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Human Pathophysiology > Chapter 6 > Flashcards

Chapter 6 Flashcards

1
Q

where are capillaries

A

vessels between arteries and veins

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2
Q

how many layers do capillaries have

A

1 (tunica intima)

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3
Q

what is the role of capillaries

A

regulate fluids, electrolytes, and nutrient exchange between blood and extracellular space

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4
Q

can capillaries proliferate?

A

yes.
they help repair injured areas

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5
Q

hydrostatic pressure

A

pressure exerted by water

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6
Q

osmotic pressure

A

pressure exerted by differences in osmolarity

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7
Q

what determines osmotic pressure

A

amount of protein in fluid
albumin made by liver

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8
Q

integrity of endothelial cells

A

fluid can leak out of vessels

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9
Q

what is lymph

A

comes from blood, composed of water, proteins, WBCs, but NO RBCS

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10
Q

what happens to excess fluid that leaks out of a vessel

A

picked up by lymphatic vessels and brought back to blood

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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

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12
Q

what are the fluid compartments of the body

A

intracellular fluid, plasma, interstitial fluid

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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)

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14
Q

water in females

A

55% total body weight

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15
Q

water in males

A

60% total body weight

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16
Q

what does water balance depend on

A

lean body mass and muscle

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17
Q

what is water balance determined by

A

fluid intake and loss

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18
Q

fluid intake

A

LIQUIDS, food, metabolic water

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19
Q

fluid loss

A

URINE, stool, sweat, insensance water loss

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20
Q

what causes edema and effusion

A

alterations in pressures and/or vessels

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21
Q

edema

A

accumulation of fluid in tissues
interstitial space

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22
Q

effusion

A

accumulation of fluid in body cavities
pleural cavity

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23
Q

types of edema

A

exudate and transudate

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24
Q

exudate edema

A

high protein
inflammatory
NOT pitting

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25
Q

transudate edema

A

low protein, caused mainly by fluid
decreased osmotic pressure
increased hydrostatic pressure
pitting

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26
Q

what is pitting

A

push skin in and it remains indented

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27
Q

is edema pathological or physiological

A

pathological

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28
Q

why is edema a problem

A

results of underlying disease
mild-severe
can be fatal

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29
Q

fatal edemas

A

cerebral and pulmonary edema

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30
Q

cerebral edema

A

swelling of brain, skull limits swelling so the swelling goes inward and suppresses brain stem

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31
Q

pulmonary edema

A

impairs gas exchange

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32
Q

ascites-peritoneum

A

edema in abdominal cavity

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33
Q

anasarca

A

severe, generalized edema (all over body)

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34
Q

pericardial edema

A

fluid within pericardium preventing heart from expanding
EFFUSION

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35
Q

pleural edema

A

fluid in pleural cavity
EFFUSION

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36
Q

hydrostatic edema

A

caused by impaired venous return

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37
Q

where is hydrostatic edema most commonly observed

A

lower extremities = gravity

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38
Q

examples of hydrostatic edema

A

localized venous obstruction
thrombosis

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39
Q

osmotic edema

A

caused by low albumin

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40
Q

what causes low albumin

A

liver disease, poor nutrition (not enough protein), kidney disease

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41
Q

is osmotic edema transudate or exudate?

A

transudate

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42
Q

lymphedema

A

build up of fluid when lymphatics are damaged or blocked

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43
Q

is lymphedema exudate or transudate?

A

exudate, high protein edema

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44
Q

what is the most common cause of lymphedema

A

removal of lymph nodes, impairing lymph draining

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45
Q

secondary lymphedema

A

removal of lymph nodes due to cancer metastasizing

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46
Q

high protein edema

A

observed with inflammation
leaky capillaries releasing water and plasma proteins into interstitial space

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47
Q

dehydration

A

deficiency of body water

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48
Q

what causes dehydration

A

insufficient water intake vs. excess water loss

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49
Q

3 types of dehydration

A

dehydrated, euhydrated, overhydrated

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50
Q

how is dehydration categorized?

A

relative amount of lost body weight

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51
Q

symptoms of dehydration

A

headache, rapid pulse, thirst, low urine output, tenting

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52
Q

tenting

A

pinch skin, stays up

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53
Q

who is at risk for dehydration

A

babies, toddlers, elderly

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54
Q

normotonic

A

same tonicity thats in the body
sweat

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55
Q

hypotonic

A

low tonicity compared to body
urine

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56
Q

hypertonic

A

high tonicity compared to body
diarrhea

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57
Q

third spacing

A

moved into another space
edema or dehydrated, not both

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58
Q

characteristics of third spacing

A

low urine, low BP, increased weight, puffiness

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59
Q

what causes third spacing

A

shift of fluid from intravascular space into another body space or cavity; ascites, severe burns, low oncotic pressure (low albumin)

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60
Q

cations

A

sodium
potassium
calcium
magnesium

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61
Q

anions

A

bicarbonate
chloride
phosphate

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62
Q

potassium

A

primary intracellular cation
plays role in repolarization, action potentials

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63
Q

control of K+

A

intake, excretion (kidneys)

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64
Q

why is it important to keep ECF levels low

A

increase K+ then K+ stays inside cell
avoids leaking

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65
Q

hypokalemia

A

too low K+ in blood

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66
Q

hyperkalemia

A

too much K+ in blood

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67
Q

what does hypokalemia do to the membrane

A

hyperpolarizes it
cells fire less easily
inhibition of Na+/K+ pump
cardiac arrhythmias

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68
Q

what causes hypokalemia

A

diuretics (increases urine output to reduce body water)
eating disorders

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69
Q

what does HYPERkalemia do to membrane

A

decreases resting membrane potential closer to 0

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70
Q

effects of hyperkalemia

A

depolarizes membrane
cells fire more easily
creates ectopic beats from non-conducting myocardium

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71
Q

pH of extracellular fluid

A

7.4

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72
Q

blood pH

A

7.35-7.45

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73
Q

what pH levels does death occur at

A

<6.8 or >8.0

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74
Q

acidosis

A

pH below 7.35
increase H+ levels

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75
Q

alkalosis

A

pH above 7.45
decreases H+ levels

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76
Q

intracellular buffering system

A

phosphate buffer

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77
Q

what does the phosphate buffer do

A

minimizes changes in pH

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78
Q

plasma buffer

A

carbonic acid-bicarbonate pair

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79
Q

protein buffering (hemoglobin)

A

proteins have negative charge, serving as buffers for H+

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80
Q

renal buffering

A

major corrector of pH
secretion of H+ in urine and reabsorption of HCO3-

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81
Q

ion exchange buffer system

A

exchange of K+ for H+ in acidosis and alkalosis

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82
Q

acid-base imbalances

A

respiratory acidosis
respiratory alkalosis
metabolic acidosis
metabolic alkalosis

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83
Q

what is principal effect of acidosis

A

depression of CNS through decrease in synaptic transmission vcfc

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84
Q

what does acidosis lead to

A

disorientation
coma
death

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85
Q

respiratory acidosis

A

carbonic acid excess caused by elevated blood levels of CO2

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86
Q

hypercapnia

A

high CO2

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87
Q

what causes respiratory acidosis

A

depression of respiratory center in brain controlling breathing rate
drugs/head trauma
paralysis of respiratory or chest muscles (ALS)
emphysema (COPD)

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88
Q

respiratory acidosis compensation

A

kidneys eliminate H+ ions and retain bicarb ions

89
Q

what causes metabolic acidosis

A

loss of bicarb through diarrhea or renal dysfunction
accumulation of acids

90
Q

compensation of metabolic acidosis

A

increased ventilation
renal excretion of H+ ions if possible

91
Q

what does alkalosis cause in nervous systems

A

over excitability of CNS and PNS

92
Q

what can alkalosis lead to

A

nervousness
muscle spasms/tetany
convulsions
loss of consciousness
death

93
Q

respiratory alkalosis

A

low PCO2

94
Q

hypocapnea

A

low PCO2

95
Q

what is the primary cause of respiratory alkalosis

A

hyperventilation
O2 deficiency at high altitudes
diseases caused by hypoxia
acute anxiety
fever
early salicylate intoxication
cirrhosis
gram-negative sepsis

96
Q

compensation for respiratory alkalosis

A

kidneys conserve H+ ion and excrete bicarb ion

97
Q

causes of metabolic alkalosis

A

excess vomiting
diuretics
endocrine disorders
heavy ingestion of antacids
severe dehydration

98
Q

compensation for metabolic alkalosis

A

retain H+ ions
most commonly occurs w/renal dysfunction so you can’t count on kidneys
hypoventilation limited by hypoxia

99
Q

rates of correction

A

buffers function instantly
respiratory mechanisms take minutes-hours
renal mechanisms take hours-days

100
Q

what is the best system for correction

A

renal system

101
Q

kidney control

A

eliminates large amounts of acid
excretes bases
conserve and produce bicarb ions
most effective pH regulator

102
Q

what happens to pH balance if kidneys fail

A

fails

103
Q

hyperemia/congestion cause

A

increased volume of blood in affected body part

104
Q

active hyperemia

A

dilation of arterioles, more blood flow

105
Q

causes of active hyperemia

A

blushing
exercise
inflammation

106
Q

passive hyperemia (congestion)

A

impaired venous outflow (failure of venous blood to return to heart)

107
Q

what does passive hyperemia lead to

A

heart failure, leads to pulmonary edema

108
Q

hemorrhage

A

escape of blood into tissue due to blood vessel damage

109
Q

hemostasis

A

stops hemorrhage

110
Q

how does hemostasis stop hemorrhaging

A

vascular factors, platelets, coagulation factors

111
Q

when does coagulation occur

A

when blood vessels come into contact w/tissue outside of vessel or foreign material

112
Q

phases of normal hemostasis

A

I. vascular system (vasoconstriction)
II. platelet plug
III. coagulation (clot)

113
Q

Phase I - vascular system

A

vasoconstriction

114
Q

vasoconstriction

A

narrows lumen of vessel to minimize loss of blood
brings hemostatic components of blood into closer proximity to vessel wall

115
Q

Phase II - platelets

A

cell fragments of megakaryocytes

116
Q

where are platelets found

A

bone marrow

117
Q

in resting state, how often due platelets circulate

A

10 days

118
Q

what activates platelets

A

contact w/basement membrane due to cell injury

119
Q

what is the role of platelets

A

plug the defect
round and sticky, aggregate to build a hemostatic plug

120
Q

what do platelets release

A

secretions causing more platelets to aggregate

121
Q

platelet secretions

A

ADP, vasoactive amines, thromboxane A2

122
Q

ADP causes…

A

shape change
granule release
thromboxane A2 production

123
Q

where does thromboxane A2 come from

A

arachidonic acid

124
Q

vasoactive amines

A

epinephrine (causes vasoconstriction)

125
Q

thromboxane A2

A

amplifies initial aggregation of platelets into large platelet mass

126
Q

von willebrand factor

A

secreted by endothelial cells as scaffold for platelets

127
Q

von willebrand factor

A

secreted by endothelial cells as scaffold for platelets

127
Q

von willebrand factor

A

secreted by endothelial cells as scaffold for plateletsP

128
Q

Phase III - coagulation

A

liquid to semi-solid

129
Q

pathways of coagulation

A

extrinsic
intrinsic

130
Q

extrinsic coagulation pathway

A

tissue factor
stuff in tissue being released

131
Q

intrinsic coagulation pathway

A

stimulated by basement membrane

132
Q

what do you need for coagulation

A

calcium
vitamin K

133
Q

fibrin

A

final outcome of coagulation

134
Q

what does fibrin help

A

helps platelets plug

135
Q

platelets and coag factors

A

DIFFERENT but work TOGETHER

136
Q

how do platelets and coag factors work together

A

by providing binding sites

137
Q

what activates platelets

A

thrombin

138
Q

plasminogen

A

activated to plasmin by TPA

139
Q

tissue plasminogen activator

A

TPA
activates plasminogen

140
Q

what dissolves fibrin

A

plasmin

141
Q

use for TPA clinically

A

acute treatment
stroke

142
Q

petechiae

A

smallest, pinpoint hemorrhage

143
Q

intermediate blood loss

A

purpura
ecchymosis

144
Q

hematoma

A

BIG
indicative of hemophilia

145
Q

types of bleeding

A

bleeding from large vessels or capillaries

146
Q

what causes bleeding from large vessels

A

trauma
coagulation deficiency

147
Q

what causes bleeding from capillaries

A

low platelet count
vasculitis

148
Q

consequence of a massive hemorrhage

A

blood loss, hypovolemic shock, death

149
Q

consequence of hematoma

A

compression of tissues

150
Q

consequence of intracerebral hemorrhaging

A

stroke, death

151
Q

consequence of chronic hemorrhage

A

slow blood loss, iron deficiency

152
Q

types of abnormal hemostasis

A

abnormalities of small blood vessels
abnormality of platelet formation
deficiency of one or more plasma coag factors
liberation of thromboplastic material into circulation

153
Q

thrombocytopenia

A

low platelet count leading to petechiae

154
Q

what causes thrombocytopenia

A

genetic (hemopoetic stem cell)
radiation
leukemia
autoimmune
hypersplenism

155
Q

types of blood coag deficiencies

A

hemophilia A/B
von willebrand’s disease

156
Q

hemophilia

A

X-linked hereditary disease
MALES

157
Q

types of hemophilia

A

A/B

158
Q

hemophilia A

A

classic
deficiency in Factor VIII

159
Q

hemophilia B

A

christmas disease
deficiency in Factor IX

160
Q

clinical findings of hemophilia A

A

spontaneous/traumatic subcutaneous bleeding
blood in urine
bleeding in mouth, lips, tongue
bleeding in joints, CNS, GI tract

161
Q

treatment for hemophilia A

A

transfusions of whole blood
give missing factor VIII

162
Q

how to test for hemostasis

A

CBC for platelet count
bleeding time
clotting time

163
Q

partial thromboplastin time (PTT)

A

measures time it takes for blood plasma to clot after adding artificial surface (something foreign)
intrinsic and overall efficiency

164
Q

prothrombin time (PT)

A

time to clot after adding tissue factor
used to activate extrinsic pathway

165
Q

thrombin time

A

fibrinogen assay
measures level of fibrinogen

166
Q

anti-coagulants

A

warfarin
heparin

167
Q

warfarin

A

anti-coag
reduces amount of vitamin k availability
decreases risk of clot formation

168
Q

heparin

A

inactivates thrombin

169
Q

anti-platelets

A

aspirin
plavix

170
Q

aspirin

A

inhibits thromboxane A2 formation

171
Q

plavix

A

inhibits ADP

172
Q

disseminated intravascular coagulation (DIC)

A

widespread clotting inside blood vessels all over the body

173
Q

does DIC affect blood flow

A

yes, can obstruct small vessels

174
Q

what does DIC cause

A

hemorrhaging because of consumption of clotting factors & platelets

175
Q

is DIC primary or secondary

A

ALWAYS secondary to some other pathology

176
Q

hemostasis thrombosis abnormality

A

inappropriate activation of hemostatic process in uninjured or slightly injured vessel
NEVER NORMAL

177
Q

are clots and thrombosis the same

A

no, a clot is the normal response to a external injury

178
Q

thrombosis requirements

A

requires a combination of endothelial injury, abnormal local blood flow, hypercoagulability

179
Q

where does thrombosis normally occur

A

large veins or arteries damaged by atherosclerosis

180
Q

what does thrombosis form

A

thrombus

181
Q

what is a thrombus

A

pathologic processes overwhelm regulatory mechanisms
platelet aggregation
blood coagulation-fibrin
further platelet agglutination
WBC adhere to platelets
clot grows larger

182
Q

does thrombosis depend on coagulation

A

no, not initially but can grow by adding clot

183
Q

outcomes of thrombus

A

grows, breaks loose and becomes embolus, dissolve, rechannel

184
Q

embolus

A

piece of thrombus breaks off and moves around

185
Q

arterial thrombus

A

can be non-occlusive but grows to occlude artery causing ischemia and necrosis

186
Q

venous thrombus

A

thrombophlebitis, deep vein thrombosis (DVT)

187
Q

thrombophlebitis

A

abnormal venous clot leading to inflammation of the vein

188
Q

where do venous thrombus’ form

A

around valves in heart because of good spots to pool

189
Q

can a venous thrombus result in death

A

yes, or can be unharmful

190
Q

deep vein thrombosis

A

risk of thromboembolism

191
Q

emoblism

A

intravascular object that ravels in bloodstream

192
Q

sources of embolism

A

thrombi
athersclerotic debris
marrow fat
air
amniotic fluid

193
Q

ischemia

A

lack of oxygen to tissue

194
Q

what causes ischemia

A

obstruction

195
Q

what do long periods of ischemia do

A

long periods result in infarct

196
Q

ischemic necrosis

A

necrosis (death of tissue) due to ischemia

197
Q

what else ischemia be caused by that is NOT obstruction

A

torsion
drowning
carbon monoxide

198
Q

torsion

A

twisting of blood vessels

199
Q

drowning

A

water in bronchioles causes them to close
NO oxygen

200
Q

carbon monoxide

A

oxygen cannot be released from hemoglobin

201
Q

white infarction

A

bloodless, due to arterial obstruction in dense solid tissue

202
Q

red infarction

A

bloody, occurs in loose spongy tissue

203
Q

tissues with dual blood supply

A

lungs
liver

204
Q

factors influencing development of infarct

A

single/dual vascular supply
rate at which obstruction develops
sensitivity of downstream tissue due to oxygen deprivation
oxygen content of blood

205
Q

shock

A

inability of cardiovascular system to meet O2 demands of body

206
Q

what could shock be the final stage of

A

severe hemorrhage
bacterial sepsis
burns
myocardial infarction
severe soft tissue damage

207
Q

end result of shock

A

multi-organ failure/death

208
Q

cardiogenic shock

A

heart failure due to pump failing and cannot maintain perfusion pressure

209
Q

hypovolemic shock

A

decreased blood volume

210
Q

obstructive shock

A

fluid in pericardium preventing expansion of the heart

211
Q

septic shock

A

systemic bacterial infection
disseminated intravascular coagulation

212
Q

anaphylactic shock

A

systemic vasodilation
blood pressure decreases

213
Q

sepsis

A

associated w/bacterial infection
lipopolysaccharides (LPS)
endotoxins

214
Q

effects of sepsis

A

promotes thromobosis
microvascular occlusion
DIC

215
Q

treatment for sepsis

A

antibiotics

216
Q

stages of shock

A

non-progressive
progressive
irreversible

217
Q

irreversible shock

A

circulatory collapse
marked hypoperfusion of vital organs
loss of vital functions
multiorgan failure
death

218
Q

complications of shock

A

acute respiratory distress syndrome
acute renal failure
GI tract complications
DIC
multiple organ dysfunction syndrome

Human Pathophysiology (8 decks)

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