DM & Hypoglycemia Flashcards
Obesity
its role with T2DM
classifications
other diseases associated with obesity
Strong association between T2DM and obesity - not a straightforward relationship but strong correlation
- fitness plays a role strongly
BMI calculations: bodyweight / square of height
overweight: 25-29.9
obese: 30+
class 1: 30-35
class 2: 35-40
class 3: 40+
Other Diseases
- CVD (atherosclerosis, stroke, HTN)
- T2Dm
- gallbladder disease
- osteoarthritis (knees’ decrease in mobility)
- cancer
role of Childhood T2Dm
risk factors
prevention
- obesity is a facotr here too: increase obesity = increaed risk for development of T2DM
- inactivity is also a factor
- youths from minorities
Risk Factors
- family history
- insulin resistant conditions (like increase coags and lipids)
- obesity and physical inactivity
- race and ethnicity
- westernization (energy dense diet & reduced activity)
Prevention
- in-school interventions
- elimate candy and sodas
- 30-45 vigorous excerise
- appropropriate diet
Relationship between Obestiy and Insulin Resistance
- how does reduction in weight play a role
- increased weight and greater percentage of fats in the body = the greater the resistance to insulin
- a decrease in weight by even 5-10%, significantly reduces insulin resistance (going from “unfit” to fit is the biggest change)
The role of apettie in T2Dm
- role of leptin
- Ghrelin
Appetite
- supressed due to the actions of leptin (released by adipose tissue)
- activation of hunger is due to release of ghrelin from the stomach
Leptin
- secreted by the adipocytes
- control energy intake
- deficiency in lepitn leads to hyperphagia
- work in parallel with insulin: when insulin is released: that triggers leptin release as well
- insulin and leptin controlling indicates a high level of control for energy intake
in obesity: with increased adiposity the release of leptin from the increased number of cells: becomes slow/sluggished: they’re too full/satisfied: so they dont release the leptin
Ghrelin
- produced by the stomach (fundus)
- epsilon cells cells of the pancreas
- arcuate nucleus of the hypothalmus
- stimuate appetite
- a counter-regulatory for leptin
- in bariatric surgery: there is a decreased ghrelin so that helps to facilitate early satiety
Explain the mechanism of insulin resistance
- how does it correlate with weight
- patho behind it
increased weight, increased insulin resistance
- a decrease in the cerebro-cortical and overall systemic sensitivity to insulin a down reglation of insulin receptors occurs in the body and in the brain due to too much glucose in the blood, “over stimualte”
- hyperinsulinemia develops as a compensation in attempts to “pvercome” the decreased response to try to attempt to decrease weight gain
over time….
- insulin released from the pancrease fails
- and the lack of insulin increases appetite and weight gain
Increase insulin resistance…
- arcuate nucleus decrease response to insulin
- this allows increase wieght and increased eating behaviors
- obestiy results
- fat cells dysregulated in their response
- viscious cycle established
Normal Glucose Behavior v DM
normally: there is a fasting baseline level (70-100)
- within 1st half hour get increases
- next within the next 1 1/2 hour get returned to baseline
in DM: there is no or dimished release of insulin thus the level of glucose in the blood remains
Explain how impaired glucose tolerance occurs
- decreased ability of glucose to enter the cells due to lack of insulin response
- this triggers the process of gluconeogenesis to occur within cells & is trigger by glucagon (triggering breakdwon of glucose stores: glycogenolysis)
in insulin resistance
- intestinal absorbtion and renal reabsorbtion arenet altered
- areas wehre the GLUT 4 transporters arent active (like the brain) are unaffected
in sum
- decreased glucose uptake
- increase protein breakdown
- increase lipolysis
Hyperglycemia
what are they pathoologys that result
due to hyperglycemia
- hyperosmalr blood
- glycosuria with water loss
- sodium and potassium loss
- dehydration
- decreased glucose into cells
- cells turn to lipids for energy
Explain the process of glucose deposition into the various tissues and the complications it causes
The kidney: increased glucose creates excess glucose, allowing for the glucose to deposit into the basement membrane of the golmereulus
- over time the BM thickens, and leads to damange via the immune reponse which occurs: leads to spilling of the glucose and susequent issues
The skin: glucose deposits within the skin, leading to thikening and dysfunction
The muscle: glucoe deposits in the BM here too, leading to improper muscle physiology
what are some acute complications of DM in terms of glucose control
- due to insulin administration
hypoglycemia the act of low glucose within the body
- ususally due to improper insulin administration or other disease states (like sepsis untreated)
Coma
- as a result of hyperglycemia
- as a result of hypoglycemia
- due to lactic acidosis (due to gluconeogenesis releasing of acidic byproducts)
What is the bodies natural response to hypogylcemia normally
what hormones kick in
at what glucose level are neurologic effects noted
how do you treat in DM
when there is a low level of glucose within the body
- counter regulatory hormones are triggered on: named glucagon this happens at blood sugars of 60 (normal again: 70-100)
- epinephrone (a CR hormone) triggers autonomic symmptoms (tremor, sweaty, etc.) between 50-60
- neuro-gylcopenic (brain issues due to lack of glucose) effects being when glucose concentration is ** < 50**
a coma can occur at ** 30 with severe brain damage**
IN Dm pts.
- the counter-regulatory response is often impaired (the glucagon surge)
- thus, most times the move to treat with oral sugar or infusion is needed
Treatment
- oral intake of sugar, foods with sugar or sugar tabels
- unconscious pt: glucose infucsion or glucagon kit
Types of Comas related to DM and glucose
hyperglycemic coma (DKA, HHS)
(elaborate on ^^)
hypogycemic comas
lactic acidosis
Hyperglycemic
- DKA related
- hyperglycemic, hyperosmotic, non-ketotic coma (HHS)
DKA
- seen in T1DM
- a MAJOR insulin deficiency leads to hyperglycemic serum
- results in beta-oxidative pathways of energy prodcution inside the cells for energy: release of the ketones as by products
- acidic nature of the ketones affects brain cells & leads to coma
HHS
- a mild, to moderate insulin defiency (T2DM)
- because the body is making some amount of insulin, there is no DKA presentation
- instead, plasma osmolarity > 300
- underlying renal and cardiac issues
- trigger by too much glucose in the serum, inability to use it in cells, leads to spilling into the urine, leads to osmotic diuersis from the glucose pulling the fluid into the urine, to dehydration (NO KETONES heres!!)
- because there is some insulin, prevents the lipids from conveting to lipolysis and the creation of ketones does not occur
Chronic Complications of DM
Kidney
(can see occular, kidney, CV, Skin, bone/joint and infection complications)
Kidney
- thickening of the basement membrane leads to glomerulosclerosis
- microalbuminuria due to compensatory hyperfilteration
- hypertension
- pylenonephritis
Chronic Complications of DM
Neurologic
- patho unknown, maybe related to C-peptide deficiency
- peripheral sensory issues
- motor neuropathy
- autonomic neuropathy
Chronic Complications
Cardiovascular
- atherosclerosis: due to glycoslyation: increased LDL oxydation leads to atherosclerosis
- platelet adheasions
- coagulation issues
- hypertension
- most people with T2DM die of CVD complications
