Pathophysiology yp by mikeholy

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									Pathophysiology 2006-06-14 6yp
The exam consists of 2 types of questions
a question w/ 5 possible answers where you have to choose the best possible one
complex sentence joined w/ “because” where you answer according to the following
If both sentences are true & there is a logical association between them.
If both sentences are true but there is NO logical association between them.
If the 1st sentence is true but the 2nd is false.
If the 1st sentence is false but the 2nd is true.
If both sentences are false.

1.    During an insufficiency of a liver, the serum concentration may drop down of:
     -a. vasopressin
     -b. testosterone
     -c. aldosterone
     -d. prolactin
     -e. none of these

2.    The body responds to METABOLIC ACIDOSIS by:
     -a. decreased renal ammonia production.
     -b. increased ventilation - hyperventilation
     -c. excreting large amounts of potassium – actually retention of K
     -d. retaining carbon dioxide
     -e. decreasing bicarbonate absorption

3.    NOT a secondary adaptive mechanisms of INTRAVASCULAR VOLUME DEFICIT:
     -a. activation of RAA system
     -b. secretion of ADH
     -c. activation of sympathetic NS
     -d. increase of diuresis
     -e. reduction of ANP secretion

4.    Fanconi syndrome:
     -a. generalized reabsorptive defect
     -b. synonym for acute tubular necrosis
     -c. synonym for renal hypoplasia
     -d. a & b are correct
     -e. none of the above

5.    What biochemical changes are characteristic for renal osteodystrophy in chronic renal
     -a. hypocalcemia
     -b. hypophosphatemia
     -c. hyperparathyroidism
     -d. a & c are correct
     -e. none of the above

6.    The most common cause of CHRONIC RENAL FAILURE is:
     -a. diabetes mellitus
     -b. renal hypoplasia
     -c. polycystic disease
     -d. acute pyelonephritis
     -e. amyloidosis

7.    What is the most common mechanism of glomerular injury in primary
     -a. immunologic injury (Ag-Ab complexes)
     -b. metabolic (diabetes mellitus)
     -c. toxic (drugs)
     -d. vascular
     -e. ischaemic

8.    What is NOT characteristic for nephrotic syndrome?
     -a. hypoalbuminemia
     -b. proteinuria >3g/24hrs
     -c. hypertension
     -d. hyperlipidemia
     -e. edema

9.    Hepatorenal syndrome is a functional insufficiency of kidneys BECAUSE no
      anatomical changes can be found in these organs.
     -a. 1st true, 2nd false
     -b. 1st false, 2nd true
     -c. both false
     -d. both true w/ logical connection
     -e. both true w/ no logical connection

10. Choose the false statement below.
   -a. Aggravation of RVHF typically leads to pulmonary edema.
   -b. Respiratory disorders in course of chronic CHF most often have restrictive &
       obstructive component.
   -c. The most frequent cause of cardiac arrest is ventricular fibrillation.
   -d. Dyspnea occurring the course of LVHF is frequently aggravated in horizontal position.
   -e. Cyanosis occurs whenever the concentration of deoxyHb exceed normal Hb

11. OLIGURIC means that urine output is:
   -a. less than 600 mL/day
   -b. less than 1000 mL/day
   -c. less than 400 mL/day
   -d. less than 1500 mL/day
   -e. less than daily fluid intake
Oliguria - abnormally small production of urine; can be a symptom of kidney disease or
obstruction of the urinary tract or edema or an imbalance of fluids & electrolytes in the body

12. The main cause of portal hypertension caused by an Intrahepatic barrier is:
   -a. postinflammatory cirrhosis
   -b. alcoholic cirrhosis
   -c. biliary cirrhosis
   -d. metabolic cirrhosis
   -e. congenital hepatic fibrosis

13. Which can be a possible reason for anemia in renal disease?
   -a. reduced erythropoietin level
   -b.   decreased erythrocyte survival (toxins)
   -c.   decreased level of transferrin (proteinuria)
   -d.   susceptibility to bleedings (toxins destroy platelets)
   -e.   all answers are correct

   -a. hypoxemia & hypercapnia
   -b. hypoxemia & hypocapnia
   -c. hypercapnia
   -d. hypoxemia
   -e. none of the above

15. A localized edema may be caused by:
   -a. a breast cancer operation
   -b. a wasp bite
   -c. venous insufficiency
   -d. contact w/ an allergen
   -e. all answers are correct

16. IATROGENIC PNEUMOTHORAX may be caused by:
   -a. a pleural puncture
   -b. a lung puncture
   -c. a fluid evacuation from the pleural cavity
   -d. all the above correct
   -e. none of the above correct

17. Symptom(s) typical for left ventricular heart failure (LVHF) is(are):
    -a. orthopnea
    -b. dilation of peripheral veins
    -c. hydroperitoneum
    -d. congestive hepatic cirrhosis
    -e. all the above
Left Heart Failure: symptoms of decompensated heart failure include dyspnea on exertion,
orthopnea, fatigue & paroxysmal nocturnal dyspnea (cardiac asthma). Nocturnal cough,
Confusion & memory impairment (in advanced stages), & diaphoresis & cool extremities at rest.
Signs of decompensated left heart failure include: cardiomegaly, Pathologic S3 Gallop, S4,
Crackles at the lung bases due to pulmonary edema (fluid accumulation in the lungs), Dullness
to percussion & tactile fremitus of lower lung fields. Increased intensity of pulmonic component
of 2nd heart sound.

18. Heart infarction can be complicated by:
   -a. ventricular fibrillation
   -b. acute pulmonary edema
   -c. acute mitral regurgitation
   -d. a & c are correct
   -e. all answers are correct

19. Which of the pathologies below makes you think that the reason of edemas may NOT
    be a liver disease?
   -a. hepatorenal syndrome
   -b. portal hypertension
   -c. secondary hyperaldosteronism
   -d. hyperalbuminemia
   -e. renal failure

20. Patients with latent chronic renal failure usually have:
   -a. oliguria
   -b. dysuria
   -c. uremia
   -d. isosthenuria
   -e. anuria

21. The main causes of LIVER INSUFFICIENCY is:
   -a. cardiovascular disease
   -b. metabolic disease
   -c. intoxications & drug abuse – 15%
   -d. infections – 60%
   -e. none of the above

22. Edemas are the clinical manifestation of abnormally large amounts of fluid in the
    interstitial tissue spaces of the body. Which of the disorders below is NOT subject of
    this definition.
   -a. Quincke’s edema
   -b. lymphedema
   -c. cerebral edema
   -d. pulmonary edema
   -e. all answers are correct

23. Which of the following statements is TRUE?
   -a. anterior infarct usually involve occlusion of the L coronary artery, in particular the L
       anterior descending
   -b. normal size of the heart is typical for ischaemic cardiomyopathy
   -c. myocardial infarction is principally diagnosed on ECG
   -d. elevation in total creatine kinase is specific for myocardial injury
   -e. macrophage/monocyte infiltration and fibrovascular disease response typically occurs
       w/in 7 weeks after myocardial infarction

24. Which of the conditions listed below usually precedes the onset of insulin-independent
    diabetes mellitus?
   -a. chronic viral insulinitis
   -b. nephrotic syndrome
   -c. chronic hyperinsulinemia
   -d. acute pancreatitis
   -e. understimulation of insulin receptors in peripheral tissues

25. Pseudocyanosis may occur in the course of:
   -a. passive hyperrhemia
   -b. ischaemia
   -c. chronic respiratory insufficiency
   -d. elevated RBC count
   -e. all of the conditions listed above
26. Which of the following factors is responsible for homosexualism in males?
   -a. having a difficult childhood
   -b. having some unpleasant experiences with women in adolescence
   -c. insufficient stimulation of the brain by androgens during fetal development
   -d. overstimulation of the brain by estrogens during fetal development
   -e. none of the factors listed above can be regarded as responsible

27. Female look accompanied by 46,XY karyotype is a symptom of:
   -a. congenital deficiency of steroid 21-alfa-hydroxylase
   -b. tissue resistance to androgens
   -c. pituitary dysfunction
   -d. hypothalamic dysfunction
   -e. none of the above

28. Which of the following laboratory tests is the most useful when making a differential
    diagnosis between a hemolytic and aplastic anemia?
   -a. MCV
   -b. MCHC
   -c. ESR
   -d. reticulocytosis
   -e. a & b are true

29. Which of the following findings can be observed in pernicious anemia?
   -a. leukocytosis
   -b. autoimmune inflammation of gastric mucosa
   -c. decreased MCV
   -d. decreased MCHC
   -e. none of the above

30. Which of the following defects underlies syderoblastic anemia?
   -a. impaired globin synthesis
   -b. synthesis of pathological form of transferrin
   -c. impaired iron incorporation in the porphyrin part of hemoglobin
   -d. impairment of iron absorption in the small intestine
   -e. none of the above

31. Which of the following conditions is NOT a complication of ischaemic heart disease?
   -a. circulatory failure
   -b. pulmonary edema
   -c. cor pulmonale
   -d. cardiac arrhythmias
   -e. myocardial infarction

32. Which of the following conditions is NOT a complication of a nephrotic syndrome?
   -a. obesity
   -b. hyperlipoproteinemia
   -c. edemas
   -d. immune deficiency
   -e. impaired blood clotting
33. Which of the following conditions can not be regarded as a risk factor for
   -a. tobacco addiction
   -b. hyperinsulinemia
   -c. cholelithiasis
   -d. arterial hypertension
   -e. elevated level of homocysteine in the blood

34. Among rheumatic diseases:
   -a. some have autoimmune background
   -b. some are caused by metabolic disorder
   -c. some have genetic predisposition
   -d. a & c are true
   -e. all are true

35. Which of the following systems are involved in connective tissue diseases?
       1. locomotor
       2. central nervous
       3. peripheral nervous
       4. cardiac
       5. skin
   -b. 1 & 5
   -c. 1 & 2 & 3
   -d. 1 & 4
   -e. none of the above
   -f. all of the above

36. Classification of rheumatic diseases for academic and epidemiological reasons is
    possible BECAUSE these diseases could be grouped according to genetic background
    or underlying pathomechanisms.
   -a. 1st true, 2nd false
   -b. 1st false, 2nd true
   -c. both false
   -d. both true w/ logical connection
   -e. both true w/ no logical connection

37. Rheumatic diseases are curable now BECAUSE new biological drugs are available.
   -a. 1st true, 2nd false
   -b. 1st false, 2nd true
   -c. both false
   -d. both true w/ logical connection
   -e. both true w/ no logical connection

38. A symptom of suprachiasmatic nucleus dysfunction can be:
   -a. disturbances in circadial biological rhythms
   -b. increased sex drive
   -c. choreoatetosis
   -d. increased appetite
   -e. none of the above

39. Decreased body temperature (hypothermia) may be a symptom of:
   -a.   streptococcal infection
   -b.   thyroid gland hyperfunction
   -c.   over-epithelialization of sweat glands
   -d.   all of the above
   -e.   none of the above

40. What will be the most reasonable strategy of pharmacological management of
    cardiogenic shock?
   -a. alfa1-adrenergic drugs
   -b. alfa1-adrenolytic drugs
   -c. beta1-adrenergic drugs
   -d. beta2-adrenolytic drugs
   -e. none of the above

41. Which condition can lead to hypernatremia?
   -a. glycosuria
   -b. intoxication w/ diuretic drugs
   -c. SIADH
   -d. generalized edemas
   -e. all of the above

42. Which of the following substances can be present in the urine of a healthy man during
    routine examination?
   -a. glucose
   -b. fructose
   -c. acetoacetate
   -d. bilirubin
   -e. hemoglobin

43. Which of the following drugs can be used in the treatment of bronchial asthma?
   -a. cholinergic drugs, stimulating muscarinic receptors
   -b. alfa1-adrenolytic drugs
   -c. beta1-adrenolytic drugs
   -d. cholinolytic drugs, blocking muscarinic receptors
   -e. none of the above

50. Risk factors for osteoarthritis include the following EXCEPT:
    -a. obesity
    -b. abnormal anatomic structure
    -c. mechanical overload
    -d. age
    -e. exocrinopathy
51. Abnormal loading of normal tissue in the locomotor system accelerates osteoarthritis
    BECAUSE initiation of autoimmune processes leads to development of connective
    tissue diseases.
   -a. 1st true, 2nd false
   -b. 1st false, 2nd true
   -c. both false
   -d. both true w/ logical connection
   -e. both true w/ no logical connection

The most often affirmed antibodies in ADDISON-BIERMER’S DISEASE are:
Anti-parietal cell – 90% of pts w/ pernicious anemia
None-of the above
ADDISON-BIERMER’S DISEASE - pernicious anaemia or megaloblastic anaemia, secondary to
vitamin B12 deficiency. Characterized by faulty maturation of erythrocytes w/ formation of
abnormally large megaloblastic precursors. Occurs most commonly in middle-aged. Aassociated
w/ weakness, pallor, shortness of breath, digital paresthesia, numbness, lack of coordination,
spasticity, difficulty in walking, decreased sense of taste & smell, mental dullness, & sometimes
psychoses. GI changes include achylia gastrica, diarrhea, & constipation. Both sexes affected.

Patient 24h after 1st dose of sulfonamides*, normochromic & normocytic anemia were observed
along w/ jaundice as well as hemoglobinuria. The most probable diagnosis would be:
Deficiency of Glu-6-PD – X-linked; sulfonamides induce hemolysis in these pts. Normochromic
& normocytic anemia
Inborn spherocytosis – see explanation for 3 below
Drepanocytosis – sickle cell anemia
Anemia w. sideropenia – decreased production of RBCs
PRCA – pure red cell aplasia
PURE RED CELL APLASIA – attacks Erythroid precursors; normoblastic normochromic anemia &
absence of reticulocytes; Injury to stem cells in utero ~90% of congenital cases Diamond-
Blackfan syndrome; 10% is familial; acute self-limited secondary to virus/drug-induced
impairment of erythroid progenitor cells. acquired chronic associated w/ thymomas &
autoimmune disorders, damage is immune & T-cell mediated;
*also antiepileptics, azathioprine, chloramphenicol, isoniazid, procainamide.

Jaundice, raised MCHC & increased osmotic sensibility of erythrocytes in 16yo boy suggests:
Anemia w/ sideropenia – decreased production of RBCs
Inborn spherocytosis
Wiskott-Aldrich syndrome – Xlinked recessive immunodeficiency w/ thrombocytopenia & eczema
Hemophilia A
None of the above
SPHEROCYTOSIS – autosomal dominant hemolytic anemia, pancytopenia, increased incidence of
thrombosis; Most COMMON inherited intracorpuscular HA in whites; prominent splenomegaly;
Increased MCHC; Erythrocyte osmotic fragility to NS: Manifest spectrin deficiency.

Is an intracorpuscular defect acquired at stem cell level
Makes red blood corpuscles more sensitive to the lytic effect of complement
The thrombocytopenia is of PNH symptoms
Manifests in course of mycoplastic infections
All the above are incorrect
PNH - surface proteins missing in all blood cells, including platelets & white cells due to a
biochemical defect, a genetic mutation leading to the inability to synthesize the glycosyl-
phosphatidylinositol (GPI) anchor that binds these proteins to cell membranes. The
corresponding gene PIGA (phosphatidylinositol glycan class A) in the deletions or point
mutations on X chromosome; Complement-regulating surface proteins lacking in all
hematopoietic cells (CD55, C8 binding protein, & CD59); Hemolytic anemia due to
intravascular destruction of RBCs by complement; dark urine during the night w/ partial clearing
during the day; Thrombosis of the veins sudden catastrophic complication w/ severe abdominal
pain & rapidly enlarging liver & ascites (Budd-Chiari syndrome) due to lack of CD59 on platelet
membranes that induces platelet aggregation & is highly thrombogenic; Deficient hematopoiesis
w/ hypoplastic bone marrow; PTs w/ PNH have 10-20% chance of developing aplastic anemia
& 5% of patients w/ aplastic anemia eventually develop PNH.

Erythropoietin level increases
Reticulocytosis occurs
Enlarged demand on cobalamin is observed – due to –a.
Enlarged demand on folic acid occurs – due to –a.
All the above
HA – increased Red Cell destruction; increased ucBR, acholuric jaundice (no BRuria);
hyperBRemia leads to “pigment-containing gallstones”; increased urine urobilinogen; Hb-emia
& Hb-urea; haptoglobins disappear; hemosiderosis; INC ERYTHROPOIESIS leading to normoblastic
erythroid hyperplasia, RETICULOCYTOSIS, polychromatophilia.

Many decreases in structure of bones, increase of [Ca2+], albuminuria, & presence of
monoclonal protein characterize
mercuric Cl poisoning
myeloma multiplex
chronic nephritis
MULTIPLE MYELOMA - is a debilitating malignancy that is part of a spectrum of diseases ranging
from monoclonal gammopathy of unknown significance (MGUS) to plasma cell leukemia.
Characterized by a proliferation of malignant plasma cells & a subsequent overabundance of
monoclonal paraprotein. antibody-forming cells are malignant. Can be asymptomatic or
insidious. Infections, renal failure, pathologic fractures, & spinal cord compression. Treatment
(longer life, less pain, fewer complications) but no cures. Pathophysiology: plasma cell
proliferation can lead to leukopenia, anemia, & thrombocytopenia. plasmacytomas (soft tissue
masses) or lytic lesions in the skeleton. Bone pain, hypercalcemia, & spinal cord compression.
Impaired humoral immunity especially against encapsulated organisms. hyperviscosity,
amyloidosis, & renal failure.

Choose the incorrect answer about SICKLE CELL ANEMIA (chronic hemolytic anemia):
sickling (w/ Na metabisulfate) occurs when there is a high [deoxyHbS]
single amino acid is altered in the Beta chain of HbS – point mutation of beta-globin
the disease may be diagnosed in fetal DNA – from amniotic cells or chorionic villus
solubility of deoxyHbS is abnormally low
HbS has an unchanged electrophoretic mobility, relative to normal Hb

PNH is a clonal disease BECAUSE it causes hemolysis engaging the complement.
–a. both sentences are true & there is a logical association between them

IRON DEFICIENCY ANEMIA is characterized by
Problems w/ concentration
lip-sores at angle of mouth
All the above
IDA – hypochromic microcytic anemia due to dietary lack or loss from chronic bleeding. pallor,
fatigue, dyspnea upon exertion, glossitis, gastritis, koilonychias. w/ Plummer-Vinson syndrome

is used to diagnose anemia of VitB12 deficiency.
is performed w/ use of radioactive cobalamin
shows the level of absorption of VitB12 in alimentary canal
all are correct
all are incorrect

Choose incorrect answer.
Shortage of Glu-6-PD has Heinz bodies located w/in red blood corpuscles.
For an average human the 24h loss of iron is less than 1mg.
Sickle cell anemia is autosomal recessive disorder.
In course of hemophilia A factor IX is deficient. – hB is factor IX; hA is factor VIII
Mucoviscidosis is caused by mutation of ion channel gene located on chromosome 7.

EOSINOCYTOSIS can be caused by:
allergic disorder                                    1, 2, 3, 4
skin diseases (psoriasis)                            1, 2
drug reactions                                       1, 2, 4
parasitic infections                                 1, 4
                                                     1, 3, 4

Lab results indicate - Hb = 9 g/dL; Hct = 30%; MCV = 78 fL; MHC = 25 pg. The patient suffers
pernicious anemia
anemia of B12 deficiency
megaloblastic anemia
microcytic anemia
all are correct

diabetes mellitus
anemia of iron deficiency

The most common cause of ELEVATED CREATINE level in blood is:
acute pyelonephritis
polycystic disease
acute glomerulonephritis
renal stones

pH = 5.5            sg = 1.005 proteins +++
pH = 7.5            sg = 1.010 proteins ++
pH = 5.5            sg = 1.025 proteins -
pH = 7.5            sg = 1.030 proteins -
pH = 7.5            sg = 1.030 proteins ++

Urinalysis is: pH 5.5; sg = 1.020; proteins 0.02mg/dL, WBC (?); RBC 0-1 va; urine vol. is 1500
mL/day. The result is:
abnormal, the patient develops 1st signs of renal failure
abnormal, the patient has proteinuria
abnormal, the patient has E.coli in the urinary tract
abnormal, the patient requires 24 hr urine analysis

Which is not the most common symptom of CHRONIC RENAL FAILURE:
acidosis                                    dysuria
nycturia                                    uremia
hyperkalemia                                proteinuria
oliguria                                    leukocyturia
HT & anemia

Most characteristic features of RENAL FAILURE are:
Hypocalcemia                                   Metabolic acidosis
Hypokalemia – actually hyperkalemia            Metabolic alkalosis
Anemia                                              1, 2, 5, 7
Polycythemia                                        1, 4, 6, 7
Hyperphosphatemia – leads to acidosis               3, 4, 5, 6
1, 2, 4, 5
1, 3, 5, 7

proteinuria > 3.5-4 g/day                        hematuria
hypoalbuminemia < 2.5-3 g/dL                     1, 2, 5, 6
edema – decreased PCOP                           1, 2, 4, 6
hyperlipidemia – increased hepatic lipoprotein   1, 2, 3, 5
synthesis                                        1, 2, 3, 4
hypertension                                     1,2,4,5

In patient w/ CHRONIC RENAL FAILURE, altered regulation of serum calcium & phosphate
leads to:
Primary hypothyroidism
Secondary hypoparathyroidism
Secondary hyperparathyroidism - hypophosphatemia, so inc PTH sec,PTH resp for Ca & P
transport to bone
Primary hyperthyroidism
Primary hyperparathyroidism

sudden attack of asthma
valvular pneumothorax
chronic bronchitis –COPD
recurrent embolism & thrombus of pulmonary aa.
C & D are correct

All the above
None of the above

Main cause of ATELECTASIS is:
lack of surfactant
a rupture of the subplural alveolus
acute LVHF
alfa1antitrypsin deficiency
lack of collagen

all the above correct
none of the above correct

Which condition listed below predisposed to UROLITHIASIS
congestion of urinary tract
infection of urinary tract
inability to move
all the above correct

Factor directly responsible for CNS manifectations of END-STAGE RENAL FAILURE is:
hypersecretion of PTH – causes seizures & depression; RF is most common cause of
deficiency of free calcium ions in blood
hyperproduction of angiotensin I
insufficient hydroxylation of VitD to its metabolically active form

is a risk factor for atherosclerosis.
can occur in the course of hypothyroidism.
is typical for nephritic syndrome.
is all the above.
A & C are correct

May appear in a HEALTHY MANS URINE:
free bilirubin
glucose –bGlu >200mg/dL
fructose - could be due to hereditary inability to metabolize fructose, also in obese individuals
acetoacetic acid – produced in liver leading to excessive FA breakdown as in DM

PSEUDOCYANOSIS may occur in the course of:
passive hyperthermia
ischaemia – associated w/ hypoxemia
chronic respiratory insufficiency – not here either
elevated RBC count - would prevent PC
all the above – definitely not
Pseudocyanosis – a bluish tinge of skin &/or mucous membranes NOT associated w/
hypoxemia or peripheral vasoconstriction. Mostly related to metals (eg, silver nitrate, silver
iodide, silver, lead) or drugs (eg, phenothiazines, amiodarone, chloroquine hydrochloride).
Clinical presentation of rapid intermittent abdominal pain, red colored urine, skin changes,
mental & neurological disturbances, & elevated iron content in the blood are highly typical for:
hemolytic anemia – lysis of RBCs releasing Iron
Goodpasture’s syndrome – hematuria w/ “red cell casts” & smokey brown urine.
Henoch-Schonlein purpura

The onset of NON-INSULIN DEPENDENT DM is usually preceded by:
chronic viral insulitis
nephrotic syndrome – occurs at onset of NID-DM
chronic hyperinsulinemia
acute pancreatitis
hypostimulation of insulin receptors in periphery
NID-DM most commonly in obese. Pancreas produces some insulin. insulin insensitivity.. so
you have chronic hyperinsulinemia; Nephrotic syndrome protein- & mineral- urea leading to
edema.Diabetes is the most common cause of nephrotic syndrome in adults.

arterial HT, hypokalemia, acidosis
arterial HT, hyperkalemia, acidosis
arterial HT, hypokalemia, alkalosis
orthostatic HT, hyponatremia, weight loss
orthostatic HT, hypernatremia, weight loss

PULMONARY EDEMA as a result of MI is due to:
acute LVHF
acute RVHF
chronic RVHF
chronic LVHF
Plays a crucial role in the pathogenesis of ANAPHYLACTIC SHOCK:
bradykinin & C3
histamine & leukotrienes
prostaglandins & thromboxanes
prostacyclin & serotonin
tachykinin & hageman’s factor
AS – rapid onset Urticaria, bronchospasm, laryngeal edema, shock; IgE mediated release of
histamine; marked eosinophilia; no complement involvement.

ALFA-ADRENERGIC DRUGS contraindicated in:
septic shock
neurogenic shock
anaphylactic shock
cardiogenic shock – carvedilol & labetelol
hypovolemic shock

Most life threatening manifestation of THYROID STORM concern:
alimentary tract
circulatory system
respiratory system
TS – acute, severe exacerbation of thyrotoxicosis; increased Catecholamine response &
hyperthyroid state; life threatening cardiac, hepatic, renal; Grave’s disease most common form
of hyperthyroidism (increase T4 leading to goiter)

Blockade of H1 RECEPTORS in CNS typically results in:
increased appetite
sexual frigidity
drowsiness – most common SE
all the above

Most frequent non-extrapyramidal (mental) symptoms of HUNTINGTON’S DISEASE include:
myoclonic jerks - extrapyramidal
painful skeletal mm. cramps
mental disorders & dementia
ataxia, astasia, abasia
Mental- loss of cognitive ability & changes in personality that may develop into dementia.
Physical- General lack of coordination & involuntary movements causing an unsteady gait. Most
people with HD eventually exhibit chorea, which is jerky, random, uncontrollable, rapid
movements, although some exhibit very slow movement & stiffness (bradykinesia,dystonia).
Typically, the abnormal movements begin at the extremities & then later progress. Patients also
show loss of facial expression (they are called "masks in movement"). HD autosomal dominant;
increased # of paternal CAG repeats on Chr.4; decreased BDNF (brain derived neutortropic
PUTAMEN) & FRONTAL CORTEX; onset 30-40yoa w/ athetoid movements, deterioration &
hypotonicity, fecal & urinary incontinence, anorexia & wt. loss, ALL LEADING TO DEMENTIA &
DEATH; onset is earlier in subsequent generations.

HYPERKALEMIA is not due to:
diarrhea – causes hypokalemia
massive necrosis
massive hemolysis
end-stage renal failure
Addison’s disease

Possesses proven DEPRESSANT properties:
serotonin – increased serotonin is MOA of ANTIDEPRESSANTS
CYCLO-OXYGENASE 2 (COX2) inhibitors inhibit the production of prostaglandin E2 & of
proinflammatory cytokines, & have been reported to have antidepressive effects.

Hyponatremia due to SIADH will be accompanied by:
Lack of secondary hypovolemia & hypotension
increased appetite
decreased MCV
SIADH- water retention, hyponatremia, anorexia, nausea, disorientation, coma, convulsions, &

Henoch-Schonlein purpura – allergic purpura; primary hemostasis
Marfan syndrome – defect in connective tissue
Ehlers-Danlos syndrome – primary hemostasis; inherited abnormalities of collagen/elastin
DIC – primary & secondary hemostasis
VonWillebrand’s disease – primary & secondary; most common inherited bleeding disorder of
def vWF

The cause of thrombocytopenia should always be diagnosed BECAUSE thrombocytopenia may
be a symptom of neoplastic disease.
a.     If both sentences are true & there is a logical association between them.

Symptoms of BLOODY DIARRHEA can be:
prolonged bleeding after dental surgery
nose bleed
extravasations on skin
all the above

abdominal pain
changes in urine tests
joint pain
skin changes
all the above
Henoch-Schonlein purpura – purpura (hemorrhagic urticaria), fever, arthralgias, gastrointestinal
symptoms (abdominal pain, nausea, vomiting, diarrhea, bloody stools), painful menstruation, &
glomerulonephritis. Leukocytoclastic angiitis. Hypersensitivity vasculitis from immune rxn.
usually seen in children, but people of any age may be affected. It is more common in boys.
Many people w/ Henoch-Schonlein purpura had an upper respiratory illness in the previous
weeks. PE skin lesions (vasculitis) & joint tenderness. UA microHb-uria. No specific treatment.
Most resolve spontaneously w/out treatment. If symptoms persist, therapy w/ corticosteroids.
Complications - recurrence of symptoms, renal impairment.

DIC may lead to:
acute renal failure
acute respiratory failure
secondary bleeding diathesis
all the above

DIC may be triggered by:
entry of tissue factor into circulation
endothelial damage – causing release of tissue thromboplastin
direct activation of factor X & prothrombin – leads to depletion of factors II, V, VIII
A & B are correct
A & B & C are correct
DIC – release of tissue thromboplastin, activation of intrinsic pathway of coagulation &
fibrinolytic system.

Abnormal function of GpIIb/IIIa RECEPTOR is present in:
hemophilia A
hemophilia B
Glanzmann’s thrombasthenia
VonWillebrand’s disease
all the above
GLANZMANN’S THROMBASTHENIA - inaggretability of platelets due to hereditary lack of platelet
GPIIb/IIIa (required for formation of fibrinogen bridges)

In hemophilia B intracranial bleeding may occur BECAUSE & is caused by lack of factor VIII.
If the 1st sentence is true but the 2nd is false. – should be factor IX

hemophilia A - secondary
acute liver failure primary & secondary; deficiency of all coagulation factors except vWF
leading to inc PT, APTT, Thrombin Time, Bleeding Time.
hemophilia B - secondary
VonWillebrand’s disease - primary & secondary; most common hereditary bleeding disorder.
all the above

Normal bleeding time, prolonged APTT may be observed in:
hemophilia A
hemophilia B
intox w/ oral anticoagulants – prolonged BT
A & B are correct
A & B & C are correct
HEMOPHILIA A is a genetic disease of:
X-linked recessive – factor VIII def.
X-linked dominant
Autosomal recessive
Autosomal dominant
May be autosomal or X-linked

RECURRING THROMBOSIS is not influenced by:
lack protein C – leads to thrombosis
lack of protein S – leads to thrombosis
lack of antithrombin III – leads to thrombosis
lack of VitK –needed for thrombus formation

Symptoms of VIT-K DEFICIENCY can be caused by:
problems w/ digestion & absorption
long therapy w/ broad spectrum antibiotics
oral anticoagulants
all the above
VKD – decreased activity of clotting factors II, VII, IX, X; prolonged PT, APTT; in adults most
often caused by fat malabsorption due to pancreatic or small bowel disease; in neonates causes
hemorrhagic disease caused by deficient exogenous VitK in breast milk due to fat malabsorption
in mother

BUDD-CHIARI SYNDROME is caused by thrombosis of:
hepatic v.
portal v.
hepatic a.
coronary a.
none of the above

isolated HT in the pulmonary a.
hypertrophy of the R. ventricle of the heart – predominates in chronic
dilation of the R. ventricle – due to primary pulmonary HT or COPD
all the above
none of the above

Rheumatic diseases are curable now BECAUSE new biological drugs are available.
d.   If the 1st sentence is false but the 2nd is True.

Abnormal loading of normal tissue in locomotor system accelerates Osteoarthritis BECAUSE
initiation of autoimmune processes leads to development of connective tissue diseases.
a.       If both sentences are true but there is no logical association between them.
OA is a degenerative connective tissue disease of type II collagen. Not autoimmune.

Degradation of chondroid tissue in OA is caused by metalloproteinases BECAUSE these
proenzymes are secreted by hepatocytes & activated through IL-1.
If the 1st sentence is true but the 2nd is false.
Metaloproteinases are type IV collagenases of epithelial & basement membranes; IL-1 is a
potent pro-inflammatory cytokine that induces CHONDROCYTES & SYNOVIAL cells to synthesize
MMPs; may play significant role in tumor invasion, including carcinomas, melanomas,
sarcomas. Adenomas of breast & colon have less MMPs; metalloproteinases inhibitors;

Mechanism NOT involved in the pathogenesis of RHEUMATOID ARTHRITIS is:
hyperplasia of synovium
inflammation of synovium
osteocyte formation
fibrosis of synovium
pannus formation

Reactive arthritis is characterized by HLA-B27 positivity BECAUSE this Ag is involved in
presentation of bacterial Ag to immune competent cells.
If the 1st sentence is false but the 2nd is true.
REACTIVE ARTHRITIS bacteria cause. knees, ankles, toes, also eyes, skin, muscles. 50% HLA-
B27 positive but also found in other diseases.
Sjogren syndrome is named inflammatory endocrinopathy BECAUSE in this disease the
inflammatory damage of glandular tissue occurs.
If the 1st sentence is false but the 2nd is True.
SJOGRENS syndrome is a autoimmune exocrinopathy of tears & saliva glands; 90%
rheumatoid factor positive; hallmark symptoms dry mouth & dry eyes (sicca symptoms), skin,
nose, and vaginal dryness, may affect kidneys, blood vessels, lungs, liver, pancreas, and brain.
9/10 are women; onset p 40yoa; 2nd most common autoimmune rheumatic disease. BLOOD TESTS
for ANA (SSB/La & SSA/Ro) & rheumatoid factor; SCHIRMER TEST measures the production of
tears; SLIT-LAMP EXAMINATION dryness on the surface of the eye; SALIVARY GLAND FUNCTION
saliva amount produced; LIP BIOPSY lymphocytes around inflamed salivary glands.

ELEPHANTIASIS can be the symptom of:
venous insufficiency – just edema
infection w/ filarial worms
long air travel – also edema
lymphatic vessel failure – obstruction of lymphatic vessels
A & B are correct
LYMPHATIC FILARIASIS by far most common cause of ELEPHANTIASIS; Wuchereria bancrofti,
Brugia malayi, & Brugia timori (nematodes/roundworms) transmitted by mosquitoes; parasite
occupies lymph vessels that drain the lower extremities, producing massive enlargement and
deformity of the legs and genitalia; swelling results from the obstruction of these lymphatic
vessels or from the immune response to the parasite and their endosymbiotic bacteria; found
almost exclusively in the tropics; W.bancrofti=bancroftian filariasis; Onchocerca volvulus
causes many disorders in addition to elephantiasis.

NOT a secondary adaptive mechanisms of INTRAVASCULAR VOLUME DEFICIT:
activation of RAA system
secretion of ADH
activation of sympathetic NS
increase of diuresis
reduction of ANP secretion

SYSTEMIC EDEMAS may accompany
hepatic failure
all the above
A & B are correct

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