NRSG exam Flashcards
How is BGL regulated?
Food consumed –> carbohydrate broken down into glucose –> increased BGL –> detected by pancreas –> beta cells release insulin
Low BGL –> alpha cells release glucagon
What does glucagon do?
Stimulates the liver to convert glycogen back into glucose
Stimulates the conversion of amino acids into glucose
Stimulates the liver to convert triglycerides and free fatty acids to glucose
What is DM?
Group of metabolic diseases characterised by chronic hyperglycemia due to issues with insulin secretion and/ or action
Define T1 DM
Beta cell destruction resulting in insulin deficiency (total lack of insulin production)
Define T2 DM
Impaired insulin action due to:
- increased insulin resistance at target tissues due to reduced number of insulin binding sites and/ or decreased amount of insulin binding to receptors
- decreased beta cell responsiveness to insulin
- Decreased insulin production as disease progresses
What are the causes of T1 DM?
Autoimmune destruction of beta cells
Environmental and genetic factors trigger autoimmune response
What are the causes of T2 DM?
Ethnicity Age Overweight >35 years Genetics Gestational DM
What are the acute complications of T1 DM?
DKA
What are the acute complications of T2 DM?
HHS
Describe the pathophysiology of T1 DM
Genetic factors + environmental factors –> immune response against beta cells –> beta cell destruction –> no insulin produced –> GLUT4 transporters are not activated –> glucose unable to be taken up by cells –> cell starvation –> compensatory release of glucagon by alpha cells + continued impaired glucose uptake –> hyperglycemia –> T1 DM
Describe the pathophysiology of T2 DM
Non-modifiable risk factors (age, genetics, ethnicity) + modifiable risk factors (lifestyle, diet, weight) –> increased adiposity –> increased free fatty acids (proinflammatory cytokines) –> chronic cell inflammation –> increased ROS –> oxidative stress –> liver and muscle cell damage –> decreased insulin production/ ineffective function –> increased BGL –> compensatory glucagon release from alpha cells + continued impaired glucose uptake –> hyperglycemia –> T2 DM
Explain how DM leads to the 3 Ps
- Polyphagia: impaired glucose uptake prevents cells from making ATP –> liver cells, muscle cells and adipose tissue break down glycogen and triglyceride stores to make glucose and ATP –> these stores eventually depleted –> cell starvation –> increased appetite
- Polyuria: excess glucose removed from blood by the kidneys –> glucose is a osmotic diuretic and draws water with it to the kidneys –> increased urine production
- Polydipsia: polyuria –> dehydration –> increased thirst sensation –> worsens polyuria –> worsens polydipsia
What is DKA?
Dangerously high blood ketones and metabolic acidosis related to hyperglycemia
Develops over hours - days
How does DKA occur?
Lack of insulin –> cells unable to take up and use glucose –> adipose tissue broken down to make ATP –> ketones produced as by-product and accumulate in blood –> ketoacidosis
Also: severe hyperglycemia –> osmotic diuresis –> fluid shifts from cells and loss of fluid through urine –> dehydration
What are the clinical manifestations of DKA?
Ketonic breath
Kussaml’s respirations
Polyuria
Polydipsia, sunken eyes, tachycardia, dry skin, headache, seizures, coma
Hypotension
Impaired cerebral functioning, lethargy, ALOC, seizures
BGL >11, ketones in urine
What are the clinical manifestations of DKA?
Ketonic breath
Kussaml’s respirations
Polyuria
Polydipsia, sunken eyes, tachycardia, dry skin, headache, seizures, coma
Hypotension
Impaired cerebral functioning, lethargy, ALOC, seizures
BGL >11, ketones in urine
What is HHS?
Severe hyperglycemia, dehydration and high serum osmolality without ketoacidosis
Develops over days - weeks
How does HHS occur?
Severe hyperglycemia –> excess glucose causing osmotic diuresis –> fluid shifts out of cells and into BVs –> excess glucose excreted in urine –> water follows –> dehydration –> increased osmotic solutes in blood –> hyperosmolality (high concentration of osmotically active solutes in blood) –> continued fluid loss –> hypotension, hypovolemia, dehydration, impaired perfusion –> ALOC, seizures, coma
Why is there no ketone production in HHS?
HHS is a complication of T2DM; in T2DM insulin is still being produced (although it can’t be used) –> insulin inhibits ketogenesis (the breakdown of adipose tissue to make ATP), which is what produces the ketones
What are the clinical manifestations of HHS?
Polyuria Polydipsia Sunken eyes Hypotension Tachycardia Headache Fatigue Seizures ALOC Coma BGL >30mmol/L No blood/ urine ketones
What are the interventions for DKA and HHS in order of priority and the rationale for each?
- IV fluid resuscitation - 24 - 72 hours; increase intravascular volume so fluid moves back into cells
- Reverse hyperglycemia - IV insulin infusion +/- dextrose infusion; the underlying cause of the condition
- Correct acid-base and electrolyte imbalance - regular BGLs, monitor urine ketones, K+, Na+, urea, cardiac monitoring, fluid balance
- Regular vitals
What causes hyoglycemia?
medication OD, not eating enough, exercise
What are the clinical manifestations of hypoglycemia?
Trembling Dizziness Diaphoresis Hunger Headaches Lack of coordination and concentration Vision changes seizures ALOC Coma
What is the management of hypoglycemia?
- Check BGL
- Eat 15 - 20g fast acting carbohydrate
- Re-check BGL
- Eat 20g slow acting carbohydrate
If unconscious: - Position on side, ensure airway patency
- IV dextrose bolus or IM glucagon (if no IV access)
- One pt alert and stable eat 20g slow acting carbohydrate
What does insulin do?
Enables glucose uptake into cells
Stores glucose as glycogen in muscle and liver cells
Inhibits the liver from producing glucose
Stimulates glucose to be stored as triglycerides in adipose tissue
What is the role of OHAs?
Increase insulin action or encourage glucose uptake
What happens to RBCs if DM is poorly managed?
Persistent hyperglycemia –> glucose irreversibly bound to RBCs –> AGEs produced (toxic metabolites)
How does DM lead to retinopathy?
Hyperglycemia –> glucose bound to RBCs –> AGEs formed –> vasoconstriction –> hypertension –> increased pressure in retina and hemorrhage –> decreased perfusion –> ischaemia –> cell damage/ death
How does DM lead to nephropathy?
Hyperglycemia –> glucose bound to RBCs –> AGE formation –> vasoconstriction –> hypertension –> increased glomerular blood flow –> increased GFR –> impaired filtration –> microalbuminuria –> kidney damage –> renal failure
How does DM cause neuropathy
Hyperglycemia –> glucose bound to RBCs –> AGE formation –> vasoconstriction –> decreased nerve perfusion –> ischemia –> impaired nerve function and demyelination –> impaired nerve impulse transmission:
- peripheral neuropathy: pins & needles, numbness in peripheries
- autonomic neuropathy: incontinence, digestive issues
How does DM lead to ATH
Hyperglycemia –> glucose binds to RBCs –> AGE formation –> decreased nitric oxide –> vasoconstriction –> hypertension –> endothelial injury
Also leads to increased vascular permeability –> monocytes and LDLs enter endothelium
AGE also promotes platelet aggregation
How does hyperglycemia lead to peripheral vascular disease?
ATH formation due to AGE –> reduced peripheral perfusion –> ischemia -> pain, pallor, paresthesia, pulselessness –> necrosis
How does hyperglycemia increase infection risk?
- Hyperglycemia impairs chemotaxis –> prevents WBCs migrating to site of inflammation –> prevents phagocytosis
- Hyperglycemia inhibits complement cascade activation –> complement cascade activation cause bacteria to become porous due to formation of protein channels –> fluid enters –> bacteria swell and burst
- AGE –> vasoconstriction –> impaired blood flow and delivery of WBCs, O2 etc required for healing
- High glucose environment good for bacterial growth
- Vision and sensation changes –> loss of early warning signs
