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

Pathophysiology of Diabetes Flashcards

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
Q

What pathway in adipose tissue creates a precursor for gluconeogenesis?

A

Lipolysis: fat breakdown via hormone-sensitive lipase

Triglyceride broken down to 3 fatty acids + glycerol

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26
Q

How are the products of lipolysis used for energy uptake?

A

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)

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27
Q

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

A

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

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28
Q

Where does ketogenesis occur?

A

The liver

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29
Q

Describe the pathway of ketogenesis?

A

Fatty acids released by adipose lipolysis

Oxidized by the liver at a high rate

Acetyl CoA and ketone body production

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30
Q

What states of the body promote ketogenesis?

A

Prolonged fasting

Absence of insulin

Very low carb diet

High levels of glucagon and stress hormones

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31
Q

Which pancreatic cells synthesize insulin?

A

Beta cells of the islets of Langerhans

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32
Q

Which pancreatic cells synthesize glucagon?

A

Alpha cells

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33
Q

What is the significance of the structure of an insulin molecule?

A

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

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34
Q

What are incretins?

A

Peptides that stimulate the secretion of insulin

Examples: GLP-1 and GIP

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35
Q

What breaks down incretins?

A

DPP-4 enzyme

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36
Q

Which incretin can inhibit glucagon?

A

GLP-1

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37
Q

Insulin secretion: oral glucose vs. IV glucose response

A

There is more insulin secreted in response to oral glucose vs. IV glucose

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38
Q

Describe the feedforward mechanism of glucose in the GI tract

A

Glucose in the GI tract increases insulin secretion, anticipating a rise in blood glucose

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39
Q

When is glucagon production the highest?

A

In the early morning

40
Q

What is a counter-regulatory or counter insulin hormone?

A

A hormone that tends to increase blood glucose

Opposite effects of insulin

41
Q

What is glucagon’s role in the liver?

A

Increases glycogenolysis

Increases gluconeogenesis

Increases ketone body formation

Decreases triglyceride synthesis

Minor role in lipolysis

42
Q

What tissue lacks receptors for glucagon?

A

Skeletal muscle

43
Q

What are examples of counter-insulin hormones?

A

Glucagon

Cortisol

Epinephrine

Placental hormones

Growth hormone

44
Q

Stress hormones _____ blood glucose levels

A

INCREASE

45
Q

What effect does increased BG have on healing?

A

If not attended to, increased blood glucose can delay healing time significantly

46
Q

Growth Hormone

A

Released during hypoglycemia

Acts as counter insulin

Excess –> acromegaly –> diabetes

47
Q

What doubles a child’s risk of developing T1DM?

A

The risk is doubled
if a parent developed Type 1 DM before age 11

48
Q

If both parents have T2DM, what is their children’s risk of developing it?

A

If both parents have Type 2 DM, their
children have about a 50% risk of developing Type 2 DM

49
Q

Type 2 DM is an example of what kind of disease?

A

Polygenic and multifactorial

50
Q

What is monogenic diabetes?

A

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
Q

Type 1 DM is what kind of disease? What does this mean/what happens?

A

Autoimmune disease

Results in the destruction of pancreatic beta cells, meaning no insulin production

Pancreatic alpha cells remain –> continue producing glucagon

52
Q

What is insulitis?

A

Infiltration of pancreatic beta cells by pro-inflammatory leukocytes

53
Q

What are classic DM presentations?

A

Polyuria

Polydipsia

Polyphagia

Weight loss

Hyperglycemia and hyperlipidemia

54
Q

What causes the three “polys”? (polyuria, polydipsia, polyphagia)

A

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
Q

What is usually a patient’s state when they are diagnosed with T1DM?

A

Often extremely ill at diagnosis

May be in DKA

40%-60% of children under 15 years old in DKA at dx

56
Q

How does unopposed glucagon action in T1DM affect ketogenesis?

A

Ketone formation occurs which contributes to metabolic acidosis, as well as osmotic diuresis

57
Q

Diabetic Ketoacidosis (DKA) is an example of a ____ of T1DM

A

Sequela

58
Q

What precipitating events can lead to DKA?

A

Illness, stress, not injecting insulin, kinked insulin pump catheter, etc.

59
Q

Describe how DKA occurs in patients with T1DM (eh used the diagram)

A

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
Q

What are the effects of recurrent hypoglycemia on the brain?

A

Reduced counterregulatory responses
- Decreased or no glucagon response
- Decreased epinephrine and cortisol responses

61
Q

What is hypoglycemia unawareness?

A

Lack of autonomic symptoms reduces conscious perception of hypoglycemia

VERY DANGEROUS

62
Q

Who is at risk to be screened for T2DM?

A

All patients age 35 or older

Overweight or obese children and adolescents who have at least one risk factor

63
Q

What is acanthosis nigricans?

A

Skin condition potentially indicating diabetes

Areas of dark, velvety discoloration in body folds and creases

Affected skin can become thickened (axillae, groin, neck)

64
Q

Why might people with T2DM go 10 years without a diagnosis?

A

Changes are gradual

Pancreas initially compensates for insulin resistance by increasing insulin production

Patients are often asymptomatic

65
Q

The key combinations in T2DM:

A

Insulin resistance

Beta cell dysfunction

Precipitates by genetic predisposition and/or lifestyle, habits, environment

66
Q

What is insulin resistance?

A

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
Q

Glucagon in T2DM

A

Secreted at abnormally high levels

Working against insulin action

Increases hepatic glucose production

68
Q

Insulin paracrine effect in the pancreas:

A

Secretion of insulin in the Islets of Langerhans keeps glucagon levels low

69
Q

How does the body try to compensate for insulin resistance?

A

Pancreatic cell hyperplasia and hypersecretion of insulin

Pancreatic cells then begin to fail and die

70
Q

What is prediabetes?

A

T2DM is usually preceded by prediabetes. Indicated by:

  • Impaired glucose tolerance
  • Impaired fasting glucose
  • Hemoglobin A1c 5.7%-6.4%
71
Q

Hyperosmolar Hyperglycemic State

A

Similar to DKA

  • Greater fluid loss
  • Low level of insulin often prevents ketosis from developing
  • Higher hyperglycemic
  • Hyperosmolar state with severe intracellular dehydration
72
Q

HHS Initiating Events

A

Acute illness (infection)

Decreased fluid intake

Increased stress hormone loss due to fever

Leads to increased stress hormone reaction

Hyperglycemia

73
Q

How can hypoglycemia occur in patients with T2DM?

A

Insulin
Oral medications that stimulate insulin release
Older Adults

74
Q

Criteria for diagnosing diabetes

A

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
Q

What is Hemoglobin A1c?

A

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
Q

American Diabetes Association recommends that most people with diabetes maintain an A1c of:

vs.

AACE recommends:

A

Less than 7.0%

6.5% or less

77
Q

Goals of Glycemic Control

A

Preprandial glucose: 80-130 mg/dL

1 to 2 hours postprandial glucose: < 180 mg/dL

HgbA1c: < 7.0%

78
Q

Microvascular DM Sequelae

A

Retinopathy – major cause of blindness

Nephropathy – major cause of CKD

79
Q

Macrovascular DM Sequelae

A

Dyslipidemia

80
Q

Describe neuopathy

A

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
Q

Describe how foot ulcers can develop in patients with chronic DM

A

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
Q

Describe how infections occur in patients with chronic DM

A

Decreased blood flow

Abnormal leukocyte function

Increased sepsis risk

83
Q

What are the two types of diabetic retinopathy?

A

Proliferative: new blood vessels, fragile, disorganized

Non-proliferative: blood vessels leaky, can lead to macular edema

84
Q

Important teaching point for diabetic retinopathy:

A

Dilated retinal exams are the standard of care

85
Q

What is gastroparesis?

A

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
Q

Important Patient Teaching Point: Foot Ulcers

A

Regular self foot checks and regular podiatrist visits can minimize the risk of wounds and amputation

87
Q

General Patient Teaching for T1 and T2 DM

A

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
Q

What is gestational diabetes?

A

Disorder of glucose intolerance of variable severity with onset during pregnancy

Increases risk of both mother and child developing T2DM

89
Q

Risk factors for gestational diabetes

A

Severe obesity

Prior history of gestational diabetes

Previous large babies (macrosomia)

Presence of glycosuria

Strong family history of T2DM

90
Q

What test is done to test for gestational diabetes?

A

Oral glucose tolerance testing (OGTT) at 24-28 weeks gestation

91
Q

Gestational Diabetes Pathophysiology

A

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
Q

If the pregnant person experiences hyperglycemia, what happens to the fetus?

A

Fetus will increase production of insulin, but then risk HYPOglycemia at birth

93
Q

Sequelae of gestational diabetes

A

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
Q

Management of Gestational Diabetes

A

Dietary counseling, exercise, and
blood glucose/ketone monitoring; medications, including insulin may be needed

95
Q

Non-pharmacologic Management of Prediabetes and T2DM

A

Education and self-management

Diet and weight loss

Increased physical activity

Decreased sedentary time

96
Q

Qualifications for metabolic surgery

A

Recommended if BMI > 40

OR

BMI 35.0-39.9 + hyperglycemia not adequately controlled with lifestyle interventions and optimal medical therapy

97
Q

Types of Metabolic/Bariatric Surgery

A

Gastric Band

Gastric Sleeve

Gastric pouch

NURS 1650 - Here We Go Again (20 decks)

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