Physiology of Endocrine System & Diabetes Flashcards

Flashcards about the physiology of the endocrine system, focusing on diabetes mellitus.

What were the presenting symptoms of the 20-year-old male patient in the case study?

A 20-year-old male patient presented to the emergency department with vomiting and abdominal pain, along with a 2-week history of polyuria, polydipsia, 20-pound weight loss, and blurred vision.

What were the key laboratory findings that led to the DKA diagnosis?

The patient's initial blood glucose level was 1192 mg/dL, and clinical presentation and laboratory findings were consistent with diabetic ketoacidosis (DKA).

What was the insulin regimen the patient was discharged from the hospital on?

30 units of NPH/regular human insulin 70/30 mixture before breakfast, 15 units of regular human insulin before dinner, and 20 units of NPH insulin at bedtime.

What is Type 1 Diabetes Mellitus?

A syndrome characterized by hyperglycemia and insulin deficiency resulting from the loss of beta cells in pancreatic islets.

What are the two types of Type 1 Diabetes Mellitus?

Nonimmune (type 1B) and autoimmune (type 1A).

What are the two main factors that contribute to the destruction of beta cells in Type 1A diabetes?

Genetic and environmental factors.

With what is type 1 diabetes most strongly associated?

Major histocompatibility complex (MHC), specifically histocompatibility leukocyte antigen (HLA) class II alleles (HLA-DQ and HLA-DR).

What are some environmental factors that include Type 1 diabetes?

Viral infections (especially enteroviruses), exposure to infectious microorganisms (such as Helicobacter pylori), exposure to cow’s milk proteins and a lack of vitamin D.

The destruction of insulin-producing beta cells in the pancreas starts with the formation of what?

Autoantigens.

Ingested autoantigens activate what types of lymphocytes?

T helper 1 (Th1) and T helper 2 (Th2) lymphocytes.

What do activated Th1 lymphocytes release?

Interleukin-2 (IL-2) and interferon.

How do autoantigen-specific T cytotoxic lymphocytes function?

Destroy islet cells through the secretion of toxic perforins and granzymes.

Activated Th2 lymphocytes produce what?

IL-4.

B lymphocytes produce what?

Islet cell autoantibodies (ICAs) and anti-glutamic acid decarboxylase (antiGAD65) antibodies.

What autoantibodies are also associated with type 1 diabetes mellitus?

Insulin autoantibodies (IAAs).

Without insulin and amylin, what happens in the body?

The body cannot promote glucose disappearance or limit glucose appearance from the bloodstream, resulting in hyperglycemia.

Type 1 diabetes does not present clinically until what percentage of beta cells has been destroyed?

80-90%.

How might Type 1 diabetics present?

Abrupt onset of diabetic ketoacidosis, polyuria, polyphagia, polydipsia, or rapid weight loss with marked hyperglycemia.

What is needed to diagnose the difference between Type 1 and Type 2 diabetes?

The presence of ketones in the urine and/or autoantibodies in the blood can distinguish type 1 from type 2 diabetes.

What are the central nervous system symptoms of Type 1 Diabetes?

Polydipsia, Polyphagia, Lethargy, Fatigue, Acute Confusion.

Give three trade names for rapid-acting insulin

NovoRapid, Apidra, Humalog

Give two trade names for short-acting insulin.

Humulin-R, Novolin grToronto

Give two trade names for intermediate-acting insulin

Humulin-N, Novolin ge NPH

Give two trade names for long-acting insulin

Levemir, Lantus

When insulin interacts with its receptor, what occurs?

Increasing the number of glucose transporters in the plasma membrane.

What is insulin's action on carbohydrate metabolism in the liver?

Stimulates glycolysis, promotes glucose storage as glycogen, inhibits glycogenolysis, and inhibits gluconeogenesis.

What is insulin's action on carbohydrate metabolism in the muscle?

Stimulates glucose uptake (GLUT4) and promotes glucose storage as glycogen.

What is insulin's action on carbohydrate metabolism in the adipose tissue?

Stimulates glucose transport into adipocytes, promotes the conversion of glucose into triglycerides and fatty acids.

What is the effect of insulin on lipogenesis?

Insulin favours the synthesis of triacylglycerols from glucose by providing more glycerol 3-phosphate & NADPH and increases activity of acetyl CoA carboxylase.

What is the effect of insulin on lipolysis?

Insulin decreases the activity of enzyme -hormone-sensitive lipase & reduces the release of fatty acids from stored fat.

What is the effect of insulin on ketogenesis?

Insulin reduces ketogenesis by decreasing the activity of HMG COA synthase.

What are the effects of insulin on protein metabolism?

Stimulates the entry of amino acids into the cells, enhances protein synthesis, and reduces protein degradation.

Who are credited with the experiments to isolate insulin?

Charles Best and Frederick Banting.

What were the presenting symptoms of the 34-year-old woman in Scenario 2?

Complaints of chronic fatigue, increased thirst, constant hunger, and frequent urination.

What in the patients history may have contributed to her condition?

She has a history of gestational diabetes and reports that, after her delivery, she went back to her traditional eating pattern, which is high in carbohydrates.

In Scenario 2, what were the patient's BP and random plasma glucose measurements?

152/97 mm Hg, and a random plasma glucose is 291 mg/dL.

In Scenario 2, what did the primary care provider suspect?

Type 2 diabetes mellitus (DM).

In Scenario 2, what were the laboratory test results?

Fasting glucose 184 mg/dL, HbA1C 8.8%, Total cholesterol 256 mg/dL, Triglycerides 346 mg/dL, LDL 155 mg/dL, HDL 32 mg/dL, UA +glucose, ketones.

What is a key difference in the onset of Type 1 vs Type 2 diabetes?

Sudden vs. Gradual

If a patient with Type 2 Diabetes has an HbA1c that rises to 48 mmol/mol (6.5%), what should be the course of treatment?

Offer standard-release metformin, aiming for an HbA1c level of 48 mmol/mol (6.5%).

If a patient with Type 2 Diabetes has an HbA1c that rises to 58 mmol/mol (7.5%), what should be the course of treatment?

Consider dual therapy, triple therapy or insulin-based therapy depending on patient specific requirements.