200 Important Points with Definitions to

Remember in General Pathology

By
Dr. Ejaz Waris !sso"iate Professor #istopathology !$D%
1. Hyperplasia is an increase in the number of cells in an organ or tissue,
usually resulting in increased volume of the organ or tissue.
2. Hypertrophy refers to an increase in the size of cells, resulting in an
increase in the size of the organ.
3. Atrophy is the shrinkage in the size of the cell by loss of cell
substance.
4. etaplasia is defined as a reversible change in !hich one adult cell
type "epithelial or mesenchymal# is replaced by another adult cell
type.
$. %ell s!elling is the earliest sign of a reversible cell in&ury.
'. (ree radical is a chemical species that have a single unpaired electron
in an outer orbit.
). *ecrosis is a spectrum of morphological changes that follo! cell death
in a living tissue largely resulting from the progressive degradative
action of enzymes on the lethally in&ured cell.
+. *ecrosis has si, ma&or type- coagulative, %aseous, .i/uefactive,
fibrinoid,gangrenous and (at.
0. Apoptosis "1reek falling off# is defined as a path!ay of programmed
cell death that is aimed at a highly regulated intracellular programme
in !hich cells destined to death by activated enzyme that degrade the
cell2s 3*A and nuclear and cytoplasmic proteins.
14. orphologically an apoptotic cell sho!s5 a# cell shrinkage, b#
chromatin condensation c# formation of cytoplasmic blebs and
apoptotic bodies, d# phagocytosis by macrophages.
11. Apoptosis has t!o phases a# 6nitiation phase e,trinsic and intrinsic
path!ays b#7,ecution phase c#phagocytosis of dead cell
12. 1enes promoting apoptosis are5 ba,,bak,bim
13. 1enes inhibiting apoptosis are bcl 2 family.
14. 6nitiator caspase are + 8 0, !hile e,ecutioner caspases are mainly 3 8
'.
1$. 3ystrophic calcification is al!ays seen in damaged tissues !hile
metastatic calcification may occur in normal tissues !henever there is
hyperplasia.
1'. 6nflammation is a comple, reaction to in&urious agents such as
microbes and damaged, usually necrotic cells that consists of vascular
responses, migration and activation of leukocytes, and systemic
reactions.
1). 6nflammatory response consist of 9:; main components5 vascular 8
cellular, and divided into 9:; main patterns5 Acute and %hronic.
1+. <asodilatation is one of the earliest manifestation of acute
inflammation, if follo!s a transient vasoconstriction of arterioles
lasting fe! seconds.
10. 6ncreased vascular permeability leading to the escape of a protein=rich
fluid "e,udate# into the e,travascular tissue in the HA.. A>? of acute
inflammation.
24. (ormation of endothelial gaps in venules is the most common cause of
vascular leakage.
21. .eukocytes Adhesion molecular families have a ma&or classes5 a#
@electins "7,. 8 A types#, b# 6ntegrins, c# 6mmunoglobulin family of
adhesion molecules and d# ucin like glycoproteins.
22. @electins mainly involved in rolling of leukocytes, A7%A in
transmigration and immunoglobulin family in adhesions.
23. %hemota,is is defined as uni directional migration of leukocytes
to!ards the site of in&ury under chemical gradient action.
24. ost important chemotactic agents are %$a,.9B4 and bacterial
products.
2$. a&or opsonins are5 %3b 8 (c fragment of 6g1 proteins
2'. H242=A;=Halide systein is the most efficient bactericidal system in
neutrophils.
2). %hediak=Higashi @yndrome is an autosomal recessive condition
characterized by failure of fusion of phagosome !ith lysosome.
2+. %hronic granulomatous disease of childhood results from inherited
defects in the components of *AA3H o,idase !hich generates
supero,ide, leading to body infections.
20. <asoactive amines are histamine and serotonin !hich are the main
players of early inflammation.
34. Alasma Aroteins are5 %omplement system proteins, clotting system
and fibrinolytic system.
31. Arostaglandins are vasodilators.
32. A% "%$B')+0# is the membrane attack comple,, !hich finally kills
the bacteria.
33. Activated Hageman factor initiates (;C> systems involved in
inflammatory responses ?inin, %lotting, fibrinolytic and complement
system
34. @>@=A "slo! releasing substance of anaphyla,is# constitutes .9%4,
.934 8 .974 promote vasoconstriction, bronchospasm 8 increased
vascular permeability.
3$. .ipo,ins are bioactive products generated from transcellular
biosynthetic mechanisms involving neutrophils and platelets.
3'. 6.=1 8 9*( are t!o of the AD;> cytokines that mediate inflammation.
3). a&or chemokines include5 6.=+, %A=1, eota,in, 6A=1, .ymphotactin
and >A*97@.
3+. *itric o,ide plays ma&or role in production of vasodilation by rela,ing
vascular smooth muscle in ischemic conditions.
30. 9he ma&or mediators of pain are Bradykinin 8 Arostaglandins
44. Aotent vasodilators are 5 <asoactive Amines, Arostaglandins 8 *;.
41. Acute inflammation is defined as a rapid response to an in&urious agent
that serves to deliver mediators of host defense E leukocytes and
plasma proteins to the site of in&ury.
42. %hronic inflammation is defined as an inflammation of prolonged
duration, in !hich active inflammation, tissue destruction and attempts
at repair are proceeding simultaneously.
43. *eutrophils are the main cells of acute inflammation "e,udates# !hile
ononuclear cells "!ith one nucleus are the main cells of chronic
inflammation .ononuclear cells include .ymphocytes, onocytes,
acrophages and Alasma cells.
44. acrophages are the prima donna "main !orking cell# of chronic
inflammation, !hile lymphocytes are present in increased number.
4$. 1ranuloma is a focus of chronic inflammation, consisting of
microscopic aggregation of macrophages that are transformed into
epithelium like cells surrounded by a collar of mononuclear leukocytes.
3on2t confuse it !ith 1ranulation tissue !hich has capillaries,
fibroblasts, and a variable amount of inflammatory cells.
4'. %lassical tuberculous granulomas is composed of epithelioid cells,
.anghan2s multinucleated giant cells, caseation necrosis and collar of
lymphocytes. 9here are t!o types of 1ranulomas5 6mmune 8 foreign
body.
4). 9here are 3 types of cells in the body5 %ontinously dividing labile cells,
Fuiscent or stable cells and Aermanent *on=dividing cells.
4+. @tem cells are cells characterized by their prolonged self rene!al
capacity and by the asymmetric replication. 9hey are of t!o types5
embryonic 8 adult stem cells.
40. <71( 8 fibroblast 1ro!th factor are mainly involved in angiogenesis.
$4. 91(=B is a gro!th inhibitor for most epithelial cells and leukocytes,
potent fibrogenic agent and a strong anti=inflammatory effect.
$1. 7,tracellualr matri, is formed of these groups of molecules 5 a#
fibronectin b# adhesive glycoproteins and c# proteoglycans 8
hyaluronic acid.
$2. %ollagens is the most common protein in the animal !orld, !ith 2)
types discovered so far. 9ypes 6, 66, 666, < 8 G# are fibrillar and most
common !hile type 6< is non fibrillar.
$3. Healing by 2
nd
intention differs from 1
st
intention in three !ays- a#
inflammatory reaction is more intense, b# uch more granulation
tissue forms and c# !ound contraction phenomenon.
$4. Accumulation of e,cessive amounts of collagen may give rise to a
hypertrophic scar !hile if scar tissue gro!s beyond the boundaries of
the original !ound and does not regress, it is called keloid.
$$. 7dema is defined as accumulation of fluid in the interstitial tissue
spaces and body cavities.
$'. .ocal increased volume of blood in a particular tissue leads to
Hyperemia and congestion. Hyperemia is an active process, resulting
from augmented tissue inflo! because of arteriolar dilation !hile
%ongestion is a passive process resulting from impaired outflo! from
tissue.
$). Heart failure cells are hemosiderin laden macrophages seen in chronic
pulmonary congestion.
$+. Aetechiae are minute 1 to 2 mm hemorrhages into skin, mucous
membranes or serosa surfaces, !hile H3 mm hemorrhages are called
Aurpura and more larger H 1 to 2 cm subcutaneous hematomas are
called 7cchymoses.
$0. <ircho!2s triad include5 a# 7ndothelial in&ury b# @tasis or turbulent
blood flo! 8 c# blood hypercoagulability.
'4. ;f the inherited causes of hypercoagulability, mutation in the factor <
gene and prothrombin gene are the most common.
'1. .ines of Iahn are laminated lines produced by alternating pale layers
of platelets admi,ed !ith some fibrin and darker layers containing
more red cells.
'2. (ate of thrombus include5 propagation embolization, dissolution,
organization and recanalization.
'3. 7mbolus is a detached intravascular solid, li/uid or gaseous mass that
is carried by the blood to a site distant from its point of origin. 9he
phenomenon is called embolism.
'4. 6nfarct is an area of ischemic necrosis caused by occlusion of either the
arterial supply or the venous drainage in a particular tissue.
'$. 9he most dominant histologic characteristic of infarction is ischemic
coagulative necrosis.
''. @hock is the systemic hypoperfusion caused by reduction either in
cardiac output or in the effective circulating blood volume, and
resulting in hypotension follo!ed by impaired tissue perfusion and
cellular hypo,ia.
'). a&or types of shock include5 cardiogenic, hypovolemic, septic,
neurogenic and anaphylactic.
'+. utation is defined as a permanent change in the 3*A.
'0. arfan2s syndrome is a disorder of the connective tissue of the body,
characterized by changes in the skeleton, eyes and cvs. ainly cause
by defects in an e,tracellular glycoprotein (irbillin=1.
)4. 7hlers=3anlos @yndrome comprise a clinically and genetically
heterogenous groups of disorders that result from some defect in the
syntesis or structure of fibrillar collagen.
)1. Amyloid is a pathologic proteinaceous substance deposited bet!een
cells in various tissues and organs of the body in a !ide variety of
clinical settings.
)2. *eoplasm is an abnormal mass, the gro!th of !hich e,ceeds and in
uncoordinated !ith that of the normal tissue and persists in the same
e,cessive manner after cessation of the stimuli !hich evoked the
change.
)3. 9umor has t!o basic components5 Aarenchyma 8 stroma, !hile
tumors are of t!o types5 Benign and alignant.
)4. Benign tumors are !ell differentiated, gro! slo!ly and don2t sho!
invasion and metastases, !hile alignant tumors range from !ell to
undifferentiated, gro! fast and sho! invasion and metastasis.
)$. @ingle most important feature to differentiate benign from malignant
tumor is 79A@9A@6@.
)'. %arcinomas mostly use lymphatic routes and sarcomas mostly use
hematogenous routes of spread.
)). (our types of genes are normally !orking in human body5 a# proto=
oncogens b# antioncogenes, c# apoptotic genes and d#3*A repair
genes
)+. Aroto=oncogenes are changed to oncogenes by three processes5
mutation, translocation and amplification.
)0. a&or oncogenes are- >A@, 7>B=B1, >79, ?69, AB., %=J% 8 *=J%.
+4. a&or antioncogenes are5 >B, 9A$3, :.=1, *(=1, B>%A=1, AA%.
+1. ;ncogenic viruses include- Human Aapilloma virus, Hepatitis B virus,
7pstein Barr virus ,?aposi @arcoma Herpes viruses 8 Human 9=%ell
leukemia virus "9he only oncogenic >*A virus#.
+2. %hemical carcinogenesis is a multistep process, divided into initiation
and promotion phases.
+3. a&or chemical carcinogens associated as include5 Asbestos !ith
esothelioma, Aniline dyes !ith 9%%, *itrates=1astric carcinoma,
Aflato,in !ith H%%, <inyl chloride !ith Angiosarcoma .iver.
+4. >adiation induced malignancies include leukemias and papillary
carcinoma thyroid.
+$. a&or paraneoplastic synbdromes include, %ushing syndrome, A3H
secretion by small cell carcinoma lung, Hypercalcemia by @/uamous
cell carcinoma lung, hypoglycemia by (ibrosarcoma and H%%,
Aolycythemia by >%% and hypertrophia osteoarthropathy by %A lung.
+'. a&or tumor markers included 5 H%1 for %horiocarcinoma, calcitonin
for medullary carcinoma thyroid, alpha fetoprotein=H%% and *on=
seminomatous germ cell tumor testis, %7A=%A colon, AAA (or %A
prostate, %A=12$ for ;varian %A , %a 10=0 for %A %olon and
pancreas ,%A 1$=3 for %A breast.
+). a&or immunomarkers for epithelial tumors are cytokeratin, for
mesenchymal tumor E vimentin, for leukocyte origin tumor E leukocyte
common antigen, @144 for neural origin tumors and for skeletal
muscle tumors E desmin.
++. 9ype 6 hypersensitivity "KanaphylacticL# or Kimmediate
hypersensitivityL# is the result of antigen binding to 6g7 on the surface
of mast cells and basophils. 9hese instantly degranulate and release
active substances into the surrounding tissue.
+0. 9ype 66 cytoto,ic hypersensitivity, antibodies attach to antigens on the
surfaces of a cell and then something in&ures or destroys the cell.
04. 6n type 666 immune=comple, hypersensitivity reaction, K@oluble
antigensL precipitate !ith antibodies, usually this happens 2=4 hours
after e,posure. 9his sort of tissue in&ury is mediated by antigen=
antibody comple,es "Kimmune comple,esL#.
01. 9ype 6< Hypersensitivity reaction is called Kdelayed hypersensitivityL.
6t is mediated by sensitized %34M9 lymphocytes !hich process
antigens in association !ith class 66 H.A molecules and release
lymphokines.
02. 6mmune reactions are divided into t!o broad categories5 A# Humoral
immunity=B=cell lymphocyte mediated via production of antibody and
;ften develops as a response to soluble antigens, and B# %ellular
immunity=9=%ell lymphocyte mediated. %34Mhelper lymphocytes5 help
B cells make antibody and also help to generate cytoto,ic 9 cells.
03. a&or histocompatibility comple, is present on all nucleated cells.
04. 9he H.A system is a key factor in most 9ransplant re&ection reactions.
>eactions are mediated by either 9 lymphocytes or by antibody.
0$. 9oll like receptors are membrane proteins that recognize a variety of
microbe derived molecules and stimulate innate immune responses
against the microbes.
0'. %34 molecule is a high affinity receptor for H6<
0). a&or autoimmune disease include Hashimoto2s thyroiditis,
>heumatoid Arthritis, @&ogren2s syndrome, ankylosing spondylitis.
0+. 1amma interferon is one of the cytokine to activate macrophages and
also play ma&or >ole in 1ranuloma formation.
00. %ytokines are mediators released from one cell and modulate the
actions of another cell.
144. @/uamous cell carcinoma is characterized by sheets, groups and
clusters of pleomorphic malignant epithelial cells !ith high *N%
ratio,hyperchromatic nuclei and pale cytoplasm.?eratin epithelial
pearls,intercellular bridges and individual cell keratinization are seen.
141. Adenocarcinoma is characterized by back to back closely packed
glands lined by pleomorphic malignant epithelial cells !ith high *N%
ratio,hyperchromatic nuclei and eosinophilic cytoplasm.:all sharing is
often noted.
142. 9!o types of vaccines include5 .ive vaccines- easles, umps,
>ubella, <aricella, Aolio etc and ?illed vaccines5 >abies, Aolio, Hepatitis
A.
143. Arotooncogenes are converted into oncogenes.
144. p$3 !orks by 3*A repair and promoting apoptosis.
14$. >B gene activates and :orks in hypophosphorylated form.
14'. >A@ gene protooncogene protein is 19A bound and :orks !ith 1AA in
cooridination !ith 19Aase.
14). 1liomas and B%% are highly malignant but dont usually metastasize.
14+. A(B is acid fase bacillus " ycobacterium tuberculosis # and called so
because it resists decolourization by %oncentrated Acids.
140. 9igered lipid effect is seen in Herat.
114. a&or complement proteins include 5
;psonization by %3b
%hemota,is by %$a
Anaphylato,in %3a, %4a, %$a
embrane breakdo!n and killing %$b,',),+,0 A% comple,
7nhancement of antibody production %3b
111. (*A% and biopsy are key investigations to early diagnose a tumor.
112. Active 6mmunity is the resistance induced after contact !ith foreign
antigens eg microorganisms, immunization !ith live or killed infectious
agents, e,posure to microbial products "to,ins, to,oids#
Aassive immunity is resistance based on antibodies preformed in
another host eg administration of antibody against tetanus, botulism,
diphtheria, rabies etc.
113. @udden death is ma&orly linked !ith embolism.
114. 24 to 4+ hours post acute inflammation ,monocytes start
accumulating.
11$. ubi/uitin proteosome path!ay 8 autophagic vacuoles are mainly
involved in atrophy.
11'. >eserve stem cells are main players in metaplasia.
11). echanical and trophic factors are involved in hypertophy.
11+. 7osinophils are players in allergic infections.
110. @e/uence of events in acute inflammation is 5
9ransient asoconstriction,vasodilation stasis, margination, rolling,
adhesion, diapedesis, chemota,is and phagocytosis.
124. acrophages seen as a part of reticuloendothelial system include5
;steoclasts E bone,microglia E brain,kupffer cells E liver,alveolar
macrophages E lung.@inus histiocytes E lymph nodes.
124. 9uberculosis is the leading cause of granuloma in Aakistan.
121. a&or granulomatous causes include5 sarcoidosis, leprosy, cat scratch
disease, fungal infections.
122. 1rading of a tumor is based on differentiation,atypia and mitoses.
123. @taging of a tumor is based on 9* E tumor,nodes,metastasis.
124. a&or autosomal dominant disorders include5 @keletal E arfan-
syndrome
*ervous E Huntington disease,neurofibromatosis
1astrointestinal E familial polyposis coli
Crinary E polycystic kidney disease
Haematopoietic E hereditary spherocytosis
12$. a&or intracellular accumulations are 5
elanin E melanoma,bile E cholestasis,carbon E anthracosis,copper E
:ilson disease
lipofuscin E aging
12'. (atty change is also kno!n as steatosis.
12). Aoint mutations are often caused by chemicals or malfunction of 3*A
replication, e,change a single nucleotide for another e.g >A@.
12+. 1iant cells are cells containing more than one nucleus.
120. a&or giant cells are 5 .anghan giant cells E 9uberculosis,9uton giant
cells E ,anthoma :arthin finkeldey giant cells E measles,>eed
@ternberg cells E Hodgkin .ymphoma
(oreign body giant cells E foreign body
134. 6g1 fi,es complement and crosses placenta.
131. 6g is the most heavy antibody.
132. 6g7 is the allergic reaction player antibody.
133. 6g A is found in secretions.
134. AB. gene is seen translocated in %..
13$. .ines of Iahn confirms a thrombus.9hey are alternate layers of
platelets !ith fibrin and >B%s2
13'. Asamomma bodies are lamellated bodies of dystrophic calcification
seen in meningioma,papillary carcinoma thyroid and serous ovarian
malignant tumors.
13). *uclear changes in a necrotic cell include5 pyknosis, karyolysis,
karryorrhe,is and loss of nucleus.
13+. acrophages get accumulated in chronic inflammation by continuous
recruitment,proliferation and immobilization.
130. 6schemic in&ury leads to coagulative necrosis.
144. a&or sensitive cell components5 maintenance of integrity of cell
membrane, aerobic respiration, protein synthesis, genetic integrity
141. .i/uefactive necrosis5 Csually caused by focal bacterial infections,
because they can attract polymorphonuclear leukocytes.
142. %oagulative necrosis is characterised by the preservation of cellular
and tissue architecture
143. (at *ecrosis5 A term for necrosis in fat, caused either by release of
pancreatic enzymes from pancreas or gut "enzymic fat necrosis# or by
trauma to fat, either by a physical blo! or by surgery "traumatic fat
necrosis#.
144. %aseous necrosis E cheese like 5 A distinct form of coagulative necrosis
seen in mycobacterial infections "e.g., tuberculosis#, or in tumor
necrosis, in !hich the coagulated tissue no longer resembles the cells,
but is in chunks of unrecognizable debris
14$. 1angrene "Ogangrenous necrosisO# is not a separate kind of necrosis at
all, but a term for necrosis that is advanced and visible grossly !ith
super added putrefaction.
14'. (ibrinoid necrosis occurs in the !all of blood vessels !hen endothelium
and smooth muscle cells are in&ured and dying.
14). Cnlike necrosis, !here the cell dies by s!elling and bursting its content
in the area, !hich causes an inflammatory response, apoptosis is a
very clean and controlled process !here the content of the cell is kept
strictly !ithin the cell membrane as it is degraded.
14+. 9he e,trinsic path!ay of apoptosis is initiated through the stimulation
of the transmembrane death receptors, such as the (as receptors,
located on the cell membrane.
140. 6n contrast, the intrinsic path!ay of apoptosis is initiated through the
release of signal factors by mitochondria !ithin the cell
1$4. 6n males bronchogenic carcinoma and in females breast carcinoma are
at the top.
1$1. Areneoplastic conditions include5 %irrhosis of liver, Atypical hyperplasia
of endometrium, .eukoplakia, 6nflammatory bo!el disease,
Adenomatous colonic polyps
1$2. 6nitiator chemicals = %ause irreversible damage to 3*A, but at
ma,imum they can cause severe dysplasia.

1$3. Aromoter chemicals itself cannot induce cancer,they propagate or
enhance the effects of initiators
1$4. ?no!n chemical carcinogens include 5A= Asbestos = .ung,
mesothelioma. 16 tract "esophagus, stomach, large intestine#
b= Arsenic = .ung, skin, hemangiosarcoma
c= Beryllium = .ung
d= %admium = prostate
e. Benzene = .eukemia
1$$. 6onizing radiation leads to dys&unction random fusion mutation.
1$'. 7,posure long term of radiations lead to leukemia and thyroid cancers.
1$). 6nitiation, .atent stage, Aromotion and alignant transformation are
recognizable stages in carcinogenesis.
1$+. ast cells are the main source of histamine and platelets the main
source of serotonin.
1$0. 9hrombo,ane A2 "9GA2#, from platelets, aggregates platelets,
constricts blood vessels. 1reat for hemostasis.
1'4. Arostacyclin "A162#, from the vessel !all, prevents platelet
aggregation, dilates vessels. 1reat for !henever hemostasis is
unnecessary.
1'1. @uppurative or purulent inflammation is characterized by the
production of large amounts of pus or purulent e,udate consisting of
neutrophils, necrotic cells, and edema fluid.
1'2. An ulcer is a local defect, or excavation, of the surface of an organ or
tissue that is produced by the sloughing (shedding) of inflammatory
necrotic tissue
1'3. 9eratoma is a tumor derived from more than one germ cell layer.
1'4. @eminomas,elanomas,Hepatomas are malignant tumors.
1'$. 7,tent to !hich the tumor cell resemble its parent cell is
differentiation.
1''. >anges of differentiation include5 !ell, moderately, poorly,
undifferentiated "anaplasia#.
1'). A malignant cells sho!s5 high *N% ratio,hyperchromatic nuclei,
prominent nucleoli, scanty cytoplasm and pleomorphism.
1'+. %arcinoma in situ is 5 (ull=thickness dysplasia e,tending from the
basement membrane to the surface of the epithelium.
1'0. 3ysplasia 5Atypical proliferation of cells characterized by nuclear
enlargement and failure of differentiation !hich falls short of
malignancy
1)4. 9he change that occurs in the stroma as tumor invades is called
desmoplasia
1)1. Benign tumors never locally invade and alignant tumors al!ays
invade the surrounding tissues.
1)2. %arcinoma of the ovary spreads through seeding of body cavities.
1)3. %ommonest places for mets deposits are liver and lungs.
1)4. Aerineural spread is seen by carcinoma of prostate and pancreas "2 A2s
#.
1)$. *uclear damage is the hall mark of irreversible cell in&ury.
1)'. @cientific study of structural changes and functional conse/uences of
in&urious stimuli on cells, tissues and organs is Aathology.
1)). etaplasia is a t!o edges s!ord because it can lead to dysplasia and
the original function of cells is lost.
1)+. etaplasia can lead to dysplasia.
1)0. A.9H;C1H A9>;AH6% %7..@ AJ HA<7 366*6@H73 (C*%96;*,9H7J
> *;9 37A3.
1+4. Aathologic hyperplasia constitutes a fertile soil in !hich cancerous
proliferation may eventually arise like bph and endometrial
hyperplasia.
1+1. 3ysplasia can regress and does not al!ays lead to cancer.
1+2. 9ransudates are fluid accumulations that are essentially salt=!ater,
accumulated because of pressure problems. 7,udates are protein=rich
fluid accumulations, due to leaky vessels.
1+3. 6n disseminated intravascular coagulation, the clotting cascades are
activated throughout the body. 9his is bad, since it tends to shut do!n
organs due to microthrombi, and also causes bleeding due to
consumption of clotting factors and activation of plasmin.
1+4. @ome people reserve the !ord OthrombusO for the ante=mortem kind,
and call post=mortem thrombi OclotsO.
1+$. Arterial thrombi usually occur over ruptured atherosclerotic pla/ues,
less often at sites of other vascular disease or old surgery.
1+'. <egetations are thrombi that occur on cardiac valves. 9hey may be
loaded !ith bacteria "Obacterial endocarditisO#, or sterile "OmaranticO,
OverrucousO, OblandO- also the thrombi of acute rheumatic fever#.
1+). 7mbolusO comes from the 1reek for Obottle stopperO.
1++. Aulmonary embolization is one of the great killers of hospitalized
patients, and that ante=mortem diagnosis is notoriously unsatisfactory
even today.
1+0. A parado,ical embolus "P crossed embolus# is one from the systemic
veins that passes through a right=to=left intracardiac shunt "i.e., a
birth defect#, to occlude a systemic artery.
104. .ong bone fractures are the main cause of fat embolism.
101. 9umor emboli are bits of cancer that invaded a vein and then broke
off. >enal cell carcinoma is famous for this.
102. :hite infarcts "Oanemic infarctsO, from Oan=O, not, and O=emeO, blood#
are usual !hen arteries are occluded in solid organs
103. >ed infarcts "Ohemorrhagic infarctsO, sounds like an o,ymoron but
isnQt# result !hen veins are occluded, or !hen arteries are occluded in
loose tissues "bo!el# or !ith a dual blood supply, or !hen the organ
!as already very congested.
104. onocytes are the largest cells in blood stream.
10$. Histiocytes are mature tissue macrophages.
10'. %ell membrane damage is the first sign of irreversible cell in&ury.
10). .ysosomal leakage confirms irreversible cell in&ury.
10+. %horistomas and hemartomas are not neoplasms.
100. (1(,91(,<71(,71( are main gro!th factors.
244. 7ndothelium gets leaky in acute inflammation due to5 1# formation of
endothelial gaps in venules 2# cytoskeletal reorganization 3# increased
transcytosis 4# direct endothelial in&ury $# leukocyte dependent in&ury
'# delayed prolonged leakage )# leakage from ne! blood vessels