Diabetes Flashcards
diabetes
metabolic disorder characterized by hyperglycemia that results from insulin secretion, insulin action, or both
- associated with extensive long term damage when uncontrolled
carbohydrate
simple sugars and complex chemical units
where are carbs broken down
duodenum and proximal jejunum
normal health human glucose trends
blood glucose rises after you eat, then will lower back to baseline
diabetes
role of liver in glucose levels
- extracts glucose
- synthesizes glucose into glycogen for storage
- glycogenolysis: break down of glycogen
liver will inc glucose levels, which stimulates the pancreas to secrete insulin
what do peripheral tissues use for energy
glucose
role of the pancreas w glucose levels
- exocrine function: secrete enzymes into the ducts of GI tract for breakdown
- endocrine function: secrete insulin directly into the blood
islets of langerhans
islands of cells in pancreas that secrete glucagon and insulin
- alpha: secrete glucagon when low blood sugar
- beta: produce and secrete insulin which inc in blood sugar
glucagon
release by alpha cells when glucose levels are low
- stimulates glycogenolysis to begin (breakdown glycogen into glucose)
insulin
released from beta cells when glucose in blood is inc to promote intake of glucose into cells
- stimulates uptake, utilization, and storage of glu
- stimulates liver to store glu
- dec plasma conc of glu
hormones that lower blood glucose
- insulin
hormones that increase blood glucose
- glucagon
- epi
- glucocorticoids
- growth hormones
together balance glucose levels against insulin to prevent hypoglycemia
insulin and lipid metabolism
- insulin promotes synthesis of fatty acids in the liver once the liver has been saturated w glycogen
- insulin inhibits the breakdown on adipose tissue which can cause a buildup of TGs in fat cells
- drives cells to use carbs instead of fat E
what happens when not enough insulin
- cannot breakdown carbs
- dec glucose
- causes rapid glucose build up in blood –> hyperglycemia
- cells can use alt sources of E like fatty acids
insulin deficiency: inc lipolysis
inc lipolysis (breakdown) and dec lipogenesis (formation)
- causes free FA in blood which is an alternate energy source, converted into cholesterol and phospholipids, and breaks down into acetyl-coA
- results in ketone bodies
ketone bodies
substances that are composed of acid breakdown byproducts
short term complications of impaired fat metabolism
increase serum ketones
- ketosis, measured by blood and urine levels of ketones
- ketosis can cause severe metabolic acidosis which can lead to coma
long term complications of impaired fat metabolism
- atherosclerosis bc his serum lipid levels
insulin deficiency: protein metabolism
body unable to store protein effectively
- inc protein catabolism
- cessation of protein synthesis
what can protein metabolism in insulin deficiency result in
- inc protein breakdown means more aa in blood
- inc use of aa as energy storage
- protein catabolism results in muscle wasting, multiple organ dysfunction, aminoacidemia, inc BUN
insulin deficit: fluid and electrolytes
inc serum glucose levels –> increased plasma oncotic pressure –> fluid shifts into intravascular compartment –> intracellular dehydration
glucose isnt being taken but, blood becomes super conc w glucose, water moves out of cells dehydrating them and in to vascular space
glycosuria
excretion of sugar in the urine
- occur when hyperglycemia inc beyond what kidneys can reabsorb
- + urine dipstick
- inc acetones in urine
polyphagia
increased hunger
- due to catabolism (breakdown) of fat and protein, cell starvation
polydipsia
excessive thirst
- due to inc serum osmolality
polyuria
excessive urination
- due to osmotic diuresis
DM
group of metabolic disorders characterized by hyperglycemia resulting from absolute or relative insulin deficiency
type 1 D
complete lack of endogenous insulin
- most common pediatric disease –> usually around 12 yr old
- can be idiopathic
- usually an autoimmune process –> genetic predisposition and env factors
t cell mediated disease destroys beta cells
clinical manifestations of type 1 D
long preclinical period of symptoms until the insulin production is almost to none
- results in hyperglycemia producing symptoms
- symptoms: 3 p’s, weight loss, fatigue, recurrent infections, prolonged wound healing, visual changes, parathesias, cardio symptoms
type 2 d
insulin resistance and some dec insulin production
- genetic - environmental aspect usually responsible
- risk factors: age, obesity, HTN, physical inactivity, family history
- suboptimal response of insulin resistant tissue
types of risk factors for type 2 D
modifiable: physical inactivity, high body fat, high blood pressure, high cholesterol
non modifiable: history of gestational, race/ethnicity, over 45 yo, family history
type 2 clinical manifestation
usually just vague/non specific manifestations of hyperglycemia like fatigue, recurrent infections, visual changes, prolonged wound healing
- usually diagnosis by dr testing bc of risk factors
complications associated w type 2
- impaired insulin secretion
- peripheral insulin resistance
- increased hepatic glucose production
- altered production of hormones and cytokines by adipose tissue
acute complications of d
DKA: type 1, insulin deficiency so hyperglycemia, acidosis, ketonuria
HHNS: type 2, less profound insulin deficiency but more significant fluid deficiency (fluid shifting)
hypoglycemia
rapid onset, blood sugar below 55-60
- usually related to medications
- symptoms: pallor, sweating, tachycardia, palpations, hunger, restlessness, anxiety, tremors, convulsions, coma
problems w poorly controlled diabetes
- insulin resistance/deficit, chronic hyperglycemia, accumulation of advanced glycation end products, activation of metabolic pathways that cause damage
micro vascular
damages to capillaries
- retinopathies, nephropathies, neuropathies
- frequency and severity of lesions are proportional to disease
- accompanied by hypoxia and ischemia
- associated w capillary membrane thickening (microangiopathy: small vessel disease)
macrovascular
damage to large vessels
- coronary artery, peripheral vessels, cerebral vascular
diabetic neuropathy
loss of pain, temperature, and vibration sensations that can lead to ulcers, infection, possible amputation
- most common complication
- cause ischemia and demyelination, delaying conduction
diabetic retinopathy
results from relative hypoxemia, damage to retinal blood vessels, red blood cell aggregation and HTN
–> small vessels become occluded causing infarction
- leading cause of blindness world wide
diabetic nephropathy
glomerular basement membrane thickens and become sclerosed –> nonfunctional
- diabetes cause chronic kidney disease and end stage kidney disease
macrovascular complications
atherosclerosis: thickening, hardening of large arteries
- coronary artery disease, peripheral vascular disease, stroke, inc risk of infection
- thought to be result of oxidative stress, endothelial dysfunction, alterations in mineral metabolism, inc cytokine production
diabetes and infection
- diminished warning sign bc peripheral and retinal neuropathies
- tissue hypoxia when skin becomes impaired and health cells cant get there to heal
- rapid proliferation of pathogens bc of excess glucose feeding them
- dec WBC
