Ọrịa shuga mellitus - etiopathogenesis, nyocha, nhazi ọkwa

Ọrịa shuga na-abụghị insulin (NIDDM, ọrịa shuga 2) - Ọrịa heterogeneous ji insulin inspa mechie yana nsị insulin nke anụ ahụ na - egbochi insulin.

1) ihe nketa - mkpụrụ ndụ ihe mebiri emebi (na chromosome 11 - mebiri insulin, na chromosome 12 - insulin receptor synthesis insurement, ntụpọ mkpụrụ ndụ ihe dị n’ime sistemụ glucose site na mkpụrụ ndụ or-mkpụrụ ndụ ma ọ bụ akwara), ebugharị nke ukwuu, na ejima abụọ, NIDDM na-etolite na 95-100% okwu.

2) oke nri na oke ibu - ihe oriri nwere kalori nwere otutu ihe ndi mmadu na enye obi uto karia, ihe ndi ozo, ihe o alcohol nu alcohol nu na mmanya ubara, ya na ndu ume ala, na-enye aka na izopu insulin na mmepe nke iguzogide insulin.

Pathogenesis nke NIDDM kpatara mmebi iwu na ọkwa atọ:

1. Imebi insulin insulin - ntụpọ igodo nke mbụ na NIDDM, achọpụtara ma n ’ụzọ mbụ ọrịa ahụ siri kwupụta:

a) mmebi iwu ruru eru- na NIDDM, ọkwa insulin ọbara na-ebu ọnụ na-ebelata nke ukwuu, proinsulin na-ebu ụzọ

b) nsogbu ụkọ - na ahụike, na nzaghachi na nchịkwa glucose, a na - achọpụta insulin nke insulin: ọnụ ọgụgụ nke mbụ nke nzuzo na - amalite ozugbo mkpali glucose, na - ejedebe site na nkeji nke iri, n'ihi ntọhapụ nke insulin echekwara site na mkpụrụ ndụ β-cell, na njiri nke abụọ nke nzuzo na - amalite mgbe nkeji 10 gasịrị. jiri ya na mmeghe ma ọ bụ mgbe nkeji iri atọ gasịrị ma ọ bụ mgbe emesịrị nchịkwa glucose, ogologo oge, na-egosiputa nzuzo nke insulin arụkọtara ọhụrụ na nzaghachi na mkpali nke mkpụrụ ndụ with na glucose, na NIDDM enweghị usoro mbu yana akụkụ nke abụọ nke insulin na-agbazi.

c) mmebi iwu - NIDDM gosipụtara insulinopenia siri ike n'ihi mbelata nke β-sel nke agwaetiti Langvrhans, itinye ego nke amyloid na agwaetiti (mebere site na amylin, nke mkpụrụ ndụ β-mekọtara yana insulin ma sonye na ntụgharị nke proinsulin ka insulin), “glucose na-akpata ọnya" nsogbu nke ndagwurugwu nke Langerhans na mbelata insulin), wdg.

2. Nchịkwa insulin nke akwara anụ ahụ:

a) prereceptor - ejikọtara ya na ngwaahịa nke mkpụrụ ndụ ihe nketa gbanwere, arụghị ọrụ

insnwe insulin ma ọ bụ ntụgharị nke proinsulin na insulin ezughị ezu

b) onye nnata - ejikọtara yana ọnụ ọgụgụ nke ndị na - anabata insulin na - arụ ọrụ, njikọta nke ndị na - anabata ndị na - adịghị arụ ọrụ nke ukwuu, ọdịdị nke ọgwụ mgbochi antireceptor.

c) postreceptor - Mbelata na ọrụ nke tyrosine kinase nke nnabata insulin, mbelata ọnụ ọgụgụ ndị na - ebuga glucose (ihe na - edozi ihe dị n'ime sel ahụ nke na - ahụ na ọ bụ glucose na - abanye n'ime ụlọnga),

Na mmepe nke nguzogide insulin, mgbasa nke insulin antiagonists n’ọbara (mgbochi insulin, homonụ insulin: homonụ ibu, cortisol, homonụ thyroid, thyrotropin, prolactin, glucagon, CA) dịkwa mkpa.

3. Mmụba na-emeju umeji imeju - n'ihi ịba ụba gluconeogenesis, imeju glucose mepụta glucose site na imeju, mebiri usoro circadian nke ịtọ glucose (enweghị mbelata nke mmepụta glucose n'abalị), wdg.

Nkpugheputa nke ogwu nke NIDDM:

1. Mkpesa ndị na-esonụ bụ njirimara ha:

- nkwuputa izugbe na adighi ike aru (n'ihi erughi otu ike, glycogen na protein n’ime akwara)

- akpịrị ịkpọ nkụ - na oge ọgbụgba DM, ndị ọrịa nwere ike ị drinkụ mmiri 3-5 ma ọ bụ karịa kwa ụbọchị, hyperglycemia dị elu, akpịrị ịkpọ nkụ na-akpọ nkụ, akpịrị kpọrọ nkụ (n'ihi akpịrị ịkpọ nkụ na belata agịga ọnụnụ)

- ugboro ugboro ma na-eme ka ọsụgharị ma ehihie ma abalị

- oke ibu - ọtụtụ mgbe, mana ọ bụghị oge niile

- itching nke anụahụ - ọkachasị ụmụ nwanyị nọ na mpaghara ọmụmụ

2. Ebumnuche, steeti akụkụ na sistem:

A) akpụkpọ:

- akpụkpọ akpọnwụ, belata turgor na elasticity

- ọnya anụ ahụ pustular, ụkwara ntutu ugboro ugboro, hydroadenitis, epidermophytosis nke ụkwụ

- akpụkpọ anụ xanthomas (papules na nodules nke agba edo edo, juputara na lipids, nke dị na ala, ụkwụ, ikpere na ikpere aka, aka) na xanthelasma (oghere egbugbere ọnụ na-acha odo odo na akpụkpọ nke nkuanya)

- Rubeosis - mmụba nke akpukpo anụ ahụ na ịmịcha nke anụ ahụ na cheekbones na cheeks (ọrịa shuga)

- lipoid necrobiosis nke anụ ahụ - ọtụtụ mgbe na ụkwụ, nke mbụ enwere okpu-acha ọbara ọbara-aja aja ma ọ bụ odo nodules ma ọ bụ ntụpọ gbara gburugburu ókèala erythematous nke cha cha dị, akpịrị dị n’elu ha jiri nwayọ nwayọ, na-egbu maramara, na-enwe oke ikikere (“mpempe akwụkwọ”), mgbe ụfọdụ emetụta mpaghara ọnya, na-agwọ nwayọ nwayọ, na-ahapụ mpaghara mmebi

b) nri digestive:

- ọrịa ọgbụgba, ịtọpụ ezé

- alveolar pyorrhea, gingivitis, ọnya afọ ma ọ bụ stomatitis aphthous

- gastritis na-adịghị ala ala, duodenitis na mmepe nke nke atrophy, belatara ihe nzuzo nke mmiri ọ gastụ gastụ gastric,

mbelata nke ọrụ moto nke afọ ruo gastroparesis

- nsị nsia: afọ ọsịsa, steatorrhea, ọrịa malabsorption

- ịba ọcha n'anya nke imeju, cholecystitis na-adịghị ala ala, gallbladder dyskinesia, wdg.

sisitemu obi:

- mmalite mmepe nke atherosclerosis na ọrịa obi na ọrịa na - enwe ọtụtụ nsogbu (MI nwere ọrịa shuga nwere ike ime na - enweghị ihe mgbu - Cardiac hypesthesia syndrome nke Parishioner, na - abụkarị transmural, na - esiri ike ịga n'ihu, yana ọtụtụ nsogbu)

- ọbara mgbali ọbara (oge nke abụọ n'ihi nephroangiopathies, atherosclerosis nke akwara gbasara akwara, wdg)

- "obi na-arịa ọrịa shuga" - dysmetabolic myocardial dystrophy

sistem iku ume:

- nsogbu nke akwara afọ na --eme ya okpomoku, ugboro ugboro, nsogbu

- oria na-efe efe (n'ihi microangiopathy nke ngụgụ)

- ọnya na-arịa ụkwara akwara na-arịa ọrịa ụkwara akwara na-arịa ya

e) sistem: ntụgharị uche nke ọrịa na - efe efe na mbufụt nke urinary tract (cystitis, pyelonephritis), wdg

Nchoputa nke NIDDM: lee ajụjụ 74.

1. Nri - ga- agbaso ihe ndị a chọrọ:

- be physiological na mejupụtara na ruru nke isi ihe (60% carbohydrates, abụba 24%, protein 16%), na-ekpuchi niile ume akwụ ụgwọ dabere ogo nke ọrụ anụ ahụ na n'ịhụ na mmezi nke nkịtị "ezigbo" ahu ahu, na ngafe nke ahu ahu a hypocaloric nri na-egosi. site na ngụkọta oge nke 20-25 kcal kwa 1 n'arọ nke ịdị ahịrị / ụbọchị

- 4-5 ugboro nri na nkesa na - esote nri nke kalori kwa ụbọchị: 30% - maka nri ụtụtụ, 40% - maka nri ehihie, 10% - maka nri ehihie, 20% - maka nri abalị.

- kpochapu ahihia n’iru ahihia, inu mmanya, mee ka ihe ndi n’ahu ghara idi

- amachi abụba sitere na anụmanụ (40-50% nke abụba kwesịrị ịbụ ihe oriri)

A na-eme nri n'ụdị monotherapy rue, megide nzụlite nke iji ya, ọ ga-ekwe omume ịkwụghachi ụgwọ zuru oke maka ọrịa shuga.

2. Ibelata ibu, mmega ahụ zuru oke (na iribiga oke aru, enwere ike iji ya dozie ihe - usoro a ga --eme ihe na - egbochi mgbochi nke catecholamines, meridia (sibutramine) 10 mg 1 oge / ubochi, maka onwonye onwa nke 3-5 n'arọ buru ibu.

3. Ọgwụ ọgwụ - ọgwụ hypoglycemic ọgwụ (na ndị ọrịa nwere ụdị insulin-chọrọ ụdị 2 ọrịa shuga + ọgwụ insulin na ọgwụ ọgwụ a gwakọtara ọnụ: mixtard-30, profaịlụ humulin-3, insuman comb-25 GT na usoro nchịkwa okpukpu abụọ tupu nri ụtụtụ na nri abalị):

a) zoro ezo - ọgwụ na - eme ka mkpụrụ ndụ ndị mejupụtara insulin insulin rụchaa

1) sulferilurea dị iche iche - chlorpropamide (m ọgbọ) 250 mg / ụbọchị na 1 ma ọ bụ 2 doses, glibenclamide (maninyl) 1.25-20 mg / ụbọchị, gụnyere micronized ụdị mannyl 1.75 na 3.5, glipizide, glycoslazide (ọrịa shuga) 80-320 mg / ụbọchị, glycidone, glimepiride (amaryl) 1-8 mg / ụbọchị

2) usoro amino acid - nke kachasị mma maka nhazi nke hyperglycemia postprandial: novonorm (repaglinide) nke 0.5-2 mg tupu nri ruo 6-8 mg / ụbọchị, starlix (nateglinide)

b) biguanides - mmụba na ọnụnọ nke insulin ikike itinye n'ọrụ nke glucose, belata gluconeogenesis, nwekwuo ojiji nke glucose site na eriri afọ na mbelata glucose ọbara site na eriri afọ: N, N-dimethylbiguanide (siofor, metformin, glucophage) 500-850 mg 2 ugboro / ụbọchị

c) a-glucosidase inhibitors - belata nnabata nke carbohydrates na nri diges: glucobai (acarbose) na 150-300 mg / ụbọchị na usoro atọ kewara nri.

d) glitazones (thiosalidinediones, insulin na-enyocha ihe) - mee ka ọgbụgba anụ ahụ dị na insulin na-abawanye na insulin: actos (pioglitazone) 30 mg 1 oge / ụbọchị

4. Mgbochi na ọgwụgwọ nke nsogbu ndị na-egbu oge NIDDM - iji nweta ihe ịga nke ọma nke nsogbu ahụ ọ dị mkpa:

a) iji kwụọ ụgwọ mmebi nke metabolism metabolism na normoglycemia, aglycosuria site na ọgwụgwọ zuru oke na nke NIDDM

b) kwụọ ụgwọ maka metabolism abụba na usoro ọgwụgwọ nwere ike ịmịlata mmanụ: nri nwere mgbochi nke abụba, ọgwụ (statins, fibrates, na -eme nicotinic acid, wdg)

c) hụrụ ọkwa ọbara mgbali elu (ọgwụ mgbochi mmiri, ọkachasị ndị na - egbochi ACE, nke na - enwekwa nsogbu nephroprotective)

g) iji hụ nhazigharị nke coagulation na usoro anticoagulation ọbara

Mgbochi nke nsogbu ịta ahụhụ gụnyere na-ejigide ụgwọ ọrụ nke carbohydrate metabolism ogologo oge na nchọpụta mbụ nke mmalite nke mbido ọrịa shuga:

1) ọrịa mamịrị retinopathy - Ọ dị mkpa ị na-eme nyocha ego mgbe niile otu ugboro n'afọ na afọ ise mbụ, yana otu ugboro kwa ọnwa 6, na neoplasm nke arịa azụ, a na-egosi coagulation laser.

2) Ọrịa mamịrị na-arịa ọrịa mamịrị - ọ dị mkpa iji kpebie microalbuminuria otu ugboro kwa ọnwa isii, mgbe ihe iriba ama nke akwara gbasara akụrụ na-apụta - nri nwere mgbochi nke protein anụmanụ (ihe ruru 40 g kwa ụbọchị) yana sodium chloride (ihe ruru 5 g kwa ụbọchị), ojiji nke ACE inhibitors, ọgwụgwọ detoxification, yana iji ya na-akawanye njọ nke ọrụ akụrụ - ịba ọcha n’anya na nsogbu ndị ọzọ.

NIDDM Mgbochi: ezigbo ndu (zere hypodynamia na oke ibu, emela ihe ọ ,ụ alcoholụ na-aba n'anya, ị smokingụ sịga, wdg, nri na-edozi ahụ, iwepụ mgbakasị ahụ) + mmezi zuru oke site na nri ma ọ bụ oge mbụ nke hyperglycemia, na-esochi anya oge nke ọkwa shuga ọbara.

Ọrịa ụkwara ume ọkụ (ọrịa na-adịghị ala ala) nke ọrịa shuga mellitus: microangiopathies (ọrịa mamịrị retinopathy, ọrịa nephropathy), macroangiopathy (ọrịa mamịrị n'ụkwụ ụkwụ), polyneuropathy.

Angiopathy na-arịa ọrịa shuga - ọnya na-arịa ọrịa vaskụla na-agbasa n'ọrịa shuga, na-agbasa ma obere arịa (microangiopathy) yana akwara nke caliber na nnukwu caliber (macroangiopathy).

Ọrịa shuga microangiopathy - kpọmkwem ọrịa shuga mellitus ọnya nke obere arịa (arterioles, capillaries, venules), na-egosipụta mgbanwe na ha owuwu (ndim nke ala okpuru ulo, endothelial ịgbasa, itinye ego nke glycosaminoglycans na arịa mgbidi, arterioles mgbidi hyalinosis, microtromboses, mmepe nke microaneurysmpe nke a na -akụta ọnụ na -anara ọnụ nke a) :

1. Ọrịa mamịrị retinopathy - isi ihe kpuru ìsì na ndị ọrịa nwere ọrịa shuga, ọrịa na-adịghị ala n’ihu (ọnụnọ nke microaneurysms, ọbara ọgbụgba, edema, exudates siri ike na retina), preproliferative (+ mgbanwe na veins retinal: idoanya, mmekpa ahụ, loops, mwepu, ịgbanwere arịa ọbara) na ịmụba (+ ọdịdị nke arịa ọhụrụ). , oke ọbara ọgbụgba ugboro ugboro na retina ya na njiri mara ya na usoro kpụkọtara ọnụ nke anụ ahụ), mkpesa mkpesa banyere ijiji, ntụpọ, mmetụta nke oke ọhịa, ihe ndị na-egbu mara mma. s visual acuity.

Nchọpụta maka ọrịa mamịrị retinopathy nke mamịrị.

"Ọlaedo edo" bụ foto agba agba nke fundus, Fọlọgo nke angiography nke retina; ophthalmoscopy kpọmkwem bụ ugbu a kachasị enweta maka nyocha.

Nyochaa 1st mgbe afọ 1,5-2 gachara nchoputa nke oria shuga, na enweghi ọrịa mamiri retinopathy, nyocha ọ dịkarịa ala 1 oge na 1-2 afọ, ọ bụrụ na ọ dị - ọ dịkarịa ala 1 oge kwa afọ ma ọ bụ karịa, yana ngwakọta nke ọrịa mamịrị retinopathy na afọ ime. , AH, CRF - usoro nyocha nke onwe ya, yana mbelata ihe mberede na anya - nyocha ozugbo site n'aka onye ọkachamara na - ahụ maka ọrịa.

Cipleskpụrụ maka ọgwụgwọ maka ọrịa mamịrị retinopathy mamịrị:

1. Ọgwụ ọgwụ: ụgwọ kachasị ụgwọ maka metabolism metabolism (ọgwụ na-ebelata shuga, insulin ọgwụgwọ), ọgwụgwọ nke concomitant mgbagwoju anya, antioxidants (nicotinamide) maka ọrịa mamịrị retinopathy na-enweghị proliferative na mkpụrụ ndụ dị elu, heparins dị ala nke pere mpe na mbido mbụ nke usoro ahụ.

2. A na-etinye fotocoagulation nke arịa azụ na mbido mbụ nke ọrịa mamịrị retinopathy (mpaghara - foci nke laser coagulation na mpaghara nke usoro pathologies ma ọ bụ ọbara ọgbụgba preretinal, etinyere - coagulates) n'ọtụtụ ahịrị na mpaghara paramacular na parapapillary, panretinal - eji proliferative retinopathy, site na 1200 ruo 1200 etinyere akụrụngwa na usoro nyocha na retina, ụzọ niile site na mpaghara paramacular na parapapillary na mpaghara equatorial nke retina).

3. Cryocoagulation - egosipụtara maka ndị ọrịa nwere ọrịa retinopathy na-arịa ọrịa ụbụrụ, na-agbagha site n'ọbara ugboro ugboro na anụ ahụ, ihe na-abawanye ike na neovascularization na anụ ahụ na-abawanye, na-ebu ụzọ na ọkara nke nku anya, na mgbe izu gasịrị na ọkara nke elu, ọ na-enye aka melite ma ọ bụ dozie ọhụụ ezumike, igbochi ọhụụ zuru ezu, igbochi ọhụụ zuru ezu, igbochi ọhụụ zuru ezu. ìsì.

4. Vitrectomy - egosiri maka ọbara ọgbụgba na-emetụta ugboro ugboro na mgbanwe na - esochi mgbanwe mgbanwe fibrotic na vitreous na retina

2. Ọrịa mamịrị na-arịa ọrịa mamịrị - n'ihi nodular ma ọ bụ mgbasa mgbasa nephroangiosclerosis nke gbasara akụrụ glomeruli.

Clinical na ụlọ nyocha ngosipụta nke ọrịa mamịrị nephropathy.

1. Na mbido mbụ, ekpughere ihe ngosipụta adịghị, na ọkwa ngosipụta nke ọrịa, ịbawanye ụba proteinuria, ọbara mgbali elu, ọrịa nephrotic, ụlọ ọgwụ na-aga n'ihu nke ọdịda akwara adịghị ala ala.

2. Microalbuminuria (urinary albumin excretion, karịa ụkpụrụ nkịtị, mana ọ gaghị eru ogo proteinuria: 30-300 mg / ụbọchị) - akara izizi nke nephropathy mamịrị, na ngosipụta microalbuminuria oge niile, ọkwa ngosipụta nke ọrịa ahụ ga-etolite na afọ 5-7.

3. Hyperfiltration (GFR> 140 ml / min) - nsonaazụ mmalite nke mmetụta hyperglycemia na ọrụ akụrụ na ọrịa shuga, na-eme ka mmebi akụrụ, na-abawanye na oge ọrịa shuga, GFR ji nwayọọ nwayọọ na-agbadata na nha maka ịrị elu proteinuria na ogo ogo nke ọbara mgbali elu.

N'oge ngwụsị nkebi nke ọrịa mamịrị nephropathy proteinuria mgbe niile, mbelata na GFR, mmụba na azotemia (creatinine na urea ọbara), ịbawanye ụba na nkwụsi ike nke ọbara mgbali elu, na mmepe nke ọrịa nephrotic syndrome bụ ihe e ji mara ya.

Otiti mmepe nke ọrịa mamịrị nephropathy:

1) hyperfunction nke akụrụ - mụbara GFR> 140 ml / min, mụbara ọbara gbasara akwara, ọbara mgbali akwara, albuminuria nkịtị.

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Etiopathogenesis na nchọpụta ọrịa shuga

Dabere na ndị ọkachamara na WHO (1999), a kọwara ọrịa shuga dị ka ọrịa metabolic nke etiologies dị iche iche, nke nwere hyperglycemia na-adịghị ala ala nke nwere carbohydrate na-emetụta, abụba na protein metabolism metụtara ntụpọ na nchekwa insulin, mmetụta nke insulin, ma ọ bụ ha abụọ.

Ọkpụkpụ metabolism bụ isi na - ebute ọrịa glucose na amino acids site na membranes cytoplasmic n'ime anụ ahụ na - eme insulin. Mmachi nke ebu mmiri na - ebugharị ihe ndị a na - akpata ihe ndị ọzọ metabolic na - eme.

N'afọ ndị na-adịbeghị anya, echiche ahụ emepechaala na ọrịa shuga bụ mkpụrụ ndụ ihe nketa yana ọrịa nje na-arịa ọrịa hyperglycemia na-adịghị ala ala, ụdị ndị bụ isi nke ụdị shuga II na ọrịa shuga. Ọtụtụ mgbe, enweghị ike ịmata ọdịiche dị na etiological na ihe na-akpata mmepe nke ọrịa ahụ.

Ebe obu na ekpughere ngosiputa ihe omimi nke oria mellitus na nkwenye biochemical na ogha nke ndi mmadu, otutu nsogbu nke vaskụla mbubreyo (mmepe nke pụtara na oge nke ọrịa metabolic afọ karịa afọ 5-7), ka ekpughere, mgbe ahụ, na 1999 ndị ọkachamara WHO mere atụmatụ maka nhazi nke ọrịa na ihe ọhụrụ. ihe nlere nyocha nke ulo ogwu maka oria oria (table. 33.1).

A na-atụ aro ka ọ ghara iji mkpụrụ okwu “shuga insulin” na “ọrịa insulin na-abụghị” na ịhapụ naanị aha “ụdị shuga II na ọrịa shuga”. Nke a bụ n'ihi pathogenesis nke ụdị ndị a, ma ghara iburu n'uche usoro ọgwụgwọ na-aga n'ihu. Na mgbakwunye, enwere ike ịgbanwere ụdị insulin na-enwere onwe ya iji mezue ịdabere na ya nwere ike ịda na ọkwa dị iche iche nke ndụ onye ọrịa (Isiokwu 33.3).

Isiokwu 33.3. Ọrịa glycemic: ụdị etiological na ọkwa nlere (WHO, 1999)

Typesdị ọrịa shuga na-arịakarị II, nke na-akpata ihe karịrị 90% nke ọrịa shuga niile.

Elldị nke ọrịa shuga mellitus gụnyere nsogbu nke metabolism metabolism metụtara mbibi nke β-mkpụrụ ndụ nke agwaetiti pancreatic na mkpụrụ ndụ ihe nketa na ebuso ya agha.

A na-amata ndị ọrịa afọ iri afọ atọ, ụkọ insulin zuru oke, ọchịchọ nke ketoacidosis yana mkpa ịhazi insulin nke na - apụ apụ.

N'ọnọdụ ebe mbibi na mbelata nke ọnụ ọgụgụ b mkpụrụ ndụ sitere na usoro mgbochi ma ọ bụ autoimmune, a na-ahụta ọrịa shuga autoimmune. A na-ahụta ụdị ọrịa shuga mellitus site na ọnụnọ nke autoantibodies dị iche iche.

Ihe a na –ebu n ’isi ya jikọtara ya na agwakọta nke HLA complex DR3, DR4 ma ọ bụ DR3 / DR4 yana ụfọdụ agbụrụ nke HLA DQ. A na-ekwusi ike na ụdị ọrịa shuga m (autoimmune) nwere ike ịbanye ọnọdụ nke mmepe site na Normoglycemia na-enweghị mkpa maka nchịkwa insulin iji mezue mbibi nke mkpụrụ ndụ b. Mbelata ma ọ bụ mwepu nke mkpụrụ ndụ b kpamkpam na-eduga n'ịdabere na insulin kpamkpam, na-enweghị nke onye ọrịa ahụ zụlitere ọchịchọ nke ketoacidosis, coma. Ọ bụrụ na etiology na pathogenesis amabeghị, mgbe ahụ, a na-ekwupụta ikpe ndị dị otú ahụ ụdị ọrịa shuga "ọrịa shuga" idiopathic.

Elldị nke abụọ nke ọrịa shuga mellitus na-agụnye nsogbu nke carbohydrate metabolism, nke a na-ejikọ ọnụ na ọkwa dị iche iche n'etiti ogo nke nguzogide insulin na ntụpọ nke njikọ insulin. Dịka iwu, n'ọrịa shuga II, ihe abụọ a metụtara na pathogenesis nke ọrịa ahụ, n'ime ndị ọrịa ọ bụla, ha na-ekpebisi ike na oke dị iche.

A na-ahụkarị ụdị shuga II mgbe afọ 40 gachara. Ọtụtụ mgbe, ọrịa ahụ na-amalite nwayọ nwayọ, nwayọ, na-enweghị ketoacidosis ọrịa mamịrị n'oge mberede. Ọgwụgwọ, dịka iwu, achọghị nchịkwa insulin ngwa ngwa iji zọpụta ndụ. Na mmepe nke ụdị ọrịa mellitus nke ọrịa shuga II (ihe dị ka 85% nke ọrịa shuga niile), usoro mkpụrụ ndụ ihe nketa (ezinụlọ) dị ezigbo mkpa.

Ọtụtụ mgbe, a na-ewere ihe nketa dị ka polygenic. Ọnọdụ ọrịa shuga na oke ọrịa na-abawanye na afọ, na ndị okenye karịa afọ 50 na-abịaru nso 100%.

A na-agwọ ndị ọrịa nwere ụdị shuga nke II na insulin maka ọrịa hyperglycemia dị elu, mana mgbe mwepu nke ketoacidosis na-apụtakarị adịghị nke ọma.

Ọrịa metabolism

Na usoro ọmụmụ nke ọrịa shuga nke II, ọrụ oke mkpali na-arụ site na oke ibu, ọkachasị n'ụdị nke eriri afọ.

Diabetesdị ọrịa shuga a na-emetụta hyperinsulinemia, ịba ụba insulin na-eguzogide anụ ahụ, ịba ụba mmepụta glucose, na mmebi nke cell na-aga n'ihu.

Nlegide insulin na-etolite n’ime akwara ndị na-emetụta insulin, nke gụnyere akwara ọkpụkpụ, akwara adipose, na imeju. A maara mmekọrịta dị n'etiti ọkwa insulin na oke ibu.

N'okpuru ọnọdụ hyperinsulinism na oke ibu, mmụba dị n'ọbara nke somatostatin, corticotropin, abụba abụba, uric acid na ihe ndị ọzọ na - egbochi ihe, nke n'otu aka emetụta ọkwa nke glucose na insulin na plasma ọbara, na aka nke ọzọ, ịmalite nke mmetụta "physiological" agụụ. Nke a na - eduga n'ịdị ọcha nke lipogenesis karịa lipolysis. A na - emeri ihe mgbochi insulin na oke ibu site na ụba ọkwa insulin plasma.

Onweghi nri nri diabetogenic, mana ịba ụba nke abụba buru ibu na oke ezuru nri nke nri n’enye nri na - eme ka mbelata nke insulin.

Mbelata ahụ dị 5-10%, ọbụlagodi ma ọ bụrụ na oke ibu ka dịgide, na-eduga na mgbazi nke ntụpọ nnabata, mbelata nke ịba ụba na insulin na plasma, mbelata ogo glycemia, atherogenic lipoproteins na mmụba na ọnọdụ izugbe nke ndị ọrịa.

Ọrịa shuga n'ọrịa ụfọdụ ndị ọrịa buru ibu nwere site na mmụba nke erughi insulin site na nke a kpam kpam. Ya mere, oke ibu, n'aka nke ọzọ, bụ ihe dị egwu maka ibute ọrịa shuga, n'aka nke ọzọ, ngosipụta ya n'oge. Elldị nke abụọ nke ọrịa shuga mellitus bụ usoro nje.

Nchọpụta otu WHO nke 1999 mere, gosipụtara echiche nke ọrịa metabolic dịka ihe dị mkpa na nsogbu vaskụla.

N’agbanyeghi enweghi nkwekorita ekwenyero maka arumazu nke metabolic, echiche ya gunyere abuo ma obu ndi ozo n’ime ha:

- metabolism na-arịa ọrịa glucose ma ọ bụ ọnụnọ nke ọrịa shuga.
- insulin iguzogide,
- mmụba nke ọbara mgbali elu karịa 140/90 mm RT. Art.,
mụbara triglycerides na / ma ọ bụ cholesterol dị ala lipoprotein dị obere(LDL),
- oke ibu,
- microalbuminuria karịrị 20 mcg / min.

Ojiji nke usoro nri siri ike iji belata oke ahụ n'ahụ ndị ọrịa buru ibu, ikpughe ihe ndị dị ize ndụ nke ọrịa metabolic na-edugakarị na nhazi ma ọ bụ mbelata nke glycemia na mbelata ugboro ugboro nsogbu.

Nsogbu nke Ọrịa Shuga

Ọtụtụ ndị ọrịa (ihe dị ka 5%) nwere oke nsogbu na nsogbu ha, agbanyeghị nkwụghachi ụgwọ nke metabolism; n'akụkụ ọzọ nke ndị ọrịa (20-25%), a naghị ahụkarị nsogbu dị iche iche n'ihi ntakịrị ịkọ mkpụrụ ndụ ihe nketa.

N'ọtụtụ ndị ọrịa (70-75%), ogo nke ịkọ mkpụrụ ndụ nwere ike ịdị iche, ọ bụkwa na ndị ọrịa a na ijigide ezigbo ụgwọ ọrụ maka metabolism metabolism nwere mmetụta inhibitory n'ụzọ nke angiopathy na neuropathy.

Ọrịa mamịrị (ọrịa shuga) na microangiopathy na neuropathy bụ ụfọdụ n'ime ngosipụta kachasị njọ nke ọrịa shuga, n'agbanyeghị ụdị ya. Na mmepe nke nsogbu ndị a, ha na-etinye oke mkpa na nchịkọta nke protein (njikọ ha na mkpụrụ ndụ glucose dị ka nsonaazụ nke enzymatic na, na ọkwa ikpeazụ, mmeghachi kemịkal kemịkalụ nke mgbanwe ọrụ ọrụ cellular na akwara ndị na-abụghị insulin), na mgbanwe na ihe mgbazigharị nke ọbara.

Lymịkọta protein ndị dị na haemoglobin na-eduga na-agbagha ụgbọ njem gas. Na mgbakwunye, enwere nsogbu nke membranes dị n'okpuru ala n'ihi ihe mebiri usoro nke protein akpụkpọ ahụ. N'ime ndị ọrịa nwere ọrịa shuga, a chọpụtara usoro nke ịba ụba nke glucose na protein nke ọbara, lipoproteins, irighiri akwara ozi, na akụkụ akwara njikọ.

Ogo nke glycation bụ ihe kwekọrọ na ịba glucose. Mkpebi hemoglobin glycosylated (HbA1b, HbA1c) ka ọ bụrụ usoro nke ngụkọta hemoglobin abụrụla ụzọ a ga-esi na-eleba anya na nkwụghachi nke metabolism metabolism na ndị ọrịa nwere ọrịa mellitus. Site n'ọbara hyperglycemia na-agbanwe mgbe niile, ruo 15-20% nke haemoglobin niile nwere ike ị nweta ahụrịị. Ọ bụrụ na ọdịnaya nke HbA1 karịrị 10%, mgbe ahụ mmepe nke ọrịa mamịrị retinopathy bụ nkwubi okwu ga-ebu amụma.

A na-ahụta maka mmepe nke angio- na neuropathy na-atụle ntụpọ glucose oke n'ime sel anụ ahụ nwere insulin. Nke a na - eduga na nchịkọta nke sorbitol mmanya na - egbu cyclic, nke na - agbanwe nrụgide osmotic n'ime sel ma si otú a na - enyere aka na mmepe nke edema na arụ ọrụ. Nnukwu intracellular nke sorbitol na - aputa na akwara nke sistem, retina, lens, na mgbidi nke nnukwu arịa.

Usoro pathogenetic nke imepụta microthrombi na ọrịa shuga bụ nkwarụ nke homeostasis, viscosity ọbara, microcirculation: nchịkọta nke platelet, thromboxane A2, njikọ nke prostacyclins na arụ ọrụ ọbara fibrinolytic.

Imirikiti ndị ọrịa na-arịa ọrịa shuga na-arịa ọrịa nephropathy. Ọ gụnyere mamịrị glomerulosclerosis, nephroangiosclerosis, pyelonephritis, wdg Micro- na macroangiopathy na-emetụtakwa mmepe nke nsogbu ndị a. N'afọ ndị na-adịbeghị anya, egosipụtara mmekọrịta dị n'etiti ọnụnọ protein na mmamịrị na njedebe ikpeazụ nke akụrụ na ndị ọrịa nwere ọrịa mellitus.

Ọ dị mkpa ịchọpụta microalbuminuria, ewezuga ọrịa ndị dị na intercurrent. Ogo albumin excretion dị ihe karịrị 20 μg / min bụ akara mgbapụta nke microalbuminuria, ogo nke albumin na ọkwa creatinine karịa 3 na-enye gị ohere ịtụkwasị obi na-akọ ọkwa oge abalị gafere karịa 30 μg / min.

A na - ahụta mgbanwe site na nsọtụ ala na syndrome nke afọ ọria mamịrị. A na -emepusi akụkụ nke mpaghara ala ndị ọrịa na-arịa ọrịa shuga mellitus ugboro 15 karịa karịa na ndị bi.

Ọnọdụ nke ọrịa mamịrị ụkwụ na-emetụta ogo, afọ nke ọrịa, glycemia, ise anwụrụ, ogo ọbara mgbali elu. Ọrịa shuga na-ejikọtaghị ya na microangiopathy dịka ya na polyneuropathy, na-ehichapụ atherosclerosis nke arịa ukwu na nke etiti na nsọtụ ala (macroangiopathy), ma ọ bụ na njikọ nke ihe ndị a.

Degwọ ọrịa shuga ogologo oge na-aka njọ nke ọrịa na-ebilite, na-eduga n'ịbelata mgbochi, ihe na-efe efe na usoro mkpali, na adịghị ala ala ha.

Ọ kwesiri iburu n'uche na ọtụtụ ndị dọkịta ụdị ọrịa shuga II na-achọpụta dị ka ọrịa nke usoro ịla ala. Bureaulọ ọrụ European nke International Federation of Diabetologists na WHO European Bureau na 1998 tụpụtara ụkpụrụ ọhụụ maka ịkwụ ụgwọ maka metabolism na ihe ize ndụ nke nsogbu ndị ọrịa nwere ụdị II, nke a gosipụtara na Isiokwu. 33,4.

Isiokwu 33.4. Nkwụghachi ụgwọ Iwuọrịa shuga mellitusụdị II

Na afo efu (tupu nri mmol / L (mg / dL) 6.1 (> 110)> 7.0 (> 126)

Etiology nke ọrịa

Ọrịa shuga 1dị nke Abụọ bụ ọrịa si n'ọrịa, mana ịkọwa mkpụrụ ndụ ihe nketa na-ekpebi uto ya site na naanị atọ. Ihe puru omume pathology na nwatakiri nwere nne nwere oria n’azu enweghi ihe kariri 1-2%, nna n’enwe oria - site na 3 ruo 6%, nwanne - ihe dika 6%.

Enwere ike ịchọpụta otu ma ọ bụ ihe nro nke huruwuru nke ọnya akwara, nke gụnyere ọgwụ mgbochi mmiri na agwaetiti nke Langerhans na 85-90% nke ndị ọrịa:

• ihe mgbochi iji glutamate decarboxylase (GAD),
• ọgwụ mgbochi ọrịa tyrosine phosphatase (IA-2 na IA-2 beta).

N'okwu a, enyere ihe dị mkpa na mbibi nke mkpụrụ ndụ beta ihe ndị na-egbochi mgbochi sel. Ọrịa shuga 1dị nke mbụ na-ejikọkarị na HLA haplotypes dịka DQA na DQB.

Ọtụtụ mgbe, a na-ejikọ ụdị ọrịa a na nkwarụ endocrine ndị ọzọ autoimmune, dịka ọmụmaatụ, ọrịa Addison, autoimmune thyroiditis. Non-endocrine etiology na-arụkwa ọrụ dị mkpa:

• vitiligo
• ọrịa rheumatic
• alopecia
• Ọrịa Crohn.

Na pathogenesis nke ọrịa shuga

Ọrịa shuga 1dị nke mbụ na-eme onwe ya obi ma ọ bụrụ na usoro igbu onwe ya na-ebibi mkpụrụ ndụ nke mkpụrụ ọgwụ beta nke 80 ruo 90%. Ọzọkwa, ike na ọsọ nke usoro a na - efe efe mgbe niile na-adịkwa iche. Ọtụtụ mgbe, n'oge oge ochie nke ọrịa na ụmụaka na ndị na-eto eto, a na-ebibi mkpụrụ ndụ ngwa ngwa, na-egosipụta ngwa ngwa.

Site na mmalite nke ọrịa ahụ na mgbaàmà mbụ ọ na-arịa na mmepe nke ketoacidosis ma ọ bụ ketoacidotic coma, ọ dịghị ihe karịrị izu ole na ole nwere ike ịgafe.

N'aka ozo, oria a na-adighi ahukebe, na ndi okenye karia ogo iri-ario, oria nwere ike gaba n'ihu na nzuzo (oria shuga shuga mellitus Lada).

Ọzọkwa, n'ọnọdụ a, ndị dọkịta chọpụtara ụdị ọrịa shuga mellitus nke 2 ma tụọ ndị ọrịa ha ka ha nwee ike kwụọ ụgwọ insulin na nkwadebe sulfonylurea.

Agbanyeghị, ka oge na-aga, akara nke enweghị homonụ na-amalite ịpụta:

1. ketonuria
2. ifelata
3. doro anya hyperglycemia megide ndabere nke mbadamba mgbe niile iji belata shuga ọbara.

Ọrịa pathogenesis nke ụdị shuga 1 sitere na ụkọ homonụ zuru oke. N'ihi ekwe omume ịba oriri shuga na akụrụngwa na-adabere na anụ ahụ (akwara na abụba), ụkọ ike na-etolite ma, n'ihi nke a, lipolysis na proteolysis na-akawanye ike. Usoro yiri nke ahụ na-ebute oke ibu.

Site na mmụba nke glycemia, hyperosmolarity na-apụta, tinyere osmotic diuresis na akpịrị ịkpọ nkụ. Site na enweghi ume na homonụ, insulin na - egbochi mmiri nke glucagon, cortisol na homonụ nke uto.

N'agbanyeghị glycemia na-eto, a na-akpali gluconeogenesis. Ceme ngwa ngwa nke anụ ahụ na - eme ka mmụba abụba bukwuo ibu.

Ọ bụrụ na insulin na - adịghị ike, mgbe ahụ, a na - egbochi ikike liposynthetic nke imeju, na abụba n'efu na - etinye aka na ketogenesis. Nchịkọta nke ketones na-ebute mmepe nke ketosis mamịrị na nsonaazụ ya - ketoacidosis na-arịa ọrịa shuga.

Na-emegide ihe mmụba na-abawanye n'iyi na acidosis, Coma nwere ike ịmalite.

Ya, ọ bụrụ na enweghị ọgwụgwọ (ọgwụgwọ insulin na ezumike mmiri zuru oke), n'ihe fọrọ nke nta ka ọ bụrụ 100% nke ikpe ga-akpata ọnwụ.

Mgbaàmà nke Ọrịa Shuga 1

Pathodị ọrịa a na - adịkarị ụkọ - ọ bụghị ihe karịrị 1.5-2% nke ụdị ọrịa niile. Ihe egwu ga - eme na ndụ gị niile bụ 0.4%. Ọtụtụ mgbe, mmadụ na-achọpụta ọrịa shuga dị ka afọ 10 ruo 13. Otutu ngosi banyere oria a na - aputa ihe ruru afo iri anọ.

Ọ bụrụ na ikpe ahụ bụ nke a na-ahụkarị, ọkachasị na ụmụaka na ndị ntorobịa, mgbe ahụ ọrịa ahụ ga-egosipụta onwe ya dị ka ihe atụ doro anya. O nwere ike itolite n’ime ọnwa ole ma ole ma ọ bụ izu ole na ole. Ọrịa na-efe efe na ọrịa ndị ọzọ na-efe efe nwere ike ịkpasu iwepụta ọrịa shuga.

Ọrịa ga - amata ụdị ọrịa shuga niile:

• polyuria
• akpụkpọ ahụ,
• polydipsia.

A na-ekwupụta ihe ịrịba ama a ụdị ọrịa 1. N'ehihie, onye ọrịa nwere ike ị drinkụ mmiri ma nwee ọ fluidụghị mmiri 5-10 nke mmiri.

Kachasị maka ụdị ọrịa a ga-abụ oke ibu dị oke oke, nke ọnwa 1-2 nwere ike iru 15 n'arọ. Na mgbakwunye, onye ọrịa ga-ata ahụhụ site na:

• ike adighi ike
• iro ụra
• arụmọrụ belatara.

Na mbido, enwere ike ibute ya site na agụụ na-enweghị ezi uche, nke Anorexia dochiri anya mgbe ketoacidosis na-abawanye. Onye ọrịa ahụ ga-enweta isi e ji mara acetone site n’oghere ọnụ (enwere ike inwe isi mkpụrụ), ọgbụgbọ na pseudoperitonitis - ọnya afọ, akpịrị oke, nke nwere ike ibute ọgbụgba.

N'ọnọdụ ụfọdụ, ihe ịrịba ama mbụ nke ụdị shuga 1 na ndị ọrịa ụmụaka ga-abụ mmụọ na-aga n’ihu. Enwere ike ikwu ya na, site na nzụlite oria a na-asọ oyi (ịwa ahụ ma ọ bụ nke na-efe efe), nwatakịrị ahụ nwere ike ịdaba.

N’oge na-adịghị anya, mgbe onye ọrịa ji afọ iri atọ na-arịa ọrịa shuga (ya na ọrịa shuga na-arịa ya), ọrịa ahụ nwere ike ọ gaghị eme onwe ya ka ọ na-enwu, na-achọpụta ya kpam kpam na mberede n’oge a na-eme nyocha shuga ọbara.

Mmadu aghaghi ifelata, polyuria na polydipsia ga adi nma.

Nke mbu, dọkịta nwere ike ichoputa oria oria abuo ma bido kwa ogwugwo na ogwu iji belata shuga n’ime mbadamba ihe. Nke a ga -, mgbe oge ụfọdụ gasịrị, na - ekwe nkwa ụgwọ ntaramahụhụ a ga - anabata ya. Agbanyeghị, mgbe afọ ole na ole gasịrị, ọ na - abụkarị mgbe otu afọ gasịrị, onye ọrịa ahụ ga - enwe ihe ịrịba ama kpatara mmụba nke erughi insulin:

1. ifelata dị egwu
2. ketosis
3. ketoacidosis
4. enweghi ike ijikwa ọkwa shuga na ọkwa a chọrọ.

Akara nke ịchọpụta ọrịa shuga

Nyere ụdị 1 nke ọrịa a bụ ihe ejiri mara ya na ọria pụtaranụ ma bụrụkwa ọrịa na-adịghị ahụkebe, a na-eme nnyocha nyocha iji chọpụta ọkwa shuga dị n'ọbara. Ohere inweta ọrịa shuga developingdị nke mbụ n'ime ndị ikwu dị ntakịrị, nke, yana enweghị ụzọ dị irè maka nchọpụta mbụ nke ọrịa ahụ, na-ekpebi ezighi ezi nke nyocha zuru oke nke ihe nrịbama immunogenetic nke ọrịa.

Detechọpụta ọrịa a n'ọtụtụ oge a ga-esite na ịkọwapụta nnukwu glucose ọbara n'ime ndị ọrịa nwere mgbaàmà nke ụkọ insulin zuru oke.

Nnyocha mmadụ iji chọpụta ọrịa a bụ nke a na-ahụkarị.

Ọ bụghị ebe ikpeazụ bụ nchọpụta ọdịiche. Ọ dị mkpa iji gosipụta nchoputa ahụ n'ọnọdụ ndị nwere obi abụọ, ya bụ ịchọpụta glycemia agafeghị oke na enweghị ihe doro anya doro anya nke ụdị ọrịa shuga 1, karịsịa na ngosipụta na nwata.

Ebumnuche nke nyocha dị otú ahụ nwere ike ịbụ iche ọdịiche nke ọrịa ahụ na ụdị ọrịa shuga ndị ọzọ. Iji mee nke a, tinye usoro iji chọpụta ọkwa nke basal C-peptide na awa 2 mgbe erichara.

Omuma ihe banyere odi omuma nke ihe omimi n’uche ihe di nkpa bu ihe ndi choputara ihe omumu banyere oria nke oria 1:

• ihe mgbochi na usoro ogige nke akwara,
• Glutamate decarboxylase (GAD65),
• phoroshatase (IA-2 na IA-2P).

Usoro ọgwụgwọ

Usoro ọgwụgwọ maka ụdị ọrịa shuga ọ bụla ga-adabere n'ụkpụrụ atọ bụ:

1. belata shuga ọbara (n'ọnọdụ anyị, ọgwụ insulin),
2. nri nri
3. mmụta ndidi.

Ọgwụ insulin maka ụdị ọrịa 1 bụ ihe a na-eji dochie anya. Ebumnuche ya bụ ime ka i theomi insulin na-eme ka ihe dị mma iji nweta nkwụghachi ụgwọ a na-anabata. Ọgwụ insulin na-arụ ọrụ nke ọma ga-agbadata mmepụta nke homonụ.

Ihe a chọrọ kwa ụbọchị maka homonụ ahụ ga-ahazịrị ọkwa nke nzuzo ya. 2 oge ị ofụ ọgwụ ọgwụ ogologo oge ekpughere ma ọ bụ ntụtụ 1 nke insulin ogologo Glargin nwere ike inye ahụ ahụ insulin.

Oru nke homonụ nke basal ekwesịghị gafere ọkara ihe a chọrọ kwa ụbọchị maka ọgwụ.

A ga-eji mmiri ọgwụ insulin mee ka mmadụ sie ike ma ọ bụ nzụlite nke insulin ga - anọchi obere oge ma ọ bụ nke obere oge ekpughere tupu nri. Na nke a, a na-agbakọta usoro usoro ọgwụgwọ ahụ dabere na njirisi ndị a:

• ego nke carbohydrate a ga-eripịa n’oge nri,
• ọ̀ dị ọ̀tụ̀tụ̀ shuga dị n'ọbara, kpebisiri ike tupu ntụtụ insulin ọ bụla (nke ejiri glucometer tụrụ).

Ozugbo ekpughere ụdị shuga mellitus nke 1 na ozugbo ọgwụgwọ ya malitere ogologo oge zuru oke, mkpa maka ịkwadebe insulin nwere ike ịdị obere ma ga-erughị 0.3-0.4 U / n'arọ. A na-akpọ oge a “honiimuunu” ma ọ bụ oge mgbaghara nke na-adịgide.

Mgbe usoro nke hyperglycemia na ketoacidosis, na-eme ka insulin na-ebelata mmepụta insulin site na ịlanarị mkpụrụ ndụ beta, a na-enweta ụgwọ ọrụ insulin na-enweta ụgwọ ọrụ homonụ na metabolic. Ọgwụ a na-eweghachi arụ ọrụ nke mkpụrụ ndụ akwara, nke werezie obere insulin nke insulin.

Oge a nwere ike ịdị site na izu ole na ole rue ọtụtụ afọ. Na ngwụcha, na agbanyeghị na, n'ihi mbibi nke mkpụrụ ndụ beta-cell, usoro mgbaghara ga-akwụsị ma chọọkwa ọgwụgwọ siri ike.

Na-arịa ọrịa shuga na-arịa insulin na-abụghị insulin (ụdị 2)

Typedị ọrịa a na-etolite mgbe anụ ahụ nwere ike ghara ịmịcha shuga ma ọ bụ mee ya na oke na-ezughi ezu. Nsogbu yiri nke ahụ nwekwara aha ọzọ - ezughi ezu nke extrapancreatic. Usoro etiology nke ihe a di iche nwere ike di iche:

• mgbanwe na nhazi nke insulin na mmepe nke oke ibu, ịreatụbiga nri ókè, ndụ ebughi oke ibu, ọbara ọgbụgba, na agadi na ọnụnọ riri ahụ,
• ọ bụ ọrụ arụ ọrụ ndị nnabata insulin na n'ihi ihe mebiri ọnụ ọgụgụ ma ọ bụ otu ha,
• erughị nri shuga na-emepụta site n’akwara akwara,
• Usoro ọmụmụ intracellular, nke nnyefe nke mkpali n'ahụ ya na sel siri ike nnabata insulin,
• gbanwee insulin insulin na pancreas.

Nkewa oria

Dabere ogo ịrịa ọrịa shuga 2 ga-ekewa:

1. ogo di ala. Ihe e ji mara ya bụ ịkwụ ụgwọ enweghi insulin, na-a theụ ọgwụ ike na nri nwere ike belata shuga ọbara n’oge dị mkpirikpi,
2. ọkara. Can nwere ike kwụọ ụgwọ maka mgbanwe metabolic nyere na ọ dịkarịa ala ọgwụ ọgwụ 2-3 iji belata glucose. Na ọkwa a, a ga-ejikọta ọdịda metabolism na angiopathy,
3. ogbo siri ike. Iji dozie ọnọdụ ahụ chọrọ iji ọtụtụ ụzọ nke ịdalata glucose yana ịba insulin. Onye ọrịa ahụ nọ n’ọgbọ a na-enwekarị nsogbu.

Gini bu oria abuo?

Ihe omuma kpochapu nke oria ojoo nke oria aghaghi ime nke abuo:

• ngwa ngwa. Ngwa ngwa ịtọgbọ insulin chịkọbara na aza glucose,
• oge na-adịghị. Mwepụta nke insulin iji belata shuga dị n'ọbara nwere nwayọ. Ọ na-amalite ịrụ ọrụ ozugbo usoro ọsọ ọsọ dị, mana ọ dabere na nkwụcha ike nke carbohydrates.

Ọ bụrụ na enwere ihe ọmụmụ nke mkpụrụ ndụ beta nke na-adịghị eche maka mmetụta nke homonụ nke pancreas, enweghị mgbanwe n'ọtụtụ carbohydrates n'ọbara ji nke nta nke nta tolite. 2dị ọrịa shuga abụọ nke ọrịa mellitus, usoro ngwa ngwa anaghị adị, oge na-adịghị nwayọ na-amalitekwa. Mmepụta insulin dị obere ma maka nke a, agaghị enwe ike ịkwado usoro ahụ.

Mgbe enweghị ọrụ nnabata insulin ma ọ bụ usoro nnabata, hyperinsulinemia na-amalite. Site n'ọkwa insulin dị n'ọbara, anụ ahụ na-amalite usoro nke ụgwọ ya, nke agbadoro ime ka nguzosi nke homonụ ahụ sie ike. A pụrụ ịhụ mgbaàmà a e ji amata ọbụna na mmalite nke ọrịa ahụ.

Foto doro anya banyere ọrịa ahụ na-etolite mgbe hyperglycemia na-adịgide adịgide ruo ọtụtụ afọ. Sugar sugarụbiga ọbara ókè ókè na-emetụta mkpụrụ ndụ beta. Nke a na - abụ ihe mere ha ji agbaze ma na - eyi, na - eme ka mbelata mmepụta insulin.

Site na ntule, mgbanwe insulin ga-egosiputa site na mgbanwe nke ibu na nguzo nke ketoacidosis. Na mgbakwunye, akara nke ọrịa shuga nke ụdị a ga-abụ:

• polydipsia na polyuria. Ọrịa metabolic na-etolite n'ihi hyperglycemia, nke na-akpalite mmụba nke ọbara ọbara osmotic. Iji mezie usoro ahụ, anụ ahụ malitere iwepu mmiri na electrolytes,
• itching nke anụahụ. Ọkpụkpụ akpụkpọ n'ihi oke mmụba nke urea na ketones n'ime ọbara,
• ibu oke ibu.

Nchịkwa insulin ga-akpata ọtụtụ nsogbu, ma nke mbụ na nke abụọ. Yabụ, ìgwè mbụ nke ndị dọkịta gụnyere: hyperglycemia, mbelata nke mmepụta glycogen, glucosuria, igbochi mmeghachi ahụ nke anụ ahụ.

Ndi otu nsogbu abụọ kwesiri ịgụnye: mkpali nke mwepụta nke lipids na protein maka mgbanwe ha ka ọ bụrụ ka ọ na - eme ka ọ bụrụ nri na - egbochi protein nke protein na-edozi ahụ, belata nnabata nke carbohydrates, na - egbochi mmiri ngwa ngwa nke homonụ.

Ọrịa shuga 2dị nke Abụọ bụ ihe zuru oke. N'ozuzu, ezigbo ihe ngosiputa nke oria bu oria nwere ike karie oge opekata mpe ugboro abụọ.

Ọzọkwa, ndị ọrịa na-achọ enyemaka ahụike naanị mgbe mmalite nke nnukwu nsogbu dị egwu. Maka nke a, endocrinologists na-ekwusi ike na ọ dị mkpa ịghara ichezọ banyere nyocha ahụike mgbe niile. Ha ga - enyere aka ịchọpụta nsogbu ahụ ozugbo enwere ike ma bido ọgwụgwọ ngwa ngwa.