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BLOCK A > Pathology > Flashcards

Pathology Flashcards

1
Q

10 steps on approaching disease

A
  1. Disease epidemiology and history
  2. Disease etiology
  3. Disease pathogenesis
  4. Pathogenetic alterations
  5. Pathophysiology
  6. Clinical manifestations + lab data
  7. Diagnosis (+ differential diagnoses)
  8. Therapies, procedures and complications
  9. Predictive and prognostic factors
  10. Therapy
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2
Q

What anatomic pathology comprises

A

= diagnostic pathology

  • Autopsy pathology
  • Surgical pathology
  • Cytopathology
  • Specialty labs, ancillary techniques
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3
Q

Steps of tissue preparation and are they automated?

A
  1. Fixation (10% formalin water) - aqueous (NA)
  2. Dehydration with alcohol (A)
  3. Clearing with xylene (increasing translucency) - organic (A)
  4. Infiltration by paraffin wax - organic (A)
  5. Embedding (NA)
  6. Cut on microtome for LM (NA)
  7. Staining with H&E (A)
  8. Coverslipping (A)
  9. Distribution
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4
Q

Prussian blue stain characteristics

A

Stains for ferric iron (blue)
Useful for diagnosing hemochromatosis (deficiency in iron absorption)

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5
Q

Masson trichrome characteristics

A

IDs CT, muscle and collagen
3 colours:
Collagen = blue
Muscle = red
Cytoplasm = light red or pink
Nuclei = dark blue

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6
Q

Ziehl-Neelsen stain

A

aka acid-fast stain

ID tuberculosis

Stains the lipid coat

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7
Q

Grogott stain

A

Stains fungal organisms
(Silver stains carbohydrate capsule)
Eg. Aspergillus infection

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8
Q

EM main uses

A

Renal glomerular diseases and virology

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9
Q

Diff between IF and IMHC

A

Immunofluorescence uses the same principle as IMHC but with tissues sensitive to loss by paraffin embedding, so it is done on frozen sections and the Abs are stained.

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10
Q

Cytopathology definition

A

Branch of anatomic pathology looking at whole cells rather than tissues.

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11
Q

5 types of necrosis

A
  1. Coagulative necrosis
  2. Liquefactive necrosis
  3. Caseous necrosis
  4. Fat necrosis
  5. Fibrinous necrosis
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12
Q

Hypertrophy =

A

increase in cell size thru increased protein synthesis, induction of structural genes and re-expression of developmental genes

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13
Q

Hyperplasia =

A

increase in cell number thru GF/GH signalling pathway activation, activation of cell cycle regulators and new productions from stem cells

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14
Q

Atrophy mechanisms

A

lysosomal enzyme pathway, Ub-proteasome pathway, autophagic vacuoles

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15
Q

3 examples of intracellular accumulations?

A

lipofuscin, iron, melanin

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16
Q

5 cardinal signs of inflammation

A

heat, pain, swelling, redness, loss of function

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17
Q

Leukocyte migration process

A
  1. Margination
  2. Rolling
  3. Adhesion
  4. Transmigration
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18
Q

What are the three arachidonic acid metabolites?

A

2 pro-inflammatory: prostaglandines and leukotrienes
1 anti-inflammatory: lipoxins

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19
Q

granulomatous inflammation cells

A

macrophages clustered up looking like epithelia, and surrounded by lymphocytes and plasma cells

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20
Q

4 systemic effects of chronic inflammation

A

fever
leukocytosis
production of acute phase proteins (CRP)
septic shock (in severe situations)

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21
Q

5 factors that can impair wound healing

A
  1. Infection
  2. Protein deficiency
  3. Treatments such as glucocorticoids, which act as anti-TNF alpha
  4. Poor perfusion
  5. Increased production of keloids by the ecm (abnormal wound healing characteristic)
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22
Q

Balances in tissue remodeling

A

Pro: TGF-beta; tissue inhibitors of MMPs

Anti: MMPs

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23
Q

Squamous cell benign neoplasm

A

Squamous papilloma

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24
Q

Urothelium benign neoplasm

A

Urothelial papilloma

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25
Q

Glandular benign neoplasm

A

Adenoma / papillary adenoma

26
Q

Squamous cell malignant neoplasm

A

Squamous cell carcinoma

27
Q

Urothelium malignant neoplasm

A

Urothelial carcinoma

28
Q

Glandular malignant neoplasm

A

Adenocarcinoma

29
Q

Melanocyte benign neoplasm

A

Nevus

30
Q

Melanocyte malignant neoplasm

A

Melanoma

31
Q

Germ cell malignant neoplasm

A

Dysgerminoma

32
Q

Germ cell benign neoplasm

A

Benign cystic teratoma

33
Q

Fibroblast benign neoplasm

A

Fibroma

34
Q

Fibroblast malignant neoplasm

A

Fibrosarcoma

35
Q

Adipocyte benign neoplasm

A

Lipoma

36
Q

Adipocyte malignant neoplasm

A

Liposarcoma

37
Q

Smooth muscle cell benign neoplasm

A

Leiomyoma

38
Q

Smooth muscle cell malignant neoplasm

A

Leiomyosarcoma

39
Q

Endothelium benign neoplasm

A

Hemangioma

40
Q

Endothelium malignant neoplasm

A

Angiosarcoma

41
Q

Osteocyte benign neoplasm

A

Osteoma

42
Q

Osteocyte malignant neoplasm

A

Osteosarcoma

43
Q

Hematopoietic stem cell malignant neoplasm

A

Leukemia

44
Q

Lymphoid cell malignant neoplasm

A

Lymphoma

45
Q

Breast (mixed neoplasm) benign neoplasm

A

Fibroadenoma

46
Q

Breast (mixed neoplasm) malignant neoplasm

A

Phyllodes tumor

47
Q

What is transcoelomic metastasis?

A

Metastasis thru the peritoneal cavity

48
Q

number of carcinogens known to humans (group 1)

A

126

49
Q

number of carcinogens in group 2A

A

2A: probably carcinogenic, 94

50
Q

number of carcinogens in group 2B

A

2B: possibly carcinogenic, 322

51
Q

number of carcinogens in group 3

A

3: not classifiable as to carcinogenicity in humans, 50 agents

52
Q

5 occupational carcinogens

A

silica
benzene
radon gas
arsenic
asbestos

53
Q

4 medicinal drugs that are carcinogenic

A

anti cancer drugs: busulphan, chlorambucil
hormonal: estrogens
immunosuppressants: cyclosporine

54
Q

Consequences of ionizing radiations + examples

A

X-rays, gamma-rays and beta particles
Ex. Hiroshima and Nagasaki = increase in leukemia, breast cancer and thyroid CA

Mechanism = damage to chromosomes: mutations and translocations

55
Q

Consequences of UV light on cancer

A

Impacts skin basal cells and squamous cells: carcinomas, melanomas.

Mechanism = formation of pyrimidine dimers, damaging DNA and overwhelming DNA repair mechanisms.

56
Q

Consequences of electromagnetic fields on cancer

A

Possibly carcinogenic; leukemias in children

57
Q

Bacteria causing cancer

A

H pylori (indirect/promoter: cell damage, inflammation, cytokines), causing gastric carcinoma.

58
Q

Viruses having direct effects on cancer?

A

HPV (cervix CA), EBV (lymphoma), HBV (liver CA)

59
Q

Why are cancer stem cells difficult to eliminate by therapy?

A
  • slow dividing (not amenable to chemotherapeutic drugs targeting rapidly-dividing cells)
  • express multiple drug resistance (MDR-1) factors
60
Q

Mutated ras?

A

= proliferation of cells even when there is stop signal

BLOCK A (8 decks)

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