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PATH > Unit 2: Changes in Blood flow and body fluid balance > Flashcards

Unit 2: Changes in Blood flow and body fluid balance Flashcards

1
Q

fluid pressure balance in normal tissues

A

hydrostatic pressure and oncotic pressure are balanced and near 0
- contribute little to fluid exchange

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2
Q

fluid pressure in normal capillaries: venous end

A

vein end: vascular hydrostatic pressure (fluid out) < vascular oncotic pressure (fluid in)
- this drives fluid back into blood vessels, carrying away the metabolic waste byproducts

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3
Q

what is osmosis

A

the tendency of a fluid to move from a solution of lesser concentration to one of greater concentration when 2 solutions are separated by a semipermeable membrane

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4
Q

what is oncotic pressure (colloid osmotic pressure)

A

osmotic pressure that is exerted by proteins within the plasma portion of blood
- pressure draws water into vessels and hence circulatory system

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5
Q

what is hydrostatic pressure

A

pressure of water influenced by…
- the activity of the heart as a pump
- the elasticity and recoil of blood vessels
- the quantity of blood within a vessel

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6
Q

what is the result of increased hydrostatic pressure (or diminished plasma osmotic pressure)

A

extravascular fluid accumulation (edema)

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7
Q

what is ultrafiltrate

A

fluid which has passed out of the normal capillary containing water, salts and small organic molecules
- excludes large protein molecules in the blood

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8
Q

what happens to remaining ultra filtrate that does not return to the capillary (and small proteins that may have also moved out)

A

they drain from the tissue via the lymphatic system, the lymphatic vessels drain into the bloodstream
- SO the fluid does return to the bloodstream, just not at the level of the capillary bed

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9
Q

what is edema

A

accumulation of excess fluid in extracellular spaces

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10
Q

where does edema occur

A

can occur in any tissue but most easily seen in the skin and associated subcutaneous tissues

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11
Q

what is localized edema

A

the result of a localized disturbance of the fluid exchange mechanism in the tissue
- e.g. bug bite

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12
Q

what is pitting edema

A

edema of the skin
- if focal pressure is applied to the edema area, a small focal depression or pit will be produced - pressure forced fluid out of the area

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13
Q

what is generalized edema

A

excess fluid is seen in many tissues
- e.g. congestive heart failure

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14
Q

what is effusion

A

when tissue fluid accumulates in body cavities such as the pleural space, pericardial sac of the peritoneal cavity

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15
Q

What is ascites

A

a watery effusion in the peritoneal (abdominal) cavity

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16
Q

what is anasarca

A

massive edema of the whole body, including body cavities

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17
Q

what is the pleural space

A

the space between the surface of the lungs and the pleura lining the chest wall

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18
Q

what is the pericardial sac

A

the membraneous sac that surrounds the heart, separating it from the adjacent lungs

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19
Q

what is the peritoneal cavity

A

the abdominal cavity, limited by the diaphragm, the abdominal walls and the pelvic floor
- contains the abdominal organs

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20
Q

normal state of the major body cavities

A
  • contain only a small amount of fluid
  • prevents friction between adjacent serosal or pleural surfaces
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21
Q

what happens in an abdominal (peritoneal) effusion

A

abdominal contents are surrounded by a reddish watery fluid (instead of a small amount of clear fluid like in normal)

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22
Q

dog example - signs of localized edema

A
  • swelling of limb
  • swelling is the same temperature as skin
  • feeling of a firm mass
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23
Q

what happens with obstructed venous drainage of the capillary bed

A
  • hydrostatic force at the venular end of the capillary bed would be increased
  • fluid leaves capillaries normal at the arteriole end (HP>OP) but cannot return to capillaries at veinous end
  • HP still exceeds OP therefore fluid remains in tissue spaces as edema
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24
Q

what determines the extent of edema that occurs with venous obstruction

A
  • size of vessel obstructed
  • how completely it is obstructed
  • extent of collateral venous circulation
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25
Q

what is the lymphatic system responsible for

A
  • removing the small protein molecules which leave the capillaries normally
  • removing small amounts of fluid that do not return to the capillaries via the oncotic pressure
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26
Q

venous obstruction vs lymphatic obstruction and edema

A

venous = immediate
lymphatic = over time

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27
Q

stages of lymphatic obstruction edema

A
  • initially small amounts of fluid remain in interstitium
  • accumulation of small molecules overtime leads to increased tissue colloid oncotic pressure (favours fluid remaining in the tissue spaces)
  • pull of oncotic pressure is not sufficient to move fluid back into the capillaries
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28
Q

what happens if lymphatic obstruction edema persists

A

the oedematous tissue may undergo fibrosis - affected area becomes firm and thickened

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29
Q

causes of localized edema

A
  • venous obstruction
  • lymphatic obstruction
  • acute inflammation
  • acute allergic reactions
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30
Q

how does localized edema form from acute inflammation and acute allergic reactions

A
  • increase in capillary permeability allows fluid and plasma proteins to move out of the capillaries and into the tissues
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31
Q

why does someone with congestive heart failure have swelling or pitting edema of the legs and ankles?

A
  • heart fails as a forward pump
  • venous blood “backs up” in systemic circulation
  • fluid gradually builds up in interstitial as it cannot move back up
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32
Q

what is dependent edema

A

edema in dependent parts of the body such as the lower legs and ankles because of effects of gravity

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33
Q

dependent edema in case of right sided heart failure

A

fluid will collect in the sacral region of the back and the buttocks

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34
Q

what happens with left-sided heart failure (failure to pump oxygenated blood to tissues)

A
  • decreased cardiac output
  • increased hydrostatic pressure in pulmonary vessels
  • lungs become edematous (retain fluid)
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35
Q

what happens when hydrostatic pressure is increased in pulmonary circulation

A

fluid leaves the capillaries but there is not much interstitial space for it to collect in, so fluid moves into the alveolar spaces

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36
Q

what is pulmonary edema

A

fluid moves into the alveolar space - interferes with gas exchange in the lungs and makes it difficult to breath

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37
Q

what is Dyspnea

A
  • shortness of breath (due to pulmonary edema)
  • in mid failure: only occurs with exertion
  • in severe failure: occurs at rest
  • more pronounced when lying down
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38
Q

signs and symptoms of pulmonary edema

A
  • non-productive cough
  • wheezing (due to bronchospasm initiated by high left atrial pressures)
  • extreme shortness of breath
    frothy blood-tinged fluid in the airways
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39
Q

what can cause congestive heart failure

A

anything which decreases cardiac output…
- decreasing contractility of heart muscles
- causing mechanical abnormality
- increased resistance to forward outflow
- electrical disturbance (arrhythmias)

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40
Q

what plays a major role in the volume of pulmonary edema

A

sodium and water retention by the body

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41
Q

how does left-sided heart failure lead to sodium and water retention

A
  • decreased “forward” cardiac output from left ventricle
  • decreased blood flow to the kidneys
  • decreased glomerular filtration pressure
  • renin production in the kidneys (leading to renin-angiotensin system)
  • system results in sodium and water retention
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42
Q

renin-angiotensin system

A
  1. decreased blood flow to kidneys
  2. decreased glomerular filtration rate
  3. increased renin production by juxtaglomerular apparatus
  4. renin increases angiotensin release
  5. angiotensin converted to angiotensin II which increases aldosterone production by adrenal cortex
  6. leads to increased sodium retention
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43
Q

Aldosterone results in retention of salt and water within the blood which in turn…

A
  1. increases blood volume (and vascular hydrostatic pressure)
  2. decreased vascular oncotic pressure by diluting blood albumin
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44
Q

what is hypoproteinemia

A
  • low levels of serum protein
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45
Q

what are the major causes of generalized edema

A
  • hypoproteinemia
  • congestive heart failure
  • renal failure
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46
Q
  • hypoalbuminemia
A

low levels of albumin
- decreases the plasma osmotic pressure
- leads to sodium and water retention (attempt to increase vascular volume) - ultimately decreases albumin further due to dilution

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47
Q

common result of heart failure and hypoproteinemia

A

decrease glomerular filtration - lead to sodium and water retention - worsening edema

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48
Q

Causes of hypoproteinemia

A
  1. low serum protein: insufficient dietary protein, decreased albumin synthesis, increased loss of albumin
  2. albumin and globins
  3. nephrotic syndrome: due to disease of the glomerulus in the kidney
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49
Q

what is a syndrome

A

a set of symptoms that occur together - not a specific disease

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50
Q

effect of effusions in the pleural and pericardial space

A
  • restricts the expansion of the lungs - leads to dyspnea
  • restricts filling of the heart - leads to decreased cardiac output
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51
Q

what may lead to cerebral (brain) edema

A
  • head trauma
  • cerebral vascular accidents
  • infections
  • tumours
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52
Q

cerebral edema

A
  • pressure within the cranium leads to headache
  • as pressure increases parts of the brain are forces to herniate down
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53
Q

plasma vs serum

A

plasma: fluid part of the blood in which blood cells are suspended - composed of water, electrolytes and protein
serum: fluid that remains after blood has been allowed to clot in a tube - fibrinogen id depleated

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54
Q

what is a hemorrhage

A

presence of blood in the interstitial tissues, within a body cavity, or externally

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55
Q

what is petechiae

A

small pinpoint focal hemorrhage

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56
Q

what is purpura

A

multiple 3-5mm sized, oval to irregularly shaped hemorrhages

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57
Q

what are ecchymoses (bruises)

A

large areas of heorrhage

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58
Q

what is hematoma

A

a large blood blister - area where blood has pooled within the tissue

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59
Q

what is a cause of petechiae

A

lack of sufficient numbers of platelets

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60
Q

what are hemoperitoneum, hemothorax and hemoperricardium (respectively)

A

hemorrhage into the peritoneal, pleural and pericardial spaces

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61
Q

what is hyphema

A

hemorrhage into the fluids within the eye

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62
Q

why is hemoperricardium particularly problematic

A

if enough blood accumulates within the enclosed pericardial space, the pressure of that blood can reach an equilibrium with to even overcome the BP of the heart - causes collapse of the right atrium and ventricle

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63
Q

what happens if the chambers of the heart collapse

A

blood can no longer enter the chambers and acute heart failure ensures

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64
Q

what is spontaneous hemorrhage

A

hemorrhage without trauma, such as excessive bleeding after a skin wound or following surgery
- can occur from nose, gums, lungs etc.

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65
Q

what is epistaxis

A

spontaneous nose bleeds

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66
Q

how does injury from blood vessels lead to hemorrhage

A

the hydrostatic pressure of the blood will cause blood to leave the vessel as soon as the vessel wall is damaged

67
Q

what is hemostasis

A

the process of blood clotting that prevents excessive bleeding after blood-vessel damage
- fine balance between… primary hemostasis, secondary hemostasis and fibrinolysis

68
Q

what initially controls hemostasis

A

contraction of smooth muscle in the arteriolar wall (vasoconstriction) - effective in small vessels

69
Q

steps in hemostasis

A
  1. vasoconstriction
  2. platelet activation and aggregation
  3. activation of clotting factors and formation of fibrin
  4. clot resorption
70
Q

what happens in the platelet activation and aggregation step of hemostasis (step 2)

A
  • platelets bind via Gplb receptors to vWF on exposed ECM and are activated
  • platelets undergo a shape change and granule release
  • released ADP and TXA2 induce additional platelet aggregation through Gpllb-IIIa receptor binding to fibrinogen
  • this form the primary plug
71
Q

what happens in the activation of clotting factors and formation of fibrin step of hemostasis (step 3)

A
  • local activation of the coagulation cascade
  • results in fibrin polymerization, cementing platelets into the secondary plug
72
Q

what happens in the clot resorption step of hemostasis (step 4)

A
  • counterregulatory mechanisms mediated by tPA and thrombomodulin
  • confine the hemostatic process to the site of injury
73
Q

what are the 4 primary responses involved in normal hemostasis

A
  1. transient arteriolar vasoconstriction
  2. primary hemostasis
  3. secondary hemostasis
  4. formation of a permanent plug
74
Q

what are the 3 general components needed for hemostasis

A
  1. platelets
  2. vascular wall
  3. the coagulation cascade
75
Q

what is the role of platelets in hemostasis

A

forming the platelet plug (primary hemostasis)

76
Q

what happens to platelets when the vessel walls are injured

A

platelets are exposed to constituents of the extracellular matrix, subendothelial collagen and a variety of adhesive glycoproteins

77
Q

what is the role of fibrinogen

A

acts to connect large numbers of platelets together to form large aggregates

78
Q

what are the effects of PGI2 and TXA2 on blood vessels

A

PGI2: vasodilation - helps lower BP and increase blood flow
TXA2: vasoconstriction - increases BP and reduces blood flow to site of injury

79
Q

what are the effects of PGI2 and TXA2 on platelet aggregation

A

PGI2: inhibits it - increases cAMP within platelets which leads to decreased activation, prevents thrombosis
TXA2: activates platelet aggregation - amplifies clotting process, crucial in hemostasis

80
Q

what is the purpose of the endothelial wall in hemostasis

A

critical in preventing blood clots - have antithrombotic properties
- when endothelium is disrupted due to blood vessel injury and extracellular matrix is exposed it becomes prothrombic

81
Q

what are the prothrombotic properties of endothelial cells

A
  • synthesis of VWF
  • induced by cytokines or bacterial endotoxin to secrete tissue factor
  • binding to activated coagulation factors to augment their activities
  • secretion of inhibitors of plasminogen activators
82
Q

what is the coagulation cascade

A

a series of enzymatic conversions which convert inactive proenzymes into their active form ignorer to initiate the next step

83
Q

what are additional factors that optimize coagulation

A
  • calcium ions
  • a phospholipid surface
  • vitamin K (for synthesis of prothrombin and clotting factors)
84
Q

initiation of clotting in the laboratory

A

intrinsic: initiated by adding phospholipids and calcium to a negatively charged surfaces
extrinsic: initiated by adding phospholipids and calcium to tissue factor

85
Q

initiation of the coagulation cascade in vivo

A

Tissue factor is the main initiator - amplified by feedback loops involving thrombin

86
Q

common result of the coagulation cascade

A
  • conversion of the proenzyme prothrombin to thrombin
  • allows conversion of fibrinogen to fibrin
  • fibrin then makes a mesh network that is the basis of the clot
87
Q

what is the purpose of fibrinolysis

A

counteracts clotting
- proenzyme plasminogen is incorporated into a developing clot, is later activated within the clot (to plasmin) when it needs to be dissolved

88
Q

role of plasmin

A

breaks down fibrin snd interferes with its polymerization
- fibrin breakdown products are weak anticoagulants

89
Q

what are the main coagulation dissorders

A
  1. deficiency of coagulation factors
  2. increased anticoagulant activity
90
Q

common clinical manifestations of coagulation dissorders

A
  • bleed excessively following minor trauma
  • spontaneous bleeding
91
Q

Hemphilia

A
  • sex-linked inherited disease
  • deficiency in factor VIII
  • bleeding spontaneously - often in subcutaneous tissue, muscle and joints
  • subsequent fibrosis cases muscle contractors and joint stiffness
92
Q

Von Willebrand’s disease

A
  • inherited disease
  • reduced levels of circulating VWF and the entire factor VIII complex is deficient
  • disorders in platelet function
  • bleeding tendencies related to both VWF and platelets
93
Q

what do anticoagulants do

A

“induce” factor deficiencies and can lead to bleeding problems
- e.g. warfarin and heparins

94
Q

how are platelet disorders characterized

A

“small bleeds” in the skin, particularly petechiae and purpura

95
Q

what is thrombocytopenia

A
  • decreased platelet numbers
  • caused by deficient production or maturation of platelets in bone marrow, abnormal distribution of platelets within body, or increased destruction of platelets
96
Q

what is thrombocytopathia

A
  • abnormalities in platelet function
  • platelet counts are normal
97
Q

clotting vs thrombosis

A

clotting: protective and prevents excessive hemorrhage
thrombosis: clotting “gone wrong” or within a vessel

98
Q

what is Virchow’s Triad

A

3 factors for the development of thrombosis
1. endothelial injury
2. alteration in normal blood flow
3. hypercoagulability

99
Q

endothelial injury and thrombosis development

A

changes in endothelial vessels can either lead to acute or chronic thrombosis
acute: caused by trauma or surgery, inflammation and lack of blood supply. post-surgical period = high thrombosis risk, can be prevented with anticoagulants
chronic: more common, example is atherosclerosis

100
Q

what is atherosclerosis and its clinical significance

A

chronic endothelial injury, primarily affecting arteries. it can…
- cause symptomatic disease involving arteries supplying the heart, brain, kidneys and lower extremities
- compromise of blood flow in smaller arteries, leading to schema
- thrombus formation
- aneurysm formation due to weakening of vessel walls
- embolism

101
Q

who is more at risk for atherosclerosis

A
  • older people
  • women following menopause
  • those with diabetes mellitus
  • those with a sedentary lifestyle
  • people who smoke
  • people with chronic inflammatory disease
102
Q

alterations In normal blood flow and thrombosis development

A

caused by stasis or pooling of blood

103
Q

2 changes that occur to alter normal blood flow

A
  1. turbulence: blood flow becomes fast yet erratic causing greater interaction with the endothelium
  2. stasis/pooling: blood flows much slower than normal because of failure of forward pressure, downstream obstruction of flow of abnormal flow qualities to the blood itself such as hyperviscosity
104
Q

normal blood flow

A
  • in larger vessels blood flows in a layered pattern
  • the central column of blood cells moves very swiftly
  • blood adjacent to the endothelium moves more slowly
105
Q

what is polycythemia

A

an increase in RBC numbers which leads to increased viscosity of the blood (hyper viscosity and blood stasis)

106
Q

relative vs absolute polycythemia

A

relative: often occurs because of dehydration ( can also occur because of hyper coagulability)
absolute: has significant clinical effects similar to blood stasis

107
Q

Appropriate adaptive physiological polycythemia

A
  • deficient oxygenation of blood which causes release of erythropoietin form the kidney to increase RBC mass
  • athletes use this to give them an edge when competing at sea level
108
Q

inappropriate non-physiological polycythemia

A
  • caused by increases erythropoietin levels which increase RBC mass
  • seen with tumours
  • injectable erythropoietin can be used illegally
109
Q

what is hypercoagulability

A

any alteration in the balance of clotting and fibrinolytic mechanisms which favour thrombosis
- causes include factor V or prothrombin mutations

110
Q

what is economy class syndrome

A
  • the development of deep venous thrombosis in the legs of passengers in cramped seating on long distance air flights
111
Q

what is ischemia

A

a reduction or failure of blood supply to tissues

112
Q

what is an infract

A

localized failure of blood supply will lead to necrosis of the tissue
“ischemic necrosis”

113
Q

effects of ischemia

A
  • can cause hypoxia
  • can lead to functional changes in tissue
  • cause gradual death of specialized cells of an organ or tissue
  • loss of coronal neurons (failure of recent memory)
  • pain in skeletal and cardiac muscle
  • can lead to infraction if blood supply fails
114
Q

infraction due to arterial obstruction (heart attack)

A
  • when an area of the myocardium is deprived of blood due to occlusion of a coronary artery, death of cardiac myocytes occurs
115
Q

critical level of major coronary artery narrowing

A
  • 75% or greater = critical
  • the artery is unable to meet a moderate increase in myocardial oxygen demand therefore myocardial ischemia occurs
116
Q

manifestations of coronary artery atherosclerosis

A
  • atherosclerotic plaque causes a narrowing of the vessel
  • results in changes in blood flow and endothelial damage
  • these changes cause endothelial injury, alterations in blood flow and alterations in blood clotting factors - prime for a thrombotic event to occur and result in ischemia
117
Q

what is a prognosis

A

the “forecast” as to the most likely outcome of a disease
- an attempt to predict the recovery of a disease
- accuracy depends on physicians knowledge

118
Q

what factors influence the outcome of arterial obstruction

A
  1. the availability of collateral circulation: development of alternate pathways if primary means of delivery are obstructed
  2. the integrity of the collateral arteries
  3. the tissues susceptibility to ischemia: brain and heart are very susceptible
  4. the tissue metabolic rate: state of demand for that tissue
  5. the rate of development of the obstruction: sudden obstructions are more severe for ischemic changes
119
Q

what is the femoral artery

A

one of the major arteries supplying the lower limbs

120
Q

cat ischemia example - sources of stiffness and pain in legs due to ischemia and pulmonary edema

A
  1. lack of femoral pulses: blood flow to femoral arteries is obstructed, lack of blood supply to muscles therefore lack of oxygen to tissues
  2. congestive heart failure: cardiac output has decreased and blood flow is slowed, may develop a thrombus
  3. Thrombosis: could be the cause of obstruction of the arteries
121
Q

what does idiopathic mean

A

a disease of an unknown cause

122
Q

feline cardiomyopathy - common idiopathic condition

A
  • hypertrophy of the left ventricle
  • increased turbulence and stasis flow - probably contribute to thrombosis of the left atrium
  • emboli travel from the left atrium to the bifurcation of the distal aorta
123
Q

what is an embolus

A

a free-floating intravascular solid, liquid or gaseous mass that is carried by the blood to a different site
- majority originate as part of a dislodged thrombus (thromboembolism)

124
Q

what do emboli do

A
  • obstruct arteries and arterioles (rather than veins) as they become narrower until the embolus is too large to pass
  • blocks the lumen of the artery preventing blood from reaching the tissue
125
Q

organs that have dual blood supply

A
  1. lungs: both pulmonary and bronchial arterial blood supply
  2. liver: both hepatic artery and portal veins supply blood
126
Q

embolus and organs without dual blood supply

A

if the embolus is sufficient in a tissue lacking alternate blood supply, then insufficient blood reaches the tissues - leads to infraction

127
Q

what do arterial infracts look like in dense tissues vs tissues with dual blood supply

A
  • pale (sine the area lacks blood and venous circulation is still intact)
  • hemorrhagic appearance - since some blood continues to flow in this area so hemorrhage occurs from necrotic small vessels
128
Q

what happens over time to arterial infracts with hemorrhage appearence

A

the body will react with inflammation to the necrotic tissue and a red line may develop around the margin of the infract - necrotic tissue may be removed and replaced by scar tissue, so the infract appears sunken

129
Q

development of edema by obstructed veins

A
  • the increased hydrostatic pressure favours fluid remaining in the interstitial
  • tissue hydrostatic forces increase - acts to limit further swelling but the net result leads to edema
  • results in local venous capillary congestion
130
Q

development of infract from obstructed veins

A
  • local venous capillary congestion occurs
  • venous hydrostatic forces may rise rapidly and cause capillary rupture and hemorrhage
  • if deoxygenated blood cannot leave, hypoxia results
  • leads to increased capillary permeability and hemorrhage will occur and create a venous infract
131
Q

outcome of venous obstruction based on hoe severe

A

local edema - congestion - hemorrhage
- depends on the size of the vein, how quickly the obstruction develops, availability of collateral drainage

132
Q

what is torsion

A

the twisting of the pedicle of an organ

133
Q

testicular torsion

A
  • when a testicle becomes twisted on its own axis, completely obstructing all venous drainage through the spermatic cord, and leading to edema and hemorrhagic infraction
134
Q

what is tachycardia

A

faster than normal heart rate

135
Q

what is tachypnea

A

abnormally rapid breathing

136
Q

lesions due to testicular torsion

A
  1. a twist in the mesentery at the root of the colon, causing collapse of the veins draining the affected loop of bowel
  2. a segment of large intestine that is congested to hemorrhage and edematous
137
Q

what do intestine accidents result in

A
  • venous infraction of the affected organ
    *not arterial because BP within veins is much lower than arteries
  • shock is a common sequel to this
138
Q

what is repercussion injury

A

when resolving tissue ischemia actually promotes and exacerbates the severity of the initial injury

139
Q

by what 2 processes are reperfusion injuries mediated (respectively)

A
  1. increased sensitivity of oxidative stress
  2. inflammation
140
Q

what can happen if you restore blood supply to a tissue after venous outflow is impaired

A
  • you can release any inflammatory mediators and toxic byproducts from cell death into the bloodstream - will likely cause shock
141
Q

what is the best treatment for a reperfusion injury of the intestine

A

to surgically remove that loop of intestine to relieve the torsion and avoid systemic concequences

142
Q

what is disseminated intravascular coagulation (DIC)

A

a thrombohemorrhagic disorder resulting from widespread activation of coagulation - which leads to widespread thrombosis in microcirculation of the body - often fatal complications

143
Q

how can DIC form

A
  • it is the result of severe underlying disease
  • does not occur without triggers
  • not a disease but a syndrome
144
Q

consumptive coagulopathy

A

the latter stage of DIC

145
Q

how can DIC be triggered

A
  1. by the release of tissue factor, or other thromboplastin substances into the circulation
  2. by widespread endothelial injury
146
Q

what diseases is DIC often associated with

A
  • sepsis
  • malignancy (cancer)
  • obstetric complications
  • severe trauma
  • burns
147
Q

relationships in DIC and the bleeding tendency

A

massive tissue destruction, sepsis and endothelial injury leads to the release of tissue factor - activates primary and secondary clotting cascades… - results in widespread thrombosis - results in tissue hypoxia and then ischemia
- fibrinolysis cascade is activated at the same time as the clotting cascade to breakdown clots - problem as platelets were previously consumed from endothelial damage

148
Q

the obstruction of the microcirculation by micro thrombi can cause…

A

widespread impaired tissue perfusion, leading to tissue hypoxia, shock and micro infarction in many organs

149
Q

how is DIC diagnosed

A

clinical signals such as…
- damages RBCs (happens when passing through fibrin strands of microthrombi)
- thrombocytopenia - thrombocytes are “consumed” in thrombus formation

150
Q

major goal of DIC therapy

A

to stop the cycle of thrombosis and fibrinolysis

151
Q

what is shock

A

a physiologic state characterized by a generalized reduction of passage of body fluids to an organ/tissue
- related to a decrease in either effective cardiac output or ineffective circulating blood volume

152
Q

what are the causes of shock

A
  1. hypovolemia (decreased BV)
  2. Septic shock
  3. Cardiogenic shock
  4. neurogenic shock
  5. anaphylactic shock
153
Q

what is hypovolemia shock

A
  • associated with hemorrhage (blood loss) or fluid loss which leads to decreased plasma and blood volume
154
Q

what is septic shock

A
  • associated with widespread vasodilation that increases the capacity of the vascular bed causing maldistribution of fluid
  • leads to tissue hypo perfusion and organ dysfunction
  • triggered by microbial infections, severe tissue trauma and inflammation - leads to SIRS
155
Q

what is cariogenic shock

A
  • associated with failure of the heart to function effectively as a pump
  • results from primary diseases of the heart and with conditions obstructing blood flow in the heart or filling of the ventricle
156
Q

what is neurogenic shock

A
  • results from anesthesia or spinal cord injury and results loss of vascular tome and maldistribution of body fluids
157
Q

what is anaphylactic shock

A

results in systemic vasodilation and increased vascular permeability - but is triggered by IgE-mediated hypersensitivity

158
Q

phases of shock

A
  1. non-progressive or compensated phase
  2. progressive or non compensated phase
  3. terminal phase
159
Q

non-progressive/compensated phase of shock

A
  • various neurohumoral reflex mechanisms to maintain cardiac output and blood pressure
  • decreased blood pressure causes increased heart rate and stroke volume
  • peripheral vasoconstriction helps maintain blood pressure in vital organs by diverting blood from peripheral vascular beds
  • fluid retention by kidneys to help retain body fluid and maintain BP and volume
160
Q

progressive/non-compensated phase

A
  • development of widespread tissue hypoxia which begins to affect function of vital tissues and organs
  • decreased blood flow to brain
  • urinary output declines further
  • prolonged vasoconstriction acts to further impair tissue perfusion
  • leads to acidosis and lysosomal enzyme release
161
Q

what are effects of prolonged vasoconstriction

A
  • myocardial contractile function worsens
  • decreased renal blood flow (ischemic injury of kidneys)
  • hypoxia in the lungs - causes edema and hemorrhage (leading to “shock-lung” and dyspnea)
  • ischemic necrosis of the intestine (endotoxic or septic shock)
  • DIC
162
Q

terminal result of shock

A
  • failure of the reflex peripheral vasoconstriction
  • movement of blood into these vascular beds causes a steady fall in BP - perfusion of brain and heart is inadequate
  • multiple organ dysfunction
  • cerebral and myocardial hypoxia
  • death
163
Q
A

PATH (11 decks)

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