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Summary Porth Essentials of pathophysiology 4th edition Ch 33 best set: Diabetes Mellitus and the Metabolic Syndrome: Hormonal Control of Nutrient Metabolism and Storage. Updated Fall 2024/2025. £11.04   Add to cart

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Summary Porth Essentials of pathophysiology 4th edition Ch 33 best set: Diabetes Mellitus and the Metabolic Syndrome: Hormonal Control of Nutrient Metabolism and Storage. Updated Fall 2024/2025.

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Porth Essentials of pathophysiology 4th edition Ch 33 best set: Diabetes Mellitus and the Metabolic Syndrome: Hormonal Control of Nutrient Metabolism and Storage. Updated Fall 2024/2025.

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  • August 27, 2024
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Porth Essentials of pathophysiology 4th
edition Ch 33 best set: Diabetes Mellitus
and the Metabolic Syndrome: Hormonal
Control of Nutrient Metabolism and
Storage. Updated Fall 2024/2025.
are tightly regulated between 70 and 99 mg/dL (4.0 and 5.5 mmol/L).




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1

SGLT2 inhibitors

2

normal fasting blood glucose levels

3

alcohol consumption affect on glucose in diabetics

4

,Prediabetes Lab Values

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topics:
I. Hormonal Control of Nutrient Metabolism and Storage
1. Nutrient Metabolism and Storage
a. Glucose Metabolism and Storage
b. Fat Metabolism and Storage
c. Protein Metabolism and Storage
2. Glucose-Regulating Hormones
a. Insulin
b. Glucagon
c. Amylin, Somatostatin, and Gut-Derived
Hormones
d.. Counterregulatory Hormones

SUMMARY CONCEPTS
The body predominantly metabolizes glucose and fatty acids for energy.The brain depends exclusively on
glucose for its energy. The liver stores excess glucose as glycogen.
Fats, which serve as an ef cient source of fuel for the body, are stored in adipose tissue as triglycerides,
which consist of three fatty acids linked to a glycerol molecule. In situations that favor fat breakdown,
such as fasting or diabetes mellitus, the triglycerides in adipose tissue are broken down and the fatty
acids are used as fuel or transported to the liver, where they are converted to ketones.
Proteins, which are made up of amino acids, are essential for the formation of all body structures. Unlike
glucose and fatty acids, there is onlya lim ited facility for storage of excess amino acids in the body.
Because fatty acids cannot be converted to glucose, the body must break down proteins and use the
amino acids for gluconeogenesis.
Energy metabolism is controlled by a number of hormones, including insulin, glucagon, epinephrine,
growth hormone, and the glucocorticoids. Of these hormones, only insulin has the effect of lowering the
blood glucose level. It does this by facilitating the transport of glucose into body cells and decreasing the
liver's production and release of glucose into the bloodstream. Insulin also has the effect of decreasing
lipolysis and the use of fats as a fuel source.
Other hormones—glucagon, epinephrine, growth hormone, and the glucocorticoids—maintain or
increase blood glucose concentrations. Glucagon and epinephrine prom ote glycogenolysis, and glucagon
and the glucocorticoids increase gluconeogenesis. Epinephrine and glucagon also increase the use of fat
for energy by increasing the release of fatty acids from adipose tissue cells. Growth hormone decreases
the peripheral utilization of glucose.

II. Diabetes Mellitus
1. Classification and Etiology
a. Categories of Risk for Diabetes
b. Type 1 Diabetes Mellitus
c. Type 2 Diabetes Mellitus and the Metabolic Syndrome
d. Other Specific Types of Diabetes
e. Gestational Diabetes

,2. Clinical Manifestations of Diabetes
3. Diagnostic Tests
a. Blood Tests
b. Urine Tests
4. Diabetes Management
a.Dietary Management
b. Exercise
c. Oral and Injectable Antidiabetic Agents
d. Insulin
e. Pancreas or Islet Cell Transplantation
f. Management of Diabetes in Children
5. Acute Complications
a. Diabetic Ketoacidosis
b.Hyperglycemic Hyperosmolar State
c. Hypoglycemia
6. The Somogyi Effect and Dawn Phenomenon
7. Chronic Complications
a. Theories of Pathogenesis
b. Diabetic Neuropathies
c. Diabetic Nephropathies
d. Diabetic Retinopathies
e. Macrovascular Complications
f. Diabetic Foot Ulcers
g. Infections

SUMMARY CONCEPTS
Diabetes mellitus is a disorder of carbohydrate,
protein, and fat metabolism resulting from an imbalance between insulin availability and insulin need. In
type 1 diabetes, there is destruction of beta cells and an absolute insulin deficiency.Type 2 diabetes is
characterized by a lack of insulin availability or effectiveness. Diabetes can also occur secondary to some
other condition that destroys beta cells (e.g., pancreatic disorders) or endocrine diseases that cause
increased production of glucose by the liver and decreased use of glucose by the tissues (e.g., Cushing
syndrome). Gestational diabetes develops during pregnancy.
The metabolic syndrome represents a constellation of metabolic abnormalities characterized by obesity,
insulin resistance, high triglyceride levels and low HDL levels, hypertension, cardiovascular disease, and
increased risk for development of type 2 diabetes.
The most commonly identified symptoms of type 1 diabetes are polyuria, polydipsia, polyphagia, and
weight loss despite normal or increased appetite. Although persons with type 2 diabetes may present
with one or more of these symptoms, they are often asymptomatic initially. The diagnosis of diabetes
mellitus is based on clinical signs of the disease, fasting blood glucose levels, random plasma glucose
measurements, and results of the glucose tolerance test. Glycosylation involves the irreversible
attachment of glucose to the hemoglobin molecule; the
measurement of glycosylated hemoglobin (A1C) provides an index of blood glucose levels over several m
onths. Self-monitoring of capillary blood glucose provides a means of maintaining near-normal blood
glucose levels through adjustment of insulin dosage.

, Dietary management of diabetes focuses on maintaining a well-balanced diet, controlling calories to
achieve and maintain an optimum weight, and regulating the distribution of carbohydrates, proteins, and
fats.
Pharmacologic agents used in the management of diabetes include injectable insulin, injectable non-
insulin agents including amylin and GLP-1 analogs, and oral diabetic drugs. Type 1 diabetes (and
sometimes type 2 diabetes) requires treatment with injectable insulin. Oral antidiabetic drugs include
the insulin secretagogues, biguanides, α-glucosidase inhibitors, thiazolidinediones, and incretin-based
therapies. These drugs require a functioning pancreas and may be used in the treatment of type 2
diabetes.
The metabolic disturbances associated with diabetes affect almost every body system. The acute
complications of diabetes include diabetic ketoacidosis, hyperglycemic hyperosmolar state, and
hypoglycemia in people with insulin-treated diabetes.The chronic complications of diabetes affect the
microvascular system (including the retina, kidneys, and peripheral nervous system) and the
macrovascular system (coronary, cerebrovascular, and peripheral arteries). The diabetic foot is usually a
combination of both microvascular and macrovascular dysfunction. Infection is also a frequent
occurrence and is more likely to be severe in the diabetic patient.

diabetes mellitus (DM)

Abnormality in blood glucose regulation and nutrient storage related to an absolute or relative
deficiency of insulin and/or resistance to the actions of insulin.

Metabolic disorder caused by the absence or insufficient production of insulin secreted by the pancreas,
resulting in hyperglycemia and glucosuria (resulting from defects in insulin secretion, insulin action, or
both)

An endocrine disorder marked by an inability to maintain glucose homeostasis. The type 1 form results
from autoimmune destruction of insulin-secreting cells; treatment usually requires daily insulin
injections. The type 2 form most commonly results from reduced responsiveness of target cells to
insulin; obesity and lack of exercise are risk factors.

Diabetes is a disorder of carbohydrate, protein, and fat metabolism resulting from a lack of insulin avail-
ability or a reduction in the biologic effects of insulin. It can represent an absolute insulin de ciency,
impaired release of insulin by the pancreatic beta cells, inadequate or defective insulin receptors or
postreceptor regulation, or the production of inactive insulin or insulin that is destroyed before it can
carry out its action.




normal fasting blood glucose levels

are tightly regulated between 70 and 99 mg/dL (4.0 and 5.5 mmol/L).

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