Management of diabetic ketoacidosis

Mainstay of treatment are: fluid therapy, insulin therapy, potassium replacement and antibiotics for precipitating infections.
Typical requirement of fluid is 6 litres in 1st 24 hours, ideally with a central line. Start with 1 litre normal saline in 1st 30 minutes. Caution is needed in cardiac and renal impairment.
Aims of insulin therapy: reduce lipolysis and ketone body formation; reduce hepatic glucose output, increase peripheral glucose utilization. Low dose, IV, regular insulin. Subcutaneous and intra muscular insulin may not be absorbed well. Reduce the dosage when blood sugar …

Oxygen therapy can be normobaric or hyyperbaric. During oxygen therapy, ventilation and airway maintenance should be adequate so that oxygen reaches the lung for gas exchange. Reserve of oxygen in the body is 1.5 litres, which lasts for about 6 minutes in circulatory arrest assuming a consumption of 250 ml/min. Hb contains 800 ml and alveoli contains about 400 ml of oxygen. Pre-oxygenation prior to induction of anaesthesia leads to denitration and increase in the alveolar oxygen content, enabling tolerance of longer period of apnea.
Circulatory gradient of oxygen: Oxygen …

Hepatic encepahalopathy is a neuropsychiatric syndrome with multiple manifestations. It is caused by liver failure and / or portosystemic shunting of blood. It is potentially reversible.
Loss of function / or mass of hepatocytes can cause hepatic encephalopathy. The former occurs in acute fatty liver of pregnancy.
Pathogenesis of hepatic encephalopathy
Various agents are implicated in the pathogenesis of hepatic encephalopathy:
Direct ammonia toxicity
Mercaptan, short chain fatty acids
Aromatic amino acids
GABA
Types of hepatic encephalopathy
1. Acute liver failure
2. Major portosystemic shunt without cirrhosis as in non-cirrhotic portal hypertension
3. Chronic liver disease
Overt vs minimal hepatic encephalopathy
Overt hepatic …

“Metabolic memory” is the name given to the situation of diabetic vascular stresses persisting after normalization of glucose values. The emergence of metabolic memory in diabetes mellitus emphasises the need for early aggressive treatment and normalization of glucose levels. The mechanism of the memory appears to be due to non enzymatic glycation of cellular proteins and lipids as well as due to an excess of cellular reactive oxygen and nitrogen species. These reactive species originate at the level of glycated mitochondrial proteins and may maintain stress signaling independant of glucose …

American Diabetes Association (ADA) target levels for lipoproteins in diabetic dyslipidemia are as follows:
Low density lipoprotein (LDL ) < 100 mg /dl
High density lipoprotein (HDL) > 45 mg / dl
Triglyceride (TG) <150 mg /dl

Insulin secretion in the body follows and inverted U pattern, during the natural history of type 2 diabetes mellitus, which is termed the ‘Starling’s curve of the pancreas’. Insulin concentration in blood initially increases as the sensitivity to insulin decreases as a consequence of situations like obesity. But when the glucose tolerance deteriorates as in impaired glucose tolerance or overt type 2 diabetes mellitus, the insulin levels come down.

 Normal blood glucose: Fasting 70-100 mg dl; Following glucose load: <140 mg/dl
Pre-diabetes
Hyperglycemia not sufficient to meet the diagnostic criteria of diabetes mellitus
Impaired fasting glucose (IFG) 100 – 125 mg/dl
Impaired glucose tolerance (IGT) 140 -199 mg/dl (after 75 gm glucose load)
Both basal hyperglycemia and postprandial hyperglycemia can increase HbA1c and cardiovascular complications
Types of diabetes mellitus
Type 1 Diabetes Mellitus: beta cell deficiency
Type 2 Diabetes Mellitus: beta cell defect + insulin resistance
Gestational Diabetes Mellitus (GDM)
ADA 1997, WHO 1999 – Diagnostic criteria for diabetes mellitus
Symptoms of hyperglycemia (polyuria, polydipsia and unexplained weight loss) and …

Sepsis is a generalised inflammatory response to infection. Systemic inflammatroy response syndrome (SIRS) can occur in many conditions other than sepsis as well.
Low tidal volume ventilation is useful in ARDS. Activated protein C is useful in severe sepsis, especially if Apache score is more than 25.
Severity of sepsis
Sepsis with organ dysfunction is considered severe sepsis: 25 -30% mortality. If there is significant hypotension, it is called septic shock: 60 -70% mortalitly.
Increase in oxygen extraction in a normal individual occurs due to “capillary recruitment”. But in severe sepsis, this does not …

It is a heterogenous group of conditions with cytopenias, hypercellular / dysplastic marrow and is a premalignant condition. Dyserythropoesis manifest as ring sideroblasts.
In MDS, there is decreased normal hemopoetic stem cells, proliferation of dyspoetic marrow cells, selective outgrowth of MDS cells and malignant transformation.
Most patients with MDS die of cytopenias than of leukemia. Transfusion dependence is also an important prognostic factor in MDS. Those who need more transfusions have a poorer prognosis.
5q deletion (5q minus) syndrome has been identified as an important factor in MDS, but this …

Carcinoma: cytokeratin
Sarcoma: desmin / vimentin
Malignant polycythemia rubra vera: V617F JAK2 mutation
FLT3 mutation predicts prognosis in AML
Chromosome 13 abnormality will indicate poor response to conventional treatment in multiple myeloma