Glucose Regulation 🍬🩸

Glucose regulation

Maintaining optimal blood glucose levels

Alpha cells in pancreas

Releases glucagon

• Glucagon triggers GLUCOSE RELEASE from the LIVER

• Raises blood sugar (triggered when BG is low at 70 mg dl)

Beta cells in pancreas

Releases insulin

• Insulin BINDS to insulin receptors in the CELLS to allow GLUCOSE INTO THE CELLS

• Facilitates movement of glucose across cell membranes INTO cells

Delta cells in pancreas

Neurotransmitter that inhibits production of both glucagon and insulin

• Known as somatostatin

Which area of the pancreas are alpha, beta, and delta cells in

Islets of Langerhans

T1DM

Beta cells are DESTROYED

• NO INSULIN MADE

• Can be autoimmune-triggered (e.g. chicken pox VIRUS) or genetically predisposed

• Acute/occurs within days or few weeks

• Most common in CHILDREN

T2DM

Insulin is still produced but the body RESISTS IT or cannot use it

• Can be controlled and prevented/stopped

• Chronic

• common in MIDDLE/OLDER adults

Risk factors to T2DM

• Family Hx of diabetes

• Obesity/lack of physical exercise

• Race

• Hx of gestational diabetes

• PCOS

• Hypertension

What race is at most risk for T2DM

1. American Indians

2. Alaska natives

Prevention methods to T2DM

• Lifestyle changes

  • Dietary management

  • Exercise

• Medication

• Maintenance of blood glucose levels

Treatment to T2DM

Oral glycemic and insulin therapy

Metabolic syndromes that can INCREASE risk for T2DM

• Obesity (Apple/pear body types)

• Hyperglycemia (high sugar)

• Hypertension (high bp)

• Hyperlipidemia (high fat/cholesterol)

Metabolic syndrome is pronounced if AT LEAST 3 of these are present

Hyperglycemia levels?

• More than 140 mg/dl

• More than 180 mg/dl is (SEVERE)

Hypoglycemia levels?

• Less than 70 mg/dl

• Less than 50 mg/dl (SEVERE)

Euglycemia levels

• 70-140 mg/dl

A1C pre-diabetic levels

5.7-6.4%

A1C normal levels

Below 5.7%

A1C diabetic levels

+ 6.5%

Fasting blood glucose for pre-diabetics (FPG)

100-125 mg/dl

Fasting blood glucose for diabetics (FPG)

+126 mg/dl

Fasting blood glucose normally (FPG)

Less than 70-100 mg/dl

2 hour OGTT for normal people

Less than 140 mg/dl

2 hour OGTT for prediabetic

140-200 mg/dl

2 hour OGTT for diabetics

+200 mg/dl

What is A1C

Reflects the percentages of glycated hemoglobin (hemoglobin w/glucose attached)

• Reflects average blood glucose over the past 2-3 months

Why is fasting plasma glucose (FPG) taken

To measure the amount of sugar in the body when it is at its lowest

• Provides a stable baseline

• DM is confirmed after 2 FPG tests are +126 mg/dl

How else is diabetes mellitus declared positive in a person

Levels +200 mg/dl w/ANY of the 3 tests WITH classic hyperglycemia symptomscan also be taken to declare DM

What is OGTT (oral glucose tolerance test)

A more sensitive test used to diagnose GESTATIONAL DIABETES MELLITUS

• No fasting is needed

• Give 75g of glucose dissolved in water, evaluate in 2 hours, and repeat

• 2 tests +200 mg/dl confirm for GDM

Hyperglycemia symptoms?

• Polyphasia

• Polyuria

• Polydipsia

• Dehydration (bc of high urine)

• Fatigue (bc of LACK of glucose USE/LACK OF ENERGY)

• Weight loss

• Poor wound healing

• Fruity mouth odor

• Kussmaul respiration

HAPPENS OVER AN EXTENDED PERIOD OF TIME (LONG TERM)

Why does weight loss occur in hyperglycemia

Water loss and breakdown of fat and muscle causes for mass and fluids to be lost

What is glycosuria

Exceeding glucose in the urine (more than 180 mg/dl)

• CAN PLACE PATIENT IN DANGER OF INFECTIONS

• Causes intimate itchiness in hyperglycemia

Why does poor healing occur in hyperglycemia

Vessels are damaged by high blood glucose levels, reducing oxygen and nutrient delivery to injured tissues

Why does Polyphagia occur in hyperglycemia

Glucose cannot enter cells bc of lack of insulin, causing lack and NEED for energy, stimulating hunger

Hypoglycemia symptoms?

• Reduced cognition

• Tremors (nervousness)

• Diaphoresis

• Weakness

• Hunger (Polyphasia)

• Headache

• Vision problems

• Irritability

• Anxiety

• Unconsciousness

• Seizures

HAPPENS IN A SHORT/RAPID PERIOD OF TIME (MORE DANGEROUS)

What hormones are released when body hits hypoglycemic levels?

• Glucagon

• Cortisol

• Epinephrine

Triggered when blood glucose hits levels BELOW 70 mg/dl

What does epinephrine do during hypoglycemia

Stimulates glucagon release (in pancreas) increasing GLUCOSE release from the liver TO the blood causing:

• Palpitations

• Diaphoresis

• Tremors

• Anxiety

Activates ANS

What are the FIRST warning signs of hypoglycemia

• Diaphoresis

• Tremors

• Palpitation/tachycardia

• Anxiety

• Hunger

• Irritability

3 glucose-related EMERGENCIES occurring to DM patients

1. DKA

2. HSS

3. Hypoglycemia

What causes hypoglycemia

• Too much insulin

• Not enough food/carbohydrates

• Increased activity/exercise

ALCOHOL/DRUG INTAKE MAY ALSO CAUSE HYPOGLYCEMIA

What symptoms occur in hypoglycemia as blood sugar remains low

Vision problems and reduced cognition

Late symptoms to hypoglycemia

• Confusion

• Paralysis

• Seizure

• Coma

what may occur if hypoglycemia goes untreated

• Seizures

• Coma

• DEATH

FIRST step to treat hypoglycemia

TAKE THE BLOOD GLUCOSE LEVELS!

• Find what type of hypoglycemia they have

• Are they ALOC

Treatment to ALERT AND CONSCIOUS hypoglycemic patients

25-50% glucose solution (gels/tabs)

• Use the rule of 15-15 (15 g of rapid-acting sugar→ 15 minutes→ 15 g of sugar again if levels remain low)

Treatment to ALTERED ALOC hypoglycemic patients

Parenteral (IV) glucose

• D50, D10, D5

• Glucagon can be administered via SQ injection

What if blood glucose hits levels BELOW 50 mg/dl

Coma

Seizures

Altered behavior

GO TO THE HOSPITAL ASAP

What does diabetes mean

Sweet urine

What does diabetes MELLITUS mean

Group of disorders characterized by CHRONIC HYPERGLYCEMIA/ HIGH BLOOD SUGAR

• Causes abnormalities in carbohydrate, protein, and fat metabolism

In children w/T2DM, what is the first line of therapy

LIFESTYLE CHANGES

• Manage sexual maturity, insulin sensitivity, physical growth, self-management

DO NOT GIVE hypoglycemic agents first (ONLY METFORMIN may be used if REALLY NEEDED)

Acanthosis nigricans

Insuline resistance marker in T2DM

• Darkening of skin folds (e.g. neck, thigh, axillae, etc)

T1DM older adults

May need more recovery time after surgery/illness

• increased risk due to CVS (bad A1C, cholesterol, triglycerides, and HTN management)

T2DM in older adults

Harder to diagnose (due to age-related changes in glucose)

• Polypharmacy risks

• high hypoglycemia risk

• DONT MANIFEST CLASSIC SYMPTOMS

Gestational diabetes

Diabetes occurring during pregnancy (6-7% of all pregnancies)

• Women diagnosed w/ T1DM/T2DM before pregnancy are still considered T1DM/T2DM patients

What does GDM place patient AT RISK for

• Hydramnios

• Preeclampsia

• UTIs

• Congenital anomalies

• LGA

What complications can GDM cause

Retinopathy (should see ophthalmologist during pregnancy)

As insulin NEEDS INCREASE due to placental MATURATION/HORMONES, it causes

1. Preexisting disease

2. Metabolic abnormalities (due to stress)

3. Altered maternal metabolism (due to hormones)

What if someone has T1DM before pregnant

A1C levels → 6-6.5%

• lower due to high RBC turnover

• Increased retinopathy risk

• Get counseling

What if someone has T2DM before pregnancy

A1C levels → 6-6.5%

• Weight management

• Insulin may be needed

Gluconeogenesis

MUSCLE + FAT are broken down by the LIVER in an attempt to produce MORE glucose

• Used even when glucose is already present as CELLS continue to demand for glucose (due to lack of insulin)

• Body attempts to use AMINO ACIDS and GLYCEROL as energy

What do kidneys have to do with hyperglycemia?

Because of the high blood glucose levels, kidneys try to balance fluid and electrolytes with the process of Osmotic Diuresis

Osmotic diuresis

Increased urination by kidneys due to excessive amounts of solutes (glucose) in the bloodstream

• Increase urine → glucose (electrolytes) leaving the body BUT ALSO causing WATER to be released

• Causes DEHYDRATION and LOSS OF ELECTROLYTES

What are ketones

Chemicals released as a byproduct of lypolysis (breakdown of fat) during glyconeogenesis.

• Fat breakdown can lead to metabolic acidosis as ketones accumulate (increased ketoacids)

What are the side effects of metabolic acidosis from ketones

CNS depression and COMA

• Causes Kussmaul respirations

• Leads to fruity smelly breath

• Leads to DKA

DKA

Diabetic Ketoacidosis

• Emergent/complications of T1DM

• Can occur when ENERGY requirements (need for glucose) INCREASES during PHYSICAL/EMOTIONAL STRESS

DKA levels

Greater than 300 mg/dl

4 metabolic problems of DKA

1. Hyperosmolarity

2. Metabolic acidosis

3. Extracellular VOLUME depletion

4. Electrolyte imbalance

What causes hyperosmolarity in DKA

Hyperglycemia (high blood glucose) and dehydration (loss of water)

What causes metabolic acidosis in DKA

Accumulation of ketoacids

What causes extracellular volume depletion in DKA

Osmotic diuresis (loss of fluids from increased urine)

What causes electrolytes to imbalance in DKA

Osmotic diuresis (loss of water AND electrolytes)

DKA symptoms

• Thirst

• Flushed

• Warm/dry

• Kussmaul respiration

• N/V

• Blurred vision

• Weight loss

• ALOC

FIRST step to treat DKA

8-10 L of ISOTONIC FLUIDS to replace fluid losses

• IV w/ 0.9% or .45% NS

SECOND step to treat DKA

Regular insulin infusion (only insulin given through IV)

• Humulin R

• Novolin R

What should you do after DKA has been treated

Monitor for:

• Potassium depletion (Monitor cardiac function if this happens)

How can potassium depletion occur if we’re treating for DKA

1. In the beginning, lack of insulin keeps K outside the cells

2. Osmotic diuresis causes K to leave the body

   • THERE IS TOTAL BODY LOW POTASSIUM LEVELS (serum potassium may look normal)

3. Once treatment starts and insulin allows glucose, POTASSIUM MOVES INTO THE CELLS

4. As potassium moves INTO the cells and OUT THROUGH URINE (bc of IV fluids)

   • SERUM POTASSIUM DEPLETION OCCURS

   • Watch for cardiac changes

Hyperosmolar Hyperglycemic Syndrome (HSS)

A hyperosmolar state (high blood osmolarity) due to osmotic diuresis

• Extremely high blood glucose levels (more than DKA)

• Ketones are absent

• Extreme dehydration

• Osmolarity may exceed 320

• Body STILL makes enough insulin to prevent ketosis BUT not enough to prevent hyperglycemia

Why do HSS patients experience dehydration

Osmotic diuresis

• Presence of high glucose causes for MORE URINE OUTPUT

• causing EXCESSIVE dehydration w/high levels of glucose prevailing

HSS symptoms

• Dry skin/mucous

• Extreme thirst

• ALOC

• Seizures

• Lethargy

• N/V

• Abdominal pain

FIRST step to treat HSS

8-10 L of ISOTONIC FLUIDS via IV to replace fluid losses

• 0.9% or 0.45% NS

SECOND step to treat HSS

Insulin infusion

• Monitor for potassium depletion as AGGRESSIVE REHYDRATION can cause K to lower as urine continues

• Monitor cardiac levels

Osmotic diuresis

Increased urination due to presence of certain substances in fluid filtered by the kidneys

What diabetic patient experiences HSS

T2DM patients because they can STILL make insulin, glucose is STILL entering cells, but it is not enough to prevent hyperglycemia

What factors can place a patient at risk for HHS

• Infection

• Surgery

• Acute illness

• Chronic illness

HSS levels

Greater than 600 mg/dl

What diabetic patient experiences DKA

T1DM because they don’t make insulin at all so the cells continue to look for glucose even if it is already there

Symptoms of T1 and T2 diabetes are the same, so how do they differ?

T2 is preventable and can be changed as their onset is gradual, compared to T1 which can happen in a shorter time and does not have a preventable period

Which group requires exogenous insuline lifelong?

T1DM

How is HSS and DKA different

HSS does NOT use fat breakdown, so it produces no metabolic acidosis (no ketones)

How are both the HSS & DKA similar

If untreated, they may lead to:

• Cerebral edema

• COMA

• Death

What are chronic complications of hyperglycemia

Microvascular and Macrovascular complications

What are acute complications of hyperglycemia

HSS and DKA

Microvascular complications

Damage to small vessels causing diabetic:

• Retinopathy

• Nephropathy

• Neuropathy

• Sexual dysfunction

Diabetic retinopathy

Recommend ANNUAL eye exams

• Causes loss of vision due to high blood glucose accumulating near the retina

Diabetic nephropathy

Disease of kidneys identified early by the PRESENCE of ALBUMIN in urine, HTN, and EDEMA

• Glomeruli walls thicken bc of glucose, impairing and damaging renal function

• Glomeruli filter is becomes “leaky”

• Albumin, normally stored in blood, leaks out into urine

First indication of diabetic nephropathy/vascular damage

Microalbuminuria (small amounts of albumin in the urine)

• HTN only accelerates diabetic nephropathy (manage w/aggressive hypertensives)

Diabetic neuropathy

Disorder in peripheral NERVES and AUTONOMIC NERVOUS SYSTEM (ANS)

• Blood vessels walls that supply nerves THICKEN

• Nutrient supply to nerves DECREASES

• Leads to loss of SENSATION

Sexual dysfunction

Damage to nerve tissue and vascular tissue

What can reduction in HbA1C levels do

Prevent eye and kidney Microvascular complications

Macrovascular complications

Damage to medium and large vessels causing:

• Cardiovascular disease (CVD)

• Stroke

• Peripheral Vascular disease (PVD)

• Reduced immunity

What increases risks for complications to a Macrovascular level?

• HTN

• Smoking

• Hyperlipidemia (high cholesterol)

• Obesity