Escolar Documentos
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Cultura Documentos
BIOSCIENCE 2
FACULTY OF MEDICINE
UNIVERSITY OF BRAWIJAYA
2008
Printed By: Davin Pratama Cahyadi 0710710036 FKUB PD-A. 2007/ 0818550590
www.brawijaya-fk2007.co.cc (Y!Group Kolega 2007) || davincmail-fkub@yahoo.com.sg
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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PDA. 2007/ 0818550590 Basic Structure and Functions
Bioscience 2 1st Semester 2008
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davincmail-fkub@yahoo.com.sg
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.
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
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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.
II. Describe the History of Anatomy that involves the following name. Galen,
Andreas Vesalius and William Harvey (Carolla).
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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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davincmail-fkub@yahoo.com.sg
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
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
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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
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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
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)
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
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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.
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.
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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.
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
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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.
b. Occupations or habits:
- Risor = laughter
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
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D. Make a schematic picture of the synovial joint with their component
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.
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.
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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
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
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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
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
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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 :
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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
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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.
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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.
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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)
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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
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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)
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
2. Explain how the eyeball can move describe extrinsic muscles of eyeball
(extra-ocular muscles)
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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.
Telencepahalon ( Brain
hemisphere )
Diencephalon (
Thalamus,
epitahalamus,
hypothalamus )
Nervous Cerebrum
System Cerebellum Mesencephalon (
Brainstem )
Metencephalon (
Cerebellum )
Central Myelencaphalon (
Nervous Medulla oblongata )
System
lateralis
Columna / Funiculus
posterior
Columna / Funiculus
anterior
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 .)
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CELLULAR ADAPTATION,
CELL INJURY and CELL DEATH
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.
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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.
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Nature and Severity of Injurious Cellular Response
Stimulus
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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
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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
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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.
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
31. List two patterns of reversible cell injury can be recognized under the light
microscope :
1. Cellular swelling
2. Fatty change / steatosis
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.
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ACUTE AND CHRONIC INFLAMMATION
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.
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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
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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
2.2 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.
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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.
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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.
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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.
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
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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 )
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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 )
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.
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.
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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.
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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
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)
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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.
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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
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
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
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
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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