Pathology Flashcards

1
Q

What is pathology?

A

When physiological processes go wrong= state of disease.

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2
Q

What is aetiology?

A

The cause of disease

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3
Q

What are aetiological agents?

A

Things that cause disease.

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4
Q

What categories do aetiological agents come in?

A
  • infections
  • traumatic
  • nutritional
  • chemical
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5
Q

what is the development of disease process?

A
  1. stimulus
  2. cellular injury
  3. cellular response
  4. structural and functional changes
  5. clinical signs
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6
Q

What causes the stimulus in the development of disease?

A

aietology

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7
Q

What will the cellular response consist of?

A

General Pathological processes:

  • altered growth or differentiation
  • inflammation and healing
  • degeneration
  • blow flow and circulatory changes
  • neoplasia
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8
Q

What structural and functional factors may change in the development of disease?

A
  • molecular
  • cellular
  • tissue/organ level
  • gross, micro or biochemical level
  • may change during the period of the disease
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9
Q

Why do you need to understand the aetiopathogenesis of disease?

A
  1. explains clinical signs
  2. enables a list of differential diagnoses to be produced
  3. decide which diagnostic tests to use to get a definitive diagnosis
  4. helps predict prognosis
  5. basis for treatment, control and prevention
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10
Q

What are congenital malformations?

A

structural, functional, metabolic or behavioural disorders

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11
Q

When do congenital abnormalities occur?

A

During intrauterine life and can be present at birth, but may become apparent later in life.

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12
Q

what is a teratogen?

A

foreign antigen that interfere with normal development of the embryo/ foetus, giving rise to a congenital malformation

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13
Q

What factors influence whether teratogens will cause congenital malformations?

A
  • Agent factors
  • Species susceptibility
  • Maternal factors
  • Embryo/foetus factors
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14
Q

What type of agent factors influence teratogen influence?

A
  • Dose level
  • Frequency of exposure
  • Route of exposure- topical/ingested?
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15
Q

What maternal factors influence teratogens?

A
  • Genetic makeup

- Metabolism

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16
Q

What foetal factors influence teratogens?

A
  • Stages of development= most important
  • Genetic makeup
  • Metabolism
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17
Q

What could happen during the embryonic stage of development?

A

Organogenesis is happening- where organs are created from germ cells.
Sensitivity to teratogens: High
Result: death, abortion, major morphological abnormalities

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18
Q

What could happen during the foetal stage of development?

A

Histogenesis and functional maturation- growth and maturation of organs
Sensitivity to teratogens: Low
Result: death, abortion, growth retardation, minor morphological abnormalities

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19
Q

What are the two factors that cause congenital malformations?

A
  • Genetic

- Environmental

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20
Q

Give examples of Genetic factors affecting congenital malformations.

A
  • Gene Mutations- monogenic or polygenic

- Chromosomal abnormalities- numerical, structural, gamete meiosis.

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21
Q

What developmental failures can occur?

A
Agenesia
Hypoplasia
Dysraphia
Atresia
Failure of migration
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22
Q

What developmental excess issues can occur?

A

Hamartoma

supernumerary tissue

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23
Q

What is agenesia?

A

Lack of formation of a tissue or organ

24
Q

What is Hypoplasia?

A

Partial failure to develop

Mechanisms: insufficient cellular proliferation or arrested development

25
Q

What is atresia?

A

Failure of development of an opening/ orifice

EG: Atresia Ani- anal opening fails to develop.

26
Q

What is dysraphia?

A

Failure of tissues to fuse or merge

EG: cleft palate

27
Q

What is failure of migration?

A

Organs not located in correct anatomical position

28
Q

What is Hamartoma?

A

Extra tissue at a normal site, developmental excess

29
Q

What is supernumerary tissue?

A

an excess number of tissues/ features, EG: Teats or toes

30
Q

Examples of internal injurious stimuli

A

oxygen deprivation, nutritional imbalance, immune system reactions,
genetic abnormalities, ageing, workload imbalance

31
Q

Examples of environmental injurious stimuli

A

Infectious agents, physical agents, chemicals, drugs and toxins

32
Q

What is the difference between hypoplasia and atrophy?

A

Hypoplasia is a developmental failure where the cells don’t reach the right size
Atrophy is a reduction in the size or functionality, of a normal cell

33
Q

What are the causes of hypertrophy and hyperplasia?

A
  1. Increased workload
  2. Increased hormonal stimulation
  3. Reactive response to inflammation
  4. Age related change
34
Q

What are the causes of atrophy

A
  1. Decreased workload
  2. Destruction and loss of cells with lack of requirement
  3. Deprivation of nutrients or growth factors.
35
Q

What is Metaplasia?

A

change from normal cell type to another that is better able to withstand insult/stress
protective/ adaptive

36
Q

What is Dysplasia?

A

A reversible or partly reversible change characterised by disorderly growth

  • at sites of chronic inflammation
  • epidermal/ epithelial tissue
  • neoplastic disease
37
Q

What is the chronological order of the 3 phases of the acute inflammatory response?

A

Vascular, exudative, cellular

  • Capillaries fill the area with fresh blood= heat and reddening
  • Endothelial cells move apart so that the capillaries become more leaky/ permeable- into interstitial space =swelling
  • Leukocytes recruited to the area
38
Q

What is oedema?

A

accumulation of excess fluid in the interstitial area, may be localised or generalised.

39
Q

Main mechanisms of cellular injury?

A
  • impaired energy production
  • impaired cell membrane function
  • biochemical pathway derangement
  • Nucleic acid damage
40
Q

What are the causes of mitochondrial damage?

A
  • Apoptosis

- Free radicals- causes lipid peroxidation of membranes

41
Q

Consequences of membrane damage

A
  • mitochondrial dysfunction- ATP depletion
  • plasma membrane dysfunction- Loss of osmotic balance, loss of cellular contents, metabolites and influx of fluids
  • Leakage of lysosomal enzymes into cytosol
42
Q

What sort of cell injuries cause cellular swelling?

A
  1. Hypoxia- not enough O2
  2. Cell membrane injury-free radical attack- lipid peroxidation, membrane attack complexes, toxins inactivating pumps and channels.
43
Q

What is lipidosis?

A

Altered lipid metabolism and accumulation of lipids.

Excessive triglyceride accumulation in hepatocytes

44
Q

What is necrosis?

A

Death of cells within living tissue

unregulated mechanisms where multiple cells are affected and stimulates inflammation

45
Q

What cytoplasmic changes occur in necrosis?

A

-increased cytoplasmic eosinophilia= deeper red/ pink

46
Q

What nuclear changes occur in necrosis?

A
  1. Karyolysis= nuclear fading
  2. Pyknosis= nuclear condensation
  3. Karyorrhexis= nuclear fragmentation
47
Q

What are the different types of necrosis?

A
  • Coagulative
  • fat
  • caseous
  • gangrene- dry, gaseous, and wet
  • liquefactive
48
Q

Why is pus formed?

A

When pyogenic organisms attract many neutrophils to the site of infection

49
Q

What are the two types of pathological calcification?

A

Dystrophic and Metastatic

50
Q

What is dystrophic calcification?

A

extensive mineralisation at sites of necrosis

51
Q

What is metastatic calcification?

A

Associated with disturbed calcium metabolism resulting in elevated blood calcium and deposition of calcium salts in tissues (hypercalcaemia)

52
Q

Where can metastatic calcification occur?

A
  • stomach mucosa
  • lungs, pleura
  • blood vessel walls
  • endocardium
53
Q

What are the causes of hypercalcaemia?

A
  • parathyroid gland producing excessive parathyroid hormone
  • parathyroid hormone related peptide produced by other tissues
  • chronic kidney disease
  • Vitamin D toxicity/ poisoning with some rodenticides.
54
Q

What is prehepatic icterus?

A

excessive bilirubin production due to haemolysis, before it’s taken up by the liver.

55
Q

What is hepatic icterus?

A

Hepatocyte damage and decreased metabolism of bilirubin

56
Q

What is post hepatic icterus

A

obstruction of bile duct and excretion.