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Pathology

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metaplastic change in lungs

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Pathology

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6 years ago

Date created

Mar 1, 2020

Cards (49)

Section 1

(49 cards)

metaplastic change in lungs

Front

normal columnar epithelium to squamous epithelium

Back

hyperplasia

Front

number of cells increases

Back

Coagulative Necrosis

Front

usually related to ischemia, tissue dies and undergoes necrosis,

Back

ulcer

Front

typically in skin or mucosal surface; overlying cells at the site of inflammation die off; exposed and inflamed tissue left

Back

Most predominant cells in acute inflammation

Front

neutrophils* and macrophages *=mostly

Back

Vascular events of acute inflammation recruitment

Front

1)increased vascular blood flow -histamine and NO cause vasodilation 2)increased vascular permeability -endothelial cells retract, allows more permeability -happens most in post-capillary venules -can also be seen in pathological states (ex: burns, inappropriate retraction, get leakage)

Back

Where can cytokines travel and what do they do when they get there?

Front

-brain:create fever -liver: increase plasma proteins production (to enhance complement and kinin systems) -bone marrow: up regulate lymphocyte maturation

Back

migration

Front

process by which cells move from the lumen through the vessel wall and into the local tissue

Back

Fibrinoid

Front

accumulation of antibody complexes that form and stick in blood vessels, appears bright pink, can lead to clots in blood vessels

Back

atrophy

Front

decrease in organ or tissue size from decrease in cell size, number of cells don't change

Back

Transudate

Front

protein scarce fluid that results from increased hydrostatic pressure as a result of the vasodilation seen during inflammation. Often seen in Chronic Heart Failure (CHF)

Back

metaplasia

Front

change in cell type

Back

hypertrophy

Front

increase size of organ or tissue through increased cell size but doesn't change number of cells

Back

Types of Necrosis:

Front

1. Coagulative 2. Liquefactive Necrosis 3. Caseous 4. Fat Necrosis 5. Fibrinoid Necrosis

Back

What does selectin binding do in acute inflammation?

Front

leukocytes bind and roll along the endothelium

Back

Chronic Inflammation Common Infections

Front

Virus, bacteria, parasite, or fungi (typically low toxicity and elicit delayed type hypersensitivity reaction, ex: mono or syphilis)

Back

Inflammatory cytokines examples

Front

TNF-a & IL-1

Back

Liquefactive Necrosis

Front

see lots of neutrophils, abscess forms, seen in brain or in specific types of infection

Back

tumor

Front

swelling

Back

Exudate

Front

protein rich fluid that results from the increased vascular permeability seen during acute inflammation

Back

Cellular events of acute inflammation recruitment

Front

margination, adhesion, migration, chemotaxis, recognition

Back

Abscess

Front

when pus becomes localized to a specific region, should be removed surgically to avoid fibrosis or rupture

Back

metaplastic change in esophagus

Front

changes from squamous to glandular epithelium (secretes mucin protectively)

Back

Recruitment (acute inflammation)

Front

mediators released from the receptors to attract the necessary cells for the inflammatory response causing vascular and cellular events to occur

Back

margination

Front

leukocytes traveling in blood tend to locate themselves on the outer edge of the lumen, rather than in the center, regulated by selectins and integrins

Back

Chronic Inflammation Causes

Front

Infections, toxic substances, and hypersensitivity diseases

Back

chemotaxis

Front

-Process by which leukocytes follow the gradient of a certain chemical towards a higher concentration -Chemical can be cytokines from macrophages, dendritic cells, etc., or bacterial components recognized as foreign -Actual cell mobilization due to Actin Polymerization, which resembles cells pulling themselves forward on a rope.

Back

What are a type of anti-inflammatory mediator used at the end of an inflammatory immune response?

Front

lipoxins

Back

metaplastic change in cervix

Front

the ectocervix is exposed to outside and is lined by squamous epithelium and indocervix is glandular, HPV tends to infect this metaplastic area

Back

Caseous Necrosis

Front

combination of liquefactive and coagulative, occurs in specific type of granuloma

Back

Anti-inflammatory cytokines examples

Front

TGF-b & IL-10

Back

Cellular accumulations

Front

Lipid, protein, exogenous materials (ex tattoo ink and carbon dioxide) , endogenous materials (ex hemosiderin)

Back

What is the general order of events in acute inflammation?

Front

Recognition (of pathogen or damage)--> Recruitment (of inflammatory cells) --> Removal (of damaged cells or pathogens) --> Termination (of inflammatory processes)--> Repair(there are different ways this can happen)

Back

Things that may occur with acute inflammation

Front

Rubor (redness) Tumor (swelling) Calor (heat) Dolor (pain) Odor (caduceus)

Back

Recognition (by leukocytes)

Front

Use these receptors on their cell membranes: - Toll Like Receptors (recognize bacterial carbohydrate, peptide and lipid parts) - G Protein Coupled Receptors (recognize bacterial carbohydrate, peptide and lipid parts) - Opsonin Receptors (recognize Igs and complement proteins) - Cytokine Receptors (recognize IL's)

Back

What does integrin binding cause in acute inflammation?

Front

firmer adhesion of the leukocyte occurs and rolling from selectins stops

Back

Complications of acute inflammation

Front

ulcer, abscess, fibrosis, and scarring

Back

Outcomes of inflammation

Front

1)Healthiness/ Resolution (all back to normal) 2)Abscess Formation (pus forms and remains) 3)Chronic Inflammation (leads to fibrosis and loss of tissue function)

Back

calor

Front

heat

Back

dolor

Front

pain

Back

Fat Necrosis

Front

occurs in fat cells, loses white colors and cells die

Back

Removal (acute inflammation)

Front

Phagosome (extracellular microbe) + Lysosome (deadly enzymes) = Phagolysosome (dead microbes), essentially we phagocytose and destroy the foreign substance

Back

Recognition (acute inflammation)

Front

Carried out by sentinel cells using receptors that have pattern recognition for things that don't usually exist in a human

Back

adhesion

Front

TNF-a & IL-1 secreted; increases the production of Selectins & Integrins on the endothelium near their location. Leukocytes then more likely to use their proteins to bind the Endothelium in that region

Back

Chronic Inflammation

Front

1)has variable onset 2)prolonged duration 3)causes tissue destruction 4)ongoing healing and fibrosis occurs 5)lymphocytes are the major cells but macrophages and plasma cells also important

Back

pus

Front

type of exudate rich in leukocytes and fibrin debris; Can be seen in Purulant (also known as Supurative) Inflammation

Back

physiologic stressors

Front

1. increased demand 2. decreased nutrients 3. increased/decreased stimulation 4. hypoxia 5. microbial infections 6. metabolic alterations

Back

Rubor

Front

redness

Back

Edema

Front

fluid build-up in the interstitial space, which can be either Exudate or Transudate

Back