Six Factors that Affect Pain

Pain is a sensory and emotional experience that the unpleasant result of tissue damage, actual and potential. Similarly, understanding the pain of Brunner & Suddarth, 2002.

This pain can only be felt by a person without being perceived by others, and will include patterns of thought, activity someone directly, as well as changes in a person's life. Pain is an important signs and symptoms which may indicate the occurrence of a physiological disorder.

For a nurse or other health professionals should consider the factors that influence pain in the face of patients who experience pain. It is very important in the accurate assessment of pain and for nursing action.

Here are Six Factors that Affect Pain, including:

1. Age Factor. Age is an important variable that affects the pain, especially in children and adults. Developmental differences were found between the two age groups may affect how children and adults react to pain. Children difficulty to understand the pain and think that what nurses can cause pain. Children who do not have a lot of vocabulary, have difficulty verbally describing and expressing pain to parents or caregivers. Children can not express the pain, so the nurse should assess pain responses in children. In adults often report pain if it is pathological and malfunction.

2. Anxiety Factor. Although it is generally believed that the anxiety will increase the pain, may not be entirely true in all circumstances. Research does not show a consistent relationship between anxiety and pain also showed that preoperative stress reduction training at lower postoperative pain. However, the relevant anxiety, or dealing with the pain can increase the patient's perception of pain. In general, an effective way to relieve pain is to direct the treatment of pain rather than anxiety (Smeltzer & Bare, 2002).

3. Gender Factor. Gender factor this in conjunction with the factors that affect pain is that men and women did not have significant differences regarding their response to pain. It is doubtful that gender is an independent factor in the expression of pain. For example, boys must be brave and not cry in which a woman can cry at the same time.

4. Family and Social Support Factors. Other factors that also affect the response to pain is the presence of people nearby. People who are in a state of pain often rely on family for support, help or protect. The absence of family or close friends might make the pain increased. The presence of parents is particularly important for children in the face of pain (Potter & Perry, 1993).

5. Cultural Factors. Beliefs and cultural values ​​influence the way individuals cope with pain. Individuals learn what is expected and what is acceptable to their culture. This includes how to react to pain (Calvillo & Flaskerud, 1991). Recognizing the cultural values that have one and understand why these values ​​differ from the values ​​of other cultures helps to avoid evaluating a patient's behavior based on a person's expectations and cultural values. Nurses are aware of cultural differences will have a greater understanding of the patient's pain and be more accurate in assessing pain and behavioral responses to pain are also effective in relieving pain patients (Smeltzer & Bare, 2003).

6. Coping Pattern Factor. When a person is experiencing pain and undergoing treatment at the hospital is very unbearable. Continually client lost control and was not able to control the environment, including pain. Clients often find a way to overcome the effects of physical and psychological pain. It is important to understand the sources of individual coping during painful. Sources of coping is like communicating with family, exercise and singing can be used as a plan to support the client and the client reduce pain.

Signs and Symptoms of Yaws

Clinical symptoms of yaws, consists of 3 Stadium, namely:

Stage I:

This stage is also known as infectious stage. The average incubation period of 3 weeks or in the range of 3-90 days. Initial form of papilloma lesions on port d 'entre shaped like strawberries, wet surfaces, damp, festering, recovered spontaneously without leaving a trace, sometimes accompanied by an increase in body temperature, headache, sore bones and joints later, papules spread which resolved after 1-3 months. Lesions intinial last a few weeks and a few months later recovered. These lesions are often found around the mouth, the anus and vagina, and similar kandilomatalata on syphilis. These symptoms were healed without leaving scars, although sometimes with pigmentation. In addition there is a kind of papilloma on palms or feet, and usually humid. Symptoms of the skin, can be macula, macula Papulosa, papules, micropapula, nodules, without showing damage to the structure of the epidermis and no exudation. The form of the primary lesion is an infectious form.

Stage II

Or a period of transition: at this stage, where the lesion was found Treponema pallidum pertenue. This positive Treponema be several weeks to several months after stage I. At this stage, no infectious yaws with various clinical forms, such as hyperkeratosis. Abnormalities in the bones and joints, often the fingers and limb bones, which can lead to atrophy occurs nails, and gangosa deformation, which is a form of necrotizing disorder and can cause damage to the nasal bone and septum nasi with images of loss of nose shape, gondou (a form of hypertrophic osteitis), although rarely encountered. Joint disorders, hydrarthrosis and juxta articular nodules (subcutaneous nodules, easy to move, chewy, multiple), usually found in the ankle, near the caput fibulae, Acral areas or plantar and palmar.

Stage III:

At this stage, there Guma or indolent ulcer with steep edges or resonate, when cured, these lesions leave scars, keloids and contractures can form. If there is infection in the bone can lead to defects and damage to the bone. Damage often occurs on the palate, nasal bone, the tibia.

Physical Examination and Investigations of Stroke

Physical Examination of Stroke

1. The general state
   Awareness: Generally, decreased consciousness
   The voice spoke: Some disorders are difficult to understand, sometimes can not talk
   Vital signs: increased blood pressure, pulse rate varied.


2. Examination of Integument
   Skin: If the client is less oxygen skin will look pale. If less fluid, it's ugly skin turgor. In addition, it should also be assessed signs of pressure sores, especially on areas that stand out as the client CVA Bleeding should bed rest 2-3 weeks
   Nails: Need to see a finger clubbing, cyanosis
   Hair: Generally no abnormalities


3. Examination of the head and neck
   Head: Shape normocephalic
   Advance: Generally not symmetrical is lopsided to one side
   Neck: Stiff neck rare (Satyanegara, 1998)


4. Examination of the chest
   In breathing audible breath sounds sometimes obtained ronchi, wheezing breath sounds or additional, irregular breathing due to decreased cough reflex and swallowing.


5. Examination of the abdomen
   Obtained decrease intestinal peristalsis caused by bed rest periods, and sometimes there are bloated.


6. Examination of inguinal, genital, anal
   Sometimes there incontinensia or urinary retention.


7. Examination of the extremities
   Often obtained paralysis on one side of the body.


8. Examination of neurology
   • Cranial Nerve
     Generally there is interference with cranial nerve VII and XII central.
   • Motor
     Almost always happens paralysis / weakness on one side of the body.
   • Sensory
     Hemihypesthesia can occur.
   • Reflex
     In the acute phase of physiological reflexes are paralyzed side will disappear. After several days of physiological reflexes will reappear didahuli with pathological reflexes.

Investigations of Stroke

1. Radiological Examination
   • CT scan: hyperdense focal obtained, sometimes get in the ventricles, or spread to the brain surface. (Linardi Widjaja, 1993)
   • Magnetic resonance imaging (MRI) to show the area that experienced hemorrhagic. (Marilynn E. Doenges, 2000)
   • Cerebral angiography: to find the source of bleeding such as aneurysms or vascular malformations. (Satyanegara, 1998)
   • X-ray of the thorax: to show the state of the heart, whether there is an enlargement of the left ventricle, which is one sign of chronic hypertension in patients with stroke. (Jusuf Misbach, 1999)
   
   
2. Laboratory Tests
   • Lumbar puncture: a red liquor inspection is usually found in massive bleeding, minor bleeding while liquor is usually normal color (xanthochromia) during the first days. (Satyanegara, 1998)
   • Routine blood tests
   • Chemical examination of blood: in acute stroke hyperglycemia may occur. Blood sugar can reach 250 mg in the serum and then gradually fell back. (Jusuf Misbach, 1999)
   • Complete blood count: fatherly look for abnormalities in the blood itself. (Linardi Widjaja, 1993)

Basic Concept of Nursing Care Plan for Stroke

Assessment is an early stage and the foundation of the nursing process to identify client problems, in order to give direction to nursing actions. Assessment phase consists of three activities: data collection, data classification and formulation of nursing diagnoses. (Lismidar, 1990)

Data Collection

Data collection is to collect information about the overall health status of the client's physical, psychological, social, cultural, spiritual, cognitive, developmental level, economic status, ability to function and lifestyle of patients. (Marilynn E. Doenges et al, 1998)

a) The identity of the client
Includes name, age (most often in old age), sex, education, address, occupation, religion, ethnicity, date and time of hospital admission, registration number, medical diagnosis.
b) The main complaint
Limb weakness typically found next to the body, speech pelo, and can not communicate. (Jusuf Misbach, 1999)
c) History of present illness
Hemorrhagic stroke often take place very suddenly, when the client is doing the activity. Usually occurs headache, nausea, vomiting and even seizures to unconsciousness, paralysis symptoms besides half body or other brain dysfunction. (Siti Rochani, 2000)
d) History of previous illness
A history of hypertension, diabetes mellitus, heart disease, anemia, history of head trauma, a long oral contraceptives, use of anti-coagulant drugs, aspirin, vasodilators, addictive drugs, obesity. (Donna D. Ignativicius, 1995)
e) A family history of disease
There is usually a family history of hypertension or diabetes mellitus. (Hendro Susilo, 2000)
f) Psychosocial History
Stroke is a disease that is very expensive. The cost for testing, treatment and care of the family finances that can disrupt these cost factors can affect the stability of the emotions and thoughts of clients and families.


The Patterns of Health Functions

1) Pattern perception of healthy living and governance
There is usually a history of smoking, alcohol use, use of oral contraceptives.
2) The pattern of nutrition and metabolism
Complaints difficulty swallowing, loss of appetite, nausea and vomiting in the acute phase.
3) The pattern of elimination
It usually occurs in the urinary incontinence and bowel habit constipation usually occurs due to decreased intestinal peristalsis.
4) The pattern of activity and exercise
There is the difficulty of the move as weakness, sensory loss or paralise / hemiplegia, tiredness.
5) The pattern of sleep and rest
Usually clients are having difficulties to rest because of muscle spasms / muscle pain.
6) The pattern of relationships and roles
A change in the relationship and role as client has difficulty communicating due to impaired speech.
7) The pattern of perception and self-concept
Clients feel helpless, hopeless, irritable, uncooperative.
8) The pattern of sensory and cognitive
At the client's pattern of sensory impaired vision / blurring sight, touch / touch down on the face and extremity pain. On the pattern of cognitive decline typically memory and thought processes.
9) Patterns of sexual reproduction
It usually occurs due to decreased sexual desire of some of the treatment of stroke, such as anti-seizure drugs, anti-hypertensive, histamine antagonists.
10) The pattern of response to stress
Clients often find it difficult to solve due to the disruption of thinking and difficulty communicating.
11) The pattern of values ​​and beliefs
Clients rarely practicing because of unstable behavior, weakness / paralysis on one side of the body.

Hyperparathyroidism Definition, Etiology, Pathophysiology and Clinical Manifestations

Definition of Hyperparathyroidism

Hyperparathyroidism is excessive production of parathyroid hormone by the parathyroid glands, characterized by decalcification of bone and the formation of kidney stones, which contain calcium. Hyperparathyroidism is divided into two, namely primary and secondary hyperparathyroidism. Primary hyperparathyroidism occurs two or three times more often in women than men and in patients aged 60-70 years. While secondary hyperparathyroidism with manifestations similar to patients with chronic renal failure. Renal rickets, caused by retention of phosphorus will increase the stimulation of the parathyroid glands and increased secretion of parathyroid hormone. (Brunner & Suddath, 2001)

Hyperparathyroidism is a character of a disease caused by excess secretion of parathyroid hormone, amino acid polypeptide hormone. Secretion of parathyroid hormone is directly regulated by the concentration of calcium ion fluid. The major effect of parathyroid hormone is increased by increasing the concentration of liquid calcium and phosphate calcium release from bone matrix, increases the absorption of calcium by the kidneys, and the kidneys to increase production. Parathyroid hormone also causes phosphaturia, if dehydrated phosphate. Hyperparathyroidism is usually divided into primary, secondary and tertiary. (Lawrence Kim, MD, 2005, section 2).

Etiology of Hyperparathyroidism

According to Lawrence Kim, MD. 2005, the etiology of hyperparathyroidism are:

1. Approximately 85% of cases of primary hyperparathyroidism caused by single adenoma.
2. While the other 15% involves various glands (eg various adenoma or hyperplasia). Usually hereditary and frequency associated with other endocrine disorders.
3. Few cases of primary hyperparathyroidism caused by parathyroid carcinoma. Etiology of adenoma and hyperplasia in most cases unknown. Family cases can occur either as part of various endocrine neoplasia syndrome, hyperparathyroidism tumor syndrome, or hyperparathyroidism derivatives. Familial hypercalcemia and hypocalcuric and neonatal severe hyperparathyroidism are also included into this category.
4. Some surgeons and pathologist reported that enlargement of the gland adenoma types are generally multiple doubles. In about 15% of patients with hyper-function of all glands; chief cell parathyroid hyperplasia.

Pathophysiology of Hyperparathyroidism

Hyperparathyroidism can be primary (ie caused by hyperplasia or parathyroid neoplasm) or secondary, where cases are usually associated with chronic renal failure.

In 80% of cases of primary hyperparathyroidism caused by parathyroid adenomas are benign; 18% of cases caused by hyperplasia of the parathyroid glands: and 2% of cases are caused by parathyroid carcinoma (damjanov, 1996). Normally there are four parathyroid glands. Parathyroid adenoma or carcinoma is characterized by enlargement of the gland, with the other glands remained normal. In parathyroid hyperplasia, four enlarged glands. Because the diagnosis of adenoma or hyperplasia can not be enforced preoperative, so it is important for the surgeon to examine the four gland.

If one identified an enlarged adenomatous gland, the gland is usually removed and others left intact. If it is an enlarged lymph fourth surgeon will lift the third and leave one lymph gland that should be sufficient to maintain the homeostasis of calcium-phosphate.

Secondary parathyroid hyperplasia can be distinguished from primary hyperplasia, because the four symmetrically enlarged glands. Enlarged parathyroid glands and hiperfungsi are compensatory mechanisms that are triggered by the retention of the format and hypercalcemia associated with chronic kidney disease. Osteomalacia caused by hipovitaminosis D, as in rickets, can lead to the same effect.

Hyperparathyroidism is characterized by excess PTH in the circulation. PTH mainly working on bone and kidney. In bone, PTH increases calcium resorption from the renal tubules Limen. Thereby reducing the excretion of calcium in urine. PTH also increases the active form of vitamin D3 in the kidneys, which in turn facilitates the uptake of calcium from food in the intestines. Hypercalcemia and hypophosphatemia thus compensatory, is abnormlitas biochemical detected through blood analysis. Serum PTH concentrations also increased. (Rumahorbor, Hotma, 1999)

Excess production of parathyroid hormone is accompanied by kidney failure can cause a wide range of bone disease, which often occurs tulng is osteitis fibrosa cystica, a disease of increased bone resorption due to increased levels of parathyroid hormone. Other bone diseases are also common in these patients, but did not appear in person. (Lawrence Kim, MD, 2005, section 5)

Excess amounts of PTH secretion causes hypercalcemia can cause direct effects on receptors in bone, intestinal tract, and kidneys. Physiologically PTH secretion is inhibited by high serum calcium ions. The mechanism is not active in the state of adenomas, or gland hyperplasia, hypersecretion of PTH which coincides with hypercalcemia. Reabsorption of calcium from bone and increased absorption from the gut is a direct effect of the increase in PTH.

At the time of serum calcium levels approaching 12 mg / dL, renal tubular reabsorption of calcium causing excessive hypercalciuria circumstances. This can increase the incidence nefrolithiasis, which raises can decreased creatinine clearance and renal failure. Elevated levels of extracellular calcium can be deposited on soft tissue. The pain arises due to calcified nodules form on the skin, subcutaneous tissues, tendons (calcific tendonitis), and cartilage (chondrocalcinosis). Vitamin D plays an important role in calcium metabolism by PTH causes needed to work in the target organ.

Clinical Manifestations of Hyperparathyroidism

Patients may not be, or have signs and symptoms due to the disruption of multiple organ systems. Symptoms of apathy, fatigue complaints, muscle weakness, nausea, vomiting, constipation, hypertension, and cardiac arrhythmias may occur: all this is related to elevated levels of calcium in the blood. Psychological manifestations may range from irritability and emotional state of neurosis to psychosis caused by the direct effect of calcium on the brain and nervous system. Increased calcium levels will decrease the potential excitation of nerve and muscle tissue.

Stone formation in one or both kidneys associated with increased excretion of calcium and phosphorus is one of the complications of primary hyperparathyroidism. Kidney damage caused by precipitation of calcium phosphate in the pelvis, and renal parenchyma resulting in kidney stones (renal calculi), obstruction, pyelonephritis and renal failure.

Musculoskeletal symptoms accompanying hyperparathyroidism may occur due to demineralization of bone or bone tumors, which appears in the form of benign giant cells due to excessive osteoclast growth. Patients may experience skeletal pain and tenderness, especially in the back and joints; pain when supporting the body; pathologic fractures; deformity, and shortening of the body. Bone loss associated with hyperparathyroidism is a risk factor for fracture.

The incidence of peptic ulcer and prankreatitis increased in hyperparathyroidism and can cause symptoms gastroitestinal. (Brunner & Suddath, 2001)

Anatomy and Physiology of Parathyroid Gland

Anatomy of the Parathyroid Gland

Parathyroid glands grown from endoderm tissue, ie, the third and fourth pharyngeus sulcus. Parathyroid glands from four pharyngeus sulcus tend to unite with the upper pole of the thyroid gland, parathyroid glands that form the cranial. Glands from third pharyngeus sulcus is part of caudal parathyroid glands, which are sometimes fused with the lower pole of thyroid. However, the position is often highly variable. Caudal portion of the parathyroid glands can be found in the posterolateral lower pole of the thyroid gland, or in the thymus, even in the mediastinum. Parathyroid glands sometimes found in the thyroid gland parenchyma. (R. Sjamsuhidajat, Wim de Jong, 2004, 695)

Normally there are four parathyroid glands in humans, which is located just behind the thyroid gland, two embedded in the superior pole of the thyroid gland and two in the inferior pole. However, the location of each of the parathyroid and the numbers can be quite varied, parathyroid tissue is sometimes found in the mediastinum.

Each of the parathyroid glands are approximately 6 millimeters, 3 millimeters wide and two millimeters thick and has a blackish brown fat macroscopic picture. Parathyroid gland contains mainly the adult primary cells (chief cells) containing Golgi apparatus striking plus the endoplasmic reticulum and secretory granules that synthesize and secrete parathyroid hormone (PTH). Tues oksifil fewer but larger granules containing oksifil and a large number of mitochondria in the cytoplasm In humans, before puberty is only rarely found, and after that the number of these cells increases with age, but the majority of young animals and humans, the cell is not found oksifil . Oksifil cell function is still unclear, these cells may be modified or the rest of the main cells that no longer secrete various hormones.

Physiology of the Parathyroid Gland

Parathyroid glands secrete parathyroid hormone (PTH), which together with Vitamin D3, and calcitonin regulate calcium levels in the blood. PTH synthesis is controlled by the plasma calcium levels, which inhibited the synthesis when high calcium levels and stimulated when calcium levels are low. PTH stimulates renal tubular reabsorption of calcium, increases the absorption of calcium in the small intestine, whereas inhibiting reabsorption of phosphate and calcium release from bone. So PTH will actively work on three major target point within the control of calcium homeostasis in the kidney, bone and intestine. (R. Sjamsuhidayat, Wim de Jong, 2004, 695)