection inflammation tumor iatrogenic vascular malformation focal tissue necrosis ```
28
what are some of the systemic causes of hemorrhage?
``` coagulopathy (naturally occurring or iatrogenic) vascular defects (vasculitis) ```
29
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)
30
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
31
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
32
what are ecchymoses?
bruises - blood diffuses through the tissue due to trauma have degraded and phagocytized RBCs
33
what is hematoma?
localized collection of blood outside the blood vessels, usually in liquid form within the tissue like blood under toenail
34
what is hemoptysis?
coughing up blood
35
what is hematemesis?
vomiting blood
36
what is melena?
black, tarry feces - associated with GI hemorrhage
37
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
38
what is hypoxia versus anoxia?
low O2 supply versus no O2 supply
39
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
40
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)
41
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
42
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
43
what is backward heart failure?
failure to pump blood out of the veins | aka congestive failure
44
what is forward heart failure?
failure to pump blood into the arteries with sufficient pressure to perfuse the organs can cause ischemia
45
what is global heart failure?
failure having elements of both backward and forward failure usually a sign of diffusely diseased myocardium
46
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
47
what are the consequences of congestive (right-sided) heart failure?
chronic congestion of the liver | increased venous pressure leading to dependent edema
48
what can be the causes of increased interstitial fluid?
increased capillary pressure | diminished colloid osmotic pressure
49
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)
50
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
51
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
52
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
53
what does acute pulmonary congestion look like?
engorged alveolar capillaries with alveolar septal edema and focal intra-alveolar hemorrhage
54
what does chronic pulmonary congestion look like?
septa thickened and fibrotic | alveoli have hemosiderin-laden macrophages = heart failure cells
55
what happens in acute hepatic congestion?
central vein and sinusoids distended | centrilobular hepatocytes ischemic and periportal hepatocytes just develop fatty change
56
what does chronic passive hepatic congestion look like?
in cetrilobular regions = grossly red-brown and slightly depressed, surrounding zones = nutmeg liver
57
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
58
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
59
when do septic infarctions occur?
when infected cardiac valve vegetations embolize or when microbes seed necrotic tissue - infarct zone becomes abscess
60
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
61
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
62
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
63
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
64
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
65
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
66
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
67
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
68
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)
69
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

Path Quiz 1 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions