Since the most likely diagnosis is anal fissure, the correct treatment is topical nitrates.

Anal fissures are a common cause of painful, bright red rectal bleeding. Most fissures are idiopathic and present as a painful mucocutaneous defect in the posterior midline (90% cases). Fissures are more likely to be anteriorly located in females, particularly if they are multiparous. Diseases associated with fissure-in-ano include:
1. Crohn’s disease
2. Tuberculosis
3. Internal rectal prolapse

Diagnostic options are as follows:
In most cases, the defect can be visualised as a posterior midline epithelial defect. Where symptoms are highly suggestive of the condition and examination findings are unclear, an examination under anaesthesia may be helpful. Atypical disease presentation should be investigated by colonoscopy and EUA, with biopsies of the area.

For management of anal fissure:
1. Stool softeners are important as hard stools may tear the epithelium and result in recurrent symptoms. The most effective first-line agents are topically applied GTN (0.2%) or Diltiazem (2%) paste.
2. Resistant cases may benefit from injection of botulinum toxin or lateral internal sphincterotomy. Advancement flaps may be used to treat resistant cases.

Middle suprarenal arteries arise from either side of the abdominal aorta, opposite the superior mesenteric artery.

The classic presentation of a ureteric colic is acute, colicky flank pain radiating to the groin. The pain is often described as the worst pain the patient has ever had experienced. Ureteric colic occurs as a result of obstruction of the urinary tract by calculi at the narrowest anatomical areas of the ureter: the pelviureteric junction (PUJ), near the pelvic brim at the crossing of the iliac vessels and the narrowest area, the vesicoureteric junction (VUJ). Location of pain may be related but is not an accurate prediction of the position of the stone within the urinary tract. As the stone approaches the vesicoureteric junction, symptoms of bladder irritability may occur.

Calcium stones (calcium oxalate, calcium phosphate and mixed calcium oxalate and phosphate) are the most common type of stone, while up to 20% of cases present with uric acid, cystine and struvite stones.

Physical examination typically shows a patient who is often writhing in distress and pacing about trying to find a comfortable position; this is, in contrast to a patient with peritoneal irritation who remains motionless to minimise discomfort. Tenderness of the costovertebral angle or lower quadrant may be present. Gross or microscopic haematuria occurs in approximately 90% of patients; however, the absence of haematuria does not preclude the presence of stones.

Burkitt’s lymphoma is a type of non-Hodgkin’s lymphoma. Histologically it is characterised by a starry sky appearance due to numerous neoplastic macrophages which are required to clear the rapidly dividing tumour cells/blast cells. Burkitt’s lymphoma commonly affects the jaw bone, forming a huge tumour mass. It is associated with translocation of c-myc gene and has three types: 1) endemic/African type, 2)sporadic and 3)immunodeficiency-associated. The first type is strongly associated with EBV.

Glucose is reabsorbed almost 100% via sodium–glucose transport proteins (apical) and GLUT (basolateral) in the proximal convoluted tubule. Glycosuria or glucosuria is a condition of osmotic diuresis typical in those suffering from diabetes mellitus. Due to a lack of insulin, plasma glucose levels are above normal. This leads to saturation of receptors in the kidneys and glycosuria usually at plasma glucose levels above 11 mmol/l. Rarely, glycosuria is due to an intrinsic problem with glucose reabsorption within the kidneys (such as Fanconi syndrome), producing a condition termed renal glycosuria.

Anal squamous cell cancer is believed to be directly linked to the presence of a complex inflammatory process most commonly caused by HPV infection (particularly with serotypes 16 and 18) in the histologically unique area of the anal squamocolumnar epithelium. In one Scandinavian study, serotype 16 HPV DNA was detected in 73% of anal cancer specimens, and serotype 16, 18, or both were detected in 84% of specimens. In contrast, no rectal cancer specimens contained HPV DNA.

The rectus sheath is a tendinous sheath that encloses the rectus abdominis muscle. It covers the entire anterior surface however on the posterior surface of the muscle the sheath is incomplete ending inferiorly at the arcuate line. Below the arcuate line, the rectus abdominis is covered by the transversalis fascia. The linea alba is a band of aponeurosis on the midline of the anterior abdominal wall, which extends from the xiphoid process to the pubic symphysis. It is formed by the combined abdominal muscle aponeuroses. This is a useful site for midline incision during abdominal surgery because it does not carry many blood vessels. All of the other answer choices are related to the inguinal canal.
The falx inguinalis (sometimes called the inguinal falx or conjoint tendon), is the inferomedial attachment of the transversus abdominis with some fibres of the internal abdominal oblique – it contributes to the posterior wall of the inguinal canal.
The inguinal ligament is the ligament that connects the anterior superior iliac spine with the pubic tubercle – it makes the floor of the inguinal canal.
The internal (deep) inguinal ring is the entrance to the inguinal canal, where the transversalis fascia pouches out and creates an opening through which structures can leave the abdominal cavity.

Complications of intravenous drug abuse, such as subcutaneous abscess, joint infections, osteomyelitis, overdose, hepatitis, and infective endocarditis, account for an increasing number of admissions in accident and emergency departments throughout the UK. The organisms that usually cause chronic osteomyelitis in intravenous drug users are Gram‐negative rods such as Pseudomonas aeruginosa and Gram‐positive cocci such as staphylococci. Early treatment is essential to prevent progressive bone destruction. TB tends to affect the thoracic spine and in other causes of osteomyelitis the lumbar spine is affected.

Dead space refers to inhaled air that does not take part in gas exchange. Because of this dead space, taking deep breaths slowly is more effective for gas exchange than taking quick, shallow breaths where a large proportion is dead space. Use of a snorkel by a diver increases the dead space marginally. Anatomical dead space refers to the gas in conducting areas such as mouth and trachea, and is roughly 150 ml (2.2 ml/kg body weight). This corresponds to a third of the tidal volume (400-500 ml). It can be measured by Fowler’s method, a nitrogen wash-out technique. It is posture-dependent and increases with increase in tidal volume. Physiological dead space is equal to the anatomical dead space plus the alveolar dead space, where alveolar dead space is the area in the alveoli where no effective exchange takes place due to poor blood flow in capillaries. This physiological dead space is very small normally (< 5 ml) but can increase in lung diseases. Physiological dead space can be measured by Bohr’s method. Total ventilation per minute (minute ventilation) is given by the product of tidal volume and the breathing rate. Here, the total ventilation is 600 ml times 12 breaths/min = 7200 ml/min. The problem mentions alveolar ventilation to be 6000 ml/min. Thus, the difference between the alveolar ventilation and total ventilation is 7200 – 6000 ml/min = 1200 ml/min, or 100 ml per breath at 12 breaths per min. This 100 ml is the dead space volume.

It is not possible to tell if an inguinal hernia is direct or indirect just by palpating it. Despite the fact that indirect inguinal hernias commonly come out of the superficial inguinal ring to enter the scrotum, direct inguinal hernia might still do this.
Femoral hernia goes through the femoral ring into the femoral canal (has nothing to do with the superficial inguinal ring).
Superficial inguinal lymph nodes lie in the superficial fascia parallel to the inguinal ligament; it would therefore feel more superficial and would not be mistaken for a hernia protruding through the inguinal ring.

Minimal-change disease (MCD) refers to a histopathologic glomerular lesion, typically found in children, that is almost always associated with nephrotic syndrome. The most noticeable symptom of MCD is oedema, which can develop very rapidly. Due to the renal loss of proteins muscle wasting and growth failure may be seen in children. Renal function is usually not affected and a proteinuria of more than 40 mg/h/m2 is the only abnormal finding in urinalysis.

Priapism is defined as a prolonged penile erection lasting for >4 h in the absence of sexual stimulation and remains despite orgasm.

The classification of priapism is conventionally divided into three main groups. The commonest classification is into non‐ischaemic (high flow), ischaemic (low flow), and stuttering (recurrent) subtypes.

The EAU guidelines refer to the subtypes as ischaemic (low flow, veno‐occlusive) and arterial (high flow, non‐ischaemic). Of these, ischaemic priapism is the commonest, with refractory cases at risk of smooth muscle necrosis in the corpus cavernosum leading to sequelae of corporal fibrosis and erectile dysfunction (ED).

One of the key considerations in the management of priapism is the duration of the erection at presentation.
The EAU guidelines do differentiate the periods such that the intervention varies accordingly, which is particularly important for prolonged episodes that are refractory to pharmacological interventions and allow a step‐wise intervention.

Ischaemic priapism is a medical emergency as the progressive ischaemia within the cavernosal tissue is associated with time‐dependent changes in the corporal metabolic environment, which eventually leads to smooth muscle necrosis. As the duration of the penile erection becomes pathologically prolonged, as in the case of low‐flow priapism, the partial pressure of oxygen (pO2) progressively falls as the closed compartment prevents replenishment of stagnant blood with freshly oxygenated arterial blood.
Investigations using corporal blood aspiration, that in itself can be a therapeutic intervention leading to partial or complete penile detumescence, helps to differentiate ischaemic from non‐ischaemic priapism subtypes based on the pO2, pCO2 and pH levels. The AUA guidelines state that typically the blood gas analysis would give a pO2 of <30 mmHg and pCO2 of >60 mmHg and a pH of <7.25 in ischaemic priapism, whereas non‐ischaemic blood gas analysis would show values similar to venous blood. Once the diagnosis of priapism has been made, the initial management involves corporal blood aspiration followed by instillation of α‐agonists directly into the corpus cavernosum.
The EAU guidelines recommend several possible agents for intracavernosal injection, as well as oral terbutaline after intracavernosal injection.
Phenylephrine – 200 μg every 3–5 min to a maximum of 1 mg within 1 h.
Etilephrine – 2.5 mg diluted in 1–2 mL saline.
Adrenaline – 2 mL of 1/100 000 solution given up to 5 times in a 20‐min period.
Methylene blue – 50–100 mg intracavernosal injection followed by aspiration and compression.

Shunt surgery allows diversion of blood from the corpus cavernosum into another area such as the corpus spongiosum (glans or urethra) or the venous system (saphenous vein). Both the EAU and AUA guidelines recommend surgical intervention using firstly distal shunts and then proximal shunts in cases where aspiration and instillation of pharmacological agents fails to achieve penile detumescence. The EAU guidelines recommend that distal shunts should be attempted before proximal shunts, although the specific technique is left to the individual surgeon’s preference. The EAU guidelines also define a time point (36 h) when shunt surgery is likely to be ineffective in maintaining long‐term erectile function and may serve to reduce pain only. This is an important consideration when contemplating early penile prosthesis placement.

Early ECG changes of hyperkalaemia, typically seen at a serum potassium levels of 5.5-6.5 mEq/L, include the following:
– Tall, peaked T waves with a narrow base (best seen in precordial leads)
– Shortened QT interval
– ST-segment depression

Severe abdominal pain tends to favour infection with Campylobacter jejuni.

Infection with Campylobacter jejuni is one of the most common causes of gastroenteritis worldwide. In developed countries, the incidence of Campylobacter jejuni infections peaks during infancy and, again, during early adulthood. Most infections are acquired by the consumption and handling of poultry. A typical case is characterized by diarrhoea, fever, and severe abdominal cramps. Obtaining cultures of the organism from stool samples remains the best way to diagnose this infection. Complications of C. jejuni infections are rare, and most patients do not require antibiotics. Careful food preparation and cooking practices may prevent some Campylobacter infections.

Answer: Cystine stone

Cystinuria is a genetic cause of kidney stones with an average prevalence of 1 in 7000 births. Cystine stones are found in 1 to 2 percent of stone formers, although they represent a higher percentage of stones in children (approximately 5 percent). Cystinuria is an inherited disorder. Inherited means it is passed down from parents to children through a defect in a specific gene. In order to have cystinuria, a person must inherit the gene from both parents.
Cystine is a homodimer of the amino acid cysteine. Patients with cystinuria have impairment of renal cystine transport, with decreased proximal tubular reabsorption of filtered cystine resulting in increased urinary cystine excretion and cystine nephrolithiasis. The cystine transporter also promotes the reabsorption of dibasic amino acids, including ornithine, arginine, and lysine, but these compounds are soluble so that an increase in their urinary excretion does not lead to stones. Intestinal cystine transport is also diminished, but the result is of uncertain clinical significance.

Cystinuria only causes symptoms if you have a stone. Kidney stones can be as small as a grain of sand. Others can become as large as a pebble or even a golf ball. Symptoms may include:

Pain while urinating
Blood in the urine
Sharp pain in the side or the back (almost always on one side)
Pain near the groin, pelvis, or abdomen
Nausea and vomiting

Struvite stones are a type of hard mineral deposit that can form in your kidneys. Stones form when minerals like calcium and phosphate crystallize inside your kidneys and stick together. Struvite is a mineral that’s produced by bacteria in your urinary tract. Bacteria in your urinary tract produce struvite when they break down the waste product urea into ammonia. For struvite to be produced, your urine needs to be alkaline. Having a urinary tract infection can make your urine alkaline. Struvite stones often form in women who have a urinary tract infection.

Calcium oxalate stones are the most common type of kidney stone. Kidney stones are solid masses that form in the kidney when there are high levels of calcium, oxalate, cystine, or phosphate and too little liquid. There are different types of kidney stones. Your healthcare provider can test your stones to find what type you have. Calcium oxalate stones are caused by too much oxalate in the urine.

What is oxalate and how does it form stones?
Oxalate is a natural substance found in many foods. Your body uses food for energy. After your body uses what it needs, waste products travel through the bloodstream to the kidneys and are removed through urine. Urine has various wastes in it. If there is too much waste in too little liquid, crystals can begin to form. These crystals may stick together and form a solid mass (a kidney stone). Oxalate is one type of substance that can form crystals in the urine. This can happen if there is too much oxalate, too little liquid, and the oxalate “sticks” to calcium while urine is being made by the kidneys.

Uric acid stones are the most common cause of radiolucent kidney stones in children. Several products of purine metabolism are relatively insoluble and can precipitate when urinary pH is low. These include 2- or 8-dihydroxyadenine, adenine, xanthine, and uric acid. The crystals of uric acid may initiate calcium oxalate precipitation in metastable urine concentrates.
Uric acid stones form when the levels of uric acid in the urine is too high, and/or the urine is too acidic (pH level below 5.5) on a regular basis. High acidity in urine is linked to the following causes:
Uric acid can result from a diet high in purines, which are found especially in animal proteins such as beef, poultry, pork, eggs, and fish. The highest levels of purines are found in organ meats, such as liver and fish. Eating large amounts of animal proteins can cause uric acid to build up in the urine. The uric acid can settle and form a stone by itself or in combination with calcium. It is important to note that a person’s diet alone is not the cause of uric acid stones. Other people might eat the same diet and not have any problems because they are not prone to developing uric acid stones.
There is an increased risk of uric acid stones in those who are obese or diabetic.
Patients on chemotherapy are prone to developing uric acid stones.

Only cystine stone is inherited.

Non-neoplastic (non-adenomatous) colonic polyps include hyperplastic polyps, hamartomas, juvenile polyps, pseudopolyps, lipomas, leiomyomas and others.
An autosomal dominant condition, Peutz–Jeghers syndrome is a disease that is characterized by multiple hamartomatous polyps in the stomach, small bowel and colon. Symptoms of this syndrome include hyperpigmentation of the skin and mucous membranes, especially of the lips and gums.
Juvenile polyps develop in children, and once they outgrow their blood supply, they autoamputate around puberty. In cases of uncontrolled bleeding or intussusception, treatment is needed.
Inflammatory polyps and pseudopolyps occur in chronic ulcerative colitis and Crohn’s disease. There is an increased risk of cancer with multiple juvenile polyps (not with sporadic polyps).

Direct inguinal hernias occur because of weakness in the abdominal muscles. The ilioinguinal nerve is important for innervating the muscles of the lower abdominal wall and damage during appendicectomy therefore prevents the man from being able to contract abdominal muscles to pull the falx inguinalis over the weak fascia.
The genitofemoral nerve innervates the cremaster muscle and injury to it would cause inability to elevate the testes.
The subcostal nerve and the ventral primary ramus of T10 innervate the muscles, skin and fascia of the upper abdominal wall.
The iliohypogastric nerve supplies the skin over the upper part of the buttock behind the area supplied by the subcostal nerve.

Sigmoid arteries are branches of the inferior mesenteric artery (IMA). Sigmoid artery gives off branches that supply the lower descending colon, the iliac colon and the sigmoid colon.

The duodenum is the only organ in the list that would not be affect by the clumping of the splenic artery as it is supplied by common hepatic artery (through the gastroduodenal artery) and the superior mesenteric artery (through the inferior pancreaticoduodenal artery). The splenic artery is the artery that supplies the spleen with oxygenated blood. The splenic artery before reaching the spleen also gives off branches that supply the stomach and the pancreas. The greater curvature and the fundus of the stomach is supplied the short gastric artery which branches off from the splenic artery. The left portion of the greater curvature of the stomach together with the greater omentum is supplied by the left gastro-omental artery of the splenic artery. The body and tail of the pancreas is supplied by branches of the splenic artery through the dorsal and superior pancreatic arteries and the caudal pancreatic arteries respectively.

The skin over the cheek and the maxilla are innervated by the trigeminal nerve (CN V). The trigeminal nerve has three major branches and it is the largest cranial nerve. The three branches of the trigeminal nerve are; the ophthalmic nerve, the maxillary nerve and the mandibular nerve. The trigeminal nerves ganglion is a sensory nerve ganglion know as the trigeminal ganglion (also referred to as the Gasser’s ganglion or the semilunar ganglion). It is contained in the dura matter in a cavity known as the Meckel’s cave, which covers the trigeminal impression near the apex of the petrous part of the temporal bone.