Trans 1- Cell adaptation Flashcards by Rhaizza Mae Guerra

the study (logos) of disease (pathos)

Pathology

How well did you know this?

Not at all

Perfectly

Disease is due to cellular abnormalities:

o Altered ability to proliferate
o Dysfunction
o Disturbed homeostasis

How well did you know this?

Not at all

Perfectly

Cells react to adverse stimuli by:

o Cellular adaptation
§ Hypertrophy
§ Hyperplasia
§ Atrophy
§ Metaplasia
o Reversible injury
o Irreversible injury and cell death
o Apoptosis
o Necrosis

How well did you know this?

Not at all

Perfectly

Types of cellular adaptation

Hypertrophy
Hyperplasia
Atrophy
Metaplasia

How well did you know this?

Not at all

Perfectly

response to hormonal or

endogenous influences

physiologic

How well did you know this?

Not at all

Perfectly

response of the cell to injurious

stimuli which enable them to escape injury

pathologic

How well did you know this?

Not at all

Perfectly

are continuously cycling

skin cells

How well did you know this?

Not at all

Perfectly

are stable and will go to G1 if needed.

“Prometheus and his liver regeneration.”

Hepatocytes

How well did you know this?

Not at all

Perfectly

are permanent cells and non-dividing. They cannot regenerate.

Heart muscles and Neurons

How well did you know this?

Not at all

Perfectly

Increase in the number of cells

* Encountered in cells which are capable of dividing

Hyperplasia

How well did you know this?

Not at all

Perfectly

Hyperplasia is encountered where

epithelium
blood cells
connective tissues

How well did you know this?

Not at all

Perfectly

In hyperplasia, these are PHYSIOLOGIC if normal stressor

o Breasts in pregnancy

o Menstrual endometrium

How well did you know this?

Not at all

Perfectly

In hyperplasia, these are PATHOLOGIC if normal stressor

o ACTH from pituitary adenoma

o High estrogen

How well did you know this?

Not at all

Perfectly

• Increase in the size of cells due to an increase in the
cellular contents
• Encountered in cells which are not capable of or have
limited capacity to divide

Hypertrophy

How well did you know this?

Not at all

Perfectly

Hypertrophy is encountered where

in myocytes and skeletal muscles

How well did you know this?

Not at all

Perfectly

In hypertrophy, these are PHYSIOLOGIC if normal stressor

Skeletal Muscles with Exercise

How well did you know this?

Not at all

Perfectly

In hypertrophy, these are PATHOLOGIC if normal stressor

Hypertensive cardiomegaly

How well did you know this?

Not at all

Perfectly

Histological Comparisons between Pregnancy and Normal Uterus

Pregnancy has bigger cells compared to the Normal Uterus

How well did you know this?

Not at all

Perfectly

A normal heart weighs

250 g

How well did you know this?

Not at all

Perfectly

Decrease in the size of a previously normal cell

* Not hypoplasia, Cells under hypoplasia never developed to begin with.

Atrophy

How well did you know this?

Not at all

Perfectly

In atrophy, these are PHYSIOLOGIC if normal stressor

non-pregnant uterus and

brain in senility

How well did you know this?

Not at all

Perfectly

In atrophy, these are PATHOLOGIC if normal stressor

loss of stimulus (blood, innervation, endocrine, disuse, mechanical compression

How well did you know this?

Not at all

Perfectly

Poliio virus affects

anterior motor neurons

How well did you know this?

Not at all

Perfectly

Gyri become smaller, sulci become wider

Atrophy Normal Brain

How well did you know this?

Not at all

Perfectly

More fat rather than beefy-looking

Skeletal Muscle Atrophy

Renal atrophy due to atherosclerosis or incidental cancer

renal atrophy

Change of Epithelium from one to another in an abnormal location (Chronic cervicitis, Chronic bronchitis, Barrett Esophagus). Gastro-esophageal junction demarcation is not clear. Due to reflux.

Metaplasia

from squamous epithelium of normal esophagus to the glandular type along the gastroesophageal junction

Glandular metaplasia

• Not an adaptive response • Limbo/grey area between normal and neoplastic tissue • Alteration in the size, shape and organization of the cellular components of a tissue • Disorganized, haphazard cellular growth • Like metaplasia, reflects persistence of injurious influences and may regress • Pre-neoplastic, step before cancer.

Dysplasia

Normal cellular constituent

water, lipids, proteins, carbohydrates

may be acquired or congenital in origin (ex. lysosomal storage diseases)

enzymatic defects

foreign material engulfed by macrophages, cell cannot degrade the substance nor transport it to other sites (ex. carbon particles, silica)

Exogenous deposition

accumulations that appear as rounded, eosinophilic | droplets in the cytoplasm

protein

homogenous, glassy, pink appearance

mallory hyaline

Steatosis (fatty change) resulting from abnormal | metabolism

fat

Fat accumulation is frequent in liver but also occurs in

heart, muscle and kidney

major organ in fat metabolism

liver

Fat appearance

Gross: with progressive accumulation, the liver enlarges and becomes increasingly yellow In extreme instances, it may weigh 2 to 4 times normal and be bright yellow, soft and greasy Microscopic: small vacuoles around nucleus -> join together to create cleared spaces, pushing the nucleus to the cell's periphery -> cells may rupture and the enclosed fat globules will coalesce to form fatty cysts

exogenous deposition of pigments | § phagocytosed by dermal macrophages

tattoo

most common, air pollutant

carbon

accumulations blacken the organ (e.g. of the lungs, lymph nodes)

athracosis

Picked up by macrophages in alveoli and | transported to regional lymph nodes

carbon

Wear-and-tear pigment

Lipofuscin

§ Yellow brown, finely granular cytoplasmic, often perinuclear pigment § From lipid peroxidation and free radical injury

Lipofuscin

may be pathologic (as in melanoma) or | physiologic

melanin

Endogenous source is hemolysis

iron

elevated circulating iron, asymptomatic

hemosiderosis

symptomatic

Hemochromatosis

accumulation of copper in vital organs

Wilson's disease

Copper deposits in the cornea manifests as

Kayser-Fleischer ring

bile-stained liver; also presents with nodularities which are hallmarks of liver cirrhosis

Cholestasis

Bile deposition in brain

kernicterus

results to deposition of bile in different parts of the body

Hyperbilirubinemia

* Controlled breakdown of cells in response to DNA damage or as part of normal growth and development * Greek: “falling off” or falling away” * Chromatin condensation and fragmentation * No inflammation * Ultrastructurally, clumping chromatin is better visualized

apoptosis

catalytically active cysteine aspartic acid proteases (caspases)

initiation

Apoptosis mechanism

o Intra and extracellular pathways o Caspases cleave DNA o DNA fragments are phagocytosed

Stimuli: Hypoxia toxins

Coagulation Necrosis

Stimuli: Physiologic and pathologic factors

Apoptosis

Histologic Appearance: Cellular Swelling

Coagulation Necrosis

Histologic Appearance: Single cells Chromatin condensation Apoptotic bodies

Apoptosis

DNA breakdown: Random, diffuse

Coagulation Necrosis

DNA breakdown: Internucleosomal

Apoptosis

Mechanisms: ATP depletion Membrane injury Free radical change

Coagulation necrosis

Mechanisms: Gene activation Endonucleases Proteases

Apoptosis

Tissue reaction: Inflammation

Coagulation Necrosis

Tissue reaction: No inflammation Phagocytosis of apoptotic bodies

Apoptosis

Uncontrolled breakdown of cells due to injury

necrosis

* Most common form * Protein is denatured, less enzymatic breakdown * More eosinophilic cytoplasm, less basophilic nucleus * Preserved architecture * Most organs * e.g. Acute myocardial infarction

Coagulative Necrosis

o More enzymatic breakdown o Occurs in lipid-rich, low-protein tissue (e.g. brain) o Architecture is lost

Liquefactive necrosis

o Can be enzymatic (as in pancreatitis) or traumatic | o Gross appearance: soapy white deposits

Fat necrosis

o “Cheesy” appearance (resembling cream cheese or kesong puti); classic description of tuberculosis § Not evident for all cases of TB o Architecture not distinct microscopically; presents with granuloma

Caseous necrosis

o With pus | o e.g. renal abscess, brain abscess

Suppurative necrosis

o Complication of coagulative, caseous, or liquefactive necrosis o Normal serum calcium and calcium metabolism

Dystrophic

o Hypercalcemia | o Abnormal calcium metabolism

Metastatic

Trans 1- Cell adaptation Flashcards

(74 cards)