The dose is calculated, using the conversion factor, as follows:

(Conversion factor used to convert oral morphine to subcutaneous diamorphine = Divide the total daily dose of oral morphine by 3)
Hence,
60mg*2 = 120mg
120mg/3 = 40mg

The side effects of opioids can be transient or persistent, and these include constipation, nausea, and drowsiness. Therefore, all patients taking opioids should also be prescribed a laxative and an anti-emetic (if the nausea is persistent). Dose-adjustment may be necessary in cases of persistent drowsiness. Moreover, strong opioids can also provide quick relief from metastatic bone pain, as compared to NSAIDs, bisphosphonates, and radiotherapy.

One of the questions the therapist poses himself while informing a patient is: whom shall I inform about the diagnosis, treatment and prognosis? If we unconditionally accepted the view that information belongs to the patient from an ethical and legal standpoint, we would automatically exclude the partner and the family. Therefore, the therapist should raise another question: what is the benefit to the patient? To answer the question and the resulting dilemma, we have to leverage the long experience of family therapy and tailor it to the cases we are dealing with. It should be taken into consideration that patient and family are a dynamic system which was balanced before the onset of the disease, but is now disrupted, entering into crisis. Therefore, the denial mechanisms and personality characteristics we have previously elaborated on, and communication among members play a crucial role in determining the information strategy and the way family should be approached. In this particular case, the most appropriate person to inform the patient is the consultant, meaning the one currently responsible for the patient’s care. The patient most probably has already developed some form of close and trustful relationship with his consultant.

5-ASA is not an acute treatment; it is for maintenance therapy for ulcerative colitis and/or Crohn’s. The most benefit is seen in patients with ulcerative colitis.

The walls of the ascending limb of the loop of Henle are not permeable to water. The tubular fluid thus becomes increasingly dilute as it ascends toward the cortex, whereas the interstitial fluid around the loops of Henle in the medulla becomes increasingly more concentrated.

The ascending limb actively reabsorbs NaCl but has an extremely low transepithelial osmotic water permeability, even in the presence of vasopressin. This combination of NaCl reabsorption without water reabsorption serves two vital functions: it provides NaCl to increase the osmolality of the medullary interstitium, tubules, vasculature, and collecting ducts; and it dilutes the luminal fluid within the thick ascending limb.

The development of hepatic fibrosis reflects an alteration in the normally balanced processes of extracellular matrix production and degradation. [6] The extracellular matrix, the normal scaffolding for hepatocytes, is composed of collagens (especially types I, III, and V), glycoproteins, and proteoglycans. Increased collagen in the space of Disse (space b/w sinusoids and hepatocytes) leads to capillarization of sinusoids, and stellate cells also have contractile properties when activated. This is fibrosis processes. This can lead to the development of portal hypertension.

Chvostek and Trousseau signs can be elicited in patients with hypocalcaemia. Chvostek sign is the twitching of the upper lip with tapping on the cheek 2 cm anterior to the earlobe, below the zygomatic process overlying the facial nerve. Trousseau sign (a more reliable sign present in 94% of hypokalaemic individuals and only 1% to 4% of healthy people) is the presence of carpopedal spasm observed following application of an inflated blood pressure cuff over systolic pressure for 3 minutes in hypokalaemic patients.

The correct answer is patchy inflammation. Superficial ulceration as well as non-patchy inflammation are seen in ulcerative colitis (UC) in the colon and rectum; you would expect to see transmural inflammation in Crohn’s disease and it can be patchy and located anywhere from mouth to anus. Crypt distortion and crypt abscesses are seen in both UC and Crohn’s, however they are more common in ulcerative colitis.

The diagnosis for the aforementioned case is thrombotic thrombocytopenic purpura (TTP). TTP is classically characterised as a pentad of thrombocytopaenia, microvascular haemolysis, fluctuating neurological signs, renal impairment, and fever.

The differential diagnosis for severe thrombocytopaenia is immune thrombocytopenic purpura (ITP). ITP is more common than TTP. However, a patient of ITP would not present with the range of symptoms seen in this scenario.

In TTP, there is deficiency of a protease which breaks down large multimers of von Willebrand factor. This leads to abnormally large and sticky multimers of von Willebrand factor which cause platelets to clump within the vessels.

Untreated TTP has a mortality rate of up to 90%. Therefore, rapid plasma exchange (PEX) may be a life-saving intervention. Platelet transfusion in TTP is only indicated if there is an ongoing life-threatening bleed. Intravenous methylprednisolone is indicated after treatment with PEX has been completed. There is no current role of intravenous immunoglobulin in the routine management of TTP. However, there have been reports of its successful use in PEX- and steroid-refractory cases. Intravenous argatroban is indicated in heparin-induced thrombocytopaenia (HIT), but there is no history of recent heparin administration or hospitalisation in this patient nor are the clinical signs consistent with HIT.

Management options for TTP include PEX as the treatment of choice. Steroids and immunosuppressants are also given. Antibiotics are not recommended as they may worsen the outcome of the disease. For cases resistant to PEX and pharmacologic therapy, vincristine is given.

Hypertrophic cardiomyopathy is an autosomal dominant condition. Patients present with sudden cardiac death, dyspnoea, syncope and presyncope, angina, palpitations, orthopnoea and paroxysmal nocturnal dyspnoea, Congestive heart failure and dizziness. Physical findings include double or triple apical impulse, prominent a wave in the JVP, an ejection systolic crescendo-decrescendo murmur and a holosystolic murmur at the apex and axilla of mitral regurgitation.
ECG shows ST-T wave abnormalities and LVH, axis deviation (right or left), conduction abnormalities (P-R prolongation, bundle-branch block), sinus bradycardia with ectopic atrial rhythm, atrial enlargement, abnormal and prominent Q wave in the anterior precordial and lateral limb leads.
2D echocardiography shows abnormal systolic anterior leaflet motion of the mitral valve, LVH, left atrial enlargement, small ventricular chamber size, septal hypertrophy with septal-to-free wall ratio greater than 1.4:1, mitral valve prolapse and mitral regurgitation, decreased midaortic flow, partial systolic closure of the aortic valve in midsystole

CMV infection is usually asymptomatic in adults. However, if the mother is infected for the first time during pregnancy then there is high chances of this infection passing on to the foetus. CMV infection can cause blindness, deafness, learning difficulties, restricted growth etc. Hepatitis B, herpes simplex, syphilis and HIV do not present with these classical signs of CMV infection in new-borns. It is estimated that 10 stillbirths occur in England and Wales every year due to CMV infection. The foetus is most at risk in early pregnancy. There is no effective prevention.

A Mongolian spot can be present in new born babies which usually appears over the back and fades with time. There is nothing to worry about.

Occupational asthma (OA) could be divided into a nonimmunological, irritant-induced asthma and an immunological, allergy-induced asthma. In addition, allergy-induced asthma can be caused by two different groups of agents: high molecular weight proteins (>5,000 Da) or low molecular weight agents (<5,000 Da), generally chemicals like the isocyanates.
Isocyanates are very reactive chemicals characterized by one or more isocyanate groups (–N=C=O). The main reactions of this chemical group are addition reactions with ethanol, resulting in urethanes, with amines (resulting in urea derivates) and with water. Here, the product is carbamic acid which is not stable and reacts further to amines, releasing free carbon dioxide.

Diisocyanates and polyisocyanates are, together with the largely nontoxic polyol group, the basic building blocks of the polyurethane (PU) chemical industry, where they are used solely or in combination with solvents or additives in the production of adhesives, foams, elastomers, paintings, coatings and other materials.

The complex salts of platinum are one of the most potent respiratory sensitising agents having caused occupational asthma in more than 50% of exposed workers. Substitution of ammonium hexachlor platinate with platinum tetra amine dichloride in the manufacture of catalyst has controlled the problem in the catalyst industry. Ammonium hexachlorplatinate exposure still occurs in the refining process.

Rosin based solder flux fume is produced when soldering. This fume is a top cause of occupational asthma.

Bakeries, flour mills and kitchens where flour dust and additives in the flour are a common cause of occupational asthma.

Cadmium was not found to cause occupational asthma.

Palmar xanthomas are found in type III hyperlipoproteinemia. Her total cholesterol level and triglyceride level support the diagnosis.

Prostacyclin (PGI2) generated by the vascular wall is a potent vasodilator, and the most potent endogenous inhibitor of platelet aggregation so far discovered. Prostacyclin inhibits platelet aggregation by increasing cyclic AMP levels. Prostacyclin is a circulating hormone continually released by the lungs into the arterial circulation. Circulating platelets are, therefore, subjected constantly to prostacyclin stimulation and it is via this mechanism that platelet aggregability in vivo is controlled.

According to NICE guidelines (2013) all people who have had an acute MI, treatment should be offered with ACE inhibitor, dual antiplatelet therapy (aspirin plus a second antiplatelet agent), beta-blocker and a statin.

Sleep paralysis is a temporary inability to move or speak that occurs when you’re waking up or falling asleep. Paralysis is often accompanied by hallucinations

REM is a stage of sleep when the brain is very active and dreams often occur. The body is unable to move, apart from the eyes and muscles used in breathing, possibly to stop the person from acting out the dreams and hurting himself.

It’s not clear why REM sleep can sometimes occur while one is awake, but it has been associated with:
-not getting enough sleep (sleep deprivation or insomnia)
-irregular sleeping patterns – for example, because of shift work or jet lag
-narcolepsy – a long-term condition that causes a person to suddenly fall asleep at inappropriate times
-a family history of sleep paralysis
-sleeping on one’s back

The most likely diagnosis is idiopathic Parkinson’s disease because of the unilateral presentation. In addition, cogwheel rigidity is a classic presenting symptom. Neuroleptic-induced parkinsonism is usually bilateral and symmetrical. Essential tremors do not cause rest tremors.

In the PCR, DNA amplification is performed by thermostable enzymes; invariably either family A DNA polymerases from thermophilic and hyperthermophilic Bacteria or family B DNA polymerases from hyperthermophilic Archaea. Family Y DNA polymerase from the hyperthermophilic archaeon Sulfolobus solfataricus, Sso-polY, is also an enzyme marketed for PCR, but with specialist applications. Each thermostable DNA polymerases has different characteristics and to achieve optimal results, the choice of a PCR enzyme depends on the application itself.

The patient is most likely complaining of the effects of hyperkalaemia, due to missing his dialysis sessions. Additionally, because the patient presents with a risk of cardiac arrest (based on pulmonary oedema and ECG findings), the best intervention is to give calcium gluconate that will address the hyperkalaemia as well as improve the cardiac condition.

Scabies is an infection caused by a microscopic mite known as Sarcoptes scabies. The chief presenting complaint is itching especially in skin folds and mostly during night. It spreads from one person to another through skin contact, and therefore it is more prevalent in crowded areas like hospitals, hostels and even at homes where people live in close contact with each other. Treatment options include benzyl benzoate, ivermectin, sulphur and permethrin.

Bicarbonate therapy is not indicated in mild and moderate forms of DKA because metabolic acidosis will correct with insulin therapy. The use of bicarbonate in severe DKA is controversial due to a lack of prospective randomized studies. It is thought that the administration of bicarbonate may actually result in peripheral hypoxemia, worsening of hypokalaemia, paradoxical central nervous system acidosis, cerebral oedema in children and young adults, and an increase in intracellular acidosis. Because severe acidosis is associated with worse clinical outcomes and can lead to impairment in sensorium and deterioration of myocardial contractility, bicarbonate therapy may be indicated if the pH is 6.9 or less.

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

People aged 16 or over are entitled to consent to their own treatment. This can only be overruled in exceptional circumstances. Children under the age of 16 can consent to their own treatment if they’re believed to have enough intelligence, competence and understanding to fully appreciate what’s involved in their treatment. This is known as being Gillick competent.

Otherwise, someone with parental responsibility can consent for them.
This could be:
the child’s mother or father
the child’s legally appointed guardian
a person with a residence order concerning the child
a local authority designated to care for the child
a local authority or person with an emergency protection order for the child.
Giving the blood transfusion is therefore both clinically and ethically the right course of action.
Jehovah’s Witnesses frequently carry a signed and witnessed Advance Decision Document listing the blood products and autologous procedures that are, or are not, acceptable to them It is appropriate to have a frank, confidential discussion with the patient about the potential risks of their decision and the possible alternatives to transfusion, but the freely expressed wish of a competent adult must always be respected.

A patient with a gradual onset of schizophrenia is to be associated with a poor prognosis.

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.

Hashimoto thyroiditis is the most common cause of hypothyroidism in developed countries. In contrast, worldwide, the most common cause of hypothyroidism is an inadequate dietary intake of iodine. This disease is also known as chronic autoimmune thyroiditis and chronic lymphocytic thyroiditis.

Many drugs are responsible for causing drug induced lupus. However, it is most commonly associated with hydralazine, procainamide and quinidine.

Glioblastoma multiforme, also considered as grade IV astrocytoma, is the most malignant form of the tumour and accounts for about 20% of all cerebral tumours. These often remain clinically silent until they have reached a large enough size. In adults, glioblastoma multiforme usually occurs in the cerebral hemispheres, especially the frontal and temporal lobes of the brain. About half occupy more than one hemisphere at presentation, and some are multicentric. Biopsy shows high cellularity with mitoses, pleomorphism, and vascular hyperplasia. Prognosis is extremely poor, with only 20% surviving beyond 1 year and 10% beyond 2 years.

The classic history in this high risk patient is suggestive of a dissecting aortic aneurysm. His transoesophageal echocardiogram confirms the diagnosis. ST elevation in ECG is probably due to the extension of the dissection of the aorta which results in compromised coronary blood supply.

Metabolic acidosis is associated with cocaine overdose.
In overdose, cocaine leads to agitation, tachycardia, hypertension, sweating, hallucinations, and finally convulsions.
Metabolic acidosis, hyperthermia, rhabdomyolysis, and ventricular arrhythmias also occur.
Chronic use may be associated with premature coronary artery disease, dilated cardiomyopathy, and increased risk of cerebral haemorrhage.
There are 3 stages for acute cocaine toxicity:
Stage I: CNS symptoms of headache, vertigo, pseudo hallucinations, hyperthermia, hypertension.
Stage II: increased deep tendon reflexes, tachypnoea, irregular breathing, hypertension.
Stage III: Areflexia, coma, fixed and dilated pupils, hypotension, ventricular fibrillation, apnoea, and respiratory failure.

Treatment:
– Airway, breathing, and circulation to be secured. The patient’s fever should be managed, and one should rule out hypoglycaemia as a cause of the neuropsychiatric symptoms.
– Cardiovascular toxicity and agitation are best-treated first-line with benzodiazepines to decrease CNS sympathetic outflow.
– The mixed beta/alpha blocker labetalol is safe and effective for treating concomitant cocaine-induced hypertension and tachycardia.
– Non-dihydropyridine calcium channels blockers such as diltiazem and verapamil have been shown to reduce hypertension reliably, but not tachycardia.
– Dihydropyridine agents such as nifedipine should be avoided, as reflex tachycardia may occur.
– The alpha-blocker phentolamine has been recommended but only treats alpha-mediated hypertension and not tachycardia.

The patient has small cell lung cancer presented by paraneoplastic syndrome; Ectopic ACTH secretion.

Small cell lung cancer (SCLC), previously known as oat cell carcinoma is a neuroendocrine carcinoma that exhibits aggressive behaviour, rapid growth, early spread to distant sites, exquisite sensitivity to chemotherapy and radiation, and a frequent association with distinct paraneoplastic syndromes.
Common presenting signs and symptoms of the disease, which very often occur in advanced-stage disease, include the following:
– Shortness of breath
– Cough
– Bone pain
– Weight loss
– Fatigue
– Neurologic dysfunction
Most patients with this disease present with a short duration of symptoms, usually only 8-12 weeks before presentation. The clinical manifestations of SCLC can result from local tumour growth, intrathoracic spread, distant spread, and/or paraneoplastic syndromes.
SIADH is present in 15% of the patients and Ectopic secretion of ACTH is present in 2-5% of the patients leading to ectopic Cushing’s syndrome.