Typhoid Fever 8.

Clinical character (feature) of typhoid fever:

1. Source of infection of typhoid fever 1. fever
1. typhoid fever patient at the initial period of 2. marked intoxication
disease 3. hepatolienal syndrome
2. typhoid fever patient at the height of disease 4. relative bradycardiac
3. acute bacterium carrier 5. confluence rash in articulation area
4. chronic bacterium carrier 9. Exanthema peculiarities in typhoid fever
5. domestic and agriculture animals 1. profuse spot – papule rash
2.Leading pathogenicity S. typhi factors: 2. poor rosealus rash
1.exotoxin 3. phenomenon of ‘pouring in addition ‘
2. IL-1 ,TNF-α 4. concentration of rash in the distal portion of
3. cytotoxin extremities
4. endotoxin 5. localization of rash on the anterior abdominal
5. Vi – antigen wall
3. Prolonged persistence mechanism of typhoid fever 10. Exanthema peculiarities in typhoid fever
infectious agent in the human organism 1. descending character of sequence of rash spread
1. antigen drift 2. circular localization of rash elements
2. formation of spores 3. localization of rash on palm and sole
3. antigen shift 4. appearance of the rash on the 5th day of illness
4. L – transformation 5. appearance of the rash from 8th – 10th day of
5. formation of capsule illness
4. Mechanism of pathogenesis of typhoid fever 11. Characteristic clinical feature of typhoid fever
1. bacteremia 1. edematous tongue with furs and teeth prints at
2. endotoxinemia margins
3. sensitibilization on the level of the intestinal 2. dullness of percutaneous sound in R iliac area
lymphoid tissue 3. anasarca
4. parenchymal diffusion of infectious agent into 4. hepatolienalic syndrome
the structure of mononuclear phagocytes systems 5. Gowrov – Godelye’s syndrome
5. persistence of infectious agent in macrophages 12. Clinical feature of typhoid fever height
5. Mechanism of pathogenesis of typhoid fever 1. toxic encephalopathy
1. cytotoxic action of infectious agent on small 2. hyperpyrexia
intestine epithelium 3. exanthema
2. translocation of infectious agent through M-cells 4. enamthema
in lymphoid follicles 5. Padalka’s symptoms
3. multiplication of infectious agent in intestinal 13. Typhoid fever complication
lymphoid tissue 1. intestinal bleeding
4. hematogenic dissemination of infectious agent 2. infectious toxic shock
5. infectious agent multiplication in lymphatic 3. intestinal perforation
formation of parenchymal organ 4. stomach perforation
6. Specific path morphologic changes in typhoid 5. infectious – exhaustion psychosis
develop in: 14. Typhoid fever complication
1. lymphatic formation of small intestine 1. intestinal bleeding
2. mucous membrane of the stomach 2. stomach bleeding
3. erythrocyte (red blood cell) 3. infectious toxic shock
4. hepatocyte 4. infectious toxical myocarditis
5. epithelium of the mucous membrane intestine 5. dehydration
7. Morphologic changes in the intestine in typhoid 15. Sign of development of intestinal bleeding in
fever: typhoid fever:
1. cribriform swelling of Peyer patches (Peyer’s 1.acute pain in abdomen
gland ) and solitary follicles 2. tachycardia against background of temperature
2. necrosis of intestine lymphatic formation decreasing
3. ulcers formation 3.tachycardia against background of temperature
4. ulcers healing with stricture formation increasing
5. formation of chronic ulcerous process 4. melena
5. rebound tenderness symptoms of peritonium
16. Sign of development of intestinal bleeding in 23. Typical changes in clinical blood analyzes in
typhoid fever: period of typhoid fever height
1. hemoglobin drop 1. leukocytosis
2. coffee ground vomit 2. leucopenia
3. increase hematocrit 3. eosinophilia
4. decrease hematocrit 4. relative lymphocytosis
5. revealing of occult blood in feces 5. aneosinophilis
17.Sign of development of intestinal bleeding in 24. Clinical diagnosis of typhoid fever is confirmed:
typhoid fever 1. increasing of antibody titer in Widal’s reaction
1. arterial pressure drop in pair serum in the course of disease
2. melena 2. detection of infectious agent antigen in ELISA
3. tachycardia 3. bacteriological examination of blood, feces,
4. pain in right iliac area urine
5. growing pale of skin 4. discharging of infectious agent from food
18. Sign of development of intestinal perforation in 5. bacteriological examination of feces
typhoid fever 25. Field of diagnostic search in typhoid fever
1. tongue thickening with teeth prints 1. shigellosis
2. appearance of local symptom of rebound 2. salmonellosis, generalized form
tenderness of peritoneum 3. paratyphoid fever A and B
3. growing local painful symptomatic in R iliac 4. Yersinosis
area 5. cholera
4. relative bradycardiac 26. Principals of therapy of patients with
5. tenesmus uncomplicated typhoid fever
19. Sign of development of peritonitis in typhoid 1. antibacterial therapy
fever 2. disintoxication therapy
1. muscular tension of anterior abdominal wall 3. serum therapy
2. Padalka’s symptoms 4. hemostatic therapy
3. musculative peristalsis absence 5. rehydration therapy
4. pouring in addition of rash elements 27. Antibacterial preparation of typhoid fever
5. increasing of leucocyte 1. ‘Salazoperizidine’
20. Signs of development of peritonitis in typhoid 2. Fluoroquinolone
fever 3. Nitrofuran
1. intoxication symptoms 4. Cephalosporin II and III generation
2. rebound tenderness symptoms 5. Penicillin
3. coffee ground vomit 28. Medical tactics in typhoid fever height
4. roentgenologic signs of air presence in 1. obligate hospitalization in infectious in-pt.
abdominal cavity department
5. appearance of Reiter’s syndrome 2. observation by local doctor at home
21. Basic clinical sign in typhoid fever diagnosis 3. antibacterial therapy
1. prolonged high fever 4. cytostatic therapy
2. hepatolienal syndrome 5. disintoxication therapy
3. type of rash as ‘gloves’ and ‘socks’ 29. Medical tactics of typhoid fever height
4. roseolus rash 1. strict bed regime
5. arthritis of major joints 2. ward regime
22. Clinical diagnostic of typhoid fever is confirmed 3. home regime
by : 4. dietary menu No. 13
1. clinical blood analysis 5. dietary menu No. 4
2. clinical urine analysis 30. Tactics of antibacterial therapy in uncomplicated
3. bacteriological examination of blood course of typhoid fever
4. bacteriological examination of feces 1. using maximum permissible dose of
5. bacteriological examination of urine preparation
2. using average therapeutic doses of preparation
3. treatment by the scheme of prolonged
uninterrupted course
4. treatment to the 3rd day normal temperature
5. treatment to the 10th day normal temperature
Viral hepatitis 9. Acute viral hepatitis C is characterized by:
1. Factors of risk development of viral hepatitis with 1. high frequency of anicteric forms
parenteral mechanism of contamination. 2. high frequency development of chronic hepatitis
1. IV introduction of narcotics( drug abuse) 3. presence of autoimmune reaction
2. blood transfusion 4. inclination to fulminant course
3. smoking 5. marked cholestasis sign
4. confused sex partners (multiple sexual contacts) 10. Variants of the course of preicteric period in viral
5. pregnancy hepatitis A
2. Basic risk group of viral hepatitis E 1. Influenza likely ( flu like)
1. drug addicts 2. allergic
2. homosexual 3. dyspeptic
3. children 4. mononucleous likely
4. pregnant 5. astheno – vegetative
5. medical officers 11. Variants of the course of preicteric period in viral
3. Viral hepatitis A patient represent epidemiologic hepatits B
hazard 1. influenza likely (flu like)
1. at the end of incubation period 2. arthral
2. at the preicteric period 3. dyspeptic
3. at the icteric period 4. mononucleous likely
4. in 12 months from the beginning of the disease 5. astheno - vegetative
5. all life 12. Clinical criteria of the severe course of acute viral
4.Viral hepatitis B patient may represent hepatitis
epidemiologic hazard 1. bradycardia inversion is followed by tachycardia
1. at the end of incubation period 2. hemorrhagic syndrome
2. at the preicteric period 3. decreasing size of liver against background of
3. at the icteric period increasing jaundice
4. in 12 months from the beginning of the disease 4. presence of persistent skin itching
5. all life 5. increasing size of liver against background of
5. Cells corresponding for immune lysis of increasing jaundice
hepatocytes 13. Clinical criteria of the severe course of acute viral
1. CD4+ T lymphocytes hepatitis
2. cytotoxic lymphocyte 1. secondary hepatic sign
3. macrophages 2. hemorrhagic syndrome
4. natural killer 3. fever in icteric period
5. fibroblast 4. recurrent vomiting, hiccup in icteric period
6. Viral hepatitis B persistence mechanism 5. inversion of sleep
1. viral variability 14. Clinical laboratory criteria of the severe course of
2. antigen drift acute viral hepatitis
3. integration in hepatocyte genome 1. increasing activity of alkaline phosphatase
4. extrahepatic replication 2. decreasing prothrombin index
5. antigen shift 3. decreasing size of liver against background of
7. Viral hepatitis C persistence mechanism increasing jaundice
1. low immunogenicity 4. increasing of direct bilirubin
2. rapid mutation of superficial viral proteins 5. decreasing of albumin concentration
3. integration in hepatocyte genome 15. Possible result of viral hepatitis A
4. extrahepatic replication 1. Recovery
5. antigen shift, drift 2. formation of chronic viral hepatitis
8. The role pay in intoxication development in viral 3. development of hepatocellular carcinoma
hepatitis 4. development of biliary ducts dyskinesis
1. nitrogen containing products of superficial viral 5. autoimmune hepatitis
proteins 16. Possible result of viral hepatitis B
2. combined (direct) bilirubin 1. recovery
3. lipopolysaccharides of intestinal flora 2. chronic viral hepatitis
4. viral antigen 3. hepatocellular carcinoma
5. free (indirect) bilirubin 4. biliary duct dyskinesis
5. autoimmune hepatitis
17. Possible result of viral hepatitis B 26. Markers of post-vaccination immunity against
1. hepatic cirrhosis HBV
2. recovery 1. HBs Ag
3. hepatocellular carcinoma 2. anti HBe
4. development of chronic viral hepatitis 3. anti HBcor Ig M
5. cholelithic disease 4. anti HBcor Ig G
18. Possible result of viral hepatitis C 5. anti HBs
1. recovery 27. Markers of acute viral Hepatitis D (co-infection)
2. chronic viral hepatitis 1. HBs Ag
3. hepatocellular carcinoma 2. HBe Ag
4. hepatic cirrhosis 3. anti HBcor Ig M
5. autoimmune hepatitis 4. anti HDV Ig M
19. Sign of precoma I 5. HDV RNA
1. emotional lability 28. Markers of acute viral Hepatitis D (co-infection)
2. increasing of jaundice and dyspeptic syndrome 1. anti HBs
3. disturbance of coordination of point movement 2. anti HAV – Ig M
4. yawning dizziness ( giddiness) 3. anti HBcor Ig M
5. increasing of size of liver 4. anti HDV Ig M
20. Sign of precoma II 5. HDV RNA
1. disorder consciousness (sopor) 29. Markers of acute viral Hepatitis D
2. complete loss of consciousness (superinfection)
3. locomotors excitement 1. anti HDV Ig M
4. convulsions 2. anti HBs
5. ‘bang tremor’ 3. HDV RNA
21. Markers of initial period of acute viral hepatitis A 4. anti HDV Ig G
determined in clinical practice 5. HBs Ag
1. HAV – Ag 30. Field of differential diagnostic search in viral
2. anti HAV – Ig G hepatitis
3. anti HAV – Ig M 1. leptospirosis
4. anti HEV – Ig M 2. infectious mononucleosis
5. HBs Ag 3. Yersinosis
22. Markers of viral hepatitis C 4. carcinoma of head of pancrease
1. anti HBcor – Ig G 5. toxical hepatitis
2. anti HBcor – Ig M 31. Basic therapy of acute viral hepatitis
3. RNA HCV 1. regime
4. anti HCV – Ig M 2. diet
5 anti HCV – Ig G 3. disintoxication therapy
23. Markers of viral hepatitis B in icteric period 4. hormone therapy
1. HBs Ag 5. interferon therapy
2. HBe Ag 32. Agents of pathogenic therapy for treatment of
3. anti HBcor – Ig M severe form of acute viral hepatitis
4. anti HDV – Ig G 1. Lactulose
5. anti HBe 2. Hepasol
24. Markers of acute viral hepatitis B in pre-icteric 3. Interferon
period 4. Chilled plasma
1. HBs Ag 5. Essential forte
2. HBV DNA 33. Agents for treatment of viral hepatitis
3. anti HBcor – Ig M complicated form
4. anti HBcor – Ig G (total) 1. lactulose
5. anti HBe 2. Hepamers
25. Marker of HBV post-infection immunity 3. Legalon
1. HBs Ag 4. Essential forte
2. HBe Ag 5. Corticosteroid
3. anti – HBcor Ig M
4. anti – HBcor Ig G (total)
5. anti - HBs
34. Agents of pathogenic therapy for treatment of Botulism
cholestatic form of acute viral hepatitis 1. Quality of botulism agent
1. Ursofalk 1. anaerobe
2. Ursosan 2. production of exotoxin
3. Interferon 3. production of endotoxin
4. Ribavirin 4. spore formation
5. Cholestiramine 5. L transformation ability
35. Criteria of discharging of viral hepatitis patient 2. Quality of botulism agent ( botulinus toxin)
1. clinical recovery 1. thermolability
2. normalization of transaminase activity 2. thermostability
3. normalization of albumin 3. hyperspecificity
4. disappearing of antibodies to viral hepatitis 4. neurotropism
5. disappearing of viral antigens 5. cytotoxicity
36. Dispensary examination of viral hepatitis 3. Botulism forms by mechanism of contamination
includes 1. water
1. carrying out of contrast roentegenography of 2. alimentary
biliary ducts 3. newborns
2. determining of bilirubin 4. wound
3. USD (ultrasound of hepatoduodenal diagnostic 5. sexual
area) 4. Risk of botulism disease connected with usage in
4. determining of transaminase activity food
5. carrying out serologic examination 1. meat – jelly, jellied
2. salt river fish
3. fancy cake with cream
4. canning products
5. salad of fresh cabbage
5. Cause of development of pareisis and paralysis in
botulism
1. potentiation of acetylcholine secretion in
neuromuscular synapse
2. blocking of acetylcholine secretion in
neuromuscular synapse
3. suppression of functional cell activity of
peripheral nuclei of motor nerve
4. hypercatecholemia
5. hypoxia
6. Causes of respiratory insufficiency in botulism
1. aspiration of vomiting mass
2. pleuritis
3. paresis of respiratory masculation
4. pneumothorax
5. pneumonia
7. Symptoms caused by acetylcholine release in
nerve endings
1. ammimia
2. paresis of accommodation
3. paresis and paralysis of skeletal musculature
4. convulsion (spasm)
5. meningeal syndrome
8. Variants of initial botulism period:
1. gastroenteric
2. influenza like
3. arthral (articular)
4. opthalmoplegic
5. acute respiratory insufficiency
9. Clinical signs of botulism 18. Characteristic serologic disorder in botulism
1. sharp dryness of mucous membrane 1. bulbar
2. edema of stomatopharynx mucouse membrane 2. meningeal tonic syndrome
3. uncontrolled vomiting 3. cerebellar
4. bulbar syndrome 4. disturbance of sensitivity
5. arterial hypertension 5. spastic (convulsion) syndrome
10. Clinical signs of botulism 19. Iatrogenic complication of botulism
1. hypersalivation 1. serious disease
2. opthalmoplegic syndrome 2. dysbiosis
3. hood symptoms 3. suppuration of tracheostomical wounds
4. muscular debility (myasthenia) 4. anaphylactic shock
5. Padalka’s symptoms 5. paresis and paralysis
11. Clinical signs of botulism 20. Complication in botulism
1. mydriasis 1. pneumonia
2. miosis 2. edema and swelling of brain
3. Gowtov – Godelye syndrome 3. cardiomyopathy
4. Meningeal symptoms 4. acute hepatic encephalopathy
5. ptosis 5. Waterhouse – Friderichsen syndrome
12. Opthalmoplegic syndrome in botulism include 21. Complication in botulism
1. mydriasis 1. pneumonia
2. miosis 2. neuritis
3. symmetrical ptosis 3. cardiomyopathy
4. blepharospams 4. fasciitis
5. disturbances of accomodation 5.neuralgia
13. Opthalmoplegic syndrome in botulism include 22. Botulism laboratory diagnosis method
1. acute developed myopia 1. biological test – neutralization reaction of toxin
2. disturbance of ocular convergence on white mice
3. disturbance of accommodation 2. bacteriological examination of suspicious
4. strabismus product
5. absence or reduction of pupil response of light 3. bacterioscopy
14. Bulbar syndrome in botulism include 4. reaction of direct hemaagglutination
1. mydriasis 5. detection of botulinus toxin in biomedium of
2. disturbance of phonation organism by ELISA
3. ptosis 23. Field of differential diagnostic search in botulism
4. disturbance of articulation 1. epilepsy
5. disturbance of swallowing 2. methyl alcohol poisoning
15. Bulbar syndrome in botulism include 3. tetanus
1. disturbance of phonation 4. Russian tick borne (spring summer)
2. disturbance of mucous membrane encephalitis
3. disturbance of articulation 5. Poliomyelitis
4. arterial hypertension 24. Field of differential diagnostic search in botulism
5. disturbance of swallowing 1. acute disturbance of cerebral circulation
16 Bulbar syndrome in botulism include 2. pile loadstool poisoning
1. snuffling voice 3. alcohol poisoning
2. decrease of vital capacity (respiratory capacity) 4. rabies
3. choking in swallowing (difficult swallowing) 5. atropine poisoning
4. flow of fluid into nasal cavity in swallowing 25. Principals of botulism treatment
5. slurring speech 1. gastric lavage
17. Symptoms of wound botulism 2. dehydration therapy
1. bulbar syndrome 3. immunosuppression therapy
2. opthalmoplegic syndrome 4. disintoxication therapy
3. myasthenia syndrome 5. interferon therapy
4. gastroenteric syndrome in initial period disease
5. fever and leukocytosis
26. Principals of botulism treatment
1. specific detoxication therapy
2. beta blocker
3. antimicrobial therapy
4. hyperbaric oxygenation
5. blockers of calcic canals
27. Remedies for treatment of botulism patient
1. horse specific antitoxic serum
2. hepasterin
3. antitoxic antibotulism fresh frozen donor
plasma
4. hepa-merz
5. antibotulism immunoglobin
28. Indication for administration of artificial
pulmonary ventilation to botulism patients
1. pneumonia
2. tachypnea more than 40 a minute, growing of
bulbar disorder
3. hydrothorax
4. decreasing of vital capacity up to the value of
respiratory volume
5. infectious toxic shock
29. Indication for administration of artificial
pulmonary ventilation to botulism patients
1. apnea
2. orthopnea
3. availability of hyposemia and hypercapnia
4. hemopericardium
5. obstruction of respiratory tracts
30. Rules of discharging of botulism patient in
hospital
1. absence paresis and paralysis
2. control inoculation of blood, urine and feces
3. restoration of swallowing, phonation articulation
4. findings of blood count
5. negative result of direct hema-agglutination
reaction
Shigellosis
1. Pathogenic factors of Shigella sp.
1. LPS
2. Shiga toxin
3. invasine protein
4. fibrinolysine
5. blocker of choline esterase receptors
2. Pathogenic factors of Shigella sp.
1. O-antigen
2. Invasine protein
3. Exotoxin
4. LPS
5. H - antigen
3. Source of shigellosis
1. patients with acute shigellosis
2. patients with chronic shigellosis
3. Carrier of shigella spp.
4. domestic animals
5. rodents
4. Pathogenesis mechanism of shigellosis
1. Damaging action of shigella cytotoxin on
intestinal epithelium
2. translocation of Shigella spp. through M cell to
lymphoid tissue
3. multiplication of Shigella spp. in regional
lymph node
4. invasion of Shigella spp. n muscle layer of
bowels wall
5. invasion of Shigella spp. in interstitial
epithelium, colonization of tunica mucosa of
bowel wall
5. Pathogenesis stages of shigellosis
1. Secretion of invasine proteins and exotoxins by
Shigella spp.
2. Destruction of tunica mucosa of bowel wall
3. Phagocytosis of SHigella spp. by macrophage
proinflammatory cytokines release
4. affection nof nerve plexus intestine
5. hypersecretion of mucus by goblet (crypt) cell
6. Pathogenesis stages of shigellosis
1. endotoxinemia
2. Shigella spp. intracellular surviving
3. Damaging action of cytokine on intestinal
epithelium
4. bacteriemia
5.motility disturbance of intestine
7. Multiplication of Shigella spp. is occur in
1. blood
2. parenchymal orgnas
3. tunica mucosa of colon
4. lymphoid tissue of small intestine
5. lymphoid tissue of large intestine
8. Types of diarrhea mechanism involved in 16. Typical signs of colitis variants of shigellosis
shigellosis 1. poor watery stool with mucus and blood
1. hypersecretory admixture
2. hyperexudative 2. tenesmus
3. hyperkinetic 3. cramp like epigastric pain
4. hyperosmolar 4. false urge of defecation
5. hyperoncotic 5. <rice> water stool
9. In the course of colitis variant of shigellosis 17. Clinical signs of colitis variant of shigellosis
mainly affected 1. acute onset of disease with temperature rise
1. small intestine and intoxication
2. terminal part of small intestine and cecum 2. frequent defecation with reducing amount of
3. right proximal part of large intestine stool
4. sigmoid colon and rectum 3. abundant( bulky) watery stool with stinking
5. duodenum odour
10. Pathomorphology changes in shigellosis 4. pathological admixture in feces
1. catarrhal prostosigmoiditis 5. painful and spasmodic sigmoid colon
2. catarrhal hemorrhagic prostosigmoiditis 18. Clinical signs of colitis variant of shigellosis
3. erosive ulcerative prostosigmoiditis 1. Schyitkin- Blumberg sign (peritonieum
4. granulomatous prostosigmoiditis irritation sign)
5. fibrinogenous necrotic prostosigmoiditis 2. abdominal pains in response to palpation of
11. Most severe clinical form of shigellosis large intestine
associated with: 3. imperative urge to defecate
1. Shigella Sonnei spp. 4. tenemus
2. Shigella Bodyii spp 5. Rosving sign
3. Shigella Dysenteria spp, 19. Character of stool in colitis variant of shigellosis
5. Shigella New Castle spp. 1. poor stool with mucus and blood admixture
12. Clinical classification of shigellosis is included 2. Scybalous <sheep stool
1. etiological causative agnet 3. <Ribbon-like> stool
2. number of previous cases 4. Abundant (bulky) watery stool with stinking
3. variants of disease odour
4. duration of incubation period 5. Fecal formed stool with scarlet (ruby-coloured)
5. duration of disease blood
13. Clinical variants of shigellosis 20. Criteria of severity of colitic variant of shigellosis
1. gastritis 1. tenesmus
2. gastroenteritis 2. stool frequency
3. gastroenterocolitis 3. presences of pathological admixture in feces
4. enterocolits 4. degree of dehydration
5. colitis 5. degree of intoxication
14. Feature of clinical course of acute shigellosis 21. Clinical signs of gastroenterocolitis variant of
1.Abortive shigellosis
2. Obliterated 1. stool with mucus and blood admixture
3. Fluminant 2. epigastric pains
4. Prolonged 3. vomiting
5. Recurrent 4. cramp like pain in left abdominal region
15. Feature of clinical course of chronic shigellosis 5. mesogastric (paraumbilical) pain
1. Continuous 22. Criteria of severity of gastroenterocolitis variant
2. Subacute of shigellosis
3. Recurrent 1. degree of dehydration
4. Progressive 2. degress of intoxication
5. Malignant 3. presence of multiple organ failure
4. intensity of colitis syndrome
5. presence of complication
23. Complication of colitis variant of shigellosis Brucellosis
1. infectious toxic shock 1. Species of Brucella, pathogenic to human
2. hypovolemic shock organism
3. rectal prolapse 1. Brucella militensis
4 intestinal bleeding 2. Brucella abortus
5. endocariditis 3. Brucella suis
24. Complication of shigellosis 4. Brucella ovis
1. intestinal perforation 5. Brucella neotomae
2. peritonitis 2. Pathogenic factors of Brucella condition
3. infectious toxic shock 1. Endotoxin
4. hemolytic-uremic syndrome 2. Fribinolisine
5. toxic megacolon 3. Resistance to phagocytosis
25. Principals of laboratory diagnosis of shigellosis 4. Action of cytotoxin
1. detection of antibodies 5. Enterotoxin
2. detection of antigen in biological medium 3. Ways of Brucella transmission
3. bacteriological investigation of stool 1. alimentary
4. skin allergic test 2. contact
5. biological test in mice 3. sexual
26. Area of differential diagnosis searching in case of 4. respiratory
shigellosis 5. transmissible
1. food poisoning 4. Pathogenesis stage of Brucellosis
2. amebiasis 1. passage Brucella through non-impaired skin
3. Yersinosis 2. foramation of primary effect
4. nonspecific tularemic colitis 3. development of incomplete phagocytosis
5. rectosigmoid tumor 4. lymphatic transport of Brucella’s into regional
27. Principals of therapy of shigellosis lymph node
1. specific antitoxic serum therapy 5. multiplication and accumulation of Brucella in
2. etiotropic therapy the regional lymph node
3. disintoxication therapy 5. Pathogenesis stage of Brucellosis
4. rehydration therapy 1. Passage of Brucella through impaired skin
5. probiotics prescription 2. complete phagocytosis with release of Brucella
28. Most effective treatment in shigellosis endotoxin
1. chloramphenicol 3. incomplete phagocytosis Brucella persistence
2. fluoroquinolones 4. Multiplication of Brucella in blood stream
3. tetracycline 5. multiplication of Brucella in hepatocyte
4. co-trimaxazole 6. The fundamental phases in the pathogenesis of
5. nitrofuran Brucellosis
29. Rules of discharge from the hospital in case 1. lymphogenous
shigellosis 2. hematogenous
1. Control proctosigmodoscopy 4. phase of exogenous dissemination
2. negative result of bacteriological investigation 5. phase of residual metamorphosis
of feces to dysbacteriosis 7. The fundamental mechanism of acute brucellosis
3. negative result of indirect agglutination with development
shigella diagnosticum 1.bacterima
4. clinical recovery 2. toxinemia
5. negative result of bacteriological investigation 3. formation of granulomas in parenchymal
of feces to Shigella spp. organs
30. Consequences of shigellosis 4. dissemination into lymphatic nodes and
1. postdysenteric colits multiplication
2. peritoneal commisures 5. fibrosis in the target organ
3. Reiter’s syndrome
4. Reye’s syndrome
5. dysbacteriosis
8. The fundamental mechanism of subacute 15. Clinical form of brucellosis
brucellosis development 1. acute brucellosis
1. allergic rebuilding of the microorganism 2. localized brucellosis
2. formation of granuloma in parenchymal organs 3. chronic brucellosis
3. repeated episodes of lympho- hematogenous 4. residual brucellosis
dissemination 5. second focus form
4. development of fibrositis and cellulitis 16. Clinical form of acute brucellosis
5. fibrous scars in the organs and tissue 1. irregular fever
9. The formation of chronic brucellosis form in 2. fibrositis, cellulitis
connected with 3. hepatolienal syndrome
1. granulomatous inflammation 4. arthritis
2. immune-complex reaction 5. sweating
3. anaphylactic reaction 17. Clinical form of acute brucellosis
4. immediate hypersensitivity 1. sacrolitis
5. cytotoxic reaction 2. irregular fever
10. The formation of chronic brucellosis form in 3. arthralgia, myalgia
connected with 4. chills, sweating
1. lasting Brucella’s persistent in the organ of 5. orchitis
mononuclear phagocytic system 18. Peculiarity of fever reaction during brucellosis
2. community of antigenic Brucella’s 1. satisfactory condition during fever
determinants and host tissue 2. irregular or constant type of fever
3. immunopathological reaction development 3. chills or sweating
4. contagion;s mechanism 4. regular changes of fever period and apyrexia
5. infectious dose 5. duration fever is not more than 5 days
11. The fundamental mechanism of chronic 19. Clinical sign of subacute brucellosis
brucellosis development 1. irregular fever
1. immunopathological reaction development 2. regular change of fever period and apyrexia
2. Brucella’s multiplication in the bloodstream 3. dehydration
3. discontinuation of new focus formation 4 fibrositis
4. reactive inflammatory procession development 5. cellulitis
5. fibrous scars in the organs and tissue 20. Clinical sign of subacute brucellosis
12. The fundamental mechanism of residual 1. migrant erythema
brucellosis development 2. ‘wave-like’fever
1. fibro-sclerotic changes 3. hepatolienal syndrome
2. functional disturbances in the different organ 4. arthritis
3. the absence of Brucella;s in the organism 5. fibrinous conjunctivitis
4. bactermia episodes 21. Clinical sign of chronic brucellosis
5. the lasting latent Brucella in the organism 1. ankyloses
13. The fundamental sign of acute brucellosis 2. polyarthiritis
1.hyperplasia of lymphatic nodes and endothelial 3. orchitis
element 4. the absence of exacerbation and recurrence of
2. proliferative vasculitis with increase blood brucellosis
vessels permeability 5.polyradiculonervitis
3. dystrophic disturbance and serous 22. Clinical sign of chronic brucellosis
inflammation 1. bursitis
4. formation of granulomas in the parenchymal 2. presence exacerbation and recurrence of illness
organs 3. duration of illness to 4th month
5. granuloma scelrosis 4. oophoriits, salpingitis
14. Clinical form of brucellosis 5. chronic atrophied acrodermitis
1. acute brucellosis 23. Clinical peculiarity of brucellosis
2. subacute brucellosis 1. changes in the area of Brucella inoculation
3. septic form 2. plural clinical manifestation
4. chronic brucellosis 3. inclination to chronic course
5. typhoid like form 5. absence of cyclical course of disease
 24. Methods of brucellosis diagnosis
1. clinical epidemiological method
2. bacterioscopy
3. allergologic
4. endoscopy
5. immunologic
25. Methods of brucellosis diagnosis
1. immunologic
2. serologic
3. roentgenologic examination
4. bacteriologic
5. isotopic radiography
26. Laboratory studies which confirm brucellosis
1. Rite’s reaction
2. Coomb’s reaction
3. Haddleson reaction
4. Hoff Bower reaction
5. Vidal reaciton
27. Principals on antibacterial therapy during
brucellosis
1. the duration of treatment course to 5th day of
normal temperature
2. lasting 5 – 6 weeks treatment
3. combination of different on antibacterial drugs
4. bacteriological control after treatment
completion
5. repeated course of antibacterial drugs during
relapse
28. Most effective drugs in treatment of brucellosis
1. ofloxacin
2. doxycycline
3. rifampicin
4. penicillin
5. primachin
29. Duration of etiotropic therapy by brucellosis
1. to the 5th day of apyrexia
2. to the 10th day of apyrexia
3. not less than 4 -6 weeks
5. to the appear negative result of blood culture
30. Drugs for eititropic therapy of brucellosis
1. doxycycline + streptomycin
2. doxycycline + rifampicin
3. cotrimaxazole + rifampicin
4. levomicetine + metronidazole
5. penicillin + lincomycin

*cholera, food poisoning and Yersinosis not included… please refer to other MCQ notes..
Sorry for not compiling the these three topics inside 

Anyhow the second sem ones are complete .. ENJOY 

Erysipelas 8. Types of inflammation typical in erysipelas
1. Pathogenicity of erysipelas pathogen 1. serous
1. Peptidoglycan 2. croupous
2. Streptolysin 3. hemorrhages
3. A-polysaccharide 4. purulent
4. Exotoxin 5. productive
5. Lipoteichoic acid 9. Erysipelas classification according to local
2. Pathogenicity factors of erysipelas pathogen manifestation prevalence
1. Lipopolysaccharide 1. localized
2. Hyaluronic acid 2. disseminated
3. Streptokinase 3. scarlet fever resembling
4. Hyaluronidase 4. generalized
5. Fibrinolysin 5. metastatic
3. Factors predispose to erysipelas development 10. Erysipelas classification according to the nature
1. lower extremities varicose of local manifestation
2. pyschoemotional stress 1. erythematous
3. lymph stasis 2. erythematous – hemorrhagic
4. insolation 3. erythematous – plegmonous
5. obesity 4. erythematous – bullous
4. Factors predispose to erysipelas development 5. gangrenous
1. overcooling 11. Erysipelas classification according to the nature
2. diabetes mellitus of local manifestation
3. erysipeloid 1.erythematous
4. postmastectomy syndrome 2. catarrhal
5. chronic suppurative infection foci 3. erythematous – phlegmenous
5. Provocative factors in erysipelas 4. bullous – hemorrhagic
1. psychoemotional stress 5. bullous – necrotic
2. lymphovenous insufficiency 12. Erysipelas classification according to number of
3. endocrine disturbances episodes of the disease
4. intercurrent infections 1. primary
5. abrupt changes of temperature 2. recurrent
6.The main stages of primary erysipelas pathogenesis 3. repeated
1. entrance of pathogen through intact skin 4. relapsing
2. proliferation in lymphatic dermal capillaries, 5. frequently relapsing
incomplete phagocytosis 13. Criteria of frequently relapsing erysipelas
3. bacteriemia, toxiemia 1. 3 or more relapse a year within the same
4. formation of immunopathology infection in focus localization
the dermis 2. seasonal relapsing
5. formation of purulent inflammation focus in 3. one relapse a year with the same focus
subcutaneous localization
7.The mains stages of relapsing of erysipelas 4. the development of the relapse 6 months later
pathogenesis with a different locus
1. persistence of L form of the pathogen in the 5. the development of hemorrhagic erysipelas
body of a person recovering from erysipelas form
2. protracted dermal sensitization to 14. Symptoms characterizing acute erysipelas period
streptococcal antigens 1. severe intoxication preceding local erysipelas
3. reinversion of L form of pathogen to bacterial manifestation
form 2. jerking pain in the focus area at rest
4. formation of granulomatous inflammation 3. erythema with distinct border
pool in dermis 4. regional lymphangitis
5. formation of purulent inflammation focus in 5. regional lymphadenitis
the dermis
15. Symptoms characterizing acute erysipelas period 23. Hemogram data in acute erysipelas period
1. normal body temperature 1. accelerated ESR
2. burning sensation in the focus 2. normocytosis
3. erythema with indistinct border 3. leucopenia with lymphocytosis
4. regional lymphangitis 4. leukocytosis with neutrophilic shift to the left
5. fluctuation in the focus area 5. anemia
16. Symptoms characterizing acute erysipelas period 24. The area of differential diagnosis search in
1. the development of the local focus on the erysipelas
second day of disease 1. phlegmon
2. the development of the local focus on the 10th 2. erysipeloid
day of disease 3. contact dermatitis
3. erythema with indistinct border 4. anthrax
4. poly lymphadenopathy 5. shingles
5. sensation of the burning and the bloating in 25. Principles of treatment of uncomplicated
the focus erysipelas
17. Characteristics of the focus in the erysipelas 1. antibacterial treatment
1. erythema with distinct border and irregular 2. desensitization therapy
contour 3. dehydration therapy
2. hemorrhages 4. Vishensky’s ointment dressing
3. hardening along the course of superficial veins 5. Detoxication therapy
4. presence of bullous with hemorrhagic content 26. Remedies of complex erysipelas treatment
5. fluctuation in the center of erysipelas focus 1. Vishensky’s ointment
18. Clinical sign of erysipelas 2. Laser therapy
1. erythema with distinct border 3. ichtyol ointment
2. pustulosis in the inflammation focus 4. Ultraviolet irradiation, ultrahigh frequency
3. dotty hemorrhages on the erythema 5. Magnet therapy
background 27. Antibiotics used for the treatment of primary
4. ulcers on the skin uncomplicated erysipelas in the acute period
5. absence of jerking pain in the focus of rest 1. benzyl penicillin sodium salt
19. Clinical signs of bullous – hemorrhagic 2. prolonged penicillin
erysipelas 3. macrolides
1. the presence of pustule 4. metronidazole
2. pulsating pain in the inflammation focus 5. levomyctin
3. fluctuation in the area of inflammation focus 28. Methods of erysipelas relapses prevention
4. the presence of bullous with hemorrhagic 1. full value of treatment of primary erysipelas
content on the erythema background 2. prophylactic administration of fluoroquinolone
5. distinct erythema contour, hemorrhages 3. two course antibacterial treatment with
20. Erysipelas complication lincomycin
1. sepsis 4. prophylactic administration of aminoglycosides
2. appendicitis 5. acoiding abrupt temperature change
3. procitis 29. Methods of erysipelas relapse prevention
4. toxico – infection shock 1. plasmapheresis
5. thrombophlebitis 2. bicillin prevention course
21. Erysipelas complication 3. vaccinotherpay
1.absecess 4. treatment of predisposing therapy
2. phlegmonous 5. indomethacin administration during relapse of
3. purulent periadenitis free period
4. obliterating endarteritis 30. Antibiotics used for the treatment of relapsing
5. deep skin necrosis uncomplicated erysipelas in the acute period
22. Erysipelas consequences 1. I – II generation of cephalosporin
1. lymphaedema 2. prolonged penicillin
2. fibroedema 3. fluoroquinolone
3. abscess 4. drugs of lincosamine group
4. phlegmon 5. aminoglycoside
5. sepsis
31.Antibioics used for erysipelas relapse prevention Influenza
1. III generation of cephalosporin 1. Main structural proteins of type A influenza virus
2. prolonged penicillin 1. superoxidedismutase
3. fluoroquinolone 2. neuramidase
4. drugs of lincosamine group 3. lipopolysaccharides
5. aminoglycosides 4. hemagglutinase
32.Indication for lincomycitin administration in the 5. murein acid
treatment of erysipelas 2. The most often way of influenza transmission
1. frequent erysipelas relapse 1. household contacts
2. sever course of erysipelas 2. transmissible
3. prevalence of the focus 3. fecal – oral
4. development of complication 4. air borne (droplets infection)
5. erysipelas localization on the upper extermities 5. parenteral
33. Indication for erysipelas patients treatment with 3. Mechanism causing changeability of influenza
biccilin virus
1. frequent erysipelas of the disease 1. antigen shift
2. development of complication 2. apoptosis
3. distinct seasonality of relapse 3. antigen shift
4. advanced age of patient 4. L – transformation
5. residual manifestation such as skin induration 5. H - transformation
and lymphadenitis 4. Peculiarities of immune response in influenza
1. antibody formation
2. induction of interferon
3. proliferative inflammation
4. cell cytotoxicity reaction in epithelium tract
5. granuloma formation
5. Stages of influenza pathogenesis
1. virus adhesion on the cells of columnar
(cylindrical) epithelium of the upper respiratory
tract
2.virus adhesion on the cells of simple squamous
epithelium of the upper respiratory tract
3. virus reproduction in trachea mucosa
4. virus reproduction in the bronchi mucosa
5. virus reproduction in mucous of gastrointestinal
tract
6. Stages of influenza pathogenesis
1. virus reproduction in mucous of trachea and
bronchi
2. virus production in synovial membrane
3. dystrophy and necrosis of upper respiratory
tract cells
4. development of inflammation in mucous of
upper respiratory tract
5. development of inflammation in synovial
membrane
7. Complaints of influenza patients
1. a headache
2. stuffiness in nose
3. abundant nasal discharge
4. a dry scratch feeding in the throat of swelling
5. profuse watery stool
8. Fever characteristics in non-complicated course of 16. Clinical symptoms of non-complicated influenza
influenza 1, gradual onset of disease
1. paroxysmal fever 2. retroorbital pain
2. wavelike during 2 weeks 3. hypersalivation
3. febrile duration up to 5 days 4. increasing of the headache in eyeball
4. febrile lasting more than 7 days movement
5. recurrent 5. maculopapular exanthema
9. Clinical symptoms of non-complicated influenza 17. Clinical symptoms of non-complicated influenza
1. subictericness of the skin 1. acute onset of the disease
2. injection of sclera vessels 2. stepped increasing of temperature during 5
3. hyperemia of the face skin days
4. a dry scratch feeling in the throat 3. parotid glands enlargement
5. aphonia 4. hyperemia of face and neck
10. Clinical symptoms of non-complicated influenza 5. injection of sclera vessels
1. dry cough 18. Clinical symptoms of non-complicated influenza
2. feeling of substernal stuffiness 1. abundant rhinorrhea
3. fever more than 5 days 2. pharygoconjunctivits
4. stuffiness in the nose 3 tracheobronchitis
5. marked rhinorhea 4. fibrosing alveolits
11. Clinical symptoms of complicated influenza 5. myelitis
1. nasal bleeding 19. Leading syndrome of influenza
2. meningism 1. intoxication syndrome
3. hyperpyrexia 2. icteric syndrome
4. icteriness of the skin 3. catarrhal syndrome
5. hepatolienal syndrome 4. hepato-lienal syndrome
12. Clinical symptoms of complicated influenza 5. hemorrhagic syndrome
1. hemorrhagic exanthema 20. Criteria of influenza severity
2. Reye’s syndrome 1.infection toxic shock
3.Reiter’s syndrome 2. articular syndrome
4. Raynaud’s syndrome 3. respiratory syndrome
5. nasal bleeding 4. diarrhea syndrome
13. Clinical symptoms in severe course of non- 5. hemorrhagic syndrome
complicated influenza 21. Pathogenic complication of influenza
1. Padalka’s syndrome 1. infectious toxic shock
2. hemorrhagic enanthema 2. respiratory distress syndrome
3. hemorrhagic exanthema 3. hepato-renal insufficiency
4. colitic syndrome 4. thrombophlebitis
5. orthostatic collapse 5. myocardial dystrophy
14. Clinical symptoms in severe course of non- 22. Pathogenic complication of influenza
complicated influenza 1. acute respiratory insufficiency
1. tachycardiac more than 120 bpm 2. brain edema
2. lacunar tonsillitis 3. infective toxic shock
3. otitis media suppurative ( purulent) 4. peritonitis
4. respiratory rate more than 40 respiration a 5. acute renal insufficiency
minute 23. Influenza complication caused by activation of
5. blood-streaked sputum conditioned pathogenic flora
15. Clinical symptoms of non-complicated influenza 1. septical state
1. acute onset of disease 2. respiratory distress syndrome
2. bilateral ptosis 3. hepato-renal insuffciency
3. temperature increase to 39˚C-40˚C in the first 4. maxillary sinusitis
hours of the disease 5. pneumonia
4. decrease acuity of vision
5. headache of the frontal-temporal area
24. Principles of influenza diagnosis Meningococcal Infection
1. epidemic findings 1. Pathogenic factors of N. meningitides
2. clinical findings 1. LPS
3. allergiology diagnosis 2. H antigen (motility properties)
4. endoscopy diagnostica 3. Exotoxin
5. immunodiagnostic 4. Stability to phagocytosis
25. Methods of influenza laboratory diagnosis 5. L - transformation
1. immunofluorescent method 2. Pathogenesis mechanism of meningococcal
2.serodiagnosis infection
3. allergologic method 1. Adhesion and multiplication of meningococcal
4. virology method on mucous layer of upper respiratory tract
5. biological method 2. Phagocytosis of meningococci by macrophages
26. Field of differential diagnostic search in influenza 3. Discharge of LPS
1. meningococcal indection 4. Production of hemolysin
2. typhus 5. production of cytotoxin
3. cholera 3. Pathogenesis mechanism of meningococcal
4. adenoviral infection infection
5. rabies 1.Endotoxinemia, bacteriemia
27. Principals of non-complicated influenza 2. production of cytotoxin by macrophages after
treatment interaction with LPS
1.antibiotic therapy 3. disturbance of permeability of endothelium of
2. anti-influenza donor γ-globulin microcirculation vessels
3. disintoxication therapy 4. penetration of meningococci after blood brain
4. vitamin therapy barrier
5. hormontherapy 5. development of granulomatous inflammation
28. Indication for hospitalization in influenza virus 4. Pathogenesis mechanism of meningococcal
1. absence of influenza inoculation infection
2. presence of influenza patient in the family 1. development of necrotic supportive changes in
3. severe course organs and tissues
4. elderly 2. hyper production of liquor (cerebrospinal fluid)
5. presence of sever accompanying illness 3. increasing of permeability of blood brain barrier
29. Etiotropic influenza therapy 4. neutrophils perivascular infiltration
1. rimatadin 5. disturbance of hemostasis
2. reopirin 5. Pathmorphology changes in meningococcemia
3. oseltamivir 1. dystrophic changes in parenchymatous organs
4. terraflu 2. < septic spleen>
5. lumivudin 3. granuloma in prenchymatous organs
30. Indication for antibacterial therapy in influenza 4. Plethora of cerebral membranes vessels
1. severe course 5. Hemorrhages in adrenal glands
2. presence of secondary bacterial complication 6. Pathmorphology changes in meningococcemia
3. high titer of antibodies 1. granulomatous in derma
4. typical specificity of influenza virus 2. lipodystrophy of subcutaneous fat
5. belonging of a patient to risk group 3. necrosis of vascular wall in places of
thrombosis
4. serohemorrhages impregnation of derma
5. parietal or obstructive thrombus
7. Clinical classification of meningococcal infection
1. primary localized form
2. typhoid like form
3. hemotogenic generalized form
4. scarlatinous like form
5. rare form
 8. Primary localized forms of meningococcal 17. Clinical sign of meningococcemia
infection 1. acute onset of disease with high fever
1. rhinitis 2. watery stool
2. nasopharygitis 3. hemorrhagic rash
3. laryngotracheitis 4. ring shaped (annular) erythema
4. carrier state 5. myalgia, arthralgia
5. pneumonia 18. Clinical sign of meningococcemia
9. Hematogenic-generalized form of meningococcal 1. acute onset of disease with intoxication sign,
infection hemorrhages on conjuctive
1. meningococcemia 2. acute onset of disease with intoxication sign,
2. meningitis abundant punctulated rash with thickening in
3. meningoencephalitis natural fold sites
4.mixed form 3. acute onset of disease with intoxication sign,
5. typhoid like form abundant large spotted rash on the face
10. Rare form of meningococcal infection 4. acute onset of disease with intoxication sign,
1. brain abscess papulo-vesicular rash on hairy part of head
2. arthritis 5. acute onset of disease with intoxication sign,
3. iridocylitist hemorrhagic rash on distal part of extremities
4. hepatitis 19. Typical complication of meningococcemia
5. endocardidits 1. paresis of facial nerve
11. Clinical forms of meningococcal infection 3. endotoxic (infectious toxic shock)
1. rhinitis 3. acute hepatic failure
2. nasopharyngitis 4. acute adrenal failure
3. meningitis 5. acute renal failure
4. meningococcemia 20. Typical complication of meningococcemia
5. hepatitis 1. DIC syndrome
12. Clinical forms of meningococcal infection 2. Waterhouse – Friederichsen syndrome
1. meningitis 3. Myelitis
2. colitis 4. Bulbar syndrome
3. meningoencephalitis 5. Acute renal failure
4. antritis ( sinusitis) 21. Symptoms complex of brain edema (swelling) at
5. mixed form meningococcal meningitis
13. Meningeal symptoms is included 1. increasing sign of meningeal symptoms
1. focal neurologic symptomatology 2. impairment of consciousness, psychomotor
2. hyperesthesia symptoms agitation
3. reactive pain symptoms 3. increasing of hemorrhagic syndrome
4. pathologic refelc 4. convulsion
5. musculotinic tension symptoms 5. hyperemia, puffiness, hyperhidrosis of face
14. Meningococcal nasopharyngeal symptoms skin
1. rise in temperature, headache 22. Symptoms complex of brain edema (swelling)
2. stuffiness in nose with impaction (herniation) at meningococcal
3. tickleness and soreness in throat meningitis
4. dysphagia 1. occulomotorius disorder (ptosis, mydriasis,
5. eyesight decreasing diverged strabismus)
15. Meningococcal nasopharyngitis syndrome 2. sudden (sharp) motor anxiety
1. hemorrhagic exanthema 3. Waterhouse – Friederichsen syndrome
2. fever with chill 4. loss of consciousness
3. dry cough 5. appearance of pathological type of respiration
4. tickleness and soreness in throat 23. Clinical signs of meningococcal
5. rigidity of neck muscle meningoencephalitis
16. Clinical sign of meningococcemia 1. fever, headache, vomiting
1. gradual onset of disease 2. Stephansky symptoms
2. vesicular rash 3. meningeal symptoms
3. <star – shaped> hemorrhagic rash 4. focal neurologic symptomatology
4. affection of articulation 5. hemorrhagic exanthema
5. intoxication syndrome
 24. Criteria of severity of meningococcal infection 31. Clinical signs in presence with meningococcal
1. intensity of intoxication syndrome infection can be suspected
2. intensity of hemorrhagic syndrome 1. acute onset of disease with apparent
3. degree of changes in pigmental metabolism intoxication sign
4. intensity of meningeal syndrome 2. icterinous of skin and sclera
5. degree of anemia 3. positive meningeal symptoms
25. Criteria of severity of meningococcal infection 4. hemorrhagic skin
1. degree of dehydration 5. diarrheal symdrome
2. intensity of meningeal syndrome 32. Area of differential diagnosis search in meningeal
3. degree of dysuria syndrome presence
4. spreading of hemorrhagic rash of face skin 1.influenze, severe course
5. degree of purulent inflammatory changes in 2. meningococcal infection
liquor 3. spotted fever
26. Clinical laboratory characters of meningococcal 4. botulism
meningitis 5. leptospirosis
1. intensive headache, vomiting 33. Principals of therapy of meningococcal infection
2. neurtrophilic leukocytosis, SDE increased 1. etiotropic therapy
3. increasing of liquor pressure 2. disintoxication therapy
4. lymphocytosis pleocytosis 3. cytostatic therapy
5. detection of diplococci in liquor 4. rehydration therapy
27. Clinical laboratory characters of meningococcal 5. antishock therapy
meningitis 34. Principals of therapy of meningococcal infection
1. purulent inflammatory changes in liquor 1. administration of specific antitoxic horse serum
2. common brain symptomatology 2. antimicrobial therapy
3. appearance of paresis and paralysis 3. correction of hemostasis disturbances
4. <star like> hemorrhagic rash 4. glucocorticoid administration
5. signs of brain membrane irrtiation 5. vaccine therapy
28. Which of meningitis can be suspected in liquor is 35. Drugs for meningococcal infection treatment
muddy, flow on under high pressure, cytosis 1. gentamicin
count 47X103 /mm2, neutrophilic 98%, proteins 2. penicillin
2.64g/L, sugar content 1.4 mmol 3. ceftraizone
1. meningococcal meningitis 4.chloramphenicok
2. tuberculous meningitis 5. erythromycin
3. pneumococcal meningitis 36. Principals of meningococcal meningitis treatment
4. parotitis meningitis 1.oligatory urgent hospitalization
5. cytomegalovirus meningitis 2. planned hospitalization
29. Typical change in liquor in meningococcal 3. early prescribing of antimicrobial based on
meningitis clinical sign
1. neutrophilc cytosis 4. prescribing of antimicrobial only after
2. lymphocytic cytosis bacteriological examination of liquor
3. decreased concentration of glucose 5. choice of antimicrobial with relation to their
4. increased concentration of glucose penetration to BBB
5. cell protein dissociation 37. Antimicrobial used in meningococcal meningitis
30. Typical change in liquor in meningococcal 1. Penicillin
meningitis 2. Chloramphenicol
1. positive Wasserman reaction 3, Ciprofloxacin
2. positive Noone-Appelt reaction 4. Erythromycin
3. protein cell dissociation 5. Cephalosporin
4. cell protein dissociation 38. Criteria of termination of etiotropic therapy in
5. positive Pandi reaction meningococcal infection
1. Normalization of hemodynamic
2. not earlier than 21 days of normal temperature
3. liquor sanation
4. not earlier than 10 days of normal temperature
5. decreasing of specific antibody titer
39. Criteria of liquor sanitation in meningococcal Plague
meningitis 1. Pathogenic factor of Y. peptis
1. cytosis content less than 100 in mm2 1. Enterotoxin
2. cytosis count no more than 200 in mm2 2. Hacterlocidias
3. neutrophil count less than 25% 3. v/w antigen
4. neutrophil count 50% 4. pesticin
5. absence of bacteria in liquor 5. choline esterase blocker
2. Source of plague infection
1. Plague sick patient
2. Mammalia
3. Rodents
4. Ticks
5. Fleas
3. The spread way of plague infection
1. Transmissible
2. Contact
3. Alimentary
4. Air borne (droplet infection)
5. Sexual
4. Pathomorphological changes in lymph node in
plague
1. Necrosis of lymphoid tissue
2. Granulomatous inflammation
3. Serohaemorrhagic inflammation
4. Fibrinous inflammation
5. Presence of Y. peptis
5. Clinical form of plague
1. Cutaneous
2. Bubonic
3. Secondary bubonic form
4. Primary pneumonia form
5. Secondary pneumonia form
6. Clinical form of plague
1. primary septic form
2. secondary septic form
3. primary bubonic form
4. secondary bubonic form
5. dermatobubonic form
7. Clinical form of plague
1.anginous bubonic form
2. oculobubonic form
3. abdominal form
4. typhoid like form
5. septic form
8. Skin manifestation in plague
1 hemorrhagic rash
2. erythema nodosum
3. ‘gloves like’ and ‘sock like’ erythema
4. hemorrhagic carbuncle
5. phyletema
9. Characteristic of plague in primary bubone 17. Clinical manifestation of plague
1. card-like necrosis in cavity of bubo 1. painful bubo with hemorrhagic impregnation
2. sharp pain leading to forced position of of surrounded tissue
extremities 2. high temperature
3. adhesion with surrounded tissue, disappearance 3. psychomotor excitation
of bubo’s circuis 4. urticarial rash
4. hemorrhagic impregnation of tissue 5. deforming arthritis
5. abundant lymphangitis 18. Clinico-epidemiological sign of plague diagnostic
10. Clinical syndrome of plague 1.the stay in the endemic region 2 weeks before
1. infectious toxic shock illness
2. encephalitis 2. mosquitoes bite
3. hemorrhagic 3. acute infection pyschosis
4. bulbar 4. reddened face, scleritis, conjunctivitis,
5. paralytic hemorrhages
11. Clinical sign of pneumonic plague 5. dry mucous membrane of pharynx, chalk like
1.severe intoxication tongue
2. relatively satisfactory condition of patient 19. Methods of plague diagnostic
3. arising pulmonary insufficiency 1. skin allergic test
4. evident auscultation sign of lobar pneumonia 2. serologic
5. low grade auscultative sign 3. bacteriology
12. Clinical manifestation of pneumonic plague 4. X-ray study
1. cough with difficult separate purulent sputum 5. immunology
2. chest pain 20. Methods of plague diagnostic
3. friction rub 1. coprology
4. cough with fluid bloody sputum 2. thick blood ____
5. pronounced dyspnea, the sense of air 3. serologic
deficiency 4. biological
13. Clinical manifestation of intoxication syndrome 5. bacterioscopy
in plague 21. Differential diagnosis of bubonic plague
1. delirium, progressive encephalopathy 1. tularemia
2. descending paresis paralysis 2. benign nodular lymphoma
3. ascending paresis, paralysis 3. anthrax
4. hemorrhagic syndrome 4. suppurative lymphadenitis
5. absolute tachycardiac, hypotension 5. suppurative scleroadenitis
14. The primary septic form of plague is 22. Differential diagnosis of septic plague
characterized: 1. hemorrhagic fever
1. primary bubo 2. meningococcemia
2. secondary bubo 3. leptospirosis
3. rapid progression intoxication 4. viral hepatitis B
4. hemorrhagic syndrome 5. Lyme disease
5. hyperleucocytosis 23. Differential diagnosis of pnuemonia plague
15. Outbreak of bubonic plague 1. croupour pneumonia
1. adenophlegmon 2. severe acute respiratory syndrome (SARS)
2. secondary of pneumonic plague 3. onithosis
3. secondary septic plague 4. legionelossis
4. Reiter syndrome 5.infectious mononucleosis
5. Bechet’s syndrome 24. Principals of plague treatment
16. Clinico-epidemiological sign of plague 1.administration of antitoxic serum
diagnostic 2. antibacterial therapy
1. the way of the patient in the endemic region 10 3. disintoxication therapy
days before illness 4. desensitization therapy
2. the way of the patient in the endemic region 5 5. cytostatic therapy
days before illness
3. rapid progressive intoxication syndrome
4. early development of hemorrhagic syndrome
5. microadenopathy
25. Antimicrobial drug for plague treatment Tularemia
1. streptomycin 1. Properties of Fr. Tularemia
2. tetracycline 1. Fibrinolysis production
3. doxycycline 2. exotoxin production
4. chloramphenicol 3, resistance to phagocytosis
5. biseptol 4. O antigen presence
5. protein lipopolysaccharide complex presence
2. Ways of tularemia transmission
1. transmissible
2. alimentary
3. air born (droplet infection)
4. contact
5. sexual
3. Typical character of inflammation during
tularemia
1. fibrinous
2. granulomatous
3. serious hemorrhagic
4. purulent
5. gangrenous
4. Clinical form of tularemia
1. infectious allergic form
2. ulcerobubonic form
3. oculobubonic form
4. tuberculoid form
5. pulmonary form
5. Clinical form of tularemia
1. generalized form
2. bubonic form
3. scarlet like form
4. abdominal form
5. pulmonary form
6. Clinical sign of bubonic tularemia
1. ‘wave – like ‘ fever
2. hepatolienal syndrome
3. absence of lyphangitis
4. periadenitis
5. legible circuits of bubos
7. Characteristic of bubos during tularemia
1. modereate tenderness during palpation
2. full blown palpatory tenderness forced position
of extremities
3. inflammatory changes of surrounded tissue
4. absence of inflamed surrounded tissue
5. legible circuits and mobility
8. Oculobubonic tularemia is characterized by
1. papule conjunctivitis
2. erosion unlcer conjunctivitis
3. bilateral ptosis
4. blepharospasm
5. strabimus
9. Angionous bubonic tularemia is characterized by 18. The principle of treatment in tularemia
1. edema of subcutaneous fat spreading the neck 1. antibacterial therapy
and on the check 2. vaccinotherapy
2. necrotic tonsillitis 3. desintoxication therapy
3. paresis of soft palate 4. dehydration therapy
4. submaxillary lymphadenitis 5. desensitization therapy
5. predominant involvement of non tonsil 19. Treatment of tularemia
10. Pulmonary tularemia is characterized by 1. antibiotic
1. tracheobronchitis 2 nonsteroidal antiinflammotory drugs
2/ enlarges paratracheal and mediastinal lymph 3. immunosuppressive therapy
node 4. radial therapy
3. pneumonia 5. surgical therapy
4. purulent pleuritic 20. Effective antibiotic in tularemia
5. hemorrhagic pulmonary edema 1. streptomycin
11. Abdominal form of tularemia is characterized by 2. doxycycline
1. evident dehydration 3. chloramphenicol
2. mesenteric lymphadenitis 4. primaquine
3. hepatolienal syndrome 5. penicillin
4. symptoms of intoxication 21. Effective antibiotic in turaremia
5. hepatic absecess 1. erythromycin
12. Variants of course of pneumonia tularemia 2. rimfampicin
1. influenza like 3. gentamycin
2. bronchial 4. cephatriaxon
3. pneumonic 5. penicillin
4. Tuberculosis like
5.miliary
13. Types of fever in tularemia
1. permanent
2. remitant
3. intermittent
4. undular
5. atypical
14. Possible symptoms complex in tularemia
1. infectious toxix
2. infectious allergic
3. dehydration
4. primary effect
5. hemorrhagic
15. Laboratory diagnostic method of tularemia
1. endoscopy
2. serological
3. bacteriological
4. allergological
5. bacterioscopy
16. Laboratory diagnostic method of tularemia
1. agglutination reaction
2. reaction indirect hemagglution
3. Mantu test
4. allernocutanous test with tularemia
5. Bjurme test
17. The region of differential diagnostic in tularemia
1. felinosis
2. lymphogranulomatosis
3, purulent lymphadenitis
4. bubonic form of plague
5. pharyngeal diphteria
 HIV infection
1. Ways of HIV infection transmission
1. parenteral
2. sexual
3. perinatal
4. transmissible
5. household contact
2. Target cell of HIV
1. monocyte
2. neuroglia cell
3. CD 8+ lymphocyte
4. erythrocyte
5. CD 4+ lymphocyte
3. HIV infectious is characterized
1. presence of latent phase of disease
2. swift development of the disease
3. slow gradual development of the disease
4. activation of opportunistic infection
5. development of oncologic disease
4. In HIV infection lesion of immune system is
characterized by
1. functional disturbance of T lymphocyte
2. functional disturbance of B lymphocyte
3. functional disturbance of natural killer
4. appearance of autoimmune disturbance
5. decreasing of phagocytic function of
neutrophil
5. HIV in infected organism present in
1. plasma
2. neuroglia cell
3. vitreous
4. cells of macrophageal mononuclear system
5. sperm
6. Immunopathology of HIV infection is
characterized by
1. disorder of recognizing of hererologus
antigens by macrophage system
2. disorder of antibody genesis process
3. decreasing of CD 4 + T lymphocyte level
4. decreasing of secondary antibody level
5. hypergammaglobunemia
7. Damage of immune system of HIV is
characterized by
1. decreasing CD 4 + T lymphocyte level
2. high level of CIC (circulating immune
complex)
3. high level of immunoglobulin of all class
4. high level of B – lymphocytw
5 . lymphocytosis
8. Incubation period of HIV infection (A1) is
characterized by
1. high level of viraemia
2. exacerbation of opportunistic infection
3. falling of B lymphocyte numbers
4. decreasing of CD4+ T lymphocyte numbers
5. pancytopenia
9. Latent phase (A1,A2) of HIV infection is
characterized by
1. detection of HIV antibody
2. acute retroviral syndrome
3. decreasing of body mass
4. growing of weakness
5. intestinal disorder
10. Manifestation of acute retroviral (mononucleosis
like syndrome)
1. fever
2. polylymphadenopathy
3. erythematomacular rash
4. stomatitis
5. lymphomonoctyosis
11. Appearance of opportunistic infection in HIV
infection is caused by
1. congenital immunodeficiency
2.acquired immunodeficiency
3. social status of patients
4. repeated infection
5. absence of inoculation
12. Stage of primary manifestation of HIV infection
is characterized by
1. fever reaction more than 3 months
2. stable polylymphadenopathy
3. diarrhea of unknown genesis more than 2
month
4. decreasing of body mass more than 20%
5. visceral manifestation of Karposi Sacroma
13. Stage B2 B3 and C1 of secondary disease of HIV
infection is characterized
1. superficial damage of skin and mucous
membrane of fungous flora
2. superficial damage of skin and mucous
membrane of bacterial flora
3. superficial damage of skin and mucous
membrane of viral flora
4. cachexia
5. oncologic processes of central nervous system
14. Stage C2 of secondary disease of HIV infection is
characterized by
1. recurrent damage of skin and mucous
membrane of fungous, bacterial and viral flora
2. stable damage of skin and mucous membrane
of fungous, bacterial and viral flora
3. tuberculosis of extra pulmonary localization
4. pneumocytosis
5. local form of Karposi Sacroma
15. Stage C3 of secondary disease of HIV infection is
characterized by
1. cachexia
2. generalize bacterial viral fungous disease
3. localized form of Karposi sarcoma
4. toxoplasmosis of central nervous system
5. pnuemocytosis
16. Damage of respiratory organs in HIV infection is 22. Laboratory finding of AIDS stage in HIV
caused by infection
1. mycobacterium 1. pancytopenia
2. pneumocystitis carinii 2 polyclonal hypergammaglobulin
3. cytomegalovirus 3. decreasing of CD4+ T lymphocyte level less
4. toxoplasma than 200 cells in 1 mcl
5. cryptosporidium 4. appurtenance of gp160 in serum of blood
17. Clinical sign, indicating on necessity of 5. appearance of p24 in serum of blood
examination of HIV infection 23. Final diagnosis of HIV infection is put on basis of
1. diarrhea of unclear genesis during 2 – 3 weeks 1. clinical sign
2. fever of unclear genesis 2 -3 weeks duration 2. by appearance of antibody of HIV in ELISA
3. stable night sweating 3. by twice repeated appearance of antibody to
4. stable bilateral polylymphadenopathy more HIV glycoprotein in immunoblotting
than 2 groups of lymphanodule (except inguinal 4. by appearance of p24 in immunoblotting
lymphanodule) 5. by appearance of absolute decreasing of CD4+
5. first detection mycobacterial infection T lymphocyte
independently of localization and agent type 24. Principals of HIV infection treatment
18. It is necessary to suspect HIV infection in the 1. antiretroviral therapy
case of detection of 2. treatment of opportunistic infection
1. histologically confirm Karposi Sacroma in 3. cytostatic therapy
persons youngers than 60 4. substituting immunotherapy (introduction γ
2. toxoplasmosis of brain globulin , donor plasma
3. tuberculosis of any location 5. immunomodulant therapy
4. lymphoma of brain 25. Absolute evidence to the beginning of
5 stable candidiasis of skin and mucous antiretrovirus therapy is CD4+ lymphocyte level
membrane (lungs, gastrointestinal tract and 1. > 500 cells in 1mcl
urogenital system) 2. 200 – 499 cells in 1mcl
19. Obligatory laboratory examination in HIV 3. <200 celss in 1 mcl
antibody must be carried out 4. 500 – 1000 cells in 1 mcl
1.donor of blood organ biosubstrate 5. > 1000 cells in 1 mcl
2. patients of surgical hospital before planned
investigation
3. all pregnancy women
4. all newborns
5. all medical officer
20. Laboratory method of HIV infection diagnosis
1. detection fo HIV antibody in serum of blood
by ELISA method
2. detection of decreasing CD4+ T lymphocyte in
blood
3. detection of antibody to HIV glycoproteins in
blood serum by immnuobloting method
4. detection of hypergammaglobulin
5. detection of p24 in serum of blood
21. Prognostic unfavorable laboratory indices of HIV
infection are
1. lymphopenia
2. high level of CIC ( circulating immune
complex)
3. pancytopenia
4. falling of CD4+ T lymphocyte level
5. high level of CD8+ T lymphocyte level
Malaria 9. Pathogenetic mechanism of pyrogenic effect in
1. Sources of malaria infection malaria
1. agriculture animals 1. influence of metabolic parasites products
2. birds 2. granulomatous inflammation in
3. malaria patient parenchymatous organs
4. domestic animals 3. influence of decay product on invaded
5. parasitic carrier erythrocyte
2. Ways of malaria transmission 4. effect of mediators of inflammation and
1. transmissible immunity
2. parenteral 5. effect of plasmodium endotoxin
3. vertical 10. Availability of brady and tachy form of malaria
4. alimentary sporozoites in characteristic of malaria
5. household contacts 1. malariae
3. Malaria carrier 2. ovale
1. mosquitoes 3. falciparum
2. gnats 4. vivax
3. pincers 5. any etiology
4. louse 11. Development of erythrocyctic malaria
5. fleas recurrences is characterized in malaria
4. Relatively stable to malaria contamination 1. vivax
person, suffering from 2. falciparum
1. sickle cell anemia (crescent cell anemia) 3. malariae
2. diabetes mellitus 4. ovale
3. thalassemia 5. none of the above listed
4. thyrotoxicosis 12. Development of exoerythrocytic malaria
5. glucose 6 phosphate dehydrogenase deficiency occurrence is characteristic in malaria
5. When insect stings malaria agent penetrate into 1. vivax
the organism in the form of 2. falciparum
1. gametocyte 3. malariae
2. schizonts 4. ovale
3. tachysporozoites 5. none of the above listed
4. baradysporozoites 13. Development of perennial parasitemia is possible
5. trophozoites in malaria
6. Vital cycle of malaria agent falciparum in human 1. vivax
organism include 2. falciparum
1. exoerythrocytic (tissue) schizogony 3. malariae
2. erythrocytic schizogony 4. ovale
3. gametogenesis 5. none of the above listed
4. hibernation (persistence of hypnozoites in 14. For malaria is characteristic of anemia
hepatocytes) development
5. sporogony 1. aplastic
7. Vital cycle of malaria agents of vivax and ovale 2. iron deficiency
in human organism include 3. B12 deficiency
1. exoerythrocytic (tissue) schizogony 4. hemolytic
2. erythrocytic schizogony 5. folic acid deficiency
3. gametogenesis 15. Characteristic clinical signs of non-complicated
4. hibernation (persistence of hypnozoites in malaria
hepatocytes) 1. alternation of feverish paroxysm and apyrexia
5. sporogony periods
8. Pyrogenic effect in malaria caused by 2. hepatolienal syndrome
1. proteins of agents 3. polylymphadenopathy
2. endotoxin of plasmodium 4. hemolytic anemia
3. decay product of invaded erythrocyte 5. pnuemonia
4. inflammatory reaction in place of invasion
5. development of immunopathology reaction
16. Stages of malaria paroxysm
1. chill
2. headache
3. fever heat
4. myalgia
5. sweat
17. Clinical malaria periods
1. initial fever
2. secondary focus manifestation
3. residual manifestation
4. early recurrences
5. late recurrences
18. Clinical malaria periods
1. polylymphadenopathy
2. initial fever
3. typical malaria parosyxm
4. convalescence
5. catarrhal
19. For vivax malaria is characterized
1. alternation of paroxysms with 1 day apyrexia
2. alternation of paroxysms with 2 day apyrexia
3. alternation of paroxysms with 3 day apyrexia
4. exoerythrocytic cycle
5. erythrocytic cycle
20. For vivax malaria is characterized
1. benign (non-complicated) course
2. development of cerebral form
3. hemolytic anemia
4. initial fever
5. nephrotic syndrome
21. For falciparum malaria is characterized
1. prolonged fever of irregular type
2. alternation of paroxysms with 2 days apyrexia
3. alternation of paroxysms with 3 day apyrexia
4. exoerythrocytic recurrences
5. erythrocytic recurrences
22. For falciparum malaria is characterized
1. often formation of complication
2. severe course in unimmune persons
3. formation of stable postinfection immunity
4. polymorphisms of temperature curve
5. incubation period of 6 – 8 months
23. For malariae malaria is characterized
1. hemoglobinuric fever
2. early establishment of periodicity attacks
3. benign (non-complicated) course
4. cerebral form
5. possibility of nephrotic syndrome development
24. For malariae malaria is characterized
1. alternation of paroxysms with 1 day apyrexia
2. alternation of paroxysms with 2 day apyrexia
3. alternation of paroxysms with 3 day apyrexia
4. perennial erythrocyctic schizogony on low
level
5. prolonged (to 6 weeks) incubation period
25. Complication of falciparum malaria
1. cerebral form
2. hemoglobinuric fever
3. edema of lungs adult respiratory distress
syndrome
4. endocarditis
5. polyarthritis
26. Complication of falciparum malaria
1. infective toxical shock
2. acute renal insufficiency
3. purulent meningitis
4. cerebral form
5. hepatocirrhosis
27. Criteria of severe malaria course
1.articular syndrome
2. acute respiratory insufficiency
3. acute renal insufficiency
4. hepatolienal syndrome
5. encephalopathy
28. Criteria of severe malaria course
1. encephalopathy
2. anuria
3. prolonged course of disease
4. appearance of black colour urine
5. development of recurrence
29. Criteria of severe of malaria falciparum
1. leukocytosis more than 12 x 109 /L
2. level of parasitemia
3. detection of plasmodium in ring stage
4. level of gametocyctemia
5. appeaeance in peripheral blood of erythrocytic
containing trophozoites and schizonts
30. Laboratory criteria of severe course of malaria
falciparum
1. parasitemia more than 5000 in 1 mcl
2. number of parasite in smear more than 10 in
visual field
3. decreasing level of hemoglobin
4. decreasing of hematocrite
5. leukopenia
31. Examination methods that necessary for
diagnosis confirmation and species malaria
determination
1. microscopy of thick blood film
2. biochemical analysis of blood
3. microscopy of blood smear
4. blood culture
5. serologic method
32. Reliable method of laboratory malaria diagnostic
1. serologic
2.microscopy
3. biological
4. biochemical
5. allergological
33. Field of differential diagnostic in malaria Leptospirosis
1. brucellosis 1. Factors of leptospirosis pathogenicity
2. leptospirosis 1. cytotoxin production
3. viral hepatitis 2. the presence of endotoxin (lipopolysaccharide)
4. influenza of severe course 3. enterotoxin production
5. amebiasis 4. mobility
34. Hematoschizotropic drugs used for malaria 5 resistance to phagocytosis
treatment 2. The modes of leptospirosis transmission
1. vivax 1. aerosol
2. falciparum 2. contact
3. malariae 3 alimentary
4. ovale 4. transmissive
5. none of the above mentioned 5. aqueous
35. Histoschizotropic drugs used for malaria treatmet 3. Pathogenesis mechanism in leptospirosis
1. vivax 1. the formation of primary affect
2. falciparum 2. penetration of the pathogen through damaged
3. malariae skin layers, primary leptospiraemia
4. ovale 3. proliferation of the pathogen in the cells of
5. none of the above mentioned MPS
36. Gametocytic drugs expediency to use for 4. pronounced regional lymphadenitis with
prevention of malaria spreading periadenitis
1. vivax 5. hematogenic leptospira dissemination
2. falciparum endotoxinemia
3. malariae 4. Pathogenesis mechanism in leptospirosis
4. ovale 1. damage of vascular endothelium by leptospira
5. none of the above mentioned and their toxin
37. For treatment of severe course of falciparum 2. enhanced permeability of the vessels of
malaria parenterally are introduced the following microcirculating bed
drug 3. the development of granulomatous process in
1. quinine their liver
2.chloroquine 4. secretory diarrhea development
3. artemisinine 5. hemolysis of erythrocyte
4. fanzidar 5. Pathogenesis mechanism in leptospirosis
5. primaquine 1. damage of hepatocyte followed by
38. Preparation for malaria falciparum treatment parenchymal jaundice
1. quinine 2. damage of renal tubules epithelium
2.chloroquine 3. skeletal muscle involvement (rabdomyolisis)
3. artemisinine 4. permeation through hematoencephalic barrier
4. halofantrine 5. development of granuolomatous process in
5. mefloquine ( lariam) CNS
6. Clinical and epidemiological signs of
leptospirosis
1. acute onset of the disease pronounced
intoxication fever
2. severe muscle pain
3. signs of liver and kidney damage
4. bathing in open basins, staying in rural area
5. copious watery stool
7. Icteric syndrome in leptospirosis is due to
1. hemolytic activity of the pathogen
2. cytolysis of hepatocyte
3. development of mesenchymal inflammation
and intreahepatic cholestasis
4. development of cholangitis
5. decrease of guanosine- triphosphate transferase
products
8. Clinical symptoms of leptospirosis 17. Methods of laboratory diagnosis of leptospirosis
1. watery diarrhea leading to dehydration 1. bacterioscopical
2. muscular pain in particular of calf muscle 2. bacteriological
3. regional lymphadenitis 3. serological
4. liver enlargement 4. PCR-diagnostic
5. acute onset high fever intoxication 5. biological assay
9. Clinical symptoms of leptospirosis 18. Methods of laboratory diagnosis of leptospirosis
1. Padalka’s sumptoms 1. dark field microscopy of crushed blood drop
2. hemorrhagic syndrome 2. agglutination – lysis reaction
3. scanty roseaole rash on the anterior abdominal wall 3. complement binding assay
4. muscular pain in particular pain in calf muscle 4. indirect hemagglutiniation reaction
5. positive pounding symptoms 5. skin allergic assay
10. Clinical symptoms of leptospirosis 19. The range of differential diagnostic search in
1. marked hyperemia and puffiness of the face leptospirosis
2. conjunctival injection bleeding into sclera 1. viral hemorrhagic fever
3. swelling of subcutaneous fat 2. viral hepatitis
4. ulcerative necrotic tonsillitis 3. meningococcal infection
5. icteric skin and sclera vessels on the background of 3. typhus
fever 5. severe course of flu
11. Clinical syndrome of leptospirosis 20. The principles leptospirosis treatment
1. opthalmoplegic 1 hospitalization
2. colitic 2. etiotropic therapy
3. hepatolienal 3. non-specific toxication therapy
4. intoxication 4. specific detoxicaton therapy
5. renal 5. extracorporal detoxication
12. Clinical syndrome of leptospirosis 21. Antimicrobial agents for leptospirosis treatment
1. meningeal 1. gentamycin
2. hemorrhagic 2. tetracycline
3. myalgia 3. ampicillin
4. icteric 4. penicillin
5. exanthema 5. rifampicin
13. Criteria of leptospirosis course severity
1. degree of intoxication
2. acuteness of kidneys damage symptoms
3. acuteness of hemorrhagic manifestation
4. presence of relapse
5. serologic reaction titer
14. Criteria of leptospirosis course severity
1. acuteness of dehydration
2. the state of hemodynamic
3. sign of CNS damage involvement
4. acuteness of icteric syndrome
5. presence of hemorrhagic syndrome
15. Signs of kidney damage in leptospirosis
1. ansarca
2. anuria
3. urinary residues modification
4. oligoanuria
5. positive symptoms of Pastenatsky
16. Leptospirosis complications
1. iritis, iridocyclits
2. acute hepato-renal failure
3. external and internal bleedings
4. meningoencephalitis
5. toxico-infecitous shock