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Flashcards in Midterm 2 Deck (383):
1

What makes up half of body weight

muscle

2

which muscle types are innervated by ANS

cardiac and smooth are involuntary

3

muscle fibre

single skeletal muscle cell, lie in parallel bundles in CT

4

Myoblast

Small cells fuse into skeletal fibres in embryo

5

Myofibril

80% of fibre is tick and thin filaments for contraction

6

Proteins in filaments

Thick is myosin
Thin is actin

7

Order of muscle elements big to small

Muscle
Fibre
Myofibril
Thick and thin filaments
Myosin and actin

8

muscle coverings

Dense CT of collagen and elastin

9

3 layers covering muscle

Epimysium
Perimysium--> divides into bundles/fasicles
Endomysium--> covers each fibre

10

A band

Dark, stacked thick filaments with some thin--> only A bands have thick bands

11

H zone

Lighter area in middle of A band where thin filaments don't reach

12

M line

Proteins hold thick filaments vertically together
Extends down middle of A band in centre of H zone

13

I band

Remaining thin filaments not projecting into A band

14

Z line

Dense vertical line in the middle of each I band connecting sacromeres

15

Sacromere

Area between 2 Z lines. Functional unit of skeletal muscle

16

Titin

Elastic protein extends down M line of thick filaments to Z line on other end of sarcomere to stabilize thick filaments

17

Cross bridge

Myosin head extends from each thick filament towards surrounding thin
Hexagon--> extend from 6 directions on thick

18

How many thick filaments surround a thin in a CB

3

19

Myosin

2 subunits twisted like a golf club. Heads form CBs between thick and thin

20

2 cross bridge sites

Actin binding site
Myosin ATPase site for splitting

21

Thin filament componenets

Actin
Tropomyosin
Troponin

22

Actin

2 twisted strands are backbone of thin. Binding site for mysosin

23

Regulatory proteins

Troponin and tropomyosin block cross bridge activity at rest

24

Troponin

3 polypeptide units--> 1 for tropomyosin binding, 1 for actin and one for Ca

25

Ca in CB activity

Binds to regulatory proteins to change shape and slip from blocking position

26

Sliding filament mechanism

Contraction--> thin filaments slim over stationary thick filaments towards A band centre
Z lines are pulled together so sarcomere shortens

27

Concentric contraction

Contract fibres, Z lines move, whole muscle shortens
H zone smaller and I band narrows
A bands unchanged

28

How does filament length change during SLM

it doesnt, the thin ones just slide in . HAHA tricked you

29

Powers troke

CB hinges to centre of sarcomere pulling in thin filaments, myosin/actin bond breaks and shape reverts, cycle continues

30

Excitation Contraction Coupling

Stimulates contraction when teased at NMJwhen permeability changes increase AP rate. spreads across T tubules and SR to link to contraction

31

Transverse tubules

Surface membrane at NMJ dips into muscle fibre between every A and I band to conduct AP by inducing P changes in SR

32

Sarcoplasmic Reticulum

Modified ER encircles myofibril and separates segments around A and I band

33

Lateral sacs

End of each SR segment, separated by a gap to T tubule, release Ca when stimulated

34

Foot proteins

Extend SR in gap between lateral sac and tubule. 4 units for Ca channels

35

Ryanodine receptors

On lateral sac side Zip with complementary units on dihydropyridine receptors on T tubule

36

Ca release

voltage gated sensors activated by AP on T tubule so CA is released into cytosol from lateral sacs. Bind to actin and links myosin CB

37

ATP powered cross bridge cycle

ATP split with enzymes, attach to myosin before actin. Actin binding causes power stroke. ADP released and a new ATP joins to continue cycle

38

Rigor mortis

Skeletal muscles locked in contraction when Ca lingers so actin can bind, but there is no ATP after death to let CB detach

39

Relaxation

contraction stops when the CAATPase put in SR moves Ca back into lateral sacs. Reg proteins move back into blocking position

40

Latent period

Time delay between stimulation and contraction because AP is done before contractile apparatus is involved

41

contraction time

From contraction onset to peak tension is 50 msec.

42

Relaxation time

From peak tension to complete relaxation is 50 msec

43

How many skeletal muscles

600

44

twitch

Single AP in muscle fibre makes weak contraction

45

2 factors effecting gradation of whole skeletal muscle tension

Number of fibres recruited to contract
Tension produced by each fibre

46

Motor unit

Motor neuron links with each individual fibre on muscle it innervates so they contract simultaneously. Motor units spread out evenly

47

Asynchronous Recruitment of motor units

alternate units to sustain activity of sub maximal contractions

48

4 factors effecting fibre tension

Frequency of stimulation
Length of fibre at onset
Extent of fatigue
Thickness of fibre

49

Twitch summation

Repeated stimulation of fibre to achieve tension. Same magnitude APs piggy back

50

Tetanus

Muscle fibre is stimulated rapidly and doesnt relax at all. Smooth, sustained maximal strength. CB cycling continues until titanic contraction

51

NS regulations on contraction strength

Number of motor units recruited
Frequency of stimulation

52

Optimal muscle length

Thin filaments optimally overalap thick where CBs project. Relationship between length and the titanic contraction that can be developed. Central thick filaments only have myosin tails

53

greater than optimal length

passive stretching causes tin to be pulled from thick so they don't match up

54

Less than optimal length

Thin filaments opposite side overlap to limit opportunity for CB. Thick filaments forced against Z line to impede shortening

55

Series elastic component

stretchy springs between tension gathering elements--> sarcomere shortens and ES stretches

56

Isotonic contraction

Force production is unchanged. Tension is constant while fibre length changes

57

Isometric contraction

Length is unchanged, tension developed at constant length

58

Dynamic contraction

Lift things when tension exceeds load

59

Static contraction

Tension develops but load is to heavy so muscle can't shorten to move. submaximal postural

60

Eccentric contraction

Dynami contraction produces tension while lengthening muscle, actin is pulled apart and Z lines move away--? lowering weight

61

concentric contraction

Dynamic, produces tension while muscle shortens

62

Work

Force x distance

63

Power arm

Portion of lever between fulcrum and point of upward force

64

Load arm

Between fulcrum and downward force

65

3 steps in contraction requiring ATP

Split ATP on myosin head
Bind fresh ATP to myosin head
Active transport of Ca to SR to relax

66

Creatine Phosphate

first energy for contraction, catalyzed by creaatine kinase. Shifts after a minute

67

Oxidative phosphorylation

In muscle mitochondria. Can keep pace with moderate exercise

68

Myoglobin

Muscle fibres store small amounts of oxygen transferred from blood

69

Carb loading

liver holds stores of glycogen

70

Increased cystolic ADP and P

interferes with CB cycling and Ca release and uptake

71

Muscle fatigue

Fibres dont respond to stimulation with same degree of contraction. Increase ADp, , lactic acid, deplete oxygen nd glycogen

72

CNS fatigue

lack of adequate stimulus to motor neurons

73

Excess post exercise o2 consumption

EPOC to repay O2 deficit, restore nutrients. Caused by too much epinephrine

74

Type 1 muscle fibres

Slow twitch, innervated by bigger alpha 2 neurons with higher threshold
Take energy through slow oxidative processes. Red in colour from mitochondria and myoglobin

75

Type 2 fibres

Fast glycolytic or fast oxidative glycolytic defending on enzymes. White due to less mitochondria and myoglobin

76

Satellite cells

growth and tissue rear found between sarcolemma and basal lamina of muscle fibres, Donate nuclei for regernation

77

Hypertrophy

Increase in muscle mass caused by resistance training

78

Fibres in a motor unit

All the same type. Cant convert between fast and slow, but Fg can become FOG

79

Atrophy

Myosin and actin decrease, fibres shrink. Can be from disuse or disinnervation

80

muscular dystrophy treatment

Stem cell form myoblasts, fuse together and placed in muscle

81

3 things controlling motor neuron ouput

Afferent neuron input
Primary motor cortex
Brain stem

82

corticospinal motor system

Fibres originate in pyramidal cells and terminate on motor neurons in pinalcord. For fine volunatry movements like hands

83

Multineuronal

extrapyramidal, synapse in RF and thalamus, for posture

84

motor control

Inhibitory and excitatory inputs on same neuron

85

Spastic paralysis

Increased muscle tone from disrupted inhibition

86

Flaccid Paralysis

Loss of excitatory input causes lack of voluntary movement but spinal reflexes work

87

Hemiplegia

Flaccid paralysis from stroke on opposite side of primary cortex

88

Muscle spindles

Collections of intrafused fibres monitor muscle length. Each has a efferent/afferent nerve supply and non-contractile centre

89

gamma motor neuron

Efferent neuron supplies intramural fibres

90

Alpha neuron

Efferent supply for extrafusal fibres

91

Primary ending (annulospiral)

Afferent ending wrapped around central portion of intrafusal fibres sensitive to stretch and speed

92

Secondary endings

Flower spray. Clustered at end of intrafusal fibres sensitive to change in length

93

golgi tendon organs

In tendons, detect changes in muscle tension . afferent Bundles in CT tighten during contraction. Reaches consciousness

94

Stretch reflex

afferent neuron synapses on alpha motor neuron that innervates extrafusal fibres on same muscle. Negative feedback for optimal length

95

patellar tendon

extensor knee muscle activated by spindle receptors

96

Coactivation

Gamma and alpha motor neurons activate to take slack out of spindle as muscle shortens

97

Smooth/cardiac muscle structure

Sliding actin, stationary myosin, Ca release and CBc

98

Smooth muscle cells

Spindle shaped, single nucleus, small, arranged in sheets not down full length. No myofibril, sarcomere , striations or Z lines

99

3 filament types in smooth muscle

thick myosin
thin actin (only tropomyosin)
intermediate filaments

100

Dense bodies

Contain Z line protein, positioned down length of smooth muscle and held by intermediate filaments along with actin

101

Smooth contractile units

Diagonal lattice, not parallel

102

Light chains

Proteins regulate smooth muscle function as regulatory proteins don't block Cbs. Chain must be phosphorylated by myosin light chain kinaseto interact with myosin

103

Contract diff between skeletal and smooth

Skeletal is a physical change in thin filaments
smooth is chemical change in thick

104

smooth muscle excitation

receptors in PM act as Ca channels. ECF calcium influences cross bridge because there is no SR or T tubule response required.

105

smooth muscle relax

Ca uptake into SR and myosin is dephosphorylated to relax

106

Multi unit smooth msucle

partway between skeletal. Many units work separately by neurogenic stimulation. Innervated by ANS

107

Single unit smooth muscle

visceral smooth muscle. Contract as single unit with gap junctions

108

Functional synctium

Group of muscle cells function electrically and mechanically together. Self excitable. Constant fluctuating potential

109

2 types of spontaneous depolarizations

pacemaker potential
slow wave potential

110

Pacemaker potential

membrane gradually depolarizes from passive ionic flux due to changes in channel permeability. AP initiated at threshold and then repolarized

111

Slow wave potential

alternating hyperpolarizing/depolarizing swigs caused by change in Na active transport. Threshold reached on depolarizing swing causing AP burst

112

Myogenic activity

Contractile activity stimulated by muscle itself

113

myogenic smooth muscle

Self excitable cells can't contract. AP goes to non pacemaker cells in functional sanctum via gap junctions. Cant alter number of fibres recruited but can modify tension by varying systolic Ca

114

Smooth muscle tone

not enough Ca to maintain low tone level without APs

115

smooth muscle innervation

both branches of Ans. Don't imitate contraction in single unit but can modify strength . Receptors everywhere, not just at NMJ in skeletal

116

smooth muscle optimal length

Wide range where max contraction can be reached . Thick/thin overlap even when stretched

117

Stress relaxation response

Smooth muscle initially increases tension, eventually get used and return to original tension. Cbs detach slowly

118

Smooth muscle contraction time

Response is much slower than skeletal (3 sec). Slow Ca removal prolongs contraction. Same stretch but uses way less energy than skeletal

119

Latch phenomenon

in smooth muscle CBs latch onto thin filaments for longer contraction with less ATP

120

Cardiac muscle

Striated, both reg proteins present.
Clear length/tension relationship
Lots of mitochondria and myoglobin

121

Cardiac excitation Ca

Ca entry from ECF and SR through voltage gated dihydropyridine receptors. Ca channels in T tubules trigger release

122

Cardiac excitation

Pacemaker activity, gap junctions
Innervated by ANS
Fibres in branching network

123

Atria

upper chambers receive blood returning from heart

124

Heart septum

separates o2 poor right side for o2 rich left side

125

heart blood flow

venae cavae
right atrium
tricuspid
RV
semilunar
Pulmonary artery
pulmonary vein
semilunar
LA
Bicuspid
LV
aorta

126

pulmonary circuit

pumps same amount of blood. Low pressure, low resistance

127

Atriventricular Valves

Open during ventricular filling when atrial pressure is greater

128

Chordae tendinae

Fibrous cords attached to cusps to prevent back flow. attached to papillary muscles on V walls

129

Semi lunar valves

At major arteries leaving ventricles. 3 cups open duringg high V pressure

130

heart skeleton

fibrous frame keeps all valves on same plane

131

3 layers of heart wall

Endothelium-- thin epithelial
myocardium: muscle, bulk
Epicardium: thin external

132

Intercalated discs

Cardiac cells form branches joined by desmosomes

133

Autoryhmicity

Synchronized APs from heart made by autoryhmic cells at pacemaker potential. Contractile cells pump (99%)

134

heart activation

decreased K out, constant Na in, increased Ca in. No voltage gated Na channels so its always open and permeable

135

T type Ca channel

1 of 2 voltage gated Ca channels opens so influx depolarizes membrane to threshold

136

heart rising phase

after threshold L type Ca channels cause influx of positivity

137

heart falling phase

K efflux with active voltage gated channels

138

4 places of autorhymic cells

Sinoatrial node
Atrioventricular node
Bundle of His
Purkinje fibres

139

SA node

In right atrial wall. Fastest AP initiation so it it is the pacemeaker

140

Bundle of His

special cell tract originating at AV node, to atrial outerwalls

141

Purkinje fibres

Terminal fibres extend from bundle of hisand through myocardium

142

latent pacemaker

SA node pace is 70, if it breaks down then AV node takes over at 50 AP/min

143

complete heart block

Conducting tissue between A and V is damaged

144

Ectopic focus

Area becomes depolarized quick and is new pacemaker causing premature V contraction

145

Fibrillation

Random excitation of cardiac cells can cause death if in ventricles

146

Interatrial pathway

Sa node
Right A
Left A
depolarizes atrium at same time

147

Internodal pathway

Sa Node to AV nodes electrical contact between A and V

148

AV nodal delay

100 msec allows ventricular filling as AP travels through AV node

149

Ventricular excitation

AV nodal delay
Bundle of his down septum
purkinje fibres
ventricular myocardium (way bigger, needs faster propagation than atria)

150

Cardiac contractile cells rising

-90 resting potential. Rise to +30 with Na entry. Na P plummets

151

cardiac plateau

membrane stays at peak positive maintained by P changes in L type Ca and K
Slow in Ca prolongs it
K P drops to prevent efflux

152

cardiac falling phase

Ca channels inactivated, rapid K efflux, return to rest

153

Ca induced ca release

AP causes Ca diffusion in from T tubule, triggers release from lateral sacs, triggers much larger intracellular release of ca sparks.Cardiac CB activity is dependant on Ca stores unlike skeletal

154

is cardiac or skeletal contraction faster

Cardiac is slower to allow blood to eject

155

ECF concentration and cardiac

elevated K lessens gradient and reduces resting potential causing octopic focus and arrythmia

156

cardiac refractory perios

long due to plateau phase--> Ca prolongs it

157

electrocardiogram

Meaures comparison of activity between 2 nodes, not actual potential

158

Lead

ECG connected between 2 recording elctrodes

159

ECG waves

P- atrial depolarization
QRS complex-- ventricular depolarization
T-- ventricular repolarization
Atrial repol. recorded as QRS

160

3 points without flow in ECG

PR-- AV nodal delay between P and QRS
ST- plateau between QRS and T
TP- heart repolarized, resting after T wave

161

Tachycardia vs bradycardia

T is 60/min
B is less than 60

162

ECG heart rate

Distance between QRS waves

163

Atrial flutter

Rapid but regular atrial depolarization sat 200/min so AV node can't respond to every impulse

164

atrial fibrillation

irregular, uncoordinated depolarizations with no P waves and sporadic QRS. Causes pulse deficit

165

Pulse deficit

Difference between heart rate and pulse

166

Heart block

Fail to conduct to V so every second atrial impulse spread to V

167

cardiac myopathies

damage of heart muscle

168

myocardial ischemia

inadequate O2 supply to tissue causes necrosis and abnormal QRS waves

169

Cardiac repolrization

Diastole, relaxation and filling

170

End diastolic volume

volume of blood in V after diastole when contraction is complete and A and V are filled

171

isometric ventricular contraction

All valves closed, no blood entry/exit, muscle fibre length constant

172

Stroke volume

Amount of blood ejected out of V in contraction

173

End systolic volume

amount of blood left in V after contraction

174

V diastle

T wave for repolarization
V isstill filling so pressure is below atrial P
happens at the same time as atrial depolarization

175

PV loop of LV

AB: V filling, diastole
BC: isovolumetriccontraction, V P rises to AP
CD: P rises with contraction, blood ejected
DA: isovolumetric relaxation: Pul valve closing

176

Systolic pressure volume relationshi

LV develops max pressure at any volume

177

First heart sound

low pitched, soft, long lub from AV valves closing and onset of V systole

178

Second heart sound

High pitch shorter dub
semilunar valves closing, onset of V diastole

179

Laminar blood flow

Slides over itself easily and makes no sound

180

Stenoic valve

Stiff and doesnt open completely so a lot of pressure needed to eject blood--> whistle sound

181

insufficient/incomplete valve

can't close so blood gushes back and regurgitates --> leaky valve

182

Systolic and diastolic murmur

S: between first and second heart sounds
D: between second and first

183

Cardiac output

volume of blood pumped by each ventricle per minute, not total amount of blood pumped by heart

184

2 cardiac output factors

heart rate and stroke volume
70 beats/min, 5L/min

185

Cardiac reserve

diff between output at rest and at max exercise. up to 25 L/min

186

Vagus nerve

PNS connection to heart supplies atrium, SA and AV nodes and ventricles. Release ACH to bind to G protein and muscarine reducing CAMP

187

SNS activity in heart

norepinephrine binds with beta adrenergic and G protein to accelerate CAMP. Speed depolarization of Sa node and reduce AV delay

188

PNS stimulation of heart

influence SA to decrease HR, increase K P to reduce APs. decrease AV node excitability to delay V contraction. Shorten plateau phase. Limited effect on ventricles

189

cardiac control centre

in brainstem. balances inhibition by vagus nerve and stimulation by SNS

190

extrinsic and intrinsic control of stroke volume

Ex: extent of SNS stimulation to heart
Intrinsic: change venous return

191

Frank stealing law of heart

Cardiac muscle length determined by degreee of diastolic filling--> lengthening increases output

192

Ejection fraction

Stroke volume/ EDV

193

After load

Arterial BP. V must match pressur not open valves

194

compensatedHeart failure

can't keep up with demand, less contractility, smaller SV. Compensate with SNsactivity to raise HR, increase EDV and fibre length

195

decompensated HF

fibres stretched too far on descending arm of curve . Forward failure when SV is too small. Backward failure when veins dam up

196

Nourish heart

Watertight endothelium no passage, walls too thick for diffusion so you need coronary circulation. Mostly uses fatty acids

197

Coronary artery disease

Diminished flow to heart during activity
Profound artery spasm, plaques

198

Plaques

Lipid rich core, smooth muscle overtop with collagen cap when oxidized cholesterol gets in an injury

199

Plaque forming

Cholesterol accumulation below endothelium, monocyte attraction causes inflammation
Injest LDL till macrophage becomes foam cell
bulge through muscle and into lumen

200

angina pectoris

lactic acid build u when heart goes anaerobic due to myocardial schema and O2 deprivation

201

Thromboembolism

Sudden occlusion of coronary artery by free embolus

202

Flow rate

Proportional to pressure gradient and inversey proportional to vascular resistance

203

Pressure gradient

diff in pressure between beginning and end of vessel from high to low

204

resistance

hindrance of blood flow by friction so pressure must increase to compensate. Depends on viscosity, vessel length and radius, less resistance in large radius

205

Poiseuilles law

factors effecting flow rate are flow pressure and resistance. determined by radius

206

Microcirculation

arterioles capillaries and venues only visible under microscope

207

vessel pressure resevoir

Arteries. large radius and little resistance

208

Artery structure

endothelium surrounded by thick CT. greater volume during systole, recoil during diastole

209

Blood pressure

Force exerted on vessel wall by blood. 120/80

210

how is arterial BP measured

invasively with cannula needle

211

Sphygmomanometers

Externally applied arm cuff on brachial artery. Blood flows when pressure exceeds cuff

212

Kortokoff sounds

when determining BP. First sound at highest cuff P is systolic pressure
Second sound when diastolic pressure reached

213

Exercise hypertension

rise in systolic pressure

214

Pulse pressure

difference between systolic and diastolic pressure causes pulse

215

Mean arterial pressure

Average pressure driving blood forward. Closer to diastolic

216

Arterioles

Major resistance vessels with small radius causes pressure drop. Encourage down flow to organs and a more constant pulse

217

Areriole structure

Little elastic in walls, surrounded by thick smooth muscle which contracts to decrease flow

218

Vascular tone

partial smooth muscle constriction with myogenic activity. SNS norepinephrine enhances tone

219

Active hypermia

local anterior vasodilation when cells need more O2

220

metabolic changes inducing arteriolar radius change

decreased O2, acid build up, increased K, increased osmolarity, adenosine or prostaglandin release

221

2 vasoactive mediators released by endothelium

NO: dilation by inhibiting Ca entry
endothelium: contraction and is potent

222

Reactive hypermia

ALot of blood to area when blocked flow restored to change composition to normal

223

Autoregulation

Arteriolar mechanisms keep constant blood flow when arterial pressure changes. Stretch detectors. Brain is best at auto and skeeltal is worst

224

Extrinsic arteriolar control

SNS innervation everywhere except brain. Increased SNs for contraction. Influences TPr and BP

225

Total peripheral flow

F= P/R-- mean arterial pressure/resistance of peripheral vessels

226

norepinephrine

SNS for vasoconstriction, attach to adrenergic receptors but there isn't any in brian so it needs local factors

227

PNS influence on arterioles

none except in penis and clit

228

Integrating centre for BP control

Cardiovascular control centre for SNS output

229

adrenergic receptor types

B2: vasodilation in heart/skeletal with epic.
A1: nor. binds for constriction in kidneys and digestion

230

Vasopressin

Regulate amount of water kidneys retain. vasoconstrictor

231

Angiotensin

renin-angiotensin- aldosterone pathway promotes salt and water retention. vasoconstrictor

232

carrier mediated transport

nno in capillaries except in BBB. all is diffusion

233

Capillary pores

water filled gaps at junctions permit passage of water solubles, while lipid solubles like gas goes through PM. no pores in brain only tight junctions. Liver has huge pores

234

Cap permeability

endothelial cells adjust by widening pores with myosin/actin so plasma proteins can escape

235

Metaarteriole

between arteriole and venuole. Smooth muscle pre capillary sphincters control flow to caps that don't have muscle in response to metabolic changes

236

Bulk flow

protein free plasma leaves capillary, mixes with IF and is reabsorbed so all materials move as a unit

237

Ultrafiltration

High cap pressure so fluid is forced out of pores but proteins stay

238

Reabsorption

inward driving pressure moves fluid into cap

239

capillary BP

hydrostatic pressure exerted on walls by blood forces stuff out

240

Plasma colloid osmotic pressure

Force by colloidal dispersion of plasma proteins encourages fluid to flow in

241

IF hydrostatic pressure

fluid pressure on the outside of cap wall forces fluid in

242

IF colloid osmotic pressure

small fraction of leaked proteins returned to blood by lymphatic system

243

histamine effecting IF

pathologic protein leak causes fluid to rush out

244

Lymphatic system

one way vessel network returns fluid from IF to blood

245

Initial lymphatics

Small terminal lymph vessels permeate almost all tissues. Overlapping endothelial shingles make valves with inward pressure

246

Lymph

Lymphatic vessel with lymph in it converge into larger ones and empty near right atrium. Larger vessels have smooth muscle, skeletal muscle pushes it forwrad

247

4 causes of edema

reduced plasma proteins
increased cap wall permeability by hist.
increased venous pressure
blocked lymph vessels

248

venuloarteriolar signalling

Match capillary flow in and out of an organ

249

veins

large radius, little resistance, flow speeds as it approaches heart. Thinner walls and less smooth muscle. Little myogenic ability. Little elasticity

250

Capacitance vessles

veins are blood reservoir, hold a lot of blood with little pressure because they stretch with little recoil. 60% of circulating blood

251

venous return

volume of blood entering each atrium from veins per minute. pressure is low but atrial pressure is 0. leaky valve rising atrial pressure can cause dam in veins

252

5 factors in venous return

SNS vasoconstriction, skeletal muscle contraction, venous valves, respiration, cardiac suction

253

Decreased venous volume =

more cardiac output from larger EDV

254

Vein vasoconstriction

unlike arterioles constriction increases flow due to decreased capacity

255

Standing

gravity distends veins, cap BP increases and fluid goes into feet

256

varicose veins

vein valves can't support weight of column so vein distends and blood pools

257

Respiratory pump

chest pressure below atmospheric so veins experience pressure out. enhances return

258

cardiac suction

Atrial pressure is below 0 during contraction, increases pressure for blood in veins to flow into atria. Negative V pressure sucks in blood from atria

259

Barroreceptor reflex

triggered change in MAP so heart and vessels adjust cardiac output and TPR--> typical reflex pathway. carotid sinus and aortic arch. Changes in AP firing mark chnage

260

2 reflexes override barroreceptors

LA volume receptors and hypothalamus receptors control plasma volume

261

Secondary hypertension

10% occurs secondary to another problem. loss of renal flow, excessive secretion by adrenal gland, neurogenic defect

262

Primary hypertension

defect in salt magement by kidneys, poordiet low in K and Ca. Defective Na/K pump for contraction

263

endogenous digitalis

increase contractility, constrict vessels, retain salt

264

Prehypertension range

up to 139/89

265

orthostatic hypotension

insufficient compensation to gravity shifts so venous return is reduced

266

circulatory shock

BP too low so blood flow to tissues isn't mainytained
hypovolemic- loss of blood
carcinogenic: weak heart
neurogenic: loss of SNS vascular tone
vasogenic: widespread diction

267

blood loss response

increase SNS, vasoconstriction to increase TPR and cardiacouput

268

Autotransfusion

Capillary volume drops so fluid rushes in , liver makes more proteins

269

myocardial toxic factor

released from pancreas in fluid loss and shock

270

Blood

5L 8% of weight
erythrocytes, leukocytes and platelets ain plasma

271

Hematocrit

packed cell volume shows blood content
48% RBC, 58% plasma, the rest is 1%

272

inorganic plasma elements

Na and Cl electrolytes for excitability and fluid districution

273

3 types of plasma proteins

albumins
globulins
fibrinogen: blood clot factor

274

Albumin

most abundant, contribute to colloid osmotic pressure. Bin to poorly soluble things for transport

275

Globulin

Alpha: inactive circulating. Regulate salt
Alpha/beta: blood clot, highly selective carriers
Gamma: immunoglonulins for defence

276

Hemoglobin

globin protein of 4 polypeptide chains each attached to a non protein heme group. attach to O2, Co2, H, CO and NO

277

Glycolytic enzymes

in RBC for active transport of ion concentrations in cell, glycolysis

278

Carbonic anhydrase

Enzyme for CO2 transport, turns into bicarbonate

279

Erythropoiesis

new RBCs made in red bone marrow

280

Redbone marrow

Make RBCs, stays in sternum, ribs and long limbs. Makes leukocytes, platelets and stem cells

281

yellowbone marrow

fatty stuff replaces RBM after childhood, can't make RBCs

282

Erythropoietin

hromones secreted by kidneys during low O2 to stimulate RBC production. Turn stem cells into RBC. synthetic ETP diminhes need for transfusions

283

Reticulocytes

develop in RBM and become RBC when in demand

284

Pernicious anemia

inability to absorb B12 for RBc production due to lack of intrinsic factor in stomach lining

285

Aplastic anemia

bone marrow destruction causes lack of RBCs

286

Renal anemia

no ETP release

287

Hemolytic anemia

rupture of too many RBc by invaders

288

Sickle cell disease

Hemoglobin makes rigid RBC clumps

289

primary Polycythemia

Too many RBCs so blood is too thick from tumour in bone marrow

290

secondary Polycythemia

appropriate compensation to improve O2 capacity at altitudes

291

Relative Polycythemia

dehydration increases blood cell concentration

292

Polymorphonuclear granulocytes

neutrophils, eosinophils and basophils have lobes on nucleus and lots of granules

293

mononuclear agranulocytes

monocytes and lymphocytes have one nucleus and few granules. leukocytes are smallest

294

lymphoid tissues

most lymphocytes made here. the rest are in RBM

295

normal WBC count

7000/mm3

296

neutrophil

Release traps to kill bacteria.first defenders can attack in or out of cell. Increase in infection

297

Eosinophil

Phagotize parasites. Increased in allergies and parasite infection

298

Basophil

Chemotactic factor production like mast cells . Store histamine and heparin

299

monocytes

mature into macrophages in tissues, make antigens, cytokines. Can last for years

300

Lymphocytes

cytokine, antigen recognition, antibodies, memory

301

B lymphocytes

make antibodies to circulate in humorla immunity

302

T lymphocyte

Directly kill cells in cell mediated immunity. live for hundreds of days

303

Mononucleoisis

increaesd abnormal lymphocyte caused by eptstein barr

304

Leukemia

uncontrolled WBC production reduces defence

305

Platelets

shed off of RBM bound megakaryocytic made form stem cells. Lack nuclei but have organelles and enzymes in granules. Myosin/actin to contract. Live for 10 days

306

Thrombopoietin

Hormone released by liver increases megakaryocytic number in bone marrow

307

hemostasis

Hole in wall with greater pressure inside. Fix it by vascular spasm, platelet plug, clotting

308

Vascular spasm

torn vessel constricts to slow blood flow

309

Platelets aggregation

exposed collagen in CT, platelets adhere
ADP from granules makes platelets sticky
NO and prostacyclin prevent plug from spreading
Actin/myosin contract to make plug tight

310

Fibrinogen

plasma protein turned into fibrin, adheres to damaged surface ad traps blood cells. Enfoced by Factor XIII

311

Thrombin

Converts fibrinogen to fibrin
Activate Factor XIII in positive feeddback
Prothrombin is inactive precursor that circulates

312

CLotting cascade

Factor X turns prothrombin into thrombin
12 factor chain reaction ends in thrombin turning fibrinogen into fibrin

313

Intrinsic clot pathway

Factor 12 hangman starts pathway when met collagen.

314

Extrinsic clot pathway

Shortcut to imitate clot in blood escaped from tissues. tissue thromboplastin directly activates factor X

315

Clot retraction

Platelets in clot contract and squeeze out serum. Dissolved by fibrinolytic plasmin. Phagocytes remove debris

316

tissue plasminogen activator

Diposes fibrin that is regularly made to prevent inappropriate clotting

317

Hemophilia

Deficiency in clotting factor causes thrombocytopenia purport spots

318

peyers patches

Gut associated lymphoid tissues. Placed easily to intercept invaders. Spleen is largest

319

Innate IS

Non specific response immediately on exposure. Nuetrophil and macrophages most important

320

Tollike recepetors

membrane protein studs make phagocytes bind with bacterial markers. Makes phagocyte release chemicals that trigger wider responses

321

Inflammation

Non specific response to bring phagocytes and plasma proteins to area. Histamine release and deem

322

Arterioles in invasion

Dilate, increase permeability and slow blood flow to bring more blood to area--> swelling brings defenders in

323

Who arrives first to invader

Neutrophils and then monocytes

324

Margination

Leukocytes stick to endothelial lining of capillaries. selection makes them slow down to find signlas

325

Diapedesis

adhered leukocytes amoeba through capillary pores

326

Chemotaxis

guide phagocytes with chemicals to damage, bind with phagocyte PM to increase CA entry and let it move to injury

327

Opsonin

Chemicals coat a cell marked for destruction . Bind to bacteria and phagocyte to hold them together

328

Phagocytosis

Engulfs material, fuse to lysosome to destroy them with hydrolytic enzymes

329

Phagocytes release these to inflame

No
lactoferrin: makes iron unavailable
Histamine
Kallikerin: plams proteins become kinins
Pyrogen: induces fever when pathogens i blood
leukocyte mediator: dcerease iron in plasma

330

Interleukin 1

enhanced proliferation of B and T lymphocytes

331

NSAIDS

nonsteroidal antiinflammatory drugs like aspirin suppress immune repsonse

332

Glucocorticoids

suppress inflammation like in allergies, lessen ability to fight infection

333

Interferon

released from virus infected cells, interferes with replication by warning neighbours to make enzymes. Slow virus and cancer

334

Complement system

carb chains on invaders (innate)
antibodies produced against invader (adaptive). Steps wotk on their own to augment inflammation . Confined to invader membrane

335

Membrane attack complex

5 plasma proteins make a donut that inches a hole in cell and it explodes

336

Adaptive immunity

speciifc responses for material body has been exposed to. Mediated by T and B lymphocytes which only defend against one pathogen

337

antibody/humoral immunity

produce antibodies by B cells

338

Cell mediated immunity

active T cells destroy cells

339

Thymus

Lymphoid tissue in chest where T cells mature. B cells mature in bone marrow

340

Antigen

Foreign molecule triggers specific immune rresponse

341

B cells

lymphocytes with surface antibody become either plasma cell or memory cell after binding with antigen

342

Plasma cell

produce antibodies to combine with antigen that stimulated it. ER becomes big, protein factories

343

Immunogolbulins

Antiobdies that have gone into blood

344

Antibody

4 interlinked polypeptide chains in Y shape. Arms determine specificity, tail for function

345

Antigen binding fragments

arms of antibody bind to one type of antigen lock and key

346

Constant region

Antibody tail is the same in each immunoglobulin

347

5 antibody classes

IGM: surface receptor for antigen attach.
IgG: most #, most specific
IGE: worms and allergies
IGA: digestive, respiratory and urninary secretions, mike and tears
IGD: on B cell surface

348

Neutralization

antibodies interact with bacteria to stop harm from host cell

349

Agglutination

Foreign cells bind together in clump from antibodies. Precipitates out of solution when it gets too big

350

Immune complex disease

Too many antigens can't be cleared away so complement system keeps going

351

Clonal selection theory

all offspring for B cell make antibody for one antigen even if they haven't been exposed. When antigen enters a clone is chosen to respond

352

Memory cells

B cellsr emain dormantt and expand clones for a goos response next time

353

Active vs passive immunity

Active: produce antibodies
Passive: transfer from another like mom to kid in milk

354

antiserum

Foreign anitbodies injected to fight an infection

355

ABO system

surface membranes of RBC have a specific antigen
AB have both
O have none
No antibodies in AB blood
O has anti A and Anti B antibodies

356

Transfusion reaction

incompatible blood makes recipient antibodies fight the donor cells. less effect from donor antibodies

357

Universal donor

O. Can only recieve AB

358

Universal Recipient AB

Lack antibodies so they can recieve any blood

359

rH factor

RBC antigen only some people have with no natural antibodies. Only RH negative people make antibodies on exposure--> negative poeple need negative, positive can get either

360

Erythroblastosis

RH negative mom makes antibodies on positive fetus

361

Antigen presenting cell

Macrophages cluster around T cell, eat invader and present antigen to activate B cells

362

MHC molecule

engulfed antigen peptides bind to it. Compartment for peptide loading

363

Dendritic cells

antigen presenting cells in very tissue migrate to T cell and cluster on activation

364

B cell growth factor

helper T cell help B function with interleukin 1 secreted by macrophages

365

T cells

Fight against invaders in cells where B cells can't reach

366

T receptor

Only activated when antigen is on surface. Only recognize foreign antigen in combination with self antigen

367

2 t cels

CD8: cytotoxic, kill foreign cells
CD4: helper T cells enhance activated B cells turning into macrophages and plasma cells

368

Regulatory T cell

suprpess innate and adaptive immune responses--> AIDS

369

Memory T cells

Primary and secondary responses like B cells . continued exposure to antigen makes it apoptosis

370

cytotoxic T cells

Hit men mix viral antigen with self antigen to make red flag. Release perforin to MAC. Release granzymes into pores

371

Helper T cells

release cytokine GF for leukocytes.
TH1: cytotoxic T cell response for infections
TH2: promote antibody mediated immunity

372

Cytokines

all chemicals other than antibodies secreted by leukocytes
B cell GF
T cell GF
Chemotaxins
Macrophage inhibition factor: prevents migration

373

Tolerance

prevent IS from attacing own tissues

374

6 tolerance mechnaism

clonal deletion: for self antigens
clonal anergy: won't activate with foreign antigen
recpeot editing: change type
inhiition by regulatory T cells
Immunicological ignornace: self antigen hidden
Immune privilige: trigger apoptosis if leukocyte approaches

375

MHC molecule

Major Histocompatibility complex link with T recpetolike hotdog. T cell must have MHC protein to become active

376

Class 1 MHC glycoprotein

cytotoxic T cells need it to respond to foreign antigen, found on all nucleated cell bodies]

377

Class 2 MHC glycoprotein

only found on immune cells, recognized by helper T cells

378

Immune surveillance

T cells, NK cells and macrophages, interferon attack cancer cells. NK cells dont need exposure so they're first

379

severe combined immunodeficiency

hereditary lack of B and T cells
Can be acquired form daaged lymphoid tissues

380

Allergies

immediate or delayed, acquired sensitivity to allergens

381

mmediate allergic reaction

pollen, bees, food bind to IGE antibodies, B cells involved
Sensitiation period where no symtpoms, but memory forms. Delayed is T cell mediated

382

Hypodermis

Anchors skin to underlying muscle or bone. CT/adipose

383

4 epidermis cell types

Melanocytes
keratinocytes
langerhans cells: migrate to bone marrow, APC
granstein: brake on immune response