This site is 100% ad supported. Please add an exception to adblock for this site.



undefined, object
copy deck
What is hydropic swelling?
acute sublethal reversible injury
can cause cell swelling, large pale cytoplasm, membrane blebbing, mito swelling, detachment of ribosomes from ER, ER swelling, nucleolar disaggregation
what is hypertrophy
increase in cell size accompanied by augmented functional capacity
what is metaplasia?
conversion of one cell type into another.

usualy fully reversible, but may have associated risk of neoplastic transformaiton
what is dysplasia
alteration in size, shape and organization of cellular components of tissue
what are some intracellular storage problems?
iron (liver)
lipofuscin (yellow stuff)
inherited lysosomal storage diseases
Name the types of necrosis
1) coagulative
2) liquefactive
3) enzymatic fat
4) caseous
5) fibrinoid
What is coagulative necrosis?
denaturation of proteins, nuclear dissolution with PRESERVATION of cell outline.

Characteristic of hypoxic cell death/ischemia
What is liquefactive necrosis?
cellular digestion to a liquid, viscous mass.

Characteristic of focal bacterial or fungal infections
What is fat necrosis?
focal areas of fat destruction, frequently associated with release of activated pancreatic enzymes into pancreatic tissue during pancreatitis
What is caseous necrosis?
Subset of coagulative necrosis

Associated with TB and granulomatous inflammation
What is fibrinous necrosis?
alteration of injured BV with insudation and accumulation of blood proteins causing vessel wall to stain intensely with eosin.
What are the stages histologically of coagulative necrosis?
1) cytoplasm and organelle swelling, blebbing, ribosome detachment (reversible injury)
2) rupture of membranse, organeles, nuclear pyknosis (irreversible)
3) more rupturing....
What is the most important cause of coagulative necrosis?
describe the histologiocal stages of apoptosis
1) condensation of chromatin; compaction of cytoplasm
2) shrinkage, blebbing, nuclear fragmentation
3) cell fragmentatin as membrane bound apoptotic bodies
4) phagocytosis of those bodies
What is karyorrhexis?
fragmentation of nucleus
What are the categories of etiology (mnemonic)
1) vascular
2) inflammatory
3) neoplastic
4) drug
5) infectious
6) congenital
7) allergic
8) trauma
9) endocrine
How does eosin stain?
stains basic things pink/red
How does hematoxylin stain/
stains acidic (neg charged) (??) things blue.
What is in a granulomain the lung?
activated Mphages
giant cells
caseous necrotic core
What is inflammation
The reaction of living tissue and its microcirculation to pathogenic insult

Generation of inflammatory mediators

movement of fluid and leukocytes from blood into extravascular tissue
What are the characteristics of accute inflammation?
Immediate reaction to tissue injury
Rapid onset
Innate immnunity
Neutrophils mainly
prominent VASCULAR response
What are the characteristics of chronic inflammation
Persistant rxn to tissue injury
slow response
mainly mononuclear cells: lymphocytes, plasma cells, monos
less prominennt vascular response
Causes of accute inflammation
microbial infection
tissue necrosis
physical agents
chemical irritants
immune-mediated hypersensitivity
causes of chronic inflammation
persistant tissue injury & acute inflammation
microorgs resistant to phagocytosis or intracellular killing
foreign bodies
autoimmune disorders
primary granulomatous diseases
What are some primary granulomatous diseases that can trigger chronic inflammation?
Crohn's disease
Name some chemotactic factors that are inflammatory mediators
Name some vasoactive mediators of inflammation

Name some outcomes of inflammation
1) abscess: excessive tissue destruction
2) persistant inflammation-->chronic inflam w/fibrosis
3) resolution
4) fibrosis (scar)
What are the classic signs of acute inflammation

and loss of function
What are the major manifestations of acute inflammation?
1) rapid vascular response wiht altered microvasculature (dilation, flow up)
2) increased vascular permeability with accumulation of fluid and plasma components
3) intravascular stimulation of platelets
4) interaction of chemical mediators
5) emigration of neutrophils (PMNs)
6) Phagocytosis, intracellular kiling
what is effusion
excess fluid in body cavities
What are the causes of increased vascular permeability in acute inflammation
1) contraction of vascular endothelial cells makes gaps (Fast, short lived)
2) direct injury to the vessel
3) leukocytes injure vesssel from insiide and get out
What are some plasma derived mediators of edema?
1) Hageman factor (triggers clotting system), triggers bradykinin production

2) Complement activation system (C3a, C5a)
What are some cell derived mediators of edema?
1) Histamine (mast cell degranulation)
2) platelets (serotonin)
3) inlfammatory cells (PAF, PG, Leukotrienes)
4) Endothelium (NO, PAF, PGs)
What is transudate?
edema fluid with LOW protein content
What is exudate?
edema fluid with HIGH protein content
What is serous exudate
hi protein

absence of prominent cellular componenets
what is fibrinous exudate?
contains large amts of fibrin from activation of coag
what is prurulent exudate?
prominent cellular components, usually neutrophils
What is suppurative inflammation?
Subset of purulent exudate

purulent + liquefactive necrosis (pus)
what does hageman factor activation cause?
(=factor XII)

kinin generation
clot formation
anaphylatoxin generation (via complement cascade)
fibrin degradation product formation (fibrinolyiss)
what does fibrinolysis do wrt vascular permeabilty/
augments it
how else does hageman factor increase vascular permeability/
activates complement cascade, which produces anaphylatoxins (c3a, c5a)

generates kinins (bradykinin)
name a comoplement cascade opsin
name complement cascade anaphylatoxins
c3a, c5a
name a complement cascade chemoattractant
what is the MAC
c5b - c9
lyses cell

started by c5b
which is the most important anaphylatoxin
what effects do anaphylatoxins have?
smooth muscle contraction (broncho and vasoconstriction)
increased vascular permeability
Name some more cell derived vasoactive mediators
1) AA metabolites (PG, TX, LT)
2) PAF
3) platelets
4) mast cell, basophil: hist, leukotrienes
5) endothelial cells: prostacyclin
What are the 2 ways AA can be metabolized?
Cyclooxygenase path-->PG and thromboxanes

Lipoxygenase path-->leukotrienes
What is PAF? What does it do?
1) generated by activated inflammatory cells (neutros, masts), endo cells, injured cells
2) induces platelet aggregation
3) enhances platelet release of serotonin
4) increase vascular permeability
5) recruits leukocytes
6) vasodilator
7) enhances phagocytosis
8) stimulates synthesis of AA pathways
What are the platelet derived mediators?
1) serotonin (-->vasc perm up_
2) TxA2 (AA-->cyclooxygenasepath-->SM constriction
3) cationic proteins (vasc perm up)
4) histamine
what does PGI2 do?
anti aggregatory for platelets
inhibits PMN respons
What are mast celll and basophil derived mediators?
leukotrienes (sm contract, vasc perm up)
what is haptotaxis?
chemotaxis along a fixed, insolumble chemotactic gradient
what chemotaxins are the initial neutrophil recruiters?
what are the 3 stages of leukocyte emigration? what are they mediated by/
1) rolling: selectins, addressins
2) adhesion; integrins, ICAM
3) transmigration: PCAM
what is in neutrophil granules?
phospholipase A2
what is the major bacteriocidal agent?
(hypochlorous acid)
Name all of the bacteriocidal compounds
superoxide anion (respiratory burst)
hydrogen peroxide (substrate for other ROS)
OH radical: another potent bactericide
what are symptoms of a myeloperoxidase deficiency?
no HOCl, recurrent fungal infections
what is chronic granulomatous disease?
no NADPH oxidase, so you get no H202, which is a substrate for the real potent bactericides
what are some diseases caused by inflammatory cells damamging tissue by releasing enzymes and ROS??
rheumatoid arthritis
hemostasis definition
arrest of hemorrhage following vascular injury
what are the 2 paths of the coagulation cascade
1) Intrinsic cascade. FXII contacts thrombogenic surface.

2) Extrinsic cascade: blood is exposed to extravascular (subendothelial) tissue factor (TF)
Coagulation, generally
conversion of soluble plasma fibrinogen to insoluble fibrillar polymer fibrin, catalyzed by thrombin
What is probably the most important factor in thrombus progression and stabilization?
Thrombin production
Steps to no in clotting cascade
1) TF combines with VII
2) TF:VIIa catalzyses X-->Xa and IX--IXa
3) These steps are inhibited by TFPI tho
4) Meanwhile, THROMBIN Activates XI to XIa.
5) Thrombin also activates V and VIII and XIII.
6) these precursors help the steps in 2 progress better
7) this all leads to more creation of thrombin from prothrombin
8) finally, thrombin converts fibrinogen to soluble fibrin, and then soluble fibrin converst to insoluble fibrin via activated XIIIa
Whaat is VWF
Von Willebrand factor

enhances platelet adhesion by binding both to platelet membrane and fibrinogen
What do activated platelets do?
1) release granule contents (ADP, TxA2) that recruits more platelets and promotes aggregation
2) other factors released promote clotting cascade and thrombus formation
What does endothelium do to regulate the thrombus?
releases NO and PGI2 (prostacyclin), which INHIBIT platelet aggregation
Descibe hemophilia A
1) inherited coagulopathy
2) MOST COMMON X-linked recessive inherited bleeding disorder
3) absent/low F XIII
4) spontaneous bleeding into joints, muscles, organs
5) dr. brinkhous worked on this
Describe hemophilia B
1) less common X-linked recessive bleeding disorder
2) clinically indistinguishable from type A
3) "Christmas disease"
Describe vWD
2) AUTOSOMAL DOMINANT (cf hemophilias, X-linked recessive)
3) abnormal/deficient vWF
4) also associated with reduced F XIII levels, since vWF is a carrier for F XIII
5) excessive blood loss from superficial injuries, operative and post traumatic injuries
Incidence of acquired coagulopathies
GREATER than thhat of the inherited coagulopathies (hemophilia, vWD)
Vitamin K deficiency
1) decrease in a bunch of factors (II, VII, IX, X)
2) malapsorption in the gut of stuff
Liver disease and coagulopathy
1) can cause impaired vit K absorption, leading to vit K deficiency-type coagulopathy
2) thrombocytopenia due to hypersplenism
3) reduced synthesis of clotting factors, fibrinogen
Characteristics of DIC
an acquired coagulopathy characterized by widespread thrombosis AND hemorrhage secondary to the consumption of all of the platelets and coag factors elsewhere.

Also widepsread ischemia due to thrombosis
General cauases of DIC
1) tissue injury
2) endothelial cell injury
what are the major factors predisposing to thrombosis?
1) changes in blood constituents
2) changes to internal surface of BV
3) changes in patterns of blood flow
what is the most common cause of death in western industrialized countries?
arterial thrombosis, with the complication of embolization
definition of embolism
passage through arterial or venous system of ANY material capable of lodging in the lumen and occluding it
Materials able to cause embolism
amniotic fluid
atheromatous debris
foreign objects
Where can arterial emboli cause infarct
(usually cardiac source, e.g. mural thrombi)

1) brain
2) intestine
3) lower extremeties
4) kidney
5) heart
Describe amniotic fluid embolism
1) uncommon but lethal childbirth complication
2) sudden dyspnea, hypertension, SCA
3) ebolization of fetal material/debris
4) associated with DIC and ARDS
what is fat embolism associated with
bone fractures
what causes the nasty rotted off fingers?
Buerger disease
(necrosis secondary to thrombosis)
what cells are responsible for organizing a thrombus? how?
Phagocytes: injest thrombotic material
Fibroblasts: replace it with fibrosis
name some signs of greater thrombus reorganization
clefts form in the thrombus, line themselves with endothelial cells! meanwhile fewer nucleii are seen inside the thrombus.
what things can happen to a thrombus after formation
1) can be lysed either by endogenous enzypmes or drugs
2) can be replaced by fibrous tissue/reorganized
how are venous thrombi distinuishable from just blood in the lumen
1) you see signs of repair and healing
2) you see mphages injesting RBCs
3) you see endothelial proliferation in the adjacent vein wall
why do you get hemorrhagic infacts in the lung
not an end-artery system like spleen or kidney. There is another, o2 rich arterial blood supply to lung (bronchial arteries, cf pulmonary arteries). this shoots in blood distal to the thromboembolism into necrotic vessels...hemorrhage ensues
what is the most frequent cause of AAA?
atherosclerosis with medial destruction
What are possible consequences of AAAs
1) they may give rise to emboli of atheroma or mural thrombus

2) they may rupture and cause massive/fatal hemorrhage
Simplified clot cascade steps
1) vascular/endothelial injury releases TF
2) TF combines with VII to make TF:VIIa, which activates IX and X
3) IX and XIIIa activates X
4) Xa and Va catalzye prothrombin-->thrombin
5) thrombin converts fibrinogen to fibrin
what is chronic inflammation characterized by?
interetitial fibrosis and influx of mainy MONONUCLEAR leukocytes (lymphocytes, monocytes, macrophages)
what things induce chronic inflammation
1) stimulus not readily degradable
2) stimulus is incide a cell
3) stimulus IS a cess
4) recurrent injury
5) inflammation is induced by a T lymphocyte mediated immune response (contact dermatitis)
What are the most important effecter cells of chronic inflammation?
mononuclear phagocytes and lymphocytes
how are monocytes/macrophages activated and recruited?
1) monocytopoeisis, trigered by CSFs
2) vascular transmigration and chemotaxis
3) activation, via gamma interferon, LPS, polynucleotides
how are lymphocytes activated and recruited/
1) immune activation via antigen recognition y T lymphocyte antigen recceptors, B lymphocte antigen receptors, or antibodies

2) activation involves ccytokines
whhat are cytokines? Who releases them
= major molecular mediators of chronic inflammation

released by

1) mononuclear phagocytes
2) lymphocytes
3) non leugocytes like endothelial cells, fibroblasts
what do activated macrophages release?
1) lytic enzymes
2) phlogogenic lipid metabolites
30 toxic oxygen metabolites
4) plasma mediators or their activators (complement proteins, etc)
Describe granulomatous inflammation
A special form of chronic inflammation characterized by granulloma formation.

Granuloma is a dense accumulation of predominantly mononuclear phogocytes, typically with many showing difenrentiation into "epithelioid cells"
what causes many of the systemic signs and symptoms of choonic inflammation?
what is granulation tissue
tissue characterized by small new blood vessels with plump endothelium and active fibroblasts laying down collagen.
are b lymphocytes involved in chronic inflammation mediation?
what kind of things do the cytokines IL-1 and TNNF cause?
1) activation of leukocytes
2) CNS effects--fever, somnolence, anorexia
3) skeletal muscle proteolysis, bone resorption--myalgias
4) proliferation of tissue cells (proud flesh)
are multinucleated giant cells found in granulomas
sometimes, not always
what is success of repair dependent on?
severity of injury
proliferative capacity of injured cells
nature of the inflammatory response
other mitigating/aggravating circumstances.
stages of "organization" of a MI
1) coagulative necrosis with acute inflammation
2) chronic inflammation w/early granulation tissue
3) Late granulation tissue
4) Focal fibrosis (scar)
What is sarcoidosis? what can be involved
multisystemic disease of unknown etiology invovling noncaseating granulomatous infection in many organs, including:

uveal tract
hilar/mediastinal nodes
bone marrow
is there always a gross process evident in viral myocarditis?
what does granulation tissue eventually do
remodels into dense fibrous tissue
in addition to sarcoidosis, what can cause granulomatous inflammation/
fungal infection
what are the nodules in a cirrhotic liver made up of?
regenerating hepatocytes
what is a characteristic of keloid microoscopicallly?
wide, pink, accellular bands of stained collagen. not normal skin/dermis componenets. Large, darkly staining fibroblasts
what is the major pathological process in viral myocarditis
chronic inflammation
which cytokines are most important in directly causeing the systemic signs of chronic inflammatory disease/
IL-1 and TNF
is infiltration with mononuclear leukocytes characteristic of acute, chronic, neither, or both viral myocarditis?
hyperplasia, def
increase in cell number
usually associated with increase in tissue mass
can be physiologic or pathologic
metaplasia, def
change of one differentiated cell type into another.

Dysplasia, def
1) abnormal appearing cells
nuclear enlargment/irregularity

2) disorderly arranged cells
loss of polarity
loss of maturation
abnormal location of mitotic figures
Neoplasia, def
abnormal growth of tissue
excessive growth
uncoordinated and autonomous
histology of benign neoplasms
resemble normal tissue
histologically well differentiated
low mitotic rate
generally well circumscribed
does not metastasize
osteoma is...
benign bone neoplasm
benign Cartilage neoplasm
benign neoplasm of gland
what are sarcomas?
tumors that arise in CT like bone, muscle, fat
where do carcinomas arise
what group are sarcomas more common in?
is dysplasia reversible?
what is grading
a HISTOLOGICAL determination of how differentiated tumor cells are compared to the tissue they came from
what are the 3 parts of a cancer staging
tumor (0-4)
nodes (0-4)
metastasis (0, +)
what is anaplasia
very poorly differentiated neoplasm
skeletal muscle-derived
smooth muscle derived
is leiomyoma at risk to turn into leiosarcoma?
how does tumor get from gut to liver
hematogenous spread
what is desmoplasia
scarring response to tumor
what is chronic myelogenous leukemia
cancer of white blood cells
bcr-abl tranlocation
targeted by magic bullet gleevec

Deck Info