Lecture 1: Intro to study of disease Flashcards

1
Q

Morbid anatomy

A

Study of diseased organs and tissues
- visible
- post-mortem
- gross examination.

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2
Q

Histopathology

A

The microscopic study of tissues - morphology and architecture
Histology - tissues
Cytology - cells

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3
Q

Anatomical pathology

A
  • Clinical/hospital pathology
  • Macro and microscopic study of disease
  • observational science
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4
Q

General pathology

A
  • mechanisms of disease
  • study of processes underlying disease conditions
  • experimental science
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5
Q

Aetiology

A

Cause or origin of disease

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6
Q

Pathogenesis

A

Mechanism of disease development

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7
Q

cyto-

A

related to cells
i.e. Cytotoxicity

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8
Q

dys-

A

disordered
i.e. dysplasia

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9
Q

hyper-

A

more than normal
i.e. hyperplasia

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10
Q

hypo-

A

less than normal
i.e. hypothyroidism

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11
Q

leuko-

A

white
i.e. leukocyte

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12
Q

meta-

A

change of one state into another
i.e. metaplasia

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13
Q

neo-

A

new
i.e. neoplasia

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14
Q

-aemia

A

relating to blood
i.e. anaemia

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15
Q

-cytosis

A

increase number of cells (in blood)
i.e. leukocytosis

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16
Q

-itis

A

inflammatory process
i.e. appendicitis

17
Q

-oid

A

resemblance to something
i.e. epithelioid

18
Q

-oma

A

swelling or growth
i.e. atheroma

19
Q

-opathy

A

diseased state
i.e. adenopathy

20
Q

-osis

A

state or condition
i.e. acidosis

21
Q

-penia

A

lack of something
i.e. lymphopenia

22
Q

-plasia

A

growth disorder
i.e. anaplasia, metaplasia

23
Q

What is crohn’s disease

A

Inflammatory bowel disease which first appears in young adults

24
Q

What are some symptoms o crohn’s disease

A

Diarrhea, abdominal pain, fever, fatigue, blood in stood

25
Histological features of Crohn's disease
Affected areas are inflamed with leukocytes, crypts from repeated inflammation and regeneration, noncaseating granuloma.
26
What is granuloma
aggregation of macrophages
27
Aetiology of Crohn's disease
Genetic susceptibility, pathogenic variant of NOD2, a receptor which recognises bacterial products and eliminates invaded bacteria, altered communities of gut flora, environmental actors such as NSAIDs, diet, hygiene, overactive immune system responses, Th1 and Treg cells.