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Cutar Creutzfeldt-Jakob

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Cutar Creutzfeldt-Jakob
Description (en) Fassara
Iritransmissible spongiform encephalopathy (en) Fassara
Field of study (en) Fassaraneurology (en) Fassara
Cututtukan cututtuka (ƙwarewar kiwon lafiya)
Sanadiprion (en) Fassara
Symptoms and signs (en) FassaraDementia, myoclonus (en) Fassara, ataxia (en) Fassara, vision disorder (en) Fassara, akinetic mutism (en) Fassara, apathy (en) Fassara, psychosis (en) Fassara, paralysis (en) Fassara, rashin nauyi, motor dysfunction (en) Fassara, Rashin jituwa, acalculia (en) Fassara, prosopagnosia (en) Fassara, anxiety, Harin tsoro, paranoia (en) Fassara, paresthesia (en) Fassara, pyramidal sign (en) Fassara, phobia (en) Fassara, tremor (en) Fassara, anisocoria (en) Fassara, scotoma (en) Fassara, hemianopia (en) Fassara, diplopia (en) Fassara, delusion (en) Fassara, stridor (en) Fassara
dystonia (en) Fassara
Physical examination (en) FassaraTarihin kiwon lafiya, neurological diagnostic techniques (en) Fassara, magnetic resonance imaging (en) Fassara, electroencephalography (en) Fassara, autopsy (en) Fassara, neurological examination (en) Fassara
histopathology (en) Fassara
Genetic association (en) FassaraPRNP (mul) Fassara da MTMR7 (en) Fassara
Suna sabodaHans Gerhard Creutzfeldt da Alfons Maria Jakob (mul) Fassara
Identifier (en) Fassara
ICD-10-CMA81.00 da A81.0
ICD-9-CM046.1 da 046.19
OMIM123400
DiseasesDB3166
MedlinePlus000788
eMedicine000788
MeSHD007562
GeneReviewsNBK1229
Disease Ontology IDDOID:11949

Cutar Creutzfeldt-Jakob (CJD) cuta ce da ba za a iya warkar da ita ba, koyaushe mai haɗari, cuta ce ta neurodegenerative wacce ke cikin ƙungiyar spongiform encephalopathy (TSE), wanda aka fi sani da cututtukan prion.[1][2] Alamomin farko sun haɗa da matsalolin ƙwaƙwalwar ajiya, canje-canje na halayyar, rashin daidaituwa, rikicewar gani da rikicewar ji.[1] Alamomin da suka biyo baya sun haɗa da Rashin hankali, motsi mara kyau, makanta, kurma, rauni, da kuma coma.[1] Kimanin kashi 70% na masu fama da cutar sun mutu a cikin shekara guda bayan ganowa.[1]

An fara bayyana yanayin ne a shekarar 1920.[1] Walther Spielmeyer ne ya gabatar da sunan "Cutar Creutzfeldt-Jakob" a 1922, bayan likitocin kwakwalwa na Jamus Hans Gerhard Creutzfeldt da Alfons Maria Jakob .

CJD ya samo asali ne daga prion, [1] wani nau'i mai kamuwa da cuta, wanda ba daidai ba ne na furotin da ake kira furotin prion. [2] Kimanin kashi 85% na shari'o'in CJD suna faruwa ne saboda dalilan da ba a sani ba ('sporadic CJD'), yayin da kusan kashi 10-15% na shari'ar an gaji su ne a hanyar autosomal.[3] A lokuta masu wuya, bayyanar kwakwalwa ko ƙwayoyin kashin baya daga mutumin da ya kamu da cutar ya haifar da yaduwar cutar, kuma wani nau'i daban-daban na CJD ya haifar da bayyanar nama daga shanu tare da encephalopathy na bovine spongiform ('Mad Cow Disease'). [2][3] Babu wata shaida cewa CJD na yau da kullun na iya yaduwa tsakanin mutane ta hanyar hulɗa na yau da kullum ko ƙarin jini, kodayake wannan yana yiwuwa a cikin Bambancin cutar Creutzfeldt-Jakob.[2][4][5]

Alamomi da alamomi

[gyara sashe | gyara masomin]

Alamar farko ta CJD yawanci ci gaba ne mai saurin kai gaba, wanda ke haifar da asarar ƙwaƙwalwa, canje-canje na mutum, da hallucinations. Myoclonus (motsi mai banƙyama) yawanci yana faruwa a cikin kashi 90% na shari'o'in, amma yana iya kasancewa a farkon farawa.[3] Sauran siffofi masu yawa sun haɗa da damuwa, baƙin ciki, paranoia, alamun damuwa, da kuma psychosis.[4]

Wannan yana tare da matsalolin jiki kamar raunin magana, daidaituwa da rashin aiki (ataxia), canje-canje a cikin tafiya, da kuma Matsayi mai tsauri. A mafi yawan mutanen da ke fama da CJD, waɗannan alamun suna tare da motsi ba tare da son rai ba. Ba a saba gani ba, alamun da ba a saba gani kamar abin da ya faru na baƙo.[5] Tsawon cutar ya bambanta sosai, amma CJD na lokaci-lokaci (ba a gada ba) na iya zama mai kisa a cikin watanni ko ma makonni.[6]

Yawancin mutanen da abin ya shafa sun mutu watanni shida bayan bayyanar bayyanar bayyanarsa ta farko, sau da yawa na cutar huhu saboda raunin tari. Kimanin kashi 15% na mutanen da ke da CJD sun rayu na tsawon shekaru biyu ko fiye.[7]

Alamomin CJD suna haifar da ci gaba da mutuwar Kwayoyin jijiyoyi kwakwalwa, waɗanda ke da alaƙa da haɓaka sunadarai na prion da ba daidai ba a cikin kwakwalwa. Lokacin da aka bincika kwayar kwakwalwa daga mutumin da ke da CJD a ƙarƙashin microscope, ana iya ganin ƙananan ramuka da yawa inda ƙwayoyin jijiyoyi suka mutu. Sassan kwakwalwa na iya kama da soso inda prions ke kamuwa da yankunan kwakwalwa.[8]

Dalilin da ya sa

[gyara sashe | gyara masomin]

CJD wani nau'in cututtukan spongiform encephalopathy (TSE), wanda prions ke haifar da shi.[9] Prions sunadarai ne da ba daidai ba waɗanda ke faruwa a cikin neurons na tsarin juyayi na tsakiya (CNS). CJD prion yana da haɗari saboda yana inganta sake ninka sunadarai na prion na sel zuwa cikin yanayin da ke fama da rashin lafiya.[10]

Adadin kwayoyin furotin da ba daidai ba zai karu sosai, kuma wannan tsari yana haifar da yawan sunadarai masu yawa a cikin sel da suka shafi. Wannan tarin sunadarai da ba daidai ba yana rushe aikin tantanin halitta kuma yana haifar da mutuwar tantanin halitta. Canje-canje a cikin kwayar halitta don furotin na prion na iya haifar da ɓarna na yankunan alpha helix a cikin takalma na beta. Wannan canji a cikin tsari yana kashe ikon furotin na yin narkewa. Da zarar an watsa prion, sunadarai masu lahani sun mamaye kwakwalwa kuma sun sa wasu kwayoyin furotin na prion su ɓace a cikin madauki mai dorewa. Wadannan cututtukan neurodegenerative ana kiransu Cututtukan prion.[11]

  1. 1 2 3 4 5 "Creutzfeldt–Jakob Disease Fact Sheet | National Institute of Neurological Disorders and Stroke". NINDS. March 2003. Archived from the original on 4 July 2017. Retrieved 16 July 2017. Cite error: Invalid <ref> tag; name "NIH2003" defined multiple times with different content.
  2. ↑ "Creutzfeldt–Jakob Disease, Classic (CJD)". CDC. 2 October 2018. Retrieved 21 November 2018.
  3. ↑ "A 49-Year-Old Man With Forgetfulness and Gait Impairment". reference.medscape.com/viewarticle/881806_3. Archived from the original on 2017-07-06. Retrieved 2017-07-09.
  4. ↑ Murray ED, Buttner N, Price BH. (2012) Depression and Psychosis in Neurological Practice. In: Neurology in Clinical Practice, 6th Edition. Bradley WG, Daroff RB, Fenichel GM, Jankovic J (eds.) Butterworth Heinemann. April 12, 2012. ISBN 1437704344, 978-1437704341
  5. ↑ Noor, Huzaifa; Baqai, Muhammad Hadi; Naveed, Hufsa; Naveed, Tooba; Rehman, Syed Sarosh; Aslam, Muhammad Shaheer; Lakdawala, Fatima Mustafa; Memon, Waleed Abdullah; Rani, Sanjana; Khan, Haneen; Imran, Alizeh; Farooqui, Sabeeh Khawar (2024-12-15). "Creutzfeldt-Jakob disease: A comprehensive review of current understanding and research". Journal of the Neurological Sciences. 467. doi:10.1016/j.jns.2024.123293. ISSN 0022-510X. PMID 39546829 Check |pmid= value (help).
  6. ↑ Brown P, Cathala F, Castaigne P, Gajdusek DC (November 1986). "Creutzfeldt–Jakob disease: clinical analysis of a consecutive series of 230 neuropathologically verified cases". Annals of Neurology. 20 (5): 597–602. doi:10.1002/ana.410200507. PMID 3539001. S2CID 7995631.
  7. ↑ Gambetti, Pierluigi. "Creutzfeldt–Jakob Disease (CJD)". The Merck Manuals: Online Medical Library. Archived from the original on 2011-06-04. Retrieved 2011-06-04.
  8. ↑ Atalay, Fatma Oz; Tolunay, Sahsine; Ozgun, Gonca; Bekar, Ahmet; Zarifoglu, Mehmet (2013). "Creutzfeldt–Jakob disease: report of four cases and review of the literature". Turkish Journal of Pathology. 31 (2): 148–152. doi:10.5146/tjpath.2013.01195. ISSN 1018-5615. PMID 24272930.
  9. ↑ "Creutzfeldt–Jakob Disease, Classic (CJD) | Prion Diseases | CDC". www.cdc.gov (in Turanci). 1 February 2019. Retrieved 17 June 2019. Classic CJD is a human prion disease
  10. ↑ Clarke AR, Jackson GS, Collinge J (February 2001). "The molecular biology of prion propagation". Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences. 356 (1406): 185–195. doi:10.1098/rstb.2000.0764. PMC 1088424. PMID 11260799.
  11. ↑ Geschwind, MD (2015). "Prion Diseases". Continuum. 21 (6): 1612–1638. doi:10.1212/CON.0000000000000251. PMC 4879966. PMID 26633779.