week 10 part 1 Flashcards
diabetes mellitus
a chronic disorder of metabolism characterized by elevated plasma glucose levels resulting from defects in insulin secretion, insulin action or both
extrapulmonary issue
limits lung expanison
- spinal disorder or disorder of muscle weakness
pulmonary fibrosis
result of long-term exposure to irritants
-decreased barriers permeability at alveoli
-decreased compliance (more effort for inspiration, dyspnea and cough)
pulmonary edema
fluid collect around and in alveoli
this will impact the efficiency of diffusion
- increased fluid out of capillaries and into the interstitial fluid
-inflammation within the lungs
-low blood plasma protein levels
-pulmonary hypertension
(left-sided heart failure)
pulmonary embolus
a blood clot that blocks the flow of blood
-within deep veins
- risk factors - dehydration/trauma
-symptoms of chest pain, dysnea
consequences of insulin deflict
- result in a decreased glucose uptake into many cells for metabolic and anabolic processes
-insulin is required for translocation of the GLUT-4 glucose transporter to the cell surface
–glucose enters through this transporter in muscle
how are insulin and glucose linked
insulin increases the ability for cells to take up glucose
what does not require insulin for glucose transport
liver, red blood cells, and brian(they have a different transporter for glucose)
- but insulin is still important for anabolic processes in the tissue
3 types of diabetes mellitus
type I and type II and gestational diabetes
gestational diabetes
Type II diabetes develops during pregnancy but
disappears after delivery
signs and symptoms of diabetes
Polyuria (frequent urination)
* Polydipsia (thirst)
* Polyphagia (hunger)
* Weight loss (T1DM) / weight gain (T2DM)
* Fatigue
* Additional acute symptom: ketoacidosis (serious) – more common in T1DM
T1DM
onset of symptoms usually abrupt and dramatic
why do you think polyuria is a symptoms of diabetes
because the kidneys need to excrete excess glucose
diabetic ketoacidosis
ketone bodies are produced as a byproduct of fat breakdown
- made in the liver and used for ATP production in cels around the body
- excess can be excreted in urine
(meaning if there is too much ketone present in the blood at one time – metabolic acidosis
ketone bodies byproduct
fatty acid metabolism
diabetic ketoacidosis symptoms
Nausea/vomiting, fruity breath (acetone), deep breathing,
lethargy, confusion, coma
Complications of ChronicHyperglycemia
- retinopathy-microvascular damage to high blood glucose
- nephropathy-nerve degeneration due to ischemia
- vascular disease –atherosclerosis
type 1 diabetes
- characterized by autoimmune destruction of Beta cells of the pancreatic islets leading to a lack of insulin (beta cells break down over time)
(possible predisposing factors: genetic and environmental )
Type I Diabetes: Progressive Loss of β
Cell Mass
insulin treatment
the goal is to replace insulin and to tightly monitor blood glucose levels
ex with pumps or injection
type II diabetes
- non-insulin-dependent diabetes
- characterized by abnormal insulin secretion and action
- insulin resistance and beta cell destruction
- leads to chronic hyperglycemia
T2DM Diagnosis & Monitoring: The Glucose Tolerance
Test
- fasting blood glucose at least 126mg/dl (this is high)
- oral glucose tolerance test
also monitoring long-term blood glucose levels measuring
-Glycated Hemoglobin - Gives a good reflection of the blood glucose profile
over the past 8-12 weeks
T2DM - Symptoms
- commonly asymptomatic
-symptoms are subtle, occur late in the disease - long term consequences very serious
T2 risk factors
-genetics
* nutrition
* physical inactivity
* Age (over age 45)
* Obesity
* Previous gestational diabetes or gave birth to child > 9 lb
* Dyslipidemia: elevated blood lipids (LDL, TG, total Chol)
* Could be a result of genetic and/or lifestyle factors
lifestyle factors
Two defects characterized in T2DM
- impaired insulin action in liver skeletal muscle and adipocytes (insulin resistance)
- impaired insulin secretion (loss of b cell mass and function)
these both lead to chronic hyperglycemia
Etiology & Pathogenesis of T2DM
genetic predisposition + overnutrition, obesity = insulin resistance causes increased stress on B cells
potential mechanism of insulin
- primarily due to defects in the signal transduction pathways leading to GLUT-4 expression at the cell surface
- insulin receptor downregulation (due to chronic increase in blood insulin
insulin resistance at insulin primary at liver
- over production of glucose by the liver in both the fasting and fed states
- increased gluconeogenesis
insulin resistance at insulin primary Skeletal Muscle
- Impaired glucose uptake during fed state
- Primarily due to impairments in insulin signal transduction pathway
insulin resistance at insulin primary adipose tissue
Increased lipolysis Increased FFA production Spills over into blood & peripheral
tissues
* Contributes to atherosclerosis risk
treatment option for T2DM
- diet and exercise
- insulin injections
- oral hypoglycemic drugs
- incretin-based therapies
obesity
- complex multifactorial disease
- characterized by BMI
- diet composition & physical activity status
- The location matters….
- Visceral (abdominal) adiposity is associated more highly with chronic disease risk factors
- Metabolic health matters…
- Adipose tissue is an endocrine organ that can impact metabolism and inflammatory status
epidemic obesity
-driven by charges in the global food system
-combined with either local environmental factors
variation within the population due to interaction between environment and individual factors
obesity pathophysiology
adipose tissue is active - with autocrine& endocrine functions
- produces adipose-derived cytokines adipokines
- some adipokines are protective but many are pathogenic are they accumulated
result
Chronic low-grade inflammation
Leptin resistance (leptin is a hormone that normally suppresses appetite and increases
energy expenditure)
Insulin resistance
obesity treatment
goal: weight loss of body weight in first 6 months
treatment modalities
multimodal lifestyle intervention that includes dietary modification increase PA
Pharmacotherapy – Drugs that aim to reduce food intake e.g. by
decreasing hunger, slow gastric emptying, reduce absorption of fat
* Medical Devices:
* Intragastric balloons
* Vagus nerve blocker (specific to GI area) suppresses neural
communication between stomach and brain increased satiety
Typical Progression of Metabolic Syndrome
(MetS)
genetic predisposition –accumulated body fat – develop MetS– progression to diseases
