Wednesday, December 31, 2014

ស្បែក និង ភ្នាសរាងកាយ (Skin & Body Membranes)





ប្រភេទធំចំបងចំនួន ២ នៃភ្នាសរាងកាយ គឺ Epithelial Membranes ដែលត្រូវគេហៅផងដែរថាភ្នាសគ្របដណ្តប់ / ភ្នាសស្រទាប់ និង ជាលិកាដែលតភ្ជាប់ អាស្រ័យតាមការប្រភេទនៃជាលិកាដែលបានបង្កើតពួកគេ ។ 

ភ្នាសគ្របដណ្តប់ / ភ្នាសស្រទាប់ (Epithelial Membranes) ចែកចេញជាប្រភេទរងធំ ចំនួន ៣ រួមមាន:-

ភ្នាសស្បែក (Cutenaoeus Membranes) គឺ ស្បែករបស់យើង 

ភ្នាសស្បែកស្តើង (ដែលរអឹលដូចសំបោរ) - Mucous Membranes: គឺ ជាភ្នាសស្បែកទ្រនាប់នៃបន្លប់រាងកាយដែលបើកចំហទៅខាងក្រៅ ដូចជាសរីរាង្គប្រហោងមួយចំនួន រួមមាន សរីរាង្គផ្លូវដង្ហើម សរីរាង្គផ្លូវទឹកមូត្រ សរីរាង្គរំលាយអាហារ និង សរីរាង្គបន្តពូជ ។ ល ។

ភ្នាសស្រទាប់ (ដែលមានផ្ទុកសេរ៉ូម serum) - Serous Membranes: សមាសភាពនៃភ្នាសនេះរួមមានកោសិកាស្តើងរាងសំប៉ែត (រកឃើញនៅក្នុងស្រទាប់គ្របដណ្តប់ ដូចជា ស្បែក និង សរសៃ ឈាម និង បំពង់អាហារ epithlium squanous) ដែលត្រដាងលើស្រទាប់ស្តើងនៃជាលិកាតភ្ជាប់ ។

Source: Elaine N. Marieb, Essential of Human Anatomy and Physiology

បន្លប់សព៌ាង្គកាយ និង សរីរាង្គ(Body Cavities & Organs)



បន្លប់សព៌ាង្គកាយផ្នែកខាងក្រោយ (Dorsal body cavity)
បន្លប់សព៌ាង្គកាយផ្នែកខាងក្រោយ ចែកចេញជាចំណែករងចំនួន ២ ដែលបានតភា្ជប់ជាមួយគ្នា គឺ បន្លប់ឆ្អឹងលលាដ៏ក្បាល និង បន្លប់ឆ្អឹងខ្នង ។

បន្លប់ឆ្អឹងលលាដ៏ក្បាល គឺ ទីប្រហោងស្ថឹតនៅខាងក្នុងលលាដ៍ក្បាល ។ បន្លប់ឆ្អឹងខ្នងពង្រីកចេញពីបន្លប់ឆ្អឹងលលាដ៏ក្បាលទៅទល់ចុងជួរនៃឆ្អឹងខ្នង ។ សសៃរប្រសាទឆ្អឹងខ្នង ឬ ខួរឆ្អឹងខ្នងបានការ ពារដោយឆ្អឹងខ្នង ។

បន្លប់សព៌ាង្គកាយផ្នែកខាងមុខ (Ventral body cavity)

បន្លប់សព៌ាង្គកាយផ្នែកខាងមុខ រួមទាំងរចនាសម្ព័ន្ធទាំងឡាយនៃទ្រូង ពោះ និងសរីរាង្គក្នុង (អ្នក ផងទាំងឡាយ តែងតែហៅថាគ្រឿងក្នុង) ។ បន្លប់សព៌ាង្គកាយផ្នែកខាងមុខ ចែកចេញជាចំណែក រងចំនួន ២  គឺ បន្លប់ទ្រូង និង បន្លប់ពោះ ។ បន្លប់ទ្រូងត្រូវបានបំបែកចេញពីបន្លប់សព៌ាង្គកាយផ្នែកខាងមុខដោយបន្ទះសាច់ដុំស្តើង - Diaphragm (ស្ថឹតនៅខាងក្រោមសួត និង បេះដូងដែលបាន បំបែកទ្រូងចេញពីពោះ) ។ 

តំបន់កណ្តលនៃបន្លប់ដើមទ្រូង ដែលត្រូវគេបានហៅថា Mediastinum បំបែកចេញជា បន្លប់សួតខាងឆ្វេង និង ខាងស្ដាំ។ សរីរាង្គនៅបន្លប់នេះ រួមមាន បេះដូង សួត និង សិរីរាង្គផ្សេងៗ ទៀតត្រូវបានការពារដោយគ្រោងនៃឆ្អឹងជំនីរ ។

ផ្ទៃខាងលើនៃតំបន់ពោះ-អាងត្រគាក និង បន្លប់ទាំងឡាយ (Abdominopelvic surface)

ខាងឆ្វេង - ចតុភាគមណ្ឌល ។ ខាងស្តាំ - តំបន់ទាំង ៩ នៃ ទីតាំងរចនាសម្ព័ន្ធរាងកាយទាំង ៤

(រូបភាពខាងលើ) ខាងស្តាំ "តំបន់ទាំង ៩ នៃ ទីតាំងរចនាសម្ព័ន្ធរាងកាយទាំង ៤" រួមមាន
  • តំបន់ផ្ចិត (Umbilical Region) គឺ ជាតំបន់កណ្តាល ជ្រៅទៅក្នុង និង នៅជុំវិញផ្ចិត
  • តំបន់ផ្នែកខាងលើនៃក្រពះ (Epigastric Region
  • តំបន់ផ្នែកខាងក្រោមនៃក្រពះ (Hypogastric Region)
  • តំបន់ខាងឆ្វេង និង ខាងសា្តំនៃផ្នែកខាងលើនៃឆ្អឹងត្រគាក (right and left Iliac Region)
  • តំបន់ខាងឆ្វេង និង ខាងសា្តំនៃចឡក (right and left Lumbar Region)
  • តំបន់ខាងឆ្វេង និង ខាងសា្តំនៃផ្នែកខាងក្រោមចុងផុតនៃឆ្អឹងជំនីរ  (right and left Hypochon- driac Region)



ទិដ្ឋភាពពីមុខនៃបន្លប់រាងកាយផ្នែកខាងមុខ បង្ហាញពីសរីរាង្គទាំងឡាយដែលមាននៅក្នុងបន្លប់នោះ


Source: Elaine N. Marieb, Essential of Human Anatomy & Physiology.









Friday, December 26, 2014

ថ្នាំគ្រាប់ថ្មីសម្រាប់ព្យាបាលជម្ងឺទឹកនោមផ្អែមប្រភេទទី ២ (New Tablet For Type 2 Diabetes Treatment)



Jardiance គឺ ជា ថ្នាំព្យាបាលជម្ងឺទឹកនោមផ្អែមប្រភេទទី ២ សម្រាប់មនុស្សពេញវ័យ - លេប ១ គ្រាប់ក្នុងមួយថ្ងៃ គួបផ្សំនឹងរបបអាហារនិងការធ្វើលំហាត់ប្រាណ ដើម្បីបន្ថយជាតិស្ករក្នុងឈាម (A1C)  ។

Jardiance មិនសមស្របសម្រាប់អ្នកដែលមានជម្ងឺទឹកនោមផ្អែមប្រភេទទី ១ ឬ សម្រាប់អ្នកដែលមានជម្ងឺទឹកនោមផ្អែម ដែលមានបញ្ហា Ketoacidosis (កំណើននៃសារធាតុ Ketone នៅក្នុងឈាម ឬ ទឹកមូត្រ) ។

Jardiance (Empagliflozin), an antidiabetic used to improve glycemic control in patients with type 2 diabetes mellitus in addition to diet and exercise, has recently been approved by US Food and Drug Administration (FDA) 


Thursday, December 25, 2014

ទីតាំងរចនាសម្ព័ន្ធនៃរាងកាយ និង ផ្នែកនៃរាងកាយ (Body Planes & Sections)








ទីតាំងរចនាសម្ព័ន្ធនៃរាងកាយ និង ផ្នែកនៃរាងកាយ (Body Planes & Sections)

Sagittal Section: គឺ ការកាត់តាមបណ្តោយរាងកាយ បែងចែករាងកាយទៅជាផ្នែក - ខាងស្ដាំ និង ខាងឆ្វេង 

Midsagittal ឬ Median Sectionគឺ ការកាត់ចំចំណុចកណ្តាលនៃរាងកាយ (ផ្នែកខាងស្ដាំនិងខាងឆ្វេង គឺ មានទំហំស្មើគ្នា)

Frontal Section  ជួនកាលគេហៅថា Coronal Sectionគឺ ការកាត់តាមបណ្តោយ ចំហៀងរាងកាយ ឬ សរីរាង្គណាមួយ បែងចែករាងកាយ ឬ សរីរាង្គចេញជាផ្នែកខាងមុខ (Anterior) និង ផ្នែកខាងក្រោយ (Posterior) 

Transverse or Cross Section : គឺ កាត់មួយ ដែលបែងចែករាងកាយ ឬ សរីរាង្គ ចេញជាផ្នែកខាងលើ និង ខាងក្រោម

Reference: Essentials of Human Anatomy & Physiology. Elaine N. Marieb

តើផលប្រយោជន៍សុខភាពនៃជាតិដែកមានអ្វីខ្លះ? (What Are The Health Benefits of Iron?"

iron symbolកង្វះជាតិដែកអាចបង្ករអោយមានបញ្ហាកង្វះឈាមក្រហម ។   
កត្តាមួយចំនួនដែលបណ្តាលអោយមានបញ្ហាកង្វះឈាមក្រហម រួមមាន :-
  • ការស្រូបយកជាតិដែកចូលមិនបានបរិបូរណ៏ ឬ មានសភាពមិនប្រពៃ
  • កង្វះអាហារូបត្ថម្ភក្នុងរបបអាហារជាពិសេស ជាតិអា ស៊ីដហ្វូលីក (folate) ប្រូតេអ៊ីន និង វីតាមីន C ។ 
  • អាចបណ្តាលមកពី ឬ ការរងរបួសកាន់តែមានសភាពធ្ងន់ធ្ងរឡើង
  • ការបាត់បង់ឈាម (ហូរឈាម)
  • ជម្ងឺក្រពះពោះវៀន ដែលធ្វើអោយប៉ះពាល់ដល់ការស្រូបយកជាតិដែក ។

អ្នកដែលរងផលប៉ះពាល់ពីកង្វះជាតិដែក ភាគច្រើន គឺ កុមារ និង ស្រ្តីស្ថឹតក្នុងវ័យអាចមានគ៌ភ។
អនុសាសន៍ - ជាតិដែកប្រចាំថ្ងៃ អាស្រ័យលើអាយុ និង ភេទ
កុមារអាយុ ១ - ៣ ឆ្នាំ : ៧ មីលីក្រាម អាយុ ៤ - ៨ ឆ្នាំ : ១០ មីលីក្រាម។
ប្រុស៩ - ១៣ ឆ្នាំ : ៨ មីលីក្រាម ១៤ - ១៨ ឆ្នាំ : ១១ មីលីក្រាម ១៩ ឆ្នាំឡើងទៅ : ៨ មីលីក្រាម។
ស្ត្រី៩ - ១៣ ឆ្នាំ : ៨ មីលីក្រាម ១៤ - ១៨ ឆ្នាំ : ១៥ មីលីក្រាម ១៩ - ៥០ ឆ្នាំ : ១៨ មីលីក្រាម      ៥១ ឆ្នាំឡើងទៅ : ៨ មីលីក្រាម។
អ្នកមានផ្ទៃពោះ២៧ មីលីក្រាម ។
Iron deficiency anemia is the world's most common nutritional deficiency disease and is most prevalent among children and women of childbearing age. Anemia develops due to an inadequate amount of iron in the diet or poor iron absorption.
Iron deficiencies can be caused or exacerbated by injury, blood loss, hemorrhage or gastrointestinal diseases that impair iron absorption. Inadequate intake of folate, protein and vitamin C can also contribute to iron deficiency.
MNT Knowledge Center feature is part of a collection of articles on the health benefits of popular vitamins and minerals. It provides an in-depth look at recommended intake of iron, its possible health benefits, foods high in iron and any potential health risks of consuming iron.

សារធាតុនៅក្នុងក្រហមរំហោាចការឆ្លើយតបទៅនឹងភាពតានតឹងដើម្បីលើកកម្ពស់សុខភាព (Red Wine Compound Activates Stress Response To Promote Health Benefits)


Excerpt from Medical New Today, "Red wine compound activates stress response to promote health benefits"

A glass of red wine
ការសិក្សាមួយចំនួនកន្លងមក បានរកឃើញថា សារធាតុ Resveratrol ដែលបានរកឃើញនៅក្នុងស្រាក្រហម និង ផ្លែទំពាំងបាយជូរ បានភ្ជាប់ទៅនឹងអត្ថប្រយោជន៍សុខភាពមួយចំនួន:- ការថយចុះនៃហានិភ័យនៃជម្ងឺដែលទាក់ទងទៅនឹង វ័យ ដូចជា ជម្ងឺសសៃរឈាមបេះដូង (cardiovascular disease) អាចជួយព្យា បាលជម្ងឺមហារីកមួយចំនួន អាចការ ពារនឹងបញ្ហាបាត់បង់សោតវិញ្ញាណ និង ការចងចាំ ។ល។ ពេលថ្មីៗនេះ អ្នកវិទ្យាសាស្ត្រពីវិទ្យាស្ថានស្រាវជ្រាវ Scripps នៅ La Jolla CA បានផ្តល់យោបល់ថ្មីថា សារធាតុ Resve-ratrol បានរំញោច ហ្សែនដែលឆ្លើយតបទៅនឹងភាពតាន តឹង ហើយទទ្ទឹមនឹងនោះ ហ្សែននេះក៏បានរំញោចហ្សែនមួយចំនួនទៀតដើម្បីជួយការពាររាងកាយ ។  

By now, most of us have heard of resveratrol - a compound found in red wine and grapes that has been linked to an array of health benefits, such as reduced risk of age-related diseases. Researchers have long investigated how resveratrol promotes such benefits. Now, scientists from The Scripps Research Institute in La Jolla, CA, offer a new suggestion; the compound stimulates a stress response gene, which activates a number of genes that protect the body.

A glass of red wine
Drinking two glasses of red wine can trigger the stress response that promotes numerous health benefits, according to the researchers.
The research team, led by Mathew Sajish of the Skaggs Institute for Chemical Biology at The Scripps Research Institute (TSRI), publish their findings in the journal Nature.
Past research has associated resveratrol with longevity and reduced risk of cardiovascular disease (CVD). Last year, Medical News Today reported on a study claiming the compound could help treat several cancers by sensitizing diseased cells to treatment, while another study claimed resveratrol can protect against hearing loss and cognitive decline.
More recently, however, some studies have blasted the health benefits of resveratrol. In May, researchers from Johns Hopkins University School of Medicine in Baltimore, MD, claimed people who consume a diet rich in resveratrol are at no lower risk of CVD or cancer than those who consume small amounts of the compound.
Sajish and senior investigator Paul Schimmel - also of the Skaggs Institute for Chemical Biology at TSRI - note that some researchers have questioned the health benefits of resveratrol because many studies have used "unrealistically high doses" of the compound.
In this latest study, the researchers set out to determine if resveratrol really is beneficial for health and if so, how the compound promotes such benefits.

Resveratrol binds to TyrRS enzyme to activate protective genes

Sajish and Schimmel investigated resveratrol's association with tRNA synthetases - enzymes that aid translation of genetic material during protein synthesis.
In particular, the researchers focused on a specific tRNA synthetase called TyrRS - an enzyme that binds with an amino acid called tyrosine before linking up with encoding genetic material - after a former investigator at TSRI found that it can relocate to the cell nucleus under stressful conditions, effectively adopting a protective role.
Since resveratrol has been shown to have similar properties to tyrosine and has been associated with a comparablestress response, Sajish says he wanted to see whether TyrRS is a target for the compound.
Using X-ray crystallography and other tests to compare resveratrol with TyrRS, the researchers found that resveratrol mimics tyrosine, so much so that TyrRS was able to bind with resveratrol. The team explains that this attachment led TyrRS away from its protein translation activity and pushed it toward the cell nucleus.
Once in the nucleus, the researchers found that the TyrRS-resveratrol combination switched on a gene called PARP-1 - known to play a role in stress response and DNA repair and to have a major influence on aging. What is more, activating PARP-1 also switched on a number of other protective genes, including FOXO3A and SIRT6 - associated with longevity - and the tumor-suppressor gene p53.
The team notes that their findings were confirmed when they injected mice with resveratrol.

'A couple of glasses of red wine' could evoke protective effect of resveratrol

Interestingly, Sajish and Schimmel found that the TyrRS-PARP1 pathway can be activated with doses of resveratrol up to 1,000 times lower than doses that have been used in past studies investigating the compound's health benefits.
"Based on these results, it is conceivable that moderate consumption of a couple glasses of red wine would give a person enough resveratrol to evoke a protective effect via this pathway," says Sajish, adding:
"This stress response represents a layer of biology that has been largely overlooked, and resveratrol turns out to activate it at much lower concentrations than those used in prior studies.
With these findings we have a new, fundamental mechanism for the known beneficial effects of resveratrol."
He adds that because previous research has used such high doses of resveratrol, this may have confounded some results.
Resveratrol triggers a similar stress-response pathway in plant cells, according to the researchers, and they believe the compound has grown to produce a similar effect in human cells. "We believe that TyrRS has evolved to act as a top-level switch or activator of a fundamental cell-protecting mechanism that works in virtually all forms of life," says Sajish.
Earlier this month, MNT reported on a study by researchers from the University of Colorado Cancer Center claimingresveratrol has both cancerous and anti-cancerous properties.
Written by 

Orientation & Directional Terms


សព្ទបច្ចេកទេសទឹស/ទីតាំង ត្រូវបានប្រើដោយបុគ្គលិកសុខាភិបាល និង អ្នកជំនាញផ្នែកកាយវិភាគវិទ្យា ដើម្បីពន្យល់ច្បាស់លាស់អំពីទីតាំង ឬ តំបន់រចនាសម្ព័ន្ធរាងកាយ ទំនាក់ទំនងរវាងផ្នែកមួយនៃរាងកាយ នឹង ផ្នែកមួយផ្សេងទៀត ។ 

ឧទាហរណ៍ ស្បែកស្ថឹតនៅខាងលើ/ខាងក្រៅនៃគ្រោងឆ្អឹង  - The skin is superficial (external) to the skeleton ។ 

រូបភាពខាងលើបានពន្យល់ច្បាស់លាស់អំពីអត្ថន័យនៃប្រជុំសព្ទបចេ្ចកទេសនិមួយៗ ព្រមទាំងឧទា ហរណ៍ផងដែរ ។

ទីតាំងកាយវិភាគវិទ្យា (Anatomical Position)




ទីតាំងកាយវិភាគវិទ្យា (Anatomical Position)
សញ្ញាសំគាល់ផ្នែកខាងមុខនៃរាងកាយ (Anterior body landmarks)

  • Abdominal - ផ្នែកខាងមុខនៃដងខ្លួន ខាងក្រោមឆ្អឹងជំនីរ
  • Acromial - ចំណុចនៃស្មា
  • Anetcubital - ផ្ទៃខាងមុខនៃកែងដៃ
  • Axillary - ក្លៀក
  • Brachial - ដៃ
  • Buccal - តំបន់ថ្ពាល់
  • Carpal - កដៃ
  • Cervical - តំបន់ក
  • Coxal - ត្រគាក
  • Crural - ជើង
  • Digital - ម្រាមដៃ ម្រាមជើង
  • Femoral - ភ្លៅ
  • Fibular - ផ្នែកខាងក្រោយនៃជើង
  • Inguinal - តំបន់ក្រលៀន
  • Nasal - ច្រមុះ
  • Oral - មាត់
  • Orbital - តំបន់ភ្នែក
  • Patellar - ផ្នែកខាងមុខនៃជង្គង់
  • Pelvic - តំបន់ខាងមុខនៃអាងត្រគាក
  • Pubic - តំបន់ប្រដាប់ភេទ
  • Tarsal - តំបន់កែងជើង
  • Thoracic - ទ្រូង
  • Umbilical - ផ្ចិត 


សញ្ញាសំគាល់ផ្នែកខាងក្រោយនៃរាងកាយ (Posterior Body Landmarks)

  • Calcaneal - កែងជើង
  • Cephalic - ក្បាល
  • Deltoid - ផ្នែកកោងនៃសា្មដែលបង្កើតដោយសាច់ដុំស្មា
  • Femoral - ភ្លៅ
  • Gluteal - គូទ ឬ ផ្ពាល់គូទ
  • Lumbar - តំបន់ខ្នង នៅចន្លោះឆ្អឹងជំនីរ និង ត្រគាក
  • Occipital - ផ្នែកខាងក្រោយនៃក្បាល
  • Olecranal - ផ្នែកខាងក្រោយនៃកែងដៃ
  • Popiteal - ផ្នែកខាងក្រោយនៃជង្គង់
  • Sacral - តំបន់នៅចន្លោះត្រគាក
  • Scapular - តំបន់ឆ្អឹងសា្លបប្រជៀវ 
  • Sural - តំបន់កំភួនជើង
  • Vertebral - តំបន់ឆ្អឹងខ្នង
  • Platar - តំបន់បាតជើង

Reference: Elaine N. Marieb, Essential of Human Anatomy & Physiology, 

Wednesday, December 24, 2014

ប្រព័ន្ធទាំង ១១ នៃរាងកាយ (11 Systems Of The Body)


ប្រព័ន្ធទាំង ១១ នៃរាងកាយ



ប្រព័ន្ធស្បែក (Integumentary system): ជាប្រព័ន្ធគ្របដណ្តប់ផ្នែកខាងក្រៅនៃរាងកាយ ។ ស្បែកការ ពាររាងកាយរបស់យើងពីការជ្រៀបទឹកចូល និង ការពារជាលិកាផ្នែកខាងក្នុងពីការ រងរបួស ។ ស្បែកបញ្ចេញជាតិអំបិល និង អ៊ុយ រ៉េ (Urea) តាមរយះញើស (Perspi ration) និង ជួយគ្រប់គ្រងសីតុណ្ហ ភាពរាងកាយរបស់យើង  

ចំណាំ - Receptors ជាម៉ូលេគុលប្រូតេអ៊ីន (Protein molecule) ជាធម្មតាត្រូវបានរកឃើញនៅលើភ្នាសនៃប្លាស្មា ឬ លោហិតម្ភ (Plasma) ជាអ្នកទទួលសញ្ញាគីមី (Chemical signals) ពីបរិវេណខាងក្រៅនៃកោសិកា (Cell) 

Receptors សីតុណ្ហភាព សម្ពាធ និង ការឈឺចាប់ គឺ ស្ថឹតនៅក្នុងស្បែក ហើយពួកគេផ្តល់នូវសញ្ញាប្រាប់ពួកយើងអំពីបញ្ញាអ្វីៗ ដែលកំពុងកើតមានឡើងនៅលើផ្ទៃរាងកាយរបស់យើង ។


ប្រព័ន្ធឆ្អឹង (Skeletal system)

ប្រព័ន្ធឆ្អឹងរួមមាន ឆ្អឹង (Bones) ឆ្អឹងខ្ចី (Cartilages) សរសៃពួរ (Ligaments) និង សន្លាក់ (Joints) ។ វាគាំទ្ររាងកាយ និង ផ្តល់នូវក្របខ័ណ្ឌដែលសាច់ដុំឆ្អឹងប្រើប្រាស់ដើម្បីបង្កើតនៅចលនាណា មួយ  វាក៏មានមុខងារ ក្នុងការការពារ (ឧទាហរណ៍) លលាដ៍ក្បាលរុំព័ទ្ធ និង ការពារខួរក្បាល) ។ ការកកើតនៃកោសិកាឈាម (Hematopoiesis) គឺ កើតមានឡើងនៅក្នុងប្រហោងនៃគ្រោងឆ្អឹង ។ សារធាតុរឹងនៃឆ្អឹង មានដើរតួនាទីជាឃ្លាំងសម្រាប់ផ្ទុកសារធាតុខនិជទាំងឡាយ ។


ប្រព័ន្ធសាច់ដុំ (Skeletal system) 

សាច់ដុំនៃរាងកាយរបស់យើងមានមុខងារតែ មួយគត់ គឺ កន្រ្តាក់ ឬ បង្រួញខ្លី ។ សាច់ដុំជាម៉ាស៊ីននៃរាងកាយ។ រាល់ការចល័តនៃរាងកាយ គឺ ឆ្លុះបញ្ចាំងពីសកម្មភាពនៃសាច់ដុំ - សាច់ដុំធំ ថ្លោសដែលភ្ជាប់ទៅនឹងឆ្អឹង ។ នៅពេលដែលសាច់ដុំកន្រ្តាក់យើងអាចឈរត្រង់ ដើរ បោះបាល់ ឬ ញញឹម ។ សាច់ដុំនេះ គឺខុសប្លែកពីសាច់ដុំបេះដូង និង សរីរាង្គប្រហោងផ្សេងទៀតៗ ដែលដឹកជញ្ជូនវត្ថុរាវ (ដូចជាឈាម និង ទឹកនោម) ឬ សារធាតុផ្សេងទៀតៗ (ដូចជា អាហារ) តាមច្រកយ៉ាងច្បាស់លាស់នៅក្នុងរាងកាយរបស់យើង ។


ប្រព័ន្ធសសៃរប្រសាទ (Nervous system)

ប្រព័ន្ធសរសៃប្រសាទ គឺ ជាប្រព័ន្ធត្រួតពិនិត្យរាងកាយដែលឆ្លើយតបជាបន្ទាន់នឹងសា្ថនភាពណា មួយ ។ ប្រព័ន្ធនេះ រួមមាន ខួរក្បាល (Brain) សរសៃប្រសាទឆ្អឹងខ្នង ឬ ដែលទូទៅតែងតែហៅថា ខួរឆ្អឹងខ្នង (Spinal cord) សសៃរប្រសាទ (Nerves) និង receptors ខាងវិញ្ញាណ ។



Receptors ខាងវិញ្ញាណ ចាប់/ទទួលការផ្លាស់ប្តូរទាំងឡាយ ដូច ជា ពន្លឺ (Light) សំឡេង (Sound) ឬ ការផ្លាស់ប្តូរសីតុណ្ហភាពទាំងឡាយ (Changes in temperature) ពីខាងក្រៅនៃរាងកាយ និង ខាងក្នុងនៃរាងកាយ ដូចជា ការថយចុះនៃអុកស៊ីហ្សែន (Decrease in oxygen)  ឬ សន្ទឹងភាពនៃជាលិកា (Stret-ching of tissue) ។


ខណៈដែល Receptors ខាងវិញ្ញាណ រកឃើញការផ្លាស់ប្តូរទាំងនេះ នោះវាផ្ញើរសារ (តាមរយៈសញ្ញាអគ្គិសនី ដែលបានត្រូវគេហៅថា "សន្ទុះសរសៃប្រសាទ" - Nerve impulse) ទៅប្រព័ន្ធប្រសាទកណ្តាល (ខួរក្បាល និង សរសៃប្រសាទឆ្អឹងខ្នង) ។ ប្រព័ន្ធសរសៃប្រសាទកណ្តាល ធ្វើការវាយតម្លៃលើពត៌មានទាំងនេះ ហើយឆ្លើយតបដោយធ្វើអោយមានសកម្មភាពពីប្រព័ន្ធប្រត្តិបត្តិរាងកាយសមស្របណាមួយ (Body effectors) ដូចជា សាច់ដុំ ឬ ក្រពេញ  

References: Elaine N. Marieb, Essentials of Anatomy & Physiology




កាយវិភាគសាស្ត្រ & សរីរវិទ្យា (Anatomy & Physiology)


រាងកាយរបស់មនុស្ស: ការណែនាំ (The Human Body: An Orientation)

កាយវិភាគសាស្ត្រ (Anatomy): គឺ ជាការសិក្សាអំពីរចនាសម្ព័ន្ធរាងកាយ រូបរាងនៃរាងកាយ និង ទំនាក់ទំនងរបស់ពួកគេ ។  

កាយវិភាគសាស្ត្រ មាន ២ ប្រភេទ: កាយវិភាគសាស្ត្រទូទៅ ឬ ទ្រង់ ទ្រាយខាងក្រៅ (Gross anatomy) និង កាយវិភាគសាស្ត្រមីក្រូទស្សន៍ ឬ លម្អឹត (Microscopic anatomy) ។

  •  សំដៅទៅលើការសិក្សាអំពីរចនាសម្ព័ន្ធរាងកាយដោយប្រើប្រាស់ឧប ករណ៍ ដូចជា មីក្រូទស្សន៍ ឬ ឧបករណ៍ពង្រីក ដើម្បីមើលរចនាសម្ព័ន្ធតូចៗ ទាំងឡាយនៅក្នុងរាងកាយរបស់យើង 

សរីរវិទ្យា (Physiology): គឺ ជាការសិក្សាអំពីរបៀបដែលរាងកាយ និង ផ្នែកទាំងឡាយរបស់រាងកាយធ្វើការ ឬ បំពេញមុខងាររបស់គេ (physio = ធម្មជាតិ = សិក្សាអំពី) 

សរីរវិទ្យាក៏មិនខុសគ្នាពីកាយវិភាគសាស្ត្រដែរ វាមានបំណែងចែករងជាច្រើន ។ ឧទាហរណ៍: សរីរវិទ្យាសសៃរប្រសាទ (Neuro-physiology) ពន្យល់អំពីដំណើរការរបស់ប្រព័ន្ធប្រសាទ និង សរីរវិទ្យាបេះដូង (Cardiac-physiology) គឺ ជាការសិក្សាអំពីមុខងារនៃបេះដូង (ជាប៉ូមសកម្មដែលចលនាដោយសាច់ដុំ) ដើម្បីរក្សាបញ្ជូនឈាមទៅរាល់ផ្នែកនៃរាងកាយ ។

ទំនាក់ទំនងរវាងកាយវិភាគសាស្ត្រ និង សរីរវិទ្យា (Relationship between anatomy & physiology)

ការពិត កាយវិភាគសាស្ត្រ និង សរីរវិទ្យា តែងតែពាក់ព័ន្ធគ្នា ។ ផ្នែកទាំងឡាយនៃរាងកាយរបស់យើងបានបង្កើតជាអង្គភាពមួយយ៉ាងជិតស្នឹទ្ធនិងគ្នា ហើយផ្នែកទាំងនោះមានការងាររបស់គេដើម្បីធ្វើឱ្យរាងកាយរបស់យើងអាចប្រតិបត្តិការទាំងស្រុង ។ ឧទាហរណ៍: សួតមិនដូចបេះដូងដែលចលនាដោយសាច់ដុំ ដែលអាចប៉ូម និង បញ្ជូនឈាមទូទាំងរាងកាយនោះទេ ប៉ុន្តែដោយសារ តែជញ្ជាំងថង់ខ្យល់របស់សួតវាស្តើង ម៉្លោះហើយពួកគេអាចផ្លាស់ប្តូរខ្យល់និងផ្តល់អុកស៊ីហ្សែនទៅ ឱ្យរាងកាយ ។ 

A new blood glucose management algorithm for type 2 diabetes: a position statement of the Australian Diabetes Society


Summary
  • Lowering blood glucose levels in people with type 2 diabetes has clear benefits for preventing microvascular complications and potential benefits for reducing macrovascular complications and death.
  • Treatment needs to be individualised for each person with diabetes. This should start with selecting appropriate glucose and glycated haemoglobin targets, taking into account life expectancy and the patient's wishes. For most people, early use of glucose-lowering therapies is warranted.
  • A range of recently available therapies has added to the options for lowering glucose levels, but this has made the clinical pathway for treating diabetes more complicated.
  • This position statement from the Australian Diabetes Society outlines the risks, benefits and costs of the available therapies and suggests a treatment algorithm incorporating the older and newer agents.
Large randomised controlled trials (RCTs) have demonstrated that controlling blood glucose level (BGL) in people with type 2 diabetes (T2D) is important for preventing microvascular complications.1,2Lowering BGL may also reduce myocardial infarction, though not necessarily stroke or all-cause mortality.3
In 2009, the Australian Diabetes Society (ADS) published a position statement recommending individualisation of glycaemic targets.4 The general glycated haemoglobin (HbA1c) target for most people with T2D is ≤ 53 mmol/mol (7%), however:
  • in people without known cardiovascular disease, a long duration of diabetes, severe hypoglycaemia or another contraindication,4 the target is ≤ 48 mmol/mol (6.5%);
  • in people with reduced hypoglycaemia awareness or major comorbidities, the target may increase to ≤ 64 mmol/mol (8%);
  • in people with limited life expectancy, aim for symptom control; and
  • in women planning a pregnancy, aim for the tightest achievable control without severe hypoglycaemia; preferably ≤ 42 mmol/mol (6.0%).
Despite the increasing range of therapies available, achieving glycaemic targets can be difficult. To assist with selecting glucose-lowering pharmacotherapy for people with T2D, the ADS developed this position statement (Box 1). Its aim is to describe the place of the various drug classes in the glucose-lowering therapeutic algorithm (Box 2), drug options in the setting of renal impairment (Appendix 1) or hepatic impairment, the Pharmaceutical Benefits Scheme (PBS) prescribing restrictions for obtaining subsidised products in Australia (Appendix 2), and the current PBS-subsidised and unsubsidised costs (Appendix 3). A more detailed version of the statement that will be updated annually is available on the ADS website (http://www.diabetessociety.com.au).

Drugs

Metformin

Metformin decreases hepatic glucose output, lowers fasting glucose levels and is generally weight-neutral. It decreases HbA1c level by up to 15–22 mmol/mol.5 Gastrointestinal side effects are common. Metformin should be started at low doses and titrated. People with gastrointestinal side effects should be offered one of the slow-release formulations, which cost about 40% more per dose (Appendix 3). Metformin is contraindicated for patients who have severe renal, hepatic or cardiac failure (Appendix 1).

Sulfonylureas

Sulfonylureas have favourable long-term safety and outcome data and are cheap and effective, with decreases in HbA1c level of up to 7–16 mmol/mol when combined with metformin.6-8 They trigger insulin release in a glucose-independent manner. Their main side effects are hypoglycaemia and weight gain. The risk of hypoglycaemia is highest with sulfonylureas with long half-lives and renally excreted active metabolites, such as glibenclamide.7

Dipeptidyl peptidase-4 inhibitors

Dipeptidyl peptidase-4 (DPP-4) inhibitors decrease inactivation of glucagon-like peptide-1 (GLP-1), thereby increasing its availability. GLP-1 improves β-cell function and insulin secretion and slows gastric emptying. A meta-analysis reported decreases in HbA1c level of 7–8 mmol/mol, except for vildagliptin (11 mmol/mol).9 Common side effects include gastrointestinal disturbance and nasopharyngitis, which often subside over 10–14 days. Rash is a rare but potentially serious side effect. Postmarketing surveillance has reported an association between DPP-4 inhibitors and pancreatitis. People with diabetes have an increased background risk of pancreatitis and it remains unclear whether DPP-4 inhibitors augment this risk.10
At the time of writing, there were five DPP-4 inhibitors available in Australia that were approved for PBS-subsidised use with eithermetformin or a sulfonylurea but not both. Triple therapy and monotherapy are not PBS-subsidised; nor is dual therapy with insulin or sodium–glucose cotransporter 2 (SGLT2) inhibitors (Appendix 2).

Thiazolidinediones

Thiazolidinediones (TZDs) are transcription factor peroxisome proliferator-activated receptor PPARγ agonists, which lower BGL through insulin sensitisation. Side effects include weight gain, fluid retention, heart failure and an increased risk of non-axial fractures in women.11Pioglitazone is associated with an increased risk of bladder cancer. In a limited number of people, TZDs combine well with metformin and sulfonylureas.

Acarbose

Acarbose is an α-glucosidase inhibitor that slows intestinal carbohydrate absorption and reduces postprandial BGL. Its main side effects are bloating and flatulence, which lead to discontinuation in up to 25% of people. If tolerated, it can be effective, particularly when combined with metformin.

Sodium–glucose cotransporter 2 inhibitors

Two SGLT2 inhibitors (canagliflozin and dapagliflozin) were listed on the PBS in 2013. These drugs inhibit a renal sodium–glucose cotransporter to produce urinary glucose loss and decrease BGL. Urinary glucose loss is the mechanism for the weight loss associated with these drugs. Side effects include dehydration, dizziness and increased risk of genitourinary infections. The first two can be prevented with adequate fluid intake, and the latter diminished with meticulous hygiene. Use with loop diuretics should be avoided. SGLT2 inhibitors have diminished efficacy in people with renal impairment. PBS reimbursement requires use with metforminor a sulfonylurea but not both.

Glucagon-like peptide-1 receptor agonists

GLP-1 receptor agonists (GLP-1RAs) are administered by subcutaneous injection. They stimulate β-cell insulin release and slow gastric emptying, which contributes to weight loss but may cause nausea and vomiting. Effects on BGL are slightly superior to those of oral agents. An increased risk of pancreatitis (about 50% above a baseline of one to two episodes per 1000 patient-years in T2D) has been reported.10 These agents should be avoided in patients with a history of pancreatitis or pancreatic malignancy.

Insulin

Insulin has extensive effects on metabolism and is generally necessary for cellular glucose uptake. Short-, intermediate- and long-acting insulins are available, as well as premixed preparations. The major side effects are hypoglycaemia and weight gain. In many people, insulin is initiated only after an unnecessarily prolonged period of hyperglycaemia. Insulin is the most potent glucose-lowering agent. With adequate dosage and dietary adherence, it can almost always achieve target BGL. Insulin should be considered early if BGL is very high.

Treatment algorithm

The algorithm in Box 2 summarises the available clinical evidence for pharmacotherapeutic strategies to achieve target HbA1c levels in people with T2D. At each step, there are proven and effective approaches. Indications that may be PBS-subsidised are highlighted in the algorithm by a red border. It should be noted that use of a medication outside PBS-approved indications requires that it be purchased through private prescription. The current cost of these medications is given in Appendix 3. The algorithm is structured with a usual approach to treatment initiation, and intensification and alternative approaches at each stage.

First-line treatment

First-line treatment is appropriate diet and exercise. This should be reinforced at every stage. Both weight loss and prevention of weight gain are important.
When lifestyle measures alone no longer achieve desired targets, metformin should be added if there is no contraindication. If metformin is not tolerated or is contraindicated, a sulfonylurea should be used. Other medications are also available but, apart from acarbose and insulin, are not PBS-subsidised as initial treatment.

Second-line treatment

If glucose control is not achieved with a single agent, there are many second-line treatment options. Sulfonylureas are good second-line agents, achieving similar decreases in HbA1c level as other second-line oral agents, for about 25% of the daily cost (Appendix 3). For patients who experience problematic hypoglycaemia, weight gain or other side effects, an alternative agent should be considered. The most common alternative second-line agent is a DPP-4 inhibitor. These are available in combination tablets with metformin, which may improve compliance.
SGLT2 inhibitors are another option and are PBS-subsidised with eithermetformin or a sulfonylurea. Addition of acarbose is another second-line alternative. GLP-1RAs can also be used with metformin or a sulfonylurea as second-line therapy. As always, insulin is an option that should be considered, especially if the HbA1c level is > 75 mmol/mol (9%) after use of an oral agent, as the likelihood of achieving good glycaemic control with oral agents alone becomes lower.

Third-line treatment

After failure of dual oral therapy, treatment options become more complex. Metformin should be continued for its insulin-sensitising effects unless contraindications develop. Ineffective therapies should be ceased and substituted with a different medication. Comparative evidence from RCTs to inform prescribing is scarce. The options are triple oral therapy or the addition of a GLP-1RA or insulin.

Triple oral therapy

Metformin, sulfonylurea and DPP-4 inhibitor: Limited RCTs examining the addition of sitagliptin12 and linagliptin13 to metformin–sulfonylurea have demonstrated reductions in HbA1c level of 7–10 mmol/mol versus baseline and placebo, respectively,12,13 but with small increases in weight that are significant in some studies. With triple therapy, the advantage of lower risk of hypoglycaemia with DPP-4 inhibitors appears to be lost.12,13 It is reasonable to escalate from metformin and a sulfonylurea or metformin and a DPP-4 inhibitor to triple therapy with all three. However, this combination is not currently PBS-subsidised.
Metformin, sulfonylurea and thiazolidinedione: Trials of triple therapy with metformin, a sulfonylurea and a TZD show HbA1c lowering of about 11 mmol/mol, but with an increase in weight of 3–5 kg and increased hypoglycaemia.14 Pre-emptive decreases in the sulfonylurea dose should be considered. Pioglitazone is PBS-subsidised for triple oral therapy with metformin and a sulfonylurea.
Metformin, sulfonylurea and SGLT2 inhibitor: Limited trials indicate that triple therapy with metformin, a sulfonylurea and an SGLT2 inhibitor may be an effective combination, but this is not PBS-subsidised. A 52-week RCT comparing the addition of canagliflozin or a DPP-4 inhibitor to metformin–sulfonylurea found that HbA1c level decreased by 11 mmol/mol with the SGLT2 inhibitor versus 7 mmol/mol with the DPP-4 inhibitor. There were greater reductions in weight and blood pressure with the SGLT2 inhibitor, and no difference between groups in hypoglycaemia.12
Metformin, sulfonylurea and acarbose: Acarbose is PBS-approved for triple therapy with metformin and a sulfonylurea. One double-blinded crossover trial of this combination reported a 1.9% decrease in weight and a 15 mmol/mol decrease in HbA1c level with the addition of acarbose.15 Acarbose in other dual-therapy combination studies more commonly decreases HbA1c level by about 6–9 mmol/mol.16

Injected agents

Metformin, sulfonylurea and GLP-1RA: Triple-therapy studies of metformin, a sulfonylurea and a GLP-1RA are few but show reductions in HbA1c level of about 11 mmol/mol, with a little weight loss.17-19Hypoglycaemia is common but may be attenuated by reducing sulfonylurea dosage. The available GLP-1RAs have approval from the Therapeutic Goods Administration for use with metformin and sulfonylurea, but only exenatide is PBS-subsidised.
Insulin: Insulin can be used at any stage in the treatment cascade. It is commonly initiated as once-daily basal insulin added to oral drugs, particularly metformin. Alternatively, it can be initiated as once- or twice-daily premixed insulin, again usually in combination with metformin. Insulin therapy can be intensified by combining long-acting insulin with multiple injections of short-acting insulin.
Recent studies have explored combining insulin with newer therapies, including DPP-4 inhibitors, SGLT2 inhibitors and GLP-1RAs, with good effect. These combinations are not PBS-subsidised.

Glucose-lowering therapy in people with renal or hepatic impairment

In the setting of renal dysfunction, pharmacokinetic changes develop that may increase the risk of hypoglycaemia and side effects. Changes are most evident with chronic kidney disease stages 4 and 5, and must be considered when deciding on therapy (Appendix 1). Drug doses may need reduction or cessation. Among the oral agents, glipizide and gliclazide can be used at a reduced dose up to stage 4, as can sitagliptin. Linagliptin is acceptable without dose adjustment, even with dialysis.
Liver disease may also affect pharmacokinetics. Most drugs do not need discontinuation in the setting of mild–moderate hepatic impairment. Drug half-lives, doses, interactions and risks of drug-specific adverse effects should be considered. There is little experience with use of the newer drug classes in people with advanced hepatic impairment.

Glucose-lowering therapy in older people

In older people, glycaemic targets need to be moderated in light of life expectancy, cognitive impairment or frailty.4 This may mean that the glycaemic target should be symptom control only, or ≤ 64 mmol/mol (8%). Assessment of estimated glomerular filtration rate is important, as serum creatinine level is not as reliable a marker of renal function. Cardiac dysfunction is more common in older people, and severe congestive cardiac failure is a contraindication to metformin. Use of multiple drugs should prompt regular review, to minimise polypharmacy. Drugs should be used at the minimum doses needed to achieve practical and safe glycaemic targets.

Conclusions

Diabetes is a progressive condition and, as such, glycaemic targets should be reviewed at regular intervals. The importance of diet and exercise should be reinforced at each step of the therapeutic pathway.
With the range of therapies now available in Australia, there is considerable scope for individualising therapy. If the patient experiences adverse effects with one glucose-lowering agent, another should be substituted. This will often take the form of combination therapy. With diabetes education and an engaged patient, it is now possible to achieve good glycaemic control in more people with T2D.
The Australian Diabetes Society (ADS) council appointed the authors to draft the position statement, with a focus on results of recent trials of triple therapy and newer agents.
The draft statement was reviewed by the current ADS council and revised, then sent to all ADS members for comment and revision.
Provenance: 
Not commissioned; not externally peer reviewed.