DIABETES MELLITUS

DM is a chronic multisystem disease with both biochemical and anatomical/structural consequences. Affects carbohydrate, fat, and protein metabolism caused by the lack of insulin (type 1), which results from the marked and progressive inability of the pancreas to secrete insulin because of autoimmune destruction of the beta cell, or (type 2) an array of dysfunction resulting from a combination of resistance to insulin action and inadequate insulin secretion.

Chronic manifestation:

Nonenzymatic glycosylation

1)      Small vessel diseased:

a)      Retinopathy: hemorrhage, exudation, microaneurysm, vessel proliferation.

b)      Glaucoma.

c)      Nephropathy: nodular sclerosis, progressive proteinuria, CRF, arteriosclerosis leading to hypertension, Kimmelstiel-Wilson nodules.

2)      Large vessel atherosclerosis:

a)      CAD.

b)      Peripheral vascular occlusive disease/gangrene.

c)      Cerebrovascular disease.

Osmothy damage

1)      Neuropathy: motor, sensory, and autonomic degeneration.

2)      Cataracts (sorbitol accumulation).

Variable	DM type 1	DM type 2
1° defect	Viral or immune destruction of β cells	↑ resistance to insulin
Insulin necessary in treatment	Always	Sometime
Age onset	< 30	> 40
Obesity	No	Yes
Genetic predisposition	Weak, polygenic	Strong, polygenic
HLA system	Yes ( HLA-D3, D4, DQ)	No
Glucose intolerance	Severe	Mild to moderate
Ketoacidosis	Common	Rare
β cells	↓	Variable with amyloid deposits
Serum insulin levels	↓	Variable
Classic symptoms	Common	Sometime

                                                                               

Diabetic Ketoacidosis: One of the most important complications of type 1 diabetes. Usually, due to increases insulin requirements from stress (e.g. infection). Excess fat breakdown and increase ketogenesis from elevated free fatty acids, which are then made into ketone bodies.

Finding: Kusmaul respiration, nausea/vomiting, abdominal pain, psychosis/delirium, dehydration. Fruit breath odor due to exhaled acetone.

Hyperglycemia, ↑ H+, ↓ HCO3-, ↑ blood ketone levels, leukocytosis, hyperkalemia, but depleted intracellular K+.

Complications: life-threatening mucormycosis, Rhizopus infection, cerebral edema, cardiac arrhythmia, heart failure.

Treatment: Fluids, insulin, and K+. Glucose if necessary to prevent hypoglycemia.

Diabetes Insipidus: intense thirst and polyuria, inability to concentrate urine owing to lack of ADH.

 

Central DI: Pituitary tumor, trauma, surgery, histiocytosis X.

Nephrogenic DI: hereditary or secondary to hypercalcemia, lithium, demeclocycline (ADH antagonist).

Finding: Urine specific gravity <1.006 and serum osmolality >290 mOsm/L.

Treatment: Adequate fluid intake. For central DI, intranasal desmopressin (ADH analog); for Nephrogenic DI, hydroclorotiazide, indomethacine, or amiloride.

 

 

Literature consulted

Lawrence, M. J., Stephen, J., & Maxine, A. (2005). CURRENT Medical Diagnosis & Treatment. USA: Mc Graw Hill.

Le, T., Bhushan, V., Grimm, L., & Vasan, N. (2009). First AID for the USMLE step 1. USA: Mc Graw Hill.

Perez, A., & Capel, I. (2007). Diabetes Mellitus. In C. Aut, Cliniguia actualizacion de diagnostico y tratamiento (pp. 633-644). Spain: EviSciencie.

Veitia Suarez, M., Astorgano de la Puente, C., Delgado Gomez, M., & Casal Codesido, J. (2010). Cetoacidosis Diabetica. In M. Vazquez Lima, & J. Casal Codesido, Guia de Actuacion de Urgencia (pp. 258-261). Spain: Ofelmaga, s.l.