Etica En Salud Pública

Páginas: 7 (1524 palabras) Publicado: 3 de diciembre de 2012
PATHOPHYSIOLOGY:
Diabetic Ketoacidosis (DKA) and Hyperglycemic Hyperosmolar State (HHS)

Abbas E. Kitabchi, Ph.D., M.D.
Maston K. Callison Professor of Medicine
The University of Tennessee Health Science Center Memphis, Tennessee

Objectives
Monday, December 13, 2010 (8:00 a.m. – 9:00 a.m.)

1. Be able to define the diagnostic criteria and typical total body deficit of water andelectrolytes in DKA and HHS. 2. To know the precipitating factors of development of DKA and HHS. 3. Be able to calculate serum osmolality on the basis of serum glucose, sodium and BUN. 4. Understand the pathophysiology of DKA and HHS which leads to abnormality of proteins, fat and CHO metabolism. 5. Understand how the above leads to polyuria, polydipsia, polyphagia, loss of electrolytes, dehydration,weight loss and coma. 6. Understand which metabolic pathways are altered in DKA and HHS (i.e., gluconeogenesis, glycolysis, lipolysis, lipogenesis, protein synthesis, ketogenesis, etc.) based on the state of insulin deficiency. 7. Be able to differentiate, biochemically, the pathogenesis of DKA versus HHS.

DIABETES: First Description
“Diabetes [Mellitus] is a remarkable disorder, and not onevery common to man… The disease is chronic in its character, and is slowly engendered, though the patient does not survive long when it is completely established, for the marasmus produced is rapid, and death speedy. Life too is odious and painful, the thirst is ungovernable, and the copious potations are more than equaled by the profuse urinary discharge; for more urine flows away, and it isimpossible to put any restraint to the patient’s drinking or making water. For if he stops for a very brief period, and leaves off drinking, the mouth becomes parched, the body dry; the bowels seem on fire, he is wretched and uneasy, and soon dies, tormented with burning thirst.”
ARETAEUS OF CAPPODOCIA (ca. 120 A.D. - 200 A.D.)

Diagnostic Criteria in Diabetic Ketoacidosis(DKA) and HyperglycemicHyperosmolar Syndrome (HHS)*
Mild DKA Moderate DKA Severe DKA HHS Diagnostic criteria and classification Plasma glucose >250 mg/dl >250 mg/dl >250 mg/dl >600 mg/dl (mg/dl) Arterial pH 7.25-7.30 7.00-10 >12 >12 Variable Mental Status Alert Alert/Drowsy Stupor/Coma Stupor/Coma * Nitroprusside reaction method ** 2[measured Na+ (mEq/L)] + glucose (mg/dl)/18 *** (Na+)– [(Cl- + HCO3- (mEq/L)] * Kitabchiet al., Diabetes Care 2006

Other Hyperglycemic States
Diabetes Mellitus Hyperglycemic Hyperosmolar State Impaired Glucose Tolerance Stress Hyperglycemia

Other Metabolic Acidotic States
Lactic Acidosis Hyperchloremic Acidosis Drug-induced Acidosis Uremia

Hyperglycemia

Acidosis

DKA

Ketosis

Other Ketotic States
Alcoholic Ketoacidosis Starvation Ketosis Ketotic Hypoglycemia Gluconeogenesis

Fat

Ingested Carbohydrate

Blood Glucose

Oxidation

Hepatic Glycogen

Lactic Acid

Muscle Glycogen

Oxidation

Effect of Insulin-Induced Hypoglycemia in Normal Subjects
Glucagon (pg/ml) 250 200 150 100 50 0 25 20 15 10 5 0 Prolactin (ng/ml) 100 80 60 40 20 0 0 10 20 30 45 60 120 100 80 60 40 20 0 Minutes 0 10 20 30 45 60 120 Cortisol (µg/ml) 250 200 150 10050 0 1000 800 600 400 200 0 Glucose (mg/dl) 0.5 0.4 0.3 0.2 0.1 0 0 10 20 30 45 60 120 Norepinephrine (pg/ml) Epinephrine (pg/ml) 250 200 150 100 50 0 250 200 150 100 50 0 C-peptide (pmole/ml) ACTH (pg/ml) Growth Hormone (ng/ml)

Minutes

Minutes

Precipitating Factors for DKA and HHS
% of Admissions Precipitating Factor Infection - Pneumonia - Septicemia - Urosepsis - Abscess -Gastorenteritis New-onset diabetes Discontinued insulin Unknown/miscellaneous DKA* 35 18 9 5 3 30 20 15
* Slovis et al. (1987)

HHS** 60 35 5 5 10 5 33 7
**Pedan et al (1984)

Kitabchi & Rumbak. Hosp Prac 24:129-160, 1989

ACUTE INSULIN DEFICIENCY
and Increased Counterregulatory Hormones (Effect on Carbohydrate Metabolism)
GLUCOSE USE BLOOD GLUCOSE
(Hyperglycemia)

GLYCOGEN BREAKDOWN
and...
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