General Pathology Flashcards
Increase in cell size
Hypertrophy
Increase in cell number
Hyperplasia
Shrinkage of cell
Atrophy
Reversible change in which one adult cell type is replaced by another
Metaplasia
MC metaplasi
Columnar to squamous(smoking)
Uterus
Hyperplasia then hypertrophy
Breast during puberty and pregnancy
Hyperplasia
Liver donation
Hyperplasia
Endometrium
Hyperplasia
Prostate gland
Hyperplasia (BPH)
Gums on phenytoin exposure
Hyperplasia
Type of metaplasia in Barretts esophagus
Squamous to columnar
Type of metaplasia in the cervix
Squamous to columnar
Most common primary esophageal cancer
Squamous cell cancer
MC location of esophageal squamous cell cancer
Middle third
Most common location of esophageal adenocarcinoma
Distal third
Precursor for esophageal adenocarcinoma
Barretts esophagus
Tx to reverse Barrett’s esophagus
Nissen fundoplication
Hallmark of intestinal metaplasia
Presence of intestinal goblet cells
Disorganized cellular architecture,irreversible
Dysplasia
Most common cause of cell injury
Hypoxia
MCC of hypoxia
Ischemia
Mechanisms of cell injury
Damage to cell by peroxidation caused by Free radicals/ROS
ATP Depletion
Increase cell membrane permeability
Influx of calcium-2act as 2nd messenger for enzymes: proteases, atpases, phospholipases, endonucleases
Reversible/irreversible:
Cell swelling/vacuolar degeneration
Reversible
Reversible/irreversible:
Bleb on cell surface
Reversible
Reversible/irreversible:
Nuclear chromatin clumping
Reversible
Reversible/irreversible:
ER swelling
Reversible
Reversible/irreversible:
Cell membrane defect and myelin figures
Irreversible
Reversible/irreversible:
Lysis of ER
Irreversible
Reversible/irreversible:
Influx of calcium
Irreversible
Reversible/irreversible:
Calcification
Irreversible
Reversible/irreversible: Nuclear changes (karyolysis,pyknosis, karyorrhexis)
Irreversible
Programmed cell death
Apoptosis
Pro apoptotic:
Bax
Bad
Bak
Anti apoptotic
Bcl2
What activates pro apoptotic proteins
DNA damage and protein misfolding
Major mechanism/pathway of apoptosis in all mammalian tissue
Mitochondrial pathway
Responsible for protein folding
Chaperones
3 diseases associated with protein misfolding
Alzheimers
Parkinsons
Huntington
Responsible for pathogenesis of alzheimers
Tau protein
First drug used in alzheimers
Tacrine
Spectrum of morphologic changes that follow cell death in living tissues
Necrosis
Irreversible condensation of chromatin
Pyknosis
Fragmentation of nucleus
Karyorrhexis
Disintegration and dissolution of nucleus
Karyolysis
Apoptosis/necrosis:
Reduced cell size
Apoptosis
Apoptosis/necrosis:
Physiologic, eliminate unwanted cells
Apoptosis
Apoptosis/necrosis:
Intact cell contents
Apoptosis
Apoptosis/necrosis:
No inflammation
Apoptosis
Apoptosis/necrosis:
Pyknosis,karyorrhexis, karyolysis
Necrosis
Apoptosis/necrosis:
Enzymatic digestion
Necrosis
Apoptosis/necrosis
Frequent with inflammation
Necrosis
Aka tombstone necrosis
Coagulative
Preserved architecture, ghost cells
Coagulative
Involve solid organs except brain
Coagulative
Digestion of dead cells–pus
Liquifactive
Acute cerebral infact
Liquifactive
Cheese like material
Caseous
TB
Caseous
Enzymatic necrosis, saponification
Fat necrosis
Involves arteries, vasculitis, organ transplant
Fibrinoid
DM foot, buergers disease,PAOD
Gangrenous
Most common cause of fatty change
Alcohol
Abnormal accumulation if fat within parenchymal cells
Fatty change
Substance responsible for caseous necrosis in tb
Phosphatides
Classic microscopic description of malignant hypertension
Onion skin appearance
Wear and tear pigment
Lipofuschin
Intracellular accumulation mechanism
Abnormal metabolism
Enzyme deficiency
Inability to degrade/transport substances
Fatty accumulation in heart
Flabby heart/tigered effect
Strawberry gallbladder
Gallbladder cholesterolosis
Neurofibrillary tangles
Alzheimers
Russel bodies
Multiple myeloma
Pink eosinophilic inclusions in plasma cells
Russel bodies
Carbon dust
Anthracosis
Inhalation of silica dioxide
Silicosis
Eggshell calcification of lymph nodes
Silicosis
Predispose to mesothelioma and brochogenic cancer
Asbestosis
MC lesion of asbestosis
Pleural plaque
Calcification of walls of muscular artery involving internal elastic membrane
Mockenberg medial sclerosis
Glucoceribrosidase
Gauchers disease
Hexosaminidase A
Tay sachs disease
Sphingomyelinase
Niemann pick disease
Iron deposit
Hemosiderin
MCC of hemosiderosis
Transfusion
Iron deposit,no organ damage
Hemosiderosis
Iron deposit with organ damage
Hemochromatosis
Bronze diabetes
Hemochromatosis
Green to brown to black pigment
Bilirubin
P. Falciparum
Maurer dots
P. Malariae
Zieman dots
P. Ovale
James dots
P. Vivax
Schuffner dots
Hepatolenticular degeneration
Wilsons disease
Brown black pigment
Melanin
Homogentisic acid accumulation
Black urine
Alkaptonuria
Black nails
Ochronosis
Calcium deposit in dead/dying tissues
Normal seum calcium
Dystrophic calcification
Psammoma bodies
Dystrophic calcification Papillary thyroid cancer Serous ovarian cancer Meningioma Mesothelioma
Calcium deposits in normal tissues due to increased serum calcium
Metastatic calcification
Seen as glassy, homogenous,pink appearance
Hyaline change
Hallmark of chronic inflammation
Fibrosis
Hallmark of acute inflammation
Increased capillary permeability
Retraction of endothelial cell leading to increased permeability is due to
Histamine
Outcomes of acute inflammation
Resolution
Scar/fibrosis
Chronic inflammation
Anaphylatoxin
C3a-C5a
Cytokine that induces fever
IL-1 TNF
Chemotactic factors
Bacterial products
C5a
LTB4
IL-8
Cellular events in leukocyte extravasation
Margination Rolling Adhesion Diapedesis/transmigration Chemotaxis Phagocytosis
Neutrophils will cling to capillary wall
Margination
Leukocytes line the endothelial surface/ pavementing
Rolling
Endothelial molecules for rolling
E selectin
P selectin
Glycam1
CD34
Neutrophils squeeze through capillary wall
Diapedesis
Unidirectional movement of wbc towards site of injury
Chemotaxis
One of the most powerful chemo attactants
Bacterial products
Engulfment and killing of microbes
Phagocytosis
Endothelial molecules for adhesion
ICAM1
VCAM1
Leukocyte molecule for rolling
Sialyl x modified protein
L selectin
Leukocyte molecules for adhesion
CD11/18
VLA 4
Defective leukocyte adhesion due to mutation in beta chain of CD11/18
Leukocyte adhesion defect 1
Defective adhesion due to mutation in fucosyltransferase required for synthesis of sialylated oligosaccharides
Leukocyte adhesion deficiency 2
Decrease in oxidative burst due to NADH deficiency
Chronic granulomatous disease
Process of coating a particle by opsonin to target it for ingestion
Opsonization
3 major opsonins
Fc fragment
C3b
Plasma lectin
1st line of defense of the innate immune system
Neutrophils
Defense against parasitic infection
Allergic and immunologic diseases
Eosinophils
Major source of histamine
Mast cells
Derived from circulating monocytes
Macrophages
Another name for tissue macrophages
Histiocytes
Bean shaped nuclei
Monocytes
Involved in immune reactions and immediated antibody response
Lymphocytes and plasma cells
Cells that produce antibodies
Plasma cells
Transudate/Exudate
Hypocellular
Transudate
Transudate/Exudate
Cellular
Exudate
Transudate/Exudate
Protein poor
Transudate
Transudate/Exudate
Rich protein
Exudate
Transudate/Exudate
Specific gravity less than 1.012
Transudate
Transudate/Exudate
Due to increased hydrostatic pressure
Transudate
Transudate/Exudate
Due to infection or malignancy
Exudate
Membrane attack complex
C5b to C9
Potent vasodilator produce from the action of nitric oxide synthetase from arginine
Nitric oxide
Powerful vasodilator, a vasoactive amine produced by mast cell and basophil
Histamine
Nodular collection of specialized macrophages/epithelioid cells surrounded by a rim if lymphocytes,MN giant cell, with or without caseous necrosis
Granuloma
Examples of non caseating granulomatous disease
Sarcoidosis
Crohns disease
Steps in scar formation
Angiogenesis
Granulation tissue
Remodelling
At how many day does neovascularization and granulation tissue fill up the incision space
Day 5
Characterized by arterial dilation, secondary to sympathetic stimulation or vasoactive substances
Active hyperemia
Impaired venous outflow due to venous obstruction
Passive congestion
Zone of liver most prone to toxic and viral injury
Zone 1
Zone of liver least oxygenated and most prone to ischemia
Zone 3
Chronic passive congestion of liver
Nutmeg liver
Steps in hemostasis
Primary hemostasis:platelet plug formation
Secondary hemostasis: fibrin clot formation
Virchows triad
Stasis
Hypercoagulability
Injury to blood vessel wall
