Review (not include choice questions)

Give the definition

Atrophy
Shrinkage in the size of the cell by loss of cell substance is known as atrophy( 萎
缩).
Physiologic, pathologic
Thymus atrophy after adolescence
Genital system
Senile atrophy
 decreased workload
( atrophy of disuse 废用性萎缩)
 Loss of innervation
(denervation atrophy 去神经性萎缩): poliomyelitis
 Inadequate nutrition
(Dystrophic atrophy 营养不良性萎缩)

Hypertrophy
Hypertrophy ( 肥大 ) refers to an increase in the size of cells and, with such
change, an increase in the size of the organ.
• Compensatory hypertrophy
• Endocrine hypertrophy
• Physiologic hypertrophy
• Pathologic hypertrophy

Metaplasia
Metaplasia(化生) is a reversible change in which one matured cell type (epithelial or
mesenchymal) is replaced by another matured cell type.
columnar squamous

Granulation tissue
After injury, fibroblasts and vascular endothelial cells begin proliferating to form a
specialized type of tissue that is the hallmark of healing, called granulation tissue.

Infarction
An infarct is an area of ischemic necrosis caused by occlusion of either the
arterial supply or the venous drainage in a particular tissue.

99% of all infarcts result from thrombotic or embolic event, and almost all result
from arterial occlusion.

Heart failure cells

Macrophage in the lungs duuring left heart failure cells that offen carry amount of
haemosiderin , hemosidirine containing macrophage in the alveoli the main cause
are left heart failure and chronic pulmonary adema .

Nutmeg liver
Is the congestive hepatopathy also know as netmeg liverand chronic congestion of
the liver .
Is liver dysfunction due to venous congestion ussually cardiac dystaction right heart
failure or congestive heart failure .

Inflammation
Various exogenous and endogenous stimuli can provoke a complex and protective
reaction in the vascularized connective tissue called inflammation.

Exudation
 Exudation is the mark of acute inflammation: The escape of fluid, proteins,
and blood cells from the vascular system into the interstitial tissue or body
cavities is known as exudation(渗出).

Organization
The process of proliferated granulation tissue replacing necrotic tissues or other
foreign bodied is termed organization.

Granulomatous inflammation
Granulomatous inflammation is a distinctive pattern of chronic inflammatory
reaction in which the predominant cell type is an activated macrophage with a
modified epithelial-like (epithelioid) apperence. Hallmark is granuloma

Embolism
An embolus (栓子) is a detached intravascular solid, liquid, or gaseous mass that is
carried by the blood to a site distant from its point of origin.

99% emboli: thromboembolus

fat globule, air bubble and amniotic fluid

Atypia
 There are various degrees of differences between tumor and its normal origin
in the areas of cell morphology and tissue architecture.
 These differences are called atypia.

Precancerous lesions
 Refers to the lesions that have the potential to progress to carcinomas such as
Leukoplakia
 Chronic cervicitis and cervical erosion
 Proliferative fibrocystic change of the breast
 Polypous adenoma of colon and rectum
 Chronic atrophic gastritis and gastric ulcer
 Chronic ulcerative colitis
 Chronic skin ulcer
 Cirrhosis of the liver

Carcinoma in situ
 When dysplastic changes are marked and involve the entire thickness of the
epithelium, still with intact basement membrane, the lesion is called
carcinoma in situ.

Neoplasm
 Neoplasm(tumor): a lesion resulting from the autonomous or relatively
autonomous abnormal growth of cells which persists after the initiating
stimulus has been removed.

Borderline tumor
 Borderline tumor
--its cellular morphology and biologic behavior lie between benign tumor and
malignant tumor and may progress to malignant tumor

Dysplasia
denotes a loss of architectural organization and a loss of cell uniformity in epithelium
pleomorphism and mitoses are more prominent than in the normal
usually graded: mild, moderate, severe
Dysplasia is a non-neoplastic proliferation.
Mild to moderate dysplasia is potentially reversible.
Dysplasia may or may not progress to cancer.

Teratoma
 Teratoma
--contains recognizable mature or immature cells or tissues representative of more
than one germ layer and sometimes all three.

ectoderm: skin, hair, sebaceous glands, neural tissue

mesoderm: muscle, fat, bone, cartilage
endoderm: gut epithelium, thyroid gland

 Benign teratoma (dermoid cyst): common in the ovary

  Malignant teratoma: common in the testis

Atheromatous plaque
consist of arised focal lession facilating with the intima having a soft yellow
grumous core of lipid covered by afirm white fibrous cap .

Myocardial infarction
MI refers to a massive myocardial necrosis induced by sustained ischemia of
coronary perfusion zones.
Severe, crushing substernal chest pain can not be relieved by rest or nitroglycerin
significantly.

Concentric hypertrophy
Hypertrophy growth or hollow organ with out over all enlagement in which the
walls thickned it is capacity or volume diminished .

Aschoff body
A granulomatous are nodules found in the hearts of individuals with rheumatic fever
.they result from inflamation in the heart muscle and are characteristics of rheumatic
heart disease .
COPD
 A disease state characterized by poorly reversible airflow limitation that is
usually both progressive and associated with an abnormal inflammatory
response of the lungs
 airflow limitation that is not fully reversible
 pulmonary function tests
post-bronchodilator FEV1<80% of the predicted value,
FEV1/FVC<70%

Pulmonary emphysema
An abnomal condition of lungs marked by decrease respiratory function associated
with smoking or chronic bronchitis or old age .

centroacinar,
The central or proximal parts
of the acini are affected, whereas distal alveoli are normal.
panacinar
The acini are uniformly enlarged from the level of the respiratory bronchiole to the
terminal blind alveoli.

periacinar emphysema
The proximal portion of the acinus is normal, but the distal part is dominantly
involved.
Silicosis
a lung disease caused by inhalation of crystalline silicon dioxide (silica).
the most prevalent chronic occupational disease in the world.
a slowly progressing, nodular, fibrosing pneumoconiosis.

Chronic cor pulmonale

Definition: right ventricular hypertrophy, dilation, and potentially failure secondary
to prolonged pulmonary hypertension caused by disorders of the lungs, chest
movement or pulmonary vasculature.

Intestinal metaplasia
Intestinal metaplasia:
（肠上皮化生）
Both antral and body-fundic mucosa may become replaced by goblet cells,
absorptive cells and peneth cells of intestinal morphology, both along the surface
epithelium and in the proliferated glands.

Early gastric carcinoma

A lesion confined to the mucosa and submucosa, regardless of the area and the
presence or absence of perigastric lymph node metastases.

Interface hepatitis
Is the association with a high incidence of late graft fibrosis in a group of tightly
monitored pediatrics orthotopic liver transplantation .

Bridging nerosis
Bridging necrosis: necrosis of contiguous hepatocytes may span adjacent lobules in a
portal to portal, portal to central, or central to central fashion.

pseudolobule
loss of normal hepatic architecture some with pseudo lobule formation .

nephrotic syndrome
it is a clinical complex, usually of acute onset, characterised by hematuria with dysmorphic red
cells and red blood cell casts in the urine, some degree of oliguria and azotemia and
hypertension.
Cellular crescent

The glomeruli show segmental necrosis and GBM breaks, with resulting proliferation of
parietal epithelial cells in response to the exudation of plasma proteins including fibrin into
Bowman’s capsule. These distinctive lesions of proliferation are called crescents due to their
shape as they fill in the bowman’s space.
Ghon complex
Is a lession seen in the lung that is cause by tuberculosis .the lessions consist of
calsified focus of infection and and an associated with lymph node .

Tubercle
Is the swelling that is the characteristics lesion of tuberculosis .

caseous necrosis
A form of biological tissue death ,caseous meaning it has a cheese like appearence
.the dead tissue appear as asoft and white proteinnaceous dead cell mass . caseous
necrosis it deals with tb .

tuberculoma
a non neoplastic mass usually in the

Typhoid nodule lungs or brain caused by a loalized tuberculous infection , A tumor

like mass resulting from enlargemnt of caseous turburcle .
Un common manifestation of tuberculosis this pattern may be the result of an
extended primary infection .
Typhoid nodules:
Are primary aggregated of altered macrophages (typhoid cell ) that phagoctose
bacteria ,erythroctes and degenerated lymphocytes .

Eosinophilic abscess or acute egg nodule

Of the liver is caused by various disorders including allergic dis order ,parasitic
infestations ,neoplastic disease and hyperosinophilic syndrome .

Pseudotubercle or chronic egg nodule/granuloma

A nodule or granuloma resembling a tubercle of tuberculosis but due to other
causes .

Pipe stem cirrhosis

Cirrhosis of the liver with finger like fibrosis pridominantly around portal tracts
,seen in schistosomiasis. Leads to portal hypertention but rarely to function failure
of the liver .

Amoebic liver abscess

Type of liver abscess caused by amoebiasis ,histolically which forms collection of
pus in the liver .

Answer the following questions in details and some important points:

1. The features of all kinds of patterns of necrosis.
refers to a spectrum of morphologic changes that follow cell death in living tissue.
Irreversible cell injury
Features of patterns of necrosis
Coagulative necrosis
Denature of structural proteins and enzymic proteins
Preservation of the basic structural outline of the coagulated tissue

Liquefactive necrosis
is characteristic of the liquid state due to complete enzymatic digestion of the dead
cells

a. Caseous necrosis (干酪样坏死 )

A distinctive form of coagulative necrosis

Tuberculosis
White and cheesy, soft
Amorphous granular debris, the tissue architecture completely disappears
Gangrene necrosis
Gangrene is a result of secondary changes following tissue necrosis. Because of
putrefactive organism infection, massive necrosis exhibit special changes such as
black or dark green color.

Three types of gangrene

Dry gangrene: distal part of limbs, coagulative necrosis, dry, shrunken, black
Wet gangrene: internal organs, intestine,lung
Gas gangrene:severe open wounds, anaerobic bacteria

Distinctive patterns of necrosis

Caseous necrosis,
A distinctive form of coagulative necrosis
Tuberculosis
White and cheesy, soft
Amorphous granular debris, the tissue architecture completely disappears

Gangrene,
Gangrene is a result of secondary changes following tissue necrosis. Because of
putrefactive organism infection, massive necrosis exhibit special changes such as
black or dark green color.
Limbs, internal organs
Fibrinoid necrosis,
Collagen fibers of stroma and the walls of small arteries
In allergic diseases
A pile of granular, striped disorganized substances, fibrin

Fat necrosis

2. What are the structure and function of granulation tissue?

Pink, soft,granular appearance
Component: a. proliferative fibroblasts
B. new small blood vessels
C. inflammatory cells
Function of granulation tissue
 Protect the wound surface and resist infection
 Fill in the wound and other tissue defects
 Organize or encapsule necrosis,thrombus,inflammatory exudates,and other
foreign materials

3. Describe the morphologic changes of pulmonary congestion and hepatic

congestion

Pulmonary congestion
 Acute pulmonary congestion: alveolar capillaries engorged with blood
 Chronic pulmonary congestion: numerous hemosiderin-laden
macrophages(heart failure cells 心衰竭细胞), septa thickened and fibrotic

Hepatic congestion
 Acute hepatic congestion: the central vein and sinusoids are distended with
blood, centrilobular necrosis and hemorrhage
 Chronic hepatic congestion: nutmeg liver, cardiac cirrhosis

4. Categories and features of the acute and chronic inflammations.

Categories and features of the acute

Morphologic patterns in acute inflammation

Exudatative inflammation
1. Serous inflammation
Serous inflammation is marked by the outpouring of a thin fluid .
Serous effusion: thin fluid from blood serum or secretions of mesothelial cells

2. Fibrinous inflammation
A fibrinous exudate: fibrin
A pink meshwork of fibrin exudate

3. Suppurative or purulent inflammation

 Purulent inflammation is characterized by the product of large amounts of
pus or purulent exudate consisting of neutrophils, necrotic cells, and edema
fluid.
 Pyogenic bacteria
 Surface purulence and empyema:
empyema: mucosa, chorion
 Phlegmonous inflammation:
inflammation: loose connective tissue, diffuse suppurative
inflammation, acute appendicitis
 Abscess:
Abscess: Abscesses are focal localized collections of purulent inflammatory
tissue caused by suppuration buried in a tissue, an organ, or a confined
space.

4. Hemorrhagic inflammation

Categories and features of chronic inflammations

Patterns of chronic inflammation

 Non specific chronic inflammation
Features:
A. collection of chronic inflammatory cells
B. fibrosis
C. degeneration and necrosis are slight

Inflammatory polyp
Proliferation of epithelium of mucosa, gland and granulation tissue
Nasal polyp, cervical polyp, intestinal polyp

Inflammatory pseudotumor
 Inflammatory pseudotumor is a clear boundary tumor-like mass formed by
the inflammatory proliferation of tissues.
 Orbit and lung

 Granulomatous inflammation
Feature
granuloma
 Infectious granuloma: rheumatism, tuberculosis, typhoid, schistosomiasis,
leprosy
 Foreign body granuloma: suture
5. Please tell the pathways of metastasis of malignant tumors.
 a discontinuous spread of the tumor
 Methods of metastasis include: (1) lymphatic spread, (2) hematogenous
spread, and (3) seeding of body cavities.

6. Describe the differences between

Benign and malignant tumors,

characteristics Benign tumors Malignant tumors

Differentiation Well differentiated; low atypia; structure may beSome lack of differentiation with
atypical of tissue origin anaplasia; high atypia; structure is often
atypical
mitosis Normal or rare, without pathological mitotic numerous, with abnormal mitotic
figures figures
Rate of growth Usually progressive and slow; may come to a Erratic and may be slow to rapid;
standstill or regress
Growth pattern Usually cohesive and expansile, well-demarcated Locally invasive, infiltrating the
masses that do not invade or infiltrate the surrounding normal tissues; sometimes
surrounding normal tissues may seem cohesive and expansile but
with microscopic invasion
Metastasis Absent Frequently present; the larger and less
differentiated the primary, the more
likely are metastases
Secondary changes Rare with necrosis and bleeding Usually with necrosis, ulceration, and
hemorrhage
recurrence Rare Frequently present
Influences to humanMild,mainly result in pressure and obstruction Severe, may destroy the normal tissues,
body sometimes result in cachexia

Carcinoma and sarcoma,

carcinoma sarcoma

Derivation Epithelial tissues Mesenchymal tissues

Morbidity High, more seen in adults above 40Low, more seen in youngsters
years old
Gross appearances Hard, dry, gray-white Soft, wet, gray-red, like the flesh
of fish
Microscopically Nests formation, No nests, widespread,
well demarcated betweenpoorly demarcated between
parenchyma and mesenchyma, moreparenchyma and mesenchyma,
fibrous tissues few fibrous tissues and more blood
vessels
Reticular fiber Few more

Metastasis Most by lymphatic routes Most by blood vessels

Immunohistochemistry Epithelial markers Mesenchymal markers

(e.g. cytokeratin) (e.g. vimentin)

neoplastic and non-neoplastic hyperplasia.

neoplastic
 Monoclonal
 Immature with abnormal
structure and function
 Out of control (autonomous):
persists after the initiating
stimulus has been removed
 Unnecessary and harmful to the
body
non-neoplastic
 Includes regeneration,
hyperplasia,and metaplasia
 Polyclonal
 Mature with normal structure
and function
 All are controlled proliferation
and abate after the initiating
stimulus has been removed
 Necessary and beneficial to the
body

7. Morphology of atherosclerosis in
Arteries ,utility of electron beam tomography to detect non calsified

Heart, the heart in renal failure ,mophological change of the heart morphology of
coronary atherosclerosic lession in patients with chronic renal failure

Kidney,
Atherosclerotic contracted kidney

Brain
Cerebral atrophy, cerebral infarct, cerebral hemorrhage

8. Differences of two types of myocardial infarction and its complications

(1)Subendocardial infarction
• involves the inner one third or at most one half of the ventricular wall;
• extends laterally beyond the perfusion territory of a single coronary artery;
 • diffuse stenosing coronary atherosclerosis and reduction of coronary flow
but neither plaque disruption nor superimposed thrombosis;
• Multifocal and small.
2) transmural infarction
• involves the full or nearly full thickness of the ventricular wall;
• locates in the distribution area of a single coronary artery;
• usually associated with total thrombotic occlusion induced by acute plaque
change;
• transmural and large.
Complications
(1) Myocardial rupture
Rupture of the ventricular free wall leads to hemopericardium and cardiac
tamponade
Rupture of a necrotic papillary muscle,
resulting in the acute onset of severe mitral regurgitation
(2) Fibrinous pericarditis
(3) Mural thrombus
(4) Ventricular aneurysm

9. Pathologic changes of benign hypertension in

Vessels,
a. Arterioles
Hyaline arteriolosclerosis

Leakage of plasma components across vascular endothelium Hyaline degeneration of the wall
Increasing ECM production by smooth muscle cells (SMCs)
Apoptosis of SMCs

Wall
Renal arteriolosclerosis: thickening
homogenous, pink and hyaline deposition within the wall and lumen
narrowing
b. Small muscular arteries
Fibroelastic hyperplasia:
increased collagen and elastic fibrin in the intima, destruction of internal elastic membrane;
medial SMCs proliferation and hypertrophy, increased collagen and elastic fibrin

wall thickening and lumen narrowing

c. Large arteries -- accompany with As

Heart,
Morphology:
Concentric hypertrophy
thickening of the LV wall, 1.5-2cm;
increased weight, >400 g;
without dilation of the LV
Eccentric hypertrophy
with dilation of the LV

Kidney,
Gross appearance
Benign nephrosclerosis or primary granulo-contracted kidney:
symmetrically contracted; decreased in size and weight; hardened;
fine, leathery granularity of the surface;
on section, cortical narrowing

Brain
① hypertensive encephalopathy
headaches, nausea, vomiting and
visual impairment
hypertensive crisis: loss of consciousness,
convulsions 抽搐
②cerebral softening
microinfarct (lacunar infarct, 腔隙性梗死)
③cerebral hemorrhage
large fatal
microaneurysm

10. Essential morphology of the rheumatism and changes in the heart

(1)alteration and exudation
sites: heart, joints, skin, arteries, lung.
features: mucoid degeneration and fibrinoid necrosis , serous, fibrinous exudate, and
leukocytes infiltration.
outcomes: complete resolution, fibrosis, granulomas.
2) Proliferation or granulomas
Sites: interstitial connective tissues of the heart, perivascular
Hallmark: Aschoff bodies
①central fibrinoid necrosis
②Anitschkow cells（Aschoff cell）
Macrophage-derived,
Abundant amphophilic cytoplasm,
Central round-to-ovoid nuclei (the chromatin is disposed in a central slender, wavy
ribbon),
owl-eye cells or caterpillar cells
③Aschoff giant cells
④lymphocytes and plasma cells

(3) Fibrosis
 Aschoff bodies spindle scar

Changes in the heart

11. Describe the differences between lobar pneumonia and lobular pneumonia
difference name Lobar pneumonia Lobular pneumonia
Site of the lesion alveoli Bronchioles
Distribution Entire lobe or more Lobules, patchy
Nature of Fibrinous inflammation Suppurative
inflammation
Patients Adults Infants and aged
Etiology Streptococcus pneumoniae Staphylococci, streptococci,
(pneumococcus, type 1, 3, 7) pneumococci (type 4, 6, 10)
Characterized by wide-spread fibrinosuppurative An acute suppurative
consolidation of large areas and inflammation characterized by
even hole lobes of the lungs patchy consolidation, which
originates from bronchioles
Pathogenesis Respiratory defense An extension of a preexisting
mechanisms are impaired. bronchitis or bronchiolitis
Some interfering factors: loss Having overt inductive factors
or suppression of the cough Complications of other diseases
reflex.
Injury to
the mucociliary apparatus.
Interferenc
e with the phagocytic or.
bacterici
dal action of macrophages
The resistance of the host is
lowered.

12. Comparison of peptic ulcer of stomach and ulcerative gastric carcinoma

peptic ulcer of stomach Ulcerative gastric car.

Size <2cm >2cm
Shape regular, round to oval irregular, like a volcanic
crater
Depth Deep shallow
Margins Regular and neat Irregular and heaped up
Base Smooth and clean Un even, hemorrhage and
necrosis
Surrounding mucosal Radiate like whell spokes Interrupted, nodular mass
folds

13. Basic pathologic changes of viral hepatitis

Inflammation mainly concerning with alterative changes of hepatic parenchyma

Alteration hepatocyte degeneration

and necrosis
Exudation inflammatory infiltration
Proliferation mesenchymal reactive
proliferation and
hepatocyte regeneration

14. Morphology of chronic hepatitis and severe hepatitis

Chronic hepatitis
symptomatic, biochemical, or serologic evidence of continuing or relapsing viral
hepatitis for more than 6 months, with histologically documented inflammation and
necrosis, mainly transformed from HBV and HCV hepatitis
3 subtypes:
①mild chronic hepatitis:
chronic inflammatory infiltration and fibrous proliferation within portal tracts,
widening of portal tracts;
focal necrosis, mild piecemeal necrosis ;
well preserved lobular architecture
②moderate chronic hepatitis
moderate piecemeal necrosis and characteristic bridging necrosis;
formation of fibrous bands within lobules;
most lobular architecture preserved
③severe chronic hepatitis
severe piecemeal necrosis and extensive bridging necrosis;
hepatocyte irregular regeneration;
hepatic lobules subdivided by fibrous septa

Severe hepatitis
1 acute several hepatitis
- Massive necrosis with out hepatocytes regeneration
- Hyperemia hemorrhage
- Kupffer cell hyperplasia and hypetrophy
2 sub acute severe hepatitis (both necrosis and regeneration)
-submassive necrosis with nodular regeneration
- over inflamatory infiltration
- bile duct proliferation and cholestasis .
15. Cirrhosis: definition, morphology, clinical features
definition
Chronic liver disease characterized by diffuse parenchymal injury, bridging fibrous
septa and nodular regeneration of hepatocytes, that result in disruption and
reorganization of the architecture of the entire liver.
Morphology

1. Portal Cirrhosis
Etiology: chronic viral hepatitis
Morphology
Histologic features:
 Disruption of the normal architecture of hepatic lobules, pseudolobule
formation
 regular, uniformly sized
 delicate fibrous septa
 few infiltrates within the septa
 mild proliferation and cholestasis of the small bile ducts
Gross view: shrunken, lightened, hardened,
Surface finely granular/micronodular, uniform-sized
Cut surface each nodule is surrounded by delicate fibrous septa.
Color yellow, yellow green

2. Postnecrotic Cirrhosis
Etiology: subacute severe hepatitis
Morphology
Gross view: shrunken, lightened, hardened
Surface coarse nodules with variable sizes
Cut surface variable but most broad septa
Color yellow green or yellow brown
Histologic features:
 Disruption of the normal architecture of hepatic lobules, pseudolobule
formation
 Irregular, variably sized
 Focal or zonal necrosis, even involved the entire lobules
 Broad fibrous septa
 Large amount infiltrates within septa
 Overt proliferation of small bile ducts

Clinical features
 Portal hypertension
1. Ascites
2. Portosystemic shunts
3. Splenomegaly
 Hepatic dysfunction
 1. hypogonadism, gynecomastia
2. spider angioma, palmar erythema
3. Bleeding tendency
4. Jaundice
5. Hepatic encephalopathy

16 the major features of acute diffuse proliferative GN, rapidly progressive GN,
membranous glomerulopathy, minimal change disease, membranoproliferative GN,
mesangioproliferative GN, IgA nephropathy and diffuse sclerosing GN Acute diffuse
proliferative Glomerulonephritis (GN)
 Is characterized by diffuse proliferation of glomerular cells, associated with influx of
leukocyte
 Diffuse endocapapillary proliferative glomerulonephritis (morphology)
 Or poststreptococcal, postiniferative glomerulonephritis (etiology)
 Children 6 to 10 years of age frequently affected
 Acute nephritic syndrome

Rapid progressive Glomerulonephritis (RPGN)

 Is a clinical syndrome characterized by a rapid and progressive loss of renal function
associated with severe Oliguria and death from renal failure within weeks to months.
Histology feature: Presence of the cresecents

Membranous Glomerulonephritis
 Most common in adult
 Also named membranous nephropathy
 Is characterized by diffuse thickening of the glomerulacapillary wall and the accumulation of
electron-dence, immunologlobulin-containing deposits along the subeithelial side of the
basement membrane

Minimal change disease (lipoid Nephritis)

 Most frequents in children (2-6 years of age)
 Diffuse effacement of foot processes of epithelial cells
 Normal appearance by light microscopy

Membranoproliferative Glomerulonephritis
 Is manifested histologycally by altenation in the basement membrane and proliferation of
the mesangial cells
 Also named mesangiocapillary glomerulonephritis

Mesangioproliferative Glomerulonephritis
 Proliferation of mesangial cells and increased matrix
 Common in young adults
 Asymptomatic hematuria, nephritic syndrome
 IgA Nephropathy
 Mesangial deposition of IgA

17Basic lesions, conversion rule of TB

Immune status M.tubeculosis
pathologic
lesions Amount of
Immunity hypersensitivity characteristics
virulence
serous or
exudative weak powerful many strong
serofibrinous
more
proliferative few lower tubercle
powerful weaker

Necrotic weak most powerful many strong caseous necrosis

18 Comparison of primary and secondary pulmonary TB in the following aspect: susceptible

host, immunity, characteristics of the lesions, dissemination, conversions and clinic
courses
Site name Primary pulmonary T.B secondary pulmonary T.B
Susceptible host Children adults
Immunity No previous immunity or There is previous
hypersensitivity immunity and
hypersensitivity to
tubercle bacilli.
Characteristic of lesions Ghon complexs Coexistence of new and
old lesions; localization.
Dissemination Usually lymphatic or mainly along the airway
hematogenous but rarely
by airway
Conversion
Clinic course Short, 95% of the patients Long, fluctuating.
are healed.

19 tuberculoma) Characteristics of the lesions and clinic implications in

common PTB (focal PTB, infiltrative PTB, chronic fibrocavernous PTB,
caseous pneumonia and
 20 Characteristics of the intestinal lesions for typhoid fever and bacillary
dysentery
Typhoid fever

a) Bacillary dysentery refer to an pseudomembranous inflamation caused by

the genus shigella ,which affect predominatly rectosigmoid colon
The lession is located at sigmoid colon or rectum
1 clinical manifestations
-bellyache ,diarrhea
- tenesmus
- stool:loose stools contain blood ,pus and mucus
--Fever
b) intestinal lesions for typhoid fever
1) favorable site : peyer pather and isolated lymphoid nodule in terminal
2) clinical staging : medullary swelling ,necrosis ,allceration ,healing
3) clinic manifestation ,persistant high fever ,relative infrequent pulse tumefaction
of liver and spleen .

21 Favored sites and morphology about Schistosomiasis in the gut

a)Favorite site sites are rectum sigmoid colon , descending colon
b) Morphology of schistosomias is cercaria penetrating the skin the cercaria
produce cercarial dermatitis due to type 1 and iv hypersensitivity which
presents as pruritic rash .
schistomiasis moving into the pulmonary tissue schistosomiasis causes congestion ,
Edema, puntate hemorrhage, infiltration of esinophils and monocytes and vasculitis.
- Adults: schistosome- toxic injury of metabolites and excretion of the
decomposed production of dead worm cause eosinophilic abscess.
- eggs: acute egg granuloma, chronic egg granuloma.
- Circulating antigens: type III allergy at blood vessles joint, kidney

22 Morphology and clinical manifestations about Schistosomiasis in the liver.

Acute stage:
- The liver is enlarged with a nodular or bosselated gleason’s capsule. Yellow or
gray nodules are found on the capsular surface and liver parenchyma. The acute egg
nodules are distributed near the portal area. Hepatocytes may show atrophy,
degeneration and necrosis. Portal inflammation may occur in some cases.
- portal blood vessles and hepatic sinuses are congested usually with infiltration
of eosinophil, lymphocytes, plamocytes and macrophages.
Chronic stage:
- Fibrous egg nodules and scar are formed. Some tributeries are atrophied,
obstructed and disappeared due to the pressure. Hepatocytes may presently
degeneration, atrophy and proliferation, but no regenerative nodule is
formed. Kupffler cells proliferate to phagocytes schistosomal pigment.
- The liver is hardered atrophied discollorated and disformed.

Clinical manifestations:
- Presinusoidal portal hypertension
- Sever congestive splenomegaly
- Esophageal varices and ascites.

23 Differences between Pipe-stem cirrhosis and portal cirrhosis.