Brainscape's Knowledge GenomeTM

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


See full index

MODULE 4 - Infectious Agents > CELLULAR BIOLOGY - Cell Injury > Flashcards

CELLULAR BIOLOGY - Cell Injury Flashcards

1
Q

List the five ways cells can respond to adaptive change

A

Hypertrophy
Hyperplasia
Atrophy
Metaplasia
Dysplasia

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

How are permanent cells repaired?

A

Permanent cells are repaired through replacement by connective tissue causing a loss of specialised function

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

What is hypertrophy?

A

An increase in organ/tissue size due to an increase in cell size

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

Which cells is hypertrophy seen in?

A

Stable and permanent cells

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

What are the physiological causes of hypertrophy?

A

Increased mechanical or metabolic workload
Hormone stimulation

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

Give an example of hypertrophy caused by increased mechanical workload?

A

Hypertrophy cardiomyopathy

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

Give an example of hypertrophy caused by hormone stimulation?

A

Hypertrophy secondary to hyperthyroidism

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

What age and sex of cat is predisposed to Feline Hypertrophic Cardiomyopathy?

A

Middle aged male cats

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

What are the pathological causes of hypertrophy?

A

Abnormal increase in hormone stimulation
Physical obstruction
Genetics

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

What are the limiting factors of hypertrophy?

A

Limited vascular and nutritional supplies for the enlarged cells

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

What is hyperplasia?

A

An increase in organ/tissue size due to an increase in the number cells (proliferation)

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

Which cells is hyperplasia seen in?

A

Labile and stable tissues

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

What are the causes of hyperplasia?

A

Hormonal stimulation
Growth factors
Pathological

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

Give an example of hormone induced hyperplasia. What is the clinical significance of this condition?

A

Cystic endometrial hyperplasia which can progress to a pyometra

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

Give an example of infection induced hyperplasia

A

Porcine proliferative enteropathy

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

What is atrophy?

A

A decrease in organ/tissue size due to a decreased nutrient supply and/or function leading to decreased protein synthesis and increased protein and organelle breakdown

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

What are the causes of physiological atrophy?

A

Altered/decreased hormonal stimulation
Apoptosis of individual cells

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

What are the causes of pathological atrophy?

A

Nutrient deficiency (cachexia)
Disuse
Denervation
Pressure
Loss of endocrine stimulation

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

What is denervation atrophy?

A

The atrophy of skeletal muscle fibres due to neural damage

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

What is indicated by post mortem serous atrophy of fat?

A

Suggests starving/emaciation but it can be caused by a wide range of other things

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

What is metaplasia?

A

The replacement of an adult cell type with another adult cell type

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

What is adaptive substitution in regards to metaplasia?

A

The replacement of sensitive cell types with another cell type that is able to withstand adverse environments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are some of the causes of metaplasia?

A

Chronic chemical injury
Chronic mechanical injury
Chronic inflammation
Vitamin A deficiency
Hormonal stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is dysplasia?

A

The disordered arrangement of epithelial cells with loss of differentiation, loss of cell polarity and features of atypia (abnormalities)

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

What is hypoplasia?

A

The incomplete or underdevelopment of an organ/tissue leading to a below average number of cells

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

What is a common example of hypoplasia which frequently leads to reduced fertility?

A

Unilateral or bilateral testicular hypoplasia

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

What is aplasia/agenesis?

A

The complete lack of organ/tissue development

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the seven causes of cell injury?

A

Oxygen deprivation
Physical agents
Chemical agents and drugs
Infectious agents
Immunologic dysfunction
Genetic defects
Nutritional deficiencies and imbalances

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

List four examples of reversible cell injury

A

Hydropic change
Lipidosis
Glycogen accumulation
Neuronal chromatolysis

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

What are the cellular characteristics of reversible cell injury?

A

Generalised cell swelling
Blebbing of the plasma membrane
Chromatin condensing

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

What is hydropic change?

A

Acute cellular swelling caused by a failure of energy-dependent ion transport pumps which cause an electrolyte imbalance and thus a water overload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

On gross examination, how to organs with hydropic change appear?

A

Enlarged
Pale
Turgid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

On microscopic examination, how to cells with hydropic change appear?

A

Pale cytoplasm
Vacuolated cytoplasm
‘ballooning degradation’ (clear cytoplasm) in severe cases

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

What is lipidosis?

A

An abnormal metabolism of lipids

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

What can cause lipidosis?

A

Increased mobilisation of lipid stores
Nutritional disorders
Endocrine diseases

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

In which specific cells types is lipidosis more likely to occur?

A

Hepatocytes
Myocardial cells
Renal tubule cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

On gross examination, how to organs with lipidosis appear?

A

Enlarged
Pale/yellow
Soft
Greasy

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

On microscopic examination, how to cells with macrovesticular lipidosis appear?

A

Single round vacuoles in the cytoplasm causing peripheral displacement of the nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

On microscopic examination, how do cells with microvesticular lipidosis appear?

A

Multiple small round vacuoles in the cytoplasm with no peripheral displacement of the nucleus
- indicates more severe lipidosis

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

What are some causes of glycogen accumulation?

A
  • Diabetes mellitus
  • Glycogen storage disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are some specific causes of hepatic glycogen accumulation?

A

“Steroid hepatopathy’ (prolonged
corticosteroid/glucocorticoid treatment)
Hyperadrenocorticism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the gross appearance of the liver in a glucocorticoid (steroid) hepatopathy?

A

Enlarged
Pale brown to tan
Firm
Non-greasy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is neuronal chromatolysis?

A

The chromatolysis of neuronal ganglia caused by autonomic nervous system disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Give an example of a disease caused by neuronal chromatolysis?

A

Equine dysautonomia (equine grass sickness)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the cellular characteristics of irreversible cell injury?

A

Severe endoplasmic reticulum and mitochondrial swelling
Lysosome rupturing
Blebbing of the plasma membrane followed by membrane rupturing
Nuclear membrane rupture and chromatin fragmentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Which ion is found in the cytoplasm of cells undergoing irreversible cell injury?

A

Increased cytoplasmic Ca2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What causes oxidative stress in cells?

A

Free radicals/reactive oxygen species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

List how free radicals/reactive oxygen species are produced in cells

A

Normal metabolic functions
Absorption of radiation
Activated leukocytes due to inflammation
Iron and copper catalysing the formation of free radicals
Nitrogen oxide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the two main mechanisms of cells death?

A

Apoptosis
Necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is hypoxia?

A

Partial oxygen deficiency to the cells/tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is anoxia?

A

Complete oxygen deficiency to the cells/tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What are the possible causes of hypoxia?

A

Heart failure
Respiratory failure
Ischaemia
Anaemia
Blockage of cell respiratory enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is ischaemia?

A

Partial reduction or complete loss of blood supply caused by local impairment of blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What are the possible causes of Ischaemia?

A

Thrombosis
Mechanical interference with blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What occurs within cells affected by ischaemia?

A

Ischaemia leads to a lack of oxygen in the mitochondria, decreasing oxidative phosphorylation and thus there will be a lack of ATP production. This causes a decrease in the actions of the Na+/K+ ATPase pump, an increase in anaerobic glycolysis and the detachment of ribosomes from the endoplasmic reticulum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

How does a decrease in the actions of the Na+/K+ ATPase pump due to ischaemia affect a cell?

A

Leads to cellular swelling and membrane blebbing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

How does increased anaerobic glycolysis due to ischaemia affect a cell?

A

The production of lactic acid decreases the cellular pH causing the clumping of chromatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

How does ribosome detachment from the endoplasmic reticulum due to ischaemia affect the cell?

A

Results in reduced protein synthesis and increased lipid deposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is infarction?

A

Necrosis due to ischaemia

60
Q

What can happen if ischaemic tissue is restored with a blood supply?

A

This can result in ischaemia-reperfusion injury which is the paradoxical exacerbation of cell injury due to increased reactive oxygen species, the influx of inflammatory cells and the activation of complement

61
Q

List the morphological changes seen in necrotic cells

A

Eosinophilia
Nuclear shrinkage
Fragmentation
Dissolution

62
Q

List the morphological changes seen in apoptotic cells

A

Chromatin condensation
Formation of apoptotic bodies

63
Q

List the five different types necrosis

A

Coagulative necrosis
Liquifactive necrosis
Caseous necrosis
Gangrenous necrosis
Enzymatic necrosis

64
Q

Where in the body is coagulative necrosis seen?

A

Liver
Heart
Kidney
Skeletal muscle

65
Q

What does it mean when necrotic cells become ‘individualised’?

A

The cells lose adherence to their basement membranes and adjacent cells

66
Q

What is a characteristic cytoplasmic change in cells undergoing early stage necrosis?

A

Increased eosinophilia due to a loss of RNA (which is responsible for cytoplasmic basophilia)

67
Q

What is a characteristic cytoplasmic change in cells undergoing late stage necrosis?

A

Rupture of the cells membrane causes the release of cellular contents into the extracellular space

68
Q

What are the four possible nuclear changes seen in cells undergoing necrosis?

A

Pyknosis
Karyorrhexis
Karyolysis
Absence

69
Q

Describe pyknosis

A

Nucleus becomes sunken, dark, homogenous and round

70
Q

Describe karyorrhexis

A

Nuclear membrane ruptures and dark nuclear remnants are released into the cytoplasm

71
Q

Describe karyolysis

A

Nucleus becomes pale due to chromatic dissolution by DNAses

72
Q

Describe absence

A

Nucleus is completely dissolved or lysed

73
Q

What are the possible causes of coagulative necrosis?

A

Hypoxia
Infarction
Bacterial toxins
Chemical toxins

74
Q

Give examples of nephrotoxins which can cause renal tubular degradation and coagulative necrosis

A

Plants differing between species
Heavy metals (mercury, lead)
Chemicals (ethylene glycol)
Therapeutic drugs (antibiotics and chemotherapeutics)

75
Q

How does ingestion of ethylene glycol cause acute renal tubular coagulative necrosis?

A
  • When ethylene glycol is ingested, it is metabolised by the liver into glycoxylate which causes renal tubular epithelial degradation
  • Glycoxylate is converted into oxylate which causes oxylate crystal deposition in the renal tubules, leading to tubule obstruction, mechanical damage and necrosis
76
Q

Give three examples of viral infections which can cause coagulative necrosis

A

Infectious bovine rhinotracheitis
Canine parvovirus enteritis
Canine infectious hepatitis

77
Q

Which virus causes infectious bovine rhinotracheitis?

A

Bovine herpes 1

78
Q

Which virus causes canine parvovirus enteritis?

A

Canine parvovirus 2

79
Q

Which virus causes canine infectious hepatitis?

A

Canine adenovirus 1

80
Q

What are the clinical consequences of infectious bovine rhinotracheitis?

A

Thick plaques of fibronecrotic exudate covering the laryngeal and tracheal mucosa contributed by secondary bacteria

81
Q

What are the clinical consequences of canine parvovirus enteritis?

A

Segmental necrosis and haemorrhage of the intestine

82
Q

What are the clinical consequences of canine infectious hepatitis?

A

Friable, enlarged liver with fibrin on the capsular surface
Oedema of the gallbladder

83
Q

Describe the gross appearance of caseous necrosis

A

Dead tissue converted into a granular, friable mass (resembling cottage cheese)
Dystrophic calcification seen in the centre of the lesions

84
Q

Describe the microscopic appearance of caseous necrosis

A

Accumulation of lysed cells
No tissue architecture

85
Q

What is a classic cause of caseous necrosis?

A

Tuberculosis

86
Q

What is an example of caseous necrosis seen in sheep and goats?

A

Caseous Lymphadenitis (CLA)

87
Q

Which bacteria causes Caseous Lymphadenitis (CLA) in sheep and goats?

A

Corynebacterium Pseudotuberculosis

88
Q

Describe the routes of infectious of corynebacterium pseudotuberculosis causing caseous lymphadenitis

A

Caused by arthropod bites or contaminated drips and bacterial spread via ruptured abscesses and oral/nasal secretions

89
Q

What is the incubation time for corynebacterium pseudotuberculosis?

A

3 months

90
Q

How does caseous lymphadenitis have a significant economic impact?

A

Due to carcase condemnation

91
Q

Where in the body does liquefactive necrosis most commonly target?

A

The central nervous system

92
Q

What causes liquefactive necrosis in the central nervous system?

A

Hypoxic or toxic neural necrosis

93
Q

What occurs during liquefactive necrosis of the central nervous system?

A

Enzymatic dissolution of the neuropil and due to the little connective tissue in the central nervous system, the cavity is filled with fluid and debris

94
Q

Give an example of a common disease which causes liquefactive necrosis

A

Polioencephalomalacia caused by bovine thiamine deficiency

95
Q

What causes liquefactive necrosis in tissues outside the central nervous system?

A

Pyogenic bacteria infection causing the formation of an abscess

96
Q

What are the three types of gangrenous necrosis?

A

Moist gangrene
Dry gangrene
Gaseous gangrene

97
Q

Describe how moist gangrene occurs

A

Initial coagulative necrosis followed by infarction and the active action of saprophytic bacteria

98
Q

Describe the gross examination of moist gangrene

A

Soft, moist, reddish-brown tissue with a putrid smell and sometimes gas bubbles

99
Q

Describe how dry gangrene occurs

A

Coagulative necrosis secondary to infarction with mummification (dehydration)

100
Q

Where in the body is dry gangrene most commonly seen?

A

In the extremities i.e. distal limbs, tail, ears, udders

101
Q

List some possible causes of dry gangrene

A

Toxin ingestion
Frostbite

102
Q

Describe the gross examination of dry gangrene

A

Shrivelled, dry, black/brown tissue

103
Q

What is the other name used to describe gas gangrene

A

Malignant oedema

104
Q

Describe how gas gangrene occurs

A

Anaerobic bacteria infiltrates the body via a penetrating wound or via ingestion, proliferates and produces toxins causing gas gangrene

105
Q

Describe the gross appearance of gas gangrene

A

Dark red/black semi-haemorrhagic exudate tissue, gas bubbles and coagulative necrosis of the muscle

106
Q

Give an example of anaerobic bacteria that can cause gas gangrene

A

Clostridium Chauvoei (blackleg)

107
Q

What are three ways fat necrosis can occur?

A

Enzymatically via pancreatitis
Traumatically via crushed fat around the pelvis after dystocia or crushed sternal fat in recumbent animals
Idiopathic

108
Q

What is dystocia?

A

A difficult birth

109
Q

List three possible consequences of necrosis

A

Inflammatory reactions in viable tissue
Digestion and liquefaction of necrotic tissue
Regeneration of normal tissue or fibrous scarring

110
Q

What are the two main causes of apoptosis?

A
  • Physiological
  • Pathological
111
Q

What are the two main apoptotic pathways?

A
  • Intracellular (mitochondrial)
  • Extracellular (death receptors)
112
Q

What are cellular accumulations?

A

Degenerative changes caused by metabolic alterations

113
Q

What are some examples of intracellular accumulations?

A
  • Excessive normal cellular components (e.g lipids, proteins, water, carbohydrates)
  • Abnormal exogenous or endogenous substances
  • Pigments
114
Q

What are some examples of extracellular accumulations?

A
  • Amyloid
  • Calcification
  • Urates
115
Q

What are some of the causes of intracellular accumulations?

A
  • Increased rate of metabolism of endogenous substances
  • Genetic or acquired defects in metabolism, packaging, transport or secretion of substrates
  • Failure of enzymatic machinery to degrade or transport abnormal exogenous substances
116
Q

Give an example of intracellular exogenous accumulation

A

Lipofuscin

117
Q

In which types of cell/tissues does lipofuscin occur?

A
  • Stable cells/tissues
  • Permanent cells/tissues
118
Q

Give an example of intracellular endogenous accumulation

A

Haemosiderin

119
Q

What is haemosiderin?

A

A form of storage iron derived from the breakdown of erythrocytes

120
Q

In which organs does hemosiderin most commonly accumulate?

A

Organs involved in erythrocyte degradation (liver, spleen)

121
Q

How is haemosiderin accumulation presented both grossly and microscopically?

A

Golden yellow or brown pigmentation

122
Q

What is local haemosiderin accumulation associated with?

A

Bruising

123
Q

What is generalised haemosiderin accumulation associated with?

A

Haemolytic anaemia and/or haemochromatosis

124
Q

Which stain is used to identify haemosiderin accumulation?

A

Perls blue stain due to the iron content in haemosiderin

125
Q

Give three examples of extracellular accumulations

A
  • Amyloid
  • Calcification/mineralisation
  • Gout
126
Q

What are amyloids?

A

Extracellular proteinaceous material consisting of a diverse group of beta sheet glycoproteins

127
Q

Why can amyloids accumulate so easily?

A

Amyloid is resistant to normal proteolytic mechanisms so can easily accumulate and cause cell/tissue compression

128
Q

List some of the clinical consequences of amyloid accumulation (amyloidosis)

A
  • Atrophy
  • Cell death (necrosis/apoptosis)
129
Q

Which stain should be used to identify amyloid accumulation?

A

Congo red

130
Q

Which kind of amyloidosis is the most common in animals?

A

Secondary (relative systemic) amyloidosis

131
Q

Describe what causes secondary (relative systemic) amyloidosis

A

The sustained production of the lipoprotein, serum amyloid A (SAA), by the liver in response to chronic inflammation and/or necrosis

132
Q

Where in the body is secondary (relative systemic) amyloidosis commonly seen?

A
  • Kidneys
  • Liver
  • Spleen
  • Lymph nodes
133
Q

What can cause primary amyloidosis?

A
  • Plasma cell tumours (VERY RARE IN ANIMALS)
  • Seen in the islet cells of cats with type two diabetes mellitus
134
Q

What is the gross appearance of kidneys with renal amyloidosis?

A
  • Waxy
  • Enlarged
  • Pale
  • Swollen cortex
135
Q

What is calcification?

A

Calcium deposition in necrotic or normal tissue

136
Q

What are the two types of calcification?

A
  • Dystrophic
  • Metastatic
137
Q

What is dystrophic calcification associated with?

A

Necrotic tissues - most commonly in coagulative, caseous and fat necrosis

138
Q

Why do necrotic cells/tissues undergo calcification?

A

Dead/dying cells cannot regulate cytoplasmic calcium influx so the calcium accumulates in the mitochondria

139
Q

What is metastatic calcification associated with?

A

Normal tissues secondary to hypercalcaemia

140
Q

What are the five common causes of metastatic calcification?

A
  • Renal failure
  • Vitamin D toxicosis
  • Hyperparathyroidism (primary or secondary)
  • Paraneoplastic hypercalcaemia
  • Destruction of bone from primary or metastatic neoplasms
141
Q

Which stain should be used to identify mineralisation/calcification deposits?

A

Von Cossa staining

142
Q

What is gout?

A

Gout is deposition of sodium urate crystals (Tophi)

143
Q

Why is gout only seen in birds and reptiles?

A

As birds and reptiles excrete uric acid as semi-solid urates

144
Q

What are the two different types of gout?

A
  • Articular gout
  • Visceral gout
145
Q

List three possible causes of visceral gout

A
  • Vitamin A deficiency
  • High protein diet
  • Renal injury
146
Q

Describe the gross examination of gout

A

Grey/white granular deposits on the visceral serosa

147
Q

Describe the microscopic examination of gout

A

Radial deposits surrounded by inflammation and fibrosis

MODULE 4 - Infectious Agents (20 decks)

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