Modul 1General Pathomorphology Text tests



Download 0.93 Mb.
Page2/10
Date conversion14.05.2018
Size0.93 Mb.
1   2   3   4   5   6   7   8   9   10

  1. Swollen cells

  2. Edematous appearance

  3. Clumped cytoplasm

  4. * Large droplets of fat

  5. Large clear spaces.

  • Among the complications of peptic ulcer by Samson emit:

    1. common processes

    2. local processes

    3. Local hemosyderoz

    4. dystrophic processes

    5. * inflammation

  • Among the complications of peptic ulcer by Samson allocate:

    1. bleeding

    2. perforation

    3. Penetration

    4. anemia

    5. * ulcer-scar Processes

  • Among the complications of peptic ulcer by Samson emit:

    1. atrophic gastritis

    2. hypertrophic gastritis

    3. chronic pancreatitis

    4. sepsis

    5. * malignization ulcers

  • Among the complications of peptic ulcer by Samson emit:

    1. common processes

    2. local processes

    3. Local hemosyderoz

    4. dystrophic processes

    5. * Combined complications

  • Are distinguished chronic cholestatic hepatitis, characterized by:

    1. hyalinosis hepatocytes

    2. sclerosis hepatocytes

    3. fibrosis hepatocytes

    4. disintegration of erythrocytes in vessels segments

    5. * cholestasis, cholangitis and holanhiolitom

  • Are distinguished chronic persistent hepatitis, in which prevails:

    1. sclerosis hepatocytes

    2. hyalinosis hepatocytes

    3. fibrosis hepatocytes

    4. necrosis of hepatocytes

    5. * cell infiltration of portal fields and vnutrishnochastochkovoyi stroma

  • Artificial particles differ in cirrhosis:

    1. largest

    2. placed

    3. hiperhromnistyu

    4. presence of fat droplets

    5. * broken angioarchitectonics

  • As a result of chronic alcoholic hepatitis, disorders of nutrition and metabolism occurs:

    1. necrotic cirrhosis

    2. atrophic cirrhosis

    3. biliary cirrhosis

    4. posttoksychnyy cirrhosis

    5. * Portal cirrhosis

  • Autoimunizatsiyu in viral hepatitis associated with:

    1. specific liver tromboplastynom

    2. liver specific albumin

    3. specific liver trombohenom

    4. basis of virus protein

    5. * liver specific lipoprotein

  • Ballooning degeneration of hepatocytes is caused by:

    1. * Accumulation of water and cellular swelling

    2. Retaining of biliary material

    3. Accumulation of iron or copp

    4. Accumulation of fat droplets

    5. Accumulation of lipofuscin.

  • Ballooning degeneration of hepatocytes results from:

    1. * Viral hepatitis

    2. Alcoholic liver disease

    3. Biliary material accumulation

    4. Obesity

    5. Diabetes mellitus.

  • Choose stage in necrosis morphogenesis:

    1. Paranecrosis irreversible change

    2. Coagulation

    3. Distrophy

    4. Autophagy

    5. * Cell death

  • Choose stage in necrosis morphogenesis:

    1. Prinecrosis reversible change

    2. * Necrobiosis irreversible degenerative changes;

    3. Coagulation

    4. Distrophy

    5. Autophagy

  • Choose stage in necrosis morphogenesis:

    1. * Paranecrosis reversible change

    2. Prinecrosis reversible change

    3. Coagulation

    4. Distrophy

    5. Autophagy

  • Choose stage in necrosis morphogenesis:

    1. Paranecrosis irreversible change

    2. Coagulation

    3. Distrophy

    4. Autophagy

    5. * Cell autolysis

  • Choose tipe of necrosis according to the cause:

    1. * Traumatic necrosis

    2. Coagulative necrosis

    3. Liquefactive necrosis

    4. Caseous necrosis

    5. Gangrenous necrosis

  • Choose tipe of necrosis according to the cause:

    1. * Toxic necrosis

    2. Coagulative necrosis

    3. Liquefactive necrosis

    4. Caseous necrosis

    5. Gangrenous necrosis

  • Choose tipe of necrosis according to the cause:

    1. * Trophoneurotic

    2. Coagulative necrosis

    3. Liquefactive necrosis

    4. Caseous necrosis

    5. Gangrenous necrosis

  • Choose tipe of necrosis according to the cause:

    1. * Vascular

    2. Coagulative necrosis

    3. Liquefactive necrosis

    4. Caseous necrosis

    5. Gangrenous necrosis

  • Choose tipe of necrosis according to the clinico-morphological forms:

    1. Vascular necrosis

    2. Toxic necrosis

    3. Trophoneurotic necrosis

    4. Traumatic necrosis

    5. * Coagulation (dry) necrosis

  • Choose tipe of necrosis according to the clinico-morphological forms:

    1. Vascular necrosis

    2. Toxic necrosis

    3. Trophoneurotic necrosis

    4. Traumatic necrosis

    5. * Colliquative (liquefactive) necrosis

  • Choose tipe of necrosis according to the clinico-morphological forms:

    1. Vascular necrosis

    2. Toxic necrosis

    3. Trophoneurotic necrosis

    4. Traumatic necrosis

    5. * Gangrene necrosis

  • Coagulative necrosis is characterized by all of the following pathologic features, EXCEPT:

    1. Denaturation of cytoplasmic proteins

    2. Karyorrhaxis

    3. Karyopiknosis

    4. Breakdown of cell organelles

    5. * Lipid deposition

  • Duration of toxic liver dystrophy:

    1. 1 year

    2. 2 months

    3. 5 months

    4. about 1 week

    5. * about three weeks

  • During the first days in toxic liver dystrophy characterized by fatty dystrophy of hepatocytes:

    1. on the periphery

    2. around vessels

    3. around ducts

    4. total dystrophy

    5. * the center slice

  • During the first days in toxic liver dystrophy characterized by fatty dystrophy of hepatocytes in the center slice, then she quickly changed:

    1. cirrhosis

    2. * necrosis and collapse autolitychnym

  • Early potentially reversible changes in myocardial cells induced by anoxia include all of the following conditions, EXCEPT:

    1. Failure of oxidative phosphorylation

    2. Depletion of ATP

    3. * Inhibition of anaerobic glycolysis and glycogenolysis

    4. Decrease in cellular pH

    5. Increase in intracellular Na and water and loss of intracellular K.

  • Faecalis mass in patients with bleeding peptic ulcer gaining color and consistency of tar, the evacuation is called:

    1. coffee huscheyu

    2. raspberry jelly

    3. metrorahiyeyu

    4. conjee

    5. * with ground (melaena)

  • Fatty change is seen by light microscopy as:

    1. Intracellular granules

    2. Basophilic granules

    3. Extracellular granules

    4. * Vacuoles in the cytoplasm around the nucleus

    5. Eosinophilic granules.

  • For acute gastritis characteristic of erosion -

    1. single

    2. No erosion

    3. point

    4. smuhopodibni

    5. * Multiple

  • For chronic gastritis characterized by the presence in blood of antibodies to gastric parietal cells -

    1. reflux gastritis

    2. focal acute gastritis

    3. Helicobacter-associated chronic gastritis

    4. acute diffuse gastritis

    5. * autoimmune chronic gastritis

  • For pathogenesis in this type of gastritis -

    1. chemical gastritis

    2. exogenous toxic gastritis

    3. autoimmune gastritis

    4. erosive gastritis

    5. * bacterial gastritis

  • Formation of false particles in liver cirrhosis leads to:

    1. necrosis of hepatocytes

    2. sclerosis hepatocytes

    3. Communities hemosyderozu

    4. ischemic foci

    5. * disturbed circulation in the liver

  • Give the definition of Peptic ulcer -

    1. ulcer, which reaches the muscular layer

    2. superficial mucosal ulcer

    3. damage submucosa

    4. damage to all layers of stomach

    5. * violation of the integrity of epithelial cover under the influence of acid and pepsin

  • Hepatic cell injury induced by CC14 is character ized by all of the following changes, EXCEPT:

    1. Lipid peroxidation

    2. Disaggregation of ribosomes

    3. * Depletion of intracellular lipids

    4. Influx of calcium

    5. Mitochondrial damage.

  • Hepatitis - acute or chronic liver disease, characterized by dystrophic changes and nekrobiotychnymy:

    1. stroma in combination with inflammatory infiltration of parenchyma

    2. capillary bed in conjunction with inflammatory infiltration of parenchyma

    3. peryportalnoyi stroma in combination with inflammation of hepatocytes

    4. in the capsule and on the periphery of the body

    5. * parenchyma in combination with stromal inflammatory infiltration

  • Hepatitis B, which accompanies infectious diseases, intoxications, called:

    1. intoksykatsiynym hepatitis

    2. stagnant hepatitis

    3. primary infectious hepatitis

    4. necrotic

    5. * secondary hepatitis

  • Hepatitis, which can accompany gastrointestinal tract pathology, called:

    1. intoksykatsiynym hepatitis

    2. stagnant hepatitis

    3. primary infectious hepatitis

    4. combined

    5. * secondary hepatitis

  • Hie causes related to CCl4-induced hepatic cell injury are all of the following, EXCEPT.

    1. Processing by mixed function oxidases free radical formation

    2. Free radical formation lipid peroxidation of intracellular membranes

    3. * Failure of protein synthesis-disaggregation of ribosomes

    4. Decreased apolipoprotein synthesis intracel lular lipid accumulation

    5. Plasma membrane damage mitochondrial calcification.

  • In long-standing hypertension and diabetes mellitus, the walls of arterioles, especially in the kidney, become:

    1. Serous

    2. Thined

    3. * Hyalinized

    4. Ulcered

    5. Pigmented.

  • In patients with peptic ulcer bleeding observed vomiting "coffee huscheyu, its color is due to the presence of:

    1. hydrochloric hemosiderin;

    2. hematoidin salt;

    3. hydrochloric hemomelaninu

    4. hydrochloric hematoporfirynu

    5. * hydrochloric hematin;

  • In patients with peptic ulcer bleeding vomiting occurs:

    1. with ground

    2. with tenesmus

    3. with convulsions

    4. with admixtures of bile

    5. * "Coffee huscheyu"

  • In remission at the edges of chronic ulcers appears:

    1. necrosis and hemorrhage;

    2. necrosis and inflammation;

    3. fibrynoyidnyy necrosis, inflammation, krovylyvy.

    4. multilayered epithelium

    5. * scar tissue bottom of the ulcer is covered with a thin layer of epithelium;

  • In seeming speck liver cirrhosis often:

    1. No sine

    2. no connective tissue partitions

    3. No regeneration

    4. existing fat droplets

    5. * A central vein in developing connective membrane sinusoid

  • In the acute phase of ulcer disease in days and the edges of ulcers appears:

    1. overgrowth of granulation tissue, amputation neuroma;

    2. mucosal hypertrophy, plethora;

    3. scar tissue from hipervaskulyaryzatsiyeyu.

    4. epithelial metaplasia

    5. * Area fibrynoyidnoho necrosis with purulent exudate;

  • In the course of toxic liver dystrophy distinguish stage:

    1. Yellow hypertrophy

    2. Yellow hypothrophy

    3. Yellow gonadal

    4. amiloidosis

    5. * yellow atrophy

  • In the course of toxic liver dystrophy distinguish stage:

    1. Yellow hypertrophy

    2. Yellow hypothrophy

    3. Yellow gonadal

    4. yellow necrosis

    5. * yellow atrophy

  • In the course of toxic liver dystrophy distinguish stage:

    1. red aplasia

    2. red anaplasia

    3. red aheneziyi

    4. red infarct

    5. * red atrophy

  • In the course of toxic liver dystrophy distinguish stage:

    1. cicatrization

    2. Restitution

    3. substitution

    4. cicatrization

    5. * restoration

  • In the red stage dystrophy in toxic liver dystrophy becomes:

    1. gray

    2. Muscat

    3. fat

    4. green

    5. * yellow with a red krapom

  • In the red stage dystrophy in toxic liver dystrophy often develops:

    1. renal failure

    2. heart failure

    3. cholangiocellular failure

    4. ICE syndrome

    5. * liver failure

  • In ulcer-destructive ulcer complications include:

    1. stenosis

    2. tetaniyu

    3. hlorhidropeniyu

    4. malignization

    5. * perforation

  • In ulcer-destructive ulcer complications include:

    1. stenosis

    2. tetaniyu

    3. hlorhidropeniyu

    4. malignization

    5. * Penetration

  • In viral hepatitis liver cells damaged by the mechanism:

    1. anaphylactic reaction

    2. apoptosis

    3. response alternatives

    4. ischemic necrosis

    5. * allergic-type reactions tsytolitychnoho

  • In viral hepatitis liver cells damaged by the mechanism:

    1. apoptosis

    2. response alternatives

    3. anaphylactic reaction

    4. hypoxia

    5. * slow-type hypersensitivity

  • Liver cirrhosis in at (bulk has:

    1. almost no changes

    2. uniformly reduced

    3. not reduced

    4. significantly increased

    5. * reduced

  • Liver in toxic dystrophy of the liver becomes less feeble, yellow comes in stages:

    1. red atrophy

    2. Sclerosis

    3. fibrosis

    4. necrotic foci

    5. * yellow atrophy

  • Morphological features of secondary biliary cirrhosis are:

    1. necrosis of hepatocytes

    2. necrosis peryportalnyh tracts

    3. necrosis portal tracts

    4. fatty dystrophy of hepatocytes

    5. * expansion and rupture bile capillaries, which causes peripheral necrosis of hepatocytes

  • Name changes in the gastric mucosa, which arise as a result of regular intake of alcohol -

    1. slyzoprodukuyuchyh atrophy cells

    2. appearance kelyhopodibnyh cells

    3. rare occurrence of erosions

    4. polimorfnoyadernymy infiltration of leukocytes

    5. * peeling of epithelial cells and reduce mucus secretion

  • Name changes of gastric juice in chronic autoimmune gastritis -

    1. No change

    2. hiperhlorhidriya

    3. dilution of gastric juice

    4. thickening of gastric juice

    5. * hipohlorhidriya until ahlorhidriyi

  • Necrotic cells are characterized by all of the following features, EXCEPT:

    1. Increased eosinophilia

    2. * Hyaline-like droplets in the cytoplasm

    3. Glassy appearance

    4. Lysis of cytoplasm

    5. Fragmentation of cytoplasm

  • One of manifestations of metabolic derangements in cells is:

    1. Apoptosis

    2. * The intracellular accumulation of abnormal amounts of various substance and necrosis

    3. Hypertrophy and necrosis

    4. Metaplasia

    5. Atrophy

  • One of the following changes in cells is apoptotic:

    1. Karyolysis

    2. * Nuclear pyknosis

    3. Plasmolysis

    4. Breakdown of mitochondrias

    5. Cellular swelling

  • One of the following variants of necrosis can be found in myocardial infarct:

    1. * Coagulative necrosis

    2. Liquefactive necrosis

    3. Caseous necrosis

    4. Gangrenous necrosis

    5. Fat necrosis.

  • One of the following variants of necrosis can be found in tuberculosis:

    1. * Caseous necrosis

    2. Gangrenous necrosis

    3. Liquefactive necrosis

    4. Fat necrosis

    5. Fibrinoid necrosis.

  • One of the following variants of necrosis is associated with syphilis:

    1. Coagulative necrosis

    2. Liquefactive necrosis

    3. * Caseous necrosis

    4. Gangrenous necrosis

    5. Fat necrosis.

  • One of the following variants of necrosis is associated with acute pancreatitis:

    1. Coagulative necrosis

    2. Liquefactive necrosis

    3. Caseous necrosis

    4. Gangrenous necrosis

    5. * Fat necrosis

  • One of the possible causes of intracellular accumulation of metabolic substances and necrosis:

    1. * Genetic defects

    2. Inflammation

    3. Embolism

    4. Necrosis

    5. Activation of oncogenes.

  • Overgrowth of connective tissue on the course portal tracts in the form of sprouts, the penetration of particles in the liver, dividing them into small artificial characteristic:

    1. necrotic cirrhosis

    2. toxic cirrhosis

    3. biliary cirrhosis

    4. focal hepatic

    5. * portal cirrhosis

  • Penetration is accompanied by changes in adjacent tissues of the gastrointestinal juice by:

    1. local inflammation

    2. local inflammation

    3. kariolizysu

    4. fester

    5. * digesting its tissues and inflammation

  • Penetration ulcers (penetratio) - is entering its:

    1. the thick mucous

    2. the thick muscle membrane

    3. to serosa

    4. in peritoneal

    5. * beyond the stomach or duodenum in other organs

  • Pericardial hepatitis divided into:

    1. hemorrhagic and fibrinous

    2. hnylisnyy and membranous

    3. hemorrhagic and necrotic

    4. purulent and hnylisnyy

    5. * serous and purulent

  • Portal cirrhosis of morphology are:

    1. velykovuzlykovoyu form of cirrhosis

    2. hypertrophic form of cirrhosis

    3. diffuse form of cirrhosis

    4. focal form of cirrhosis

    5. * dribnovuzlovoyu form

  • Precancerous stomach are:

    1. sharp erosion surface

    2. ulcer

    3. acute catarrhal gastritis

    4. carcinomatosis

    5. * chronic gastric ulcer

  • Precancerous stomach are:

    1. sharp erosion surface

    2. ulcer

    3. acute catarrhal gastritis

    4. intestinal metaplasia

    5. * severe dysplasia of gastric mucosal epithelium.

  • Primary biliary cirrhosis is the result:
  • 1   2   3   4   5   6   7   8   9   10


    The database is protected by copyright ©dentisty.org 2016
    send message

        Main page