Diabetes Complications Flashcards
hyperglycemic emergencies - overview
*occur when there is either too little insulin, or too much glucagon/cortisol/epinephrine/NE
*includes: 1) DKA; 2) hyperosmolar hyperglycemic state (HHS)
diabetic ketoacidosis (DKA) - pathophysiology
*an effect of insulinopenia or relative insulinopenia (too little insulin)
*not enough insulin to suppress fatty acids from being released from fat and sent to liver (lipolysis)
*liver mitochondria cannot handle all the fatty acids, and the excess become ketones
*glucose rises, as does serum ketones: beta-hydroxybutyrate > acetoacetate
*the serum ketones cause an anion gap metabolic acidosis
diabetic ketoacidosis (DKA) - presentation
*typically occurs in T1DM, but can occur in extreme cases of T2DM
*presenting signs/symptoms:
-hyperglycemia
-polyuria/polydipsia
-Kussmaul respirations (rapid deep breathing, respiratory compensation for metabolic acidosis)
-GI sx: abdominal pain, N/V (due to acidemia)
-fruity breath odor (due to exhaled acetone, a breakdown product of acetoacetate)
hyperosmolar hyperglycemic state (HHS)
*there is enough insulin to suppress fatty acid release from adipose tissue, but not enough insulin to drive the glucose into the cells
*therefore: glucose increases, but no ketones are produced
*takes longer to present with sx compared to DKA
*has a higher mortality than DKA, likely due to high osmolality leading to coma
4 key problems in hyperglycemic emergencies
- dehydration: due to osmotic diuresis from hyperglycemia; can be severe and life threatening
- hyperosmolality: more of an issue in HHS; causes osmotic fluid shift (intracellular → extracellular); occurs in brain as well
- acidosis: in DKA; mental obtundation, coma, cardiac dysfunction, etc
- electrolyte abnormalities: HYPOKALEMIA (potassium shifts out of cells into extracellular space due to acidemia and insulin deficiency; then K+ is lost in urine)
dilutional hyponatremia
*sodium level is a concentration, influenced by intravascular fluid status
*in severe hyperglycemia, water is drawn into intravascular space, which will decrease the sodium concentration (i.e. dilutional hyponatremia)
*must calculate a corrected sodium based on how high the blood sugar is
treatment of DKA
- IV fluids
- potassium
- insulin
- assess need for bicarbonate
note - do not correct too rapidly d/t risk of cerebral edema
treatment of HHS
- IV fluids
- insulin
- potassium
note - do not correct too rapidly d/t risk of cerebral edema
prevention of hypoglycemia in a normal (non-diabetic) state
- as blood sugar approaches 70 mg/dl (low end of normal), insulin secretion from beta cells ceases
- at glucose < 70 mg/dL, alpha cells secrete glucagon
- as glucose continues to fall, epinephrine and cortisol are secreted to help increase sugar
hypoglycemia in diabetes
*this is iatrogenic due to insulin (you are giving insulin) or insulin secretagogues (sulfonylureas)
*only failsafe against hypoglycemia is epinephrine/cortisol
*the more hypoglycemia you have, the less of an adrenergic response you have → hypoglycemic unawareness
symptoms of hypoglycemia - general
- adrenergic symptoms: tremors, sweating, anxiety, hunger
- neuroglycopenic symptoms: AMS, seizures, CNS toxicity
adrenergic symptoms of hypoglycemia
*due to epinephrine (released in attempt to increase blood glucose)
1. tremulousness
2. diaphoresis
3. anxiety
4. hunger
neuroglycopenic symptoms of hypoglycemia
*lack of glucose to brain, usually glucose < 50
1. altered mental status
2. seizures
3. CNS toxicity (mimics anoxic brain injury)
4. cardiac arrest
treatment of hypoglycemia
*mild to moderate (pt is still alert and oriented) = consume 15g of sugar and recheck in 15 mins
*severe hypoglycemia (pt requiring assistance, can’t consume carbs) = give glucagon injection; if pt is hospitalized, give IV dextrose
macrovascular complications of diabetes: atherosclerotic coronary vascular disease (ASCVD)
*coronary artery disease, cerebral vascular disease, peripheral artery disease
*pts with DM are 2-4x more likely to develop ASCVD
*pathogenesis is complex and not fully understood, but advanced glycation end products (AGEs) play a role
advanced glycation end products (AGEs)
*form when glucose reacts with proteins and lipids in the endothelial wall, leading to direct & indirect damage
*leads to inflammation and a cascade of events in the endothelial wall
microvascular complications of diabetes - overview
*small blood vessels/capillaries are particularly susceptible to advanced glycation end products (AGEs)
*most commonly affected vessels include:
-retinal vessels
-vessels supplying small nerve fibers
-arterioles of nephrons
diabetic retinopathy - epidemiology
*leading cause of blindness in developed countries
*up to 90% of patients with T1DM will develop some degree of diabetic retinopathy
*in T2DM, 50-60% will develop diabetic retinopathy
*2 types: non-proliferative and proliferative
*classic findings = exudates and cotton wool spots
non-proliferative diabetic retinopathy
*starts with microaneurysms, which then bleed
*vessel walls become more permeable, and fluid/lipids leak into retina, causing macular edema, hard exudates
proliferative diabetic retinopathy
*vessel damage/occlusion can lead to hypoxia → neovascularization
*new blood vessels are weak/fragile and have a tendency to bleed
diabetic nephropathy
*most common cause of ESRD in the US
*50% of T1DM pts will develop CKD, 30% of T2DM pts
*earliest sign = small amounts of albumin lost in urine (albuminuria)
*histology: GBM thickening, nodular glomerulosclerosis, Kimmelstein-Wilson nodules
*treatment = ACE inhibitors/ARBs
diabetic neuropathy - overview
*damage to small nerve fibers, most commonly sensory nerves
*symmetric and length-dependent: longer nerves are affected first (i.e. sx typically start in FEET and eventually have a stocking-glove distribution)
*some pts experience painful neuropathy, some simply lose sensation
*main contributing factor to diabetic foot wounds/amputations
*can also cause autonomic neuropathy - cardiac issues & orthostatic hypotension
diabetic neuropathy - screening & treatment
*screening: monofilament test, annual foot exams
*treatment: gabapentin, SNRIs
other complications of diabetes
*heart failure
*gastroparesis
*diabetic foot wounds/amputations
*periodontal disease
*infections
*sexual dysfunction
*skin manifestations
*metabolic dysfunction-associated steatotic liver disease (MASLD)
*diabetic myonecrosis (muscle infarction)
