Based on the given clinical scenario, the most probable diagnosis in this patient is acute paranoid schizophrenia.

Schizophrenia is a functional psychotic disorder characterized by the presence of delusional beliefs, hallucinations, and disturbances in thought, perception, and behaviour.

Clinical features:
Schneider’s first-rank symptoms may be divided into auditory hallucinations, thought disorders, passivity phenomena, and delusional perceptions:

Auditory hallucinations of a specific type:
Two or more voices discussing the patient in the third person
Thought echo
Voices commenting on the patient’s behaviour

Thought disorder:
Thought insertion
Thought withdrawal
Thought broadcasting

Passivity phenomena:
Bodily sensations being controlled by external influence
Actions/impulses/feelings – experiences which are imposed on the Individual or influenced by others

Other features of schizophrenia include
Impaired insight (a feature of all psychoses)
Incongruity/blunting of affect (inappropriate emotion for circumstances)
Decreased speech
Neologisms: made-up words
Catatonia
Negative symptoms: incongruity/blunting of affect, anhedonia (inability to derive pleasure), alogia (poverty of speech), avolition (poor motivation).

Treatment:
For the initial treatment of acute psychosis, it is recommended to commence an oral second-generation antipsychotics such as aripiprazole, olanzapine, risperidone, quetiapine, etc.
Once the acute phase is controlled, switching to a depot preparation like aripiprazole, paliperidone, zuclopenthixol, fluphenazine, haloperidol, pipotiazine, or risperidone is recommended.
Cognitive-behavioural therapy (CBT) and the use of art and drama therapies help counteract the negative symptoms of the disease, improve insight, and assist relapse prevention.
Clozapine is used in case of treatment resistance.

This is a classic clinical presentation, with alcohol intake and nausea/vomiting that leads to hematemesis, of a Mallory-Weiss tear. In Mallory-Weiss tear, they typically present as a hemodynamically stable patient after a night of binge drinking and excessive resultant vomiting. Given his EGD did not show any other pathology and he is now stable, he can be discharged home.

Memantine is an antagonist of the NMDA (N-Methyl-D-Aspartate)-receptor subtype of glutamate receptor. It is used to slow the neurotoxicity thought to be involved in Alzheimer’s disease and other neurodegenerative diseases.

Drug interactions:
When given concomitantly with other NMDA-receptor antagonists (e.g., ketamine, amantadine) increase the risk of psychosis.
Dopamine agonists, L-dopa, and anticholinergics enhance effects of memantine.
Antispasmodics (e.g., baclofen)  enhance effects, as memantine has some antispasmodic effects.
Drugs excreted by cationic transporters in the kidney (e.g. quinine, cimetidine, ranitidine) reduce excretion.

Common adverse effects include dizziness, headache, confusion, diarrhoea, and constipation.

Apraclonidine eye drops are initially used to confirm a Horner’s pupil. Apraclonidine stimulates both alpha-1 and alpha-2 receptors. When added to the affected eye, it causes pupil dilation by >2mm because of the relative super sensitivity of this pupil to alpha-1 receptor activity. In a normal pupil, however, it causes constriction due to the more potent activity at the alpha-2 receptor which triggers re-uptake of noradrenaline in the synaptic cleft.

Hydroxy amphetamine is then used to distinguish between first/second or third order neurones. In other words, it will distinguish either a lesion in the brainstem, cervical cord, chest or neck and one affecting above the superior cervical ganglion at the carotid bifurcation. In a normal pupil or a first/second order Horner’s, the pupil will dilate secondary to increased levels of noradrenaline released from the post-synaptic neurones. In a third order neurone, this will not occur. There is no fourth or fifth order neurone.

A single dose of intravenous magnesium sulphate is safe and may improve lung function and reduce intubation rates in patients with acute severe asthma. Intravenous magnesium sulphate may also reduce hospital admissions in adults with acute asthma who have had little or no response to standard treatment.

Consider giving a single dose of intravenous magnesium sulphate to patients with acute severe asthma (PEF <50% best or predicted) who have not had a good initial response to inhaled bronchodilator therapy. Magnesium sulphate (1.2–2 g IV infusion over 20 minutes) should only be used following consultation with senior medical staff.

Lead poisoning is characterised by abdominal pain, fatigue, constipation, peripheral neuropathy (mainly motor), and blue lines on gum margin in 20% of the adult patients (very rare in children).

For diagnosis, the level of lead in blood is usually considered with levels greater than 10 mcg/dL being significant. Furthermore, the blood film shows microcytic anaemia and basophilic stippling of red blood cells. Urinary coproporphyrin is increased (urinary porphobilinogen and uroporphyrin levels are normal to slightly increased). Raised serum and urine levels of delta-aminolaevulinic acid may also be seen, making it sometimes difficult to differentiate from acute intermittent porphyria.

Carcinoembryonic antigen (CEA) is a known tumour marker for colorectal cancer. It is not used diagnostically, but in patients with a known diagnosis of colorectal cancer associated with raised CEA levels, it can be used to monitor disease activity and help with the early identification of disease recurrence.

Tumour markers can be divided into:
1. Monoclonal antibodies
CA 125: Ovarian cancer, primary peritoneal cancer
CA 19-9: Pancreatic cancer
CA 15-3: Breast cancer

2. Tumour specific antigens
Prostate specific antigen (PSA): Prostatic carcinoma
Alpha-feto protein (AFP): Hepatocellular carcinoma, teratoma
Carcinoembryonic antigen (CEA): Colorectal cancer
S-100: Melanoma, schwannomas
Bombesin: Small cell lung carcinoma, gastric cancer

3. Enzymes
Alkaline phosphatase (ALP)
Neuron specific enolase (NSE)

4. Hormones
Calcitonin
Antidiuretic hormone (ADH)
Human chorionic gonadotropin (hCG)

The patient has a non-functioning pituitary tumour as her hormone profile is normal.
Non-functioning pituitary tumours are relatively common. A large number of these tumours are incidentally found pituitary microadenomas (<1 cm) and are usually of no clinical importance.

The ECG findings are suggestive of anterior myocardial infarction and the most likely artery affected is the left anterior descending artery. Occlusion of the right coronary artery will be shown by ST elevation in lead II, III, aVF and occlusion of the circumflex artery will show changes in leads I, aVL, V5 and V6. To have ST elevation, there should be complete occlusion of the artery.

Indications for permanent pacemaker implantation

-Sinus node dysfunction
-Acquired Atrioventricular(AV) block (Complete third-degree AV block with or without symptoms, Symptomatic second degree AV block, Mobitz type I and II, Exercise-induced second or third degree AV block in the absence of myocardial infarction, Mobitz II with widened QRS complex)
-Chronic bifascicular block
-After acute phase of myocardial infarction
-Neurocardiogenic syncope and hypersensitive carotid sinus syndrome
-Post cardiac transplantation
-Hypertrophic cardiomyopathy
-Pacing to detect and terminate tachycardia
-Cardiac resynchronization therapy in patients with severe systolic heart failure
-Patients with congenital heart disease

Retinitis pigmentosa primarily affects the peripheral retina resulting in tunnel vision. Night blindness is often the initial sign. Tunnel vision occurs due to loss of the peripheral retina (occasionally referred to as funnel vision).
Fundoscopy exam reveals black bone spicule-shaped pigmentation in the peripheral retina, and mottling of the retinal pigment epithelium.

The patient is most likely to have Postpartum thyroiditis which goes through 2 phases; hypothyroid and a hyperthyroid phase.
The hyperthyroid phase of postpartum thyroiditis occurs between 2 and 10 months postpartum. Most commonly, it presents at 3 months. Symptoms more common in women with hyperthyroid postpartum thyroiditis include palpitations, fatigue, heat intolerance, and irritability/nervousness. The frequency of asymptomatic hyperthyroidism is 33%.
Untreated, the hyperthyroidism resolves spontaneously within 2–3 months. This phase is diagnosed by the combination of a low serum TSH concentration in the presence of thyroid peroxidase antibodies, in women who are TSH receptor antibody-negative. Free T4 levels are typically elevated but may be normal.
Treatment of hyperthyroidism, when necessary, is based on symptom severity and should be a joint decision of patient and physician. Beta-blockers such as propranolol are given to alleviate palpitations, irritability, and nervousness. The morbidity associated with treatment is the side effects of beta-blockade. The downside of withholding treatment is allowing the woman to remain symptomatic. Antithyroid medicines (thioureas) are not a potential treatment alternative, because the hyperthyroidism is caused by destructive thyroiditis resulting in the release of preformed thyroid hormone.

After renal transplantation, cytomegalovirus has been identified to affect 1/4 of the post-op patients. It is the most common viral infection causing morbidity and mortality in post-op patients in the first 3 months.

The history is suggestive of acute gingivostomatitis, which is a manifestation of primary HSV-1 infection. Patients present with gingivitis and vesicular lesions which develop on the oral mucosa, tongue, and lips and later rupture and coalesce, leaving ulcerated plaques.

The patient should be prescribed IV iron and subcutaneous erythropoietin to enhance erythropoiesis to address the dropped haemoglobin.

Classic Kallmann syndrome (KS) is due to isolated hypogonadotropic hypogonadism. Most patients have gonadotropin-releasing hormone (GnRH) deficiency, as suggested by their response to pulsatile GnRH therapy. The hypothalamic-pituitary function is otherwise normal in most patients, and hypothalamic-pituitary imaging reveals no space-occupying lesions. By definition, either anosmia or severe hyposmia is present in patients with Kallmann syndrome.

Vincristine is part of the antimitotic agents, cell cycle specific (M phase). It binds to microtubules in the spindle apparatus and prevents their proper function, finally arresting mitosis.

The next step in managing this patient is to give 10 mg and continue administering in 10 mg increments each hour until symptoms are under control.

Methadone alleviates opioid withdrawal symptoms and reduces cravings. Methadone is useful for detoxification from longer-acting opioids such as morphine or methadone itself.
Methadone should be used with caution if the patient has:
Respiratory deficiency
Acute alcohol dependence
Head injury
Treatment with monoamine oxidase inhibitors (MAOIs)
Ulcerating colitis or Crohn’s disease
Severe hepatic impairment
The dose must be reviewed on a daily basis and adjusted based upon how well the symptoms are controlled and the presence of side effects. The greater the dose of opioids used by the patient, the greater the dose of methadone required to control withdrawal symptoms.

To avoid the risk of overdose in the first days of treatment The recommended dosing of methadone is 30mg in two doses of 15mg morning and evening.

It is important to note that a methadone dose equivalent to what the patient reports they are taking should never be given.
It is rare to need more than 40 mg per 24 hours: beware of overdosing which can lead to respiratory arrest.

Scleritis, or inflammation of the sclera, is usually painful whereas episcleritis is not painful.

Keratoconjunctivitis sicca is usually bilateral and associated more with dryness, burning and itching.

There are five prognostic factors which indicate poor prognosis in HOCM:
-family history of HOCM-related sudden cardiac death
-unexplained recent syncope
-large left ventricular wall thickness (MLVWT ≥ 30 mm)
-multiple bursts of nsVT on ambulatory electrocardiography
-hypotensive or attenuated blood pressure response to exercise

The peak incidence of seizures is expected 36 hours following the onset of alcohol withdrawal.

Pathophysiology:
Chronic alcohol consumption enhances GABA mediated inhibition in the CNS (similar to benzodiazepines) and inhibits NMDA-type glutamate receptors. Alcohol withdrawal is thought to lead to the opposite (decreased inhibitory GABA and increased NMDA glutamate transmission).

Clinical course in alcohol withdrawal:
Symptoms begin 6-12 hours following the onset of alcohol withdrawal
Seizures occur 36 hours following the onset of withdrawal
Delirium tremens (coarse tremor, confusion, delusions, auditory and visual hallucinations, fever, tachycardia) occurs approximately 72 hours after the onset of alcohol withdrawal.

Management
First-line: benzodiazepines e.g. lorazepam, chlordiazepoxide.
Carbamazepine is also effective in the treatment of alcohol withdrawal.
Phenytoin is said not to be as effective in the treatment of alcohol withdrawal seizures.

The most COMMON site of inflammation from ulcerative colitis is the rectum, making this the correct answer. This is simply a fact you need to memorize. In general, ulcerative colitis only occurs in colorectal regions– nothing in the small bowel (unless there is backwash into the terminal ileum) and nothing further up the GI tract. In Crohn’s it can affect the entire GI tract from mouth to anus.

Immunity against mumps develops over a long time. There is nothing to be done except to proceed with the usual vaccination schedule.

From the given answers, complete heart block with a narrow complex QRS complex is associated with the least risk of asystole. Transvenous pacing is indicated by the other given responses.

Herpes zoster oticus is a viral infection of the inner, middle, and external ear. It manifests as severe otalgia with associated cutaneous vesicular eruption, usually of the external canal and pinna. When associated with facial paralysis, the infection is called Ramsay Hunt syndrome.

Age of the patient, headache only on one side, and loss of vision on that side suggest temporal arteritis, also known as giant cell arteritis. The laboratory hallmark of this condition is a raised ESR.

Left ventricular ejection fraction = (stroke volume / end diastolic LV volume ) * 100%

Stroke volume = end diastolic LV volume – end systolic LV volume

Pulse pressure = Systolic Pressure – Diastolic Pressure

For medical management of carcinoid syndrome, there are two somatostatin analogues available, Octreotide and Lanreotide. Somatostatin is an amino acid peptide which is an inhibitory hormone, which is synthesized by paracrine cells located ubiquitously throughout the gastrointestinal tract. Both somatostatin analogues provide symptom relief in 50% to 70% of patients and biochemical response in 40% to 60% patients. Many studies have shown that Octreotide and Lanreotide also inhibit the proliferation of tumour cells.

Smoking cessation is the most effective intervention in stopping the progression of COPD, as well as increasing survival and reducing morbidity. This is why smoking cessation should be the top priority in the treatment of COPD. Long term oxygen therapy (LTOT) may increase survival in hypoxic patients. The rest of the options dilate airways, reduce inflammation and thereby improve symptoms but do not necessarily increase survival.

Desmopressin test (done to differentiate nephrogenic diabetes insipidus from central diabetes insipidus), and serum lithium levels can together confirm a diagnosis of lithium-induced nephrogenic diabetes insipidus.

Bipolar disease is most often managed with mood stabilizers like lithium. This patient develops gastrointestinal symptoms followed by an acute confusional state associated with polyuria and polydipsia. These symptoms are suggestive of diabetes insipidus.

In a case where these symptoms occur in a bipolar patient under treatment, lithium-induced nephrogenic diabetes insipidus should be considered as the most probable cause.

Lithium intoxication can present with symptoms of nausea, vomiting, mental dullness, action tremor, weakness, ataxia, slurred speech, blurred vision, dizziness, especially vertical nystagmus and stupor or coma. Diffuse myoclonic twitching and nephrogenic diabetes insipidus can also occur. Such a clinical syndrome occurs above the serum level of lithium of 1.5–2.0 mEq/L.

Management:
– Correcting electrolyte abnormalities in patients with acute disease is critical and often life-saving.
– Treatment should be initiated with parenteral fluids to replete hypovolemia (normal saline at 200-250 mL/h), followed by administration of hypotonic fluid (0.5% normal saline).
– On the restoration of the volume status of the patient forced diuresis should be initiated by the administration of parenteral furosemide or bumetanide accompanied by continued intravenous hypotonic fluid administration to maintain volume status.
– Polyuria is managed with hydrochlorothiazide combined with amiloride, acetazolamide.