Pathophysiology of Constipation

Defecation as well on urination is a physiological process that includes working smooth muscles, and fiber latitude, central and peripheral innervation, coordination of the reflex system, good awareness and physical ability to reach a place of defecation. The difficulty of diagnosis and management of constipation is because of the many mechanisms involved in the normal process of defecation (urge to defecate normally stimulated by rectal distension through four stages, among others: the stimulus baffle recto-anal reflex, muscle relaxation of the internal sphincter, external sphincter muscle relaxation and muscles in the pelvic region, and an increase in intra-abdominal pressure).

Disruption of one of these mechanisms can result in constipation. Defecation starting peristalsis of the large intestine to the rectum to deliver feces removed. Feces enter and stretch the ampulla of the rectum followed by relaxation of the internal anal sphincter. To avoid spontaneous spending stool, occurring reflex contraction of the external anal sphincter and pelvic floor muscle contraction that is innervated by the pudendal nerve. The brain receives stimuli desire for defecation and external anal sphincter relaxation was ordered to, so the rectum expel its contents with the help of muscle contractions of the abdominal wall. This contraction will raise the pressure in the stomach, and muscle relaxation of the sphincter ani elevators. Both sympathetic and parasympathetic innervation involved in the process of defecation.

The pathogenesis of constipation varied, multiple causes, including several overlapping factors. Although constipation is a lot of complaints in the elderly, colonic motility was not affected by age. Normal aging process does not result in a slowing of gastrointestinal trip. Pathophysiological changes that cause constipation not due to age but is particularly the case for those with constipation.

Study with radiopaque sign ingested by healthy elderly people who do not get a change of the total time of bowel movements, including motor activity of the colon. About time bowel movements by following the radiopaque markers are swallowed, normally less than 3 days already incurred. In contrast, studies in older people who suffer from constipation, bowel movements showed an extended time of 4-9 days. In those treated or bedridden, can be extended to 14 days. Radioactive markers used mainly slow the course of the left colon and the slowest time of the expenditure of the sigmoid colon. Electrophysiological examination to measure motor activity of the colon of patients with constipation showed reduced motor responses of the sigmoid due to reduced intrinsic innervation because myentericus plexus degeneration. Found also reduced nerve stimulation in circular smooth muscle that can lead to an increased time bowel movements.

Individuals over the age of 60 years are also shown to have plasma levels of beta-endorphins are increased, accompanied by an increase in endogenous opiate binding to receptors in the gut. This is evidenced by the effect of dosage opiate constipation that can cause relaxation of colonic tone, reduced motility, and inhibits gastric-colonic reflex.

In addition, there is a tendency of decrease in sphincter tone and strength of smooth muscles associated with age, particularly in women. Patients with constipation have a greater difficulty to remove the small, hard stools that attempts to push harder and longer. This can result in pressure on the pudendal nerve, causing further weakness.

Pathophysiology of Heart Failure

In case of heart failure, the body has several adaptations, both in the heart and systemically. If both ventricular stroke volume is reduced, therefore the emphasis contractility or afterload was increased, the volume and end-diastolic pressure in the two chambers of the heart increased. This will increase the length of myocardial fibers end-diastolic, systolic rise time becomes shorter. If this condition persists, ventricular dilatation occurs. Cardiac output at rest can still be good, but the increase in diastolic pressure that lasts longer / chronicle will spread to both the atrium and the pulmonary circulation and the systemic circulation. Finally, capillary pressure will increase which will lead to transudation of fluid and edema arising systemic or pulmonary edema. Decrease in cardiac output, especially if associated with a reduction in arterial pressure or decreased renal perfusion, will activate several neural and humoral systems. Increased activity of the sympathetic nervous system will stimulate myocardial contraction, heart rate and veins; recent changes that will increase central blood volume, which in turn increase the preload. Although these adaptations are designed to increase cardiac output, adaptation itself can interfere with the body. Therefore, tachycardia and increased myocardial contractility can stimulate the occurrence of ischemia in patients with coronary artery disease earlier and increased preload may worsen pulmonary congestion.

Activation of the sympathetic nervous system will also increase peripheral resistance; adaptation designed to maintain perfusion to vital organs, but if activation is increased instead will decrease the flow to the kidneys and tissues. Peripheral vascular resistance may also be a major determinant of ventricular afterload, so that excessive sympathetic activity can improve the function of the heart itself. One important effect is a decrease in cardiac output decreased renal blood flow and filtration rate decreased glomerolus, which will cause sodium and fluid retention. Sitem renin - angiotensin - aldosterone system will also be activated, leading to increased peripheral vascular resistance and penigkatan selanjutnta left ventricular afterload as sodium and fluid retention. Heart failure is associated with increased levels of arginine vasopressin in the circulation increases, which also is vasokontriktor and inhibiting the excretion of fluids. In heart failure increased atrial natriuretic peptide due to increased atrial pressure, which indicates that here there is resistance to the effects of natriuretic and vasodilator.

Pathophysiology of Osteomyelitis

Pathophysiology of Osteomyelitis

Staphylococcus aureus is the cause of 70-80 percent of bone infection. Other pathogenic organisms commonly found in osteomyelitis include: Proteus, Pseudomonas and E.coli. There is an increased incidence of penicillin-resistant infections, nosocomial, gram negative and anaerobic.

Onset of osteomyelitis after orthopedic surgery can occur within the first 3 months (acute fulminant stage I) and is often associated with accumulation of hematoma or superficial infection. Late onset infection (stage 2) occurred between 4 and 24 months after surgery. Osteomyelitis long onset (stage 3) is usually due to haematogenous spread and occurred 2 years or more after surgery.

Initial response to infection is one of inflammation, increased Vascularization and edema. After 2 or 3 days, thrombosis in blood vessels occurs in the area, resulting in ischemia with bone necrosis associated with an increased and can spread to soft tissue or joints in the vicinity, unless the infection process can be controlled, then the bone will form an abscess.

Abscess formed in the walls forming the dead tissue, but as in the abscess cavity in general, the bone tissue dies (sequestrum) is not easy to melt and flow out. Cavity can not be deflated and healed, as occurs in soft tissues. New bone growth occurs (involukrum) and surrounds the sequestrum. Although there appeared to be healing, but the sequestrum remains vulnerable to infectious chronic recurrent abscesses issue.

Source : http://nanda-nursing-care-plan.blogspot.com/2012/07/pathophysiology-of-osteomyelitis.html