Physiopathology 3nd YearInd Semester * (nd, 3-00, 14-15, npBods) 7 | Blesing rectum colts iscily harcez bye) 2” A, Soft and equ defection, th blood -B._ Abdominal pin : C. “Raabsontion: = : D,_ Caches : (Alot these disorder, 2: Carino-embrynic antigen isthe timor marker forthe folowing mors; with one exception’ A. Brescancer : BB Ovaria cancer : C. Gastic Cancer toe 1° Pancreatic cancer E. Colon cancer 3, Choose the FALSE statement) A. Vascular purpuas include hereditary disorders, of angiogenesis or vasclrsuctre -and acquired disorders incured by vascular image. Patients with hereditary hemorhagic telangiectasia display repeated noscbends ©. Parpra simplex is the most common vascular bleeding disorder, ‘D) Age-related vesculer pupure is hereditary disorder E, Allergic purpura is an avic or chronic vasculitis.” 4. Choose the FALSE statements) ‘A; Hemomage may be amajor feature of vitamin C deficiency, B, ‘Laige intramuscular hemorthage and hemarthrosisocéur in patients with vita C. deficiency. «Ascorbic acid’ an exit ofetr fr hyn of poi and Ine residues in collagen D, In ascorbic acid deficiency unhydroxylated procollagen and collagen ae unable to” ‘assume stable confirmation a" ‘The vitamin C deficiengy does not affect har follicles,5. Chocise the TRUE stement about septic purpura fulminansin pe A. Itmay be caused by difét invasion of endothelium. "BL Ttmay be caused by the release of bacterial toxins damaging the endothelium. ‘©. Endoloxins relesed by Nelsserid meningitis may cause ¢vruletpurpur with necrizing vasculitis . + D. Allofthe above E, None of tie above . <6 Choose the TRUE sttementx AS” Hemophilia type A hast identical clinical manifestations with hemophilia type B. 1B. Ineasily affected patients with herfophilia type A bleeding into joints and muscles sana dexintve hangs Pain an imi gas of miovsment may occur in eves ated patients with 4 hemophtintype A 3) 1D, Factor VII deficiency and factor IX deficiency doesn't have sex-linked genetic seansmissions “7.” Hemophilia type B is inerted as an autosomsl dominant disorder. "7. Cisplatin causesix co Disropt membane phospholipids a Mitigcondra injury Renal vasodilation CColapse of glomerular filtration ‘Obstruction of tubules re . - é D. 8, Clinical signs in the inating phase of acute renal following, EXCEPT AL Inereased pulse rate B. Decreased jug 20,” Oliguria : “ B. Hypertension é E Thist caused by hypovolemia are the: oo 0 0 nsw ooo eee | DE; ciB| ciel tere} | Alcic, (B/D B| Bipip pie |E{olc| E|D BiB} D{C|D 1ai3/4 sieiris |Bip c|D ee i cfc) sel | Bja|c{[B] cai c B| |E * These answers may or uno be correct.17. Wipe dese cn nied bye flowing exepex 9, Duodeho‘gasric reflux components with detcgent effect on gastric mucosa afe:x Arthritis AY Deoxiocoli acid : : : Potiserosits ’ B. Chenodeoxycholicacid | Cie acid Lisolesithin Adenopathy Constipation | (mo owe Fever, > Alf these components . « 10, Find out the false afignation concerning aut prerenafituresx™ A. Functional excretion of 1 B,_ Urine osmolarity > $00 mosmikg “© Renal fitureindex> 1 ‘D. Urine specifig gravity > 1018” E. Urine Ne concentration <10 mmol. ° > * 5 11, Find out the fale afirmaton cone Urine osmolarity <250 mostvkg Fractional excretion of Na <1 Renal fire index 1 wy mon Urine specific gravity < 1012 12, Find out the fle afirmaticn concerning the diagnos of real glucosuies =>“ A. - Glucosuri inthe absece of hyperlicemia ae R)Canstantghicosiria with ite Fiction slate to it . C. Normal storage of carbohydrates ~ D. Hyperliemia in the absence ofglucostria E, / Normal uilsation of exbohy@iies _ 13. Find out tte hase -afirmation concerning the later stage of chronic renal failure:x. A. Hypertrophy of the surviving nephrons ( B, Policia withiyposicmi’. 2) Glomerular filtration te <25% ' 'B. Azoteia appears in any sudden sess The pts asta eu of compet angchanisie14, Follows statemens on the evolitin of ype 2 diabetes ae te, with one exception x ‘AL Genetic predisposition; lack of exercise and obesity cause insulin resistance Bw ‘The ta cells ae desvoyed by atime mechani _ -, Tastn cesses aes la ts sere more inn < * DL Compensatory Iypernslinisn maintains the siycemic contol E, After 101020 years of hyperin incmia, beta-ells depletion occurs 15, Following statements on type 2 diabetes are true, with one exception:x A Isa rors diode hat woren with age and dbs dition B. Over 50% of the population over 50 years has type 2 diabetes C. Th gests conponeis alos 00% 1. Gyo fa disibiton sic wih inlinesiance E Sedentatty worsens type 2 diabetes 16, From the next sentences about ihe mechanism of hemolytic anemia due to glucose-6- phosphate-dehydrogénase'(G6PD), one is NOT TRUE:x. Av NADPH proves the een power at conversoxisied ghtathon to edused ghishione in, Nomallyntaetlaredced glutathione inate the oxidants which mig ine te cals (> Srtinoyes ata ecient in GERD ar more ess 0 xian cased by inet or xan drags" Unde onan tes, etoglihin is denatured a pits as Hein bodes on Ge ethoryietenbane .,_F. G6PD isan enzyine ofthe hexose monophosphate shunt pathway that maintains "> glutathione in ts active form i “tame tet i DONT ss ne oft mne e > taocyopat ne nada Quinine 83, Which ofthe fllowii sttgmeis is alsexx [Na+ has a mgjor effect on extracellular water Exuacellolar hyperosmolality leads to cellular debydraion Exiracellular hypoosmolality leads to cell shrinking ‘Water moves freely across cell membranes to maintain osmolality, mole Osmolality must be te same for bth intra and extracellular spaces 84, Which ofthe statements relating to type 2 diabetes is false ‘A, 1040 15% of patients with diabetes have type 2 diabets 1B. Genetic factors have a 90% prevalence inthe pathogesesis of type 2 diabetes C. Type? diabetes isthe result of insulin resistance associated with insulinadeficency 1D, Insulin resitance is secondary to excess fatty acids in the muscle and visceral adipose tissue E Noinsulils 85, Which os the following statements describe the polyol pahway setvation:x A B c D. E, Glucose stiches to proteins to form glycoprotein by enzymatic mechanishi Glucose metabolism in the absence on insulin, ve aldose reductase pathway Glucose is atefed to ammo groups of proteins (lication) Auto-oxidation of glucose > ‘Activation of protein kinase C 86, Widespread injury to endotieliai cells may trigger dsseirinated intavasculse __spagulation inthe following conditions EXCEPT ONE:x A. Systeme pus erythenaiosus © Bums Cerebral edema Infections with vaious microorganisms B. c D. E Endotoxemie7. Volatile acids produced by the body are following, with one exception:x ‘4.18. From the subsequent ist chose examples of drugs inkl AL Casbnic acid . B) Lastcacia : Acetic acid of : D. Bete-hydroxybusic acid a E. Propionic acid esa & 80, Which of the following mechanisms are mainly responsible for the pathogenesis ofthe 19, Gast ulcer is located more frequently:x cardiogenic shack . : Greater curvature AL Cell membrane injury Aawsiicrall, * i : 'B. Endothelial coll injury with disseminated intravascular coaguston cae ae C. » Peripheral vascilaton and poating ofthe blood ee : ‘D. Inadequate blood ot plasma volume eet - » . Failure ofthe myocardial pump eee a os . : scopmwmennesne 20, General ymponsofeace ae the flowing wih on exception, > 8 Whi othe flowing seis a my mono eager fe fe Cats gioee * A. Inadequate blood or plasma volume Pree + bate at 'B. Failure of the myocardial pump C._ Weight oss . . ._ Peipiral asdilaton ad pootng ofthe blood Dp. Hypoenaulatinsymes * Dy Cell membrane injury t E, _ Parancoplatic syndromss - - E_ Endothelial ell injury with disseminated intravascuer coagulation ae : ae ae ee 21. Heavy proieinaiaeanea~ 4 £2, Which ofthe fllowing statement scribe the polo patna activation x ONAL >gpratcins?. ¢ [ "A. Glucose attaches to proteins to form glycoproteins by enzymatic mechanism Bi 141.Sg proteinsim? is “ Glucose bola in the absence of insulin, vidoe reductase pathway ©. 02g prteinsn® | C. Glucose is attached to amind groups of proteins (glication) Di. 1Se1.8g proteins? : a 7 D. Aulo-oxiation of glucose E. 2aproeinn, e : E,_ Activation of protein kinase C oS > : ©22, Hematologic sbiomalites that appear in chron rena are are the loving 75. The Plasma concentration of which filtered glucose begins to escepe proximal tubular EXCEPTS, : capacity i Incentderytopoesis . ¢ AL 11Simiolt *Fisis ofthe tne marow B. 0-1 mmolt 5 Herilyis € 10'mmott ‘Gastisestnal bemortbages D. 1$:5:mmoit Blod oss exggeated in hmodiss E, $.78mmol 23, Hyperosmolar hyperglycemic coma is chatacterized by the following parameters, with.” 76, The Sensation of hits is stimulated bythe following mectanisms, with one exception:x “one excepion:x Sa. Increased Nat concentration A. Hypetosmeliy 8.) tnréased volemia 8. Hoppe ; arr 2G Masivekeonnin + : : ¢ . D. Crane inset“ ~ i “E Hypematremia ~ 71. Viral oncogenes that mimic the effects of growth factors ee the following, with one 2A. deity whish ae on widespread cringens . exception A, Biologic facts AL vais B. Physical factors” | ‘ B. von ~YC) Chemie tas : C yeb BD, Social factars, ie D. vee E., Psychological factors E. Vas 25. nal ates of inzeancular hey desease in the sera hapoyobin evel i 78, Vian K defisieney may be the result ofthe following event:x chrasterse because : AL Dietary deticieny of viamin K AP The unbound ee hemoglobin i exerted though he ides ‘ ee ” 'B, When hemoglbin escipes int he plasms, its promptly bound by haptoglobin . ‘C, Within the tubslar cells, irom released from the hemoglobin produces hemosiderosis s ofthe real tutu epithetiam ak eel D. The hem groups are cataboized within the reticaloendthlial sytem bilrbin CE. Allofthe above E, Excessive bilimbin excreted by the liver into the gastrointestinal tract leads to se eee aan ee p+» increased formation of urobilinogen171. The next peripheral blood and bone marrow characteristics are present in pernicious anemia, A 5 EXCEPJ ONEx ‘Mean éell hemoglobin concentration (MCHC) isnot elevated ‘Neuthropils are larger than normal and hypersogmentated ‘In the bone mare, there are megalablastic changes inal stages of red cell development ‘Mean cell hemoglobin concentration (MCHC) i elevated Inthe bone marrow, granulocytic precursors and megakaryocyts are abnormally large 72. The next peripheral blood changes are present in iton deficiency anemia, EXCEPT ONE. ‘A, Decreased serum iron B, Decreased serum ferritin” C. Total plasma iron binding Zapacity is low D. Red blood eels are microcytic and hypochromic E.” Many cells ean be seen as anulocytes "73. The next sentences about thalascemias are true, EXCEPT ONE A mo ole Have in common dfestive synthesis of or chain ofthe normal hemoglobin teteamer in the Pthalosscmia synthesis of chain ae impaired ‘Ae characterized by a hypochromicané micreytc anemia -Ar characerined by reduced or absent of the complete hemoglobin mlecsle In Cooley anemia, itis pronounced rédution o absence of chains production 74, The next sentences referring to « and B adenergic are true, EXCEPT ONE: Stimulation ofa receptors result in vasodiason Stimulation off receptors ofthe heart results in increase in myo (trope action) receptor predominate in the heart Broceptors are not innervated and respond to cifeulating cathecholamines ial contractility ‘timlation off receptors resuitin vasailaton 26. In lipid metabolism, liver occurs through the following functions exceptx > mo oe 27. In’shock, sustained catecholamine production eauses capil Synthesis of endogenous TG Synthesis of exogenous TG Esterfiation of free cholesterol Synthesis of bile acids 7 Formation of ketones ary congestion whic allows ial esis of smb naan aeolian oe cme, EXCEPTONER = ‘ A 5 © a E Procapillarysphinctér olaxation and more capillary congestion Coll damage cansing rleace nf vasoactive substances Ines capay presto ofintnascr id int extacelllar compartment Increase epost nd ue person ‘Opening of two-third ofthe capillaries which are normally closed at any onetime 28. nthe prézreson sige ofa evolution can appear the following phesojes of malignancy, with one excepionx A BD é Db E Increased growth proliferation rite Cat airetiion msned : : (Cellular hetrogensity Evasion of apoptosis» Metastasis 3 . 2. tntermitnt proteinuria mabe aust the folowing, EXCEEI'X rppop> Fever eget ite Siandng poston 5 Increase lotr lation Exercise | 1~ 30, Nephooe! hematuria demonsuates the following, EXCEPT:x ” AL Santina el disease . Prdseité ofpaliogenic bacteria =~ Glomerular inflamation ibular injures; eno Schon syndrom” 31. Nephroi diabetes insipidus has the elowing causes, EXCEPT x A, Piclonenbitis . > (Bi) Trauma ie 1D Cocweet “+ D. Multiple mela, ce BY Analiesieneptropathy - “32; Normally the Protein/creatinine ratio is:x ‘ B.. .>6.01 4 : D) <4 : 33, Oné of the following conditions may cause neurogenic thock:x A. Heat rupture B. Severe hemotriage ce C.. Septvemia . - ) in i ~E, * Massive fluid lois through vomiting or diarrhea 67. The sin fntions of theives in pron metabolism area Sitesis of emia . Synthesis of globuias Synthesis of Loing fos Sybex of anino-ransease )allothde fino log ow > * 68. The mechanism by which hypovolagmia may be associated with metabolic alkalosis ix AL Loss of sodium Loss of bicarbonate Tncreased sodium reabsorption Tncreased water reabsorption nope Hemoconcentrasion CR) Increased production of Ketones TB. Increased production of atic acid C. Increased elimination of bicarbonate 1D. Shift of potassium out ofthe cells 5 Increased sodium reabsorption 70, The most frequent microeytc and hypochfomie anemia ix Acute blood loss anemia Megalobiastic anemia Tron deficiency anemia Hemolytic anemia moo wy Aplastic anemia(63, The main causes of hepatic congestion arerx Sever right heat fitore Constitive pericarditis ~ Budd Chiari syndrome Occlusion of hepatic venules rp OpP All these causes (64. The main clinical manifestations in acute gastritis ar the following, except A (belching) B. Diffuse pain in lft bypéchondeium C) Anorexia & D. Navsea E. Heartburn, 65, The main complications of increasing size of esophageal diverticula are the following, exceptx A. Diverticulitis BD Hoarseness (Gi Headache \ Hipo-salivation E. Oculo-pupillary disorders '66. The main complications of recurring vomiting are the following except Dehydration, Metabolic acidosis Gastrogenietetony Increase of non-protein nitrogen in serum moo we Uremia 34. On of te et sees feng tptogei mca of erediay sphieroeytoss isNOT TURE A. This an autosomildéminan disorder . B. . Itis caused by a spectrin defigiency ee Cz, lis characerized by splenic trapping of RBCS nis cand by hemoglobin chains synthesis defiieney tis characterized by reduced membrane stability and spontaneous loss of RBC membrane a 35, Pemiciois anemia is also calledx A. Iron defigiency anemia “(BL Biermer anemia . $ ‘Sideroblastic anemia 8 ©. Apa nemia : D, E.Thaleemia 36. Physiopathology maid meni ‘which contribute to the occurrence of acute gastritis 5 *arex AL Altestio of gastric mncosal barrier © 8.” Duodeno-gastri reflux C. Changes of gastric microcirculation ,__Altration of postaglandin metabolism (ED allot tem. . 2 37, Plasma protease inhibitors that can neutralize coagulation enzymes incfude the following EXCEPT ONE A. Antithrombin : B. Alpha 2 macrogobulin : Alpha 1 anipoieace ce D2 Fibrinogen . E, Heparin cofactor I ®38. Polyvore diy wary velune $9. The following mess could ea wo hyperlyenia, wth ne exception Sy A So0mL* ° : AL Increased GH 8, 15002000m1 B. Inersssed ACTH : foe teen ADH . ~ D. Stress : BL Lack finslin 38, Protobncoges ecime oncogenic by fllowing mgchaniss, with one excopton:x 60, Th iver failure phenonsna ae ini! visible when iver pareclyna is desiwyed at AL Point mutations, > es : : B. Chromosome earangéineats: ® aul “(G2 ttyi ca ooieproncigen 3 6% _D., Gene amplfeaion > = oe oa Dom Em Fo, Co ee : - - disseminated inzascular eoaglation inthe following conditions EXCEPT ONE>x 81, The main sis of cue panes sx AL Otstevoa complication - ‘ : AL Gatisones B. Acute promyebeyticleukémia : B. Chronic cholecystitis ©. Adeoocarcnomas : ions aschotism “D. Endofoxemia : D.-_ Vira infeeons * CE} High abitade eceplopay 7 E, Allofthese 4. Severe thrombocytopenia often results isa typical pattem of bleeding such 53. 62, The msi aus of chronic live fire are the following, exepc A Maliplepetsncindeskin : | < BL Smal eocymese at sts oF minor aime SB Liversinhors Mucosa teeding : ©. Primary ver cancer Si [oo (Ey antoesteie - E Ziventiome‘5. The following clinical signs characterize extracellular volume deficit, with one exception. A. Persistence of skin fold oe ry mucous membranes and reduce axillary sweating Hypotesion Bradicardia Oliguria moglo » ‘56. The following conditions lead to metabolic acidosis with high anionic gap, exceptx * AL Ketoacidasis Severe diarthea - Cronic kidney disease Lactic acidosis, Ingestion of saiclaes. : poop > 51. The following conditions may eause cardiogenic shock, with ONE EXCEPTION: Cardiac tamponade ‘Pulmonafy embolism General Anesthesia Myocardial infarction Heart rupture ‘8 The following laboratory signs characterise excel yaue ven, with on exception Hiaermoert increased ESR increased =~ . “Total protein decreased Creatinine decreased Urea decreased“ room 42, Specify ow many gene musstons for malignany:x As 24, : 2 34 4s 56 > 48, The inl ioe ioctl wih deine ineavesul ogultin incu the following EXCEPT ONEX + AL Obstet eomplicatogs Bie Diaritea © Toxemia. D._ Lang ercinsinas F Bwensivesugery <4. Teloeal manent nae paths he floning sis Eicon ONes ‘A. Paleand cool skin (8) PogrstiveBradyara : - ©. Tachypnes 2° D.. Normal blood pressure. : : * B. Decreased urinary output due to decreased revial perfusion 48, The components of lod coagulation reaction inclde te following sri factors EXCEPT ONEx, : ae ‘A, Tissue thromboplastin” ‘B) Fibrinogen * °C. « Tissue factor _* ~ . , Procoagulant phospholipid . FE. Thrombafhodtlin46. The components ofsood coagulation reactions include the following plasma factors 50, The following are ceisequenegs hyperpolassemia, with one exception:x ~ EXCEPT ONEX Le : « AD Thirst A Bbnogen : : B.- Progressive muscle weakness B. Protiembin, 5s C.Veatrieular bition 5 Se Petals D._ Prosninent U'wave : E. Anbythmias 51. The following ao the consequences of hyponatraemia, with one exception:x ~The daify ion rebyitements for adult males ae about i : AL. Decrease lass osnliy A S108, . . ‘B) Cellular dehydration Ass a “Etat bypereson gy ‘$-10 mg . i. ‘D. Vomiting 2D tie: : B Anorela B 5.10ug se 52. The flowing aes re invaved in nub lao, ith one exception 45, Te allowing sr tues of equ nsui resismce, wih on exceionx : : A,” Diuretics : _ AY Obesity : B,_Recent massive vomiting 5 B. Wevemarye det 8 : CG. Revent gastric aspirtion Seeing * : : “ypoaldosteronism : : : “ Hypopotssienia oe a 4 = ae ee 53. The following changes charutrize metabolic alkalosis, wth one exception x 49, The following are causes of hyperkalemia, with one exception:x - - : : cera : me oA. Hypokalaemia As” Intravenous adninistatio solutions containing K* Bo ope Tas “—B. " Deereaseg glomerular fitraton rate . ©. HCO3-> 26 mEgL LG Alisa aiese : D. PaCO2>45 mmig __,D Acute metaole alkteiss, : ED PaCO2<35 mmlig E, Heemelysis 2 te aise ee 54, The folowing hangsschrecterizing respiratory lisloss, wth one exceton:x ~, . AL plo 74s . i : a : B, HCO3-<22mEq/L : : . TE) HCOR-> 30/1 : : D. raC2<30 mm Hg : E, Decreased essa on