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Cells to systems > Lecture 13 > Flashcards

Lecture 13 Flashcards

1
Q

What causes cell degeneration

A
  • the result of sublethal injury

- results in reversible morphologic change

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2
Q

What is essential to homeostasis

A

The cellular membranes are essential to homeostasis by
regulating what substances enter and leave the
cell and its organelles

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3
Q

Causes of cell injury

A
  • Hypoxia
  • Impaired blood flow – cardiac disease/ ischemia
  • Impaired O2 transport – respiratory disease/ anemia/ toxins
  • Physical agents
  • trauma, thermal, UV radiation, ionising radiation
  • Microbes
  • viruses, bacteria - toxins, fungi, helminths, protozoa
  • Inflammation and immunologic dysfunction
  • Nutritional imbalances
  • Genetic derangement
  • eg. lysosomal storage diseases
  • Workload imbalance
  • Chemicals, drugs, toxins
  • Aging
  • Combination - potentiating
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4
Q

Hypoxia

A
  • Impaired blood flow – cardiac disease/ ischemia

* Impaired O2 transport – respiratory disease/ anemia/ toxins

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5
Q

Physical agents Causes of cell injury

A

• trauma, thermal, UV radiation, ionising radiation

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6
Q

Microbes Causes of cell injury

A

• viruses, bacteria - toxins, fungi, helminths, protozoa

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7
Q

What is the cell injury mechanism activated by

A 
different injurious stimuli
• ATP depletion
• Oxygen derived free radicals
• Permeabilization of cell membranes
• Mitochondrial damage
• Disruption of biochemical pathways
• DNA damage
• Often overlapping mechanisms
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8
Q

how does ATP depletion work

A

Ishemia(reduce blood) causes reduction in oxidative phosphorylation, thus reduce ATP

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9
Q

How does Oxygen derived free radicals work

A

radiation toxins reperfusion

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10
Q

What do you see in Reversible injury

A 
swelling of the cell
Damage to membrane ion pumps
swollen mitochondria, ER, lysosomes
changes to plasma membrane
Altered protein synthesis
accumulation of metabolites
Nuclear changes
clumped chromatin
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11
Q

What happens in hypoxia

A 
• Largely reflects ↓ATP → impaired Na+
/K+
- ATPase pumps
• → influx Na+
, Ca++ accompanied by H2O
• → efflux K+
, Mg++
• ↓ATP → switch to anaerobic metabolism
• → ↓ glycogen in cell
• → ↓ pH
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12
Q

Where does hydropic degeneration happen

A

– liver, renal tubular epithelium, pancreatic

islet cells

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13
Q

Where does Ballooning degeneration happen

A

epidermis and upper alimentary tract –

keratinocytes

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14
Q

Where does Cytotoxic oedema happen

A

astrocytes in the CNS

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15
Q

How does hydropic degeneration work

A

Due to hypoxia, sodium channel pumps in H2O and causes water to move to cytosol and cytocavitary system and all other organelles due to osmotic pressure. Which then end up having hydropic degeneration

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16
Q

When does ballooning degeneration develop

A

before vesicle formation

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17
Q

When might there be a chance that epithelial cells of the stratum spinosum contain intracytoplasmic eosinophilic
parapoxvirus inclusions

A

earlier stage

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18
Q

When does cytotoxic oedema occur

A

Accumulation of ammonia

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19
Q

What happens when there is an accumulation of ammonia?

A
  • ammonia taken up by astrocytes > converted
    to osmotically active glutamine, which causes cytotoxic astrocytic swelling >
    rise in intracranial pressure and compromised astrocytic function
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20
Q

What dictates the result after acute cell swelling

A
  • Depends upon
  • number of cells affected and
  • regenerative capabilities of the cell – brain and heart vs liver and kidney
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21
Q

What are the outcomes of injurious insult

A
  • Recover and regain function – Back to normal after removal
  • If severe, lengthy or repetitive injury see
  • Impaired cell metabolism with intracellular accumulations
  • Irreversible cell damage and cell death
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22
Q

What make cell can accumulate intracellular material via

A 
• Disturbance/s to metabolism
→ accumulation of by-products
• Genetic mutations
→ accumulation of abnormal product
OR
inability to process intracellular by-product
• Exogenous substances
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23
Q

Is intracellular accumulation harmful

A

Can be innocuous but may be harmful

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24
Q

What Lipidosis/ Steatosis/ Fatty change affect

A

a range of tissues – liver especially

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25
Q

What are the possible mechanisms for Lipidosis/ Steatosis/ Fatty change

A
  1. ↑ delivery of FFAs
  2. ↓ utilization of FFA
  3. ↓ synthesis of apoprotein
  4. ↓ impaired lipoprotein formation
  5. ↓ release of lipoproteins
    1. and 5. most common sites – require energy and protein
26
Q

What is one way to see if If lipidosis is severe

A

the affected

tissue may float in formalin fixative

27
Q

What does diffuse lipidosis usually indicates

A

the increased mobilization of free fatty acids in association with
negative energy balance resulting in mobilization of fat reserves
eg periparturient cow – ketosis or pregnancy toxaemia in sheep

28
Q

Where are the two major sight of glycogen storage

A

liver and skeletal muscle

29
Q

What is the most common cause of glycogen

accumulation in hepatocytes of dogs

A

Hyperadrenocorticism

30
Q

What causes Excess cortisol in dogs

A 
• corticosteroid drugs
• functional ACTH-producing pituitary tumour
• functional cortisol-
producing adrenocortical 
• Induces hepatocellular transcription
of glycogen synthetase
31
Q

What is the diagnosis for vacuolar hepatopathy

A

• Hydropic degeneration, glycogen accumulation, lipid accumulation,
ballooning degeneration, other
• Not possible to differentiate the cause of hepatocellular vacuolation

32
Q

What is glycogen storage disease

A
  • Inherent disorders of glycogen metabolism – Various types
  • Pompe’s Disease – def lysosomal acid maltase (acidic α-glucosidase)
  • Inherited – autosomal recessive - esp Brahman and Shorthorn
33
Q

Is Lysosomal storage diseases inherited

A
  • Inherited or induced defects of metabolism
  • Genetic defect
  • Exogenous toxin
34
Q

What is Lysosomal storage diseases

A

Accumulation of storage material in lysosomes

• Range of storage materials - lipids and carbohydrates

35
Q

What are the early clinical signs of Congenital alpha-mannosidosis

A

early – blindness, ataxia, head tremors, intention tremors

36
Q

What causes Acquired alpha-mannosidoses

A
  • Swainsonine intoxication

* plants such as Swainsona species (Darling pea)

37
Q

What is Acquired alpha-mannosidoses

A

• indolizidine alkaloid (swainsonine)
• inhibits lysosomal α-mannosidase
• Induces clinical disease and lesions to
congenital α-mannosidase deficiency

38
Q

What is amyloid

A

• Extracellular deposits of fibrillar protein
tissue damage and functional compromise
• Abnormal folding of proteins which become insoluble and aggregate
to form fibrils (amyloid)

39
Q

What happen to the abnormal folding of proteins in amyloid

A

• Deposited in the extracellular space

40
Q

What are the two forms of amyloid proteins

A

normal proteins with an inherent tendency to fold improperly

mutant proteins that are prone to misfolding and aggregation

41
Q

What is AA amyloid

A

AA amyloid
• most common form in animals – reactive – associated with chronic inflammation
• formed via serum amyloid A – acute phase protein via liver/inflammation

42
Q

What is AL amyloid

A
  • most common form in humans – occasionally animals

* formed via λ or occasionally κ Ig light chains – plasma cell neoplasia

43
Q

What is IAPP amyloid

A
  • deposited in pancreatic islets of cats and primates

* formed via islet amyloid polypeptide – secreted by β cells in pancreas - ?

44
Q

What is Aβ amyloid

A

• Cerebral plaques and cerebral blood vessels – Alzheimer’s in humans and dementia
in dogs

45
Q

Where does AA amyloid in absysinnians deposit to

A

– renal glomeruli and medulla – renal protein loss and kidney
failure

46
Q

Where does AA amyloid in siamese cats deposit to

A

– liver – hepatic rupture

47
Q

Where does AA amyloid in shar peis deposit to

A

renal medulla – renal protein loss and kidney failure

48
Q

How is pancreatic amyloidosis formed by

A

Formed by islet amyloid polypeptide
Produced by the β- cells

Deposition of amyloid in pancreatic islets (Islets of Langerhans) with loss of β- cells

49
Q

What is tunica intima in the artery

A
  • endothelium
  • basement membrane
  • internal elastic lamina
50
Q

What is tunica media in the artery

A
  • smooth muscle
  • collagen, reticular, and elastin fibres
  • external elastic lamina
51
Q

What is tunica adventitia in the artery

A
  • connevtive tissue
  • vasa vasorum (microvessels)
  • lymphatic vessels
  • nerve fibre
  • peripheral layer
52
Q

What causes Fibrinoid change

A

Damage to endothelial cells, basement

membrane or smooth muscle of media

53
Q

What happens when there is fibrincoid change

A

Leakage of immunoglobulin, fibrin, complement
into blood vessel wall forming fibrinoid
Deeply eosinophilic deposits = fibrinoid change
Vascular damage can reflect vasculitis arising in
association with
sepsis, viral infection, endotoxemia

54
Q

What is flame figures

A

• Seen in association with eosinophilic inflammation
• Discharged eosinophil granules and nuclear debris
encrusted on intact collagen
• Mantle of surrounding macrophages = campfire

55
Q

What are some Range of hypersensitivity reactions to agents

A

arthropod bites
food and environmental allergens
fungal infections
equine and canine mast cell tumors

56
Q

Which animal is most common to have flame figures

A

Especially in the cat and horse

57
Q

What is Eosinophilic granuloma complex in cats

A

EGC is a group of lesions – range of locations

Characterized by florid eosinophilic inflammation often with flame figures

58
Q

What can intracellular accumulations be

A
  • lipid, glycogen, protein, pigment
59
Q

What is FFA

A

free fatty acids

60
Q

what can cause a large accumulation of glycogen

A

Hyperadrenocorticism

61
Q

What cause glycogen storage disease

A

The inability for lysosoman acid maltase to metabolize glycogen

62
Q

is SAA protein caused by chronic inflammation

A

yes

Cells to systems (25 decks)

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