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Foundations 2 > Cell Adaptation, Injury, Death > Flashcards

Cell Adaptation, Injury, Death Flashcards

1
Q

Definition of Cellular Adaptation and Causes

A

Reversible functional + structural responses to stimuli

  1. changes in physiologic state (normal)
  2. changes in pathologic state (bad, disease)
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2
Q

Definitions of hypertrophy, atrophy, hyperplasia, metaplasia

A

H: increase in cell size + metabolic activity (doesn’t divide)
A: decrease in cell size/number + metabolic activity
HP: increase in cell number (orderly) [callouses, breast tissue in pregnancy]
MP: transformation of one differentiated cell type to another (within tissue category - mostly epithelial - Barrett’s esophagus)

all are types of adaptations

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3
Q

What are the differences between conditionally dividing cells and non-dividing cells? (Examples)

What is a possible non-stress related cause to smooth muscle hypertrophy?

A
  1. don’t normally divide but can (kidney, liver)
  2. fully differentiated cells that do not divide, no replacement if they die (neurons, skeletal muscle, cardiac muscle)

Hypertrophy in response to hormonal stimulation

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4
Q

Types of physiologic and pathologic stimuli

A
  1. Puberty, Pregnancy, Hormone-Mediated

2. Traumatic Injury, Infection, Environmental Toxins

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5
Q

Characteristics of Dysplasia (Examples)

A
  1. disordered growth in epithelial tissues (pre-malignant)
  2. loss of cell uniformity and architectural organization
  3. pleomorphism (variation in cell size/shape)
  4. anaplasia (lack of cell differentiation)
  5. increased nuclear:cytoplasm ratio and increased mitoses
    Ex: HPV - induces squamous dysplasia (cervical intraepithelial neoplasia), evolves into invasive squamous carcinoma
    Carcinoma in situ: abnormal changes in entire thickness of epithelia from basal layer to surface
    can regress if stimuli is removed
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6
Q

Neoplasm Terminology (Adeno, Squamous, Leiomyo, Rhabdo, Chondro, Osteo)

A

Glandular Epithelium, Squamous Epithelium, Smooth muscle, skeletal muscle, cartilage, bone

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7
Q

Neoplasm Terminology (carcinoma, sarcoma, lymphoma, melanoma, -oma) plus the exception

A 
malignant epithelial (MOST COMMON - breast, prostate, lung), malignant mesenchymal (connective tissue/muscle/bone), malignant lymphatic, malignant melanocytic, usually benign
GI tract adenomas are NOT benign - dysplastic lesions that can evolve to carcinomas!
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8
Q

Tumor Grade vs. Tumor Stage

A

Grade: Degree of Histologic Differentiation, subjective, depends on anaplasia, mitotic activity

Stage: Evaluation of extent of tumor spread - clinically important
T: size + tissue involved by main mass (T1-T4)
N: number and type of lymph nodes (N0-N3)
M: metastatic spread + where (M0-M1)

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9
Q

When does cell injury occur?

What causes cell injury?

A

Occurs when (1) stress is acute/intense, (2) when cell’s ability to adapt to chronic/mild stress is exceeded

caused by external agents and internal disturbances (oxygen deprivation, physical/chemical/infectious agents, immune system, genetic disease, nutritional abnormalities)

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10
Q

How does oxygen deprivation cause cell injury?

A
  1. Decreased ATP generation - Na/K ATPase deficiency - increased intracellular Na ions - cell swelling
  2. Increased anaerobic glycolysis - reduced glycogen and increased lactate production - decreased pH (acidosis)
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11
Q

How does mitochondrial damage cause cell injury?

A
  1. Form mitochondrial transition pore - loss of mito membrane potential and function
    a. Decreased ATP production and increased ROS - necrosis
    b. leakage of apoptotic proteins - apoptosis
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12
Q

How does cell injury lead to irreversible damage?

A
  1. influx of Ca (+ Ca released from IC stores - mito and smooth ER)
    a. Opens mito transition pore - necrosis/apoptosis
    b. activates enzymes - lipid breakdown - membrane damage
  2. production of ROS
    a. lipid peroxidation - membrane damage
    b. DNA damage - mutations - dysplasia
    c. protein modifications - misfolding
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13
Q

How do genetic polymorphisms affect cell injury?

What is the time course of cell injury?

A
  1. Polymorphisms alter the response of an individual’s cells to a stressor
  2. TIME LAG between molecular/biochemical change and morphologic changes
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14
Q

How does hypoxia lead to reperfusion injury?

A
  1. Hypoxia - impairs mito ox-phos - decreased ATP + Membrane damage (ROS)
  2. Re-oxygenation after transient ischemia - causes severe tissue damage
  3. Reperfusion injury: sudden burst of ROS generation - explosive necrosis
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15
Q

Changes between reversible injury and irreversible injury

A
  1. cell swelling (more cytoplasm), eosinophilia (pinker), cytoplasmic vacuoles/blebbing, microvilli loss, nuclear condensation, mild mito swelling
  2. MISSING NUCLEI = NECROSIS, membrane disruption - lose border b/w cells - may be artifact of sample processing, swollen mito, election dense deposits, accumulation of lipids/proteins/indigestible material/LSD
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16
Q

Features of Necrosis (biochemical + histologic)

A
  1. local death of GROUPS of cells, always PATHOLOGIC, INFLAMMATION present, NO ATP required, NO protein synthesis, transcription ceases, RANDOM DNA degradation
  2. Cell swelling, increased eosinophilia (pinkness) due to loss of RNA, smoother/glossy look due to protein degradation, loss of nuclear material, ghost-like and inflammatory response
    karolysis - loss of basophilia
    karyorrhexis - nuclear fragmentation
    pyknosis - nuclear shrinkage
17
Q

Features of Apoptosis (biochemical + histologic)

A
  1. tightly regulated genetic suicide program, physiologic or pathologic, NO unregulated inflammation, NEEDS ATP, DE NOVO transcription and new proteins synthesized, DNA fragment ladders
  2. death of SINGLE cells, cytoplasmic blebbing, cell shrinkage, chromatin condensation, nuclear fragmentation, organelles intact, phagocytosis without inflammation
18
Q

Difference between Apoptosis Intrinsic and Extrinsic Pathway

A

Intrinsic (Mitochondrial): Cell injury - BCL2 effectors (BAX,BAK) - cytochrome C - caspases - apoptosis

Extrinsic (Death Receptor): Receptor-Ligand (Fas/INF) - caspases - apoptosis

19
Q

List the forms of necrosis

A
  1. Coagulative (MI/toxic agents) - absent nuclei - but cytoplasms present due to denatured enzymes can’t break down protein)
  2. Liquefactive (BRAIN ischemia) - cell outlines not intact, cell mush, necrotic liquid tissue, no visible nuclei
  3. Caseous (TB) - cheese-like, surrounding inflammatory cells w/central necrosis
  4. Fat (Acute Pancreatitis) - due to alcohol/gall stones - activate lipases - increase in FFA - react with Ca to make soap (saponification) - chalky deposits visible
  5. Fibrinoid (Immune Rxns in blood vessels) - bright, pink, amorphous material - vasculitis
  6. Gangrenous (GANGRENE, variant of coagulative), soft tissues of lower limbs, occurs due to hypoxia/ischemia

Foundations 2 (12 decks)

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