Which of the following antihypertensives is considered safe in pregnancy?

# Which of the following antihypertensives is considered safe in pregnancy?

A. ACE inhibitors

B. Methyldopa

C. Losartan

D. Warfarin

Correct Answer: B. Methyldopa

Pharmacological Profile and Safety : Methyldopa is the correct choice because it has a long-standing safety record and is widely considered a first-line agent for chronic hypertension in pregnancy.

Mechanism: It is a centrally acting alpha-2 adrenergic agonist. It works by decreasing sympathetic outflow to the heart, kidneys, and blood vessels.
Safety: It does not harm the blood flow between the uterus and the placenta, nor does it negatively affect the fetus's blood circulation. It has been used safely for over 40 years.
Side Effects: While safe for the baby, it can cause sedation (drowsiness), dry mouth, and postural hypotension (dizziness upon standing) in the mother.

Analysis of Incorrect Options

A. ACE Inhibitors (e.g., Enalapril, Lisinopril) These are strictly contraindicated (unsafe) in pregnancy, especially in the second and third trimesters.

Risk: They block the baby’s kidney function (renin-angiotensin system), leading to fetal hypotension and renal failure.
Outcome: This causes a decrease in amniotic fluid (oligohydramnios), which can result in Potter’s sequence (limb deformities, facial defects) and underdeveloped lungs (pulmonary hypoplasia).

C. Losartan (Angiotensin Receptor Blocker - ARB) These are also contraindicated.

Risk: Like ACE inhibitors, ARBs act on the renin-angiotensin system. They carry similar severe risks, including kidney failure and defects in skull bone formation.

D. Warfarin This option is incorrect for two reasons:

Classification: Warfarin is an anticoagulant (blood thinner), not an antihypertensive drug.
Safety: It is a known teratogen (causes birth defects). It is associated with Fetal Warfarin Syndrome, which includes nasal hypoplasia (underdeveloped nose) and bone defects.

Clinical Note: Other Safe Options In addition to Methyldopa, current medical guidelines often recommend these agents for hypertension in pregnancy:

Labetalol: A mixed alpha/beta-blocker (often preferred for its faster action and fewer side effects compared to Methyldopa).
Nifedipine: A calcium channel blocker (specifically extended-release versions).

Wernicke's encephalopathy is attributed to:

# Wernicke's encephalopathy is attributed to:

A. Severe riboflavin deficiency

B. Severe thiamine deficiency

C. Excessive blood alcohol content

D. Excessive GGT levels

The correct answer is B. Severe thiamine deficiency.

Pathophysiology and Mechanism

Wernicke's encephalopathy (WE) is an acute, life-threatening neurological condition caused specifically by a deficiency in Thiamine (Vitamin B1).

Metabolic Role: Thiamine, in its active form thiamine pyrophosphate (TPP), is a crucial cofactor for several enzymes in the Krebs cycle and the pentose phosphate pathway, including:
- Transketolase
- Alpha (α) Ketoglutarate dehydrogenase
- Pyruvate dehydrogenase
Neuronal Injury: Deficiency leads to an inability to metabolize glucose, causing a decrease in ATP production and an accumulation of glutamate. This results in excitotoxicity, oxidative stress, and eventual neuronal cell death.
Targeted Areas: The lesions classically affect areas of high metabolic requirement, specifically the mammillary bodies, the dorsomedial thalamus, the locus coeruleus, the periaqueductal gray, and the ocular motor nuclei.

Why the other options are incorrect

A. Severe riboflavin deficiency (Vitamin B2): This typically presents with ariboflavinosis, characterized by cheilosis, angular stomatitis (relevant to dentistry), glossitis, and seborrheic dermatitis, not the acute neurological signs of WE.
C. Excessive blood alcohol content: While chronic alcohol abuse is the leading cause of thiamine deficiency (due to poor diet, impaired absorption, and reduced hepatic storage), alcohol itself does not directly trigger the specific neuropathology of WE. WE can occur in non-alcoholic contexts, such as hyperemesis gravidarum, starvation, or prolonged parenteral nutrition without supplementation. Therefore, the attribution of the disease is the vitamin deficiency, not the alcohol.
D. Excessive GGT levels: Gamma-glutamyl transferase (GGT) is a liver enzyme used as a marker of hepatobiliary disease and chronic alcohol consumption. It is a diagnostic marker, not a pathogenic cause of encephalopathy.

Clinical Relevance

WE is characterized by the classic clinical triad (though the complete triad is seen in only a minority of patients):

Ophthalmoplegia (nystagmus, lateral rectus palsy)
Ataxia (gait imbalance)
Confusion (mental status changes)

If untreated, Wernicke's encephalopathy can progress to Wernicke-Korsakoff syndrome, resulting in permanent anterograde and retrograde amnesia and confabulation.

MCQs in Oral Medicine and Radiology - Radiation safety and Protection

MDS Entrance: Radiation Safety & Protection

Radiation Safety & Protection

MDS Entrance Preparation | Oral Medicine & Radiology

Radiation Safety MCQs

60+ High-yield questions covering biological effects, units, protection principles (ALARA), regulatory limits, and equipment safety. Designed for MDS aspirants.

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Orchestrating the Smile: The Orthodontist’s Role in Cleft Lip and Palate Care - Dr. Raman Dhungel

Treatment of cleft lip and palate (CLP) is one of the most complex, yet rewarding, challenges in our profession. It is not a sprint; it is a marathon that spans from birth to early adulthood. As orthodontists, we do not work in a silo. We are the architects within a Multidisciplinary Team (MDT) that includes oral surgeons, plastic surgeons, speech-language pathologists, ENTs, and pediatricians.

While the surgeons repair the tissues, the orthodontist’s role is to guide the underlying foundation—the bone and dental arches—to ensure that the repair looks good, functions well, and allows the child to speak clearly.

A multidisciplinary approach to cleft lip and palate care

Beyond Braces: The Orthodontist as a Long-Term Partner

Our involvement begins long before the first permanent tooth erupts. In the cleft patient, the maxilla (upper jaw) is often segmented, collapsed, and growth-restricted due to scar tissue from early surgeries. The orthodontist’s primary goal is to normalize the dental arch form to facilitate surgical closure and allow for normal speech and chewing.

Clinical Milestones: The Roadmap of Care

Successful management of CLP relies on doing the right thing at the right time. Intervening too early can hamper growth; intervening too late can compromise the result. Here is the standard timeline of orthodontic intervention:

1. Infancy (0 – 12 Months): The Foundation

Objective: Reduce the severity of the cleft deformity before the primary lip repair.
Intervention: Presurgical Infant Orthopedics (PSIO) or Nasoalveolar Molding (NAM).
Action: We use passive appliances to approximate the cleft lip and alveolar segments and mold the flattened nose. This reduces tension on the surgical site, leading to better esthetics and less scar tissue.

2. Primary Dentition (2 – 6 Years): The Observation Phase

Objective: Monitor growth and speech.
Intervention: Usually minimal.
Action: Unless there is a functional shift of the jaw (a severe crossbite causing the jaw to slide), we often wait. This preserves the cooperation of the young child for the more critical phases ahead.

3. Early Mixed Dentition (7 – 9 Years): The Critical Turning Point

Objective: Prepare the maxilla for the Secondary Alveolar Bone Graft (SABG).
Intervention: Maxillary Expansion (Quad Helix or RME).
Action: The maxillary segments are often collapsed. We must expand the upper jaw to align the segments and create a bed for the surgeon to place the bone graft.
Timing is Key: This must be done before the permanent canine erupts, so the canine can erupt naturally into the newly grafted bone, ensuring periodontal health.

4. Permanent Dentition (12 – 16 Years): Comprehensive Alignment

Objective: Establish functional occlusion and smile esthetics.
Intervention: Fixed Mechanotherapy (Braces).
Action: We align the permanent teeth, correct rotations common in the cleft area, and manage missing teeth (often the lateral incisor) by either closing the space or preparing it for a future implant.

5. Skeletal Maturity (17+ Years): The Final Polish

Objective: Correction of skeletal discrepancies.
Intervention: Orthognathic Surgery.
Action: Many cleft patients have a maxilla that does not grow forward enough (Class III skeletal pattern). Once growth is complete, we work with surgeons to advance the upper jaw (Le Fort I osteotomy) to achieve the final facial profile and bite.

Conclusion

The management of cleft lip and palate is a testament to the power of collaboration. As orthodontists, we are privileged to watch these patients grow from infants into confident young adults. It is our precise management of the hard tissues that allows the soft tissue work of our surgical colleagues to truly shine.