Yu gɛt ay blɔd shuga? Lɛ wi lan ɔltin bɔt aypa glycemia!

Sɔntɛnde, yu kin fil lɛk se yu nɔ de fil fayn? Jɔs taya, ɔ yu de tɔsti ɔltɛm? Dɛn tin ya kin bi sayn dɛn we de sho se yu blɔd shuga dɔn ay smɔl. Tide, wi go tɔk bɔt dis sik we dɛn kɔl ay blɔd shuga, ɔ wetin dɔktɔ dɛn kɔl ``Hyperglycemia.'' Nɔ wɔri, dis na sɔntin we bɔku pipul dɛn gɛt, ɛn i impɔtant fɔ no bɔt am.

Wetin di ay blɔd shuga min? (Haypa glycemia) .

Fɔ tɔk am simpul wan, `(Hyperglycemia)` min se di shuga, ɔ glukɔs, na yu blɔd tu bɔku. Dis kin apin we wi bɔdi gɛt tumɔs smɔl insulin , ɔ we wi bɔdi nɔ ebul fɔ yuz insulin fayn fayn wan (dɛn kɔl dis insulin rɛsistɛns) .

Bɔku tɛm, aypa glycemia kin min se yu gɛt dayabitis . Bɔku tɛm, pipul dɛn we gɛt dayabitis kin gɛt ay shuga na dɛn blɔd. If dɛn nɔ trit dis ay blɔd shuga lɛvɛl fɔ lɔng tɛm, i kin pwɛl yu nerv dɛn, blɔd vesel dɛn, tisu dɛn, ɛn ɔgan dɛn.

Sɔntɛnde, if di blɔd shuga go ɔp tumɔs, i kin mek pɔsin gɛt wan sik we dɛn kɔl dayabitik ketoacidosis (DKA) we kin mek pɔsin in layf de pan denja wantɛm wantɛm. Dis kin denja mɔ fɔ pipul dɛn we gɛt dayabitis we de tek insulin ɛn di wan dɛn we nɔ gɛt tayp 1 dayabitis we dɛn nɔ no. Dis nid fɔ go to dɔktɔ wantɛm wantɛm.

Aw bɔku shuga na di blɔd dɛn kin tek am se ‘ay’?

Dis na sɔntin we wi nid fɔ ɛksplen smɔl.

• Fɔ pɔsin we dɛn nɔ no se i gɛt dayabitis, if in blɔd glukɔs lɛvɛl pas 125 mg/dL (miligram pan wan dɛsilita) afta i dɔn fast fɔ at le 8 awa , dɛn kin tek am se na ``Hyperglycemia''.
• If pɔsin in fast glukɔs lɛvɛl de bitwin 100 mg/dL ɛn 125 mg/dL, dɛn kin tek am se i gɛt prɛdiabɛtis . Dis min se i gɛt bɔku prɔblɛm fɔ gɛt dayabitis.
• If di glukoz lεvεl we yu de fast kin hכy pas 125 mg/dL, dεn kin no se dεn gεt dayabitis – bכku tεm dis na tayp 2 dayabεtis. We dɛn no se pipul dɛn gɛt tayp 1 dayabitis, dɛn blɔd shuga lɛvɛl kin rili ay (i pas 250 mg/dL).

Fɔ pɔsin we gɛt dayabitis, if yu blɔd glukɔs lɛvɛl pas 180 mg/dL wan ɔ tu awa afta i it, dɛn kin tek am se na ``Hyperglycemia.`` Bɔt dɛn valyu ya kin difrɛn difrɛn wan dipen pan yu blɔd shuga gol. Yu fɔ tɔk to yu dɔktɔ fɔ no di rayt tin we yu want fɔ du.

Wetin na dis ‘shuga’ (Glucose) we de insay di blɔd?

Glukose, ɔ jɔs ‘shuga’, na di men tin we de gi wi bɔdi ɛnaji, we de kɔmɔt frɔm di kabɔhaydrɛt dɛn we wi de it. Dis na di men tin we wi bɔdi de gi wi trɛnk. Dis glukoz de kכmכt frכm yu bכdi to εvri sεl na yu bכdi εn dεn de yuz am as εnεji.

If yu nɔ gɛt dayabitis, sɔm natura l prɔses dɛm na wi bɔdi de ɛp fɔ kip di blɔd glukɔs lɛvɛl na wɛl bɔdi lɛvɛl. Di men tin we kin mek dis apin na wan ɔmon we dɛn kɔl insulin , we wi pankrias kin mek.

Bɔku tɛm, di blɔd shuga we bɔku kin apin bikɔs i nɔ gɛt insulin ɔ insulin rɛsistɛns. Dis na wetin kin mek pɔsin gɛt dayabitis. Pipul wae gɛt shuga nid fɔ tek mɛrɛsin (we na mɛrɛsin wae dɛn kin it ɔr sintetik insulin) ɛn/ɔ mek chenj na dɛn layf fɔ kɔntrol dɛn blɔd shuga lɛvɛl.

Aw dis sik kin kɔmɔn?

Hyperglycemia ɛn dayabitis na tin dɛn we kin apin to pɔsin. Fɔ ɛgzampul, wan pan ɛvri tɛn pipul dɛn na Amɛrika gɛt dayabitis. Di blɔd shuga we bɔku kin bɔku bak pan pipul dɛn we gɛt dayabitis. Dis sik dɔn rili kɔmɔn naw na wi kɔntri.

Wetin na di sayn dɛm we de sho se yu gɛt bɔku blɔd shuga?

We di shuga na yu blɔd go ɔp, yu nɔ go notis ɛni big sayn wantɛm wantɛm. Bɔt yu kin bigin fɔ notis dɛn sayn ya smɔl smɔl.

Di sayn dɛm wae kin apun kwik kwik wan:

• Tɔsti pasmak (polydipsia) ɛn/ɔ fil angri.
• Nid fɔ pis bɔku tɛm.
• Ɛd we de at (ed we de at).
• Di vishɔn we nɔ klia smɔl.

Di sayn dɛm we kin apin we di shuga lɛvɛl de go ɔp as tɛm de go:

• Jɔs fil fɔ taya pasmak.
• We yu de lɔs yu wet (fɔ no rizin).
• uman dεm kin gεt vagina yist infεkshכn .
• Infεkshכn dεm na di skin .
• Wund dɛn kin tek tɛm fɔ wɛl.

If yu ɔ yu pikin gɛt ɛni wan pan dɛn sik ya, i rili impɔtant fɔ go to dɔktɔ fɔ advays.

Di glukɔs lɛvɛl wae pipul dɛm wae gɛt shuga kin bigin fɔ gɛt dis sik kin difrɛn frɔm pɔrsin to ɔda pɔrsin. Bɔrku pipul nɔr kin gɛt big big sik te dɛn blɔd shuga rich 250 mg/dL ɔ pas dat. Bɔt pipul dɛm wae nɔr dɔn no yet se dɛn gɛt shuga kin gɛt sɔm kayn sik wae dɛn nɔr gɛt bɛtɛ blɔd.

If yu de tek insulin ɔ ɔda mɛrɛsin fɔ dayabitis, i impɔtant fɔ no di fɔs sayn dɛn we de sho se yu gɛt bɔku shuga na yu blɔd ɛn fɔ chɛk yu blɔd shuga ɔltɛm. If dɛn nɔ trit dis sik (haypa glycemia) kin mek pɔsin gɛt dayabitik ketoacidosis (DKA).Dis kin mek yu gɛt wan denja sik we dɛn kɔl ketoacidosis. dis na we di bכdi de bi asid bikoz fכ insulin nכ de εn di tin dεm we dεn kכl kεtכn de inkrεs. Dis kin afɛkt pipul dɛm bak wae gɛt tayp 1 dayabitis wae dɛn nɔr dɔn no. Dis kin bi imejensi, we kin mek pɔsin kɔma ɔ ivin day.

Denja kondishɔn: Di sayn dɛm fɔ dayabitik ketoacidosis (DKA):

• Nɔs ɛn vɔmit.
• Dihaydreshɔn - we wata de lɔs na di bɔdi.
• Pɔsin we de fil pen na di bɛlɛ.
• Briz we de smɛl frut.
• Dip, labored brith ɔ kwik brith (Kussmaul breathing).
• At bit kwik kwik wan.
• Kɔnfyushɔn ɛn disorienteshɔn.
• Nɔbɔdi nɔ kin no natin.

If yu ɔ yu pikin gɛt dɛn sayn ya fɔ `(DKA)`, go to dɔktɔ wantɛm wantɛm!

Wetin mek di blɔd shuga kin go ɔp lɛk dis? Wetin na di tin dɛn we kin mek i apin?

Di men rizin we mek pɔsin gɛt bɔku blɔd shuga na we i nɔ gɛt insulin. Dis kin bi bikɔs ɔf di insulin rɛsistɛns ɔ prɔblɛm wit wi pankrias we de mek insulin.

Ɔda ɔmon dɛn bak kin mek di blɔd shuga bɔku. fכ egzampl, we di kכ tisol (dεn kכl dεm bak "strεs כmon") כ di כmon we de gro kin mek bak di bכdi shuga go kכmכt.

Insulin Resistans fɔ mek yu nɔ gɛt insulin

Di tin we kin mek pɔsin gɛt aypa glycemia na we pɔsin nɔ kin gɛt insulin . Dis na we yu mɔsul, fat, ɛn liva sɛl dɛn nɔ de ansa fayn to insulin.

We yu sɛl dɛn nɔ de ansa fayn to insulin, yu bɔdi nid mɔ insulin fɔ kɔntrol yu blɔd shuga. If yu bɔdi nɔ ebul fɔ mek insulin (ɔ if yu nɔ tek insulin), yu blɔd shuga de go ɔp.

Insulin resistance na di men tin we kin mek pɔsin gɛt tayp 2 dayabitis. Bɔt i kin apin bak pan pipul dɛn we nɔ gɛt shuga ɛn pipul dɛn we gɛt ɔda kayn shuga. I kin bi fɔ sɔm tɛm ɔ fɔ lɔng tɛm.

Sɔm tin dɛn we kin mek pɔsin nɔ gɛt insulin:

• Fat: Sayɛnsman dɛn biliv se we pɔsin fat, mɔ di bɔku bɔku fat we de na di bɛlɛ ɛn rawnd di ɔgan dɛn (wi kin kɔl am `visceral fat` ), na di men tin we kin mek pɔsin nɔ gɛt insulin.
• We pɔsin nɔ de du ɛnitin we i de du na in bɔdi.
• Na it we gɛt bɔku tin dɛn we dɛn dɔn prosɛs, we gɛt bɔku kabɔhaydrɛt ɛn we gɛt sɛtyuret fat.
• Sɔm mɛrɛsin dɛn: Fɔ ɛgzampul , kɔtikosterɔyd, sɔm blɔd prɛshɔn mɛrɛsin, sɔm HIV tritmɛnt, ɛn sɔm saykayatrik mɛrɛsin. Dɛn tin ya kin mek yu nɔ gɛt insulin, fɔ sɔm tɛm ɔ fɔ lɔng tɛm, i kin dipen pan aw lɔng yu tek dɛn.

Sɔm ɔmon kɔndishɔn dɛn kin mek bak insulin nɔ de wok:

• Cushing’s syndrome (di kɔtisol we de bɔku).
• Acromegaly (di ɔmon we de mek pɔsin gro ɔp).
• di bεlε: We di bεlε de, di כmon dεm we di plasεnta de kכmכt kin mek di insulin rεsistεns. Dis kin mek sɔm pipul dɛn gɛt gestational diabetes .

Sɔm jɛnɛtik kɔndishɔn dɛn we dɛn kin gɛt frɔm dɛn mama ɛn papa kin gɛt fɔ du bak wit insulin rɛsistɛns:

• `Rabson-Mendenhall sindrom`
• `Donohue sindrom`
• `Mayotonik distrofi`
• `Alström sindrom`
• `Werner sindrom`

Prɔblɛm dɛn we de na di pankrias

If yu pankrias pwɛl, dat kin mek yu nɔ gɛt bɔku insulin, ɛn dis kin mek yu gɛt aypa glycemia. Sɔm pan di pankrias sik dɛm wae kin mek yu gɛt aypa glycemia ɛn dayabitis na:

• Ɔtoimyun sik: Insay tayp 1 dayabitis, yu imyun sistɛm kin atak di sɛl dɛn we de mek insulin na yu pankrias fɔ rizin we yu nɔ no. Dis min se yu pankrias nɔ kin ebul fɔ mek insulin igen, we kin mek yu gɛt aypa glycemia. Wan sik we dɛn kɔl Latent Autoimmune Diabetes in Adults (LADA) kin kam bak bikɔs ɔf wan ɔtoimyun riakshɔn, bɔt i kin divɛlɔp sloslo pas tayp 1 dayabitis.
• Kronik pankrias: Dis kכndyushכn kin mek di pankrias inflameshn fכ lכng tεm, we kin pwεl di sεl dεm we de mek insulin. Dis kin mek yu nɔ gɛt insulin (haypa glycemia). Pankriaytis na wan tin we dɛn no se kin mek pɔsin gɛt Tayp 3c dayabitis .
• Pankrias kansa: Pankrias kansa kin pwɛl di sɛl dɛn we de mek insulin, ɛn dis kin mek dɛn nɔ gɛt insulin (hyperglycemia). Na lɛk 25% pan di pipul dɛm we gɛt pankrias kansa kin gɛt dayabitis 6 to 36 mɔnt bifo dɛn no di kansa.
• Sistik fibrosis: Pipul dεm we gεt sistik fibrosis kin gεt skata na dεn pankrias bikoz dεn de mek mכkus pasmak. dis de ridyus di insulin we dεn pankrias de mek, we de mek dεn gεt haypa glycemia εn cystic fibrosis-related diabetes (CFRD) .

Di tin dɛn we kin mek di shuga bɔku fɔ sɔm tɛm

Sɔntɛnde, pipul dɛm wae gɛt shuga ɛn wae nɔr gɛt shuga kin gɛt bɔrku shuga na dɛn blɔd fɔ sɔm tɛm (hyperglycemia).

• Bɔdi strɛs, lɛk sik, ɔpreshɔn, ɔ injuryDis kin mek di blɔd shuga go ɔp fɔ sɔm tɛm.
• Akyu imɔshɔnal strɛs , lɛk wan bad bad tin ɔ strɛs we gɛt fɔ du wit wok, kin mek bak di blɔd shuga go ɔp. Dis kin bi bikɔs di ɔmon dɛn we dɛn kɔl kɔtisol ɛn/ɔ epinefrin (adrenaline) de kɔmɔt .

Speshal rizin dɛm wae kin mek yu gɛt ay blɔd shuga pan pipul dɛm wae gɛt shuga

Bɔku rizin dɛn de we mek pipul dɛn we gɛt dayabitis kin gɛt bɔku shuga na dɛn blɔd. Dis kin apin if tin lɛk it ɛn dayabitis mɛrɛsin nɔr balans.

Kɔmɔn tin dɛm wae kin mek yu gɛt ``Hyperglycemia`` pan pipul dɛm wae gɛt shuga:

• Nɔ tek insulin inof, tek di rɔng kayn insulin, tek insulin we dɔn pas, ɔ prɔblɛm wit di say we dɛn injekt insulin (e.g., prɔblɛm wit di say we dɛn injɛkshɔn fɔ pɔsin we de yuz insulin pɔmp).
• Di kɔrɛkt tɛm fɔ it insulin ɛn kabɔhaydrɛt.
• Di kayn kabɔhaydrɛt we yu de it nɔ go mach di insulin we yu bɔdi kin mek ɔ di insulin we yu injɛkt.
• Yu nɔ de tek inof pan yu ɔral dayabitis mɛrɛsin.
• Fɔ nɔ de du tin bɛtɛ pas aw i kin bi.
• Dawn phenomenon: Na in blɔd shuga de go ɔp na mɔnin.

Wetin na di prɔblɛm dɛn we kin apin if di blɔd shuga kɔntinyu fɔ go ɔp?

If yu gɛt ay blɔd shuga lɛvɛl (chronic hyperglycemia) fɔ bɔku ia, i kin pwɛl yu blɔd vesel ɛn tisu dɛn. Dis kin mek yu gɛt difrɛn prɔblɛm dɛn. Sɔm pan dɛn na:

• Retinopathy, we kin afɛkt di yay .
• Nefropathy, we kin afɛkt di kidni dɛn .
• Nyuropathy, we kin afɛkt di nerv dɛn .
• Gastroparesis, we kin mek di bɛlɛ nɔ ebul fɔ ɛmti .
• At sik .
• Strok .

De impɔtant tin fɔ mɛmba na dat ɔda tin dɛm lɛk di jɛnɛtik inflɔwɛns ɛn aw lɔng yu dɔn gɛt dayabitis, kin afɛkt bak di divɛlɔpmɛnt fɔ di prɔblɛm dɛm wae gɛt shuga.

If yu blɔd shuga go ɔp wantɛm wantɛm ɛn bad bad wan (acute hyperglycemia) i kin mek yu gɛt wan sik we go mek yu layf de pan denja we dɛn kɔl dayabitik ketoacidosis (DKA) .

Aw yu kin no bɔt dis?

Dɔktɔ dɛn kin tɛl dɛn fɔ du blɔd tɛst fɔ chɛk fɔ si if pɔsin gɛt ay blɔd ɛn fɔ no if i gɛt dayabitis. Dɛn tɛst ya kin bi:

• Fast glukɔs tɛst dɛn.
• Glukɔs tolɛreshɔn tɛst dɛn.
• A1c tɛst.

Pipul wae gɛt shuga kin tɛst dɛn blɔd shuga na os (yuz glukɔs mita). Dis kin mek dɛn ebul fɔ wach aw dɛn blɔd shuga de ɛn chɛk fɔ si if dɛn gɛt aypa glycemia. If yu yuz wan kɔntinyu glukɔs monitarin (CGM) sistem , i kin wɔn yu we yu blɔd shuga bɔku. Bɔt sɔntɛnde dis teknɔlɔji nɔ kin kɔrɛkt, so if di CGM ridin dɛn nɔ mach wetin yu fil, i impɔtant fɔ chɛk yu blɔd shuga wit glukɔs mita.

Aw fɔ kɔntrol di ay blɔd shuga? (Tritmɛnt)

If yu tek insulin fɔ kɔntrol yu dayabitis, di men we fɔ trit di ay blɔd shuga na fɔ injekt insulin. Ɔlman nid difrɛn insulin. Yu ɛn yu dɔktɔ go disayd togɛda wetin na di bɛst doz fɔ trit ɛn mek yu nɔ gɛt ay blɔd shuga fɔ yu. If yu chenj di it we yu de it ɛn yu plan fɔ du ɛksɛsayz, dat kin ɛp bak fɔ kɔntrol yu blɔd shuga ɛn mek yu nɔ gɛt aypa glycemia.

Pipul dɛm wae gɛt tayp 2 dayabitis wae nɔr nid fɔ tek insulin kin kɔntrol dɛn aypa glycemia wit chenj na dɛn layf (lɛk aw dɛn de it ɛn ɛksesaiz) ɛn dɛn kin tek mɛrɛsin fɔ dayabitis. Yu ɛn yu dɔktɔ go disayd us plan we bɛtɛ fɔ yu.

Us kayn op yu kin gɛt we yu de liv wit dis sityueshɔn?

Di prɔgnosis fɔ pipul dɛm wae gɛt haypa glycemia de dipen pan aw dɛn kin kɔntrol dɛn dayabitis ɔltogɛda.

Bɔku tin dɛn kin afɛkt aw pɔsin go ebul fɔ kɔntrol in dayabitis:

• Akses to wɛlbɔdi savis.
• Akses fɔ ɛdyukeshɔn bɔt dayabitis.
• Akses to dayabitis mɛnejɛmɛnt tɛknɔlɔji ɛn mɛrɛsin.
• Abiliti fɔ gɛt tin dɛn fɔ it fayn ɛn fɔ du ɛksɛsayz.
• Sɔpɔt frɔm di wan dɛn we wi lɛk.
• Mental hεlth kכndishכn dεm (e.g. pwεl hat, wae yu de wɔri).
• Ɔda tin dɛn we kin apin to pɔsin in bɔdi.

If yu gɛt bɔku bɔku blɔd blɔd fɔ lɔng tɛm, dat kin mek yu gɛt siriɔs prɔblɛm dɛn, ɛn bɔku tɛm dɛn nɔ kin ebul fɔ chenj dɛn prɔblɛm ya. Bɔku stɔdi dɛn dɔn sho se we pɔsin nɔ trit am fɔ lɔng tɛm, i kin mek di pɔsin in layf shɔt ɛn i kin mek di kwaliti fɔ layf wɔs.

De tin wae impɔtant pas ɔl na fɔ no se yu kin liv wɛl bɔdi layf wit dayabitis. Dɛn tin ya rili impɔtant fɔ mek pɔsin tink gud wan:

• Di we aw pipul dɛn de liv dɛn layf kin chenj.
• Fɔ du ɛksasaiz ɔltɛm.
• Di chenj dɛn we de apin na di it we dɛn de it.
• Fɔ chɛk di blɔd shuga ɔltɛm (espɛshali fɔ di wan dɛn we de tek insulin).

Stɔdi dɔn sho se pipul dɛn we gɛt dayabitisif yu mεnten di A1C lεvεl dεn dכn 7% i kin ridyus di risk fכ komplikεshכn dεm.

Aw fɔ mek yu nɔ gɛt bɔku blɔd shuga ɔltɛm?

Bɔt i sɔri fɔ no se i nɔ kin izi fɔ mek yu nɔ gɛt bɔku blɔd shuga kpatakpata we yu gɛt dayabitis. Bɔt yu kin chenj yu plan fɔ mɛn yu shuga fɔ tray fɔ ridyus di bɔku bɔku blɔd shuga.

Dis kin izi fɔ du wans yu ɛn yu dɔktɔ dɔn ɔndastand wetin de mek yu gɛt ay blɔd shuga. Gi yu dɔktɔ bɔku tin bɔt ɛni tɛm we yu blɔd shuga bɔku. Sɔntɛnde, di sɔlv fɔ di prɔblɛm kin simpul lɛk fɔ chenj di tɛm we yu de tek yu mɛrɛsin, it, ɔ ɛksesaiz.

Dɛn step ya kin ɛp fɔ mek yu nɔ gɛt bɔku blɔd shuga:

• Tek ɔl yu mɛrɛsin dɛn lɛk aw dɛn tɛl yu fɔ tek.
• Fɔ fala yu dɔktɔ in advays bɔt aw fɔ it ɛn ɛksesaiz.
• Chek yu blɔd shuga ɔltɛm.

Ustɛm yu fɔ go to dɔktɔ bɔt di ay blɔd shuga?

If yu gɛt dayabitis ɛn yu de gɛt bɔku bɔku blɔd shuga, go to yu dɔktɔ we de ɛp yu fɔ kɔntrol yu dayabitis. I kin ɛp yu fɔ ajɔst yu manejmɛnt plan. Dis kin inklud fɔ chenj di mɛrɛsin we yu de tek, di tin dɛn we yu fɔ it, ɔ di we aw yu de du ɛksɛsayz.

Ustɛm yu fɔ go na Imejɛnsi Tritmɛnt Yunit (ETU) ?

If yu gɛt sayn dɛm fɔ `(DKA)` (e.g. fɔ vɔmit ɛn fɔ tɔsti pasmak wit ay blɔd shuga), go na imejensi rum wantɛm wantɛm. `(DKA)` nid fɔ gɛt mɛrɛsin kwik kwik wan.

Wetin na di difrɛns bitwin di ay blɔd shuga (Hyperglycemia) ɛn di lɔw blɔd shuga (Hypoglycemia)?

• Hyperglycemia na we di blɔd shuga de go ɔp. "Hyper-" min "high" ɔ "pas."
• Hypoglycemia na we di blɔd shuga nɔ bɔku. "Hypo-" min "lɔ."

Hyperglycemia kin rili kɔmɔn pan pipul dɛm wae gɛt shuga. We yu de chɛk yu blɔd shuga ɔltɛm ɛn go to yu dɔktɔ we gɛt dayabitis, dat kin ɛp yu fɔ kɔntrol yu shuga ɛn aypa glycemia. Mɛmba se, ay blɔd shuga nɔto sɔntin we yu fɔ de du ɔltɛm. No se tin dɛn de we yu kin du fɔ mek i nɔ gɛt am. If yu de fil se yu de fil bad fɔ kɔntrol yu dayabitis, tɔk to yu dɔktɔ. Tugeda, una kin mek wan plan fɔ rich yu manejmɛnt gol dɛn.

Mɛsej we dɛn kin kɛr go na os

So, frɔm wetin wi dɔn tɔk bɔt, yu fɔ ɔndastand wetin na di ay blɔd shuga, ɔ ``Hyperglycemia'', di tin dɛm wae kin mek yu gɛt am, di sayn dɛm, ɛn aw fɔ kɔntrol am.

De tin wae impɔtant pas ɔl na fɔ go to dɔktɔ if yu gɛt dɛn kayn sik ya. If dɛn no am kwik ɛn dɛn de manej am fayn, yu go ebul fɔ liv fayn layf ɛn gladi at.

• Yu fɔ no di shuga we yu gɛt na yu blɔd.
• Yuz di mɛrɛsin we dɛn gi yu di rayt we.
• It fayn it .
• Ɛksesaiz ɔltɛm.
• Tray fɔ ridyus strɛs .

If yu du dɛn tin ya rayt, dɛn go ɛp yu bad bad wan fɔ protɛkt yusɛf frɔm ``Hyperglycemia`` ɛn di prɔblɛm dɛn we kin kam wit dayabitis. Nɔto yu wan de, ɛn bɔku pipul dɛn de we go ɛp yu fɔ du dis waka.

` Haypa glycemia, dayabitis, blɔd shuga, insulin, simptom dɛm, DKA, Insulin Resistance