Pathology Question Set 12

by Lecturio USMLE

Questions about the lecture
My Notes
  • Required.
Save Cancel
    Report mistake

    About the Lecture

    The lecture Pathology Question Set 12 by Lecturio USMLE is from the course Pathology - High Yield Questions.

    Included Quiz Questions

    1. Botulinum toxin binds presynaptically to inhibit release of acetyl choline at neuromuscular junction.
    2. Botulinum toxin binds presynaptically to cause excessive release of acetyl choline at neuromuscular junction.
    3. Botulinum toxin binds to glycine receptor to block inhibitory neuronal output.
    4. Botulinum toxin binds irreversibly to nicotinic receptors at neuromuscular junction and blocks effects of acetyl choline.
    5. Botulinum toxin binds presynaptically to inhibit Renshaw cell release of glycine.
    1. Anti-GD1a antibodies are most common antibodies causing AIDP.
    2. Most common isotype of the autoantibodies causing AIDP is IgG.
    3. During pathogenesis of AIDP, complement deposition occurs along outer surface of the Schwann cells.
    4. Examination of cerebrospinal fluid (CSF) can be normal within 48 hours of onset of symptoms of AIDP.
    5. Reduced amplitudes of compound muscle action potentials (CMAPs) are one of the earliest electrodiagnosis features of AIDP.
    1. α1 adrenergic receptor on radial muscle of iris
    2. β2 adrenergic receptor on ciliary muscle
    3. α1 adrenergic receptor on pupillary sphincter muscle
    4. α2 adrenergic receptor on pupillary sphincter muscle
    5. α2 adrenergic receptor on radial muscle of iris
    1. The gene locus which is mutated in this condition is on chromosome 9.
    2. The condition is inherited as autosomal dominant condition.
    3. Gait ataxia in this condition is a pure sensory ataxia.
    4. Vertical nystagmus is characteristically seen in patients suffering from this condition.
    5. Restrictive cardiomyopathy is seen in approximately 50% of the patients.
    1. Subcutaneous nodules are commonly associated with arthritis and are an early manifestation.
    2. HLA-DR4 and HLA-DR7 alleles are associated with susceptibility to the condition.
    3. Choreic movements commonly involve head and upper limbs.
    4. The least common site for erythema marginatum is face.
    5. Any strain of group A streptococcus has potential to cause the condition.
    1. Prothrombin gene mutation that causes predisposition to prothrombotic state is inherited in autosomal dominant pattern.
    2. Used of oral contraceptives is the most common acquired cause of thrombophilia.
    3. Virchow’s triad consists of inflammation, hypercoagulability, and platelet activation.
    4. Neutrophils have no role in pathogenesis of deep vein thrombosis.
    5. Histones in prothrombotic networks prevent platelet aggregation.
    1. Gene for mitogen-activated protein (MAP) kinase phosphatase-1 is activated by inhaled corticosteroids, which produces anti-inflammatory effects.
    2. β2-agonists reverse bronchoconstriction but do not control underlying inflammation because inflammatory cells do not express β2 adrenergic receptors.
    3. Theophylline activates histone acetyltransferase and therefore exerts anti-inflammatory activity in bronchial asthma.
    4. Antileukotrienes exert their beneficial effects in bronchial asthma by blocking cys-LT2-receptors.
    5. Omalizumab acts by blocking both circulating IgE and cell-bound IgE to produce therapeutic effects in bronchial asthma.
    1. Transforming Growth Factor β-1 (TGFβ1) gene variations can modify severity of cystic fibrosis.
    2. Cystic fibrosis transmembrane conductance regulator protein (CFTR) is involved in active transport of chloride and bicarbonate anions across plasma membranes of epithelial tissues.
    3. Inflammatory response in airways in patients with cystic fibrosis airway is characterized by predominant lymphocytic infiltration.
    4. Approximately 50% of males with cystic fibrosis have azoospermia.
    5. Penetrance of CFTR mutations is high and genotype determines the clinical manifestations.
    1. In patients with high-level nasal resistance, the opening of mouth during sleep prevents apnea/hypopnea episodes.
    2. Most common site of collapse of pharyngeal airway during sleep apnea is at level of base of tongue.
    3. Overnight blood pressure monitoring in the patient may not show a fall during sleep from blood pressure while awake.
    4. Episodes of apnea and hypopnea are more likely to occur during deeper stages of non-rapid eye movement (NREM) sleep.
    5. Gynoid obesity is associated with apnea and hypopnea more frequently as compared to android obesity.
    1. Hypocholesterolemia
    2. Hypoalbuminemia
    3. Raised serum α1-antitrypsin levels
    4. Hyponatremia
    5. Raised serum γ-glutamyl transpeptidase
    1. H. pylori infection is more commonly present in gastric ulcers than in duodenal ulcers.
    2. 90% of duodenal ulcers are located in first part of duodenum within 3 cm of the pylorus.
    3. Base of duodenal ulcer often contains eosinophilic necrosis.
    4. Bicarbonate secretion is decreased in duodenal bulb of patients with an active duodenal ulcer.
    5. H. pylori infection and non-steroidal anti-inflammatory drugs (NSAIDs) have synergistic effects in pathogenesis of peptic ulcer disease.
    1. Mucosal atrophy
    2. Increased number of intraepithelial lymphocytes
    3. Crypt hyperplasia
    4. Reduced height of villi
    5. Cuboidal appearance of surface epithelial cells
    1. Increased caloric intake in patients with Gilbert syndrome reduces bilirubin levels.
    2. Conjugation of bilirubin by UDP-glucuronosyltransferase disrupts the internal oxygen bonding that limits aqueous solubility of bilirubin.
    3. Most common UGT1A1 mutations causing Crigler-Najjar syndrome type I are missense mutations.
    4. Failure of phenobarbital to reduce serum bilirubin rules out Crigler-Najjar syndrome type II.
    5. Human UGT1 gene complex is is located on chromosome 5.
    1. Anti-CRMP5
    2. Anti-Hu
    3. Anti-Ri
    4. Anti-amphiphysin
    5. Anti-Yo
    1. Hyaline casts in urine sediment
    2. Fractional excretion of Na+ (FeNa) < 1%
    3. Urine sodium concentration < 10 mg/dL
    4. Urine creatinine: plasma creatinine ratio > 40
    5. Urine specific gravity > 1.018
    1. Chronic liver disease is associated with increased HbA1C levels.
    2. Iron deficiency is associated with increased HbA1C levels.
    3. Alcoholism is associated with increased HbA1C levels.
    4. Vitamin E supplementation may reduce HbA1C levels.
    5. Vitamin B12 supplementation may reduce HbA1C levels.
    1. To lower dietary calcium intake
    2. To lower animal protein intake
    3. To increase dietary potassium intake
    4. To lower dietary sodium intake
    5. To lower sucrose intake
    1. Complement fixation by anti-TPO antibodies is the most important mechanism for thyroid cell destruction in Hashimoto’s thyroiditis.
    2. Annual risk of developing clinical hypothyroidism is ~4% when subclinical hypothyroidism is associated with positive TPO antibodies.
    3. Thyrotropin-binding inhibitory immunoglobulin (TBII) assays cannot distinguish between TSI (thyroid stimulating immunoglobulin)- and THS-R-blocking antibodies.
    4. Transplacental passage of TSH-R(TSH-Receptor)-blocking antibodies may induce transient neonatal hypothyroidism.
    5. Hashimoto’s thyroiditis is associated with CTLA-4 polymorphisms.
    1. Smooth muscles of the gastrointestinal tract may be involved.
    2. After the calves, the next most common site of muscular hypertrophy is muscles of forearm.
    3. Asymptomatic carriers have normal serum CK levels.
    4. The severity of cardiac involvement correlates with the degree of skeletal muscle weakness.
    5. All the patients suffering from the conditions have carrier mothers.
    1. Interleukin 5
    2. Interleukin 3
    3. Interleukin 4
    4. Interleukin 9
    5. Interleukin 13

    Author of lecture Pathology Question Set 12

     Lecturio USMLE

    Lecturio USMLE

    Customer reviews


    5,0 of 5 stars
    5 Stars
    4 Stars
    3 Stars
    2 Stars
    1  Star