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    5.0

    1

    After consumption of rich food a patient has nausea and heartburn, steatorrhea. This

    condition might be caused by:

    A Bile acid deficiency

    B Increased lipase secretion

    CDisturbed tripsin synthesis

    D Amylase deficiency

    EDisturbed phospholipase synthesis

    2

    Galactosemia is revealed in the child. Concentration of glucose in the blood is not

    considerably changed. Deficiency of hat en!yme caused this illness"

    A Galactose#$#phosphate uridyltransferase

    BAmylo#$,%#glucosidase

    C &hosphoglucomutase

    D Galacto'inase

    E(e)o'inase

    3

    *atty of phospholipids is disordered due to fat infiltration of the liver. Indicate hich of the

    presented substances can enhance the process of methylation during phospholipids

    synthesis"

    A +ethionine

    BAscorbic acid

    CGlucose

    D Glycerin

    ECitrate

    4

    Characteristic sign of glycogenosis is muscle pain during physical or'. Blood e)amination

    reveals usually hypoglycemia. This pathology is caused by congenital deficiency of the

    folloing en!yme:

    A Glycogen phosphorylase

    B Glucose %#phosphate dehydrogenase

    CAlpha amylase

    D Gamma amylase

    E ysosomal glycosidase

    5

    An infant has apparent diarrhea resulting from improper feeding. -ne of the main diarrhea

    effects is plentiful e)cretion of sodium bicarbonate. hat form of acid#base balance disorder

    is the case"

    A +etabolic acidosis

    B +etabolic al'alosis

    C/espiratory acidosis

    D/espiratory al'alosis

    E0o disorders of acid#base balance ill be observed

    6

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    +ethotre)ate 1structural analogue of the folic acid hich is competitive inhibitor of the

    dihydrofolatreductase2 is prescribed for treatment of the malignant tumour.-n hich level

    does methotre)ate inhibit synthesis of the nucleic acids"

    A +ononucleotide synthesis

    B /eplication

    C Transcription

    D /eparation

    E &rocessing

    7

    /0A#polymeraseB1II2 is bloc'ed due to amanitine poisoning 1poison of death#cup2. It

    disturbes:

    A 3ynthesis of m#/0A

    B 3ynthesis of t#/0A

    C/everse transcription

    D &rimers synthesis

    E+aturation of m#/0A

    8

    &ain along large nervous stems and increased amount of pyruvate in the blood ere revealed

    in the patient. Insufficiency of hat vitamin can cause such change"

    A 4$

    B 45

    C 66

    D &antothenic acid

    E Biotin

    9

    &atient ith encephalopathy as admitted to the neurological in#patient department.

    Correlation of increasing of encephalopathy and substances absorbed by the bloodstream

    from the intestines as revealed. hatsubstances that are created in the intestines can

    cause endoto)emia"

    A Indole

    B Butyrate

    CAcetacetate

    D Biotin

    E-rnithine

    10

    7)amination of a patient suffering from cancer of urinary bladder revealed high rate of

    serotonin and hydro)yanthranilic acid. It is caused by e)cess of the folloing amino acid in the

    organism:

    A Tryptophan

    BAlanine

    C(istidine

    D +ethionine

    ETyrosine

    11

    A mother consulted a doctor about her 8#year#old child ho develops erythemas, vesicular

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    rash and s'in itch under the influence of sun. aboratory studies revealed decreased iron

    concentration in the blood serum, increased uroporphyrinogen I e)cretion ith the urine. hat

    is the most li'ely inherited pathology in this child"

    A 7rythropoietic porphyria

    B +ethemoglobinemia

    C(epatic porphyria

    D Coproporphyria

    E Intermittent porphyria

    12

    A 9 year old child ith fever as given aspirin. It resulted in intensified erythrocyte haemolysis.

    (emolytic anemia might have been caused by congenital insufficiency of the folloing

    en!yme:

    A Glucose %#phosphate dehydrogenase

    B Glucose %#phosphatase

    CGlycogen phosphorylase

    D Glycerol phosphate dehydrogenase

    E #glutamiltransferase

    13

    Blood of a $5 year old boy presents lo concentration of uric acid and accumulation of

    )anthine and hypo)anthine. This child has genetic defect of the folloing en!yme:

    A ;anthine o)idase

    BArginase

    Cs2

    dystrophy. hich blood en!yme changes ill be of diagnostic value in this case"

    A Creatine phospho'inase

    B actate dehydrogenase

    C &yruvate dehydrogenase

    D Glutamate dehydrogenase

    EAdenylate cyclase

    16

    A patient is ill ith diabetes mellitus that is accompanied by hyperglycemia of over ?,5

    millimole@l on an empty stomach. The level of hat blood plasma protein allos to estimate

    the glycemia rate retrospectively 1=# ee's before e)amination2"

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    A Glycated hemoglobin

    BAlbumin

    C *ibrinogen

    D C#reactive protein

    ECeruloplasmin

    17

    In case of enterobiasis acrihine # the structural analogue of vitamin B5 # is administered.The synthesis disorder of hich en!ymes does this medicine cause in microorganisms"

    A *AD#dependent dehydrogenases

    B Cytochromeo)idases

    C &eptidases

    D 0AD#dependet dehydrogenases

    EAminotransferases

    18

    A $#year#old girl often e)periences acute respiratory infections ith multiple spotty

    haemorrages in the places of clothes friction. (ypovitaminosis of hat vitamin is present at

    the girl"

    A E

    B 4%

    C 4$

    D F

    E 45

    19

    (ydro)ylation of endogenous substrates and )enobiotics reuires a donor of protons. hichof the folloing vitamins can play this role"

    A Hitamin C

    B Hitamin &

    C Hitamin B%

    D Hitamin 7

    E Hitamin A

    20

    The formation of a secondary mediator is obligatory in membrane#intracellular mechanism of

    hormone action. &oint out the substance that is unable to be a secondary mediator:

    A Glycerol

    B Diacylglycerol

    C Inositol#9,=,8#triphosphate

    D CA+&

    ECa5

    21

    A = y.o. child ith signs of durative proteinic starvation as admitted to the hospital. The signs

    ere as follos: groth inhibition, anemia, edemata, mental deficiency. Choose a cause ofedemata development:

    A /educed synthesis of albumins

    B /educed synthesis of globulins

    C/educed synthesis of hemoglobin

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    D /educed synthesis of lipoproteins

    E/educed synthesis of glycoproteins

    22

    /esearchers isolated 8 isoen!ymic forms of lactate dehydrogenase from the human blood

    serum and studied their properties. hat property indicates that the isoen!ymic forms ere

    isolated from the same en!yme"

    A Cataly!ation of the same reactionB The same molecular eight

    C The same physicochemical properties

    D Tissue locali!ation

    E The same electrophoretic mobility

    23

    -n some diseases it is observed aldosteronism ith hypertension and edema due to

    sodium retention in the organism. hat organ of the internal secretion is affected on

    aldosteronism"

    AAdrenal glands

    B Testicle

    C-varies

    D &ancreas

    E(ypophysis

    24

    An e)periment proved that

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    EAfter contact ith a sic' dogs

    27

    Tere is observed inhibited fibrillation in the patients ith bile ducts obstruction, bleeding due

    to lo level of absorbtion of some vitamin. hat vitamin is in deficit"

    A J

    BF

    CDD K

    ECarotene

    28

    A 85 year#old patient ith bronchial asthma as treated ith glucocorticoids. *ever reaction

    appeared as a result of postinLective abscess. The patient had subfebrile temperature, hich

    didnMt correspond to latitude and severity of inflammatory process. hy did patient have lo

    fever reaction"

    A Inhibited endogen pyrogens production

    B Hiolation of heat loss through lungs

    C Inflammatory barrier formation in inLection place

    D Hiolation of heat#producing mechanisms

    E Thermoregulation center inhibition

    29

    A 98#year#old man under the treatment for pulmonary tuberculosis has acute#onset of right

    big toe pain, selling, and lo#grade fever. The gouty arthritis as diagnosed and high

    serum uric acid level as found. hich of the folloing antituberculosis drugs are 'non for

    causing high uric acid levels"A &yra!inamide

    B Cycloserine

    C Thiaceta!one

    D /ifampicin

    EAminosalicylic acid

    30

    During metabolic process active forms of the o)ygen including supero)ide anion radical are

    formed in the human body. ith help of hat en!yme is this anion activated"

    A 3upero)ide dismutase

    B Catalase

    C &ero)idase

    D Glutathionepero)idase

    EGlutathionereductase

    31

    A patient presents high activity of D($,5, aspartate aminotransferase, creatine

    phospho'inase. In hat organ 1organs2 is the development of a pathological process the

    most probable"A In the heart muscle 1initial stage of myocardium infarction2

    B In s'eletal muscles 1dystrophy, atrophy2

    C In 'idneys and adrenals

    D In connective tissue

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    E In liver and 'idneys

    32

    Buffer capacity of blood as decreased in the or'er due to e)hausting muscular or'. 7ntry

    of hat acid substance to the blood can this state be e)plained"

    A actate

    B &yruvate

    C $,9#bisphosphoglycerateD N#'etoglutarate

    E 9#phosphoglycerate

    33

    hile e)amining the child the doctor revealed symmetric chee's roughness, diarrhea,

    disfunction of the nervous system. ac' of hat food components caused it"

    A 0icotinic acid, tryptophane

    B ysine, ascorbic acid

    C Threonine, pantothenic acid

    D +ethionine, lipoic acid

    E &henylalanine, pangamic acid

    34

    A$9#year#old boy complains of general ea'ness, di!!iness, tiredness. (e is mentally

    retarded. Increased level of valine, isoleucine, leucine is in the blood and urine.

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    37

    Aspirin has antiinflammatory effect due to inhibition of the cycloo)ygenase activity. evel of

    hat biological active acids ill decrease"

    A &rostaglandins

    B eucotriens

    CCatecholamines

    D Biogenic amines

    E Iodinethyronyns

    38

    At the aboratory e)periment the eu'ocyte culture as mi)ed ith staphylococci. 0eutrophile

    leu'ocytes engulfed and digested bacterial cells. This processes are termed:

    A &hagocytosis

    B &inocytosis

    CDiffusion

    D *acilitated diffusion

    E-smosis

    39

    7)amination of a patient revealed typical presentations of collagenosis. This pathology is

    characteri!ed by increase of the folloing urine inde):

    A (ydro)yproline

    BArginine

    CGlucose

    D +ineral salts

    EAmmonium salts

    40

    +ar'ed increase of activity of O4#forms of C&P 1creatinephospho'inase2 and D(#$ ere

    revealed on the e)amination of the patient>s blood. hat is the most li'ely pathology"

    A +iocardial infarction

    B (epatitis

    C/heumatism

    D &ancreatitis

    ECholecystitis

    41

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    A 0eutrophils

    B 7osinophils

    C Basophils

    D imphocytes

    E+onocytes

    43

    AT& synthesis is totaly bloc'ed in a cell. (o ill the value of membrane rest potentialchange"

    A It ill disappear

    B It ill be slightly increased

    C It ill be considerably increased

    D *irst it ill increase, then decrease

    E *irst it ill decrease, then increase

    44

    The concentration of albumins in human blood sample is loer than normal. This leads to

    edema of tissues. hat blood function is damaged"

    A +aintaining the oncotic blood pressure

    B +aintaining the &h level

    C+aintaining the body temperature

    D +aintaining the blood sedimentation system

    EAll ansers are correct

    45

    7)amination of a patient suffering from freuent haemorrhages in the inner organs and

    mucous membranes revealed proline and lysine being included in collagen fibers.Impairment of their hydro)ylation is caused by lac' of the folloing vitamin:

    A C

    B 7

    C P

    D A

    ED

    46

    A 5 year old patient complains of general ea'ness, di!!iness, uic' fatigability. Blood

    analysis results: (b# g@l. +icroscopical e)amination results: erythrocytes are of modifiedform. This condition might be caused by:

    A 3ic'le#cell anemia

    B (epatocellular Laundice

    CAcute intermittent porphyria

    D -bturative Laundice

    EAddison>s disease

    47

    A = year old patient complained about intense pain, slight selling and reddening of s'inover the Loints, temperature rise up to 9oC. Blood analysis revealed high concentration of

    urates. This condition might be caused by disturbed metabolism of:

    A &urines

    B Collagen

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    CCholesterol

    D &yrimidines

    ECarbohydrates

    48

    A patient has yello s'in colour, dar' urine, dar'#yello feces. hat substance ill have

    strengthened concentration in the blood serum"

    A

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    53

    A patient ith high rate of obesity as advised to use carnitine as a food additive in order to

    enhance Qfat burningQ. hat is the role of carnitine in the process of fat o)idation"

    A Transport of **A 1free fatty acids2 from cytosol to the mitochondria

    B Transport of **A from fat depots to the tissues

    C It ta'es part in one of reactions of **A beta#o)idation

    D **A activationEActivation of intracellular lipolysis

    54

    An e)perimantal animal that as 'ept on protein#free diet developed fatty liver infiltration, in

    particular as a result of deficiency of methylating agents. This is caused by disturbed

    generation of the folloing metabolite:

    A Choline

    B D-&A

    CCholesterol

    D Acetoacetate

    E inoleic acid

    55

    A patient consulted a doctor about symmetric dermatitis of open s'in areas. It as found out

    that the patient lived mostly on cereals and ate too little meat, mil' and eggs. hat vitamin

    deficiency is the most evident"

    A 0icotinamide

    B Calciferol

    C *olic acidD Biotin

    E Tocopherol

    56

    A =% year old oman suffering from chololithiasis developed Laundice. (er urine became

    dar'#yello and feces became colourless. Blood serum ill have the highest concentration of

    the folloing substance:

    A ConLugated bilirubin

    B

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    58

    A =5#year man suffering from gout has increased level of urinary acid in the blood. Allopurinol

    as prescribed to decrease the level of urinary acid. Competitive inhibitor of hat en!yme is

    allopurinol"

    A ;anthino)idase

    BAdenosinedeaminase

    CAdeninephosphoribosiltransferaseD (ypo)antinphosphoribosiltransferase

    EGuaninedeaminase

    59

    A 9 year old patient suffers from rheumatism in its active phase. hat laboratory

    characteristic of blood serum is of diagnostic importance in case of this pathology"

    A C#reactive protein

    B

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    the graft became sollen and changed colourR on the $$#th day graft reLection started. hat

    cells ta'e part in this process"

    A T#lymphocytes

    B 7rythrocytes

    C Basophils

    D 7osinophils

    E B#lymphocytes

    64

    A 9 y.o. oman had been ill for a year hen she felt pain in the area of Loints for the first time,

    they got sollen and s'in above them became reddened. &rovisional diagnosis is

    rheumatoid arthritis. -ne of the most probable causes of this disease is a structure alteration

    of a connective tissue protein:

    A Collagen

    B +ucin

    C+yosin

    D -voalbumin

    E Troponin

    65

    Autopsy of a $5#year#old girl revealed: multiple cutaneous hemmorhages 1mostly into the s'in

    of buttoc's, loer e)tremities2, serous and mucous memrane hemmorhages, cerebral

    hemmorhages. Adrenal glands sho focal necrosis and massive hemmorhagesR 'idneys

    sho necrotic nephrosis, suppurative arthritis, iridocyclitis, vasculitis. hat is the most

    probable diagnosis"

    A +eningococcemia

    B 7pidemic typhus

    C &eriarteritis nodosaD 3ystemic lupus erythematosus

    E/adiation sic'ness

    66

    7)amination of a 5?#year#old patient revealed pathological changes in liver and brain. Blood

    plasma analysis revealed an abrupt decrease in the copper concentration, urine analysis

    revealed an increased copper concentration. The patient as diagnosed ith ilsonMs

    degeneration. To confirm the diagnosis it is necessary to study the activity of the folloing

    en!yme in blood serum:

    A CeruloplasminB Carbonic anhydrase

    C ;anthine o)idase

    D eucine aminopeptidase

    EAlcohol dehydrogenase

    67

    A patient complains about dyspnea provo'ed by the physical activity. Clinical e)amination

    revealed anaemia and presence of the paraprotein in the !one of gamma#globulins. To

    confirm the myeloma diagnosis it is necessary to determine the folloing inde) in thepatientMs urine:

    A Bence Sones protein

    B Bilirubin

    C(aemoglobin

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    D Ceruloplasmin

    EAntitrypsin

    68

    As a result of e)hausting muscular or' a or'er has largely reduced buffer capacity of blood.

    hat acidic substance that came to blood caused this phenomenon"

    A actate

    B &yruvateC $,9#bisphosphoglycerate

    D 9#phosphoglycerate

    E #

    69

    A 5#year#old child ith mental and physical retardation has been delivered to a hospital. (e

    presents ith freuent vomiting after having meals. There is phenylpyruvic acid in urine.

    hich metabolism abnormality is the reason for this pathology"

    AAmino#acid metabolism

    B ipidic metabolism

    CCarbohydrate metabolism

    D ater#salt metabolism

    E &hosphoric calcium metabolism

    70

    A patient as delivered to the hospital by an emergency team. -bLectively: grave condition,

    unconscious, adynamy. Cutaneous surfaces are dry, eyes are sun'en, face is cyanotic. There

    is tachycardia and smell of acetone from the mouth. Analysis results: blood glucose # 5,$

    micromole@l 1standard is 9,9#8,8 micromole@l2, urine glucose # 9,8 1standard is # 2. hat isthe most probable diagnosis"

    A (yperglycemic coma

    B (ypoglycemic coma

    CAcute heart failure

    D Acute alcoholic into)ication

    EAnaphylactic shoc'

    71

    &rofuse foam appeared hen dentist put hydrogen pero)ide on the mucous of the oral cavity.

    hat en!yme caused such activity"

    A Catalase

    B Cholinesterase

    CAcetyltransferase

    D Glucose#%#phosphatdehydrogenase

    E+ethemoglobinreductase

    72

    A %5 y.o. oman complains of freuent pains in the area of her chest and bac'bone, rib

    fractures. A doctor assumed myelomatosis 1plasmocytoma2. hat of the folloing laboratorycharacteristics ill be of the greatest diagnostical importance"

    A &araproteinemia

    B (yperalbuminemia

    C &roteinuria

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    D (ypoglobulinemia

    E(ypoproteinemia

    73

    A neborn child has convulsions that have been observed after prescription of vitamin B%.

    This most probable cause of this effect is that vitamin B% is a componet of the folloing

    en!yme:

    A Glutamate decarbo)ylaseB &yruvate dehydrostase

    C0etoglubarate dehydromine

    D Aminolevulinate synthase

    EGlycogen phosphorylase

    74

    0appies of a neborn have dar' spots that itness of formation of homogentisic acid.

    +etabolic imbalance of hich substance is it connected ith"

    A Thyrosine

    B Galactose

    C+ethionine

    D Cholesterine

    E Tryptophane

    75

    &athological changes of the liver and brain ere revealed in a 5?#year#old patient.The copper

    concentration is abruptly decreased in blood plasma and increased in the urine. ilson>s

    disease as diagnosed. Activity of hat en!yme in the blood serum should be e)amined to

    prove diagnisis"A Ceruloplasmin

    B Carboanhydra!e

    C ;anthio)idase

    D eucinamineopeptida!e

    EAlcoholdehydrogena!e

    76

    A 8#year#old patient complains about general ea'ness, appetite loss and cardiac

    arrhythmia. The patient presents ith muscle hypotonia, flaccid paralyses, ea'ened

    peristaltic activity of the boels. 3uch condition might be caused by:

    A (ypo'aliemia

    B (ypoproteinemia

    C(yper'aliemia

    D (ypophosphatemia

    E(yponatremia

    77

    An $#year#old patient has enlarged inguinal lymphnodes, they are painless, thic'ened on

    palpation. In the area of genital mucous membrane there is a small#si!ed ulcer iththic'ened edges and QlauerQ bottom of greyish colour. hat is the most probable diagnosis"

    A 3yphilis

    B Tuberculosis

    C epra

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    D Trophic ulcer

    EGonorrhea

    78

    Concentration of pyruvate is increased in the patient>s blood, the most of hich is e)creted

    ith urine. hat avitaminosis is observed in the patient"

    AAvitaminosis 4$

    BAvitaminosis 7CAvitaminosis 49

    D Avitaminosis B%

    EAvitaminosis 45

    79

    Carnitine including drug as recomended to the sportsman for improving results. hat

    process is activated most of all ith help of carnitine"

    A Transport of fatty acids to the mitochondria

    B 3ynthesis of steroid hormones

    C 3ynthesis of 'etone bodies

    D 3ynthesis of lipids

    E Tissue respiration

    80

    A patient ith suspected diphtheria ent through bacterioscopic e)amination. 7)amination of

    throat sab revealed rod#shaped bacteria ith volutin granules. hat etiotropic preparation

    should be chosen in this case"

    AAntidiphtheric antito)ic serum

    B BacteriophageCDiphtheria antito)in

    D 7ubiotic

    E Interferon

    81

    &atient ith diabetes mellitus e)perienced loss of consciousness and convulsions after

    inLection of insulin. hat is the result of biochemical blood analysis for concentration of the

    sugar"

    A $,8 mmol@

    B , mmol@

    C $, mmol@

    D 9,9 mmol@

    E 8,8 mmol@

    82

    A oman ho has been 'eeping to a clean#rice diet for a long time as diagnosed ith

    polyneuritis 1beriberi2. hat vitamin deficit results in development of this disease"

    A Thiamine

    BAscorbic acidC &yrido)ine

    D *olic acid

    E/iboflavin

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    83

    /emoval of gall bladder of a patient has disturbed processes of Ca absorption through the

    intestinal all. hat vitamin ill stimulate this process"

    A D9

    B &&

    CC

    D B$5

    E P

    84

    A %9#year#old oman developed signs of rheumatoid arthritis. Increase of hich indicated

    blood values level could be helpful in proving diagnosis"

    AAdditive glycosaminoglycans

    B ipoproteids

    CAcid phosphatase

    D General cholesterol

    E/#glycosidase

    85

    A $,8#year#old child presents ith both mental and physical lag, decolori!ing of s'in and hair,

    decrease in catecholamine concentration in blood. hen a fe drops of 8 solution of

    trichloroacetic iron had been added to the childMs urine it turned olive green. 3uch alteration

    are typical for the folloing pathology of the amino acid metabolism:

    A &henyl'etonuria

    BAl'aptonuria

    C Tyrosinosis

    D AlbinismE ;anthinuria

    86

    A patient complains of freuent diarrheas, especially after consumption of fattening food, and

    of body eight loss. aboratory e)amination revealed steatorrheaR hypocholic feces. hat can

    be the cause of this condition"

    A -bturation of biliary tracts

    B +ucous membrane inflammation of small intestine

    C ac' of pancreatic lipase

    D ac' of pancreatic phospholipase

    E

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    A child is languid, apathetic. iver is enlarged and liver biopsy revealed a significant e)cess of

    glycogene. Glucose concentration in the blood stream is belo normal. hat is the cause of

    lo glucose concentration"

    A o 1absent2 activity of glycogene phosphorylase in liver

    B o 1absent2 activity of he)o'inase

    C(igh activity of glycogen synthetase

    D o 1absent2 activity of glucose %#phosphatase

    EDeficit of a gene that is responsible for synthesis of glucose $#phosphaturidine transferase

    89

    A %8 year old man suffering from gout complains of 'idney pain.

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    93

    A 98 y.o. patient ho often consumes alcohol as treated ith diuretics. There appeared

    serious muscle and heart ea'ness, vomiting, diarrhea, A $@% mm (g, depression.

    This condition is caused by intensified e)cretion ith urine of:

    A &otassium

    B 3odium

    CChlorine

    D Calcium

    E &hosphates

    94

    After inta'e of rich food a patient feels nausea and sluggishnessR ith time there appeared

    signs of steatorrhea. Blood cholesterine concentration is U,5 micromole@l. This condition as

    caused by lac' of:

    A Bile acids

    B Triglycerides

    C *atty acids

    D &hospholipids

    EChylomicrons

    95

    7)amination of a man ho hadn>t been consuming fats but had been getting enough

    carbohydrates and proteins for a long time revealed dermatitis, poor ound healing, vision

    impairment. hat is the probable cause of metabolic disorder"

    A ac' of linoleic acid, vitamins A, D, 7, P

    B ac' of palmitic acid

    C ac' of vitamins &&, (

    D o caloric value of dietE ac' of oleic acid

    96

    A ==#year#old oman complains of common ea'ness, heart pain, considerable increase of

    body eigt. -bLectively: moon#li'e face, hirsutism, A $%8@$ mm (g, height # $%= cm,

    eight # $9 'gR fat is mostly accumulated in the region of nec', upper shoulder girdle,

    stomach. hat is the main pathogenetic mechanism of obesity"

    A Increased production of glucocorticoids

    B Decreased production of thyroidal hormones

    C Increased production of insulinD Decreased production of glucagon

    E Increased production of mineralocorticoids

    97

    An e)perimental animal has been given e)cessive amount of carbon#labeled glucose for a

    ee'. hat compound can the label be found in"

    A &almitic acid

    B +ethionine

    CHitamin A

    D Choline

    EArachidonic acid

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    98

    After a serious viral infection a 9#year#old child has repeated vomiting, loss of consciousness,

    convulsions. 7)amination revealed hyperammoniemia. hat may have caused changes of

    biochemical blood indices of this child"

    A Disorder of ammonia neutrali!ation in ornithinic cycle

    BActivated processes of aminoacids decarbo)ylation

    CDisorder of biogenic amines neutrali!ation

    D Increased purtefaction of proteins in intestines

    E Inhibited activity of transamination en!ymes

    99

    7)amination of a patient ith freuent hemorrhages from internals and mucous membranes

    revealed proline and lysine being a part of collagene fibers. hat vitamin absence caused

    disturbance of their hydro)ylation"

    A Hitamin C

    B Hitamin P

    C Hitamin A

    D Thiamine

    E Hitamin 7

    100

    A 9%#year#old female patient has a history of collagen disease.

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    e)creted by urine can characteri!e the state of antito)ic function of liver"

    A (ippuric acid

    BAmmonium salts

    C Preatinine

    D

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    A /enin

    B &epsin

    CGastrin

    D 3ecretin

    E ipase

    109

    The penetration of the irritable cell membrane for potassium ions has been increased duringan e)periment. hat changes of membrane electric status can occur"

    A (yperpolari!ation

    B Depolari!ation

    CAction potential

    D ocal response

    E0o changes

    110

    A sportsman as recommended to ta'e a medication that contains carnitine in order to

    improve his results. hat process is activated by carnitine the most"

    A *atty acids transport to mitochondrions

    B 3ynthesis of steroid hormones

    C 3ynthesis of 'etone bodies

    D 3ynyhesis of lipids

    E Tissue respiration

    111

    To prevent postoperative bleeding a % y.o. child as administered vicasol that is a synthetic

    analogue of vitamin P. 0ame post#translational changes of blood coagulation factors thatill be activated by vicasol:

    A Carbo)ylation of glutamin acid

    B &hosphorylation of serine radicals

    C &artial proteolysis

    D &olymeri!ation

    EGlycosylation

    112

    A = y.o. boy has had recently serious viral hepatitis. 0o there are such clinical presentations

    as vomiting, loss of consciousness, convulsions. Blood analysis revealedhyperammoniemia. Disturbunce of hich biochemical process caused such pathological

    condition of the patient"

    A Disturbed neutrali!ation of ammonia in liver

    B Disturbed neutrali!ation of biogenic amines

    C Increased putrefaction of proteins in boels

    D Activation of aminoacid decarbo)ylation

    E Inhibition of transamination en!yms

    113

    During e)amination of an $$#month#old infant a pediatrician revealed osteoectasia of the

    loer e)tremities and delayed minerali!ation of cranial bones. 3uch pathology is usually

    provo'ed by the deficit of the folloing vitamin:

    A Cholecalciferol

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    B Thiamin

    C &antothenic acid

    D Bioflavonoids

    E/iboflavin

    114

    7)amination of a patient suffering from chronic hepatitis revealed a significant decrease in the

    synthesis and secretion of bile acids. hat process ill be mainly disturbed in the patientMsboels"

    A *at emulsification

    B &rotein digestion

    CCarbohydrate digestion

    D Glycerin absorption

    EAmino acid absorption

    115

    The energy inputs of a healthy man have been measured. In hat position as the patient if

    his energy inputs ere less than the main e)change"

    A 3leep

    B /est

    C 7asy or'

    D 0ervous e)ertion

    ECalmness

    116

    Glutamate decarbo)ylation results in formation of inhibitory transmitter in C03. 0ame it:

    A GABAB Glutathione

    C(istamine

    D 3erotonin

    EAsparagine

    117

    In course of histidine catabolism a biogenic amin is formed that has poerful vasodilatating

    effect. 0ame it:

    A (istamine

    B 3erotonin

    CDio)yphenylalanine

    D 0oradrenalin

    EDopamine

    118

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    119

    After a sprint an untrained person develops muscle hypo)ia. This leads to the accumulation of

    the folloing metabolite in muscles:

    A actate

    B Petone bodies

    CAcetyl CoA

    D Glucose %#phosphate

    E-)aloacetate

    120

    +yocyte cytoplasm contains a big number of dissolved metabolites of glucose o)idation.

    0ame one of them that turns directly into a lactate:

    A &yruvate

    B -)aloacetate

    CGlycerophosphate

    D Glucose %#phosphate

    E *ructose %#phosphate

    121

    7motional stress causes activation of hormon#sensitive triglyceride lipase in the adipocytes.

    hat secondary mediator ta'es part in this process"

    A Cyclic adenosine monophosphate

    B Cyclic guanosine monophosphate

    CAdenosine monophosphate

    D Diacylglycerol

    E Ions of EW5

    122

    A patient has been diagnosed ith al'aptonuria. Choose an en!yme hose deficiency can be

    the reason for this pathology:

    A (omogentisic acid o)idase

    B &henylalanine hydro)ylase

    CGlutamate dehydrogenase

    D &yruvate dehydrogenase

    EDio)yphenylalanine decarbo)ylase

    123

    A patient diagnosed ith carcinoid of boels as admitted to the hospital. Analysis revealed

    high production of serotonin. It is 'non that this substance is formed of tryptophane

    aminooacid. hat biochemical mechanism underlies this process"

    A Decarbo)ylation

    B Desamination

    C+icrosomal o)ydation

    D Transamination

    E *ormation of paired compounds

    124

    A genetics specialist analy!ed the genealogy of a family and found that both males and

    females may have the illness, not across all the generations, and that healthy parents may

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    have ill children. hat is the type of illness inheritance"

    AAutosomal recessive

    BAutosomal dominant

    C ;#lin'ed dominant

    D ;#lin'ed recessive

    E V#lin'ed

    125

    Analysis of amniotic fluid that as obtained as a result of amniocentesis 1puncture of

    amniotic sac2 revealed cells the nuclei of hich contain se) chromatin 1Barr>s body2. hat can

    it be evidence of"

    A Development of female fetus

    B Development of male fetus

    CGenetic disorders of fetus development

    D Trisomy

    E &olyploidy

    126

    Hitamin B$ deficiency results in disturbance of o)idative decarbo)ylation of

    N#'etoglutaric acid. This ill disturb synthesis of the folloing coen!yme:

    A Thiamine pyrophosphate

    B 0icotinamide adenine dinucleotide 10AD2

    C *lavine adenine dinucleotide 1*AD2

    D ipoic acid

    ECoen!yme A

    127

    A child>s blood presents high content of galactose, glucose concentration is lo. There are

    such presentations as cataract, mental deficiency, adipose degeneration of liver. hat

    disease is it"

    A Galactosemia

    B Diabetes mellitus

    C actosemia

    D 3teroid diabetes

    E *ructosemia

    128

    According to clinical indications a patient as administered pyrido)al phosphate. hat

    processes is this medication intended to correct"

    A Transamination and decarbo)ylation of aminoacids

    B -)idative decarbo)ylation of 'etonic acids

    CDesamination of purine nucleotide

    D 3ynthesis of purine and pyrimidine bases

    E &rotein synthesis

    129

    A =8 y.o. oman suffers from Cushing>s syndrome # steroid diabetes. Biochemical

    e)amination revealed: hyperglycemia, hypochloremia. hich of the under#mentioned

    processes is the first to be activated"

    A Gluconeogenesis

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    B Glycogenolysis

    CGlucose reabsorption

    D Glucose transport to the cell

    EGlycolysis

    130

    Autopsy of a =%#year#old man revealed multiple bron#and#green layers and hemmorhages

    on the mucous membrane of rectum and sigmoid colonR slime and some blood in colonlumenR histologically # fibrinous colitis. In course of bacteriological analysis of colon contents

    3.3onne ere found. hat is the most probable diagnosis"

    A Dysentery

    B Cholera

    C 3almonellosis

    D Versiniosis

    ECrohn>s disease

    131

    A patient had been ill ith bronchial asthma for many years and died from asthmatic fit.

    (istologic lung e)amination revealed: lumen of bronchioles and small bronches contain a lot

    of mucus ith some eosinophils, there is sclerosis of alveolar septums, dilatation of alveole

    lumen. hat mechanism of development of hypersensibility reaction too' place"

    A /eagin reaction

    B Cytoto)ic reaction

    C Immunocomple) reaction

    D Cytolysis determined by lymphocytes

    EGranulomatosis

    132

    Desulfiram is idely used in medical practice to prevent alcocholism. It inhibits aldehyde

    dehydrogenase. Increased level of hat metabolite causes aversion to alcochol"

    AAcetaldehyde

    B 7thanol

    C+alonyl aldehyde

    D &ropionic aldehyde

    E+ethanol

    133

    A $#year#old child ith symptoms of muscle involvement as admitted to the hospital.

    7)amination revealed carnitine deficiency in his muscles. hat process disturbance is the

    biochemical basis of this pathology"

    A Transporting of fatty acids to mitochodrions

    B /egulation of Ca5level in mitochondrions

    C 3ubstrate phosphorylation

    D actic acid utili!ation

    EActin and myosin synthesis

    134

    The patient ith complaints of permanent thirst applied to the doctor. (yperglycemia, polyuria

    and increased concentration of $?#'etosteroids in the urine ere revealed. hat disease is

    the most li'ely"

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    A 3teroid diabetes

    B Insulin#dependent diabetes mellitus

    C+y)oedema

    D Type I glycogenosis

    EAddison>s disease

    135

    Inde) of p( of the blood changed and became ?,9 in the patient ith diabetus mellitus.Detecting of the components of hat buffer system is used hile diagnosing disorder of the

    acid#base euilibrium"

    A Bicarbonate

    B &hosphate

    C(emoglobin

    D -)yhemoglobin

    E &rotein

    136

    As a result of posttranslative modifications some proteins ta'ing part in blood coagulation,

    particularly prothrombin, become capable of calcium binding. The folloing vitamin ta'es part

    in this process:

    A P

    B C

    CA

    D B$

    E B5

    137

    -bLective e)amination of a patient revealed: slender figure, big s'ull, highly developed frontal

    region of face, short e)tremities. hat constitutional type is it characteristic for"

    A /espiratory

    B +uscular

    CDigestive

    D Cerebral

    E+i)ed

    138

    A 9#year#old patient died during intractable attac' of bronchial asthma. (istologice)amination revealed mucus accumulation in bronchial lumen, a lot of fat cells 1labrocytes2 in

    the all of bronches, many of them are in the state of degranulation, there are also a lot of

    eosinophils. hat pathogenesis of bronchial changes is it"

    AAtopy

    B Cytoto)ic, cytolytic action of antibodies

    C Immunocomple) mechanism

    D Cellular cytolysis

    EGranulomatosis

    139

    Diabetes mellitus causes 'etosis as a result of activated o)idation of fatty acids. hat

    disorders of acid#base euilibrium may be caused by e)cessive accumulation of 'etone

    bodies in blood"

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    A +etabolic acidosis

    B +etabolic alcalosis

    CAny changes oun>t happen

    D /espiratory acidosis

    E/espiratory alcalosis

    140

    A oman ith 1I2 bllod group has born a child ith AB blood group. This oman>s husbandhas A blood group. hat genetic interaction e)plains this phenomenon"

    A /ecessive epistasis

    B Codominance

    C &olymery

    D Incomplete dominance

    EComplementation

    141

    Depressions and emotional insanities result from the deficit of noradrenalin, serotonin and

    other biogenic amines in the brain. Their concentration in the synapses can be increased by

    means of the antidepressants that inhibit the folloing en!yme:

    A +onoamine o)idase

    B Diamine o)idase

    C #amino#acid o)idase

    D D#amino#acid o)idase

    E &henylalanine#=#monoo)ygenase

    142

    A 9 year old child ith symptoms of stomatitis, gingivitis and dermatitis of open s'in areasas delivered to a hospital. 7)amination revealed inherited disturbance of neutral amino acid

    transporting in the boels. These symptoms ere caused by the deficiency of the folloing

    vitamin:

    A 0iacin

    B &antothenic acid

    C Hitamin A

    D Cobalamin

    E Biotin

    143

    During hypersensitivity test a patient got subcutaneous inLection of an antigen hich caused

    reddening of s'in, edema, pain as a result of histamine action. This biogenic amine is

    generated as a result of transformation of the folloing histidine amino acid:

    A Decarbo)ylation

    B +ethylation

    C &hosphorylation

    D Isomeri!ation

    EDeamini!ation

    144

    A patient ith suspected diagnosis Qprogressing muscular dystrophyQ got his urine tested.

    hat compound ill confirm this diagnosis if found in urine"

    A Preatine

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    B Collagen

    C &orphyrin

    D +yoglobin

    ECalmodulin

    145

    A patient complained about di!!iness, memory impairment, periodical convulsions. It as

    revealed that these changes ere caused by a product of decarbo)ylation of glutamic acid.0ame this product:

    A GABA

    B &yrido)al phosphate

    C TD&

    D AT&

    E T(*A

    146

    A sportsman needs to improve his sporting results. (e as recommended to ta'e a

    preparation that contains carnitine. hat process is activated the most by this compound"

    A *atty acids transporting

    BAmino acids transporting

    CCalcium ions transporting

    D Glucose transporting

    E Hitamin P transporting

    147

    A doctor e)amined a child and revealed symptoms of rachitis. Development of this desease

    as caused by deficiency of the folloing compound:A $,58 XYZ[#dichydro)ycholecalciferol

    B Biotin

    C Tocopherol

    D 0aphtauinone

    E/etinol

    148

    aboratory e)amination of a child revealed increased concentration of leucine, valine,

    isoleucine and their 'etoderivatives in blood and urine.

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    D D-&A

    EDopamine

    150

    It as found out that some compounds, for instance fungi to)ins and some antibiotics can

    inhibit activity of /0A#polymerase. hat process ill be disturbed in a cell in case of

    inhibition of this en!yme"

    A TranscriptionB &rocessing

    C/eplication

    D Translation

    E/eparation

    151

    hen blood circulation in the damaged tissue is restored, then lactate accumulation comes

    to a stop and glucose consumption decelerates. These metabolic changes are caused by

    activation of the folloing process:

    AAerobic glycolysis

    BAnaerobic glycolysis

    C ipolysis

    D Gluconeogenesis

    EGlycogen biosynthesis

    152

    During starvation muscle proteins brea' up into free amino acids. These compounds ill be

    the most probably involved into the folloing process:

    A Gluconeogenesis in liverB Gluconeogenesis in muscles

    C 3ynthesis of higher fatty acids

    D Glycogenolysis

    EDecarbo)ylation

    153

    3urgical removal of a part of stomach resulted in disturbed absorption of vitamin B\$5], it

    is e)creted ith feces. The patient as diagnosed ith anemia. hat factor is necessary for

    absorption of this vitamin"

    A Gastromucoprotein

    B Gastrin

    C(ydrochloric acid

    D &epsin

    E *olic acid

    154

    A neborn develops dyspepsia after the mil' feeding. hen the mil' is substituted by the

    glucose solution the dyspepsia symptoms disappear. The neborn has the subnormal

    activity of the folloing en!yme:A actase

    B Invertase

    C+altase

    D Amylase

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    E Isomaltase

    155

    &atients ho suffer from severe diabetes and don>t receive insulin have metabolic acidosis.

    This is caused by increased concentration of the folloing metabolites:

    A Petone bodies

    B *atty acids

    Cs syndromeC Turner>s syndrome

    D 0iemann#&ic' disease

    E+acArdle disease

    158

    In clinical practice tuberculosis is treated ith i!onia!id preparation # that is an antivitamin

    able to penetrate into the tuberculosis bacillus. Tuberculostatic effect is induced by the

    interference ith replication processes and o)idation#reduction reactions due to the buildup

    of pseudo#coen!yme:

    A 0AD

    B *AD

    C *+0

    D TD&

    ECo^

    159

    A neborn child as found to have reduced intensity of suc'ing, freuent vomiting, hypotonia.

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    ECori cycle

    160

    A male patient has been diagnosed ith acute radiation disease. aboratory e)amination

    revealed a considerable reduction of platelet serotonin level. The li'ely cause of platelet

    serotonin reduction is the disturbed metabolism of the folloing substance:

    A 8#o)ytryptofane

    B TyrosineC(istidine

    D &henylalanine

    E 3erine

    161

    Dietary inta'e of a 9 year old nursing oman contains $ mg of calcium, $9 mg of

    phosphorus and 5 mg of iron per day. It is necessary to change content of these mineral

    substances in the folloing ay:

    A To increase phosphorus content

    B To increase calcium content

    C To reduce fluorine content

    D To increase iron content

    E To reduce iron content

    162

    Cardinal symptoms of primary hyperparathyroidism are osteoporosis and renal lesion along

    ith development of urolithiasis. hat substance ma'es up the basis of these calculi in this

    disease"

    A Calcium phosphateB

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    165

    A =U#year#old driver complains about unbearable constricting pain behind the breastbone

    irradiating to the nec'. The pain arose 5 hours ago. -bLectively: the patientMs condition is

    grave, he is pale, heart tones are decreased. aboratory studies revealed high activity of

    creatine 'inase and D($. hat disease are these symptoms typical for"

    AAcute myocardial infarction

    BAcute pancreatitisC 3tenocardia

    D Cholelithiasis

    EDiabetes mellitus

    166

    &lasmic factors of blood coagulation are e)posed to post#translational modification ith the

    participation of vitamin P. It is necessary as a cofactor in the en!yme system of

    #carbo)ylation of protein factors of blood coagulation due to the increased affinity of

    their molecules ith calcium ions. hat amino acid is carbo)ylated in these proteins"

    A Glutamic

    B Haline

    C 3erine

    D &henylalanine

    EArginine

    167

    &harmacological effects of antidepressants are connected ith inhibition of an en!yme

    cataly!ing biogenic amines noradrenaline and serotonine in the mitochondrions of cerebral

    neurons. hat en!yme participates in this process"A +onoamine o)idase

    B Transaminase

    CDecarbo)ylase

    D &eptidase

    E yase

    168

    An oncological patient as prescribed methotre)ate. ith the lapse of time target cells of the

    tumour lost susceptibility to this drug. There is change of gene e)pression of the foloing

    en!yme:

    A Dehydrofolate reductase

    B Thiaminase

    CDeaminase

    D *olate o)idase

    E *olate decarbo)ylase