In this article, we will discuss the Biochemical Features of Diabetic Ketoacidosis. So, let’s get started.
The characteristic metabolic abnormalities diagnostic of DKA are depicted below. There is hyperglycemia, ketonemia, hyperkalemia, hyperphosphatemia, acidosis and elevated blood urea and serum creatinine
- Increased (Following levels are increased in DKA)
- Blood glucose (250-600 mg/dL)
- Plasma ketone level
- Plasma osmolality (300-320 mOsm/mL)
- Hematocrit value
- WBC count (>11000/L)
- Blood urea, creatinine
- Serum FFA and triglycerides
- Anion gap
- Serum amylase and lipase (20-25% cases)
- Decreased (Following levels are decreased in DKA)
- Serum sodium (125-135 mEq/L)
- Serum magnesium
- Serum potassium initially increase, later decreased
- Bicarbonate (<15 mEq/L)
- PCO2 (20-30 mmHg)
- pH 6.8 to 7.3
In this article, we will discuss the Precipitating Factors and Differential Diagnosis of Myxoedema Coma. So, let’s get started.
The factors that push the patient of hypothyroidism into myxoedema coma are given below:
- Infection, e.g. pneumonia
- Exposure to cold
- Dilutional hyponatremia
- GI bleeding
- Stroke (CVA)
- CNS depressants, e.g. tranquillisers, sedatives and antidepressants
- Cardiovascular disease (e.g. CHF), myocardial infarction
- Respiratory disease (infection, COPD)
Hypoventilation leading to hypoxia and hypercapnia plays a major role in pathogenesis. Hypoglycemia and dilutional hyponatremia also contribute to the development of myxoedema coma.
The conditions which are associated with coma and hypothermia may mimic myxoedema coma. These include:
1. Brainstem infarction in older persons may lead to both coma and hypothermia
2. Hypothermia due to any cause and renal failure may itself induce physiological changes simulating myxoedema such as delayed relaxation of deep tendon reflexes. Coma is due to hypothermia and renal failure.
In this article, we will discuss the Diagnosis of Acute Adrenal Crisis or Insufficiency. So, let’s get started.
- Eosinophil count may be high
- Plasma cortisol (morning and evening): It will be low (<3 mcg/dl at 8 am). A plasma cortisol in normal range in acutely ill patient does not rule out adrenal insufficiency
- Short one hour ACTH (cosyntropin) stimulation test: In adrenal insufficiency, serum cortisol does not rise in response to ACTH (i.e. cortisol level remains below the cut off limit of 500-550 nmol/L sampled one hour after ACTH stimulation)
- ACTH levels will help to diagnose whether adrenal insufficiency is primary (high level) or secondary (low level). Low plasma cortisol with high level ACTH simultaneously suggests primary adrenal insufficiency/crisis
- Serum DHEA levels <1000 ng/ml in all patients with Addison’s disease
- Serum Na+ and K+ levels: Serum Na+ is normal to low and K+ is high. Blood sugar levels low. Serum calcium level may be high
- Screening for steroid auto antibodies for autoimmune adrenalitis: They are positive in 50% cases with autoimmune Addison’s disease/crisis. Antibodies to 21-hydroxylase help confirm the diagnosis of autoimmune adrenal disease/crisis. Antibodies to thyroid may be present in 45% cases
- CT scan of adrenal glands may reveal the underlying cause (hemorrhage, infiltration or masses)
- Blood, sputum or urine culture may be positive of bacterial infection if it is the precipitating cause of the crisis.
In this article, we will discuss the Differential Diagnosis and Complications of Acute Pancreatitis. So, let’s get started.
Differential diagnosis includes the following conditions i.e.
- Perforated peptic ulcer
- Acute cholecystitis and biliary colic
- Acute intestinal obstruction
- Inferior myocardial infarction
- Mesentery vascular occlusion
- Dissecting aortic aneurysm
- Diabetic ketoacidosis
They are both local and systemic:
- Pancreatic necrosis
- Pancreatic fluid collection, e.g. abscess, pseudocyst
- Pancreatic ascites
- Involvement of adjoining organs and vessels
- Obstructive jaundice
- Pulmonary, e.g. pleural effusion, pneumonitis, ARDS, atelectasis and mediastinal abscess
- Renal, e.g. oliguria, azotemia, ATN (acute tubular necrosis) and renal artery/venous thrombosis
- Cardiovascular, e.g. hypotension, pericardial effusion and sudden death
- Hematological, e.g. disseminated intravascular coagulation
- GI hemorrhage, e.g. peptic ulcer disease, hemorrhagic pancreatic necrosis, portal vein thrombosis
- Metabolic, e.g. hyperglycemia, hypertriglyceridemia, hypocalcemia and encephalopathy
- CNS, e.g. psychosis, fat emboli.
In this article, we will discuss the Pathophysiology of Pituitary Apoplexy. So, let’s get started.
Hemorrhage and necrosis of the pituitary adenoma are the cardinal pathological features of pituitary apoplexy and occur due to:
1. Pituitary adenomas are more vulnerable to bleeding than other tumors.
2. A rapidly growing adenoma outstripes its blood supply and produces ischemia followed by necrosis and secondary hemorrhage.
3. Compression of a large pituitary stalk carrying blood vessels by an expanding tumor mass may render the entire anterior lobe ischemic followed by secondary hemorrhage.
4. Fragility of the tumor blood vessels predispose to bleeding.
5. Sheehan syndrome (pituitary necrosis following postpartum uterine hemorrhage) is characterized by amenorrhea and inability to lactate. Hypopituitarism develops acutely usually with severe secondary adrenal insufficiency.