200 Important Points
Transcript of 200 Important Points
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200 Important Points with Definitions toRemember in General Pathology
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 anincrease in the size of the organ.
3. Atrophy is the shrinkage in the size of the cell by loss of cellsubstance.
4. etaplasia is defined as a reversible change in !hich one adult cell
type "epithelial or mesenchymal# is replaced by another adult cell type.
$. %ell s!elling is the earliest sign of a reversible cell in&ury.
'. (ree radical is a chemical species that have a single unpaired electron
in an outer orbit.
). *ecrosis is a spectrum of morphological changes that follo! cell death
in a living tissue largely resulting from the progressive degradativeaction of enzymes on the lethally in&ured cell.
+. *ecrosis has si ma&or type- coagulative, %aseous, i/uefactive,
fibrinoid,gangrenous and (at.
0. Apoptosis "reek falling off# is defined as a path!ay of programmed
cell death that is aimed at a highly regulated intracellular programmein !hich cells destined to death by activated enzyme that degrade the
cells *A and nuclear and cytoplasmic proteins.
1. orphologically an apoptotic cell sho!s5 a# cell shrinkage, b#
chromatin condensation c# formation of cytoplasmic blebs andapoptotic bodies, d# phagocytosis by macrophages.
11. Apoptosis has t!o phases a# 6nitiation phase etrinsic and intrinsicpath!ays b#7ecution phase c#phagocytosis of dead cell
12. enes promoting apoptosis are5 ba,bak,bim
13. enes inhibiting apoptosis are bcl 2 family.
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14. 6nitiator caspase are + 8 0, !hile eecutioner caspases are mainly 3 8 '.
1$. ystrophic 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 asmicrobes 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+.
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2). %hediak=Higashi @yndrome is an autosomal recessive conditioncharacterized by failure of fusion of phagosome !ith lysosome.
2+. %hronic granulomatous disease of childhood results from inherited
defects in the components of *AH oidase !hich generates
superoide, leading to body infections.
20.
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42. %hronic inflammation is defined as an inflammation of prolongedduration, in !hich active inflammation, tissue destruction and attempts
at repair are proceeding simultaneously.
43. *eutrophils are the main cells of acute inflammation "eudates# !hile
ononuclear cells "!ith one nucleus are the main cells of chronicinflammation .ononuclear cells include ymphocytes, onocytes,
acrophages and lasma cells.
44. acrophages are the prima donna "main !orking cell# of chronic
inflammation, !hile lymphocytes are present in increased number.
4$. ranuloma 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.
ont confuse it !ith ranulation tissue !hich has capillaries,fibroblasts, and a variable amount of inflammatory cells.
4'. %lassical tuberculous granulomas is composed of epithelioid cells,
anghans multinucleated giant cells, caseation necrosis and collar of lymphocytes. 9here are t!o types of ranulomas5 6mmune 8 foreign
body.
4). 9here are 3 types of cells in the body5 %ontinously dividing labile cells,
Fuiscent or stable cells and ermanent *on=dividing cells.
4+. @tem cells are cells characterized by their prolonged self rene!alcapacity and by the asymmetric replication. 9hey are of t!o types5embryonic 8 adult stem cells.
40.
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$3. Healing by 2nd intention differs from 1st intention in three !ays- a#inflammatory reaction is more intense, b# uch more granulation
tissue forms and c# !ound contraction phenomenon.
$4. Accumulation of ecessive 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, resultingfrom 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 chronicpulmonary congestion.
$+. etechiae are minute 1 to 2 mm hemorrhages into skin, mucous
membranes or serosa surfaces, !hile 3 mm hemorrhages are called
urpura and more larger 1 to 2 cm subcutaneous hematomas arecalled 7cchymoses.
$0.
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'$. 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, andresulting in hypotension follo!ed by impaired tissue perfusion and
cellular hypoia.
'). a&or types of shock include5 cardiogenic, hypovolemic, septic,
neurogenic and anaphylactic.
'+. utation is defined as a permanent change in the *A.
'0. arfans syndrome is a disorder of the connective tissue of the body,
characterized by changes in the skeleton, eyes and cvs. ainly causeby defects in an etracellular glycoprotein (irbillin=1.
). 7hlers=anlos @yndrome comprise a clinically and genetically
heterogenous groups of disorders that result from some defect in thesyntesis or structure of fibrillar collagen.
)1. Amyloid is a pathologic proteinaceous substance deposited bet!eencells 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 eceeds and inuncoordinated !ith that of the normal tissue and persists in the sameecessive manner after cessation of the stimuli !hich evoked the
change.
)3. 9umor has t!o basic components5 arenchyma 8 stroma, !hile tumors
are of t!o types5 Benign and alignant.
)4. Benign tumors are !ell differentiated, gro! slo!ly and dont 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 malignanttumor is 79A@9A@6@.
)'. %arcinomas mostly use lymphatic routes and sarcomas mostly use
hematogenous routes of spread.
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)). (our types of genes are normally !orking in human body5 a# proto=oncogens b# antioncogenes, c# apoptotic genes and d#*A repair
genes
)+. roto=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%.
+. a&or antioncogenes are5 >B, 9$3, :.=1, *(=1, B>%A=1, A%.
+1. ;ncogenic viruses include- Human apilloma virus, Hepatitis B virus,
7pstein Barr virus ,?aposi @arcoma Herpes viruses 8 Human 9=%ellleukemia virus "9he only oncogenic >*A virus#.
+2. %hemical carcinogenesis is a multistep process, divided into initiationand promotion phases.
+3. a&or chemical carcinogens associated as include5 Asbestos !ith
esothelioma, Aniline dyes !ith 9%%, *itrates=astric carcinoma,Aflatoin !ith H%%, adiation induced malignancies include leukemias and papillarycarcinoma thyroid.
+$. a&or paraneoplastic synbdromes include, %ushing syndrome, AH
secretion by small cell carcinoma lung, Hypercalcemia by @/uamouscell carcinoma lung, hypoglycemia by (ibrosarcoma and H%%,olycythemia by >%% and hypertrophia osteoarthropathy by %A lung.
+'. a&or tumor markers included 5 H% for %horiocarcinoma, calcitonin
for medullary carcinoma thyroid, alpha fetoprotein=H%% and *on=
seminomatous germ cell tumor testis, %7A=%A colon, A (or %Aprostate, %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, formesenchymal tumor E vimentin, for leukocyte origin tumor E leukocytecommon antigen, @1 for neural origin tumors and for skeletal
muscle tumors E desmin.
++. 9ype 6 hypersensitivity "KanaphylacticL# or KimmediatehypersensitivityL# is the result of antigen binding to 6g7 on the surface
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of mast cells and basophils. 9hese instantly degranulate and releaseactive substances into the surrounding tissue.
+0. 9ype 66 cytotoic hypersensitivity, antibodies attach to antigens on the
surfaces of a cell and then something in&ures or destroys the cell.
0. 6n type 666 immune=comple hypersensitivity reaction, K@oluble
antigensL precipitate !ith antibodies, usually this happens 2=4 hoursafter eposure. 9his sort of tissue in&ury is mediated by antigen=
antibody complees "Kimmune compleesL#.
01. 9ype 6< Hypersensitivity reaction is called Kdelayed hypersensitivityL. 6t
is mediated by sensitized %4M9 lymphocytes !hich process antigensin association !ith class 66 HA molecules and release lymphokines.
02. 6mmune reactions are divided into t!o broad categories5 A# Humoralimmunity=B=cell lymphocyte mediated via production of antibody and
;ften develops as a response to soluble antigens, and B# %ellularimmunity=9=%ell lymphocyte mediated. %4Mhelper lymphocytes5 help
B cells make antibody and also help to generate cytotoic 9 cells.
03. a&or histocompatibility comple is present on all nucleated cells.
04. 9he HA 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 responsesagainst the microbes.
0'. %4 molecule is a high affinity receptor for H6<
0). a&or autoimmune disease include Hashimotos thyroiditis,>heumatoid Arthritis, @&ogrens syndrome, ankylosing spondylitis.
0+. amma interferon is one of the cytokine to activate macrophages andalso play ma&or >ole in ranuloma formation.
00. %ytokines are mediators released from one cell and modulate the
actions of another cell.
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1. @/uamous cell carcinoma is characterized by sheets, groups andclusters of pleomorphic malignant epithelial cells !ith high *N%
ratio,hyperchromatic nuclei and pale cytoplasm.?eratin epithelialpearls,intercellular bridges and individual cell keratinization are seen.
11. Adenocarcinoma is characterized by back to back closely packedglands lined by pleomorphic malignant epithelial cells !ith high *N%
ratio,hyperchromatic nuclei and eosinophilic cytoplasm.:all sharing isoften noted.
12. 9!o types of vaccines include5 ive vaccines- easles, umps,>ubella, abies, olio, Hepatitis
A.
13. rotooncogenes are converted into oncogenes.
14. p$3 !orks by *A repair and promoting apoptosis.
1$. >B gene activates and :orks in hypophosphorylated form.
1'. >A@ gene protooncogene protein is 9 bound and :orks !ith A in
cooridination !ith 9ase.
1). liomas and B%% are highly malignant but dont usually metastasize.
1+. A(B is acid fase bacillus " ycobacterium tuberculosis # and called so
because it resists decolourization by %oncentrated Acids.
10. 9igered lipid effect is seen in Herat.
11. a&or complement proteins include 5
;psonization by %3b%hemotais by %$a
Anaphylatoin %3a, %4a, %$aembrane 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 infectiousagents, eposure to microbial products "toins, tooids#
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assive immunity is resistance based on antibodies preformed inanother 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, chemotais and phagocytosis.
12. 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.
12. 9uberculosis is the leading cause of granuloma in akistan.
121. a&or granulomatous causes include5 sarcoidosis, leprosy, cat scratch
disease, fungal infections.
122. rading 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,neurofibromatosisastrointestinal E familial polyposis coliCrinary E polycystic kidney diseaseHaematopoietic E hereditary spherocytosis
12$. a&or intracellular accumulations are 5
elanin E melanoma,bile E cholestasis,carbon E anthracosis,copper E
:ilson disease
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lipofuscin E aging
12'. (atty change is also kno!n as steatosis.
12). oint mutations are often caused by chemicals or malfunction of *A
replication, echange a single nucleotide for another e.g >A@.
12+. iant 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
13. 6g fies 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%s
13'. samomma bodies are lamellated bodies of dystrophic calcification
seen in meningioma,papillary carcinoma thyroid and serous ovarianmalignant tumors.
13). *uclear changes in a necrotic cell include5 pyknosis, karyolysis,
karryorrheis 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.
14. a&or sensitive cell components5 maintenance of integrity of cellmembrane, aerobic respiration, protein synthesis, genetic integrity
141. i/uefactive necrosis5 Csually caused by focal bacterial infections,
because they can attract polymorphonuclear leukocytes.
http://en.wikipedia.org/wiki/Point_mutationhttp://en.wikipedia.org/wiki/Nucleotidehttp://en.wikipedia.org/wiki/Point_mutationhttp://en.wikipedia.org/wiki/Nucleotide
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142. %oagulative necrosis is characterised by the preservation of cellularand 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 fatnecrosis#.
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$. angrene "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 endotheliumand 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 keptstrictly !ithin the cell membrane as it is degraded.
14+. 9he etrinsic 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 therelease of signal factors by mitochondria !ithin the cell
1$. 6n males bronchogenic carcinoma and in females breast carcinoma areat the top.
1$1. reneoplastic conditions include5 %irrhosis of liver, Atypical hyperplasia
of endometrium, eukoplakia, 6nflammatory bo!el disease,Adenomatous colonic polyps1$2. 6nitiator chemicals = %ause irreversible damage to *A, but at
maimum they can cause severe dysplasia.
1$3. romoter chemicals itself cannot induce cancer,they propagate orenhance the effects of initiators
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1$4. ?no!n chemical carcinogens include 5A= Asbestos = ung,mesothelioma. 6 tract "esophagus, stomach, large intestine#
b= Arsenic = ung, skin, hemangiosarcomac= Beryllium = ung
d= %admium = prostate
e. Benzene = eukemia
1$$. 6onizing radiation leads to dys&unction à random fusion à mutation.
1$'. 7posure long term of radiations lead to leukemia and thyroid cancers.
1$). 6nitiation, atent stage, romotion 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$0. 9hromboane A2 "9GA2#, from platelets, aggregates platelets,constricts blood vessels. reat for hemostasis.
1'. rostacyclin "62#, from the vessel !all, prevents platelet
aggregation, dilates vessels. reat for !henever hemostasis isunnecessary.
1'1. @uppurative or purulent inflammation is characterized by theproduction of large amounts of pus or purulent eudate consisting of
neutrophils, necrotic cells, and edema fluid.
1'2. An ulcer is a local defect, or excavation, of the surface of an organ or
tissue that is produced by the sloughing (shedding) of inflammatory necrotic tissue
1'3. 9eratoma is a tumor derived from more than one germ cell layer.
1'4. @eminomas,elanomas,Hepatomas are malignant tumors.
1'$. 7tent to !hich the tumor cell resemble its parent cell isdifferentiation.
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.
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1'+. %arcinoma in situ is 5 (ull=thickness dysplasia etending from thebasement membrane to the surface of the epithelium.
1'0. ysplasia 5Atypical proliferation of cells characterized by nuclear
enlargement and failure of differentiation !hich falls short of
malignancy
1). 9he change that occurs in the stroma as tumor invades is calleddesmoplasia
1)1. Benign tumors never locally invade and alignant tumors al!aysinvade 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. erineural spread is seen by carcinoma of prostate and pancreas "2 s#.
1)$. *uclear damage is the hall mark of irreversible cell in&ury.
1)'. @cientific study of structural changes and functional conse/uences of in&urious stimuli on cells, tissues and organs is athology.
1)). etaplasia is a t!o edges s!ord because it can lead to dysplasia and
the original function of cells is lost.
1)+. etaplasia can lead to dysplasia.
1)0. A9H;CH A9>;H6% %7@ AJ HA *;9 7A.
1+. athologic hyperplasia constitutes a fertile soil in !hich cancerous
proliferation may eventually arise like bph and endometrialhyperplasia.
1+1. ysplasia can regress and does not al!ays lead to cancer.
1+2. 9ransudates are fluid accumulations that are essentially salt=!ater,
accumulated because of pressure problems. 7udates are protein=richfluid accumulations, due to leaky vessels.
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1+3. 6n disseminated intravascular coagulation, the clotting cascades areactivated throughout the body. 9his is bad, since it tends to shut do!n
organs due to microthrombi, and also causes bleeding due toconsumption of clotting factors and activation of plasmin.
1+4. @ome people reserve the !ord OthrombusO for the ante=mortem kind,and call post=mortem thrombi OclotsO.
1+$. Arterial thrombi usually occur over ruptured atherosclerotic pla/ues,
less often at sites of other vascular disease or old surgery.
1+'. 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 oymoron but
isnQt# result !hen veins are occluded, or !hen arteries are occluded inloose 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.
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10). ysosomal leakage confirms irreversible cell in&ury.
10+. %horistomas and hemartomas are not neoplasms.
100. ((,9(,