Type 2 Diabetes Mellitus: Symptoms, Medications & Treatment

Type 2 Diabetes: This lecture reviews type 2 diabetes mellitus including its definition, symptoms, risk factors, diet, pathophysiology, treatment, medications, and more!


Guest Author

Guest Author: Charlotte Watson

The lecture and tables below were written by guest author Charlotte Watson, and the medical illustrations were created and provided by EZmed.


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Type 2 Diabetes Mellitus

Definition

Diabetes mellitus is a metabolic disorder in which the body’s ability to produce or respond to insulin is impaired, resulting in elevated blood glucose (blood sugar) levels.

The medical term for high blood glucose levels is hyperglycemia.

Diabetes mellitus comes from the Greek word “diabetes” meaning to pass through, and the Latin word “mellitus” meaning sweet.

This makes sense as sweet glucose ‘passes through’ the body and into the urine in diabetes mellitus.

Diabetes mellitus can be classified into 2 main types:

  1. Type 1 Diabetes Mellitus

  2. Type 2 Diabetes Mellitus

This lecture will focus on Type 2 Diabetes Mellitus (T2DM).  

Type 2 diabetes is a metabolic disorder in which the body’s response to insulin is reduced, called insulin resistance.

Insulin production is initially increased by the pancreatic beta cells to try to counteract the insulin resistance.

However, over time there is a progressive decrease in insulin production and secretion leading to insufficient insulin levels.

The combination of insulin resistance and impaired insulin secretion results in hyperglycemia and type 2 diabetes.

Type 2 diabetes is more common than type 1 diabetes, making up over 90% of diabetes diagnoses.

The prevalence of type 2 diabetes is increasing due to rising obesity rates.

Type 2 diabetes usually develops in older age groups (over 45 years old) with a peak incidence of diagnosis at 60 years old.

However, the incidence has increased in children and adolescents due to rising obesity levels, physical inactivity, etc.

More on type 2 diabetes and how insulin works below!

Type 2 Diabetes Mellitus Definition: Type 2 diabetes is a metabolic disorder in which the body’s response to insulin is reduced (insulin resistance) and there is decreased insulin secretion by the pancreas, resulting in high blood glucose levels.

Overview

In this lecture, we will discuss the following about type 2 diabetes:

  • Definition

  • Signs & Symptoms

  • Risk Factors

  • Causes

  • Pathophysiology

  • Diagnosis

  • Treatment

  • Complications

  • Type 1 vs Type 2 Diabetes

The following pertinent information will also be reviewed:

  • Anatomy and Function of the Pancreas

  • Function of Insulin

Don’t miss the table at the end and leave a comment below if this lecture was helpful!

Type 2 Diabetes Mellitus: This lecture reviews type 2 diabetes definition, symptoms, causes, risk factors, pathophysiology, diagnosis, treatment, and more!


Symptoms of Type 2 Diabetes

Type 2 diabetes is a condition caused by insulin resistance and decreased insulin secretion, resulting in high blood glucose levels.

Many cells require insulin for glucose uptake.

In other words, insulin helps transport glucose from the blood and into cells (see insulin function below).

Once inside the cell, glucose can then be used as energy or fuel for the cell.

Without insulin, glucose remains in the blood and blood glucose levels increase as a result.

The elevated blood glucose levels, along with the inability of cells to take up glucose, result in a number of symptoms.

Signs and Symptoms of Type 2 Diabetes Include: 

  • Polyuria (increased urine output)

  • Increased urinary frequency

  • Polydipsia (increased thirst)

  • Polyphagia (increased hunger or appetite)

  • Unexplained weight loss

  • Blurred vision

  • Fatigue

  • Recurrent urinary tract infections

  • Recurrent skin infections

  • Recurrent candida (yeast) infections

  • Acanthosis nigricans (darkening of the skin around the neck, groin, and axilla/armpits)

  • Paresthesias (numbness, burning, prickling, or tingling sensation - typically in the hands, legs, and feet)

  • Slow healing of cuts or sores

Type 2 diabetes typically has a slower onset than type 1 diabetes, with symptoms developing over months to years (type 1 symptoms develop within days to weeks).

Type 2 Diabetes Symptoms: Signs and symptoms of type 2 diabetes include increased thirst (polydipsia), increased hunger (polyphagia), unexplained weight loss, fatigue, increased urine output (polyuria), blurred vision, numbness, etc.


Risk Factors for Type 2 Diabetes

There are both modifiable and non-modifiable risk factors for developing type 2 diabetes.

You are more likely to develop type 2 diabetes if you are/have:

  • Modifiable risk factors

    • Obese/Overweight

    • Low physical activity

    • Unbalanced diet

    • Prediabetes (higher than normal blood sugar, but not enough to be considered type 2 diabetes)

  • Non-modifiable risk factors

    • Family history of diabetes

    • Older than 45 years old

    • South Asian, African, Hispanic, American Indian, or Caribbean ethnicity

    • Low birth weight

    • Previous pregnancy with gestational diabetes

    • History of polycystic ovary syndrome (PCOS) or other metabolic diseases

Many of the modifiable risk factors listed above are the cause of insulin resistance - See the “Cause of Type 2 Diabetes” section below!

The genetic inheritance of type 2 diabetes is very strong, especially when compared to type 1 diabetes.

A child who has one parent with type 2 diabetes will have a 40% chance of developing it.

Type 2 Diabetes Risk Factors: Risk factors for developing type 2 diabetes include obesity, low physical activity, unbalanced diet, prediabetes, family history, age, ethnicity, gestational diabetes, etc.


Anatomy of the Pancreas 

In order to better understand the cause and pathophysiology of type 2 diabetes, let’s briefly review the anatomy and function of the pancreas and insulin.

The pancreas is an accessory organ of the abdomen.

The pancreas is located behind the stomach in the epigastric and left hypochondriac regions of the abdomen.

Anatomically, the pancreas is located along the transpyloric plane.

The transpyloric plane is an imaginary line midway between the suprasternal notch (jugular notch) and the upper border of the pubic symphysis, at approximately the level of the L1 vertebrae.

The pancreas can be divided into 5 main parts:

  1. Head

  2. Uncinate Process

  3. Neck

  4. Body

  5. Tail

The head of the pancreas sits within the curve of the duodenum, and the tail is located by the hilum of the spleen.

The pancreas (except for the tail) is retroperitoneal - This includes the head, neck, and body.

The tail of the pancreas is intraperitoneal.

Anatomy of the Pancreas: Location and labeled diagram of the pancreas and its parts including the head, uncinate process, neck, body, and tail.


Function of the Pancreas

The pancreas has both exocrine and endocrine roles:

Exocrine Function

The pancreas produces digestive enzymes which are secreted into the duodenum via the main pancreatic duct.

Pancreatic digestive enzymes include lipase, amylase, and proteases (such as trypsin and chymotrypsin).

The pancreatic digestive enzymes aid in the digestion of fats (lipase), carbohydrates (amylase), and proteins (proteases).

Endocrine Function

The pancreas produces and secretes hormones into the bloodstream.

  • Islets of Langerhans = Clusters of pancreatic endocrine cells that release specific hormones

    • Made up of 3 main types of cells:

      • Alpha Cells = Release glucagon

      • Beta Cells = Release insulin

      • Delta Cells = Release somatostatin

These hormones aid in glucose control.

The beta cells will be relevant in this lecture as they are responsible for producing and releasing insulin into the blood.

Function of the Pancreas: Digestive (exocrine) and hormone (endocrine) functions of the pancreas including glucagon (alpha cells), insulin (beta cells), and somatostatin (delta cells) release


Function of Insulin 

As previously mentioned, insulin is produced and released by the beta cells of the pancreas.

Insulin is responsible for regulating blood glucose levels in the body by allowing the movement of glucose into cells.

Insulin is continuously released by the pancreatic beta cells (see above) at a low level throughout the day, which helps to:

  • Maintain the resting blood glucose levels at a healthy range between eating and during the night

  • Allow constant low-level uptake of glucose into cells for cellular processes, such as cellular growth and DNA replication

Blood sugar rises after eating a meal, and the beta cells release insulin in a biphasic pattern.

  • Firstly, beta cells rapidly release stored insulin from granules inside the cell

  • Secondly, beta cells increase insulin synthesis for a smaller, second-phase release

How Does Insulin Work?

Once the beta cells of the pancreas release insulin into the blood, insulin binds to insulin receptors on the surface of body cells.

The binding of insulin to insulin receptors on cells activates a signaling cascade.

This cascade increases the recruitment of the glucose transporter GLUT4 from within intracellular storage vesicles to the plasma membrane of the cell.

GLUT4 is the major transporter responsible for the uptake of glucose from the bloodstream and into the cell.

An increase in GLUT4 glucose transporters at the plasma membrane will increase glucose uptake into the cell.

The cell can then use the glucose as energy or fuel to carry out its functions.

How Does Insulin Work? Insulin receptor signaling pathway: Insulin binds to insulin receptors which increases the recruitment of GLUT4 glucose transporters to the plasma membrane. GLUT4 allows for glucose uptake into the cell.


What Causes Type 2 Diabetes?

Type 2 diabetes develops when the pancreatic beta cells secrete less insulin than the body requires (decreased insulin levels), and the cells in the body stop responding to insulin (insulin resistance).

In other words, type 2 diabetes is an insulin-resistant condition with associated pancreatic beta cell dysfunction.

It is suggested insulin resistance can be caused by:

  • Metabolic Syndrome (3 or more of the following)

    • High blood glucose

    • Low levels of HDL (good) cholesterol

    • High levels of triglycerides

    • Large waist circumference

    • High blood pressure

  • Obesity - Adipose tissue promotes insulin resistance through inflammatory mechanisms

  • Lack of exercise

  • Poor diet

  • Genetics - Abnormal gene functioning can lead to insulin resistance and/or pancreatic beta cell dysfunction

Pathophysiology

Both insulin resistance and inadequate insulin secretion must be present for type 2 diabetes to occur.

In type 2 diabetes, insulin receptors on cell surfaces become resistant to insulin.

This means that glucose cannot be taken up into the cell from the bloodstream - See insulin function above.

Cells become deprived of glucose and blood sugar levels inappropriately rise.

More simply, the blood is full of sugar (glucose) but the sugar cannot enter the cells due to reduced insulin action and eventual overall lack of insulin.

To compensate for insulin resistance and to maintain normal glucose levels, the pancreatic beta cells will initially increase insulin synthesis and release.

The increase in insulin production and secretion is a temporary fix to overcome the lack of sensitivity of insulin and allow the body’s cells to take up glucose.

However, the increase in insulin production and secretion will eventually lead to accelerated beta cell changes and/or damage.

Simply put, the pancreatic beta cells “tire out” and do not make as much insulin.

This will cause a subsequent decrease in insulin production and secretion.

When the levels of insulin secreted by beta cells are not enough to compensate for the lack of sensitivity of insulin receptors, the patient will begin to experience symptoms of diabetes.

Type 2 Diabetes Pathophysiology: Type 2 diabetes is caused by insulin resistance and inadequate insulin secretion by the pancreatic beta cells, resulting in high glucose levels (hyperglycemia).

Effects on the Liver

The combination of insulin resistance and inadequate insulin secretion leads to a further increase in blood glucose levels by the liver.

As insulin is not recognized by insulin receptors on the liver, the liver can no longer take glucose up from the blood to store it.

This causes the liver to inappropriately respond as if the blood sugar is low (when in fact it is actually high), resulting in increased gluconeogenesis and glycogenolysis.

Gluconeogensis = The formation of glucose in the liver; Glycogenolysis = The breakdown of stored glycogen in the liver, released as glucose into the blood

Both processes increase blood glucose levels. 

Type 2 Diabetes Pathophysiology: Insulin resistance on liver cells and decreased insulin secretion by the pancreas can make the liver “think” blood glucose levels are low, leading to increased gluconeogenesis, glycogenolysis, and even higher blood glucose levels as a result.


Diagnosis & Tests

Diagnosis of type 2 diabetes involves measuring blood glucose levels through one of the following methods:

  • Hemoglobin A1C

  • Fasting blood sugar test

  • Oral glucose tolerance test

  • Random blood sugar test

Patients with symptoms of diabetes may only require 1 biochemical test to confirm their diagnosis of type 2 diabetes.

However, patients with no symptoms typically require 2 separate investigations on different occasions.

Both tests must have results which confirm the diagnosis of type 2 diabetes.

The investigations and their outcomes are shown in the table below.

Table 1: Standard units for United States, France, and Italy

Table 2: Standard units for United Kingdom (UK), Canada, and Australia

Prediabetes = Blood sugar levels are higher than normal, but not high enough to be diagnosed as type 2 diabetes

  • Prediabetes is also referred to as impaired fasting glucose, impaired glucose tolerance, or impaired glucose regulation depending on the test used

***Diagnostic values for both charts are based on the American Diabetes Association

Type 2 Diabetes Diagnosis (USA): Chart showing blood glucose levels for normal, prediabetes, and diabetes using hemoglobin A1C, fasting blood sugar test, oral glucose tolerance test, and random blood sugar test

 

Type 2 Diabetes Diagnosis (UK, Canada, Australia): Chart showing blood glucose levels for normal, prediabetes, and diabetes using hemoglobin A1C, fasting blood sugar test, oral glucose tolerance test, and random blood sugar test

Hemoglobin A1C

Hemoglobin A1C (HbA1c) is a simple blood test that measures the patient’s average blood sugar levels for the past 2-3 months (8-12 weeks). 

It measures the amount of glucose attached to hemoglobin (the protein in red blood cells that carries oxygen).

HbA1c does not require the patient to fast (not eating/drinking caloric intake) prior to the test.

HbA1c levels can be interpreted as:

  • Less than 5.7% (39 mmol/mol) = Normal

  • 5.7-6.4% (39-47 mmol/mol) = Prediabetes

  • 6.5% (48 mmol/mol) or higher on 2 separate occasions = Diabetes

HbA1c is affected by red blood cell turnover, therefore should not be used diagnostically in patients who have pathology affecting these cells, such as hemoglobinopathies, hemolysis, ongoing iron deficiency anemia, or HIV.

HbA1c is also not recommended in pregnant patients (OGTT below is more commonly used).

STUDY TIP - It is important to remember that although an elevated HbA1c can diagnose type 2 diabetes, a low HbA1c cannot rule it out! 

Fasting Blood Sugar Test

A fasting blood sugar test (also known as fasting plasma glucose, FPG) is a blood test that checks the blood sugar levels after having not consumed any food or drink (except water) for at least 8 hours prior to the test.

Patients usually begin fasting at midnight and have the blood test performed in the morning prior to breakfast.

Fasting blood glucose levels can be interpreted as:

  • Less than 100 mg/dL (5.6 mmol/L) = Normal

  • 100-125 mg/dL (5.6-6.9 mmol/L) = Prediabetes

  • 126 mg/dL (7 mmol/L) or higher on 2 separate tests = Diabetes

Oral Glucose Tolerance Test (OGTT)

The oral glucose tolerance test (OGTT) involves taking a fasting blood glucose level first, followed by the patient drinking a beverage containing 75g of glucose.

The blood glucose is then measured again, 2 hours after drinking the sugary beverage to analyze how the blood sugar level has changed.

This test is more commonly used to test pregnant patients.

  • A 2 hour blood glucose level of less than 140 mg/dL (7.8 mmol/L) = Normal

  • A 2 hour blood glucose level of 140-199 mg/dL (7.8-11.0 mmol/L) = Prediabetes

  • A 2 hour blood glucose level of 200 mg/dL (11.1 mmol/L) or higher = Diabetes

Random Blood Sugar Test

A random blood sugar test (also known as random plasma glucose) is a blood test that checks the blood sugar levels at any random time regardless of when the last meal was.

Regardless of when the last meal was, a blood glucose level of:

  • 200 mg/dL (11.1 mmol/L) or higher = Diabetes

Other Tests

On investigation for type 2 diabetes, the patient should also have their lipid profile tested and a urinalysis performed to check for proteinuria (protein in the urine) and ketones.

If ketones are present in the urine, it may indicate the patient has type 1 diabetes.

Renal (kidney) and liver function tests should also be performed via blood work. 


Treatment of Type 2 Diabetes 

The management of type 2 diabetes involves the input from a multidisciplinary team.

Due to the potential complications of diabetes, the patient will be seen by a variety of specialists including general practitioners, ophthalmologists, diabetic nurses, healthcare assistants, podiatrists, and dietitians. 

The treatment and management of type 2 diabetes involves the following:

  1. Education and Lifestyle Changes

    1. Diet

    2. Exercise

  2. Medication

    1. Oral diabetes medications

    2. Insulin

  3. Careful Glucose Monitoring

Type 2 Diabetes Treatment: Management of type 2 diabetes includes diet, exercise, medications, insulin, and glucose monitoring with HbA1c and fingersticks

1. Education and Lifestyle Changes

As previously mentioned, type 2 diabetes is commonly caused by a metabolic syndrome and factors that can often be modified such as obesity, poor diet, lack of exercise, etc (see causes above).

The first line treatment for patients with prediabetes or type 2 diabetes, prior to starting any medications, should be conservative management with lifestyle and diet modifications to reduce blood sugar levels.

Diet and exercise can also help prevent the progression of prediabetes to type 2 diabetes.

Patients will be encouraged to eat a balanced diet, exercise regularly, and stop smoking.

Diet may include:

  • More fiber-rich fruits and vegetables - Apples, berries, bananas, broccoli, leafy greens, etc.

  • More high fiber, complex carbohydrates (good carbs) - Brown rice, brown bread, whole wheat, whole grains, etc.

  • Less low fiber, simple carbohydrates (bad carbs) - White rice, white bread, pastas, etc.

  • Less simple sugars - Soda, candy, fruit juice concentrates, etc.

  • Low calorie diet

Exercise may include:

  • Aerobic Exercise - 150 minutes/week (walking, biking, swimming, etc.)

  • Resistance Exercise - 2-3 times/week (yoga, weightlifting, etc.)

  • Limit inactivity (take breaks from couch to walk around, etc.)

If the patient is overweight, then the primary care staff may encourage the patient to lose 5-10% of their body weight.

Losing this proportion of weight has been shown to decrease cardiovascular risk, improve glycemic control, and prevent diabetic complications. 

Patients will also be invited to an educational program to develop the skills, knowledge, and confidence to self manage their diabetes.

2. Medication

If diet, exercise, and lifestyle modifications alone are not sufficient to treat type 2 diabetes and maintain target glucose levels, then medications may need to be added.

Medications include:

  1. Oral diabetes medications (antidiabetic/hypoglycemic agents)

  2. Insulin

2.1. Oral Diabetes Medications - Hypoglycemic Agents

Oral diabetes medications are routinely used before insulin for the treatment of type 2 diabetes.

Examples of oral diabetes medications include:

  • Biguanides (metformin)

  • Thiazolidinediones (pioglitazone, rosiglitazone)

  • Sulfonylureas (glimepiride, glyburide, glipizide)

  • SGLT-2 Inhibitors (dapagliflozin, canagliflozin, empagliflozin)

  • DPP-4 Inhibitors (alogliptin, linagliptin, saxagliptin, sitagliptin)

  • GLP-1 Mimetics/Agonists (exenatide, liraglutide)

  • Meglitinides/Glinides (nateglinide, repaglinide)

    • Similar to sulfonylureas but act more quickly

  • Alpha-Glucosidase Inhibitors (acarbose, miglitol)

Type 2 Diabetes Medications: Treatment chart showing a list of diabetes medication drug classes, examples, mechanism of action, side effects, and contraindications

CKD = chronic kidney disease; HDL = high-density lipoprotein; UTI = urinary tract infection; AKI = acute kidney injury; DKA = diabetic ketoacidosis; GI = gastrointestinal

Metformin is generally the first-line medication prescribed for type 2 diabetes, while the other drugs listed above are considered second-line.

Metformin is usually started at a low dose to prevent gastrointestinal irritation, and will gradually be increased until the patient’s HbA1c levels begin to decrease.

The A1C target for a patient on monotherapy with metformin is ≤ 6.5% (48 mmol/mol).

Goals vary based on patient characteristics and may be ≤ 7% (53 mmol/mol) for some patients.

If target glucose levels are not achieved on metformin, then a second oral medication may be added to the treatment regimen.

If the patient’s initial HbA1c is ≥ 7.5% (58 mmol/mol), then the patient may need to start metformin and another second-line oral diabetes medication immediately. 

Considerations when choosing medications:

  • If the patient has cardiovascular disease or chronic heart failure (or is at risk of), then SGLT-2 inhibitors or GLP-1 agonists may be considered as they have been shown to reduce cardiovascular morbidity and mortality.

  • Pioglitazone has been shown to increase the risk of developing bladder cancer, and should not be given to patients with ongoing or a history of bladder cancer. It is also contraindicated in heart failure.  

The HbA1c target for patients on dual therapy is ≤ 7% (53 mmol/mol).

If dual therapy is not sufficient to lower the blood sugar, another agent can be added.

The HbA1c target for patients on triple therapy is still ≤ 7% (53 mmol/mol).

If this is not achieved, one of the drugs could be exchanged for a GLP-1 receptor agonist, or insulin therapy may be required. 

2.2. Insulin therapy 

If diet, exercise, lifestyle modifications, and oral diabetes medications are not sufficient to treat type 2 diabetes and maintain target glucose levels, then insulin may be required.

In some instances, insulin may be recommended first as an initial treatment.

When given insulin, patients with type 2 diabetes typically continue their oral diabetes medication, but use an intermediate-acting or long-acting insulin (“basal” insulin) at bedtime or twice daily. 

Healthcare providers will work with each individual patient to recommend the best insulin regimen, and over time insulin regimens may need to be adjusted.

3. Glucose Monitoring

Hemoglobin A1C

HbA1c levels should be measured by primary care staff to estimate the patient’s average blood glucose level over the past 2-3 months (8-12 weeks).

Levels are typically checked every 3 to 6 months until the patient’s HbA1c is stable and their treatment has been finalized, and then it can be reduced to every 6 months. 

Unlike type 1 diabetes, the HbA1c target for type 2 diabetics may be more personalized in order to aid patient motivation.

In addition to HbA1c monitoring, blood sugars may be checked daily or multiple times per day using a capillary “pinprick” blood glucose test.

Important: HbA1c goals may vary from patient to patient and the table below is a general guideline.

Type 2 Diabetes A1C Chart: Target goals for HbA1c in type 2 diabetes mellitus

Annual Review

Patients with diabetes in the UK will be invited to an “annual review” with a member of the multidisciplinary team from their primary care practice.

This will involve a full screen of the patient’s diabetic history, how they are managing their diabetes, and a full examination.

The examination will involve measuring the patient’s weight, abdominal circumference, and BMI (body mass index) to assess cardiovascular risk.

A full cardiovascular and peripheral vascular exam will also be completed, along with inspection of the feet to check for neuropathy and foot ulcers/sores.

The patient must also be seen in a yearly eye clinic to check for diabetic retinopathy.

The modifiable risk factors of type 2 diabetes will be assessed, such as hypertension.

Hypertension in diabetic patients are typically managed with an ACE inhibitor or angiotensin II receptor blocker (ARB).

Statins may be used to manage hyperlipidemia. 

Sick Day Rules

A patient with type 2 diabetes must abide by what are known as “sick-day rules”.

Stress, such as acute illness, increases the level of cortisol produced and released by the adrenal glands.

This causes the blood glucose levels to increase without increased oral intake.

If the patient is able to check their capillary blood glucose, this should be done more frequently, and it is vital that they remain well hydrated.

If the patient is on medications for their type 2 diabetes (metformin, sulfonylureas, GLP-1 analogues or SGLT-2 inhibitors), then adjustment in dosing and/or frequency may need to be made when sick**.

Injectable insulin typically should not be stopped**.

**Important: Medication adjustments for sick days will vary from patient to patient. The patient and their provider will need to discuss specific recommendations and guidelines that are tailored to that patient.


Complications of Type 2 Diabetes

Complications of type 2 diabetes occur when blood glucose levels are not managed correctly.

The duration of uncontrolled hyperglycemia is proportional to the severity of the complications. 

Microvascular Complications

Sustained inappropriately high blood sugar levels can damage small blood vessels.

This can lead to:

  • Diabetic Retinopathy (Eyes) - May cause loss of vision in both eyes

  • Diabetic Nephropathy (Kidneys) - May require dialysis

  • Diabetic Neuropathy (Nerves) - Diabetic peripheral neuropathy has a high mortality rate due to infection, and can often lead to lower limb amputation due to gangrene.

Macrovascular Complications

High blood sugar can cause plaque formation in blood vessels, called atherosclerosis.

This can increase the risk of:

  • Cardiovascular Disease

  • Heart Attack (Myocardial Infarction)

  • Stroke

  • Peripheral Vascular Disease (PVD)

Type 2 Diabetes Complications: Microvascular complications include diabetic retinopathy, nephropathy, and neuropathy; Macrovascular complications include cardiovascular disease, heart attack, stroke, and peripheral vascular disease

Hyperosmolar Hyperglycemic State (HHS)

Patients with type 2 diabetes may present to the hospital in a hyperosmolar hyperglycemic state (HHS, also known as hyperosmolar hyperglycemic nonketotic state [HHNS]).

You may also see HHS referred to as syndrome instead of state.

HHS can be caused by stress on the body (infections, strokes, heart attacks, dehydration), poor glucose control (therapy noncompliance), or certain medications (corticosteroids), etc.

The patient will present with a high blood glucose (over 600 mg/dL or 33 mmol/L), high osmolality, and profound dehydration which can lead to low blood volume (hypovolemia).

This makes the blood very viscous (thick), increasing the risk of acute kidney injury (AKI) and thromboembolic events, such as heart attack and stroke.

Management of HHS involves IV fluid replacement and IV insulin. 


Type 1 vs Type 2 Diabetes

Type 1 vs Type 2 Diabetes: Chart showing type 1 vs type 2 diabetes differences including symptoms, diagnosis, treatment, etc.


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