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Low Yield Semmelweis > Pathophys-Written Questions - Semester 2 > Flashcards

Pathophys-Written Questions - Semester 2 Flashcards

1
Q
  1. Which of the following causes vitamin B12 deficiency?
    a. Pregnancy
    b. Antiepileptic drugs
    c. Veganism
    d. Hemolytic anemia
    e. Jejunal resection
A

c. Veganism

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2
Q
  1. Which one of the following is caused by vitamin B12 deficiency?
    a. vitiligo
    b. peripheral neuropathy
    c. carcinoma of the stomach
    d. macrocytic anemia
A

b. peripheral neuropathy

d. macrocytic anemia

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3
Q

3a. Folate deficiency may cause:
a. Peptic ulcer
b. Spinal cord damage
c. Duodenal atrophy
d. Hemolytic anemia
e. Neural tube defect

A

e. Neural tube defect

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4
Q

3b. Which of the following may NOT cause folate deficiency?
a. inflammation
b. pregnancy
c. gluten sensitivity
d. antiepileptic drugs
e. veganism

A

e. veganism

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5
Q
  1. Which statement is true about the reduction of folate?
    a. it is inhibited by methotrexate
    b. it occurs during thymidylate synthesis
    c. it is inhibited by sulfonamides
    d. vegan people are affected more
    e. it needs vitamin B12
A

a. it is inhibited by methotrexate

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6
Q
  1. The lab reports for a patient with low MCV show high serum ferritin and low TIBC. What is the most likely cause for this patient’s anemia?(1)
    a. hypothyroidism
    b. iron deficiency
    c. thalassemia
    d. hemoglobinopathy
    e. anemia secondary to inflammation
A

e. anemia secondary to inflammation

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7
Q
  1. Specific signs and symptoms of iron deficiency anemia may include:
    a. intermittent glossitis
    b. angular cheilitis
    c. Plummer-Vinson syndrome
    d. dermatitis
A

a. intermittent glossitis
b. angular cheilitis
c. Plummer-Vinson syndrome
d. dermatitis

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8
Q
  1. Select the following that enhance iron absorption
    a. calcium
    b. citric acid
    c. ascorbic acid (Vitamin C)
    d. polyphenols (tea)
A

b. citric acid

c. ascorbic acid (Vitamin C)

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9
Q
  1. Iron is absorbed in the (1):
    a. duodenum
    b. stomach
    c. jejunum
    d. ileum
    e. colon
A

a. duodenum

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10
Q
  1. Signs/Symptoms of iron deficiency anemia may include all of the following except (1):
    a. Dizziness (vertigo)
    b. Pallor of conjunctiva
    c. Tachypnoe
    d. Abdominal pain
    e. Tachycardia
A

d. Abdominal pain

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11
Q
  1. Which of the following does not cause iron deficiency anemia? (1)
    a. Infection
    b. Increased requirement
    c. Decreased intake
    d. Malabsorption
    e. Chronic blood loss
A

d. Malabsorption

could be correct but the less probable option

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12
Q
  1. Which are characteristic laboratory finding(s) for IDA?
    a. Increased RDW
    b. Decreased sTfR
    c. Ovalocytes, elliptocytes, microcytes
    d. Decreased MCV, MCH, MCHC
A

a. Increased RDW

d. Decreased MCV, MCH, MCHC

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13
Q
  1. Which of the following normally contains >10% of body iron? (1)
    a. lymphocytes
    c. heart
    d. transferrin
    e. macrophages
A

e. macrophages

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14
Q
  1. What is the most important test for iron stores?
    a. se transferrin
    b. bone marrow biopsy
    c. se Fe
    d. TIBC
    e. se ferritin
A

e. se ferritin

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15
Q
  1. Where is most of non-heme iron found in the body?(1)
    a. in red blood cells
    b. free in plasma
    c. bound to transferrin
    d. bound to IF
    e. stored in the liver
A

e. stored in the liver

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16
Q
  1. Which of the following statements is correct?
    a. Hemorrhage is the major cause of iron deficiency in Hungary
    b. A molecule of transferrin may transport 4 atoms of iron
    c. A unit of blood contains 200-250 mg iron
    d. A man needs to absorb about 1 mg of dietary iron daily
A

c. A unit of blood contains 200-250 mg iron

d. A man needs to absorb about 1 mg of dietary iron daily

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17
Q
  1. Which of the following laboratory findings coincide with megaloblastic anemia?
    a. increased LDH
    b. increased serum bilirubin
    c. increased transferrin
    d. increased serum iron
A

a. increased LDH

b. increased serum bilirubin

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18
Q
  1. Which of the following is a normochromic, normocytic anemia:
    a. anemia of chronic renal disease
    b. sideroblastic anemia
    c. iron deficiency
    d. megaloblastic anemia
    e. thalassemia
A

a. anemia of chronic renal disease

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19
Q
  1. Microcytic anemia may be caused by:(1)
    a. Acute bleeding
    b. alpha Thalassemia
    c. Renal damage
    d. Folate deficiency
    e. Alcohol
A

b. alpha Thalassemia

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20
Q
  1. Which of the following is NOT a cause of microcytic anemia? (1)
    a. pancytopenia
    b. lead poisoning
    c. thalassemia
    d. iron deficiency anemia
    e. anemia of chronic disease
A

a. pancytopenia

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21
Q
  1. The most common form of sideroblastic anemia is:(1)
    a. Acquired, alcohol related
    b. Hereditary, X-linked
    c. Hereditary, autosomal recessive
    d. hereditary, autosomal dominant
    e. acquired, lead poisoning
A

a. Acquired, alcohol related

B6 def. is caused

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22
Q

21/22. Which of the following is NOT true about sideroblastic anemia?(1)

a. It may respond to erythropoietin
b. it may be inherited
c. it may cause splenomegaly
d. it may be caused by folate deficiency
e. it is most frequently caused by myelodysplasia

A

d. it may be caused by folate deficiency

B6 could cause but not folate

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23
Q
  1. All of the following statements regarding sideroblastic anemias are correct, EXCEPT:(1)
    a. sideroblastic anemic diseases result from impaired iron utilization and defective Hb formation
    b. they may cause splenomegaly
    c. they can be hereditary or acquired
    d. iron stores in the bone marrow are decreased
    e. they can be treated with pyridoxine to stimulate heme-synthesis
A

d. iron stores in the bone marrow are decreased

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24
Q
  1. Aside from the gradual onset signs of anemia, what other clinical presentations do you expect to see in aplastic anemia?
    a. associated thrombocytopenia, e.g. history of bleeding from the gums
    b. neutropenia, e.g. repeated bacterial infections
    c. purpura
    d. koilonychia, “spoon nails
A

a. associated thrombocytopenia, e.g. history of bleeding from the gums
b. neutropenia, e.g. repeated bacterial infections
c. purpura

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25
Q
  1. Aside from the gradual onset signs of anemia, what other clinical presentations do you expect to see in aplastic anemia?
    a. purpura
    b. koilonychia, “spoon nails”
    c. associated thrombocytopenia, e.g. history of bleeding from the gums
    d. neutropenia, e.g. repeated bacterial infections
A

a. purpura
c. associated thrombocytopenia, e.g. history of bleeding from the gums
d. neutropenia, e.g. repeated bacterial infections

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26
Q
  1. Aplastic anemia is a condition where:
    a. there is deficiency of iron
    b. there is deficiency of vitamin B12
    c. there is deficiency of vitamin B6
    d. the bone marrow does not produce enough blood cells
    e. red blood cells are destroyed very fast in the circulation
A

d. the bone marrow does not produce enough blood cells

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27
Q
  1. What can cause aplastic anemia?
    a. pregnancy
    b. drugs and chemicals
    c. viral infection
    d. idiopathic
A

a. pregnancy
b. drugs and chemicals
c. viral infection
d. idiopathic

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28
Q
  1. Select the statement about red blood cells that is incorrect?
    a. Red blood cells contain hemoglobin
    b. Deoxyhemoglobin carries oxygen
    c. Mature red blood cells lack nuclei
    d. Red blood cells lack mitochondria
    e. proerythroblast has EPO receptors
A

b. Deoxyhemoglobin carries oxygen

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29
Q
  1. Signs/symptoms of sickle cell anemia may include:
    a. Tachycardia
    b. Dizziness (vertigo)
    c. Abdominal pain
    d. Pallor of conjunctiva
A

a. Tachycardia
b. Dizziness (vertigo)
c. Abdominal pain
d. Pallor of conjunctiva

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30
Q 
31. Which are characteristic finding(s) for PNH, 
Paroxysmal nocturnal hemoglobinuria?
a. increased expression of CD55/CD59 
b. dark urine in the morning
c. Budd-Chiari syndrome
d. positive Ham test
A

b. dark urine in the morning
c. Budd-Chiari syndrome
d. positive Ham test

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31
Q
  1. What could be the clinical manifestation(s) of PNH?
    a. decreased GFR
    b. bone marrow aplasia, pancytopenia
    c. normal se haptoglobin
    d. iron deficiency
A

b. bone marrow aplasia, pancytopenia

d. iron deficiency

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32
Q
  1. Signs/symptoms of porphyrias may include:
    a. abdominal pain
    b. dermatitis
    c. peripheral neuropathy
    d. gallstone
A

a. abdominal pain

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33
Q
  1. Which of the following is NOT true about autoimmune hemolytic anemia?
    a. it may complicate B cell chronic lymphocytic leukemia
    b. it may be associated with IgM antibodies in serum
    c. it may be due to drugs
    d. it is associated with pernicious anemia
    e. it is associated with a positive direct antiglobulin test
A

d. it is associated with pernicious anemia

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34
Q
  1. Hemolytic anemia can be caused by:
    a. thalassemia
    b. G6PD deficiency
    c. PK deficiency
    d. inflammation
A

a. thalassemia
b. G6PD deficiency
c. PK deficiency

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35
Q
  1. Where in the body is erythropoietin produced?
    a. spleen
    b. thyroid
    c. liver
    d. kidney
A

c. liver

d. kidney

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36
Q
  1. The primary cause of anemia of chronic renal disease is:
    a. hydremia
    b. blood lost in the urine
    c. deficiency of iron
    d. hemolysis resulting from capillary thrombosis
    e. decreased erythropoietin synthesis
A

e. decreased erythropoietin synthesis

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37
Q
  1. When red blood cells are removed from the circulation, part of their components are recycled while others are disposed. Select the incorrect statement about destruction of red blood cells:
    a. biliverdin and bilirubin impart color to bile
    b. macrophages in the liver and spleen destroy worn out red blood cells
    c. iron is stored in RES in the form of ferritin
    d. the greenish pigment, biliverdin, is recycled to the bone marrow
    e. iron is carried to the bone marrow by a protein called transferrin
A

d. the greenish pigment, biliverdin, is recycled to the bone marrow

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38
Q
  1. What test would you do, besides history, CBC and blood smear, to confirm Thalassemia? (1)
    a. Hb electrophoresis
    b. se bilirubin
    c. TIBC
    d. se ferritin
    e. se Fe
A

a. Hb electrophoresis

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39
Q
  1. Which of the following is true about alpha-thalassemia?
    a. Presence of Bart’s Hb
    b. Reduced production of alpha chain due to a point mutation
    c. The Mentzer index usually is >13
    d. Presence of HbH
A

a. Presence of Bart’s Hb

d. Presence of HbH

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40
Q
  1. Which of the following is true about α-thalassemia?
    a. it is rare except in the Far East
    b. it causes a microcytic hypochromic blood picture
    c. it ameliorates β thalassemia
    d. it may cause haemoglobin H disease
A

b. it causes a microcytic hypochromic blood picture

d. it may cause haemoglobin H disease

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41
Q
  1. Which would you expect to see on a blood smear for beta thalassemia?
    a. Heinz bodies
    b. hypochromic microcytic anemia
    c. multinucleated neutrophils
    d. target cells
A

b. hypochromic microcytic anemia

d. target cells

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42
Q
  1. Which of the following is true about β-thalassemia?
    a. reduced production of β chain due to a point mutation
    b. presence of HbH
    c. increased HbF
    d. the Mentzer index usually is >13
A

a. reduced production of β chain due to a point mutation

c. increased HbF

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43
Q
  1. Which of the following statements is true about β-thalassemia trait?(1)
    a. it is associated with a reticulocytosis
    b. it may cause hemoglobin H disease
    c. it is associated with splenomegaly
    d. it is associated with a raised hemoglobin A2 level
    e. it is associated with iron overload
A

d. it is associated with a raised hemoglobin A2 level

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44
Q
  1. Where is beta thalassemia the most common?
    a. Mediterranean
    b. Arabian peninsula
    c. West Africa
    d. Southeast Asia
A

a. Mediterranean
b. Arabian peninsula
d. Southeast Asia

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45
Q
  1. Spherocytes in the blood film may occur in: (1)
    a. Iron deficiency anemia
    b. Reticulocytosis
    c. Thalassemia major
    d. Autoimmune hemolytic anemia
    e. Glucose-6-phosphate dehydrogenase (G6PD) deficiency
A

d. Autoimmune hemolytic anemia

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46
Q
  1. It is true about hereditary spherocytosis (1):
    a. it can be treated by splenectomy
    b. it is due to pyruvate kinase deficiency
    c. it is caused by an inherited defect in hemoglobin
    d. it is more frequent in southern Europe
    e. It is more common in males
A

a. it can be treated by splenectomy

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47
Q
  1. Spherocytes in the blood film may occur in:(1)
    a. thalassemia major
    b. autoimmune hemolytic anemia
    c. glucose-6-phosphate dehydrogenase (G6PD) deficiency
    d. reticulocytosis
    e. iron deficiency anemia
A

b. autoimmune hemolytic anemia

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48
Q
  1. Anemia secondary to uremia is characteristically: (1)
    a. macrocytic
    b. microcytic, hypochromic
    c. hemolytic
    d. megaloblastic
    e. normocytic, normochromic
A

e. normocytic, normochromic

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49
Q
  1. A 50-year-old patient is suffering from pernicious anemia. Which of the following laboratory data are most likely on this patient?(1)
    a. WBC 12.5 G/l; PLT 1250 G/l
    b. WBC 6.5 G/l; PLT 80 G/l
    c. WBC 4 G/l; PLT 750 G/l
    d. WBC 5 G/l; PLT 50 G/l
    e. WBC 12.5 G/l; PLT 250 G/l
A

d. WBC 5 G/l; PLT 50 G/l

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50
Q
  1. Which of the following is associated with pernicious anemia?(1)
    a. thyroid antibodies in serum
    b. systemic lupus erythematosus
    c. ileocecal resection
    d. alcoholism
    e. malabsorption of B12-intrinsic factor complex
A

e. malabsorption of B12-intrinsic factor complex

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51
Q
  1. Myelodysplastic syndrome (MDS) is characterized by:
    a. Favorable responsiveness to chemotherapy
    b. Decreasing prevalence among elderly people
    c. Granulocytes with hyperlobulated nuclei
    d. A wide array of red blood cell shape deformities
A

c. Granulocytes with hyperlobulated nuclei

d. A wide array of red blood cell shape deformities

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52
Q
  1. 2 Myelodysplastic syndrome (MDS) is characterized by:
    a. Hypocellularity in the bone marrow
    b. Simultaneous involvement of multiple cell lines
    c. Frequent progression to acute leukemia
    d. Gradually progressive anemia
    e. Favorable responsiveness to chemotherapy
A

b. Simultaneous involvement of multiple cell lines
c. Frequent progression to acute leukemia (“the real danger”)
d. Gradually progressive anemia

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53
Q
  1. 3 Myelodysplastic syndrome (MDS) is characterized by:
    a. Predominant involvement of the megakaryocytic cell line
    b. Anemia
    c. Increasing prevalence among elderly people
    d. Elevated platelet count
A

b. (Refractory) Anemia

c. Increasing prevalence among elderly people

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54
Q
  1. Symptoms/alterations in polycythemia vera (PV)?
    a. Decreased erythropoietin level
    b. Decreased hematocrit
    c. Long standing febrile state
    d. Itching
A

a. Decreased erythropoietin level

d. Itching

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55
Q
  1. Symptoms/alterations in polycythemia vera (PV), except?
    a. Itching
    b. Increased hematocrit
    c. Decreased erythropoietin level
    d. Long standing febrile state
A

d. Long standing febrile state

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56
Q
  1. A factor in the molecular pathomechanism of chronic myeloid leukemia (CML)? (1)
    a. Decreased protein degradation
    b. Abnormally increased intracellular signaling
    c. Increased relocation of membrane lipids
    d. Increased intracellular phosphatase activity
    e. Decreased mitochondrial energy production
A

b. Abnormally increased intracellular signaling

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57
Q
  1. Which is a characteristic, frequent, acquired genetic
    alteration in chronic myeloid leukemia (CML)?(1)
    a. Calreticulin gene mutations
    b. 9:22 chromosome translocation
    c. Abl kinase gene mutations
    d. Gene rearrangement of the cyclin D gene
    e. K-ras gene mutations
A

b. 9:22 chromosome translocation

* This is the Philadelphia Chromosome: Bcr-Abl translocation.

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58
Q
  1. As a result of 9:22 translocation in chronic myeloid leukemia (CML):(1)
    a. Apoptosis of affected cells is increased
    b. mRNA transcription decreases
    c. A chimeric protein is produced with increased kinase activity
    d. Activity of the bcr protein increases
    e. Cell differentiation becomes blocked at an early stage
A

c. A chimeric protein is produced with increased kinase activity

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59
Q
  1. Acute lymphoblastic leukemia (ALL) is characterized by:
    a. All cell forms of the lymphoid lineage are present in the periphery
    b. Simultaneous involvement of multiple cell lines
    c. Favorable responsiveness to chemotherapy
    d. It is less frequent in adults compared to children
A

c. Favorable responsiveness to chemotherapy

d. It is less frequent in adults compared to children

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60
Q
  1. 2 Acute lymphoblastic leukemia (ALL) is characterized by:
    a. T lymphocytes are more frequently affected than B lymphocytes
    b. High chance of in utero mutation generation
    c. Recurrent genetic alterations can be identified by cytogenetic testing
    d. Poor response to chemotherapy
A

b. High chance of in utero mutation generation

c. Recurrent genetic alterations can be identified by cytogenetic testing

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61
Q
  1. As a result of high sensitivity detection of minimal residual disease: (1)
    a. The cost of diagnostic testing can be decreased
    b. Novel inherited mutations can be identified
    c. Novel tumor specific molecular alterations can be identified
    d. Treatment of relapse can be initiated earlier
    e. Disease classification can be improved
A

d. Treatment of relapse can be initiated earlier

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62
Q
  1. The most frequent hematological tumor: (1)
    a. Acute myeloid leukemia (AML)
    b. Primary myelofibrosis (PMF)
    c. Non-Hodgkin lymphoma
    d. Myelodysplastic syndrome (MDS)
    e. Follicular lymphoma
A

c. Non-Hodgkin lymphoma

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63
Q
  1. Pathogenic factors of renal failure in myeloma multiplex (MM), except:
    a. Decreased perfusion
    b. Light chain deposition
    c. Nephrocalcinosis
    d. Amyloidosis
A

a. Decreased perfusion

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64
Q
  1. 1 Pathogenic factors of renal failure in myeloma multiplex (MM), except:
    a. Decreased perfusion
    b. Amyloidosis
    c. Light chain deposition
    d. Nephrocalcinosis
A

a. Decreased perfusion

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65
Q
  1. 1 Pathogenic factors of renal failure in myeloma multiplex (MM), except:
    a. Decreased perfusion
    b. Nephrocalcinosis
    c. Light chain deposition
    d. Amyloidosis
A

a. Decreased perfusion

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66
Q
  1. Pathogenetic factors of anemia in myeloma multiplex (MM):
    a. Latent iron deficiency
    b. Bone marrow infiltration by plasma cell expansion
    c. Decreased erythropoietin production due to renal failure
    d. Hemodilution
A

b. Bone marrow infiltration by plasma cell expansion

c. Decreased erythropoietin production due to renal

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67
Q
  1. Predominantly affected cell lines in myeloma multiplex (MM):
    a. Plasma cells
    b. Myeloblasts
    c. B lymphocytes
    d. Megakaryocytes
A

a. Plasma cells

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68
Q
  1. Consequences of the bone lesions in myeloma multiplex (MM):
    a. Increased osteoblast activity
    b. Elevated serum calcium level
    c. Erythroid hyperplasia in the newly formed bone marrow space
    d. Pathological fractures
A

b. Elevated serum calcium level

d. Pathological fractures

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69
Q
  1. Abnormal condition(s) preceding myeloma multiplex (MM):
    a. Myelodysplastic syndrome (MDS)
    b. Primary myelofibrosis (PMF)
    c. Polycythemia vera (PV)
    d. Monoclonal gammopathy of undetermined significance (MGUS)
A

d. Monoclonal gammopathy of undetermined significance (MGUS)

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70
Q
  1. Characteristic alteration in myeloma multiplex (MM):
    a. Renal failure
    b. Elevated plasma total protein level
    c. Anemia
    d. Elevated blast count in the periphery
A

a. Renal failure
b. Elevated plasma total protein level
c. Anemia

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71
Q
  1. 1 Characteristic alteration in myeloma multiplex (MM):
    a. Elevated plasma cell count in the periphery
    b. Decreased plasma total protein level
    c. Osteolytic bone lesions
    d. Thrombocytosis
A

c. Osteolytic bone lesions

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72
Q
  1. Which of the following is an immature cell in platelet differentiation? (1)
    a. Common myeloid progenitor cell
    b. Common lymphoid progenitor cell
    c. Mesodermal stem cell
    d. Mesenchymal stem cell
    e. None of the above
A

a. Common myeloid progenitor cell

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73
Q
  1. As a result of uncovering the driver mutation in myeloproliferative neoplasms (MPN):(1)
    a. There is a predominance of the chemotherapeutic treatments
    b. Bone marrow examination can be omitted in the majority of the cases
    c. There is a cost decrease of diagnostics
    d. There is a favorable change in prognosis
    e. None of the above
A

b. Bone marrow examination can be omitted in the majority of the cases

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74
Q
  1. 1 As a result of uncovering the driver mutation in myeloproliferative neoplasms (MPN):
    a. Novel, targeted therapies become feasible
    b. The invasive bone marrow examination can frequently be omitted
    c. The incidence of MPN diseases decreases
    d. The diagnostics become less expensive
A

a. Novel, targeted therapies become feasible

b. The invasive bone marrow examination can frequently be omitted

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75
Q
  1. Which cell lines are affected in myeloproliferative neoplasms (MPN)?
    a. Dendritic cell
    b. Thymocyte
    c. Megakaryocyte
    d. Natural killer cell
A

c. Megakaryocyte

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76
Q
  1. Which is a characteristic feature of myeloproliferative neoplasm? (1)
    a. Bone destruction
    b. Elevated erythropoietin level
    c. Splenomegaly
    d. Initial symptom is frequently bone pain
    e. Rapid progression
A

c. Splenomegaly

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77
Q
  1. Acute myeloid leukemia (AML) is characterized by:
    a. Blast ratio in the bone marrow exceeds 20%
    b. Anemia is a characteristic symptom at presentation
    c. It is associated with elevated platelet count
    d. All cell forms of the myeloid lineage are present in the periphery
A

a. Blast ratio in the bone marrow exceeds 20%

b. Anemia is a characteristic symptom at presentation

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78
Q
  1. Acute myeloid leukemia (AML) is characterized by:
    a. Blast ratio in the bone marrow exceeds 20%
    b. Anemia is a characteristic symptom at presentation
    c. It is associated with elevated platelet count
    d. All cell forms of the myeloid lineage are present in the periphery
A

a. Blast ratio in the bone marrow exceeds 20%

b. Anemia is a characteristic symptom at presentation

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79
Q
  1. Acute myeloid leukemia (AML) is characterized by:
    a. In the majority of cases, the malignant clone has increased differentiation capacity
    b. It is the result of a series of acquired mutations affecting the myeloid stem cell
    c. It causes death in a couple of weeks/months without treatment
    d. Myeloblasts are rarely seen in the periphery
A

b. It is the result of a series of acquired mutations affecting the myeloid stem cell
c. It causes death in a couple of weeks/months without treatment

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80
Q
  1. It is true for acute myeloid leukemia (AML):
    a. All cell forms of the myeloid lineage are present in the periphery
    b. It is more common in adults than ALL
    c. A pathological bone fracture is the most frequent symptom at presentation
    d. Blast ratio in the bone marrow does not exceed 20%
A

b. It is more common in adults than ALL

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81
Q
  1. Main AML subclasses according to the World Health Organization (WHO) classification:
    a. AML with myelodysplastic alterations
    b. Therapy related AML
    c. AML with recurrent genetic abnormality
    d. AML associated with Epstein-Barr virus infection
A

a. AML with myelodysplastic alterations
b. Therapy related AML
c. AML with recurrent genetic abnormality
* Lecture slide 44

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82
Q
  1. In AML, genes affected by mutation in more than 10% of the cases:
    a. Kirsten rat sarcoma viral oncogene homolog (K-RAS)
    b. Nucleophosmin 1 (NPM1)
    c. Janus kinase 2 (JAK2)
    d. Break point cluster region (BCR)
A

b. Nucleophosmin 1 (NPM1)

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83
Q
  1. Which of the following diseases is associated with increased AML-transformation risk? (1)
    a. Follicular lymphoma
    b. Primary myelofibrosis (PMF)
    c. Essential thrombocytosis (ET)
    d. Polycythemia vera (PV)
    e. Myeloma multiplex (MM)
A

b. Primary myelofibrosis (PMF)

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84
Q
  1. Which is an environmental factor playing a role in leukemogenesis?
    a. Down syndrome
    b. Deep vein thrombosis
    c. Human T lymphotropic virus (HTLV) infection
    d. Chronic alcohol consumption
    e. Vitamin K deficiency
A

c. Human T lymphotropic virus (HTLV) infection

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85
Q
  1. Symptoms/alterations in essential thrombocytosis (ET)?
    a. Itching
    b. Decreased hematocrit
    c. Decreased erythropoietin level
    d. Splenomegaly
A

d. Splenomegaly

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86
Q
  1. Which is a characteristic, frequent, acquired genetic alteration in essential thrombocytosis (ET)?(1)
    a. 9:22 chromosome translocation
    b. Gene rearrangement of the cyclin D gene
    c. Abl kinase gene mutations
    d. K-ras gene mutations
    e. Calreticulin gene mutations
A

e. Calreticulin gene mutations

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87
Q
  1. Which disease is characterized by the total absence of differentiation? (1)
    a. Myelodysplastic syndrome (MDS).
    b. Chronic myeloid leukemia (CML).
    c. Essential thrombocytosis (ET).
    d. All of the above.
    e. Acute myeloid leukemia (AML).
A

d. All of the above.

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88
Q
  1. Which genetic factor plays a role in leukemogenesis? (1)
    a. Down syndrome
    b. Sickle cell anemia
    c. Thalassemia major
    d. Glucose-6-phosphate dehydrogenase deficiency
    e. Epstein-Barr virus infection
A

a. Down syndrome
*Leukemogenesis =Generation of Cancer
(Other Genetic factors: Down, Bloom, Klinefelter, Wiskott-Aldrich syndromes, Fanconi anaemia, neurofibromatosis)

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89
Q
  1. Which are the environmental factors playing a role in leukemogenesis, Except one?
    a. Industrial solvents
    b. Epstein-Barr virus infection
    c. Anti-tumor chemotherapy
    d. Ionizing irradiation
    e. Sickle cell anemia
A

e. Sickle cell anemia

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90
Q
  1. The following are myeloid diseases, Except (1):
    a. Polycythemia vera (PV)
    b. Essential thrombocytosis (ET).
    c. Myelodysplastic syndrome (MDS).
    d. Myeloma multiplex (MM)
    e. Chronic myeloid leukemia (CML).
A

d. Myeloma multiplex (MM)

It is a Monoclonal Gammopathy

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91
Q
  1. Chemotherapeutic target(s) in leukemias:
    a. mRNA synthesis
    b. Purine synthesis
    c. %*50%Glycolysis
    d. Terminal oxidation
A

b. Purine synthesis

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92
Q
  1. Targeted therapeutic options in leukemias:
    a. Proteasome inhibitors
    b. Cyclooxygenase inhibitors
    c. Tyrosine kinase inhibitors
    d. Proton-pump inhibitors
A

c. Tyrosine kinase inhibitors
* For example, the drug imatinib (Gleevec) stops the action of a protein within the leukemia cells of people with chronic myelogenous leukemia - FIRST DRUG TO BE RELEASED EARLIER THAN EXPECTED BY THE SUPPORT OF FDA.

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93
Q
  1. Which is a common symptom of leukemia at presentation? (1)
    a. Jaundice
    b. Febrile state without obvious cause
    c. Headache
    d. Altered vision
    e. Nausea and vomiting
A

b. Febrile state without obvious cause

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94
Q
  1. Which is a common symptom of acute leukemia at presentation?
    a. Punctuated skin bleedings
    b. Painful swelling of the lower extremity
    c. Altered vision
    d. Nausea and vomiting
    e. Headache
A

a. Punctuated skin bleedings
* Multiple ecchymoses. Bleeding may be caused by thrombocytopenia, coagulopathy that results from disseminated intravascular coagulation (DIC), or both.

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95
Q
  1. Which is a clonal hematopoietic disease with primary bone marrow localization?(1)
    a. Hodgkin disease
    b. Chronic myeloid leukemia (CML)
    c. Mantle cell lymphoma
    d. Follicular lymphoma
    e. None of the above
A

b. Chronic myeloid leukemia (CML)

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96
Q
  1. The French-American-British (FAB) classification is primarily based on: (1)
    a. Cytogenetic alterations
    b. Prognosis
    c. Molecular alterations
    d. Histopathological picture
    e. Genetic mutations
A

d. Histopathological picture

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97
Q
  1. Which one is a targeted diagnostic procedure of clonal hematologic diseases? (1)
    a. Fine needle biopsy
    b. Scintigraphy
    c. Computed tomography
    d. Gastroscopy
    e. Flow cytometry
A

e. Flow cytometry

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98
Q
  1. Factors in the molecular pathomechanism of leukemia, except?(1)
    a. Decreased differentiation
    b. Increased mitochondrion production
    c. Increased DNA synthesis
    d. Decreased apoptosis
    e. Increased proliferative signaling text
A

b. Increased mitochondrion production

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99
Q
  1. 1 Factors in the molecular pathomechanism of leukemia, except?(1)
    a. Increased proliferative signaling
    b. Increased DNA synthesis
    c. Increased mitochondrion production
    d. Decreased differentiation
    e. Decreased apoptosis
A

b. Increased mitochondrion production

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100
Q
  1. Element of molecular pathomechanism of leukemia? (1)
    a. Predominance of glycolysis in cellular energy production
    b. Increased mitochondrion production
    c. Plasma membrane reorganization
    d. Increased intracellular signaling leading to enhanced cell proliferation
    e. Accelerated differentiation
A

d. Increased intracellular signaling leading to enhanced cell proliferation

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101
Q
  1. The World Health Organization (WHO) classification is primarily based on:(1)
    a. Cytochemistry reaction pattern
    b. Cellular origin and genetic alterations
    c. Cytogenetic alterations
    d. Histopathological picture
    e. Prognosis
A

b. Cellular origin and genetic alterations

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102
Q
  1. What is the cause of thrombocytopenia in liver cirrhosis?
    a. decreased bile secretion
    b. direct effect of metabolic alterations on the bone marrow
    c. splenomegaly – hypersplenia
    d. hyperbilirubinemia
    e. malabsorption
A

c. splenomegaly – hypersplenia

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103
Q
  1. Thrombocytopenia can occur, except in:
    a. acute leukemia
    b. in autoimmune disease
    c. following massive transfusion
    d. acute inflammation
    e. in measles infection
A

d. acute inflammation

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104
Q
  1. Thrombotic thrombocytopenic purpura (TTP) is characterized by:
    a. ADAMTS13 deficiency
    b. increased platelet aggregation
    c. von Willebrand factor protein of ultra large size
    d. renal failure
A

a. ADAMTS13 deficiency
b. increased platelet aggregation
c. von Willebrand factor protein of ultra large size
d. renal failure?

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105
Q
  1. Idiopathic thrombocytopenic purpura (ITP) is characterized by:
    a. it is associated with vitamin K deficiency
    b. decreased platelet aggregation
    c. it is more common in females than males
    d. decreased platelet release reaction
    e. bleedings into the joints
A

c. it is more common in females than males

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106
Q
  1. Which of the following statements is true regarding the regulation of platelet production?
    a. Hypoxemia is an important stimulus of platelet production.
    b. The stimulating hormone, thrombopoietin is produced in the bone marrow.
    c. No hormone is known to inhibit platelet production.
    d. The segmented nuclei of the megakaryocytes are incorporated in the platelets.
    e. Platelet production is decreased in inflammation.
A

c. No hormone is known to inhibit platelet production.

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107
Q
  1. Surface receptor that plays a role in platelet activation:
    a. prostacyclin
    b. histidine decarboxylase
    c. thromboxane A2
    d. glycoprotein IIb/IIIa
    e. endocannabinoid
A

d. glycoprotein IIb/IIIa

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108
Q
  1. Which step of platelet activation takes place the earliest?
    a. aggregation
    b. contraction of the cytoskeleton
    c. adhesion
    d. elevation of intracellular calcium levels
    e. release of dense granule content
A

c. adhesion

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109
Q
  1. Platelets are characterized by:
    a. the majority of blood group antigens are expressed on their surface
    b. they are capable to divide
    c. surface expression of HLA class I antigens
    d. a lack of granules
    e. they generate energy by glycolysis
A

c. surface expression of HLA class I antigens

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110
Q
  1. Platelet production can be inhibited by:
    a. vitamin B12 deficiency
    b. all answers are correct
    c. chemotherapy
    d. bone marrow manifestation of malignant disease
    e. measles virus infection
A

b. all answers are correct

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111
Q
  1. Direct interaction partner of thrombin, except:
    a. subendothelial smooth muscle cells
    b. platelets
    c. lymphocytes
    d. monocytes
    e. endothelial cells
A

a. subendothelial smooth muscle cells

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112
Q
  1. Interaction partner of thrombin:
    a. lymphocytes
    b. monocytes
    c. fibrinogen
    d. platelets
    e. all the answers are correct
A

e. all the answers are correct

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113
Q
  1. 1 Acquired risk factor for deep vein thrombosis:
    a. dehydration
    b. nephrotic syndrome
    c. hypertension
    d. obesity
A

a. dehydration
b. nephrotic syndrome
d. obesity

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114
Q
  1. 2 Acquired risk factor for deep vein thrombosis:
    a. sustained immobilization
    b. overdose of vitamin K
    c. asthma bronchiale
    d. malignant disease
A

a. sustained immobilization

d. malignant disease

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115
Q
  1. Causative factor responsible for increased deep vein thrombosis risk in malignant diseases:
    a. anemia
    b. decreased food intake
    c. cachexia due to the tumor
    d. decreased physical activity
A

d. decreased physical activity

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116
Q

14 Genetic factors increasing the risk of deep vein thrombosis:

a. activated protein C resistance
b. Gilbert’s syndrome
c. Leiden mutation
d. alfa-1 antitrypsin deficiency

A

a. activated protein C resistance

c. Leiden mutation (Factor V def.)

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117
Q
  1. 1 Laboratory alteration suggesting deep vein thrombosis:
    a. decreased erythrocyte sedimentation rate (ESR)
    b. decreased hemoglobin level
    c. decreased activated partial thromboplastin time (aPTT)
    d. elevated plasma D-dimer level
A

d. elevated plasma D-dimer level

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118
Q
  1. 2 Laboratory alteration suggesting deep vein thrombosis:
    a. elevated plasma total protein level
    b. elevated plasma fibrin degradation peptide (FDP) level
    c. elevated plasma D-dimer level
    d. decreased plasma calcium level
A

b. elevated plasma fibrin degradation peptide (FDP) level

c. elevated plasma D-dimer level

119
Q
  1. Endothelial cells synthesize:
    a. prostaglandin E2
    b. serotonin
    c. protein C
    d. von Willebrand factor
    e. elastase
A

d. von Willebrand factor

120
Q
  1. Which of the following statements is true regarding the role of endothelial cells in coagulation?
    a. upon tissue injury, endothelial cells physically prevent the exposure
    of the subendothelium
    b. by the production of protein C, endothelial cells inhibit the coagulation process
    c. none of the other answers are correct
    d. endothelial cells inhibit platelet activation
    e. endothelial cells have an overall anticoagulant activity
A

e. endothelial cells have an overall anticoagulant activity

Thrombomodulin

121
Q
  1. Mechanism of bleeding of vascular origin, except:
    a. amyloidosis
    b. hypertension
    c. immune complex deposition
    d. connective tissue atrophy
    e. altered TGF-β signaling
A

b. hypertension

122
Q
  1. 1 Its concentration increases in inflammation:
    a. protein C
    b. factor X (Stuart-Prower)
    c. thrombomodulin
    d. factor II (prothrombin)
    e. factor VIII (anti-hemophilic)
A

e. factor VIII (anti-hemophilic)

123
Q
  1. 2 Its concentration increases in inflammation:
    a. anti-hemophilic factor (VIII)
    b. fibrinogen (I)
    c. prothrombin (II)
    d. free fatty acids
A

a. anti-hemophilic factor (VIII)

b. fibrinogen (I)

124
Q
  1. Part of the coagulation process, except:
    a. release of thromboxane A2 from platelets
    b. release of fibrin degradation peptides
    c. release of tissue factor
    d. release of serotonin from platelets
    e. mast cell degranulation
A

e. mast cell degranulation

125
Q
  1. Vitamin K dependent coagulation factor, except:
    a. factor VIII (anti-hemophilic)
    b. factor II (prothrombin)
    c. factor X (Stuart-Prower)
    d. factor IX (Christmas)
    e. factor VII (proconvertin)
A

a. factor VIII (anti-hemophilic)

126
Q
  1. 1 Vitamin K dependent coagulation factors:
    a. von Willebrand factor
    b. tissue factor
    c. proconvertin (VII)
    d. prothrombin (II)
A

c. proconvertin (VII)

d. prothrombin (II)

127
Q
  1. 2 Vitamin K dependent coagulation factors:
    a. Stuart-Prower factor (X)
    b. fibrinogen (I)
    c. Christmas factor (IX)
    d. prothrombin (II)
A

a. Stuart-Prower factor (X)
c. Christmas factor (IX)
d. prothrombin (II)

128
Q
  1. 1 Typical laboratory results in vitamin K antagonist treatment:
    a. normal activated partial thromboplastin time (aPTT)
    b. normal prothrombin time (PT)
    c. normal platelet count
    d. prolonged thrombin time (TT)
A

c. normal platelet count

129
Q
  1. 2 Typical laboratory results in vitamin K antagonist treatment:
    a. prolonged prothrombin time (PT)
    b. prolonged bleeding time
    c. decreased platelet count
    d. prolonged activated partial thromboplastin time (aPTT)
A

a. prolonged prothrombin time (PT)

d. prolonged activated partial thromboplastin time (aPTT)

130
Q
  1. Anticoagulation mechanisms/factors:
    a. prostacyclin
    b. antithrombin III
    c. protein S
    d. heparin cofactor type II
A

a. prostacyclin
b. antithrombin III
c. protein S
d. heparin cofactor type II

131
Q
  1. Anticoagulation mechanisms/factors:
    a. protein C
    b. thrombomodulin
    c. thromboxane A2
    d. dilution
A

a. protein C
b. thrombomodulin
d. dilution

132
Q
  1. Characteristics in hemophilia type A:
    a. deficiency of factor VIII
    b. mucous membrane and skin bleedings
    c. males are affected
    d. deficiency of factor IX
A

a. deficiency of factor VIII
b. mucous membrane and skin bleedings
c. males are affected

133
Q
  1. Characteristics in hemophilia type B:
    a. deficiency of factor VIII
    b. joint and muscle involvement
    c. deficiency of factor IX
    d. autosomal recessive inheritance
A

b. joint and muscle involvement

c. deficiency of factor IX

134
Q
  1. Major therapeutic methods in disseminated intravascular coagulation (DIC):
    a. anti-thrombotic treatment
    b. raising of the blood pressure
    c. supplementation of coagulation factors
    d. vitamin K supplementation
A

a. anti-thrombotic treatment

c. supplementation of coagulation factors

135
Q
  1. 1 Laboratory alterations in disseminated intravascular coagulation (DIC):
    a. decreased platelet number
    b. elevated fibrinogen level
    c. decreased hemoglobin level
    d. prolonged activated partial thromboplastin time (aPTT)
A

a. decreased platelet number
c. decreased hemoglobin level
d. prolonged activated partial thromboplastin time (aPTT)

136
Q
  1. 2 Laboratory alterations in disseminated intravascular coagulation (DIC):
    a. decreased activated partial thromboplastin time (aPTT)
    b. prolonged thrombin time (TT)
    c. elevated D-dimer level
    d. decreased fibrinogen level
A

b. prolonged thrombin time (TT)
c. elevated D-dimer level
d. decreased fibrinogen level

137
Q 
30. Disseminated intravascular coagulation (DIC) can be caused by the 
following, except:
a. septic abortion
b. polytraumatic state
c. acute promyelocytic leukemia (APL)
d. pancreatitis
e. hypertension crisis
A

e. hypertension crisis

138
Q
  1. Coagulation factors with serine protease activity:
    a. Stuart-Prower factor (X)
    b. fibrin stabilizing factor (XIII)
    c. anti-hemophilic factor (VIII)
    d. von Willebrand factor
A

a. Stuart-Prower factor (X)

139
Q
  1. 1 Acquired coagulation factor deficiency can occur:
    a. in chronic pancreatitis
    b. in liver cirrhosis
    c. in diabetes mellitus type I
    d. in heart valve insufficiency
A

b. in liver cirrhosis

140
Q
  1. 2 Acquired coagulation factor deficiency can occur:
    a. in biliary obstruction
    b. in autoimmune diseases
    c. in disseminated intravascular coagulation (DIC)
    d. in renal tubular acidosis
A

a. in biliary obstruction
b. in autoimmune diseases
c. in disseminated intravascular coagulation (DIC)

141
Q
  1. The most frequent inherited coagulation deficiency:
    a. activated protein C resistance
    b. von Willebrand disease
    c. hemophilia type B
    d. hemophilia type A
    e. dysfibrinogenemia
A

b. von Willebrand disease

142
Q
  1. Potential mechanism of bleedings due to vascular alterations, EXCEPT:
    a. mechanical injury
    b. inflammation affecting the small vessels
    c. weakening of the vessel wall connective tissue
    d. immune complex deposition
    e. atherosclerosis
A

e. atherosclerosis

143
Q
  1. Major indications of routine laboratory coagulation testing:
    a. bleeding tendency in a genetically related family member
    b. skin bleeding
    c. preparation for surgery
    d. long term febrile states
A

a. bleeding tendency in a genetically related family member
b. skin bleeding
c. preparation for surgery

144
Q
  1. Bleeding due to coagulation factor deficiency is characterized:
    a. First manifestation may be gingival bleeding.
    b. Its prevalence is the same in both genders.
    c. Frequent association with skin bleeding.
    d. Deeper localization, in the joints.
    e. It is more common in women.
A

d. Deeper localization, in the joints.

145
Q
  1. Which of the following statements are true regarding
    antithrombin III deficiency:
    a. An important anticoagulant mechanism is missing.
    b. Direct thrombin inhibition is altered.
    c. It is more common than the Leiden mutation.
    d. Its main manifestation is deep vein thrombosis.
A

a. An important anticoagulant mechanism is missing.

d. Its main manifestation is deep vein thrombosis.

146
Q
  1. Streptokinase affects:
    a. kallikrein activation
    b. thrombin inactivation
    c. enhancement of antithrombin III effect
    d. conversion of plasminogen to plasmin
    e. inhibition of fibrinogen binding of thrombin
A

d. conversion of plasminogen to plasmin

147
Q
  1. Interaction partner of von Willebrand factor: Select one:
    a. coagulation factor VIII
    b. fibrinogen
    c. glycoprotein IIb/IIIa receptor of platelets
    d. plasminogen
    e. activated protein C
A

a. coagulation factor VIII

148
Q
  1. Alterations in von Willebrand disease:
    a. decreased platelet function
    b. mucous membrane bleedings
    c. decreased factor VIII level
    d. prolonged bleeding time
A

b. mucous membrane bleedings
c. decreased factor VIII level
d. prolonged bleeding time

149
Q
  1. Tubular adaption does NOT occur in excretion of:
    a. Phosphate ion
    b. Sodium ion
    c. Hydrogen ion
    d. Potassium ion
    e. Urea, creatinine
A

a. Phosphate ion

150
Q
  1. Effects of PTH:
    a. Rise of cAMP activity
    b. Calcification of tissues
    c. Rise of intracellular Ca2+
    d. Increase of proteins synthesis
A

a. Rise of cAMP activity
c. Rise of intracellular Ca2+ (In distal Tubule)
d. Increase of proteins synthesis

151
Q
  1. Which of the following statements are true for
    tubuloglomerular feedback:
    a. If the filtrate decreases, secretion of renin will decrease too
    b. It is influenced by amount of NaCl passing into distal tubules
    c. The activity of the JGA complex changes
    d. Increased filtration is followed by constriction of the efferent arteriole
A

a. If the filtrate decreases, secretion of renin will decrease too
b. It is influenced by amount of NaCl passing into distal tubules

152
Q
  1. Which of the following statements are true for hyperfiltration:
    a. It is a glomerular adaption process
    b. Has no role in progression of kidney failure
    c. Moderates the decrease of total GFR
    d. Glomerular hypertrophy occurs
A

a. It is a glomerular adaption process

d. Glomerular hypertrophy occurs

153
Q
  1. Which of the following are nephrotoxins:
    a. Aminoglycosides
    b. Melamine
    c. Lead
    d. Carbon tetrachloride
A

a. Aminoglycosides
b. Melamine
c. Lead
d. Carbon tetrachloride

154
Q
  1. Stages of chronic kidney disease based on eGFR:

a. Severity reduced kidney function (stage 4) If 15 ml/min

A

a. Severity reduced kidney function (stage 4) If 15 ml/min

155
Q
  1. Metabolic causes of chronic kidney failure:
    a. Cystinosis
    b. Gout
    c. Hyperoxaluria
    d. Hypercalciuria
A

a. Cystinosis
b. Gout
c. Hyperoxaluria
d. Hypercalciuria

156
Q
  1. Causes of chronic kidney failure EXCEPT:
    a. Goodpasture syndrome
    b. polyarteritis nodosa
    c. SLE
    d. transfusion reaction
    e. Wegener granulomatosis
A

d. transfusion reaction (Acute)

157
Q
  1. Congenital or hereditary causes of chronic kidney diseases, EXCEPT:
    a. Cryoglobulinemia
    b. Alport syndrome
    c. Hyperoxaluria
    d. Polycystic kidney
    e. Cystinosis
A

a. Cryoglobulinemia

158
Q
  1. Causes of secondary hyperparathyroidism in chronic kidney failure:
    a. Decreased renal synthesis of Vitamin D
    b. Metabolism of PTH is decreased in kidney
    c. Increased phosphate excretion
    d. Increased Ca2+ absorption
A

a. Decreased renal synthesis of Vitamin D

159
Q
  1. In the polyuric phase of chronic kidney disease:
    a. Rediffusion of urea increases in intact collecting tubules
    b. SNGFR decreases
    c. Osmotic concentration of the medulla increases
    d. Osmotic load of distal tubules rises
A

a. Rediffusion of urea increases in intact collecting tubules
d. Osmotic load of distal tubules rises
Not sure here - text if you are

160
Q
  1. Causes of prerenal kidney failure EXCEPT;(1)
    a. bacteriemia
    b. peritonitis
    c. transfusion reaction
    d. pulmonary embolism
    e. renovascular thrombosis
A

d. pulmonary embolism

161
Q
  1. In prerenal azotemia:((1)
    a. sodium concentration in the urine is high
    b. there are granular casts in urine
    c. the urine/plasma creatinine ratio is low
    d. osmolarity of the urine is high
    e. osmolarity of the urine is low
A

d. osmolarity of the urine is high

* According to Wiki

162
Q
  1. Causes of renal parenchymal kidney failure
    a. crush syndrome
    b. overdose of diuretics
    c. hepatorenal syndrome
    d. schölein-Henoch purpura
A

a. crush syndrome
b. overdose of diuretics
c. hepatorenal syndrome
d. schölein-Henoch purpura

163
Q
  1. Effect of tubular obstruction:
    a. GFR increase
    b. Intratubular pressure increases
    c. Perfusion of the afferent arteriole increases
    d. Glomerular filtration pressure decreases
A

b. Intratubular pressure increases

d. Glomerular filtration pressure decreases

164
Q
  1. In acute tubular injury
    a. Concentration of intracellular H+ rises
    b. Concentration of intracellular K+ rises
    c. Concentration of intracellular Ca2+ rises
    d. Concentration of intracellular Na + rises
A

a. Concentration of intracellular H+ rises
b. Concentration of intracellular K+ rises
c. Concentration of intracellular Ca2+ rises
d. Concentration of intracellular Na + rises

165
Q
  1. 1 in Uremia: (1)
    a. Natriuretic peptide level rises
    b. Glucagon level rises
    c. PTH level rises
    d. insulin level rises
A

c. PTH level rises

166
Q
  1. 2 in Uremia: (1)
    a. EPO level increases
    b. Leptin level decreases
    c. Vitamin D level increases
    d. Phosphate level decreases
    e. Bicarbonate level decrease
A

a. EPO level increases

167
Q
  1. What is true for NGAL:
    a. It has low molecular weight
    b. It is an early marker of acute kidney failure
    c. Its serum level rises only in renal failure
    d. Can be measured only from the urine
A

a. It has low molecular weight

b. It is an early marker of acute kidney failure

168
Q
  1. Which of the following are true for causes of acute kidney failure:
    a. Renal parenchymal 60-80%
    b. Prerenal 20-40%
    c. Renal parenchymal 30-40%
    d. Postrenal 5% or less
A

b. Prerenal 20-40%

c. Renal parenchymal 30-40%

169
Q
  1. Significant processes in the pathomechanism of acute kidney failure:
    a. Dilation of efferent arteriole
    b. Constriction of the afferent arteriole
    c. Increased glomerular permeability
    d. Decreased activity/activation of RAAS
A

b. Constriction of the afferent arteriole

170
Q
  1. What is it true for acute kidney failure:(1)
    a. it causes hypokalemia
    b. it causes metabolic acidosis
    c. the type without oliguria is more common
    d. Its major cause is the obstruction in the urinary tract
    e. The BUN level does not rise
A

b. it causes metabolic acidosis

171
Q
  1. Principles of therapy in acute kidney failure:
    a. Avoid vasoconstrictors
    b. Recovery of intravascular volume
    c. Diuretics
    d. Therapy of the primary diseases
A

b. Recovery of intravascular volume
c. Diuretics
d. Therapy of the primary diseases

172
Q
  1. The average volume of the interstitial space in men:
    a. 5 l
    b. 8 l
    c. 12 l
    d. 20 l
    e. 25
A

c. 12 l

10. 5 for 70Kg

173
Q
  1. Which ion concentration is the highest in the EC space?
    a. H+
    b. Mg++
    c. Cl–
    d. K+
    E. Ca++
A

c. Cl–

98. 00–107.00 (mM)

174
Q
  1. Which ion concentration is the lowest in the EC space?
    a. Ca++
    b. H+
    c. Cl–
    d. Mg++
    e. K+
A

b. H+

pH=7.4, H+ = 4x10^5~ mM

175
Q
  1. The average daily Na+ intake is:
    a. 5 mmol
    b. 20 mmol
    c. 80 mmol
    d. 120 mmol
    e. 200 mmol
A

d. 120 mmol

176
Q
  1. Which of the following are idiogenic osmoles?
    a. taurine
    b. Cl–
    c. glycine
    d. Na+
A

a. taurine

c. glycine

177
Q
  1. Tonicity of the plasma is increased by:
    a. Urea
    b. K+
    c. Glucose (in untreated DM)
    d. Na+
A

a. Urea
c. Glucose (in untreated DM)
d. Na+

178
Q
  1. The dynamic changes in water excretion by the kidneys occur in order to stabilize:
    a. the cell volumes
    b. the potassium level of the plasma
    c. the osmolarity of the blood
    d. the total protein level of the plasma
    e. the glucose level of the blood
A

c. the osmolarity of the blood

179
Q
  1. Which route is the most significant for Na+ excretion?
    a. respiration
    b. urine
    c. sweating
    d. stool
    e. squamous cells
A

b. urine

180
Q
  1. Possible symptoms of hyponatremia, EXCEPT (1):
    a. nausea, vomiting
    b. headache
    c. abdominal pain
    d. intense thirst
    e. confusion
A

d. intense thirst

Low Na = Low Osmolality = Inactivation of Thirst Centers/Osmoreceptors

181
Q
  1. Which is the proper treatment of hyponatremia?
    a. V2 receptor antagonist
    b. restricting water intake
    c. mineralocorticoids
    d. Infusing normal saline
    e. Insulin
A

a. V2 receptor antagonist

182
Q
  1. It may cause either hypo- or hypernatremia depending on the case:
    a. Hypothyroidism
    b. Conn’s syndrome
    c. Diarrhea
    d. SIADH
    e. Primary Polydipsia
A

c. Diarrhea

183
Q
  1. Above which value is considered hypernatremia severe?
    a. 140 mmol/l
    b. 145 mmol/l
    c. 150 mmol/l
    d. 155 mmol/l
    e. 160 mmol/l
A

d. 155 mmol/l

184
Q
  1. The most common cause of hypernatremia:
    a. Excessive intake of sodium
    b. Cushing’s syndrome
    c. Overdose of diuretics
    d. Conn’s syndrome
    e. Restricted water intake
A

e. Restricted water intake

185
Q
  1. It may be a symptom of hypernatremia
    a. fever
    b. nausea, vomiting
    c. spasticity
    d. irritability
A

a. fever
b. nausea, vomiting
c. spasticity
d. irritability

186
Q
  1. It is a Colloid Solution:
    a. Lactated Ringer (Hartmann’s)
    b. Dextran
    c. 0.9% NaCl
    d. 5% glucose
    e. Ringer
A

b. Dextran

The rest are crystalloid

187
Q
  1. The infusion of which solution produces the largest increase of blood volume?
    a. Ringer
    b. 0.9 % NaCl
    c. 5% glucose
    d. 5 % albumin
    e. Lactated Ringer (Hartmann’s)
A

d. 5 % albumin

The only Colloid among the answers

188
Q
  1. Disadvantages of colloid solutions in volume therapy, EXCEPT(1):
    a. they may cause kidney injury
    b. they may cause coagulopathy
    c. they cause interstitial edema
    d. they are more expensive
    e. they may cause anaphylactic reaction
A

c. they cause interstitial edema

189
Q
  1. Ca. how much 5% glucose solution must be infused to increase the blood volume by 1 liter?
    a. 1–2 liters
    b. 2–4 liters
    c. 4–6 liters
    d. 6–8 liters
    e. 10–14 liters
A

b. 2–4 liters

Slide 34: 1.4L/0.37=3.783

190
Q
  1. Which statement is true for normal saline?
    a. it has equal tonicity to the plasma
    b. it gets excreted faster than lactated Ringer
    c. it does not cause any change in the acid-base balance
    d. it is recommended for resuscitation
A

a. it has equal tonicity to the plasma

191
Q
  1. AVP production is stimulated by
    a. MDMA
    b. Hypotension
    c. CNS lesions
    d. Excessive physical activity
A

a. MDMA
b. Hypotension
c. CNS lesions
d. Excessive physical activity

192
Q
  1. It is true for the central form of diabetes insipidus -
    a. 50% of the cases are idiopathic
    b. it responds well to V2 receptor antagonists
    c. nycturia
    d. plasma osmolarity is usually elevated
A

a. 50% of the cases are idiopathic
c. nycturia
d. plasma osmolarity is usually elevated

193
Q
  1. Water poisoning may occur in -
    a. Schizophrenia
    b. Ketosis
    c. Cushing’s syndrome
    d. Marathon runners
A

a. Schizophrenia

d. Marathon runners

194
Q
  1. Who are more likely to have a fatal outcome in case of water poisoning? -
    a. women
    b. children
    c. alcoholics
    d. elderly people
A

b. children

Low body Mass - Low TBW

195
Q
  1. SIADH may be caused by -
    a. mutation of the gene of the V2 receptor
    b. malignant tumor
    c. drug effect
    d. CNS lesions
A

b. malignant tumor
c. drug effect
d. CNS lesions
(Slide 27)

196
Q
  1. Must be excluded for the diagnosis of SIADH -
    a. osmotic diuresis
    b. hypothyroidism
    c. diarrhea
    d. Addison’s disease
A

a. osmotic diuresis

b. hypothyroidism

197
Q
  1. Useful in the treatment of SIADH -
    a. Glucocorticoids
    b. Restriction of water intake
    c. V2 receptor antagonists
    d. 3% NaCl infusion + loop diuretics
A

b. Restriction of water intake
c. V2 receptor antagonists
d. 3% NaCl infusion + loop diuretics

198
Q
  1. The normal H+ concentration in the arterial blood:
    a. 7.35-7.45 nmol/l
    b. 36-44 nmol/l
    c. 36-44 μmol/l
    d. 10-30 nmol/l
    e. 68-74 nmol/l
A

b. 36-44 nmol/l

199
Q
  1. Which of the following buffer system has the highest capacity in the blood?
    a. phosphate
    b. albumin
    c. sulfate
    d. hemoglobin
    e. bicarbonate
A

e. bicarbonate

200
Q
  1. Buffer components of the blood, EXCEPT(1):
    a. H3PO4/H2PO4–
    b. H2SO4/SO42-
    c. hemoglobin
    d. albumin
    e. H2CO3/HCO3–
A

a. H3PO4/H2PO4–

Intracellular and Urine

201
Q
  1. The daily volatile acid production is:
    a. 15 mol/kg bw
    b. 15 mmol
    c. 1 mmol/kg bw
    d. 15 mol
    e. 15 mmol/kg bw
A

d. 15 mol

CO2 - Slide 2

202
Q
  1. The daily nonvolatile acid production is:
    a. 1 mmol/kg bw
    b. 15 mmol/kg bw
    c. 15 mol/kg bw
    d. 15 mol
    e. 15 mmol
A

a. 1 mmol/kg bw

Slide 2

203
Q
  1. Important organs in H+ production and excretion, EXCEPT(1):
    a. kidney
    b. liver
    c. lung
    d. sweat glands
    e. bone
A

d. sweat glands

204
Q
  1. The effects of alkalemia, EXCEPT(1):
    a. increased excitability
    b. peripheral vasodilation
    c. tissue hypoxia
    d. muscle twitching
    e. dizziness, numbness
A

b. peripheral vasodilation

Happens in Acidosis

205
Q
  1. The role of liver in the regulation of acid-base balance, EXCEPT(1):
    a. production of plasma proteins
    b. CO2 production
    c. glycogen storage
    d. metabolism of organic acids
    e. metabolism of ammonium
A

c. glycogen storage

It is a role that those not involve acid-base regulation

206
Q
  1. Which of the molecules made by the distal tubular cells from glutamine?
    a. 2NH4+/2H2PO4–/2HCO3–
    b. 4NH4+/glucose/2HCO3–
    c. 2NH4+/glucose/2HCO3–
    d. NH4+/glucose/HCO3–
    e. 2NH4+/2HCO3–
A

c. 2NH4+/glucose/2HCO3–

Slide 11

207
Q
  1. Which statements are true? (One or more)
    a. a respiratory alteration is chronic if stHCO3– is increased
    b. a respiratory alteration is acute if aHCO3– is in the normal range
    c. a metabolic acidosis is compensated if ΔpCO2 ≈ BE
    d. a metabolic alkalosis is compensated if ΔpCO2 ≈ BE
A

a. a respiratory alteration is chronic if stHCO3– is increased
b. a respiratory alteration is acute if aHCO3– is in the normal range

(Not sure about this one yet - pm)

208
Q
  1. Which of the following statement is true?
    a. 88% of the filtered HCO3– reabsorbed in the distal tubules
    b. the distal tubular cells make 2 molecules of NH4+ and 1 molecule of HCO3– from glutamine
    c. significant amount of H+ excreted in the proximal tubular cells
    d. the kidney filtrates about 15 mol HCO3– daily
    e. the filtered titratable acidity originates mainly from H2PO4–
A

e. the filtered titratable acidity originates mainly from H2PO4–
(Slide 11)

209
Q
  1. Cause of respiratory acidosis:
    a. salicylate overdose
    b. emphysema
    c. low pO2
    d. fever
    e. respiratory center lesions
A

b. emphysema

Slide 14, Here they give choices from Slide 20 that might seem similar

210
Q
  1. The causes of respiratory acidosis EXCEPT(1):
    a. paralysis of the respiratory muscles
    b. emphysema
    c. drug abuse
    d. ARDS
    e. pneumonia
A

e. pneumonia

Slide 14

211
Q
  1. The causes of respiratory alkalosis EXCEPT(1):
    a. respiratory center lesions
    b. ARDS
    c. fever
    d. low pO2
    e. salicylate overdose
A

b. ARDS

Slide 20

212
Q
  1. Indicative of respiratory acidosis:
    a. pCO2 >45 mmHg and pH<7.35
    b. pCO2 < 26 mmHg and pH <7.35
    c. pCO2 >26 mmHg and pH<7.35
    d. pCO2 = 40 mmHg and pH <7.35
    e. pCO2 < 45 mmHg and pH <7.35
A

a. pCO2 >45 mmHg and pH<7.35

Slide 14

213
Q 
16. Which of the following data may indicate a simple
 respiratory acidosis? (One or more)
a. pCO2 > 40 mmHg; stHCO3– = 24 mmol/l  
b. pCO2 > 40 mmHg; stHCO3– > 24 mmol/l 
c. pCO2 < 40 mmHg; stHCO3– > 24 mmol/l 
d. pCO2 < 40 mmHg; stHCO3– < 24 mmol/l
A

a. pCO2 > 40 mmHg; stHCO3– = 24 mmol/l

214
Q
  1. In chronic respiratory acidosis (pCO2 = 55 mmHg):
    a. aHCO3– < stHCO3-
    b. aHCO3– = stHCO3–
    c. aHCO3– ↑↑; stHCO3– ↑
    d. stHCO3– ↑; aHCO3– not changed
A

c. aHCO3– ↑↑; stHCO3– ↑

215
Q
  1. The most common cause of AG acidosis, except:
    a. Addison’s disease
    b. inflammation
    c. diabetic ketoacidosis
    d. ethanol
    e. lactic acid
A

c. diabetic ketoacidosis
MUD PILES - Slide 29

−M ethanol
−U remia
−D iabetic ketoacidosis
−P araldehyde
−I nfection, iron, INH
−L Lactate acidosis
−E thylene glycol
−S alicylate
216
Q
  1. Which of the following may cause AG acidosis?
    a. diarrhea
    b. none of them
    c. lactic acidosis
    d. diabetic ketoacidosis
A

c. lactic acidosis
d. diabetic ketoacidosis
MUD PILES - Slide 29

−M ethanol
−U remia
−D iabetic ketoacidosis
−P araldehyde
−I nfection, iron, INH
−L Lactate acidosis
−E thylene glycol
−S alicylate
217
Q
  1. Which of the following may cause an AG acidosis with an increased osmolar gap?
    a. ketoacidosis
    b. ethylene glycol poisoning
    c. methanol intoxication
    d. lactic acidosis
A

b. ethylene glycol poisoning
c. methanol intoxication
Slide 32
(“External Sources will cause increased osmolar Gap”)

218
Q
  1. Causes of hyperchloremic acidosis:
    a. hypoaldosteronism
    b. upper airway infection
    c. hyperosmolar nonketotic coma
    d. Aspirin therapy
A

a. hypoaldosteronism
c. hyperosmolar nonketotic coma
HARD UP - Slide 32

•H ypoaldosteronism, hyperosmolar
nonketotic coma
• A cetazolamide – CAH inhibitor
• R TA
• D iarrhea
• U reterosigmoidostomy, - ileostomy
• P ancreatic fistula
219
Q
  1. Indicative of hyperchloremic acidosis, if the urinary AG (UAG):
    a. UAG < -10 mmol/l
    b. UAG is not suitable to make the diagnosis
    c. UAG > +10 mmol/l
    d. UAG < +10 mmol/l
    e. –10 mmol/l < UAG < +10 mmol/l
A

c. UAG > +10 mmol/l

Slide 36

220
Q
  1. Characteristic of ethylene glycol poisoning:
    a. it may cause metabolic alkalosis
    b. it may cause kidney failure
    c. AG > 14 mmol/l
    d. osmolar gap increased
A

b. it may cause kidney failure (Oxalate Crystals)
c. AG > 14 mmol/l
d. osmolar gap increased

https://en.wikipedia.org/wiki/Ethylene_glycol_poisoning

221
Q
  1. The effects of acidemia, EXCEPT(1):
    a. increased sympathetic transmission
    b. cardiac depression
    c. decreased release of neurotransmitters
    d. decreased parasympathetic transmission
    e. decreased catecholamine effect
A

b. cardiac depression

https: //en.wikipedia.org/wiki/Acidosis#Signs_and_symptoms

222
Q
  1. Indicative of respiratory alkalosis:
    a. pCO2<35 mmHg and pH<7.45
    b. pCO2 = 40 mmHg and pH > 7.45
    c. pCO2 > 45 mmHg and pH > 7.35
    d. pCO2 < 35 mmHg and pH > 7.45
    e. pCO2 < 45 mmHg and pH < 7.35
A

d. pCO2 < 35 mmHg and pH > 7.45

ROME - Respiratory Opposite Metabolic Equal

223
Q
  1. Which of the following data indicate a simple metabolic alkalosis?
    a. pCO2 = 40 mmHg; stHCO3– > 24 mmol/l
    b. pCO2 < 40 mmHg; stHCO3– < 24 mmol/l
    c. pCO2 < 40 mmHg; stHCO3– = 24 mmol/l
    d. pCO2 > 40 mmHg; stHCO3– > 24 mmol/l
    e. pCO2 < 40 mmHg; stHCO3– > 24 mmol/l
A

a. pCO2 = 40 mmHg; stHCO3– > 24 mmol/l

224
Q
  1. Metabolic alkalosis may be due to -
    a. Conn’s syndrome
    b. Ethanol intoxication
    c. Ethylene glycol poisoning
    d. Diarrhea
A

a. Conn’s syndrome

225
Q
  1. Which of the following data indicate clearly a mixed acid base disorder?
    a. pCO2 >40 mmHg; stHCO3– < 24 mmol/l
    b. pCO2 < 40 mmHg; stHCO3– < 24 mmol/l
    c. pCO2 < 40 mmHg; stHCO3– = 24 mmol/l
    d. pCO2 < 40 mmHg; stHCO3– > 24 mmol/l
A

a. pCO2 >40 mmHg; stHCO3– < 24 mmol/l

226
Q
  1. Characteristic of type 1 RTA- (one or more):
    a. can occur in sickle cell anemia
    b. decreased production of NH4+ by the distal tubular cells
    c. can be caused by Amphotericin B therapy
    d. classic type, associated with a defect of the distal H+/ATP-ase activity
A

a. can occur in sickle cell anemia
b. decreased production of NH4+ by the distal tubular cells
c. can be caused by Amphotericin B therapy
d. classic type, associated with a defect of the distal H+/ATP-ase activity
(Slides 41-43)

227
Q
  1. Characteristic of type 1 RTA, EXCEPT(1):
    a. urine pH > 5.5
    b. can be caused by SLE
    c. hypercalciuria
    d. distal HCO3– reabsorption ↓
    e. distal H+ secretion ↓
A

d. distal HCO3– reabsorption ↓

Slides 41-43

228
Q
  1. Characteristic of type 2 RTA, EXCEPT(1):
    a. proximal HCO3– reabsorption ↓
    b. may cause hypokalemia
    c. my cause hyperkalemia
    d. can be due to drugs inhibiting carbonic anhydrase
    e. loss of Na+ and K+
A

c. may cause hyperkalemia

Slides 38-40

229
Q
  1. Characteristic of type 4 RTA, EXCEPT(1):
    a. can develop due to NSAID therapy
    b. diabetic nephropathy may cause it
    c. hyperkalemia
    d. serum renin activity is always high
    e. can be due to Addison’s disease
A

d. serum renin activity is always high

Slide 44

230
Q
  1. True statement(s) about the glycosaminoglycans linkage to the protein core -
    a. The core protein is rich in serine in these places
    b. The trisaccharide unit consist of 2 galactose and a xylose molecule
    c. With the statements above is possible that the proteoglycans have a structure like a bottle brush
    d. There is a specific trisaccharide unit
A

a. The core protein is rich in serine in these places
b. The trisaccharide unit consist of 2 galactose and a xylose molecule
c. With the statements above is possible that the proteoglycans have a structure like a bottle brush
d. There is a specific trisaccharide unit

231
Q
  1. True statement(s) about the glycosaminoglycans:
    a. they are rigid
    b. they are located on the surface of the cells
    c. they provide the structural integrity of the cells
    d. because of their low compressibility they are ideal for lubricating the joints
A

a. they are rigid
b. they are located on the surface of the cells
c. they provide the structural integrity of the cells
d. because of their low compressibility they are ideal for lubricating the joints

232
Q
  1. True statements about the glycosaminoglycan molecules: (1)
    a. their basic units are monosaccharides
    b. they play an important role in the synthesis of collagen
    c. they bind to a core protein molecule
    d. they are not important in wound healing
A

c. they bind to a core protein molecule

233
Q
  1. In glycosaminoglycan molecules the disaccharide units are containing a: (1)
    a. N-glucuronidated hexosamine molecule
    b. N-methylated hexosamine molecule
    c. N-acetylated hexosamine molecule
    d. N-ethylated hexosamine molecule
A

c. N-acetylated hexosamine molecule

234
Q
  1. True statements about the glycosaminoglycans and proteoglycans:
    a. They filter the macromolecules
    b. Because of their positive charge they cannot move closer when compressed
    c. They filter the tumor cells
    d. They hold water
A

a. They filter the macromolecules

d. They hold water

235
Q
  1. True statements about proteoglycan (PGs) in connection with wound healing:
    a. In wound healing epithelial cells synthesized dermatan and chondroitin-sulfate
    b. The amount of PGs is decreasing via remodeling
    c. The amount of PGs in scar is decreasing with aging
    d. The proteoglycan synthesis is increased in the first 3 weeks
A

b. The amount of PGs is decreasing via remodeling

d. The proteoglycan synthesis is increased in the first 3 weeks

236
Q
  1. Typical GAGs in a human being are:
    a. Dermatain-sulfate
    b. Chondroitin-sulfate
    c. Keratin-sulfate
    d. Heparin
A

b. Chondroitin-sulfate
d. Heparin

**correct: Dermatan-sulfate, keratan-sulfate

237
Q
  1. Typical location of heparin-sulfate is/are:
    a. Cell surface
    b. Basement membranes
    c. Cornea
    d. Cartilage
A

a. Cell surface
b. Basement membranes

Lecture slide 21

238
Q
  1. Dermatan-sulfate is mainly present in:
    a. skin
    b. heart valves
    c. cartilage
    d. blood vessels
A

a. skin
b. heart valves
d. blood vessels

Lecture slide 21

239
Q
  1. Dermatan-sulfate is mainly present in:
    a. ligaments
    b. meniscus
    c. cartilage
    d. joint capsule
A

b. meniscus
d. joint capsule

Lecture slide 23

240
Q
  1. Hyaluronates are mainly present in:
    a. vitreous humor
    b. cartilage
    c. bones
    d. synovial fluid
A

a. vitreous humor
b. cartilage
c. bones
d. synovial fluid

Lecture slide 22,21

241
Q
  1. True statements about the hyaluronic acid:
    a. it is the largest glycosaminoglycan
    b. its occurrence is about 10-20% in skin
    c. its occurrence is about 50-60% in aorta
    d. it is present in all connective tissues
A

a. it is the largest glycosaminoglycan
b. its occurrence is about 10-20% in skin
d. it is present in all connective tissues

Lecture slide 22,21

242
Q
  1. Which are cell binding proteins?
    a. Collagen
    b. Laminin
    c. Elastin
    d. Fibronectin
A

b. Laminin

d. Fibronectin

243
Q
  1. The statement(s) about the toughness of collagen:
    a. With aging the number of cross-links between the molecules are increasing
    b. The collagen cannot be stretched
    c. The toughness of collagen is mainly depending on its triple helix structure
    d. With aging the collagen will be more elastic
A

a. With aging the number of cross-links between the molecules are increasing
b. The collagen cannot be stretched
Lecture slide 12

244
Q
  1. True statements about the structure of collagen:
    a. Its molecular weight is around 200-300 kD
    b. Collagen’s basic unit is coiled into a left handed helix molecule
    c. Collagen is 10% of total protein in a newborn baby
    d. Collagen is synthetized from the preprocollagen molecule
A

a. Its molecular weight is around 200-300 kD
c. Collagen is 10% of total protein in a newborn baby
d. Collagen is synthetized from the preprocollagen molecule

Lecture slide 9 - 12

245
Q
  1. True statement(s) about the synthesis of collagen:
    a. Van der Waals bounds are between the collagen fibrils
    b. The procollagen triplexes are leaving the cell via exocytosis
    c. Vitamin C is needed to the normal function of procollagen peptidases
    d. The final triple helix formation is happening in the extracellular space
A

b. The procollagen triplexes are leaving the cell via exocytosis
d. The final triple helix formation is happening in the extracellular space

Lecture slide 9 - 12

246
Q
  1. Which cells are not structural elements of the connective tissue? (1)
    a. Chondroblasts
    b. Neurons
    c. Smooth muscle cells
    d. Endothelial cells
A

b. Neurons

247
Q
  1. True statements about the extracellular matrix (ECM), EXCEPT(1):
    a. annulus fibrosus and nucleus pulposus are connective tissues
    b. it helps for the inflammatory cells to spread the inflammation
    c. macromolecules are filtered by the ECM
    d. it is a filler material to cushion organs
A

b. it helps for the inflammatory cells to spread the inflammation

248
Q
  1. Prolyl-lysyl hydroxylase enzyme requires:
    a. iron
    b. O2
    c. alpha-ketoglutarate
    d. ascorbic acid
A

a. iron
b. O2
c. alpha-ketoglutarate
d. ascorbic acid

Lecture slide 9

249
Q
  1. The most frequent amino acids in collagen are:
    a. alanine
    b. glycine
    c. proline
    d. Hydroxyproline
A

b. glycine
c. proline
d. Hydroxyproline

250
Q
  1. True statements about the Marfan syndrome:
    a. among artists and athletes there is an increased number of patients with Marfan syndrome than in the normal population.
    b. no gender predilection is known.
    c. it is pan-ethnic.
    d. its inheritance is autosomal recessive.
A

b. no gender predilection is known.
c. it is pan-ethnic.

Lecture slide 32

251
Q
  1. True statement about Marfan syndrome (1):
    a. A Marfan syndrome patient can have an average height
    b. healthy lifestyle is good prevention for Marfan syndrome
    c. Marfan syndrome is an acquired disorder
    d. Marfan syndrome is a disease of modern civilization
A

a. A Marfan syndrome patient can have an average height

Lecture slide 32

252
Q
  1. The genetic background of Marfan syndrome is:
    a. Marfan syndrome patients always have a fibrillin-1 gene mutation
    b. the mutation affects the fibrillin-1 gene
    c. 75% of patients have affected parents
    d. 25% is because of new mutation
A

b. the mutation affects the fibrillin-1 gene
c. 75% of patients have affected parents
d. 25% is because of new mutation
(Can also affect the TGF-R)
Lecture slide 32

253
Q
  1. True statement about the elastin:
    a. it plays an important role in the structure of bones and cartilages
    b. the ability of stretch depends on the desmosine cross-links
    c. it is synthetized from a prepro-elastin molecule
    d. its synthesis is totally different from the synthesis of collagen
A

b. the ability of stretch depends on the desmosine cross-links

Lecture slide 13

254
Q
  1. True statement about optimal daily diet?(1)
    a. The highest representation within lipids is that of polyunsaturated fatty acids.
    b. The amount of dietary fiber intake is 15-20 g.
    c. The amount of water intake is approx. 1-1.5 ml/kcal.
    d. The amount of protein intake is 1-1.5 g/kg.
    e. Energy content of protein intake exceeds that of lipids.
A

c. The amount of water intake is approx. 1-1.5 ml/kcal.

Slide 6

255
Q
  1. Essential nutrient:(1)
    a. dietary fiber
    b. palmitic acid
    c. alanine
    d. gliadin
    e. amylum (starch).
A

a. dietary fiber

Slide 5

256
Q
  1. Essential nutrient, except: (1)
    a. dietary fiber
    b. ascorbic acid
    c. amylum (starch)
    d. linoleic acid
    e. lysine
A

c. amylum (starch)

Slide 5

257
Q
  1. What is the ratio of carbohydrate energy intake within the total energy intake? (1)
    a. none of the answers are correct
    b. approx. 50%
    c. approx. 20%
    d. approx. 30%
    e. approx. 40%
A

b. approx. 50%

Slide 6

258
Q
  1. What are the effects of dietary fiber?(1)
    a. They increase the transit time of consumed foods.
    b. They decrease gas production of intestinal bacteria.
    c. They increases the protective capabilities of intestinal lymphocytes.
    d. They slow down carbohydrate absorption.
    e. They increase amino acid absorption.
A

d. They slow down carbohydrate absorption.

Slide 7

259
Q
  1. True statements about dietary fibers, except:(1)
    a. They slow down carbohydrate absorption.
    b. They contribute to the maintenance of favorable intestinal bacterial flora.
    c. They decrease the transit time of consumed foods.
    d. They are an easily utilized carbohydrate energy source.
    e. As a consequence of hydration, they thicken the lining of the intestine.
A

d. They are an easily utilized carbohydrate energy source.

Slide 7

260
Q
  1. Essential amino acid:(1)
    a. arginine
    b. alanine
    c. lysine
    d. tyrosine
    e. glutamic acid
A

c. lysine

Slide 5

261
Q
  1. Vitamins are characterized by: (1)
    a. The human body is able to synthesize them in small amounts.
    b. At least weakly consumption is necessary due to storage
    c. They are not utilized for energy generation.
    d. None of the answers are correct
    e. In all cases, they are absorbed as active substances.
A

c. They are not utilized for energy generation.

Slide 18

262
Q
  1. Vitamins are characterized by, except: (1)
    a. They can be absorbed as provitamins as well as active substance.
    b. None of the answers are correct.
    c. They serve as energy source in starvation.
    d. They belong to micronutrients.
    e. The human body is not able to synthesize them but animals and plants are.
A

c. They serve as energy source in starvation.

Slide 18

263
Q
  1. Water soluble vitamins are characterized by:
    a. In certain cases, symptoms of excess intake can appear.
    b. Excess amounts will be excreted with the urine.
    c. Due to small B12 reserves, daily intake is needed.
    d. In this group, the highest amount is needed of vitamin B1.
    e. A daily amount exceeding 50 mg is needed of vitamins belonging to the B family.
A

b. Excess amounts will be excreted with the urine.

Slide 20

264
Q
  1. Which belongs to macronutrients? (1)
    a. ergocalciferol
    b. amylum (starch)
    c. tocopherol
    d. iodine
    e. none of the answers are correct
A

b. amylum (starch)

Slide 4

265
Q
  1. Which belongs to micronutrients, except:(1)
    a. ascorbic acid
    b. potassium
    c. folic acid
    d. iron
A

b. potassium

Slide 44

266
Q
  1. Which belongs to micronutrients?(1)
    a. none of the answers are correct
    b. beta-carotene
    c. calcium
    d. linoleic acid
    e. amylum (starch)
A

b. beta-carotene

Slide 4 (Precursor of VitA - Wiki)

267
Q
  1. Belong(s) to trace elements, except: (1)
    a. iodine
    b. calcium
    c. magnesium
    d. iron
A

b. calcium
c. magnesium

Slide 44

268
Q
  1. Which belong(s) to trace elements?
    a. selenium
    b. iron
    c. magnesium
    d. Cobalt
A

b. iron
c. magnesium

Slide 44: Se and Cb are “Ultra-trace” elements

269
Q
  1. 1 Which belong(s) to trace elements?
    a. manganese
    b. iodine
    c. iron
    d. zinc
A

a. manganese
b. iodine
c. iron
d. zinc

Slide 44

270
Q
  1. Zinc containing proteins participate in:
    a. intracellular proteolysis
    b. DNA-stabilization
    c. spermatogenesis
    d. binding of steroid hormone receptors to DNA
A

c. spermatogenesis
d. binding of steroid hormone receptors to DNA

Slide 45 and MCB

271
Q
  1. Disease related to dietary deficiencies, except:
    a. nyctalopia (night blindness)
    b. scurvy
    c. ulcerative colitis
    d. xerophthalmia
    e. iron deficiency anemia
A

c. ulcerative colitis

Slide 15, UC is Autoimmune Disease

272
Q
  1. Disease related to dietary deficiencies, except: (1)
    a. marasmus
    b. megaloblastic anemia
    c. peptic ulcer
    d. goiter
    e. pellagra
A

c. peptic ulcer

Slide 15

273
Q
  1. Which disease may be related to dietary deficiencies?(1)
    a. sickle cell anemia
    b. peptic ulcer
    c. goiter
    d. ulcerative colitis
    e. irritable bowel syndrome
A

c. goiter

Slide 15

274
Q
  1. What participates in vitamin B12 turnover?
    a. reticulocyte transferase
    b. intrinsic factor
    c. transcobalamin
    d. hepcidin
A

b. intrinsic factor
c. transcobalamin

Slide 32

275
Q
  1. Organ(s)/tissue(s) primarily altered in vitamin B12 deficiency?
    a. pancreas
    b. reproductive system
    c. nervous system
    d. adrenal gland
A

c. nervous system

USMLE First aid 2020

276
Q
  1. Biochemical reactions catalyzed by vitamin B12:
    a. transamination
    b. homocysteine-methionine conversion
    c. methylmalonyl coenzyme A conversion
    d. glycogenolysis
A

b. homocysteine-methionine conversion
c. methylmalonyl coenzyme A conversion

USMLE First aid 2020

277
Q
  1. Sources of vitamin B12:
    a. legumes
    b. meat
    c. citrus fruits
    d. fish
A

b. meat
d. fish

USMLE First aid 2020

278
Q
  1. What is the symptom of vitamin B1 deficiency?
    a. all of the answers are correct
    b. microcytic anemia
    c. ataxia
    d. atrophy of the small intestine mucus membrane
    e. gastritis
A

c. ataxia

in Wernicke encephalopathy - USMLE First aid 2020

279
Q
  1. 2 What is the symptom of vitamin B1 deficiency?
    a. peripheral neuropathy
    b. cardiomyopathy
    c. ataxia
    d. all of the answers are correct
    e. memory alterations
A

d. all of the answers are correct

in Wernicke encephalopathy, Korsakoff syndrome, Beriberi disease - USMLE First aid 2020

280
Q
  1. What is the symptom of vitamin B3 (niacin) deficiency? (1)
    a. glossitis
    b. obstipation
    c. none of the answers are correct
    d. microcytic anemia
    e. proctitis
A

a. glossitis

USMLE First aid 2020

281
Q
  1. What is the characteristic role of the vitamin B complex?
    a. intracellular signaling material
    b. intermediate metabolism product
    c. allosteric stimulant
    d. regulator of translation
    e. coenzyme
A

e. coenzyme

USMLE First aid 2020

282
Q
  1. Increased folic acid requirement is characteristic in:
    a. increased physical activity
    b. iron deficiency anemia
    c. autoimmune diseases
    d. inflammation
    e. pregnancy
A

e. pregnancy

Reduces the genetic risk for neural tube defects - USMLE First aid 2020

283
Q
  1. What is the consequence of folic acid deficiency?
    a. decreased fatty acid metabolism
    b. altered protein synthesis
    c. fetal neural tube defects
    d. none of the answers are correct
    e. microcytic anemia
A

c. fetal neural tube defects

USMLE First aid 2020 (Depends on genetics as well)

284
Q
  1. Consequences of folic acid deficiency, except:(1)
    a. altered protein synthesis
    b. altered DNA-synthesis
    c. decreased erythroid proliferation
    d. fetal neural tube defects
    e. macrocytic anemia
A

a. altered protein synthesis

Slide 31

285
Q
  1. Consequences of vitamin A deficiency:
    a. microcytic anemia
    b. decreased lipid metabolism
    c. xerophthalmia
    d. altered protein synthesis
A

c. xerophthalmia

Slide 38

286
Q
  1. Organ(s) affected by the functions of vitamin A:
    a. reproductive system
    b. eyes
    c. epidermis
    d. bones
A

a. reproductive system
b. eyes
c. epidermis
d. bones

Slide 38

287
Q
  1. 2 Organ(s) affected by the functions of vitamin A:
    a. bones
    b. hematopoiesis
    c. epidermis
    d. peripheral nerves
A

a. bones
b. hematopoiesis
c. epidermis

Slide 38

288
Q
  1. Source(s) of vitamin A:
    a. retinoic acid
    b. beta-carotene as provitamin
    c. retinol
    d. retinitis
A

b. beta-carotene as provitamin
c. retinol

Slide 38

289
Q
  1. What are the effects of vitamin D:
    a. enhancement of calcium absorption in the intestine
    b. enhancement of lymphocyte proliferation
    c. enhancement of fluid retention in the kidneys
    d. inhibition of parathyroid hormone synthesis
A

a. enhancement of calcium absorption in the intestine
d. inhibition of parathyroid hormone synthesis

Slide 39

290
Q
  1. Deficiency of vitamin K is characterized by:
    a. a prolonged prothrombin time
    b. newborns are at increased risk
    c. an elevated platelet count
    d. keloid wound healing
A

a. a prolonged prothrombin time
b. newborns are at increased risk

Slide 42

291
Q
  1. Predisposing condition for vitamin K deficiency:
    a. chronic pancreatitis
    b. broad spectrum antibiotic treatment
    c. gastro-esophageal reflux
    d. peptic ulcer
A

a. chronic pancreatitis
b. broad spectrum antibiotic treatment

Slide 42

292
Q
  1. What are the effects of vitamin K:
    a. it stimulates amino acid absorption in the intestine
    b. it stimulates protein synthesis in the liver
    c. it is required for gamma-carboxylation
    d. it inhibits bile acid secretion
A

b. it stimulates protein synthesis in the liver
c. it is required for gamma-carboxylation

Slide 42

293
Q
  1. Primary alteration(s) in vitamin C deficiency:
    a. keloid wound healing
    b. bone weakening
    c. skin structure alterations
    d. mucus membrane bleedings
A

b. bone weakening
c. skin structure alterations
d. mucus membrane bleedings

Scurvy - Slide 35

294
Q
  1. Primary vitamin C activity(ies)?
    a. hydrating agent
    b. proteolysis enhancer
    c. reducing agent
    d. antioxidant
A

a. hydrating agent
c. reducing agent
d. antioxidant

Slide 33

Low Yield Semmelweis (37 decks)

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