Circulatory Disorders Flashcards

1
Q

Describe arteries VS veins.

A
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2
Q

Describe interstitial space.

A

-space between tissue compartments
-medium thru all metabolic prod pass between microcirculation & the cells
-CT

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3
Q

Describe fluid distribution & homeostasis.

A
  1. Homeostasis = state of steady internal conditions maintained by living things
  2. Total body water = 60% of total BW
    -intracellular fluid 40%
    -ECF 20%
    >interstitial 15%
    >plasma 5%
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4
Q

Describe hydrostatic pressure VS osmotic pressure.

A

water distribution between plasma & interstitum determined by osmotic & hydrostatic pressure differences between the 2 compartments
1. Hydrostatic
-fluid moves out of vasculature
2. Osmotic
-fluid into vasculature
-plasma proteins
[starling equation]

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5
Q

Describe edema & the different types.

A

*abnormal accumulation of excess ECF in the interstital spaces or in body cavities
*fluid is both outside the vascular & cellular fluid compartment

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6
Q

Describe inflammatory edema.

A

Inc vascular permeability
-immune reaction -> release inflam mediators -> vasodilation
-endothelium can be directly damaged by agents

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7
Q

Describe non inflammatory edema.

A

-inc hydrostatic pressure or dec plasma osmotic pressure causes extravascular fluid to accumulate
-tissue lymphatics remove excess volume & return it to the circ via thoracic duct but if the capacity for lymphatic drainage is exceeded = tissue edema

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8
Q

Describe the different types of non inflam edema.

A
  1. Inc hydrostatic pressure -> due to impaired venous blood flow (congestion)
    -generalized (CHF)
    -localized (tightly bandaged limb - vein occlusion)
  2. Dec oncotic pressure -> hypoproteinemia
    -generalized edema
    -proteins not absorbed from diet/not produced/loss
  3. Lymphatic obstruction
    -localized edema
    -damage/obstruction of lymphatics
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9
Q

Describe transudates VS exudate.

A
  1. Transudates
    -non inflam
    -inc blood hydrostatic pressure, dec osmotic pressure, lymphatic obstruction
    -low protein, SG, nucleated cells
  2. Exudate
    -inc vascular permeability
    -high protein, SG, nucleated cells
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10
Q

Describe the gross appearance of edema.

A

-wet, gelatinous & heavy, swollen, fluid weeps from cut surfaces, yellow

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11
Q

Describe generalized edema common locations.

A

-SQ edema
1. Ventrum of ab/thorax “brisket”
2. Ventral cervical/mandibular “bottle jaw”
-parasites
-hypoproteinemia
3. Limbs “stocking up”
-protein losing enteropathy

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12
Q

Describe different types of edema PM.

A
  1. Pitting edema in SQ = pressure applied, area of edema leaves a depression/dent due to excessive interstital fluid forced to adjacent areas
  2. Ascites/hydroperitoneum = fluid (transudates) in peritoneal cavity (CHF)
  3. Hydrothorax = fluid in thoracic cavity
  4. Pericardial effusion = ‘mulberry heart disease’
    >inflam
    >fibrin
    >exudate
  5. Anasarca = gen edema w profuse accumulation of fluid in SQ tissue
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13
Q

Describe the mechanism of development & common locations of generalized edema.

A
  1. Mech of development
    -inc hydrostatic pressure
    >heart failure
    -dec colloidal osmotic pressure
    >hypoproteinemia
  2. Common locations
    -ab cavity = hydro abdomen (ascites)
    -thoracic cavity = hydrothorax
    -pericardium = hydropericardium
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14
Q

Describe localized edema mechanisms of development.

A

-local impaired venous drainage
-local lymphatic blockage
-local inflam

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15
Q

Describe the histological appearance of edema.

A

-spaces distended
-blood vessels may be filled w RBCs
-lymphatics are dilated
-collagen bundles separated
-eosinophilic if inflam

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16
Q

Describe pulmonary edema & its gross appearance.

A

-accumulation of fluid in interstitum & alveoli of lungs
-common cause of death
GROSS:
-lungs swollen, heavy, wet
-interlobular septa distended w fluid
-froth in airways on cut surface

17
Q

Describe pulmonary edema in left sided heart failure VS increased endothelial permeability.

A
  1. Left sided heart failure
    -inc hydrostatic pressure in pulmonary circ -> non inflam edema
    -flood alveolar space w transudates
  2. Inc endothelial permeability
    -damage to pulmonary capillary endothelium w acute inflam -> inflam edema or toxins (ex. Pneumonia)
    -sudden, diffuse, direct inc in vascular permeability = massive inflam in distant organ/sepsis/toxins
    -
18
Q

Describe chronic pulmonary edema.

A

-associated w cardiac failure
-alveolar walls become thickened -> fibrosis
-congestion, microhemorrhages -> accumulation of heart failure cells
-chronicity -> fibrosis of pleura & alveolar septa

19
Q

Describe cerebral edema causes & gross appearance VS histological appearance.

A
  1. Causes
    -trauma to brain
    -obstruction of venous outflow
    -inflam
  2. Gross appearance
    -brain heavier
    -sulci are narrow
    -gyri are swollen & flattened
  3. Histological appearance
    -expansion of virchow robin spaces
20
Q

Describe cerebellar coning VS herniation.

Coning
A
  1. Coning
    -herniation of cerebellum thru foramen magnum
  2. Herniation
    -herniation of cd cerebral cortex beneath tentorium cerebelli
Herniation
21
Q

Describe the clinical significance of edema.

A

-depends on extent, location, duration
-tissue become firm & distorted due to inc in fibrous CT after prolonged edema

22
Q

Describe hyperemia/congestion.

A

-local inc in blood vol & flow within vascular bed
-hyperemia = inc of arteriole mediated engorgement of vascular bed
>oxygenated blood (red)
-congestion indicates passive venous engorgement
>blood not oxygenated

23
Q

Describe the 2 types of hyperemia.

A
  1. Physiological
    -digestion: inc blood flow to GIT during digestion
    -exercise: inc blood flow to muscles during exercise
    -dissipate heat: inc blood flow to the skin to dissipate heat & cool down
    -neurovascular (blushing): involuntary inc in blood flow to the face
  2. Pathological
    -caused by underlying pathological process (inflam)
    -arteriolar dilation occurs 2ndary to inflam stim (mediators)
    -5 cardinals signs of inflam
    -associated w edema
24
Q

Describe gross VS histological findings of hyperemia.

A
  1. Gross
    -red color of tissue (eye, gums, etc)
    -swelling, warmth
    -localized
  2. Histology
    -capillaries (+/-) arterioles dilated & filled w blood
    -accompanied by edema
    -inflam
    -hastens movement of metabolites into area & flushes catabolites from area
25
Q

Describe congestion & its classification.

A

-engorgement of vascular beds caused by dec outflow of blood
-vascular bed engorged w poorly oxygenated blood
>tissues are dark red or blue depending on degree of stagnation
CLASSIFICATION:
1. According to duration = acute or chronic
2. According to extend = localized & generalized systemic change like in CHF

26
Q

Describe gross VS histology findings of congestion.

A
  1. Gross
    -red to blue/black -> depending on degree of stagnation of blood
    -tissues might be cooler than normal
    -cut surfaces ooze blood & wet bc edema
    *EX: gastric volvulus
  2. Histology
    A) acute
    -engorged capillaries, (-/+) edema
    B) chronic
    -hypoxia, atrophy, cell degen & necrosis
27
Q

Describe pulmonary congestion.

A

-results of L side heart failure & associated w edema
>high hydrostatic pressure

28
Q

Describe hepatic congestion.

A

-subacute to chronic congestion = result of R side congestive heart failure

29
Q

Describe hyperemia VS congestion.

A
  1. Hyperemia
    -active
    -results in accumulation of oxygenated blood -> erythema
  2. Congestion
    -passive
    -results in red cell stasis & accumulation of deoxygenated hemoglobin -> cyanosis
Hyperemia on L & congestion on R