Which of the following are complications of insulin therapy? (Select all that apply).

Choice A rationale: Stroke, also known as a cerebrovascular accident, is a significant macrovascular complication of diabetes mellitus. Chronic hyperglycemia damages the endothelial lining of blood vessels, leading to the formation of atherosclerotic plaques. These plaques can rupture, forming thrombi that obstruct blood flow to the brain, causing ischemic stroke. Hypertension, a common comorbidity, also increases stroke risk by damaging vessel walls.
Choice B rationale: Kidney failure, specifically diabetic nephropathy, is a major microvascular complication. Persistent hyperglycemia causes glomerular hyperfiltration and damage to the small blood vessels and filtering units (glomeruli) in the kidneys. This leads to protein leakage (albuminuria), which progresses to a decrease in the glomerular filtration rate, ultimately resulting in end-stage renal disease and the need for dialysis or kidney transplantation.
Choice C rationale: Blindness, specifically diabetic retinopathy, is a primary microvascular complication. Chronic high blood glucose levels damage the tiny capillaries supplying the retina, causing them to leak fluid or close off completely. This can lead to the growth of new, fragile blood vessels (proliferative retinopathy) that are prone to bleeding, scarring, and retinal detachment, causing irreversible vision loss or blindness.
Choice D rationale: Respiratory failure is not a direct complication of diabetes mellitus. While conditions like diabetic ketoacidosis can lead to Kussmaul respirations (deep, rapid breathing) as a compensatory mechanism, this is not considered respiratory failure. Respiratory failure is more often associated with primary pulmonary diseases, severe infections, or neuromuscular disorders.
Choice E rationale: Cirrhosis, a late-stage liver disease, is not a direct complication of diabetes mellitus. While non-alcoholic fatty liver disease (NAFLD) is prevalent in individuals with diabetes and metabolic syndrome, and can progress to cirrhosis, it is not an inevitable or direct consequence of the disease itself. Cirrhosis is more directly caused by chronic viral hepatitis, alcohol abuse, or other liver diseases.

Choice A rationale: The Dawn phenomenon is a morning hyperglycemia that results from the normal circadian release of growth hormone and cortisol. These hormones increase glucose production in the liver, leading to elevated blood glucose levels. Unlike the Somogyi phenomenon, it is not preceded by a nocturnal hypoglycemic episode.
Choice B rationale: Insulin resistance is a physiological condition in which cells fail to respond to the normal actions of insulin. The body's cells do not effectively absorb glucose, leading to elevated blood glucose levels. It is a chronic condition and does not involve an acute nocturnal hypoglycemic event followed by a rebound hyperglycemia.
Choice C rationale: Lipodystrophy is a complication of insulin therapy characterized by changes in subcutaneous fat tissue at injection sites. It can present as either lipoatrophy (denting of the skin) or lipohypertrophy (thickening of the skin). This is a localized skin condition and not a systemic metabolic phenomenon related to blood glucose fluctuations.
Choice D rationale: The Somogyi phenomenon is a rebound hyperglycemia that occurs after an episode of undetected hypoglycemia, typically overnight. The low glucose triggers the release of counter-regulatory hormones (glucagon, epinephrine, cortisol, and growth hormone) which stimulate the liver to release glucose, leading to an elevated morning blood glucose level.