Chapter 6 Flashcards
where are capillaries
vessels between arteries and veins
how many layers do capillaries have
1 (tunica intima)
what is the role of capillaries
regulate fluids, electrolytes, and nutrient exchange between blood and extracellular space
can capillaries proliferate?
yes.
they help repair injured areas
hydrostatic pressure
pressure exerted by water
osmotic pressure
pressure exerted by differences in osmolarity
what determines osmotic pressure
amount of protein in fluid
albumin made by liver
integrity of endothelial cells
fluid can leak out of vessels
what is lymph
comes from blood, composed of water, proteins, WBCs, but NO RBCS
what happens to excess fluid that leaks out of a vessel
picked up by lymphatic vessels and brought back to blood
what happens if excess fluid that leaks out of a vessel is left outside of a vessel
too much fluid in interstitial space, blood volume gets too LOW
what are the fluid compartments of the body
intracellular fluid, plasma, interstitial fluid
imbalance of fluids
fluid may not be able to keep up (diarrhea=losing too much fluid)
may shift abnormally (goes into different compartment)
water in females
55% total body weight
water in males
60% total body weight
what does water balance depend on
lean body mass and muscle
what is water balance determined by
fluid intake and loss
fluid intake
LIQUIDS, food, metabolic water
fluid loss
URINE, stool, sweat, insensance water loss
what causes edema and effusion
alterations in pressures and/or vessels
edema
accumulation of fluid in tissues
interstitial space
effusion
accumulation of fluid in body cavities
pleural cavity
types of edema
exudate and transudate
exudate edema
high protein
inflammatory
NOT pitting
transudate edema
low protein, caused mainly by fluid
decreased osmotic pressure
increased hydrostatic pressure
pitting
what is pitting
push skin in and it remains indented
is edema pathological or physiological
pathological
why is edema a problem
results of underlying disease
mild-severe
can be fatal
fatal edemas
cerebral and pulmonary edema
cerebral edema
swelling of brain, skull limits swelling so the swelling goes inward and suppresses brain stem
pulmonary edema
impairs gas exchange
ascites-peritoneum
edema in abdominal cavity
anasarca
severe, generalized edema (all over body)
pericardial edema
fluid within pericardium preventing heart from expanding
EFFUSION
pleural edema
fluid in pleural cavity
EFFUSION
hydrostatic edema
caused by impaired venous return
where is hydrostatic edema most commonly observed
lower extremities = gravity
examples of hydrostatic edema
localized venous obstruction
thrombosis
osmotic edema
caused by low albumin
what causes low albumin
liver disease, poor nutrition (not enough protein), kidney disease
is osmotic edema transudate or exudate?
transudate
lymphedema
build up of fluid when lymphatics are damaged or blocked
is lymphedema exudate or transudate?
exudate, high protein edema
what is the most common cause of lymphedema
removal of lymph nodes, impairing lymph draining
secondary lymphedema
removal of lymph nodes due to cancer metastasizing
high protein edema
observed with inflammation
leaky capillaries releasing water and plasma proteins into interstitial space
dehydration
deficiency of body water
what causes dehydration
insufficient water intake vs. excess water loss
3 types of dehydration
dehydrated, euhydrated, overhydrated
how is dehydration categorized?
relative amount of lost body weight
symptoms of dehydration
headache, rapid pulse, thirst, low urine output, tenting
tenting
pinch skin, stays up
who is at risk for dehydration
babies, toddlers, elderly
normotonic
same tonicity thats in the body
sweat
hypotonic
low tonicity compared to body
urine
hypertonic
high tonicity compared to body
diarrhea
third spacing
moved into another space
edema or dehydrated, not both
characteristics of third spacing
low urine, low BP, increased weight, puffiness
what causes third spacing
shift of fluid from intravascular space into another body space or cavity; ascites, severe burns, low oncotic pressure (low albumin)
cations
sodium
potassium
calcium
magnesium
anions
bicarbonate
chloride
phosphate
potassium
primary intracellular cation
plays role in repolarization, action potentials
control of K+
intake, excretion (kidneys)
why is it important to keep ECF levels low
increase K+ then K+ stays inside cell
avoids leaking
hypokalemia
too low K+ in blood
hyperkalemia
too much K+ in blood
what does hypokalemia do to the membrane
hyperpolarizes it
cells fire less easily
inhibition of Na+/K+ pump
cardiac arrhythmias
what causes hypokalemia
diuretics (increases urine output to reduce body water)
eating disorders
what does HYPERkalemia do to membrane
decreases resting membrane potential closer to 0
effects of hyperkalemia
depolarizes membrane
cells fire more easily
creates ectopic beats from non-conducting myocardium
pH of extracellular fluid
7.4
blood pH
7.35-7.45
what pH levels does death occur at
<6.8 or >8.0
acidosis
pH below 7.35
increase H+ levels
alkalosis
pH above 7.45
decreases H+ levels
intracellular buffering system
phosphate buffer
what does the phosphate buffer do
minimizes changes in pH
plasma buffer
carbonic acid-bicarbonate pair
protein buffering (hemoglobin)
proteins have negative charge, serving as buffers for H+
renal buffering
major corrector of pH
secretion of H+ in urine and reabsorption of HCO3-
ion exchange buffer system
exchange of K+ for H+ in acidosis and alkalosis
acid-base imbalances
respiratory acidosis
respiratory alkalosis
metabolic acidosis
metabolic alkalosis
what is principal effect of acidosis
depression of CNS through decrease in synaptic transmission vcfc
what does acidosis lead to
disorientation
coma
death
respiratory acidosis
carbonic acid excess caused by elevated blood levels of CO2
hypercapnia
high CO2
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)
respiratory acidosis compensation
kidneys eliminate H+ ions and retain bicarb ions
what causes metabolic acidosis
loss of bicarb through diarrhea or renal dysfunction
accumulation of acids
compensation of metabolic acidosis
increased ventilation
renal excretion of H+ ions if possible
what does alkalosis cause in nervous systems
over excitability of CNS and PNS
what can alkalosis lead to
nervousness
muscle spasms/tetany
convulsions
loss of consciousness
death
respiratory alkalosis
low PCO2
hypocapnea
low PCO2
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
compensation for respiratory alkalosis
kidneys conserve H+ ion and excrete bicarb ion
causes of metabolic alkalosis
excess vomiting
diuretics
endocrine disorders
heavy ingestion of antacids
severe dehydration
compensation for metabolic alkalosis
retain H+ ions
most commonly occurs w/renal dysfunction so you can’t count on kidneys
hypoventilation limited by hypoxia
rates of correction
buffers function instantly
respiratory mechanisms take minutes-hours
renal mechanisms take hours-days
what is the best system for correction
renal system
kidney control
eliminates large amounts of acid
excretes bases
conserve and produce bicarb ions
most effective pH regulator
what happens to pH balance if kidneys fail
fails
hyperemia/congestion cause
increased volume of blood in affected body part
active hyperemia
dilation of arterioles, more blood flow
causes of active hyperemia
blushing
exercise
inflammation
passive hyperemia (congestion)
impaired venous outflow (failure of venous blood to return to heart)
what does passive hyperemia lead to
heart failure, leads to pulmonary edema
hemorrhage
escape of blood into tissue due to blood vessel damage
hemostasis
stops hemorrhage
how does hemostasis stop hemorrhaging
vascular factors, platelets, coagulation factors
when does coagulation occur
when blood vessels come into contact w/tissue outside of vessel or foreign material
phases of normal hemostasis
I. vascular system (vasoconstriction)
II. platelet plug
III. coagulation (clot)
Phase I - vascular system
vasoconstriction
vasoconstriction
narrows lumen of vessel to minimize loss of blood
brings hemostatic components of blood into closer proximity to vessel wall
Phase II - platelets
cell fragments of megakaryocytes
where are platelets found
bone marrow
in resting state, how often due platelets circulate
10 days
what activates platelets
contact w/basement membrane due to cell injury
what is the role of platelets
plug the defect
round and sticky, aggregate to build a hemostatic plug
what do platelets release
secretions causing more platelets to aggregate
platelet secretions
ADP, vasoactive amines, thromboxane A2
ADP causes…
shape change
granule release
thromboxane A2 production
where does thromboxane A2 come from
arachidonic acid
vasoactive amines
epinephrine (causes vasoconstriction)
thromboxane A2
amplifies initial aggregation of platelets into large platelet mass
von willebrand factor
secreted by endothelial cells as scaffold for platelets
von willebrand factor
secreted by endothelial cells as scaffold for platelets
von willebrand factor
secreted by endothelial cells as scaffold for plateletsP
Phase III - coagulation
liquid to semi-solid
pathways of coagulation
extrinsic
intrinsic
extrinsic coagulation pathway
tissue factor
stuff in tissue being released
intrinsic coagulation pathway
stimulated by basement membrane
what do you need for coagulation
calcium
vitamin K
fibrin
final outcome of coagulation
what does fibrin help
helps platelets plug
platelets and coag factors
DIFFERENT but work TOGETHER
how do platelets and coag factors work together
by providing binding sites
what activates platelets
thrombin
plasminogen
activated to plasmin by TPA
tissue plasminogen activator
TPA
activates plasminogen
what dissolves fibrin
plasmin
use for TPA clinically
acute treatment
stroke
petechiae
smallest, pinpoint hemorrhage
intermediate blood loss
purpura
ecchymosis
hematoma
BIG
indicative of hemophilia
types of bleeding
bleeding from large vessels or capillaries
what causes bleeding from large vessels
trauma
coagulation deficiency
what causes bleeding from capillaries
low platelet count
vasculitis
consequence of a massive hemorrhage
blood loss, hypovolemic shock, death
consequence of hematoma
compression of tissues
consequence of intracerebral hemorrhaging
stroke, death
consequence of chronic hemorrhage
slow blood loss, iron deficiency
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
thrombocytopenia
low platelet count leading to petechiae
what causes thrombocytopenia
genetic (hemopoetic stem cell)
radiation
leukemia
autoimmune
hypersplenism
types of blood coag deficiencies
hemophilia A/B
von willebrand’s disease
hemophilia
X-linked hereditary disease
MALES
types of hemophilia
A/B
hemophilia A
classic
deficiency in Factor VIII
hemophilia B
christmas disease
deficiency in Factor IX
clinical findings of hemophilia A
spontaneous/traumatic subcutaneous bleeding
blood in urine
bleeding in mouth, lips, tongue
bleeding in joints, CNS, GI tract
treatment for hemophilia A
transfusions of whole blood
give missing factor VIII
how to test for hemostasis
CBC for platelet count
bleeding time
clotting time
partial thromboplastin time (PTT)
measures time it takes for blood plasma to clot after adding artificial surface (something foreign)
intrinsic and overall efficiency
prothrombin time (PT)
time to clot after adding tissue factor
used to activate extrinsic pathway
thrombin time
fibrinogen assay
measures level of fibrinogen
anti-coagulants
warfarin
heparin
warfarin
anti-coag
reduces amount of vitamin k availability
decreases risk of clot formation
heparin
inactivates thrombin
anti-platelets
aspirin
plavix
aspirin
inhibits thromboxane A2 formation
plavix
inhibits ADP
disseminated intravascular coagulation (DIC)
widespread clotting inside blood vessels all over the body
does DIC affect blood flow
yes, can obstruct small vessels
what does DIC cause
hemorrhaging because of consumption of clotting factors & platelets
is DIC primary or secondary
ALWAYS secondary to some other pathology
hemostasis thrombosis abnormality
inappropriate activation of hemostatic process in uninjured or slightly injured vessel
NEVER NORMAL
are clots and thrombosis the same
no, a clot is the normal response to a external injury
thrombosis requirements
requires a combination of endothelial injury, abnormal local blood flow, hypercoagulability
where does thrombosis normally occur
large veins or arteries damaged by atherosclerosis
what does thrombosis form
thrombus
what is a thrombus
pathologic processes overwhelm regulatory mechanisms
platelet aggregation
blood coagulation-fibrin
further platelet agglutination
WBC adhere to platelets
clot grows larger
does thrombosis depend on coagulation
no, not initially but can grow by adding clot
outcomes of thrombus
grows, breaks loose and becomes embolus, dissolve, rechannel
embolus
piece of thrombus breaks off and moves around
arterial thrombus
can be non-occlusive but grows to occlude artery causing ischemia and necrosis
venous thrombus
thrombophlebitis, deep vein thrombosis (DVT)
thrombophlebitis
abnormal venous clot leading to inflammation of the vein
where do venous thrombus’ form
around valves in heart because of good spots to pool
can a venous thrombus result in death
yes, or can be unharmful
deep vein thrombosis
risk of thromboembolism
emoblism
intravascular object that ravels in bloodstream
sources of embolism
thrombi
athersclerotic debris
marrow fat
air
amniotic fluid
ischemia
lack of oxygen to tissue
what causes ischemia
obstruction
what do long periods of ischemia do
long periods result in infarct
ischemic necrosis
necrosis (death of tissue) due to ischemia
what else ischemia be caused by that is NOT obstruction
torsion
drowning
carbon monoxide
torsion
twisting of blood vessels
drowning
water in bronchioles causes them to close
NO oxygen
carbon monoxide
oxygen cannot be released from hemoglobin
white infarction
bloodless, due to arterial obstruction in dense solid tissue
red infarction
bloody, occurs in loose spongy tissue
tissues with dual blood supply
lungs
liver
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
shock
inability of cardiovascular system to meet O2 demands of body
what could shock be the final stage of
severe hemorrhage
bacterial sepsis
burns
myocardial infarction
severe soft tissue damage
end result of shock
multi-organ failure/death
cardiogenic shock
heart failure due to pump failing and cannot maintain perfusion pressure
hypovolemic shock
decreased blood volume
obstructive shock
fluid in pericardium preventing expansion of the heart
septic shock
systemic bacterial infection
disseminated intravascular coagulation
anaphylactic shock
systemic vasodilation
blood pressure decreases
sepsis
associated w/bacterial infection
lipopolysaccharides (LPS)
endotoxins
effects of sepsis
promotes thromobosis
microvascular occlusion
DIC
treatment for sepsis
antibiotics
stages of shock
non-progressive
progressive
irreversible
irreversible shock
circulatory collapse
marked hypoperfusion of vital organs
loss of vital functions
multiorgan failure
death
complications of shock
acute respiratory distress syndrome
acute renal failure
GI tract complications
DIC
multiple organ dysfunction syndrome
