Among the veins listed, only the left brachiocephalic vein is anterosuperior to the ascending aorta. The right brachiocephalic vein being on the right side would not be affected by the aortic aneurysm.
The azygos vein lies deep in the chest on the right side.
The internal thoracic vein lies interior to the anterior wall of the chest.
The left superior intercostal vein is close to the aortic arch, crossing it laterally. This vein drains the 2nd to 4th interspaces on the left side.
The Right internal jugular vein joins the right brachiocephalic vein which would not be affected by the aneurysm.

Calcium is necessary for coagulation to occur. Citrate being a chelator and combining with calcium ions to form un-ionised compound will prevent coagulation. Following transfusion the citrate is removed by the liver with in a few minutes. Oxalate also works on the same principle but it is toxic to the body.

Lactase, an enzyme belonging to β-galactosidase family of enzymes, brings about the hydrolysis of the disaccharide lactose into galactose and glucose. In humans, it is present along the brush border membrane of the cells lining the small intestinal villi. Deficiency of lactase causes lactose intolerance.

Angio-oedema, is the rapid swelling of the skin, mucosa and submucosal tissues. The underlying mechanism typically involves histamine or bradykinin. The version related to histamine is to due an allergic reaction to agents such as insect bites, food, or medications. The version related to bradykinin may occur due to an inherited C1 esterase inhibitor deficiency, medications e.g. angiotensin converting enzyme inhibitors, or a lymphoproliferative disorder.

Early antibiotic treatment of anthrax is essential. A delay may significantly lessen the chances for survival of the patient. Treatment for anthrax infection include large doses of intravenous and oral antibiotics, such as fluoroquinolones (ciprofloxacin), doxycycline, erythromycin, vancomycin, or penicillin.

High-probability ECG features of MI are the following:
ST-segment elevation greater than 1 mm in two anatomically contiguous leads
The presence of new Q waves

Intermediate-probability ECG features of MI are the following:
ST-segment depression
T-wave inversion
Other nonspecific ST-T wave abnormalities
Low-probability ECG features of MI are normal ECG findings. However, normal or nonspecific findings on ECGs do not exclude the possibility of MI.

Special attention should be made if there is diffuse ST depression in the precordial and extremity leads associated with more than 1 mm ST elevation in lead aVR, as this may indicate stenosis of the left main coronary artery or the proximal section of the left anterior descending coronary artery.

Localization of the involved myocardium based on the distribution of ECG abnormalities in MI is as follows:
– Inferior wall – II, III, aVF
– Lateral wall – I, aVL, V4 through V6
– Anteroseptal – V1 through V3
– Anterolateral – V1 through V6
– Right ventricular – RV4, RV5
– Posterior wall – R/S ratio greater than 1 in V1 and V2, and – T-wave changes in V1, V8, and V9
– True posterior-wall MIs may cause precordial ST depressions, inverted and hyperacute T waves, or both. ST-segment elevation and upright hyperacute T waves may be evident with the use of right-sided chest leads.

Hyperacute (symmetrical and, often, but not necessarily pointed) T waves are frequently an early sign of MI at any locus.
The appearance of abnormalities in a large number of ECG leads often indicates extensive injury or concomitant pericarditis.
The characteristic ECG changes may be seen in conditions other than acute MI. For example, patients with previous MI and left ventricular aneurysm may have persistent ST elevations resulting from dyskinetic wall motion, rather than from acute myocardial injury. ST-segment changes may also be the result of misplaced precordial leads, early repolarization abnormalities, hypothermia (elevated J point or Osborne waves), or hypothyroidism.
False Q waves may be seen in septal leads in hypertrophic cardiomyopathy (HCM). They may also result from cardiac rotation.
Substantial T-wave inversion may be seen in left ventricular hypertrophy with secondary repolarization changes.
The QT segment may be prolonged because of ischemia or electrolyte disturbances.
Saddleback ST-segment elevation (Brugada epsilon waves) may be seen in leads V1-V3 in patients with a congenital predisposition to life-threatening arrhythmias. This elevation may be confused with that observed in acute anterior MI.
Diffuse brain injuries and haemorrhagic stroke may also trigger changes in T waves, which are usually widespread and global, involving all leads.
Convex ST-segment elevation with upright or inverted T waves is generally indicative of MI in the appropriate clinical setting. ST depression and T-wave changes may also indicate the evolution of NSTEMI.
Patients with a permanent pacemaker may confound recognition of STEMI by 12-lead ECG due to the presence of paced ventricular contractions.
To summarize, non-ischemic causes of ST-segment elevation include left ventricular hypertrophy, pericarditis, ventricular-paced rhythms, hypothermia, hyperkalaemia and other electrolyte imbalances, and left ventricular aneurysm.

Answer: Inflammatory bowel disease

The inflammatory bowel diseases (IBDs), including ulcerative colitis and Crohn disease, are chronic inflammatory disorders of the gastrointestinal tract most often diagnosed in adolescence and young adulthood, with a rising incidence in paediatric populations. Inflammatory bowel disease is caused by a dysregulated mucosal immune response to the intestinal microflora in genetically predisposed hosts. Although children can present with the classic symptoms of weight loss, abdominal pain, and bloody diarrhoea, many present with nonclassical symptoms of isolated poor growth, anaemia, or other extraintestinal manifestations.

Colorectal Carcinoma (CRC) is rare in patients less than 20 years of age.

The special part of the equipment is the T tube itself. As the name refers, it is a special tube in the shape of T with a shorter transverse part (20 cm) that stays inside the CBD (after trimming) and a long longitudinal part (60 cm) that extends from the middle of the transverse part to an end that connects with a drainage bag. This portion extends from the CBD to outside the abdominal cavity when applied. It comes with different circumference sizes (10, 12, 14, 16, 18 Fr). T tube can be made of different materials like latex, silicone, red rubber and polyvinyl chloride (PVC). PVC is very inert causing the least tissue reaction with lack of tissue tract formation making it the least favourable material for T tube placement purposes. Silicon has many favourable physical properties, but it can disintegrate with poor handling making it not a practical option for long-term placement. Latex has the desired properties to be the most commonly used. Red rubber is an alternative if latex can not be used or is not available.

Carcinoid syndrome occurs in ∼20% of cases of well-differentiated endocrine tumours of the jejunum or ileum (midgut neuroendocrine tumours (NET) and consists of (usually) dry flushing (without sweating; 70% of cases) with or without palpitations, diarrhoea (50% of cases) and intermittent abdominal pain (40% of cases); in some patients, there is also lacrimation and rhinorrhoea.
Carcinoid syndrome occurs less often with NETs of other origins and is very rare in association with rectal NETs. It is usually due to metastasis to the liver, with the release of vasoactive compounds, including biogenic amines (e.g., serotonin and tachykinins), into the systemic circulation. However, it may also occur in the absence of liver metastases if there is direct retroperitoneal involvement, with venous drainage bypassing the liver. Pain due to hepatic enlargement may also be a presenting feature, as may upper right abdominal pain (similar to that of pulmonary infarction) secondary to either haemorrhage into, or necrosis of, a hepatic secondary tumour. Wheezing and pellagra are less common presenting features. CHD is present in ∼20% of patients at presentation and usually indicates that the syndrome has been present for several years.

The aim of treatment should be curative where possible but it is palliative in the majority of cases.
Surgery is the only curative treatment.
Administration of specific medications to treat symptoms should, therefore, start as soon as clinical and biochemical signs indicate the presence of hypersecretory NETs, even before the precise localisation of primary and metastatic lesions is confirmed.

The only proven hormonal management of NETs is by the administration of somatostatin analogues.
Somatostatin analogues bind principally to SSTR subtypes 2 (with high affinity) and 5 (with lower affinity), thus inhibiting the release of various peptide hormones in the gut, pancreas and pituitary; they also antagonise growth factor effects on tumour cells, and, at very high dosage, may induce apoptosis. The effects of somatostatin analogues are demonstrable as biochemical response rates (inhibition of hormone production) in 30–70% of patients and as symptomatic control in the majority of patients.
There are two commercially available somatostatin analogues: octreotide and lanreotide.

The fundus of the bladder is related anatomically to the anterior surface of the vagina and the urethra as well. If there was a malignant growth in the anterior surface of the vagina, then most likely the fundus of the bladder would be involved as well aspotentially the urethra.