Beruflich Dokumente
Kultur Dokumente
Final
Summary
Chapter
1:
Cellular
reactions
to
aggression
(Based
on
1,2,3,4,5,6,7
chapters
from
Mr.Paiusans
material
and
personal
extras)
Alessandro
Motta,
Medicine
Class
in
English,
3rd
Year,
UVVG
On this chapter we can jump a lot of notional material and focus on some keywords and few categories lists. Hypoxia: reduction of tissue oxygenation Anoxia: missing of tissue ox. Noxious Agents affecting tissues health status: Chemicals such as: strong acids/bases, poisons, everyday chemicals, substances found in workplaces, social chemicals (alcohol, cigarettes) Physical agents: mechanical traumas, extreme temperatures, ionizing radiation, electricity etc. Infective/biological: bacteria, viruses, fungi Adaptive cellular changes are performed by tissues to fight these aggressions, usually follows a recover but they could trigger also pre-cancerous stages, these is a quick revise: Hypertrophy: increase of volume/weight, either physiological (muscle) or pathological (cardiac) Hyperplasia: similar to the abovementioned but with an increase in numbers of tissues components, physiological in pregnancies, pathological for hormonal causes Atrophy: or involution is defined as the reduction in volume of a tissue or organ, previously normally developed. Either physiological (thymus, senility) or path. (Severe chronic diseases or prolonged immobilization) Metaplasia: means the transformation of a specialized tissue in other specialized tissue, but more resistant to the action of harmful agents. Dysplasia: It is more common in the epitheliums, due to action of extremely harmful agents. It is often associated with metaplasia or hyperplasia, and is being called atypical hyperplasia. It is considered more degenerative than an adaptive reaction. If these stages are not enough to the survival of our damaged tissues it can develop two types of death: NECROSIS: uncontrolled cellular death, derived by traumas, noxious agents and anoxia. APOPTOSIS: process characteristic for programmed cell death during organogenesis and hormone-dependent involution occurs in adults (e.g. endometrium during menstruation). It is seen also in certain diseases, such as certain viral infections (viral hepatitis) 1
Types of cell necrosis: 1. Coagulation: triggered by brutal loss of oxygen supply (infarct), necrotic tissues are visually opaque, dry, and gray-whitish, with slightly higher consistency. Considered a structured necrosis. 2. Liquefaction: found in cerebral infarctions (ramollissement) and in the areas of necrosis in case of suppurative bacterial infections. Unstructured. 3. Caseous: Represent a variety of coagulation necrosis, characteristic of tuberculosis infection. Macroscopic, the cazeum looks like fresh cheese or casein. Unstructured. 4. Fat: called also steatonecrosis, fat necrosis is common seen in acute pancreatitis. In this disease occurs autodigestion of the organ due to local activation of enzymes from pancreatic juice composition. Lipase will decompose peripancreatic fat, with the release of free fatty acids that will combine with calcium, triggering a local saponification process. Unstructured. 5. Gangrenous: superimposed a process of putrefaction. It is caused by bacteria that trigger degradation of local structures, with gas release that gives a fetid smell and emphysematous consistency of affected tissues. Primary gangrene (gas gangrene) is produced by a group of anaerobic bacteria, and often occurs as a complication of traumatic wounds. The tissues are very dilated through the gas bubbles (crepe on palpation) and extremely painful. Secondary gangrene may be dry or wet. Dry form is more common in diabetes. This is a nice interactive video with great explanations of necrosiss steps: http://www.susanahalpine.com/anim/KubyHTML/Celdeath.htm
Dystrophies
types
one
by
one
super-summary
(revise
them
one
by
one
from
the
word
file
before
the
exam,
I
do
not
want
to
loose
time
with
details):
Hydro-proteic:
cells
are
no
longer
able
to
maintain
fluid
and
electrolyte
homeostasis, this
leads
to
swelling
(intumescent)
cells.
Increase
in
cell
volume
is
due
to
the
swelling
of
mitochondria.
Are
early
lesions
that
occur
after
many
cell
aggressions,
and
are
often
reversible.
Nucleo-proteic:
depositing
in
tissues
of
uric
acid
and
urate,
of
endo,
or
exogenous
origin.
The
most
important
complication
of
hyperuricemia
is
the
gout.
Acute
attack
of
gout
is
manifested
as
arthritis,
with
all
signs
of
acute
joint
inflammation.
In
chronic
gout,
uric
acid
crystals
are
deposited
in
peri-articular
tissues,
forming
so-called
gout
tophi.
Chromo-proteic:
pigments
are
colored
substances,
accumulated
in
some
diseases.
Two
main
subtypes:
1. Melanin:
brown-blackish
endogenous
pigment,
physiological
accumulation
occurs
in
pregnancies
and
pathological
one
in
Addisons
disease
2. Bilirubin:
yellow-green,
produced
by
spleen,
liver
or
bone
marrow
from
hemoglobin,
first
stage
in
unconjugated,
then
in
the
liver
becomes
associated
with
glucuronic
acid
(conjugated).
The
consequence
of
accumulation
is
the
Jaundice,
which
can
be:
Pre-hepatic
(
unconjugated
in
bloodstream)
Hepatic
(
unconjugated
and
conjugated
in
b.s.)
Post-hepatic
(conjugated
in
b.s.)
Fat: by triglycerides triggers steatosis, with fomations of vacuoles and fatty cysts, a typical one is the Hepatic steatosis. By cholesterols triggers atherosclerosis, xanthomatosis or cholesterolosis. Carbohydrate: Diabetes mellitus is a metabolic disturbance, characterized mainly by hyperglycemia, resulted from a relative or absolute deficiency of metabolically active insulin. The etiology of this condition is not completely elucidated. There are two types of diabetes: insulin-dependent (juvenile) and non-insulin-dependent. This disease affects kidneys, pancreas, SNS, and gives also retinopathies, vascular diseases. Mineral: related to calcium metabolism disorders. Abnormal deposit of calcium in tissues is called pathological calcification, classification name them as dystrophic and metastatic. Hyaline: is a substance with a variable structure, incompletely studied, but essentially consists of proteins or glycoproteins. deposits can occur in both physiological and pathological conditions. Normally, hyaline occurs in the ovarian corpus luteum involution, in uterine arteries after menopause, and old scars. Pathological hyaline deposits are found in the serous membranes after chronic inflammations or in the benign or malignant tumors mass. Amyloid: pathological protein substance stored in various interstitial tissues and organs, in association with various clinical manifestations. Pathogenesis of 3
amyloidosis
is
not
sufficiently
elucidated
so
far,
but
immunological
mechanisms
appear
to
be
particularly
important.
It
can
be
divided
in
primary
and
secondary.
Fibrinoid:
eosinophilic
substance,
homogeneous
or
finely
granular,
showing
similar
tinctorial
affinity
with
fibrin.
The
chemical
composition
is
complex,
including
proteins
and
mucopolysaccharides
and
sometimes
fibrin
and
gamma
globulin.
Are
part
of
collagenosis
disease.
Mucinous
and
mucoid:
Mucin: occurs
in
catarrhal
mucosal
inflammations,
and
in
some
neoplasm
(mucinous
carcinoma).
These
tumors
are
characterized
by
an
intracellular
accumulation
of
mucin,
which
pushes
the
nucleus
to
the
periphery
Mucoid:
accumulations
occur
in
certain
connective
tissue
pathological
conditions
such
as
myxedema,
or
in
certain
mesenchymal
tumors
such
as
myxomas.
Acute lung stasis occurs in the left heart failure, sudden, and has the major consequence pulmonary edema. Chronic lung stasis occurs due to left heart failure slowly installed, allowing pulmonary circulation to adapt to congestion. Lung weight and volume are increased, low elasticity and crepitation, rusty red color. Stasis liver occurs most commonly as a result of right heart failure, with increased pressure in the inferior vena cava. Mostly blood is stagnating in the veins and capillaries of centrilobular sinusoids. 1. Hemorrhages: loss of blood from circulatory system It could comes from the vessels interruption or by erythrodiapedesys (extravasation of blood trough healthy vessel, common of inflammation process) We can have several clinical forms of hemorrhages, external and internal are rough divisions. Then further ones: Interstitial Petechiae: punctiform hemorrhages, capillary origin, produced in the skin, mucous or serous Ecchymosis: larger hemorrhagic spots, diffuse, without tissue swelling. Purpura: spontaneous tegumentary hemorrhage, with diameters ranging between petechia and ecchymosis Hematoma: establishment of a collection of blood that deforms interstitial tissue. Apoplexy: large area of hemorrhagic tissue infiltration, to which are added and alteration of affected tissue. The term is used especially for cerebral and utero- placental hemorrhages Hemorrhages of serous cavities: Hemothorax, hemoperitoneum, hemopericardium, hemarthrosis and hematocele(testicular). From internal organs to the outside: Hematemesis: vomiting of blood coming from the digestive tract hemorrhages (gastric ulcer, cirrhosis with rupture of esophageal varices) Hemoptysis: expectoration of blood from broncho-pulmonary hemorrhages (lung tuberculosis, broncho-pulmonary cancers) Melena: digested blood through stool (duodenal ulcers) Proctorrhagia: removing fresh blood through stool (hemorrhoids) Hematuria: blood elimination in the urine (urinary stones) Menorrhagia: abundant and prolonged menstruation Metrorrhagia: inter-menstrual hemorrhages Epistaxis: hemorrhage from nasal fosses. The seriousness of the hemorrhage may depends of course by the quantity of blood loss but also by the place of installation (check out how dangerous are small cerebral hemorrhages), even 20% of blood loss from circulation have clinical relevance, even less for chronic bleedings in debilitated patients.
There are four clinical anatomical forms of thrombosis: Cardiac Mural: by formation either in atrium, ventricles or valves Arterial:less common due to speed of bloodstream Venous: most common, called phlebothrombosis, predominantly in the lower limbs due to stagnant blood. Capillary: can occur during acute inflammation in a particular syndrome which is called disseminated intravascular coagulation. If patient survives the first occlusion the thrombus can undergo other pathways such as extension, disaggregation, mobilization (thromboembolism) or reorganization of the vessels and reabsorption. 3. Embolism: transport in bloodstream of insoluble masses named embolus, that could stop in a vessel far away from its origin, and could create an infarction of that area. Categories of emboli by nature: solid, liquid, and gaseous. These are the most common and their consequences may vary upon their nature: Thromboembolism, 99% of all of them, they could evolve in pulmonary (most silent -> dyspnea or giving right heart failure) or systemic (depends where the embolus stops). Fat: consequence of long bones fractures, released by adipose panicle. Gas: because of difficult pregnancy, pneumothorax or in case of deep diving with a sudden decompression. Amniotic fluid: due to difficult births, may cause mothers exitus (death). 4. Infarction: area of ischemic necrosis tissue produced as a result of brutal and complete interruption of arterial irrigation which serves that territory An infarct differs from an ischemia only because the interruption of oxygen supply is more rapid and involves an entire vascular portion. Thrombosis and embolisms usually cause it. Consequences may vary according to the oxygen sensitivity, the vascular architecture and the functional status of the organ/area. They are classified as follows:
2. Thrombosis: formation process on the cv system of semi-solid masses called thrombi. It is a pathological process, which is an extension of abnormal hemostasis. Basically, there are three thrombogenic factors: Endothelial/endocardial lesions Alterations in blood flow Blood hypercoagulability By the morphological point of view a thrombus can be: White, of conglutination, fibrin smaller amount, in arteries, hard, slow-grow Red, coagulation, in veins, fibrin and blood cells components, soft, Mixed, levels of intercalated white and red components
Regular: have triangular shape per section, pointing to the hilum and the periphery toward the organ. Of course, seen spatially, these infarcts have a conical shape Irregular: in circulation anastomotic organs. This is seen in the myocardium, which are normally small anastomoses between three major coronary trunks: anterior descending left, left circumflex and right coronary. Others will at least for a while, complement occlusion of one of them. White: (anemic) occur in the organs with compact terminal circulation: kidney, spleen, myocardium Red: (hemorrhagic) are found in soft organs, with double circulation (lung) or anastomotic (gut). Venous obstruction, regardless of their location, is hemorrhagic infarcts.
5. Edema: abnormal accumulation of fluid in the interstitial space and / or in body cavities. These are key steps of its mechanism of formation: Increased hydrostatic pressure; Reduced oncotic pressure within blood vessels; Increased tissue oncotic pressure; Increased blood vessel wall permeability e.g. inflammation; Obstruction of fluid clearance via the lymphatic system; Changes in the water retaining properties of the tissues themselves. Raised hydrostatic pressure often reflects retention of water and sodium by the kidney. It may be also localized (as ascites for peritoneum or hydrothorax for lungs) or generalized and called anasarca (as a consequence of hearth, renal failure or nutritional causes) The Shock: circulatory collapse, resulting in tissue hypoperfusion and hypooxygenation. It is an acute imbalance between content (blood mass) and container (blood vessels), generated mainly by three mechanisms: decreased cardiac output; generalized peripheral vasodilatation; reduction of circulating blood volume. It can be defined and divided also in terms of how it generates: Cardiogenic Hypovolemic Septic Anaphylactic Ill not describe them one by one because I think each of us knows them from physiopathology, dont ya ?!
Inflammations are vascular, cellular and humoral reactions against harmful agents. This tries to destroy, dilute or neutralize noxious and protect body against aggression, may excess protective mechanisms and become harmful itself. Inf. involves all elements present in vascularized connective tissue. There are two kinds of inflammatory events: ACUTE: called also exudative, it lasts minutes to few days, usually ends with full resolution/no damages, is characterized by exudate production and leukocytes migration. Typical and classical morph pathological signs: CALOR, increased temperature due to hyperemia RUBOR, erythema formation triggered by vasodilatation TUMOR, swelling, tissue distension, edema DOLOR, local pain, due to compression of nerves terminations and release of chemical mediators FUNCTIO LAESA, reduction of functional properties Mechanism: Transitory short vasoconstriction (histamine/serotonine) Vasodilation of afferent arterioles accumulation of blood Active Hyperemia Increased extravasation of fluid with high protein content more colloid- osmotic pressure more fluid migration Exudate formation Decreased blood velocity accumulation of leukocytes Leukocytes will adhere through adhesive molecules to endothelial cells and will leave vessels with a process named diapedesis 8
Leukocytes of inflammation process Polymorphonuclear: most common, first activity Monocytes Macrophages: replacing abovementioned after 1-2 days, longer life, proliferates in the in the inflammatory outbreak, phagocytes larger particles Lymphocytes: usually for chronic inflammation but present in acute inflammations of viral etiology Polymorphonuclear/eosinophils: characteristics for allergic reactions or parasitical ones. How does leukocytes are involved in inflammatory process? 1st step Chemotaxis: is a migration process of leukocytes to aggression foci through chemical gradient Phagocytosis: ingestion of material particles, acts in several stages: Opsonization: overlaying material to immobilize foreign particles Formation of the phagosome, a vesicle formed by Pseudopodia from the macrophage/monocytes Phagosome and lysosome cytoplasm form the phagolysosome, triggering leukocyte degranulation Intracellular bacterial destruction What are the possible evolutions of an Acute Inflammation? Complete Resolution Incomplete resolution Conversion into chronic inflammation Which are the categories of acute inf.? Catarrhal: viral/pollution etiology rhinitis 1 watery exudate, 2 viscous, 3 mucopurulent Pseudomembranous: usually of mucosae diphtheria pseudomembranous exudations low invasive rate but rapid multiplication of bacterias Serous: of serosas accumulation in cavities parenchymal organs/teguments often at 1 stage of inflammation Fibrinous: serous membranes/lungs fibrin-rich exudate healing with sequels Suppurative (purulent): due to pyogenic germs toxins produce local necrosis as abscesses (circumscribed) or Phlegmon (diffused) Hemorragic: exudate + RBCs, encountered in TB, cancer or anthrax.
CHRONIC: or proliferative, has long-acting effect, with proliferations of granulation tissues (with macrophages) These inflammatory manifestations interpenetrate with destruction phenomena and attempts of regenerations; hence it could start as a de novo process, not only after an acute phase. Three key differences from the Acute to the Chronic: Monocytes inf. infiltrate with macrophages Tissue alteration Granular tissue proliferation Macrophages are characteristics forming granulomas Lymphocytes lead antibody-mediated immunity and cell-mediated one. The leucocytic positive feedback: Lymphocytes Monokines Macrophages Plasmocytes: local source of antibodies Plomorphonuclear: can be found in chronic inf. Tissue Necrosis: due to chemical mediators released by macrophages action Granulation: formation of new tissue Lymphokines
Here we can find several different types of Chronic Inf.: Non-specific Proliferative are exudative reactions and proliferation of granulation tissue (E.g.: chronic hepatitis, nonspecific nephritis/myocarditis) Granulomatous inf. with partial specificity, can just suggest the etiology, are not taken in account for a sure diagnosis: 1. Granulomas from infectious diseases (typhoid fever, viral inf., chlamidia) 2. Foreign body granulomas, induced by exo/endogenous bodies 3. Granulomas with relatively uncommon diseases (collagen disorders, sarcoidosis, legionnaires, etc.) Specific granulomatous inf. (microbial/parasitic nature, easy to identify) In this last type we have to pay attention about TB, Syphilis and parasitic inf. TB: tuberculosis generates a series of uncommon morphological reactions: Exudative: most early stage, like pulmonary macrophages alveolitis, serous/fibrinous exudate, resolution usually after 10 days, gives caseous necrosis / TB follicle / carnification Proliferative: single lesion complex Kosters tubercular follicle (conglomerate of macrophages) (composed by Langhans giant cells + epitheloid cells + lymphocytic infiltrate) Alterative: coagulation necrosis called cazeification (most common pathway)
10
Nodular: circumscribed military (1mm) / simple (1mm to 3cm) / acinous (larger, alveolar-like shape) / tuberculoma (pseudotumoral, 10 cm) Ulcerative: resulting from caseous masses gives either ulcers or caverns and are source of hemoptysis Diffuse: from caseous bronchopneumonia It has a primary and a secondary form: Primary: first contact with Koch bacillus, primo infections is called Ranke primary complex, with various compliances and evolutions Secondary: re-infection, reactivation of dormant bacilli. Syphilis: an infectious disease with chronic evolution, caused by treponema pallidum spirochete, considered as a venereal disease. It could be either gained or congenital, for gained it could be: Primary: starts three weeks after infection, manifestation located on external genital organs, the specific lesion is called syphilitic chancre, gives ulcerations. It disappears after 5 weeks of evolution. Secondary: multiple and superficial rash, it has several ways of evolutions, and once again disappears for a third apparent healing period. Tertiary: an evolution of previous stages, can lasts from few months up to 30 years, characterized by nodular lesions or diffused ones. Congenital type: result of trans-placental infection from mother to child, it could be fetal, infantile or late congenital. Parasitic inflammation: chronic granulomatous inflammatory processes, specific of different forms of parasites. Vegetal: candidosis, actinomycosis. Animal: toxoplasmosis, trichinellosis
11
Complete
resolution
is
a
healing
mechanism
in
conditions
of
minimal
tissue
damage
with
focal
or
unicellular
limited
necrosis. Destroyed
cells
are
replaced
through
proliferation
of
specialized
cells
in
the
vicinity.
Reparation
is
characterized
by
organization
(replacement
of
damaged
cells
by
an
unspecialized
connective
tissue,
resulting
in
a
fibrous
scars),
and
these
are
the
stages
of
this
process:
Phagocytosis
by
macrophages
Proliferation
endothelial
cells
and
fibroblasts
from
the
edge
of
affected
area
Endothelial
cells
penetrate
in
the
area,
building
a
capillary
network,
that
will
restore
the
blood
flow
Fibroblast
migrate
along
new
network,
making
a
conjunctive
skeleton
Proliferation
of
collagen
fibers
with
formation
of
a
scar
Cutaneous
Wound
Healing
is
a
mixed
process,
consisting
of
a
combination
of
specific
mechanisms
of
regeneration
and
repair.
Depending
on
the
amount
of
destroyed
tissue,
the
persistence
of
inflammatory
reactions,
surgical
approach,
to
wound
healing
is
of
two
types:
First
intention: uninfected
wounds,
with
minimal
lack
of
substance,
such
as
surgical
incisions.
It
takes
place
as
follow
a
blood
clot
emerge
on
the
edges
to
prevent
dehydration
or
infections,
then
will
act
normal
inf.
response
associated
with
the
formation
of
unstratified
epithelial
layer,
follows
the
granulation
(small
amount),
removing
the
clot
and
what
remain
is
just
a
linear
scar.
Second
Intention:
in
unsutured
wounds
or
more
extensive
ones,
it
has
some
stages
as
the
1
type
but
with:
more
granulation
tissue,
uncomplete
epidermic
restoration,
smaller
scar
but
with
stronger
contractions
(deformations
of
affected
segment)
12
which in turn will destroy the target cells. Clinical Manifestations: haemolitic anemia, basedow disease. 3. Type III: IgM, IgG and IgA form antigen-antibody complex, that can be deposited in various tissues; lesions may occur by attraction and activation of neutrophils and thrombocytes. Is involved in collagenosis. 4. Type IV: mediated by lymphocytes type T, involved in rejection of grafts and transplants. In Immune reactions of transplant rejection are involved cell-mediated and antibodies immunity. It has three subcategories: (E.g. is Kidneys transplant) Super-Acute: is mediated by antigen-antibody reaction in vascular endothelium and manifestation is immediate after surgery. Kidney appears cyanotic and secret few drops of hematic urine. Acute: from days to years, involves cellular and immune mechanisms. Cellular one is manifested by a rich interstitial monocyte inf. infiltrate while humoral by necrotizing vasculitis and thrombosis / neutrophilic infiltration Chronic: months or years, announced by a progressive increase of serum creatinine, vascular lesions, cellular inf. infiltrate are mainly plasma cells and eosinophils.
Autoimmune diseases to focus on in this chapter are lupus, scleroderma and AIDS. Systemic Lupus Erythematosus: affects skin, joints, kidneys and serous membranes. It causes necrotizing vasculitis, glomerulonephritis, tegumentary (butterfly shaped facial erythema, hives, rashes and ulcerations); joint level (non-erosive synovitis) Scleroderma: excessive fibrosis of the skin and internal organs. Morphologically: formation of collagen tissue deposits. Can be diffuse or localized; the skin is initially edematiate and after atrophyzed. Microscopically gives deposits of collagen in the dermis and hyaline thickening. The digestive tract is affected at esophagus level; mucosa and interlobular arterioles in kidney are thick because of collagen as abovementioned. At heart level it can cause pericarditis and myocardial fibrosis, it can cause also thickening of alveolar and vascular walls in lungs. AIDS: given by the HIV retrovirus, contracted by sexual contact, parenteral use of needles or congenital. It spreads in the collapse of the immune system, cell mediated immunity initially and lately humoral immunity. There are 2 phases, an asymptomatic period of variable duration and period of clinically manifest disease (AIDS-related complex = ARC) And now starts the interesting part ! 13
Chapter
7:
Tumors
This
is
the
harder
one,
though
to
summarize
and
to
study,
but
probably
the
most
critical
at
the
exam.
A
neoplasm
(Tumor)
is
an
abnormal
mass
of
tissue,
as
a
result
of
an
uncontrolled
and
excessive
irreversible
proliferation.
Cancer
could
develop
in
almost
all
kinds
of
tissues.
The
term
is
related
to
Tumor
as
swelling
in
classic
inflammations.
Nowadays
tumors
are
defined
for
their
microscopic
characteristics
and
divided
in
benign
and
malignant
(cancer).
It
could
starts
either
by
epithelium
or
conjunctive.
It
is
made
up
of
two
aspects:
the
parenchyma
(neoplastic
cells
mass)
and
the
stroma
(sustaining/nutritive
role).
Incidence
of
tumors
depends
on
several
aspects:
geographic
factors,
age,
sex,
race,
inherited
predisposition
and
acquiring
of
pre-neoplastic
lesions
or
conditions.
Carcinogenesis:
means
the
process
of
formation
from
normal
to
malignant
cells,
and
there
are
a
series
of
factors
that
are
involved,
such
as:
Chemicals
(aromatic
hydrocarbons
=
cigarettes
smoke
triggers
lung
carcinoma)
Viruses
(IMPORTANT):
Papilloma
virus
(cervical
cancer),
Epstein-Barr
Virus
(for
Burkitt
Lymphoma)
Radiant
Energy
(ultraviolet
for
malignant
melanoma,
or
ionizing
radiation
specially
for
leukemias)
They
can
alter
the
genetic
unit
of
cells
in
2
ways:
inactivation
of
tumor
suppressor
genes
or
activation
of
some
tumor
stimulating
genes
(oncogenes).
Bio
morphological
Characters
of
Tumors
in
comparsion:
Types:
Evolutional
feat.
1.
Benignant
Slow
grow,
period
of
stagnation
or
regression
2. No
local
invasion,
no
relapse
after
surgery
3. No
metastasis
4. No
cachexia
or
death
Do
not
destroy
surrounding
tissues,
only
compression
of
adjacent
structures
Systemic
effects
generally
absent
Malignant
1. Generally rapid evolutions 2. Local invasion and post- operative recurrence 3. Gives metastasis 4. Cachexia and death Infiltrates invades and destroys surrounding tissues. Systemic effects are noisy, generates metastases and abnormal substances (paraneoplastic syndromes)
Clinical effects
14
Macroscopic feat.
High consistency and color similar to original tissue. Usually encapsulated, oval and well defined formations in parenchymal organs. In teguments/mucosae grow vegetant polyps (sessile or pedicle)
Decreased consistency and soft tumor tissue. White-gray for carcinomas and reddish- hemorrhagic for sarcomas. In parenchymal organs are irregular, not well delimited and without envelopes. On teguments have 3 kinds of grows: vegetant-fungal, diffuse on surface, infiltrative.
Microscopic feat.
Immature cells, no original cells morphology (anaplasia), Mature differentiated malignant cells may stop in numerical increased cells, various evolution stages, with morpho/functionally similar to irregular shape, volume, original cells. Architecture dimension (polymorphism). generally is not disturbed, Increase usually in volume nuclei are uniform in shape and with irregular membranes, configurations, rare mitosis and bizarre/monstrous giant cells. seems typical. Architecture is deeply altered. Nuclei have important changes. Check below
Cytologically speaking malignant tumors have some key features: Nucleal features: Different shape and size (nuclear polymorphism) High volume leading to a compartment ratio in favor of the nucleus Nucleolema has many irregularities with thickening and invagination Nucleoly are hyperplastic, hypertrophic, prominent with dense nuclear material Mitosis is frequent and atypical unequal bipolar or multipolar DNA highly variable, giving polyploidy and/or aneploid Cytoplasmic features: Reduced cytoplasm and content Increased basophilia (increased RNA) Great capability of phagocytosis (cannibalism) Simpler organization as anaplasia increase Invasion and metastasis form of malignant tumors: most important characteristic, which explains post-operative recurrences. Favorited by abnormal mobility, decrease adhesion between malignant cells, and secretions of proteolytic enzymes. Metastasis: process of tumor mobilization, giving birth to new tumor at distance from its origin. It could follows different pathways, such as: 1. Lymphatic: early, specific for carcinomas. Could colonize a lymph node on his road, replace it and attack a new one 15
Prognosis criteria: In clinical practice is used a system with 3 degrees of differentiations: G1 high differentiation (favorable) G2 medium G3 low differentiation (severe evolution) Hence the tumor staging is the assessment used for describing macroscopically and microscopically (after biopsy) the status of a tumoral invasion, it is called TNM international system, and uses imaging techniques associated with histological analysis: T refers to the primitive tumor, the number means its size N refers to the lymphnodal status, follows a number that describes how many are involved and their distribution M presence and extension of metastases E.g. TxN0M1 = tumor not evaluable, no lymph nodes involved, 1 metastasis far from the origin
2. Hematogenous: specific and early in sarcomas, lately in carcinomas, more severe than the first case. Even if more tumoral cells are destroyed in circulation a very few quantities could attack: liver, lungs, bone, adrenal cortex, CNS. Sometimes they tend to be similar to the first place of invasion, hence metastatic tumors tends to be less dangerous than firsts. 3. Along serous cavities: organs neighboring (Krukenberg tumor, ovarian metastasis through peritoneum) 4. Along perineural spaces: cause nerve compression, really painful, nerves atrophies and loss of functionality 5. Trough cerebro-spinal fluid: the only one possible for CNS tumors, cells migration is made through sub-arachnoid space 6. Along tubular organs: such as bronchi, ureters; e.g. pelvis renalis carnicoma metastazing in bladder 7. By direct contact: can occur in post-operative scars after excisions of malignant tumors, a cancer may be inoculated from one lip to the other
16
Methods
of
diagnosis
(nonsense
subchapter,
isnt
a
little
premature
to
make
them???
:D
)
Are
used
several
types
of
methods,
usually
cytological
studies
or
even
better
histopathological,
by
biopsies
taken
during
surgery
or
post-operative.
Are
widely
used
for
therapeutic
orientation.
THATs
IT!
Now
my
little
padawan
and
me
will
try
to
make
a
small
table
to
summarize
every
kind
on
tumor
we
could
face
during
the
exam!
B=
Benign
/
M
=
Malignant
TYPE
NAME
TISSUE
Features
Can
develop
anywhere
in
the
body,
has
viral
etiology
(HPV)
and
can
develop
malignancy.
Appear
as
a
pedicle
(narrow)
or
sessile
(broad
base
of
imp.).
Microscopically
has
several
typical
layers
arising
from
a
central
axis:
stratum
spinosum,
granulosum
and
cornosum;
all
of
them
are
thickened
Can
develop
anywhere,
appears
as
poorly
defined
masses,
non-encapsulated
with
infiltrations
in
surrounding
tissues,
low
consistency
and
whitish
color,
with
necrosis/hemorrhagic
areas.
Types
of
growth:
vegetative,
diffusive,
and
infiltrative.
May
triggers
ulceration.
Can
arise
from
exocrine
or
endocrine
glands,
can
develop
in
internal
organs
(single
or
multiple
nodular
masses)
or
on
membrane
surfaces
(GI
tract,
polyps)
attached
by
a
pedicle.
Papilloma B
Carcinoma M
Adenoma
Epithelial glandular
Adeno- M carcinoma
Epithelial glandular
Occurs more frequent in GI tract, breast, pancreas, endometrium. May be sessile or polypoid, with infiltrations and ulcerations, poorly defined masses, non-encapsulated containing cystic cavities. Particular proliferation by either benign or malignant charters. Known as pre-invasive carcinoma, or carcinoma stage 0 or in situ. Doesnt present big changes in the mucosa and tegument. Derived from epithelial cells of spinous layer, common located o skin/mucosal surface of squamous in metaplasia (tongue, vagina, anus). Divided in keratinized or non-keratinized. Develops from basal cell layer of the epidermis, is composed of cords of small dark cells with little cytoplasm, nuclear polymorphism. Palisade layout at periphery of tumor island.
Epithelial
Epidermis
17
TYPE
NAME
TISSUE
Features
Fibroma
Connective common
Can develop anywhere, appears as nodular formation, circumscribed, encapsulated, pearly white color. Rich of connective fibers (collagen- reticulin) and cells (fibroblasts, fibrocytes) More cells = softer, more fibers = harder.
Mixoma
Connective common
Soft tumor, poorly demarcated, gelatinous, can reach large size. Local infiltrative growth, star- shaped cells floating in mocoid mass. Difficult surgical excision may re-occur.
Sarcoma
Connective common
Can develop anywhere, lower incidence than carcinoma, but could spreads at young age. Generally large, low consistencies, reddish-pink like fish-fresh meat. With necrosis and hemorrhage.
Fibro sarcoma
Connective common
Less aggressive growth in sarcomas family, rare metastasis, usually relapses after surgery.
Connective common
More aggressive evolution, fast growing, infiltrative. With early hematogenous metastasis.
Polymorphi c sarcoma
Connective common
Highest degree of malignancy, no more reminiscent of connective tissue from origin, undifferentiated cells with highly polymorphism and atypical mitosis. Evolution is fulminating.
18
TYPE
NAME
TISSUE
Features
Lipoma
Adipose
Occurs mainly in subcutaneous adipose tissue, with a symmetrical distribution. Consists of hyperplasied unequal adult type of fat cells. Small peripheral nuclei, poor blood supply.
Lipo - sarcoma
Adipose
Generally appears like a single nodular tumor, apparently well demarcated, can reach giant sizes. Looks gelatinous and with cystic areas. There is a well differentiated and a poor-differentiated subtype.
Most
frequently
in
extremities
(phalanges),
can
develop
towards
bony
surface
(Ecchondroma)
or
into
the
depth
of
bone
(Enchondroma).
Consists
of
islands
of
hyaline
cartilage
separated
by
vascularized
fibrous
septa.
Condroma
Cartilagenous
Condro - sarcoma
Cartilagenous
Rare one, occur often de novo as malignant. Usually large tumors, poorly defined, smooth or lobulated.
Most
common
location
in
skull
and
paranasal
cavities,
it
is
small,
round
and
hard.
Growing
towards
the
bone
surface
into
the
depth.
There
are
3
types
of
osteoma:
osteoid,
compact,
spongeous.
Has
a
benign
evolution,
in
10%
act
as
malignant.
Localized
in
long
bone
diaphysis,
looks
soft,
reddish-brow,
with
hemorrhagic
necrosis
and
cystic
formations.
2
types
of
cells:
multinucleated
giant
osteoclasts
and
small
connective
cells
(fibrous
type)
Usually
located
in
metaphysis,
of
long
bones,
large
proliferations
showing
bony
white
hard
areas
alternated
with
soft
fleshy
masses,
and
area
of
necrosis
and
hemorrhage.
3
kinds:
osteogenic
(osteoids),
osteoblastic
(osteoblasts),
osteolytic
(few
bony
element
lysis)
Osteoma
Bone
Osteo - clastoma
Bone
Osteo - Sarcoma
Bone
19
TYPE
NAME
TISSUE
Features
Leyomioma
Muscolar smooth
Anywhere in a smooth muscle, usually in the uterus. Has a characteristic fasciculated aspect, Damascus cloth. Slow growth, with possible stagnation or involution.
Leyomyosar coma
Muscolar smooth
Well-differentiated form are difficult to distinguish from the benign one, just a large number of atypical mitosis helps diagnosis. Frequent vascular lacunae.
Rhabdomyo ma
Striated Muscolar
Mainly developed in skeletal muscle, appear as small nodular formation with hypertrophic muscle fibers, incompletely differentiated.
Rhabdomyo sarcoma
Striated Muscolar
Similar location of abovementioned, can also arise in organs that normally have no striated muscles fibers (embryonic remnants). Several types, the most common is pleomorphic one, occurs in advanced ages. The embryonic type (Botrioid) may appear in youg girls genitalia.
It
Is
a
conglomeration
of
blood
vessels
with
irregular
caliber
and
disordered
arrangements.
3
types:
capillary,
cavernous
and
sclerosing.
Hemangiom a
Blood Vessels
Hemangio - sarcoma
Blood Vessels
Low consistency tumor, spongy, haemorrhagic, consisting of capillary lumens bonded by atypical endothelial cells. We can remember the hemangio- pericytoma and kaposis sarcoma.
20
TYPE
NAME
TISSUE
Features
Proliferations
of
melanocytes,
found
in
the
basal
layer
of
epidermis.
Frequently
colored
in
brown,
rarely
uncolored.
Most
of
them
are
acquired
during
life,
but
can
be
found
congenital.
3
types:
junctional,
intradermal
and
compounds.
Some
of
them
have
potential
of
malignancy,
specially
those
in
palms,
plants
or
mucous
membranes.
Nevi
Melanic Pigmentary
Melanoma
Melanic Pigmentary
May develop as de novo or due to malignization of a nevus, for chronic exposure to irritants. Is one of the most aggressive giving early lymphatic and hematogenous metastasis.They appears as flat formations or polypoid masses with tendency to ulcerations. Melanoma acroma is without pigmentation.
Both
of
them
have
high
malignancy
and
are
very
aggressive.
Is
the
most
common
tumor
of
this
kind,
affects
usually
men,
with
two
peaks
of
incidence
(20/60
years
old).
Etiopathogenesis
unknown.
Starts
in
a
single
lymph
node
located
in
cervical
region,
then
affects
adjacent
ones.
Simultaneously
affects
spleen,
liver
and
bone
marrow.
Rubber
like
elasticity
and
whitish
color.
Partial
or
total
removal
of
lymphnodes
structure
by
polymorphic
cellular
infiltrates.
Pathognomonic
element
is
the
Sternberg-Reed
Cell.
Highly
heterogeneous
group
of
malignancy
due
to
possibility
of
neoplastic
proliferation
of
B
and
T-lymph
cells.
Begins
in
lymph
nodes,
spleen,
liver
and
bone
marrow.
From
here
tumor
can
infiltrate
any
tissue,
also
in
peripheral
blood
(leukemia
lymphoma).
They
are
sometimes
they
increase
in
fibrosis
process,
soft,
whit
or
yellowish
with
necrosis.
Very
controversial
classification.
Hodgkins Lymphoma
Blood Vessels
Blood Vessels
It
has
been
a
though
work,
trust
me,
I
was
impressed
by
how
synthetic
this
chart
can
be
20
pages
from
all
the
morphopathology
material
is
really
a
great
effort!
Hope
you
all
will
find
them
useful
as
we
guess,
have
a
nice
rehearsing
time
with
this
summary.
Sincerely
my
team
wishes
you
the
best
for
this
exam!
Darth Vader: Ale Motta (the Boss) (in Yoda version for his patience) My padawan: Luke (Anakin) Serenas My Lord Sith: Luca Darth Silvestrus Your beloved colleagues specially wish for each of us. May the force be with you
21