What are the normal, pre-diabetic and diabetic levels for hemoglobin A1c
Normal: Is less than 5.7%
Prediabetic: 5.7% to 6.4%
Diabetic: 6.5% and above
Epinephrine, cortisol (increasing cortisol increases BP), and glucagon are all examples of what
counter regulatory hormones used during hypoglycemia
What is the over all role of insulin
the overall role of insulin is to push glucose into the cell so that it can be metabolized
if it doesnt get pushed into the cell then it stays outside of the cell leading to hyperglycemia and micro and macrovascular damage over time
What are the indicators for type II diabetes and what are some reasons that someone gets diagnosed with Type II DM
age, race, comorbidities (HTN, Obese etc.), high blood sugar but not extremely high
Recurrent infections, slow healing wounds, and incidental finding (come into ER for something unrelated)
How does infection increase blood pressure?
Our body needs more energy when fighting an infection so our body releases cortisol which increases blood pressure and sugar levels causing hyperglycemia
What is the normal glucose range
70-110
What are the two clinical manifestations in both hypo and hyperglycemia?
Blurry vision
-hypo: because brain and lens arent communicating
hyper: because swelling of the lens
hunger: cells are starving for both
What is the pathophysiology of type I DM
It is autoimmune in nature for the most part and it is caused by the destruction of the beta cells in the pancreas leading to a lack of insulin production and release. Because of the lack of insulin glucose never goes into the cell causing severe hyperglycemia
*a person can have type I DM for up to 10 years before it is diagnosed (it takes time to destroy all the beta cells)
What are some of the diagnostic labs used to identify type II diabetes
A1C, fasting blood glucose, OGTT
What would be the treatment for the somogyi and the dawn effect?
Treatment for somogyi would be to eat a little snack at bed time
treatment for the dawn would be to alter medications
what level for a random blood glucose test would be considered diabetic?
200 or above
List some of the current diabetes statistics
29 million living with diabetes in the US
86 million are prediabetic
it is the 7th leading cause of death
Leading cause of: kidney failure, lower limb amputation, and adult onset blindness (when poorly controlled)
What are the clinical manifestations of Type I DM
Polyuria: excess glucose in the urine causing osmotic diuresis (too much sugar in the blood so the body is trying to get rid of it through the urine)
Polydipsia: fluid is lost in the urine and fluid shifts from vascular space because of dehydration
Polyphagia: Lack of nutrients entering cells leads to increased hunger
explain the difference between a random BG and A1C
Random blood glucose is similar to a picture, it is a quick snapshot
A1C is the average of previous 3 months and is the best measure for DM (you do not need to repeat an A1C)
Explain the trends for the somogyi and the dawn effect
Somogyi and dawn effect both start and end at the same place but for the dawn effect there is a steady incline in glucose levels in the body while the somogyi there is a big dip in the middle of the night and a big rise after (dip is due to too much insulin and rise is due to counter regulatory hormones like epi)
Normal is less than 140
prediabetic is 140 to 199
diabetic is 200 or greater
Oral Glucose tolerance test
What are the clinical manifestations of hyperglycemia in diabetics
-Excessive thirst because urinating frequently which alerts the thirst center in the brain to tell the body to drink more water
-Blurred vision because of swelling of the lens
-Dry skin because of increased peeing leading to dehydration
-Hunger because cells are starving
-Excessive urination
What is the normal physiology of glucose when you eat a meal high in carbs
In a normal person blood sugar goes up when you eat a ton of carbs
1)pancreas via beta cells release insulin2) the release of insulin causes cells to take up more glucose and causes the liver to take up glucose storing it as glycogen
3)Blood glucose levels will then drop returning the body to homeostasis
Explain the pathophysiology behind type II diabetes
Cells are desensitized to insulin but some insulin my still be released. As a result there is an increase in glycogen break down in the liver to produce glucose (gluconeogenesis)
Where do the micro and macrovascular changes occur as a result of uncontrolled DM
Macro vascular:
-Coronary arteries: heart attack
-Carotid: stroke
-Micro: kidneys, eyes, nervous system
What are the normal, prediabetic, and diabetic levels for Fasting blood sugar
Normal is less than 99
Prediabetic is 100 to 125
Diabetic is 126 and above
What are the clinical manifestations of Hypoglycemia in diabetics?
-Tachycardia because when the body is low on sugar so it releases catecholamines like epinephrine to try to create sugar to burn off fat which increases HR
-Sweaty for same reason above
-Shakiness/ tremors for same reason (these catecholamines are called counter regulatory hormones
-Hunger because cells are starving
-blurred vision because lens cannot focus correctly (brain and body aren't communicating efficiently)
What is the normal physiology when you dont eat enough carbs
1) the pancreas via alpha cells releases glucagon
2) glucagon causes the liver to release glycogen and begin gluconeogenesis (making glucose molecules)
Explain the difference between DKA and HHS/HNS
DKA
-Occurs in type I DM and happens very suddenly/ is often the first time someone is diagnosed with T1DM
-Adipose tissue is broken down and as a result releases ketones which results in metabolic acidosis and in an effort to blow off CO2 Pt will have kussmals respirations
-Patient will have fruity breath
HHS
-Occurs in type II diabetics
- Happens over time because T2DM have some insulin so they can manage their own bs to some extent
Explain the pathophysiology and clinical manifestations of Diabetic Gastroparesis
Pathophysiology:
-vagal nerve stimulation is responsible for peristalsis
-Prolonged hyperglycemia damages the vagal nerve and decreases peristalsis which leads to a decrease in gastric emptying
*this happens more frequently in Type I diabetics because of their severely high hyperglycemic levels and this only happens to long-term poorly controlled diabetics
Clinical manifestations:
-N/V: not emptying stomach so trying to get food out somehow
-Feeling of fullness
-bloating
-Heartburn
-anorexia
-weight loss/ malnutrition