AD1 > Pathology > Flashcards

Pathology Flashcards

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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?

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A

Lack of formation of a tissue or organ

24
Q

What is Hypoplasia?

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A

Partial failure to develop

Mechanisms: insufficient cellular proliferation or arrested development

25
What is atresia?
Failure of development of an opening/ orifice | EG: Atresia Ani- anal opening fails to develop.
26
What is dysraphia?
Failure of tissues to fuse or merge | EG: cleft palate
27
What is failure of migration?
Organs not located in correct anatomical position
28
What is Hamartoma?
Extra tissue at a normal site, developmental excess
29
What is supernumerary tissue?
an excess number of tissues/ features, EG: Teats or toes
30
Examples of internal injurious stimuli
oxygen deprivation, nutritional imbalance, immune system reactions, genetic abnormalities, ageing, workload imbalance
31
Examples of environmental injurious stimuli
Infectious agents, physical agents, chemicals, drugs and toxins
32
What is the difference between hypoplasia and atrophy?
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
What are the causes of hypertrophy and hyperplasia?
1. Increased workload 2. Increased hormonal stimulation 3. Reactive response to inflammation 4. Age related change
34
What are the causes of atrophy
1. Decreased workload 2. Destruction and loss of cells with lack of requirement 3. Deprivation of nutrients or growth factors.
35
What is Metaplasia?
change from normal cell type to another that is better able to withstand insult/stress protective/ adaptive
36
What is Dysplasia?
A reversible or partly reversible change characterised by disorderly growth - at sites of chronic inflammation - epidermal/ epithelial tissue - neoplastic disease
37
What is the chronological order of the 3 phases of the acute inflammatory response?
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
What is oedema?
accumulation of excess fluid in the interstitial area, may be localised or generalised.
39
Main mechanisms of cellular injury?
- impaired energy production - impaired cell membrane function - biochemical pathway derangement - Nucleic acid damage
40
What are the causes of mitochondrial damage?
- Apoptosis | - Free radicals- causes lipid peroxidation of membranes
41
Consequences of membrane damage
- 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
What sort of cell injuries cause cellular swelling?
1. Hypoxia- not enough O2 2. Cell membrane injury-free radical attack- lipid peroxidation, membrane attack complexes, toxins inactivating pumps and channels.
43
What is lipidosis?
Altered lipid metabolism and accumulation of lipids. | Excessive triglyceride accumulation in hepatocytes
44
What is necrosis?
Death of cells within living tissue | unregulated mechanisms where multiple cells are affected and stimulates inflammation
45
What cytoplasmic changes occur in necrosis?
-increased cytoplasmic eosinophilia= deeper red/ pink
46
What nuclear changes occur in necrosis?
1. Karyolysis= nuclear fading 2. Pyknosis= nuclear condensation 3. Karyorrhexis= nuclear fragmentation
47
What are the different types of necrosis?
- Coagulative - fat - caseous - gangrene- dry, gaseous, and wet - liquefactive
48
Why is pus formed?
When pyogenic organisms attract many neutrophils to the site of infection
49
What are the two types of pathological calcification?
Dystrophic and Metastatic
50
What is dystrophic calcification?
extensive mineralisation at sites of necrosis
51
What is metastatic calcification?
Associated with disturbed calcium metabolism resulting in elevated blood calcium and deposition of calcium salts in tissues (hypercalcaemia)
52
Where can metastatic calcification occur?
- stomach mucosa - lungs, pleura - blood vessel walls - endocardium
53
What are the causes of hypercalcaemia?
- 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
What is prehepatic icterus?
excessive bilirubin production due to haemolysis, before it's taken up by the liver.
55
What is hepatic icterus?
Hepatocyte damage and decreased metabolism of bilirubin
56
What is post hepatic icterus
obstruction of bile duct and excretion.
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