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Overview
1 What is A & P?
o 1.1 Anatomy: How the body is put together — its organization.
o
1.1.1 Chemical
1.1.2 Cellular
1.1.3 Tissue
1.1.4 Organ
1.1.5 System
1.1.6 Organism
1.2 Physiology: how the structures of the body function (at all levels of organization).
1.2.1 Metabolism
1.2.2 Irritability / Responsiveness
1.2.3 Growth
1.2.4 Differentiation
1.2.5 Reproduction o 1.3 Homeostasis
1.3.1 What is it?
1.3.1.1 Maintenance of internal environment...
1.3.1.2 ...at the optimal range of conditions. — the body can tolerate successively less environmental variation in each of the above environments.
1.3.2 Cellular activities tend to upset homeostasis. (ex.; acidosis — most metabolic byproducts are acidic)
1.3.3 Homeostasis is maintained by feedback systems ( = system where effect changes control of effect)
1.4 Terminology o
2 Energy - “the ability to do work” o 2.1 Potential vs. kinetic energy o 2.2 Forms of energy:
3 Elements (exhibit 2.1)
4 Atomic Structure and Valence o 4.1 Protons, Neutrons, Electrons o o
4.2 Atomic number = p;Mass number = p + n
4.3 Electron shells - pairs of electrons - valence
5 Chemical Bonds:
5.1 Ionic o o o
5.2 Covalent
5.3 Hydrogen — weak bonds between covalently-bonded H and another covalently-bonded atom
6 Chemical Reactions (review starting on pg. 32) o 6.1 Exergonic o 6.2 Endergonic
o 6.3 Synthesis (anabolic) o 6.4 Decomposition (catabolic)
7 Compounds o 7.1 Inorganic compounds
7.1.1 Acids
7.1.2 Bases
7.1.3 Salts
7.1.4 H2O
7.1.4.1 solvent for other chemicals.
7.1.4.2 vital component of some important reactions
7.1.4.3 high heat capacity
7.1.4.4 high heat of vaporization
7.1.4.5 lubricant
8 Tissue Types and their origins o 8.1 A tissue is a group of cells, similar in origin, specialized and organized for a specific function.
o 8.2 Tissues generally are given their function by the cells they contain, -and- by the extracellular matrix that surrounds these cells. Not surprisingly, this is also how we classify tissues.
8.2.1 There are four principal types of tissue:
9 Extracellular Materials o 9.1 Extracellular fluid - dissolves, mixes solutes (ions, nutrients, wastes, gases).
Subdivided into:
9.1.1 Blood plasma - liquid portion of blood o 9.2 Matrix - primarily important in connective tissues, it consists of a ground substance plus protein fibers. The ground substance is composed of complex
molecules; can be a fluid, gel, or solid.
10 Cell Junctions - points of contact between adjacent cells. The different kinds of junctions have distinct functional differences: o 10.1 Tight junctions (zonula occludens) - fluid-tight seals. Common in epithelial tissues, girdling the whole cell near the free surface. “stitches” adjacent cells together. Common anywhere a tight seal is needed,
often found in places were the control of passage of substances through membranes is important - molecules can’t leak around the cells, they must go right through them. Ex: digestive, bladder.
o 10.2 Anchoring junctions (desomosomes) o 10.3 Communicating junctions
11 Epithelial Tissues o o
11.1 General features:
11.1.1 One surface of tissue is free
11.1.7 Avascular
11.1.8 Innervated
11.1.9 High mitotic rate
11.1.2 Cells closely packed, very little extracellular material
11.1.10 Derived from all three germ layers
11.1.3 Cells are arranged in single- or multiple-layered sheets
11.1.4 Differentiated into an apical surface and a basal surface
11.1.5 Attached to adjacent connective tissue via basement membrane
11.1.6 Many cell junctions
11.2 General functions:
11.2.1 Protection (skin), filtration (capillary endothelium), lubrication
(pleura), secretion (duodenum), absorption (ileum), transportation
(alveoli), excretion (sweat glands), sensory reception (skin)
11.2.2 Covering & lining epithelium
11.2.2.1 the two criteria: how many layers (1 layer = simple; > 1 layer = stratified) and shape (squamous, cuboidal, columnar) of
cells. for the stratified types, usually only the outer layers look like squamous or columnar cells; the underlying layers all look cuboidal.
11.2.2.2 types:
11.2.2.2.1 simple squamous--single layer of flattened cells
(nuclei often squashed & spread out) - good for diffusion, osmosis, filtration; bad for abrasion, friction
11.2.2.2.2 simple cuboidal--single layer of cube-shaped/ spherical cells (nuclei evenly spaced) - more room for internal ‘machinery’, and usually associated with secretion/absorption
11.2.2.2.3 simple columnar--single layer of cylindrical cells
(nuclei crowded close together) - lots of internal components, often very metabolically active, lots of activity. 2 kinds:
11.2.2.2.4 nonciliated--cells often with microvilli and goblet cells (produce mucus) - lining of digestive, reproductive, respiratory, & parts of urinary tracts
11.2.2.2.5 ciliated--cells with cilia present - cilia create movement in mucus or fluid - parts of respiratory and reproductive systems, paranasal sinuses
11.2.2.2.6 stratified squamous--multiple layers of cells;
usually only outer layers look squamous. abrasion-resistant, relatively impervious. St. sq. epi. can be either:
11.2.2.2.7 keratinized St. Sq. E.--large amounts of the protein keratin are deposited in the cells, rendering them tough and waterproof; outer surface is dry
11.2.2.2.8 nonkeratinized St. Sq. E. --lack of keratin means that outer layers are moist, absorb/lose water easily
11.2.2.2.9 stratified cuboidal--rare - found in sweat gland ducts, portions of the male urethra
11.2.2.2.10 stratified columnar--rare - found in the conjunctiva, urethra, some exocrine gland ducts
11.2.2.2.11 pseudostratified ciliated columnar--appears multilayered, but all cells are in contact with basement
membrane. Cells reaching free surface have cilia; functions similar to simple ciliated columnar tissue. lines most of respiratory tract
11.2.2.2.12 transitional--can change from a stratified cuboidal appearance to a stratified squamous appearance to allow structures to stretch without breaking - found lining the urinary bladder
11.2.3 Glandular epithelium - glands can be single celled or multicellular-- because of their relatively high metabolic rates, they are (not surprisingly) made of cuboidal or columnar cells.
11.2.3.1 Exocrine glands secrete their products into ducts; their classification is based on how they secrete... is the product released by itself, or is part or all of the gland’s cells released also?
11.2.3.2 Endocrine glands secrete their products (hormones) into the bloodstream through the extracellular fluid (pituitary, thyroid, etc.) We will deal with them in detail later.
12 Connective Tissues o 12.1 General Features
12.1.1 High proportion of extracellular material, especially ground
o
substance and fibers
12.1.2 Not found on free surfaces (1 exception - synovial membrane)
12.1.3 Most connective tissues are vascularized (exc. tendons, cartilage)
12.1.4 Innervated (exc. cartilage)
12.1.5 Major characteristics of tissue determined by matrix, which can be fluid, gelatinous, fibrous, or calcified
12.2 Matrix
12.2.1 Ground substance
12.2.2 Fibers o o
12.3 Cells
12.4 Types & Functions
12.4.1 Loose connective tissues
12.4.1.1 Areolar CT
12.4.1.2 Adipose CT
12.4.1.3 Reticular CT
12.4.2 Dense connective tissues
12.4.2.1 Dense regular CT
12.4.2.2 Dense irregular CT
12.4.2.3 Elastic CT
12.4.3 Cartilaginous connective tissues
12.4.3.1 Hyaline cartilage
12.4.3.2 Fibrocartilage
12.4.3.3 Elastic cartilage
12.4.4 Bone tissue
12.4.5 Blood tissue
13 Muscle Tissue o 13.1 General features o 13.2 Types
13.2.1 Skeletal (striated)--Very long, cylindrical cells; multinucleate,
striated, voluntary
13.2.2 Cardiac--Branching cells, usually with 1 nucleus; striated; connected by intercalated disks; involuntary
13.2.3 Smooth--Small, spindle-shaped, 1 nucleus, not striated, many gap junctions, involuntary
14 Nervous Tissue
o 14.1 General features
15 Membranes o 15.1 Mucous
o 15.2 Serous o 15.3 Synovial
16 Skin o o
16.1 Anatomy
16.2 Epidermis
o o
16.2.1 Stratum basale (str. germinativum)
16.2.2 Stratum spinosum
16.2.3 Stratum granulosum
16.2.4 Str. lucidum (present in thick skin only)
16.2.5 Str. corneum
16.3 Dermis
16.3.1 Reticular layer
16.3.2 Papillary layer
16.4 Physiology
16.4.1 Protection
16.4.2 Thermoregulationheat lost by dilating blood vessels, sweating,direct conduction of heatheat saved by constricting blood vessels, insulation of subcutaneous fat, shivering(brown fat in o 16.5 Skin color
17 Epidermal Derivatives o o
16.4.3 Absorption/Excretion
16.4.4 Synthesis
17.1 Hair
17.2 Glands
16.4.5 Sensory reception
16.4.6 Fluid regulation
16.4.7 Blood reservoir
infants)(arrector pili muscles)
17.2.1 Sudoriferous
17.2.2 Sebaceous
17.2.3 Ceruminous
o 17.3 Nails
18 Homeostasis o 18.1 Wound healing
18.1.1 Epidermal wound healing
18.1.2 Deep wound healing o 18.2 Burns
18.2.1 1st-degree
18.2.2 2nd-degree
19 Aging
20 Disorders
18.2.3 3rd-degree o 20.1 Skin cancerBasal cell — St. basale - low chance of metastasis - most frequentSquamous cell — St. spinosum - greater chance of met., less frequentMelanoma — in melanocytes - high chance of met., rare
21 Functions of the skeletal system: o o o o o o
21.1 Support of soft tissues:
21.2 Protection of organs:
21.3 Motion
21.4 Homeostasis of Ca and P
21.5 Hemopoeisis
21.6 Energy storage
22 Gross anatomy of bone o 22.1 Diaphysis o 22.2 Epiphysis o o
22.3 Epiphyseal plate (or line)
22.4 Articular cartilage
o 22.5 Periosteum o 22.6 Medullary / marrow cavity o 22.7 Endosteum
23 Microscopic anatomy of bone o o o
23.1 Osteoprogenitor cells
23.2 Osteoblasts
23.3 Osteocytes o 23.4 Osteoclasts o 23.5 Matrix:
24 Bone formation and growth o 24.1 Formation
24.1.1 Intramembranous
24.1.2 Endochondral: Most bones in body formed this way; takes advantage of growth properties of hyaline cartilage.
24.1.2.1 Hyaline cartilage forms model of bone; surrounded by perichondrium
24.1.2.2 Cartilage model grows interstitially and appositionally; chondrocytes in mid-region hypertrophy, burst, release acids, trigger calcification - chondrocytes die from lack of nutrient diffusion. (calcified cartilage)Nutrient artery penetrates mid region, carrying osteoprogenitor cells with it - starts formation of
1
ossification centerBone collar forms under perichondrium of
midregion.
24.1.2.3 At 1
o. c., osteoblasts lay matrix over calcified cartilage, forming spongy bone. Close behind, the osteoclasts break down the matrix, leaving a cavity, which fills with red marrow.
24.1.2.4 Epiphyseal arteries enter the ends of the bone, and induce the development of 2
o.c.’s there. No medullary cavities form,
o and cartilage replacement is never quite complete (it remains on articular surfaces).
24.2 Growth
24.2.1 zone of resting cartilage
24.2.2 zone of proliferating cartilage
24.2.3 zone of hypertrophic cartilage
24.2.4 zone of calcified cartilage
25 Bone homeostasis o 25.1 Remodelling:
25.1.1 hormones: hGH (general activity), sex hormones (increase in o.b. at
puberty)
25.1.2 calcium status of the body; if calcium is needed, it gets taken from o
bone (& v.v.)
25.1.3 Mechanical stress (compression
more matrix; tension
more fibers)
25.2 Fracture
25.2.1 fracture hematoma--blood clot, within periosteum; swelling, inflammation. forms framework for repair
25.2.2 procallus--capillaries invade, fibroblasts start forming granulation tissue. mass called procallus. fibroblasts lay down collagen fibers, osteoprogenitor cells turn into chondroblasts and form fibrocartilage at the procallus (soft callus)
25.2.3 soft callus--as blood vessels grow back inwards, osteoprogs. form osteoblasts, which make spongy bone. Eventually, the fibrocartilage is all converted to spongy bone (hard callus)
25.2.4 hard callus--after several months, osteoblasts & osteoclasts remodel the callus back towards the original shape.
25.3 Aging
25.4 Calcium regulation: o o
26 Components of the skeletono 26.1 Types of bones:
26.1.1 Long
26.1.2 Flat
26.1.3 Unusual
26.1.3.1 wormian bones - flat bones that form from additional
centers of ossification in the skull. most common in the lambdoidal suture.
26.1.3.2 sesamoid bones - ‘seed-shaped’ bones that form as reinforcements within tendons. The two sesamoids that everyone has are the patellae (kneecaps). Others form as a result of longterm stress on a tendon where it passes over an articulation, especially in the metacarpals and phalanges of the hands and feet.
o 26.2 Axial Skeleton - selected comments.
26.2.1 Skull
26.2.1.1 Paranasal
26.2.1.2 Mastoid o
26.2.2 Vertebral column
o 26.3 Appendicular Skeleton - selected comments
27 Introduction
28 Classification
28.1 Structural classification — presence / absence of synovial cavity, type of connective tissue between bones:
o 28.2 Functional classification — degree of motion-
29 Types of joints (by functional classification) o 29.1 Synarthroses — immobile joints
29.1.1 Suture — fibrous joint, thin layer of dense CT. Sometimes sutures fuse completely; (for example, the frontal and occipital bones) these fusions are called synostoses.
29.1.2 gomphosis — fibrous joint, peg in socket, dense CT
29.1.3 synchondrosis — hyaline cartilage instead of dense CT; epiphyseal
o plate
29.2 Amphiarthroses — slightly mobile joints
29.2.1 syndesmosis — fibrous; like a suture, but more dense CT, so
slightly mobile (distal tibia / fibula)
29.2.2 symphysis — like a synchondrosis, but with fibrocartilage;
(intervertebral discs, pubic symphysis) o 29.3 Diarthroses
29.3.1 All diarthroses are synovial joints, and are bounded by articular cartilage and articular capsule.
29.3.2 How strong/mobile is a joint?
29.3.3 Types of movement:
29.3.4 Types of diarthroses:
29.3.5 Special movements:
30 Disorders:
o 30.1 Shoulders & Knees o 30.2 Arthritis & gout
31 Types of Muscle Tissue o 31.1 Skeletal muscle o 31.2 Cardiac muscle o 31.3 Smooth muscle
32 Functions of Muscle Tissue o 32.1 Movement (voluntary and involuntary)
32.1.1 Skeletal motion
32.1.2 Organ movement (sphincters, spleen, stomach)
o 32.2 Stability o 32.3 Thermogenesis
33 Characteristics of M. T.
o o o o
33.1 Irritability
33.2 contractability
33.3 extensibility
33.4 elasticity
34 Anatomy / Innervation of MT o 34.1 Nerve and blood supply o 34.2 Connective tissues
34.2.1 Fascia: o
34.2.1.1 Superficial
34.2.1.3 Deep
34.2.1.2 adipose, areolar CT
34.2.1.4 dense irreg. CT
34.2.2 Epimysium -- whole muscle
34.2.3 Perimysium -- holds fascicles together
34.2.4 Endomysium -- holds fibers together
34.2.5 All of these may be continuous with tendons or aponeuroses
34.3 Fibers (= cell)
34.3.1 Each fiber is the result of embryonic fusion, so multiple nuclei
34.3.2 up to approx. 12 in longplasma membrane = sarcolemmacytoplasm
= sarcoplasmendoplasmic reticulum = sarcoplasmic reticulum
34.3.3 fibers are full of myofibrils (striated): these are the contractile elements
34.3.3.1 myofilaments:myofibrils contain tiny threadlike structures, myofilaments.these are characterized as thick or thin.
The filaments overlap.in a relaxed muscle, little overlap; in a contracted muscle, much overlap.
34.3.3.1.1 the thick filaments are composed of myosin,; approx 200 molecules per. a big bundle of golf clubs; the
golf club handles form the filament; the heads form cross bridges
34.3.3.1.2 the thin filaments of actin, troponin, tropomyosin; main chain is twisted strand of actin molecules, with myosin-binding sites pointed outwards. troponin-tropomyosin cover the outside of the thin filament, and control whether myosin and actin can contract.this is why we say that actin and myosin are contractile; troponin and tropomyosin are regulatory.
34.3.3.1.3 a 3rd kind of filament, elastic filaments, seems to help stabilize thick filaments.
34.3.3.2 sarcomeres:myofibrils are made up of a series of repeating units, sarcomeres. each contains a series of light and dark regions. at each end is a Z-line (or disk). the light & dark effect (& therefore the striated bit) is the result of greater or lesser overlap of myofilaments.
34.3.4 The sarcoplasmic reticulum:The endoplasmic reticulum of other cells becomes the sarcoplasmic reticulum in muscle cells. The SR is more organized and regular than ER. SR encircles each myofibril. SR forms sacs called terminal cisterns which encircle a myofibril. SR is normally full of a Ca++ solution. Between each terminal cistern is a transverse tubule, a tube that wraps around the myofibrils and also communicates with the outside of the cell; its full of extracellular fluid.
35 Muscle movement: microscopic o 35.1 Contraction: The sliding filament model
35.1.1 Calcium’s role
35.1.2 ATP’s role
35.1.2.1 when myosin spontaneously binds to actin, it undergoes a
shape change; the heads spring towards the middle of the sarcomere, carrying the actin & thus the thin filaments with them.
35.1.2.2 as the myosin changes shape, ADP is released from the myosin head. after myosin has sprung, ATP spontaneously o o o
reattaches to it. This causes the myosin head to detach from actin
35.1.2.3 the ATP is split, the myosin head recocks, and the myosin head rebinds to actin (if available).
35.2 Relaxation
35.3 Motor Units:
35.4 Neuromuscular Junctions
35.4.1 Synapsesa tiny gap between two irritable cells, across which a
signal can jump under the right circumstances. usually you think of these between neurons, but muscle fibers get stimulated the same way.
35.4.2 Parts:
35.4.2.1 axon terminals(quick review: a nerve cell is a neuron; each neuron has a long, cable-like axon extending from it) at the o o
end of each motor neuron axon, the axon branches into axon terminals. at the tip of each terminal is a synaptic end bulb. within the bulb are synaptic vesicles (phospholipid membrane-lined packages) packed with neurotransmitters
35.4.2.2 synaptic clefta very small gap between the axon end bulb
and the sarcolemma of the muscle cell (specialized in this area; called the motor end plate).
35.4.2.3 motor end platesthe sarcolemma below the axon terminal is specialized as the motor end plate. it is studded with neurotransmitter receptors, 30 - 40 million of them
35.4.2.4 neurotransmitters (acetylcholine, in this case)transmit the
(basically) electrical nervous impulse across the synapse as a chemical signal. the neurotransmitter permits the nervous signal to excite the motor unit.
35.4.3 How it works:
35.4.4 What if it doesn’t work?
35.5 Muscle Tone
35.6 Muscle Metabolism: where does the energy come from?
35.6.1 ATP supplies in cell — 3-5 sec. worth in cellanaerobic
35.6.2 Phosphagen system — creatine phosphate (found only in muscle cells) gives up phosphate group to synthesize ATP (CP + ADP
C +
ATP) 15 sec. worth in cellanaerobic
35.6.3 Glycogen-lactic acid — 30 -40 sec. worth in cell. breakdown of glycogen in muscle cells to form glucose; breakdown of glucose (also from bloodstream) to form pyruvic acid (then to lactic acid). 2 ATP /
glucose. lactic acid mostly diffused to blood; some cells (cardiac) can oxidize LA to make more ATP.anaerobic
35.6.4 Aerobic — after 40 sec. slower than glycolysis, but efficient;
36
ATP / glucose. glucose comes from usual sources (glycogen, bloodstream) and O2 comes from blood and myoglobin. As long as the bloodstream supplies sufficient O2 and glucose, ATP is generated.aerobic
36 Muscle tension
o o o o
36.1 Twitch:
36.2 Types of stimulation
36.2.1 Multiple motor unit summation / recruitment
36.2.2 Wave summation / temporal summationstimulus after refractory, before relaxation- contraction increased (increased Ca++ release); helps to control smoothness of muscle contractions
36.2.3 Tetany
36.2.4 Treppe - staircase effect
36.3 Types of muscle contraction o
37 Fiber types
36.3.1 Isotonic — constant load:
36.3.2 Isometric — constant length
37.1 Slow twitch / slow oxidative / slow red
37.2 Fast twitch
37.2.1 fast oxidative / fast red -- lots of myoglobin & mitochondria; ATP from aerobic; fast ATP production, some fatigue; intermediate glycogen
37.2.2 fast glycolytic / fast white -- little myoglobin & mitochondria; ATP
from glycolysis; quick fatigue; lots of glycogen
38 Cardiac muscle o 38.1 Anatomy o 38.2 Physiology
39 Smooth muscle o o
39.1 Anatomy
39.2 Physiology
40 Heart Anatomy o 40.1 Layers of the heart:
40.1.1 pericardium:
40.1.2 epicardium (see above)
40.1.3 myocardium:
40.1.4 endocardium: o 40.2 Chambers: o 40.3 Valves:
41 Blood flow through the heart
o 41.1 heart is really 2 pumps in one- r side deoxy, l oxy
42 Conduction system o 42.1 About 1% of cardiac muscle cells are autorythmic - these are concentrated in the sinoatrial (SA) and atrioventricular (AV) nodes. They also form the cells of the conduction system. These cardiac muscle cells are specialized to behave more like neurons, transmitting action potentials from one place to another.
o 42.2 Timing of events during heartbeat:
42.2.1 SA node generates action potential (AP).
42.2.2 AP travels through atrial walls, spreads to all parts of atria; atria
contract (from base downwards to valves)
42.2.3 AP reaches AV node
42.2.4 After a delay (
0.1 seconds) the AV node continues the AP,
sending it on:
42.2.5 AP travels from the AV node
AV bundle
branch bundles
purkinje fibers at
300 cm/sec.
42.2.6 purkinje fibers pass the AP to regular cardiac muscle cells
42.2.7 ventricles contract (from apex upwards to valves)
43 Contraction physiology o 43.1 A big functional difference between cardiac muscle cells and skeletal muscle cells has to do with how long they remain depolarized following stimulation.
Skeletal muscle cells repolarize fast; cardiac cells stay depolarized for a long time
(.25 sec). A flow of Ca+ into the cells keeps them depolarized.A muscle cell can only contract while Ca+ is present - eventually Ca+ gets pumped out, and the cardiac cell relaxes.The cardiac refractory period is longer than the period of contraction (in skeletal muscle it is much shorter).
44 Cardiac cycle o 44.1 Relaxation o 44.2 Ventricular filling o 44.3 Ventricular contraction
45 Cardiac output o 45.1 Stroke volume(EDV-ESV;
70ml) x heart rate(
75bpm) = cardiac output(
5.25 l/min). This is approximately the total volume of blood in the body.
[2]
45.1.1 Preload:
45.1.2 Contractility:
45.1.3 Afterload: o 45.2 Heart rate
45.2.1 Nervous control
45.2.1.1 Feedback to brain:
45.2.1.2 Output to heart:
45.2.2 Hormonal control
46 Developmental details
47 Anatomy of Blood Vessels o 47.1 Arteries - carry blood away from the heart to tissues
47.1.1 Elastic arteries = more elastic, less muscle; pressure reservoir
47.1.2 Muscular (Distributing) arteries = adjustment of flow to regions of o o o o
the body
47.1.3 Anastomoses
47.2 Arterioles
47.3 Capillaries
47.4 Venules
47.5 Veins
48 Physiology of Circulation o 48.1 Velocity of flow — total trip time: approx. 1 min.
o 48.2 Volume of flow o 48.3 Capillary exchange
48.3.1 Diffusion
48.3.2 Vesicular transport — rare (large, polar molecules; antibodies)
48.3.3 Bulk Flow — movement of fluids because of pressure diffs.
48.3.3.1 increased BP due to poor venous return (clots, cardiac fail.)
48.3.3.2 decreased plasma proteins (burns, malnutrition, kidney disease)
48.3.3.3 increased capillary permeability (histamines)
48.3.3.4 Fluid retention
48.3.3.5 Blockage of lymph vessels (loss of vessels, filarial worms) o 48.4 Venous return
49 Control of flow and pressure o
o
49.1 Cardiovascular center — regulates heart rate, contraction, vessel diameter - rate of flow and patterns of flow
49.2 Neural Regulation of Blood Pressure o 49.3 Hormonal Regulation of Blood Pressure o o
49.3.1 Renin- Angiotensin- Aldosterone:
49.3.2 Epinephrine - Norepinephrine
49.3.3 Antidiuretic hormone (ADH)
49.3.4 Atrial natriuretic peptide (ANP)
49.3.5 Parathyroid hormone (PTH) & calcitriol o 49.4 Autoregulation
50 Shock & Homeostasis
50.1 Causes:
50.2 Stages: (specifically, we’ll talk about hypovolemic shock)
50.2.1 Stage I/Compensated/non-progressive shock
50.2.1.1 strong vasoconstriction of less-essential organs
50.2.1.2 activation of RAA system
50.2.1.3 release of ADH
50.2.1.4 local autoregulation - hypoxic cells cause vasodilation
50.2.2 Stage II/Decompensated/Progessive shock
50.2.2.1 When BP drops sufficiently (60 mmHg), blood no longer
pumps through coronary arteries; heart becomes hypoxic; reduces contraction, even less pumping
50.2.2.2 loss of BP (40-50 mmHg) at vasomotor center (part of cardiovascular center) of brain; neurons become hypoxic, decrease
vasoconstrictor impulses
50.2.2.3 local autoregulation causes greatly increased permeability of capillaries - fluid loss to tissues
50.2.2.4 decreased cardiac output reduces blood speed in vessels, allowing clots to form. Obstructions block blood flow, slow blood further, cut off tissues
50.2.2.5 accumulation of acid wastes in cells disrupts cellular
metabolism
50.2.2.6 acid by-products (mostly lactic - anaerobic metabolism) cause acidosis throughout system, depressing CNS, inc. vasomotor center.
50.2.3 Stage III/irreversible shock
51 Circulatory routes
52 Blood Functions -
53 Components of blood:
54 Hemopoiesis (hematopoiesis)
55 Red blood cells o 55.1 Production
o 55.2 Destruction o 55.3 hematocrit — % RBC’s in blood -fem 38 - 46%; mal 40 - 54% anemia, polycythemia
56 White blood cells o o
56.1 function - attack pathogens, dead cells, foreign cells, sick cells
56.2 Types:
56.2.1 eosinophils — control inflammation, attack multicellular parasites
56.2.2 neutrophils — phagocytize foreign objects
56.2.3 basophils — promote inflammation, slow clotting
56.2.4 Monocytes — monoblast
monocyte
{leave blood}
macrophage
56.2.5 Lymphocytes — lymphoblast
lymphocyte (T or B cells, NK cells)
56.2.6 Platelets — cell fragments, not whole cells.
o 56.3 WBC counts- useful in determining what is going on:
57 Hemostasis o 57.1 Spasm o 57.2 Platelets
o 57.3 Coagulation
58 Blood typing
59 Disorders:
60 Lymphatic system o 60.1 Lymphatic formation, flow, and vessels
60.1.1 Formation and flow of lymph
60.1.3 Lymph ducts
60.1.2 Lymph capillaries (lymphatics) o 60.2 Lymphatic tissues
60.2.1 Lymph nodes
60.2.1.1 Anatomy
60.2.1.2 Function
60.2.2 Lymph nodules
60.2.3 Thymus gland
60.2.4 Spleen
One characteristic shared by all living things, though, is hierarchical organization.
We’ll find it useful to look at the body using this hierarchy as a guide.
Chemical the level of atoms and molecules; at this level, principles of chemistry and physics are most important. This seems like it’s outside the scope of this course, but it’s very important - all of physiology eventually depends on chemical reactions. You need to know at least a little of this to understand the rest of what’s going on.
Cellular
the level of cells, which are structures made of highly organized groups of molecules. As a general rule, you can say that the cell is the fundamental unit of living things - all living things are cells or made up of cells. Single celled organisms have to have one cell do everything - a
‘jack of all trades’ cell. Larger organisms have the ability/necessity of allowing cells to specialize for certain funtions.
Tissue
Groups of cells, organized to perform a specific function, are called tissues; for example, muscle tissue, nervous tissue, connective tissue. Tissues are the building blocks used to put together large, multicellular organisms like people.
Organ
Groups of tissues, organized to perform a specific function, are called organs. The tissues in an organ each perform the roles typical for that tissue; but the result is that the organ can perform complex roles that would be impossible for the tissues by themselves, for example the stomach.
But the stomach by itself is not very useful - it has to be connected to a set of other organs to work.
System
Groups of organs, organized to perform a specific function - the digestive system as an example.
As a whole , the system is responsible for getting energy into the body; this means it has individual parts (organs) that are responsible for ingesting food, breaking it down (mechanically and chemically), absorbing nutrients, detoxifying (some) bad chemicals, and getting rid of what’s not usable by the body.
Organism
Groups of organ systems, organized to perform a specific function - to be a complete, functioning organism (in this case, a human being). Just as an organ by itself is not very useful without the other organs that support it, an organ system is not independent of the other organ systems of the body. For us, what that really means is that what happens in one system is almost never just restricted to that one system - the effects ripple outward to many other systems as well.
Physiology is the study of the principal processes of life:
Metabolism a general term that covers all the chemical changes and reactions that occur within the body; the chemistry that controls the day-to-day business of living. this covers digestion, respiration, synthesis, excretion, etc.
Irritability / Responsiveness
the ability to detect and respond to changes in the (internal or external) environment. This happens at many structural levels - cells detect & respond to changes in extracellular fluid, organs can respond to changes outside the body (or to instructions from the nervous or endocrine systems), the organism as a whole can respond to internal or external events.
Growth generally, we mean an increase in size because of an increase in cell number or cell-produced materials.
Differentiation the changes that cells and tissues undergo as they divide and mature. in general, cells (or cell lineages) and tissues start out unspecialized, then become increasingly specialized as time goes on.
Reproduction in this case, reproduction occurs at 2 distinct levels: most of our cells reproduce repeatedly throughout our lifetimes (producing cell lineages) and in addition, the organism as a whole is capable of reproduction, though in this case additional help is required.
What is it?
You, as an organism, can operate at a wide range of conditions.
Your cells, however, cannot.
Maintenance of internal environment...
Environments:
External — outside the body
Extracellular — fluids outside the individual cells
Intracellular — internal cell environment
...at the optimal range of conditions. — the body can tolerate successively less environmental variation in each of the above environments.
What sort of conditions must be controlled?pH — 6.8 - 7.3% H
2
Oion concentrations (0.9 % saline)oxygennutrientstemperaturewastes
Cellular activities tend to upset homeostasis. (ex.; acidosis — most metabolic byproducts are acidic)
Homeostasis is maintained by feedback systems ( = system where effect changes control of effect)
nervous & endocrine systs. main actors here. negative feedback: — thermoregulation, blood sugar positive feedback: — labor - stretching uterus causes release of oxytocin, causes contraction, causes more stretching...
body regionsFig. 1.5directional termsExhibit 1.3 planes [1] Figure 1.7, 1.8cavitiesFigure 1.9 quadrant Chemical Background
as the saying goes, it can not be created or destroyed — but it can be converted from one form to another. We can categorize energy by what it’s doing
:
Potential energy is stored energy.
Kinetic energy is the energy spent doing work.
Radiant — energy of the electromagnetic spectrum; kinetic Electrical — energy from the flow of charged particles; potential & kinetic Heat — energy from the vibration of atoms and molecules; potential & kinetic Chemical — energy contained within chemical bonds; potential Mechanical
— energy from the movement of objects; potential & kinetic
Major: Minor: Trace:
Oxygen Calcium Cobalt
Carbon Phosphorus Selenium
Hydrogen Potassium Zinc
Nitrogen Sulfur
Sodium
Chlorine
Magnesium
Iodine
Iron
Chromium
Transfer of electrons — results in ions which dissociate in H
2
O (easily dissolved), polar cation - + -charge; anion - -charge
Sharing of electrons — not ionic; does not dissociate; may or may not be polarsingle, double, triple bonds
Exergonic
Endergonic
Synthesis (anabolic)
Decomposition (catabolic)
compounds are combinations of 2 or more different elements. They can be divided into 2 categories, inorganic and organic .
Compounds that do not contain C and H . Many inorganic substances dissolve into ions . In general, most inorganic molecules that we are concerned with will fall into one of the following
4 categories.
Acids an acid is a substance which, when it dissolves, increases the amount of H + ions in solution. it may do this directly, by adding more H + to the solution (HCl
H + + Cl ) or indirectly, by reducing the amounts of OH
-
in solution (proteins & amino acids may do this*). *Note: organic compounds can be acids (and bases) too!!!
Bases a base is a substance which, when it dissolves, decreases the amount of H + ions in solution.
Most often, it will do this by adding OH ions to the solution, which will combine with the H + ions to form water (NaOH
Na
+
+ OH
-
; OH
-
+ H
+
H work as well (H
+
+ NaHCO
3
Na
+
+ H
2
CO
3
H
2
2
O ). Other negatively-charged ions will
O + CO
2
).
H
+
and OH
-
ions are very, very reactive- they tend to interfere with other molecules. That’s why solutions that have lots of one or the other (HCl, NaOH) are dangerous. H
+
and OH
-
combine with each other to form water, so if you have lots of both, nothing much will happen. In fact, pure water is a combination of H
2
O, H
+
, and OH
-
. The scale that measures the imbalance of H
+ and OH
-
is the pH scale. Strictly speaking, pH is the
Salts a salt is a substance that dissolves into
Cl
-
; NaHCO
3
Na
+
+ HCO
3
-
+ and particles (
; other important ions - Ca ions
++
), neither of which is H
, K
+
)
+ or OH
-
.
Many of these ions are vitally important to physiological processes in the body (NaCl
Na
+
+
H2O
70% of body weight; some important chemical properties — solvent for other chemicals. water is a very good solvent; a wide range of materials will dissolve, at least slightly, in water. solutions can be ionic (like NaCl in solution) or molecular (like glucose in solution).
Water’s secret is its polarity . This means that each water molecule acts like a little battery, with a pole and a + pole. These are not ‘complete’ + and charges, so they are indicated with a
symbol in front:
+ ,
. These differently-charged ‘poles’ of the molecules are attracted to and can surround (and therefore dissolve) other substances whose molecules have + and regions
(and are themselves ‘polar’).
Even when water can’t dissolve something, it often is very good at suspending it; that is, it can keep materials floating around without letting them clump together - for a while, at least.
Most important chemical reactions in the body take place in an aqueous environment. vital component of some important reactions two important examples — dehydration synthesis, hydrolysis
high heat capacity it takes a lot of energy to raise the temperature of water; it is an excellent buffer for heat. that enables it to help the body maintain temperature homeostasis. a related property is water’s: high heat of vaporization this means the amount of energy required to evaporate liquid water. (it’s a lot of energy). this is why evaporating sweat can be an effective cooling mechanism lubricant water is the major component of mucus, serous fluid, digestive fluids, saliva, etc.
Tissues / Types
There are four principal types of tissue:
Epithelial Covering, lining, glandular ectoderm, mesoderm, endoderm
Connective Support, binding, energy reserve, immune cells mesoderm
Muscular Movement mesoderm
Nervous Signal transmission ectoderm
Blood plasma - liquid portion of blood
One surface of tissue is free
Cells closely packed, very little extracellular material
Cells are arranged in single- or multiple-layered sheets
Differentiated into an apical surface and a basal surface
Attached to adjacent connective tissue via basement membrane
Many cell junctions
Avascular
Innervated
High mitotic rate
Derived from all three germ layers
Protection (skin), filtration (capillary endothelium), lubrication (pleura), secretion (duodenum), absorption (ileum), transportation (alveoli), excretion
(sweat glands), sensory reception (skin)
Covering & lining epithelium the two criteria: how many layers (1 layer = simple; > 1 layer = stratified) and shape
(squamous, cuboidal, columnar) of cells. for the stratified types, usually only the outer layers look like squamous or columnar cells; the underlying layers all look cuboidal. types: simple squamous--single layer of flattened cells (nuclei often squashed & spread out) - good for diffusion, osmosis, filtration; bad for abrasion, friction simple cuboidal--single layer of cube-shaped/ spherical cells (nuclei evenly spaced) - more room for internal
‘machinery’, and usually associated with secretion/absorption simple columnar--single layer of cylindrical cells (nuclei crowded close together) - lots of internal components, often very metabolically active, lots of activity. 2 kinds: nonciliated--cells often with microvilli and goblet cells (produce mucus) - lining of digestive, reproductive, respiratory, & parts of urinary tracts ciliated--cells with cilia present - cilia create movement in mucus or fluid - parts of respiratory and reproductive systems, paranasal sinuses stratified squamous--multiple layers of cells; usually only outer layers look squamous. abrasion-resistant, relatively impervious. St. sq. epi. can be either: keratinized St. Sq. E.--large amounts of the protein keratin are deposited in the cells, rendering them tough and waterproof; outer surface is dry nonkeratinized St. Sq. E. --lack of keratin means that outer layers are moist, absorb/lose water easily stratified cuboidal--rare - found in sweat gland ducts, portions of the male urethra stratified columnar--rare - found in the conjunctiva, urethra, some exocrine gland ducts pseudostratified ciliated columnar--appears multilayered, but all cells are in contact with basement membrane. Cells reaching free surface have cilia; functions similar to simple ciliated columnar tissue. lines most of respiratory tract transitional--can change from a stratified cuboidal appearance to a stratified squamous appearance to allow structures to stretch without breaking - found lining the urinary bladder
Glandular epithelium - glands can be single celled or multicellular-- because of their relatively high metabolic rates, they are (not surprisingly) made of cuboidal or columnar cells.
Exocrine glands secrete their products into ducts; their classification is based on how they secrete... is the product released by itself, or is part or all of the gland’s cells released also?
Holocrine glands entire cell releasedsebaceous glands
Apocrine glands apex of cell releasedmammary glands
Merocrine glands substance onlysalivary, digestive
Endocrine glands secrete their products (hormones) into the bloodstream through the extracellular fluid (pituitary, thyroid, etc.) We will deal with them in detail later.
High proportion of extracellular material, especially ground substance and fibers
Not found on free surfaces (1 exception - synovial membrane)
Most connective tissues are vascularized (exc. tendons, cartilage)
Innervated (exc. cartilage)
Major characteristics of tissue determined by matrix, which can be fluid, gelatinous, fibrous, or calcified
Ground substance
Contains molecules that determine the ‘consistency’ (fluid, gel, solid) of the matrix. The most important are:
Hyaluronic acid - thick, slippery substance - lubricant, glue-like
Chondroitin sulfate - jellylike, provides support
Adhesion proteins - help to anchor cells
Fibers
Provide support, strength. Embedded in the ground substance between the cells of the connective tissue. 3 kinds:
Collagen fibers - very strong, resistant to stretching, but flexible; long single fibers made of collagen
Elastic fibers - smaller than collagen fibers, can be stretched without breaking, less strong than collagen fibers, flexible; single or branching, made with elastin & fibrillin
Reticular fibers - short, branching fibers, less strong than collagen, inelastic; used as support; made of collagen
Cells in connective tissue are most often named for the matrix they secrete. Cell names can end in blast (cells actively secreting matrix), cyte (cells metabolically maintaining matrix, but not forming new matrix), and sometimes clast (cells breaking down matrix). Not all of these three kinds of cells will be found in a specific tissue.
Cell names start with the kind of matrix being made:
Fibro-cells making or maintaining fibrous CT (fibroblast, but no “fibrocytes”
)
Chondro-cells making or maintaining cartilage (chondroblast, chondrocyte)
Osteo-cells making or maintaining or breaking down bone (osteoblast, osteocyte, osteoclast)
Loose connective tissues
Areolar CT
Cells: Fibers: Ground Substance: Function: many types collagen, elastic, reticular fluid to gelatinous support, ‘packing’, elasticity
Adipose CT
Cells: Fibers: Ground Substance: Function: adipocytes few (but all types present) fluid; mostly squeezed out energy storage, cushioning
Reticular CT
Cells: Fibers: Ground Substance: Function: reticulocytes reticular fluid to gelatinous support (esp. in glands)
Dense connective tissues
Dense regular CT
Cells: Fibers: Ground Substance: Function: fibroblasts collagen (in parallel) fluid strong, inelastic support
Dense irregular CT
Cells: Fibers: Ground Substance: Function: fibroblasts collagen (irregular) fluidto gelatinous strong, multidirectional support
Elastic CT
Cells: Fibers: Ground Substance: Function: fibroblasts elastic (often in sheets) fluidto gelatinous stretchable, moderate strength
Cartilaginous connective tissues
Hyaline cartilage
Cells: chondroblasts, chondrocytes
Fibers:
Ground
Substance: collagen gelatinous
Function: flexible support, low friction, shockabsorbing
Fibrocartilage
Cells: chondroblasts, chondrocytes
Fibers: collagen (LOTS of collagen)
Ground
Substance: gelatinous
Function: strongest cartilage; support, slight flexibility
Elastic cartilage
Cells: Fibers: Ground Substance: Function: chondroblasts, chondrocytes elastic gelatinous maintains shape, support
Bone tissue
Cells: osteoblasts, osteocytes, osteoclasts
Fibers: Ground Substance: collagen calcium phosphate, calcium carbonate
Blood tissue
Cells: Fibers: Ground Substance: Function: red & white blood cells (none) liquid (plasma) transport, immune system
Function: support, protection
Contains cells that respond to an electrical stimulus by contracting
Often interspersed with connective tissues, especially dense regular connective tissue
Skeletal (striated)--Very long, cylindrical cells; multinucleate, striated, voluntary
Cardiac--Branching cells, usually with 1 nucleus; striated; connected by intercalated disks; involuntary
Smooth--Small, spindle-shaped, 1 nucleus, not striated, many gap junctions, involuntary
Contains cells that respond to an electrical stimulus by generating & conducting another electrical stimulus (neurons)
Also contains cells that act as physical & metabolic support for neurons
Epithelial layer + underlying CT makes an epithelial membrane. Mucous & serous membranes are the most common kinds within the body; cutaneous membrane (skin) lines the outside. In addition, synovial membranes have connective tissue but no epithelium.
Line body cavities & surfaces that open to the exterior; lots of goblet cells, generally cuboidal or columnar cells over irregular CT; produces mucus (& many other secretions besides)
Line cavities that do not open to the exterior; generally simple squamous epithelium over areolar
CT; produces serous fluid (watery, lubricating fluid)
line joint cavities, tendon sheaths; areolar CT with additional elastic fibers and adipocytes; produce synovial fluid, slippery lubricating & nutrient fluid.
Integumentary System
Two layers, epidermis (stratified squamous epi.; ectoderm) and dermis (dense irregular CT; mesoderm) underlain by 3rd layer, hypodermis (loose CT); also called the subcutaneous fascia; area of fat storage. One of the larger organs of the body.
A strat. squam. epi. (keratinized); acts as hydrophobic protective barrieravascular30-50 cells thick; most layers are dead cellspalms, soles have 5 distinct layers — “thick” skin; found in hihgfriction areasother areas have 4 distinct layers — “thin” skin
Cell types: keratinocytesmelanocytesothers
Epidermal layers: follow the course of an individual cell from start to finish
Stratum basale (str. germinativum) a single layer of keratinocytes, which secrete the BM of epidermis and divide on a 17-20 day cycle. also found here are cell bodies of melanocytes. One keratinocyte daughter cell remains in
S.B., while the other is pushed up into the:
Stratum spinosum about 10 cells thick; keratinocytes start to flatten out, amount of keratin increases. some of these cells can still undergo mitosis. processes of melanocytes extend among the keratinocytes, k’s. pick up melanin from these. Next:
Stratum granulosum
2-5 cells thick, keratinocytes continue to flatten, granules of keratohyalin form; lipids released into gaps between cells; envelope of keratin proteins begins to form under cell membrane; organelles and nucleus begin to die & disintegrate
Str. lucidum (present in thick skin only)
2-3 cells thick keratinocytes dead, no internal structure visible (except keratin fibers); appears transparent, hence name
Str. corneum
20+ layers thick; dead cells, heavily keratinized, held together by desmosomes. cells flat, scalelike; surrounded by lipids; as desmosomes break, cells are shed (desquamate) these cells are cornified = dead & full of keratin total trip time = 2-4 weeks? 50 days?
Recapping thick vs. thin skin —
Thick:5 layers, many layers of S.C. palms fingertips, soles of feet, toespapillary layer of dermis forms curving, parallel ridges
generally thicker than epidermis; many blood vessels, nerve fibers, glands, hair follicles present. mainly dense irregular CT with elastic fibers also; adipocytes and immune components (mast cells and macrophages) present also.Dermal layers (deep
shallow)
Reticular layer very fiber-rich; collagen fibers irregular, elastic fibers more regular;
skin stretches better in some directions than others - must be taken into account when making surgical incisions. over-stretching causes striae “stretch marks” this layer contains lymph vessels, adipocytes, bases of hair follicles
Papillary layer contains projections (papillae) extending up towards epidermis - few fibers, more cells - many blood vessels which supply epidermis bedsores (decubitus ulcers) demonstrate importance of good blood flow through dermis
Protection physical barrier to microorganisms, physical traumasecretions retard pathogen growth (pH 4 -
6.8)retards UV penetration
Thermoregulationheat lost by dilating blood vessels, sweating,direct conduction of heatheat saved by constricting blood vessels, insulation of subcutaneous fat, shivering(brown fat in infants)(arrector pili muscles)
Absorption/Excretion absorption limited to fat-soluble, hydrophobic compounds, small amounts of O
2
& CO
2
urea
(ammonia excretion) in sweat, also excess salt
Synthesis
3 main ‘products’ of the skin:melanin, keratin, vitamin D (regulates metabolism, absorption of
Ca
+
and Phosphorus)
7-dehydroxycholesterol (in skin cells) + UV
vit. D3; (carried to liver)
25hydroxycholecalciferol; (carried to kidneys)
calcitriol = most active form. so the skin is actually an endocrine gland.
Sensory reception receptors detect heat, cold, pain, light touch, pressure; hair follicles have receptors that detect hair movement
Fluid regulation prevention of water loss across skin (dehydration in burn patients)
Blood reservoir
Dermal layers contain up to 10% of blood volume
Skin color is determined by 3 pigments — melanin, carotene, hemoglobin (locations) melanin production highly variable. UV exposure increases rate of synthesisalbinism = genetic inability to produce melanin - total lack of pigmentvitiligo = patchy melanin distribution - cause unknown, may be autoimmune against melanocytes
Other unusual colorations: jaundice, cyanosis, erythema (redness)
functions? (UV and thermoregulation, sensation, protection of orifices, pheromonal?)Very high mitotic activity cellsHairs grow from follicles, epidermal evaginations into the dermis (why?)
Hair develops from dividing cells in matrix of bulbcolored by melanin, sometimes with iron and sulfur added. tyrosinase decreases with age,
loss of pigment. hormonal effects - androgens
Sudoriferous
Sebaceous
Ceruminous
Depending on depth- epidermal vs. deep
Epidermal wound healing
(abrasion, 1st or 2nd degree burn) keratinocytes of the St. B. migrate inwards from the edges of the wound until they meet; contact inhibition prevents excess growth; keratinocytes then proliferate and reform layers.
Deep wound healing involves CT, so is harder to heal, takes longer, more complex.
inflammatory phase: blood pours into wound from broken vessels; clot forms, and seals the wound from the outside. blood vessels in the area dilate, become more permeable
redness, swelling, warmth; brings WBC’s and antibodies to area for immune function. mesenchyme (fibroblast) cells migrate in also. migratory phase: clot
scab; epithelial cells migrate beneath scab to bridge wound; fibroblasts produce collagen fibers & matrix (granulation tissue); blood vessels begin to regrow. proliferative phase: like migratory phase, but more of it. maturation phase: as epidermis is restored to normal thickness, scab is lost as epithelial cells dequamate. repaired CT is often richer in fibers than normal tissue, often low in blood vessels.
Overlying epi. often without hair, melanocytes.
anything that denatures proteins is a burn- heat, chemical, radiation, electricity. because they disrupt the StSE, they demonstrate how important it is.
1st-degree epidermis only; redness, no blistering; skin functions remain
2nd-degree full thickness of epidermis, and some (or most) dermis; redness, blistering, fluid accumulation; epidermal derivatives deep in the dermis usually not affected; healing takes place from edges and from intact epi. derivatives; several weeks to heal if protected from infection; because of dermal damage, may scar if enough dermis is involved.
3rd-degree full thickness of skin, destroying epidermis, all derivatives, dermis and contents; color varies; edema, loss of sensation; healing can only occur from edges of burn; infection risk high, fluid loss great
Effects are predictable: fibroblasts slow fiber production, so # of fibers and strength (& elasticity) reduced. Keratinocyte mitosis slows, hairs grow more slowly, glands produce less, melanin production tends to be reduced, healing ability lessened.
Skeletal System
attachment of muscles, tendons, and (indirectly) organs
most obvious examples - the brain surrounded by the cranium and base of skull, lungs, heart & major blood vessels surrounded by ribcage, vertebral canal
Provide something for muscles to work against
Primary reservoirs of these elements, whose most important role is in nerve and muscle tissue function (not skeletal support)
Bone marrow is the site of blood tissue formation, which means O
2
and CO
2
transport, and immune system components
Bone marrow is an important site of adipose tissue formation.
Major parts: (of a typical ‘long’ bone, like a femur or humerus)
The main shaft of the bone
The proximal and distal ends of the bone, generally flared out & flattened for articulation with other bones
The junction of the epiphyses with the diaphysis. During active growth, this region is not bone tissue at all - it is hyaline cartilage
A thin layer of hyaline cartilage that covers the epiphyses where they articulate with other bones.
A two-layered membrane that covers the bone (except at the articular cartilages). The outer layer is dense irregular CT; the inner layer is elastic CT with many bone cells.
The cavity that is found within the diaphysis of long bones, where some of the marrow is found - this is not present in many bones.
a thin membrane composed mainly of bone-producing and bone-removing cells.
Bone is a connective tissue, so it has matrix surrounding cells. Matrix is 25% H
2
O, 25% collagen fibers, 50% mineral salts.
A. Cells are of four types:
Osteoprogenitor cells
unspecialized, can divide repeatedly; found mostly in the periosteum and endosteum
Osteoblasts form from osteoprogenitor cells; actively form bone, no longer can divide
Osteocytes mature osteoblasts; no secretion of matrix, but still metabolically active
Osteoclasts derived from immune cells; secrete acids & enzymes that help break down bone
calcium phosphate + calcium carbonate, mostly; crystallization of these salts along matrix fibers
= calcification. fibers - tensile strength, flexibilityCaPO - compressive strength, hardness
Intramembranous
Endochondral: Most bones in body formed this way; takes advantage of growth properties of hyaline cartilage.
Hyaline cartilage forms model of bone; surrounded by perichondrium
Cartilage model grows interstitially and appositionally; chondrocytes in mid-region hypertrophy, burst, release acids, trigger calcification - chondrocytes die from lack of nutrient diffusion. (calcified cartilage)Nutrient artery penetrates mid region, carrying osteoprogenitor cells with it - starts formation of 1
ossification centerBone collar forms under perichondrium of midregion.
At 1
o. c., osteoblasts lay matrix over calcified cartilage, forming spongy bone. Close behind, the osteoclasts break down the matrix, leaving a cavity, which fills with red marrow.
Epiphyseal arteries enter the ends of the bone, and induce the development of 2
o.c.’s there. No medullary cavities form, and cartilage replacement is never quite complete (it remains on articular surfaces).
Bones grow either by appositional growth, which can add to their girth, or by cartilage replacement at epiphyseal plates. The plate has 4 regions:
( epiphysis ) zone of resting cartilage zone of proliferating cartilage zone of hypertrophic cartilage zone of calcified cartilage
( diaphysis )
Eventually, osteoblast growth overtakes chondrocyte growth, and lengthening stops.
Despite appearances, bone is continually remodelling itself; osteoblasts and osteoclasts continually make and break bone.Several factors alter the rate at which o.b.’s and o.c.’s work: hormones: hGH (general activity), sex hormones (increase in o.b. at puberty) calcium status of the body; if calcium is needed, it gets taken from bone (& v.v.)
Mechanical stress (compression
more matrix; tension
more fibers)
Effects of weight-bearing activities- lack of same (1% loss/week)
fracture hematoma--blood clot, within periosteum; swelling, inflammation. forms framework for repair procallus--capillaries invade, fibroblasts start forming granulation tissue. mass called procallus. fibroblasts lay down collagen fibers, osteoprogenitor cells turn into chondroblasts and form fibrocartilage at the procallus (soft callus) soft callus--as blood vessels grow back inwards, osteoprogs. form osteoblasts, which make spongy bone. Eventually, the fibrocartilage is all converted to spongy bone (hard callus) hard callus--after several months, osteoblasts & osteoclasts remodel the callus back towards the original shape.
2 main effects: loss of calcium, largely due to reduced sex hormone production; and reduced protein synthesis, leading to increased brittleness.
One of the most common conditions caused by aging is osteoporosis — extremely thin and brittle bones caused by reduced osteoblast function. It is most common in women- bones are usually smaller to begin with, so loss is more damaging; menopause greatly reduces the production of estrogens, so osteoblast activity slows. Very low body fat content can also cause osteoporosis (men & women) because the presence of adipose tissue stimulates sex hormone production - very low-fat diets, or inadequate total calories in the diet can also cause it.
Osteoarthritis is the result of breakdown of the articular cartilages. Once bone tissue is exposed, the bone attempts to “fix” itself by reacting as though a fracture has occurred, and the joint can become fused.
ca++ required for: muscle contraction, nerve conduction, enzymes, blood clotting
Long
The ‘typical’ bone - has a diaphysis of compact bone, epiphyses of spongy bone, and a medullary cavity; forms endochondrally
Flat
Bones without medullary cavities - spongy bone all the way through. Can form endochondrally or intramembranously
Unusual
Bones that may or may not be present. The two most common types are: wormian bones - flat bones that form from additional centers of ossification in the skull. most common in the lambdoidal suture. sesamoid bones - ‘seed-shaped’ bones that form as reinforcements within tendons. The two sesamoids that everyone has are the patellae (kneecaps). Others form as a result of longterm stress on a tendon where it passes over an articulation, especially in the metacarpals and phalanges of the hands and feet.
Skull
Housing for brain, special sensory organs; entryway for respiratory and digestive systems. To help reduce the weight of this large mass of bone, the bones of the facial region contain air-filled sinuses-
Paranasal sinuses in the maxillary, frontal, ethmoid, and sphenoid bones; also act as ‘resonating chambers’ for vocal cords. Lined with mucous membrane, draining into nasal cavity.
Mastoid located in mastoid process of temporal bone - weight reduction
Vertebral column
Divisions -
# vertebrae Division
7 cervical
12 thoracic
5
5
3-5 lumbar sacral coccygeal
Curves-
4 in adults: cervicalposteriorsecondarythoracicanteriorprimarylumbarposteriorsecondarysacralanteriorprimar y
1 in fetus, anterior abnormal curves- scoliosis - lateral bendkyphosis - exaggerated thoracic curve vertebrae separated by disks- annulus fibrosus - fibrocartilage, very strong & flexiblenucleus pulposus - elastic connective tissue, very elastic
The limb girdles demonstrate a compromise between strength and flexibility (in other words, the more flexible a joint, the weaker it is).
— pectoral girdle weakly attached to body, glenoid oriented laterally, designed for tensile forces, arboreality
— pelvic girdle strongly attached, less mobility, greater weight concerns -supporting viscera, and weight of the body on legs differences resulting from sex hormone influences:bipedalism & childbirth angle of leg bones - keeping weight centered
Articulations
articulation (joint) = point of contact between two or more bones, between cartilage and bone, or between teeth and bone.
The anatomy of a joint determines its function; the range of motion it can produce, the amount of support it provides.
fibrous: dense CT between bones, no joint cavity cartilagenous: cartilage between bones, no joint cavity synovial: . joint cavity; structure complex
synarthrosis: no movement amphiarthrosis: slight movement diarthrosis: free movement
Suture — fibrous joint, thin layer of dense CT. Sometimes sutures fuse completely; (for example, the frontal and occipital bones) these fusions are called synostoses. gomphosis — fibrous joint, peg in socket, dense CT synchondrosis — hyaline cartilage instead of dense CT; epiphyseal plate
syndesmosis — fibrous; like a suture, but more dense CT, so slightly mobile
(distal tibia / fibula) symphysis — like a synchondrosis, but with fibrocartilage; (intervertebral discs, pubic symphysis)
All diarthroses are synovial joints, and are bounded by articular cartilage and articular capsule.
The capsule surrounds the cavity and unites the articulated bones. There is an outer fibrous capsule which unites with external ligaments and a synovial membrane.
There are often other accessory structures - ligaments, bursae, articular discs (menisci); ‘torn cartilages’ are damaged articular discs
How strong/mobile is a joint?
Determined by: shape of bones, strength of ligaments, muscle tension, hormonal influences
Types of movement:
Flexion/extension (hyperextension)
Rotation/ circumduction adduction/abduction
Types of diarthroses: gliding/arthrodial {side-to-side}[carpals, tarsals] hinge/ ginglymus {flexion/extension}[elbow] pivot/trochoid {rotation}[atlas-axis] ellipsoidal/condyloid {fl.-ex.; ad.-ab.}[carpals-radius]
saddle/sellaris [trapezium-1st metacarpal] ball-and-socket/spheroid
Special movements: elevation/depression protraction/retraction inversion/ eversion dorsiflexion/plantar flexion supination/pronation
dislocations of shoulder - rotator cuff injury the shoulder joint consists of: articular capsuleglenoid labrumcoracohumeral ligament, glenohumeral ligamentstendons of infraspinatus, supraspinatus, teres minor, subscapularis muscles the knee consists of: articular capsule extracapsular ligaments: patellar, medial & lateral patellar retinacula, medial & lateral collaterals, popliteals infracapsular ligaments: anterior & posterior cruciate articular discs
(menisci) {attached by transverse & coronary ligaments}
rheumatoid osteoarthritis autoimmune disease- most common in small, distal joints
‘wear & tear’ disease- most common in weight-bearing joints gout, gouty arthritis multiple causes- buildup of uric acid at joints, esp. distal
Muscles
Skeletal motion
Organ movement (sphincters, spleen, stomach)
why are nerves and blood so important to muscles?(irritability/nutrients/O
2
/wastes)
Fascia:
Superficial adipose, areolar CT
Deep dense irreg. CT
Epimysium -- whole muscle
Perimysium -- holds fascicles together
Endomysium -- holds fibers together
All of these may be continuous with tendons or aponeuroses
Each fiber is the result of embryonic fusion, so multiple nuclei up to approx. 12 in longplasma membrane = sarcolemmacytoplasm = sarcoplasmendoplasmic reticulum = sarcoplasmic reticulum fibers are full of myofibrils (striated): these are the contractile elements myofilaments:myofibrils contain tiny threadlike structures, myofilaments.these are characterized as thick or thin. The filaments overlap.in a relaxed muscle, little overlap; in a contracted muscle, much overlap. the thick filaments are composed of myosin,; approx 200 molecules per. a big bundle of golf clubs; the golf club handles form the filament; the heads form cross bridges the thin filaments of actin, troponin, tropomyosin; main chain is twisted strand of actin molecules, with myosin-binding sites pointed outwards. troponin-tropomyosin cover the outside of the thin filament, and control whether myosin and actin can contract.this is why we say that actin and myosin are contractile; troponin and tropomyosin are regulatory. a 3rd kind of filament, elastic filaments, seems to help stabilize thick filaments. sarcomeres:myofibrils are made up of a series of repeating units, sarcomeres. each contains a series of light and dark regions. at each end is a Z-line (or disk). the light & dark effect
(& therefore the striated bit) is the result of greater or lesser overlap of myofilaments.
The sarcoplasmic reticulum:The endoplasmic reticulum of other cells becomes the sarcoplasmic reticulum in muscle cells. The SR is more organized and regular than ER. SR encircles each myofibril. SR forms sacs called terminal cisterns which encircle a myofibril. SR is normally full of a Ca++ solution.
Between each terminal cistern is a transverse tubule, a tube that wraps around the myofibrils and also communicates with the outside of the cell; its full of extracellular fluid.
Muscles don’t accordion-pleat, they slide.
The thin filaments in the sarcomere are pulled toward each other, along the thick filaments. The filaments do not change in length. What causes the pull?
Calcium’s role
In a relaxed muscle, Ca
++ concentration is low; pumps actively transport Ca
++
out of sarcoplasm into the SR. When a muscle cell gets the message from a neuron, special channels open, flooding
Ca
++
into the sarcoplasm around the filaments. Ca
++
binds to troponin, changing that molecule’s shape-- this bends troponin-tropomyosin away from the myosin-binding sites on actin.
ATP’s role
In relaxed muscle, myosin is in an energized state. ATP attaches to myosin heads - myosin splits
ATP to ADP + P, & uses the energy to “cock” itself, in preparation for muscle contraction. This activated myosin spontaneously binds to actin if the binding sites are available . Otherwise, it just sits, waiting. Once binding sites become available on actin, several steps happen in rapid succession: when myosin spontaneously binds to actin, it undergoes a shape change; the heads spring towards the middle of the sarcomere, carrying the actin & thus the thin filaments with them. as the myosin changes shape, ADP is released from the myosin head. after myosin has sprung, ATP spontaneously reattaches to it. This causes the myosin head to detach from actin the ATP is split, the myosin head recocks, and the myosin head rebinds to actin (if available).
As long as Ca
++
and ATP levels are high, this cycle repeats.
Once the signal to contract ceases, the Ca
++
gates close, and Ca
++
pumps rapidly remove Ca
++ from the sarcoplasm; so thin filament binding sites covered.
Muscle cells/fibers are innervated by motor neurons. A single motor neuron will innervate multiple muscle cells. The number of muscle cells / neuron is an indication of how fine the muscular control over a structure is; the fewer fibers/neuron, the greater the control. Range:2 -
2000 fibers/neuron, mean 150 (fingers, lips vs. rectus fem.)
Synapsesa tiny gap between two irritable cells, across which a signal can jump under the right circumstances. usually you think of these between neurons, but muscle fibers get stimulated the same way.
Parts:
axon terminals(quick review: a nerve cell is a neuron; each neuron has a long, cable-like axon extending from it) at the end of each motor neuron axon, the axon branches into axon terminals. at the tip of each terminal is a synaptic end bulb. within the bulb are synaptic vesicles (phospholipid membrane-lined packages) packed with neurotransmitters synaptic clefta very small gap between the axon end bulb and the sarcolemma of the muscle cell (specialized in this area; called the motor end plate). motor end platesthe sarcolemma below the axon terminal is specialized as the motor end plate. it is studded with neurotransmitter receptors, 30 - 40 million of them neurotransmitters (acetylcholine, in this case)transmit the (basically) electrical nervous impulse across the synapse as a chemical signal. the neurotransmitter permits the nervous signal to excite the motor unit.
How it works:
As a nervous impulse (much, much more on that later) reaches the axon terminals, it causes the symaptic vesicles to release their neurotransmitters into the synaptic cleft. The acetylcholine is picked up by the receptors on the end plate, and this triggers opening of Na + channels in the sarcolemma at the motor end plate. The flood of Na
+
into the muscle cell causes a change in electric voltage across the sarcolemma (because this is a big flow of + ions). This voltage change is “contagious”; it spreads along the muscle cell from the point of stimulation. (Most neuromuscular junctions are located near the midpoint of a muscle cell’s length).The voltage change travels down into the transverse tubules (T-tubules; remember them?). This voltage change in the T-tubules induces Ca
++
channels in the adjacent terminal cisterns of the sarcoplasmic reticulum (SR) to open. Ca
++
floods into the sarcoplasm, and the muscle contracts.
What if it doesn’t work?
If no nervous signal crosses the neuromuscular junction, then obviously no contraction can take place; myasthenia gravis is an example - autoimmune disease, antibodies block ACh receptors on motor end plate, progressively reducing ability of ACh to stimulate muscle cell. MG tends to affect muscles of face & neck; may progress to limbs, respiratory muscles (usually not). How to treat? — increase levels of ACh by reducing AChE (acetylcholinesterase inhibitors), reduce antibody levels with steroids. (other treatments exist).
If Na + channels don’t close, then the electrical signal never stops, Ca ++ continually floods into the cell, muscles continue contraction as long as ATP present (tetany); can be caused by; repeated nervous stimulation, outside electrical stimulation, bacterial toxins (tetanus), neurotoxins (nerve gas - AChE inhibitor).
Random, asynchronous firing of motor units; if lacking, hypotonia; if increased, then hypertonia
(spasticity or rigidity)
ATP supplies in cell — 3-5 sec. worth in cellanaerobic
Phosphagen system — creatine phosphate (found only in muscle cells) gives up phosphate group to synthesize ATP (CP + ADP
C + ATP) 15 sec. worth in cellanaerobic
Glycogen-lactic acid — 30 -40 sec. worth in cell. breakdown of glycogen in muscle cells to form glucose; breakdown of glucose (also from bloodstream) to form pyruvic acid (then to lactic acid). 2 ATP / glucose. lactic acid mostly diffused to blood; some cells (cardiac) can oxidize LA to make more
ATP.anaerobic
Aerobic — after 40 sec. slower than glycolysis, but efficient;
36 ATP / glucose. glucose comes from usual sources (glycogen, bloodstream) and O2 comes from blood and myoglobin. As long as the bloodstream supplies sufficient O2 and glucose, ATP is generated.aerobic
A single contraction of a motor unit in response to a single neuron action potential. (remember, it’s all-or-none) latent period -(Ca ++ release - 2 msec)contraction - 10 -100 msecrelaxation -(Ca ++ back to SR - 10
- 100 milliseconds) after stimulation, a refractory period (5 - 300 msec; skeletal - cardiac) occurs.
The refractory period is caused by the inability of a new AP to initiate.
Multiple motor unit summation / recruitment increase in # of MU’s firing; helps to control force of muscle contractions
Wave summation / temporal summationstimulus after refractory, before relaxation- contraction increased (increased Ca++ release); helps to control smoothness of muscle contractions
Tetany
20-30 stim/sec — incomplete (partial relaxation)80 + — complete (no relaxation at all)
Treppe - staircase effect stims too far apart for summation will cause increasing contractions, to threshold. same explanation as others? (buildup of Ca ++ )
(Most movements are a combination of all of these)
Isotonic — constant load: concentric - muscle shorteningeccentric - muscle lengthening (more likely to cause soreness?)
Isometric — constant length
Most muscles in the body contain a mix of fibers; all fibers of a motor unit are identical.
Different individuals may vary in their fiber makeup - leg muscles of sprinters tend to have lots of fast-twitch fibers (60%) while marathoners tend to have less (20%).
lots of myoglobin & mitochondria; ATP from aerobic; slow, steady ATP production; slow fatigue rate; little glycogen
fast oxidative / fast red -- lots of myoglobin & mitochondria; ATP from aerobic; fast ATP production, some fatigue; intermediate glycogen fast glycolytic / fast white -- little myoglobin & mitochondria; ATP from glycolysis; quick fatigue; lots of glycogen
cells are shorter, wider, and branched (compared to skeletal muscle); more mitochondria; usually only one nucleus. similar arrangement of sarcomeres; less SR. connected at ends to each other by intercalated disks- desmosomes & gap junctions. these allow muscle contractions to be spread from one cell to the next. also - some cardiac cells are autorythmic.
almost exclusively aerobic; twitch is much longer than in skeletal muscle because channels that allow Ca+ to enter stay open longer. Na
+ gates prolong refractory period to about .3 seconds - this helps prevent summation and tetany.
visceral smooth muscle - VSM - lots of gap junctions, contracts as unit; forms sheets of contracting tissuemultiunit smooth muscle - MSM - few gap junctions, few cells per neuron; rare, in eye, arrector pili, bronchioles
small, spindle-shaped; single nucleus; thick & thin filaments present, but not in sarcomeres; no T tubules, little SR
Heart
located in mediastinum; 4 chambers; 2 atria, 2 ventricles; cone-shaped, with apex pointing down
& left, base at top.
pericardium: fibrous pericardium — dense irreg.; anchors heart to diaphragm (does not stretch -- tamponade = compression of heart by accumulated fluid) serous pericardium — makes space around heart. outer parietal, inner visceral (aka epicardium) layers. fluid between them pericardial fluid. epicardium (see above) myocardium: bulk of heart muscle — made up of cardiac muscle cells. formed into spiral shape, more or less aligned along axis of heart; atrial & ventricular components independent. endocardium: endothelial lining of atria & ventricles. continuous with lining of blood vessels.
atria: thin walled upper chambers — flappy parts called auricles; ventricles: larger, thick-walled chambers separated by interventricular septum. connective tissues separate atria & ventricles. atria separated by interatrial septum, with fossa ovalis. surfaces of chambers ridged. thicknesses correlate with distance blood must be pumped.
rt AV = tricuspid;l AV = mitral/bicuspid; flaps cusps; chordae tendineae connect to cusps and papillary muscles of ventricles. (prevent regurgitation)semilunar valves — 3 cusps; to arterial trunks
3 circuits are involved; pulmonary, systemic, cardiac
Besides the nodes, the conduction system is made of: the AV bundle (bundle of His)the left & right bundle branchesthe purkinje fibers (conduction myofibers)
SA node cells have an autorythmic rate of about 90 beats/minute. This is faster than other autorythmic cardiac cells, so the SA node ‘sets the pace’ for the rest of the heart - that is, it is the natural pacemaker. The AV node cells contract autorythmically at about 50 beats/min., but the faster beats coming from the SA node ‘override’ that slower pace. The rest of the conducting fibers beat at about 30 beats/min.
The speed of the SA node can be varied by signals from the nervous and endocrine systems.
SA node generates action potential (AP).
AP travels through atrial walls, spreads to all parts of atria; atria contract (from base downwards to valves)
AP reaches AV node
After a delay (
0.1 seconds) the AV node continues the AP, sending it on:
AP travels from the AV node
AV bundle
branch bundles
purkinje fibers at
300 cm/sec. purkinje fibers pass the AP to regular cardiac muscle cells ventricles contract (from apex upwards to valves)
Everything that happens in the heart, from the end of one heartbeat to the end of the next, is referred to as one cardiac cycle. The basic idea is that both atria relax & contract together, and both ventricles relax & contract together, but the atria and ventricles are slightly out of phase.
Relaxation all chambers relaxed. ventricular cells repolarize, ventricular pressure drops. pressure of blood in arterial system forces semilunar valves closed. when pressure drops enough (below blood pressure in atria [controlled by venous blood flowing into them]), the AV valves open and blood starts to fill the ventricles.
Ventricular filling chambers still relaxed. blood flows into the ventricles from the atria; the SA node beats, depolarizing the atrial cells (P wave). atria contract, forcing additional blood into ventricles
(about 130ml total EDV)
Ventricular contraction atria contracted, ventricles relaxed; impulse from SA passes into AV node, then takes
.1 seconds to travel to the AV bundle. Then ventricles start to contract, pushing up pressure in ventricles; AV valves close; isovolumetric contraction - pressure rises rapidly. when ventricular pressure exceeds aortic pressure (80mmHg) and pulmonary trunk pressure (20mmHg) semilunar valves open, forcing blood into aorta and pulmonary trunk. during all this, the atria relax. then,
the ventricular cells begin repolarization (T) and relaxation, leaving some blood in the ventricles
(about 60ml total ESV)
The whole cycle takes about 0.8 seconds, about half relaxation (diastole) and half contraction
(systole). When the heart rate speeds up, systole remains constant - diastole gets shorter.
[2]
Regulation of stroke volume:
Preload: stretch on heart before contraction; the more cardiac muscle is stretched, the more it contracts —
Frank Starling law — duration of diastole and venous pressure determine preload- as rate increases, diastole is shorter, less preload; increase in venous pressure increases preloadF-S law helps to equalize output of both ventricles; a strong contraction in one ventricle will result in an increase of blood filling the other ventricle, which then contracts more strongly - out put of both sides stays equal
Contractility:
Strength of contraction for a given preload; can be increased by + inotropic agents
(digitalis,epinephrine), decreased by - i. a. (acidosis, anoxia)
Afterload: pressure that must be exceeded to expel blood from ventricle (20 mmHg pulmonary, 80 mmHg aortic [same as diastolic blood pressure]);
Congestive heart failure: pumping becomes less effective, more blood remains in heart at end of systole - eventually, heart muscle becomes overstretched, contracts less forcefully; + feedback; left side = pulmonary edema; right side = peripheral edema
Nervous control
Feedback to brain: proprioceptors , chemoreceptors , baroreceptors monitor peripheral activity & report to brain; also, input from other parts of the brain ( sensory and limbic stimulus);
Output to heart: cardiovascular center in medulla sends signals via cardiac accelerator & vagus nerves:
Cardiac accelerator nerves : sympathetic division of nervous system - nerve endings release norepinephrine onto heart muscle; increase heart rate, strength of contraction
Vagus nerves : - parasympathetic division of NS - nerve endings release acetylcholine; decrease heart rate (but don’t affect strength of contraction much)
Hormonal control
Epinephrine & norepinephrine from the adrenal glands have the same effect as the cardiac accelerator nerves; thyroid hormones also elevate heart rate and strength of contraction.
During early development, the atria and ventricles are not divided in two. Septa develop and separate the chambers about the 8th week. A small opening - the foramen ovale - remains, connecting the atria. This normally closes at birth, leaving a depression, the fossa ovalis .
Hemodynamics
Parts-tunica interna (endothelium, basement membrane, elastic lamina) tunica media (elastic fibers, sm. muscle) (contractility, elasticity) tunica externa (elastic & collagen fibers)
Elastic arteries = more elastic, less muscle; pressure reservoir
Muscular (Distributing) arteries = adjustment of flow to regions of the body
Anastomoses
Arteries may branch together, or with veins directly = alternate routes of flow
Arteries that don’t - end arteries; occlusion = necrosis
Tiny — tunics become thinner & thinner - smooth muscle (t.m.) helps to regulate flow to capillaries
Excxhange = endothelium + basement membrane; no t. m. or t. e. flow regulated by precapillary sphincters
Continuous — the usual (brain = held together by tight junctions)
Fenestrated — pores in endothelium - where diffusion of small particles/ions important
Sinusoids — incomplete, wide, gappy
tunica interna + tunica externa
three layers again - little muscle, mostly elastic CT; often contain valves to ensure proper flow
Sinuses — wide veins without muscle to control diameter (eg; sinuses in brain, coronary sinus)
Veins act as reservoirs of blood; 60% of total; important for diversion to other organs, or in case of hemorrhage
rate of flow inverse of cross-sectional area (4cm
2
/ 40cm/sec : 5000cm
2
/ 0.1cm/sec : 14cm
2
/
15cm/sec)
5.25 l/min: Cardiac output = stroke vol. X heart rate. but in addition, pressure diffs. and resistance affect flow. CO = MABP/R.
Blood Pressure=generated by ventrcular contraction, volume of blood
Resistance increases as blood travels through smaller & smaller vessels - greatest in arterioles.
Resistance depends on 3 things; viscosity (cells [or proteins]/ volume) blood vessel length blood vessel diameter — 1/r
4
SVR Systemic Vascular Resistance = all resistance offered by systemic vessels — since most resistance is in arterioles, major function is to control SVR
5% of blood, but all of exchange, in capillaries. 3 methods:
Diffusion
Vesicular transport — rare (large, polar molecules; antibodies)
Bulk Flow — movement of fluids because of pressure diffs.
At arterial end of caps.: net flow out of blood (filtration)10 mmHg at venous end: net flow back in (reabsorption)9mmHg
1 mmHg lost, retrieved by lymphatic system
Edema — increase in IF — caused by: increased BP due to poor venous return (clots, cardiac fail.) decreased plasma proteins (burns, malnutrition, kidney disease) increased capillary permeability (histamines)
Fluid retention
Blockage of lymph vessels (loss of vessels, filarial worms)
pressure in rt. atrium about 0mmHg, allowing easy flow from veins; if rt AV valve is blocked, then things back up skeletal muscle pump repiratory pump
The body has three mechanisms by which it can regulate blood pressure:
vasoconstriction
vasodilation
antidiuresis (water retention) increase in BP decrease in BP increase in BP
diuresis (water loss through urine) decrease in BP
increase in heart rate & contraction force increase in BP
decrease in heart rate & contraction force decrease in BP
input from cortex, limbic system, hypothalamus (non-feedback) input from baroreceptors in carotid sinus, aorta via CN IX (feedback) input from proprioceptors, chemoreceptors (feedback) out put is via autonomic NS; ennervation to SA, AV, and myocardium output to vagus = decrease heart rate & forceoutput to cardiac accelerator = increase heart rate & forceoutput to blood vessels = dilate/constrict vessels
carotid sinus reflex-(pressure to brain) baroreceptors stim. by stretch
decreased rate, dilation aortic reflex - (systemic pressure) baroreceptors stim. by stretch
decreased rate, dilation atrial reflex - (venous pressure) baroreceptors in rt. atrium: stretch
increased rate, force chemoreceptors monitor CO
2
, O
2
, H
+
; if too little ox. or too much others, sympathetic response
Renin- Angiotensin- Aldosterone: if volume or flow
, kidneys release renin {converts angiotensinogen to} angiotensin
{converted in lungs to angiotensin II, which} 1)vasoconstricts, 2)stimulates aldosterone secretion
(increases Na
+
and H
2
O retention)
Epinephrine - Norepinephrine if volume or flow
, these increase rate & force, vasoconstrict viscera, dilate cardiac & skeletal musc.
Antidiuretic hormone (ADH)
Strong vasoconstrictor - response to hemorrhage
Atrial natriuretic peptide (ANP)
if venous pressure high, vasodilation
Parathyroid hormone (PTH) & calcitriol
PTH - vasodilator; calcitriol - vasoconstrictor
vasodilation or vasoconstriction, depending - most often triggered by O
2
levels in tissues
inadequate cardiac output, such that O
2
delivery is affected.
hypovolemia — loss of plasma (burns, dehydration, diarrhea, kidney disease) or whole blood
(hemorrhage) loss of vasomotor tone — brain damage to medulla, ‘fainting’ (syncope)
Stage I/Compensated/non-progressive shock negative feedbacks attempt to reverse drop in cardiac output - effective if blood loss not more than 15% of total. strong vasoconstriction of less-essential organs activation of RAA system release of ADH local autoregulation - hypoxic cells cause vasodilation
Stage II/Decompensated/Progessive shock above 15% volume loss, feedback mechanisms inadequate. Harmful positive feedbacks now start to appear. Stage II is reversible if caught in time.
When BP drops sufficiently (60 mmHg), blood no longer pumps through coronary arteries; heart becomes hypoxic; reduces contraction, even less pumping loss of BP (40-50 mmHg) at vasomotor center (part of cardiovascular center) of brain; neurons become hypoxic, decrease vasoconstrictor impulses local autoregulation causes greatly increased permeability of capillaries - fluid loss to tissues
decreased cardiac output reduces blood speed in vessels, allowing clots to form.
Obstructions block blood flow, slow blood further, cut off tissues accumulation of acid wastes in cells disrupts cellular metabolism acid by-products (mostly lactic - anaerobic metabolism) cause acidosis throughout system, depressing CNS, inc. vasomotor center.
Stage III/irreversible shock if stage II conditions are not reversed, damage to heart, CNS, liver, kidneys, & the rest becomes fatal.
Systemic; cardiac; pumonary; hepatic portal; fetal
Blood
Transport — of gases, nutrients, waste products
Regulation of body systems — by hormone transport, pH regulation Protection — immune components
Blood trivia - volume: 5 - 6 liters (male) 4 - 5 liters (female)about 7.5% of total body weightpH range of 7.35 -
7.45temperature about 38
C (100.4 F)
Component
Plasma
Water
Proteins
Ions, nutrients, gases, hormones, metabolic intermediates, wastes
Formed elements
Erythrocytes (RBC’s)
Other cells:
Percent of total
55
Primary function
50 Solvent
4
1
45 buffers, osmotic pressure, immune response
(antibodies), clotting agents pH buffers, osmotic pressure, energy, building materials, regulation, metabolism, excretion
43 gas transport
2 immune functions,clot formation
Leukocytes (WBC’s), platelets
Blood cell formation takes place in red bone marrow.
Some cells in marrow are hemopoietic stem cells , or hemocytoblasts these give rise to all blood cells.
These cells then divide and produce 5 other kinds of cells:
Cell type: eventually forms: proerythroblast erythrocyte (RBC) myeloblast granulocytes (neutrophils, eosinophils, basophils) (WBC) monoblast agranulocytes (monocytes) lymphoblast lymphocytes megakaryoblast platelets
anucleate, lack cellular machinery, produce what little ATP they need anaerobically; oxygencarrying, stuffed w/ hemoglobin (33% of weight); 5.4 mill/mm
3
(males), 4.8 million/mm
3
(females) turnover of 2 million per second. hemoglobin ‘carries’ oxygen, releasing it in tissues where concentrations are low. O
2
-carrying part called the heme group ; rest is globin protein. hemoglobin also helps transport CO
2
- about
1/4 of CO
2
is picked up by the globin portion.
a.k.a. erythropoiesis — controlled by kidney cells- response to low O
2
(erythropoietin) erythropoietin stimulates reticulocyte production; reticulocytes mature into erythrocytes in 1 - 2 days. complete procedure takes
4 days.
lacking repair mechanisms, RBC’s wear out in about 110 - 120 days. Macrophages in the liver, spleen, lymph nodes, & red marrow phagocytize the RBC, splitting & releasing heme + globin . heme is split: Fe
3+
is transported back to bone marrow, non- Fe
3+
portion metabolized: biliverdin
bilirubin
yellow, brown pigments released in urine & feces. globin broken down to amino acids, reused.
granulocytes + monocytes — non-specific cellular response; neutrophils 1st, macrophages 2nd, eosinophils 3rd
Granulocytes — ‘granular’ under microscope. all are mobile, usually leave blood vessels after transport to inflamed area myeloblasts form promyelocytes, then differentiate into either: eosinophils — control inflammation, attack multicellular parasites neutrophils — phagocytize foreign objects basophils — promote inflammation, slow clotting
Agranulocytes — less distinct in staining; a mixed bag.
Monocytes — monoblast
monocyte
{leave blood}
macrophage some fixed, some wandering; phagocytotic
Lymphocytes — lymphoblast
lymphocyte (T or B cells, NK cells)
B cells make antibodies; T cells kill other cells -or- coordinate lymphocyte response (more on that later)
Platelets — cell fragments, not whole cells. megakaryoblast
megakaryocyte
metamegakaryocyte
breaks into fragments
high neutrophil bacterial infection, burns, stress, inflammation low neutrophil radiation, drugs, B
12
deficiency, lupus high eosinophil parasites, autoimmune disease, allergic reaction
low eosinophil adrenal gland malfunctions, stress high basophil leukemia, hypothyroidism, allergic reaction low basophil pregnancy, hyperthyroidism, stress high lymphocyte viral infection, autoimmune disease, leukemia low lymphocyte prolonged severe illness, high steroid levels, immunosuppression high monocyte viral, fungal infections, TB, leukemia, chronic disease
stopping blood loss. must be quick, local to region of damage. 3 mechanisms:
immediate, strong contraction of smooth muscle in vessel walls near damage - reduces blood flow through damaged vessel
adhesion (platelets stick to tissues underlying ruptured endothelium; platelets become activated , then)
release (of the chemicals within platelets; these cause further activation, local vasoconstriction, and make the platelets sticky)
aggregation (platelets stick together, blocking rupture)
blood is a very reactive liquid - if disturbed, it tends to solidify & form clots. complex cascade reaction; once blood comes into contact with certain (most) substances, coag. is initiated — results in deposition of insoluble protein fibers prothrombinase {converts}
prothrombin {into}
thrombin {converts}
fibrinogen {into}
fibrin {inhibits thrombin} lack of certain factors results in hemophilia after clot formation, it retracts, pulling edges of vessel together
eventually, clot is dissoved
(fibrinolysis) by enzymes incorporated into the clot
surfaces of RBC’s contain a variety of molecules that act as antigens : something that the immune system can make antibodies against. ABO system best known, other kinds of antigens exist as well.
Blood type: A B AB O
RBC antigens: antigen A antigen B antigens A & B none
Plasma antibodies anti-B anti-A none anti-A, anti-B
Rh factor:
RBC with the antigen are Rh
+
, those without are Rh
-
plasma does not contain anti-Rh antibodies unless there is sensitization hemolytic disease newborn (HDN) - Rh- mother carries Rh+ fetus - fetal blood leaks to maternal, mother makes antibodies. if further fetuses are Rh+, maternal antibodies can attack fetal blood cells
anemia - iron deficiency, pernicious, hemorrhagic, hemolytic, sickle-cell, thalassemia polycythemia, leukemia
Lymphatic System
An ‘accessory’ circulatory system, consisting of closed-ended tubules, carrying lymph (basically just interstitial fluid) from the body tissues to the cardiovascular system. Functions:
Draining excess interstitial fluid
Transport of dietary lipids
Protection against pathogens
Formation and flow of lymph blood plasma seeps/gets squeezed out of capillary walls, becomes interstitial fluid. bulk flow pushes this into the lymphatics. the walls of lymphatics are effectively 1-way valves, keeping lymph from backflowing into tissues. lymph movement similar to venous flow - dependent on actions of skeletal muscles, helped by valves. lymph pushed from abdomen to thorax.
Lymph capillaries (lymphatics) lymphatics are found just about everywhere, except - CNS, bone marrow, avascular tissues. anchoring filaments help hold lymphatics in place among tissue cells.
Special types:each villus of the intestines has a single lymphatic ( lacteal ) running down its axis.
These pick up lipids from digested food and carry it to the bloodstream (milky
‘lacteal’)
lymph capillaries converge to become vessels, which enter groups of lymph nodes. leaving the nodes, the vessels converge to become lymphatic trunks; these converge into 2-
Lymph ducts thoracic duct - starts at cisterna chyli, runs superiorly and eventually drains into the left subclavian vein. drains most of body right lymphatic duct - much smaller, collects lymph from rt. side of body superior to diaphragm
Lymph nodes
1mm to 1 in. in diameter - scattered throughout the body, but concentrated in the groin, axillae, viscera, neck. act as ‘filtering’ sites for lymph - screen out pathogens/foreign cells.
Anatomy outer capsule (DICT) extends supporting trabeculae into center; lots of reticular tissue internally. internal cells organized as cortex (containing follicles , regions of packed lymphocytes [T-cells,
B-cells] & macrophages) and medulla (lymphocytes & macrophages arranged as cords); sinuses allow flow of lymph through the node.
Function lymph flows through in 1 direction only. as it does, the reticular fibers act to filter out objects present in lymph. if foreigh / pathogenic, lymphocytes & macropahges take care of them. also, the presence of these objects in the node can cause T & B cells to set off immune responses throughout the body (antibodies, ex.)
Lymph nodules not surrounded by capsule, generally small, scattered through mucous membranes (mucosaassociated lymphoid tissue - MALT) occasionally these form aggregations - tonsils, peyer’s patches
Thymus gland site of most T-cell production (hence name) - mainly important as a childhood organ, atrophies after puberty.
much T-cell maturation takes place early in life
Spleen aside from its role breaking down RBC’s, spleen also is a site of B-cell proliferation- some macrophages (& phagocytosis) occur there also
1.
↑ the frontal plane is often called the coronal plane.
2.
↑ We should note that these “average” measurements are derived, as usual, from adult european males.
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This page was last modified on 19 October 2011, at 10:28.
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