INI-CET 2023 May Session (Sample Paper Discussion @ Medico)

Q1:

All of the following are in anterior relationship with the 3rd part of the duodenum except:

Options:

  1. Gallbladder fundus
  2. Root of mesentery
  3. Superior mesenteric vessels
  4. Jejunal coils

Improved Explanation:

Answer: 1. Gallbladder fundus

Anatomical Relationships of the Third Part of the Duodenum (D3):

  • Anteriorly:

    • Superior Mesenteric Vessels: The superior mesenteric artery (SMA) and vein (SMV) cross anterior to D3.
    • Root of Mesentery: The mesentery of the small intestine originates here and lies over D3.
    • Jejunal Coils: Loops of the jejunum may overlie D3.

  • Posteriorly:

    • Aorta
    • Inferior Vena Cava (IVC)
    • Right Ureter

  • Superiorly:

    • Head of Pancreas

Gallbladder Fundus:

  • Located in the right upper quadrant (RUQ) of the abdomen.
  • Lies anterior to the first part of the duodenum (D1) and the transverse colon.
  • Not in anterior relationship with the third part of the duodenum (D3).

Illustrative Table:

Structure Relationship to D3
Superior Mesenteric Vessels Anterior
Root of Mesentery Anterior
Jejunal Coils Anterior
Gallbladder Fundus Not related

Clinical Relevance:

  • Surgical Importance: Understanding these relationships is crucial during abdominal surgeries to avoid vascular injury and other complications.
  • Pathology Considerations: Compression of D3 by the SMA can lead to Superior Mesenteric Artery Syndrome, causing duodenal obstruction.

Q2:

In which of the following vitamin deficiencies is xanthurenic acid seen in urine?

Options:

  1. Vitamin B9 (Folic acid)
  2. Vitamin B6 (Pyridoxine)
  3. Vitamin B12 (Cobalamin)
  4. Vitamin B1 (Thiamine)

Improved Explanation:

Answer: 2. Vitamin B6 (Pyridoxine)

Role of Vitamin B6 (Pyridoxine):

  • Coenzyme Functions: Essential for amino acid metabolism, neurotransmitter synthesis, and hemoglobin formation.
  • Tryptophan Metabolism: Acts as a coenzyme for enzymes in the kynurenine pathway, converting tryptophan to niacin (Vitamin B3).

Xanthurenic Aciduria:

  • Pathogenesis: Vitamin B6 deficiency impairs the enzyme kynureninase, leading to the accumulation of xanthurenic acid.
  • Clinical Significance: Elevated levels of xanthurenic acid in urine are indicative of vitamin B6 deficiency.

Metabolic Pathway Overview:

  1. Tryptophan → Kynurenine (via tryptophan dioxygenase)
  2. Kynurenine → 3-Hydroxykynurenine (requires B6)
  3. 3-Hydroxykynurenine → Xanthurenic Acid (accumulates when B6 is deficient)

Illustrative Table:

Vitamin Deficiency Characteristic Urinary Metabolite
Vitamin B6 Xanthurenic acid
Vitamin B9 FIGLU (Formiminoglutamic acid)
Vitamin B12 Methylmalonic acid
Vitamin B1 No specific metabolite in urine

Clinical Features of Vitamin B6 Deficiency:

  • Neurological Symptoms: Peripheral neuropathy, irritability, seizures (especially in infants).
  • Dermatological Symptoms: Seborrheic dermatitis, glossitis, cheilosis.
  • Anemia: Microcytic hypochromic anemia due to impaired heme synthesis.

Clinical Relevance:

  • Diagnosis: Measurement of urinary xanthurenic acid after a tryptophan load test.
  • Management: Vitamin B6 supplementation corrects the deficiency and associated symptoms.

Q3:

Which hormone acts through the JAK-STAT pathway?

Options:

  1. Calcitonin
  2. Leptin
  3. Aldosterone
  4. Vasopressin

Improved Explanation:

Answer: 2. Leptin

JAK-STAT Pathway Overview:

  • JAK (Janus Kinase): A family of intracellular, non-receptor tyrosine kinases.
  • STAT (Signal Transducer and Activator of Transcription): Transcription factors activated by phosphorylation.
  • Mechanism:
    1. Hormone binds to its receptor.
    2. Receptor-associated JAKs become activated.
    3. JAKs phosphorylate STATs.
    4. Phosphorylated STATs dimerize and translocate to the nucleus.
    5. STAT dimers regulate gene expression.

Hormones and Cytokines Utilizing JAK-STAT Pathway:

  • Leptin: Regulates appetite and energy expenditure.
  • Growth Hormone (GH): Stimulates growth and metabolism.
  • Prolactin: Promotes milk production.
  • Cytokines: Interleukins (e.g., IL-2, IL-6), interferons.

Hormones Not Using JAK-STAT Pathway:

  • Calcitonin: Acts via cAMP second messenger system (G-protein-coupled receptor).
  • Aldosterone: Binds to intracellular mineralocorticoid receptors, affecting gene transcription.
  • Vasopressin (ADH):
    • V1 receptors: Activate IP3/DAG pathway.
    • V2 receptors: Activate cAMP pathway.

Illustrative Table:

Hormone/Cytokine Signaling Pathway
Leptin JAK-STAT
Growth Hormone JAK-STAT
Prolactin JAK-STAT
Calcitonin cAMP (GPCR)
Aldosterone Intracellular receptor
Vasopressin V1: IP3/DAG; V2: cAMP (GPCR)

Clinical Relevance:

  • Leptin Resistance: Can lead to obesity due to impaired satiety signaling.
  • Pharmacological Targeting: JAK inhibitors are used in treating certain myeloproliferative disorders and autoimmune diseases.

Q4:

Which drug is used for trastuzumab-resistant HER2-positive breast cancer?

Options:

  1. Lapatinib
  2. Sorafenib
  3. Vemurafenib
  4. Erlotinib

Improved Explanation:

Answer: 1. Lapatinib

HER2-Positive Breast Cancer:

  • HER2 (Human Epidermal Growth Factor Receptor 2): Overexpressed in ~20% of breast cancers.
  • Trastuzumab (Herceptin): Monoclonal antibody targeting HER2; resistance can develop.

Lapatinib:

  • Mechanism of Action: Small molecule tyrosine kinase inhibitor (TKI) that inhibits both HER2 and EGFR (HER1) tyrosine kinases.
  • Clinical Use: Indicated for patients with advanced or metastatic HER2-positive breast cancer who have progressed on trastuzumab therapy.
  • Administration: Oral; often combined with capecitabine.

Other Drugs in Options:

  • Sorafenib: Multikinase inhibitor; used for renal cell carcinoma and hepatocellular carcinoma.
  • Vemurafenib: BRAF inhibitor; used for melanoma with BRAF V600E mutation.
  • Erlotinib: EGFR TKI; used for non-small cell lung cancer (NSCLC) with EGFR mutations.

Illustrative Table:

Drug Target Clinical Use
Lapatinib HER2 and EGFR tyrosine kinases HER2-positive breast cancer (trastuzumab-resistant)
Sorafenib RAF, VEGFR, PDGFR kinases Renal cell carcinoma, hepatocellular carcinoma
Vemurafenib Mutated BRAF V600E kinase Melanoma
Erlotinib EGFR tyrosine kinase NSCLC with EGFR mutations

Clinical Relevance:

  • Overcoming Resistance: Lapatinib provides an alternative mechanism of action to overcome trastuzumab resistance.
  • Side Effects: Diarrhea, rash, and hepatotoxicity; monitoring is necessary.

Q5:

A diabetic patient was started on a drug that decreased HbA1c from 7.6% to 6.8%. After a few weeks, she started complaining of itching around the vulvovaginal area. What is the most likely drug she started?

Options:

  1. Canagliflozin
  2. Acarbose
  3. Linagliptin
  4. Metformin

Improved Explanation:

Answer: 1. Canagliflozin

Canagliflozin:

  • Class: Sodium-Glucose Co-Transporter 2 (SGLT2) Inhibitor.
  • Mechanism of Action: Inhibits SGLT2 in the proximal renal tubules, reducing glucose reabsorption, resulting in increased urinary glucose excretion (glycosuria).
  • Effectiveness: Lowers HbA1c by approximately 0.5-1%.
  • Common Adverse Effects:
    • Genital Mycotic Infections: Increased glucose in urine promotes growth of Candida species, leading to vulvovaginal candidiasis.
    • Urinary Tract Infections (UTIs)
    • Polyuria and Dehydration
    • Hypotension

Other Options:

  • Acarbose: α-Glucosidase inhibitor; delays carbohydrate absorption; side effects include flatulence and abdominal discomfort.
  • Linagliptin: Dipeptidyl peptidase-4 (DPP-4) inhibitor; side effects are minimal.
  • Metformin: Biguanide; first-line therapy; side effects include gastrointestinal upset and, rarely, lactic acidosis.

Illustrative Table:

Drug Class Common Side Effects
Canagliflozin SGLT2 Inhibitor Genital infections, UTIs, polyuria
Acarbose α-Glucosidase Inhibitor Flatulence, diarrhea
Linagliptin DPP-4 Inhibitor Nasopharyngitis, minimal side effects
Metformin Biguanide GI upset, risk of lactic acidosis

Clinical Relevance:

  • Patient Counseling: Advise on genital hygiene to reduce infection risk.
  • Monitoring: Regular assessment for signs of infection and renal function.

Q6:

Which of the following is true about lithium?

Options:

  1. Fine tremors are seen at therapeutic blood levels
  2. Lithium is not absorbed from the gut
  3. It does not cause teratogenicity
  4. Approved for absence seizures

Improved Explanation:

Answer: 1. Fine tremors are seen at therapeutic blood levels

Lithium:

  • Use: Mood stabilizer for bipolar disorder; effective in treating mania and preventing mood swings.
  • Absorption: Well absorbed orally; not protein-bound; excreted unchanged by the kidneys.
  • Therapeutic Side Effects:
    • Fine Tremors: Common even within therapeutic levels; often involves hands.
    • Polyuria and Polydipsia: Due to nephrogenic diabetes insipidus.
    • Hypothyroidism: Interference with thyroid hormone synthesis.
    • Weight Gain
    • Gastrointestinal Disturbances: Nausea, diarrhea.
  • Teratogenicity:
    • Ebstein's Anomaly: A congenital heart defect associated with first-trimester exposure.
    • Contraindicated during pregnancy, especially in the first trimester.

Incorrect Statements:

  • Not Absorbed from Gut: False; lithium is well absorbed orally.
  • Does Not Cause Teratogenicity: False; it is teratogenic.
  • Approved for Absence Seizures: False; lithium is not indicated for epilepsy.

Clinical Relevance:

  • Monitoring: Requires regular monitoring of serum lithium levels due to narrow therapeutic index.
  • Interactions: NSAIDs, ACE inhibitors, and diuretics can increase lithium levels.
  • Management of Tremors: May respond to dose adjustment or addition of beta-blockers (e.g., propranolol).

Q7:

Which electrolyte abnormality is most associated with prolonged QT interval?

Options:

  1. Hypocalcemia
  2. Hypernatremia
  3. Hypokalemia
  4. Hypermagnesemia

Improved Explanation:

Answer: 1. Hypocalcemia

Effects of Electrolyte Abnormalities on QT Interval:

  • Hypocalcemia:

    • Prolongs QT Interval: Specifically prolongs the ST segment due to delayed ventricular repolarization.
    • ECG Findings: Prolonged QT interval increases risk of ventricular arrhythmias (e.g., torsades de pointes).

  • Hypokalemia:

    • ECG Changes: Flattened T waves, prominent U waves, but generally does not prolong the QT interval significantly.

  • Hypermagnesemia:

    • Effects: Can cause bradycardia and hypotension at high levels but not typically associated with prolonged QT interval.

  • Hypernatremia:

    • Effects: Neurological symptoms due to osmotic shifts; minimal direct impact on ECG or QT interval.

Illustrative Table:

Electrolyte Abnormality Effect on QT Interval
Hypocalcemia Prolonged QT Interval
Hypokalemia U waves, minimal QT effect
Hypermagnesemia May cause bradycardia
Hypernatremia No significant ECG effect

Clinical Manifestations of Hypocalcemia:

  • Neuromuscular Excitability: Muscle cramps, tetany, paresthesias.
  • Signs: Positive Chvostek's sign (facial muscle contraction), Trousseau's sign (carpal spasm).
  • Cardiac Risks: Prolonged QT can lead to arrhythmias.

Clinical Relevance:

  • Treatment: Calcium supplementation (calcium gluconate) is administered to correct hypocalcemia.
  • Monitoring: Regular monitoring of electrolytes and ECG is important in at-risk patients.

Q8:

A patient with suspected meningitis had gram-negative diplococci isolated from cerebrospinal fluid. What is the most likely organism?

Options:

  1. Neisseria meningitidis
  2. Haemophilus influenzae
  3. Streptococcus pneumoniae
  4. Listeria monocytogenes

Improved Explanation:

Answer: 1. Neisseria meningitidis

Neisseria meningitidis:

  • Characteristics:
    • Gram-negative, kidney-shaped diplococci.
    • Oxidase-positive.
    • Possesses a polysaccharide capsule (important for virulence and serogroup classification).
  • Transmission: Person-to-person via respiratory droplets; colonizes the nasopharynx.
  • Pathogenesis:
    • Capsule: Prevents phagocytosis.
    • Endotoxin (Lipooligosaccharide - LOS): Triggers inflammatory response leading to symptoms.
  • Clinical Presentation:
    • Meningitis: Fever, headache, neck stiffness, photophobia.
    • Meningococcemia: Petechial or purpuric rash, hypotension, disseminated intravascular coagulation (DIC), Waterhouse-Friderichsen syndrome (adrenal hemorrhage).

Differential Diagnosis:

  • Haemophilus influenzae:
    • Gram-negative coccobacilli.
    • Requires chocolate agar with factors V (NAD+) and X (hemin).
  • Streptococcus pneumoniae:
    • Gram-positive lancet-shaped diplococci.
    • Alpha-hemolytic, optochin-sensitive.
  • Listeria monocytogenes:
    • Gram-positive rods with tumbling motility.
    • Can cause meningitis in neonates and immunocompromised adults.

Illustrative Table:

Organism Gram Stain Shape
Neisseria meningitidis Gram-negative Diplococci
Haemophilus influenzae Gram-negative Coccobacilli
Streptococcus pneumoniae Gram-positive Lancet-shaped diplococci
Listeria monocytogenes Gram-positive Rods (bacilli)

Clinical Relevance:

  • Empiric Treatment: High-dose intravenous antibiotics (e.g., ceftriaxone or penicillin G).
  • Prevention:
    • Vaccination: Available against certain serogroups.
    • Chemoprophylaxis: Rifampin or ciprofloxacin for close contacts.

Q9:

Which of the following organisms is responsible for blackwater fever?

Options:

  1. Plasmodium vivax
  2. Plasmodium falciparum
  3. Plasmodium malariae
  4. Plasmodium ovale

Improved Explanation:

Answer: 2. Plasmodium falciparum

Blackwater Fever:

  • Definition: A severe complication of falciparum malaria characterized by intravascular hemolysis leading to hemoglobinuria, resulting in dark (black-colored) urine.
  • Mechanism:
    • Massive destruction of red blood cells (RBCs) infected with P. falciparum.
    • Free hemoglobin released into the bloodstream is filtered by the kidneys.
  • Clinical Features:
    • High fever, chills, anemia, jaundice.
    • Dark urine due to hemoglobinuria.
    • Risk of acute renal failure.

Plasmodium Species Comparison:

Species Severe Complications Relapse Potential
P. falciparum Blackwater fever, cerebral malaria, severe anemia No (no hypnozoites)
P. vivax Milder disease Yes (hypnozoites in liver)
P. ovale Milder disease Yes (hypnozoites in liver)
P. malariae Chronic infection, nephrotic syndrome No relapse potential

Clinical Relevance:

  • Urgent Treatment: Requires prompt administration of effective antimalarials (e.g., intravenous artesunate).
  • Supportive Care: Management of anemia, renal function monitoring, and hydration.
  • Prevention: Use of insecticide-treated bed nets, prophylactic medications for travelers, mosquito control measures.

Q10:

A patient presented with a foul-smelling vaginal discharge. Microscopic examination revealed epithelial cells covered with coccobacilli. What is the diagnosis?

Options:

  1. Trichomoniasis
  2. Candida infection
  3. Bacterial vaginosis
  4. Gonorrhea

Improved Explanation:

Answer: 3. Bacterial vaginosis

Bacterial Vaginosis (BV):

  • Etiology: Disruption of normal vaginal flora, leading to overgrowth of anaerobic bacteria such as Gardnerella vaginalis, Mycoplasma hominis, and Mobiluncus species.
  • Signs and Symptoms:
    • Thin, homogenous, gray-white vaginal discharge.
    • Fishy odor, which may be more noticeable after intercourse.
  • Diagnosis:
    • Clue Cells: Vaginal epithelial cells coated with adherent bacteria (appear as stippled or fuzzy borders under microscopy).
    • Amsel's Criteria: At least three of the following:
      1. Homogeneous, thin discharge.
      2. Vaginal pH > 4.5.
      3. Positive Whiff Test (fishy odor when 10% KOH is added).
      4. Presence of clue cells on wet mount microscopy.

Differential Diagnoses:

  • Trichomoniasis:
    • Frothy, yellow-green discharge.
    • Motile trichomonads seen on wet mount.
    • Vulvar itching and strawberry cervix.
  • Candida Infection (Candidiasis):
    • Thick, white, "cottage cheese" discharge.
    • Pseudohyphae and budding yeast on microscopy.
    • Intense pruritus and erythema.
  • Gonorrhea:
    • Purulent cervical discharge.
    • Gram-negative diplococci on Gram stain.

Illustrative Table:

Condition Discharge Characteristics Microscopy Findings
Bacterial Vaginosis Thin, gray-white, fishy odor Clue cells
Trichomoniasis Frothy, yellow-green, malodorous Motile trichomonads
Candidiasis Thick, white, curd-like, odorless Yeast cells, pseudohyphae
Gonorrhea Purulent, mucopurulent Gram-negative diplococci

Clinical Relevance:

  • Treatment: Metronidazole (oral or intravaginal) or clindamycin (intravaginal).
  • Complications: BV is associated with increased risk of pelvic inflammatory disease (PID), adverse pregnancy outcomes, and increased susceptibility to sexually transmitted infections (STIs).
  • Prevention: Avoidance of douching and maintenance of healthy vaginal flora.
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