w4 management of acute and chronic illness diabetes Flashcards
what are acute complications of diabetes mellitus?
-Hypoglycemia
-Counter-Regulatory Mechanisms
Somogyi effect
dawn phenomenon
-Diabetic ketoacidosis (DKA)
-Hyperosmolar hyperglycemic Nonketotic Syndrome (HHNKS)
also known as Hyperglycemic Hyperosmolar State (HHS)
what is hypoglycemia
-Lowered plasma glucose level children and adults: less than 4 mmol/L (3.9 or less) -Called insulin shock, insulin reaction -Clinical manifestations tachycardia, palpitations, diaphoresis, tremors, pallor, and arousal anxiety -Treatment oral or IV glucose D50W glucagon: prescribed for emergency use
what are symptoms of hypoglycemia? Neurogenic Adrenergic Symptoms (activation of the SNS)
- tachycardia
- palpitations
- diaphoresis
- tremors
- pallor
- arousal anxiety
- hunger
what is hypoglycemia? Neuroglycopenic Symptoms
abrupt cessation of glucose delivery to brain
- headache
- dizziness
- blurred vision
- irritability
- fatigue
- poor judgment
- confusion
- seizures
- coma
- death
somogyi effect
-Hypoglycemia ~3:00am
too much intermediate-acting insulin given at dinner time followed by rebound hyperglycemia
-Hyperglycemia caused by secretion of counter-regulatory hormones (epinephrine, GH, corticosteroids)
stimulated by hypoglycemia → gluconeogenesis
-+++ carbohydrate intake may contribute to rebound hyperglycemia
-Treatment
decrease evening insulin level
what is dawn phenomenon?
-Early morning rise in BG without nocturnal hypoglycemia
different from Somogyi effect!
-Related to nocturnal growth hormone elevation
decreases metabolism of glucose by muscle and fat
-Treatment
alter timing and dose of insulin
increase dose of evening insulin
diabetic ketoacidosis (DKA)
-Absolute or relative deficiency of insulin and increase in counter-regulatory hormones
-Precipitating factors
-poor adherence to insulin treatment
-interruption of insulin admin
-infection
-trauma
-surgery
-MI
-Increased fat mobilization with release of fatty acids
leads to production of keto acids
what is happening in DKA?
-Most common in type 1 diabetes
-Less likely in type 2 diabetes
but can happen!
- Extreme hyperglycemia, osmotic diuresis
- Body metabolizes lipids to ketone bodies to create source of energy for cells
- Ketone bodies reduce pH of blood causing metabolic acidosis
What is the pathophysiology of DKA ?
-Caused by increased levels of circulating ketones in absence of antilipolytic effect of insulin
-Because glucose is unable to enter cells, lipids are used as energy source and keto acids are produced as waste products
-High levels of keto acids lower pH of blood, causing diabetic ketoacidosis
drop in pH triggers buffering system associated with metabolic acidosis
-May progress to coma and possible death if untreated
What are signs and symptoms of DKA
- ketonuria
- polyuria
- dehydration
- thirst
- Kussmaul respirations
- acetone (fruity) breath odor
What are the treatments of DKA
insulin
-decrease BG levels
fluids
-replace lost fluid volume (osmotic diuresis d/t hyperglycemia)
electrolytes
-K+ most important electrolyte
can shift into and out of cells!!!
What is the pathophysiology of HHNKS
Factors
-insulin deficiency and increased levels of counter-regulatory hormones (glucagon, catecholamines, cortisol, growth hormone)
-increased gluconeogenesis and glycogenolysis
inadequate use of glucose by peripheral tissues, primarily muscle
-Proinflammatory mediators (TNF-α, IL-6, IL-1β) promote insulin resistance and release of counter-regulatory hormones
-contributes to insulin resistance and hyperglycemia
-Insulin levels sufficient to prevent excessive lipolysis but not to use glucose properly
-characterized by a lack of ketosis
What are the clinical manifestations of HHNKS
-glycosuria, polyuria, dehydration, neurologic changes
Lab findings
-BG often more than 33 mmol/L
-absent or low urine ketones
What are the treatments for HHNKS
- insulin infusion combined with fluid replacement
- electrolyte replacement
What is Chronic Hyperglycaemia AKA Glucose Toxicity in type 1
Hyperglycemia more than 6 mmol/L:
-chronic hyperglycemia =glucose toxicity =harmful metabolic effects
-tight glycemic control is important!!!
-reverse or slow glucotoxic effects of chronic hyperglycemia
Type 1 diabetes:
-progressive autoimmune destruction of pancreatic beta cells
-occurs from absolute insulin deficiency and increase glucagon
What is Chronic Hyperglycaemia AKA Glucose Toxicity in type 2
- pancreas usually continues to produce some insulin but insulin produced is
- either insufficient for needs of body (beta cell exhaustion)
- is poorly utilized by tissue (insulin resistance)
- or both
- pulse hepatic glucose production
How Does Recurrent or Persistent Hyperglycemia Cause Chronic Complications?
-With recurrent or persistent hyperglycemia, glucose becomes irreversibly bound to collagen and other proteins, blood vessel walls, interstitial tissue, and within cells causing damage
- thickens basement membranes
- increases permeability in small blood vessels and nerves
- induces release of inflammatory cytokines and growth factors
- stimulate cellular proliferation in glomeruli, smooth muscle of blood vessels, and collagen -synthesis with fibrosis
- induces lipid oxidation, oxidative stress, and inflammation
- inactivates NO with loss of vasodilation and diminished endothelial function
- causes procoagulant changes with promotion of platelet adhesion and reduced fibrinolysis
- promotion of beta-cell apoptosis and insulin resistance
How does Hyperglycemia affect the Metabolic Pathways?
-Hyperglycemia induces overproduction of oxygen free radicals (oxidative stress)
- Activation of several metabolic pathways
- Inflammation
- Associated with insulin resistance and dyslipidemia
- Results in atherogenesis and damage to large and small vessels
What are the Chronic Complications of Diabetes Mellitus ?
-Microvascular disease .damage to capillaries .diabetic retinopathy .diabetic nephropathy .diabetic neuropathies
-Macrovascular disease .damage to medium and larger arteries .coronary artery disease .MI .cerebral vascular disease .peripheral vascular disease
-Infection
What are the Chronic Complications of Diabetes Mellitus ?
-Microvascular disease .damage to capillaries .diabetic retinopathy .diabetic nephropathy .diabetic neuropathies
-Macrovascular disease .damage to medium and larger arteries .coronary artery disease .MI .cerebral vascular disease .peripheral vascular disease
-Infection
What are the characteristics of Microvascular Disease
-Damage to capillaries
-Characteristics hyperglycemia (must be present) hypoxia and ischemia thickening of capillary basement membrane endothelial cell hyperplasia thrombosis pericyte degeneration
What is Diabetic Retinopathy ?
-Leading cause of blindness worldwide
-Develops more rapidly in type 2 diabetes
-Maculopathy
.progressive process that accompanies retinal capillary permeability, vessel occlusion, ischemia
-Macular edema
.fluid accumulation and retinal thickening
-Treatment
.laser treatment, vitrectomy, intravitreal steroids, antivascular endothelial growth factor, and renin-angiotensin system inhibitors
What is the Screening For Retinopathy ?
Type 1 diabetes
every year starting 5 years after diagnosis in all individuals 15 years of age or older
Type 2 diabetes
-children, adolescents, and adults at time of diagnosis
-interval for follow-up assessment should be tailored to severity of retinopathy
-in those with no or minimal retinopathy, recommended interval is 1 to 2 years
What is Diabetic Nephropathy ?
-Most common cause of end-stage kidney disease
-Progressive changes
.glomerular enlargement, glomerular basement membrane thickening
-Microalbuminuria
.first manifestation
-Treatment
.tight glucose control
.ACEIs or ARBs
.aggressive treatment of hypertension