Altered cellular and tissue biology Flashcards

1
Q

cellular adaption definition

A

the cell’s response to escape and protect itself from injury

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2
Q

Adaptive changes in cells

A

atrophy = DEC cell size

hypertrophy = INC cell size

hyperplasia = INC cell number

metaplasia = reversible replacement of one mature cell type by another less mature cell type

dysplasia = deranged cellular growth; not a true cellular adaption (atypical hyperplasia)

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3
Q

Atrophy physiologic

A

occurs in early development; thymus shrink in childhood

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4
Q

Atrophy pathologic

A

results from DEC in workload, use, pressure, blood supply, nutrition, hormonal stimulation, nervous stimulation

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5
Q

Atrophy disuse

A

bedridden

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6
Q

Hypertrophy

A

caused by INC work demand or hormones

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7
Q

Hypertrophy physiologic

A

pregnancy

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8
Q

Hypertrophy pathologic

A

HTN, Heart valve dysfunction

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9
Q

Hyperplasia

A

INC rate of cellular division

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10
Q

Hyperplasia physiologic

A

compensatory = allows organs to regenerate (LIVER)

hormonal = replaces lost tissue or supports new growth (uterus/breast)

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11
Q

Hyperplasia pathologic

A

endometrium/BPH

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12
Q

Dysplasia

A

abnormal changes in size, shape, and organization of mature cells

atypical hyperplasia

does NOT indicate CA

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13
Q

Metaplasia

A

reversible replacement of one mature cell by another less mature cell

ex: replacement of normal bronchial columnar ciliated epithelial cells by stratified squamous epithelial cells

reprogramming of stem cells

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14
Q

Cellular injury

A

leads to injury of tissues and organs, determining structural patterns of disease

REVERSIBLE = injured cells recover
IRREVERSIBLE = injured cells die

causes cell stress

acute vs chronic and reversible vs irreversible

can involve necrosis, apoptosis, accumulation, pathologic calcification

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15
Q

Cellular injury CAUSES

A

1) lack of oxygen
2) free radicals
3) toxic chemicals
4) infectious agents
5) physical and mechanical factors
6) immunologic reactions
7) genetic factors
8) nutritional imbalances
9) physical trauma

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16
Q

Cellular injury BIOCHEMICAL mechanisms

A

1) ATP depletion
2) mitochondrial damage
3) accumulation of O2 and O2-derived free radicals
4) membrane damage (ATP depletion)
5) protein folding defects
6) DNA damage defects
7) calcium level alterations

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17
Q

Cellular injury can lead to CELL DEATH by…

A

1) DEC ATP production
2) failure to activate transport mechanism
3) cellular swelling
4) detachment of ribosomes from ER
5) cessation of protein synthesis
6) mitochondrial swelling from calcium accumulation
7) vacuolation
8) leakage of digestive enzymes from lysosomes, autodigestion of intracellular structures
9) lysis of plasma membrane
10) death

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18
Q

CI: Ischemia-Reperfusion Injury

A

DUE to:
1) oxidative stress
2) radicals that cause membrane damage and mitochondrial calcium overload
3) mitochondrial permeability transition pore

MECHANISM of injury in:
1) tissue transplantation
2) ischemic syndromes: myocardial, hepatic, intestinal, cerebral, renal, stroke

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19
Q

CI: Free radicals and ROS - oxidative stress

A

INC of different reactive species
Detrimental oxidation of:
1) lipids
2) proteins
3) nucleic acids

Mitochondrial effects: dysfunction caused by ROS, inefficient antioxidants

20
Q

CI: Chemical Injury

A

direct toxicity to the cell = damage to or destruction of plasma membrane

reactive free radicals and lipid peroxidation

EX: lead, CO, ethyl alcohol, mercury, social or street drugs

21
Q

CI: Carbon Monoxide

A

colorless and odorless

produces hypoxic injury

CO’s affinity for Hgb is much greater than that of oxygen; if quickly binds w/ the Hgb, preventing oxygen molecules from doing so

22
Q

CI: Lead

A

exposure in children = learning/behavior problems, speech/hearing problems, brain/nervous system damage, slowed growth/development

common source: paint in old homes

PREVENTION is key

23
Q

CI: Ethanol (alcohol)

A

folate deficiency

metabolized by liver

protective effect w/ the cardiovascular system

acute alcoholism affects CNS
chronic alcoholism affects liver and stomach

24
Q

CI: Mercury

A

major sources: fish & healthcare

AVOID in pregnant women, nursing mothers, young children

in street drugs

25
Q

CI: Unintentional and Intentional injury

A

falls
motor vehicle injuries
opioid overdose
poisonings
sports r/t injuries in children
firearms
medical care
suicide

26
Q

CI: Asphyxial injuries

A

cause: failure of cells to receive or use oxygen

suffocation
strangulation
chemical asphyxias
drowning

27
Q

CI: Infectious injuries

A

pathogenicity of microorganism

disease producing potential:
1) invasion and destruction
2) toxin production
3) production of hypersensitivity rxns

28
Q

CI: Immunologic and inflammatory injuries

A

phagocytic cells

immune and inflammatory substances: histamine, antibodies, lymphokines, complement, proteases

causes membrane alterations

29
Q

CI: Injurious genetics and epigenetic factors

A

nucleus alterations

alterations in plasma membrane structure, shape, receptors, or transport mechanism

EX: sickle cell anemia

30
Q

CI: Injurious nutritional imbalances

A

proteins, carbs, lipids, vitamins, minerals

deficient intake
excessive intake

31
Q

CI: Temperature extremes and climate change

A

HYPOTHERMIC INJURY
slows cellular metabolic processes; produces ROS

HYPERTHERMIC INJURY
1) heat cramps, heat exhaustion, heat stroke
2) malignant hyperthermia, neuroleptic malignant syndrome
3) drug induced hyperthermia
4) burns
5) overheating, SIDS

32
Q

CI: Sudden INC/DEC atmospheric pressure

A

blast injury

decompression sickness or caisson disease = bends (diver disease)

high-altitude sickness:
1) high-altitude pulmonary edema HAPE
2) high-altitude cerebral edema HACE
3) acute mountain sickness AMS

33
Q

CI: Ionizing radiation

A

x-rays

mechanism of action:
1) early or late tissue rxn
2)stochastic

bystander effects: cells not directly radiated = horizontal transmission

genomic instability: over time; vertical transmission; time lethal and nonlethal mutations appear

34
Q

Manifestations of CI: cellular accumulations (infiltrations)

A

water = cellular swelling

lipids/carbs = affect liver (fatty liver)

glycogen = genetic disorders

proteins = renal convoluted tubule and immune B lymphocytes

pigments = melanin, hemoproteins, bilirubin

calcium

uric acid = gout

35
Q

Manifestations of CI: systemic manifestations

A

fatigue and malaise
loss of well being
altered appetite
fever
leukocytosis
INC HR
PAIN

36
Q

Types of CELLULAR DEATH

A

1) NECROSIS = Inflammatory changes, autolysis

2) Apoptosis = NO inflammatory changes
type 1 = programmed cell death
type 2 = autophagic cell death

37
Q

Necrosis

A

Sum of cellular changes after local cell death and the process of cellular autodigestion (autolysis)

Process:
pyknosis = shrinking of nucleus
karyorrhexis = fragmentation of nucleus
karyolysis = nuclear dissolution and chromatic lysis

38
Q

Types of Necrosis: Coagulative

A

kidneys, heart, and adrenal glands

protein denaturation

changes protein albumin

39
Q

Types of Necrosis: Liquefactive

A

neurons and glial cells in the brain

hydrolytic enzymes form liquid-filled cyst or form pus

40
Q

Types of Necrosis: Caseous

A

TB pulmonary infection

combination of coagulative and liquefactive necrosis

cheese-looking substance that is walled off

41
Q

Types of Necrosis: Fat

A

breast, pancreas, other abdominal structures

action of lipases

42
Q

Gangrenous necrosis

A

clinical term
dry vs. wet
gas gangrene

43
Q

Apoptosis

A

programmed cellular death

ER stress results in apoptotic cell death

active process of cellular destruction

44
Q

Autophagy

A

“recycling center”

eats itself

self-destructive process

survival mechanism

45
Q

Aging and Altered cellular and tissue biology

A

degenerative extracellular changes:
1) collagen binding and cross-linking
2) INC free radicals’ effects on cells
3) structural alterations
4) peripheral vascular disease and oxidative stress

cellular aging:
1) atrophy, DEC functioning, loss of cells

tissue and systemic aging: progressive stiffness and rigidity

frailty:
1) complex clinical syndrome
2) involves oxidative stress, dysregulation of inflammatory cytokines and hormones, malnutrition, physical inactivity, muscle apoptosis

46
Q

Somatic death

A

death of entire person

NO inflammatory response

postmortem changes:
1) complete cessation of respirations and circulation
2) algor mortis: reduced temp
3) livor mortis: purple skin discoloration
4) rigor mortis: muscle stiffening
5) postmortem autolysis: release of enzymes and lytic dissolution