DM Flashcards
DM literal meaning
blood sugar in urine, the urine tastes sweet, thats why MD use to drink to diagnose
DM is what kind of disease resulting from a ?
DM is a metabolic disease resulting from a defect in insulin secretion, action, or both, and is chronic, systemic disorder characterized by hypoglycemia and disruption of carbs, fat, and protein metabolism
What is responsible for DM ?
The chronic state of hypoglycemia is responsible for dysfunction and impairment in tissues and organs
Type I DM is called
insulin dependent/ juvenile
Type I DM is an
autoimmune response at the islet cells of the pancreas associated with an absolute deficiency of insulin production and secretion, typically before 14, peak onset 11
A patient with Type I DM requires
exogenous insulin to maintain life
Type II DM previously known as (On test)
Non-insulin dependent DM (NIDDM) or adult onset DM
Type II DM derived from a
combo of cellular resistance to insulin and an inadequate adjustment via secretion to the desensitized receptors, which are the alpha subunits on tyrosine kinase
Autoimmune component of Type II DM
happens in middle to late adulthood
does not impact affect of pancreatic beta cells
immune cells attack body cuz they see the cells as foreign invaders/ bad shit
Individuals have endogenous insulin production, yet
ineffective insulin action at the cellular level, so exogenous insulin is not effective in type II DM
Type II DM is associated with what
obesity, inactivity/ prolonged sedentary nature, smokers, age, gene susceptibility
Beta cells are unable to do what in type II DM
unable to increase production of insulin to compensate for the cell receptor hyposensitivity
When the body cannot use glucose the way that it should is considerd what?
preDB
When less glucose moves into the celll, plasma glucose levels rise =
preDB
Decreased insulin sensivity is
PreDB
The cells stop responding to the action of insulin (insulin resistance)
PreDB
Blood glucose levels are above normal but do not yet meet the criteria for diabetes diagnosis
preDB
100 mg/dl to 125 mg/dl plasma glucose levels
preDB
DB severe complications of: due to oxidative stress/ systemic inflammation include diseases and SX
Heart disease stroke Kidney disease blindness loss of limbs
WHAT IS THE MOST COMMON ENDOCRINE DISEASE?
DM
insulin is an antagonist to the hormone
cortisol
cortisol causes
hypoglycemia and stress to sys, and makes cells desitivied to insulin receptor, resitin
Since 1970 DM rates have increased due to
prolonged life expectancy
increased incidence of obesity
diabetes insipidus caused by
trauma to hypothalamus
lack of ADH production
Watching 2 or more hours of TV daily is a RF for
DM
Skipping breakfeast is a RF for
DM cuz coritsol is released to conserve glucose
Insulin is secreted by
beta cells (Tyrosine kinase) of pancreas
Insulin helps to
transport glucose into cells for fuel or for storage (glycogen/adipose)
insulin stimulates what mTOR stimulates
protein synthesis
insulin stimulates not carbs but
FFA storage
When glucose levels after meal,
beta cells increase secretion of insulin into the blood stream, thus, lowering plasma glucose levels
Blood glucose levels drop as the cells take up glucose, this does what?
reestablishes plasma homeostasis
Deposit large amounts of glucose in the liver as per glycogen storage, but unable if
insulin resistant or insensitive, which increases glucose secretion due to lack of phosphorylation of glucose to glucogen
Kidneys excrete excess
glucose in an attempt to balance blood sugar levels, making sweet urine yum
Kidney action of DM is due to
excessive water loss to osmotic diuretic force generated from glucose excretion, forces water out increasing urination
Increased fat mobilization occurs causing
excessive ketone formation creating decreased pH, increasing acidity
By-products of fat metabolism in combo with glucose excretion by the kidneys increase the
osmotic pressure and rapid dehydration can happen in conjuncton with elctrolyte imbalance
Muscle and most other body tissues are most blank to glucose
impermeable
What is used to increase permeability to glucose?
insulin increases cell membrane permability to glucose more than 10 fold/times
Liver is moderately
only organ to do this
permeable to glucose, both in and out, when insulin is or isn’t present
Glucose can leave Liver
easily unless it has been phosphorylated, not converted to glycogen via glycogen synthase
Insulin promotes the activity of the
glucokinase enzyme, which phosporylates glucose and enzymes that promote glycogen synthesis (vital for later portion of exercise)
Insulin promotes protein what
storage in muscle cells as amino acids
Insulin promoting protein storage cuases promotion and enhances
protein synthesis, stimulates AA uptake across the plasma membrane
Protein and insulun increases
DNA/RNA transcriptional mechanism and inhbits protein catabolism, break down AA causing muscle wasting in DM due to protein synthesis lacking
Lipid and insulin stimulates the synthesis and storage of
TGs, which inhibits the enzyme that break down stored llipids, (HSL) Hormone sensitive lipase
DM has plasma lipid levels rise by approx
500%
DM results in
atherosclerosis
DM can cause
cardiovascular complications, and impaired protein use occurs for fuel
DM 3 three complication vascular/ neurology
Large blood vessels (atheroscelorss)
small blood vessels (retina damage)
nerves (neuropathies)
DM and mitochondria
excess superoxide production in the mitochondria
DM causes lack of the body to
heal or regenerate results in increased susceptibility to infection, or lack of ability to heal from infection (weak immune sys)
DM can result in
sensory, motor, and/or autonomic neurppathy
DM and ecg with autonomic neuopathy
ECG not accurate secondary to autonomic neuropathy
Sensory example with DM
Poor temp regulation/ BP regulation with exercise
There frequent what in DM
frequent ulceration
healthy A1C desire less than
5
Hemoglobin A1C indicates the average
hemoglobin exposure to glucose over a prolonged time period for approx. 30-60 days
insulin molecule is comprised of
large polypeptide of 51 amino acids
insulin facilitates
the entrance of glucose into peripheral tissues
Alpha cells of pancreas yield
glucagon
Beta cells of pancreas produce
insulin
Delta cells of pancreas produce
somatostatin
somatostatin regulates
GI absorption and motility
F cells of pancreas produce
pancreatic polypeptide
GLUT proteins are
glucose transporters from the intracellular storage sites to the cell membrane of skel muscle and other peripheral tissues
GLUT proteins synthesized and stored in the
Golgi system of the cell
GLUT-4:
glucose transporter in muscle and fat cells
GLUT4 promote
facilatated diffusion for glucose transport across the plasma membrane
Insulin binds to a specific insulin receptor (a paired receptor)
Tyrosine kinase
Alpha subunit =
receptor site
Beta:
enzyme that reuslts in autophosporylation through a tyrosine kinase mechanism that initiates a series of biochemical cellular reactions
Insulin Receptor Substrates (IRSs) get
phosphorylated by tyrosine
IRSs initate changes in
various metabolic pathways that result in increase glucose uptake
IRSs initiate the translocation of
glucose transporters from intracellular storage sites to the cell membrane
IRSs and GLUT proteins promote
facilated diffusion via glut4
As plasma glucose [ ] rise, what happens
beta cells increase synthesis/ release of insulin
increased plasma glucose causes insulin to take it into cells, which reduces
blood glucose [ ] to normal
increased plasma glucose causes insulin to take it into cells, controlled by other factors:
cortisol, thyroxine (T4), lipid, and AA [ ]
Insulin release inhibits what
glucagon synthesis/release from the alpha cells
Reduced insulin release is correlated w/
increased glucagon
Factors afecting insulin release
Elevated blood glucose
rising AA and Fatty acid levels
ACh through parasympathetic pathways
Somatostatin and sympathetic nervous system pathways
Rising AA and fatty acid levels increases
insulin secretion
ACh through parasympathetic pathways increases
insulin secretion
Somatostatin and sympathetic nervous system pathways
decreases insulin release allowing increase in blood glucose levels
Hyperglycemia
lack of insulin mediated tissue glucose uptake
Microangiopathy and why?
abnormalities in small diameter blood vessels because of thickening of the basement membrane causing occulsions causing ischemia to tissues
hyperglycemia and microangiopathy damage by DM
Retina
kidneys
poor wound healing
Microangiopathy disease
large vessel thickening resulting in atherosclerosis, diseases include HTN, MI, CVA, and these conditions also demonstrate insulin resistance even when not combined with DM
adverse effects of exogenous insulin for type I DM
hypoglycemia
Immunosuppressants for type I DM
has an autoimmune origin, drugs that suppress the immune sys are becoming more common
sulfonylureas act directly on
pancreatic beta cells
sulfonylureas stimulate the release of
endogenous insulin
sulfonylureas released directly into the
hepatic portal vein travelling to the liver, which inhbits hepatic glucose production
sulfonylureas effect, increased insulin prodcution also aids in
glucose entry into muscle tissue
sulfonylureas most succesful for individuals with early
type II DM and still have good beta cell function
biguanides act directly on the
liver to decrease hepatic glucose production, also increase sensitvity of peripheral tissues to insulin
Alpha-glucosidase inhibitors inhbit
sugar breakdown in the intestines and also delays glucose absorption from the intestines
Thiazolidinediones similar mech to
biguanides
Dietary management non-pharm intervention for DM
total caloric intake and percentage of those being carbs
Weight loss non-pharm intervention for DM reduce the amount of
tissue that requires insulin, therby reducing the need for exogenous drugs
