BIOL 320: EXAM 2
178 Cards in this Set
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thrombocytopenia
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deficiency of circulating platelets; caused by destruction of RBM
treatment = transfusion
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hemophilia
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inability to form prothrombin activator; repeated bleeding in joints; deficiency of VIII, IX, or XI
treatment = transfusions
**genetic
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von willebrand disease
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most common hereditary bleeding disorder; abnormal menstrual bleeding, bleeding of gums, bruising...
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agglutinogens
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RBC antigens (substances foreign to the body); define ABO blood types
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agglutinins
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plasma antibodies (protective cells that attack agglutinogens)
are specific to type of antigen NOT present in blood type
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transfusion reactions
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agglutination (clumping) of RBCs in presence of an antibody
1. small BVs clot and rupture
2. Hb released into blood
symptoms=fever, chills, low BP, incr HR
treatment: alkaline fluid infusion and diuretics (avoid kidney failure)
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rhesus (Rh) factor
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C, D, E = most common antibodies
Rh+ = RBCs carry D antigen
anti-Rh antibodies not spontaneously formed
1st exposure: body primed to Rh-, no rxn
2nd exposure: transfusion reaction; donor RBCs rupture
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erythroblastosis fetalis
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"hemolytic disease of the newborn"
for Rh- mother with Rh+ baby, RhoGAM serum given containing anti-Rh to prevent sensitization
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pericardium
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outer: fibrous pericardium (protects, anchors, prevents bld overflow)
inner: serous pericardium (parietal layer, pericardial cavity, visceral layer)
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layers of heart wall
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1. visceral layer of serous pericardium (epicardium)
2. myocardium (muscle bundles)
3. endocardium (squamous epithelium)
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valve function (relaxed heart, atria contract, ventricles contract)
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relaxed hrt: bld flows thru AV valves to atria
atria contract: squeeze remaining blood from atria to ventricles
ventricles contract:
1. high ventricular pressure closes AV valves
2. papillary muscles hold valves shut
3. bld leaves via SL valves
Relaxed heart: vol of bld in aor…
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chordae tendinae
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"heart strings"; anchor AV valves to papillary muscles
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heart sounds (lub-dub)
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lub = AV valves closing (systole)
dub = SL valves closing (diastole)
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valve stenosis
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AV or SL valves fail to open during systole/diastole
blood flow restricted
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heart murmur
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blood reflux through valves; turbulent flow
valves partially open when they sholuld be shut
common in children (thin heart walls)
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path of bloodflow through heart
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IVC/SVC
right atrium
tricuspid valve
right ventricle
pulmonary SL valve
pulmonary trunk/arteries
LUNGS
pulmonary veins
left atrium
mitral valve
left ventricle
aortic SL valve
aorta
body (then repeat)
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left coronary artery branches
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anterior interventricular artery
circumflex artery
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right coronary artery branches
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right marginal artery
posterior interventricular artery
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anastomoses
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merger of blood vessels
fxn = make sure blood flow continues
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three veins draning the heart
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great cardiac vein
middle vardiac vein
small cardiac vein
**give feedback to coronary sinus
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angina pectoris - cause
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cause = set off by temper fit; fleeting def. of bld to myocardium; temporary blockade of coronary vessels; low BF allows accumulation of lactic acid
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angina pectoris - symptoms and tx
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symptoms = chest pain, heaviness, aching, burning, squeezing
tx = beta blockers, nitrates, blood thinners, and big 3 (diet, exercise, no smoking)
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myocardial infarct (heart attack/coronary) - cause
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cause = blockade of coronary arteries..blood flow blocked..heart tissue begins to die
**not only from decreased O to heart
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myocardial infarct (heart attack/coronary) - symptoms, verification, tx
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symptoms = chest pain, dizziness, nausea, palpitations, impending doom
verification = ECG, blood gas analysis
tx = ambulance: ox therapy, nitroglycerin tablets, aspirin, heparin
hospital: angioplasty, stenting, thrombolytics, bypass surgery
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heartburn - cause and tx
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cause = GERD, inflam in upper ab. cavity
tx = PB, mylanta, tums (antacids)
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microscopic anatomy of heart
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mono/binucleated
short, fat, striated cells
intercalated discs
-gap junctions (transmitting currents)
-desmosomes (prevent separation during contraction)
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AP mechanism of contractile cells
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1. depolarization- Na fast channels open; - to + charge
2. plateau phase- Ca slow channels open; maintains + charge
3. repolarization- Ca channels inactivated, K channels open; + to - charge
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unique characteristics of cardiac cells (3)
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1. automaticity (some self-excitable)
2. single contractile unit
3. long cardiac refractory period (prevents tetany of hrt)
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intrinsic conduction system of autorhythmic (noncontractile) heart cells
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1. pacemaker potential (slow)- Na channels open and K channels close
2. depolarization- Ca channels open, membrane becomes more +
3. repolarization- Ca channels inactivated, K channels open; + to - charge
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sequence of excitation in heart
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1. sinoatrial (SA) node - "pacemaker"; rate 72-75 bpm
2. internodal pathway
3. atrioventricular (AV) node- .1 sec delay
4. Bundle of His (AV bundle)
5. bundle branches
6. purkinje fibers
7. papillary muscles
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sympathetic ANS regulation of HR
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cardioacceleratory center- incr HR and force of contraction
innervation= SA and AV nodes, heart muscle, coronary arteries
neurotransmitter= NE
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parasympathetic ANS regulation of HR
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cardioinhibitory center- decreases HR
nodes
cranial nerve= vagus nerve X
neurotransmitter= ACh
**main regulator of HR ("brakes system")
innervation= SA and AV
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bainbridge reflex
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sympathetic reflex
baroreceptors in aorta --> BP low --> CAC --> speeds up HR
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endocrine regulation of HR (2 hormones)
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epinephrine- brief, fast increase in HR
thyroxin- slower, long-lasting increase in HR
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P wave
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depolarization wave from SA node through atria (small wave)
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QRS wave
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ventricular depolarization (steep wave)
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T wave
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ventricular repolarization (small wave)
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P-Q interval
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from beg of atrial excitation to beg of ventricular excitation
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P-R interval
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atrial depolarization and contraction
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Q-T interval
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from beg of ventricular depolarization to beg of ventricular repolarization
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S-T segment
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entire ventricular myocardium depolarized
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ECG tracing of heart depol/repolarization (6 steps)
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1. atrial depolarization (P wave)
2. impulse delayed at AV node
3. vent depolarization (QRS complex); atrial repolarization
4. vent depolarization complete
5. vent repolarization (T wave)
6. vent repolarization complete
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junctional rhythm of heart
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SA node nonfunctional
P waves absent
heart paced by AV node @ 40-60 bpm
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second-degree heart block (sinus rhythm)
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some p waves not conducted through AV node
excess ratio of P waves to QRS waves (2:1)
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ventricular fibrillation
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chaotic, irregular heart rhythm
ECG deflections seen in acute heart attack and electrical shock
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arrhythmia
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irregular HB
common causes- nicotine, caffeine
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fibbrilation
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rapid, uncoordinated HB
defibrillation- resets conduction system
AFib- observed to see if worsens
VFib- MUST defibrillate
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ectopic focus
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excitable group of cells that causes premature heart beat outside the normally functioning SA node of heart
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bradycardia
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very low heart rate; bpm<60; body temp is low
causes- overative P-ANS (CIC); drugs, symptom of brain edema; in most pro athletes
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tachycardia
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very high HR; bpm>100 @ rest; can lead to VFib
causes- increase in body/ambient temps, stress, heart disease, drugs
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cardiac output
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amount of blood pumpedo ut be each ventricle in 1 min
CO (ml/min) = HR x SV
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stroke volume
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volume of blood pumped out by 1 ventricle with each beat
correlated w/ force of ventricular contraction
SV (ml/beat) = EDV - ESV
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frank starling law of heart
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greater vol blood entering heart during diastole (EDV) means greater volume of blood being ejected during systole (ESV)
**preload controls SV
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preload
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degree to which cardiac muscles are stretched just before they contract (greater preload = greater SV)
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contractility
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contractile strength acheived at a given muscle length;
influenced by incr Ca, incr S-ANS, epinephrine, digitalis, TH
incr contractility = incr SV and decr ESV
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afterload
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pressure that must be overcome for ventricles to eject blood
greater BP= excess straining on SL valves
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venous return
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amount of blood returning to heart and stretching ventricles
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vagal tone
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dominany inhibitory effect on heart; vagal nerves innervating it
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NE incr heart contractility via cAMP secondary messenger system
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1. NE incr entry of extracellular Ca
2. NE causes incr release of SR Ca
3. NE causes SR uptake pumps to incr Ca uptake from sarcoplasm
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congenital heart defects - ventricular septal defect
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interveltricular septum fails to form; blood mixes between ventricles
more blood shunted from left to right
tx= replacing wall
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coarctation of aorta
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part of aorta narrowed; increases the workload of the left ventricle
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tetralogy of fallot - symptoms
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1. pulmonary stenosis
2. VSD
3. overriding aorta
4. R ventricle hypertrophy
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tetralogy of fallot - detection, tests, decline, tx
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initial detection- cyanosis, blue tint 1-2 days post-birth
tests- chest xray, ultrasound, ECG
decline- bypasses close
tx- "blue baby" surgery; OHS if severe
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sclerosis/thickening of valve flaps
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common site- mitral valve (where BF greatest)
result- heart murmur
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cardiac reserve decline
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cardiac reserve= ability of heart to respond to sudden/prolonged stress
symp. control= SANS control decr with age, less efficient
heart rate more variable
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fibrosis of cardiac muscle
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cardiac cells die and are replaced by fibrous tissue
stroke volume decreases
fibrosis of nodes- incr incidence of arrhythymias
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atherosclerosis
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contributing factors- inactivity, smoking, stress
consequences- hypertensive HD, incr incidence of heart attack and stroke, and coronary
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tunics of blood vessels
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1. tunica intima
2. tunica media
3. tunica externa
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tunica intima
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1. endothelium - simple squamous epithelium
2. sub endothelial layer (in BVs > 1 mm)
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tunica media
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1. smooth muscle (reg. by vasomotor nerve fibers of ANS)
2. elastic fibers
**important in blood flow and BP
thickest in muscular arteries
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tunica externa
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1. loose collagen fibers
2. vaso vasorum - system of tiny blood vessels that nourish external tissues of BV wall (in larger BVs)
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elastic arteries
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"conducting arteries"
largest arteries
mostly elastic tissue and smooth muscle
fxn= pressure reservoirs
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muscular arteries
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"distributing arteries"
mostly sm. muscle and fibrous tissue (collagen)
fxn= deliver blood to body organs; **vasoconstriction
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arterioles
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smallest arteries
mostly sm. muscle and fibrous tissue
fxn= incr/decr blood flow into capillary beds
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capillaries
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"back alleys and driveways"
smallest BVs
*only composed of tunica intima (endothelium)
fxn= exchange of materials bw blood and interstitial fluid
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continuous capillaries
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least permeable capillaries
location= skin and muscle
composition= pericytes, basement membrane, tight jxn, IC cleft (not in blood brain barrier)
fxn = transport of solutes
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pericytes
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located on surface of some capillaries
"smooth muscle-like" cells
fxn= stabilize capillary wall, help control permeability
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fenestrated capillaries
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partially permeable
location= kidneys, SI, endocrine glands
composition= large fenestrations (pores; increase permeability)
fxn= solute movement
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sinusoidal capillaries/ sinusoids
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most permeable
location= liver, speen, BM, adrenal medulla
composition= discontinuous endothelium, hepatic macrophages
fxn= passage of large substances; macrophages destroy bacteria
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vascular shunt
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**precapillary sphincters closed
blood flow=
terminal arteriole
metarteriole
thoroughfare channel
postcapillary venule
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true capillaries
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"exchange vessels"
**precapillary sphincters open - blood flows through vascular shunt AND true capillaries
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venules
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formed when capillaries unite
smalllest= postcapillary venules
-only endothelium, very porous
larger= 1 or 2 layers of sm muscle (tunica media) and thin tunica externa
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veins
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formed when venules voin
fxn= carry blood from capillary beds toward heart
thickest layer=tunica media
largest= venae cavae
fxn= capacitance vessels and blood reservoirs
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occurence of BVs in circulatory system (5)
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60% - systemic veins and venules
15% - systemic arteries and arterioles
12% - pulmonary BVs
8% - heart
5% - capillaries
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structural adaptations of veins (2)
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1. large-diameter lumens
2. venous valves
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venous valves
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prevent blood from flowing backwards in veins
formed from folds of tunica media
most abundant in veins of limbs, absent in thoracic/abdominal cavities
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varicose veins
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veins that have become twisted and dilated bc of leaky valves
contributing factors= heredity, elevated venous pressure
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hemorrhoids
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varicosities in anal veins
caused by elevated venous pressure in abdomen, prevents blood from draining from veins of anal canal
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vascular anastomoses
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when vascular channels join
fxn= provide alternate pathways (collateral channels) for bld to reach given body region
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blood flow
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vol of bld flowing through vessel/organ/circulation at given period
equivalent to CO, relatively constant
F = change in BP/resistance
units: ml/min
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blood pressure (BP)
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force perunit area exerted on vessel wall exerted by contained blood
**means systemic BP in largest arteries near heart
units: mm Hg
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peripheral resistance
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opposition to blood flow; amount of friction blood encounters passing through vessels
factors: blood viscosity, total BV length, BV diameter
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factors affecting peripheral resistance (3)
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1. blood viscosity - thickness of blood (incr viscosity=incr resistance)
2. total BV length - incr length=incr resistance
3. blood vessel diameter - most variable; decr diameter=incr resistance
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poiseuille's law
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blood flow inversely proportional to= resistance (viscosity, vessel length)
blood flow directly proportional to= vessel diameter (decr. resistance) and change in pressure
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arterial blood pressure - factors (2)
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1. how much elastic arteries close to heart can be stretched (compliance)
2. vol of bld forced into them at given time
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systolic pressure
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aortic pressure peak
result of L ventricle contraction, which expels bld into aorta
avg= 120 mm Hg
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diastolic pressure
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lowest aortic pressure
aortic valves close (preventing backflow), walls of aorta recoil
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pulse pressure
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systolic - diastolic pressure
felt as pulse during systole
increased by incr SV, incr contractility, and arteriosclerosis (chronic)
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mean arterial pressure (MAP)
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pressure that propels blood to tissues
MAP= diastolic pres. + (pulse pres./3)
decr with incr distance from heart
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3 functional adaptations important for venous return
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1. respiratory pump
2. muscular pump
3. layer of sm muscle around veins (constricts under S-ANS control)
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respiratory pump
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incr pressure in ventral cavity moves blood up towards heart
inahalation = incr ab. pressure (forces bld in local veins --> hrt) AND decr. chest pressure (thoracic veins expand, spd bld entry to R atrium)
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muscular pump
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sk muscle causes deep adj veins to contract/relax, "milking" blood toward heart
**successive valves prevent backflow
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factors regulating BP (3)
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1. cardiac output (CO= SV x HR) in L/min
2. peripheral resistance (viscosity, BV length and diameter)
3. blood volume
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CO regulation by BP - normal
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HR control= cardioinhibitory center of parasympathetic ANS; in medulla
SV control= venous return (usually limits SV); EDV
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CO regulation by BP - under stress
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HR control= cardioacceleratory center of sympathetic ANS (acts on SA node)
SV control: CAC center; epinephrine/neural reg; venous return
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short term BP controls
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counteract changes in BP by altering peripheral resistance (and CO)
goals:
1. maintain MAP by altering BV diameter
2. alter bld distribution according to demands of organs
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vasomotor center
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neural integration center that oversees changes in diameter of BVs
fxn= transmits efferent impulses along vasomotor fibers to sm muscle of BVs (mainly arterioles)
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vasomotor tone
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constant state of moderate constriction in arterioles
incr S-ANS activity = vasoconstriction, incr BP
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controls of vasomotor activity (3)
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input from:
1. baroreceptors
2. chemoreceptors
3. higher brain centers
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baroreceptors
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pressure-sensitive mechanoreceptors
respond to change in arterial pressure/stretch
location= carotid sinuses (brain) and aortic arch
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baroreceptor reflexes - high BP
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baroreceptors in aortic arch and carotid sinuses stimulated by stretch
stimulate= CIC (P-ANS)
inhibit= CAS (S-ANS) and vasomotor center
result:
1. decr HR, contractility, and CO (decr S-ANS)
2. vasodilation (decr VM activity)
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baroreceptor reflexes - low BP
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baroreceptors in carotid sinuses/aortic arch inhibited
stimulate= CAC and VM center
inhibit= CIC (P-ANS)
result:
1. incr HR, contractility, and CO (incr S-ANS)
2. vasoconstriction (incr VM activity)
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chemoreceptors
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respond to changes in bld levels of CO2, H+, and oxygen)
location= carotid and aortic bodies; large neck arteries
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chemoreceptor reflexes
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stimulated by: incr in bld CO2, decr pH or oxygen
stimulates= CAC and VM center
result:
1. incr CO (CAC)
2. vasoconstriction (incr VM activity)
-->incr BP
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short term mechanism of BP regulation
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altering peripheral resistance (VM activity) and CO (CAC/CIC)
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long term mechanism of BP regulation
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altering blood volume; mediated by kidneys
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direct renal mechanism (long term BP reg)
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incr in BV or BP = incr rate of fluid filtering in kidneys; increase in urinary output (decr BV)
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renin-angiotensin mechanism
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indirect renal regulation of BP
decr BP...kidneys release renin...renin stim angiotensin II production...BP increases
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angiotensin II mechanisms for increasing BP (3)
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1. potent vasoconstrictor (incr R)
2. stim secretion of aldosterone (incr renal Na reabsorption)
3. stim secretion of ADH (incr water reabsorption)
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high BP medications
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1. diuretics
2. beta blockers
3. angiotensin-converting enzyme (ACE) inhibitor
4. Ca channel blockers
angiotensin II receptor blockers
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autoregulation of blood flow - metabolic controls
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decrease:
1. pH
2. blood oxygen
increase:
1. CO2 (D)
2. potassium (D)
3.prostaglandins (D)
4. adenosine (D)
5. NO (D)
6. endothelins (C)
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autoregulation of blood flow - myogenic controls
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vascular sm muscle responds to stretch (incr pressure) by increasing tone (resists stretch, causes vasoconstriction)
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extrinsic mechanisms of blood flow - nervous system
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sympathetic nervous system causes vasoconstriction of BVs to incr BP
**major role of NO
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extrinsic mechanisms of blood flow - hormones (5)
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1. epinephrine - alpha receptors (C)
2. NE - beta receptors (D)
3. angiotensin II (C)
4. ADH (C)
5. ANP (D)
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alpha adrenergic receptors
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binds to epinephrine
location= most tissues
fxn= sm muscle contraction, arteriolar constriction
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beta adrenergic receptors
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binds to NE
location= arterioles supplying sk and heart muscle
fxn= sm muscle relaxation, arteriolar dilation
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intrinsic mechanism of blood flow
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distribution of BF to organs/tissues as needed
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extrinsic mechanisms of blood flow
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1. maintain MAP
2. redistribute bld during exercise and thermoregulation
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angiogenesis
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long-term autoregulation of BF
increasing # of BVs in region, enlargement of existing BVs
common in heart when coronary vessel partially occluded
in ppl who live in high altitudes (air has les ox)
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skeletal muscle blood flow - at rest
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approx 1 L/ min
25% capillaries open
myogenic and general neural mechanisms predominate
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skeletal muscle blood flow - during activity
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incr in BF to area proportional to met. activity
local controls override S-ANS (which would normally cause vasoconstriction)
BF can increase 10x or more during activity
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brain blood flow
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remains constant (neurons intolerant of ischemia or lack of BF)
metabolic and myogenic controls
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brain blood flow - metabolic controls
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low BF:
decr pH and incr CO --> vasodilation of cerebral vessels --> incr BF
**Oxygen not as impt
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brain blood flow - myogenic controls
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decr in MAP= cerebral vessels dilate to ensure BF
incr in MAP= cerebral vessels constrict, protecting small vessels further down from rupturing
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factors increasing MAP by increasing CO (4)
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1. incr activity of muscular/respiratory pump
2. decr release of ANP
3. fluid loss (hemorrhage, sweating)
4. crisis stressors (exercise, trauma, incr BT)
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factors increasing MAP by increasing peripheral resistance (5)
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1. fluid loss
2. crisis stressors (exercise, trauma, incr BT)
3. bloodborne chemicals (epi, NE, ADH, AT II)
4. dehydration
5. incr body size
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extrinsic factors affecting BP (8)
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age
sex
weight
race
mood
posture
SE status (diet)
physical activity
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orthostatic hypotension
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temporary decr in BP and dizziness after rising suddenly from reclining or sitting position
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chronic hypotension
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ong-lasting; due to poor nutrition
anemia --> decr # bld proteins --> decr viscosity --> decr BV/BP
**warning sign for hypothyroidism, addison's disease, or severe tissue wasting
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acute hypotension
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most impt sign of circulatory shock
threat to patients undergoing surgery or in ICU
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transient hypertension
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normal
causes= fever, physical exertion, emotional upset
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normal
causes= fever, physical exertion, emotional upset
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damage to BVs, baroreceptors, hrt muscle
risk factors= age, sex diet...; heredity, stress, smoking
**major cause of hrt failure, vascular disease, kidney failure, stroke
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secondary chronic hypertension
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due to other disorders (kidney disease, hyperthyroidism, cushing's disease)
tx= fixing above diseases
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circulatory shock
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BVs inadequately filled, blood can't circulate normally
result= inadequate BF to meet tissue needs
if persists, can lead to cell death and damaged organs
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hypovolemic shock
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from large-scale loss of blood (acute hemorrhage, V&D, extensive burns)
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vascular shock
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BV normal but decreased cirulation bc of extreme vasodilation
**anaphylactic shock
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obstructive shock
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inadequate BF due to obstruction of BVs
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cardiogenic shock
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"pump failure"
heart cant sustain adequate circulation
cause= myocardial damage from numerous MIs
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anaphylactic shock
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vascular shock caused by loss of VM tone due to bodywide systemic allergic reaction
triggered by massive histamine release
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atherosclerosis
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most common form of arteriosclerosis
deposits of lipid/cholesterol build up on vessel walls
result= turbulent BF..incr resistance.. BF blocked
increased risk= MIs, strokes, blood clots (embolus, thrombus)
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arteriosclerosis
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walls of arteries become thick/tough; decr elasticity
result= hypertension
family of genetic disorders
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foramen ovale and ductus arteriosus
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fetal shunts bypassing nonfunctional lungs
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ductus venosus
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fetal shunts bypassing nonfunctional liver
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umbilical veins and arteries (in utero)
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circulate bld b/w fetal circulation and placenta (where gas/nutrients exchanged with mother's blood)
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common circulatory complications caused by aging (3)
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1. high BP
2. atherosclerosis
3. varicose veins
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AB blood group
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antigens= A, B
antibodies= none
recipient for= A, B, AB, O (universal recipient)
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B blood group
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antigens= B
antibodies= anti-A
recipient for= B, O
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A blood group
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antigens= A
antibodies= anti-B
recipients for= A, O
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O blood group
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antigens= none
antibodies= anti-A, anti-B
recipient for= O (universal donor)
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functions of lymphatic system (3)
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1. fat absorption
2. role in immunity
3. fluid balance
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lymphatic vessels collect... (4)
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1. cells
2. fluids
3. proteins
4. metabolic waste
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lymphatic vessel functions (3)
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1. return excess tissue fluid to bld stream
2. return leaked proteins to bld
3. carry absorbed fats from intestine to blood (lacteals)
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lymph
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interstitial fluid that has entered the lymphatic system at leakages of capillary beds
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pathway of blood through lymph system to heart
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1. lymphatic capillaries
2. collecting vessels
3. lymphnodes
4. R lymphatic or thoracic duct
5. subclavian veins
6. heart
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volume of blood in lymphatic system (ml/min...L/day)
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1.5 ml/min
2.16 L/day
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mechanisms of lymphatic capillary permeability (2)
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1. flaplike minivalves (endothelial cells loosely overlapping)
2. incr volume in interstitial fluid opens minivalves (collagen "anchoring" filaments)
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lymphatic trunks
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1. R/L lumbar trunks
2. R/L broncomediastinal trunks
3. R/L subclavian trunks
4. R/L jugular trunks
5. intestinal trunk
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right lymphatic duct
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drains lymp from upper limbs and right side of head and thorax
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thoracic duct
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drains lymph from rest of the body (not upper limbs or R head/thorax)
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unique characteristics of lymphatic collecting vessels
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compared to veins - more internal valves, thinner walls, more anastomoses
in skin, travel with superficial veins
deep vessels travel with arteries
nutrients via vaso vasorum
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characteristics of lymph transport (4)
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1. no central pump
2. pressurized by: sm muscle, sk muscle, breathing, arteries
3. flow matches tissue activity
4. valves ensure ONE-WAY flow
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macrophages
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lymphoid cells; phagocytes; "big eater"; engulfs microbes, trash, debri, etc.
help activate T-cells
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lymphocyte functions (2)
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1. protect body from antigens (bacteria, viruses, mismatched RBCs, etc)
2. mature into attack cells
lymphocytes arise in RBM, cycle b/w circ. vessels, lymph tissues, and loose CT
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T-lymphocytes
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act in thymus gland; responsible for directing immune response
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B-lymphocytes
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act in bone marrow; produce plasma cells (secrete antibodies into blood)
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components of lymphoid tissue (6)
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1. macrophages (occupy fibers)
2. lymphocytes (occupy medullary sinus)
3. reticular fibers (supportive, contain reticular cells)
4. dendritic cells (capture antigens and bring back to lymph nodes)
5. reticular cells (produce fibers)
6. medullary sinus
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regional concentrations of lymph nodes (3)
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1. cervical (neck)
2. axillary (chest, armpits)
3. inguinal (groin)
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lymph nodes- function, primary cell type
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cluster along lymph vessels, embedded in CT
fxn= isolate/destroy foreign substances
primary cell type= macrophages
**more afferent (in) than efferent (out) vessels
become enlarged during infection
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BIOL 320: EXAM 1