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NURS 1650 - Here We Go Again > Pathophysiology of Diabetes > Flashcards

Pathophysiology of Diabetes Flashcards

(97 cards)

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1
Q

Are GLUT-2 transporters insulin-dependent? How do they allow the entrance of glucose and where?

A

They are not insulin dependent

Entrance of glucose into hepatocytes via facilitated diffusion

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2
Q

Which GLUT transporter uses translocation? Explain how it works

A

GLUT-4 is insulin dependent and uses translocation

When insulin attaches to GLUT-4, the GLUT-4 transporters move to the cellular membrane to uptake glucose

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3
Q

What is SGLT?

A

Sodium-glucose cotransport

Mechanism of glucose uptake from the GI tract and renal tubules

Secondary active transport mechanism

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4
Q

What role does SGLT have in presenting a clinical manifestation of DM?

A

Hyperglycemia in DM may overwhelm the number of transporter (limited amount!)

Results in glucosuria because glucose is not being reabsorbed

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5
Q

Glycogen

A

Stored form of glucose in the liver

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6
Q

Glycogenesis

A

Synthesis of glycogen

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7
Q

Glycogenolysis

A

Breakdown of glycogen

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8
Q

Glycolysis

A

Breakdown (metabolism) of glucose

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9
Q

Gluconeogenesis

A

Synthesis of new glucose, mainly by the liver

From non-carb sources

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10
Q

How does glucose become an energy source for cells?

A

Glucose

Glucose-6-phosphate (G6P)

Glycolysis –> Pyruvate

Pyruvate enters mitochondria

oxygen available Pyruvate converted to acetyl CoA, which enters the Krebs cycle

ETC produces ATP

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11
Q

In a fed state what form of metabolism is occuring?

A

Anabolism

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12
Q

In a fed state, where is glucose going in relation to the bloodstream? (GI tract, neural tissue, pancreas, muscle, liver, adipose)

A

GI –> Glucose is entering the bloodstream from the GI tract

Liver –> glycogenesis and glycolysis is occuring, glucose is entering the liver from the bloodstream

Adipose tissue –> glucose is entering adipose tissue

Pancreas –> is releasing insulin to promote the uptake of glucose

Neural tissue –> uptaking glucose

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13
Q

How does physical activity affect insulin?

A

Physical activity enhances insulin sensitivity

Muscle contraction enhances GLUT-4 translocation to the cell surface

Important teaching point for patients

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14
Q

What does lipoprotein lipase do?

A

Breaks down triglycerides from VLDLs and chylomicrons into fatty acids that can diffuse into the adipocyte with glycerol

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15
Q

How does insulin affect the activity of lipoprotein lipase?

A

Insulin promotes lipoprotein lipase activity

Insulin promotes fat storage

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16
Q

Where is lipoprotein lipase found?

A

Vascular endothelial cells throughout the body

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17
Q

What does hormone-sensitive lipase do?

A

Promotes the breakdown of stored triglycerides

Adipocyte then can release free fatty acids and glycerol

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18
Q

In a fasting state, what form of metabolism is occuring?

A

Catabolism

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19
Q

What two pathways produce glucose in the liver during a fasting state?

A

Glycogenolysis

Gluconeogenesis

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20
Q

Describe the effects of phosphorylation and dephosphorylation on glucose

A

Phosphorylation “traps” glucose into cells following its entry. This is a reversible action due to glucose-6-phosphate enzyme.

In a fasting state, the G6P enzyme dephosphorylates the glucose, making it into free glucose that can be transported out of the cell

All cells can carry out this reaction

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21
Q

What are gluconeogenic precursors? What precursors CANNOT be used in gluconeogenesis?

A

Lactate, amino acids, and glycerol

Fatty acids CANNOT be used

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22
Q

What hormone predominates during a fasting state?

A

Glucagon

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23
Q

What hormone predominates during a fed state?

A

Insulin

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24
Q

What two pathways in muscle create the precursors for gluconeogenesis?

A

Glycogenolysis: breakdown muscle glycogen to G6P. G6P undergoes glycolysis and is converted into lactate

Proteolysis: protein breakdown releases amino acids

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25
What pathway in adipose tissue creates a precursor for gluconeogenesis?
Lipolysis: fat breakdown via hormone-sensitive lipase Triglyceride broken down to 3 fatty acids + glycerol
26
How are the products of lipolysis used for energy uptake?
Glycerol is used for gluconeogenesis Fatty acids travel the circulation to muscle to be used as fuel and to the liver (causing the production of ketone bodies)
27
In a fasting state, where is glucose going in relation to the bloodstream? (GI tract, neural tissue, pancreas, muscle, liver, adipose)
GI Tract: no glucose movement Neural Tissue: continued glucose uptake from the bloodstream Pancreas: releases glucagon into the bloodstream to increase BG levels Adipose: FFA moving into the bloodstream Muscle: FFA and glucose uptake from the bloodstream Liver: Glucose enters the bloodstream via glycogenolysis and gluconeogenesis
28
Where does ketogenesis occur?
The liver
29
Describe the pathway of ketogenesis?
Fatty acids released by adipose lipolysis Oxidized by the liver at a high rate Acetyl CoA and ketone body production
30
What states of the body promote ketogenesis?
Prolonged fasting Absence of insulin Very low carb diet High levels of glucagon and stress hormones
31
Which pancreatic cells synthesize insulin?
Beta cells of the islets of Langerhans
32
Which pancreatic cells synthesize glucagon?
Alpha cells
33
What is the significance of the structure of an insulin molecule?
Proinsulin: contains insulin and a connecting peptide (c-peptide) The c-peptide is used to measure endogenous insulin production (no insulin means no c-peptide) Can also help differentiate causes of hypoglycemia
34
What are incretins?
Peptides that stimulate the secretion of insulin Examples: GLP-1 and GIP
35
What breaks down incretins?
DPP-4 enzyme
36
Which incretin can inhibit glucagon?
GLP-1
37
Insulin secretion: oral glucose vs. IV glucose response
There is more insulin secreted in response to oral glucose vs. IV glucose
38
Describe the feedforward mechanism of glucose in the GI tract
Glucose in the GI tract increases insulin secretion, anticipating a rise in blood glucose
39
When is glucagon production the highest?
In the early morning
40
What is a counter-regulatory or counter insulin hormone?
A hormone that tends to increase blood glucose Opposite effects of insulin
41
What is glucagon's role in the liver?
Increases glycogenolysis Increases gluconeogenesis Increases ketone body formation Decreases triglyceride synthesis Minor role in lipolysis
42
What tissue lacks receptors for glucagon?
Skeletal muscle
43
What are examples of counter-insulin hormones?
Glucagon Cortisol Epinephrine Placental hormones Growth hormone
44
Stress hormones _____ blood glucose levels
INCREASE
45
What effect does increased BG have on healing?
If not attended to, increased blood glucose can delay healing time significantly
46
Growth Hormone
Released during hypoglycemia Acts as counter insulin Excess --> acromegaly --> diabetes
47
What doubles a child's risk of developing T1DM?
The risk is doubled if a parent developed Type 1 DM before age 11
48
If both parents have T2DM, what is their children's risk of developing it?
If both parents have Type 2 DM, their children have about a 50% risk of developing Type 2 DM
49
Type 2 DM is an example of what kind of disease?
Polygenic and multifactorial
50
What is monogenic diabetes?
AKA "neonatal diabetes", typically diagnosed before 6 months of age Result from mutations in genes that regulate pancreatic beta cell function // do not involve autoantibodies Different from T1DM
51
Type 1 DM is what kind of disease? What does this mean/what happens?
Autoimmune disease Results in the destruction of pancreatic beta cells, meaning no insulin production Pancreatic alpha cells remain --> continue producing glucagon
52
What is insulitis?
Infiltration of pancreatic beta cells by pro-inflammatory leukocytes
53
What are classic DM presentations?
Polyuria Polydipsia Polyphagia Weight loss Hyperglycemia and hyperlipidemia
54
What causes the three "polys"? (polyuria, polydipsia, polyphagia)
Hyperglycemia overwhelms the kidneys' ability to reabsorb glucose Osmotic diuresis and excessive urination occurs (polyuria) Dehydration occurs leading to thirst reaction (polydipsia) Loss of satiety signals (insulin) lead to polyphagia // perception of starving due to no glucose uptake by certain tissues (bc no insulin)
55
What is usually a patient's state when they are diagnosed with T1DM?
Often extremely ill at diagnosis May be in DKA 40%-60% of children under 15 years old in DKA at dx
56
How does unopposed glucagon action in T1DM affect ketogenesis?
Ketone formation occurs which contributes to metabolic acidosis, as well as osmotic diuresis
57
Diabetic Ketoacidosis (DKA) is an example of a ____ of T1DM
Sequela
58
What precipitating events can lead to DKA?
Illness, stress, not injecting insulin, kinked insulin pump catheter, etc.
59
Describe how DKA occurs in patients with T1DM (eh used the diagram)
Severe hyperglycemia is occuring, but the body perceives that it is starving for glucose (since it is not being taken up by muscle of fat cells) The liver continues to make glucose (via continued glucagon stimulation) Adipose tissue also stimulated by glucagon, epinephrine, and cortisol --> activation of hormone-sensitive lipase --> metabolism of triglycerides, generation of free FA and glycerol FFA used for the formation of ketone bodies
60
What are the effects of recurrent hypoglycemia on the brain?
Reduced counterregulatory responses - Decreased or no glucagon response - Decreased epinephrine and cortisol responses
61
What is hypoglycemia unawareness?
Lack of autonomic symptoms reduces conscious perception of hypoglycemia VERY DANGEROUS
62
Who is at risk to be screened for T2DM?
All patients age 35 or older Overweight or obese children and adolescents who have at least one risk factor
63
What is acanthosis nigricans?
Skin condition potentially indicating diabetes Areas of dark, velvety discoloration in body folds and creases Affected skin can become thickened (axillae, groin, neck)
64
Why might people with T2DM go 10 years without a diagnosis?
Changes are gradual Pancreas initially compensates for insulin resistance by increasing insulin production Patients are often asymptomatic
65
The key combinations in T2DM:
Insulin resistance Beta cell dysfunction Precipitates by genetic predisposition and/or lifestyle, habits, environment
66
What is insulin resistance?
Insulin does not have the usual effectiveness at reducing glucose production by the liver and promoting glucose uptake into muscle and fat More and more insulin may be required to obtain the same effect GLUT-4 transporters may be reduced in number and/or have less activity
67
Glucagon in T2DM
Secreted at abnormally high levels Working against insulin action Increases hepatic glucose production
68
Insulin paracrine effect in the pancreas:
Secretion of insulin in the Islets of Langerhans keeps glucagon levels low
69
How does the body try to compensate for insulin resistance?
Pancreatic cell hyperplasia and hypersecretion of insulin Pancreatic cells then begin to fail and die
70
What is prediabetes?
T2DM is usually preceded by prediabetes. Indicated by: - Impaired glucose tolerance - Impaired fasting glucose - Hemoglobin A1c 5.7%-6.4%
71
Hyperosmolar Hyperglycemic State
Similar to DKA - Greater fluid loss - Low level of insulin often prevents ketosis from developing - Higher hyperglycemic - Hyperosmolar state with severe intracellular dehydration
72
HHS Initiating Events
Acute illness (infection) Decreased fluid intake Increased stress hormone loss due to fever Leads to increased stress hormone reaction Hyperglycemia
73
How can hypoglycemia occur in patients with T2DM?
Insulin Oral medications that stimulate insulin release Older Adults
74
Criteria for diagnosing diabetes
Hemoglobin A1c > 6.5% FPG > 126 mg/dL 2-hr plasma glucose > 200 mg/dL Patient with classic symptoms of hyperglycemia or hyperglycemic crisis = random plasma glucose of > 200 mg/dL
75
What is Hemoglobin A1c?
Hemoglobin A1c is formed when the N- terminal valine of the beta chains of hemoglobin A is modified by the addition of glucose. The resulting molecule is stable and can be measured. An algorithm converts the percentage of A1c in the serum to an average blood glucose over approximately the last 3 months.
76
American Diabetes Association recommends that most people with diabetes maintain an A1c of: vs. AACE recommends:
Less than 7.0% 6.5% or less
77
Goals of Glycemic Control
Preprandial glucose: 80-130 mg/dL 1 to 2 hours postprandial glucose: < 180 mg/dL HgbA1c: < 7.0%
78
Microvascular DM Sequelae
Retinopathy -- major cause of blindness Nephropathy -- major cause of CKD
79
Macrovascular DM Sequelae
Dyslipidemia
80
Describe neuopathy
Sequelae of chronic DM Polyneuropathy (distal, stocking then glove) Very painful or can cause loss of sensation Autonomic neuropathy -- orthostatic hypotension, tachycardia, silent MI, gastroparesis, sexual dysfunction
81
Describe how foot ulcers can develop in patients with chronic DM
Neuropathy + vessel disease + poor wound healing Patients may not feel pain/trauma on their foot, leading to ulcer (and poor wound healing contributes) Can lead to amputation
82
Describe how infections occur in patients with chronic DM
Decreased blood flow Abnormal leukocyte function Increased sepsis risk
83
What are the two types of diabetic retinopathy?
Proliferative: new blood vessels, fragile, disorganized Non-proliferative: blood vessels leaky, can lead to macular edema
84
Important teaching point for diabetic retinopathy:
Dilated retinal exams are the standard of care
85
What is gastroparesis?
Syndrome of objectively delayed gastric emptying in the absence of mechanical obstruction and cardinal symptoms: Nausea, vomiting, early satiety, bloating, and/or upper abdominal pain
86
Important Patient Teaching Point: Foot Ulcers
Regular self foot checks and regular podiatrist visits can minimize the risk of wounds and amputation
87
General Patient Teaching for T1 and T2 DM
Keep diabetes under control, self-care is key! Keep BP well-controlled Regular monitoring of A1c, fasting BG, kidney function, and lipids Regular PCP visits, regular dilated retinal exams, frequent foot checks, referral to podiatrist as needed
88
What is gestational diabetes?
Disorder of glucose intolerance of variable severity with onset during pregnancy Increases risk of both mother and child developing T2DM
89
Risk factors for gestational diabetes
Severe obesity Prior history of gestational diabetes Previous large babies (macrosomia) Presence of glycosuria Strong family history of T2DM
90
What test is done to test for gestational diabetes?
Oral glucose tolerance testing (OGTT) at 24-28 weeks gestation
91
Gestational Diabetes Pathophysiology
Increased counter insulin hormones (human placental lactogen, estrogen, progesterone, cortisol, human placental growth hormone) As the placenta grows larger, more and more of these hormones are produced Leads to maternal insulin resistance and higher levels of circulating glucose
92
If the pregnant person experiences hyperglycemia, what happens to the fetus?
Fetus will increase production of insulin, but then risk HYPOglycemia at birth
93
Sequelae of gestational diabetes
Infant: metabolic abnormalities, stillbirth, macrosomia, neonatal hypoglycemia. Increased risk of T2DM later Pregnant Person: Dev. of T2DM or impairment in glucose tolerance later in life
94
Management of Gestational Diabetes
Dietary counseling, exercise, and blood glucose/ketone monitoring; medications, including insulin may be needed
95
Non-pharmacologic Management of Prediabetes and T2DM
Education and self-management Diet and weight loss Increased physical activity Decreased sedentary time
96
Qualifications for metabolic surgery
Recommended if BMI > 40 OR BMI 35.0-39.9 + hyperglycemia not adequately controlled with lifestyle interventions and optimal medical therapy
97
Types of Metabolic/Bariatric Surgery
Gastric Band Gastric Sleeve Gastric pouch

NURS 1650 - Here We Go Again (20 decks)

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