Lecture 14: Regulating Flow, Coagulation and Peturbation of Flow Flashcards

1
Q

Define active hyperaemia

A

Increased BV due to arteriolar dilation and expansion of the perfused capillary bed

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2
Q

Define passive hyperaemia/ congestion

A

Increased blood volume within the vasculature of a tissue due to impairment of venous outflow

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3
Q

What is another name for passive hyperaemia

A

Venous (passive) congestion

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4
Q

Give examples for which active hyperaemia occur

A

Stomach when eating
Muscles when exercising
local inflammation
–> associated with increase tissue metal, O2 consumption

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5
Q

Is the early response to injury active or passive hyperaemia??

A

Active –> facilitated by NO, prostaglandins

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6
Q

Why is active hyperaemia localised??

A

Local mediators

There is insufficient blood vol to permit a generalised effect whilst maintaining systemic blood pressure!

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7
Q

Give examples for which passive hyperaemia occurs

A

Rectal prolapse
Upstream of causal lesion e.g. bloat line
luminal obstruction of vein due to thumbs
intestinal strangulation - volvulus or torsion

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8
Q

Can passive hyperaemia be localised?

A

Yes- e.g. bloat line

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9
Q

Can passive hyperaemia be generalised?

A

Yes e.g. congestive heart failure –> severe generalised oedema

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10
Q

where does the blood pool during left sided congestive heart failure

A

in the lungs

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11
Q

what does the lung look like grossly during acute stage of left sided congestive heart failure

A

diffuse dark red/ purple
wet, rubbery
LUNGS DO NOT COLLAPSE WHEN U OPEN THE THORACIC CAVITY
foam surfactant in bronchioles/bronchi/trachea

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12
Q

what does the lung look like grossly during chronic stage of left sided congestive heart failure

A

diffuse interstitial fibrosis –> palpable stiffness of lung
diffuse tan discolouration
may see some MO with heamosiderin in hits (engulf RBC)

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13
Q

where does the blood pool during right sided congestive heart failure, where is it most obvious?

A
  • cranial and caudal vena cave
  • splanic viscera
  • THE LIVER
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14
Q

what does the liver look like grossly during acute stage of right sided congestive heart failure

A

swollen, dark red/purple
venous blood ooze from cut surface
hilar lymphatics distended

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15
Q

what does the liver look like histologically during acute stage of right sided congestive heart failure

A

central vein and periacinar (zone 3) distended w/ blood

–> hydropic or fatty necrosis

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16
Q

what does the liver look like grossly during chronic stage of right sided congestive heart failure

A

fibrosis
grossly obvious nutmeg liver pattern - zonal pattern
sinusoids dilated with blood

17
Q

what are the other consequences of right sided heart failure

A
hydrothorax
hydopericardium
congestion of spleen
congestion of kidney 
congestion of intestinal viscera 
ventral/dependent oedema
18
Q

what are the different gross appearances of congestion vs. hyperaemia

A

congestion - dark red/ purple cf. cyanotic

no associated increase in tissue temp

19
Q

what are the consequences of congestion

A

–> venous hypertension

local tissue hypoxia –> degeneration atrophy of parenchyma

20
Q

what is oedema

A

accumulation of excess body fluid

21
Q

what are the x5 major mechanisms of oedema formation

A
  • increase plasma hydrostatic pressure
  • decrease plasma colloid pressure
  • lymphatic obstruction
  • increase vascular permeability
  • (sodium retention)
22
Q

what is an increased plasma hydrostatic pressure usually a consequence of?

A

venous hypertension

23
Q

how does venous hypertension result in increased plasma hydrostatic pressure

A

plasma hydrostatic pressure is capillary bed usually a reflection of capillary venous pressure
- increase in venous pressure is relayed upstream, negates the net absorptive pressure, fluid filtered out is failed to be reabsorbed

24
Q

why does systemic hypertension not result in oedema?

A

reflex = vasoconstriction, protect capillary beds

25
Q

what are some localised vs generalised causes of increased plasma hydrostatic pressure?

A

localised - local obstruction of venous flow ie/ occlusion of vein by thrombosis
generalised - conditions of impaired VR to heart

26
Q

what is a decreased plasma colloid pressure usually referable to?

A

hypoalbuminea

27
Q

how low must serum albumin be before hypoalbuminea?

A

<10-15g/L

28
Q

what are the most common causes of hypoalbuminea?

A
  • decreased hepatic synthesis; malnutrition/starvation, chronic hepatic insufficiency
  • loss of protein: severe burns, protein losing enteropathy,
29
Q

is the oedema caused by hypoalbuminmia likely to be localised or generalised and why

A

GENERALISED –> lose protein from everywhere
decrease plasma colloid pressure –> net movement of fluid into interstitum –> decrease effective circulating blood volume –> RAAS activated –> retention of Na, –> exacerbation of oedema

30
Q

is lymphatic obstruction causing oedema normally localised or generalised?

A

localised

31
Q

name 3 things that can obstruct lymph vessels

A
  • parasite
  • lymphangitis
  • trauma
32
Q

is oedema caused by an increase in vascular permeability normally localised or generalised?

A

localised to the cause of inflammation

33
Q

what is the clinical significance of oedema

A
  • impaired wound healing
  • secondary bacterial infections
  • fibroplasia and permanent fibrosis
34
Q

what are two life threatening locations to have oedema?

A
  • cerebral

- pulmonary

35
Q

what are the references for transudate, modified and exudate oedema?

A

transudate: <25 protein, <1.5x10^9 cells
modified: 25-75 protein, 1.0-7.0x10^9 cells
exudate: >30 protein, >7.0x10^9 cells