Diabetes mellitus type 1 overview: Difference between revisions
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{{Diabetes mellitus}} | {{Diabetes mellitus}} | ||
{{CMG}}; | {{CMG}}; {{AE}} [[Priyamvada Singh|Priyamvada Singh, M.B.B.S.]] [mailto:psingh13579@gmail.com]; {{CZ}}{{VD}}{{F.DF}} | ||
==Overview== | ==Overview== | ||
Diabetes mellitus type 1(T1D ) is a [[metabolic]] disorder that is primarily characterized by deficiency in [[insulin]]. T1D has 2 forms of presentations 1) Classic new onset, which commonly present with persistent [[thirst]], frequent [[urination]], and [[dehydration]] 2) Diabetic [[ketoacidosis]], which commonly presents with abdominal pain, vomiting and flu-like symptoms. Patients with classic onset presentation of T1D are usually well appearing. Whereas T1D patients presenting with [[diabetic ketoacidosis]] is usually remarkable for [[tachycardia]], [[tachypnea]] (kussumal breathing) and [[dehydration]]. T1D is characterized by an absolute [[insulin]] deficiency. For these patients, a basal-bolus regimen with a long-acting analog and a short- or rapid-acting insulin analog is the most physiologic insulin regimen and the best option for optimal [[glycemic]] control. | |||
==Historical Perspective== | |||
Term "diabetes" was first described in the literature by a Egyptian scientist Eberes papyrus in 1500 BC. Discovery of insulin by Friedrick Banting in 1921-22, was considered as an important landmark in understanding the nature of disease. | |||
==Classification== | |||
American Diabetic Association(ADA), classifies T1D based on etiology into 1) Immune mediated and 2) Idiopathic | |||
==Pathophysiology== | |||
Type 1 diabetes is a disorder characterized by abnormally high blood sugar levels. T1D is the result of interactions of [[Genetics|genetic]], [[Environmental Science|environmental]], and [[Immunology|immunologic]] factors that ultimately lead to the destruction of the pancreatic [[Beta cell|beta cells]] and [[insulin]] deficiency. | |||
==Causes== | |||
There are no established causes for type 1 DM. Studies have found that cause of T1D is the result of interactions of [[Genetics|genetic]], [[Environmental Science|environmental]], and immunologic factors. | |||
== | ==Differentiating Diabetes Mellitus Type 1 from other Diseases== | ||
[[Type 1 DM]] must be differentiated from [[type 2 DM]], MODY-DM, [[psychogenic polydipsia]], [[diabetes insipidus]], transient hyperglycemia, steroid therapy, [[Renal tubular acidosis|renal tubular acidosis type-1]], [[glucagonoma]], [[cushing's syndrome]], and [[hypothyroidism]]. | |||
==Epidemiology and Demographics== | |||
Epidemiology and demographics of type 1 DM varies with geography, [[age]], [[race]] and [[Genetics|genetic]] susceptibility. | |||
==Risk Factors== | |||
Risk factors for type 1 DM include family history, [[genetics]], geography, [[congenital rubella]] infection, maternal [[Enterovirus|entero-viral]] infection, [[cesarean]] infection, higher [[birth weight]], older [[maternal]] age, low [[maternal]] intake of vegetables, enteroviral infection, frequent [[respiratory]] or [[enteric]] infections, early exposure to cereals, root vegetables, eggs and cow's milk, infant weight gain, persistent or recurrent entero-viral infections, overweight or increased height velocity, high [[glycemic]] load, [[fructose]] intake, dietary nitrates or [[nitrosamines]], [[puberty]], [[psychological]] stress and low [[vitamin D]] levels. | |||
==Screening== | |||
According to the American Diabetic Association, screening for type 1 DM is not recommended.<sup>[[Diabetes mellitus type 1 screening|[1]]]</sup> | |||
==Natural History, Complications and Prognosis== | |||
If left untreated, patients with [type 1 DM] may progress to develop complications of the [[Hyperglycemia|hyperglycem]]<nowiki/>ia state, which commonly include [[Diabetic ketoacidosis|diabetes ketoacidosis]] and [[hyperglycemia]] [[hyperosmolar]] state. [[Prognosis]] is generally good with compliance with medications. | |||
==Diagnosis== | |||
The diagnosis of type 1 DM is based on the ADA criteria, which include [[FPGS|FPG]] ≥126 mg/dL (7.0 mmol/L), or 2-h PG ≥200 mg/dL (11.1 mmol/L) during an [[OGTT]], or [[A1C]] ≥6.5% (48 mmol/mol), or classic symptoms of [[hyperglycemia]] or [[hyperglycemic]] crisis, a random [[plasma]] [[glucose]] ≥200 mg/dL (11.1 mmol/L). | |||
===History and Symptoms=== | |||
Type 1 DM has 2 forms of presentations 1) Classic new onset, which commonly present with persistent thirst, frequent urination, and dehydration 2) [[Diabetic ketoacidosis]], which commonly presents with [[abdominal pain]], [[vomiting]] and [[flu]]-like symptoms. | |||
===Physical Examination=== | |||
Patients with classic onset presentation of type 1 DM are usually well appearing. Whereas patients with [[diabetic ketoacidosis]] present with [[tachycardia]], [[tachypnea]] (kussumal breathing) and [[dehydration]]. | |||
===Laboratory Findings=== | |||
Laboratory findings consistent with the diagnosis of type 1 DM include [[FPGS|FPG]] ≥126 mg/dL (7.0 mmol/L), or 2-h PG ≥200 mg/dL (11.1 mmol/L) during an [[OGTT]], or [[A1C]] ≥6.5% (48 mmol/mol), or classic symptoms of [[hyperglycemia]] or [[hyperglycemic]] crisis, a [[Plasma glucose|random plasma glucose]] ≥200 mg/dL (11.1 mmol/L). | |||
==Treatment== | |||
===Medical Therapy=== | |||
Type 1 diabetes is characterized by an absolute [[insulin]] deficiency. For these patients, a basal-bolus regimen with a long-acting analog and a short- or rapid-acting insulin analog is the most physiologic insulin regimen and the best option for optimal [[glycemic]] control. | |||
===Surgery=== | |||
[[Surgery]] is not the first-line treatment option for patients with type 1 DM. β-Cell replacement therapy is usually reserved for patients with either who have an indication for kidney transplantation and are poorly controlled with large glycemic excursions or in patients who already received a kidney transplant. | |||
===Primary Prevention=== | |||
Currently there are no primary preventive measures available for type 1 DM. However, there are clinical trials ongoing that aim to find methods of preventing or slowing its development. | |||
===Secondary Prevention=== | |||
Secondary prevention strategies following type 1 diabetes mellitus include: maintain optimal [[glycemic]] control, life style modifications, and monitoring for [[Microvascular disease|micro]] and [[Macrovascular disease|macrovascular]] [[complications]]. | |||
===Cost-Effectiveness of Therapy=== | |||
===Future or Investigational Therapies=== | |||
Future research mainly focuses of artificial pancreas, beta cell replacement, smart insulin, and gene therapy. | |||
==Case Studies== | |||
===Case #1=== | |||
==References== | ==References== | ||
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[[Category:Endocrinology]] | [[Category:Endocrinology]] | ||
[[Category:Emergency medicine]] | [[Category:Emergency medicine]] | ||
Latest revision as of 17:05, 9 August 2020
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Diabetes mellitus type 1 Microchapters |
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Differentiating Diabetes mellitus type 1 from other Diseases |
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Diagnosis |
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Treatment |
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Cardiovascular Disease and Risk Management |
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Case Studies |
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Diabetes mellitus Main page |
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Patient Information |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Priyamvada Singh, M.B.B.S. [2]; Cafer Zorkun, M.D., Ph.D. [3]Vishal Devarkonda, M.B.B.S[4]Fatemeh Dehghani Firouzabadi, MD [5]
Overview
Diabetes mellitus type 1(T1D ) is a metabolic disorder that is primarily characterized by deficiency in insulin. T1D has 2 forms of presentations 1) Classic new onset, which commonly present with persistent thirst, frequent urination, and dehydration 2) Diabetic ketoacidosis, which commonly presents with abdominal pain, vomiting and flu-like symptoms. Patients with classic onset presentation of T1D are usually well appearing. Whereas T1D patients presenting with diabetic ketoacidosis is usually remarkable for tachycardia, tachypnea (kussumal breathing) and dehydration. T1D is characterized by an absolute insulin deficiency. For these patients, a basal-bolus regimen with a long-acting analog and a short- or rapid-acting insulin analog is the most physiologic insulin regimen and the best option for optimal glycemic control.
Historical Perspective
Term "diabetes" was first described in the literature by a Egyptian scientist Eberes papyrus in 1500 BC. Discovery of insulin by Friedrick Banting in 1921-22, was considered as an important landmark in understanding the nature of disease.
Classification
American Diabetic Association(ADA), classifies T1D based on etiology into 1) Immune mediated and 2) Idiopathic
Pathophysiology
Type 1 diabetes is a disorder characterized by abnormally high blood sugar levels. T1D is the result of interactions of genetic, environmental, and immunologic factors that ultimately lead to the destruction of the pancreatic beta cells and insulin deficiency.
Causes
There are no established causes for type 1 DM. Studies have found that cause of T1D is the result of interactions of genetic, environmental, and immunologic factors.
Differentiating Diabetes Mellitus Type 1 from other Diseases
Type 1 DM must be differentiated from type 2 DM, MODY-DM, psychogenic polydipsia, diabetes insipidus, transient hyperglycemia, steroid therapy, renal tubular acidosis type-1, glucagonoma, cushing's syndrome, and hypothyroidism.
Epidemiology and Demographics
Epidemiology and demographics of type 1 DM varies with geography, age, race and genetic susceptibility.
Risk Factors
Risk factors for type 1 DM include family history, genetics, geography, congenital rubella infection, maternal entero-viral infection, cesarean infection, higher birth weight, older maternal age, low maternal intake of vegetables, enteroviral infection, frequent respiratory or enteric infections, early exposure to cereals, root vegetables, eggs and cow's milk, infant weight gain, persistent or recurrent entero-viral infections, overweight or increased height velocity, high glycemic load, fructose intake, dietary nitrates or nitrosamines, puberty, psychological stress and low vitamin D levels.
Screening
According to the American Diabetic Association, screening for type 1 DM is not recommended.[1]
Natural History, Complications and Prognosis
If left untreated, patients with [type 1 DM] may progress to develop complications of the hyperglycemia state, which commonly include diabetes ketoacidosis and hyperglycemia hyperosmolar state. Prognosis is generally good with compliance with medications.
Diagnosis
The diagnosis of type 1 DM is based on the ADA criteria, which include FPG ≥126 mg/dL (7.0 mmol/L), or 2-h PG ≥200 mg/dL (11.1 mmol/L) during an OGTT, or A1C ≥6.5% (48 mmol/mol), or classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose ≥200 mg/dL (11.1 mmol/L).
History and Symptoms
Type 1 DM has 2 forms of presentations 1) Classic new onset, which commonly present with persistent thirst, frequent urination, and dehydration 2) Diabetic ketoacidosis, which commonly presents with abdominal pain, vomiting and flu-like symptoms.
Physical Examination
Patients with classic onset presentation of type 1 DM are usually well appearing. Whereas patients with diabetic ketoacidosis present with tachycardia, tachypnea (kussumal breathing) and dehydration.
Laboratory Findings
Laboratory findings consistent with the diagnosis of type 1 DM include FPG ≥126 mg/dL (7.0 mmol/L), or 2-h PG ≥200 mg/dL (11.1 mmol/L) during an OGTT, or A1C ≥6.5% (48 mmol/mol), or classic symptoms of hyperglycemia or hyperglycemic crisis, a random plasma glucose ≥200 mg/dL (11.1 mmol/L).
Treatment
Medical Therapy
Type 1 diabetes is characterized by an absolute insulin deficiency. For these patients, a basal-bolus regimen with a long-acting analog and a short- or rapid-acting insulin analog is the most physiologic insulin regimen and the best option for optimal glycemic control.
Surgery
Surgery is not the first-line treatment option for patients with type 1 DM. β-Cell replacement therapy is usually reserved for patients with either who have an indication for kidney transplantation and are poorly controlled with large glycemic excursions or in patients who already received a kidney transplant.
Primary Prevention
Currently there are no primary preventive measures available for type 1 DM. However, there are clinical trials ongoing that aim to find methods of preventing or slowing its development.
Secondary Prevention
Secondary prevention strategies following type 1 diabetes mellitus include: maintain optimal glycemic control, life style modifications, and monitoring for micro and macrovascular complications.
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Future research mainly focuses of artificial pancreas, beta cell replacement, smart insulin, and gene therapy.