Diabetic Lab Values
Hyperglycemia vs. hypoglycemia
DM
DM
DM
100

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 

100

Epinephrine, cortisol (increasing cortisol increases BP), and glucagon are all examples of what

counter regulatory hormones used during hypoglycemia 

100

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 

100

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)

100

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 

200

What is the normal glucose range 

70-110

200

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 

200

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)

200

What are some of the diagnostic labs used to identify type II diabetes

A1C, fasting blood glucose, OGTT

200

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 


300

what level for a random blood glucose test would be considered diabetic?

200 or above 

300

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)

300

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 

300

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) 

300

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)

400

Normal is less than 140 

prediabetic is 140 to 199

diabetic is 200 or greater 

Oral Glucose tolerance test 

400

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


400

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 insulin

2) 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 

400

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)


400

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 

500

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 

500

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) 

500

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) 

 

500

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 

500

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  

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