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Y2S2 VETS2007 theory > Circulatory disorders > Flashcards

Circulatory disorders Flashcards

1
Q

Fx Endothelial

A

Lining all circulatory components, in a singular layer
synthesise and secrete substances which - (fluid balance, haemostasis, inflammation, immunity, angiogenesis/healing

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2
Q

3 components of microcirculation and their characteristics

A
  1. Arterioles
    major resistance
    Myocytes contract to control flow
  2. Capillaries
    enormous volume
    Slow velocity
    Sx= single endothelial layer
    Nutrient and waste exchange lx = fluid balance maintenance
  3. Postcapillary venules
    low resistance
    Store lots of blood up to 65%
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3
Q

Mechanisms for substance transport across the capillary wall


A

Direct diffusion (passive)
through endothelial cell membrane (gas and lipid soluable)
Interendothelial pores (water, ions, glucose, amino acids, waste)

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4
Q

What occurs to capillary wall transport during inflammation

A

The inter endothelial pores become large enough for large proteins (eg albumin) to escape

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5
Q

Three regional differences in capillary lining
- list and explain the lining on them

A

Continuous capillaries
complete endothelium and basal lamina
Lx muscle, Brain, thymus, skin, bone, lung etc
Allow transfer of H2O, O2 and CO2 and ion

Fenestrated capillaries
Small opening
Lx Often have a diaphragm (eg intestinal villi, kidney interstitium, choroid plexus)
Fx - can act as filter = renal glomerulus

Discontinuous capillaries
Larger gaps - discontinuous basal lamina allow large molecule or even cells to exit
Lx - hepatic and spleen
Fx -free transfer of plasma proteins, red and white blood cells, water and most molecules across endothelial cells

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6
Q

Fluid Distribution & Homeostasis
- explain the percentages of each one

A

• Total Body Water (~60% of lean body weight)
• Extracellular fluid (20%):
o Plasma (5%)
o Interstitial tissue fluid (15%)
• Intracellular fluid (40%)

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7
Q

Interstitium LX

A

Lx- space between microcirculation and the cells

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8
Q

interstitium Stx

A

Sx
made of extracellular matrix + supporting cells ( eg fibroblasts)
Has structural support and adhesive and absorptive properties
Composed of
Structural molecules: collagen, reticulin & elastin fibers.
Adhesive glycoproteins: fibronectin, laminin

Absorptive (hydroscopic) molecules: glycosaminoglycans, proteoglycan

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9
Q

Interstitium Fx (2)

A

Fx
binding cellular and structural elements into discrete organs and tissues
Medium through which all metabolic products pass through

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10
Q

Movement of fluids what affects it

A

Blood <—> intersitium <—> cells is controlled by - - physical stx
pressure gradients
Ion concentration

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11
Q

explain the things that move between blood and cells

A

In most areas, the capillary allows the free passage of water and ions and opposes the passage of plasma proteins.

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12
Q

what are the primary influence on the movement between compartments (blood, interstitium and cells)

A

Primary determinant is hydrostatic pressure end osmotic pressure

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13
Q

Starlings equation significance

A

Moving out fluid = hydrostatic pressure in the vascular system + some interstitial colloidal somatic oncotic pressure

Retaining fluid in the blood vessels
via the plasma proteins eg albumin ( most abundant) (primary way)
To a lesser extent —> Tissue hydrostatic pressure around blood vessels

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14
Q

explain Platlets

A

Primary haemostasis
Chemical and mechanical clotting contribution
For a loose plug

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15
Q

Cascade of coagulation factors

A

Secondary haemostasis
Formed in liver
Contact with damaged endothelium (among other things) = activation
Circulatory in inactive form
End result = Protein fibrin clot ( reinforcing platelet clot)

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16
Q

The circulatory disturbances (6)

A

Oedema
hyperaemia
Haemorrhage
Thrombosis
Ischaemia/Infarct
Shock

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17
Q

what is oedema

A

Imbalance in the factors controlling fluid distribution in the spaces - cellular, plasma and interstitial compartments
- the excess fluid accumulates in the interstitum

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18
Q

Histology oedema

A
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19
Q

Explain explain the fluid dynamics of arteriole end to venue end of capillaries and lymph significance, when everything is normal

A

(hydrostatic + colloidal pressure difference of vascular to interstitial compartment) ==
Art Cap end = flow out of capillary
Ven Cap end = Flow into capillary

Small net loss from vasculature = lymph
Essential that net loss = lymph drainage rate

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20
Q

4 basic processes that alter lymph creation and removal IMPORTANT

A

Decreased plasma (colloidal) osmotic pressure
Increased hydrostatic pressure
Obstruction of lymphatic drainage (least common)
Increased vascular permeability

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21
Q

Explain Decreased colloidal pressure in blood vessel (3)

A

Colloidal pressure primary = presence of albumin
Thus hypoalbuminaemia = decreased colloidal pressure

insufficient synthesis:
protein deficiency (starvation)
Liver disease (not common)

Increased loss:
Renal disease
Gastro-intestinal loss

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22
Q

Explain increased hydrostatic pressure

A

May cause oedema
can be local or generalised (generalised = eg heart failure, local = local increase in pressure)
Most common cause = local increase pressure obstruction of veins

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23
Q

Explain the side of heart failure

A

Left it causes oedema in the lungs
Right is causes oedema in the liver
(Think about the blood going backwards)

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24
Q

Explain lymphatic obstruction

A

May cause oedema (not common)
typically causes localised oedema
Mechanical pressure
Inflammation (lymphangitis)
Obstruction by neoplastic or infectious prescesses

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25
Q

Explain increase vascular permeability and its causes

A

Endothelial layer is leaking so too much water is going out to the interstitial.

Causes
-inflammation > release of inflammatory mediators > vasodilation and increased vascular permeability
-Direct endothelial damage ( eg viruses toxins)

=Localised oedema&raquo_space;»» generalised oedema

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26
Q

Local(3) vs Generalised(2) causes of oedema

A

Localised oedema causes=
Local impaired venous drainage
Local lymphatic obstruction
Local inflammation

Generalised oedema=
Increased hydrostatic pressure (heart failure)
Decreased colloid osmotic pressure (hypoproteinaemia

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27
Q

Generalised causes of oedema list with pictures

A
28
Q

Hyperaemia –> general and the two types

A

Active or passive engorgement of vascular beds
“Big vessels with lots of blood”

Active - have more blood as the arteries are pumping more blood

Passive - congestion, engorgement of vascular beds due to decreased outflow of blood (passive hyperaemia

29
Q

Hyperaemia vs haemorrhage

A

Too much blood in = hyperaemia
too much out of the blood vessel = haemorrhage

30
Q

Active hyperaemia

A

Active process
Increase in glow
More oxygenated blood (red) XXXXX
Can be either physiological or pathological

31
Q

Three eg of physiological active hyperaemia

A

Digestion
Exercise
Heat dissipation

32
Q

Three eg of pathological active hyperaemia

A

Inflammation > release of inflammatory mediators > dilation of arterioles
Often associated with oedema

33
Q

General congestion or passive hyperaemia

A

Passive process
Reduced outflow
Less oxygenated blood XXXXX
Due to blockage of venous drainage most commonly
-leads to cell death (necrosis) - how to differentiate passive vs active on histology

34
Q

how to tell macro tell if it is passive or active

A

Bright red = active
Darker = passive

35
Q

Active vs congestion hyperaemia features on histology how do you tell

A

Active hyperaemia

Congestional
- signs of cell degredation

36
Q

List the haemorrhage that have the specific name the area

A

Thorax
Peritoneum
Splenic
Epistaxis - nasal
Haemathrosis- joint

37
Q

Patechiae IMPORTANT

A

Very small pinpoint
Damage to capillaries only

38
Q

Ecchymoses

A

Large blotchy haemorrhages of larger vessels)

39
Q

Haemorrhage pathogenesis

A
  1. Loss of endothelial integrity or damage to the blood vessels
    trauma
    Vascular erosion/damage by inflammatory cells, toxin, neoplasia
  2. Platlet pathology
    decreased #
  3. Abnormal platelet Fx (genetic, drug-induced = as the platelets are produced by liver with vitamin K)
    Defects in coagulation factors
    inherited
    Acquired (decreased production - liver failure use_
40
Q

Resolution of haemorrhage (4 steps)

A
  1. activation of primary and secondary haemostasis + arrest of haemorrhage
  2. reabsorption of serum via lympathics and phagocytosis of cell debris and RBCs by macrophages

3.secretion og cytokines by macrophages –> capillaries and fibrocytes growing into the fibrin clot and secretion of fibrinolytic enzymes by macrophages –> clot removal

  1. formation of a collagenous mass (scar)
41
Q

Haemorrhage clinical implications what are the three things to look out for?

A

How much
Where
How quickly

42
Q

Reasoning for brain haemorrhage significance

A

Brain has no lympathics to drain excess fluid
No space to accomodate

43
Q

Thrombosis general

A

Inappropriate coagulation
Occurs in uninjured or mildly injured vessels
- may cause secondary necrosis

44
Q

Thrombosis pathogenesis the three (spend time thinking about this one)

A

Need two out of three at least to occur
altered blood flow
Endothelial injury
Hypercoagulability

45
Q

How does altered blood flow contribute to creation of a thrombosis

A

Coagulation factors are not running over the area is correct rate
eg turbulence causes - further endothelial injury or mixing of reagents —> quicker coagulation cascade
Eg stasis
1. No dilation of coagulation factors
2. Build up of thrombi

46
Q

How does endothelial injury contribute to creation of a thrombosis

A
  • major event
  • platelet and fibrins do not adhere to normal endothelium
47
Q

how does hyper coagulability contribute to creation of a thrombosis

A
  • increased concentration of clotting factors
48
Q

Three major consequences of thrombus

A

Ischemia
Infarction
Embolism

49
Q

Life cycle possibility of thrombus

A

Resolution
Embolisation to lungs (NEED TO UNDERSTAND MORE)
Organised and incorporated into walks

50
Q

Explain the DIC

A

Disseminated intravascular coagulation

The systemic thrombus causes lottos capillaries to blow = lots of small haemorrhage

51
Q

discuss how the thrombus looks like

A
52
Q

Ischaemia/infarct lots of info on its causes what it is

A

Area of ischaemic necrosis resulting from occlusion of either arterial supply or venous drainage

Pic

• Area of ischaemic necrosis resulting from occlusion of either arterial supply or venous drainage
Occlusion of the arteries = more common 

Causes: thrombosis, embolism, vascular occlusion from twisting of a 
vessel 

Most common in animals = pulmonary, intestinal and renal 


53
Q

Explain the infarction in the kidney

A

Renal infarct secondary to a thrombus in the artery
The bright red border is very prominent

54
Q

Explain infarction in the intestine

A

Passive hyper anemia

55
Q

Infarction —> the factors that influence the development. Characteristics of the an infarct
the three things to look for

A
  1. The vulnerability of the affected tissue to hypoxia
  2. Anatomy of blood supply
  3. Rate of vessel obstruction
56
Q

List organs that are very vulnerable to infarct and the reason why

A

brain etc
list more

57
Q

Which dies first renal or liver when cut off from blood

A

kidney

58
Q

Infarct: gross appearance

A

Wedge- shaped
Early —> ill defined and hyperaemic merging
Late ( by 48hrs) : pale

59
Q

Explain the 3. Rate of vessel obstruction

A

acute occlusion
Slow occlusion ( may have collateral circulation)

60
Q

SHOCK DEFINITON - be precise

A

Cardiovascular collapse occurring when the blood pressure is inadequate fro tissue perfusion

61
Q

What causes shock

A

Blood loss (>20% of circulating volume)
Fluid loss (vomiting, diarrhoea, burns)

62
Q

Explain cariogenic shock

A
63
Q

Explain how blood maldistribution. Causes shock and how it occurs

A

Causes systemic inflammation
Anaphylaxis (inappropriate reaction/inflammation) > Pathogenesis: blood/fluid loss > reduced blood volume > reduced blood pressure > reduced tissue perfusion

64
Q

Explain the composition of the causes of shock

A
65
Q

Shock lesions. list 9
- pulmonary
- liver
- kidney:
- Heat:
- Blood vessels:
- Brain:
- adrenal gland :
- GI tract:
- Skeletal muscle:

A
  • pulmonary congestion
  • liver congestion
  • kidney: actue tubular necrosis
  • Heat: haemorrhages and necrosis
  • Blood vessels: endothelial damage with thrombosis/DIC
  • Brain: neuronal cell death
  • adrenal gland : haemorrhage
  • GI tract: congestion and necrosis
  • Skeletal muscle; pallor

Y2S2 VETS2007 theory (12 decks)

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