Direct inguinal hernia
The direct inguinal hernia enters through a weak point in the fascia of the abdominal wall, and its sac is noted to be medial to the inferior epigastric vessels. Direct inguinal hernias may occur in males or females, but males are ten times more likely to get a direct inguinal hernia.A direct inguinal hernia protrudes through a weakened area in the transversalis fascia near the medial inguinal fossa within an anatomic region known as the inguinal or Hesselbachs triangle, an area defined by the edge of the rectus abdominis muscle, the inguinal ligament and the inferior epigastric artery. These hernias are capable of exiting via the superficial inguinal ring and are unable to extend into the scrotum. When a patient develops a simultaneous direct and indirect hernia on the same side, it is called a pantaloon hernia or saddlebag hernia because it resembles a pair of pants with the epigastric vessels in the crotch, and the defects can be repaired separately or together. Another term for pantaloon hernia is Rombergs hernia. Since the abdominal walls weaken with age, direct hernias tend to occur in the middle-aged and elderly. This is in contrast to indirect hernias which can occur at any age including the young, since their etiology includes a congenital component where the inguinal canal is left more patent (compared to individuals less susceptible to indirect hernias). Additional risk factors include chronic constipation, being overweight or obese, chronic cough, family history and prior episodes of direct inguinal hernias.
The area postrema is a circumventricular organ and as such lies outside the blood–brain barrier; it can therefore be stimulated by blood-borne drugs that can stimulate vomiting or inhibit it.There are various sources of input to the vomiting center:

The chemoreceptor trigger zone at the base of the fourth ventricle has numerous dopamine D2 receptors, serotonin 5-HT3 receptors, opioid receptors, acetylcholine receptors, and receptors for substance P. Stimulation of different receptors are involved in different pathways leading to emesis, in the final common pathway substance P appears involved. The vestibular system, which sends information to the brain via cranial nerve VIII (vestibulocochlear nerve), plays a major role in motion sickness, and is rich in muscarinic receptors and histamine H1 receptors. The cranial nerve X (vagus nerve) is activated when the pharynx is irritated, leading to a gag reflex. The vagal and enteric nervous system inputs transmit information regarding the state of the gastrointestinal system. Irritation of the GI mucosa by chemotherapy, radiation, distention, or acute infectious gastroenteritis activates the 5-HT3 receptors of these inputs. The CNS mediates vomiting that arises from psychiatric disorders and stress from higher brain centers. The medulla plays an important role for triggering the vomiting act.The vomiting act encompasses three types of outputs initiated by the chemoreceptor trigger zone: Motor, parasympathetic nervous system (PNS), and sympathetic nervous system (SNS). They are as follows:

Increased salivation to protect tooth enamel from stomach acids. (Excessive vomiting leads to dental erosion.) This is part of the PNS output.