DrQitta

Jumat, 07 September 2018

Fungsi 12 Syaraf kranialis

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Fungsi 12 Syaraf kranialis 


⦁    Syaraf olfaktorius (N.I) untuk penciuman, tipe sensori asal olfactory bulbi. pemeriksaaan yang dianjurkan klien menutup mata dan uji satu persatu hidung klien kemudian anjurkan untuk mengidentifikasi perbedaan bau-bauan yang dibeikan (kopi atau teh)
⦁    Syaraf Optikus (N.II) untuk penglihatan, tipe sensori asal otak tengah. pemeriksaan yang dianjurkan dengan menggunakan snellen cart pada jarak 5-6 meter dan pemeriksaan luas lapang pandang dengan menjalankan sebuah benda dari samping ke depan (kanan kiri dan atas bawah)
⦁    Syaraf okulomotorius (N.III) syaraf yang berfungsi untuk pergerakan mata melalui otot medial dan lateral, tipe motor keotot mata parasimpatic motor, asal otak tengah. pemeriksaan yang dianjurkan tatap mata klien dan anjurkan klien menggerakkan mata dari dalam ke luar, dangan menggunakan lampu senter uji reaksi pupil dengan memberikan rangsangan sinar kedalamnya
⦁    Syaraf troklearis (N.IV) syaraf yang berfungsi sebagai penggerak bola mata melalui otot obliq superior, tipe motor asal otak tengah bagian bawah. pemeriksaan yang dianjurkan klien melihat kebawah dan kesamping kekanan-kiri dengan menggerakkan tangan pemeriksa
⦁    Syaraf trigeminalis (N.V) saraf yang berfungsi sebagai sensasi kulit wajah, kulit kepala membrane mukosa mulut dan hidung, mengunyah tipe sensori dan motor asal pons. syaraf ini merupakan bagian dari cabang optalmikus pemeriksaan yang dianjurkan menggunakan kapas halus sentuh pada kornea klien perhatikan refleks berkedip klien, cabang dari maksilaris menggunakan sentuhan pada waja klien uji kepekaan lidah gigi. cabang mandibularis anjurkan klien menggerakan rahang atau menggigit
⦁    Syaraf Abdusens (N.VI) syaraf yang berfungsi sebagai penggerak bola mata kesamping melalui otot rectus lateralis. tipe motor, asal pons inferior. pemeriksaan yang dianjurkan klien diminta untuk melirik kanan dan kiri
⦁    Syaraf fasialis (N.VII) Syraf yang berfugsi motor otot wajah dan kulit kepala, sensori nyeri dan suhu di area tenlinga, sensasi muka, rasa dari 2/3 bagian lidah, parasimpatis motor lakrimal, submadibula dan subligual kelenjar saliva. area pons inferior pemeriksaan yang dianjurkan klien menutup mata kemudian tempatkan garam/gula ujung dan sisi lidah anjurkan klien mengidentifikasi rasa resebut
⦁    Syaraf Vestibulokoklear (N.VIII) Syaraf yang berfungsi sebagai pendengaran dan keseimbangan, tipe sensori, asal pons medulla junction. pemeriksaan yang dianjurkan tes rine weber dan bisikan, tes keseimbangan dengan klien berdiri menutup mata
⦁    Syaraf Glosofaringeus (N.IX) Syaraf yang berfungsi sensori nyeri dan suhu dari area telinga, rasa dan sensasi dari 1/3 anterior lidah dan faring, motor .. otot skelet kerongkongan (menelan), parasimpatik .., kelenjar thyroid. Asal medulla, pemeriksaan yang dianjurkan pengecapan lidah meringis mengembungkan mulut, bersiul
⦁    Syaraf Vagus (N.X) Syaraf yang berfung
⦁    Syaraf asesorius (N.XII) Syaraf yang berfungsi sebagai otot skeletal faring, laring dan stemokleidomastoideus dan otot trapesius. tipe motor, asal medulla .., pemeriksaan yang dianjurkan klien menggerakan kepala dan bahu
⦁    Syaraf Hipoglosus (N.XII) Syaraf yang berfungsi sebagai otot skelet lidah, tipe .., motor, asal medulla pemeriksaan yang dianjurkan julurkan lidah, artikulasi, sikap lidah tremor/mioklonus, kekuatan lidah.
si sebagai sensori nyeri dan suhu dari area telinga, sensasi dari faring, laring viscera torak dan abdomen, motor.., otot platinum moel, laring dan faring, parasimpatik motor.., vicera thorak dan abdomen, set dari kelenjar sektor, jantung dan inerveasi otot halus. asal medulla pemeriksaan N.IX

Jumat, 31 Agustus 2018

Wilson's Disease

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Wilson's Disease
Wilson's disease is a genetic disorder in which copper builds up in the body, mainly in the liver and brain. Without any treatment, the build-up of copper can cause serious symptoms. Treatment is with medication to remove the excess copper and/or to prevent a further build-up of copper.

What is Wilson's disease?

Wilson's disease is a condition where too much copper builds up in the body. It is a rare inherited disorder that affects about 1 in 30,000 people. It is named after Dr Samuel Wilson who first described the disorder in 1912.
If you inherit the genetic fault in Wilson's disease, your body is not able to get rid of copper. Copper is a trace metal which is in many foods. You need tiny amounts of copper to remain healthy. Normally, the body gets rid of any excess copper. People with Wilson's disease cannot get rid of excess copper and so it builds up in the body, mainly in the liver, the brain, the layer at the front of the eye (called the cornea) and the kidneys.
Too much copper in the liver cells (the hepatocytes) is harmful and leads to liver damage. Damage to brain tissue mainly occurs in an area called the lenticular nucleus. Hence, Wilson's disease is sometimes also called hepatolenticular degeneration.

What causes Wilson's disease?
In Wilson's disease, a particular gene on chromosome 13 does not work. The gene is called ATP7B. This gene normally controls the way the liver cells get rid of excess copper. Normally, the liver cells pass out excess copper into the bile. If this process does not work then the copper builds up in liver cells. When the copper storage capacity of the liver cells is exhausted, the copper spills into the bloodstream and deposits in other parts of the body, mainly the brain.

How is Wilson's disease inherited
Wilson's disease is an autosomal recessive disorder. This means that, in order to develop Wilson's disease, you need to inherit two abnormal ATP7B genes - one from your mother and one from your father.
If you inherit only one abnormal gene, you are called a carrier. Carriers do not have the disorder, as they have one normal gene which is enough to control the function of copper in the body. However, carriers can pass the abnormal gene on to their children. About 1 in 100 people are carriers of the ATP7B gene. When two people who carry the abnormal gene have a child, there is a:
⦁    1 in 4 chance that the child will have Wilson's disease (by inheriting the abnormal ATP7B gene from both parents).
⦁    2 in 4 chance that the child will not have Wilson's disease, but will be a carrier (by inheriting the abnormal ATP7B gene from one parent but the normal gene form the other parent).
⦁    1 in 4 chance that the child will not have Wilson's disease, and will not be a carrier (by inheriting the normal gene from both parents).
What are the symptoms and problems of Wilson's disease?
Although the genetic defect is present at birth, it takes years for copper to build up to the level where it is damaging. Symptoms typically start to develop between the ages of 6 and 20, most commonly in the teenage years. However, you can first develop symptoms in middle age.
Liver problems
Symptoms of liver problems often develop first. The toxic effect on the liver cells can cause inflammation of the liver (hepatitis) which may cause:
⦁    Yellowing of the skin and the whites of the eyes (jaundice).
⦁    Tummy (abdominal) pain.
⦁    Episodes of being sick (vomiting).
If left untreated, damage to liver cells causes scarring of the liver (cirrhosis). Eventually, severe cirrhosis and liver failure develop in untreated cases, causing severe problems.

Brain problems
As copper deposits in the brain it can cause various symptoms:
Physical symptoms
⦁    An odd type of tremor in the arms.
⦁    Slowness of movement.
⦁    Difficulty with speech.
⦁    Writing problems.
⦁    Difficulty swallowing.
⦁    An unsteady walk.
⦁    Headaches.
⦁    Fits (seizures).
Psychological symptoms
⦁    Depression.
⦁    Mood swings
⦁    Inability to concentrate.
⦁    Very argumentative and emotional behaviour in affected people, who may seem to have changed in personality.
Severe problems
If left untreated, the accumulation of copper in the brain can lead to:
⦁    Severe muscular weakness.
⦁    Severe rigidity.
⦁    Dementia.

Other problems
Copper may build up in the layer at the front of the eye (called the cornea). This causes a characteristic feature called Kayser-Fleischer rings - a brownish pigmentation of the cornea.
Other features that may develop include:
⦁    Anaemia.
⦁    Kidney damage.
⦁    Heart problems.
⦁    Inflammation of the pancreas (pancreatitis).
⦁    Menstrual problems.
⦁    Repeated miscarriage in women.
⦁    Premature 'thinning' of the bones (osteoporosis).

How is Wilson's disease diagnosed
If Wilson's disease is suspected, it can be diagnosed by various tests:
A blood test to measure caeruloplasmin. This is a protein that binds copper in the bloodstream. The level is low in nearly all people with Wilson's disease.
⦁    Other blood tests may also be performed. These may be done to measure your copper levels and to test your kidney and liver function.
A urine test to measure the amount of copper in the urine. This is usually tested on all the urine you produce over a 24-hour period. The amount is typically higher than normal.
⦁    An examination of the layer at the front of the eye (called the cornea) by an optician (optometrist) or an eye specialist may show the Kayser-Fleischer rings if they have developed. (They are not present in all cases.)
⦁    A small sample (biopsy) of the liver may be taken to look at under the microscope. This can show the excess copper in the liver and the extent of any scarring of the liver (cirrhosis). See separate leaflet called ⦁    Liver Biopsy for more details.
⦁    Your specialist may also request other tests -
 for example, an ⦁    MRI scan of your brain and your kidneys.

If Wilson's disease is confirmed then your brothers and sisters should be checked to see if they have the condition. Brothers and sisters of a person with Wilson's disease have a 1 in 4 chance of also having the condition.

How is Wilson's disease treated
It is essential to treat Wilson's disease. The earlier treatment is started, the better the chance of preventing long-term permanent damage to the liver or brain.
Penicillamine is a medicine used to remove copper from the body (it is called a chelating agent). The penicillamine causes the excess copper from the body to be passed out in the urine. The dose may be reduced to a maintenance dose after about a year when the initial build-up of copper has been cleared.
Trientine is an alternative to penicillamine. It too is a chelating agent and removes copper from the body.
Zinc is an option in certain circumstances. Zinc works by blocking the gut from absorbing copper from food. Therefore, it does not clear excess copper from the body, but prevents any further build-up of copper. Zinc is much less likely than penicillamine or trientine to cause side-effects. It may be an option for people who are diagnosed at the very early stages of the disease and have no symptoms. Also, a switch to zinc may be an option for people who have been initially treated with penicillamine or trientine once the initial build-up of copper has been cleared from the body. Zinc may also be taken if you are pregnant.
Note: you need treatment for life. First, to clear the excess copper, and then to prevent future accumulation of copper. Failure to take medication can lead to a return to a build-up of copper, which can be serious - even fatal.
For the few people who do not respond to treatment with medication, or are diagnosed in the late stage of the disease with severe scarring of the liver (cirrhosis) or liver failure, a liver transplant may be an option. This can be life-saving. The long-term outlook after a liver transplant is usually very good.

Diet
Foods with a high concentration of copper generally should be avoided, at least in the first year of treatment when the excess copper is being cleared from the body. These include liver, chocolate, nuts, mushrooms and shellfish, especially lobster.

What is the outlook (prognosis)?
⦁    If treatment is begun in the early stages of the disease, it usually works very well. You can expect  a normal length and quality of life.
⦁    However, without any treatment, Wilson's disease is usually fatal - typically, before the age of 40.
⦁    If symptoms have developed before treatment has started, some of the symptoms improve with treatment, but some may remain permanently. For example, some of the brain symptoms are permanent once they develop. Your specialist will be able advise about which symptoms may go and which may be permanent, once treatment begins.

Brain Cancer and Brain tumor

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Brain Cancer and Brain tumor
The treatment and outlook vary greatly depending on factors such as type of tumor and the location in the brainThe main parts of the brain include:
1.    The cerebrum : this is divided into the right side (right hemisphere) which controls the left side of the body, and the left hemisphere which controls the righr side of the body. Each hemisphere is divided into various sub-selecetion, the main divisions being the frontal lobe, tempolar lobe, parietal lobe and occipital lobe. the cerebrum is also where you think and store your memory
2.    The cerebllum : This lies behind and below the cerebrum. one of its main functions is to help control balance and co-ordination.
3.    The Brainstem : This helps to control basic bodily function such as the heartbeat, breading and blood pressure. nerves from the cerebrum also pass through the brainstem to spinal cord
4.    The meninges : These are thin layers of tissue which separete the skull from the brain. The outer layer to the skull is called the dura. the next layer is called the arachnoid. under the arachnoid tissue is the cerebrospinal fluid (CSF) which bathes the brain and spinal cord
5.    The pituitary gland. this releases various hormones into the bloodstream
    The main type of cell in the brain is called a neuron, there are millions of neurons in the brain. neurons have long thin nerve fibres which enable them to send massages to other parts of the brain and down the spinal cord to all parts of the body, the brain also contains glial cells. there are various type of glial cell, including astrocytes, oligodendrocytes and ependymal cell.

What is cancer ?
Cancer is disease of the cell in the body.the body is made up from milions of tiny cell. there are many deferent type of cell in the body and there are many deferent type of cancer have in common is that the cancer cell are abnomal multiply out of control.
Non- cancerous (benign) tumours may form in various parts of the body. benign tumors grow slowly and do not spread or invade into other tissues.there are not usually life-threatening. they often do no harm if they are left alone. however, some beningn tumours can caouse probloms. for example, some grow quite large and may cause local pressure symptoms (especially in the brain). also, some benign tumours which arise from cells in hormone glands (see piutary tumours, below) can make too much hormone which can cause anwanted effects.
A cancerous (malingnant) tumour is a lump or growth or tissue made up from cancer cells which continue to multiply. malignant tumours invade into nearby tissues and organs, which can cause damage. malignant tumours may also spread to other part of the body. this happens if some cells break off from the first (primary) tumours and are carried in the bloodstream or lymp channels to other parts of the body. these small groups of cell may then multiply to from secondary tumours (metastases) in one or more parts of the body. these secondary tumours may then grow, invade and damage nearby tissues and spread again.
Some cancers are more serious than other; some are more easily treated than other (particularly if diagnosed at an early stage); some have a better outlook (prognosis) than other . so cancer is not just one condition. in each case it is important to know exctly what type of cancer has developed, how large it has become, and whether it has spread. this will enable you to obtain reliable information on treatment options and outlook.

Primary of secondary tumours
The original site where a tumour first develops is called a primary tumor. cancerous (malignant) tumours may also spread to other parts of the body to from secondary tumours (metastases). these secondary tumours may the grow, invade and damage nearby tissues and spread again
Primary malignat brain tumours
A primary malignant brain tumour is a cancer which arieses from a cell within the brain. the cells of the tumour grow into and damage normal brain tissue, also, like non-cancerous (benign) brain tumours, they can increase the preasure inside the skull. However, unlike most other type of malignant tumours. primary brain tumours rarely spread (metastasise) to other parts of the body
There are various types of primary malignant brain tumour. the deferent types develop from diferent type of cell in the brain. As a general guide, each type is graded on a scale of 1-4 grade 1 and 2 tumours are said to be low grade and the grade 3 and 4 high -grade. the higher the grade, the more aggressive the tumour tends to be and faster it tends to grow. the treatment options and outlook (prognosis) very depending on the type and grade of the tumour

Secondary malignant brain tumours
A secondary malignant brain tumour means that a cancer which started in another part of the body has spand to the brain. many types of cancer can spread to the brain. the most common type that do this are cancers of the breast, lung, bowel, kidney, and skin (melanoma)
Defferent type of brain tumours
there are many type  of non cancerous (benign) brain tumours and primary cancerous (malignant) brain tumours. many are very rare. the following is brief description of the most common type
Meningioma
meningiomas are usually benign. they grow from cell in the tissues that surround the brain (the maninges)
Medulloblastoma
these are high-grade malignant tumours that grow in the cerebellum. they are uncommon in adults but are one of two most common brain tumours in children, there often astrocytoma in cerebellum
Gliomas
these are malignant primary brain tumours that arise of glial cells, there are various types, depending on the cell of origin- for example:
⦁    Astrocytomas (originating from astrocyte cells) there are various type of astrocytoma thery include : Astrocytomas is low grade, anaplastic astrocytoma this is a high- grade tumours and glioblastoma multiforme this is a high-grade tumour which tends to grow quickly. it is most common type of primary malignant brain tumours in adults.
⦁    Oligodenrogliomas : (originating from oligodendrocytes). these can vary in there grade
⦁    Ependymoma : (originating from ependymal cells). these are rare, but are usually low-grade

Primitive neuroectodermal tumours ( PNETs)
These are very similiar or medulloblastomas and mainly occur in children
Pituitary tumours
There are various type of tumours which arise from the diffrent cells in the pituitary gland. they tend to be benign whoever, the cell of the tumours may produce large quantities of hormones which can cause various symptoms, as they grow, they may also cause pressure symptoms, the nerves of sight (optic nerves) are near to pituitary and so a growing pituitary gland tumour may press on optic nerve and effect vision
Acoustic neuroma (schwannoma)
this is a benign tumour which aries from schwann cells which cover the nerve that goes to the ear. symptoms can include deafness on the affected side and dizziness with a spinning sensation (Vertigo)
What causes brain tumours
the cause of most non cancerous (benign) brain tumours and primary cancerous (malignant) brain tumours is not know
Genetic factor may a be a risk from some people-perhaps in about 1 in 20 cases. for example, people with the hereditary diseseases called neurofribromatosis type 1, turcot's syndrome, Li- fraumeni cancer syndrome, and tuberous slerosis have a higher-than-average risk of developing a glioma. then people with these diseases develop a glioma it trends occur in chidhood or early adult life. however, these cases are only small proportion of all glioma tumours.
How common are brain tumours
non-cancerous (benign) brain tumours and cancerous (malignant) primary brain tumours are uncommon. Overall they occur in about 12 in 100,00, people each year
the most common type in adults are benign meningioma and a glioma called glioblastoma multiforme. some type are very rare
Brain tumours can occur at any age. some type (such as medullablastoma) are more common in children and some are more common in adults. generally, the tummour that tend to occur in adults become more common with increasing age
secondary (metastatic) brain tumours are more common than benign brain tumours and malignant primary brain tumours

What are the symptoms of brain tumour
General symptoms
Early symptoms may include headaches and feeling sick. these are due to increased pressure within the skull (raised intracranial preassure). these symptoms may come and go first and tend to be worse in the morning. coughing. sneezing and stooping may make the headaches worse. epileptic seizures (convulsions) sometimes occour. increasing drowsiness may occur as tumour enlarges
Symptoms due to location in the brain
As a tumour grows it can damage the nearby brain tissue. The fungtions of the defferent parts of the body are controlled by defferent parts  of the brain. therefore, symptoms vary from case to case, depending on which part of the brain is affacted and on the size of affacted area. for example one or more of the following may develop:
⦁    Weakness of muscles in arm, leg , part of face or eyes
⦁    problems with balance, co-ordination, vision, hearing, speech, communication or swallowong
⦁    loss of smell
⦁    Dizziness or unsteadiness
⦁    Numbness or weakness in a part of the body
⦁    confution
⦁    personality changes
⦁    symptoms related to hormonal changes if you have pituitary tumour

How are brain tumours diagnosed and assessed
A doctor will examine you if a brain tumour is suspected from the symptoms. this will include checking on the functions of the brain and nerves (movemonts, reflexes, vision, etc)
An MRI scan or CT scan of the head is the common test done to confirm or rude out the presense of a brain tumour. see separate leaflets called MRI Scan and CT scan for more details. if a tumour is identifed, further more detailed scan and tests may be done. for example, a PET scan or a cerebral angiogram are sometimes done to obtain more information about tumour
A small tissue sample (a biopsi) may be needed to be sure of the type of tumour. the sample is than examined under the microscope to look for abnormal cells. to obtain a biopsy from a brain tumor you need to have a small operation, usually done under anasthetic. small hole is bored in the skull to allow a fine needle though to obtain a small type of tumour can be identified. if it cancerous (malignant), the tumour grade can be determined (see above)
Blood test and other tests on other parts of the body may be done if the tumour is thought to be a secondary (metastatic) tumour. for example, it is quite common for a  lung cancer to spread to the brain. therefore a chest X- ray may be done if this is dupected. various hormone tests may be done if a pituitary tumour is suspencted

What are the treatmants for the brain tumours
The main treatment used for brain tumours are surgery, chemotherapy, radiotherapy and medication to control symptoms such as seizues. the treatment or combination of treatments advised in each case depends on various factor, for example:
⦁    The type of brain tumour
⦁    The grede of the tumour if it is cancerous (malignant)
⦁    The exact site of the tumour
⦁    Your general health
Surgery
Surgery is often the main treatment for non- cancerous (benign) brain tumours is primary and primary cancerous (malignant) tumours. the aim of surgery is to remove (or even of the tumours) whilst doing as little damage as possible to the normal brain tissue. Your specialist will advase on whether surgery is possible option

Radiotherapy
Radiotherapy is a treatment which uses high- enery beams of radiation which are focused on cancerous tissue. this kills cancers cells or stops cancer cells from multiplying.
Radiotherapy is sometimes used insted of surgery when an operation is not possible for a malignant brain tumour. sometimes it is used in addition to surgery it is possible to remove all the tumour with surgery or to kill cancerous cell which may be left behind following surgery

Chemotherapy
chemotherapy is a treatment which uses anti- cancer medicines to kill cancer cell, or to stop them from multiplying. it may be used in addition or other treatments such as surgery or radiotherapy; again, depending on various factor such as the type of tumours

Medication to control symptoms
if you have sizeures by the tumour then anticonvulsant mediation will usually control be sizeures. painkillers may be need to ease any beadaches steroid medication is also commonly used to reduce inflamation around a brain tumour. this reduces the pressure inside the skull, which helps to ease headaches and other pressure symptoms
you should have a full discussion with specialist who you know case the will ba able to give the pros an cons, likely success rate, possible side-effects and other details about possible treatment option for your type of brain tumour

What is the outlook
it is difficult to give an overall outlook. every case is different, for example if you have a non- cancerous (benign) maningoma which is in a suitable place for surgery, the outlook is excellent
for primary cancerous (malignant) brain tumours, the outlook above is very general. the specialist who know your case can give more accurate information about your particular outlook and how well your type and stage of cancer is likely to respond to treatment.


Kamis, 23 Agustus 2018

EKG

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E.K.G
Siklus jantung normal
Laju normal : 60-100 kali/menit
P-R Normal: 0,12-0,20 detik
QRS Normal : 0,08 -0,12 detik
Gelombang P (depolarisasi atrium), QR
S (depolarisasi ventrikel), gelombang T (repolarisasi ventrikel)

Menganalisis EKG
⦁    Tentukan laju secara keseluruhan: < 60 kali/menit (bradikardi) , >100 kali/menit (takikardia)
⦁    tentukan regularisasi ( reguler/ireguler) jika ireguler apa terdapat pola tertentu?
⦁    Pemeriksaan gelombang P
i.    apakah terdapat gelombang P sebelum setiap QRS, apakah gelombang P ada atau lebih dari satu menandakan adanya gangguan
ii.    Bagaimana konfigurasi gelombang P, apakah melingkar atau seperti gergaji
iii.    apakah semuanya terlihat sama?
iv.    apakah terdapat gelombang P yang berada di dalam kompleks QRS atau gelombang T
⦁    Tentukan Interval PR
i.    apakah normal, memanjang atau memendek?
ii.    apakah dapat dihitung
iii.    apakah sama setiap denyut? adakah pola tertentu?
⦁    Pemeriksaan Kompleks QRS
i.    Apakah terdapat QRS setelah gelombang P
ii.    Apakah terlihat sama
iii.    apakah timbul lebih awal dari yang diharapkan
iv.    apakah terdapat pola tertentu pada kompleks QRS yang terjadi lebih awal

Macam macam kelainan irama jantung dan penanganannya:

1.    Takikardia supraventikuler (SVT)
⦁        laju: 150-250 kali per menit
⦁    irama: biasanya reguler
⦁    interval PR : tidak dapat ditentukan
⦁    gelombang P : biasanya tertutup gelombang T
⦁    QRS : 0,60 -0, 10 detik, > 0,10 jika dihantarkan melalui ventrikel
⦁    penyebab: nikotin, stress, ansietas, kafein
⦁    penaganan:  Manuver vagal, adenosine ( adenocard, adenoscan), amiodarone (cordarone, pacerone), diltiazem (cardizem), kardioversi, prooafenone (rythmol), flecainide (tambocor)

2. Atrial flutter
Nodus AV menghantarkan impuls ke ventrikel dengan berbagai derajat blok (2:1-2  gelombang flutter :1 QRS : 4:1- 4 gelombang flutter:1 QRS); hilangnya kontraksi atrium terlihat pada penyakit arteri koroner dan penyakit katup
⦁    laju atrial: 250-400 kalo permenit
⦁    interval PR: tidak dapat diterntukan
⦁    irama: reguler atau iregulernya tergantung derajat blok
⦁    gelombang P: gelombang seperti gergaji
⦁    laju ventrikel: lambat atau cepat tergantung derajat blok
⦁    QRS : Normal atau sempit
⦁    penanganan: Diltiazem; sotalol, propranolol, atau beta bloker, digoxin, amiodarone, propafenone, flecainide, magnesium,kardioversi listrik, ablasi radiofrekuensi; anti koagulan.

 3. Fibrasi atrial
Atrium melakukan gerakan bukan berkontraksi, tidak adanya kontraksi atrium, trombus mural dapat menyebabkan embolisme pulmural atau stroke. gejalanya seperti fatig, malaise, nadi meningkat dan penigkatan iskemia miokard
⦁    laju atrial: 400-600 kali/menit
⦁    interval PR : tidak dapat ditemukan
⦁    irama: ireguler
⦁    Gelombang P: tidak ada, glombang fibrilaturius
⦁    laju ventrikel: normal atau cepat
⦁    QRS : biasanya sempit
⦁    Penaganan : sama sepeti atrial flutter, ibutilide setelah kardioversi antikoagulan

4. Kontraksi ventrikel Premature (PVC)
Dapat uniform (satu fokus ektopik atau unifokali) atau fokus berbeda (multifokali) , klien dapat mengeluh rasa melayang, palpitasi, denyut jantung menghilang
⦁    Gelombang P : tidak ada sebelum PVC
⦁    Irama : ireguler ketika terjadi PVC
⦁    QRS : lebarm aneh, 0, 10 detik; dapat diikuti oleh pause kompensasi
⦁    penyebab : kafein, nikotin, stres, iskemia, toksisitas digoxin, ketidakseimbangan elektrolit, hipovolemia, demam, hipokalemia, hipoksia, hipermagnesemia, ketidakseimbagan asam basa
⦁    tata laksana : amiodarone, lidocaine

5. Takikardia ventikular (VT)
terdapat tiga atau lebih PVC yang terjadi bersamaan dengan bentuk dan amplitudo/ jarak yang sama . irama tidak stabil, mudah bekembang menjadi VF jika VT menetap dan tidak diobati pasien tidak memiliki denyut nadi , TD tidak terukur
⦁    Laju atrial : tidak dapat ditentukan, tidak ada gelombang P; tidak ada interval PR
⦁    laju ventikuler : > 100-250 kali permenit
⦁    irama : biasanya reguler
⦁    QRS : lebar dan aneh , >0.10 detik
⦁    penanganan : amiodarone, procainamide, lidocaine, satolol, kardioversi, sinkronisasi segera : VT tanpa denyut sama seperti VF

6. Fibrasi ventikular (VF)
Pola berantakan , tidak ada kontraksi yang efektif, tidak ada CO, tidak ada denyut , tidak ada TD. kematian otak terjadi dalam 4-6 menit. jika tidak diatasi.
⦁    laju atrial : tidak ada gelombang P; tidak ada interval PR dan tidak dapat di tentukan
⦁    laju ventrikuler : gelombang fibrasi tanpa pola
⦁    irama : ireguler
⦁    penanganan : amiodaron, procainamide, lidocaine, magnesium sulfat, defibrasi segera dengan  200-360 j, RJP epineprine, veipressin dan natrium bicarbonat; intubasi. akses IV jika tidak ada induksi hipotermia ringan 32-34 0C.

7. Blok AV Derajat 1
Masalah dalam konduksi, dapat dikembangkan menjadi blok yang lebih berat. pasien biasanya tidak memiliki gejala dan tidak ada perubahan hemodinamika.
⦁    Gelombang P : ada, sebelum QRS
⦁    irama : reguler
⦁    Interval PR : > 0,12 detik
⦁    QRS : Normal
⦁    penanganan : koreksi penyebab , pantau ketat, biasanya jinak

8. Blok AV Derajat II atau fenomena wanckebach
Hampir selalu bersifat sementara. jika bradikardia  CO2 menurun. membalik ketika kondisi yang mendasari teratasi (IM, CAD, induksi obat :  beta bloker, bloker kanal kalsium
Gelombang P : ada sampai satu gelombang P terblok tanpa adanya QRS
Irama : Ireguler
Interval PR : mulai memanjang sampai QRS menghilang
QRS : Normal
Penanganan : koreksi penyebab dasar, atropin atau pemicu sementara

9.  Blok AV derajat II- mobiz II
masalah pada bekas His atau cabang berkas. bradikardi, CO2 menurun, TD menurun, pasien simtomatik, dapat berkembang menjadi blok yang lebih serius
⦁    Gelombang P : ada namun atrial > laju ventikular ,
konduksi gelombang P : kompleks QRS dalam pola 2:1, 3:1, atau 4 :1
⦁    Irama : Reguler
⦁    Interval PR : Normal jika gelombang P diikuti dengan QRS
⦁    QRS : Normal namun QRS secara periodik menghilang, kadang-kadang lebar
⦁    penanganan : atropine untuk bradikardia, isoproterenol jika laju sangat lambat ( alat pacu)

10. Blok AV Derajat III
tidak adanya potensi antara kontraksi atrium dan ventrikel
berpotensi mengancam nyawa, (Bradikardia, CO2 menurun rastis, tekanan darah menurun, pasien simtomatik
toksisitas digoxin merupakan penyebab yang sering
⦁    Gelombang P : ada namun laju atrial > laju ventikular, konduksi gelombang P tidak berhubungan dengan kompleks QRS
⦁    irama : laju atrial dan laju ventikular reguler
⦁    interval PR : tidak ada hubungan gelombang P dengan kompleks QRS
⦁    QRS : biasanya lebar
⦁    Penanganan : atropine untuk bradikardi, isoprotenol alat pacu

Asfiksia neonatorum

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Suatu keadaan bayi baru lahir yang mengalami gangguan tidak segera bernafas secara spontan dan teratur setelah lahir. asfiksia dapat terjadi selama kehamilan atau persalinan. Asfiksia dapat disebabkan oleh penyakit infeksi akut atau kronis (toksekimia gravidarum, anemia berat, cacat bawaan, keracunan obat bius) asfeksia dalam persalinan dapat disebabkan oleh partus yang lama, placenta previa, ruptur uteria, prolapsus dll.

Untuk mendeteksi dapat menggunakan APGAR Score
Faktor penyebab :
          1.   Ibu
- terjadi hipoksia ibu
            - Gangguan aliran darah fetus
            - Primi tua, DM , anemia, ketuban pecah dini
1.    Placenta ruptur placenta, solutio placenta
2.     Fetus
prematuritas, persalinan ganda, lilitan tali pusat
3.     Lama persalinan
Persalinan lama, Operasi cesar, kelainan letak
4.       Neonatus
          Kelainan konginetal, trauma lahir sehingga menyebabkan perdarahan      intracranial, efek anastersi
Klasifikasi berdasarkan APGAR
1.       Asfeksia Berat (0-3)
2.       Asfeksia Ringan Sedang (4-6)
3.       Bayi normal atau sedikit Asfeksia (7-9)
4.       Bayi normal Dengan nilai ( 10 )
Pemeriksaan Berupa
·         Analisa gas darah
·         Elektrolit darah
·         Gula darah
·         Baby gram (RO dada)
·         USG (kepala)
Tips
Langkah yang paling umum yaitu melakukan pencegahan dimulai dari masa kehamilan dan beberapa saat setelah persalinan, adapun pencegahannya berupa:
1.       Melakukan pemeriksaan antenatal rutin minimal 4 kali kunjungan
2.       Memberikan terapi kortikosteroid antenatal untuk persalinan pada usia kehamilan kuran dari 37 minggu
3.       Melakukan pemantauan terhadap kesejahteraan janin dan  deteksi dini terhadap tanda-tanda afeksia selama persalinan
4.       melakukan perawatan neonatal :
·         Persalinan bersih dan aman
·         Stabilisasi Suhu
·         Insiasi menyusu dini
·         pencegahan infeksi serta pemberian imunisasi
Setelah persalinan ajarkan :
1.       menigkatkan upaya kardiovaskuler efektif
2.       memberi lingkungan termonetral untuk mempertahankan suhu tubuh
3.       beri asupan asi sesering mungkin setelah keadaan memungkinkan



           

Minggu, 08 Juli 2018

MENINGITIS

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Menigitis bakterialis adalah suatu infeksi puluren lapisan otak yang pada orang dewasa biasanya hanya terbatas didalam ruangan subaraknoid, namun pada bayi cendrung meluas sampai kerongga subdural sebagai suatu efusi atau empiema atau kedalam otak (meningoensefalitis)
menigitis ini disebabkan oleh diplococus pneumonia dan neiseria menigitidis, stafilokokus, dan gram negatif, pada anak anak sering disebabkan oleh hemophhylus influensa, neiseria meningitidis dan diplococus pnemonia

hal yang sering muncul yaitu:
1.      neonatus: refleks hisap kurang, muntah, diare, tangisan lemah, tonus otot lemah
2.      anak dan remaja: demam yang tinggi, sakit kepala, muntah, kejang, halusinasi, delirium dan budzinski positif (kaku kuduk)
Pemeriksaan penunjang
·         tes kultur darah, urin, dan nasofaring
·         fungsi lumbal dan kultur CSS
·         MRI, CT-scan /angiografi
·         Elektorolit serum , meningkat jika anak dehidrasi: Na + naik dan K + turun
Pengobatan
1.      obat anti inflamasi
· menigitis tuberkulosa : pemberian obat isoniasid, ripamfisin, streptomisin sulfat selama tiga bulan
· manigitis bakterial, : Sefalosporin, ampisilin 150-200 mg
2. Pengobatan darurat
· Diazepam IV 0,2-0,5 dan dilanjutkan dengan fenotonin  5 mg
· Kompres air hangat dan pemberian paracetamol
· berikan  cairan intravena dan oksigen antara 30-50 %

Sabtu, 11 Februari 2017

A CHEAP SAFE AND NATURAL MEDICINE

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Without any concern about the obliging or disobliging any man living, a mean hand has made here some little attempt, towards a plain and easy way of curing most diseases. I have only consulted herein, Experience, common sense, and the common Interest of Mankind. John Wesley, ‘The Preface’, Primitive Physic (1747) 1 John Wesley’s medical manual, Primitive Physic: Or, An Easy and Natural Method of Curing Most Diseases, was one of the most popular medical volumes published in eighteenth-century England – twenty-three editions went to press in his lifetime; the last and thirty-seventh edition was published in 1859. 2 No one was more surprised at the public’s response to Primitive Physic than Wesley himself, as is apparent in the ‘Postscript’ to the fifth edition of 1755: It was a great surprise to the Editor of the following Collection, that there was so swift and large a demand for it; that three impressions were called for in four or five years; and that it was not only re-published by the Booksellers of a neighbouring nation; but also inserted by parts in their public papers, and so propagated through the whole kingdom. This encouraged him carefully to revise the whole, and to publish it again with several alterations, which it is hoped may make it of greater use to those who love common sense and common honesty. 3 Primitive Physic was certainly in great demand, but to categorise this text as simply ‘populist’, as most historians continue to do, is to obscure its rich cultural meanings and discursive contexts. This interpretation conceals the extensive range of authoritative references drawn from a variety of European sources that are brought to bear by Wesley in Primitive Physic. On the face of it, Primitive Physic is a manual which seems to contain a strange combination of common sense and religion. There is no doubt that emphasis on the populist strains of Primitive Physic can largely be attributed to the effective nature of Wesley’s rhetoric, of which the passage previously quoted is a good example. Here, Wesley seeks to convince, comfortreassure his reader that Primitive Physic is concerned to steer an empiricist course between the Scylla of abstruse medical theory and the Charybdis of speculative philosophy.

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