Pathophysiology exam 4. 29.

Metabolic syndrome and diabetes.

Obesity is what bmi?

Underweight = <18.5

Normal weight = 18.5–24.9

Overweight = 25–29.9

Obesity = 30 or greater

Obesity has what risks?

CVD, Metabolic disorders, respiratory problems.

Metabolic syndrome. the 5 conditions.

High blood pressure (> 130/85 mmHg)

High blood glucose (fasting blood glucose ≥ 110 mg/dL)

Central/visceral adiposity (waist circumference: men > 40 in; women > 35 in)

High triglycerides (≥ 150 mg/dL)

Low HDL cholesterol (men < 40 mg/dL; women < 50 mg/dL)

How many of the conditions needed for metabolic syndrome?

atleast 3 out of 5

Metabolic syndrome risks.

Atherosclerosis

Coronary heart disease, heart attack, stroke

Type 2 diabetes

Kidney disease

Nonalcoholic fatty liver disease

MOA of insulin. Action on glucose level, glucose uptake into cells, other energy substrates, and energy storage.

Allows uptake of glucose into cells

Cells use glucose to make ATP

Lowers blood glucose

Uptake of fatty acids and amino acids

Nutrient storage & use

Excess glucose → glycogen

Fatty acids → triglycerides

Amino acids → proteins

gluconeogenesis, glycogenesis, glycogenolysis, lipolysis, lipogenesis, protein anabolism, protein catabolism

gluconeogenesis-metabolic process that creates glucose from non-carbohydrate sources like fat and protein

glycogenesis-the metabolic process where the body converts excess glucose into glycogen, a storage form of glucose, primarily in the liver and muscles, to be used later for energy. 

glycogenolysis-the process of breaking down glycogen into glucose

lipolysis-the metabolic process where triglycerides (stored fat) are broken down into glycerol and free fatty acids

lipogenesis-the metabolic process where your body converts excess carbohydrates and other substrates into fatty acids and then stores them as triglycerides (fats)

protein anabolism- building new proteins

protein catabolism-breakdown of protein

What is diabetes?

a disease in which the body’s ability to produce insulin or respond to insulin is impaired, resulting in abnormal metabolism of carbohydrates and elevated levels of glucose in the blood and urine

Type 1 vs type 2 diabetes

Type 1 is lack of insulin production

Type is poor responding to insulin.

Type 1 diebetes.

5-10% of diabetes

Peak age of diagnosis: 14 yo

Absolute insulin deficiency

Treatment: insulin

Type 2 diabetes.

Insulin resistance: cells do not respond to insulin

Causes initial hyperinsulinemia (prediabetes)

Leads to progressive loss of beta cell insulin secretion and hyperglycemia (type 2 diabetes

HOMA-IR: test for insulin resistance (uses fasting glucose and fasting insulin)

Treatment goal: increase insulin sensitivity

Physical activity

Weight loss

Proper diet/nutrition

Stress reduction

Proper sleep

• FPG, OGTT, A1C, HOMA-IR

What is each diagnostic for?

Fasting plasma glucose test (FPG)

Oral glucose tolerance test (OGTT)

Glycated hemoglobin A1c (A1C)

—Measure of long-term glucose control past 120 days.

HOMA-IR: test for insulin resistance

Chronic complications of diabetes.

Neuropathy

Foot ulcers and amputations

Retinopathy

Nephropathy

Cardiovascular disease

DKA Pathogenesis.

Occurs when the body cannot use glucose as fuel and uses fat instead (more common in type 1)

Breakdown of fat produces ketones (acidic)

Hyperosmolar Hyperglycemic State pathogenesis.

Most in type 2, underlying condition (infection), elderly

Profound hyperglycemia → glucosuria → polyuria → severe dehydration → serum hyperosmolarity

Hyperosmolar Hyperglycemic State. Symptoms and labs.

Profound hyperglycemia ( > 600 mg/dL) lab

Dehydration (up to 9 L)

Serum hyperosmolarity lab

Nonketotic lab.

Alterations in consciousness

Mortality 5-20%

DKA lab and symptoms.

Glucose, ketone, BUN labs.

• Excessive thirst

• Frequent urination

• Dry mouth and throat

• Fatigue

• Nausea and vomiting

• Abdominal pain 

• Confusion and lethargy

• Coma

• Fruity-smelling breath

• Deep, rapid breathing

• Blurred vision

• Weakness

• Weight loss

• Headache