|1. What do hypersensitivity reactions mean?||
• They are based on normal immune responses.
• Lead to inflammation and consecutive tissue damage.
|2. Which cells are the cellular mediators of tissue injury in anaphylactic hypersensitivity?||
• Mast cells.
• Circulating basophil granulocytes.
|3. Which cell type refers to anaphylactic reaction in inflammatory exsudate?||
• Eosinophil granulocytes.
|4. What is the mechanism of tissue injury in type III (immun-complex mediated)||
• Activation of complement.
• Accumlation and activation of neutrophil granulocytes.
|5. What kind of tissue damage is typical for type III hypersensitivity reaction?||
• Fibrinoid necrosis in the vessel wall (e.g. necrotising vasculitis).
|6. The effector cells in delayed (type IV.) hypersensitivity are?||
• Epithelioid cells transformed from macrophages.
|7. How long does it take from the antigen exposure (e.g. skin) to develop a delayed type hypersensitivity reaction?||
• 2-3 days.
|8. How long does it take from the antigen exposure in the skin to develop a granuloma?||
• 2-3 weeks.
|9. What is the mechanism of killing the target cell in CD8+ T-cell cytotoxic reactions?||
• Membrane perforation based osmotic lysis.
• Induction of apoptosis by Fas-ligand binding.
|10. What are the most common soft tissue tumors?||
|11. What is the most common site of a leiomyoma?||
• Uterine myometrium.
|12. What do we call myxoma?||
• Gelatinous connective tissue tumor.
• Looks like the fetal Wharton’s jelly.
|13. What is the main cell type in xanthoma?||
• Lipoid storing histiocytes.
|14. How are benign blood vessel tumors called?||
|15. What are the major forms of hemangiomas?||
• H. cavernosum.
• H. capillare.
|16. What is a biopsy?||
• A tissue sample taken for diagnostic histopathological evaluation
|17. What is the basic principle of immunohistochemical methods?||
• Specific binding of different antigens by test antibodies
• Enzyme reaction ( e.g. with peroxydase ) or a fluorescent dye the antibody is coupled with, marks the site of binding
|18. How can surgeons obtain information regarding the resection margain during surgery within ca.15 minutes?||
• By intraoperative frozen section histology.
|19. The basics of in situ hybridization are?||
• Labeled complementary DNA or RNA probe
• Specific binding showed up by histochemistry.
• End product highlights the requested sequence in situ.
|20. What is telepathology?||
• Telecommunication technology based histopathological consultation method.
|21. What conditions are required for primary wound healing?||
• Wounds made by non infected sharp devices.
• Few tissue demage.
• Good apposition of edges.
• Bleeding and inflammatory cells not significant
|22. The main features of primary wound healing?||
• Fibrin and collagen stick the edges to each other.
• Production of granulation tissue is mild.
• Production of collagen is mild.
• The remaining scar is fine.
|23. Give a classical example of primary wound healing?||
• incisions made during plastical surgery.
|24. What are the conditions of secondary wound healing?||
• Large tissue destruction.
• Lot of tissue debris.
• Infection and inflammatory reaction.
|25. What is the process of secondary wound healing?||
• the wound cavity is gradually filled with granulation tissue.
• massive collagen production.
• Terminates with a large scar.
|26. Give classical examples of secondary wound healing?||
• Dog biting.
|27. Stem cells applied for therapeutical purposes might be taken from where?||
• Bone marrow or peripheral blood of adults (adult stem cell).
• Early, blastocyst embryo (embryonal stem cell).
|28. What forms of amyloid do you know?||
• Amyloid AA (i.e. amyloid associated) occurring in patients with chronic diseases inducing pronounced tissue destruction.
• Amyloid AL (i.e. amyloid light chain) occurring in patients with abnormal proliferation of cells of B lymphocytic origin.
|29. What is the common feature of the molecular arrangement in different types of amyloidosis?||
• The macro-molecular conformation of beta-pleated sheets.
|30. How can you detect amyloid in a slide?||
• Congo-red staining.
• Bi-refringance in polarized light.
|31. What is dysplasia?||
• Preneoplastic condition.
• It occurs principally in epithelia.
• Early recognition and surgical removal prevents tumor formation.
|32. Morphological signs of dysplasia?||
• Nnuclear polymorphism.
• The cell nuclei get hyperchromatic.
• Number of mitotic figures increases.
• Disturbed cell polarity.
|33. CIN is the acronym for?||
• Cervical Intraepithelial Neoplasia.
|34. What is the meaning of the CIN categories?||
• They mark different grades of preneoplastic alteration of the squamous epithelium of the uterine cervix.
|35. What does CIN – III mean?||
• Dysplasia of the whole thickness of epithelium.
• The basement membrane is still intact, no sign of invasive growth
• It is an in situ carcinoma.
|36. What is the stagning of tumors?||
• The objective description of tumor extension in the body of a patient.
|37. What is TNM standing for?||
• The size of primary tumor in centimeters (T= primary tumor).
• Extension of lymph node involvement (N = lymph node metastasis).
• Presence of organ metastases (M = organ metastasis).
|38. What is grading of tumors?||
• Estimation of the malignancy level of a tumor based on its microscopical morphology.
|39. What is the basis of tumor ploidy determination?||
• the quantity of a DNA-binding stain (DNA index).
|40. What is DNA index?||
• DNA content of tumor cells / DNA content of normal cells.
|41. What is the meaning of homeostasis?||
• Physiological steady state.
• The cells ability for adaptation.
|42. Adaptation at cellular level by changes in cell growth||
|43. Adaptation at cellular level by changes of cellular differentiation||
|44. What is the meaning of atrophy?||
• Reduction of the functional cell volume (atrophia simplex).
|45. Factors leading to atrophy||
• Reduced activity
• Reduced blood supply
• Unsatisfactory alimentation
• Lapse of the nerve stimulation
• Lack of the hormonal stimulation
|46. The main biological mechanisms of atrophy||
• the ubiquitin-proteasome system
• cellular autophagy
|47. What is the meaning of involution?||
• Reduction of the volume of the functional cells by atrophy (atrophia simplex)
• Reduction of the number of the functional cells by apoptosis (atrophia numerica).
|48. What is the meaning of hypertrophy?||
• Organ enlagement by the increase of the volume of individual cells
|49. What is the meaning of hyperplasia?||
• Organ enlagement by the increase of the number of functioning cells.
|50. What is the meaning of cellular injury?||
• Failure of adaptation
• Loss of cellular function
|51. The mechanism of hypoxic or toxic cellular swelling||
• Sodium and water influx into the cells.
|52. The meaning of cell necrosis||
• Cell or tissue death in a living organism.
• The sum of morphological changes within dead cells.
|53. The pathomechanism of coagulative necrosis||
• Coagulation of cells/tissue proteins.
• Denaturation of cytoplasmic proteins including hydrolytic enzymes.
|54. The forms of coagulative necrosis||
• Caseous necrosis (necrosis caseosa)
• Fibrinoid necrosis (in arterial walls)
• Slough necrosis (necrosis crustosa)
• Zenker-type necrosis (etc. typhus, tetanus)
|55. The basic features of liquefactive necrosis||
• In tissues rich in fluid and lipoid and poor in proteins.
• Predominant swelling and fluidizing.
• Can be secondary to coagulative necrosis.
|56. The basic features of enzymatic fat cell necrosis||
• Escape of pancreatic lipase.
• Neutral fat is digested into fatty acid and glycerol.
• Formation of calcium soaps from fatty acids.
|57. What are the major criterias for treatment decision in malignant disease?||
• Histopathological grading.
• Pathological staging.
|58. What is the pathology-based definition of differentiation?||
• The deviance of the tumor cell phenotype from its cell-of-origin.
|59. What is the pathology-based definition of anaplasia?||
• Lack of cellular differentiation.
|60. What types of tumor-progression are you aware of?||
• Clinical progression (size, dissemination).
• Biological/histopathological progression (dedifferentiation/anaplasia).
|61. The main point of molecular cancer screening?||
• detection of germ line mutations,
• that may be associated with genetic disorders which may predispose for cancer.
|62. Presentation forms of gene amplification in chromosomal preparations?||
• Chromosomally integrated homogeneous staining region (HSR).
• Extra chromosomal double minutes.
|63. Name gene amplifications with basic clinical impact?||
• N-MYC gene amplification in neuroblastomas.
• HER-2/NEU amplification in breast cancer.
|64. List two well-known prognostic histopathological protocols?||
• Nottingham Prognostic Index (NPI) in breast cancer.
• Gleason-score in prostate cancer.
|65. What is the basis of different skin colors?||
• The intensity of melanin synthesis in the melanocytes.
• The number of melanocytes in the skin does not differ.
|66. What is a lentigo?||
• Epidermal melanocyte hyperplasia.
|67. What is a melanocytic naevus?||
• Benign tumor of the melanocytes (neoplasia).
|68. Forms of the melanocytic naevi are?||
• Junctional naevus.
• Compound naevus.
• Intradermal naevus.
|69. What is the precancerous lesion of the malignant melanoma?||
• Dysplastic naevus.
|70. What are the macroscopic features of benign melanocytic lesions?||
• They are macular.
• They are hyperpigmented (dark brown).
|71. What are the risk factors for metastatizing in malignant melanomas?||
• Depth of penetration.
• Mitotic rate.
• Epidermal ulceration.
• Epithelioid cell type.
|72. What do we understand under congestion?||
• Intravascular stasis.
|73. What kinds of congestions are known?||
• arterial (active)
• venous (passive)
|74. How would you define hyperaemia?||
• Increased blood flow in small vessels of tissues and organs.
• Active arterial stasis.
|75. Definition of oedema||
• Extravascular and interstitial accumulation of transudate fluid.
|76. What are the morphologic features of oedema?||
• macroscopically: tissue swelling, increase in weight
• microscopically: widening of the extracellular space
|77. What kind of oedemas are known? Name examples||
• circumscribed: urtica, papula, vesicula, bulla
• diffuse oedema – anasarca
• focal oedema – laryngeal oedema
• intracavital oedema or hydrops – hydrothorax, hydropericardium, ascites
• lymphoedema – elephantiasis
|78. What kinds of pathomechanisms cause oedema?||
• rise in hidrostatic pressure
• drop of plasma oncotic pressure
• increase of vascular permeability
• lymphatic stasis
|79. Name examples of increased hydrostatic pressure||
• chronic right heart failure
• venous thrombosis
• hepatic cirrhosis with parenchymal decompensation
|80. Name examples of decreased plasma oncotic pressure!||
• chronic renal failure
• hepatic cirrhosis with parenchymal decompensation
• starvation (inanitio)
• low protein malnutrition
|81. Give examples for increased capillary permeability!||
|82. Give examples of oedema caused by lymphatic congestion.||
• excision of a lymphnode (block-dissection)
• neoplastic lymphnodes
• inflammation and scarring of lymphnodes
|83. What are the major causes of pulmonary oedema?||
• acute right heart failure (acute pulmonary oedema)
• chronic left heart failure (induratio brunea pulmonum)
• hypoperfusion (ARDS=Adult Respiratory Distress Syndrome)
|84. What are the major forms of brain oedema?||
• focal (brain abcess)
• diffuse (encephalitis, right heart failure, superior vena cava syndrome)
|85. What is thrombosis?||
• Intravascular coagulation of blood in living organisms.
|86. What types of thrombi do you know?||
• red thrombus – coagulation
• white thrombus – precipitation (conglutination)
• mixed or laminated thrombus (red and white components)
• hyalin thrombus (fibrin microthrombus usualy in DIC)
• complex thrombus
|87. What types of thrombosis can be distinguished?||
• venous (phlebothrombosis, deep veins in the lower extremities, portal vein)
• intracavital thrombus of the heart (mural thrombus or vegetatio globulosa)
|88. What facilitates the development of thrombosis?||
• endothelial lesion
• deceleration of the bloodflow (congestion)
• dilatated vessels (turbulence)
• increased blood coagulation (hyperviscosity syndrome, thrombocytosis, activation and
accumulation of coagulation factors)
|89. What is embolisation?||
• detached intravascular solid, liquid or gas material
• that is carried by the blood flow to a distant site from its point of origin
|90. What forms of emboli can be differentiated:||
|91. Endogenous sources of emboli:||
• tissue particles
• cells (trauma, tumor)
• amniotic fluid
• atheroma (cholesterin crystals in the renal capillaries)
• gas-embolisation (Caisson-syndrome or decompression-syndrome)
|92. Exogen sources of emboli||
• air embolisation
• foreign body
|93. What is hamorrhagia?||
• In living organisms both cellular and non-cellular components of the blood extravasate.
|94. What are the causes of haemorrhagia?||
• Discontinuity of the vessel wall. (Haemorrhagia per rhexim, haemorrhagia per
• Step-over bleeding (haemorrhagia per diapedesim) occurs only at the capillaries.
|95. What are the causes of haemorrhagia per rhexim?||
• injury of the vessel wall (cut, puncture, contusion, incision)
• spontaneous rupture of the vessel wall (atherosclerosis, media necrosis, aneurysma,
|96. What can be the causes of haemorrhagia per arrosionem?||
• ulcer (stomach or duodenal)
• inflammation (TBC in lung)
• tumor (malignant tumors)
|97. What is haemothorax?||
• Accumulation of blood in the thorax.
|98. What is haemopericardium?||
• Accumulation of blood in the pericardial cavity.
|99. What is the medical expression for the accumulation of blood in the peritoneal cavity?||
• Haemoperitoneum or haemascos.
|100. What can be termed „haemocephalus internus”?||
• Accumulation of blood in the cerebral ventricules.
|101. What can be termed „haemocephalus externus”?||
• Accumulation of blood in the subarachnoideal spaces.
|102. What can be termed „haematometra”?||
• Accumulation of blood in the uterine cavity.
|103. What can be termed „haemarthros”?||
• Accumulation of blood in the synovial cavity.
|104. What can be termed „petechia”?||
• Small, spot like, 1-2 mm in diameter bleeding.
|105. What can be termed „purpura”?||
• Multiple, small bleedings ranging in diameter from 3mm to 1cm.
|106. What can be termed „suffusio” or „sugillatio”?||
• Lamellar bleeding in the subcutaneous connective tissue.
|107. What can be termed „haematoma”?||
• Extensive interstitial bleeding causing volume expansion.
|108. What can be termed „ecchymosis”?||
• 1-2 cm in diameter or larger patchy bleeding. Mostly occurs subcutaneously.
|109. What can be termed „apoplexia”?||
• Bleeding causing tissue destruction.
|110. What is „exsanguinatio”?||
• Bleeding to death. Loosing a significant amount of blood in a short time.
|111. What is the medical expression for blood in the urine?||
|112. What is the medical expression for blood in the vomitus?||
|113. What is the medical expression for blood in the sputum?||
|114. What is the medical expression for nose bleeding?||
|115. What is the medical expression for the stool containing digested blood?||
|116. What is the medical expression for the stool containing fresh blood?||
|117. Classification of the inflammation according to its extension.||
• local (circumscribed)
• generalized (sepsis)
|118. Classification of the inflammation according to its duration.||
|119. What does pus contain?||
• Tissue debris
• Neutrophil granulocytes
|120. What are the ancient classical symptoms of the acute inflammation?||
• Functio laesa
|121. How do we categorise the acut inflammation in virtue of the exudate?||
• Purulent or suppurative
|122. What is characteristic for serous inflammation?||
• Occurs in tissue interstitium and cavities of the body
• presents as serum like serous fluid
• The mildest form of inflammation.
|123. What is characteristic for fibrinous inflammation?||
• Starts with serum exudation.
• Exudate becomes sero-fibrinous
• Thick layer of fibrin may precipitate
|124. What is characteristic for purulent inflammation?||
• Bacterial infections.
• Pus production.
|125. What is folliculitis?||
• Purulent inflammation of the skin’s sporrans.
|126. What is the name of the deep inflammation skin affecting the sebaceous glands?||
|127. What is carbuncule?||
• Deep inflammation developed by the fusion of furuncules.
|128. What is pustule?||
• Pus filled vesicles of the superficial epidermis (varicella).
|129. What is characteristic for a chronic abscess?||
• 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.
|130. How do we call an anatomical cavity filled with pus?||
|131. What is a phlegmone?||
• Inflammatory exudate spreading freely along the tissue interstitium.
|132. What is characteristic for hemorrhagic inflammation?||
• Endothel injury
• Blood stained exudate
• May follow serous or purulent inflammation.
|133. What is characteristic for gangrenous inflammation?||
• Exudation is only in the background.
• The dominant feature is the tissue necrosis.
• The immune response is deficient.
• The causing microorganisms are putrifying bacterias.
|134. Types of gangrene are?||
• Dry (sicca)
• Wet (humida).
|135. What could be the outcome of the acute inflammation?||
• Complete healing (restitutio ad intergum).
• Fibrosis or scar.
• Abscess formation.
• Chronic inflammation.
|136. Types of chronic inflammation are?||
• Immun-mediated chr. inflammations.
• Non immun-mediated chr. inflammations.
• Granulomatous inflammations.
|137. Steps of tissue regeneration?||
• Production of granulation tissue.
• Resolution of granulation tissue.
|138. Types of wound healing?||
• Primary wound healing (sanatio vulneris per primam intentionem).
• Under scale wound healing (for example umbilical cord).
• Secondary wound healing (sanatio vulneris per secundam intentionem).
|139. Larger mass of eosinophil granulocytes indicate what cause of the inflammation?||
• Allergic inflammation.
• Fungal inflammation.
|140. Large mass of lymphocytes and plasma cells indicate what cause of inflammation?||
• Chronic or immunomediated inflammation
|141. Larger mass of epitheloid type macrophages indicate what cause of inflammation?||
• Type IV. immunomediated inflammation.
|142. Main reasons of anemia?||
• Decrease in red blood cell production.
|143. Circumstances leading to iron deficiency anemia?||
• Low iron intake.
• Iron malabsorption.
• Incrised demands.
• Chronic blood loss.
• Malignant diseases.
|144. What are the major features of aplastic anaemia?||
• Bone marrow stem cell disease.
• Trilinear bone marrow aplasia.
|145. Which are the chronic myeloproliferative diseases?||
• Chronic myelogenous leukemia (CML).
• Essential thrombocytemia.
• Polycythemia vera.
• Chronic idiopathic myelofibrosis.
|146. Phases of the CML?||
• Chronic phase.
• Accelerated phase.
• Blastic crisis.
|147. The characteristic genetic abnormality in CML?||
(also in AML m1)
it's a BCR-ABL fusion which causes activation of a tyrosine kinase.
|148. Phases of polycythemia vera and their characteristics?||
• Proliferative phase: trilinear proliferation.
• Postpolycythaemic phase: myelofibrosis.
|149. Characteristic signs of essential thrombocytaemia?||
• Isolated bone marrow megakaryocyte growth.
• Chronic platelet overproduction.
• Increased tendency for thrombosis.
|150. Characteristic signs of myelofibrosis?||
• Collagen fibrosis in the bone marrow.
• Extramedullary haematopoesis.
• Leukoerythroblastic blood picture.
|151. What is refractory anemia refractory for?||
• Substitution therapy.
|152. What features determine the outcome of the myelodysplastic syndrome?||
• the degree of pancytopenia
• the blast rate (leukemic transformation)
|153. What is the basic requirement for the diagnosis of acute myeloid leukemia?||
• the blast rate in the bone marrow is higher than 20%.
|154. How do we classify malignant lymphomas according to the clinical course of disease?||
|155. How do we classify malignant lymphomas according to the cellular development?||
|156. What is MGUS?||
• Monoclonal gammopathy of undetermined significance
|157. What are the characteristic features of plasma cell myeloma?||
• Monoclonal plasma cell tumor
• Monoclonal gammopathy
• Osteolytic bone lesions
• Pathologic fractures
|158. Types of Hodgkin's lymphoma?||
• Nodular lymphocyte predominant Hodgkin's lymphoma
• Classical Hodgkin's lymphoma
|159. Which cells are typical for Hodgkin's lymphoma?||
• Hodgkin cells
• mirror cells
• Sternberg-Reed cells
|160. Occurrance of Burkitt's lymphoma according to its etiology||
• Endemic (EBV associated)
• Immunodeficiency associated (HIV associated)
|161. Most frequent primary sites of extranodal lymphomas?||
• GI tract
• Respiratory tracts
|162. What is MALT standing for?||
• Mucosa associated lymphoid tissue
|163. Which microorganism has a causative role in the development of the MALT lymphoma of the stomach?||
• Helicobacter pylori
|164. What is mycosis fungoides?||
• The most common cutaneous T-cell lymphoma.
|165. What is Sezary syndrome?||
• Leukemic manifestation of the mycosis fungoides.
|List the major organ involvments in diabetes mellitus||
|Vascular changes in diabetes mellitus are||
• Hyalinos arteriolosclerosis
• Diabetic microangiopathy
|Elements of diabetic nephropathy||
• Recurrent pyelonephritis
|Forms of ischemic heart disease||
• Angina pectoris
• Acute myocardial infarction
• Chronic ischemic heart disease
• Sudden cardiac death
|Causes of reduced coronary perfusion are||
• Stenosis (atherosclerotic plaque)
• Coronary thrombosis
|The course of AMI at tissue level||
• Ischemic cell injury (swelling, myocytolysis)
• Coagulation necrosis
• Acute inflammatory infiltration
• Granulation tissue formation
|Major cardial complications of AMI||
• Cardiac arrest
• Fibrinous pericarditis
• Mural thrombosis
• Left ventricle aneurysm
• Myocardial rupture
|Major causes of cor pulmonale||
• Interstitial pulmonary fibrosis
• Tumors of the lung
|General forms of arteriosclerosis||
• Calcifying mediasclerosis (Mönckeberg)
|Stages of plaque formation in atherosclerosis||
• Fatty streaks
• Atheromatous plaque
• Fibrous atheroma
• Complicated plaque
|Clinical complications of atherosclerosis||
• Cerebral stroke
• Aortic aneurysm
• Renal insufficiency
• Peripheral arteriopathy (gangraena)
|Causes leading to chronic endothelial demage||
• Turbulent blood flow
• Toxins (nicotin)
• Viral infections
• Chronic or recurrent acute inflammations
|Major porto-caval venous anastomoses significant in portal hypertension (liver cirrhosis)||
• Esophageal venous plexus
• Retroperitoneal venous plexus
• Rectoanal (hemorrhoidal) veins
• Umbilical/abdominal veins
|Features of Barrett-esophagust?||
• Reddish spots on the esophageal mucosa
• Glandular epithelial cell metaplasia
• Complication of esophageal reflux
• Transformation potential to adenocarcinoma
|Basic components of acute gastritis||
• Mucosal erosion
• Acute inflammatory infiltration
• Superficial haemorrhage
|Basic components of chronic gastritis||
• Chronic inflammatory infiltration
• Mucosal atrophy
• Intestinal metaplasia
• Regeneratory dysplasia
|Major causes of chronic gastritis||
• Helicobacter pylori
• Autoimmune processes
|Significant factors in the development of peptic ulcers||
• H. pylori
• Non-steroid anti-inflammatory drugs
• Fast stomach emptying
|Histological layers of a chronic ulcer are||
• Superficial necrosis
• Acute inflammatory layer
• Granulation tissue layer
• Massive fibrosis
|Common complications of chronic peptic ulcers are||
• Gastric haemorrhage
|Major features of the Zollinger-Ellison syndrome are||
• Gastrin producing tumor
• Secondary glandular hyperplasia
• Formation of multiple peptic ulcers
|Benign tumors of the stomach are||
• Hyperplastic polyps
• Tumors of soft tissue and neural origin
|The most frequent non-epithelial malignant tumors of the stomach are||
|Basic features of Krukenberg-tumor||
• Bilateral ovarian metastasis
• Histological type is signet-ring cell adenocarcinoma
• Primary sites are the stomach, breast or pancreas
|Histological features of acute pancreatitis are||
• Parenchymal edema
• Acute inflammatory infiltration
• Fat necrosis
|Histological features of chronic pancreatitis||
• Parenchymal fibrosis
• Loss of acinar component
• Dilatation of ducts
|What does the acronym PanIN mean||
• Pancreatic Intraepithelial Neoplasia
|Histological features of adenocarcinoma of the pancreas||
• Tubular pattern
• Marked invasivity
|Histological features of adenocarcinoma of the pancreas||
In medicine, desmoplasia refers to the formation of adhesions or fibrosis (fibrosis refers to scar tissue) in the vascular stroma of a neoplasm. Desmoplasia originates from the Greek desmos (meaning fetter or band) and plasia (meaning to form). It is usually used in the description of desmoplastic small round cell tumors. Neoplasm (or neoplasia) is the medical term used for both benign and malignant tumors.
Basically, it's a blanket term that refers to abnormal, excessive, uncoordinated, and autonomous cellular/tissue growth.
Usually you only see desmoplasia with malignant neoplasms, which can evoke a fibrosis response by invading healthy tissue.
Infiltrating metastatic ductal carcinomas of the breast often have a scirrous, stellate appearance caused by desmoplastic formations.
|What are the common causes of ARDS||
|Major histological components in ARDS||
• Alveolar edema
• Hyaline membrane
|Bronchiectasis develops on the basis of||
• acute destructive bronchitis
|The principal mechanism of alveolar wall destruction in emphysema||
• insufficient anti-protease production
|Which histological types of bronchial carcinomas are strongly related to cigarette smoking||
• squamous cell carcinoma
• small cell lung carcinoma
|Epithelial precursor lesions of lung cancer are||
• squamous dysplasia
• atypical adenomatosus hyperplasia
• idiopathic neuroendocrine cell hyperplasia
|Paraneoplastic syndromes frequently associated with small cell lung carcinoma are||
• ACTH secretion
• ADH secretion
|The most frequent pleural primary tumors are||
• solitary fibrous tumor
• malignant mesenthelioma
|The most frequent metastatic pleural tumors are||
• lung carcinoma
• breast carcinoma
|Precancerous lesions of oral squamous cell carcinoma are||
• true (histological) leukoplakia
|Which histiological type of oral squamous cell carcinoma has the most favourable prognosis||
• verrucous carcinoma
|Hepatotrop viruses infecting through a fecal-oral route are||
• hepatitis A
• hepatitis E
|Hepatotrop viruses infecting parenterally||
• hepatitis B
• hepatitis C
• hepatitis D
|Which part of the hepatic lobule is affected by hepatocyte damage in acute hepatitis||
• centrilobular area
|Which part of the hepatic lobule is affected by hepatocyte damage in chronic active hepatitis||
• periphery of the lobule (= limiting plate)
|What is the Budd-Chiary syndrome||
• Thrombosis of the hepatic vein
|Features of focal nodular hyperlpasia of the liver are||
• Hepatocyte hyperplasia
• Well demarcated
• Central fibrous scar
|The most frequent primary carcinomas of the liver are||
• Hepatocellular carcinoma
• Cholangiocellular carcinoma
|Major features of Hirsprung disease||
• Regional lack of ganglion cells
• Functional obstruction
• Upstream dilation of the colon
|Major complications of colonic diverticulosis||
• Pericolic abscess
|Main forms of inflammatory bowel disease (IBD)||
• Crohn disease
• Ulcerative colitis
|Characteristic features of ulcerative colitis||
• Limited to the colon
• Distribution is diffuse
• Ulceration is superficial
• Pseudopolyps are marked
• Malignant potential
|Characteristic features of Crohn disease||
• Ileum and colon involved
• Skip lesions
• Deep ulcers
• Malignant potential
|Carcinomas of the large intestine are||
• Squamous cell carcinoma of the anus
|Common non-epithelial tumors of the large intestine||
|Aquired causes of hydronephrosis||
• Foreign body (stone)
|Major cause of urolithiasis||
• Supersaturation of the urine
|Major components of renal stones are||
• Calcium oxalate/phosphate
|Major causes of acute tubular necrosis||
|Forms of testicular inflammations||
|Causes of testicular inflammations||
|Testicular germ cell tumors are||
• Non-seminomatous tumors
|Non-seminomatous tumors of the testis||
• Embryonal carcinoma
• Yolk sac tumor
|The histological grading of prostate carcinomas is based on||
• The Gleason system
|Most important marker for prostate carcinoma detection and monitoring||
• Prostate specific antigen (PSA)
|Major risk factors for cervical carcinoma are||
• Multiple partners
• High-risk HPV infection
|The most effectve screening tool for the prevention of cervical cancer is||
• The Pap-smear
|Major categories of ovarian tumors||
• Surface epithelial
• Germ cell
|What is a comedo carcinoma||
• Ductal carcinoma with
• Extensive central necrosis
|DCIS is the abbreviation of||
• Ductal carcinoma in situ
|LCIS is the abbreviation of||
• Lobular carcinoma in situ
|What is Paget disease||
• Nipple infiltration by DCIS
|Morphological subtypes of invasive breast cancer are||
|Major causes of hypopituitarism||
• Pituitary apoplexia
• Pituitary adenoma
|Major cause of hyperpituitarism||
• Pituitary adenoma
|Major forms of thyroiditis||
• Chronic lymphocytic (Hashimoto)
• Subacute granulomatous (de Quervain)
• Subacute lymphocytic (postpartum)
|The enlagement of the thyroid is called||
• Goiter (struma)
|Carcinomas of the thyroid are||
• Papillary carcinoma
• Follicular carcinoma
• Medullary carcinoma
• Anaplastic carcinoma
|Endocrin neoplasms of the pancreas are||
|Major causes of the Cushing syndrome||
• Pituitary hyperfunction (adenoma)
• Adrenal hyperfunction
• Paraneoplastic (ACTH producing tumor)
|Patterns of brain herniation||
|Major forms of hydrocephalus||
• Hydrocephalus ex vacuo
|The most frequent cause of subarachnoid hemorrhage is||
• Rupture of saccular (berry) aneurysm
|Cause of epidural hematoma||
• Injury of the middle meningeal artery
|Cause of subdural hematoma||
• Disruption of the bridging veins
|Major routes of infective agents to the CNS||
• Direct posttraumatic
• Continous extension
• Nerve chanals
|Forms of infectious meningitis||
• Acute bacterial meningitis
• Viral meningitis
• Chronic meningitis (syphilis, tuberculosis)
|Major features of Creutzfeld-Jakob disease||
• Prion disease
• Spongiform transformation of the grey matter
• No inflammatory reaction
• Progress to dementia
|Major types of gliomas are||
|Most common primary tumors causing brain metastases||
• Lung cancer
• Breast carcinoma
• Renal cancer
• Gastrointestinal adenocarcinomas
|Morphological changes in Alzheimer disease||
• Cortical atrophy
• Neuritic plaques
• Neurofibrillary tangles
|List the four histological types of colorectal polyps!||
|What type of colorectal polyps do you know based on the macroscopical appearance?||
|Which are the two major genetic routes of colorectal carcinoma?||
• APC/β-catenin pathway
• microsatellite instability (mismatch repair) pathway
|List at least four of the hereditary polyposis syndromes!||
• FAP (familiar adenomatous polyposis)
|Which are the fibropolycystic liver diseases?||
• Caroli’s disease
• polycystic liver disease
• congenital hepatic fibrosis
• von Meyenburg komplex
|Which are the general macroscopical characteristics of cholesterol stones?||
• size measured in cms
• light colour
• radier arrangement on cut surface
|Name the major risk factors of cholesterol stone formation (the four F rule)||
|Which are the most important complications associated with acute calculosus cholecystitis?||
• bilestone ileus
|What is Klatskin’s tumor?||
• Extrahepatic cholangiocarcinoma,
• Arising at the anastomosis of the right and left hepatic duct
|Which are the common bone-forming tumors?||
• osteoid osteoma
|Which are the common cartilage-forming tumors?||
|Which are the most frequent complications of rickets?||
• caput quadratum
• rachitic rosary
• pectus carinatum/excavatum
• rachitic bowleg/knock knee
|Which are the most important characteristics of Ewing’s sarcoma?||
• usually pediatric
• diaphyseal appearance
• small, blue cell tumor histology
• associated with EWS gene translocation
|What is the major change in osteomalacia?||
• reduction of bone mineralization
|What is the major change in osteoporosis?||
• reduction of bone mineralization