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MODUL ANSWER

BIOSCIENCE 2

DAVIN PRATAMA CAHYADI


0710710036
PD-A 2007

FACULTY OF MEDICINE
UNIVERSITY OF BRAWIJAYA
2008

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MODUL ANSWERS

BIOSCIENCE 2

Dosen Pembimbing :
dr. Andi Ansharullah, DAAK.
dr. Onggung MH. Napitupulu, DAAK, MKes.
dr. Danik Agustin P, MKes.
Dr. med. dr. Tommy Alfandy Nazwar
dr. Rita Rosita, MKes.
dr. Endang Asmaningsih, MS.
dr. Arliek Rio Julia, MS.
dr. Bambang Soemantri, MKes.
dr. Subandi, DAHK, MKes.
dr. Djoko Santoso, DAHK, MKes.
Prof. Dr. dr. M. Rasjad Indra, MS.
dr. Sudiarto, MS.
dr. Soemardini, MPd.
Dr. dr. Endang Sri Wahyuni, MS.
Dr. dr. Karyono Mintaroem, SpPA. dr. Mudjiwiyono HE, SpPA.
dr. Soebarkah Basuki, SpPA.
dr. Eviana Norahmawati, SpPA.
dr. Supranowo, SpPA.

FACULTY OF MEDICINE
UNIVERSITY OF BRAWIJAYA
2008
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BASIC STRUCTURE AND FUNCTION

A. Introduction
The Medical Faculty of Brawijaya University curriculum is competency based.
Prior to graduation, a student must demonstrate competence in 7 area of
competence as asked by Indonesian Medical Council. To achieve this goal the
contributor of this module have try to integrate all the competence into lecture
material. The student performances are formatively assessed and summative
evaluated by level of mastery in process and material content.

B. Competency. The areas of competence integrated inside this module are.


1.Effective communication.
Competency component: Effective communication with the member of class
room during discussion.
2.Scientific basic of Medical Knowledge.
Competency component: Use concept and principle of anatomy in Public
Health care.
3.Information management.
Competency component: Use information technology to understand body
structure.
4.Self alertness.
Competency component: To developed new knowledge.
5.Ethic and professionalism.
Competency component: Demonstrates professional attitude during
teamwork and discussion.

C. Learning Objective
After finish this lecturer the student should have been able to wraps the general
idea of basic structure and function, as the prior knowledge to continue their
course.

D. Learning Method
Learning process doing by:
a. Active student learning in small group discussion.
b. Mini Lecture
c. Laboratory practical

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E. Learning Procedures
1.Small group discussion.
2.All class divide into small group, each consist of
a. 10 -12 students
b. Chairman
c. Secretary
d. Presenter
3.Each group discussion is facilitating e by a facilitator.
4.Topics of discussion are given to student 1 week prior to discussion.
5.Student self active learning.
6.Group Discussion I
7.Presentation of Group Discussion I.
8.Tutor comment.
9.Student Self active learning
10. Group discussion II
11. Presentation of conclusion.
12. Conclusion result are given to PJMK, and then from PJMK to Module
Contributor to see weather the conclusion have sufficient enough or need to
enriched, through Keynote Speaker
13. The student performance are formatively assessed and summative
evaluated by level of mastery of process and material content
14. Laboratory working will do as enrichment.

F. Learning Objective

1.Introduction 10. The Joint


2.History Of Anatomy 11. Cardiovascular System
3.Anatomical Terminology 12. Respiratory System
4.Development Of Physiology 13. Digestive System
5.Basic Structure And Function 14. Uropoetic System
6.Skeletal System 15. Reproductive System
7.Bones Structure 16. Lymphatic System
8.Growth And Development Of Bone 17. Sense Organ
9.The Muscle 18. Nervous System

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G. Learning Evaluation Process
Evaluation System is based on Brawijaya University Academic Policy whether in
value, quality, burden of value and the calling system
Burden of value
1. A. Theory ( NT ) Examination Mark : 50 %
- Process Mark :
* Discussion Mark : 40 % (given by Facilitator)
* Group Mark : 10%
2. Practicum. (NP) Sigma Practicum Mark : Practicum Frequency
3. Final Mark : (3x NT + 2 x NP) : 5

H. References

Martini, et all, Human Anatomy, 5th ed. Pearson Benjamin Cummins, San
Fransisco.
Gardner, et all, Anatomy a Regional Study of Human Structure, 4th Ed, WB.
Saunders Company.
Snell, Richard S, Clinical anatomy for Medical student, 6th Ed, Lippincotts
William&Wilkins.
Spalteholz, Warner Hand Atlas of Human Anatomy.
Drake, Richard L, et all, 2004, Grays Anatomy For Students. Elsevier Churchill
Livinstone, 2nd Ed.
More, Anthony .et all 2007: Rapid Review Gross and Developmental Anatomy
Mosby, Elsevier 2nd Ed.
Moore, Agur, 2005, Essential Clinical Anatomy, Lippincotts Williams & Wilkins,
3rd Ed.
Guyton, Text Book of Medical physiology.
Junqueira, Luiz Carlos, et all, 2003, Basic Histology, Lange Medical Books
McGraw-Hill.10th Ed.
Copenhaver, Wilfred M, et all,1978, Baileys Textbook of HISTOLOGY,
Williams&Wilkins. 17th Ed.
Chandrasoma, Parakrama, and Taylor, Clive R, 2006, Concise Pathology 3rd Ed,
McGraw Hill Company, New York.
Kumar, Abbas, Fausto, Mitchell, 2008, Robbins Basic Pathology 8th Ed, Elsevier,
New York.

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I. What is Anatomy; describe its definition, and its division.
Word roots : anatome [ Greek ] = to cut = dissecting
Ana = to learn
Tome = to cut
Meaning : Anatomy is the study of the many structures that make up the
body and how those structures relate to each other.
Division :
A. Microscopic Anatomy = Histology (Histos : tissue ; Logos : science), is the
study of human body by using microscope.
B. Macroscopic Anatomy = Gross Anatomy, is division of anatomy that can be
studied without microscope. There are two ways to approach gross anatomy.
C. Regional Anatomy or Topographic Anatomy, where human bodies studied by
regional approach. According to this approach human body can be divides
into many regions as follows.

Region Name Anatomic Name Indonesian Name


Cephalic Cephalon Kepala
Cervicalis Cervicis Leher
Thoracalis Thorax Dada
Brachialis Brachium Lengan atas
Antebrachii Antebrachium Lengan bawah
Manus Manus Tangan
Abdominalis Abdomen Perut
Gluteus Glutea Bokong
Femoralis Femur Tungkai atas
Cruris Crural Tunkai bawah
Pedis Pes Kaki

D. Systematic Anatomy, is the study of different systems i.e.:


1. System integumentum
2. System skeletal
3. System musculorum
4. System nervorum
5. System endocrine
6. System cardiovascular
7. System respiratorius
8. System lymphaticum
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9. System alimentarium
10. System urogenitalis

II. Describe the History of Anatomy that involves the following name. Galen,
Andreas Vesalius and William Harvey (Carolla).

129 -199 : Galen, Greeks Physician.


Perform dissecting on monkeys to explain human anatomy.
Arteries carry blood not air.
Observed that muscle contract in response to stimulus.
Made a hypothesis that nerves systems are sensoris division
and motoris division.

1514-1564 : Andreas Vesalius the Father of Anatomy


Perform dissection on human corp.
Published the first scientific text book of anatomy named
De Fabrica Corporis Humani

1578-1657 : William Harvey.


English physician and anatomist stated that blood is pumped by
the contraction of the heart, circulate throughout the body, and
return to the heart.

III. List the anatomical terminology related to :


A. Body position
1. Anatomical Plane and section
a. Transversal planes = horizontal = cross sectional, is the plane that
perpendicular to the long axis of the body.
b. Frontal plane is the plane that divides the body into anterior and
posterior parts.
c. Sagittal planes is the plane that perpendicular to frontal planes and
divides the body into right and left parts.
d. Median plane is the plane that parallel with the long axis of the body,
and passes through the centre of the body

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2. Anatomical direction
a. Anterior = toward front of the body
b. Posterior = toward back of the body
c. Ventral = belly side
d. Dorsal = back side
e. Superior = above side
f. Inferior = toward the feet
g. Cranial = toward head
h. Caudal = toward the tail
i. Medial = toward the midline
j. Lateral = away from the midline

3. Distance
a. Distal = away from the centre of the body
b. Proximal = toward the centre of the body
c.Superficial = nearer to the surface
d. Profundus = farther from surface

B. Movement/action
a. Flexi = movement to decrease angle between 2 bone
b. Extensi = movement to increase angle between 2 bone
c. Adduksi = movement of the limb away from the midline
d. Abduksi = movement of the limb toward midline
e. Rotasi = movement of the part of the body around its long axis
f. Circumduksi = movement in which distal part of the bone moves in
circular direction while the proximal part remain stable
g. Suppinasi = pivoting movement of fore arm in which radius is rotated
to become parallel to ulna
h. Pronasi = pivoting movement of forearm in which radius rotated
diagonally across ulna
i. Inversi = movement of sole of the foot inward
j. Eversi = movement of sole of foot outward
IV. Describe your knowledge about development of physiology.
A. What is the scope of physiology
Physiology is the study of how living organism work
It includes the study of individual molecule at one end, until study of organism
as well.
From viral physiology to Human physiology
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B. What is the goal of physiology
The goal of physiology is to explain physical and chemical factors that are
responsible for the origin, development, and progression of life.Human being
actually automation process.
Most of the human body activities are beyond his owned conscious control

V. Basic Structures and Functions


A. How many is the basic tissue types? Name all of the basic tissue types
There are four (4) basic tissue types:
1. Epithelial Tissue
2. Connective Tissue
3. Muscle Tissue
4. Nervous Tissue

B. List the classification of epithelial tissue, based on the number of cell layers
1. Simple Epithelium; consist of one layer of cells
2. Pseudo Complex (Pseudostratified) Epithelium; one layer but look like
more than one layer
3. Stratified Epithelium; more than one layer.

C. List the shape of epithelial cells, and compare location of their nucleus
1. Squamous form, the nucleus is oval, placed in the widest area of the cell
2. Cuboidal form, the nucleus is rounded, placed in the center of the cell
3. Columnar form, the nucleus is oval, placed close to the basal region

D. What is the definition and function of the epithelial tissue?


Epithelial tissue is a tissue that consist of epithelial cells (with no intercellular
substance) and rest on a basalis membrane
Functions:
1. Covering and lining surfaces (inside or outside) of organs
2. As glands

E. What is the definition and function of the endothelium?


Endothelium is a simple squamous cells layer that lining the vascular lumen
(artery and vein), and the heart chambers (atrium and ventricle)

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F. Name types of junctions found between epithelial cells
1. Epithelial cells to one another = junctional complex
2. Tight junction = zonula occludens
3. Gap junction = nexus
4. Desmosome = macula adherens
5. Epithelial cell with basalis membrane = hemidesmosome

G. Describe the histogenesis of glands


1. Glands arise from the invagination of epithelial cells to subjacent tissue
2. When there are excretion ducts ( ductus excretorius ), it become an
exocrine glands
3. When there is no excretion duct, it become an endocrine gland (ductless
gland) there are capillaries around to pick up and transport the
secretion product to the organ target

H. Explain the classification of the glands


1. Based on the numbers of cells
a. Unicellular glands : Goblet cell
b. Multicellular glands : Most of glands are multicellular
2. Based on the existence of ducts
a. Exocrine glands
b. Endocrine glands
3. Based on the secretory products
a. Serous glands have watery product
b. Mucous glands form thick secretion (mucus)
c. Complex glands :
seromucous, predominantly mucous

mucoserous, predominantly serous

4. Based on secreting mechanism (mode of secretion)


a. Apocrine : The apex region of cells is shed, follows with the secret.
Example : Mammary glands
b. Holocrine : All part of cells are shed as secret. Example :
cebaceous glands and tarsalis glands
c. Merocrine : Secretory product exits cell without broke the
cytoplasm. Example : Salivary glands and pancreas
d. Cytogenous : glands that shed living cells. Example : Tubulus
seminiferus spermatozoa; ovarium ovum

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I. Name the classification of the multicellular exocrine glands (based on their
structures)
1. Simple glands : tubular, branched tubular, coiled tubular
2. Compound gland : tubuloacinar (tubuloalveolar), branched
tubuloalveolar

J. What is the definition and function of the connective tissue?


Connective tissue is a tissue that consists of various cells and intercellular
substance. Connective tissue can be classified based on its component

Functions:
1. To binds or connect the organs
2. Have rules in wound healing
3. To form scar tissue (excessive process can lead to the keloid)

K. List the intercellular substance.


1. Amorph (no form) = ground substance
2. With form / fibers :
a. collagen
b. elastis
c. reticular

L. List the classification of the connective tissue


1. Embryonic connective tissue :
a. Mesenchymal tissue at the embryo
b. Gelatinous connective tissue. Ex: whartons jelly
2. Adult connective tissue :
a. Loose connective tissue; ex : Subcutaneous tissue
b. Dense connective tissue
h Regular CT; ex : tendon, apponeurose
h Irregular CT; ex : fascia, perichondrium, periosteum
Specialized CT
c. Fat
d. Reticular; ex: lymphatic organs
e. Pigmented; ex: choroids layers in the eye
f. Blood
g. Supporting c.t. :
h Cartilage
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Hyalin; ex. costae,trachea, bronchus, articular surface
Elastis; ex. cuping hidung, daun telinga
Fibrous; ex. discus intervertebralis
h Bones

M. Why the fat is classified as special connective tissue?


Because fat tissue is consist of fat cells without intercellular substance, but
still have connective function (to bound the tissues)

N. List the cells and intercellular substance that compose the connective tissue
1. Loose CT:
a. Moderately viscous intercellular substance, collagen, elastic, and
reticular fibers.
b. Cells : fibrocytes, macrophages, plasma cells, mast cells, fat cells
2. Dense connective tissue
a. Collagen fibers predominate in the intercellular substance
b. Cells : fibrocytes trapped in the collagen fibers.

3. Cartilages
a. Intercellular substance: matrix, collagen, elastic, or reticular fibers.
b. Cells : chondroblast / chondrocytes

4. Bones :
a. Calcium and phosphate deposits in the intercellular substance --> hard
b. Cells : osteocytes, osteoclast

5. Blood
a. Liquid intercelluller
b. Cells : eritrosit, lekosit and trombosit

O. List the classification of muscle types, in terms of motor control and location.
1. Smooth muscle : involuntary control. Ex : GIT and vascular wall
2. Skeletal muscle : voluntary control. Ex : biceps, triceps, deltoideus,
gastrocnemius
3. Heart muscle : involuntary control.

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P. Describe the structural features of smooth muscle
1. Spindle shaped
2. Nucleus : single, ovoid, central
3. Membrane cell = sarcoplasm
4. Cytoplasm = sarcoplasm

Q. Describe the structural features of skeletal muscle


1. Cells : Elongated
2. Nucleus : multiple, oval, peripheral
3. Prominent alternating light-dark bands. (A band: Anisotropic; dark. I-band :
Isotropic; light)

R. List the cells that compose the nerve tissue.


1. Neuron (= nerve cell )
2. Neuroglia (= glial cell)

S. List the classification of nervous system based on macroscopic anatomy.


1. CNS (Central Nervous System): Brain and spinal cord. Consist of Grey
matter & white matter
2. PNS (Peripheral Nervous System): Ganglion and peripheral nerve
3. Special sense organs (ex. Nerve ending : Meissner, vater Paccini, Ruffini,
Krausse, organ Golgi)

T. List the classification of neuron types based on the numbers of


processes. Give the examples
1. Unipolar : single process, find only at embryonal stage
2. Pseudo unipolar : ganglion
3. Bipolar : retina
4. Multipolar : cornu anterior medulla spinalis

U. Describe the morphology of multipolar neurons


1. Star-shape cell
2. Big rounded nucleus, placed in central of the cell.
3. Cytoplasm contains Nissls substance (granular endoplasmic reticulum)
4. Have 2 type of processes :
a. Axon : single, long
b. Dendrite : multiple, short

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V. Draw & show the axons and myelin-sheath of the neuron.
Axon is the only long process of the neuron. Most of axons are sheathed by
the myelin.

W. How does the impulse transmit to the neurons or effectors organs?


Via synapses. The structural component are :
1. Presynaptic membrane
2. Synaptic cleft
3. Post synaptic membrane.
4. Neurotransmitters are released from the presynaptic membrane into the
synaptic cleft.

VI. Skeletal System


A. List the name of bone according to their location.
1. Axial bone
a. Cranium
Neurocranium
h os occipitalis.
h os parietalis.
h os frontalis.
h os temporalis.
h os sphenoidalis.
h os ethmoidalis.

Splanchnocranium/viscerocranium
h os maxillae.
h os zygomaticus.

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h os lacrimalis.
h os nasalis.
h os conchae nasalis inferior.
h os palatina.
h os mandibulae.os vomer.
h ossicula.
h maleus
h incus.
h stapes.
h os hyoid.

B. Columna vertebrae.
h Vertebrae cervicalis.
h Vertebrae thoracalis.
h Vertebrae lumbalis.
h Vertebrae sacralis.
h Vertebrae coccygeus.

C. Thorax.
Os costae
Os sternum

2. Appendiculair bone.
a. Upper limb = Extremitas superior.= Lengan
Cingulum extremitas superior.( Shoulder girdle );
Os.clavicula
Os scapula.
Brachium = Arm = Lengan atas.
os humerus.
Antebrachium = forearm = Lengan bawah.
os ulna.
os radius.

Carpal = pergelangan tangan.


Os naviculare.
os. lunatum.
os. triquetrum
os. pisiformis.
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os. multangulum majus.
os. multangulum minus.
os. capitatum.
os. hamatum.
Os metacarpal.
Os phalanx.

b. Lower limb = Extremitas inferior.= Tungkai


Cingulum extremitas inferior.
Os ilium.
Os pubis.
Os ischii.
Femoris = thigh = tungkai atas.
os femur.
Cruris = Legs = Tungkai
os tibia.
os fibula.
Tarsalia =ankle = pergelangan kaki.
Os calcaneus
Os talus.
Os naviculare.
Os cuneiformis.I,II dan III
Os cuboidea.
os metatarsal.
Os phalanges.

B. List the classification of bones according to their shape.


a. Long bones. Relatively long and slender. They have a diaphyse, two
epiphyse and marrow cavity. E.g. Humerus radius.
b. Short bones. Are boxlike in appearance. Externa surface covered by compact
bone.E.g . os carpalia, and tarsalia.
c. Flat bones, have a thin roughly parallel surface of compact bone. Eg. os
parietale.
d. Irregular bones, have complex shape, with short, flat, notched or ridge
surface. Eg. os shenoidale.

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VII. Learn About Structure Of Bone
A. Explain the composition of bone and the structure of bones according to
organization in the mature bone.
Bones composition :
Cellular parts: osteoblast, osteocyte, and osteoclast
Bone matrix
a. Fibers : Collagen type I
b. Ground substance :
Organic material:
(i) 35% , consist of osteocolagen, glycosaminoglycans
(proteinpolysacharida), chondroitin sulfate, etc.
(ii) Form as a matrix
(iii) Acidophilic stain
Anorganic material
I. Compose 65% of bone weight.
II. Consist of calcium phosphate
III. As cement lies between tissue fibers.

B. Organization of Bone Tissue based on the texture, can be divided as :


1. Spongy/cancellous bone
- consist of slender irregular bone trabeculae, which
anastomose to form a lattice network
- There are some lamellae, that contain lacunae with the
osteocye inside.
2. Dense/compact bone= mature bone
Haversian canals (Canalis Havers) is the centre of the
concentric lamellae
The lamellae run regularly according to vascular
distribution that have role in nutrition source.
Volkmanns canals = nutrient canal; connect the
endosteum surface and the periosteum in the transversal
direction

C. Explain the Heversian system


Sistim Havers = Osteon is system that consist of :
1. Haversian canal as the centre
2. Concentric Lamellae (lamella Havers) with lacunae
3. Osteocytes within lacuna
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D. List the other lamellae of the bone
1. Lamella interstitialis .
2. Lamella circumferential externa = generalisata externa
3. Lamella circumferential interna = generalisata interna .

E. Explain about the Periosteum & Endosteum


1. Periosteum
a. The outer surface of bones.
b. A double layer connective tissue coat
h Periosteums outer : fibrous layer is dense CT
h Periosteums inner : osteogenic layer is looser CT.
2. Endosteum
a. Internal surface of bones, list oh the bone marrow cavity
b. A thinner condensed reticular CT
c. Reticular C.T and blood cell precursors.

VIII. Explain the growth and development of bones


Bone can develop by means of :
- Intramembranous ossification
- Endochondral ossification

Intramembranous ossification (Desmalis ossification)


- occurs within membrane-like mesenchymal condensation (trabeculae)
- the mesenchymal cells diffrentiate into osteoblasts and begin to
synthesize and secrete osteoid, which later becomes mineralized.
- The initial site of bone formation is the primary ossification center
- Osteoblast surround them selves with bone matrix, forming spicules that
eventually fuse into a spongy lattice of primary bone
- Mesenchyme between the spicules participates in bone marrow
development . Only a few human bones form entirely in this way : most
are flat and called membranes bones (ex.Os frontal,mandible and maxilla)

Endochondral ossification
- Involves replacing cartilage with bone and occurs in all except membrane
bones.
- Basic steps :
1. Cartilage model : a hyaline cartilage model
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2. The periosteal bone collar : capillaries penetrate the perichondrium,
and mesenchymal cells on its inner surface become osteoprogenitor
cells. Some differentiate into osteoblasts and secrete bone matrix,
creating primary bone spicules. The spicules eventually fused to form
a thin periosteal bone collar of membran bone around the cartilage
model.
3. Proliferation. Chondrocytes near the collar proliferated rapidly,
forming isogenous group of flattened cells parallel to the bones long
axis
4. Hypertrophy. The chondrocytes hypertrophy rapidly into large,
rounded cells that are not separated by matrix. The result is tubelike
superlacunae filled with columns of hypertrophic chondrocytes
5. Calcification. As hypertrophy progresses the strips of cartilage matrix
between the tubular superlacunae begin to calcified. Thus oxygen,
nutrient, and cellular wasted can no longer diffuse through the
matrix, and hypertrophic chondrocyte die
6. Formation of the primary marrow cavity. Dead cells and part of the
calcified cartilage matrix are removed by chondroclast (resembling
osteoclast). Tunnels at the center of developing bone, created by
chondrcyte proliferation and hypertrophy and enlarged by
chondroclast, become bones primary marrow cavity
7. The periosteal bud is a small cluster of blood vessels and
perivascular tissue from the periosteum that penetrates the primary
marrow cavity
8. Ossification. It reverses to the final steps (i.e. Osteoid) deposition
followed by mineralization.

IX. Muscle
A. Based on the microscopic anatomy structure; what is the classification of muscle
tissue and describe its structural features?
1. Skeletal muscle
a. Cells : Elongated. (So it can be called : fiber)
b. Nucleus : multiple, oval, peripheral
c. Prominent alternating light-dark bands. (A band: Anisotropic; dark.
I-band : Isotropic; light)
2. Smooth muscle
a. Spindle shaped
b. Nucleus : single, ovoid, central.
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c. Membran sel = sarcoplasma ;
d. Sitoplasma = sarcoplasma
3. Heart muscle
a. Cells : long, branched
b. Nucleus : one or two ovoid, central nuclei
c. Have striation as in the skeletal muscle
d. Intercalated disc : dark transverse lines between the muscle fibers

B. Describe the mechanism of muscular contraction!


1. Descript briefly the general mechanism of muscle contraction
A. An action potential travels along a motor nerve to its endings on muscle
fiber
B. At each ending, the nerve secretes a small amount of the neurotransmitter
substance acethylchloline.
C. The acethylcholine acts on a local area of the muscle fiber membrane to
open multiple acethylcholine-gated channels through protein molecules
floating in the membrane.
D. Opening of the acethylcholine-gated channels allows large quantities of
sodium ions to diffuse to the interior of the muscle fiber membrane. This
initiates an action potential at the membrane.
E. The action potential travels along the muscle fiber membrane in the same
way that action potentials travel along nerve fiber membrane.
F. Much of the action potential electricity flow through the center of the
muscle fiber, causing the sarcoplasmic reticulum to release large
quantities of calcium ion that have been stored within.
G. The calcium ions initiate attractive forces between actin and myosin
filaments, causing them to slide alongside each other, which called
contractile process
H. After a fraction of a second, the calcium ions are pumped back into
sarcoplasmic reticulum by a Ca++ membrane pump, and they remain
stored in the reticulum until a new muscle action potential comes along;
this removal of calcium ions from the myofibrils causes the muscle
contraction to caese.

2. Descript briefly sliding filament mechanism of muscle contraction


A. In the relaxed state, the end of the actin filaments extending from two
successive Z disc

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B. In the contracted state, these actin filaments pulled inward among the
myosin filaments, so that their ends overlap one another to their maximum
extent.
C. The Z disc also pulled by the actin filaments up to the ends of myosin
filaments.

3. Descript briefly the energetic of muscle contraction


A. Source of energy of muscle contraction is ATP
B. The ATP is split to form ADP which transfers energy to the contracting
machinery of the muscle fiber.
C. This energy is required to:
- Pumping calcium ions from sarcoplasma to sarcoplasmic reticulum after
the contraction is over
- Pumping sodium and potassium ions through the muscle fiber
membrane to maintain appropriate ionic invironment for propagation of
muscle fiber action potential.

4. Explain briefly the differences between isometric and isotonic contraction


A. It said isometric contraction if the muscle does not shorten during
contraction
B. It said isotonic contraction if the the muscle shorten but the tension remain
constant throughout the contraction

5. Descript briefly about summation, tetanization, and rigor mortis in mechanical


aspect of skeletal muscle
A. Summation means the adding together of individual twitch contraction yo
increase the intensity of overall muscle contraction. It occurs in two ways:
- by increasing the number of motor unit contracting simultaneoustly,
which is called multiple fiber summation, and by increasing the frequency
of contraction, which is called frequency summation and can lead to
tetanization

C. Describe the part of muscles!


1. Venter
2. Caput
3. Cauda
4. Origo
5. Insertio
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D. Describe the name of muscles based on
1. Shaped and location
a. Orbicularis oculi
b. Orbicularis oris
c. Trapezius
d. Deltoid
e. Romboid
2. Origo insertio
First part of name indicates origin
Second part of name indicates insertion:
Iliocostalis muscle
Sternocleidomastoid muscle
3. Stripe of the muscle
a. Rectus (straight) abdominis
b. Transversus abdominis,
c. Superior oblique
4. Relative position
a. Externus (superficialis):
Visible at body surface
b. Internus (profundus):
Deep muscles
c. Extrinsic:
Muscles outside an organ
d. Intrinsic:
Muscles inside an organ
5. Structure
a. Number of tendons:
bi = 2, tri = 3
b. Size
Longus = long
Longissimus = longest
Teres = long and round
Brevis = short
Magnus = large
Major = larger
Maximus = largest
Minor = small
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Minimus = smallest
6. Function
a. Movements:
- Flexor
- Extensor
- Hyperextensor
- Retractor

b. Occupations or habits:
- Risor = laughter

E. Make a schematic respresentation and describe the mechanism of citation


contraction coupling in the skeletal muscle, smooth muscle and heart muscle

X. Joint
A. Define what is joint and what is the synonim for joint.
1. Arthrology Is The Scientific Study Of Arthroses.
2. Arthrose Is The Site Where Rigid Elements Of The Skeleton Meet.
3. Synonym : Articulationes, Juncturae, Joints, Articulation, Junction

B. Describe the classification of joint b ased on the material that binds the
bones together and on the presence or absence of joint cavity
1. Fibrous Joints
2. Cartilaginous Joints(Synchondrosis)
3. Bony Fusion (Synostosis)
4. Synovial Joints

C. Clasified the joint based on their motion.


1. Synarthroses-Immovable Joints (Sutures)
2. Amphiarthroses- Slightly Movable Joints
3. Fibrous Connection)( Intervetebral Discs)
4. Diarthroses-Freely Movable Joints (Synovial)

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D. Make a schematic picture of the synovial joint with their component

E. Describe the structural classification of synovial joint


1. Plane Joints
Articular surfaces are plane and allow only gliding movements
2. Hinge Joints
Cylindrical surface of one joint fits in the trough shape of the other.
Allow movement around 1 axis
3. Pivot Joints
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The rounded end of one bone forms into a ring formed by the other
bone plus a ligament. Movement occurs in 1 axis
4. Condyloid
The egg shaped surface of one bone fits into the concave surface of
the other. allow movement in 2 axis
5. Saddle
Articular surfaces if both bones are concave and convex; biaxial joint
6. Ball and Socket
Spherical head of one bone fits into the socket of the other. Multiaxial
joint

XI. Cardiovascular System


A. What is the organ of cardiovasculair system
1. Heart ( Cor )
2. Artery
3. Capillair
4. Veins

B. Learn about heart and describe its location and its parts.
1. Location
a. Near the anterior chest wall
b. Posterior to the sternum
c. Anterior to the vertebral column (pericardial cavity)
d. Slightly left to midline of bodymediastinum

2. Parts of heart
a. Divided into four sections
b. Each chamber is like a separate room with doors that let
blood in and out
1. Right Atrium
2. Right Ventricle
3. Left Atrium
4. Left Ventricle

3. How many valves we can found inside the heart, named it.
a. Valvula atrioventricularis dextra= vavula tricuspidalis.
b. Valvula semilunaris aortae.
c. Valvula atrioventricularis sinistra.
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d. Valvula semilunaris pulmonum.

4. How the heart receive their blood supply.


a. A.coronaria sinistra.
b. A. coronaria dextra.
c. Sinus coronarius.
d. V. cordis magna.
e. V. cordis media.
f. V. cordis parva.
C. Mention two main functions of cardiovascular system.
To serve the body organ and tissues need in Nutrition and oxygen transport
to organs and tissues Metabolic end products transport from tissues to
excretory organ Hormon and communication mediator transportation
To maintain the internal environment condition for optimal life and function
of cells.
D. Descript the function of each part of cardiovascular system
Heart:
Pumping blood
Arteriy:
To transport the blood under high pressure to the tissues.
Arteriole:
To regulate blood flow to the capillaries.
Capillaries:
To exchange fluid, nutrition, electrolytes and hormones between
blood and interstitial fluid.
Venule:
To transport blood from capillaries to medium vein
Medium and large vein:
To flow back blood for tissues to the heart
Regulated blood reservoir.
E. Descript the blood volume in each part of the cardiovascular system
1. 84 % in systemic circulation:
a. 64 % in veins
b. 13 % in arteries
c. 7 % di arteriole dan kapiler sistemik
16 % in lungs and heart:
2. 7 % in heart
3. 9 % in lungs
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Blood vessel Area (cm2)
Aorta 2,5
Ateri kecil 20
Arteriole 40
Kapiler 2500
Venule 250
Vena kecil 80
Vena cava 8

F. Descript the blood pressure changing through cardiovascular system


The blood pressure and fluctuation are getting decrease while it flows
to periferal vessels. Therefore the blood flow also decreases:
- If in aorta, the blood flow is 33 cm / second
- In capillary vessels the blood flow is 0,3 mm / second
- If the length of capillary is: 0.3 1 mm
Blood will stay in capillary vessels in about 1 3 seconds
The length of time for exchange process between plasma and
interstitial fluid is remarkably short.

G. Arteri.
1. Name the three layers (tunics) that comprise blood vessel walls and the tissues
characteristic of each.
The three lagers (tunics) that comprise blood vessel walls :
1). Tunica Intima
2). Tunica Median (TM)
3) Tunica adventite (TA)

2. Name the four major types of blood capillaries and compare them in term of
diameter and the presence of fenestrae, a continuous basal lamina, and
phagocytotic cells in and around the capillary wall.
The three major types of blood capillaries :
a. Continous Capillaries
b. Fenestrated Capillaries :
c. Sinusoidal Capillaries :

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3. Learn about aorta and what is the name of its branches.

a. Aorta ascendens.
h coronaria sinistra.
h coronaria dextra.

b. Arcus aortae.
h brachiocephalica.
h carotis communis sinistra.
h subclavia sinistra.
h
c. Aorta thoracalis.
h 11 ps a. intercostalis.
h 1 ps a. subcostalis.

4. What is the branch of a. carotis communis.


a. A. Carotis interna
b. A. Carotis externa

5. Named the branche of a. subclavia


a. First part, from its origin to medial border of scalenus
anterior.Branches.
h vertebralis.
h Truncus thyrocervicalis.
h thyroidea inferior.
h cervicalis superficialis
h suprascapularis.
h thoracica interna.

b. Second part, lies behind m. scalenus anterior.


h Branches.
h Truncus costocervicalis.
h intercostalis superior.
h cervicalis profundus.

c. Third part. Extend from lateral border of m. s calenus to the


outer border of costa primum.

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6. Name the branche of aorta descendens.
a. Aorta thoracalis.
11 pasang a. intercostalis.
1 pasang a. subcostalis.
b. Aorta abdominalis.
c. Rami visceralis. Cabang:
B. A. supra renalis media.
C. A. renalisa..
D. A. spermatica interna
d. A. coeliaca.
h Gastrica sinistra
Untuk gaster dan oesophagus bagian bawah.
h Lienalis
Untuk lien
h Hepatica communis
Untuk hepar dan vesica fellea.
e. A. mesenterica superior.
f. A. mesenterica inferior.
g. Rami parietalis.
1. A. phrenica inferior.
2. A. lumbalis I-IV.
3. A. sacralis media

7. Named the branched of A. iliaca interna.


a. Trunkus Anterior.
h Iliolumbalis
h Sacralis lateralis.
h Gluteus medius.

b. Trunkus Posterior.
h A.umbilicalis.
h Vesicalis superior.
h Vesicalis inferior.
h Rectalis media.
h Obturatoria.
h Pudenda interna
h A.glutea inferior
h Uterina
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XII. Respiratory System
A. Named the organ of respiratory system.
a. Nasus = Rhinos = Nose
b. Pharynx
c. Larynx
d. Trachea
e. Pulmo = Lung

B. Learn the anatomi of external nose and explain it.


a. Apex. Is the free tip of the radix nasi ; is the part of the nose that connect
nose with os frontalis.
b. Dorsum nasi : is the part of nose between apex and radix.
c. Nares ; is elliptical orifices at inferior side of the nose .
d. Nares are separated by septum.
e. Ala nasi . Is struktur at lateral side of nares.

C. What nasal cavity


Nasal cavity are the uppermost part of respiratory tract and contains olfactory
receptor. From nares to choane
a. Shaped : wedge shape with superior apex and inferior base.
b. Separated from each other by (septum nasalis) nasal septum.
c. Separated from oral cavity by palatum durum ( hard palate).
d. Separated from cranial cavity by os frontalis , ethmoid and sphenoid.

D. Describe about lateral wall of nasal cavity


Lateral wall characterized by projection of three bones and their mucosa. This
projection is called
h Conchae nasalis superior.
h Conchae nasalis medius.
h Conchae nasalis inferior.

E. Describe about meatus nasi


Meatus nasi is air channel below each conchae nasalis. Conchae devide each
nasal cavity into four air channel i.e.
a. Meatus nasi inferior, between concha nasalis inferior and nasal floor.
b. Meatus nasi media, between inferior and middle conchae.
c. Meatus nasi superior, between the middle and superior conchae.
d. Recessus spheno ethmoidalis between the superior conchae and nasal roof.
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F. Describe about Paranasal Sinus
Paranasal Sinuses : Air spaces around the nose that lighten skull and provide
area of mucous epithelium.
There are 4 sinus paranasalis i.e.
h Sinus (Cellulae) ethmoidalis.
h Sinus (Cellulae) sphenoidalis
h Sinus maxillaris.
h Sinus frontalis

G. How many structure that drained into meatus nasi.


Meatus nasi is the place of drainage of :
h Ductus nasolacrimalis meatus nasi inferior.
h Sinus frontalis. meatus nasi media.
h Cellulae ethmoidalis. meatus nasi superior/media.
h Sinus maxillaris meatus nasi media.( hiatus semilunaris)

H. Describe about pharynx


Pharynx is ...
1. A chamber shared by digestive and respiratory systems
2. Extends from internal nares until entrances to larynx and esophagus
3. Divisions of the Pharynx
A. Nasopharynx
B. Oropharynx
C. Laryngopharynx

I. Describe about Tonsil


Tonsil are collection of lympoid tissues in the mucosa 0f pharynx, which are the
part of the bodys defense system. Tonsil occurs mainly in three areas. i.e
a. Pharyngeal tonsils (adenoid) is in the mid line on the roof of nasopharynx.
b. Palatine Tonsils are on each side of oropharynx between palatoglossus dan
palatopharyngeal arch.
c. Lingual Tonsils on the postrior of radix lingue.

J. Name Cartilago larynges :


a. Cartilago thyroid.
b. Cartilago cricoid.
c. Cartilago arythenoid.
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d. Cartilago corniculata
e. Cartilago cuneiforme
f. Cartilago epiglottis

K. What is division of cavum laryngis


Cavum laryngis devided into.
1. Vestibulum laryngis.
2. Ventriculus laryngis.
3. Cavum infra glottis
h Notes.:Glottis is the area that contains vocal fold and rima glottidis.
h Rima glottidis is the narowest part of the cavum laryngis

L. What is intrinsic ligament of larynx


Intrinsic ligament of larynx, binds all cartilage together.
a. Cricothyroid ligament.( crico vocal membrane, cricothyroid membrane).
h Connect the arch of cricoid cartilage with the thyroid
b. Vocal ligament . Are the upper free margin of this membrane.
h This ligament attached to thyroid cartilage at front and to vocal process of
arythenoid behind.
c. Ventricular (vestibular) ligament. Is the ligament situated above vocal
ligament.

M. What is the goal of respiration


h To provide oxygen to the tissues and to remove corbon dioxide from the
tissues

N. Descript four major functions to achieve these goals


a. Pulmonary ventilation: the inflow and outflow of air bet ween the atmosphere
and the lung alveoli
b. Diffusion of oxygen and corbon dioxide between alveoli and the blood
c. Transport of oxygen and carbon dioxide in the blood and body fluids to and
from the bodys tissue cells
d. Regulation of ventilation in maintaining these functions

O. Explain briefly the mechanism of pulmonary ventilation


a. The lungs can be expanded (inspiration) and contracted (expiration) in two
ways:

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h by downward and upward movement of the diaphragma to lengthen or
shorten the chest cavity
h by elevation and depression of the ribs to increase or decrease the
anteroposterior diameter of the chest cavity
b. The muscles that raise the rib cage are
h M. intercostalis externa ( the most important)
h M. sternocleidomastoideus
h M. serratus anterior
h M. Scalenus
c. The muscles that pull the rib cage downward during expiration are
h M. rectus abdominalis
h M. intercostalis interna

P. Descript about pulmonary volumes and capacities


a. There four pulmonary lung volumes:
h The tidal volume
h The inspiratory reserve volume
h The expiratory reserve volume
h The residual volume
b. There are four pulmonary capacities:
h The inspiratory capacity equal the tidal volume plus the inspiratory
reserve volume
h The functional residual capacity equal the expiratory reserve volume
plus the residual volume
h The vital capacity equal the inspiratory reserve volume plus expiratory
reserve volume

Q. Descript the minute respiratory volume, alveolar ventilation, and dead space
air in pulmonary ventilation
a. The minute repiratoty volume is the total amount of new air moved into
the respiratory passages each minute. It equal to the tidal volume times
the respiratory rate per minute
b. The alveolar ventilation is the rate at which new air reaches the alveoli,
saccus alveolaris, ductus alveolaris, and bronchiole respiratoric
c. The dead space air is the air a person breathes that never reaches the
gas exchange area but simply fill respiratory passage where gas
exchange does not occur, such as the nose, pharynx, and trachea

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R. Descript how oxygen is transported from inspiratory air to the bodys tissue
cells
a. Diffusion of oxygen from alveoli into pulmonary blood
b. Transportation of oxygen to periphersl tissues by combination with
hemoglobin and dissolved in water of the blood
c. Diffusion of oxygen from peripheral capillaries into the tissue cells

S. Descript how carbon dioxide is transported from the tissue cells to the
expiratory air in the lung
a. Diffusion of carbon dioxide from the peripheral tissue cells into capillaries
b. Transportation of carbon dioxide to the lungs as: a dissolved CO2,
combined with hemoglobin, and dissolved HCO3- Diffusion of carbon
dioxide from pulmonary blood into alveoli

XIII. Digestive System


A. Descibe the structure of the Ventrolateral Wall of the Abdominal Cavity
The ventrolateral wall of the abdominal cavity consists of layers,
from the outer most to the deepest layer are :
1. Cutan
2. Subcutan Fascia abdominis superficialis
3. Muscles and its fasciae
a. M. obliquus abdominis externus
b. M. obliquus abdominis internus
c. M. Transversus abdominis
d. M. Rectus abdominis anterior abdominal wall
4. Fascia Transversalis
5. Fascia extraperitonealis inferiorly continuous into fascia of cavum
pelvis , posteriorly it is abundant on the posterior abdominal wall,
especially around the kidneys. It is subdivided into : Fascia
preperitonealis ventral of the body; and Fascia retroperitonealis
dorsal of the body
6. Peritoneum Parietalis

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B. Draw the formation of Rectus Sheath above and below Arcuate line.

C. Draw a sagittal view of the Abdominal Cavity then clearly put the proper
number of the Peritoneum and its derivatives listed below. How many
peritoneal layers forming the saccus major and the saccus minor

?
1. Peritoneum parietalis
2. Saccus major
3. Saccus minor ( bursa omentalis )
4. Framen epiploicum Winslowi.

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D. Describe the General structural of sistema digestivus :

E. Named the layers of digestive tract


1. Each organs wall of tractus digestive has four concentric layers:
mucosa, submucosa, muscularis externa and serosa or
adventitia.
2. Mucosa : This layer borders the lumen and has three part. The
epithelium derives from endoderm throughout the tract, except in
the oral cavity and anal canal, where it derives from invaginating
ectoderm. The epithelium is stratified squamous in the oral cavity,
oral pharynx, esophagus, and anal canal; it is simple columnar in
the stomach, intestines and rectum. The lamina propria is the
loose connective tissue layer containing blood and lymphatic
vessels beneath the epithelium . The muscularis mucosa is a
thin, smooth muscle layer bordering the submucosa
3. Submucosa. This dense, irregular connective tissue layer
contains blood and lymphatic vessels and the submucosal
(Meissners) plexus of nerve, Some organ are characterized by
glands and lymphoid nodules in this layer

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4. Muscularis externa. This component consists of two layers
(inner circular and outer longitudinal) of smooth muscle
throughout most of the tract. Between them lies the myenteric
(Auerbachs) plexus.. In the upper esophagus, this layer contains
skeletal muscle, which is replaced by smooth muscle in the lower
portion. The stomachs muscularis externa has three layers :
outers longitudinal, middle circular, and inner oblique. The colons
outer longitudinal layer is gathered into three bands called the
teniae coli. Smooth and skeletal muscles encircling the anal canal
form involuntary and voluntary sphincters, respectively.
5. Serosa and adventitia. The tracts outer covering differs
according to location. The esophagus and rectum are surrounded
and held in place by connective tissue adventitia similar to that
around blood vessels. Intraperitoneal organs (stomach, jejenum,
ileum, transverse and sigmoid colon) are suspended by
mesenteries and covered by a serosa (ie, a thin layer of loose
connective tissue covered by simple squamous epithelium, or
mesothelium). Retroperitoneal organs (duodenum, ascending and
descending colon) are bound to the posterior abdominal wall by
adventitia and are covered on their anterior surfaces by serosa.
Functional structure :
The primary function of digestive tract occurs mainly in the
intestines, the small intestines absorb nutrients, and the large
intestines absorb water. To maximize the absorbtive surface
the small intestines lining has multiple permanent folds
including vili and plicae circulares. Intestine are lined by
absorptive cell (enterocytes) whose apical microvilli further
increase the surface area.

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Draw a scheme of derivatives of developing Gut to allow you
understand the region, blood supply, and the adult derivative of the Gut

REGION BLOOD SUPPLY ADULT DERIVATIVE

Liver parenchyma, Pancreas,


Foregut A. coeliacus
Gaster, First part of duodenum,
half of second part of duodenum

Second part of duodenum , thir


and fourth part duodenum ,
A. mesenterica
Midgut jejunum, ileum , cecum ,
cranialis
appendix vermiformis, ascending
colon , 2/3 proximal of colon
transversum

1/3 distal of colon transversum ,


A. mesenterica
Hindgut colon descendens, colon
caudalis
sigmoid, rectum, upper anal
canal

F. Draw a scheme representing the comparison of structures of the small


and of the large intestines.
Taenia ( libera, meso
Muscularis colica, omentalis )
Intestinum
-- Tenue Intestinum crassum
Haustrae
Caecum, Appendix
Duodenum, Colon : ascendes,
Consists of Jejunum transversus,
Ileum descendens, sigmoid,
rectum
Plica circularis Plica semilunaris
Mucosa
Kerkringi Patchers of Payer
Glandula Brunner
Plexus Auerbach
Submucosa Patches of Peyer
Meissner
(ileum)

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G. Draw a schematic division of the Liver lobes and put the number listed
in the box properly figuring the structures dividing those lobes

1. Ligamentum venosum
2. Ligamentum falciforme hepatis
( Ligamentum teres inside )
3. V.cava caudalis
4. Vesica fellea
5. Porta hepatis

C 5 4
S 1

D
2 Q
3
6.

I. Describe of the liver lobule :


1. The basic structural component of the liver is hepatocyte.
Hepatocyte are polyhedral with 6 or more surfaces, and have
a diameter of 20 30 um.. These epithelial cells are grouped
in interconnected plates.In the light microscope sections,
structural units called liver lobules can be seen. The liver
lobules are separated from each other by a layer of
connective tissue. In some peripheral regions the lobules are
demarcated by connective tissue containing bile ducts,
lymphatic, nerves and blood vessels (a venule a branch of the
portal vein, and an arteriole a branch of the hepatic artery).
These regions the portal spaces , are present at the corners
of the lobules.
2. The hepatocytes in the liver lobule are radially, disposed and
are arranged like the bricks of a wall. These cellular plates are
directed from the periphery of the lobule to its center and
anastomose freely, forming sponge like structure. The space
between these plates contains capillaries, the liver sinusoids.
Sinusoidal capillaries are irregularly dilated vessel composed
of a discontinuous layer of fenestrated capillar.

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3. The endothelial cells are separated from the underlying
hepatocytes by discontinuous basal lamina and a
subendothelial space known as the space of Disse, which
contains microvilli of the hepatocytes. In addition to the
endothelial cells, the sinusoids contain macrophages known
as Kupffer cell. These cells are found on the luminal surface of
the endothelial cells. Their main functions are to metabolize
aged erythrocytes & digest haemoglobin.

4. Blood supply : The liver is unusual in that it receives blood


from 2 sources: 80 % of the blood derives from the portal vein,
which carries ozygen poor, nutrient rich blood from the
abdominal viscera, and 20 % derives from the hepatic artery,
which supplies oxygen rich blood.
5. The arterial and venous blood become mixed in the sinusoids
Than blood flows through sinusoid into central veins.
6. Sinusoidal capillaries are irregularly dilated vessel composed
of a discontinuous layer of fenestrated endothelial cells.
7. The endothelial cells are separated from the underlying
hepatocytes by discontinuous basal lamina and a
subendothelial space known as the space of Disse, which
contains microvilli of the hepatocytes. In addition to the
endothelial cells, the sinusoids contain macrophages known
as Kupffer cell.

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J. What its the main function of digestive tract (Guyton)

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XIV. Urinary System
A. Identify the component of urinary system and their function :
1. Kidneys : Organs that excrete urine
2. Urinary Tract : Organs that eliminate urine
3. Ureters (paired tubes)
4. Urinary bladder (muscular sac)
5. Urethrae (exit tube)

B. Describe the main function of kidney


1. Excretion: removal of organic wastes from body fluids
2. Elimination:discharge of waste products
3. Homeostatic regulation of blood plasma volume and solute
concentration
C. Describe the blood flow through and around nephron
A. Renalis hilus renalis anterior/posterior division a.
segmentalis a. interlobaris a.arcuata a. interlobularis a.
afferen glomerulus a.efferen v.interlobularis v. arcuata v.
interlobaris v. renalis

D. Describe the general Organization of the kidney : The kidneys, which


measure approximately 11x6 cm, are beanshaped, retroperitoneal
organs encapsulated by dense connective tissue and surrounded by

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adipose tissue. Several components can be distinguished without the aid
of a microscope.
a. Renal sinus. The medial concavity of each kidney contains the
renal pelvis, the entering and exiting blood vessels and nerves and
adipose tissue.
b. Hilum. This region comprises the renal sinus and its contents
c. Cortex. This dark-staining outer region underlines the capsule. It
contains the renal corpuscles, proximal and distal convoluted
tubules, peritubular capillaries and medullary rays.
d. Medulla.This light-staining inner region partly surrounds the renal
sinus. It comprise 8 to 18 conical medulary pyramids whose bases
about the cortex and whoses apices (renal papillae) point toward
the renal sinus. It also contains the collecting ducts, loops of Henle
and vasa recta. Each renal papilla, perforated by openings the
collecting ducts, is cradled by a minor calyx into which the ducts
empty. Several minor calyces empty into a major calyx. The major
calyces empty into the renal pelvis, which in turn drains into the
ureter.
e. Renal lobes. Each human kidney has 8 to 18 lobes. Each lobe (a
medullary pyramid and its associated cortex) contains numerous
renal lobules.
f. Renal lobules. Each lobule consist of a central medullary ray and
all of the nephrons emptyng into its collecting tubules. The borders
between adjacent renal lobules are marked by interlobular arteries
and veins.

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E. Describe the Nephrons : Nephrons are the functional subunits of the
kidney. Each includes a renal corpuscle a proximal convoluted tubule,
a loop of Henle and a distal convoluted tubule.

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F. Draw the structure of renal corpuscle

G. Discuss the micturition reflex and its control


The process of urination is coordinated by the micturition reflex, which
is initiated by strech receptors in the bladder wall. Voluntary urination
involves coupling this reflex with the voluntary relaxation of the external
urethral sphincter

h Discuss the hemodialysis process and clinical correlation :


Hemodialysis is a method for removing waste products such as
potassium and urea, as well as free water from the blood when the
kidneys are in renal failure. Hemodialysis is one of three renal
replacement therapies (the other two being renal transplant; peritoneal
dialysis).
The principle of hemodialysis is the same as other methods of dialysis;
it involves diffusion of solutes across a semipermeable membrane.
Hemodialysis utilizes counter current flow, where the dialysate is
flowing in the opposite direction to blood flow in the extracorporeal
circuit. Counter-current flow maintains the concentration gradient
across the membrane at a maximum and increases the efficiency of
the dialysis. Fluid removal (ultrafiltration) is achieved by altering the
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hydrostatic pressure of the dialysate compartment, causing free water
and some dissolved solutes to move across the membrane along a
created pressure gradient.

XV. Reproductive System


A. Identify the component of female reproductive system
1. Ovaries
2. Uterine tubes : Fallopian tubes
3. Uterus
4. Vagina
5. External genitalia
6. Mons Pubis and Labia Majora
7. Labia Minora
8. Clitoris
9. Vestibule
10. Glands

B. Identify the component of female reproductive system


1. External
a. Penis
b. Scrotum
2. Internal
a. Testes
b. Epidydimis
c. Ductus deferens
d. Vesicula seminalis
e. Prostat

C. Describe the function of female reproductive system (Guyton, Ganong)


1. Oogenesis
2. Produce female sex hormones
3. Maintenance pregnancy function

D. Describe the function of male reproductive system (Guyton, Ganong)


1. Spermatogenesis
2. Produce male sex hormones
3. Sexual activities

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XVI. Lymphatic System ( Histologi)
A. List the organs that compose the lymphatic system.
1. Thymus
2. Lymphonodus (lumph nodes)
3. Spleen
4. Tonsila palatina (palatine tonsils)

B. What is the main function of the lymphatic system?


1. Immune system
2. To carry fluid from intercellular compartments to the heart

C. Explain the relationship between edema and lymphatic obstruction!


If there is obstruction in the lymphatic vessels, fluid will go to the
intercellular spaces, which cause an edema.

D. Describe the component of the lymphoid tissue that always found in the
lymphoid organs.
1. Stroma. Made of reticular connective tissue that consist of delicate
reticular fibers and reticular cells.
2. Cells :
1. (predominantly) Lymphocytes
2. Plasma cells
3. Monocytes

XVII. Sense Organ


A. Equilibrium and hearing
1. Describe the process of normal hearing
a. Sound waves enter yhe external acoustic meatus and travel toward the
tympanic membrane.
b. The auditory ossicles transfer these vibration in modified form to the
oval window.
c. Movement of the stapes at the oval window applies pressure to the
perilymph of the vestibular duct. These wave distort the cochlear duct
and the organ of Corti, stimulating the hair cells
d. Hair cells stimulation activates sensory neuron N.VIII auditory
cortex
2. Identify and describe the structure of the ear that have roles in processing
of equilibrium sensation
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The vestibular complex is the part of the inner ear that provides
equilibrium sensations by detecting rotation, gravity and acceleration.
a. The semicircular canal : the anterior, posterior, and lateral duct,
stimulated by the rotation of the head.
b. The utricle and saccule : receptors in the utricle and saccule provides
sensation of gravity and acceleration.
B. Eye
1. Identify the refractory media of the eye
a. cornea
b. Humor aqueous
c. Lensa cristalina
d. Humor vitreus

2. Explain how the eyeball can move describe extrinsic muscles of eyeball
(extra-ocular muscles)

Muscles Function Innervation

Adduction, elevation, medial


M. rectus superior
rotation (interna)

M. rectus medial Adduction


N. occulomotorius
Adduction, depression, (N. III)
M. rectus inferior
lateral rotation (externa)
Abduction, elevation, lateral
M. obliquus inferior
rotation (externa)

M. rectus lateralis Abduction N. abducens (N. VI)

M. obliquus Abduction, depression,


N. trochlearis (N. IV)
superior medial rotation (interna)

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XVIII. Nervous System
A. Describe the main structural division of the Nervous System then make a
frame to put in all the structures of each of the division.

Division Subdivision Structure

Telencepahalon ( Brain
hemisphere )

Diencephalon (
Thalamus,
epitahalamus,
hypothalamus )
Nervous Cerebrum
System Cerebellum Mesencephalon (
Brainstem )

Metencephalon (
Cerebellum )

Central Myelencaphalon (
Nervous Medulla oblongata )
System

Medulla Grey matter :


Spinalis Columna / Funiculus

lateralis
Columna / Funiculus

posterior
Columna / Funiculus

anterior

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davincmail-fkub@yahoo.com.sg Cornu lateralis


Radix posterior
Nervus Olfactorius
Nervus Opticus
Nervus Oculomotorius
Nervus Trochlearis
Nervus Trigeminus
Nervus Abducens
Nervus Facialis
Nervi Cranialis
Nervus
Peripheral Vestibulocochlearis
Nervous Nervus
System Glossopharyngeus
Nervus Vagus
Nervus Accessorius
Nervus Hypoglussus

Nervi spinales Nervi spinales

B. Discuss very briefly with your group member what you know about THE
CENTRAL NERVOUS SYSTEM
1. Central Nervous System consists of the Brain and the Spinal Cord
2. A collection of nerve cell bodies in the CNS is a Nucleus
3. A bundle of nerve fibers (axons) connectig neighboring or distant
nuclei of the CNS is a tract
4. The nerve cell bodies lie within and constitute the Graymatter; the
interconnecting fiber tract systems form the White Matter
5. Three membranous layers : Piamater, Arachnoid mater, Dura mater,
collectively constitute the Meninges.
6. The meninges and the cerebrospinal fluid ( CSF ) surround and
protect the CNS
7. The Piamater is the Innermost of the meningeal layer covering the
outer surface of brain and spinal cord.
8. The CSF is located between piamater and arachnoid mater , in the
subarachnoid space.

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9. External to the pia mater and arachnoidmater is the thick, tough
duramater, which is intimately related to the internal aspect of the
bone of the surrounding neurocranium ( braincase ).
10. The duramater of the spinal cord is separated from the vertebral
column by a fat filled space, the Epidural Space

C. Discuss very briefly with your group member what you know about THE
PERIPHERAL NERVOUS SYSTEM
1. The Peripheral Nervous System is made up of nerve fibers and nerve
cell bodies that connect the CNS with peripheral structures.
2. A collection of nerve cell bodies outside the CNS is a Ganlion. There
are both motor ( autonomic ) and sensory ganglia.
3. Peripheral nerves are either cranial or spinal nerves.
4. All of the 12 pairs of cranial nerves exit the cranial cavity trough
foramina in the cranium
5. All 31 pairs of spinal nerves ( 8 cervical, C ; 12 Thoracic, Th ; 5 lumbar
,L ; 5 sacral, S; and 1 coccygeal , Co ) , arise from the spinal cord and
exit through intervertebral foramina in the vertebral column.

D. Discuss very briefly with your group member what you know about THE
SOMATIC NERVOUS SYSTEM
1. This system is a voluntary nervous system composed of somatic parts
of the CNS and PNS, provides general sensory and motor innervation
to all parts of the body , except the viscera in the body cavities,
smooth muscles, and glands.
2. The somatic ( general ) sensory fibers transmit sensations of touch,
pain, temperature, and position from sensory receptors.
3. The somatic motor fibers permit voluntary and reflexive movement by
causing contraction of skeletal muscles, such as occurs when one
touches a candle flame.

E. Discuss very briefly with your group member what you know about THE
VISCERAL NERVOUS SYSTEM
1. Visceral afferent fibers have important relationships to the ANS both
anatomically and functionally. The sensory input of these fibers, which
provides information about the condition of the bodys internal
environment. This information is integrated in the CNS, often triggering
visceral or somatic reflexes or both.
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2. Visceral reflexes regulate blood pressure and chemistry by altering
such functions as heart and respiratory rates and vascular resistance.

F. Discuss very briefly with your group member what you know about THE
AUTONOMIC NERVOUS SYSTEM
1. The visceral efferent ( motor ) fibers of the Atonomic Nervous System
are accompanied by visceral afferent ( sensory ) fibers
2. The visceral efferent ( motor ) fibers innervate involuntarily ( smooth )
muscle, in the walls of organs and blood vessels, modified cardiac
muscle ( the intrinsic stimulating and conducting tissue of the hert ),
and glands.
3. In their role as the afferent component of autonomic reflexes and in
conducting visceral pain impulses, visceral afferent ( sensory ) fibers
also regulates visceral function.
4. The efferent nerve fibers and ganglia of the ANS are organized into
two systems or divisions : 1) Sympathetic ( thoracolumbar ) division . In
general , the effects of sympathetic stimulation are catabolic., and 2)
Parasympathetic ( craniosacral division ) .In general, the effects of its
stimulation are anabolic ( promoting normal function and conserving
energy .)

G. Explain briefly the mechanism of nerve impuls


1. Explain the mechanism of impuls transmission in nerve and synaps
2. Descript excitabilty Sel/jaringan saraf sebagai sel jaringan peka
rangsang (exitabelity)
3. Descript the mechanism of resting membrane potential and action
potential.
4. Explain the differences between IPSP & EPSP in sinaps
5. Explain the relationsive of nerve and muscle in neuromuscular junction

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CELLULAR ADAPTATION,
CELL INJURY and CELL DEATH

1. What is Pathology? Please describe!


Word roots:
Logos = to study (ilmu / studi)
Pathos = suffering (penderitaan, sakit, abnormal)
Meaning: The study (logos) of suffering (pathos)
- It is bridging discipline involving both basic science and clinical practice
- It is devoted to the study of the structural and functional changes in
cells,tissues
and organs that underlies disease

2. What are the scope of Pathology ?


Pathology covers four aspects of disease process those form the core content of
this discipline:
1. Etiology
2. Pathogenesis
3. Morphologic changes
4. Clinical significance

3. What do you know about the concept of etiologic factors? Describe it!
a. Old concept : 1 etiologic agent for 1 disease
b. New concept : 1 etiologic agent for n diseases
n etiologic agents for 1 disease
The understanding of the primary cause of the disease remains the backbone
of the diagnosis can be made, disease can be understood and the treatment
can be developed.

4. Is there any classification of etiologic factors!


There are two major classes for etiologic factors:
a. intrinsic / genetic
b. acquired / extrinsic : infectious, nutritional, chemical, physical

5. What is the definition of Pathogenesis?

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Pathogenesis refers to the sequence of events as of cells/tissues response to
the etiologic agents invasion, from the initial stimulus to the ultimate expression
of the disease.

6. Describe in short, how etiologic agents may cause clinical significance?


Etiologic agent initial stimulus response of cells / tissues clinical
significance

7. What is the definition of Morphologic Changes?


The Morphologic Changes refer to the structural alterations (shape, size,
consistency, color, content etc) in cells or tissues that clinicians notify them as the
characteristic of the disease, judge the diagnosis of the disease, and recognized
the etiologic factor/process of the disease.
8. Describe how Cellular Responses against Stress and Noxious Stimuli?
When more severe physiologic stresses and pathologic stimuli (plural form of
stimulus) are occurred, it may cause physiologic and morphologic cellular
ADAPTATION. This condition will change the cells/tissue into new steady states
condition. But it is still preserving the viability of the cell and modulating its function
as it responds to such stimuli. It means that in this condition, cells/tissue still own
their reversibility.
If the limits of adaptive response to a stimulus are exceeded, in certain
instance, the cell is exposed to an injurious agent/ stress continuously, cells/tissue
serve process that is loosely termed CELL INJURY. Cell injury is a kind of another
reversible damage. However, it depends on certain condition related to the
stimulus characteristic. If the stimulus persists or is severe enough, the cell will
reach a condition of point of no return and suffer irreversible cell injury and
ultimately CELL DEATH.

9. Draw a scheme representing the kinds of Cellular Responses to injury depends


on the nature and the severity of injurious stimulus !

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Nature and Severity of Injurious Cellular Response
Stimulus

Altered physiologic stimuli Cellular adaptations


Demand , Trophic Stimulation Hyperplasia, hypertrophy
Nutrients , stimulation Atrophyi
Chronik irritation (chemical / Metaplasia
physical)
Reduced O2 supply,chemical injury, Cell injury :
microbial infection. : Acute reversible injury
Acute & self limited Irrebersible injury cell death
Progressive & Severe (including Necrosis
DNA damage Apoptosis
Mild chronic injury Subcellular alterations in various
Organelles
Metabolic alterations, genetic or
acquired Intracellular accumulations,
Prolonged life span with cumulative calcifications
sublethal injury Cellular aging

10. Could you mention the types of cellular adaptation?:


There are four cell adaptation :
a. Hyperplasia
b. Hypertrophy
c. Atrophy
d. Metaplasia

11. What is the definition of hyperplasia?


Hyperplasia is an increasing in the number of cells in an organ or tissue, usually
enlarge the volume of organ and tissue.

12. Are there any types of hyperplasia?


Based on the pathophysiology of hyperplasia, there are two major type of
hyperplasia;
a. Hormonal hyperplasia
b. Compensatory hyperplasia

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13. Explain the mechanism of hyperplasia?:
Hyperplasia is generally caused by increasing local production of growth factor or
increasing the levels of growth factor receptors on the responding cells. It is also
caused by activation of particular intracellular signaling pathways. All of these
changes lead to the production of transcription factors that turn on many cellular
genes, including gene encoding growth factors, receptors for growth factors and
life cycle regulators. The net result of these actions is cellular proliferation.

14. Can you give some examples of Pathologic Hyperplasia based on its type?:
Caused by excessive hormonal stimulation :
Endometrial Hyperplasia
Benign Prostatic Hyperplasia (BPH)
Caused by growth factors stimulation :
Proliferating fibroblasts and blood vessels in wound healing
Viral infections : papilloma viruses skin wart and hyperplastic
epithelium in mucosa

15. What is the definition of hypertrophy?


Hypertrophy refers to the increasing in size of the cells, resulting to the
enlargement of the size of the organ. Note that the hypertrophic organ does not
contain new cells, but it just larger in amount.At this condition, the increasing
size of the cells is not due to cellular swelling, but due to the increasing amount
of structural components/ intracellular matrix and organelles. These organelles
are produced by increasing activity of intracellular synthesis by cells nucleus.

16. What conditions may precede the mechanisms of Hypertrophy? :


a. Hormonal induction: Mammary glands, uterus.
b. Mechanic: workload , stretch: cardiac myocyte, muscles of bodybuilders.

17. What is the definition of atrophy?


Atrophy refers to the shrinkage in the size of the cell caused by the loss of cells
substance. It represents a form of adaptive response that may culminate in cell
death

18. List the types of atrophy!


Atrophy can be categorized as physiologic atrophy and pathologic atrophy (local
or generalized)

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19. Please give some examples of physiologic atrophy!
- Atrophy of thyroglossus duct during early development (embryologic
developmental)
- Uterus decreasing in size shortly after parturition

20. Please mention the cause and examples of pathologic atrophy!:


a. Decreased workload (atrophy of disuse) :
- Immobilized broken limb muscle atrophy
b. Loss of innervation (denervation atrophy)
- Hemiplegi muscle atrophy
c. Diminished blood supply
A decrease in blood supply (ischemia) as a result of arterial occlusive disease
may cause progressive cell loss.
- Brain atrophy
d. Inadequate nutrition :
Marasmus (protein-calorie malnutrition), chronic inflammatory diseases and
cancer use of skeletal muscle as a source of energy cachexia (muscle
wasting)
e. Loss of endocrine stimulation.
Many endocrine glands, such as the breast, and most of reproductive organs
have dependency on other higher endocrine systems stimulation to maintain
the normal metabolism and organs function. After menopause, the
endometrium, vaginal epithelium and breast become atrophy (physiologic).
f. Aging (senile atrophy).
The aging process is associated with cell loss, This process is typically seen
in tissues containing permanent cells, particularly the brain and heart.
g. Pressure :
Tissue compression for any length of time can cause atrophy.
- an enlarging benign tumor can cause diminished of blood supply
- to surrounding tissue, cause ischemia and then become atrophy.
21. Describe the mechanism that may cause organ become atrophy!.
The exact biochemical mechanisms of atrophy are incompletely understood, but
they are likely to affect the balance between protein synthesis and degradation
(by proteolytic enzymes & cytokines, such as TNF), and the increasing of protein
degradation probably plays a key role in atrophy.
Protein degradation may cause degradation of structural components of the
cells
(mitochondria, ER, myofilament), atrophy of the cell
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22. What is the definition of metaplasia?
Metaplasia is a kind of reversible change in which one adult cell type is replaced
by another adult cell type.

23. Describe the mechanism of metaplasia!:


Metaplasia is the result of stem cells reprogramming that are known to exist in
normal tissue, or of undifferentiated mesenchymal cells present in connective
tissue.

24. List some examples and causes of metaplasia!


a.Ciliated columnar epithelial cells of the trachea and bronchi are replaced
by stratified squamous epithelial cells caused by smoke.
b.Columnar secretoric epithelial cells of the salivary gland, pancreas, or bile
ducts
are replaced by nonfunctioning stratified squamous epithelial cells caused by
stone.
c. Squamous epithelial cells of the distal esophagus are replaced by intestinal-like
columnar cells under the influence ofrefluxed gastric acid (Barrett
esophagus).
d.Connective tissue metaplasia is the formation of cartilage, bone or adipose
tissue
in tissues that normally do not contain these elements.
e.g. : myositis ossificans, there is bone formation in muscle occasionally
occurs
i. after bone fracture.

25. Draw a diagram representing result of injurious stimulus to the cell!.

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26. Describe the types and characteristic of cell injury and cell death!
a. Reversible cell injury :
Initially, injury is manifested as functional and morphologic changes that are
reversible if the damaging stimulus is removed.
Hallmarks of reversible injury :
* oxidative phosphorilation
* adenosin triphosphate (ATP)
* cellular swelling : caused by
** changes in ion concentrations
** water influx
b. Irreversible injury & cell death !:
With continuing damage, the injury becomes irreversible, at which time the
cellcannot recover.
e.g. : In ischemic myocardium, there are certain structural changes such as
amorphous densities in mitochondria, and functional changes such as
loss of membrane permeability, these are indicate of cells that have
suffered irreversible injury. Irreversibly injured cells invariably
undergo morphologic changes that recognized as cell death.

27. Describe types of cell death!


There are two types of cell death, necrosis and apoptosis.
They differ in morphologic, mechanisms and role in disease and physiology
Necrosis is always a pathologic process.
Apoptosis serves many normal functions not necessarily associated with cell
injury.

28. Describe the causes of cell injury!


a. Oxygen deprivation (hypoxia).
Hypoxia is a deficiency of oxygen, which causes cell injury by reducing
aerobic oxidative respiration.
One cause of hypoxia is inadequate oxygenation of the blood due to
cardiorespiratory failure.
Less frequent, it is loss of the oxygen-carrying capacity of the blood, as in
anemia, and CO poisoning.
b. Physical agents :
Mechanical trauma
Extremes of temperature (burns or deep cold)
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Sudden changes in atmospheric pressure
Radiation
Electrical shock
c. Chemical agents and drugs :
Glucose / salt in hypertonic concentration
Oxygen in high concentrations
Poisons : arsenic, cyanide, mercury salts
Pollutants, insecticides, herbicides
Industrial hazards : CO, asbestos
Alcohol & narcotic.
d. Infectious agents :
Viruses, rickettsiae, bacteria, fungi, parasites (tapeworms)
e. Immunologic reactions :
Anaphylactic reaction to foreign protein / drug
Autoimmune disease, reactions to endogenous self-antigens
f. Genetic derangements
Trisomy 21 Down syndrome
Sickle cell anemia
g. Nutritional imbalance :
Protein-calorie deficiensies
Vitamins deficiensies
Excesses of lipids : obesity, atherosclerosis
Metabolic disease: diabetes

29. Describe number of principles that are relevant to most forms of cell injury :
a. The cellular response to injurious stimuli depends on the type of injury, its
duration and its severity.
* chemical toxin : doses and duration
* ischemia : severity and duration
b. The consequences of cell injury depend on the type, state, and
adaptability of the injured cell.
* striated muscle cell of the leg muscle cell of the heart
c. Cell injury is resulted from functional and biochemical abnormalities in
one or more of several essential cellular components.
The most important targets of injurious stimuli are:
1. Aerobic respiration involving mitochondrial oxydative
phosphorylation & production of ATP
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2. The integrity of cell membranes, on which the ionic & osmotic
homeostasis of cell & its organelles depends
3. Protein synthesis
4. The cytoskeleton
5. The integrity of the genetic apparatus of the cell

30. List mechanisms of cell injury


* ATP depletion & decrease ATP synthesis
* Mitochondrial damage
* Influx of Intracellular Calcium & loss of Calcium Homeostasis
* Accumulation of Oxygen-derived Free Radicals (Oxidative Stress)
* Defects in Membrane Permeability

31. List two patterns of reversible cell injury can be recognized under the light
microscope :
1. Cellular swelling
2. Fatty change / steatosis

32. Describe synonym, cause, and characteristic of cellular swelling.


Synonym : hydropic change / vacuolar degeneration
Cause : Loss of function of plasma membrane energy-dependent ion
pumps incapable of maintaining ionic and fluid homeostasis.
Characteristic :
- Microscopic : small clear vacuoles within the cytoplasm
- When it affects many cells in organ, may cause pallor, increased
turgor, and increase weight of the organ.

33. Describe definition, affected cells, cause, and microscopic of fatty change /
steatosis
Definition : Fatty change is abnormal accumulations of triglycerides
within parenchymal cells.
Affected cells : Principally encountered in cells involved in & dependent on
metabolism : hepatocyte, myocardial cells.
Causes : Toxins, protein malnutrition, diabetes mellitus, obesity,
anoxia, alcohol abuse.
Microscopic : Small or large vacuoles in the cytoplasm.
To identify the fat : stained with Sudan IV or Oil Red-O

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34. Describe definition of necrosis.
Necrosis refers to a spectrum of morphologic changes that follow cell death in
living tissue, largely resulting from progressive degradative action of enzymes
on the lethally injured cell.

35. Describe morphology of the necrotic cells.


*The morphologic appearance is the result of denaturation of intracellular
protein and enzymatic digestion of the cell.
* Nuclear change : (due to nonspesific breakdown of DNA)
1. Karyolysis : the basophilia of the chromatine may fade, a change
that presumably reflects DNase activity.
2. Pyknosis : characterized by nuclear shrinkage & increased
basophilia (the DNA apparently condenses into a solid, shrunken
basophilic mass).
3. Karyorrhexis : the pyknotic or partially pyknotic nucleus undergoes
fragmentation.
With the passage of time (a day or two), the nucleus in the
necrotic cell totally disappears.
36. Describe types of necrosis.
a. Coagulative necrosis.
Occur if denaturation is the primary pattern.
The process of coagulative necrosis, with preservation of the general tissue
architecture, is characteristic of hypoxic death of cells in all tissues except
brain.
b. Liquefactive necrosis.
In the instance of dominant enzyme digestion.
Characteristic of focal bacterial or, occasionally fungal infections, because
microbes stimulate the accumulation of inflammatory cells.
Liquefaqtion necrosis completely digests the dead cells, so the tissue is
transformed into a liquid viscous mass.
e.g. Necrosis of the brain..
In acute inflammation, the material is frequenly creamy yellow called pus,
because of the presence of white cells.
c. Caseous necrosis.
Distinctive form of coagulative necrosis, encountered most often in foci of
tuberculous infecrtion.
Caseous = cheesy white on gross appearance of the area of necrosis.
d. Gangrenous necrosis.
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Usually applied to a limb, generally on the lower leg, that has lost its blood
supply and has undergone coagulation necrosis. When bacterial infection is
superimposed, coagulative necrosis is modified by liquefactive action of the bacteria
and attracted leucocytes (so-called wet gangrene)

37. What is apoptosis?


Apoptosis is pathway of cell death that is induced by tightly regulated
intracellular pogram in which cells destined to die activate enzymes that
degrade the cells own nuclear DNA and nuclear and cytoplasmic proteins.
The cells plasma membrane remain intact, but its structure is altered, and the
apoptotic cells become an avid target for phagocytosis.
Before its contents have leaked out, the dead cell is rapidly cleared.
So, there are no elicit an inflammatory reaction in the host.

38. Describe examples of apoptosis in physiologic situation.


Death by apoptosis is a normal phenomenon that serves to eliminate cells that
are no longer needed,as, for example, during development, and to maintain a
steady number of various cell populations in tissue, as the following important :
* The programmed destruction of cell during embryogenesis.
* Hormone-dependent involution in adult, such as :
** endometrial cell breakdown during the menstrual cycle,
** ovarian follicular atresia
** regression lactating breast after weaning
** prostatic atrophy after castration
* Cell deletion in proliferating cell populations (to maintain a constant
cell number).
* Death of host cells that have served their purpose
** neutrophils in acute inflammatory response
** lymphocytes at the end of an immune response
* Cell death induced by cytotoxic T cells, a defence mechanism against
viruses and tumors (eliminate virus-infected and neoplastic cells)

39. Describe examples of apoptosis in pathologic conditions.


* Cell death produced by a variety of injurious stimuli :
** radiation, cytotoxic drugs, heat, hypoxia
* Cell injury in certain viral diseases
** Councilman bodies in viral hepatitis
* Pathologic atrophy in parenchymal organs after duct obstruction,
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such as in the pancreas, parotid gland and kidney.
* Cell death in tumors, most frequenly during regression, but also in actively
growing tumors.
40. List the morphology of apoptosis.
* Cell shrinkage
* Chromatin condensation
* Formation of cytoplasmic blebs and apoptotic bodies
* Phagocytosis of apoptotic cells or cell bodies, by macrophage

41. Draw a scheme representing features of necrosis and apoptosis.

Features of Necrosis and Apoptosis


Feature Necrosis Apoptosis
Cell size Enlarge (swelling) Reduced (shrinkage)
Pyknosis karyorrhexis Fragmentation into
Nucleus
karyolysis nucleosome size fragments

Plasma Intact; altered structure,


Disrupted
membrane especially orientation of lipids
Enzymatic digestion; may Intact; may be released in
Cellular contents
leak out of cell apoptotics bodies
Adjacent
Frequent No
inflammation
Often physiologic, means of
Invariably pathologic eliminating unwanted cells;
Physiologic or
(culmination may be pathologic after
pathologic role
of irreversible cell injury) some forms of cell injury,
especially DNA damage

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ACUTE AND CHRONIC INFLAMMATION

Chapter I GENERAL FEATURES OF INFLAMMATION

I.1 What is the definition of inflammation ?


Inflammation is a complex reaction to injurious agents (such as microbes and
physical injury ) that consist of :
1. Vascular response
2. Migration and activation of leucocytes
3. Systemic reactions.

The unique feature of the inflammatory process is the reaction of fluid and
leukocytes in extra vascular tissues.
Inflammation is the local physiological response to tissue injury. It is not in itself
a disease, but it is usually a manifestation of a disease.

I.2 Explain the beneficial effects and harmfull effects of inflammation


Inflammation may have beneficial effects such as :
1. Destruction of Invading microorganism
2. Dilute the injurious agent
3. Wall off the injurious agent with formation of abscess cavity, thus
preventing spread of infection.
4. Sets into motion a series of events that try to heal and reconstitute the
damaged tissue.

Inflammation is a fundamentally a protective response, the ultimate goal of


which is to rid the organism of both the initial cause of cell injury ( e.g.,
microbes, toxin ) and the consequences of such injury ( e.g, necrotic cells and
tissue )
Without inflammation, infection would go unchecked, wounds would never
heal, and injured organs might remain permanent festering sores.
Equally inflammation may produce disease and harmfull, for example :
1. An abscess in the brain would act as a space occupying lesion that
compressing vital surrounding structures
2. Fibrosis resulting from chronic inflammation may distort the tissue and
permanently alter their function :

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For example : intestinal obstruction in intestinal tuberculosis or limited
mobility of joints in rheumatoid arthritis.
3. Inflammatory reaction underlie life threatening hypersensitivity reactions
to insect bites, drugs and toxins.

For this reason, our pharmacies abound with antiinflammatory. drugs, which
ideally would control the harmfull sequelae of inflammation yet not interfere with
its beneficial effects.

I.3 Mention two main component of the inflammatory reaction and tissue
/cells which are involved in this reaction
The inflammatory response consist of two main components:
1. Vascular reaction
2. Cellular reaction
Many tissue and cells are involved in these reactions, including:
1. Fluid and protein of plasma (coagulation factors, complement)
2. Circulating cells (neutrophils, monocytes, eosinophils, lymphocytes,
basophils and platelets)
3. Connective tissue cells (mast cells fibroblast, macrophages and
lympocytes)
4. Extracellular matrix:
a. Structural fibrous proteins (collagen, elastin)
b. Adhesive glycoproteins (filbronectin, laminin, nonfibrillar collagen,
tenascin)
c. Proteoglycan

I.4 Describe two type of inflammation according to its time course


Inflammation usually classified according to its time course as:
1. ACUTE INFLAMMATION
The initial series of tissue reactions to injury
Rapid in onset (seconds or minutes)
Relatively short duration
Lasting for minutes, several hours or few days
Main characteristic:
a. Vascular vasodilatation
b. Exudation of fluid and plasma protein (edema)
c.Emigration of leukocytes, predominantly neutrophils (PMN Cells)

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Outcome maybe resolution, suppuration (e. g. abscess), healing, or
progression to chronic inflammation.

2. CHRONIC INFLAMMATION
The subsequent tissue reactions following the initial response.
Longer duration
Histological characteristics:
a. Presence of lymphocytes , macrophages,and plasma cells (MN
Cells)
b. Proliferation of blood vessels. (Neovascularization)
c. Fibrosis
d. Tissue necrosis

1.5 Describe the nomenclature for the inflamed organ and give some
examples.
Inflammation process is usually described by the suffix itis proceeded by
the name of the organ or tissues involved, thus inflammation of the meningen
is called meningitis, inflammation of the appendix is called appendicitis, and
inflammation of the pancreas is called pancreatitis, etc.

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Chapter II ACUTE INFLAMMATION

2.1 Mention three major characteristics of acute inflammation

Acute inflammation is a rapid response to an injurious agent that serves to


deliver mediators of host defense ( leukocytes and plasma proteins ) to the site
of injury.
Acute inflammation has three major components ( characteristics) :

1. Alterations in vascular caliber that lead to an increase in blood


flow.(Vasodilatation)
2. Structural changes in the microvascular that permit plasma proteins and
leukocytes to leave the circulation.(= increased of permeability), this
process will result EDEMA.
3. Emigration of the leukocytes from the microcirculation, their accumulation in
the focus of injury and their activation to eliminate the offending agent.

2.2 What are the etiology ( stimulus/ triggered factors) of acute inflammation
Acute inflammation reactions are triggered by a variety of stimuli :
1. Physical agents like thermal injury e.g burns or frostbite, radiation; and
physical penetrating trauma e.g blunt and penetrating
2. Chemical agents.
Corrosive chemicals ( acids, alkalis, oxidizing agent ) provoke inflammation
through gross tissue damage.
3. Microbial Infections.
One of the commonest causes of inflammation is microbial infection.
Viruses lead to death of individual cells by intracellular multiplication.
Bacteria release specific exotoxin/endotoxins which are specifically initiate
inflammation. Some organisms cause immunologically mediated
inflammation through hypersensitivity reaction like parasitic infection and
tuberculous inflammation.
4. Immune Reaction / Hypersensitivity reaction
A Hypersensitivity reaction occurs when an altered state of immunological
responsiveness causes an inappropriate or excessive immune reaction
which damages the tissue.
5. Tissue Necrosis.

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Death of tissue from lack of oxygen or nutriens from any cause is a potent
inflammatory stimulus e.g necrosis in acute myocardial infarct, the edge of a
recent infarct often shows an acute inflammatory response.
6. Foreign Bodies
Such as splinters, dirt, sutures.

2.3 Mention five cardinal clinical signs of acute inflammation and explain the
pathogenesis of these signs
Clinically acute inflammation is characterized by 5 cardinal signs :
Rubor ( redness ), calor ( increased heat ), tumor ( swelling ), dolor (pain), and
functiolesa ( loss of function ).
The first four cardinal signs were described by Celsus ( 30 BC 38 AD );
the fifth was later added by Virchow in the nineteenth century.
1. Rubor ( Redness / Erythema )
An acute inflamed tissue appears red, for example skin affected by
sunburn, acute conjunctivitis or cellulitis to bacterial infection. This is due to
dilatation of vascular and increased blood flow to the inflamed area.
2. Calor ( Heat )
Increase in temperature is seen only in peripheral parts of the body, such as
the skin. It is due to increasing of blood flow ( hyperemia ) through the
region, resulting in vascular dilatation and the delivery of warm blood to the
area of injury.
Systemic fever, as a result by the activity of the chemical mediator of
inflammation also contribute to the local temperature.
3 Tumor ( swelling : edema )
Swelling results from edema ( the accumulation of fluid in the extravascular
space as part of the fluid exudate ) and to a much lesser extent, from the
physical mass of inflammation cells that migrating into the area.
4. Dolor ( Pain )
For the patient, pain is one of the best know features of acute inflammation.
It results partly from the stretching. and distortion of tissue due to
inflammatory edema and in particular, from pus under pressure in an
abscess cavity.
Pain is also due to release of chemical mediators including bradykinin, the
prostatglandins and serotonin, that stimulate nerve endings and induce
pain.
* Pain occurs only when there are appropriate Sensory nerve
endings in the inflamed site-for example, acute inflammation of the
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lung ( pneumonia ) does not cause pain unless the inflammation
involves the parietal pleura where there are pain sensitive nerve
endings.
5. Loss of Function.
Movement of an inflammed area is consciously and reflexly inhibited by
pain, while severe swelling may physically immobilise the tissue.

2.4 MORPHOLOGIC AND FUNCTIONAL CHANGES


The two main component of the acute inflammatory response are the vascular (
microcirculatory ) response and the cellular response.

2.4.1 Mention three steps vascular response in acute inflammation :


1. Vasodilatation and stasis.
2. Increased of vascular permeability.
3. Exudation of fluid.
A. Vasodilatation and stasis :
Give explanation about the process of vasodilatation and stasis of the
vascular
The first change in the microcirculatory is transient and insignificant
vasoconstriction of arterioles lasting in a few second which is followed by
marked vasodilation of arterioles , capilaries and venules and opening new
capillary bed . This vasodilatation causes an increased of blood flow in the
area which is the caused of heat and redness ( hyperemia )
Vasodilatation is induced by the action of several mediators, notably
histamine and nitric oxide on vascular smooth muscle. Vasodilation is
quickly followed by increased permeability of the microvasculature with the
out poring of protein rich fluid into the extravascular tissue.
The loss of fluid results in concentration of red cells in small vessel,
and increased viscosity of the blood, this condition will result in STASIS (
presence of dilated small vessels packed with red cells and slower blood
flow )
As stasis develops, leukocytes principally neutrophils, accumulate
along the vascular endothelium (margination) leukocytes then stick to the
endothelium ( pavementing ) and soon after ward they migrate into the
interstitial tissue.

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B. Increased vascular permeability
Explain several mechanisms of increased vascular permeability
Normal fluid exchange and vascular permeability are critically depend
on an intact endothelium.
The mechanisms which make endothelium become leaky in inflammation
are :
1. Formation of endhothelial gaps in venules ( gaps due to endothelial
contraction )
- Most common mechanism of vascular leakage.
- elicited by chemical mediators : histamine, bradykinin, leukotrienes
- Occurs rapidly after exposure to the mediator, reversible, short
lived ( 15- 30 )
- Know as IMMEDIATE TRANSIENT RESPONSE
- Clasically this type of leakage affects venules maybe because
there is a greater density of receptors for the mediators in venular
endothelium.
* Histamine binds to their receptors on endothelial cells and activates
intracellular signaling pathways that lead to phosphorylation of
contractile and cytoskeletal proteins such as myosin. These protein
contract, leading to contraction of the endothelial cells and
separation of intercellular junctions.
2 Direct endothelial injury
- Resulting in endothelial cell necrosis and detachment.
- Due to direct damage to the endhothelium by the injurious stimulus,
as severe burns or lytic bacterial infections, or chemical.
- Starts immediately after injury and sustained at a high level for
several hours until the damage vessels are thrombosed or repaired.
- Long lived ( hours to days )
- known as IMMEDIATE SUSTAINED RESPONSE.
- All level of the microcirculation are affected including venules,
capillaries, and arterioles
3 Delayed Prolonged leakage ( DELAYED RESPONSE )
- Begins after a delay of 2 to 12 hours, lasts for several hours or
even days.
- Involved venules and capillaries
- caused by mild to moderate thermal injury, X radiation or ultraviolet
radiation, and certain bacterial toxins. For example late appearing
sunburn
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- It may result from the direct effect of injurius agent leading to
delayed endothelial damage ( perhaps by apoptosis ) or the effect
of cytokines ( IL-I, TNF, IFN ) causing endothelial retraction.
4 Leukocyte mediated Endothelial injury
- When leukocytes adhere to endhothelium they may be activated
and releasing toxic oxygen species and proteolytic enzymes which
then cause endothelial injury or detachment resulting in increased
permeability
- Mostly venules and pulmonary or glomerular capillaries, where
leucocytes adhere for prolonged periods to the endothelium
5 Increased transcytosis across the endothelial cytoplasm.
Trancytosis occurs across channels consisting of clusters of vesicles
and vacuoles called the vesiculovacuolar organelle located close to
intercellular junctions.
- VEGF vascular Endothelial growth factor causes vascular leakage
by increasing the number of these channels
6 Leakage from new blood vessel formation.
- During repair endothelial cells proliferation and form new blood
vessels ( = ANGIOGENESIS )
- New vessel sprouts remain leaky until the endothelial cells mature
and form intercellular junctions
- Certain factors for angiogenesis ( VEGF ) also increase vascular
permeability.
- Endothelial cells. in foci of angiogenesis have increased density of
receptors for vasoactive mediators including histamine.

C. Exudation of Fluid
1. What is the definition of EXUDATION, EXUDATE, and TRANSUDATE ?
One of the major feature of acute inflammation is EXUDATION ( = increased
passage of fluid out of the microcirculation because of increased of permeability).
An EXUDATE approaches plasma. it is rich in plasma proteins including
immunoglobulins, complement, and fibrinogen.
Exudation should be distinguished from transudation. TRANSUDATION
denotes increased passage of fluid into tissue through vessels of NORMAL
PERMEABILITY. A transudate has a composition similar to ultrafiltrate of plasma.
2. Mention two factors which cause passage of intravascular fuid into
interstitiel ( extravascular tissue)

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The force that cause outward passage of fluid from the microcirculation into the
tissues is:
1. Increased hydrostatic pressure.
2. Decreased plasma colloid osmotic pressure.

In clinical practice, identification of edema fluid as a transudate or an exudates is of


considerable diagnostic value, since it provides clues to the cause of the disorder.

2.4.2. CELLULAR RESPONSE


Acute inflammation is characterized by the active emigration of inflammatory
cells from the blood into the area of injury. Neutrophils (polymorphonuclear
leukocytes) dominate the early phase (first 24 hours). After the first 24-48 hours
phagocytic cells of the macrophage and immunologycally active cells such as
lymphocytes and plasma cells enter area.
Leukocytes ingest offending agents, kill microbes, and get rid of necrotic tissue
and foreign substances .
But neutrophils may induce tissue damage and prolong inflammation since
the leukocytes products that destroy microbes can also injure normal host tissue.

1. What is the meaning of EXTRAVASATION, and mention each steps of the


process
The sequence of events in the journey of leukocytes from the vessel to the
interstitial tissue, called EXTRAVASATION can be divided into the following steps:
1. In the lumen:
- Margination Rolling Adhesion to the endothelium.(Pavementing)
2. Transmigration a cross the endothelium (emigration)
3. Migration in interstitial tissues toward a chemotactic stimulus.

2. Explain briefly about margination process


I MARGINATION OF NEUTROPHILS
In a normal blood vessel, the cellular elements of blood are confined to a
central axial stream, separated from the endothelial surface by a zone of plasma.
In acute inflammation, the rate of blood and the dilated vessels decreases and
the orderly flow of blood is disturbed. Erythrocytes form heavy aggregates (rouleaux)
in a phenomenon termed SLUDGING (STASIS).
As a result leukocytes move to the periphery in contact with the endothelium.
This process of leukocyte accumulation in the peripher is called MARGINATION.

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3. Explain briefly about adhesion process
. ADHESION (PAVEMENTING)
Individual and then rows of leukocytes tumble slowly a long the endothelium
and adherent transiently ( a process called ROLLING), finally coming to rest at some
point where they adhere firmly and the endothelium can be virtually lined by white
cells, an appearance called PAVEMENTING.
Pavementing is a process as a result of increased expression of various cell
Adhesion Molecules (CAMs) on leukocytes and endothelial cells. For example
expression of beta 2 integrins which include leukocyte function antigen-1 (LFA-1) is
enhanced by the action of such chemotactic factors as C5a (Complement
anaphylatoxin) and leukotriene LTB4.
The complementary CAMs on endothelial cells are similarly up regulated by the
actions of interleukin-1 (IL-1) and TNF (Tumor Necrosis Factors). This
complementary CAMs on endothelial cells include ICAM 1, VCAM 1 (from
immunoglobulin family) a ligands of integrin and ELAM-1 (Endothelial leukocyte
adhesion molecule) from selectins group.

4. What is the definition of Emigration


The adherent neutrophils actively leave the blood vessel through intercellular
junctions and pass through the basement membrane to reach the interstitial space
(=EMIGRATION)

5. What is the meaning of CHEMOTAXIS and mention factors that influence


this process
After extravasation, leukocytes emigrate in tissue toward the site of injury by
process called CHEMOTAXIS, defined must simply as locomotion oriented along a
chemical gradient. All granulocytes (neutrophil), monocytes and to a lesser extent,
lymphocytes respond to chemotactic stimuli with varying rates of speed.
The active emigration of neutrophils and the direction in which they move are
governed by CHEMOTACTIC FACTORS (= CHEMOATTRACTANS). Exogenous
and endogenous substances can act as chemotactic factors such as:
A. Endogenous substances:
1. Complement factors C5a and C3a.
2. Products of lipoxygenase pathway mainly Leukotriene B4 (LTB4).
3. Cytokine particularly IL8
B. Exogenous substances:
For example Bacterial products.
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Interaction between neutrophil surface receptors and these chemotaxins
increases neutrophil motility (via an influx of Ca2+ ions which stimulates contraction
of actin) and promotes degranulation.

6. Explain about DIAPEDESIS


Erythrocytes enter an inflamed area passively. Red blood cells are pushed out
of the vessel by hydrostatic pressure through the widened intercellular junctions
behind emigrating leukocytes. This process is called DIAPEDESIS.

7.Explain each steps in PHAGOCYTOSIS process


1. RECOGNITION
- The first step in phagocytosis
- Directly (in large or inert particles) or after OPSONIZATION (agent has been
coated with immunoglobulin or complement factors 3b ((3b)). The coating
agents are called OPSONINS.
2. ENGULFMENT
Once recognized by a neutrophil or macrophage, a foreign particle is engulfed
by the phagocytic cell to form a membrane bound vacuole called a
phagosome. which fuses with lysosomes to form a phagolysosome.
3. MICROBIAL KILLING
When the offending agent is a microorganism, it must be killed before
degradation can occur. There are several factors which effective in killing
microorganism, such as:
1. Hydrogen Peroxide (H2O2)-myeloperoldase-halide system.
This is the most important microbicidal mechanism in neutrophils
whose cytoplasmic granules contain myeloperoxidase. Superoxide is
spontaneously transformed to H2O2 in the lysosome. Myloperoxidase in
combination with halide ion (usually chloride) greathy potentiates the
microbicidal effect of H2O2 probably by forming Highly toxic ions such as
HOCl.
2. Toxic Oxygen-based radicals e. g. superoxide (O2, hydroxyl (OH), and singlet
oxygen are produced in all phagocytic cells.
Reaction of superoxide with ferric ion results in the formation of ferrous ion,
which reacts with hydrogen peroxide to form hydroxyl radicals. Hydroxyl
radicals react with bacterial cell wall phospholipids, causing loss of bacterial
cell membrane integrity (lipid peroxidation)

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3. Bactericidal agents released by neutrophil granules (hydrolases, proteases
(cathepsin G), lactoferrin and lysozyme).
Lysozyme acts by attacking muramic acid linkages in bacterial cell walls.

4. Immunologic Mechanisms
Such as macrophage activating factor, a lymphokine released by sensitized
lymphocytes, assist microbial killing by macrophages.

CHEMICAL MEDIATORS OF ACUTE INFLAMMATION

1. What is Chemical mediators ? Describe several types of chemical mediators


and its main function at the inflammation process.
Chemical mediators is chemical substances that are released from injured
tissue and cause vasodilatation, emigration of neutrophils, chemotaxis and
increased vascular permeability.
Mediators originated from plasma or from cells. Chemical mediators that
released from cells are including:
1. Vasoactive amines (Histamine and serotonin)
2. Arachidomic acid metabolite (prostatglandins, leukotrienes)
3. Neutrophil factors (proteases)
4. Lymphokine/ cytokines.

Plasma derived mediators are including


1. Complement system
2. Kinin system (Bradikinin)
3. Coagulation system
4. Fibrinolytic system

The production of active mediators is triggered by microbial products or by


host proteins, such as the proteins, of the complement kinin, and coagulation
systems that are them selves activated by microbes and damaged tissues.

A. Vasoactive Amines:
Histamine and serotonin are released from mast cells and platelets and can be
identified early in acute inflammation.
Histamine acts mainly on venules that have H1 histamine receptors.
Vasoactive amines cause VASODILATION and INCREASED PERMEABILITY

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As the main agents responsible for the immediate phase of acute inflammatory
response

B. The Kinin System


Bradykinin is the final product of the kinin system is formed by the action of
kallikrein. Kallikrein is present in its inactive form prekallikrein in plasma and
is activated by activated factor XII (Hageman factor) of the coagulation
cascade
Bradykinin causes INCREASED VASCULAR PERMEABILITY and
STIMULATES PAIN RECEPTORS

C. The Coagulation Cascade


Coagulation cascade leading to product on of fibrin, is also initiated by
Hageman factor. The fibrinopeptides that are also formed in the catabolism of fibrin
(fibrinolysis) also cause INCREASED VASCULAR PERMEABILITY and are
CHEMOTACTIC for neutophils.

D. The Complement System


C5a and C3a which are formed in the activation of complement, cause
INCREASED VASCULAR PERMEABILITY by stimulating release of histamine from
mast cells.
C5a is a powerful CHEMOTACTIC agent for neutrophils and macrophages.
C3b is an important OPSONIN.
C5a activates the lipoxygenase pathway of arachidonic acid metabolism.

E. Arachidonic Acid Metabolities


Arachidonic Acid is a fatty acid found in phospholipids in the cell membranes of
neutrophils, mast cells, monocytes, and other cells.
Release of arachidonic acid by phospholipase initiates a series of complex
reactions that produce:
1. PROSTATGLANDINS
(cause VASODILATATION, INCREASED PERMEABILITY,
CHEMOTAXIS and PAIN)
2. LEUKOTRIENES
Cause CHEMOTAXIS, INCREASED PERMEABILITY

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F. Neutrophil Factors
Proteases and toxic oxygen-based free radicals generated by neutrophil are
believed to cause endothelial damage leading to INCREASED VASCULAR
PERMEABILITY.

G. Lymphokines/ Cytokines
Cytokines are proteins produced by many cell types principally activated
lymphocytes and macrophages but also endothelium, epithelium, and
connective tissue cells.
Cytokines modulate the functions of other cell types.
Two of the major cytokines that mediate inflammation are TNF and IL-1. They
are produced mainly by activated macrophages and TNF- (lymphotoxin) is
produced by activated T lymphocytes.
The secretion of TNF and IL-1 can be stimulated by endotoxin and other
microbial products, immune complexes, physical injury and a variety of
inflammatory stimuli.
Their most important actions in inflammation are their effects on:
1. Endothelium ( leukocyte adherence )
2. Leukocytes ( cytokine secretion ( IL1, IL6 ) )
3. Fibroblast ( proliferation , collagen synthesis )
4. Induction ACUT PHASE REACTION :
FEVER
SLEEP
appetite
acute phase proteins
Hemodynamic effects ( shock )
Neutrophilia ( leukocytosis )

2. Mention chemical mediators which induce vasodilatation, increased


permeability, chemotaxis, opsonin, pain, fever, and acute phase reaction

1. VASODILATATION : Histamine, serotonin, bradykinin, prostatglan


din, nitic oxide.
2. INCREASED PERMEABILITY : Histamine, serotonin, bradykinin, comple
ment 3a and 5a, prostatglandin, leukotrienes
lysosomal protease,oxygen radicals.

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3. CHEMOTAXIS : Complement 5a, prostatglandin, leukotriene
IL1, TNF, bacterial products.
4. OPSONIN : Complement 3b.
5. PAIN : Bradykinin, prostatglandin.
6. FEVER : Endogenous pyrogens, prostatglandin, IL1
TNF.
7 ACUTE PHASE REACTION : IL 1 and TNF
( Fever, increased sleep,decreased
appetite, increased acute phase
proteins, leukocytosis )

2.6.Give some examples of morphologic variants in acute inflammation

All acute inflammatory reactions are characterized by vascular changes and


leukocytes infiltration, but specific cause, or particular tissue and site involved
introduce morphologic variations in the basic pattern.
A. SEROUS INFLAMMATION :
Marked by the outpouring of a thin fluid that is derived from the plasma or the
secretions of mesothelial cells that lining the peritoneal, pleural, and pericardial
cavities ( called effusion )
E.g. : The skin blister resulting from burn or viral infection ( chicken pox), contain
accumulation of serous fluid.

B. FIBRINOUS INFLAMMATION :
Because of severe injury and greater vascular leakage , large molecules ( fibrinogen
) pass the vascular barrier and FIBRIN is formed and deposited in the extracellular
space.Fibrinous inflammation is characteristic inflammation in the lining of body
cavities such as meninges, pericard, and pleura.

C SUPPURATIVE ( PURULENT INFLAMMATION )


Characterized by the production of large amounts of pus or purulent exudates,
consisting of neutrophils, necrotic cells, and edema fluid. A common example of an
acute suppurative inflammation is acute appendicitis.The pus may become walled
off by granulation tissue and fibrous tissue and produce ABSCESS ( collection of
pus in a solid organ ( e.g. ABSCESS OVARIUM).If hollow viscus fills with pus this is
called an EMPYEMA ( e.g empyema of gall bladder ). Accumulation of pus in the
tuba fallopii ( salphynx) is called PYOSALPHINX, and accumulation of pus in the
uterus is called PYOMETRA.
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D. CATARRHAL INFLAMMATION :
When mucus hypersecretion accompanies acute inflammation of mucous
membrane,this condition is described as catarrhal. The common cold is a good
example.

E. MEMBRANOUS INFLAMMATION :
The epithelium of mucosa becomes coated by fibrin, desquamated epithelial cells
and inflammatory cells.E.g. Grey membrane in pharyngitis or laryngitis diphteri due
to corynebacterium diphtheriae.

2.7. Mention systemic clinical signs in acute inflammation


1. Fever / Pyrexia:
Polymorphs and macrophages produce compounds known as endogenous
pyrogens which act on the hypothalamus to set the thermoregulatory
mechanisms at a higher temperature. Release of endogenous pyrogens is
stimulated by phagocytosis, endotoxins and immune complex. Fever is resulted
also by the entry of pyrogens and prostaglandins into the circulation.

2. Changes in the Peripheral White Blood Cell Count


In the pyogenic infection total number of neutrophils in the peripheral blood is
increased (neutrophil leukocytosis). This is due to accelerated release of
neutrophils from bone marrow.
Viral infections tend to produce neutropenia and lymphocytosis
Lymphocytosis also occurs in chronic infection (e.g tuberculosis)
Eosinophilia occurs in allergic condition

3. Changes in Plasma Protein Levels.


The level of certain plasma proteins typically increase when acute inflammation
is present. These acute phase reactant include: C-reactive protein, 1 antitrypsin,
fibrinogen and ceruloplasmin. Increased level of these substances lead to an
increased erythrocyte sedimentation rate, a simple and useful (though non
specific) due to the presence of inflammation.

2.8. What are the sequelae of acute inflammation ?

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The sequelae of acute inflammation depend upon the type of tissue involved and the
amount of tissue destruction, which depend in turn upon the nature of the injurious
agent. There are several possible outcomes:
1. RESOLUTION
- Means the complete restoration of the tissues to normal after acute
inflammation.
- The exudate and cellular debris are liquefied and removed by macrophages
and lymphatyc flow
- The conditions which favour resolution are:
a. Minimal cell death and tissue damage
b. Usually occur in organ/tissue which has regenerative capacity (e.g.
liver)
c. Rapid destruction of the causal agent (e.g. phagocytosis of bacteria)
d. Rapid removal of fluid and debris by good local vascular drainage.
2. REPAIR
When tissue necrosis has occurred before the agent is neutralized, repair
ensues, and dead cells are either replaced by regeneration or repaired by
scar formation.
3. SUPPURATION
- Suppuration is the formation of pus (the liquefied mass of necrotic tissue,
neutrophils and bacteria)
- Usually caused by pyogenic bacteria (staphylococcus aureus, streptococcus
pyogenes, neisseria etc)
- When an area of suppuration becomes walled off, an abscess results.
4. PROGRESSION TO CHRONIC INFLAMATION
When the noxious agent is not neutralized by the acute inflammatory
response the acute inflammation may progress to the chronic stage.

2.9 Describe steps of diagnostic for acute inflammation


- For surface structure (skin, conjunctiva, mouth, etc):Diagnosis of acute
inflammation is made based on local cardinal signs: Tumor, rubor, dolor,
color, functio laesa
- Acute inflammation in internal organs (lung, kidney) may first manifest with
systemic changes such as: Fever, alterations in the blood cell, changes in
plasma proteins
- Occasionally it is necessary to examine:
a. Inflammatory exudate:

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High protein levels, high specific grafidity, presence of acute
inflammatory cells (neutrophils,/ lymphocytes for viral infections)
b. Biopsy and microscopic examination of tissue:
Vascular vasodilatation, edema, neutrophils infiltrate, fibrin
c. Other diagnostic test:
- Microbiologic (culture and gram stained smear)
- Immunologic (serum antibody levels)

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Chapter III Chronic Inflamation

2.1. What is the definition of chronic inflammation ?


Inflammation of prolonged duration (weeks or months) in which active
inflammation, tissue destruction, and attempts at repair are proceeding
simultaneously

2.2. Explain the etiology of chronic inflammation


1. Follow acute inflammation
The commonest variety of acute inflammation is the SUPPURATIF type. If the
pus forms an abscess cavity and drainage is inadequate the abscess will have
developed thick walls composed of granulation and fibrous tissues. Good
examples of such chronic abscesses include: and abscess in the bone (in the
chronic osteomyelitis ).

2. Primary Chronic Inflammation


Chronic inflammatory begins insidiously, as a slow grade often asymptomatic
response without initial phase of acute inflammation, caused by :
A. Persestent infection
(resistance of infective agent to phagocytosis and intracellular killing) e.g.
tuberculosis, leprosy, brucellosis certain viral infection, fungal infection. These
organisms are of low toxicity and evoke an immune reaction called delayed type
hypersensitivity. The inflammatory response sometimes takes a specific pattern
called a GRANULOMATOUS REACTION

B. Prolonged exposure to potentially toxic agents either exogenous or


endogenous
a. endogenous agent: necrotic adipose tissue, bone, uric acid crystals
b. exogenous agent: silica (cause silicosis of the lung), asbestos, suture, implanted
prostheses.
These agents will induce Foreign body reactions.

C. Autoimmune disease
Autoantigens evoke a self perpetuading immune reaction that result in chronic tissue
damage and inflammation:
e.g: - Organ specific disease (Hashimoto Thyroiditis, Chronic gastritis)
- Non organ specific autoimmune disease (Rheumatoid Arthritis)

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D. Specific disease of unknown aetiology e.g. Ulcerative colitis (Chronic
inflammatory bowel disease)

E. Primary granulomatous disease e.g. Crohns disease, sarcoidosis, reactions to


beryllium.

2.3. Describe the microscopic characteristics of chronic inflammation


In contrast to acute inflammation, which is manifested by vascular change,
edema, and predominantly leukocytes infiltration,microscopically Chronic
Inflammation is characterized by:
1. Infiltration with mononuclear cells (macrophages, lymphocytes, and
plasma cells)
2. Tissue destruction (NECROSIS ), induced by the persistent offending
agent or by inflammatory cells.
3. Attempts at healing by connective tissue replacement of damaged
tissue accomplished by:
a. Proliferation of small blood vessels (angiogenesis/ neovascularization)
b. Proliferation of fibroblast (fibrosis)

2.4 Describe the macroscopic features of chronic inflammation.


The commonest appearances of chronic inflammation are
1. Granulomatous inflammation
e.g. Granulomatous inflammation with caseous necrosis in tuberculosis of the
lung
2. Chronic abscess cavity.
e.g. In chronic osteomyelitis
3. Chronic Ulcer
Such as chronic peptic ulcer of the stomach with breach of the mucosa, a
base lined by granulation tissue and with fibrous tissue extending through the
muscle layers of the walls.
4. Fibrosis or thickening of the wall of a hollow viscus organ which may be
become the most prominent feature of the chronic inflammatory reaction.
e.g. Chronic cholecystitis, Crohn disease, chronic appendicitis

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2.4.1 Explain briefly about granulomatous inflammation and describe the
microscopic characteristic of granulomatous inflammation
Granulomatous inflammation is a specific pattern of chronic inflammation,
characterized by focal accumulation of activated macrophages which often
develop an epithelial like (epithelioid) appearance.
Diseases with granulomatous inflammation are : tuberculosis, leprosy,
syphilis, cat scratch disease, sarcoidosis ,lymphogranuloma inguinale,
brucellosis, mycotic infection, berylliosis and reactions of irritant lipids
A granuloma consist of aggregation of macrophages that are transformed
into epithelium like cells (= epithelioid cells) surrounded by a collar of
mononuclear cells (lymphocytes and plasma cells)
Frequently EPITHELIOID CELLS fuse to form GIANT CELLS in the periphery
or center of granuloma.
GIANT CELLS have diameters of 40 to 50 m, large mass of cytoplasm
containing 20 or more small nuclei arranged peripherally ( = LANGHANS
TYPE GIANT CELL ) or haphazardly ( = FOREIGN BODY TYPE GIANT
CELL ).
There are two types of granuloma.
1. FOREIGN BODY GRANULOMAS
Iniciated by relatively inert foreign bodies (eg.sutures)
2. IMMUNE GRANULOMA
Caused by insoluble particles typically microbes that are capable of
inducing a cell mediated immune response. Prototype of the immune
granuloma is tuberculosis, in this disease the granuloma is referred to as a
TUBERCLE and is classically characterized by the presence of central
caseous necrosis.
In immune granuloma macrophages engulf the foreign material and
process and present some of it to appropriate. T lymphocytes. The activated
T cells produce cytokines such as IL-1, IL-2 which activates other T cells,
perpetuating the response, and IFN- which activates macrophages and
transforming them into epithelioid cells and multi nucleated giant cells.

2.4.2 Explain briefly what do you know about ABSCESS


* Abscess is localized collections of purulent inflammatory tissue caused
by suppuration buried in a solid tissue / organ, or a confined space.
* Abscess is produced by deep seeding of pyogenic bacteria into tissue.
* Abscess has a central region that appears as a mass of necrotic
leukocytes and necrotic tissue cells. There is usually a zone of
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preserved neutrophils around this necrotic focus, and outside this
region vascular dilation and fibroblastic proliferation occur. (beginning
of repair).
* Abscess may become walled off and ultimately replaced by connective
tissue.

2.4.3 Explain briefly what do you know about ULCER


* An ulcer is a local defect, or excavation, of the surface of an organ or
tissue that is produced by the shedding ( sloughing ) of inflammatory
necrotic tissue.
* Ulceration can occur only when tissue necrosis and resultant
inflammation exist on or near a surface.
* Ulcers are most commonly encountered in :
1. Inflammatory necrosis of the mucosa of the mouth, stomach,
intestines, or genitourinary tract.
2. Subcutaneous inflammation of the lower extremities in older
person who have circulatory disturbances.
* Best example of ulcer is PEPTIC ULCER of the stomach or du
odenum, in which acute and chronic inflammation coexist.
In the acute stage, there is intense polymorphonuclear infiltration and
vascular dilation in the margins of the defect.
With chronicity, the margins and base of the ulcer develop fibroblastic
proliferation, scarring, and the accumulation of mononuclear cells (
lymphocytes, macrophages, plasma cells )

2.5 Explain diagnosis process in chronic inflammation disease.


Diagnosis of the nature and cause of chronic inflammatory disease is often
difficult, precise diagnosis usually requires recourse to a full range of clinical and
pathologic studies such as :
1. Systemic features
Fever, usually low grade and insidious onset
Peripheral white blood count usually normal, sometimes lymphocytosis,
monocytosis, eosinophilia
Anemia, weight loss
Changes in plasma proteins : elevated levels of plasma immunoglobulin,
increase erythrocyte sedimentation rate

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2. Focal/local features
Necrosis
Fibrosis
Ulceration

3. Laboratory evaluation
a. Biopsy and histopathology examination of lesions:
Infiltration of MN cells
Proliferation of fibroblast
Neovascularization
Necrosis
Granuloma

b. Microbiologic culture
c.Immunologic investigation : e.g serologic markers for antibodies of syphilis,
skin test for TBC.

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Chapter III Healing and Regeneration

1. What does regeneration mean?


Growth of cells and tissues to replace lost structures, such as the growth of an
amputated limb in amphibians

2. What does healing mean?


Is a tissue response (1) to a wound (skin), (2) to inflammatory processes in
internal organs, or (3) to cell necrosis in organs incapable of regeneration

3. What are the differences between regeneration and healing?


Regeneration is growth of cells and tissues to replace lost structures, while
healing is tissue response to wound, inflammatory, and cell necrosis

4. What factors do determine the size of cell populations in adult tissues?


rates of cell proliferation, differentation, and death by apoptosis

5. How many phases are the cell cycle consist of ?,mention what are they !
G1 (presynthetic), S (DNA synthesis), G2 (premiotic), and M ( mitotic) phases.

6. Can you summarize what are the classification of human body tissues
based on their proliferative activity? Give examples for each of them !
continously dividing tissue (labile tissue), quiescent (stable tissue), and non
dividing (permanent tissue)
Labile (surface epithelia : skin, oral cavity, vagina, cervix, lining mucosa of
all the excretory ducts of the glands; columnar epithelium of the GIT and
uterus ; transitional epithelium of the urinary tract, and cells of the bone
marrow and hematopoietic tissues
stable : parenchymal cells of liver, kidneys, and pancreas ; mesenchymal
cells (fibroblast, smooth muscle) ; vascular endothelial cells ; resting
lymphocytes and other leukocytes.
permanent tissue : neurons, cardiac muscle

7. Can you determine the characteristic of stem cells?


their prolonged self renewal activity and by their asymmetric replication
8. Please describe the function of embryonic stem cells?
Stem cells first identified as pluripotent cells in embryos and also present in
many tissues in adult animals and contribute to the maintenance of tissue
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homeostasis
9. Mention the growth factors that play major role in tissue regeneration
and repair!
Epidermal Growth Factor (EGF) and Transforming Growth Factor (TGF- ),
Hepatocyte Growth Factor (HGF), Vascular Endothelial Growth Factor
(VEGF), Platelet-Derived Growth Factor (PDGF), Fibroblast Growth Factor
(FGF), TGF- and related Growth Factors, Cytokines
10. Describe the effects of signaling mechanisms in cell growth!
(1) stimulates the transcription of many genes that were silent in the resting
cells, and (2) regulates the entry of the cells into the cell cycle and their passage
through the cell cycle stages

11. What are the general modes of signaling in wound healing? Give
explanation for each of them!
autocrine, paracrine, and endocrine
a) Cells respond to molecules signal that they secrete, thus establishing
autocrine loop.
Their function are plays role in liver regeneration, proliferation of antigen
stimulated lymphocytes, and the growth of some tumors (effect of
overproduce growth factors and their receptors)
b) Cells type produce the ligand then acts on adjacent target cells that express
the appropriate receptors. Responding cells are in close proximity to the
ligand-producing cell and are generally of a different type.
Its function in tissue repair of wounds healing are common in macrophage
and has its growth effect on fibroblast (adjacent cells)
c)Hormones are sinthesized by cells of endocrine organs and act on target cells
distant from their site of synthesis, being carried by the blood vessel.
Growth factors may also circulate and act at distant sites, as in the cases of
Hepatocyte Growth Factors (HGF) that enhances proliferation epithelial,
endothelial and of hepatocytes cells

12. What is the function of Extracellular Matrix (ECM)?


It is secreted locally and assembles into a network in cells spaces. Forming a
significant proportion of the tissue volume, provides turgor to soft tissue and
minerals that give rigidity to skeletal tissue and as reservoir for growth factors
controlling cell proliferation

13. What groups of macromolecules that often associated, constitute ECM?


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1) Fibrous structural proteins (collagens, elastin), 2) Adhesive glycoproteins, 3)
Proteoglycans and hyaluronic acid (Fig 3-14).

14. Describe healing by 1st intention that follows a series of sequential


steps of healing process!
within 24 hours, neutrophils appears at the margin of incision, moving to fibrin
clot. Spurs of epithelial cells move from wound along the cut margin,
depositing membrane components. Fuse beneath surface scab and produce
thin epithelial layer.
Day 3, neuthrophils replaced by macrophage. Granulation tissue invades
incision and collagen fibers are present. Epithelial cells thicken the epidermal
layer
Day 5, incisional spaces filled granulation tissue. Collagen fibrils become
abundant and begin to bridge the incision. Epidermis recovers and yields a
mature epidermal with surface keratinization
2nd week, continued accumulation of collagen and proliferation of fibroblasts.
Blanching begins, collagen accumulation increased within incisional scar,
accompanied by regression of vascular channels.
1st month, scar is made up of a cellular connective tissue devoid of inflamatory
infiltrate, covered by intact epidermis.

15. Mention the differences between 1st and 2nd intention of healing?
(1) Large tissue defect generates a larger fibrin clot, inflamatory reaction is
more intense,
(2) much larger amounts of granulation tissue are formed
(3) wound contraction which occurs in a large surface wound
(4) scar formation and thinning of the epidermis

16. What do you know about fracture?


Continuity rupture of bone tissue and/or soft bone that frequently caused by
force/trauma.

17. What kinds of fracture do you know?


a. complete/incomplete
b. closed/simple, when the overlying tissue is intact
c. compound, when the fracture site communicates with the skin surfaces
d. comminuted, when the bone is splintered or displaced
e. pathologic fracture, already altered by a disease process
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davincmail-fkub@yahoo.com.sg
18. Describe the stages of fracture healing.
a. immediately after fracture, rupture of blood vessels results in a hematoma,
which fills the fracture gap and surround the area of bone injury, called soft
tissue callus/procallus.
b. Followed by activation of mesenchymal cells in the soft tissue and bone
sorrounding the fracture line, also differentiate in the chondroblast that make
fibrocartilage and hyaline cartilage, forming a network of the bone that called
bony callus.
c. As the callus is the greatest in the concave portion of the fracture site, and
the last stages is remodelling

19. Local and systemic host factors that influence wound healing?
(1) nutrition status (Vit C deficiency)
(2) metabolic status (DM)
(3) circulary status (inadequate blood supply)
(4) hormon (glucocorticoids)
(1, 2, 3, 4 are systemic)
(5) infection
(6) mechanical factors (early motion of wound, compressing blood vessels,
separating the edges of the wound)
(7) foreign bodies (steel, glass, bone)
(8) size, location and type of wound influence healing (poor or rich vascularized)
(5, 6, 7, 8 are local)

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davincmail-fkub@yahoo.com.sg