Professional Documents
Culture Documents
pathologies
are
treated
in
this
summary,
no
tumors
are
wri5en:
they
will
be
summarized
in
a
single
table
COMPLETE
Version
Insane
graphic
review
for
the
2
semester
exam
Alessandro
Mo5a,
UVVG,
3rd
year
1
Cardiac Pathology
Cardiac Pathologies
Angina pectoris: transient painful crises localized predominantly precordial, three types of angina: Stable angina is usually under 15 minutes, triggered by factors that overload heart (emo;ons, exercise) and resolves at rest and administra;on of coronary vasodilators (nitroglycerin); Instable angina (premyocardial infarc;on, aggravated angina) is caused by the forma;on of a non-obstruc;vely thrombus superimposed to a plaque. Prinzmetal angina is an unusual form of angina that occurs at rest, oRen during sleep, caused by arterial spasm superimposed to a atherosclerosis lesions.
Myocardial infarc6on is the most important cause of morbidity and mortality in modern society. Is an expression of brutal, complete and persistent interrup;on of blood ow through a coronary artery branch, which translates morphologically by necrosis of myocardial territory served by that artery. Comes with Atherosclerosis + superimposed thrombosis, hemorrhage into plaque, persistent arterial spasm, arteri;s, congenital coronary anomalies etc. Lab ndings: raised LDH, CPK. Types: transmural subendocardial. Chronological morphology changes: 1. First 12 hours: no macroscopical changes 2. In 1-2 days: swollen, pale yellow central area, raised neutrophils ac;on 3. In 3-7 days: necrosis area become yellowish, macrophages replace neutrophils, granula;on ;ssue forma;on 4. In 2-3 weeks: depressed area with soR texture 5. In 4-5 weeks: hard scare area, retracted, pale gray
Chronic ischemic heart disease denes slow installa;on of conges;ve heart failure due to myocardial altera;ons by chronic ischemia. Most of these pa;ents have a history of episodes of angina pectoris or myocardial infarc;on. The heart has variable dimensions, myocardium has a brown color and can some;mes be iden;ed area of infarc;on with dierent 2 seniority. There is always advanced lesions of atherosclerosis of the coronary arteries.
Cardiac Pathology
Is a systemic inammatory disease of connec;ve ;ssue, aects children from 5 to 15 years old, symptoms starts aRer 1-4 weeks from a tonsilli;s contrac;on, usually comes with streptococcal infec;ons. The Acute form (rheuma6c fever) has some extra-cardiac manifesta;ons such as: large joints impairments, tegumentary impairments and neurological damage. Cardiac manifesta;ons (rheuma;c pancardi;s) has rheuma;c involvements such as pericardi;s, myocardi;s (with Ascho granulomas) and endocardi;s. The Chronic phase is a sequel of the acute one and triggers valvular deforma;ons, CHF, endocardi;s and thromboembolism. Called eusions, triggers hydropericardium, haemopericardium and chill eusion (lymph). The accumula;on can be from 50 to 2000 ml with or without clinical manifesta;ons Acute: by biological factors, can be in form of: serous, brinous, suppura;ve or hemorragic. in Chronic one we nd a thick peritoneum, constric;ve, brous; triggered by TBC, staphylococcal sep;cemia and radioteraphy Conges6ve/dilata6ve: is the most common, triggered by alcohol/ drugs, dilata;on occurs in both ventricles, HF in 5 years Hypertrophy: in young pa;ents, for long ;me asymptoma;c, gene;c causes are studied, decreases the intraventricular volume Restric;ve: limi;ng diastolic lling, generate atrial dilata;on and retrograde venous stasis, bring to a global HF
Pericardi;s
Cardiomyopathies
dis;nct
group
of
primi;ve
disease
of
the
heart
muscle
that
did
not
cause
inamma;on
and
are
not
associated
with
hypertension,
congenital
heart
disease,
valvular
or
coronary
artery
disease.
It
is
characterized
by
heart
failure,
ventricular
volume
and
increased
ventricular
arrhythmias.
Myocardi;s
Dened as generalized inamma;on of the myocardium. Are classied into two broad categories, rheuma;c (discussed before) and non-rheuma;c such as: 1. Viral (toxic): by HIV, inuenza virus, generally reversible, worse in children and pregnancy status 2. Non-Viral: divided in bacterial, driven by hypersensivity to medicaments and a rare giant cells myocardi;s
Cardiac Pathology
Endocardi;s
Non-infec6ous
may
also
be
of
several
types:
Non-bacterial,
associated
with
metasta;c
cancer
Libman-Sacks,
associated
with
SLE
and
valvular
vegeta;on
progress
From
Carcinoid
Syndrome,
genera;ng
endocardial
plaques
at
RH
Valves
Infec6ous caused by bacterial coloniza;on, rarely fungal, of endocardium, with a severe impairment of valvular apparatus. Acute Bacterial, or ulcera;ve is driven by Staphylococcus Aureus and detroys the valves un;l the HF Sub-Acute Bacterial, or polypous is caused by streptococcus Viridians and triggers a polypoid vegeta;on that generate embolism
Valvulopathies
Mitral
Stenosis
is
caused
usually
by
rheuma;c
diseases,
the
blood
ow
from
LA
to
LV
diminishes,
ini;ally
triggers
an
atrial
dila;on,
in
;me
hypertrophy
and
pulmunary
stasis
with
risk
of
pulmunary
edema.
Mitral
Insuciency
a
very
common
valve
disease,
generated
by
a
mitral
prolapse
or
papillar
muscle
rupture,
blood
regurgita;on
in
systole
triggers
LV
hypertrophy
and
LA
hyp.
Tricuspid or pulmonary ones are very rare, associated with mitral problems. Pulmonary can be aected in congenital or in Fallots tetralogy Aor6c Stenosis is caused usually by calcica;ons or congenital condi;ons such as bicuspid valve. Blood ow diminishes from LV to Aorta, triggers a markes LV hypertrophy and bovine heart in radiology ndings
Aor6c Insuciency may be congenital or aRer a syphili;c aor;;s, blood regurgitates from Aorta to LV
Abnormali;es of embryonic development by gene;c causes or viral infec;ons or teratogen substances. With Blood Shunts from L to R side we nd ventricular septal defects, interatrial septal defects, fetal ductus arteriosus that trigger a late cyanosis. From L to R but with early cyanosis = Fallots tetralogy: pulmonary stenosis, v.septal defect, Dx posi;on of the Aorta, right ventricular hypertrophy. Without blood shunts there are transposi;ons of great vessels, coarcta;on of the Aorta and Situs Inversus (dextrocardia) Dened as the inability of the heart to deal with the body's demands, on the LEFT side is triggered by: ischemic heart disease, MI, arterial hypertension, valvulopathies, myocardiopathies. Generates dispnea, pulmonary edema, hydrothorax, low renal perfusion, cerebral anoxia. On the RIGHT side can be triggered by a previous leR heart failure, a pulmunary vascular hypertension, valvulopathies, cardiomyopathies. Triggers 4 peripheral edema, ascites and hepatomegaly
Heart Failure
Vascular System
Arteriosclerosis
Arteriolo-sclerosis
can
be
divided
in:
Hyaline,
in
chronic
ischemia,
benign
nephroangiosclerosis
Hyperplas;c,
a
concentric
thickening
of
arterioles
walls,
reduced
lumen
and
malignant
nephroangiosclerosis
Atherosclerosis or atheromatosis, has a mixed and not fully elucidated pathogenesis, has various risk factors (hypercholesterolemia, high LDL concentra;ons, hypertension, diabetes, aging, sex=male, smoking). Lesions are founded in the in;mal layer of arteries (atheromas) and are brino-lipidic plaques (with a lipidic center and a ibrous capsule). Evolu;ons: calcica;on, ulcera;on, superimposed thrombosis (occlusion of the arteria), hemorrage, aneurysm. Clinical manifesta;on: MI, chronic ischemia, aneurysm, emboliza;on
Arteri;s
Inamma;on
may
begin
in
in;ma,
media
or
adven;;a
(at
the
level
of
vasa
vasorum)
of
the
arteries.
In
terms
of
these
loca;ons
can
dis;nguish:
endarteri;s,
mesarteri;s
or
periarteri;s.
Arteri6s
types:
Thromboangi;s
obliterans,
named
Buergers
Disease
Polyarteri;s
Nodosa
Syphili;c
Arteri;s
Raynauds
disease
Aneurysms
Abnormal
dilata;ons,
localized,
permanent
of
the
blood
vessels
Atherosclero;c
Celebral
Dissec;ng
(aorta)
Arteromatous
Fistula
(post- trauma;c)
Syphili;c
Venous
Thrombosis
Forma;on
of
thrombi,
oRen
in
the
deep
veins
of
the
lower
limbs.
The
process
is
favored
by
the
stasis
at
this
level
caused
by
impeding
of
venous
return
as
a
result
of
heart
failure,
pregnancy,
prolonged
bed
repose
or
varicose
veins.
Thrombophlebi6s,
comes
with
inamma;on
and
can
be
divided
into:
bacterial,
intravenous
chemical
irrita;on
and
post-trauma;c.
Phlebothrombosis,
in
turn,
comes
without
inamma;on,
it
can
be
post-opera;ve,
obstetrical,
medical- associated
and
migratory
Varicose Veins
Are abnormally dilated veins, with a tortuous course, mainly are founded in lower limbs, but we can also nd them in form of esophageal varices (portal hypertension), hemorrhoids and varicocele
Respiratory System
3
Respiratory
System
Pathologies
Rhini6s are inamma;on of the nasal mucosa. Can be acute and chronic. Acute rhini;s, in turn, can be: Acute viral rhini6s (common cold) is caused mainly by adenoviruses. It manifests clinically with increased nasal secre;on, nasal conges;on, sneezing. Morphological substrate is represented by an acute catarrhal inamma;on of the nasal mucosa; Allergic rhini;s is caused by a type I hypersensi;vity reac;ons (IgE), following exposure to various an;gens: pollen, dust, our etc. Is manifested by abundant watery nasal secre;on, sneezing crisis. Specically, is the appearance of inammatory inltrate rich in eosinophils in the nasal mucosa; Bacterial rhini;s usually occurs as a complica;on of forms described above, characteris;c is the transforma;on of inammatory exudate from a watery into a purulent one. Chronic rhini6s, can also be of two types: Hyperplasic chronic rhini;s occurs due to repeated nasal inamma;on. It is characterized by hyperplasia of mucous glands some;mes realizing real adenomatous polyps that can extend up to the throat. They appear as mul;ple, soR, pedicled forma;ons, with bunch of grapes-looking. Chronic atrophic rhini;s (ozena) is also a possible consequence of repeated acute inamma;on. Is manifested by diminishing sense of smell due to pavimentosase metaplasia, brosis and reducing of the mucous glands. Laryngi6s are inamma;on of the larynx. May be acute or chronic. Of acute laryngi;s, the most important forms are: Catarrhal laryngi;s is in most cases caused by a viral infec;on (inuenza virus). Manifested clinically by dry throat and hoarseness. Morphologically is characterized by edema and hyperemia of the laryngeal mucosa, mucous exudate which, due to microbial superinfec;ons, becomes mucosal-purulent; Laryngeal diphtheria is now rare. It is an acute pseudomembranous inamma;on of the larynx, has a par;cular severity due to possible mechanical asphyxia;on through membranes of the pa;ent. Chronic laryngi;s may con;nue acute forms, or may have chronicity characters from the beginning, because local ac;on of chronic irrita;ve factors (smoking, pollu;on). Is manifested by hoarseness and irrita;on spas;c cough. Morphological can be described two forms: Hyperplasic laryngi;s with thickening of the pharyngeal mucosa. Some;mes may occur localized hypertrophy, pseudotumoral (singers nodules); Atrophic, dry laryngi;s. 6
Respiratory System
Bronchial Diseases
Bronchi6s are inamma;on of the large and medium bronchi. May be aected concomitant and trachea, in which case we speak of a tracheobronchi;s. Can be acute and chronic. Acute bronchi;s are ini;ated by microbes (pneumococcus, streptococcus, etc.), viruses (inuenza), or may have cause by irrita;on (pollu;on). Depending on the quality of inammatory exudate, are described several types of acute bronchi;s: catarrhal bronchi;s, ini;ally manifested by conges;on, edema and hypersecre;on of mucus, while in advanced stages occur and serous exudate. Soon there will be a microbial superinfec;on, exudate becoming purulent due to the inux of granulocytes; ulcera;ve bronchi;s is a more severe form, characterized by the occurrence of ulcers of variable depth in bronchial mucosa, at which are some;mes associated processes of necrosis and hemorrhage; pseudomembranous bronchi;s (diphtheria); gangrenous bronchi;s is rare, occurs consecu;vely to malignant tumors, infec;ons with anaerobic streptococci etc. Bronchial mucosa shows extensive necrosis with deposit of brin, necro;c material, microbial colonies. Chronic bronchi6s is characterized clinically by the appearance of more than 2 years consecu;vely of episodes of produc;ve cough for at least 3 months. It is par;cularly common in smokers and those who live in polluted urban environments. The disease is manifested with hypersecre;on of mucus, and as a result of microbial superinfec;on, there is a mucosal-purulent exudate. The main complica;ons of chronic bronchi;s include: pulmonary hypertension with cor pulmonale occurrence; squamous metaplasia of ciliated bronchial epithelium, with possibility of developing malignancies. Asthma is clinically manifested by dyspnea crisis and expiratory wheezing. From e;opathogenic point of view can be described two types: extrinsic asthma, is based on a type I hypersensi;vity reac;on, begins in childhood and usually there is an allergic family history; intrinsic asthma occurs in adults, can not be iden;ed an allergic factor and usually complicates a chronic bronchi;s. Morphologically, is characterized by hypersecre;on of mucus, by bronchial gland hyperplasia, inammatory inltrate rich in eosinophils, basement membrane thickening and bronchial muscle hypertrophy. Sputum of the pa;ents contains Charcot-Leyden crystal, produced by the disintegra;on of eosinophils. Bronchiectasis implies the existence of abnormal, persistent dilata;on of bronchi. Can be caused by several factors: sequelae of some suppura;ve pneumonia, inuenza, whooping cough; mechanical bronchial obstruc;on caused by tumors, foreign bodies etc.; congenital diseases: muciviscidosis, Kartagener syndrome (sinusi;s, situs inversus and congenital bronchiectasis by immobility cilia of bronchial epithelium). Bronchial dila;on is called bronchiectasis cavity. They can have diuse or localized character, can be single or mul;ple and may have dierent shapes: cylindrical, saccular or moniliforme (dilated por;ons alterna;ng with unaected por;ons). Bronchiectasis cavity is ini;ally dry, smooth, and aRerwards to ll with stagna;ng mucus. This mucus causes obstruc;on of the terminal bronchi and promote microbial superinfec;on, with the appearance of purulent secre;ons. Epithelium bordering the cavity is converted to metaplasia, and nally to atrophy. Bronchial wall is the seat of chronic inamma;on, with atrophy of the elas;c bers, muscle and mucous glands. In advanced stages occurs granula;on ;ssue prolifera;on with replacement brosis. 7
Respiratory System
Pulmonary Parenchyma
Pneumonia
Represents inammatory diseases of pulmonary parenchyma. Are caused by microbial or viral germs. Morphopathological subtypes: Lobar pneumonia represents the classic form of bacterial pneumonia, and is mainly caused by pneumococcus (Streptococcus pneumoniae). Currently complete evolu;on of the disease is rare, due to an;bio;c therapy. Clinically manifests with fever, chest pain and cough with sanguinolent sputum. The disease is limi;ng to a single pulmonary lobe (lobar pneumonia), oRen inferior, rarely more lobes. The star;ng point of the disease is pulmonary alveoli. Untreated, in terms of morphology, evolving into four phases: acute conges;on, red hepariza;on, grey hepariza;on, resolu;on. Lobular pneumonia (bronchopneumonia) usually occurs in debilitated persons, children and old, as a result of infec;on with pyogenic streptococci, Staphylococcus aureus, Klebsiella pneumoniae, etc. Unlike lobar pneumonia, the star;ng point of infec;on is bronchioles, with secondary extending in alveoli. Are aected more pulmonary lobules, which appear as outbreaks of condensa;on. Microscopically, bronchopneumonia outbreak appear centered by a bronchiolus with purulent bronchioli;s lesions. It is surrounded by alveoli with various types of pulmonary alveoli;s, which severity diminishes from the center to the periphery. Inters66al pneumonia is commonly caused by viral infec;on (inuenza virus, adenoviruses, etc.) or Mycoplasma pneumoniae. Pulmonary morphological changes occurring can be systema;zed as follows: inters;;al lesions, thickened alveolar septa, with dilated vessels and monocyte inammatory inltrate, without granulocytes; necro;zing bronchioli;s lesions, some;mes with the appearance of mul;nucleated giant cells; alveoli contain edema uid, red blood cells, brin. Pulmonary emphysema is permanent dila;on of terminal respiratory bronchioles and alveoli of the lungs. Disease pathogenesis is not fully elucidated. It is assumed that altera;on of alveolar walls may be caused by the ac;on of proteoly;c enzymes such as elastase, which destroys the elas;c bers at this level.
Pulmonary
TBC
Primary
tuberculosis
in
terms
of
morphology
is
characterized
by
the
appearance
of
primary
tuberculosis
complex
(Ranke),
consis;ng
of
three
elements:
primary
aect
(Ghon)
consists
of
an
area
of
caseous
necrosis
with
peripheral
tuberculous
follicles,
most
commonly
localised
subpleural
the
middle
por;on
of
the
right
lung;
connec;ng
lymphangi;s:
tuberculous
follicles
along
the
eerent
lympha;cs
of
primary
aec;on;
hilar
adenopathy,
with
the
presence
of
prolifera;v-altera;ve
lesions
in
the
lymph
nodes,
tributary
to
the
damaged
lympha;cs.
Secondary
tuberculosis
(postprimary)
develops
most
oRen
in
debilitated
persons,
immunized
by
prior
infec;on.
Source
of
bacilli
may
be
endogenous
(reac;va;on
of
latent
lesions
from
primary
disease)
or
can
talking
about
exogenous
contamina;on
by
inhala;on
of
bacilli.
The
lesions
begins
in
the
best
aerated
pulmonary
areas
(apical
posterior
part),
in
the
form
of
aggregates
of
tuberculous
follicles
(Simon
outbreak).
Follicles
conuence
and
soon
occurs
their
caseous
necrosis.
8
Respiratory System
Pneumoconiosis
Pneumoconiosis
are
professional
pulmonary
disease
caused
by
inhala;on
of
various
anorganic
powders.
Severity
of
lesions
is
variable,
depending
on
the
type
of
dust,
their
concentra;on,
dura;on
of
exposure
and
the
coexistence
of
other
pulmonary
lesions.
Types:
Silicosis,
Anthracosis,
Asbestosis
Pleuri;s
Inammatory
Types:
Sero-brinous
pleurisy
can
occur
in
rheuma;sm,
uremia,
tuberculosis,
or
may
be
a
complica;on
of
pneumonia.
It
is
characterized
by
the
appearance
of
an
intracavitary
serous
exudate,
with
brinous
inamma;on
of
pleural
serous.
Hemorrhagic
pleurisy,
with
exudate
rich
in
erythrocytes,
can
occur
in
tuberculosis,
mesothelioma,
pulmonary
infarc;on;
Purulent
pleurisy
(pleural
empyema
or
piotorax)
appears
in
pleuro-pulmonary
infec;on
with
pyogenic
germs.
Non-inammatory
pleural
eusion:
Hydrothorax
is
characterized
by
the
accumula;on
of
transudate
in
pleural
cavity.
Hemothorax
represent
accumula;on
of
blood
in
pleura,
usually
as
a
result
of
thoracic
trauma
or
rupture
of
a
aor;c
aneurysm;
Chylothorax
consists
in
accumula;on
of
of
lymph
in
pleura
due
to
an
obstruc;on
of
the
thoracic
duct;
Pneumothorax
is
represented
by
the
presence
of
air
in
the
pleural
cavity.
Depending
on
the
mechanism
can
be
described
several
types:
spontaneous,
trauma;c
or
therapeu;c.
Gastric Pathology
Gastri;s
Acute
gastric
mucosal
erosions
small
focal
defects
of
substance
in
the
gastric
mucosa
Usually
supercial,
may
extend
to
the
serous
Chronic
Idiopathic:
Supercial
gastriHs
is
a
mild
form,
characterized
by
a
chronic
inammatory
inltrate
in
the
Pep;c Ulcer
lamina propriae. Glands are not aected. Atrophic gastriHs, advanced stage. It is characterized by extensive inammatory changes in the deeper gastric mucosa. Autoimmune: (Type A) occurs due to the presence of an;bodies against parietal cells, and will be complicated with achlorhydria and pernicious anemia. Lesions are located on the gastric fundic level, being similar to those seen in idiopathic gastri;s. Infec6ous: (type B) is produced by Helicobacter pylori, present lesions of chronic supercial gastri;s located in the antrum and gastric body. Germs can be iden;ed in gastric mucus and, in ac;ve forms, appear granulocytes in the neck of glands. Hyperplas6c: (Menetrier) is characterized by a highly expressed thickening of the gastric mucosa, the presence of giant folds that give the gastric area a cerebroid aspect. It is considered a precancerous condi;on. Is usually localized on the low curvature, in antral and pre-pyloric region. Appears as a solu;on of con;nuity (crater), usually single, rounded, with a diameter of 2-3 cm, with net, prominent margins. Gastric mucosa folds converge towards ulcer. Gastric wall penetra;on is variable, ulcers can have dierent depths. Some;mes there are overcoming all the structures of stomach, the basis of ulcer being composed of a rough brous ;ssue block (callos ulcer). Microscopically, the basis of gastric ulcer consists of four layers. They are, from surface to depth: Supercial, an area with brino- Gastric leukocyte exudate, area of brinoid necrosis, area of granula;on ;ssue, area of brous ;ssue with inammatory inltrate. Caused by increased acidifying of duodenal environment. Frequently, it is localized on the anterior or posterior wall of the duodenum, in the post-pyloric area. Usually unique, but there are also double duodenal ulcers, situated opposite on the anterior and posterior wall (ulcers in the mirror). Complica;ons: Haemorrhages: from occult bleedings to massive blood loss (haematemesis or melaena) Perfora6on: more common in duodenal ulcers (peritoni;s) Penetra6on -> (liver, pancreas). Pyloric stenosis, due to ulcer healing, with occurrence of a retrac;le brous scars. 10
Duodenal
Intes6nal Pathology
Crohn's disease
Chronic inammatory disease of unknown e;ology that can aect the en;re gastrointes;nal tract, but especially the terminal ileum and colon. The disease has two specic features: the inammatory process aec;ng all layers of the intes;ne and segmental nature of the lesions (impaired segments of intes;nes alterna;ng with unaected areas). Macroscopic interested segments: appear thickened, swollen with narrowed lumen, on mucosal surface occurs linear ulcera;on that gradually became deeper, and can be transformed into stulas. Can occur mesenteric lymphadenopathy. Microscopically, it is found: the presence of a polymorphous inammatory inltrate, a brosis process that interests all intes;nal structures, oRen can be observed non-caseous granulomas; Crohn's disease can rarely develop into a cancer of the small intes;ne or colon.
Ulcera6ve
Coli6s
Chronic
inammatory
disease
of
the
colon
of
unknown
e;ology
that
aects
young
adults.
3
specic
morphological
features
that
allow
dieren;al
diagnosis
compared
to
Crohn's
disease:
impairment
limited
to
the
colon,
from
ileo-cecal
valve
up
to
anus,
the
rectum
is
the
most
severely
aected,
and
the
small
intes;ne
is
not
interested;
lesions
have
diuse
character
and
not
segmental
character;
lesions
interest
colon
mucosa
and
submucosa,
extending
in
depth
is
excep;onal.
Macroscopically,
aected
the
mucosa
is
rst
red,
granular
and
bleeds
easily
at
touch.
Then
appear
supercial
ulcers
that
extend
into
the
surface,
surrounded
by
thickened,
hyperplasic
intes;nal
mucosa,
which
protrudes
into
the
intes;nal
lumen
(inammatory
pseudo-
polyps).
Microscopically
there
is
a
congested
mucosa,
swollen
with
par;ally
destroyed
epithelium;
are
iden;ed
hemorrhagic
suusions
and
lympho-plasma
cells
inammatory
inltrate.
Specic
is
glandular
crypts
impairment,
with
appearance
of
granulocyts
inammatory
inltrate
with
large
areas
of
necrosis
(cryp;c
abscesses).
In
advanced
stages
colon
becomes
atrophied,
with
the
persistence
of
a
chronic
inammatory
inltrate
in
the
mucosa
and
submucosa.
Acute
Appendici6s
Exuda;ve
inamma;on
of
the
ileo-cecal
appendix.
Frequently
occurs
consecu;vely
to
the
appendicular
orice
obstruc;on
through
fecal
(solidied
faecal
material),
hyperplasia
of
lymphoid
structures
from
appendicular
wall,
etc.
This
process
promotes
stagna;on
of
secre;ons,
intense
prolifera;on
of
local
microbial
ora
and
nally,
bacterial
invasion
of
the
wall,
with
the
massive
inux
of
polymorphonuclears.
Morphology
types:
conges;ve
appendici;s
characterized
by
distended
appendix,
congested;
phlegmonous
appendici;s,
the
whole
appendicular
wall
is
purulent
inltrated;
gangrenous
appendici;s,
characterized
by
the
appearance
of
hemorrhagic
ulcera;on
of
the
mucosa
and
areas
of
gangrenous
necrosis
of
the
wall.
Complica;ons
of
acute
appendici;s
are
oRen
serious:
perfora;on,
usually
followed
by
the
appearance
of
a
purulent
peritoni;s;
sep;c
thrombophlebi;s
of
meso
appendicular
vein
with
11
pylephlebi;s
and
secondary
liver
abscess.
Urinary Tract
Types of Nephropathies
Glomerular
Glomerulonephri6s
With
nephro;c
syndrome
With
nephri;c
syndrome
Chronic
Tubular
Acute
tubular
necrosis
Ischemic
necrosis
Nephrotoxic
necrosis
Vascular
Nephroangiosclerosis
Benign
Malign
Inters;;al
Pyelonephri6s
Acute
Chronic
Most
glomerulonephri;s
are
the
result
of
immunological
mechanisms,
the
most
commonly
involved
of
which
are:deposit
of
circula;ng
immune
complexes
in
the
glomeruli;
local
forma;on
of
immune
complexes
by
reac;on
between
a
circula;ng
an;body
and
an
an;gen
from
glomerular
basement
membrane;
ac;va;on
of
alterna;ve
pathway
of
complement;
cell-mediated
immunological
mechanisms.
Glomerulonephri6s
characterized
by
nephro6c
syndrome:
Nephro;c
syndrome
is
a
group
of
pathological
condi;ons
arising
as
a
result
of
increased
basement
membrane
permeability
by
the
glomerular
capillary
level.
It
is
characterized
by:
proteinuria,
hypoalbuminemia,
generalized
edema,
hyperlipidemia
and
hypercholesterolemia.
In
this
category
can
be
classied:
Glomerulonephri6s
with
minimal
change
(lipoid
nephrosis)
aects
young
children
and
is
the
prototype
disease
characterized
by
nephro;c
syndrome.
Glomerulonephri6s
with
focal
and
segmental
lesions
may
appear
as
a
primi;ve
disease
(idiopathic)
or
as
a
consequence
of
systemic
disease
with
glomerular
involvement
(polyarteri;s
nodosa,
subacute
bacterial
endocardi;s
and
so
on).
Membranous
glomerulonephri6s
is
the
main
cause
of
developing
nephro;c
syndrome.
E;ology
is
unknown
and
aects
young
adults.
Some;mes
there
is
an
associa;on
with
hepa;;s
B,
syphilis,
malignancy,
systemic
lupus.
Is
characterized
by
marked
thickening
(5-10
;mes),
regular
and
diuse
of
glomerular
capillary
basement
membranes
due
to
deposits
at
this
level
of
electrondense
immune
complexes.
Glomerulonephri6s
secondary
to
systemic
diseases:
diabe6c
nephropathy
is
characterized
by
glomerulosclerosis,
which
may
be
diuse
(diuse
mesangial
hyaline
deposits)
or
nodular
(nodular
mesangial
hyaline
deposits
-
Kimmels;el-Wilson
nodules).
Are
associated
with
diabe;c
microangiopathy,
tubular
atrophy,
brosis
and
lympho-plasma
cell
inters;;al
inammatory
inltrate.
amyloid
nephropathy
occurs
in
a
systemic
amyloidosis.
Is
characterized
by
amyloid
deposit
predominantly
sub-endothelial
and
mesangial,
with
gradual
replacement
of
the
en;re
glomerular
structures.
Lesions
aec;ng
almost
all
glomeruli
in
varying
degrees.
12
Glomerulonephri6s characterized by nephri6c syndrome These glomerulonephri;s are caused by inamma;on, leading to glomerular capillary rupture with subsequent hemorrhage in the urinary tract. Nephri;c syndrome is characterized by the following elements: haematuria, oliguria, azotemia, hypertension. Proteinuria and edema may occur, but low intensity. The main types of glomerulonephri;s in this category are: Poststreptococcal acute glomerulonephri6s is most oRen a sequel of an infec;on (common tonsillar) with -hemoly;c streptococcal group A. Renal impairment occurs aRer a period of 1-2 weeks, pathogenesis being by circula;ng immune complex deposit. In children evolu;on is usually favorable, but in adult renal failure may occur. Aected kidney is hypertrophied, turgid, edematous, the surface is smooth with numerous haemorrhagic points which correspond to aected glomeruli. Glomeruli are aected diusely, being hypertrophy and hypercellularity. Subacute glomerulonephri6s (rapidly progressive) is characterized by severe evolu;on with the advent of early renal failure. Can occur poststreptococcal associated with some system diseases, or may be idiopathic. Aected glomeruli are hypertrophy, hypercellularity and may develop thrombosis and capillaries necrosis. Typically, there is a prolifera;on of parietal cells of Bowman capsule with forma;on a mul;layer structure that lls the ltering space, called epithelial crescent. Goodpasture's syndrome is most commonly seen in men around the age of 20 years. Pathogenically is characterized by development of an;bodies with anity for glomerular and pulmonar alveoli basement membranes. Clinical is manifested by glomerulonephri;s and pneumonic syndrome. Chronic glomerulonephri6s Chronic glomerulonephri;s is the nal stage of evolu;on of various glomerulopathies, clinically characterized by the occurrence of renal failure. Aected kidney is hypotrophy, increased consistency and nely granular surface on sec;on (small kidney, white, granular). The capsule is adherent and on sec;on surface there is a thin cor;cal, poorly demarcated from medullary.
Tubular
Acute
tubular
necrosis
is
the
major
cause
of
acute
renal
failure.
Acute
tubular
necrosis
may
be
the
result
of
prolonged
renal
ischemia
or
the
ac;on
of
nephrotoxic
substances.
Ischemic
necrosis
is
a
result
of
shock
of
dierent
e;ology,
characterized
by
severe
renal
hypoperfusion:
hemorrhagic
shock,
post
trauma;c
shock,
hemoly;c
shock
(incompa;ble
perfusions),
the
shock
caused
by
extensive
burns
or
crush
syndrome,
endotoxic
shock
(Sepsi
with
gram
nega;ve
germs)
and
so
on
Aected
kidney
is
hypertrophied,
swollen,
and
on
the
surface
of
sec;on
there
is
a
clear
demarca;on
between
cor;cal
and
pale
congested
medullar.
Inters;;um
is
swollen
with
discreet
granulocytaire
inltrate.
Nephrotoxic
necrosis
is
caused
by
direct
ac;on
of
a
toxic
substances
on
tubular
epithelium
(an;bio;cs,
cytosta;cs,
anesthe;cs,
mushroom
toxins,
venom
and
so
on).
Microscopically,
is
shows
extensive
necrosis
of
tubal
epithelium,
more
expressed
in
proximal
tubules.
Tubulorexis
lesions
are
much
less
common
than
in
acute
tubular
necrosis
due
to
ischemia.
13
Vascular
Caused
by
arterial
hypertension.
Benign
nephroangiosclerosis
is
caused
by
ischemia
consecu;vely
to
atherosclerosis
and
arteriolosclerosis
that
aects
renal
vessels.
Small
arteries
and
arterioles
undergoes
a
process
of
hyaline
arteriolosclerosis.
Interlobular
and
arcuate
large
arteries
shows
a
characteris;c
lesion
that
consists
in
duplica;on
of
elas;c
lamina,
brous
;ssue
hypertrophy
of
the
media,
with
narrowing
of
vasucular
lumen
(broelas;c
hyperplasia).
These
lesions
expand
over
;me
and
at
glomerular
capillaries,
leading
to
complete
atrophy
of
the
aected
glomeruli.
Renal
tubules
are
atrophied
or
hypertrophied
properly
and
inters;;um
presents
brosis
with
lympho-
plasma
cell
inltrate.
Malign
nefroangiosclerosis
is
characterized
by
the
appearance
of
hyperplas;c
arteriolosclerosis.
This
consists
in
concentric
thickening,
in
overlapping
sheets
(in
onion
bulb)
of
walls
of
arterioles,
with
consecu;vely
reduc;on
of
the
vascular
lumen.
Some;mes
it
can
appear
brinoid
necrosis
(necro;zing
arterioli;s)
and
thromboses
of
aerent
glomerular
arterioles.
These
lesions
extend
to
the
glomerular
capillaries,
causing
hyalinisa;on
of
glomeruli.
Tubules
have
varying
degrees
of
atrophy
and
inters;;um
presents
lympho-plasma
cell
and
14
granulocyte
inammatory
inltrate.
Inters;;al
Acute
pyelonephri6s
is
caused
by
bacterial
infec;on
propagated
either
by
hematogenous
path
in
the
course
of
sepsis,
either
by
ascending
path
from
the
urethra,
usually
involving
Escherichia
coli.
Are
most
commonly
aected
women,
especially
during
pregnancy.
Clinically,
the
disease
is
manifested
by
pollakiuria,
dysuria,
pyuria,
hematuria
and
bacteriuria.
In
ascending
infec;ons
appears
a
purulent
exudate
in
the
calix
and
pelvis
renalis.
In
renal
parenchyma
is
observed
radial
purulent
stria;ons
from
pelvis
renalis
into
cor;cal,
that
can
join,
producing
a
renal
abscess.
Infec;ons
by
hematogenous
path
are
leading
to
microabscesses
disseminated
in
all
renal
parenchyma.
Microscopically,
there
is
a
granulocyte
inammatory
inltrate
of
variable
intensity
that
ini;ally
interested
pyelocalyceal
inters;;um
14
and
mucosa.
Chronic
pyelonephri6s
may
con;nue
an
acute
inamma;on
or
may
have
from
the
beginning
characters
of
chronicity.
Is
an
important
cause
of
chronic
renal
failure.
Aected
kidney
is
small,
with
irregular
surface
due
to
retrac;le
scars
consecu;ve
healing
of
acute
phase
injuries.
The
capsule
is
adherent
and
pyelocalyceal
mucosa
is
thickened.
Microscopically,
lesions
have
mul;focal
disposal,
separated
by
areas
of
normal
parenchyma.
In
outbreaks
are
iden;ed
inters;;al
brosis,
the
presence
of
a
lympho-plasma
cell
inammatory
inltrate
and
various
types
of
glomerular
lesions.
Tubules
contain
hyaline
cylinders,
some;mes
making
pseudo;roidisa;on
images.
Basically,
a
chronic
pyelonephri;s
can
not
be
dis;nguished
by
chronic
glomerulonephri;s
in
both
disease
all
renal
structures
being
aected
in
varying
degrees.
14
Uterine Body
Vulva
Vulvi;s
are
mainly
caused
by
infec;ous
agents:
Human
papilloma
virus
infec6on
is
characterized
by
the
appearance
of
benign
tumor
lesions,
called
acuminate
condyloma.
These
forma;ons
appear
as
papillary,
warty,
located
on
vulvar
teguments
or
mucosa,
oRen
mul;ple
and
conuent.
Herpes
viruses
infec6on
is
common
in
the
vulva.
Ini;ally
develop
a
rash
with
blisters
lled
with
clear
uid,
then
are
converted
into
pustules
that
may
ulcerate.
Syphili6c
infec6on
is
caused
by
the
spirochete
(Treponema
Pallidum).
Bartholin
cysts
occur
due
to
glandular
excretory
ducts
obstruc;on
with
accumula;on
of
secre;on
product
and
consecu;vely
ductal
dilata;on.
Content
is
clear,
mucoid,
translucent.
Microbial
overgrowth
can
cause
the
appearance
of
an
abscess
Bartholin,
with
forma;on
of
a
circumscribed
purulent
collec;ons.
Kera6n
cysts
interested
oRen
large
labia,
are
supercial
and
small
(2-5
mm).
The
content
of
the
cys;c
consists
of
acellular
mass,
eosinophilic
of
kera;n,
bounded
by
atened
squamous
epithelium.
Mucinous
cysts
are
commonly
located
at
the
ves;bular
level,
is
separated
by
a
mucous-secre;ng
epithelium,
cuboidal
or
cylindrical
type,
frequently
with
squamous
metaplasia.
Vagina
Vagini;s
are
oRen
caused
by
pathogens
such
as
Candida
albicans,
Gardnerella
vaginalis
and
Trichomonas
vaginalis.
Cervix
Acute endometri6s oRen occur consecu;vely to a birth, an abor;on or following uterine surgery. More rarely, can occur in their absence, as in gonococcal infec;on through ascendent path from the vagina. Uterine mucosa is swollen and congested, with desquama;on of surface epithelium. Is iden;ed a mucous hypersecre;on which can then become mucopurulent or purulent. Endometriosis are characterized by the presence and prolifera;on of endometrial ;ssue non-neoplas;c anywhere else than in the mucosa of the uterus. Histologically, ectopic endometrium can be completely made up of cytogenic chorion and glands, or can contain only one of these elements. In terms of loca;on, can be described two types of endometriosis: external and internal. Internal endometriosis (adenomyosis) is the presence of islands of endometrium in myometrium thickness.
Cervici;s can be divided, depending on the nature of the e;ologic agent, in infec;ous cervici;s and noninfec;ous. Both can manifest as an acute or chronic inamma;on. It can also be aected the por;on of the the cervix from vagina (exocervici;s), or the corresponding segment of cervical canal (endocervici;s). Noninfec6ous cervici6s can be caused by chemical irrita;on, use of vaginal tampons, diaphragms and intrauterine contracep;ve devices. In acute forms, the cervix is hypertrophied, erythematous, friable. Microscopically is highlighted stromal edema, vascular conges;on, and inammatory inltrate with polymorphonuclear neutrophils in chorion. Infec6ous cervici6s may complicate those noninfec;ous or can manifest from the beginning itself. Involve the ac;on of a biological agent. ). All rst manifests as an acute cervici;s, oRen with the appearance of purulent striae on the surface of exocervix or muco- purulent secre;ons that is removed from endocervical canal. 15
Mammary Gland
Inamma;ons:
Mas;;s
Acute
mas66s
are
usually
related
to
installa;on
of
lacta;on,
usually
aec;ng
primiparous.
It
is
a
bacterial
infec;on
(staphylococcus
aureus,
streptococcus
pyogenic),
favored
by
the
appearance
of
ssures,
rhagades,
nipple
excoria;on
due
to
a
dicult
lacta;ons.
From
this
level,
the
infec;on
spreads
in
depth
by
canalicular
path.
In
breast
appear
hard
areas,
swollen
and
very
painful,
at
whose
compression
is
expressed
in
the
nipple
a
purulent
exudate.
Microscopically,
at
the
beginning
is
a
sero- brinous
acute
inamma;on,
which
can
progress
to
suppura;ve
inamma;on
of
abscess
or
phlegmon
type.
Chronic
mas66s
(mas;;s
with
plasmocytes)
are
found
in
mul;parous,
due
to
mammary
ducts
obstruc;on
by
secre;ons
condensa;on.
This
induces
a
chronic
inammatory
reac;on
with
occurrence
in
mammary
gland
mass
of
some
indurated
areas,
from
which
at
pressure
is
expressed
plugs
of
cheesy
material.
Microscopically,
can
be
iden;ed
dilated
ducts
with
epithelium
in
large
part
atrophied
and
necro;c
material
in
lumen.
Peri-and
intraductal
appears
a
granulomatous
inammatory
reac;on,
with
deposits
of
cholesterol
and
inammatory
inltrate
rich
in
plasmocytes.
Some;mes
may
occur
a
process
of
inters;;al
brosis
with
nipple
retrac;on,
similar
to
that
from
breast
cancer.
Tes;cular
Inamma;on
of
the
tes;cles
is
called
Orchi6s.
These
can
be
acute
or
chronic,
and
may
be
associated
with
inamma;on
of
the
epididymis
(orchiepididymi;s).
Acute
orchi;s
are
oRen
of
gonococcal
nature,
but
may
also
include
syphili;c
or
viral,
some;mes
complica;ng
an
epidemic
paro;di;s.
They
are
rarely
encountered
in
inamma;on
of
tuberculous
nature.
Aected
tes;cle
is
swollen,
painful
and
microscopically
shows
a
polymorphous
inammatory
inltrate,
predominantly
with
neutrophils.
Gonococcal
orchi6s
evolves
towards
suppura;on,
with
the
forma;on
of
abscess.
Acute
orchi;s
unhealed
can
become
chronic,
and
bilateral
forms
can
be
complicated
by
sterility
Prostate
Pathology
Prostate
inamma;ons
are
called
prosta66s.
They
are
oRen
bacterial
(gonorrhea,
streptococci,
coli,
etc..)
consecu;ve
of
an
urinary
infec;on.
Acute
prosta;;s
is
characterized
by
a
glandular
painful
swelling,
with
urethral
expression
of
a
sero-purulent
uid
at
compression.
Microscopically,
there
is
a
rich
granulocy;c
inammatory
inltrate
located
in
the
prosta;c
glands
and
stroma.
Chronic
prosta66s
are
the
result
of
repeated
acute
inamma;on.
Clinically,
is
manifested
by
nocturia
and
dysuria,
and
in
;me
occurs
progressive
atrophy
of
the
prostate.
Some;mes
can
occur
characteris;c
injuries
for
tuberculous
prosta;;s.
Other Condi6ons: Cryptorchidism is lack of descent of the tes;s into the scrotum. It frequently accompanies by tes;cular atrophy with sterility, and an increased rate of malignant degenera;on. Torsion of sperma;c cord, compromising blood perfusion, which can lead to tes;cular gangrene. Hydrocele is caused by the accumula;on of serous uid, with distension of the tunica vaginalis, for most of the ;me is idiopathic, but may be congenital, secondary to infec;on or as a result of lympha;c blocking of tumoral origin. Hematocele is an accumula;on of blood that relax tunica vaginalis, is usually postrauma;c, but may indicate the presence of a renal tumor. Varicocele is a varicose dilata;on of the sperma;c cord vein. Spermatocele is a cyst oRen intrates;cular containing sperm. 17
Pathology of Blood
Post-Hemorrhagic: Acute as a result of sudden, severe, internal or external hemorrhage. In the early stages there is not a decrease of hematocrit and hemoglobin concentra;on due to concomitant loss of red blood cells and plasma uid. A litle later, hypervolemia is compensated by the body through an increased produc;on of plasma liquid, with the advent of hemodilu;on. Chronic posthaemorrhagic anemias occur aRer repeated small haemorrhages (gastric ulcer, tumor, meno-metrorrhagia and so on). Anemia becomes signicant only aRer deple;on of body iron deposits (iron deciency anemias) Hemoly6c: caused by an excessive destruc;on of red blood cells, with reducing their lifespan. Destruc;on can occur in macrophages from spleen, bone marrow, or within blood vessels (intravascular hemolysis). As a compensatory response, erythropoiesis is s;mulated, anemia became manifest only when damage rate exceeds the produc;on of red blood cells. Hemoly;c anemia is characterized by the following elements: increased serum levels of unconjugated bilirubin, appearance in the blood and urine of free bilirubin (hemoglobinemia and hemoglobinuria), intensica;on of erythropoiesis, Splenomegaly Iron Deciency: can be caused by inadequate dietary intake, an increase in body iron requirements (pregnancy, growth period) or may complicate malabsorp;on syndromes and chronic hemorrhages. It is characterized by the appearance in the peripheral blood of erythrocytes of small size (microcytes), pale, hypochromic. Signicant is a decrease serum level of ferri;n, which reects a decrease of iron reserves in the body. Megaloblas6c anemias are the consequence of a reduced DNA synthesis, due to deciency of folic acid or vitamin B12. Most common cause in vitamin B12 deciency is the absence of intrinsic factor necessary for intes;nal absorp;on of the vitamin. This deciency occurs in atrophic gastri;s (pernicious anemia).
Anemias
Dyshematopoie6c: result of deciencies of factors required for normal erythrocyte matura;on, despite the existence of an adequate number of marrow precursors for their synthesis. Most important in this category are megaloblas;c and iron deciency anemia.
Aplas6c: result of altera;on of bone marrow stem cells with pancytopenia occurrence and bone marrow cell depopula;on. Impairment may be idiopathic or may be due to the ac;on of marrow toxic agents: chemotherapy, sulphonamides, benzene, radia;on, viruses, etc. Anemia is oRen macrocy;c, and leukocytes and thrombocytes are greatly reduced in number. The popula;on of normal bone marrow is replaced by fat ;ssue prolifera;on. 18
Pathology of Blood
Polycythemia
Or Erythrocytosis, is characterized by increased total mass of circula;ng erythrocytes, a process most accurately reected by increasing hematocrit. The direct consequence is increased blood viscosity, with aec;ng its ow and the possible occurrence of ;ssular hypoxia. Polycythemia may be rela;ve, occcurred as a result of the decrease in plasma volume (hemoconcentra;on), and absolute (per se), characterized by increased number of erythrocytes.
Primi6ve erythrocytosis (polycythemia vera) is a neoplas;c altera;on of mul;potent stem cells, resul;ng in prolifera;on of all marrow cell lines, but more of erythrocyte series. The disease occurs mainly in men, in old age; heredity seems to play an important role. In peripheral blood is an increase in the number of erythrocytes (over 6 million / ml) with increasing hematocrit (60%) and hemoglobin concentra;on (over 2 g%). In addi;on, increases the number of leukocytes and thrombocytes. Hematogenous marrow is hypercellular, with the presence of numerous precursors of all cell lines. Secondary erythrocytosis is the consequence of hypersecre;on of erythropoie;n. This increase is typically reac;ve, consecu;vely to a arterial hypoxia(high al;tude with rareed air, lung disease, hemoglobinopathies, etc.). Some;mes, the disease may be caused by the appearance of erythropoie;n-secre;ng tumors (renal carcinoma, liver carcinoma etc.).
Thrombocytopenia
It
is
a
decrease
in
thrombocytes
number
below
150.000/ml.
More
severe
decreases,
under
50.000/ml,
increase
the
risk
for
postrauma;c
hemorrhages
or
by
surgery,
and
at
values
less
than
20.000/ml
spontaneous
bleeding
occurs.
Thrombocytopenia
may
be
the
result
of
reduced
medullary
thrombocytopoiesis
(aplas;c
anemia,
leukemia)
or
destruc;on,
excessive
sequestra;on
of
thrombocytes
at
spleen
level.
The
most
common
manifesta;on,
but
not
pathognomonic,
of
thrombocytopenia
is
purpura
Primary
thrombocytopenic
purpura
(essen;al)
have
immune
e;ology,
being
the
result
of
appearance
in
the
blood
of
an;thrombocy;c
or
an;megakaryocy;c
an;bodies.
This
may
occur
in
adults
as
a
consequence
of
serious
chronic
diseases
(collagenosis,
leukemia,
AIDS),
or
in
children
during
viral
infec;ons.
Secondary thrombocytopenic purpura may occur due to thromboly;c ac;on of chemical agents, drugs, or secondary to myelo-or lymphoprolifera;ve neoplas;c processes.
19
Pathology of Blood
Lymphadeni;s are inamma;on of lymph nodes, secondary to the ac;on of exogenous agents, oRen biological (bacteria, viruses, parasites, etc.). Acute lymphadeni6s occur in the lymph nodes that drain lymph from ;ssular territories in which it take place an acute inammatory process. Aected lymph nodes are hypertrophied, have a low consistency and are painful at palpa;on. Microscopic lymph node histological structure is altered by the appearance of a prolifera;on of sinusal his;omacrophages (sinus his;ocytosis) and the occurrence of a subcapsular granulocy;c inltra;on (catarrhal lymphadeni;s). Some;mes inamma;on can get a suppura;ve character with extension to surrounding ;ssues.
Lymphadeni;s
Chronic lymphadeni6s may be:- Nonspecic chronic lymphadeni;s accompanies chronic infec;on with various sites, having appropriate regional topography. Lymph nodes are hypertrophied, with bro;c capsule; microscopic presents sinusal his;ocytosis and hypertrophy of lymphoid follicles. Specic chronic lymphadeni;s are characterized by the appearance of lesions characteris;c of underlying disease: in tuberculosis appear tuberculous follicles and and caseous necrosis, in syphilis, vasculi;s with plasmocytes rich in inammatory inltrate. Reac6ve splenomegaly accompanies some acute or chronic inamma;on such as bacterial, viral, parasi;c or immunological. In bacterial infec;on spleen is moderately increased in volume, red pulp being intensely populated with macrophages and polymorphonuclear neutrophils. In sep;cemia may appear abscesses and sep;c splenic infarcts, as well as involvement of capsule and surrounding structures (perispleni;s). In infec;ous mononucleosis splenomegaly is due to occurrence of an inltrate rich in lymphocytes and immunoblasts located in the sinuses and medullary cordons. In malaria, the spleen is much hypertrophied (10 kg), of gray-blackish colour due to increased an;malarial pigment content (hemateina).
Splenomegaly
Conges6ve splenomegaly occurs in portal hypertension (hepa;c cirrhosis, heart failure). The spleen is moderately hypertrophied, hard, with bro;c capsule. Microscopically, in the early stages, sinusoids are dilated, with a large number of macrophages. In advanced stages, red pulp tends to become hypocellular due to a process of brosis. Inltra6ve splenomegaly can occur in several circumstances: intrasplenic advent of cellular inltrates (macrophages in haemoly;c anemia, malignant cells in lymphoma or leukemia) or extracellular deposits of abnormal substances (amyloidosis). Others: Splenomegaly due to primi;ve or metasta;c splenic tumoral processes / Splenomegaly due to occurrence at this level of hyda;d cysts. 20
Endocrine
10
Pathology
of
Hypophysis
Injuries
associated
with
hypofunc;on
of
adenohypophysis:
Pituitary
cachexia
is
caused
by
panhypopituitarism,
can
be
produced
by
any
factor
that
destroys
the
pituitary
gland
(various
tumors,
postpartum
necrosis
of
pituitary
gland).
Selec6ve
decits
of
one
or
more
pituitary
hormones:
growth
hormone
deciency
(retarda;on
in
growth),
gonadotropin
deciency
(delayed
sexual
matura;on),
TSH
deciency
(hypothyroidism),
ACTH
deciency
(hypocor;cism).
Injuries
of
neurohypophysis:
ADH
secre6on
deciency
is
manifested
by
diabetes
insipidus
(polyuria,
dehydra;on,
permanent
thirst).
Can
occur
consecu;vely
to
any
process
that
leads
to
the
destruc;on
of
the
posterior
hypophysis
(trauma,
tumors,
inamma;on
and
so
on).
Ectopic
secre6on
of
ADH
is
the
preroga;ve
of
some
tumors
such
as
small
cell
lung
carcinoma.
It
is
characterized
by
reten;on
of
water
and
concentrated
urine.
Thyroidi;s
Acute thyroidi6s are usually bacterial, occurring as a result of infec;ous hematogenous dissemina;on, rarely spread from a neighboring organ. The thyroid is enlarged in volume and painful. The most common encountered are suppura;ve forms, abscess or phlegmon type Subacute thyroidi6s (de Quervain) have most likely a viral e;ology (mumps virus, Coxsakie etc). It is a self-limited inamma;on, characterized by focal destruc;ons of thyroid ;ssue with granulomtoase lesions. In advanced stages may occur a process of brosis with symptoms of hypothyroidism. The thyroid is enlarged in volume, not adhering to the surrounding organs, increased consistency and irregular surface
Hashimoto's thyroidi6s (diuse lymphocy;c thyroidi;s) is an autoimmune disease with familial aggrega;on, more common in women. In advanced forms is manifested by hypothyroidism. The thyroid is diusely and moderately increased in volume, with increased consistency and intact capsule, nonadhesive Riedl thyroidi6s (ligneous thyroidi;s) has unknown e;ology and may clinically mimic the carcinoma. The thyroid is usually reduced in volume, with irregular surface, adherent capsule and very high consistency.
21
Endocrine
10
Goi;er
Dene the increase in volume and weight of the thyroid, in the absence of inammatory processes or tumors. From a func;onal perspec;ve, there may be simple goiters, without endocrine disorders, and goiters associated with hyper- or hypothyroidism.
With
Euthyroidsm
(Simple,
non-toxic)
are
caused
by
iodine
deciency
due
to
either
an
insucient
exogenous
or
an
increased
need
of
the
body
(pregnancy,
growth
period,
etc..).
Iodine
deciency
leads
to
a
defec;ve
synthesis
of
thyroid
hormones,
with
consequent
decrease
of
serum
level
of
these.
This
abnormality
is
felt
by
hypophysis,
which
will
intensify
the
synthesis
of
TSH.
Under
its
ac;on
will
produces
compensatory
hypertrophy
and
hyperplasia
of
thyroid
follicular
epithelium
with
the
advent
of
goiter.
Simple
goiter
may
be
diuse
or
nodular.
Simple
difuse
goiter
is
accompanied
by
euthyroidism,
and
is
characterized
by
a
uniform
damage
of
all
thyroidian
mass.
May
be
endemic,
occurring
in
mountain
areas
(Andes,
Alps,
Carpathians).
Evolves
in
two
stages:
hyperplas;c
phase,
colloid
involu;on
phase
With
Hyperthyroidism
(toxic)
are
manifested
clinically
by
a
complex
clinical
picture:
irritability,
tremor,
heat
intolerance,
tachycardia
with
arrhythmia,
diarrhea,
menstrual
disorders
etc..
Morphologically
can
be
dis;nguished:
Diuse
toxic
goiter
(exophtalmos
goiter,
Graves
-
Basedow
Disease)
is
the
most
frequent
goiter
associated
with
hyperthyroidism.
The
disease
has
a
hereditary
component,
and
in;mate
produc;on
mechanism
is
autoimmune.
..
Clinically,
presents
signs
and
symptoms
of
hyperthyroidism,
plus
exophthalmia
and
inltra;ve
dermatopathy.
The
thyroid
is
overall
enlarged
in
volume,
but
oRen
with
unequal
lobes;
is
hard,
britle
and
highly
vascularized;
the
capsule
is
integral
and
nonadhesive.
Toxic
nodular
goiter
is
rare,
occurs
more
frequently
in
women
with
a
history
of
simple
goiter.
The
thyroid
is
uneven
increased
in
volume,
with
the
presence
of
nodules
of
varying
sizes.
With
Hypothyroidism
may
be
encountered
in
children
from
goitrous
regions,
as
a
result
of
chronic
decit
of
iodine
or
administra;on
of
an;thyroid
agents.
It
has
a
hereditary
character
resul;ng
from
co-blood
families.
Are
nodular
goiters,
in
which
predominate
microscopic
aspects
of
pseudo-thyroidian
hyperplasia.
Hypothyroidism
is
manifested
in
adults
through
myxedema
and
in
children
by
cre;nism.
Myxedema
is
characterized
by
a
localized
edema
predominantly
on
the
face,
tongue
and
hand,
dry
skin
with
tendency
to
peeling,
litle
hair
and
harshly.
To
this
can
be
added
cold
intolerance,
tendency
to
gain
weight,
mental
retarda;on,
cons;pa;on
etc.
Cre;nism
of
thyroidian
cause
is
manifested
mainly
by
severe
mental
retarda;on,
delayed
bone
development,
macroglossia
and
protuberant
abdomen.
The
thyroid
is
much
increased
in
volume,
with
marked
epithelial
hyperplasia.
22
Pathology of CNS
11
Skull
Histo Review
Cerebral Infarc;on
infarc;on (soRening) is the result of a total and persistent ischemia, caused by cerebral artery occlusion. The main causes of this event are: thrombosis, embolism. clinical consequences depend on the place of vascular obstruc;on and the possibility of development of collateral circula;on. Most commonly it is aected middle cerebral artery. In this case occurs controlateral paralysis, with motor and sensory decit, and aphasia. Cerebral infarc;on may be single or mul;ple, of various sizes, depending on the size of artery aected. In general, infarc;ons of thrombo;c cause are white, and those caused by emboli are red infarcts. Microscopically stands a liquefac;on necrosis due to the emergence of a large amount of lipids from the disintegra;on of the myelin sheath. Intracerebral hemorrhage (apoplexy) is dened as bleeding within the brain substance. Most frequently occurs in the basal nuclei, the internal capsule and thalamus.The most frequently involved in the produc;on of intracerebral hemorrhage is arterial hypertension. Under the ac;on of this there is a decrease in the resistance of walls of brain arterioles, with the forma;on of micro aneurysms, which can be easily broken. More rarely, are involved arteriovenous malforma;ons, hemorrhages diatheses or tumoral processes. Subarachnoid hemorrhage is a bleeding into the subarachnoid space. Most oRen it is the result of a ruptured aneurysm in the arteries of Willis polygon. Some;mes subarachnoid hemorrhage may also have trauma;c cause. Epidural hematoma usually occurs as a result of trauma;c fracture of the temporal bone, with the middle meningeal artery injury and accumula;on of blood in the extradural space. Clinically, it is characterized by a short asymptoma;c period, and then occur compressive cerebral phenomena and, in the absence of treatment, death. Subdural hematoma is the result of trauma;c rupture of the connec;on veins between cerebral substance and venous sinuses of the dura, with the accumula;on of blood between the arachnoid and dura mater. Typically locates in the fronto-parietal region. It is characterized by gradual appearance of signs of compression of the brain (some;mes over a period of several week).
23
Pathology of CNS
11
Meningi;s
inamma;on of the conjunc;ve membranes that cover the central nervous system organs. May be aected rough meninges, process wearing in this case the name of pachymeningi;s, or soR meninges (arachnoid, pia mater and subarachnoid space), dened with the leptomeningi;s term.
Bacterial
Meningococcal
meningi;s
aects
mostly
children,
is
characterized
by
the
appearance
of
a
sero- purulent
inammatory
exudate,
yellowish.
Exudate
contains
a
small
amount
of
brin
and
a
large
number
of
granulocytes
and
macrophages.
Brain
substance
is
edematous,
with
punctate
hemorrhages
and
peri
vascular
inammatory
inltrate.
Pneumococcal
meningi;s
is
characterized
by
the
appearance
of
green
exudate,
jelly;
has
increased
tendency
to
delimita;on
(forma;on
of
enclosed
spaces
lled
with
pus);
Staphylococcal
and
streptococcal
meningi;s
are
secondary
to
neighborly
suppura;ve
processes.
Exudate
has
sero-purulent
appearance
for
streptococcus
and
yellowish,
creamy
for
staphylococcus;
the
process
have
an
increased
tendency
for
intracerebral
abscess
forma;on,
epi-or
subdural.
Tuberculous
occurs
secondary,
in
the
context
of
generalized
miliary
tuberculosis.
It
is
a
non-purulent
inammatory
process,
with
predilect
loca;on
in
the
brain.
Here
may
occur
exuda;ve
or
prolifera;ve
(miliary
tubercles)
lesions.
May
be
complicated
by
meningeal
brosis
and
consequent
obstruc;on
of
ventricular
system.
Viral
(enterovirus,
mumps
virus,
Epstein-Barr
virus,
etc.)
predominantly
aects
young
ages,
usually
with
a
benign
evolu;on.
The
disease
is
characterized
by
the
appearance
of
an
intense
cephalalgia
and
the
diagnosis
is
made
by
spinal
puncture
(CSF
with
numerous
lymphocytes,
increased
amount
of
protein
and
normal
glucose
content).
Encephalomyeli;s
(dened
inamma;on
of
cerebral
substance
(encephali;s)
and
of
spinal
cord
(myeli;s).
Important
in
medical
prac;ce
are
inamma;ons
of
viral
e;ology,
and
of
these,
due
to
their
seriousness,
polipomyeli;s
and
rabies
encephali;s.
Poliomyeli6s
(infan6le
paralysis)
is
caused
by
one
of
three
types
of
polioviruses.
It
is
an
acute
inamma;on
that
par;cularly
interested
in
the
anterior
corns
of
the
spinal
cord,
leading
to
destruc;on
of
motor
neurons
with
paralysis
and
atrophy
of
corresponding
soma;c
muscle.
Macroscopically,
medulla
spinalis
is
with
intense
hyperemia,
edematous
(glassy)
aspect
with
hemorrhagic
suusions
on
sec;on.
Rabies
encephali6s
is
caused
by
the
rabies
virus,
transmited
by
the
bite
of
infected
animals.
From
the
entrance
gate,
virus
spreads
by
axonal
path
un;l
spinal
cord,
brain
and
internal
organs
(including
salivary
gland).
The
disease
manifests
itself
as
a
severe
encephali;s
with
increased
CNS
excitability,
violent
muscle
contrac;ons
and
convulsions
triggered
by
minimal
s;muli.
Histologically,
the
disease
is
characterized
by
neuronal
degenera;on,
perivascular
lymphocy;c
inammatory
inltrate
in
the
cerebral
hemispheres,
cerebellum
and
spinal
cord;
pathognomonic
are
Babes
-
Negri
corpuscles
24
Pathology of CNS
11
Skull
Histo Review
Mul;ple Sclerosis
Mul;ple sclerosis is the most common demyelina;ng chronic disease of the CNS. Predominantly aects young women, with a progressive evolu;on, occurring in spikes. E;ology is unknown. Characteris;c lesions are represented by plates of sclerosis visible by naked eye in the cerebral white substance and spinal cord. It presents as oval patches, irregular, in sizes up to 2 cm, translucent, with color variable, depending on their age. These correspond to areas of axonal demyelina;on. Microscopically, there is complete disappearance of the myelin sheath in these areas, with local prolifera;on of glial cells and connec;ve ;ssue.
Alzheimers Disease
Is a degenera;ve disease of unknown e;ology, which is the most important cause of demen;a. En;ty refers to demen;a occurring at any age, associated with clinical manifesta;ons and specic pathological changes. Clinical manifesta;ons: slowly progressive intellectual deteriora;on: ini;ally short term memory loss, then and the long-term memory, inability to write, count, speak, etc.. motor problems:contractures and paralyzes specic to terminal phase Morphological abnormali;es: neurobrillary disorder: intraneuronal fascicles (microtubules and neurolament) disorganiza;on in cerebral cortex neuri;c plaques (senile): eosinophils neuronal processes with center consis;ng of a amyloid deposits in the cerebral cortex and hippocampus neuronal granulocyte-vacuolar degenera;on at pyramid level Hirano bodies: dendri;c eosinophilic inclusions generalized cerebral atrophy more expressed in hippocampus and frontal areas.
This work is not subsHtute of doctor Paiusans material, even if evry single word is extracted by his word les so it will matches what we need for the nal exam May The Force Be With You Your beloved colleague, Alessandro Mo5a
25