Brainscape's Knowledge GenomeTM

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


See full index

PATH > Cell Degeneration, Injury and Death > Flashcards

Cell Degeneration, Injury and Death Flashcards

1
Q

What is Atrophy?

A

Decrease in size/number of cells after the end of normal development.

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

What is involution?

Give three examples.

A

Physiological Atrophy

  • The uterus after parturition
  • Thymus after puberty
  • Senile atrophy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Give examples of pathological atrophy.

A
  • Disuse atrophy
  • Nerve damage
  • Decreased perfusion
  • Pressure atrophy
  • Loss of endocrine stimuli
  • Senile
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is this? It is an example of which degenerative cell process?

A

Hydrocephalus.

Pressure atrophy.

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

What is this? It is an example of which cell degenerative process?

A

Hydronephrosis.

Pressure atrophy

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

Neutering an animal can cause atrophy of which organ? Why?

A

The prostate gland, due to a loss of endocrine stimuli.

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

What is this histological feature called? Explain its presence.

A

Found in atrophic cells, filled with small degenerating organelles.

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

An increase in size of a cell/organ.

What causes this?

A

Hypertrophy

Increased functional demand on the cell.

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

Give examples of pathological and physiological hypertrophy.

A

Pathological - Genetic, Obstruction, pressure overload, tumour

Physiological - Muscle training, pregnant uterus

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

Name this gross pathological feature.

A

Right ventricular hypertrophic myopathy. Caused by haemodynamic overload.

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

Name this gross pathological feature.

Explain.

A

Adenocarcinoma obstructing the small intestine. Obstruction increases force of peristalsis contraction leading to hypertrophy.

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

Name this gross pathological feature.

Explain.

A

Severe diffuse hypertrophy (X-linked dystrophin deficiency), caused by congenital deficiency of dystrophin.

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

Altered number of cells.

A

______Plasia

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

Outline two examples of physiological hyperplasia.

A
  1. Hormonal hyperplasia
    1. mammary epithelium during pregnancy
    2. uterine epithelium during pregnancy
  2. Compensatory hyperplasia
    1. Partial loss of parenchyma (eg. partial hepatectomy)
    2. Symmetrical organs, with functional loss of one organ (eg. kidneys)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Explain this gross pathological feature.

A

Unilateral hypo/aplasia of one kidney with contralateral hyperplasia of the other.

If one kidney is absent or not fully developed, the controlateral one is required to work more it therefore increases its dimension by the means of increasing number of functional cell.

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

Give examples of pathological hyperplasia and briefly explain each.

A
  • Excessive hormonal stimulation or growth factors
    • Cystic endometrial hyperplasia (dog)
    • Proud flesh
  • Regeneration
    • Nodular hyperplasia with age
  • Viral
    • Papilloma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which organs can be see in this image?

What can cause this?

A

Parathyroid and thyroid gland (hyperplasia)

Caused by chronic renal failure and abnormal calcium handling.

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

What organ can be seen in this image?

Name the gross pathological feature seen.

A

Pancreas

Nodular hyperplasia which occurs in old age.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Metaplasia

A

Exchange of one adult cell type with another adult cell type.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

True or False.

Metaplasia is an example of a reversible cellular change.

A

True.

Once the cellular stimuli is removed the original cell type will return.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Give an example of a tissue which can undergo metaplasia and name two causes.

A

The respiratory tract, replacement of respiratory epithelium by squamous epithelium due to chronic irritation or vitamin A deficiency.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Name and give example of the three categories of intracellular accumulations.

A
  1. Normal cellular constituents - water, lipid, protein, carbohydrates
  2. Abnormal substance
    1. Exogenous: mineral, products of infectious agents
    2. Endogenous: due to abnormal synthesis/ metabolism
  3. Pigment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Steatosis. State causes.

A

Intracellular accumulation of triglycerides.

Causes:

  • Toxic injury
  • Dibetes mellitus
  • Hypoxia
  • Elevated fat intake
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Describe this pathological histology feature.

A

Steatosis. Large white vacuoles can be seen within cells, these contained triglycerides before processing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe this gross pathological feature.

A

Severe diffuse lipidosis of the liver. The tissue would also be greasy to the touch.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Which stain can be used to identify lipidosis in cells?

A

Oil-red O

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What can cause abnormal protein accumulation within cells?

A
  1. Protein folding disorders - prions, genetic, age, amyloidosis
  2. Excess protein presented to cells - glomerular damage
  3. Excess protein synthesis - Russell bodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Name this histological feature. Describe its aetiology.

A

Hyaline droplets in the kidney tubules. These are caused by poor protein filtration in the glomerulus leading to proteinuria. Since a higher concentration of protein is presented to tubule cells glassy vaculoes filled with protein appear in the cell cytoplasm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Name this hitological feature.

A

Hyaline droplets (also may have a glassy appearance). Appear eosinophilic (red)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Outline the pathogenesis of protein storage disorders. Hint - prions

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Which type of abnormal proteins cause these protein folding disorders?

  1. Alzheimer`s disease
  2. Pancreatic islet amyloidosis
  3. Reactive amyloidosis
  4. Transmissible spongiform encephalopathies
A
  1. Alzheimer`s disease - amyloid-b
  2. Pancreatic islet amyloidosis - amylin
  3. Reactive amyloidosis - serum amyloid-A
  4. Transmissible spongiform encephalopathies - PrP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What can cause abnormal accumulation of glycogen within the cell?

A
  • Hyperglycemia - DM
  • Glycogen storage disease
  • Drug/steroid overuse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Name and describe this histological feature.

A

Glycogen accumulation. Cloudy vacuoles found within cell cytoplasm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Anthracosis

A

Abnormal build up of carbon compounds within cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is shown in this histological slide?

A

Build up of lipofuscin within cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Name and describe two endogenous pigments which can accumulate within cells.

A
  1. Lipofuscin
    1. insoluble
    2. yellow-brown
  2. Melanin
    1. brown-black, in melanocytes
    2. non-haemoglobin-derived
  3. Haemosiderin
    1. haemoglobin-derived, gold yellow to brown
    2. storage form of iron
  4. Bile pigments - biliverdin and bilirubin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Which type of stain is used to identify haemosiderin within cells?

A

Perl’s stain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the products of haemoglobin breakdown?

A
  1. Haem -> Haemosiderin
  2. Biliverdin -> Bilirubin -> conjugation with glucoronic acid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How is haemorrhage resolved? What feature does this result in?

A

Macrophage - dependant phagocytosis of extravasated erythrocytes.

A bruise forms - goes through multiple colour changes before resolving.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Name this pathological finding. What is it caused by?

A

Jaundice, caused by high levels of bilirubin within the blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What componants make up bile?

A

a) water
b) cholesterol
c) bile salts
Na and K salts of bile acids
d) bile pigments (bilirubin) from haemoglobin
globin = re-useable protein
haem = broken down into iron and bilirubin

42
Q

Name and describe this pathological feature.

A

Dystrophic calcification

Depositation of calcium in non-viable or dying tissues despite normal serum calcium

43
Q

What occurs in i) initiation and ii) propagation of dystrophic calcification?

A
  1. Initiation
    1. Intracellular: Ca2+ accumulates in mitochondria of dying cells
    2. Extracellular: Inititated by phospholipids in membrane-bound vesicles of dying cells
  2. Propagation
    1. Ca2+ binds membrane phospholipids and form groups in membranes. This leads to Ca deposits near membrane which form microcrystals and perforate the cell membrane.
44
Q

What type of calcification is shown in this image?

In what pathological state would this occur?

A

This image shows metastatic calcification which occurs in normal tissues with hypercalcaemia.

Hypercalcaemia can occur with:

  • Increased PTH
  • Bones catabolism
  • Vit D excess
  • Renal failure (secondary hyperthyroidism)
45
Q

What does this histo slide show?

A

Metastatic calcification of the gastric wall

46
Q

Where in tissue would you find amyloid deposits?

A

Between cells

47
Q

What is amyloid?

What is it made up of?

A

Pathological proteinaceous substance

Name amyloid as its reaction with Lugol’s iodine is “starch like”

  • 95% Fibril protein
  • 5% P component and other glycoproteins
48
Q

What pathological accumulation is shown in this image?

A

Glomerular amyloidosis

49
Q

Describe the four components of Amyloid.

A
  • AA (amyloid-associated):
  • synthesised in liver [hepatocytes]
  • AL (amyloid light chain):
  • derived from plasma cells, contains Ig light chains
  • with monoclonal B cell proliferation
  • b-amyloid protein:
  • deposited in spongiform encephalopathies
  • islet amyloid polypeptide [IAPP; amylin]
  • deposited in pancreatic islets
50
Q

Which Amyloid molecule is indicative of chronic inflammation?

AA or AL

A

AA

AL is found in myeloma tumours in humans.

51
Q

This amyloid protein is deposited in spongiform encephalopathies.

Name a condition in which this occurs.

A

Beta-amyloid protein

Alzheimer’s

52
Q

What six terms are used to classify amyloidosis?

Briefly describe each.

A
  1. Sytemic - In several organs
  2. Localised
  3. Primary - due to immunocytic disorders
  4. Secondary - a complication of chronic inflammation
  5. Hereditary
  6. Endocrine - eg islet amyloidosis
53
Q

“Programmed cell death”

A

Apoptosis

54
Q

Outline the morphological features of apoptosis.

A
  1. Cell Shrinkage
  2. Chromatin condenses
  3. Membrane blebbing
  4. Nuclear collapse
  5. Apoptotic bodies form
  6. AB’s lysed or phagocytosed
55
Q

What molecules stimulate the intrinsic and extrinsic pathways of Apoptosis?

A

Intrinsic - Growth factors or hormones

Extrinsic - FAS or TNF

56
Q

What are the biochemical features of the Apoptosis pathway?

A
  • Protein cleavage
  • Protein cross-linking
  • DNA breakdown
  • Phagocytosis recognition
57
Q

What is the common molecular goal of the intrinsic and extrinsic pathways of Apoptosis?

What phase does this molecule stimulate and what occurs?

A

Caspase 3

Caspase 3 begins the execution phase in which endonuclease destroys DNA, the cytoskeleton is cleaved and mitochondria breakdown.

58
Q

Apoptosis occurs without inflammation.

True or False

A

True Apoptotic bodies are phagocytosed unlike in necrosis when cells are lysed and leak intracellular substances into surrounding tissues.

59
Q

Outline examples of Apoptosis.

A
  • Uterine involution
  • Embryogenesis
  • cell turnover
  • atrophy
  • Tc cell induced
  • virus clearance
60
Q

This molecule is expressed by apoptotic bodies and signals their phagocytosis.

A

Phosphotidylserine

61
Q

Absence of growth factors stimulate the intrinsic pathway. What series of events does this stimulate which lead to the production of caspse 3.

A

Removal of GF/H causes cytochrom c release from mitochondria, this causes the release of casepase 9, triggering the caspase cascade.

62
Q

TNF or FAS trigger which events leading to the generation of caspase 3 for Apoptosis?

A

FAS or TNF trigger adapter proteins which signal the release of caspase 8 leading to the generation of caspase 9.

63
Q

“Irreversible exogenous injury”

A

Necrosis

64
Q

Pyknosis

A

Nuclear shrinkage and chromatin condensation

65
Q

Karyohexis

A

Fragmentation of the nucleus

66
Q

Karyolysis

A

Nuclear lysis

67
Q

The six characteristic morphological features of necrosis.

A
  1. Cell swelling
  2. Eosinophilia
  3. Pyknosis
  4. Karyohexis
  5. Karyolysis
  6. Membrane fragmentation and cell lysis
68
Q

Which two processes cause necrosis?

A
  1. Enzymatic digestion
  2. Protein denaturation
69
Q

Two types of enzyme cause cell lysis with necrosis, name them and the type of lysis they stimulate.

A
  • Lysosomal enzymes - autolysis
  • Leukocyte enzymes - heterolysis
70
Q

Caseous Necrosis

A
  • Granular friable mass
  • Cheese-like
71
Q

This slide represents which type of necrosis?

A

Caseous

72
Q

Depletion of ATP which occurs with cell injury leads to which biochemical effects?

A
  • Na+/K+ ATPase quits - Na+ & Ca2+ accumulates, water influx and cell swelling and ER dilation. K+ accumulates extracellularly.
  • Anaerobic glycolysis, decreased glycogen, lactic acid accumulates, decreased pH and decreased activity of cellular enzymes
  • Failure of the Ca2+ pump increased Ca2+ - damages cell
  • Structural disruption of the protein synthetic apparatus leading to decreased protein synthesis
73
Q

Describe the pathological condition seen in this image.

What type of stain has been used?

A

Glomerular amyloidosis

Lugol’s iodine

74
Q

What is meant by “cell injury”?

Reversible and irreversible?

A

When the limits of adaptive capability are exceeded or when adaptation is not possible.

Irreversible - Persistent or severe stimuli where the cell reaches the point of no return

75
Q

Which intracellular systems are vunerable to cell injury?

A
  • Cell membranes
  • Aerobic apparatus
  • Protein synthesis
  • Genetic apparatus
76
Q

Differenciate between reversible and irreversible cell injury.

A

Irreversible cell damage occurs with persistent or severe stimuli, cells go past the “point of no return” and undergo cell death.

77
Q

What are the five biochemical methods of cell injury?

A
  1. ATP depletion
  2. Mitochondrial damage
  3. Membrane damage
  4. Altered calcium homeostasis
  5. Oxygen free radical damage (oxidative stress)
78
Q

Outline the mechanism of ischemic cell injury.

A

Reduced O2 delivered to the cell, decreased intracellular O2 tension, this lead to reduced oxidative phosphorylation within mitochondria.

This leads to a number of

79
Q

What are the consequences of ischemia/ hypoxia?

A
  • Decreased sodium pump activity - Na+, H2O and Ca2+ influx, K+ efflux
    • ​Decreased microvilli
    • Cells swells
    • Membrane blebbing
  • Increased anaerobic glycolysis - decreased glycogen stores and pH
  • Protein sysnthesis disrupted - Ribosomes detached, decreased protein synthesis
    • ​Lipid depositation
80
Q

Describe the characteristic features of irreversible ischemic damage.

A
  • Lysosomal swelling
  • Mitochondrial vacuoles and calcification
  • Ca2+ influx on reperfusion
  • Plasma membrane damage
    • Lipid products act as detergents
    • Free radical damage
    • Cytoskeletal abnormalities
    • PLA activated - loss of phospholipids
81
Q

What are the consequences of reperfusion injury?

A

Free radical production and release of cytokines and adhesion molecules from hypoxic cells which leads to inflammation.

82
Q

Define Free Radical.

A

An extremely unstable, highly reactive chemical species with a single unpaired electron in its outer orbit.

83
Q

Name three free radical species and three potential sources.

A

OH*, H*, O2*-

  • Ionised radiation
  • Redox reactions
  • Exogenous chemicals
84
Q

What happens in free radical mediated cell injury?

A
  • DNA lesions as FRs react with thymine causing single strand breaks
  • Lipid peroxidation - FR attack double bonds of unsaturated FA’s
  • Enzymic degradation of protein cross-links
85
Q

Name three antioxidants.

A

Vitamin A,E and K

86
Q

What two ways can chemicals work to cause cell damage?

A
  • Direct binding to molecules in cell - eg mercuride, cyanide, anti-neoplastic drugs
  • Metabolite causes problem - CCl4
87
Q

Which enzymes are activated with loss of calcium homeostasis?

What effect do these enzymes have on the cell?

A
  • ATPase - decreased ATP
  • Protease - disrupts membrane and cytoskeleton
  • Phospholipase - decreased phospholipids
  • Endonuclease - nuclear chromatin damage
88
Q

Membrane damage can result from which mediators of cell injury?

A
  • decreased O2 - decreased membrane molecule synthesis
  • increased Ca2+ - increased enzyme activity
89
Q

Coagulative Necrosis

Morphology.

A
  • Pale pink cells - denatured proteins
  • Cell Outline still present
  • Hypoxic cell death - Infarcts
  • Eosinophilic cytoplasm
  • Damaged/ dense clumping nucleus
90
Q

Liquifactive Necrosis

Morphology

A
  • Enzymatic Digestion
  • Complete loss of cellular architecture
  • Focal bacterial/fungal infection
  • PMNs seen = PUS
91
Q

Caseous Necrosis

Morphology

A
  • Combination of coagulative and liquifactive
  • Obliteration of architecture surrounded by inflammatory cells
92
Q

Fat Necrosis

A
  • Focal destruction of adipose tissue
  • Chalky white gross appearance
  • Cytoplasm is pink mass of amorphous tissue
  • Loss of peripheral nuclei
93
Q

Pyknosis

A

Shrinking and condensing of cell nuclei

94
Q

Karyohexis

A

Nuclear Fragmentation

95
Q

Karyolysis

A

Lysis of the nucleus

96
Q

Describe the morphological changes undergone by a dying cell.

A
  • Cell swelling and eosinophilia
  • Nuclear changes - Pyknosis, Karyohexis, Karyolysis
  • Membrane fragmentation and lysis - Enzyme digestion or protein denaturation
97
Q

Describe the morphology of apoptosis.

A

Cell shrinks, chromatin condenses, membrane blebbing, nuclear collapse, apoptotic bodies form, cell lyses and is phagocytosed.

98
Q

What biochemical changes occur during apoptosis?

A
  • Protein cleavage
  • Protein cross links
  • DNA breakdown & nuclear collapse
  • Phygocytic recognition
99
Q

Describe the intrinsic and extrinsic causes of the caspase cascade.

A
  1. Intrinsic - growth factor/ growth hormone stimulated
    1. Cytochrome C released from mitochondria
    2. Causes caspase 9 release
  2. Extrinsic - FAS/ TNF stimulated
    1. Adapter proteins cause the release of caspase 8
100
Q

What is the common molecular goal of the caspase cascade?

A

Caspase 3

101
Q

Caspase three stimulates which processes/ molecules of apoptosis?

A
  • Exectution
    • Mitochondrial breakdown
    • Endonuclease
    • Cytoskeleton cleavage
  • This further leads to Phosphotidylserine expression by apoptotic bodies which causes phagocytosis

PATH (8 decks)

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