Inguinal hernias can present with an array of different symptoms. Most patients present with a bulge in the groin area, or pain in the groin. Some will describe the pain or bulge that gets worse with physical activity or coughing. Symptoms may include a burning or pinching sensation in the groin. These sensations can radiate into the scrotum or down the leg. It is important to perform a thorough physical and history to rule out other causes of groin pain. At times an inguinal hernia can present with severe pain or obstructive symptoms caused by incarceration or strangulation of the hernia sac contents. A proper physical exam is essential in the diagnosis of an inguinal hernia. Physical examination is the best way to diagnose a hernia. The exam is best performed with the patient standing. Visual inspection of the inguinal area is conducted first to rule out obvious bulges or asymmetry in groin or scrotum. Next, the examiner palpates over the groin and scrotum to detect the presence of a hernia. The palpation of the inguinal canal is completed last. The examiner palpates through the scrotum and towards the external inguinal ring. The patient is then instructed to cough or perform a Valsalva manoeuvre. If a hernia is present, the examiner will be able to palpate a bulge that moves in and out as the patient increases intra abdominal pressure through coughing or Valsalva.

Groin hernias are categorized into 2 main categories: inguinal and femoral.

Inguinal hernias are further subdivided into direct and indirect. An indirect hernia occurs when abdominal contents protrude through the internal inguinal ring and into the inguinal canal. This occurs lateral to the inferior epigastric vessels. The hernia contents may extend into the scrotum, and can be reduced superiorly then superolaterally. A direct inguinal hernia is protrusion of abdominal contents through the transversalis fascia within Hesselbach’s triangle. The borders of Hesselbach’s triangle are the inferior epigastric vessels superolaterally, the rectus sheath medially, and inguinal ligament inferiorly.

A femoral hernia is a protrusion into the femoral ring. The borders of the femoral ring are the femoral vein laterally, Cooper’s ligament posteriorly, the iliopubic tract/inguinal ligament anteriorly and lacunar ligament medially.

During or shortly after transfusion, febrile transfusion reactions, also known as non-haemolytic transfusion reactions, present with an unexpected temperature rise (38oC or 1oC above baseline, if baseline is 37oC). This is usually a one-off occurrence. The fever is sometimes accompanied by chills.

The most common type of transfusion reaction is febrile transfusion reactions, which occur in about 1 in every 8 transfusions.

The most common event leading to symptoms of febrile transfusion reactions is cytokine accumulation during storage of cellular components (especially platelet units). White cells secrete cytokines, and pre-storage leucodepletion has reduced this risk.

Recipient antibodies (raised as a result of previous transfusions or pregnancies) reacting to donor human leukocyte antigen (HLA) or other antigens can also cause febrile transfusion reactions. Donor lymphocytes, granulocytes, and platelets all contain these antigens.

Treatment is reassuring. Other causes should be ruled out, and antipyretics like paracetamol can help with fever relief. If another cause of fever is suspected, the transfusion should be stopped; however, if other causes of fever have been ruled out, it can be restarted at a slower rate.

Digoxin is a cardiac glycoside that is used to treat atrial fibrillation and flutter, as well as congestive heart failure. In cardiac myocytes, it works by inhibiting the membrane Na/K ATPase. Through Na/Ca exchange, this raises intracellular sodium concentration and indirectly increases intracellular calcium availability. Increased intracellular calcium levels have both a positive inotropic and negative chronotropic effect.

Digoxin therapeutic plasma levels are typically between 1.0 and 1.5 nmol/l, though higher concentrations may be required, and the value varies between laboratories. At concentrations greater than 2 nmol/l, the risk of toxicity increases dramatically.

In patients with normal renal function, digoxin has a long plasma half-life of 36 to 48 hours. This can take up to 5 days in patients with impaired renal function.

Hypokalaemia, rather than hyperkalaemia, has been shown to increase the risk of digoxin toxicity.

In the treatment of persistent and permanent atrial fibrillation, digoxin is no longer widely used. Beta-blockers, also known as rate-limiting calcium channel blockers, are now the first-line treatment for this condition.

A patient suffering from acute ischemic stroke can commonly present with hypertensive emergencies. Thrombolytic therapy is contraindicated in a patient with:
1. Systolic blood pressure greater than 185 mmHg
2. Diastolic blood pressure greater than 110 mmHg

But delaying thrombolytic therapy is associated with increased morbidity in patients with acute ischemic stroke.

Managing high blood pressure in acute ischemic stroke requires a slower and more controlled reduction in BP. In the presence of an ischaemic stroke, rapid reduction of MAP can compromise blood flow, causing further ischemia and worsening of the neurological deficit.

Intravenous labetalol is the agent of choice. The dose is 10 mg IV over 1-2 minutes. This dose can be repeated, or an infusion can be set up that runs at 2-8 mg/minute. Thrombolysis can be performed once the blood pressure is brought down to less than 180/105 mmHg.

A nitrate infusion (for example, Isoket) can be used as an alternative in patients with contraindications to the use of beta-blockers (e.g., asthma, heart block, cardiac failure).

In skeletal muscle, blood flow is closely related to metabolic rate. Due to the contraction of precapillary sphincters, most capillaries are blocked off from the rest of the circulation at rest and are not perfused. This causes an increase in vascular tone and vessel constriction. As metabolic activity rises, this develops redundancy in the system, allowing it to cope with greater demand. During exercise, metabolic hyperaemia, which is induced by the release of K+, CO2, and adenosine, recruits capillaries. Sympathetic vasoconstriction in the active muscles is overridden by this. Simultaneously, blood flow in non-working muscles is restricted, preserving cardiac output. During exercise, muscle contractions pump blood through the venous system, raising the pressure differential between arterioles and venules and boosting blood flow via capillaries.

Capillary angiogenesis is evident when muscles are used repeatedly (e.g. endurance training). It is a long-term effect, not a quick fix for increased blood flow.

The local partial pressure of alveolar oxygen is the primary intrinsic control of pulmonary blood flow (pAO2). Low pAO2 promotes arteriole vasoconstriction and vice versa. The hypoxic pulmonary vasoconstriction (HPV) reflex allows blood flow to be diverted away from poorly ventilated alveoli and towards well-ventilated alveoli in order to maximize gaseous exchange.

Absolute risk reduction (ARR) is computed as the difference between the absolute risk in the control group (ARC) and the absolute risk in the treatment group (ART).

Since Warfarin is the standard of treatment, Warfarin is considered as the control group.

ARR = ARC-ART
ARR = (20/500) – (30/300)
ARR = -0.06

This means that there is increased risk of stroke in the treatment group, which is the Ticagrelor group.

Calcium that is not protein bound is freely filtered in the glomerulus, and there is reabsorption along the nephron.About 70% is reabsorbed in the proximal tubule.About 20% is reabsorbed in the thick ascending limb of the loop of Henle.This reabsorption is mainly passive and paracellular and driven by sodium reabsorption. Sodium reabsorption causes water reabsorption, which raises tubular calcium concentration, causing calcium to diffuse out of the tubules. The positive  lumen potential also encourages calcium to leave the tubule.About 5 – 10% is reabsorbed in the distal convoluted tubule.Less than 0.5% is reabsorbed in the collecting ducts.Calcium reabsorption in the distal nephron is active and transcellular and is the major target for hormonal control.Calcium homeostasis is primarily controlled by three hormones: parathyroid hormone, activated vitamin D and calcitonin.Parathyroid hormone acts on the kidneys to increase calcium reabsorption in the distal tubule by activating Ca2+entry channels in the apical membrane and the Ca2+ATPase pump in the basolateral membrane (and to decrease phosphate reabsorption in the proximal tubule).Activated vitamin D acts to increase calcium reabsorption in the distal tubule via activation of a basolateral Ca2+ATPase pump (and to increase phosphate reabsorption).Calcitonin acts to inhibit renal reabsorption of calcium (and phosphate).

Common side effects of adenosine include:
Apprehension
Dizziness, flushing, headache, nausea, dyspnoea
Angina (discontinue)
AV block, sinus pause and arrhythmia (discontinue if asystole or severe bradycardia occur)

Muscle heals with fibrous tissue to form a scar. Once cut, it will never regain its previous bulk or power. Within the scar a small number of myocytes (muscle cells) may be seen, which are formed from satellite cells but they contribute little to the function of the muscle overall.
In more widespread ischaemic injury, such as critical ischaemic limb due to arterial compromise, or in compartment syndrome, damaged myocytes are replaced diffusely with fibrous tissue. This fibrous tissue contracts and reduces movement, and in extreme cases can pull the limb into abnormal positions such as in Volkmann’s ischaemic contracture of the forearm.

Diverticulitis refers to inflammation and infection associated with a diverticulum and is estimated to occur in 10% to 25% of people with diverticulosis. Peridiverticular and pericolic infection results from a perforation (either macroscopic or microscopic) of a diverticulum, which leads to contamination, inflammation, and infection. The spectrum of disease ranges from mild, uncomplicated diverticulitis that can be treated in the outpatient setting, to free perforation and diffuse peritonitis that requires emergency laparotomy. Most patients present with left sided abdominal pain, with or without fever, and leucocytosis. The most common location for diverticulitis is the sigmoid colon.