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Path2201 > Introduction > Flashcards

Introduction Flashcards

1
Q

What is a leision?

A

An abnormality in the structure / function of any body part caused by injury or disease

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2
Q

Compare thrombosis, embolism and infarction

A

Thrombosis:
A thrombus (blood clot) blocks blood vessels

Embolism:
Embolus (foreign material) that travels in the body becomes severely stuck and blocks the flow of blood

Infarction:
Tissue death (necrosis) due to inadequate blood supply to the are

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3
Q

What are the frameworks of knowledge in Pathology?
(Who, where, why, how, what)

A

Definition
Epidemiology
Aetiology
Pathogenesis
Morphology
Clinical manifestations
Disease outcomes

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4
Q

Epidemiology

A

patterns of disease within a population

  • frequency (incidence, prevalence)
  • gender
  • race
  • socioeconomic grouping
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5
Q

Aetiology (CHINPIG)
Unknown causes of disease?

A

Causes of disease. Can be inherited or acquired.

Chemical
Hypoxia
Infection
Nutritional
Physical
Immunologic
Genetic

Unknown causes: Idiophathic

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6
Q

Pathogenesis (How?)

A

the manner of development of a disease

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7
Q

Morphology and different types

A
  • The changes in structure (lesions) caused by injury or disease
  • macroscopic (gross pathology)
    focal/multifocal/diffuse
  • microscopic (histopathology)
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8
Q

Clinical manifecstations

A

Signs - Objective and observable
Symptoms - SUbjective experience of patient

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9
Q

Kinds of pathological investigations

A
  • Diagnostic imaging procedures: X-ray, CT, Ultrasound, MRI, etc.
  • Haematological (blood tests)
  • Biochemical
  • Microbiological (assessing microbial contamination)
  • Immunological (investigating problems with the immune system)
  • Procedural – e.g. endoscopy
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10
Q

3 disease outcomes

A
  • Complications - Lesions that develop as a direct consequence of another lesion
  • Prognosis - Likely outcome in an individual
  • Natural history - Course of untreated disease
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11
Q

link concepts of pathogenesis and clinicopathological correlation

A

Pathogenesis: How does the causative agent produce the morphological effects?

Clinicopathological correlation: How do the morphological changes produce the clinical effects and investigative abnormalities?

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12
Q

How are diseases classified and how does this change?
Use the example of pneumonia.

A

Depending on need and viewpoint:

  • Aetiological: Klebsiella pneumonia
  • Epidemiological: Hospital-acquired pneumonia
  • Pathogenetic: hypostatic pneumonia
  • Morphological: bronchopneumonia
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13
Q

What is hypoxia? What are 3 causes?

A

Deficiency of oxygen.

  • Impaired oxygenation of the blood (e.g. with any severe lung disease)
  • When the oxygen-carrying capacity of the blood is reduced (e.g. anaemia)
  • Ischaemia, refers to the inadequate blood supply (perfusion) to a tissue or organ.
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14
Q

Provide examples of hypoxia causes

A

Thrombus
Drowning
Pneumonia
Cardiac issues

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15
Q

Describe the aetiology of these chemical and drug diseases;
- Acidosis
- Diabetes

A

both recreational and illegal drugs and well as prescription drugs, as well as excessive chemicals in the body

hydrogen ions in excess = acidosis
glucose = diabetes

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16
Q

Give examples of physical agents

A

Skin cancer (pyrimidine dimers from radiation)
Burns (from heat or cold)
Physical damage (tissue damage from trauma)

17
Q

Give examples of infective agents and what they cause

A

bacteria, viruses, fungi, parasites, microorganisms

causing; gangrene, chlamydia, giardiasis

18
Q

Give examples of nutritional abnormalities

A

excessive alcohol, iron or vitamin deficiencies, overnutrition = obesity, scurvy, rickets, iron-deficiency anemia

19
Q

Give examples of Idiopathic dieases

A

Unknown cause: Parkinson’s disease, idiopathic pulmonary fibrosis, multiple Sclerosis - can be under autoimmune too

20
Q

Give examples of immunological diseases. Hypersensitivity vs autoimmune

A

Hypersensitivity: rheumatoid arthritis, organ transplant disease, tuberculosis, anaphylaxis, hay fever

Autoimmune: coeliac disease, rheumatoid arthritis, lupus, type 1 diabetes

21
Q

Give examples of genetic abnormalities. Inherited vs Acquired.

A

combination of gene variants increases the risk of developing the disease (often with adverse environmental interactions)

Inherited: down syndrome, cystic fibrosis, Huntington’s disease

Acquired: acquired epilepsies, smoking-induced COPD, lung & colorectal cancer, melanoma from UV radiation - activate cell damage

22
Q

What are the effects injury

A
  1. Biochemical lesion → 2. Functional abnormality (often the dominant effect in reversible injury) → 3. Morphological change (often non-specific)
23
Q

Give 4 examples of biochemical mechanisms that damage cells

A
  • inhib of respiration
  • loss of membrane integrity
  • alteration in enzyme/ proteins structure
  • interference w DNA synthesis of repair
24
Q

What factors influence the effects of an injury?

A
  • nature of the injurious agent
  • duration
  • severity
  • nature of target cells
25
Q

What are 4 cellular adaptations to injury?

A
  • Hypertrophy (enlargement of tissue from increased cell size)
  • increased or decreased hyperplasia (change in the number of cells)
  • metaplasia (change of cells to a form that does not normally occur in that tissue
  • atrophy (decrease in size of tissue)
26
Q

What are the 5 outcomes of injury?

A

Cellular damage, altered growth/ differentiation, inflammation, immune response, haemodynamic and vascular changes

27
Q

Discuss Benign Prostatic Hyperplasia
- epidemiology
- pathogenesis
- morphology
- outcomes

A

BPH
- common cause of prostatic enlargement
- 50% affected by 60yo
- 90% affected by 85yo
- Driven by androgens
- Results in hyperplasia of glandular and stromal cells in prostate
- may compress the urethra making hard to pass urine

28
Q

Why doesn’t skeletal muscle undergo hyperplasia? What organ undergoes both hypertrophy and hyperplasia?

A
  • # of cells is terminally differentiated
  • Uterus
29
Q

Discuss metaplasia in airway cells

A

Smoking can affect the normally columnar pseudostratified ciliated epithelial cells to become keratinised and squamous. This is reversible to a degree

30
Q

Discuss cellular swelling and provide a cause example

A
  • commong first response to cell injury
  • depletion of O2 (hypoxia) causes ion pumps to fail, sodium accumulates in the cell and draws in water -> ER and mitochondria swell –> cell died
  • reversible when injurious agent removed, up to point of cell death
31
Q

Discuss steatosis. Is it reversible? Macroscopic and microscopic morphology? Cause?

A
  • accumulation/ retention of fat in organ or tissue
  • characteristically found in the liver
  • reversible injury
  • macroscopically liver will appear enlarger, yellow and greasy
  • microscopically characterised by spherical vacuoles (lipid droplets) in hepatocytes
  • alcohol is a common cause
32
Q

Compare necrosis and apoptosis

A

Necrosis is always pathological and a result of cellular injury

Apoptosis is more tightly regulated by biochemical pathways. e.g. Skin cells after UV damage, normal cells that are no longer required, tumor cells

33
Q

Compare ischemia and hypoxia

A

stopped blood flow (which can cause hyopxia as o2 and other substrates are not entering the cell, more severe)

low oxygen (can be due or ischemia and also low haemaglobin)

34
Q

What is infarction

A

Necrosis (tissue death) due to lack of perfusion (blood delivery) due to thrombus or embolus

35
Q

Compare infarction and ischemia

A

lack of perfusion -> cell death

decreased persuion

36
Q

Discuss Gangrene

A
  • a macroscopic appearance
  • infarction is complicated by putrefaction (rotting) of infarcted tissue
  • due to superimposed bacterial infection
  • infarcted tissue turns black

Path2201 (6 decks)

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