Altered cellular and tissue biology Flashcards

1
Q

cellular adaption definition

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Atrophy physiologic

A

occurs in early development; thymus shrink in childhood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Atrophy pathologic

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Atrophy disuse

A

bedridden

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Hypertrophy

A

caused by INC work demand or hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Hypertrophy physiologic

A

pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Hypertrophy pathologic

A

HTN, Heart valve dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Hyperplasia

A

INC rate of cellular division

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hyperplasia physiologic

A

compensatory = allows organs to regenerate (LIVER)

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Hyperplasia pathologic

A

endometrium/BPH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Dysplasia

A

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

atypical hyperplasia

does NOT indicate CA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
CI: Unintentional and Intentional injury
falls motor vehicle injuries opioid overdose poisonings sports r/t injuries in children firearms medical care suicide
26
CI: Asphyxial injuries
cause: failure of cells to receive or use oxygen suffocation strangulation chemical asphyxias drowning
27
CI: Infectious injuries
pathogenicity of microorganism disease producing potential: 1) invasion and destruction 2) toxin production 3) production of hypersensitivity rxns
28
CI: Immunologic and inflammatory injuries
phagocytic cells immune and inflammatory substances: histamine, antibodies, lymphokines, complement, proteases causes membrane alterations
29
CI: Injurious genetics and epigenetic factors
nucleus alterations alterations in plasma membrane structure, shape, receptors, or transport mechanism EX: sickle cell anemia
30
CI: Injurious nutritional imbalances
proteins, carbs, lipids, vitamins, minerals deficient intake excessive intake
31
CI: Temperature extremes and climate change
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
CI: Sudden INC/DEC atmospheric pressure
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
CI: Ionizing radiation
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
Manifestations of CI: cellular accumulations (infiltrations)
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
Manifestations of CI: systemic manifestations
fatigue and malaise loss of well being altered appetite fever leukocytosis INC HR PAIN
36
Types of CELLULAR DEATH
1) NECROSIS = Inflammatory changes, autolysis 2) Apoptosis = NO inflammatory changes type 1 = programmed cell death type 2 = autophagic cell death
37
Necrosis
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
Types of Necrosis: Coagulative
kidneys, heart, and adrenal glands protein denaturation changes protein albumin
39
Types of Necrosis: Liquefactive
neurons and glial cells in the brain hydrolytic enzymes form liquid-filled cyst or form pus
40
Types of Necrosis: Caseous
TB pulmonary infection combination of coagulative and liquefactive necrosis cheese-looking substance that is walled off
41
Types of Necrosis: Fat
breast, pancreas, other abdominal structures action of lipases
42
Gangrenous necrosis
clinical term dry vs. wet gas gangrene
43
Apoptosis
programmed cellular death ER stress results in apoptotic cell death active process of cellular destruction
44
Autophagy
"recycling center" eats itself self-destructive process survival mechanism
45
Aging and Altered cellular and tissue biology
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
Somatic death
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