Unit 2 Flashcards
1
Q
vascular hydro static pressure
A
pushing fluid out of vessels
2
Q
Onconic pressure
A
drawing fluid into vessels
3
Q
What is the purpose of the net effect of driving fluid into the vessels?
A
succeed in delivering nutrients and oxygen to the tissues
4
Q
what is the difference in hydrostatic pressure and oncotic pressure in the arteriolar end and the venular end of the capillary bed?
A
in the arteriolar end of the capillary bed the vascular hydrostatic pressure is higher than the oncotic pressure and drives fluid into tissues, but in the venular end the vascular hydrostatic pressure is lower than the oncotic pressure and drives fluid back into vessels carying away metabolic waste products
5
Q
Osmosis
A
tendency of fluid to move from a solution of lesser concentration to one
6
Q
Oncotic pressure or colloid osmotic pressure
A
refers to a form of osmotic pressure exerted by proteins most notable albumin within the plasma portion of the blood
7
Q
hydrostatic pressure
A
refers to the 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
8
Q
do hydrostatic and colloid oncotic pressure affect fluid exchange and why?
A
not really because they are near zero
9
Q
increased hydrostatic pressure can lead to what?
A
extra vascular fluid accumulation (edema)
10
Q
Fluid moves at _____ or _______ between endothelial cells
A
pores or junctions
11
Q
edema
A
excess fluid in extracellular spaces
12
Q
Edema’s are mostly seen in _______ tissue
A
subqutaneous
13
Q
what is a localized edema?
A
insect bite, result of localized disturbance of fluid exchange mechanism in tissue
14
Q
what is an edema of the skin?
A
pitting edema
15
Q
effusion
A
fluid accumulates in the body cavities, pleural space, or pericardial sac or peritoneal cavity
16
Q
Ascites
A
specific name for watery effusion in the peritonial cavity
17
Q
Anasarca
A
indicative massive edema of the whole body
18
Q
Pleural space
A
between surface of the lung and pleural lining of the chest wall
19
Q
Pericardial sac
A
membrane that surrounds the heart
20
Q
Peritonial cavity
A
abdominal cavity
21
Q
what is the lymphatic system responsible for with local edema’s
A
removing small protein molecules which leave capillaries normally as well as a small amount of fluid which does not return to the capillaries via the onconic pressure
22
Q
lymphatic obstuction can cause a ______ over time as well as increased _____ ________ pressure which is usually _________
A
edema, colloid onconic, zero
23
Q
what are two important causes of localized edemas?
A
venous obstruction and lymphatic obstruction
24
Q
what causes a generalized edema?
A
if there is ventricular failure in the heart, blood backs up in the systemic circulatory system, there is a body wide venous obstruction causing an increase in hydrostatic pressure leading to a generalized edema
25
what is a dependent edema?
in dependent parts of the body such as lower legs or ankles
26
what will happen if the left side of the heart starts to fail?
blood will accumulate in the pulmonary circultion resulting in pulmonary venous congetion
27
increased pulmonary venous hydrostatic pressure means what?
fluid will remain in the lungs as edema
28
pulmonary edema
hydrostatic pressure increased, fluid leaves capillaries and moves to to alveolar space will interfere with gas exchange
29
Dyspnea
laboured or difficult breathing
30
orthopnea
condition with difficulty breathing when lying down related to positional changes in fluid accumulation
31
is congetive hert failure a disease?
no its a condition or end result
32
sodium stimulates water retention by what?
distal tubules of the kidneys
33
_________ results in retention of salt and water in the blood
aldosterone
34
increased water and salt retention in the blood can in turn do what?
- increase blood volume increasing vascular hydrostatic pressure
- decrease vascular oncotic pressure by diluting the blood albumin that largely determines the vascular oncotic pressure
35
what is this:
- caused by decrease colloid osmotic force
- insuficient dietary intake o protein
- decreased syntheisis of albumin in liver
hypoproteinemia
36
what is this:
- low levels of serum albumin
- low plasma osmotic pressure, decrease in plasma volume
- decrease glomular filtration in the kidney and increased secretion of renin leading to sodium and water retention in the kidneys
hypoalbuminemia
37
nephrotic syndrome
protein losing nephropathy, generalized edema, hypoalbuminemia, marked protinuria, its a syndrome with a bunch of symptoms together
38
plasma
fluid part of the blood which cells are suspended, composed of water and electrolytes and proteins as well as glucose enzymes products and nucleic acid metabolism
39
serum
fluid that remains after blood has been aloud to clot in a tube, similar to composition to plasma except fibrinogen and other clotting factors have been depleted by clot formation
40
hemorrhage
presence of blood in the interstitial tissues within a body cavity
41
petechia
small pinpoint focal hemorrhages
42
purpura
multiple 3-5mm sized oval to irregular shaped hemorrhages
43
ecchymoses
bruises, larger areas of hemorrhage
44
hematoma
large blood blister, area where blood has pooled in the tissue
45
peritoneal hemorrhage
hemopertoneum
46
pleural hemorrhage
hemothorax
47
percardial hemorrhage
hemopericardium, causes sudden death due to blood accumulating in the pericardial space, pressure causes collapse of right atrium and ventricle and heart failure occurs
48
hyphema
hemorrhage into the fluids within the eye
49
spontaneous hemorrhage
without trauma
50
what is hemostasis
process of blood clotting that prevents excess bleeding after blood vessel damage
51
normal hemotasis is a balance between ________ ____________ and ______________
primary hemostasis, secondary hemostasis ad fibrinolysis
52
hemostasis is initially controlled by what?
vasoconstriction, smooth muscle contraction in the arteriolar wall
53
vasoconstriction is effective for hemostasis in _______ but not in ________
small vessels but not large vessels
54
what are the 4 events that generally occur for normal hemostasis?
1. transient arteriolar vasoconstriction
2. formation of hemostatic plug (primary hemostasis)
3. secondary hemostasis including activation of the coagulation cascade that results in formation of fibrin clot
4. formation of permanent plug with concurrent counter, regulatory mechanisms or clot reabsorption (fibrinolysis)
55
the general sequece of events for hemostasis depend on what 3 componants?
1. platelets
2. vascular wall lined with endothelial cells
3. coagulation cascade
56
platelets are _______ than RBC's
smaller
57
do platelets have nucleus?
no
58
platelets form what?
the hemostatic plug
59
fibrinogen
plasma protein, important for platelet aggregation, and connects large number of platelets together to form large aggregates
60
what acts together to modulate platelet function?
two prostaglandins and thromboxane derived from platelets
61
why is intact endothelium important?
critical in preventing blood clots from forming and they have antimicrobial properties
62
when does the endothelium become prothrombotic?
when endothelium is disrupted due to blood vessel injury and ecm is exposed to the endothelium
63
what are some prothrombotic properties of endothelial cells?
- Synthesis of von Willebrand factor
- Induced by cytokines or bacterial endoxin to secrete tissue factor
- Binding to activated coagulation to augment their activities
- secretion of inhibitors of plasminogen activators
64
what does the coagulation cascade do?
series of enzymatic conversions that convert inactive pro enzymes into active enzymes
65
blood coagulation is divided into what two pathways ?
extrinsic and intrinsic
66
what are some factors needed to optimize coagulation?
calcium ions, phospholipid surface, vitamin K
67
what is needed for synthesis of prothrombin and clotting factors VII, XI, X?
vitamin K
68
what is similar between the intrinsic and extrinsic coagulation pathway?
Both extrinsin and intrinsic pathway lead to the conversion of the proenzyme prothrombin to the active enzyme thrombin, which then acts to convert fibrinogen to fibrin and amplifies the cascade
69
fibrin
polymerizes as a long insoluble strand forming a network that is the basis for a clot
70
thrombin
critical in catalyzing the final steps of the cascade and has a variety of effects on local vessels and inflammation
71
what is fibrinolysis and when does it occur?
along with the coagulation cascade is activated a fibrinolytic cascade that limits the extent of clot formation and helps in future dissolution
72
While fibrin is being formed the proenzyme _____________ is incorporated into the developing clot
plasminogen
73
within the clot plasminogen is formed into _________
plasmin/fibrinolysin
74
tissue type plasminogen activator (tPA)
synthesized by endothelial cells, management for thrombosis
75
plasmin
acts to break down fibrin, interferes with polymerization
76
the presence of fibrin split/breakdown products indicate what?
thrombotic disease
77
what are FSPs/FDPs?
weak anticlogulants
78
normal hemostasis is a balance between ________ and _______
clot formation and fibrinolysis
79
summarize how a clot forms from vessel injury
vessel injury occurs, transient vasoconstriction helps limit blood flow, platelets adhere to injured area, clot is formed to stop excessive bleeding, fibrinolysis prevents the clot from becoming overly large and interfering with blood flow
80
coagulation disorders have two categories
1. deficiency of coagulation factors
| 2. increased anticoagulant activity
81
what are the two common gene abnormalities with deficency of coagulation factors?
hemophilia A and von willebrands disease
82
Hemophilia A
Deficiency in normal functioning factor VIII, critical componant to the intrinsic pathway due to insuficient synthesis of factor VIII, Can have spontaneous bleeding in severve cases, Can be managed by plasma transfusions or by giving factor VII concentrate, to increse factor VII coagulant activity
83
von willebrands disease
Reduced levels of circulating von willebrand factor, and the entire factor VIII complex is deficient, Disorders in platelet function also present, Bleeding tendancies related to both platelet function and coagulation
84
what is an important function of vWF?
to facilitate platelet adhesion to damaged blood vessel walls
85
epistaxis
nose bleeds
86
what are wafarins and heparins used for?
anticoagulants that induce factor deficiencies and can lead to bleeding problems if not carefully minitored
87
how are platelet disorders characterized?
small bleeds in the skin typically perechiae and purpura
88
thrombocytopenia
decrease in platelet numbers, abnormal distribution, increased platelet destruction
89
thrombocytopathia
abnormalities of platelet function, platelet counts normal, don't function normally
90
what can be used to alter platelet function and can be used to prevent extreme effects of heart attacks?
asprin
91
thrombosis
clotting gone wrong within a vessel
92
virchows triad consists of
1. endothelial theory
2. alteration in normal blood flow
3. hypercoagulability
93
acute endothelial injury
injuries can be caused by trauma or surgery , inflammation and lack of blood supply
94
when is there an increased risk for thrombosis?
post surgical period
95
atherosclerosis
example of endothelial injury, as platelets tend to stick together to rough places in the endothelium, leads to atherosclerosis one of the leading causes of thrombosis in our society, symptomatic disease, Compromise of blood flow in smaller arteries
96
blood normally flows in layered ______ pattern
laminar
97
name and describe the two changes that can occur with blood flow
1. turbulance (rather than travelling in discrete columns, blood flow is fast yet erratic causing greater interaction with the endothelium)
2. stasis or pooling (blood flow much more slowly than normal because of ; failure of forward pressure, downstream obstruction or flow, or abnormal flow qualities to the blood itself such as hyper viscosity)
98
polycythemia
increase in RBCs, lead to viscous blood
99
what are the two forms of polycythemia?
1. relative (occurs in context of dehydration)
| 2. absolute ( blood stasis)
100
what is normal polycythemia?
deficient oxygenation of blood such as people or animals living at high altitudes
101
what is non physiologic polycythemia?
increased erythropoietin levels seen with certain tumours
102
3 main casues of thrombosis
changes in blood flow (turbulence and stasis), and changes in blood itself ( alterations in clotting/fibrinolysis) and endothelial damage
103
endothelial damage causes thrombosis more commonly in ______ while blood alterations with flow and composition causes thrombosis more commonly in ______
arteries, veins
104
ischemia and infraction
reduction or failure of blood supply to tissues
105
infarct
localized necrosis and inadequate blood supply and inadequate oxygen, by definition an area of ischemic necrosis
106
if the blood supply fails ischemia will lead to _______
infraction
107
anything which obstructs either the arteriole blood supply or venous drainage of the tissue can lead to what?
infraction where there is insufficient collateral circulation
108
what occurs where myocardium is deprived of blood due to occlusion of an coronary artery?
death of cyocytes occurs
109
myocardium
heart muscle
110
myocardial infraction
death of myocytes, heart attack
111
_____% or greater narrowing of lumen is considered critical
75%
112
how are acute myocardial infractions caused ?
coronary artery thrombosis
113
__________ ______ causes narrowing of the vessels
atherosclerotic plaque
114
what are the 5 factors influencing the outcome of arterial obstruction?
1. availibility of collateral circulation
2. the integrity of the collateral arteries (disease?)
3. the tissue susceptibility to ischemia
4. tissue metabolic rate
5. the rate of development of the obstruction
115
______ is more likely to cause thrombosis in the veins
stasis
116
idiopathic
disease of unknown cause
117
embolism
an embolis is a free floating intravascular solid or gaseous mass that is carried by the blood to a site different from its point of origin
118
the majority of emboli originate as what?
dislodged thrombus
119
emboli generally obstruct what?
arteries and arterioles rather than veins
120
what organs have dual blood supply? what are the blood supplies?
1. Lungs pulmonary and bronchial artery
| 2. the liver both hepatic artery and portal veins supply
121
dual blood supply can supply the lung or liver but cant prevent ______
infraction
122
obstruction occurs frequently in ______
veins
123
when the vein is obstructed hydrostatic pressure favours fluid remaining in the ________
interstitium
124
how is further swelling limited with ischemia and infraction?
tissue hydrostatic forces are increased
125
what happens when the hydrostatic pressure increases too much
capillaries can rupture and hemorrhage can occur
126
what is the outcome of venous obstruction
local edema to congestion to hemorrhage will depend on the size of the vein obstructed, how quickly the obstruction develops and availability of collateral drainage
127
whats less liekly to cause clinic problem venous or arterial obstruction?
venous because there is greater availibility of collateral vessels in the venous system
128
torison
twisting of pedicle of an organ
129
whats a reperfusion injury?
If venous outflow is impaired then any inflammatory mediators and toxic byproducts of cell death are relatively contained but If you restore blood flow to such tissue you can release all of these toxic inflammatory mediators into the bloodstream which are likely to add shock to the problem
130
DIC
thrombohemorrhagic disorder from widespread activation of coagulation which leads to widespread systemic thrombosis in microcirculation of the body with serious and fatal complications
131
is DIC a disease?
no its a syndrome
132
How is DIC a continuum?
early stages its a thrombotic process but as platelets and clotting factors are consumed it becomes a hemorrhagic process
133
how can DIC be triggered?
1. By release of tissue factor or other thromboplastic substances into the circulation
2. By widespread endothelial cell injury
134
Name some things DIC is often associated with?
sepsis, malignancy (cancer), obstructed complications, severe trauma (especially cerebral trauma), and burns
135
how is DIC diagnosed?
diagnosed by damaged RBC, RBCs are injured when passing through the fibrin stands of microthrombi, and Thrombocytopenia (thrombocytes are consumed in thrombus formation)
136
what is the goal of DIC treatment?
stop the cycle of throbosis and fibrinolysis
137
what is the pathological definition of shock?
physiologic state by generalized reduction in tissue perfusion related to decrease in either effective cardiac output or effective circulating blood volume
138
what are the 5 causes of shock?Describe each
1. Hypovolemia(decreased blood volume)
2. Septic shock (microbial infections)
3. Cardiogenic shock (failure of heart function)
4. Neurogenic shock (anesthesia or spinal cord injury, loss of vascular tone)
5. anaphlyactic shock (by immunoglobulin E mediated hypersensitivity )
139
what is the common path for all 5 forms of shock ?
reduction of tissue perfusion
140
briefly describe the stages of shock
1. neuphronal reflex come sinto play
2. decrease in blood pressure
3. peripheral vasoconstriction helps maintain blood pressure in vital organs
4. constriction in renal arteries which decrease blood flow to kidneys
5. fluid retention by the kidneys and decreased urine output
6. severe tisue hypoxia, organ failure
141
what is shock lung?
hypoxia in the lung causes edema and hemorrhage, now termed ARDS
142
ARDS
acute respiratory distress syndrome
