MIDTERM 1:

• Cell adaptations: definitions and photo recognition

o Atrophy: decrease in cell size, results in reduced tissue mass
 Physiologic.
• Ex: thymus undergoing involution during adolescence,
ovaries uterus and breasts after menopause, bones and
muscles in elderly
 Pathologic. Occurs as result of inadequate stimulation or nutrition.
• Ex: ischemic organs, general cachexia caused by cancer,
denervated muscle
o Hypertrophy: increase in cell size, results in enlarged tissue mass
 Ex: body builders, adaptation of heart due to increase workload
o Hyperplasia: increased number of cells, results in enlarged tissue mass
 Ex: hyperplastic colon, epidermal hyperplasia (psoriasis)
o Metaplasia: one mature cell type is replaced by another mature cell type,
reversible. May progress to dyslplasia if stimulus persists
 Ex: columnar cells of bronchial mucosa when irritated by cigarette
smoke over long period change into stratified epith
o Dysplasia: cells vary in size and shape, large nuclei, increased rate of
mitosis, disordered growth.
 Characterized by changes in tissues resulting from chronic
irritation or infection that may cause a precancerous change
 Ex: cervical dysplasia from abnormal paps (CIN-1 to CIN-3)
o Anaplasia: cells undifferentiated, variable nuclei, numerous mitoses,
associated with malignancy, basis for grading of tumor (well, moderate,
poorly undifferentiated)
 Dyplasia > carcinoma insitu > anaplasia
 Extremely high nuclear/ cytoplasmic ratio 1:1 instead of 1:4 or 1:6
o Neoplasia: new growth, tumor,
 Benign: less serious, don’t spread or become life threatening unless
in brain. Slow growing
 Malignant: cancer, characteristics depend on cell type origin
• Things that cause cell injury: hypoxia, anoxia
o Cell injury: may be induced by numerous pathologic mechanisms and
depending on severity of insult, may be reversible or irreversible
 Hypoxia/ anoxia: reduced or complete lack of oxygen
• Results in cessation of energy production, cell can’t survive
• Depending on length of time w/o oxygen and particular
tissue involved, determines whether injury will be
reversible/ irreversible
• Anoxia: total lack of oxygen, when pt codes, depending on
interval depends if pt will recover
• Hypoxia: decreased level of oxygen, more a chronic
problem. Ex: smoker
 • Brain cells die 4-5 minutes, heart 30 min, kidney several
hrs
 Toxins
• Direct: may be induced by substances known for their
“direct” toxic effect on cells ex: mercury
• Indirect: toxins that must be metabolically activated to injur
cells
o Ex: carbon tetrachloride in cleaning products, when
digested metabolizes to toxic compound
 Microbial agents, including bacteria and viruses: can produce
toxins to damage cells, directly invade the cell and damage it, or
can interrupt cell processes by integrating into the genome
 Genetic and metabolic disturbances: many genetic inborn errors of
interm metabolism and subsequent accumulation of toxic
metabolites in the cells
• Tay sachs disease: genetic deficiency of hexosaminidase A,
gangliosides accumulate in the lysosomes of nerve cells
and eyes. Severe mental retardation and blindness
• Know the signs of neoplasia: pleomorphism, abnormal mitotic figures, etc.
o Pleomorphism: varying in size of total cell and/or nucleus, varying nuclear
and cell contours
o Abnormal mitotic figures
• Carcinoma insitu vs. dysplasia and anaplasia (invasion)
o Dyplasia > carcinoma insitu > anaplasia
• Benign vs malignant neoplasm (picture)
o Benign: limited growth potential, good outcome
 Often encapsulated
o Malignant: grow uncontrollably, may eventually kill the host
 Lack a capsule
 Invading the surrounding tissue by infiltration
• Common suffixes that make it benign vs malignant sarcoma vs. adenoma
o Tumors are named according to the cell type which they resemble the
most, with the addition of the suffix “-oma”
 Adenoma- glandular origin
 Papilloma- squamous
 Cartilage- chondroma
o Malignant tumors of epithelial origin are called “carcinomas”
o The names for the malignant tumors of connective tissue origin are coined
from the root of the cell type and a suffix “sarcoma”
o Not all benign tumors end in “oma”
 Lymphoma, melanomas, astrocytomas, seminomas, blastomas
• Metastatic disease occurs. Some related to abnormal chromosomes
o Process where cells move from one site to another in the body
 o Only malignant tumor cells have this capacity, but not all malignant cells
are capable of causing metastasis (ex: primary brain tumors)
 Spread occurs in 3 ways
• Lymphatics
• Bloodstream
• Direct entension of the primary tumor
• Understand the difference between grading and staging
o Grading: done microscopically, based on the degree of anaplasia
o Shape and irregularity of cells, large numbers of atypical mitoses, nuclear
pleomorphism and tumor giant cells
 Grade I- well differentiated tumors
 Grade II- moderately differentiated
 Grade III- poorly or undifferentiated
o Staging: by clinically assessing the extent of tumor spread based on:
 Examination,
 Radiographic studies
 Biopsy results
 Size of the primary tumor
 Presence or absence of lymph node and distant metastasis

• TNM cancer staging system

o Tumor size, lymph node status, metastasis
• Common carcinogens. Viral words (HPV, Herpes) know the risk factors
o Chemical carcinogens: nitosamine (preserved processed foods), polycyclic
aromatic hydrocarbons (cigarette smoke), aflatoxin B1 (fungus that can
contaminate vegetables, food, etc), aromatic amines (dyes), metals and
inorganics (nickel), anticancer drugs (can themselves cause cancer!)
o Physical carcinogens: radiation
o Human carcinogens: sunlight/ UV radiation, cigarette smoke, viruses,
food, dyes, contact (tar)
• Paraneoplastic syndrome means
o In some patients, cancer produces remote effects that are not
attributable to the tumor invasion
o Caused by substances, such as hormones that are secreted by the tumor
cells, and their inappropriate secretion can cause a variety of symptoms
o Can aid in monitoring for recurrence of the cancer in pts who have had sx
resesection of the tumor or are undergoing chemo or radiation therapy
o Examples:
 Cushing’s: due to ectopic ADH, by a sm cell carcinoma, prostate,
GI tract, or pancreas cancer.
• May produce Na and H2O retention and intoxication,
leading to altered mental status, seizures, coma and even
death
 Hypercalcemia
 • Usually caused by metastatic disease of bone, although
ectopic production of a PTH- like peptide may occur in the
absence of bony metastasis
 Polycythemia
• Renal cell CA
• Erythropoietin
 Venous thrombosis
• Pancreatic CA
• thromboplastin
• Immunoglobins. Major ones. Cross placenta? Related to anaphalaxis?
o IgG:
 Most common in blood
 Produce primary and secondary response
 Activated compliment
 Crosses placenta
 Antibacterial/ anti viral
o IgM
 Binds to B lymphocytes
 Activates compliment
 Large aggregate of antibody
o IgA
 Found in secretions: saliva, breast milk
o IgE
 Binds to mast cells
 Causes release of histamine
 Related to allergens which are antigens
 Part of hypersensitivity (allergic) response
o IgD
 Activates B cells
 Responsible for humoral immunity via production of antibodies
• Hypersensitivity reactions with examples
o Type I
 Allergic reaction provoked by reexposure to a specific antigen,
local or systemic
 Mediated by IgE, histamine
 Response: immediate
 Ex: hay fever, asthma, anaphylaxis, hive
o Type II
 Ab’s bind to pts own cell surface
 Mediated by: IgG, IgM, and complement
 Response: hours to day
 Ex: autoimmune hemolytic anemia, transfusion reaction
o Type III
  Ag+ Ab form immune complexes that get deposited in tissues
(skin, kidney, joints) and start complement rxn of cell lysis
 Mediated by: IgG, IgM
 Response: hours to day
 Ex: rheumatoid arthritis, lupus, glomerulonephritis
o Type IV
 Cell mediated immunity: T cells + Ag presented by macrophages
 Mediated by: T cells
 Response: delayed, 2-3 days
 Ex: contact dermatitis (poison ivy), transplant rejection
• Cytogenetics: basic definitions, aneuploidy, translocation. Matching
o Aneuploidy: if an error occurs in meiosis/mitosis, results in a cell with
chrom complement that is not an exact multiple of 23.
 Usual cause is nondisjunction
o Nondisjunction: failure of chromosomes to separate properly during
meiosis so chromosomes pass into same daughter cell and loss of
chromosomes in other cell,
 Results in trisomy or monosomy
o Translocation: transposition of 2 segments between 2 nonhomologous
chrom
 Balanced: no loss of chromosomes
 Unbalanced: loss of chromosome material
o Robertsonian translocation
 Results when the long arms of two acrocentric chromosomes fuse
at the centromere and the two short arms are lost
o Deletions
 Breakage of chrom, loss of a fragment
o Homozygous: same allele on both of its homologous chrom
o Heterozygoys: organism has two different alleles on it homologous chrom
 The organism has more than one version of a particular gene
• Autosomonal dominant, recessive, x linked recesseive mean. What the offspring
are like. Examples of each. Inherited conditions in slide.
o Autosomal dominant: inheritance of a single copy of a defective gene
found on a non sex-chrom.
 Defective copy is sufficient to over ride the normal functioning
copy resulting in expression
 Ex: familial hypercholesterolemia, Huntington’s disease,
neurofibromatosis, Marfan syndrome
o Autosomal recessive:
 For the disorder to occur, both copies of the gene need to be
defective
 If just a single copy is inherited, the single normal gene is
sufficient to over-ride the defective one and the individual is not
affected by the disorder, but is rather a carrier
  Ex: cystic fibrosis, glycogen storage diseases, sickle cell anemia,
lysosomal storage diseases
o X- linked recessive:
 Defective gene lies on the X sex chrom
 Most common in males as there is no second X chrom carrying the
normal copy to compensate
 Less common in expression in females because of the presence of
the normal X
 Ex: Duchenne muscular dystrophy, Hemophilia A & B, Diabetes
insipidus
• Tri 21, 18, 13. klynefelters, turners. Major features with each.
o Tri 21:
 Correlation with increased maternal age
 Features: mental retardation, simian crease of hand, protruding
tongue, congenital heart defects, flat facial profile, epicanthal
folds, wide spaced toes, gentle shy and loving, hypotonia, ALL and
AML,
o Tri 18:
 Features: mental retardation, rocker bottom feet, ventricular septal
defects, micrognathia (low set ears)
o Tri 13:
 Features: mental retardation, cleft palate, ear/eye deformities,
microcephaly, cleft/lip palates, polydactyly
o Klinefelter’s
 2 or more X chrom and one or more Y chrom (XXY or XXYY)
 Features: long arms/legs, gynecomastia, lack of secondary sex
characteristics, mean IQ somewhat lower than normal,
hypogonadism
o Turner’s
 Complete or partial monosomy of the X chrom
 Features: short stature, webbing of the neck, broad shaped chest
with wide spaced nipples, cubitus valgus, coarctation of aorta,
mental status usually normal
o Cri du Chat
 Deletion of short arm of chrom #5
 Features: growth/mental retardation, microcephaly, short fingers,
characteristic meow like cry, cleft palates, GI defects
• Burns. Rule of nines. Degree of burn. Increased percent increases mortality
o Rule of nines:
 Each arm= 9% (hand to elbow= 4.5%)
 Each leg = 18%
 Ant surface of trunk = 18% (chest = 9%, belly = 9%)
 Post surface of trunk = 18%
 Head = 9 % (face = 4.5%)
  Groin = 1%
• TOTAL = 100%
o First degree (partial thickness)
 Epidermis
 Red painful, heal readily w/o scar tissue
 Ex: sunburn, mild scald
o Second degree (deep partial thickness)
 Epidermis and part of dermis
 Red, edema, blistered, hypersensitive, pain
 Healing by regeneration from edges of blistered area
 Easily infected
o Third degree (full thickness)
 Destruction of all skin layers and often underlying tissue
 Coagulated/ charred
 Can be painless initially
• Complications with burns. Pg 38-40 main headings
o Shock: low BP, hypovolemic shock, increase hematocrit, may cause
kidney failure
o Respiratory- inhalation of toxic fumes
 Carbon monoxide binds to hemoglobin in place of oxygen
 Cyanide from environmental toxins, especially if individual is
trapped
 Pneumonia – because of inflammation in respiratory tract from
inhaling hot air/ steam or irritating chemicals
• Damage to mucosal lining of trachea and bronchi
o Pain
o Infection: opportunistic bacteria and fungi are waiting to invade open
areas
 Pseudomonas, aeruginosa, staphylococcus aureus, candida,
klebsiella
• Edema. What it is and what causes it
o Fluid excess in interstitial compartment
o 4 causes:
 Increased capillary hydrostatic pressure
 Loss of plasma proteins (decrease osmotic pressure)
 Obstruction of lymphatics
 Increased capillary permeability
o Effects;
 Swelling
 Increased body wt
 Lungs: shortnes of breathe, rales
 Tissue ulcers: impaired arterial flow into tissues
o Grade 1- 4+
• Electrolytes. What is greater in or out of cell
o In:
 Na 5-10 mM
 K 110-145 mM
 Ca 100mM
 Cl 5-5 mM
o Out:
 Na 145 nM
 K 5-10 mM
 Ca 2 mM
 Cl 145 mM
• What happens when you lose electrolytes, or what causes loss of electrolytes
o Dehydration: insufficient body fluid, result from inadequate intake or
excess loss of fluids
 Effects: dry mucous membranes, low BP, increased hematocrit,
weak pulse, decreased mental function/ confusion
 Causes: vomiting, diarrhea, drainage/ suction of fluids, excess
sweating, diabetic ketoacidosis, insufficient fluid intake
o Hyponatremia: low sodium
 Causes: diuretics, excess sweating, remal failure
 Effects: fatigue, hypovolemia and decreased BP
• Swelling of brain cells: seizures, confusion
o Hypokalemia: low potassium
 Causes: diarrhea, diuretics
 Effects: cardiac arrythmias, muscle weakness, parasthesias (pins
and needles)
o Hypocalcemia: low calcium
 Causes: renal failure, malabsorption, hypoparathyroidism
 Effects: muscle twitching/ spasms, cardiac arrythmias
• Anemias. Risk factors foe each
o Hypochromic microcytic: less hemoglobin in each RBC seen as increased
paleness in center. Smaller size of each RBC
 Chronic blood loss
• Cancer
• Bleeding ulcer
• Excess menstrual loss
• hemorrhoids
 Inadequate dietary intake of iron
• Adolescence & pregnancy
 Impaired absorption of iron
• Malabsorption syndromes
 Severe liver disease
o Meglaoblastic: enlarged red cells, too few red cells, hypersegmented
neutrophils
 Vitamin B12 deficiency
• due to lack of intrinsic factor for Vitamin B12 absorption
o Intrinsic factor is made by gastric mucosa
o B12 absorption requires intrinsic factor (IF) to be
absorbed by the ileum
o Dietary deficiency as a cause is unusual and is
usually due to malabsorption caused by the
antibody formation against IF, atrophy of the gastric
mucosa (alcoholics) and ileal malabsorption
 Folic acid deficiency
 Both B12 and Folic acid are necessary for DNA synthesis

o Hemolytic: excessive destruction of red cells (sickle cell anemia,
thalassemia)
o Sickle cell
 Carrier population in Africa is high as carrier trait is protective
against malaria
 Formation of abnormal hemoglobin S (normal is A, F)
 Hgb S when deoxygenated forms a crystal and changes the shape
of the red cell
• This may damage the cell membrane causing the cell to
hemolyze
• Makes the red cell lifespan shorter (~20days)
• These red cells are not aerodynamic and get stuck
• Can carry oxygen normally but fewer red cells because of
the hemolysis which perpetuates the problem
 Signs and symptoms
• Pain with crises
o Ulcers of hands/feet
o Necrosis of bone/kidneys
o Seizures or hemiplegia
• Severe anemia
• Delayed growth and development
• Autosplenectomy [spleen dies but is still in abdomen]
resulting in increased susceptibility to infections especially
pneumonia
o Thalassemia:
 Due to genetic defect in the genes for hemoglobin (may be absent
or variant)
 Results in less normal hemoglobin and damage to red cells,
hemolysis & anemia
 Thalassemia major: homozygote
  Thalassemia minor: heterozygote
 Common in Mediterranean origins
o Aplastic
 Impairment of bone marrow and loss of stem cells
 Pancytopenia: decreased WBC, RBC, & platelets
 Causes:
• Idiopathic (~50%)
• Toxins: drugs (cancer), benzene, radiation
 S&S:
• Blood counts: pancytopenia
• Petechiae
• Infections
• Anemia symptoms
• White cell disorders. Leukemia and lymphoma difference
o Leukocytosis: elevated white count
 Can be reactive
 Infection
 Neoplastic
o Leucopenia: low white cell count
 Usually due to neutropenia (too few granulocytes)
• Due to drugs (chemotherapy), metastatic neoplasm, sepsis
 Lymphopenia: AIDS
o Leukemias:
 ALL [acute lymphoblastic leukemia]
• Proliferation of immature lymphocytes called lymphoblasts
• Common in young children
• Present with infection, bleeding, anemia because of
nonfunctional white cells and replacement of marrow by
uniform population of cells
 AML [acute myelogenous leukemia]
• Proliferation of immature granulocytic cells
• More common in young adults
 Acute monocytic leukemia
 Chronic lymphocytic leukemia [CLL]
 Chronic myelogenous leukemia [CML]
o Lymphomas: neoplastic disorders of lymph nodes
• Multiple myeloma: most common primary malignant tumor on bone
o A disorder of plasma cells (mature B lymphocytes) that produce
antibodies
o Commonly present w/ back pain and spine involvement
o Increased # of plasma cells erode bone
o The proliferating plasma cells secrete immunoglobin seen in the blood and
urine
 o Hypercalcemia, pain infections, bleeding, renal impairment
o Related w/ spontaneous fx and present with back pain
• Hodgekins. Non hodgekins
o Hodgkins: defective cell mediated (T cell) immunity (manifested by
infections)
• Cancer- - neoplastic dx of the ln
• arises form a single or chain of nodes and spreads to adjacent nodes
• predictable spreading manner
• Reed Sternberg cell (malignant cell associated)
• Epstein barr relation
• Better prognosis than non-hodg
Stages:
• stage 1 - one lymphnode region involved
• stage 2- 2 ln on the same side of diaphragm
• stage 3- ln involvement on both sides of diaphragm
• stage 4- spread of cancer outside the ln
Non- Hodgkins: (more common)
• cancer- neoplastic dx of the ln
• arises from B cells
• involves wide spread nodes and spreads by jumping form one region to
another
• at diagnosis pt usually have a wide spread disease
Staging: Same as hodgkins (not as usefull thought)

o
• Hemophilia A
o Deficit or abnormal factor VIII
o Most common inherited clotting disorder
o Severe hemorrhage from minor trauma
o Spontaneous hemorrhage in joints
o X linked recessive
• DIC- understand they are very sick. Bleed from everywhere because they’ve used
up all coagulation factors from clotting inside vessels. Risk factors: trauma, burns
• Risk factors for pulmonary emboli
• Thrombus, embolus difference
Thrombi (singular) Thrombus (plural): intra vascular collection of blood elements
(platelets and WBC), forms w/o clotting cascade and gets large by adding clot on top of
thrombus. Formation is due to endothelial injury, stasis, or hyercoagulability. (the mass
attached to something)
Examples: Pathologically, thrombi are classified on the basis of their
location:
1. Intramural Thrombi: are attached to the mural endocardium of the heart
chambers and are commonly found overlying a MI.
2. Arterial Thrombi: are attached to the arterial wall and typically cover
ulcerated atheromas in an atherosclerotic aorta or the coronary arteries.
3. Venous Thrombi: are usually found in dilated veins (varicose veins).
Long-standing venous thrombi are organized by granulation tissue, which
may give an impression of inflammation (thrombophlebitis).
4. Microvascular Thrombi: are found in arterioles, capillaries, and venules,
are typical of Disseminated Intravascular Coagulation.
Embolism: a freely movable intravascular mass carries from one site to another by the
blood, all emboli can occlude BV thus interrupting the blood supply to a an organ and
causing an infarction (the mass moving about)
Thromboemboli-
these represent fragments of thrombus carried by venous or arterial blood
Septic emboli-
Infected material
Liquid Emboli-
fat emboli that occur after bone fracture
amniotic fluid emboli caused by the entry of amniotic fluid into the uterine veins
during delivery.
Gaseous Emboli-
an air embolism can be produced by injecting air into veins.
Air that is liberated under pressure (decompression sickness aka bends)
Solid Particle Emboli-
cholesterol crystals can detach from atherosclerotic plaques
tumor cells
bone marrow emboli
Bullets or iv catheter tips

• Difference between arterial vs venous emboli

Venous thrombi:
• found in dialated veins.
o Organize by granulation tissue, giving the impression of inflammation
o Originate and carried in veins
o Typically lodge in pulm A and branches- pulm embolism
o Sources: LE, fx, pregnancy, IV caths, pelvic veins, tumor
Arterial thrombi:
o Attached to the arterial wall, typically covering ulcerated atheromas in an
athroscortic aorta or coronary arteries
o Sources: carotid A, mural thrombi of heart, cardiac valves, aorta and major
branches
• Amniotic fluid embolis
o Tear in placenta or rupture of uterine/ cervical veins causing fluid
containing fetal cells and debris to enter maternal circulation
o Occurs in the end of labor
o Catastrophic but rare
o Onset: sudden dyspnea, cyanosis, hypotensive shock, seizure, coma,
DEATH!
• Difference between active and passive hyperemia
o Hyperemia: accumulation of blood in the peripheral circulation
 Active: consequence of dilation of arterioles and mediated by
neural signs that lead to relaxation of arteriolar smooth muscle
(blushing)
 Passive congestion: increased venous back pressure and most often
occurs in a chronic form
• Consequence of CHF
 Chronic passive congestion
• Anoxia
• Pulmonary fibrosis
• Line of zahn
o layered thrombi, which show distinct layering of cellular elements and
fibrin…the white layers in these thrombi are called the “Lines of Zahn”.
• Infarction
o An insufficiency of blood supply of sudden onset that results in an area of
ischemic necrosis.
o Most are caused by either thrombosis or emboli.
o Depending on the site of vascular occlusion, infarcts may be arterial or
venous.
o On the basis of their gross appearance, infarcts may be classified as
 Red or
 white.
• Shock
o A state of hypoperfusion of tissues with blood, caused by one of three
mechanisms:
 Pump failure of the heart (Cardiogenic Shock)
 Loss of fluid from the circulation (Hypovolemic Shock)
 Severe gram negative bacteremia (Septic Shock)
• Complications of shock
o Common to all these conditions are a collapse of circulation and a
disproportion between the circulating blood volume and the vascular
space.
o Resulting hypoperfusion of tissues produces:
 tissue hypoxia
 multiple organ failure due to insufficient delivery of oxygen and
nutrients to cells and tissues.
• AIDS graph. What the T cells are doing. Kind of infections they get. Definition of
HIV to AIDS
o Look at in slides. It wouldn’t let me copy and paste for some reason…

• Laceration, abrasion, contusion, incision

 o Abrasion: scraping of the skin by a surface or force
o Contusion:
 Bleeding into the skin or underlying soft tissue
 Accentuated in:
• Hemophilia
• Alcoholism
• Elderly
o Laceration:
 Tissue Bridging
 Edges commonly abraded or contused
 Irregular Edges
 May have undermining
• Cocaine associated with heart problems, meth/ heroine addictive. Risk factors of
drug use in general. Bacterial endocarditis, skin absess
• Wound healing: intension, decubiti risk factors, keloid,
o Primary intension
 Edges of wound held close together (suture)
 Wound is clean
 Typical surgical incision
o Secondary
 Gap of the tissue margins
 Larger inflammatory response
 Longer healing period
 More scar tissue
 Heals from bottom up
o Tertiary
 great loss of tissue
 wound must heal by contraction of the wound edges, and the
formation of granulation tissue
 foreign body or infection may be suspected, and these wounds are
left open deliberately for several days until the potential
complication has resolved.
 When resolution has occurred, the wound edges can be brought
together (approximated) and the wound proceeds to heal
o Keloid:
 enlarged scar with a significant increase in collagen deposition
 have no discrete collagen bundles
 is a diffuse, random organization of the collagen bundles with no
significant regularity or associated relationship to the skin surface
as seen with normal skin.
o Contribute to ulcer formation
 Pressure
 friction
  incontinence
 poor vascular perfusion
• Inflammation: difference between major types of organisms: bacteria, fungi, etc
o Prions
 Unique proteins that have the ability to reproduce on their own and
make new particles [self perpetuating]
 Infectious
 Have no DNA
 Ex: Creutzfeldt Jacob dz; mad cow disease
o Bacteria
 Capsule: prevents phagocytosis & sticky surface increases
adhesion to target
 Pili are for attachment and determine what tissues it can attach to
 Motile (flagellum)
 Cell wall (stability)
o Viruses
 Capsid: protein shell to protect contents
 Contain RNA or DNA internally but not both
 Spikes for binding to particular tissues or target cells
 Are intracellular organisms
 Not susceptible to antibiotics
o Chlamydia, Rickettsia, Mycoplasma
 Class of organisms between viruses and bacteria
 Are susceptible to antibiotics like bacteria
 Simple structure like viruses
 Chronic inflammation reaction
 Ex. Chlamydia: vaginal infections
 Rickettsia: Rocky Mountain spotted fever
 Mycoplasma: Pneumonia
o Fungi
 Large organisms that form branching structures
 Includes yeasts
 Chronic inflammation of lymphocytes, monocytes and giant cell
granulomas at site of infection
 Ex. Candida
o Protoz Motile single cell organisms
 Create lymphocyte chronic inflammation
 Ex. Malaria, Amoebas, Giardia
o Worms
 Complex life cycles and large organisms
 Create eosinophilic chronic inflammation
 Ex. Round, pin worms
• Acute vs chronic inflammation and diseases associated with each of them
 o Acute Inflammation: Inflammation of sudden onset and of short duration.
o Chronic Inflammation: Inflammation which lasts a long time.
 Usually mediated by lymphocytes, macrophages, and plasma cells
and can appear shortly after an acute inflammation.
 Some chronic infections evolve without a typical acute phase and
represent a slow-smoldering process from their onset
• TB has a gradual onset and lasts for a long time, but
without an acute phase of the disease
• Foreign Substances: Silicosis
• Autoimmune Diseases: Rheumatoid arthritis
• Signs of acute inflammation
o 1. Calor (Heat)
o 2. Rubor (Redness)
o 3. Tumor (Swelling)
o 4. Dolor (Pain)
o 5. Functio laesa (Loss of function)
• Summary of main topics of cellular/ circulatory changes of inflammation
o 1. Circulatory Changes
 Mechanical stimulus
 Relaxation of smooth muscle at sphincters
 Increased capillary blood flow
 Gives: redness, warmth, swelling
 Rouleaux formation
• The sludged erythrocytes form stacks
• impedes and slows down the circulation even more.
 Pavementing
• WBC’s marginate and become sticky and attach to the edge
of the endothelium
o 2. Cellular Changes
 Changes within blood vessel
• Margination
• Pavementing
• Rouleaux formation
• Interleukins
o 3. Emigration
 The emigration of neutrophils through the vessel wall is an active
process that occurs in several phases
o 4. Chemotaxis
 Active movement of PMN’s along a concentration gradient is
called “Chemotaxis”, the chemo-attractant being derived from
bacteria or tissues destroyed by inflammation, or from activated
complement.
 Chemotactic substances stimulate PMN’s to move along this
gradient until they reach their source or site of the inflammation.
 o 5. Phagocytosis
 Engulfment of the bacterium
• cytoplasm of the PMN surrounds the foreign particle and
encloses it into an invagination of the cell membrane.
• Inside the PMN, the bacterium is killed by bacteriocidal
substances released from the cytoplasm of the PMN [in the
granules]
• Fever. What it is and what it’s related to. Occurs after the event as a response
o The interleukens and the Tumor necrosis factor substances get released by
tissues and white cells as part of inflammatory response
o These migrate to the hypothalamus to the thermoregulatory center causing
the elevation in temperature

• Difference between exudates and transudate

o Exudate:
 Extravascular fluid collection that is rich in protein and/or cells
 Fluid appears grossly cloudy.
o Transudate:
 Extravascular fluid collection that is basically an ultrafiltrate of
plasma with little protein and few or no cells
 Fluid appears grossly clear.
• Pseudomembranous inflammation
o A type of ulcerative inflammation that is combined with purulent exudate.
 The exudate of fibrin, pus, cellular debris and mucous forms a
pseudomembrane on the surface of ulcers
 If scraped away to expose ulcerated defects bleed profusely.
o Clostridium difficile causes pseudomembranous colitis
 Disease caused by a bacterial overgrowth secondary to intake of
broad-spectrum antibiotics resulting in life threatening diarrhea,
bacterial toxins and sepsis