A&p Exam 2

Front 1

Joints

Back 1

Tibiofemoral j. & Tibiofibular j.

Front 2

Tibiofemoral joint

Back 2

Classification-see chart
Articular capsule
Intracapsular (cruciate) ligaments
Anterior discs
Bursae
Injuries

Front 3

Articular capsule

Back 3

Patella ligement
Collateral ligament

Front 4

Patella Ligament

Back 4

Common insertion for quadriceps

Front 5

Collateral ligaments

Back 5

Tibial(medial)-attaches from medial femoral condyle to medial tibial condyle
Fibular(lateral)-extends from lateral femoral condyle to head of fibula

Front 6

Tibial (medial) collateral ligament

Back 6

-attaches from medial femoral condyle to medial tibial condyle

Front 7

Fibular (lateral) collateral ligament

Back 7

-extends from lateral femoral condyle to head of fibula

Front 8

Tibial(medial)-
attaches from medial femoral condyle to medial tibial condyle

Back 8

Broad, flat
Fibers connect to medial meniscus

Front 9

Fibular(lateral)-
extends from lateral femoral condyle to head of fibula

Back 9

Cord-like

Front 10

Intracapsular(cruciate) ligaments

Back 10

Anterior(ACL)-extends from anterior intercondylar eminence on tibia back to the medial surface of lateral femoral condyle
Posterior(PCL)-extends from posterior intercondylar fossa of tibia and lateral meniscus forward to lateral side of medial femoral condyle

Front 11

Anterior (ACL)

Back 11

-extends from anterior intercondylar eminence on tibia back to the medial surface of lateral femoral condyle

Front 12

Posterior (PCL)

Back 12

-extends from posterior intercondylar fossa of tibia and lateral meniscus forward to lateral side of medial femoral condyle

Front 13

Anterior(ACL)
extends from anterior intercondylar eminence on tibia back to the medial surface of lateral femoral condyle

Back 13

-"Clipping" injuries. Most commonly injured(70%)
-In extension, the ACL is tight
-Prevents anterior dislocation of tibia

Front 14

Posterior(PCL)
extends from posterior intercondylar fossa of tibia and lateral meniscus forward to lateral side of medial femoral condyle

Back 14

-Prevents posterior dislocation of tibia

Front 15

Articular discs

Back 15

Fibrocartilage b/w tibial&femoral condyles; deepen sockets

Front 16

Articular discs-
Fibrocartilage b/w tibial&femoral condyles; deepen sockets

Back 16

Medial meniscus
Lateral meniscus

Front 17

Medial meniscus

Back 17

"C" shaped

Front 18

Lateral meniscus

Back 18

"O" shaped

Front 19

Medial&Lateral Meniscus

Back 19

Connected to tibia anterior and posterior

Front 20

Bursae

Back 20

Many

Front 21

Injuries

Back 21

3 C's
-Cruciates (ACL)
-Collateral (Medial)
-Cartilage (Medial meniscus)
Collateral&Cartilage are attached so if one is injured usually the other is too

Front 22

Tibiofibular joint

Back 22

Proximal-Diarthrosis, synovial, gliding
Distal-Amphiarthrosis, fibrous, syndesmosis

Front 23

Nerves

Back 23

Lumbar Plexus
Sacral Plexus

Front 24

Lumbar Plexus

Back 24

from ventral rami of L1-L4

Front 25

Lumbar Plexus-from ventral rami of L1-L4

Back 25

-Branches
-Injuries

Front 26

Branches (of the Lumbar Plexus)

Back 26

Obturator nerve
Femoral nerve

Front 27

Obturator nerve

Back 27

(L2-L4)-supply mm. of medial compartment of thigh
-skin over medial thigh

Front 28

Femoral nerve

Back 28

(L2-L4)-mm. of anterior compartment of thigh
-skin over anterior medial thigh

Front 29

Injuries of the Lumbar Plexus

Back 29

Obturator nerve-loss of thigh adduction and sensation on skin of medial thigh
Femoral nerve-loss of leg/knee extension and sensation on anterior medial thigh
-difficulty with stairs

Front 30

Sacral Plexus

Back 30

from ventral rami of L4-L5 & S1-S4

Front 31

Sacral Plexus-from ventral rami of L4-L5 & S1-S4

Back 31

Branches
Injuries
Dermatomes (p.440)***

Front 32

Branches

Back 32

Sciatic nerve-->Tibial nerve & Common fibular --> Superfical & Deep fibular

Front 33

Sciatic nerve

Back 33

-branches to mm. of posterior compartment of thigh (+skin)
-divides into tibial and common fibular mm.

Front 34

Tibial nerve

Back 34

(L4-S3) supplies mm. of posterior comp. of leg (plantar flexion and flexion of toes)

Front 35

Common fibular nerve

Back 35

(L4-S2)
Superficial fibular-associated with lateral compartment
-(eversion and plantar flexion)
Deep fibular-supplies anterior compartment
-(dorsiflexion and extension of toes)

Front 36

Injuries of the Sacral Plexus

Back 36

Sciatic nerve-sensation is lost below knee
-loss of m. function below knee-"foot drop" or "drop foot"

Front 37

Histology of Skeletal Tissue

Back 37

Sarcolemma
Sarcoplasm-(cytoplasm in the cell)
Transverse tubules
Sarcoplasmic Reticulum (SR)- *Stores Calcium ions*
Myofilaments

Front 38

Myofilaments of Skeletal Tissue

Back 38

Sacromeres
Thin
Thick

Front 39

Sacromeres

Back 39

Basic structural unit of cell (+functional unit of contraction)

Front 40

Thin myofilaments

Back 40

Actin
Tropomyosin
Troponin

Front 41

Actin

Back 41

-two strings that are strung together and are twisted (helix)
i. contains a myosin-binding site

Front 42

Tropomyosin

Back 42

-arranged in loosely attached strands to the actin helix
-covers the myosin-binding site

Front 43

Troponin

Back 43

-bound to tropomyosin (troponin-tropomyosin complex)
-has Ca+2-binding sites

Front 44

Thick myofilaments

Back 44

-handles arrange themselves in parellel groups and heads projecting away from M line
-heads contain actin-binding site and an ATP binding site

Front 45

Neuromuscular Junction (NMJ)

Back 45

Motor end plate
Process

Front 46

Motor end plate of NMJ

Back 46

-region of the sarcolemma that receives the end plate (comes in contact with end bulb)
-will receive Ach in receptors (are also a Na+ channel)

Front 47

Process of NMJ

Back 47

Ach is released-->diffuses across the synaptic cleft-->binds to Ach receptors-->Na+ channels open-->Na+ rushes in -->change in membrane potential (voltage) inside m. cell-->m. action potential (MAP) forms-->moves across sarcolemma
((Cell is Depolarizing))

Front 48

Physiology of Contraction
Step 1

Back 48

MAP moves across sarcolemma and down into t-tubules from t-tubules-->into SR

Front 49

Physiology of Contraction
Step 2

Back 49

Ca+2 moves out of SR into the sarcoplasm

Front 50

Physiology of Contraction
Step 3

Back 50

Ca+2 binds to troponin and a change occurs in the shape of the troponin-tropomyosin complex (myosin-binding sites now available)-contraction cycle begins

Front 51

Physiology of Contraction
Step 4

Back 51

Previously, ATP attached to the myosin head, which acts as an ATP enzyme (ATPase) and splits ATP into ADP+P AND energy-->this energy activates the actin-binding site and is stored in the myosin

Front 52

Physiology of Contraction
Step 5

Back 52

Myosin binds to actin. Now called a cross-bridge

Front 53

Physiology of Contraction
Step 6

Back 53

ADP+P are released from cross-bridge-->myosin changes shape and pulls on actin
i. cross-bridge moves toward m-line
ii. thin filament
both i & ii=Power Stroke

Front 54

Power Stroke

Back 54

thin filaments slide over thick
(flexion of head)

Front 55

Physiology of Contraction
**Step 7**

Back 55

After power stroke, ATP binds to cross-bridge-->detaches from actin

Front 56

Physiology of Contraction
Step 8

Back 56

ATP is split (same as step #4)

Front 57

Physiology of Contraction
Step 9

Back 57

During a cycle:
a.) shorter: H+I zone (band)
b.) stay same: A band

Front 58

End result of Contraction

Back 58

Is movement

Front 59

Muscle Relaxation
Step 1

Back 59

Ach is rapidly destroyed by acetyl cholinesterase (AchE) at the synapse, therefore MAP stops

Front 60

Muscle Relaxation
Step 2

Back 60

Ca+2 are actively transported back into ST by Ca+2 active transport pumps
(Ca+2 binding is concentration dependent)

Front 61

Muscle Relaxation
Step 3

Back 61

Calsequestrin in SR acts like a Ca+2 sponge

Front 62

Muscle Relaxation
Step 4

Back 62

ATP binds to cross bridge and...

Front 63

Muscle Relaxation
Step 5

Back 63

With Ca+2 removed, the troponin-tropomyosin complex slides back over myosin-binding sites of thin filaments, therefore myosin cannot bind

Front 64

Muscle Relaxation
Step 6

Back 64

thin filaments slide back to "resting" (relaxation) pos.

Front 65

Muscle Relaxation
Step 7
In a relaxed state-

Back 65

-Ca+2 is stored in SR
-Myosin head is activated (but NOT bound to actin)
-Thin filament inactivated-->myosin-binding sites are covered by troponin-tropomyosin complex

Front 66

Muscle Relaxation
Step 8
After Death

Back 66

ATP production stops and Ca+2 leaks out of SR and myosin heads bind to actin. Cross-bridge remains formed-->no movement-->rigid=rigor mortis (about 3-24 hours)

Front 67

Sources of ATP

Back 67

ATP already present in sacroplasm (used up in milliseconds)
Phosphocreatine
Cellular Respiration

Front 68

Phosphocreatine (Creatine Phosphate)

Back 68

Creatine + Phosphate + Energy--> forms ATP
~15 seconds-used up

Front 69

Cellular Respiration

Back 69

Glycogen
Pyruvic Acid
Fatigue
Recovery

Front 70

Glycogen

Back 70

Is in mm. + liver
Glycogen-->Glucose-->2 Pyruvic acid + ATP

Front 71

Pyruvic Acid
Areobic

Back 71

PA + O2-->H2O + CO + Energy->ATP
(produces much more energy)
(prolonged activity)

Front 72

Pyruvic Acid
Anareobic

Back 72

Lactic Acid
(about 80% diffuse in blood-->liver converts it to glucose)
(remainder LA builds up in muscle)

Front 73

Fatigue

Back 73

-waste produces build up (LA)
-depletion of ATP, O2, creatine phosphate, glycogen
Both lead to inability of contraction (inhibits cross-bridge formation)

Front 74

Recovery

Back 74

after exercise the body delivers nutrients to fatigued tissues; also LA-->PA

Front 75

Control of Muscle Tension

Back 75

Motor Units
Twitch
Frequency of Stimulation
Motor Unit Recruitment + Tone
Isotonic

Front 76

Motor Units

Back 76

-1 motor neuron + all mm. fibers it innervates. (~3-3000)
-All m. fibers act together
-Avg. ~150

Front 77

Twitch

Back 77

Threshold stimulus
Subthreshold
"All-or-none"
Myogram
Latent Period
Contraction Period
Relaxation
Refractory period

Front 78

Threshold stimulus

Back 78

weakest stimulus that initiates a contraction

Front 79

Subthreshold stimulus

Back 79

too small to elicit contraction

Front 80

"All-or-none"

Back 80

m. fiber will contract completely or not at all

Front 81

Myogram

Back 81

any motion on the chart
*chart in notes

Front 82

Latent Period

Back 82

-delay b/w stimulus and beginning of contraction
-probably due to time it takes Ca+2 to be released from SR and to bind to troponin

Front 83

Relaxation

Back 83

actin transport of Ca+2 back into SR-->thin filaments slide out

Front 84

Refractory period

Back 84

Shortly after the m. receives a stimulus it is NOT capable of responding to another stimulus, therefore NO contraction can occur

Front 85

Frequency of stimulation

Back 85

1.)Treppe
2.)Wave Summation
3.)Incomplete Tetanus
4.)Complete Tetanus
5.)Ca+2 release
6.)Fatigue

Front 86

1.) Treppe

Back 86

a.)if several stimuli are applied slowly and relaxation is allowed b/w each, the contraction becomes greater over the first few times-->then maximal contraction (stairstep phenomenon)
b.)This is a "warm-up" phase of m. in order to achieve maximal contraction. Probably due to increased Ca+2 availability and enzyme activity with each contraction

Front 87

2.) Wave Summation

Back 87

If a second stimulus is applied after refractory period, but before complete relaxation, the second contraction will be stronger than the first

Front 88

3.) Incomplete Tetanus

Back 88

If multiple stimulus is applied faster, the m. only partially relaxes b/w stimuli; the m. maintains a partial, sustained contraction (unfused tetanus)

Front 89

4.) Complete Tetanus

Back 89

If stimuli are even faster, a sustained contraction occurs without any relaxation (fused tetanus)

Front 90

5.)

Back 90

Caused by release of more Ca+2 with each stimulus

Front 91

6.)

Back 91

Can be followed by fatigue

Front 92

Motor Unit Recruitment + Tone

Back 92

1.) When more motor units are needed for a motion, they are recruited--produces stronger, larger movements
2.) At any one time during contraction, some motor units are stimulated and some are not. They "take turns." Important in postural mm.
3.) Even when there's no movement, mm. remain somewhat "firm"-muslce tone
-prevent fatigue

Front 93

Isotonic vs. Isometric contractions

Back 93

Isotonic
a.) concentric
b.) eccentric
Isometric

Front 94

Isotonic

Back 94

a.) concentric-m. shortens and pulls
-angle of j. decreases
b.) eccentric-m. lengthens but still contracts
-angle of j. increases

Front 95

Isometric

Back 95

tension increases greatly in m. but little or no movement
a.) stretch=contraction
b.) important for postural mm. and stabelizing jj.

Front 96

Hypertrophy

Back 96

-increases in diameter of m. fibers due to production of more myofibrils, mitochondria, SR, etc.
1.) Caused by more forceful and/or repetitive contractions
2.) Mm. can undergo more forceful contractions
3.) Some believe the # of fibers does not change since birth. Others believe there is a limited ability for regeneration
4.) Testosterone stimulates m. cell growth

Front 97

Atrophy

Back 97

wasting away from mm.
1.) fibers and size due to progressive loss of myofibrils, etc
2.) Disuse Atrophy
3.) Dennervation Atrophy

Front 98

Disuse Atrophy

Back 98

-common in bedridden individuals, people in casts
-#of m. impulses to mm. decrease dramatically

Front 99

Dennervation Atrophy

Back 99

when a nerve is cut, the mm. lose stimulation, therefore undergo complete atrophy, shrink, and are replaced by fibrous C.T. (permenant) (~6-48 months)

Front 100

Disorders of Skeletal M.

Back 100

Myostenia Gravis
Muscular Dystrophies

Front 101

Myostenia Gravis

Back 101

-Autoimmune disease
-Progressive disease
-Most frequently in females 20-40yrs
-Treatments

Front 102

Autoimmune disease

Back 102

-body produces Antibodies against Ach receptors-->Abs bind to receptors and BLOCK Ach-->m. weakness

Front 103

Progressive disease

Back 103

-more NMJ's are affected
*drawing in notes*

Front 104

Most frequently in women 20-40 yrs

Back 104

Begins with mm. of face and neck (difficulty swallowing, chewing, and talking)-->progresses to limbs-->CAN be fatal if diaphragm is involved

Front 105

Treatments

Back 105

-immunosuppressants
-drug to increase Ach production/release
-drug to bind to the Abs and block their binding to receptor
-AchE blockers--these increase amount of Ach available

Front 106

Muscular dystrophies

Back 106

1.) Progressive degeneration of skeletal m. fibers
2.) Duchenne M.D. (DMD)-most common

Front 107

Duchenne M.D. (DMD)-most common

Back 107

a.) genetically transmitted (males only b/c 3-7 yrs)
b.) faulty metabolism of a cell protein causes sarcolemma to tear easily-->cell dies
c.) mainly voluntary skeletal m. (Doesn't affect Diaphragm)
d.) Eventually, respiratory or cardiac failure causes death b/w 20-30 yrs

Front 108

Plasma

Back 108

91.5% H2O, 8.5% plasma proteins (produced by liver)
A.) Proteins
B.) Plays role in maintaining proper blood osmotic pressure

Front 109

Proteins

Back 109

Albumins
Globulins
Fibrinogen + Prothrombin
Others include circulating hormone

Front 110

Formed Elements

Back 110

-red bone marrow-Hemopoeisis
A.)Erthyrocytes
B.)Leukocytes
C.)Platelets

Front 111

Erthrocytes

Back 111

Concave
Hemoglobin (Hb)
Erythropoietin (EPO)

Front 112

Concave

Back 112

-NO nucleus-->ejected during its development (also most organelles)
Concave-->increase surface area and helps them squeeze thru capillaries more easily

Front 113

Hemoglobin(Hb)

Back 113

-4 subunits
-each contain an Fe+2 bound in a heme group
-each Fe+2 binds ONE O2 (concentration dependent)
-Can bind CO2
-Fe+2-O2 interaction is very weak (bonding or dissociation occur readily)

Front 114

Erythropoietin (EPO)

Back 114

hormone produced by kidneys
-stimulates RBC production (as does androgens)
-"blood doping"
-increase viscocity can cause heart to pump harder
-if He+ or Hb is low=Anemia. Tissues become hypoxia:weakness, lethargy, and mental confusion

Front 115

Leukocytes

Back 115

Two groups
4 Characteristics
Types
Increase in leukocytes-->infection

Front 116

Leukocytes
Two groups

Back 116

Granular leuk
Agranular leuk

Front 117

4 Characteristics

Back 117

-Ameboid movement
-Can move thru blood vessel cells (capillaries), therefore found in blood, interstitial fluid and in lymph. **At any one time, most are in loose and dense C.T.
-Chemotaxis-attracted to specific chemical stimuli
-Some types are phagocytic

Front 118

Types

Back 118

Neutrophils
Eosinophils
Basophils
Monocytes
Lymphocytes

Front 119

Neutrophils

Back 119

50-70% of circulating WBC's
-usually first to arrive at injury site
-phagocytize and destroy with lysosomal enzymes and H2O2
-release leukotrienes-attract other phagocytes

Front 120

Eosinophils

Back 120

2-4% of circulating WBC's
-release toxic compounds onto surface of their targets
-sensitive to circulating allergens (substances that trigger allergic reactions)

Front 121

Basophils

Back 121

<1% of circulating WBC's
--release histomine-a vasodilator
--release heparine-an anticoagulent
both histomine+heparine enhance/intensify local inflammation

Front 122

Monocytes

Back 122

(largest cell) 2-8% of circulating WBC's
-migrate in/out of blood stream-->outside, called marcophages
marcophages-aggressively phagocytic
-release leukotrienes

Front 123

Lymphocyte

Back 123

20-30% of circulating WBC's
-migratory
-3 classes
--T cell
--B cell
--NK cell ("natural killer")

Front 124

Platelets

Back 124

-Fragments
-Transport chemicals for blood clotting

Front 125

Hemostasis

Back 125

Vascular Phase
Platelet Phase
Coagulation Phase
General Info

Front 126

Vascular Phase

Back 126

vascular spasm

Front 127

Platelet Phase

Back 127

-platelet plug formation
1.) damaged endothelial cells secrete anti-coagulants that inhibit platelet aggregation
-homeostasis

Front 128

Coagulation Phase

Back 128

many different clotting factors exist in plasma AND produced by damaged cells-some are proteins and calcium
3 Pathways
Extrinsic, Intrinsic, and Common Pathways

Front 129

Extrinsic Pathway

Back 129

-begins outside blood stream. *Shorter and faster*
-one clotting factor released by damaged cells combines with Ca+2 in a cascade leading to activation of factor X(ten)

Front 130

Intrinsic Pathway

Back 130

-begins inside blood stream. *Slower but longer-lasting*
-platelets release other clotting factors-->cascade-->activation of factor X(ten)

Front 131

Common Pathway

Back 131

--Factor X is activated to form enzyme prothrombinase
--Fibrin (final product)-intertwines to help form platelet plug

Front 132

General Info

Back 132

--Both pathways respond
--the common pathway stimulates both other pathways (positive feedback)-->stop blood flow
--All three require Ca+2
--Vit. K-necessary for liver to produce some clotting factors
--Aspirin inhibits vasoconstriction and platelet aggregation

Front 133

Vit. K

Back 133

-Dark greens
-Bacteria in large intestine produce ~50%

Front 134

Clot Retraction

Back 134

-fibrin shortens, platelets contract-->bleeding stops

Front 135

Disorders

Back 135

-Embolus
-Hemophilia
-Leukemia

Front 136

Embolus

Back 136

-If clotting is inadequately controlled, clots can form in blood stream-embolus. If clot b/c stuck(embolism) blood flow to a tissue stops
-Damaged tissue=infaret
---Heart-(Myocardian infaretion) M.I.
---Brain-Stroke
---Lungs-Pulmonary embolism

Front 137

Hemophilia

Back 137

-inherited disorder
-inadequate production of a clotting factor

Front 138

Leukemia

Back 138

-abnormal production of blood cells

Front 139

Heart wall (3 layers)

Back 139

Epicardium-outside (same as serous layer of pericardium)
Myocardium-
Endocardium-inside, (lining of inside of heart) simple squamous epith.

Front 140

Cardiac Muscle Tissue

Back 140

Intercalated discs
Myoglobin

Front 141

Intercalated discs

Back 141

PM interlocking,-linked by gap junction
--connect neighboring cells-->allows MAP to flow from cell-to-cell

Front 142

Myoglobin

Back 142

similar to Hb, binds O2 in a heme group

Front 143

Gross Anatomy

Back 143

Papillary mm.
Left Ventricle

Front 144

Papillary mm.

Back 144

(Cone-shaped projections)
chordae tendinae (1 papillary m. per cusp) attach; prevent prolapse of valve-->blood ejects into atria and backflow=regurgitation and causes a heart murmur

Front 145

Left Ventricle (LV)

Back 145

LV is ~2-3x thicker and 6-7x more force (but same Vol.)

Front 146

The Heartbeat

Back 146

The Conducting System
The Electrocardiogram (ECG or EKG)
The Cardiac Action Potential
Cardiac Cycle

Front 147

The Conducting System

Back 147

1-6

Front 148

1.)Autorhythmicity
Heartbeat

Back 148

-without neural stimulation

Front 149

2.)
Heartbeat

Back 149

SA node-->conducting cells-->AV node-->AV bundle (bundle of His)-->bundle branches-->apex

Front 150

3.)
Heartbeat

Back 150

SA + AV nodal cells cannot maintain a stable resting potential. After repolarization, their MP gradually depolarizes toward threshold-prepotential-->leads to AP

Front 151

4.)
Heartbeat

Back 151

Since the SA node reaches threshold first (before other heart cells), so it establishes the heart rate="pacemaker"

Front 152

5.)
Heartbeat

Back 152

The contraction follows the electrical stimulus, therefore atria contract first, then ventricles

Front 153

6.)
Heartbeat

Back 153

Caffeine increases rate of depolarization of SA node

Front 154

The Electrocardiogram (ECG or EKG)

Back 154

1.)The electrical events in heart are strong enough to be detected on surface of body-->EKG or ECG
2.)Waves: P, QRS complex, T
3.) If cardiac cells are damaged/dead, they cannot conduct an AP
4.)Excessively large QRS complex-->can indicate ventricular hypertrophy
5.)Smaller waves-->can indicate death of some cardiac tissue
6.)P-R interval
7.)S-T interval

Front 155

P wave

Back 155

depolarization of atria

Front 156

QRS complex wave

Back 156

depolarization of ventricles (+ repolarization of atria)

Front 157

T wave

Back 157

ventricular repolarization

Front 158

6.)P-R interval

Back 158

impulse begins and moves from atria to ventricles; if conduction pathway to AV node is damaged (or node itslef)-lengthens

Front 159

7.)S-T interval

Back 159

time b/w end of ventricular depolarization and repolarization; if cells are dead, this shortens and indicates an M.I.

Front 160

The Cardiac Action Potential
(compared to skeletal)

Back 160

1.)Depolarization is similar
2.)At top of peak:
3.) Repolarization
4.)Refractory period

Front 161

2.) At top of peak:

Back 161

a.)Na+ channels close
b.)Voltage-regulated Ca+2 channels open-->Ca+3 enters sarcoplasm from outside (and then from SR)
-these close slowly
c.)Na+ is being pumped out (Na+-K+ pumps)
--PLATEAU forms and so m. fiber stays contracted
a, b, + c--Little net change in charge/voltage inside the cell

Front 162

3.) Repolarization-

Back 162

"slow K+ channels" open to allow K+ to flow out of the cell

Front 163

4.) Refractory period

Back 163

is much longer to prevent summation and tetanus (+fatigue)

Front 164

Cardiac Cycle

Back 164

events from beginning to end of 1 beat

Front 165

Phases

Back 165

atrial systole
atrial diastole + ventricular systole
ventricular diastole

Front 166

Atrial systole

Back 166

atria "top off" filing of ventricle's

Front 167

Atrial diastole + ventricular systole

Back 167

i. V's contract, P increases and pushes AV valves closed (not enough P to open semilunar valves yet)
ii. Isovolumetric contraction-V's continue to build P-*All 4 valves closed
iii.P increases until semilunar valves open-->blood ejected
iv.atria fill at same time

Front 168

Ventricular diastole

Back 168

i. as V's relax, P decreases; when it is lower then P in aorta (+pulmonary trunk), blood tries to re-enter V's and semilunar valves close
ii. P continues to decrease-isovolumetric relaxation-*All 4 valves closed
iii. when P is lower than atrial P-->AV valves open-->blood moves into V's passively

Front 169

Volumes

Back 169

a.) End-Diastolic Volume (EDV)-~130ml
b.)End-Systolic Volume (ESV)- (amt. of blood left after contraction) ~50ml
Avg ~70-80ml (amt forced out in each cycle)
c.)Stroke Volume=~70-80ml
i. SV=EDV-ESV
*ii. This is the amount delivered to peripheral tissues
d.)CO=HR x SV
CO=HR x (EDV-ESV)
CO=liters/min
everything else is ml
1L=100ml

Front 170

Coxal (Hip) joint
Functional Classification
Structural Classification
Structural Type
Movements Allowed

Back 170

Diarthratic
Synovial
Ball and Socket
Flexion + Extension
Adduction + Abduction
Circumduction + Rotation

Front 171

Tibiofemoral (Knee) Joint
Functional Classification
Structural Classification
Structural Type
Movements Allowed

Back 171

Diarthratic
Synovial
Hinge
Flexion + Extension
(limited rotation)

Front 172

Patellofemoral Joint
Functional Classification
Structural Classification
Structural Type
Movements Allowed

Back 172

Diarthrotic
Synovial
Gliding Joint
Gliding

Front 173

Tibiofibular (proximal) Joint
Functional Classification
Structural Classification
Structural Type
Movements Allowed

Back 173

Diarthratic
Synovial
Gliding
Slight movement

Front 174

Tibiofibular (Distal) Joint
Functional Classification
Structural Classification
Structural Type
Movements Allowed

Back 174

Amphiarthratic
Fibrous
Syndesmosis
Slight Movement

Front 175

Tibiotalar (Ankle) Joint
Functional Classification
Structural Classification
Structural Type
Movements Allowed

Back 175

Diarthratic
Synovial
Hinge
Flexion + Extension
(Dorsiflexion/Plantarflexion)

Front 176

Intertarsal Joint
Functional Classification
Structural Classification
Structural Type
Movements Allowed

Back 176

Diarthratic
Synovial
Gliding
Slight Movement

Front 177

Tarsometatarsal Joint
Functional Classification
Structural Classification
Structural Type
Movements Allowed

Back 177

Diarthratic
Synovial
Gliding
Slight Movement

Front 178

Metatarsophalangeal ("Knuckle") Joint
Functional Classification
Structural Classification
Structural Type
Movements Allowed

Back 178

Diarthratic
Synovial
Elipsoid
Flexion + Extension
Adduction + Abduction

Front 179

Interphalangeal Joint
Functional Classification
Structural Classification
Structural Type
Movements Allowed

Back 179

Diarthratic
Synovial
Hinge
Flexion + Extension