Cellular adaptations allow cells to adjust and comply with changes in their internal and external environments as a survival strategy. There are physiological adaptations, like changes during pregnancy, and pathological adaptations, like ventricular hypertrophy in response to stress. Atrophy and hypertrophy are types of adaptations where the cell size decreases or increases, respectively. Neoplasms are abnormal cell growths that can be benign, malignant, or locally malignant depending on their behavior and prognosis. Malignant tumors can spread locally or metastasize through lymphatic or hematogenous routes.

1. Cellular Adaptation
Associate Prof.
PhD (UK), MD(Egypt)

2. Definition
 Adapt = accommodate or adjust,
to comply with changes in internal and
external environment
 It is a Survival Strategy – in response to
physiological or pathological demands

3. Types
 Physiological adaptations: usually
represent responses of cells to normal
stimulation by hormones or endogenous
chemical substances. For example, as in the
enlargement of the breast and
induction of lactation by pregnancy.
 Pathologic adaptations: they provide the
cells with the ability to survive in their
environment and perhaps escape injury. For
example as in ventricular hypertrophy

4. Atrophy
 Definition: Atrophy is reduction or
shrinkage of the size of the parenchymal
cell due to loss of cell substance. When an
adequate number of cells are involved, the
tissue or the organ becomes atrophic i.e.
diminished in size
 Causes/Types: Atrophy may be
physiological or pathological adaptation

5. A. Physiologic Atrophy
 I. Localized atrophy:
1- Atrophy of thymus after puberty.
2- Atrophy of gonads and mammary glands
after menopause.
 II. Generalized atrophy:
Aging or senile atrophy. It occurs in the brain
and the heart.

6. 6
Senile Atrophy of Brain
Aging or senile atrophy represents {Physiological
Generalized Atrophy} which is associated with
physiologic, structural alterations & cell loss.
Normal
Senile
Atrophy

7. B. Pathologic atrophy
 I. Localized atrophy:
1. Vascular or Ischaemic atrophy
2. Neuropathic atrophy
3. Disuse atrophy
4. Pressure atrophy
 II. Generalized atrophy:
1. Chronic malnutrition and Starvation
2. Increased catabolism in some
longstanding diseases such as
tuberculosis and malignancy.

8. Ischaemic Atrophy of
the kidney
8
Pathologic localized
Atrophy

9. Hypertrophy
 Definition: Hypertrophy is an enlargement
of the organ or tissue due to increase in
the size of its cells, without any change in
the
number of the cells.
 Causes/Types:
Hypertrophy may be physiological or
pathological.

10.  A. Physiologic hypertrophy:
 For example:
1. Enlarged size of uterus in pregnancy due to
hormonal stimulation.
2. Hypertrophy of striated muscles in athletes.
 B. Pathologic hypertrophy:
 For example:
Left ventricular hypertrophy.

11. Skeletal Muscle
Hypertrophy
11
Physiologic
Hypertrophy

12. Ventricular Hypertrophy
12
Pathologic Hypertrophy

13.  Definition:
 Hyperplasia is an increase in the number of
parenchymal cells resulting in enlargement of the
organ or tissue.
 It occurs due to increased recruitment of stimulated
cells from G0 (resting) phase of the cell cycle to
undergo mitosis (proliferation).
 Causes o Causes of Hyperplasia :
 It may be physiological or pathological.
13
Hyperplasia
N.B. Labile cells and stable cells can undergo hyperplasia, while
permanent cells have no capacity for proliferation except few cells as
those in hippocampus & olfactory pulp.

14. A. Physiologic hyperplasia:
I. Hormonal hyperplasia:
1) Hyperplasia of the female breast at puberty,
during pregnancy and lactation.
2) Prostatic hyperplasia in old age.
II. Compensatory hyperplasia:
1) Regeneration of the liver following partial
hepatectomy.
2) Following nephrectomy on one side, there
is hyperplasia of nephrons of the other kidney.
3) Bone marrow hyperplasia following
haemorrhage (bleeding).
14

15. 15
(A) Normal Breast
(B) Physiologic Hormonal hyperplasia of the female
breast during pregnancy and lactation.
Hyperplasia of the female breast

16. B. Pathologic hyperplasia:
1) Endometrial hyperplasia following
oestrogen excess.
2) Formation of skin warts from
hyperplasia of epidermis due to human
papilloma virus.
3) Lymphoid hyperplasia after antigenic
stimulation.
16

17. 17
Normal endometrium
Pathologic Endometrial
Hyperplasia
Pathologic Endometrial Hyperplasia

18. Metaplasia
 Definition: It is a reversible transformation of
one mature type of cells to another type of
differentiated cells of the same group. It is
precancerous.
 Causes/Types:
Metaplasia may be epithelial or
Mesenchymal.

19.  A. Epithelial metaplasia:
1. Squamous metaplasia
Occurs due to chronic irritation whether
mechanical, chemical or infective in origin.
Example: In bronchus in chronic smokers, in
case of bilharziasis of urinary bladder.
2. Columnar metaplasia
Example: In Barrett’s oesophagus
 B. Mesenchymal metaplasia:
This means the formation of mesenchymal
tissue (e.g. bone) from fibrous tissue in
tissues that normally do not contain these
elements.

20. Squamous Metaplasia
Normal
transitional
epithelium of
urinary
bladder
Squamous
Metaplasia

21. Dysplasia
 Definition: Dysplasia means the appearance
of abnormal undifferentiated cells within
the normal epithelial cells that occur due to
chronic irritation or prolonged inflammation.
 Dysplastic cells are characterized by:
1. Dysplastic cells are irregulary arranged from basal
layer to the surface layer.
2. Cellular and nuclear pleomorphism.
3. Increased nucleo-cytoplasmic ratio.
4. Nuclear hyperchromatism.
5. Increased mitotic activity than usual,
6. Increase number of epithelial layers.

22.  Degree of Dysplasia
 According to degree of cell atypia and extent
of involvement, dysplasia is graded into:
1) Mild (involves the lower ⅓ of epithelium),
2) Moderate (involves lower ⅔ of epithelium)
3) Severe/marked or carcinoma in situ “CIS”
(involves all layers i.e. whole thickness of
epithelium, without invasion of the
basement membrane). It is considered a pre-
invasive stage of cancer.
22

23. A
B C D
Mild Dysplasia
(involves the lower
⅓ of epithelium).
Moderate Dysplasia
(involves lower ⅔ of
epithelium).
Severe/marked Dysplasia or carcinoma
in situ “CIS” (involves whole thickness
of epithelium), without invasion of the
basement membrane.
Normal
Squamous
Epithelium
Grades of Dysplasia

25. Neoplasia I
Associate Prof.
PhD (UK), MD(Egypt)

26.  Definition of neoplasm or tumour:
It is a new growth formed by abnormal cell
proliferation which is uncontrolled, progressive,
irreversible and purposeless.
 Any tumor consists of: proliferating cells
(Neoplastic) and fibrovascular stroma (non
neoplastic C.T.& BVs).
 Tumors are classified According to their
behavior into :
1.Benign neoplasms (generally have good prognosis).
2. Malignant neoplasms (generally have poor prognosis)
3. Locally malignant neoplasms (locally aggressive or
intermediate tumors).

27. Comparison Between Benign and Malignant Neoplasms
MALIGNANT NEOPLASMS
BENIGN NEOPLASMS
A) TUMOR BEHAVIOR
1-Rate of growth: Often rapid.
2-Mode of growth: Invasive or
infiltrative therefore the surrounding
tissue is often invaded.
3-Prognosis:
a) Local & distant spread.
b) Recurrence is very common
c) Malignant tumors are dangerous
& cause death due to spread,
cachexia, organ destruction & failure
(e.g. liver failure, respiratory failure,
renal failure.)
1- Rate of growth: Often slow.
2- Mode of growth: Expansible
therefore the surrounding tissue is
often compressed.
3- Prognosis:
a) No spread.
b) Do not recur if well excised.
c) Not dangerous unless:
-They arise in vital organs as
brain.
-They cause obstruction.
-They may change into
malignant.

28. MALIGNANT NEOPLASMS
BENIGN NEOPLASMS
B) Tumor structure
• A tumor inside a solid organ appears
as an irregular mass.
* Tumors arising, from surface
epithelia appear as either:
1- Polypoid fungating cauliflower
Mass
2-papillary pattern
3-Ulcerative pattern: with raised
everted edges, rough necrotic floor &
indurated base.
4-lrregular infiltrative growth below the
surface.
1-GROSS FEATURES:
* In solid organs the tumor appear
globular and commonly capsulated
*Tumors, arising from a surface
(skin, mucous membranes) appear as
defined non capsulated projection
called polyp or papilloma
1 2
3 4
Well defined
& capsulated
mass
Polyp or
papilloma

29. MALIGNANT NEOPLASMS
BENIGN NEOPLASMS
B) TUMOR STRUCTURE
-The malignant cells show the criteria of
malignancy which include:
1 ) Hyperchromatism: the nuclear
chromatin increased and looks coarse &
clumpy. This result in dark-staining nuclei.
The nucleus may contain prominent
nucleolus.
2) Increase Nucleo/Cytoplasmic ratio
(1:1).
3) Abundant abnormal mitosis.
4) Tumor giant cells present with nuclear
atypia.
5) Pleomorphism: variation in size & shape
of cells.
6) Anisonucleosis: variation in size and
shape of nuclei.
2-MICROSCOPIC FEATURES:
- In benign tumors the tumor
cells are similar to the normal tissue
(perfectly differentiated):
1) Hyperchromatism: Absent
2) Normal Nucleo/Cytoplasmic ratio
(normal 1:5).
3) If present, mitosis is normal.
4) Tumor giant cells, may be present
but there is no atypia.
5) Pleomorphism: Absent.
6) Anisonucleosis: Absent.

30. 30
Mesenchymal origin
Benign: suffix “Oma”
Malignant: suffix “Sarcoma”
Epithelial origin
Benign: suffix “Oma”
Malignant: suffix “Carcinoma”
Malignant Only:
◘ Lymphoid tissue: Lymphoma
◘ Haemopoietic cells: Leukemia
◘ Mesothelium: Mesothelioma
Glandular epithelium
Surface epithelium
Malignant
Benign
Malignant
Benign
Benign & Malignant:
◘ Adipose tissue
◘ Fibrous tissue
◘ Cartilage
◘ Bone
◘ Smooth mc
◘ Skeletal mc
◘ Blood vessels
◘ Lymphoid vessels
◘ Meninges
◘ Nerve sheath
Adeno-
carcinoma
Adenoma
1. Fungating
Ca
2. Papillary
Ca
3. Malignant
Ulcer
4. Infiltrating
Ca
Papilloma
Classification of Tumours

31. Comparison between Carcinoma & Sarcoma
Sarcoma
Carcinoma
A. General features
1. Definition: Malignant tumor of
mesenchyme.
2. Much less common than carcinoma
3. Age :Usually (but not always)
below age of 20 years.
4. Growth rate: Faster than carcinoma
5. Distant spread:
- Usually faster than carcinoma
- It occurs early by blood & rarely by
lymphatics
6. Sarcoma is derived from the Greek
word “sarc” meaning flesh to describe
its fleshy consistency
1. Definition: Malignant tumor of
epithelium.
2. Most common form of malignancy
3. Age: Usually (but not always)
above age of 40 years.
4. Growth rate: Rapid
5. Distant spread:
-Usually slower than sarcoma
- It occurs early by lymphatics then
later by blood
6. carcinoma is derived from the
Greek word “Carcinos” meaning a
crab describing its infiltrating mode of
growth.

32. Sarcoma
Carcinoma
B. Gross Features
1-Most sarcomas form bulky masses.
2-Consistency: Usually soft and fleshy.
3-Colour is tinged pink due to rich
vascularity.
4-Sarcomas arising in a solid organ
forms a bulky growth , more regular
than carcinoma
5-Sarcomas do not arise from surface'
epithelium therefore do not classically
appear as ulcerating or cauliflower
masses.
or an ulcerative growth
1 -Size is usually less bulky than
sarcoma,
2-Consistency: Usually hard.
3-Colour is usually grayish.
4-Carcinoma may arise inside a solid
organ ( liver, kidney) & forms an
irregular growth.
5-Carcinoma can also arise from
surface epithelium (as skin or mucous
membranes) forming a fungating
cauliflower mass, papillary, infiltrative

33. Sarcoma
Carcinoma
C. Microscopic Features
1-Cell cohesion is often absent and the
tumor cells present singly.
2-Blood vessels are more numerous
and thin walled
3-TNM is graded as FOLLOWING:
T: usually graded as T1 or T2
according to size
N: usually graded as N0 & N1
M: graded as M0 & M1.
1-Cell cohesion: malignant cells form
sheets or groups. Cohesion decrease in
less differentiated tumours
2-Blood vessels are less and better
formed than in sarcoma.
3- TNM Staging:
T: represents tumor state & size,
graded as Tis (tumor in situ), T1,
T2, T3&T4.
N: represents the degree of
spread to Lymph nodes and is
TNM system (modified):
N0,N1,N2 & N3 (N0 means
absent)
M: represents metastases due to
blood spread and is graded as
M0 (absent) or M1 (present).
Examples T1 N0 M0 is early
cancer stage (better prognosis),
while T4 N3 M1 Is an advanced stage (
worst prognosis)

34. Oral papilloma
34
Benign tumour of surface epithelium

35. Thyroid Adenoma
35
Benign tumour of glandular epithelium

36. Lipoma
36
Lipoma: Benign Tumour of fat cells

37. Nevus
Nevus or Benign melanoma:
Benign Tumour of melanocytes
that present in epidermis of skin. 37

38. 38
Malignant tumour arising from surface epithelium in the
form of malignant ulcer

39. 39
Malignant tumour arising from stomach mucosa in the
form of malignant ulcer

40. Chondrosarcoma
with pathological
fracture

41. Characteristics of
Locally Malignant Tumours
 Locally malignant tumours is a group of
intermediate tumors that are characterized by:
1- A slower rate of growth than malignant tumors.
2- Local invasion without distant spread.
3- Microscopic features of malignancy.
4- They may changes into malignant tumors.
 Examples of locally malignant tumors:
1- Basal cell carcinoma.
2- Giant cell tumor of bone (osteoclastoma).
3- Adamantinoma

42. Osteoclastoma
Locally Malignant
tumour arising from
epiphysis of long
bone.
42

44. Neoplasia II
Associate Prof.
PhD (UK), MD(Egypt)

45. Routes of Spread of Malignant Tumours

46. Routes of Spread of Malignant Tumours
I. LOCAL (DIRECT) SPREAD:
 Tumor cells invade adjacent structures.
II. DISTANT SPREAD (METASTASIS):
 Metastasis is the development of secondary malignant
implants, discontinuous with the primary tumor .
 Metastasis can occur by:
A) LYMPHATIC SPREAD:
1- Lymphatic embolism:
2-Lymphatic permeation:
B) HEMATOGENOUS (BLOOD) SPREAD
C) SPREAD THROUGH BODY CAVITIES
D) OTHER METHODS OF SPREAD:
1- Transluminal implantation
2- Surgical implantation
3- Implantation from carcinoma of lower lip

47. A) LYMPHATIC SPREAD: Occurs more
commonly with carcinomas than sarcomas.
1- Lymphatic embolism:
Malignant cells invade the wall of lymphatic
vessels -> tumor emboli -> lymph node. Grossly:
The affected nodes are enlarged & firm. They
may become fused Fixed. Microscopically the
metastatic deposit resembles the primary tumor
from which it is derived.
2-Lymphatic permeation:
Lymphatic obstruction -lymphatic edema.
Example :Breast carcinoma -> permeation of
axillary lymphatics-> edema of the whole arm.

48. Lymphatic Spread of Malignant Tumours
Lymphatic
Permeation
Lymphatic Emboli

49. B) HEMATOGENOUS (BLOOD) SPREAD
 Emboli derived from primary tumors of organs drained
by systemic veins (vena cava) e.g. breast, and kidney->
pulmonary arteries -> lung metastases
 Emboli derived from tumors of lungs (whether primary
or metastatic) are carried through pulmonary veins to left
side of heart and systemic arterial circulation ->
metastases In different organs as liver, bones, brain...etc
 Emboli derived from tumors of organs drained by the
portal vein (tumors of gastrointestinal tract) -> liver
metastases.

50. 50

51. C) SPREAD THROUGH BODY CAVITIES:
Example: Carcinoma of stomach, colon, pancreas ...etc ->
metastatic peritoneal omental nodules.
D) OTHER METHODS OF SPREAD:
1- Transluminal implantation
malignant cells detached from transitional carcinoma of the renal
pelvis may become implanted in the mucosa of urinary bladder
forming secondary deposits.
2- Surgical implantation
Instruments contaminated with malignant cells
during surgical management of a tumor may transfer tumor cells into
the surgical wound causing secondary tumor deposits.
3- Implantation from carcinoma of lower lip

52. Mechanism and Biology of
Invasion & Metastasis
 The process of local invasion and distant
spread or metastasis (lymphatic and
haematogenous) involves the following
steps:
A. Invasion of the basement membrane
B. Passage through the extracellular matrix
C. Invasion of lymphatic or vascular channels
D. Extravasation of tumour cells
E. Survival and growth of metastatic deposit 52

53.  A- Invasion of the Basement Membrane:
 The tumour is termed invasive when the
epithelial tumour cells invade the basement
membrane then extracellular matrix.
 Loss of cellular cohesion: Normal cells are
coherent to each other by molecules called
cadherins. Tumour cells lose cadherin
expression, thus get the ability to detach.
 The tumour cells (through receptors) become
attached to the basement membrane, then they
migrate through it.
 Lysis of basement membrane occurs due to
release of proteolytic enzymes 53
Mechanism and Biology of Invasion & Metastasis

54.  B- Invasion of (Passage Through) the
Extracellular Matrix (ECM):
 After attachment of tumour cells to the basement
membrane, they migrate through it then attach
themselves to matrix components which promotes
the release of proteolytic enzymes.
 Proteolytic enzymes are released by malignant cells
which cause degradation (lysis) of ECM
components.
 Migration (motility) of tumour cells through ECM:
This is mediated by Autocrine motility factor
(AMF), a type of tumour cell cytokine
54
Mechanism and Biology of Invasion & Metastasis continued

55.  C- Invasion of Lymphatic and Vascular
channels & dissemination (spread):
 After the malignant cells have crossed the
basement membrane and invaded the
extracellular matrix, these cells penetrate the
lymphatic and vascular channels in the form
of tumour emboli (clumps).
 Less then 0.1% of malignant cells in the
blood stream survive to develop into
metastasis.
55
Mechanism and Biology of Invasion & Metastasis continued

56.  D- Extravasation of Tumour Cells:
 Tumour cells circulate (inside capillaries,
venules or lymphatics) until they get impacted
(mechanically block) in small blood vessels.
 Then they become attached (adherent) to
vascular endothelium.
 Then they attach themselves to basement
membrane, cross through it and invade the
ECM (in a similar way to previously
described)
 Once invaded ECM, they proliferate forming
secondary deposits. 56
Mechanism and Biology of Invasion & Metastasis continued

57.  E- Survival and Growth of Metastatic
Deposit:
 The extravasated malignant cells grow further
under the influence of growth factors produced
by tumour cells.
 These growth factors in particular include FGF,
and TGF-ß that stimulates angiogenesis.
 The metastatic deposits grow further if the host
immune defence mechanism fails to eliminate it.
 Metastatic deposits may further infiltrate the
same organ or spread to other sites by similar
mechanisms.
57
Mechanism and Biology of Invasion & Metastasis continued

58.  The most common sites for metastasis are liver,
bones, lungs & brain.
 It is rare & not common in muscles, spleen,
pancreas or intestine.
 Grossly: Metastases appear as scattered round
in shape nodules of variable sizes.
 Microscopically: Metastases resemble the
primary tumour.
 Bone metastasis: It is common especially in
carcinomas of breast, prostate, thyroid, lung &
kidney. It develops in vascular bone sites (ends
of long bones & vertebrae, ribs sternum, pelvis &
skull). 58
Survival and Growth of Metastatic Deposit continued.

59.  Bone metastases are commonly osteolytic
but in some tumours they are osteosclerotic
(i.e. there is new bone formation around the
metastatatic deposits).
 Effects of bone metastasis include:
A. Pathological fracture,
B. Severe pain,
C. Bone marrow destruction
59
Survival and Growth of Metastatic Deposit continued

61. Neoplasia III
Associate Prof.
PhD (UK), MD(Egypt)

62. Carcinogenesis

63. Carcinogenesis
 Definition: Carcinogenesis means induction
of cancer & agents which can induce cancers
are called carcinogens.
 Carcinogens are divided into 4 groups:
I. Chemical carcinogens
II. Physical carcinogens (mainly radiation)
III. Hormonal carcinogens
IV. Biological carcinogenesis
63

64. I. Chemical carcinogens
 The induction of cancer by chemical
carcinogens occurs after a delay of several
years.
 Other factors that influence the induction of
cancer are the dose and mode of
administration of chemical carcinogen,
individual susceptibility and various
predisposing factors explained before.
 Cellular transformation by chemical
carcinogens is a process involving 2 distinct
sequential stages: Initiation then
Promotion. 64

65.  1. Initiation:
 The change can be produced by a single dose of the
carcinogen for a short time, however larger dose for
longer duration is more effective. The change is sudden,
irreversible & permanent. These cells are called latent or
initiated cells which just have altered DNA (mutation) but
can’t proliferate to form a tumour.
 Examples of initiators carcinogens:
1) Polycyclic aromatic hydrocarbons: tobacco and cigarette
smoke cause cancer lung.
2) Aromatic amines and azo-dyes cause cancer bladder.
3) Naturally occurring products: aflatoxin causes hepatic
carcinoma.
4) Miscellaneous: Nitros compounds like nitrosamines
involved in gastric carcinoma.
5) Vinyl- chloride cause hepatic angiosarcoma
65

66.  2. Promotion:
 It is the next stage in the chemical carcinogenesis.
 Certain chemical substances (tumour promoters)
act on the latent or initiated cell to undergo
autonomous proliferation.
 They require administration for sufficient time and
in sufficient dose.
 Tumour prompters act by activation of growth
factor pathways.
 Examples of Promoters of carcinogenesis:
1) Phenols.
2) Some drugs.
66

67.  Radiation Carcinogenesis:
A. Ultraviolet light.
 In humans, excessive exposure to UV rays can cause
various forms of skin cancers e.g. squamous cell
carcinoma, basal cell carcinoma and malignant melanoma.
 UV radiation may induce mutation.
B. Ionising radiation.
 Ionising radiation of all kinds like X-rays can cause cancer.
 Radiation damages the DNA of the cell
 Most frequently radiation-induced cancers are all forms of
leukaemias, osteosarcoma, skin and lung malignancy.
67
II. Physical carcinogens

68.  1-Oestrogen: Women receiving oestrogen
therapy and women with oestrogen-secreting
tumours have increased risk of developing
endometrial carcinoma.
 2-Contraceptive Hormones: increase the risk
of developing breast cancer and may lead to
hepatic adenoma.
 3-Anabolic Steroids: Consumption of anabolic
steroids by athletes to increase the muscle
mass is unethical practice and increases the risk
of benign and malignant tumours of the liver.
 4- Androgens: its ↑ can promote prostatic Ca. 68
III. Hormonal carcinogens

69.  1. DNA & RNA oncogenic viruses: e.g.
A. High risk types of Human Papilloma Viruses (HPV types
16 and 18) are associated with the development of
cancer cervix, while HPV (types 6 and 11) may cause
genital warts or condyloma acuminata.
B. AIDS (Kaposi’s Sarcoma).
C. Hepatitis C (liver carcinoma).
D. Epstein Barr virus (nasopharyngeal carcinoma and
Burkitt’s lymphoma).
 2. Parasites (e.g. schistosomiasis) are
associated with high incidence of cancer of the urinary
bladder in Egypt.
 3. Bacteria (Helicobacter pylori) infection cause
gastric lymphoma and gastric carcinoma.
69
IV. Biological carcinogens

70. Causes of Death in Malignant
Tumours

71. Causes of Death in Malignant Tumours
1. Local organ destruction due to direct
spread.
2. Destruction of distant organs by
metastases (distant spread).
3. Tumours of hollow organs as intestine →
lumen obstruction.
4. Organ failure e.g
- Renal failure due to urinary obstruction (or bilateral renal tumours).
- Liver failure & jaundice in case of primary or metastatic liver tumours.

72. 6. Malnutrition due to:
 Loss of appetite.
 Interference with food intake (in cancer of
GIT)
7. Chronic toxemia due to secondary
bacterial infection.
8. Anaemia is common due to several
causes including:
 Recurrent hemorrhages from the tumour.
 Bone marrow destruction by metastases.

73. 9. High tumour cell metabolism may lead to folic
acid deficiency. Iron deficiency may also occur.
10. Autoimmune hemolysis occur in some cases.
11. Cachexia:
 This is marked wasting & weakness (due to anemia,
toxemia, malnutrition, organ failure)
 It's manifested by marked decrease of body weight
accompanied by profound weakness, anorexia &
anemia. The body resistance is lowered & infections
as pneumonia may terminate the patient's life.
 Recently, it has been shown that TNF or tumour
necrosis factor (released from activated
macrophages) may play an important role in
cachexia because it both suppresses the patient's
appetite and interferes with fat metabolism.

74.  12. Paraneoplastic Syndromes occur in 10% of
cases. They are a group of conditions
developing in patients with advanced cancer
which are neither explained by direct and distant
spread of the tumour nor by the usual hormone
elaboration by the tissue of origin of the tumour.
 A) Endocrine syndrome: Elaboration of
hormones or hormone-like substances by cancer
cells of non-endocrine origin is called as ectopic
hormone production. There is:
1) Hypercalcaemia.
2) Cushing's syndrome
3) Polycythaemia.
4) Hypoglycaemia 74

75.  B. Neuromyopathic syndromes. About 5%
of cancers are associated with progressive
destruction of neurons throughout the
nervous system without evidence of
metastasis in the brain and spinal cord. This
is probably mediated by immunologic
mechanisms.
 C. Haematologic and vascular syndrome,
e.g. venous thrombosis, disseminated
intravascular coagulation (DIC), leukemoid
reaction and normocytic normochromic
anaemia .
75

76.  D. Gastrointestinal syndromes:
Malabsorption.
 E. Renal syndromes. Renal vein thrombosis
or systemic amyloidosis may produce
nephrotic syndrome in patients with cancer.
 F. Amyloidosis. Primary amyloid deposits
may occur in multiple myeloma whereas
renal cell carcinoma and other solid tumours
may be associated with secondary systemic
amyloidosis.
76