exam 4 Flashcards
hemostasis
process of stop bleeding
thrombus
clot
5 major factors affecting hemostasis
integrity of small blood vessels
adequate numbers of normal platelets
normal amounts of clotting factors (liver)
normal amounts of clotting inhibitors
adequate amounts of calcium
first defense after injury
small vessels
platelets and injury
accumulate and adhere to site
plug hole in vessel
release chemicals for vasoconstriction and aggregation
release substance that initiate blood clotting
platelets characteristics
survive for 10 days
contractile proteins
become activated
prevent bleeding from capillaries
blood coagulation process
1) release prothrombin by injured vessel
2) convert prothrombin into thrombin
3) soluble fibrinogen converted into insoluble fibrin strands by thrombin
blood clot
result of clotting process
meshwork of fibrin threads and blood cells
disturbances of blood coagualtion
adnormalities of small blood vessels
abnormality of platelet numbers
deficiency of 1+ clotting factors
liberation of thromboplastic material
abnormalities of small vessels
abnormal bleeding from failure of small vessels to contract after injury
abnormality of platelet numbers
abnormal platelet formation low platelets injury or disease t bone marrow cancer of bone marrow destruction of platelets via antibodies
petechiae
small red or blue spots
pinpoint hemorrhages in skin
indicated defective or inadequate platelets
dont blanch
hemorrhagic disease
presence of petechiae and fever with infection
poor prognosis
hemophilia
x linked hereditary disease
episodes of hemorrhage in joints and organs
von willebrand disease
vWF adheres to damaged vessel wall, framework frames
helps maintain normal levels of other clotting factors
causes of abnormal blood clotting
anticoagulant drugs
inadequate synthesis of vitamen K
inadequate absorption of vitamen K
severe liver disease
causes of thrombocytopenia
injury or disease to bone marrow
leukemic or cancer cells enter bone marrow
antiplatelet antibody destroys platelets in circulation
liberation of thromboplastic material into circulation
thromboplastic chemicals released into circulation, intravascular coagulation
shock and tissue necrosis
bacterial infections
disseminated intravscular coagulation
abnormal state of bleeding and clotting
severe trauma or hemorrhage= shock, bacterial infection
many small clots in capillaries
body releases chemicals to dissolve clots
net effect: hemorrhage
high mortality
lab tests for hemostasis
platelet count
bleeding time- funktion of capillaries
clotting times
clotting time tests
PTT vs PT
thrombin time
partial thromboplastin time (PTT)
measure the time of the first phase of coagulation
lipid and calcium added to blood
prothrombin time (PT)
measure of time combines second and third phases of coagulation measure coumodin (anticoagulant)
thrombin time
bypass first two phases of blood coagulation
measure level of fibrinogen
pathogenesis of intravascular clotting
slowing or stasis of blood flow
blood vessel wall damage
increased clotting of blood
embolus
circulating clot carried into lungs or body
plugs vessels
infarct
tissue necrosis from interruption of blood flow
fat embolusim
following severe bone fracture that disrupts fatty bone marrow and adipose tissue
emulsified fat globules sucked into vein and carried into lungs, obstruct lung capillary
may block vessels in brain or organ
air emboluism
air sucked into circulation from lung injury or open chest wound
air may enter right chambers and prevents filing of heart of blood, unable to pump
foreign particle embolusim
forign matter
injected substances users
injected IV
severe respiratory distress
venous thrombosis
clot in leg from prolong bed rest
varicose veins
leg swelling
possible pulmonary embolism
clincal manifestations of pulmonary embolism
size and location in artery
cynosis or shortness of breath= deoxygenation of blood
large pulmonary emboli
right side becomes distended with blood
left ventricle unable to pump enough blood to brain and organs
systemic BP falls and go into shock
small pulmonary emboli
may pass through arteries or lodge in small arteries
lung segments undergo necrosis
dyspnea, chest pain, cough, bloody spit
gold standard for detecting pulmonary embolus
pulmonary angiogram
treatment for embolus
anticoagulants
thrombolytic drugs
angioplasty
remove clot
arterial thrombosis
may cause injury to vessel wall= ulcers
blocks blood flow
coronary artery
heart attack
major leg artery
gangrene
cerebral artery
stroke
thrombosis by increased clotting
rise in coagulation factors following surgrey or injury
estrogen or contraception pills=synthetic clotting factors
gene mutations
edema
swelling
accumulation of fluid outside vascular system
ankles
extracellular circulation between capillary and ISF
pitting edema
pit or indent formed when tissue is pressed
ascites
fluid accumulates in abdominal cavity
pathogenesis of edema
increased capillary permeability-inflammation
low plasma protein
lymphatic obstruction
factors regulating fluid flwo between capillaries and tissues
capillary BP force fluid out of capillaries
capillary permeability-fluid flow threw wall
osmotic pressure
lymphatic channels
osmotic pressure
due to proteins in blood
pulls fluid into capillaries
shock
inadequate tissue perfusion (delivery of oxygenated blod) due to low BP
hypovolemic
low blood volume
cadriogenic
failure of the heart as a pump
septic shock
excessive vasodilation secondary to release of toxins and inflammatory chemicals
anaphylactic shock
excessive vasodilation from release of inflammatory chemicals
prognosis of shock
early recognition and rapid treatment
drugs to vasoconstrict (restore BP)
IV fluids to restore blood volume
treat underlying cause
funktion of the heart
muscular pump
propels blood to tissues
heart disease
diturbance of the funktion
pericardium
double layer sac surrounding heart
fibrous pericardium
outer connective tissue
serous pericardium
parietal and visceral layers
epicardium
same layer as visceral pericardium
myocardium
thick layer of cardiac muscle
contracts to form beats
endocardium
innermost layer lining chambers and valves
smooth surface for blood flow
superior vena cava
recieves blood from regions above heart
drains into right atria
inferior vena cava
recieves blood from regions below the heart
drains into right atria
coronary sinus
collects blood that drains from myocardium
pulmonary veins
enter left atria
tricuspid valave
right side
biscupid/mitral valve
left side
pulmonary valve side
right
aortic valve side
left
pulmonary circulation
pums blood to the lungs
pick up o2
drops off co2
systemic circulation
pumps o2 rich blood to body tissues
drop off o2
picks up co2
coronary circulation
delievers o2 rich blood to myocardium and takes away co2
during diastole
coronary sinus
cardiac veins that empty into right atrium
right coronary artery
supply right side and SA node
left coronary artery
supply left side
what happens to injured heart tissue
does not regenerate
forms scar tissue that cannot conduct impulses
conduction system
muscle cells that initiate own electrical impulses
SA node in right atria
cardiac cycle
all events with blood flow through the heart during one beat
systole
contraction
diastole
relaxation
cardiac output
amount of blood pumper per minute
blood pressure
blood flow in the arteries
highest pressure
contraction
systolic pressure
lowest pressure
relax
diastolic pressure
electrocardiogram
meausres electrical activity of heart
depolarization
contraction
repolarization
relaxation
p wave
atrial depolarization
atrial systole
qrs complex
ventricular depolarization
ventricular systole
t wave
ventricular repolarization
ventricular diastole
atrial fibrilitation
atria quiver instead of contracting normally
ventricles beat faster than normal
concern of blood clot
ventricular fibriliation
ventricles quiver-incompatible with life
only treatment-defibriliation
heart block
delay or intermissions of impulse transmission from atria to ventricles
fetal blood flow diferences
blood in pulmonary trunk shunted away from fetal lungs
ductus arteriosus
opening between aorta and pulmonary trunk
after birththe ductus should close
foramen ovale
opening in atrial septum covered by flap of tissue
one way valve to bypass lungs
after birth the opening should close
abnormal heart development
effect of structural abnormality depends on type and effect on circulation
blood may be shunted between chambers-depends on size of opening
L to R shunt
systemic to pulmonary most common mixes oxygenated with deoxygenated blood o2 still reaches tissues bad affect- increase pulmonary pressure-damage to lungs
R to L shunts
pulmonary to systemic mixes deoxygenated with oxygenated blood in right chaners decreases 02 to the tissues activities restricted cynosis
4 groups of congenital heart disease
failure of normal fetal bypass channels to close
atiral and ventricular septal defects
abnormalities that obstruct blood flow
abnormal formations of aorta or pulmonary artery or connection
failure of fetal bypass channels to close
patent ductus arteriosus-surgery
patent foramen ovale-asymptomatic/surgrey
atrial and ventricular septal defects
small defects- close randomly but surgery
large defects- surgrey bc of L to R shunt
obstruction of blood flow
narrow valve opening-depends on size
dilate valve opening
pulmonary stenosis
obstruct blood flow from right ventricle
aortic stenosis
obstructs blood flow from left ventricle
coarctation of the aorta
localized narrowing of aorta (close to heart)
pressure and volume of blood decrease
high BP in brachial, low BP in legs
reconstruct aorta
tetralogy of fallot
pulmonary stenosis large ventricular septal defect enlarged aorta that overrides septal defect right ventricle hypertrophy cynosis clubbing fingers and toes increase blood viscosity treatment- opening narrowed trunk and close septal defect
valvular heart disease
rheumatic fever and heart disease
non rheumatic aortic stenosis
mitral valve prolapse
infective endocarditis
rheumatic fever
complication of strep
fever and inflammation-heart and joints
acute arthritis=scarring
can repair valves
rheumatic heart disease
complication of rheumatic fever caused by scarring ofheart valves (mitral and aortic) backflow of blood narrowed valve heart failure artificial valve
non rheumatic aortic stenosis
aortic valve has 2 cusps instead of 3
asymptomatic for years but may calcify=rigid
valve replacement
risk factoes: high cholesterol, diabetes, high BP
mitral valve prolapse
valve cusps are enlarged
prolapse into left atrium during ventricular systole
backflow of blood or murmur
infective endocarditis
bacterial infection of heart valve (mitral or aortic)
subacute- organisms of low virulence that infect abnormal or damaged heart valves
acute-highly virulent organisms that previousl normal heart valves
subacute infection endocardities
small deposits of platelets and fibrin accumulat on damged valve-bacteria=inflammation
normally body defenses destroy bacteria
prophylactic antibiotics for dental work
artificial valve
acute infective endocarditis
highly pathogenic organism spread in blood from infection elsewhere and infect valve
staph infection
vegetations form on valve
coronary heart disease
arteriosclerosis of coronary arteries
arteries narrow and accumulate fatty material
damage to lining of vessels
calcification on walls
end result- yellow, mushy debris that narrows lumen
ulcers
atheroma
collection of fatty material and debris new plaques are unstable plaques degenerative changes are irreversible permantly narrows risk factors: elevated blood lipids, high BP, smoking, diabetes
coronary heart disease symptoms
excessive demands on the heart if active
ischemia
bouts of chest pain
myocardial ischemia
reduced blood supply to heart caused by narrowing or obstruction of coronary arteries
angina pectoris
bouts of chest pain caused by ischemia
occurs on exertion and subsides when rest
unstable angina
pain occurs more often and longer
diagnosing coronary heart disease
coronary angiogram is gold stnadard
catheter in femoral artery to abdominal aorta
dye injected to show location and degree
treatment of coronary heart disase
drugs to reduce myocardial o2 consumption and improve circulation stop smoking control BP low fat/cholesterol diet lose weight exercise
percutaneous coronary inerventio (PCI)
angioplasty
similar to angiogram but affected artery are dilated with balloon and stent is placed
within 90 minutes of arriving at hospital
coronary artery bypass graft (CABG)
patients with severe sclerosis of all major coronary arteries
vein from leg used for bypass
severe myocardial ischemia complications
severe and prolonged ishcemia cause heart attack
cardiac arrest or necrosis of heart muscle
4 triggers of heart attack with CAD
sudden blockage of coronary artery
hemorrage into a plaque
arterial spasm
sudden greatly increase myocardial 02 demand
ischemia
damage due to lack of blood flow
myocardial infacrtion
necrosis of heart muscle from severe ischemia blood is insufficient to sustain muscle severe chest pain and collapse thickness of heart wall L ventricle and septum
complications of heart attack
arrhythmias
heart failure
intra cardiac thrombi
cardiac rupture
cardiac rupture
perforation thru necrotic tissue-blood leaks into pericardial sac and compresses the heart
survival of heart attack patients depends on
size of onfarct patients age complications preseence of other disease go to the hospital immediately
most helpful diagnostic tools for heart attacks
EKG
blood level of enzymes
EKG
reveals abnormalities when blood flow to heart muscle is inadequate
muscle becomes infarcted
labs fro heart attack
troponin
creatine kinase
troponin
not detectable in healthy people
peak in 24 hours
creatine kinase
only present when severe damage
thromoblytic therapy
dissolving the clot restores blood flow and salvages muscle
done before to much damage occurs
via IV
future thrombus
those who had MI have higher risks of clots
sudden death from arrhythmias
aspirin
interfers with platelet funktion
prevents them from clumping and clotting
increase chance of hemorrhage
blood lipids
elevated blood lipids important for pathogenesis of atherosclerosis
triglycerides and cholesterol
sugar elevated triglycerides
cholesterol adn CAD
high cholesterol diets leads to evelvate blood levels and premature athersclerosis
LDL
bad cholesterol
transports cholesterol from blood into cells
HDL
good cholesterol
removes cholesterol from cells and takes it to liver for excretion
protects against CAD
hypertension
high BP excessive vasoconstriction of arterioles heart pumps more forcefully=damage heart will fail bc increased workload narrow renal arteries wear out vessels arterioles thicken
treatments for high BP
drugs to dilate peripheral arteries
heart failure
heart unable to pump adequate amounts of blood to tissues
back up of blood in veins or lungs
edema
treatments for heart failure
diurectics
meds for forced contractions
meds that lower BP
aneurysms
dilation or arterial wall outpouching of portion of wall
result of arteriosclerosis
arteriosclerotic aneurysms
atheromatous deposits damage aortic wall, reduce elastictiy and weak
wall balloons outward
inside will calcify and clot
fatal if rupture
dissecting aortic aneurysms
one or more layers of aortic wall separate and form tears
blood forced between layers
severe chest and back pain
fatal unless caught early
disease of veins
venous thrombosis leg veins inflammation excessive dilation varicose veins
thrombosis in veins
post-op patients in bed
may form pulmonary embolism
early walking
varicose veins
ssuperficil veins become dilated and valves faulty
blood pools in veins
complications of varicose veins
stasis of blood in veins=poor oxygen
skin becomes thin, prone to infection
may rupture
treatment of varicose veins
stockings and elevation of legs to promote venous return
sugrey
trachea
rigid tube with C-shaped cartilage rings
carina
split of the trachea
alveoli
tiny air filled sacs for gas exchange
produce surfactant
covered in pulmonary capilarries
ventilation
movement of air into and out of lungs
breathing
respiration
gas exchange between blood and tissure or blood and lungs
gas exchange via
diffusion
high to low pressure
requirements for efficient gas exchange
large capillary surface area
unimpeded diffusion across membrane
normal pulmonary blood flow
normal pulmonary alveoli
pulmonary funktion tests
measure volume of air that can be moved into adn out of lungs under normal conditions
vital capacity
max volume of air expelled after max inspiration
pleura
thin membrance covering lungs and surface fo chest wal
pleural cavity
potential space between ungs and chest wall
intrapleural pressure
pressure of pleural cavity
has to be less than the pressure in lungs for alveoli to expand
increase pressure=lung collapse
pnemothorax
escape of air into pleural spce due to lung injury or disease
stab or gun shot=air enters chest
tension pneumothorax
positive pressure in pleural cavity
air enter sna dcannot escape
chest tube entered to release air
atelectasis
collapse of lung
obstructive atelectsis caused by bronchial obstruction from mucus
pneumonia
inflammation of the lung
exudate in lung, fills alveoli
classification of pneumonia
etiology
anatomic distribution of inflammation
predisposing factors
tuberculosis
contagious bacterial infection breath in toxic bacteria lesion in lungs=body produce antibodies and form tubercle (dead bacteria and lung tissue) necrosis occurs, tubercle coughed up antibiotics
drug resistant tuberculosis
resistance strains of organisms emerge
bronchities
inflammation of bronchial mucosa
chronic obstructive pulmonary disease
combo of emphysema and chronic bronchitis
pulmonary emphysema
destruction of alveolar structure of lungs with cycstic spaces
dysonea
chronic bronchitits
chronic inflammation of terminal bronchioles
anatomic derangement in COPD
inflammation and narrowing of terminal bronchioles swelling of bronchial mucosa dilation of pulmonary air spaces diffusion of gases loss of lung elasticity
pathogenesis of COPD
inflammatory swelling of mucosa
leukocytes accumulate in bronchioles and alveoli
coughing
retention of secretions
bronchial asthma
spasmodic contraction of smooth muscle on walls of bronchi
dyspnea and wheezing
treat with drugs to dilate bronchioles
neonatal respiratory distress syndrome
respiratory distress after birth
inadequate surfactant in lungs=alveoli collaspe
preemies
pulmonary fibrosis
thickening of alveolar septa from irritant gases and particles
lungs rigid restricting breathing
decreased diffusion
