Hemodynamic Disorders Flashcards

1
Q

___ is the increased interstitial fluid which produces swelling and is initially painless

A

edema

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2
Q

___ is the accumulation of fluid in the body cavities

A

effusion

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3
Q

What are the 4 causes of edema?

A

1-too much leakage–increased vascular permeability
2-too little reabsorption–lymphatic obstruction
3-increased capillary hydrostatic pressure
4-reduced plasma oncotic pressure

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4
Q

Retention of sodium and thus water like in kidney disease results in what cause of edema?

A

increased hydrostatic pressure

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5
Q

___ determines extracellular fluid volume and osmolarity

A

sodium

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6
Q

Hydrostatic pressure from arterioles results in an outflow of ___ of fluid into extracellular space normally

A

14 ml/min

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7
Q

Oncotic pressure in venules results in inflow of ___ of fluid into vasculature

A

12 ml/min

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8
Q

What accounts for the extra 2ml/min of fluid not involved in hydrostatic or oncotic pressure?

A

lymphatics

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9
Q

What increases hydrostatic pressure? 3 things

A

1-increased venous pressure (thrombosis, clot, CHF)
2-hypervolemia-sodium retention, acute renal failure
3-arteriolar dilation-inflammation, heat

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10
Q

What causes decreased oncotic pressure?

A

hypoproteinemia-nephrotic syndrome, cirrhosis, malnutrition

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11
Q

What are the causes of localized edema? 3

A

1- DVT
2- lymphatic obstruction
3- acute inflammation

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12
Q

What are the causes of generalized edema? 5

A
  • cardiogenic
  • nephrogenic
  • cirrhosis
  • hypoalbumininemia
  • steroids
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13
Q

___ is extreme generalized edema

A

anasarca

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14
Q

___ is an active process with increased diameter or number of vessels typically due to increased blood supply such as in inflammation

A

hyperemia

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15
Q

___ is a passive process and is due to outflow of blood from an area and it presents blue/red

A

congestion

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16
Q

___ is seen with inflammation and infection, is protein rich, and is seen with increased vascularity and hyperemia

A

exudate

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17
Q

__ is seen with CHF and hypoalbumininemia, is non-inflammatory and is a filtrate of plasma seen with congestion

A

transudate

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18
Q

___ are minute hemorrhages caused by rupture of capillaries or arterioles or low platelet counts

A

petechiae

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19
Q

___ are larger hemorrhages that are caused by rupture of capillaries or arterioles, low platelet counts, trauma, vasculitis, and increased fragility of vessels

A

purpura

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20
Q

___ are bruises

A

ecchymoses

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21
Q

a ___ is a rounded mass hemorrhage with a mass effect on tissue surrounding

A

hematoma

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22
Q

initiation and formation of the platelet plug occur in ___ hemostasis

A

primary

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23
Q

propagation of the coagulation cascade occurs in ___ hemostasis

A

secondary

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24
Q

Fibrinolysis is very important to minimize ___ of tissue distal to the clot

A

ischemia

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25
coumadin affects the ____ pathway of the coagulation cascade
extrinsic
26
heparin affects the ___ pathway of coagulation cascade
intrinsic
27
both heparin and coumadin affect the ___ pathway of coagulation cascade
common
28
Factor ___ is part of the extrinsic pathway
VII
29
Factor ___ is part of the intrinsic pathway
XII
30
___ is the most important coagulation factor
Thrombin
31
The intrinsic pathway is measured by the ____ lab test
PTT
32
The extrinsic pathway is measured by the ___ lab test
PT
33
a ___ is a stationary intravascular blood clot
thrombus
34
___ is an intravascular blood clot that travels
embolus
35
an ___ blood clot causes ischemia and infarction in tissue distal to it
arterial
36
a ___ blood clot causes emboli somewhere else
venous
37
Virchow's triad refers to the classic causes/predispositions for ___ formation; what are the 3 factors?
thrombus formation; hypercoaguable state, endothelial injury, altered blood flow (usually stasis)
38
a venous thrombus usually starts at the ___
valves
39
A ___ thrombus restricts the lumen but does not occlude it
parietal
40
a red thrombus is from ___
venous
41
a white thrombus is from ___
arterial
42
What are Virchow's triad factors in venous blood clots?
1-endothelial injury from trauma or surgery 2-abnormal blood flow-stasis 3-hypercoagulability-OCPs and older folks
43
What are Virchow's triad factors in arterial blood clots?
1-endothelial injury from atherosclerosis 2-abnormal blood flow-turbulence 3-hypercoagulability
44
What are the 3 consequences of arterial occlusion?
1-infarction or dysfunction of tissue perfused by that artery 2-infarcted tissue will undergo scarring and atrophy 3-can embolize to next capillary bed
45
What are the 4 consequences of venous occlusion?
1-edema and pain 2-infarction from embolism to next capillary bed, 3-infarction from back pressure of arterial supply 4-leakage of fibrin that retards oxygen perfusion
46
Venous emboli are usually from the deep veins of ___ and ___ system that go into the pulmonary arteries
thigh and popliteal
47
a ___ embolus gets to systemic circulation through an abnormal communication between the venous and arterial systems at the level of the heart
paradoxical embolism
48
What are the risk factors for arterial thrombi/emboli? 4
atrial fibrillation, endocarditis, MI, valve abnormalities
49
The arterial thrombi usually arise in what 3 places?
1-arteries complicated with atherosclerotic plaques 2-heart chambers 3-site of atherosclerosis/aneurysm
50
Arterial thrombi may embolize to arteries in almost any part of the body with ____ and ___ most common
lower extremities and brain
51
a ___ emboli is a special form of emboli resulting from bone fracture especially in the pelvis which usually affects the pulmonary and CNS
fat
52
a ___ emboli is a special form of emboli from atheromas--atherosclerotic debris--and may resemble a fat embolus
cholestrol
53
a ___ embolus is a special form of emboli that is usually iatrogenic--from injections or surgery--often from acute decompression sickness
gas
54
____ embolus is a special form of emboli in which fetal cells and debris enter the maternal circulation--it is often seen at the end of labor and is often catastrophic--can cause DIC
amniotic fluid
55
___ like talc and cement can also cause special forms of emboli
foreign materials
56
What are the 5 causes of arterial obstruction?
``` 1-atherosclerosis 2-arteriosclerosis 3-arterial spasm 4-compartment syndrome 5-torsion ```
57
arterial spasm is caused by
intense vasoconstriction
58
____ is when an arteriole cannot relax in absence of endothelium due to lack of NO
Furchgott phenomenon
59
Raynaud's phenomenon is often seen in the fingers and is an example of ____
arterial spasm
60
What is the path of compartment syndrome?
perfusion pressure falls below tissue pressure in closed anatomic site --> veins are affected first --> arteries are then affected --> leads to tissue necrosis or functional deficits
61
What are the 5/6 'P's of compartment syndrome?
``` Pain Paresthesia Pallor Paralysis Pulselessness Polar/poikilothermia ```
62
____ is a deformation of forearm with flexion at the wrist that follows muscle infarction and replacement with fibrous tissue
Volkmann's contracture
63
___ can cause infarction--it is a twisting that first causes venous obstruction and with further twisting causes arterial obstruction
torsion
64
____ is similar to torsion but usually occurs due to a hernia or in the colon or small bowel
strangulation
65
___ is decreased blood supply to organ
ischemia
66
damage from infarction depends on what 4 things?
1-type of vascular supply--terminal, dual 2-rate of development of occlusion (acute or chronic) 3-vulnerability of tissue to hypoxia 4-oxygen content of blood
67
Acute infarcts are often ___ due to damage to the endothelium
red
68
___ infarcts are often seen in the heart, kidneys, and spleen from arterial occlusion of terminal arteries
white
69
___ infarcts may be due to either arterial or venous blood system and hemorrhage into the infarct
red
70
___ is a kind of cardiovascular collapse where the blood supply to the body is insufficient to meet the body's demands
shock
71
What are two factors for decreased cardiac output?
1-pump failure--LV is not pumping out enough blood | 2-decreased effective circulating volume--volume is remaining in periphery instead of returning to central
72
In early shock, skin is cold and clammy--why?
the heart tries to compensate by vasoconstricting peripheral blood vessels to shunt blood to necessary organs
73
Later on in shock the skin returns to warm and pink--why?
the pt has reached the point of no return where the compensatory mechanisms fail and vasodilation returns peripheral blood
74
When the kidneys are not perfused the patient becomes ___ which damages the heart further
acidotic
75
___ shock is due to myocardial pump failure as in MI, arrhythmias, cardiac tamponade, PE
cardiogenic
76
___ shock is due to reduced amounts of blood volume as may happen with bleeding, dehydration, burns, and diarrhea
hypovolemic
77
___ shock is due to peripheral vasodilation and increased permeability as well as microbial infection
septic
78
___ shock is due to Type 1 IgE mediated hypersensitivity
anaphylactic
79
___ shock is due to severe brain or spinal cord injury which impairs vasomotor control---can't vasoconstrict
neurogenic
80
sepsis is "_____"--a systemic response to infection
SIRS plus signs of infection
81
The leading cause of septic shock is now considered to be
gram positive bacteria, followed by gram negative bacteria, and then fungi
82
What happens in septic shock?
1-bacteria have structural components of cell walls that cause immune and endothelial cell activation which release cytokines and activate complement which causes a hyperinflammatory state with leaky blood vessels
83
Induction of a procoagulant state in septic shock leads to systemic activation of ___ and deposition of fibrin-rich thrombi in small vessels which leads to ___
thrombin; DIC
84
Death of alveolar cells, acute tubular necrosis of the kidney, liver failure, myocardial cell death, bowel necrosis, and brain ischemia are all consequences of ____
multiple organ dysfunction syndrome
85
In general, how is multi-system organ failure caused?
- -microbial product starts it - -an inflammatory response is activated globally - -cytokines, etc. cause vasodilation, increased permeability and decreased perfusion
86
the ____ stage of shock has a compensatory mechanism that is activated and perfusion of vital organs is maintained
nonprogressive
87
the ___ stage of shock has tissue hypoperfusion which leads to worsening circulatory and metabolic imbalances including lactic acidosis
progressive
88
the ___ stage of shock is when there is so much cell and tissue injury that survival is not possible
irreversible
89
In shock the ____-____-___ system is activated which leads to sodium and water retention; then ___ and ___ cause selective constriction of peripheral vessels to shunt blood to vital organs (heart and brain)
renin-angiotensin-aldosterone; norepinephrine and angiotensin 2
90
How do the vessels respond to norepinephrine and angiotensin 2?
the vessels constrict
91
The vasoconstriction induced by compensatory mechanisms of shock require ATP and when the ATP is depleted there is a switch to anaerobic glycolysis which produces lactic acidosis---what does that result in?
acidosis blunts the vasomotor response and the sodium/potassium pump doesn't function and there is a point of no return where blood pressure can no longer be raised
92
____, released from the posterior pituitary gland, is rapidly poured out and leads to increased water retention and decreased urine output
vasopressin
93
Hypotension, tachycardia, cool clammy skin, tachypnea, oliguria, change in mental status, metabolic acidosis, and multi-system organ failure are all clinical signs of
shock
94
___ is a systematic hypersensitivity involving basophils and mast cells that release cytokines and things like histamine
immediate, type 1 hypersensitivity
95
____ is an autosomal dominant disease with a C1 esterase inhibitor deficiency---can cause asphyxiation and death, follows mild trauma or stress
hereditary angioedema