Chapter 6 Flashcards
(219 cards)
1
Q
where are capillaries
A
vessels between arteries and veins
2
Q
how many layers do capillaries have
A
1 (tunica intima)
3
Q
what is the role of capillaries
A
regulate fluids, electrolytes, and nutrient exchange between blood and extracellular space
4
Q
can capillaries proliferate?
A
yes.
they help repair injured areas
5
Q
hydrostatic pressure
A
pressure exerted by water
6
Q
osmotic pressure
A
pressure exerted by differences in osmolarity
7
Q
what determines osmotic pressure
A
amount of protein in fluid
albumin made by liver
8
Q
integrity of endothelial cells
A
fluid can leak out of vessels
9
Q
what is lymph
A
comes from blood, composed of water, proteins, WBCs, but NO RBCS
10
Q
what happens to excess fluid that leaks out of a vessel
A
picked up by lymphatic vessels and brought back to blood
11
Q
what happens if excess fluid that leaks out of a vessel is left outside of a vessel
A
too much fluid in interstitial space, blood volume gets too LOW
12
Q
what are the fluid compartments of the body
A
intracellular fluid, plasma, interstitial fluid
13
Q
imbalance of fluids
A
fluid may not be able to keep up (diarrhea=losing too much fluid)
may shift abnormally (goes into different compartment)
14
Q
water in females
A
55% total body weight
15
Q
water in males
A
60% total body weight
16
Q
what does water balance depend on
A
lean body mass and muscle
17
Q
what is water balance determined by
A
fluid intake and loss
18
Q
fluid intake
A
LIQUIDS, food, metabolic water
19
Q
fluid loss
A
URINE, stool, sweat, insensance water loss
20
Q
what causes edema and effusion
A
alterations in pressures and/or vessels
21
Q
edema
A
accumulation of fluid in tissues
interstitial space
22
Q
effusion
A
accumulation of fluid in body cavities
pleural cavity
23
Q
types of edema
A
exudate and transudate
24
Q
exudate edema
A
high protein
inflammatory
NOT pitting
25
transudate edema
low protein, caused mainly by fluid
decreased osmotic pressure
increased hydrostatic pressure
pitting
26
what is pitting
push skin in and it remains indented
27
is edema pathological or physiological
pathological
28
why is edema a problem
results of underlying disease
mild-severe
can be fatal
29
fatal edemas
cerebral and pulmonary edema
30
cerebral edema
swelling of brain, skull limits swelling so the swelling goes inward and suppresses brain stem
31
pulmonary edema
impairs gas exchange
32
ascites-peritoneum
edema in abdominal cavity
33
anasarca
severe, generalized edema (all over body)
34
pericardial edema
fluid within pericardium preventing heart from expanding
EFFUSION
35
pleural edema
fluid in pleural cavity
EFFUSION
36
hydrostatic edema
caused by impaired venous return
37
where is hydrostatic edema most commonly observed
lower extremities = gravity
38
examples of hydrostatic edema
localized venous obstruction
thrombosis
39
osmotic edema
caused by low albumin
40
what causes low albumin
liver disease, poor nutrition (not enough protein), kidney disease
41
is osmotic edema transudate or exudate?
transudate
42
lymphedema
build up of fluid when lymphatics are damaged or blocked
43
is lymphedema exudate or transudate?
exudate, high protein edema
44
what is the most common cause of lymphedema
removal of lymph nodes, impairing lymph draining
45
secondary lymphedema
removal of lymph nodes due to cancer metastasizing
46
high protein edema
observed with inflammation
leaky capillaries releasing water and plasma proteins into interstitial space
47
dehydration
deficiency of body water
48
what causes dehydration
insufficient water intake vs. excess water loss
49
3 types of dehydration
dehydrated, euhydrated, overhydrated
50
how is dehydration categorized?
relative amount of lost body weight
51
symptoms of dehydration
headache, rapid pulse, thirst, low urine output, tenting
52
tenting
pinch skin, stays up
53
who is at risk for dehydration
babies, toddlers, elderly
54
normotonic
same tonicity thats in the body
sweat
55
hypotonic
low tonicity compared to body
urine
56
hypertonic
high tonicity compared to body
diarrhea
57
third spacing
moved into another space
edema or dehydrated, not both
58
characteristics of third spacing
low urine, low BP, increased weight, puffiness
59
what causes third spacing
shift of fluid from intravascular space into another body space or cavity; ascites, severe burns, low oncotic pressure (low albumin)
60
cations
sodium
potassium
calcium
magnesium
61
anions
bicarbonate
chloride
phosphate
62
potassium
primary intracellular cation
plays role in repolarization, action potentials
63
control of K+
intake, excretion (kidneys)
64
why is it important to keep ECF levels low
increase K+ then K+ stays inside cell
avoids leaking
65
hypokalemia
too low K+ in blood
66
hyperkalemia
too much K+ in blood
67
what does hypokalemia do to the membrane
hyperpolarizes it
cells fire less easily
inhibition of Na+/K+ pump
cardiac arrhythmias
68
what causes hypokalemia
diuretics (increases urine output to reduce body water)
eating disorders
69
what does HYPERkalemia do to membrane
decreases resting membrane potential closer to 0
70
effects of hyperkalemia
depolarizes membrane
cells fire more easily
creates ectopic beats from non-conducting myocardium
71
pH of extracellular fluid
7.4
72
blood pH
7.35-7.45
73
what pH levels does death occur at
<6.8 or >8.0
74
acidosis
pH below 7.35
increase H+ levels
75
alkalosis
pH above 7.45
decreases H+ levels
76
intracellular buffering system
phosphate buffer
77
what does the phosphate buffer do
minimizes changes in pH
78
plasma buffer
carbonic acid-bicarbonate pair
79
protein buffering (hemoglobin)
proteins have negative charge, serving as buffers for H+
80
renal buffering
major corrector of pH
secretion of H+ in urine and reabsorption of HCO3-
81
ion exchange buffer system
exchange of K+ for H+ in acidosis and alkalosis
82
acid-base imbalances
respiratory acidosis
respiratory alkalosis
metabolic acidosis
metabolic alkalosis
83
what is principal effect of acidosis
depression of CNS through decrease in synaptic transmission vcfc
84
what does acidosis lead to
disorientation
coma
death
85
respiratory acidosis
carbonic acid excess caused by elevated blood levels of CO2
86
hypercapnia
high CO2
87
what causes respiratory acidosis
depression of respiratory center in brain controlling breathing rate
drugs/head trauma
paralysis of respiratory or chest muscles (ALS)
emphysema (COPD)
88
respiratory acidosis compensation
kidneys eliminate H+ ions and retain bicarb ions
89
what causes metabolic acidosis
loss of bicarb through diarrhea or renal dysfunction
accumulation of acids
90
compensation of metabolic acidosis
increased ventilation
renal excretion of H+ ions if possible
91
what does alkalosis cause in nervous systems
over excitability of CNS and PNS
92
what can alkalosis lead to
nervousness
muscle spasms/tetany
convulsions
loss of consciousness
death
93
respiratory alkalosis
low PCO2
94
hypocapnea
low PCO2
95
what is the primary cause of respiratory alkalosis
hyperventilation
O2 deficiency at high altitudes
diseases caused by hypoxia
acute anxiety
fever
early salicylate intoxication
cirrhosis
gram-negative sepsis
96
compensation for respiratory alkalosis
kidneys conserve H+ ion and excrete bicarb ion
97
causes of metabolic alkalosis
excess vomiting
diuretics
endocrine disorders
heavy ingestion of antacids
severe dehydration
98
compensation for metabolic alkalosis
retain H+ ions
most commonly occurs w/renal dysfunction so you can't count on kidneys
hypoventilation limited by hypoxia
99
rates of correction
buffers function instantly
respiratory mechanisms take minutes-hours
renal mechanisms take hours-days
100
what is the best system for correction
renal system
101
kidney control
eliminates large amounts of acid
excretes bases
conserve and produce bicarb ions
most effective pH regulator
102
what happens to pH balance if kidneys fail
fails
103
hyperemia/congestion cause
increased volume of blood in affected body part
104
active hyperemia
dilation of arterioles, more blood flow
105
causes of active hyperemia
blushing
exercise
inflammation
106
passive hyperemia (congestion)
impaired venous outflow (failure of venous blood to return to heart)
107
what does passive hyperemia lead to
heart failure, leads to pulmonary edema
108
hemorrhage
escape of blood into tissue due to blood vessel damage
109
hemostasis
stops hemorrhage
110
how does hemostasis stop hemorrhaging
vascular factors, platelets, coagulation factors
111
when does coagulation occur
when blood vessels come into contact w/tissue outside of vessel or foreign material
112
phases of normal hemostasis
I. vascular system (vasoconstriction)
II. platelet plug
III. coagulation (clot)
113
Phase I - vascular system
vasoconstriction
114
vasoconstriction
narrows lumen of vessel to minimize loss of blood
brings hemostatic components of blood into closer proximity to vessel wall
115
Phase II - platelets
cell fragments of megakaryocytes
116
where are platelets found
bone marrow
117
in resting state, how often due platelets circulate
10 days
118
what activates platelets
contact w/basement membrane due to cell injury
119
what is the role of platelets
plug the defect
round and sticky, aggregate to build a hemostatic plug
120
what do platelets release
secretions causing more platelets to aggregate
121
platelet secretions
ADP, vasoactive amines, thromboxane A2
122
ADP causes...
shape change
granule release
thromboxane A2 production
123
where does thromboxane A2 come from
arachidonic acid
124
vasoactive amines
epinephrine (causes vasoconstriction)
125
thromboxane A2
amplifies initial aggregation of platelets into large platelet mass
126
von willebrand factor
secreted by endothelial cells as scaffold for platelets
127
von willebrand factor
secreted by endothelial cells as scaffold for platelets
127
von willebrand factor
secreted by endothelial cells as scaffold for plateletsP
128
Phase III - coagulation
liquid to semi-solid
129
pathways of coagulation
extrinsic
intrinsic
130
extrinsic coagulation pathway
tissue factor
stuff in tissue being released
131
intrinsic coagulation pathway
stimulated by basement membrane
132
what do you need for coagulation
calcium
vitamin K
133
fibrin
final outcome of coagulation
134
what does fibrin help
helps platelets plug
135
platelets and coag factors
DIFFERENT but work TOGETHER
136
how do platelets and coag factors work together
by providing binding sites
137
what activates platelets
thrombin
138
plasminogen
activated to plasmin by TPA
139
tissue plasminogen activator
TPA
activates plasminogen
140
what dissolves fibrin
plasmin
141
use for TPA clinically
acute treatment
stroke
142
petechiae
smallest, pinpoint hemorrhage
143
intermediate blood loss
purpura
ecchymosis
144
hematoma
BIG
indicative of hemophilia
145
types of bleeding
bleeding from large vessels or capillaries
146
what causes bleeding from large vessels
trauma
coagulation deficiency
147
what causes bleeding from capillaries
low platelet count
vasculitis
148
consequence of a massive hemorrhage
blood loss, hypovolemic shock, death
149
consequence of hematoma
compression of tissues
150
consequence of intracerebral hemorrhaging
stroke, death
151
consequence of chronic hemorrhage
slow blood loss, iron deficiency
152
types of abnormal hemostasis
abnormalities of small blood vessels
abnormality of platelet formation
deficiency of one or more plasma coag factors
liberation of thromboplastic material into circulation
153
thrombocytopenia
low platelet count leading to petechiae
154
what causes thrombocytopenia
genetic (hemopoetic stem cell)
radiation
leukemia
autoimmune
hypersplenism
155
types of blood coag deficiencies
hemophilia A/B
von willebrand's disease
156
hemophilia
X-linked hereditary disease
MALES
157
types of hemophilia
A/B
158
hemophilia A
classic
deficiency in Factor VIII
159
hemophilia B
christmas disease
deficiency in Factor IX
160
clinical findings of hemophilia A
spontaneous/traumatic subcutaneous bleeding
blood in urine
bleeding in mouth, lips, tongue
bleeding in joints, CNS, GI tract
161
treatment for hemophilia A
transfusions of whole blood
give missing factor VIII
162
how to test for hemostasis
CBC for platelet count
bleeding time
clotting time
163
partial thromboplastin time (PTT)
measures time it takes for blood plasma to clot after adding artificial surface (something foreign)
intrinsic and overall efficiency
164
prothrombin time (PT)
time to clot after adding tissue factor
used to activate extrinsic pathway
165
thrombin time
fibrinogen assay
measures level of fibrinogen
166
anti-coagulants
warfarin
heparin
167
warfarin
anti-coag
reduces amount of vitamin k availability
decreases risk of clot formation
168
heparin
inactivates thrombin
169
anti-platelets
aspirin
plavix
170
aspirin
inhibits thromboxane A2 formation
171
plavix
inhibits ADP
172
disseminated intravascular coagulation (DIC)
widespread clotting inside blood vessels all over the body
173
does DIC affect blood flow
yes, can obstruct small vessels
174
what does DIC cause
hemorrhaging because of consumption of clotting factors & platelets
175
is DIC primary or secondary
ALWAYS secondary to some other pathology
176
hemostasis thrombosis abnormality
inappropriate activation of hemostatic process in uninjured or slightly injured vessel
NEVER NORMAL
177
are clots and thrombosis the same
no, a clot is the normal response to a external injury
178
thrombosis requirements
requires a combination of endothelial injury, abnormal local blood flow, hypercoagulability
179
where does thrombosis normally occur
large veins or arteries damaged by atherosclerosis
180
what does thrombosis form
thrombus
181
what is a thrombus
pathologic processes overwhelm regulatory mechanisms
platelet aggregation
blood coagulation-fibrin
further platelet agglutination
WBC adhere to platelets
clot grows larger
182
does thrombosis depend on coagulation
no, not initially but can grow by adding clot
183
outcomes of thrombus
grows, breaks loose and becomes embolus, dissolve, rechannel
184
embolus
piece of thrombus breaks off and moves around
185
arterial thrombus
can be non-occlusive but grows to occlude artery causing ischemia and necrosis
186
venous thrombus
thrombophlebitis, deep vein thrombosis (DVT)
187
thrombophlebitis
abnormal venous clot leading to inflammation of the vein
188
where do venous thrombus' form
around valves in heart because of good spots to pool
189
can a venous thrombus result in death
yes, or can be unharmful
190
deep vein thrombosis
risk of thromboembolism
191
emoblism
intravascular object that ravels in bloodstream
192
sources of embolism
thrombi
athersclerotic debris
marrow fat
air
amniotic fluid
193
ischemia
lack of oxygen to tissue
194
what causes ischemia
obstruction
195
what do long periods of ischemia do
long periods result in infarct
196
ischemic necrosis
necrosis (death of tissue) due to ischemia
197
what else ischemia be caused by that is NOT obstruction
torsion
drowning
carbon monoxide
198
torsion
twisting of blood vessels
199
drowning
water in bronchioles causes them to close
NO oxygen
200
carbon monoxide
oxygen cannot be released from hemoglobin
201
white infarction
bloodless, due to arterial obstruction in dense solid tissue
202
red infarction
bloody, occurs in loose spongy tissue
203
tissues with dual blood supply
lungs
liver
204
factors influencing development of infarct
single/dual vascular supply
rate at which obstruction develops
sensitivity of downstream tissue due to oxygen deprivation
oxygen content of blood
205
shock
inability of cardiovascular system to meet O2 demands of body
206
what could shock be the final stage of
severe hemorrhage
bacterial sepsis
burns
myocardial infarction
severe soft tissue damage
207
end result of shock
multi-organ failure/death
208
cardiogenic shock
heart failure due to pump failing and cannot maintain perfusion pressure
209
hypovolemic shock
decreased blood volume
210
obstructive shock
fluid in pericardium preventing expansion of the heart
211
septic shock
systemic bacterial infection
disseminated intravascular coagulation
212
anaphylactic shock
systemic vasodilation
blood pressure decreases
213
sepsis
associated w/bacterial infection
lipopolysaccharides (LPS)
endotoxins
214
effects of sepsis
promotes thromobosis
microvascular occlusion
DIC
215
treatment for sepsis
antibiotics
216
stages of shock
non-progressive
progressive
irreversible
217
irreversible shock
circulatory collapse
marked hypoperfusion of vital organs
loss of vital functions
multiorgan failure
death
218
complications of shock
acute respiratory distress syndrome
acute renal failure
GI tract complications
DIC
multiple organ dysfunction syndrome
