Dr. D.'s Overhead Lecture Notes Section 1 - REPLACE PAGE NUMBERS WITH PAGES FROM SIXTH EDITION1
Pathophysiology
Pathology
- study of disease
Pathophysiology
- study of abnormal function
- study of function during disease
Disease
1. Inability to adapt to maintain
homeostasis
2. Homeostasis is being lost
3. Homeostasis is lost
Homeostasis
- conditions in the body are proper
and fairly stable
- maintained by:
1. insulator
and barriers, avoiding adverse factors
- prevent change
2. negative feedback
- limit/reverse change
1. Monitor (detect)
2. Communicate
3. Adjust
Normalcy
- at or close to average
- within acceptable range
Disease at the Cell Level
Loss of homeostasis (normalcy)
- importance of:
1. Degree/intensity
2. Duration
3. Frequency
Possible results
1. Tolerate or adapt
2. Sublethal injury
3. Lethal injury ->
death
- "point of
no return"
necrosis
= localized cell death
somatic
death = whole body death
Sublethal injury -> altered states
1. Hydropic change - reversible
(p. 30 Fig. 3-2)
(sketch)
2. Fatty infiltration = fatty
accumulation = fatty degeneration - reversible (p. 31 Fig. 3-3)
2.
Normal liver, external, gross (VHP)
In normal liver, the color is even and brown and that the surface is smooth.
3.
Normal liver, cut surface, gross
The color of normal liver tissue is even and brown. It contains some blood
vessels and bile ducts.
5.
Fatty metamorphosis of liver, gross (CT)
Normal
liver, medium power microscopic *
The liver cells make up the prominent pink strands of material. Each liver
cell can be identified by its small round blue nucleus. The more open streaks
between the strands of liver cells are large capillaries (i.e., liver sinusoids)
that contain some blood cells. The large vessels in the lower left region
carry blood to the liver sinusoids, and the large vessel in the upper right
drains blood from the sinusoids. Note that the liver cell cytoplasm appears
solid in color and that most of the liver consists of liver cells and sinusoids.
36.
Fatty change, liver, microscopic *
Many of the liver cells each contain a clear fat droplet in their cytoplasm.
8.
Fatty metamorphosis of liver, microscopic
Many
of the liver cells each contain a clear fat droplet in their cytoplasm.
3. Atrophy - reversible
1.
Atrophy, muscle fibers, microscopic *
The normal cells are round. The atrophied cells are flattened.
3.
Atrophy, cerebrum, gross
Atrophy of many cells or loss of many cells can cause an entire organ to
shrink (i.e., atrophy).
4. Hypertrophy - reversible
5.
Hypertrophy, heart, gross
The wall of this heart is almost twice as thick as it should be. Thickening
of each cardiac muscle cell has caused overall thickening of the wall of
the heart. The heart muscle cells had to work very hard because of the
high blood pressure (i.e., hypertension). The same type of hypertrophy
causes skeletal muscles to thicken when they are exercised with heavy weights.
5. Hyperplasia - can end
6.
Hyperplasia, endometrium, gross
This is normal or "physiologic" hyperplasia. It occurs with normal menstrual
cycles.
Normal
prostate, medium power microscopic*
Note the thin layers of secreting cells surrounded by much non-secreting
connective tissue.
Compare this with the image of hyperplasia in the prostate.
Normal
prostate, high power microscopic *
Again, note the thin layers of secreting cells surrounded by much non-secreting
connective tissue.
Compare this with the image of hyperplasia in the prostate.
8.
Hyperplasia, prostate, microscopic*
Most of the cells are secreting cells and that there is little non-secreting
connective tissue.
Compare this with the normal prostate. This is abnormal or "pathologic"
hyperplasia. It can lead to enlargement of the prostate gland, called prostatic
"hypertrophy".
7.
Hyperplasia, prostate, gross
The hyperplasia by the prostate cells has caused overall enlargement (i.e.,
hypertrophy) of the prostate gland.
6. Metaplasia - can end (p.
109 Fig 8-1)
9.
Metaplasia, squamous, larynx, microscopic *
Compare the cells on the surface. Note that the normal cells appear on
the surface at the right side while metaplasia has occurred in the cells
on the surface at the left side.
4.
Columnar metaplasia, esophagus, microscopic *
Again, compare the cells on the surface. The normal cells are on the surface
at the right side while metaplasia has occurred in the cells on the surface
at the left side.
7. Dysplasia - can end (p.
110 Fig. 8-2)
Normal
cervix, high power microscopic *
The cells making up the thick surface layer, which fills most of the view,
are very orderly, regular, and all look the same.
6.
Dysplasia, cervix, high power microscopic *
Compare the normal cells in the thick surface layer at the left with the
irregular disorganized small cells making up the thick surface layer in
the middle and to the left.
7.
Dysplasia, cervix, Pap smear, high power microscopic *
8. Neoplasia - does not end
(pp. 111-113 Figs. 8-4 through 8-7)
The following images show masses composed of neoplastic cells.
17.
Adenomatous polyps, colon, gross
Note the reddish brown masses.
56.
Osteosarcoma of bone, gross
Note the mass on the bone.
31.
Oat cell carcinoma of lung, invasive, gross
Note the pale masses lining and filling the airways.
80.
Lung, squamous cell carcinoma, gross [XRAY]
Note the extensive pale mass. The hollowed area shows necrosis.
94.
Lung, metastatic carcinoma, gross [XRAY]
Note the many tumors. Each developed from one or more neoplastic cells
carried to the lung from a distant neoplasia.
23.
Hepatocellular carcinoma, liver, gross
Note the large tumor, which is forming smaller ones by spreading through
the liver.
45.
Metastatic adenocarcinoma, liver, gross
Note the many tumors. Each developed from one or more neoplastic
cells carried to the liver from a distant neoplasia.
9. Pigment accumulation
41.
Lipochrome in hepatocytes, microscopic *
4.
Atrophy, centrilobular region of liver, microscopic *
10. Accumulation of other substances
(e.g., calcium, ions, specific proteins)
Calcium -
Lung, tuberculosis,
secondary, with calcifications, PA chest radiograph [PATH]
Calcium deposits in lungs damaged by TB show up on X-ray as white spots
50.
Dystrophic calcification, stomach, microscopic *
Spleen, calcified
granulomas, CT scan [PATH]
Amyloid
38.
Amyloid deposition, Congo red stain, microscopic *
44.
Amyloid deposition, myocardium, microscopic *
Etc.
34.
Mallory's hyaline, liver, microscopic*
39.
Alpha-1-antitrypsin deficiency with globules in liver, PAS stain, microscopic
*
40.
Gaucher's disease, spleen, microscopic *
35.
Neurofibrillary tangles, Alzheimer's disease, microscopic *
Lethal Injury = necrosis
1. Coagulative necrosis (p.
33 Fig. 3-5)
15.
Coagulative necrosis, renal infarction, gross
With coagulative necrosis, the necrotic region is similar in structure
to the normal region.
16.
Coagulative necrosis, renal infarction, microscopic *
18.
Coagulative necrosis, splenic infarctions, gross
17.
Coagulative necrosis, adrenal infarction, microscopic *
Normal
cardiac muscle, medium power microscopic *
Compare these normal heart muscle cells with the next image of coagulative
necrosis of heart muscle.
12.
Coagulative necrosis, myocardial infarction, microscopic *
Compare these necrotic heart muscle cells with the previous image of normal
heart muscle cells.
42.
Cerebrum, coronal section, subacute infarct with edema and midline shift.
Note again that with coagulative necrosis, the necrotic region is similar
in structure to the normal region.
2. Liquefactive necrosis (p.
33 Fig. 3-6)
24.
Liquefactive necrosis, cerebral infarction, gross
25.
Liquefactive necrosis, cerebral infarction, gross
22.
Liquefactive necrosis, cerebral infarction, microscopic *
23.
Liquefactive necrosis, cerebral infarction, microscopic *
20.
Liquefactive necrosis, lung abscesses, gross
21.
Liquefactive necrosis, liver abscess, microscopic [MRI] *
3. Caseous necrosis (p. 33
Fig. 3-7)
28.
Caseous necrosis, hilar lymph node, gross
29.
Caseous necrosis, extensive in lung, gross
30.
Caseous necrosis, lung, high power microscopic *
59.
Caseous necrosis in granuloma, medium power microscopic *
60.
Caseous necrosis in granuloma, high power microscopic *
4. Gangrene
- saprophytic
bacteria
- dry vs
moist
31.
Gangrenous necrosis, foot, gross
32.
Gangrenous necrosis, lower extremity, gross
33.
Gangrenous necrosis, low power microscopic *
19.
Small intestinal infarction, gross
The necrotic area would become gangrenous when saprophytic bacteria flourish
in the necrotic tissues.
5. Enzymatic fat necrosis
1.
Normal pancreas, gross (CT) (VHP)
26.
Fat necrosis, pancreas, gross
27.
Fat necrosis, pancreas, microscopic *
Effects of necrosis
Local
1. loss of
function
2. inflammation
3. site of
infection
4. leaking
of enzymes
Systemic
5. fever
6. leukocytosis
Fates of necrotic cells
1. Removal
- phagocytosis/enzymatic
2. Peel off (p. 51 Fig. 4-11)
33.
Ulceration, gastric mucosa, gross
31.
Acute gastric ulcer, low power microscopic
Ulceration,
foot, gross
35.
Ulceration, larynx, gross
9.
Herpes simplex ulcers, gross
36.
Ulceration, esophagus, gross
Note the normal mucosal cell layer on the right and the peeling necrotic
tissue and ulcer on the left.
3. Encapsulation (p. 52 Fig. 4-13)
Response to sublethal injury/necrosis
- response to cell injury/cell death
- (review normal capillary exchange)
- cell injury/cell death ->
1. detection
(neurons/chemicals)
2. inflammation
3. resolution
or repair
Inflammation (p. 38)
- vascular reaction
- delivery of fluid, dissolved substances
+ cells
- from circulating blood
- to tissue spaces
- area of cell injury/cell death
- beneficial results
1. Dilute/remove
agent
2. Remove
damaged cells
3. Localize
and limit damage
4. Establish
conditions for repair
Capillary exchange
Normal
(sketch)
BP + small pores -> fluid leakage
(filtration) together with
BP + small pores -> proteins
retained
-> incr.COP
->
most fluid returns (osmosis)
Inflammation
(sketch)
incr.BP
+
incr.pore size -> incr.fluid
leakage -> exudate
incr.BP
+
incr.pore size -> decr.
COP
-> decr.fluid leakage
-> exudate
(See course booklet flow chart)
Cardinal Signs and symptoms
1. Pain
2. Redness
3. Warmth
4. Swelling
5. Altered function
1.
Erythema, gross
Redness and heat
2.
Erythema and edema, gross
Redness, heat, swelling, and pain
13.
Edema in larynx, gross
Redness, heat, swelling, pain, and altered function
White blood cells (WBCs) + mast cells
- general functions = defense (e.g.,
inflammation, phagocytosis, immune)
- during inflammation
1. Defense
2. Control
inflammation
- for defense
1. Phagocytosis
Neutrophil in action, GIF
animation
2. Produce opsonins -> incr. phagocytosis
3. Release enzymes -> clean up
4. Release prostaglandins
-> pain, control cells (paracrine)
5. Release pyrogens -> fever
6. Produce immune response
-> incr.
inflammation + incr. defense
- for inflammation
1. Produce histamine/chemicals
- promote inflammation
2. Produce antihistamine
- suppress inflammation
"checks and balances"
5.
Exudation, microscopic *
6.
Margination and diapedesis of neutrophils, microscopic *
8.
Neutrophil ingestion of bacteria, gram stain, microscopic *
3.
Neutrophilia, peripheral blood, microscopic *
4.
Laboratory instrument for generating CBC
Reticuloendothelial system (RES)
= macrophage-monocyte system
mobile = monocytes, neutrophils,
macrophages (histiocytes)
fixed = liver, spleen, marrow,
lungs, lymph nodes, CNS
Inflammation
with necrosis from WBCs
10.
Inflammation with necrosis, high power microscopic *
During inflammation, defense cells can damage normal tissue while trying
to remove a harmful agent.
44.
Chronic inflammation with destruction of bronchial wall, microscopic
*
9.
Inflammation with necrosis, low power microscopic *
Though generally helpful, inflammation can lead to several problems including
unwanted necrosis, clotting, swelling, pain, spreading infection or neoplastic
cells, and scar formation.
Types of exudate
5.
Exudation, microscopic *
1. Serous
- fluid
- fluid =
water + small molecules + protein
- protein = albumin, fibrin, and/or mucin
- albumin
-> serous exudate
12.
Edema in friction blister, gross
The clear liquid in the blister is serous exudate.
- fibrin -> fibrinous exudate
17.
Fibrinous exudate, pericardium, gross
18.
Fibrinous exudate, pericardium, microscopic *
7.
Exudation of fibrin, microscopic *
- mucin -> mucinous exudate
2. Purulent - fluid
+ cells (WBCs) (p. 49 Fig. 4-9)
20.
Purulent exudate, pericardial cavity, gross
21.
Purulent exudate, acute meningitis, gross
22.
Purulent exudate, acute peritonitis, gross
25.
Acute bronchopneumonia, microscopic *
Note that many defense cells in the exudate.
23.
Acute bronchopneumonia, microscopic [XRAY] *
24.
Acute cholecystitis, microscopic *
3. Suppurative (pus)
- fluid + cells + liquefactive necrosis (+ bacteria) (p. 50 Fig. 40-10)
27.
Abscess formation, lung, gross
An abscess is suppurative exudate surrounded by tissue. Suppurative exudate
may also be in an open wound.
28.
Abscess formation, lung, gross
Each of the two tiny abscesses look like a tiny pale yellow spot.
31.
Abscessing bronchopneumonia, microscopic *
32.
Abscessing bronchopneumonia, microscopic *
Types of Inflammation
1. Acute - short term/early
stage
- exudation
only
- no repair
(repair = healing /new cells)
2. Subacute - sightless
longer
- exudation
+ little repair
3. Chronic - long term
(days+)
- exudation
+ much repair
- repair
= new cells + fibers
- fibers = collagen -> scar
- scar = dense fibrous connective tissue
Acute inflammation (no scar tissue forms) vs chronic
inflammation (scar tissue forms)
43.
Chronic inflammation with scarring, bronchus, gross
Chronic inflammation occurs when injury and inflammation are either long
standing or recurring.
50.
Scarring, lung, microscopic *
51.
Healing scar, skin, low power microscopic *
42.
Acute and chronic inflammation, microscopic *
Note the fibrous scar tissue on the right.
37.
Chronic inflammation, diagram
Many cell types and chemical regulators are involved in inflammation. Note
that at the lower left, inflammation can lead to collagenous scar tissue
formation.
38.
Chronic inflammation, endometrium, microscopic *
In general, the inflammatory infiltrate of chronic inflammation consists
mainly of mononuclear cells: lymphocytes, plasma cells, and macrophages
(i.e., agranulocytes). Exudates with acute inflammation contain more polymorphonuclear
leucocytes (i.e., granulocytes or PMNs).
40.
Chronic inflammation, synovium of joint, microscopic *
45.
Chronic abscess, lung, gross
46.
Organizing abscess, microscopic (CT) *
Chronic inflammation
causes scar tissue in the liver as cirrhosis develops
2.
Normal liver, external, gross (VHP)
Note the smooth homogeneous nature of the liver. The liver consists mainly
of liver cells and small blood vessels.
3.
Normal liver, cut surface, gross
Note the smooth homogeneous nature of the liver. The liver consists mainly
of liver cells and small blood vessels.
Normal
liver, medium power microscopic *
The liver cells make up the prominent pink strands of material. Each liver
cell can be identified by its small round blue nucleus. The more open streaks
between the strands of liver cells are large capillaries (i.e., liver sinusoids)
that contain some blood cells. The large vessels in the lower left region
carry blood to the liver sinusoids, and the large vessel in the upper right
drains blood from the sinusoids. Note that the liver cell cytoplasm appears
solid in color and that most of the liver consists of liver cells and sinusoids.
37.
Cirrhosis, liver, gross
Note the lumpy nature of the liver. Bands of scar tissue, which shrink
as time passes, separate and emphasize the liver lobules. At the same time,
the lobules swell due to liver cell proliferation, fatty infiltration,
and inflammation.
9.
Macronodular cirrhosis of liver, gross
Scar tissue bands separate and emphasize the lobules.
14.
Micronodular cirrhosis and fatty change of liver, gross
Scar tissue bands separate and emphasize the lobules.
16.
Cirrhosis of liver, microscopic
Scar tissue bands separate and emphasize the lobules.
Fates of inflamed areas
1. Resolution - no necrosis/short
term (acute inflammation)
- no healing
(no new cells)
2. Repair - with necrosis/long
term injury/repeated injury
- healing
by first intention -> original cell types/
tissue structure (acute or subacute inflammation)
a. Small wound and
b. Rapidly dividing cells and
c. Favorable conditions
- healing
by second intention -> (original cell types) + scar
tissue (chronic inflammation)
(pp. 53, 54, 55 Figs. 4-15, 4-16, 4-18)
a. Large wound or
b. Slow/non-dividing cells or
c. Unfavorable conditions (e.g., ongoing/repeated injury)
Healing by second intention - healing with scar tissue formation
49.
Granulation tissue, high power microscopic *
Fibroblasts form the collagen fibers of scar tissue. Scar formation is
also called granulation. The fibrous scar tissue can be called granulation
tissue.
47.
Granulation tissue, healing myocardial infarction, microscopic *
Cardiac muscle cells do not reproduce, so necrotic myocardial cells are
replaced by scar tissue.
48.
Granulation tissue, organizing abscess, microscopic *
An abscess provides poor conditions for repair plus continued injury and
inflammation. Therefore, scar tissue forms.
Granuloma - lump
of scar tissue (granulation tissue), possibly encapsulating necrotic tissue
or a foreign body
52.
Granulomatous inflammation, extensive, lung, gross
Granulomas from tuberculosis are called tubercles. They may contain necrotic
tissue and TB bacteria.
53.
Granuloma, caseating, hilar lymph node, gross
54.
Granulomatous inflammation, lung, low power microscopic *
55.
Granulomatous inflammation, high medium power microscopic *
Granulomatous
inflammation, high power microscopic [CT]
57.
Langerhans giant cells in granuloma, high power microscopic *
58.
Epithelioid cells in granuloma, high power microscopic *
61.
Miliary granulomas, gross
Granulomas containing
foreign bodies
62.
Foreign body giant cell in granuloma, microscopic *
64.
Talc granulomatosis, pulmonary, polarized light microscopic *
65.
Silicotic nodule, lung, microscopic *
Factors for 1st vs 2nd
intention
a. size of wound
b. speed of cell division (cell type)
c. quality of conditions
Conditions (factors) affecting
repair
1. Blood supply
2. WBC supply
3. Nutritional
state
4. Foreign
bodies
5. Necrotic
tissue
6. Infection
7. Wound immobilization
8. Wound edge
apposition
9. Age
Results from repair
1. Original cell types/tissue structure
(subacute inflammation)
- normal function
restored
2. Mostly original structure (little
scar tissue) (subacute inflammation)
- normal function
restored
3. Altered structure/much scar tissue
(chronic inflammation)
- reduced/altered
function
- scar formation
= organization
- reasons
for reduced/altered function
a. fewer original cells
Granulation tissue, healing
myocardial infarction, microscopic
b. less vasculature
Scarring, lung, microscopic
c. stricture (contracture)
d. adhesions (contracture)
Adhesions of pleura, gross
e. physical presence of scar (e.g., granuloma, keloid)
Systemic effects from inflammation
1. Fever
2. Leukocytosis
3. Malaise
4. Anorexia
5. Disability
6. incr.SED
rate
Factors that promote neoplasia
1. Viruses
2. Chemicals (carcinogens)
3. Radiation
4. Physical trauma (e.g., dusts, abrasion)
5. Food additives
6. Low fiber diet
7. High fat diet
8. Stress
9. Genes
Development of neoplasia - oncogenesis
63.
Oncogenesis, diagram
Neoplasia is uncontrolled cellular proliferation. The normal genetic and
chemical controls for cell reproduction are not effective. Either controls
that stimulate cell reproduction are not turned off, or controls that inhibit
cell reproduction are not turned on.
62.
Oncogenesis, diagram
65.
Oncogenesis, examples, table
This table lists some of the genes that stimulate cell reproduction. With
neoplasia, one or more of these genes work excessively. When these genes
are excessively active and cause neoplasia, they are called oncogenes.
66.
Oncogenesis, breast cancer with c-erb-B2 positivity, immunoperoxidase stain,
high power microscopic *
This example shows the activity of an oncogene for breast cancer.
68.
Oncogenesis, lymphoma with bcl-2 positivity, immunoperoxidase stain, low
power microscopic *
This example shows the results when a gene that should cause apoptosis
(programmed cell death) does not work enough.
Characteristics of neoplasia
Benign
- does not spread
(p. 111 Fig. 8-3, p. 152)
1. Does not spread
2. Slow growth
3. Often encapsulated
4. Often normal differentiation
21.
Nevi, skin, gross
9.
Benign junctional nevus, medium power microscopic
22.
Hepatic adenoma, liver, gross
17.
Adenomatous polyps, colon, gross
38.
Adenomatous polyp, colon, low power microscopic (X-ray) *
96.
Colon, adenomatous polyp (tubular adenoma) compared to normal mucosa, medium
power microscopic *
15.
Leiomyomas, uterus, gross
16.
Leiomyoma, uterus, microscopic *
12.
Lipoma, small intestine, gross
13.
Lipoma, small intestine, low power microscopic *
14.
Lipoma, small intestine, high power microscopic *
18.
Schwannoma, peripheral nerve, gross
19.
Schwannoma, peripheral nerve, microscopic *
Malignant
(p. 111 Fig. 8-3, p. 113 Fig. 8-7,
plates 1-4, 221-23, 47, 48, 50, 51)
1. Spreads
- infiltration
- grows throughout an organ but remains attached to site of origin
(sketch)
33.
Infiltrating ductal carcinoma of breast, gross
24.
Infiltrating ductal carcinoma, gross [MAMMOGRAM]
25.
Comparison of carcinoma and fibroadenoma, gross
Note the irregular edge of the infiltrating cancer on the left and the
smooth regular boarder of the white benign neoplasm at the right.
31.
Infiltrating ductal carcinoma, low power microscopic
The neoplastic cells are the round blue cells. The pink strands of material
consists of supporting connective tissue called stroma.
33.
Infiltrating ductal carcinoma, low power microscopic
The neoplastic cells are the round blue cells. The pink strands of material
consists of supporting connective tissue called stroma.
34.
Infiltrating ductal carcinoma of breast, low power microscopic *
The neoplastic cells are the round blue cells. The pink strands of material
consists of supporting connective tissue called stroma.
- metastasis-
cells separate from the site of origin and are moved to other body area(s),
establishing new tumors.
(sketch)
- blood
- lymph
- body cavity fluid
- (surgery)
93.
Lung, metastatic carcinoma, gross [XRAY]
94.
Lung, metastatic carcinoma, gross [XRAY]
44.
Metastatic adenocarcinoma, liver, gross [CT]
45.
Metastatic adenocarcinoma, liver, gross
19.
Vertebrae, metastatic carcinoma, gross [MRI]
20.
Vertebrae, metastatic carcinoma, gross [XRAY]
21.
Metastatic carcinoma, low power microscopic [NM]
29.
Metastases to peritoneum, gross
30.
Metastases to pleura, microscopic
2. Rapid growth
3. Rarely encapsulated
4. Often anaplastic or dysplastic
(sketch)
| Effects from benign | Effects from malignant |
| - little/no competition for nutrients/O2 | - often incr. incr. competition |
| - cosmetic | - cosmetic |
| - block tube | - block tube |
| - compress tube | - compress tube |
| - press on structure | - press on structure |
| - overproduce (e.g., hormones, enzymes) | - overproduce (e.g., hormones, enzymes) |
| - site of infection or irritation | - site of infection or irritation |
| - can become malignant | - replaces/destroys normal tissue |
(sketch)
For more images and information about neoplasia,
use the apollo network and go to
file:////Fs_apollo/USER/SCHOOL/HENSON/BIOL/Webpath/334/Web-lists/Web-list-neoplasia.htm
Extrinsic vs intrinsic factors that
promote or cause disease
- Extrinsic = from outside
cells (e.g., microbes, trauma, chemicals, electricity, malnutrition, radiation,
incr./decr.
temperatures, psychosocial)
- Intrinsic = from inside
cells or the body (e.g., genes, gender, age, other disease)
- extrinsic (e.g., trauma) vs
intrinsic (e.g., sickle cell anemia) vs both (e.g., atherosclerosis
{p. 463})
DNA (genes) controls structure & function
DNA (genes) (pp. 8, 9) -> m-RNA -> proteins -> protein structures & enzymes (functional proteins) (sketch)
Enzymes -> building non-protein structures & regulate/perform "all" functions
One abnormal gene -> abnormal
structure or abnormal function
One chromosome = thousands of genes
- therefore, one abnormal chromosome
->
many abnormal structures and many abnormal functions
Karyotypes - a karyotype
is a photograph or a diagram of the chromosomes in a cell as they appear
during the metaphase stage of mitosis.
Karyotype - microscopic*
7.
Normal female 46, XX karyotype
Karyotypes - diagrammatic
1.
Normal chromosome at metaphase, diagram
2.
Normal male karyotype, diagram
Karyotype abnormalities
3.
Chromosomal abnormalities, diagram
Note that there are many types of chromosomal abnormalities.
4.
Genetic conditions and karyotypes, table
Click on a few examples.
30.
Trisomy 16 with single X chromosome (46, X, +16)
This is one of the most common chromosomal abnormalities.
Down's
syndrome = trisomy 21
In trisomy 21 ("three bodies of 21") there is an extra copy of chromosome
21, so there is a total of three copies of chromosome 21 in each
cell. Because each chromosome contains many genes, there are many extra
genes, resulting in many abnormalities. Here are a few examples.
8.
Trisomy 21 (47, XY, +21) karyotype
9.
Down syndrome, facial features, gross
10.
Down syndrome, epicanthal fold, gross
11.
External ear, low set and simplified, gross
12.
Hand, simian crease, gross
Congenital disease - a
disease that is present at birth. Not all genetic diseases cause congenital
diseases, and not all congenital diseases
are due to genetic abnormalities.
- from abnormal embryology (development
before birth)
- present at birth
- here are a few congenital
diseases that are not due to genetic abnormalities.
Abdominal hernia
5.
Omphalocele, gross
Malformed
fingers
14.
Syndactyly, hand, gross
Spina
bifida
Meningomyelocele,
gross
Congenital
syphilis
50.
Congenital syphilis, gumma in heart, gross
For
more examples of congenital diseases, many of which
may be disturbing to view -
Go
to the Pediatric-Perinatal Pathology Index
For
more information about prenatal diagnosis -
Go
to the tutorial on prenatal diagnosis.
Hereditary disease
- from abnormal genes in parents
- may develop before or after birth,
even in adulthood (e.g., certain cancers, Alzheimer's disease)
Genetic contributions to disease
Single gene vs multiple gene
disease
Genetic vs multifactorial disease
Sources of genetic abnormalities
1. Inherited from parent
- sperm +
egg -> zygote -> all cells
abnormal gene in parent cells -> abnormal gene in gamete
->
abnormal gene in all cells
- might be
expressed in only some cells (e.g., sickle cell anemia)
2. Abnormal gamete formation
- abnormal
genes from abnormal gamete formation -> abnormal gene in gamete
->
abnormal gene in all cells
- might be
expressed in only some cells (e.g., Down's syndrome)
3. Somatic cell mutation
- abnormal
gene developed in somatic (body) cell -> abnormal genes only in
cell's progeny (e.g., cancer from radiation)
Immune response
- faster and stronger with each
exposure to antigen
Characteristics
1. Self-recognition
2. Specificity (p. 62, Fig.
5-1)
3. Memory
Mechanisms
1. Humoral response
- for "unbound"
antigen
- uses B-cells
-> antibodies
2. Cell-mediated response
- for "bound"
antigen on body cells
- uses cT-cells
or
dT-cells
- T-cells contact antigen
Events of immune responses
- first encounter -> primary
response
- slow and
weak
- second/later encounter ->secondary
response (p. 78)
- faster and
stronger (memory)
- memory = memory T-cells, memory B-cells, remaining plasma B-cells,
antibody
- primary response (see
Course Booklet) (sketch)
- secondary response
(see overhead) (sketch)
Complement system
- plasma components (p. 74)
- amplifies (complement)
- kills bacteria
- incr.
phagocytosis by WBCs & macrophages
- incr.
inflammation
-> defense by WBCs
Undesirable effects from immune responses
Type I = anaphylactic
type
- histamine
->
bronchial constriction & systemic vasodilation
Larynx and epiglottis with edema,
gross
- systemic
vasodilation
-> decr. decr.BP
-> shock
Type II = cytotoxic type = autoimmunity
Type III = serum sickness
- Ag-Ab complexes
->
blocked capillaries & damaged vessels (vasculitis) (p. 137)
Type IV = delayed hypersensitivity -> allergic contact dermatitis (Plate 34, p. 13)
Fracture = break in bone matrix
- traumatic vs pathological
fracture (pp. 1028-1029)
Normal bone
1.
Normal vertebral bone, gross.
2.
Normal vertebral bone, gross.
3.
Normal vertebral bone and marrow, low power microscopic.
4.
Normal vertebral bone, polarized, medium power microscopic.
Fractures
Fracture, femur,
radiograph
Skull
fracture, base, orbital plate, gross [XRAY]
Skull fractures, head CT
scan
Intertrochanteric
fracture, femur, radiograph
Comminuted fracture,
femur, radiograph [PATH]
Comminuted spiral
fracture, femur, radiograph
Comminuted spiral
fracture, tibia, radiograph
Fracture-dislocation of
sacroiliac joint, pelvic CT scan
- effects
- decr.
function, systemic disability, fat emboli, infection (open fracture)
Healing (p. 1030)
Fracture and ORIF repair
of humerus, radiograph [PATH]
Fracture, femur at hip
joint with prosthesis, radiograph
Hip joint with prosthesis,
pelvic CT scan
1. Procallus = hematoma
2. Fibrocartilagenous callus
5.
Fracture callus, high power microscopic
(X-ray)
3. Bone formation
Fracture with new woven bone,
medium power microscopic [XRAY]
3.
Fracture with new woven bone, high power microscopic (X-ray)
Tibia, healing fracture,
CT scan
4. Bone remodeling
Osteoporosis = "porous bone"
- excess removal on inner matrix
1.
Normal vertebral bone, gross.
2.
Normal vertebral bone, gross.
3.
Normal vertebral bone and marrow, low power microscopic.
4.
Normal vertebral bone, polarized, medium power microscopic.
5.
Vertebral bone with osteoporosis, gross.
6.
Vertebral bone with osteoporosis and compressed fracture, gross.
7.
Vertebral bone with osteoporosis, low power microscopic.
41.
Vertebrae, osteoporosis, gross
42.
Vertebrae, compressed fracture, gross [MRI]
- prevention
- promote
matrix formation
- reduce matrix
removal
- strategies to promote formation
and reduce removal
- incr.
exercise, nutrition, vitamin D, estrogen (in women)
- decr.
smoking,
excess alcohol, protein, caffeine, phosphates, corticosteroids,
insoluble fiber
Osteomyelitis = infected bone
- open fracture ->incr.
exposure
Humerus, compound fracture,
gross [XRAY]
Osteomyelitis, foot,
radiograph
Osteomyelitis, great toe,
radiograph
Osteomyelitis, great toe,
nuclear medicine scan
Osteomyelitis, tibia,
radiograph
Osteomyelitis,
vertebra, MRI scan
Osteomyelitis,
vertebra, MRI scan
Osteomyelitis,
vertebra, MRI scan
6.
Chronic osteomyelitis, medium power microscopic
*
- dangers
- insidious
- systemic
spreading
- difficult
to deter
- low/interrupted
blood flow in bone
Dislocation vs subluxation
- effects
- decr.
function, systemic disability, nerve injury, vessel injury
Osteoarthritis = "degenerative joint disease"
= DJD
(sketch)
40.
Vertebrae, degenerative osteoarthritis, gross
44.
Femoral head, comparison of normal to abnormal articular cartilage, gross
(X-ray)
- causes = unknown (idiopathic)
- hypotheses
- accumulation
of small injuries
- decr.
restorative ability of cartilage (e.g., aging)
- pathogenesis
- cause(s)
->
removal of cartilage & formation of excess bone
- structural changes
- thinning
cartilage
- rough bony
projections = osteophytes
39.
Vertebrae, degenerative osteoarthritis, gross
40.
Vertebrae, degenerative osteoarthritis, gross
Femoral
head, osteoarthritis, comparison of normal to abnormal articular cartilage,
gross [XRAY]
Osteoarthritis, of knee
radiograph [PATH]
Foot
with "hammer toes", gross
Foot,
degenerative osteoarthritis, gross [XRAY]
Osteoarthritis, hands,
radiograph [PATH]
Osteoarthritis, hand,
radiograph
Osteoarthritis, hand, with
joint subluxation, radiograph
Osteoarthritis, knee, with
joint subluxation, radiograph
- functional changes
- stiffness
= difficulty moving
- decr.
range of motion (decr. ROM)
- pain
Rheumatoid arthritis = RA
46.
Hand, rheumatoid arthritis, gross
Rheumatoid arthritis,
hand, radiograph
- major characteristics
1. Chronic
flairs and remissions
2. Systemic
3. Inflammatory
- causes = unknown (idiopathic)
- hypotheses
= genes, virus
-> altered immune response (i.e., autoimmunity)
- pathogenesis
(sketch)
cause (s) identify connective tissue as foreign
yields
immune response against connective tissue (autoimmunity)
yields yields yields
Humoral response Complement system Cell-mediated
response
(B-cells, antibodies)
(cT-cells)
yields yields yields
destruction of cells and matrix (cartilage, bone, etc.) & inflammation
yields
tissue replaced by pannus (destroys tissues), scar
tissue (shrinks)
48.
Rheumatoid arthritis, pannus in joint, microscopic
yields
removal of cartilage & bone, deformity of joint (structural
changes)
46.
Hand, rheumatoid arthritis, gross
yields
stiffness,
decr.
ROM, pain (functional changes)
- locations
- primarily
affects small joints
- also affects
connective tissues in other areas = systemic effects
- blood vessels (serum sickness)
- skin (nodules)
47.
Elbow, rheumatoid nodule, gross
49.
Rheumatoid arthritis, rheumatoid nodule, microscopic
- pericardium (pericarditis)
- nerve sheaths (neuropathy)
- etc. (p. 1044)
Gout -
accumulation of uric acid
56.
Gouty arthritis, joint fluid, polarized, microscopic
55.
Gouty tophus in soft tissue, medium power microscopic
53.
Foot, gout, gross
Gout, big toe, radiograph
Gout, big toe, with joint
destruction, radiograph
Gout, hand, radiograph
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