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178 Cards in this Set

  • Front
  • Back
thrombocytopenia
deficiency of circulating platelets; caused by destruction of RBM

treatment = transfusion
hemophilia
inability to form prothrombin activator; repeated bleeding in joints; deficiency of VIII, IX, or XI

treatment = transfusions
**genetic
von willebrand disease
most common hereditary bleeding disorder; abnormal menstrual bleeding, bleeding of gums, bruising...
agglutinogens
RBC antigens (substances foreign to the body); define ABO blood types
agglutinins
plasma antibodies (protective cells that attack agglutinogens)

are specific to type of antigen NOT present in blood type
transfusion reactions
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)
rhesus (Rh) factor
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
erythroblastosis fetalis
"hemolytic disease of the newborn"
for Rh- mother with Rh+ baby, RhoGAM serum given containing anti-Rh to prevent sensitization
pericardium
outer: fibrous pericardium (protects, anchors, prevents bld overflow)
inner: serous pericardium (parietal layer, pericardial cavity, visceral layer)
layers of heart wall
1. visceral layer of serous pericardium (epicardium)
2. myocardium (muscle bundles)
3. endocardium (squamous epithelium)
valve function (relaxed heart, atria contract, ventricles contract)
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 aorta/pul. artery shuts SL valves
chordae tendinae
"heart strings"; anchor AV valves to papillary muscles
heart sounds (lub-dub)
lub = AV valves closing (systole)

dub = SL valves closing (diastole)
valve stenosis
AV or SL valves fail to open during systole/diastole

blood flow restricted
heart murmur
blood reflux through valves; turbulent flow

valves partially open when they sholuld be shut

common in children (thin heart walls)
path of bloodflow through heart
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)
left coronary artery branches
anterior interventricular artery

circumflex artery
right coronary artery branches
right marginal artery

posterior interventricular artery
anastomoses
merger of blood vessels

fxn = make sure blood flow continues
three veins draning the heart
great cardiac vein

middle vardiac vein

small cardiac vein

**give feedback to coronary sinus
angina pectoris - cause
cause = set off by temper fit; fleeting def. of bld to myocardium; temporary blockade of coronary vessels; low BF allows accumulation of lactic acid
angina pectoris - symptoms and tx
symptoms = chest pain, heaviness, aching, burning, squeezing

tx = beta blockers, nitrates, blood thinners, and big 3 (diet, exercise, no smoking)
myocardial infarct (heart attack/coronary) - cause
cause = blockade of coronary arteries..blood flow blocked..heart tissue begins to die

**not only from decreased O to heart
myocardial infarct (heart attack/coronary) - symptoms, verification, tx
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
heartburn - cause and tx
cause = GERD, inflam in upper ab. cavity

tx = PB, mylanta, tums (antacids)
microscopic anatomy of heart
mono/binucleated
short, fat, striated cells
intercalated discs
-gap junctions (transmitting currents)
-desmosomes (prevent separation during contraction)
AP mechanism of contractile cells
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
unique characteristics of cardiac cells (3)
1. automaticity (some self-excitable)
2. single contractile unit
3. long cardiac refractory period (prevents tetany of hrt)
intrinsic conduction system of autorhythmic (noncontractile) heart cells
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
sequence of excitation in heart
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
sympathetic ANS regulation of HR
cardioacceleratory center- incr HR and force of contraction

innervation= SA and AV nodes, heart muscle, coronary arteries

neurotransmitter= NE
parasympathetic ANS regulation of HR
cardioinhibitory center- decreases HR
nodes

cranial nerve= vagus nerve X

neurotransmitter= ACh

**main regulator of HR ("brakes system")
innervation= SA and AV
bainbridge reflex
sympathetic reflex
baroreceptors in aorta --> BP low --> CAC --> speeds up HR
endocrine regulation of HR (2 hormones)
epinephrine- brief, fast increase in HR

thyroxin- slower, long-lasting increase in HR
P wave
depolarization wave from SA node through atria (small wave)
QRS wave
ventricular depolarization (steep wave)
T wave
ventricular repolarization (small wave)
P-Q interval
from beg of atrial excitation to beg of ventricular excitation
P-R interval
atrial depolarization and contraction
Q-T interval
from beg of ventricular depolarization to beg of ventricular repolarization
S-T segment
entire ventricular myocardium depolarized
ECG tracing of heart depol/repolarization (6 steps)
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
junctional rhythm of heart
SA node nonfunctional
P waves absent
heart paced by AV node @ 40-60 bpm
second-degree heart block (sinus rhythm)
some p waves not conducted through AV node
excess ratio of P waves to QRS waves (2:1)
ventricular fibrillation
chaotic, irregular heart rhythm

ECG deflections seen in acute heart attack and electrical shock
arrhythmia
irregular HB

common causes- nicotine, caffeine
fibbrilation
rapid, uncoordinated HB

defibrillation- resets conduction system

AFib- observed to see if worsens

VFib- MUST defibrillate
ectopic focus
excitable group of cells that causes premature heart beat outside the normally functioning SA node of heart
bradycardia
very low heart rate; bpm<60; body temp is low

causes- overative P-ANS (CIC); drugs, symptom of brain edema; in most pro athletes
tachycardia
very high HR; bpm>100 @ rest; can lead to VFib

causes- increase in body/ambient temps, stress, heart disease, drugs
cardiac output
amount of blood pumpedo ut be each ventricle in 1 min

CO (ml/min) = HR x SV
stroke volume
volume of blood pumped out by 1 ventricle with each beat

correlated w/ force of ventricular contraction

SV (ml/beat) = EDV - ESV
frank starling law of heart
greater vol blood entering heart during diastole (EDV) means greater volume of blood being ejected during systole (ESV)

**preload controls SV
preload
degree to which cardiac muscles are stretched just before they contract (greater preload = greater SV)
contractility
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
afterload
pressure that must be overcome for ventricles to eject blood

greater BP= excess straining on SL valves
venous return
amount of blood returning to heart and stretching ventricles
vagal tone
dominany inhibitory effect on heart; vagal nerves innervating it
NE incr heart contractility via cAMP secondary messenger system
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
congenital heart defects - ventricular septal defect
interveltricular septum fails to form; blood mixes between ventricles

more blood shunted from left to right

tx= replacing wall
coarctation of aorta
part of aorta narrowed; increases the workload of the left ventricle
tetralogy of fallot - symptoms
1. pulmonary stenosis
2. VSD
3. overriding aorta
4. R ventricle hypertrophy
tetralogy of fallot - detection, tests, decline, tx
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
sclerosis/thickening of valve flaps
common site- mitral valve (where BF greatest)

result- heart murmur
cardiac reserve decline
cardiac reserve= ability of heart to respond to sudden/prolonged stress

symp. control= SANS control decr with age, less efficient

heart rate more variable
fibrosis of cardiac muscle
cardiac cells die and are replaced by fibrous tissue

stroke volume decreases

fibrosis of nodes- incr incidence of arrhythymias
atherosclerosis
contributing factors- inactivity, smoking, stress

consequences- hypertensive HD, incr incidence of heart attack and stroke, and coronary
tunics of blood vessels
1. tunica intima
2. tunica media
3. tunica externa
tunica intima
1. endothelium - simple squamous epithelium

2. sub endothelial layer (in BVs > 1 mm)
tunica media
1. smooth muscle (reg. by vasomotor nerve fibers of ANS)

2. elastic fibers

**important in blood flow and BP

thickest in muscular arteries
tunica externa
1. loose collagen fibers

2. vaso vasorum - system of tiny blood vessels that nourish external tissues of BV wall (in larger BVs)
elastic arteries
"conducting arteries"
largest arteries
mostly elastic tissue and smooth muscle
fxn= pressure reservoirs
muscular arteries
"distributing arteries"
mostly sm. muscle and fibrous tissue (collagen)
fxn= deliver blood to body organs; **vasoconstriction
arterioles
smallest arteries
mostly sm. muscle and fibrous tissue
fxn= incr/decr blood flow into capillary beds
capillaries
"back alleys and driveways"
smallest BVs
*only composed of tunica intima (endothelium)
fxn= exchange of materials bw blood and interstitial fluid
continuous capillaries
least permeable capillaries
location= skin and muscle
composition= pericytes, basement membrane, tight jxn, IC cleft (not in blood brain barrier)
fxn = transport of solutes
pericytes
located on surface of some capillaries
"smooth muscle-like" cells
fxn= stabilize capillary wall, help control permeability
fenestrated capillaries
partially permeable
location= kidneys, SI, endocrine glands

composition= large fenestrations (pores; increase permeability)

fxn= solute movement
sinusoidal capillaries/ sinusoids
most permeable
location= liver, speen, BM, adrenal medulla

composition= discontinuous endothelium, hepatic macrophages

fxn= passage of large substances; macrophages destroy bacteria
vascular shunt
**precapillary sphincters closed
blood flow=
terminal arteriole
metarteriole
thoroughfare channel
postcapillary venule
true capillaries
"exchange vessels"
**precapillary sphincters open - blood flows through vascular shunt AND true capillaries
venules
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
veins
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
occurence of BVs in circulatory system (5)
60% - systemic veins and venules
15% - systemic arteries and arterioles
12% - pulmonary BVs
8% - heart
5% - capillaries
structural adaptations of veins (2)
1. large-diameter lumens
2. venous valves
venous valves
prevent blood from flowing backwards in veins

formed from folds of tunica media

most abundant in veins of limbs, absent in thoracic/abdominal cavities
varicose veins
veins that have become twisted and dilated bc of leaky valves

contributing factors= heredity, elevated venous pressure
hemorrhoids
varicosities in anal veins

caused by elevated venous pressure in abdomen, prevents blood from draining from veins of anal canal
vascular anastomoses
when vascular channels join

fxn= provide alternate pathways (collateral channels) for bld to reach given body region
blood flow
vol of bld flowing through vessel/organ/circulation at given period

equivalent to CO, relatively constant

F = change in BP/resistance

units: ml/min
blood pressure (BP)
force perunit area exerted on vessel wall exerted by contained blood

**means systemic BP in largest arteries near heart

units: mm Hg
peripheral resistance
opposition to blood flow; amount of friction blood encounters passing through vessels

factors: blood viscosity, total BV length, BV diameter
factors affecting peripheral resistance (3)
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
poiseuille's law
blood flow inversely proportional to= resistance (viscosity, vessel length)

blood flow directly proportional to= vessel diameter (decr. resistance) and change in pressure
arterial blood pressure - factors (2)
1. how much elastic arteries close to heart can be stretched (compliance)

2. vol of bld forced into them at given time
systolic pressure
aortic pressure peak

result of L ventricle contraction, which expels bld into aorta

avg= 120 mm Hg
diastolic pressure
lowest aortic pressure

aortic valves close (preventing backflow), walls of aorta recoil
pulse pressure
systolic - diastolic pressure

felt as pulse during systole

increased by incr SV, incr contractility, and arteriosclerosis (chronic)
mean arterial pressure (MAP)
pressure that propels blood to tissues

MAP= diastolic pres. + (pulse pres./3)

decr with incr distance from heart
3 functional adaptations important for venous return
1. respiratory pump
2. muscular pump
3. layer of sm muscle around veins (constricts under S-ANS control)
respiratory pump
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)
muscular pump
sk muscle causes deep adj veins to contract/relax, "milking" blood toward heart

**successive valves prevent backflow
factors regulating BP (3)
1. cardiac output (CO= SV x HR) in L/min
2. peripheral resistance (viscosity, BV length and diameter)
3. blood volume
CO regulation by BP - normal
HR control= cardioinhibitory center of parasympathetic ANS; in medulla

SV control= venous return (usually limits SV); EDV
CO regulation by BP - under stress
HR control= cardioacceleratory center of sympathetic ANS (acts on SA node)

SV control: CAC center; epinephrine/neural reg; venous return
short term BP controls
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
vasomotor center
neural integration center that oversees changes in diameter of BVs

fxn= transmits efferent impulses along vasomotor fibers to sm muscle of BVs (mainly arterioles)
vasomotor tone
constant state of moderate constriction in arterioles

incr S-ANS activity = vasoconstriction, incr BP
controls of vasomotor activity (3)
input from:
1. baroreceptors
2. chemoreceptors
3. higher brain centers
baroreceptors
pressure-sensitive mechanoreceptors

respond to change in arterial pressure/stretch

location= carotid sinuses (brain) and aortic arch
baroreceptor reflexes - high BP
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)
baroreceptor reflexes - low BP
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)
chemoreceptors
respond to changes in bld levels of CO2, H+, and oxygen)

location= carotid and aortic bodies; large neck arteries
chemoreceptor reflexes
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
short term mechanism of BP regulation
altering peripheral resistance (VM activity) and CO (CAC/CIC)
long term mechanism of BP regulation
altering blood volume; mediated by kidneys
direct renal mechanism (long term BP reg)
incr in BV or BP = incr rate of fluid filtering in kidneys; increase in urinary output (decr BV)
renin-angiotensin mechanism
indirect renal regulation of BP

decr BP...kidneys release renin...renin stim angiotensin II production...BP increases
angiotensin II mechanisms for increasing BP (3)
1. potent vasoconstrictor (incr R)
2. stim secretion of aldosterone (incr renal Na reabsorption)
3. stim secretion of ADH (incr water reabsorption)

**also incr sensation of thirst
high BP medications
1. diuretics
2. beta blockers
3. angiotensin-converting enzyme (ACE) inhibitor
4. Ca channel blockers
angiotensin II receptor blockers
autoregulation of blood flow - metabolic controls
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)
autoregulation of blood flow - myogenic controls
vascular sm muscle responds to stretch (incr pressure) by increasing tone (resists stretch, causes vasoconstriction)
extrinsic mechanisms of blood flow - nervous system
sympathetic nervous system causes vasoconstriction of BVs to incr BP

**major role of NO
extrinsic mechanisms of blood flow - hormones (5)
1. epinephrine - alpha receptors (C)
2. NE - beta receptors (D)
3. angiotensin II (C)
4. ADH (C)
5. ANP (D)
alpha adrenergic receptors
binds to epinephrine

location= most tissues

fxn= sm muscle contraction, arteriolar constriction
beta adrenergic receptors
binds to NE

location= arterioles supplying sk and heart muscle

fxn= sm muscle relaxation, arteriolar dilation
intrinsic mechanism of blood flow
distribution of BF to organs/tissues as needed
extrinsic mechanisms of blood flow
1. maintain MAP
2. redistribute bld during exercise and thermoregulation
angiogenesis
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)
skeletal muscle blood flow - at rest
approx 1 L/ min
25% capillaries open

myogenic and general neural mechanisms predominate
skeletal muscle blood flow - during activity
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
brain blood flow
remains constant (neurons intolerant of ischemia or lack of BF)

metabolic and myogenic controls
brain blood flow - metabolic controls
low BF:
decr pH and incr CO --> vasodilation of cerebral vessels --> incr BF

**Oxygen not as impt
brain blood flow - myogenic controls
decr in MAP= cerebral vessels dilate to ensure BF

incr in MAP= cerebral vessels constrict, protecting small vessels further down from rupturing
factors increasing MAP by increasing CO (4)
1. incr activity of muscular/respiratory pump
2. decr release of ANP
3. fluid loss (hemorrhage, sweating)
4. crisis stressors (exercise, trauma, incr BT)
factors increasing MAP by increasing peripheral resistance (5)
1. fluid loss
2. crisis stressors (exercise, trauma, incr BT)
3. bloodborne chemicals (epi, NE, ADH, AT II)
4. dehydration
5. incr body size
extrinsic factors affecting BP (8)
age
sex
weight
race
mood
posture
SE status (diet)
physical activity
orthostatic hypotension
temporary decr in BP and dizziness after rising suddenly from reclining or sitting position
chronic hypotension
long-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
acute hypotension
most impt sign of circulatory shock

threat to patients undergoing surgery or in ICU
transient hypertension
normal

causes= fever, physical exertion, emotional upset
primary (essential) chronic hypertension
damage to BVs, baroreceptors, hrt muscle

risk factors= age, sex diet...; heredity, stress, smoking

**major cause of hrt failure, vascular disease, kidney failure, stroke
secondary chronic hypertension
due to other disorders (kidney disease, hyperthyroidism, cushing's disease)

tx= fixing above diseases
circulatory shock
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
hypovolemic shock
from large-scale loss of blood (acute hemorrhage, V&D, extensive burns)
vascular shock
BV normal but decreased cirulation bc of extreme vasodilation

**anaphylactic shock
obstructive shock
inadequate BF due to obstruction of BVs
cardiogenic shock
"pump failure"
heart cant sustain adequate circulation

cause= myocardial damage from numerous MIs
anaphylactic shock
vascular shock caused by loss of VM tone due to bodywide systemic allergic reaction

triggered by massive histamine release
atherosclerosis
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)
arteriosclerosis
walls of arteries become thick/tough; decr elasticity

result= hypertension

family of genetic disorders
foramen ovale and ductus arteriosus
fetal shunts bypassing nonfunctional lungs
ductus venosus
fetal shunts bypassing nonfunctional liver
umbilical veins and arteries (in utero)
circulate bld b/w fetal circulation and placenta (where gas/nutrients exchanged with mother's blood)
common circulatory complications caused by aging (3)
1. high BP
2. atherosclerosis
3. varicose veins
AB blood group
antigens= A, B

antibodies= none

recipient for= A, B, AB, O (universal recipient)
B blood group
antigens= B

antibodies= anti-A

recipient for= B, O
A blood group
antigens= A

antibodies= anti-B

recipients for= A, O
O blood group
antigens= none

antibodies= anti-A, anti-B

recipient for= O (universal donor)
functions of lymphatic system (3)
1. fat absorption
2. role in immunity
3. fluid balance
lymphatic vessels collect... (4)
1. cells
2. fluids
3. proteins
4. metabolic waste
lymphatic vessel functions (3)
1. return excess tissue fluid to bld stream
2. return leaked proteins to bld
3. carry absorbed fats from intestine to blood (lacteals)
lymph
interstitial fluid that has entered the lymphatic system at leakages of capillary beds
pathway of blood through lymph system to heart
1. lymphatic capillaries
2. collecting vessels
3. lymphnodes
4. R lymphatic or thoracic duct
5. subclavian veins
6. heart
volume of blood in lymphatic system (ml/min...L/day)
1.5 ml/min

2.16 L/day
mechanisms of lymphatic capillary permeability (2)
1. flaplike minivalves (endothelial cells loosely overlapping)

2. incr volume in interstitial fluid opens minivalves (collagen "anchoring" filaments)
lymphatic trunks
1. R/L lumbar trunks
2. R/L broncomediastinal trunks
3. R/L subclavian trunks
4. R/L jugular trunks
5. intestinal trunk
right lymphatic duct
drains lymp from upper limbs and right side of head and thorax
thoracic duct
drains lymph from rest of the body (not upper limbs or R head/thorax)
unique characteristics of lymphatic collecting vessels
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
characteristics of lymph transport (4)
1. no central pump
2. pressurized by: sm muscle, sk muscle, breathing, arteries
3. flow matches tissue activity
4. valves ensure ONE-WAY flow
macrophages
lymphoid cells; phagocytes; "big eater"; engulfs microbes, trash, debri, etc.

help activate T-cells
lymphocyte functions (2)
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
T-lymphocytes
act in thymus gland; responsible for directing immune response
B-lymphocytes
act in bone marrow; produce plasma cells (secrete antibodies into blood)
components of lymphoid tissue (6)
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
regional concentrations of lymph nodes (3)
1. cervical (neck)
2. axillary (chest, armpits)
3. inguinal (groin)
lymph nodes- function, primary cell type
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