week 10 part 1 Flashcards

1
Q

diabetes mellitus

A

a chronic disorder of metabolism characterized by elevated plasma glucose levels resulting from defects in insulin secretion, insulin action or both

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2
Q

extrapulmonary issue

A

limits lung expanison
- spinal disorder or disorder of muscle weakness

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3
Q

pulmonary fibrosis

A

result of long-term exposure to irritants
-decreased barriers permeability at alveoli
-decreased compliance (more effort for inspiration, dyspnea and cough)

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4
Q

pulmonary edema

A

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)

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5
Q

pulmonary embolus

A

a blood clot that blocks the flow of blood
-within deep veins
- risk factors - dehydration/trauma
-symptoms of chest pain, dysnea

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6
Q

consequences of insulin deflict

A
  • 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
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7
Q

how are insulin and glucose linked

A

insulin increases the ability for cells to take up glucose

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8
Q

what does not require insulin for glucose transport

A

liver, red blood cells, and brian(they have a different transporter for glucose)
- but insulin is still important for anabolic processes in the tissue

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9
Q

3 types of diabetes mellitus

A

type I and type II and gestational diabetes

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10
Q

gestational diabetes

A

Type II diabetes develops during pregnancy but
disappears after delivery

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11
Q

signs and symptoms of diabetes

A

Polyuria (frequent urination)
* Polydipsia (thirst)
* Polyphagia (hunger)
* Weight loss (T1DM) / weight gain (T2DM)
* Fatigue
* Additional acute symptom: ketoacidosis (serious) – more common in T1DM

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12
Q

T1DM

A

onset of symptoms usually abrupt and dramatic

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13
Q

why do you think polyuria is a symptoms of diabetes

A

because the kidneys need to excrete excess glucose

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14
Q

diabetic ketoacidosis

A

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

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15
Q

ketone bodies byproduct

A

fatty acid metabolism

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16
Q

diabetic ketoacidosis symptoms

A

Nausea/vomiting, fruity breath (acetone), deep breathing,
lethargy, confusion, coma

17
Q

Complications of ChronicHyperglycemia

A
  1. retinopathy-microvascular damage to high blood glucose
  2. nephropathy-nerve degeneration due to ischemia
  3. vascular disease –atherosclerosis
18
Q

type 1 diabetes

A
  • 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 )
19
Q

Type I Diabetes: Progressive Loss of β
Cell Mass

A
20
Q

insulin treatment

A

the goal is to replace insulin and to tightly monitor blood glucose levels
ex with pumps or injection

21
Q

type II diabetes

A
  • non-insulin-dependent diabetes
  • characterized by abnormal insulin secretion and action
  • insulin resistance and beta cell destruction
  • leads to chronic hyperglycemia
22
Q

T2DM Diagnosis & Monitoring: The Glucose Tolerance
Test

A
  • 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
23
Q

T2DM - Symptoms

A
  • commonly asymptomatic
    -symptoms are subtle, occur late in the disease
  • long term consequences very serious
24
Q

T2 risk factors

A

-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

25
Q

Two defects characterized in T2DM

A
  1. impaired insulin action in liver skeletal muscle and adipocytes (insulin resistance)
  2. impaired insulin secretion (loss of b cell mass and function)

these both lead to chronic hyperglycemia

26
Q

Etiology & Pathogenesis of T2DM

A

genetic predisposition + overnutrition, obesity = insulin resistance causes increased stress on B cells

27
Q

potential mechanism of insulin

A
  • 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
28
Q

insulin resistance at insulin primary at liver

A
  • over production of glucose by the liver in both the fasting and fed states
  • increased gluconeogenesis
29
Q

insulin resistance at insulin primary Skeletal Muscle

A
  • Impaired glucose uptake during fed state
  • Primarily due to impairments in insulin signal transduction pathway
30
Q

insulin resistance at insulin primary adipose tissue

A

Increased lipolysis  Increased FFA production  Spills over into blood & peripheral
tissues
* Contributes to atherosclerosis risk

31
Q

treatment option for T2DM

A
  1. diet and exercise
  2. insulin injections
  3. oral hypoglycemic drugs
  4. incretin-based therapies
32
Q

obesity

A
  • 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
33
Q

epidemic obesity

A

-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

34
Q

obesity pathophysiology

A

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

35
Q

obesity treatment

A

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

36
Q

Typical Progression of Metabolic Syndrome
(MetS)

A

genetic predisposition –accumulated body fat – develop MetS– progression to diseases