Pathology Ese Minimals Debrecen

Front 1

1. What do hypersensitivity reactions mean?

Back 1

• They are based on normal immune responses.
• Lead to inflammation and consecutive tissue damage

Front 2

2. Which cells are the cellular mediators of tissue injury in anaphylactic hypersensitivity?

Back 2

• Mast cells.
• Circulating basophil granulocytes.

Front 3

3. Which cell type refers to anaphylactic reaction in inflammatory exsudate?

Back 3

• Eosinophil granulocytes.

Front 4

4. What is the mechanism of tissue injury in type III (immun-complex mediated)
hypersensitivity?

Back 4

• Activation of complement.
• Accumlation and activation of neutrophil granulocytes.

Front 5

5. What kind of tissue damage is typical for type III hypersensitivity reaction?

Back 5

Fibrinoid necrosis in the vessel wall (e.g. necrotising vasculitis).

Front 6

6. The effector cells in delayed (type IV.) hypersensitivity are?

Back 6

• Epithelioid cells transformed from macrophages.

Front 7

7. How long does it take from the antigen exposure (e.g. skin) to develop a delayed type
hypersensitivity reaction?

Back 7

• 2-3 days.

Front 8

8. How long does it take from the antigen exposure in the skin to develop a granuloma?

Back 8

• 2-3 weeks.

Front 9

9. What is the mechanism of killing the target cell in CD8+ T-cell cytotoxic
reactions?

Back 9

• Membrane perforation based osmotic lysis.
• Induction of apoptosis by Fas-ligand binding.

Front 10

10. What are the most common soft tissue tumors?

Back 10

• Lipoma.
• Fibroma.
• Leiomyoma.

Front 11

11. what are is the most common site of a leiomyoma?

Back 11

uterine myometrium

Front 12

12. what do we call myxoma?

Back 12

* gelitaneus connective tissue tumor
* looks like Wharton's jelly

Front 13

13. what is the main cell type in xanthoma?

Back 13

lipoid storing histiocytes

Front 14

14. what are benign blood vessel tumors called?

Back 14

hemangiomas

Front 15

15. what are the major forms of hamangiomas?

Back 15

H. cavernosum
H. capillare

Front 16

16. what is a biopsy?

Back 16

a tissue sample taked for diagnostic histopathological evaluation

Front 17

17. what is the basic priniciple of immunohistochemical methods?

Back 17

* specific binding of different antigens by test antibodies
* enzyme reaction (e.g by peroxidase) or a flurescent dye the antibody is coupled with marks the site of binding

Front 18

18. how can surgerons obtain information regarding the resetion margin during surgery with ca. 15 min?

Back 18

by intraoperative frozen section histology

Front 19

19. the basics of in site hybridization are?

Back 19

* labeled complementary DNA/RNA probes
* specific binding showed up by histochemistry
* end product highlights the requested sequence in situ

Front 20

20. what is telepathology

Back 20

telecommunication technology based histopathological consultation method.

Front 21

21. what are the conditions for primary wound healing?

Back 21

* wounds made by non-infected sharp device
* few tissue damage.
* good apposition of edges
* bleeding and inflamatory cells not significant

Front 22

22. the main features of primary wound healing?

Back 22

* fibring and collagen stick the edges to each other
* production of granulation tssue is mild
* production of collagen is mild
* the remaining scar is fine

Front 23

23. give classical examples of primary wound healing

Back 23

incisions made during plastic surgery

Front 24

24. what are the conditions of secondary wound healing?

Back 24

* large tissue destruction
* lots of tissue debris
* infection and inflamation reaction

Front 25

25. what is the process of secondary wound healing

Back 25

* the wound cavity is gradually filled with granulation tussue.
* massive collagen production
* terminates with a large scar

Front 26

26. give classical example of secndary wound healing

Back 26

dog bite, burns

Front 27

27. stem cells applied for theraputical purposes can be taken from where?

Back 27

* bone marrow or peripherial blood of adutls (adult stem cell)
* early, blastocytst embryo (embryonal stem cell)

Front 28

28. what is the common feature of the molecular arragnement in diffrent types of amyloidosis?

Back 28

the macro-molecular conformation of beta pleated sheets

Front 29

29. what forms of amyloid do you know?

Back 29

* Amyloid AA (amyloid associated) occuring in patients with chronic diseases inducing pronounced tissue destruction.
* amyloid AL (amyloid light chain) occuring in patients with abnormal proliferation of cells of B type origin

Front 30

30. how can you detect amyloid in a slide?

Back 30

* congo-red staining
* bi-refringence in polarized light

Front 31

31. what is dyplasia?

Back 31

* preneoplastic condition
* it occurs principally in epithelia
* early recognition and surgical removal prevents tumor formation

Front 32

32. morphological sings og dysplasia?

Back 32

* nuclear polymorphism
* thecell nuclei get hyperchromatic.
* number of mitotic figures increases
* distrubed cell polarity

Front 33

33. CIN stands for?

Back 33

cervical intraepithelial neoplasia

Front 34

34. what is the meaning of the CIN categories?

Back 34

they mark diffrent grades of preneoplastic alteration of squamous epithelium of the uterine cervix

Front 35

35. what does CIN III mean?

Back 35

* dysplasia of the whole thickness of the epithelium.
* the basement membrane is still intact, no sign of invasive growth
* it's a carcinoma in situ

Front 36

36. what is the staging of tumors

Back 36

the objective discription of tumor extent in in the body of a patient.

Front 37

37. what does TNM stand for?

Back 37

* the size of the tumor in cenimeters (T=primary tumor)
* extension of lymph node involvement (N=lymph node metastasis)
* presence of organ metastasis (M=organ metastasis)

Front 38

38. what is the grading of tumors?

Back 38

estimation of the malignancy level of a tumor based on its microscopical morphology

Front 39

39. what is the basis of tumor ploidy determination?

Back 39

the quantity of DNA-binding stain (DNA index)

Front 40

40. what is the DNA index?

Back 40

ratio of the tumor cell DNA content/DNA content of normal cell

Front 41

41. what is the meaning of homeostasis?

Back 41

* physiological steady state
* the cells ability for adaptation

Front 42

42. adaption at the cellular level by canges in cell growth?

Back 42

* atrophy
* involution
* hypertrophy

Front 43

43. adaptation at cellular level by changes of cellular diffrentation

Back 43

metaplasia

Front 44

44. what is the meaning of atrophy?

Back 44

reduction in the functional volume of the cell (atrophia simplex)

Front 45

45. factors leading to atrophy

Back 45

* reduced activity
* reduced blood supply
* unsatisfactory alimentation
* laspe of nerve stimulation
* lack of the hormonal stimulation

Hint 45

5 answers

Front 46

46. the main biological mechanisms of atrophy

Back 46

* the ubiquitin-proteosome system
* cellular autophagy

Front 47

47. what is the meaning of involution?

Back 47

* reduction of the volume of the functional cells by atrophy (atrophia simplex)
* reduction of the number of the functional cells by apoptosis (atrophia numberica)

Front 48

48. what is the meaning of hyperplasia?

Back 48

organ enlargment by the increase of the number of functioning cells

Front 49

49. what is the meaning of hypertrophy?

Back 49

organ enlargement due to the increase of the volume of the individal cells

Front 50

50. what is the meaning of cellular injury?

Back 50

* failure of adaptation
* loss of cellular function

Front 51

51. the mechanism of hypoxic ot toxic cellular swelling?

Back 51

sodium and water influx into the cells

Front 52

52. the meaning of cell necrosis?

Back 52

* cell/tissue death in a living oragnism
* the sum of morphological changes within dead cells

Front 53

53. the pathomechanism of coagulative necrosis

Back 53

* coagulation of cells/tissue proteins
* denaturation of cytoplasmic proteins including hydrolytic enzymes

Front 54

54. the forms of coagulative necrosis

Back 54

* infarction
* caseous necrosis ("chesse like"
* Zenker-type necrosis (e.g typhus, tetanus)
* slough nectrosis (necrosis crutosa)
* fibrinoid necrosis (in arteriole wall)

Front 55

55. the basic features of the liqufactive necorsis

Back 55

* in tissues rich in fluid and lipoid and poor in proteins
* predominant swelling and fluidizing
* can be secodary to coagulative necrosis

Front 56

56. the basic features of enzymatic fat cell necrosis

Back 56

* escape of pancreatic lipase
* neutral fat is digested into fatty acid and glycerol
* can be secodary to coagulative necrosis

Front 57

57. what are the major criterias for the treatment decision in malignant disease?

Back 57

* histopatholigcal grading
* pathological staging

Front 58

58. what is the pathology based deffinition of diffrentionation?

Back 58

the deviance of the tumor cell phenotype from its cell-of-origin

Front 59

59. what is the pathology based definition of anaplasia?

Back 59

lack of cellular diffrentiation

Front 60

60. what types of tumor-progression are you aware of?

Back 60

* clinical progression(size, dissemination)
* biological/histopathological progression (de-differentiation/anaplasia)

Front 61

61. the main point of the molecular cancer screening?

Back 61

* detection of the germ line mutations
* that may be associated with genetic disoeders which may predispose for cancer

Front 62

62. presentation forms of gene amplfication on chromosomal preparations?

Back 62

* chromosomally intergrated homogenous staninig region (HSR)
* extra chromosomal double minutes

Front 63

63. Name gene amplifications with basic clinical impact?

Back 63

• N-MYC gene amplification in neuroblastomas.
• HER-2/NEU amplification in breast cancer.

Front 64

64. List two well-known prognostic histopathological protocols?

Back 64

• Nottingham Prognostic Index (NPI) in breast cancer.
• Gleason-score in prostate cancer.

Front 65

65. What is the basis of different skin colors?

Back 65

• The intensity of melanin synthesis in the melanocytes.
• The number of melanocytes in the skin does not differ.

Front 66

66. What is a lentigo?

Back 66

• Epidermal melanocyte hyperplasia

Front 67

67. What is a melanocytic naevus?

Back 67

• Benign tumor of the melanocytes (neoplasia).

Front 68

68. Forms of the melanocytic naevi are?

Back 68

• Junctional naevus.
• Compound naevus.
• Intradermal naevus.

Front 69

69. What is the precancerous lesion of the malignant melanoma?

Back 69

• Dysplastic naevus

Front 70

70. What are the macroscopic features of benign melanocytic lesions?

Back 70

• They are macular.
• They are hyperpigmented (dark brown).

Front 71

71. What are the risk factors for metastatizing in malignant melanomas?

Back 71

• Depth of penetration.
• Mitotic rate.
• Epidermal ulceration.
• Epithelioid cell type.

Front 72

72. What do we understand under congestion?

Back 72

• Intravascular stasis.

Front 73

73. What kinds of congestions are known?

Back 73

• arterial (active)
• venous (passive)

Front 74

74. How would you define hyperaemia?

Back 74

• Increased blood flow in small vessels of tissues and organs.
• Active arterial stasis.

Front 75

75. Definition of oedema

Back 75

• Extravascular and interstitial accumulation of transudate fluid.

Front 76

76. What are the morphologic features of oedema?

Back 76

• macroscopically: tissue swelling, increase in weight
• microscopically: widening of the extracellular space

Front 77

77. What kind of oedemas are known? Name examples

Back 77

• focal oedema – laryngeal oedema
• diffuse oedema – anasarca
• lymphoedema – elephantiasis
• intracavital oedema or hydrops – hydrothorax, hydropericardium, ascites
• circumscribed: urtica, papula, vesicula, bulla

Hint 77

5 answers

Front 78

78. What kinds of pathomechanisms cause oedema?

Back 78

• rise in hidrostatic pressure
• drop of plasma oncotic pressure
• increase of vascular permeability
• lymphatic stasis

Front 79

79. Name examples of increased hydrostatic pressure

Back 79

* chronic right heart failure
• venous thrombosis
• hepatic cirrhosis with parenchymal decompensation
• pregnancy

Front 80

80. Name examples of decreased plasma oncotic pressure!

Back 80

• chronic renal failure
• hepatic cirrhosis with parenchymal decompensation
• starvation (inanitio)
• low protein malnutrition

Front 81

81. Give examples for increased capillary permeability!

Back 81

• bacteriotoxins
• hypoxia
• inflammation

Front 82

82. Give examples of oedema caused by lymphatic congestion.

Back 82

• excision of a lymphnode (block-dissection)
• neoplastic lymphnodes
• inflammation and scarring of lymphnodes

Front 83

83. What are the major causes of pulmonary oedema?

Back 83

• acute right heart failure (acute pulmonary oedema)
• chronic left heart failure (induratio brunea pulmonum)
• hypoperfusion (ARDS=Adult Respiratory Distress Syndrome)

Front 84

84. What are the major forms of brain oedema?

Back 84

• focal (brain abcess)
• diffuse (encephalitis, right heart failure, superior vena cava syndrome)

Front 85

85. What is thrombosis?

Back 85

• Intravascular coagulation of blood in living organisms

Front 86

86. What types of thrombi do you know?

Back 86

• red thrombus – coagulation
• white thrombus – precipitation (conglutination)
• mixed or laminated thrombus (red and white components)
• hyalin thrombus (fibrin microthrombus usualy in DIC)
• complex thrombus

Front 87

87. What types of thrombosis can be distinguished?

Back 87

• arterial
• venous (phlebothrombosis, deep veins in the lower extremities, portal vein)
• intracavital thrombus of the heart (mural thrombus or vegetatio globulosa)

Front 88

88. What facilitates the development of thrombosis?

Back 88

• endothelial lesion
• deceleration of the bloodflow (congestion)
• dilatated vessels (turbulence)
• increased blood coagulation (hyperviscosity syndrome, thrombocytosis, activation and
accumulation of coagulation factors)

Front 89

89. What is embolisation?

Back 89

• detached intravascular solid, liquid or gas material
• that is carried by the blood flow to a distant site from its point of origin.

Front 90

90. What forms of emboli can be differentiated:

Back 90

• endogenous
• exogenous

Front 91

91. Endogenous sources of emboli:

Back 91

• thrombus
• tissue particles
• cells (trauma, tumor)
• fat
• amniotic fluid
• atheroma (cholesterin crystals in the renal capillaries)
• gas-embolisation (Caisson-syndrome or decompression-syndrome)

Front 92

92. Exogen sources of emboli

Back 92

air embolisation
• foreign body

Front 93

93. What is hamorrhagia?

Back 93

• In living organisms both cellular and non-cellular components of the blood extravasate.

Front 94

94. What are the causes of haemorrhagia?

Back 94

• Discontinuity of the vessel wall. (Haemorrhagia per rhexim, haemorrhagia per
arrosionem)
• Step-over bleeding (haemorrhagia per diapedesim) occurs only at the capillaries.

Front 95

95. What are the causes of haemorrhagia per rhexim?

Back 95

• injury of the vessel wall (cut, puncture, contusion, incision)
• spontaneous rupture of the vessel wall (atherosclerosis, media necrosis, aneurysma,
varyx)

Front 96

96. What can be the causes of haemorrhagia per arrosionem?

Back 96

• ulcer (stomach or duodenal)
• inflammation (TBC in lung)
• tumor (malignant tumors)

Front 97

97. What is haemothorax?

Back 97

• Accumulation of blood in the thorax

Front 98

98. What is haemopericardium?

Back 98

• Accumulation of blood in the pericardial cavity.

Front 99

99. What is the medical expression for the accumulation of blood in the peritoneal cavity?

Back 99

• Haemoperitoneum or haemascos

Front 100

100. What can be termed „haemocephalus internus”?

Back 100

Accumulation of blood in the cerebral ventricules

Front 101

101. What can be termed „haemocephalus externus”?

Back 101

Accumulation of blood in the subarachnoideal spaces

Front 102

102. What can be termed „haematometra”?

Back 102

• Accumulation of blood in the uterine cavity.

Front 103

103. What can be termed „haemarthros”?

Back 103

• Accumulation of blood in the synovial cavity

Front 104

104. What can be termed „petechia”?

Back 104

• Small, spot like, 1-2 mm in diameter bleeding

Front 105

105. What can be termed „purpura”?

Back 105

• Multiple, small bleedings ranging in diameter from 3mm to 1cm.

Front 106

106. What can be termed „suffusio” or „sugillatio”?

Back 106

• Lamellar bleeding in the subcutaneous connective tissue

Front 107

107. What can be termed „haematoma”?

Back 107

• Extensive interstitial bleeding causing volume expansion

Front 108

108. What can be termed „ecchymosis”?

Back 108

• 1-2 cm in diameter or larger patchy bleeding. Mostly occurs subcutaneously

Front 109

109. What can be termed „apoplexia”?

Back 109

Bleeding causing tissue destruction

Front 110

110. What is „exsanguinatio”?

Back 110

Bleeding to death. Loosing a significant amount of blood in a short time

Front 111

111. What is the medical expression for blood in the urine?

Back 111

• Haematuria

Front 112

112. What is the medical expression for blood in the vomitus?

Back 112

Haematemesis.

Front 113

113. What is the medical expression for blood in the sputum?

Back 113

Haemoptoe.

Front 114

114. What is the medical expression for nose bleeding?

Back 114

Epistaxis.

Front 115

115. What is the medical expression for the stool containing digested blood?

Back 115

Melaena

Front 116

116. What is the medical expression for the stool containing fresh blood?

Back 116

Haematocchesia.

Front 117

117. Classification of the inflammation according to its extension.

Back 117

• local (circumscribed)
• generalized (sepsis)

Front 118

118. Classification of the inflammation according to its duration

Back 118

• hyperacute
• acute
• subacute
• chronic

Front 119

119. What does pus contain?

Back 119

• Tissue debris
• Fibrin
• Neutrophil granulocytes
• Bacteria

Front 120

120. What are the ancient classical symptoms of the acute inflammation?

Back 120

• Rubor
• Tumor
• Calor
• Dolor
• Functio laesa

Front 121

121. How do we categorise the acut inflammation in virtue of the exudate?

Back 121

• Serous
• Fibrinous
• Purulent or suppurative
• Hemorrhagic
• Gangrenous

Front 122

122. What is characteristic for serous inflammation?

Back 122

• Occurs in tissue interstitium and cavities of the body
• presents as serum like serous fluid
• The mildest form of inflammation.

Front 123

123. What is characteristic for fibrinous inflammation?

Back 123

• Starts with serum exudation.
• Exudate becomes sero-fibrinous
• Thick layer of fibrin may precipitate

Front 124

124. What is characteristic for purulent inflammation?

Back 124

• Bacterial infections.
• Leukodiapedesis.
• Pus production.

Front 125

125. What is folliculitis?

Back 125

• Purulent inflammation of the skin’s sporrans

Front 126

126. What is the name of the deep inflammation skin affecting the sebaceous glands?

Back 126

• Furuncule

Front 127

127. What is carbuncule?

Back 127

Deep inflammation developed by the fusion of furuncules

Front 128

128. What is pustule?

Back 128

Pus filled vesicles of the superficial epidermis (varicella).

Front 129

129. What is characteristic for a chronic abscess?

Back 129

• it is lined with a thick wall.
• The inner layer is the so called pyogenic wall (granulation tissue infiltrated by
neutrophiles)
• The outer layer is the cell depleted scar tissue.

Front 130

130. How do we call an anatomical cavity filled with pus?

Back 130

• Empyema.

Front 131

131. What is a phlegmone?

Back 131

Inflammatory exudate spreading freely along the tissue interstitium

Front 132

132. What is characteristic for hemorrhagic inflammation?

Back 132

• Endothel injury
• Erythrodiapedesis
• Blood stained exudate
• May follow serous or purulent inflammation.

Front 133

133. What is characteristic for gangrenous inflammation?

Back 133

• Exudation is only in the background.
• The dominant feature is the tissue necrosis.
• The immune response is deficient.
• The causing microorganisms are putrifying bacterias.

Front 134

134. Types of gangrene are?

Back 134

• Dry (sicca)
• Wet (humida).

Front 135

135. What could be the outcome of the acute inflammation?

Back 135

• Complete healing (restitutio ad intergum).
• Fibrosis or scar.
• Abscess formation.
• Chronic inflammation

Front 136

136. Types of chronic inflammation are?

Back 136

• Immun-mediated chr. inflammations.
• Non immun-mediated chr. inflammations.
• Granulomatous inflammations.

Front 137

137. Steps of tissue regeneration?

Back 137

• Production of granulation tissue.
• Resolution of granulation tissue.
• Fibrosis.
• Scar.

Front 138

138. Types of wound healing?

Back 138

• Primary wound healing (sanatio vulneris per primam intentionem).
• Under scale wound healing (for example umbilical cord).
• Secondary wound healing (sanatio vulneris per secundam intentionem).

Front 139

139. Larger mass of eosinophil granulocytes indicate what cause of the inflammation?

Back 139

• Allergic inflammation.
• Fungal inflammation.

Front 140

140. Large mass of lymphocytes and plasma cells indicate what cause of inflammation?

Back 140

• Chronic or immunomediated inflammation

Front 141

141. Larger mass of epitheloid type macrophages indicate what cause of inflammation?

Back 141

• Type IV. immunomediated inflammation.

Front 142

142. Main reasons of anemia?

Back 142

• Decrease in red blood cell production.
• Hemolysis.
• Bleeding

Front 143

143. Circumstances leading to iron deficiency anemia?

Back 143

• Low iron intake.
• Iron malabsorption.
• Incrised demands.
• Chronic blood loss.
• Malignant diseases.

Front 144

144. What are the major features of aplastic anaemia?

Back 144

• Bone marrow stem cell disease.
• Trilinear bone marrow aplasia.
• Pancytopenia.

Front 145

145. Which are the chronic myeloproliferative diseases?

Back 145

• Chronic myelogenous leukemia(CML).
• Essential thrombocytemia.
• Polycythemia vera.
• Chronic idiopathic myelofibrosis.

Front 146

146. Phases of the CML?

Back 146

• Chronic phase.
• Accelerated phase.
• Blastic crisis.

Front 147

147. The characteristic genetic abnormality in CML?

Back 147

• Philaderphia-translocation

Front 148

148. Phases of polycythemia vera and their characteristics?

Back 148

• Proliferative phase: trilinear proliferation.
• Postpolycythaemic phase: myelofibrosis

Front 149

149. Characteristic signs of essential thrombocytaemia?

Back 149

• Isolated bone marrow megakaryocyte growth.
• Chronic platelet overproduction.
• Increased tendency for thrombosis

Front 150

150. Characteristic signs of myelofibrosis?

Back 150

• Collagen fibrosis in the bone marrow.
• Extramedullary haematopoesis.
• Leukoerythroblastic blood picture

Front 151

151. What is refractory anemia refractory for?

Back 151

Substitution therapy

Front 152

152. What features determine the outcome of the myelodysplastic syndrome?

Back 152

• the degree of pancytopenia
• the blast rate (leukemic transformation).

Front 153

153. What is the basic requirement for the diagnosis of acute myeloid leukemia?

Back 153

the blast rate in the bone marrow is higher than 20%.

Front 154

154. How do we classify malignant lymphomas according to the clinical course of disease?

Back 154

• Indolent
• Agressive

Front 155

155. How do we classify malignant lymphomas according to the cellular development?

Back 155

• Precursor
• Peripherial

Front 156

156. What is MGUS?

Back 156

• Monoclonal gammopathy of undetermined significance

Front 157

157. What are the characteristic features of plasma cell myeloma?

Back 157

• Monoclonal plasma cell tumor
• Monoclonal gammopathy
• Osteolytic bone lesions
• Pathologic fractures

Front 158

158. Types of Hodgkin's lymphoma?

Back 158

• Nodular lymphocyte predominant Hodgkin's lymphoma
• Classical Hodgkin's lymphoma

Front 159

159. Which cells are typical for Hodgkin's lymphoma?

Back 159

• Hodgkin cells
• mirror cells
• Sternberg-Reed cells

Front 160

160. Occurrance of Burkitt's lymphoma according to its etiology

Back 160

• Endemic (EBV associated)
• Sporadic
• Immunodeficiency associated (HIV associated)

Front 161

161. Most frequent primary sites of extranodal lymphomas?

Back 161

• GI tract
• Skin
• Respiratory tracts
• Mediastinum

Front 162

162. What is MALT standing for?

Back 162

• Mucosa associated lymphoid tissue

Front 163

Helicobacter pylori163. Which microorganism has a causative role in the development of the MALT lymphoma
of the stomach?

Back 163

Helicobacter pylori

Front 164

164. What is mycosis fungoides?

Back 164

The most common cutaneous T-cell lymphoma

Front 165

165. What is Sezary syndrome?

Back 165

Leukemic manifestation of the mycosis fungoides