Sagittal and Lambdoid Synostosis, Low set ears

 # A two-month-old boy is referred for evaluation because he has an abnormal head shape. Physical examination shows low-set ears, and short-webbed fingers. A CT scan shows sagittal and lambdoid synostosis. Which of the following genes is most likely to cause this syndrome ?

A. TWIST1

B. FGFR1

C. FGFR2

D. RAB23

The correct answer C. FGFR2.

The most likely gene to cause the syndrome described, characterized by sagittal and lambdoid synostosis, low-set ears, and short-webbed fingers in a two-month-old boy, is C. FGFR2.

Explanation:

The clinical presentation suggests a craniosynostosis syndrome, with sagittal and lambdoid synostosis indicating premature fusion of cranial sutures, and additional features like low-set ears and short-webbed fingers (syndactyly) pointing toward a syndromic form. Among the options, mutations in FGFR2 (Fibroblast Growth Factor Receptor 2) are strongly associated with syndromic craniosynostoses, particularly Apert syndrome and Crouzon syndrome, both of which can present with multisuture synostosis (including sagittal and lambdoid) and distinctive features.

Apert syndrome (caused by FGFR2 mutations) is characterized by coronal synostosis (though sagittal and lambdoid can also be involved), syndactyly (webbed fingers/toes), midface hypoplasia, and occasionally low-set ears due to associated craniofacial anomalies. The short-webbed fingers in the question align well with Apert’s syndactyly.

Crouzon syndrome (also FGFR2-related) involves craniosynostosis (often coronal, but sagittal and lambdoid can occur) and facial anomalies like low-set ears, though syndactyly is less common.

Analysis of other options:

A. TWIST1: Associated with Saethre-Chotzen syndrome, which typically involves coronal synostosis and milder limb anomalies (e.g., partial syndactyly or brachydactyly). Multisuture involvement (sagittal and lambdoid) is less common, and severe syndactyly is not typical.

B. FGFR1: Linked to Pfeiffer syndrome in some cases, but FGFR2 is more commonly implicated. Pfeiffer includes broad thumbs/toes and partial syndactyly, but sagittal and lambdoid synostosis as the primary sutures is less frequent.

D. RAB23: Associated with Carpenter syndrome, a rare condition with craniosynostosis (often sagittal or coronal), polysyndactyly (extra digits), and other anomalies. The absence of polysyndactyly or obesity in the description makes this less likely, and short-webbed fingers align better with Apert’s syndactyly.

Conclusion: FGFR2 mutations are most likely to cause a syndrome with sagittal and lambdoid synostosis, low-set ears, and short-webbed fingers, as seen in Apert syndrome, making C. FGFR2 the best answer.

Which of the following antibiotics acts by inhibiting cell wall synthesis?

 # Which of the following antibiotics acts by inhibiting cell wall synthesis?

a) Doxycycline

b) Aminoglycosides

c) Erythromycin

d) Cefepime

The correct answer is D. Cefepime.

The correct answer is d) Cefepime.

Explanation:

Cefepime is a fourth-generation cephalosporin antibiotic that inhibits bacterial cell wall synthesis by binding to penicillin-binding proteins (PBPs), disrupting peptidoglycan cross-linking, and leading to cell lysis.

Doxycycline (a tetracycline) inhibits protein synthesis by binding to the 30s ribosomal subunit, preventing tRNA attachment.

Aminoglycosides (e.g., gentamicin) also target protein synthesis by binding to the 30s ribosomal subunit, causing misreading of mRNA.

Erythromycin (a macrolide) inhibits protein synthesis by binding to the 50s ribosomal subunit, blocking peptide chain elongation.

Thus, only Cefepime acts by inhibiting cell wall synthesis.

Traumatic injury to primary tooth leads to intrusion. After how much time, the tooth usually re-erupts?

 # Traumatic injury to primary tooth leads to intrusion. After how much time, the tooth usually re-erupts?

a) 30 days

b) 3 months

c) 6 months

d) 12 months

The correct answer is C. 6 months.

Explanation:

Intrusion of a primary tooth occurs when a traumatic force displaces the tooth apically into the alveolar bone. The potential for re-eruption depends on factors such as the degree of intrusion, the integrity of the periodontal ligament, the child's age, and the absence of complications like ankylosis or damage to the underlying permanent tooth bud. In pediatric dentistry, re-eruption is a common outcome for intruded primary teeth due to the elasticity of the periodontal ligament and ongoing alveolar growth.

While some studies suggest re-eruption can occur within 2–4 months for mild to moderate intrusions, the 6-month timeframe is more plausible in clinical practice for several reasons:

Variable Healing Dynamics: Moderate to severe intrusions may require longer for the periodontal ligament to reorganize and facilitate re-eruption, especially if there is initial swelling or minor alveolar bone remodeling.

Clinical Monitoring Period: Dentists often observe intruded teeth for up to 6 months to confirm complete re-eruption or to detect complications (e.g., failure to re-erupt, ankylosis, or pulpal necrosis). The 6-month mark is a standard endpoint in guidelines (e.g., American Academy of Pediatric Dentistry) for assessing outcomes.

Conservative Estimate: The 6-month duration accounts for cases where re-eruption is slower due to partial intrusion or minor displacement, ensuring the tooth returns to its original position without intervention.

In contrast, 30 days is too short for complete re-eruption, as initial healing and tissue reorganization take longer. 3 months may suffice for milder cases but may not cover the full spectrum of intrusion severities. 12 months is excessively long unless complications delay the process significantly. Thus, 6 months is a clinically relevant and plausible timeframe for the re-eruption of most intruded primary teeth, balancing biological healing with practical observation periods.

Bulk of lamina propria of the gingiva is made of collagen type:

 # Bulk of lamina propria of the gingiva is made of collagen type:

a) I

b) II

c) III

d) IV

The correct answer is A. Type I.

The bulk of the lamina propria of the gingiva is made of collagen type I.

Explanation:

The lamina propria of the gingiva, a connective tissue layer supporting the gingival epithelium, primarily consists of collagen type I, which provides structural strength and resilience. Collagen type I is the most abundant collagen in connective tissues like the gingiva, while other types (e.g., II in cartilage, III in reticular fibers, IV in basement membranes) are less dominant in this context.

Secretin does not cause:

 # Secretin does not cause:

a) Bicarbonate secretion

b) Augments the action of CCK

c) Contraction of pyloric sphincter

d) Gastric secretion increase

The correct answer is D. Gastric secretion increase.

Secretin does not cause d) Gastric secretion increase.

Explanation:

a) Bicarbonate secretion: Secretin stimulates the pancreas to secrete bicarbonate to neutralize acidic chyme in the duodenum.

b) Augments the action of CCK: Secretin works synergistically with cholecystokinin (CCK) to enhance pancreatic enzyme and bile secretion.

c) Contraction of pyloric sphincter: Secretin promotes relaxation of the pyloric sphincter to allow chyme to pass into the duodenum.

d) Gastric secretion increase: Secretin inhibits gastric acid secretion and gastric motility to slow digestion in the stomach, making this the correct answer.

Major and frequent influence for arterial thrombus formation is:

 # Major and frequent influence for arterial thrombus formation is:

a) Alteration in blood flow

b) Hypercoagulability

c) Endothelial damage

d) Fatty streak

The correct answer is C. Endothelial damage.

For a single-choice question on thrombus formation, the answer depends on the clinical context:

1. Arterial Thrombosis (e.g., Myocardial Infarction)

Correct Answer: [c) Endothelial Damage]

Rationale: Arterial thrombi typically form at sites of disrupted atherosclerotic plaques. Endothelial injury directly exposes prothrombotic subendothelial collagen and tissue factor, triggering platelet adhesion/aggregation and coagulation activation.

2. Venous Thrombosis (e.g., DVT)

Correct Answer: [a) Alteration in Blood Flow] or [b) Hypercoagulability]

Rationale: Venous thrombi often arise from stasis (e.g., immobility) or hypercoagulable states (e.g., Factor V Leiden). If forced to choose one, prioritize [a) Alteration in Blood Flow] as stasis is the most common trigger.

Why Not Other Options?

[d) Fatty Streak] is incorrect because it represents early atherosclerosis, not active thrombosis.

Note: In practice, all three Virchow triad components (a/b/c) contribute, but exam questions often focus on the most context-specific factor.

Exam Strategy:

If the question mentions "myocardial infarction" or "artery", choose c.

If it refers to "DVT", "surgery", or "immobility", choose a.

If genetic clotting disorders (e.g., Leiden mutation) are explicitly mentioned, choose b.

Vestibular toxicity is associated with which of the following tetracyclines?

Vestibular toxicity is associated with which of the following tetracyclines?

A. Doxycycline
B. Minocycline
C. Chlorotetracycline
D. Oxytetracycline