Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology > Chapter 1 - Cell Injury, Adaptation & Death > Flashcards

Chapter 1 - Cell Injury, Adaptation & Death Flashcards

1
Q

4 Aspects of a Disease Process

A
  1. Etiology or cause
  2. Pathogenesis: sequence of cellular, biochemical, and molecular events
  3. Morphological changes: structural alterations
  4. Functional derangements and clinical manifestations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Mechanism of Cell Injury

A

Cellular response to injurious stimuli depends on the nature of the injury, duration, and severity

Consequence depends on type, state, and adaptability of the injured cell

Injury results from different biochemical mechanisms

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

Depletion of ATP

A

Reduction of ATP levels - necrotic cell death
ATP is produced via oxidative phosphorylation of adenosine diphosphate or Glycolytic pathway (absence of oxygen)

Major causes of ATP depletion - reduced supply of oxygen and nutrients, mitochondrial damage, action of some toxins

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

Mitochondrial damage

A

Supply life-sustaining energy by producing ATP

Damaged by: inc of cytosolic calcium, ROS, oxygen deprivation, mutations in mitochondrial genes

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

Influx of Calcium and Loss of Calcium Homeostasis

A

Calcium normally maintained @ v. low [ ] compared to extracellular calcium, sequestered in mitochondria and ER

Ischemic and certain toxins cause an increase in the cytosolic calcium concentrations

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

Accumulation of Oxygen-Derived Free Radicals

A

Cell injury induced by free radicals, particularly reactive oxygen species, is an important mechanism of cell damage

Unpaired e- are highly reactive and “attack” and modify adjacent molecules

Reactive oxygen species are produced normally in cells during mitochondrial respiration and energy generation

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

Defects in Membrane Permeability

A

Loss of selective membrane permeability, leading ultimately to overt membrane damage

ischemic - membrane defects may be a result of ATP depletion and calcium-mediated activation of phospholipases

membrane damaged by: various toxins, viral proteins, lytic complement components, variety of physical and chemical agents

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

Damage to DNA and Proteins

A

DNA damage too severe, suicide program - apoptosis

similar rxn triggered by improper folded proteins

Cellular metabolism, UV exposure, ionizing radiation, chemical exposure, replication errors -> Cell cycle checkpoint activation, transcriptional program activation, DNA repair, Apoptosis

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

Ischemic and Hypoxic Injury

A

Most common type of cell injury leading to cell death, due to diminished blood flow

Reduced O2 leads to reduced oxidative phosphorylation and dec ATP generation -> reduction of Na+ pump function -> efflux of K+, influx of Ca2+, Na+ and H2O = cell swelling and progressive loss of glycogen and dec protein synthesis

Irreversible = accumulation of Ca2+ rich densities in mitochondrial matrix, lack of oxidative phosphorylation and ATP generation, cell membrane damage

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

Ischemia/ Reperfusion Injury

A

Restoration of blood flow can promote recovery or exacerbate injury and cell death

Contributes to tissue damage during myocardial and cerebral infarction

Oxidative stress: reoxygenation inc generation of ROS and nitrogen species
Intracellular Calcium Overload: beings during ischemia and exacerbated during reperfusion due to calcium influx
Inflammation: ischemic injury associated w/ inflammation
Activation of complement system: IgM antibodies deposit for unknown reasons, blood flow resumed & proteins bind antibodies and activate = injury

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

Chemical Injury

A

limitation to drug therapy
liver -> frequent target to drug toxicity

direct toxicity, conversion to toxic metabolites

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

Hypertrophy

A

Inc in size of cells
No new cells
Due to synthesis & assembly of additional structural components
Striated muscle in the heart and skeletal muscles have limited capacity to divide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Hyperplasia

A

Inc in # of cells
Only take place in tissue containing cells capable of dividing

Physiologic: action of hormones when there is a need for inc capacity; action of growth factors when need for compensatory inc after damage

Pathologic: excessive or inappropriate action of hormones or growth factors acting on target cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Atrophy

A

Decrease in cell size and number

Physiologic: common during normal development

Pathologic: dec workload, loss of innervation, diminished blood supply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Metaplasia

A

Reversible change in which one differentiated cell type (epithelial or mesenchymal) is replaced by another cell type [columnar to squamous]

results form reprogramming of stem cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Dysplasia

A

Atypical changes in nuclei, “premalignant” condition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Intracellular Accumulations

A

One of the manifestations of metabolic derangements in cells

harmless or associated w/ varying degrees of injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Lipid Accumulations

A

Accumulate in cells - triglycerides, cholesterol, phospholipids

19
Q

Steatosis (fatty changes)

A

abnormal accumulations of triglycerides
Often seen in liver, heart, muscle, and kidney

Causes: toxins, protein malnutrition, diabetes mellitus, obesity, and anoxia
Alcohol abuse and fatty liver disease

20
Q

Cholesterol and Esters

A

cellular metabolism is tightly regulated
Most cells use cholesterol for synthesis of cell membrane w/out intracellular accumulations

accumulations seen in atherosclerosis, xanthomas, Niemann-Pick disease type C

21
Q

Protein accumulations

A

rounded, eosinophilic droplets, vacuoles, or aggregates in the cytoplasm

causes: renal diseases, defective intracellular transport and secretion of proteins, accumulation of cytoskeleton proteins (alzheimer’s)

“Mallory bodies” - hepatocytes in alcoholic liver disease representing aggregated intermediate filaments of the cytoskeleton

22
Q

Glycogen Accumulations

A

readily available energy, abnormality in glucose or glycogen metabolism - diabetes mellitus

23
Q

Pigment accumulations

A

colored substances

Coal dust: most common, macrophages in alveoli of lungs
Tattooing: localized exogenous pigmentation of skin

Endogenous: lipofuscin - lipochrome or wear-and-tear pigment. melanin- black/brown pigment. hemosiderin - hemoglobin-derived, golden yellow to brown

24
Q

Pathologic Calcification

A

abnormal tissue deposition of calcium salts, together w/ smaller amounts of iron, magnesium, and other mineral salts

25
Q

Dystrophic calcification

A

when deposit occurs locally in dying tissues
areas of necrosis, atheroma and damaged heart valves, tuberculous lymph node
cause of organ dysfunction
serum calcium is normal

26
Q

Metastatic calcification

A

normal tissues wherever there is hypercalcemia

1. inc secretion of PTH, 2. resorption of bone tissue, 3. Vit D related disorders, 4. renal failure

27
Q

Extracellular deposits of amyloid

A

Amyloid: abnormal, fibrillar protein deposited in intercellular matrix of blood vessel walls

AL- immunoglobulin light chains
AA- non-immunoglobulin protein associated w/ chronic inflammatory states

Deposition in kidney may produce nephrotic syndrome
may affect gastrointestinal tract
small vessels of brain

28
Q

Reversible injury

A
  • cellular swelling: appears whenever cells are unable to maintain ionic and fluid homeostasis
  • fatty changes: occur in hypoxic injury and various forms of toxic or metabolic injuries
29
Q

Irreversible Injury

A

Denaturation of intracellular proteins
Enzymatic digestion of the lethally injured cells
Elicit inflammation in surrounding tissues

30
Q

Necrosis

A

Microscopic appearance in H&E stain: pale, eosinophilic cells due to binding of eosin dye to denatured proteins

31
Q

Pyknosis

A

nuclei shrink

32
Q

Karyorrhexis

A

nuclei fragment

33
Q

karyolysis

A

nuclei disintegrate

34
Q

Coagulative necrosis

A

Architecture of the dead tissue is preserved for a span of @ least some days
ischemic leads to it
A localized area of coagulative necrosis is called an infarct

35
Q

Liquefactive Necrosis

A

digestion of the dead cells
Seen in focal bacterial, or occasionally, fungal infections
Necrotic material is frequently creamy yellow b/c of presence of dead leukocytes and is called pus

Also occurs in ischemic necrosis of brain for unclear reasons (no inflammatory cells)

36
Q

Caseous (Caseation) Necrosis

A

Associated with tuberculosis
Cheesy appearance
architecture is completely obliterated
Appearance is characteristic of a focus of inflammation known as granuloma

37
Q

Fat Necrosis

A

focal area of fat destruction

typically results from release of activated pancreatic lipases into the substance of pancreas and peritoneal cavity

38
Q

“Gangrenous” Necrosis

A

limb, lower leg, lost blood supply
ischemic coagulative necrosis
“Wet” gangrene has superimposed bacterial petrification leading to slimy appearance

39
Q

Apoptosis

A

tightly regulated suicide program -> intrinsic enzymes activated and degrade DNA and cytoplasmic proteins
normal but can be pathologic

50-70 billion cells die each day

An active, intracellular, energy-dependent process as opposed to necrosis

Doe NOT elicit an inflammatory response or damage adjacent cells

40
Q

Inducers of Apoptosis

A 
growth factor reduction
Corticosteroids
Viruses
Free Radicals
Ionizing radiation
Cytotoxic Drugs
Immune-mediated cytolysis (T-cell induced)
41
Q

Inhibitors of apoptosis

A

sex steroids
certain viral proteins
chromosomal abnormalities in malignant cellular transformation which activate the bcI-2 gene

42
Q

Diseases w/ Increased Apoptosis

A

cell loss in neurodegenerative disease, may contribute to dec. CD4 lymph in HIV, exposure to ionizing radiation

43
Q

Diseases w/ Decreased Apoptosis

A

Leads to cell accumulation, failure to inhibit may follow loss of p53 protein

inc expression of bc1-2 protein (lymphomas) -> inhibits apoptosis enabling tumor to grow, autoimmune disease (autoreactive T-cells), cell accumulation, loss of p53 proteins (switch defective cells to apoptosis before enter mitosis)

Pathology (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions