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OU Module Endo Fall 2018 > Pathophysiology of Diabetes Exam 2 > Flashcards

Pathophysiology of Diabetes Exam 2 Flashcards

1
Q

What is the primary energy source?

A

glucose

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2
Q

What is the primary macronutrient used for energy?

A

carbohydrate (CHO)

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3
Q

What are processes of catabolism of CHO?

A
  • Glycogenolysis

- Glycogenesis

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4
Q

What are processes of synthesis of glucose?

A

Gluconeogenesis

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5
Q

Glycogenolysis

A

Process of breaking down CHO for quick energy source

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6
Q

Glycogenesis

A
  • Process of converting CHO to glycogen for storage for later use.
  • Stored in skeletal muscle, liver, and fat (adipose) tissue
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7
Q

Gluconeogenesis

A
  • Process of synthesizing glucose during glucose deficiency

- Liver (primary) and kidneys

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8
Q

What are the cells that exists in the pancreas?

A
  • β-cells

- α-cells

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9
Q

β-cells

A

Produce insulin

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10
Q

α-cells

A

Produce glucagon

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11
Q

What is insulin secretion regulated by?

A
  • various nutrients
  • incretin hormones
  • pancreatic hormones
  • autonomic neurotransmitters
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12
Q

What is the primary stimulus for insulin secretion?

A
  • orally administered glucose (when you eat)

- called the incretin effect

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13
Q

Where does secreted insulin goes first?

A

into the portal vein to the liver to stop glucose production

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14
Q

What is basal release?

A

means insulin is continuously secreted from the pancreas

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15
Q

What is bolus release?

A
  • insulin secreted due to consumption
  • first phase: peak in insulin secretion, shuts down hepatic glucose production
  • second phase: delayed
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16
Q

What promotes glucose uptake?

A

insulin

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17
Q

general actions of insulin

A
  • Promotes lowering of blood glucose
  • Promotes storage of glucose
  • Promotes potassium uptake
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18
Q

function of insulin in the liver

A
  • Glucose uptake
  • Stimulates glycogen storage
  • Stimulates synthesis of triglycerides
  • Inhibits glycogenolysis
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19
Q

function of insulin in muscle

A
  • Increase glucose uptake
  • Enhances glycogen synthase
  • Increases uptake of amino acids
  • Inhibits glycogen phosphorylase
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20
Q

function of insulin in fat

A
  • Increase glucose uptake
  • Increase triglyceride production
  • Stimulates lipoprotein lipase
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21
Q

What is the major source of elimination for endogenous insulin?

A

liver

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22
Q

Glucagon-like peptide 1 (GLP-1)

A
  • one of the incretin hormones
  • Released from the L cells in the intestine in response to glucose and other nutrients upon eating
  • Stimulates insulin secretion (glucose dependent)
  • Suppresses appetite and promotes weight loss
  • Slows gastric emptying
  • Metabolized rapidly (1-2 min) by dipeptidyl peptidase 4 (DPP-4)
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23
Q

Glucose-dependent insulinotropic polypeptide (GIP)

A
  • one of the incretin hormones
  • Released from K cells in response to glucose and fat intake
  • Promotes insulin biosynthesis
  • Promotes insulin secretion (glucose dependent)
  • May prevent apoptosis
  • May stimulate glucagon
  • Metabolized rapidly (5-7 min) by DPP-4
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24
Q

Amylin

A
  • Released with insulin from β-cell

* Promotes lowering glycemia by: slowing gastric emptying, suppressing glucagon, increasing satiety

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25
Q

Glucagon

A
  • Synthesized and secreted from pancreatic alpha cells
  • Inhibited by glucose
  • Promotes increasing glucose
  • Primary effect is on the liver
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26
Q

Glucagon effect

A

In the liver:

  • Stimulates: Glycogenolysis, Gluconeogenesis, Fatty acid oxidation, Ketogenesis
  • Inhibits: Glycogen synthesis, Fatty acid synthesis
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27
Q

What are the counter-regulatory hormones?

A
  • Glucagon
  • Epinephrine
  • Cortisol
  • Growth hormone
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28
Q

Epinephrine effect

A

Stimulates hepatic glucose release via glycogenolysis and lipolysis

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29
Q

Cortisol effect

A

Stimulates hepatic uptake of amino acids which can be used to produce glucose

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30
Q

Growth hormone

A

Stimulates lipolysis and inhibits glucose uptake in muscle and adipose tissue

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31
Q

What is hemoglobin A1c?

A
  • Marker of glycemia over 2-3 month period

* Lab is a % of hemoglobin A1 molecule with glucose bound

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32
Q

What is a hemoglobin lifespan?

A

120 days

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33
Q

How can accuracy be lost in the A1c test?

A

if the patient has:

  • hemoglobinopathies
  • uremia
  • hemorrhage
  • hemolytic disorders
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34
Q

normal value for A1c

A

4-5.6%

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35
Q

normal preprandial BS

A

<100 mg/dL

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36
Q

normal postprandial BS

A

<140 mg/dL

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37
Q

normal value for A1c for someone diagnosed with DM

A

<7%

38
Q

normal preprandial BS for someone diagnosed with DM

A

80-130 mg/dL

39
Q

normal postprandial BS for someone diagnosed with DM

A

<180 mg/dL

40
Q

normal bedtime BS for someone diagnosed with DM

A

100-180 mg/dL

41
Q

correlate A1c to the estimated average blood glucose

A
  • A1c 10 = 240 mg/dL

* every 1 digit of A1c = 30 mg/dL

42
Q

A1c monitoring

A
  • Every 3 months when A1c not at goal
  • Every 6 months when A1c at goal
  • Every 12 months when A1c within pre-diabetes range
43
Q

causes of hyperglycemia

A
  • Associated with suboptimal medication doses (those with DM)
  • Excessive glucose release from the liver
  • Excessive ingestion of CHO
  • Stress, illnesses, medications
44
Q

symptoms of hyperglycemia

A
  • Polyuria / Glucosuria
  • Polyphagia
  • Polydipsia
  • Weight loss
  • Blurry vision
  • Paresthesia
  • Muscle weakness
  • Altered level of consciousness
  • Lethargy
  • Headache
  • Postural hypotension
  • DKA or HHS
45
Q

symptoms of hyperglycemia: Polyuria / Glucosuria

A
  • happens when serum glucose > 180mg/dL and glucose spills into urine
  • water follows glucose -> osmotic diuresis
  • free water and electrolytes are lost
46
Q

symptoms of hyperglycemia: Polyphagia

A

increased hunger

47
Q

symptoms of hyperglycemia: Polydipsia

A
  • unquenchable thirst
  • Caused by increasing osmolality (from hyperglycemia/free water loss)
  • ↑glucose = ↑osmolality, then hypothalamus induces sensation of thirst
48
Q

symptoms of hyperglycemia: Weight loss

A
  • Initially associated with depletion of water, glycogen and triglyceride stores
  • Then due to reduced muscle mass
  • Loss of 10-30 pounds can occur
49
Q

symptoms of hyperglycemia: Blurry vision

A

in a hyperosmolar state, water enters the lens resulting in modest swelling

50
Q

symptoms of hyperglycemia: Paresthesia

A

nerve damage from sustained hyperglycemia

51
Q

symptoms of hyperglycemia: Muscle weakness

A

due to catabolism of muscle

52
Q

symptoms of hyperglycemia: Altered level of consciousness

A

due to hyperosmolality

53
Q

symptoms of hyperglycemia: Headache

A

most patients describe as throbbing headache

54
Q

symptoms of hyperglycemia: Postural hypotension

A

due to depleted plasma volume

55
Q

hypoglycemia classifications

A
  • hypoglycemia alert value
  • clinically significant hypoglycemia
  • severe hypoglycemia
56
Q

hypoglycemia classifications: hypoglycemia alert value

A
  • ≤ 70 mg/dL

* sufficiently low for treatment with fast-acting CHO and dose adjustment of glucose-lowering therapy

57
Q

hypoglycemia classifications: clinically significant hypoglycemia

A
  • < 54 mg/dL

* sufficiently low to indicate serious, clinically important hypoglycemia

58
Q

hypoglycemia classifications: severe hypoglycemia

A
  • no specific glucose threshold

* hypoglycemia associated with severe cognitive impairment requiring external assistance for recovery

59
Q

causes of hypoglycemia

A
  • Excessive quantity of medication (those with DM)
  • More than usual physical activity
  • Inadequate food intake
60
Q

symptoms of hypoglycemia

A
  • Trembling/shaking
  • pounding heart
  • tachycardia
  • changes in body temperature
  • sweating
  • tingling in extremities
  • Slow thinking
  • blurred vision
  • slurred speech
  • lack of coordination
  • numbness
  • dizziness
  • fatigue/sleepiness
  • trouble concentrating
  • coma
  • Hunger, nausea
  • weakness
  • headache
  • general strange feeling
  • social behavioral changes
61
Q

How are autonomic symptoms happening during hypoglycemia?

A

Epinephrine is released

62
Q

hypoglycemic unawareness

A

Experiencing hypoglycemia without realizing it

63
Q

What can increase the risk of having hypoglycemic unawareness?

A
  • Previous episode of hypoglycemia in the past 24 hours
  • Multiple episodes of hypoglycemia
  • Very tight blood glucose control
64
Q

How would you treat mild hypoglycemia?

A
  • Consume 15-20g of simple CHO
  • 3-4 glucose tablets, gel, juice (preferred) • 8-10 lifesavers or 5-6 peppermint candies
  • 8oz regular milk
  • 4-6oz fruit juice or regular soda
  • 1 tablespoon honey
  • Recheck BS in 15-20 minutes
  • Repeat treatment if necessary
65
Q

How would you treat severe hypoglycemia?

A

Administer glucagon (stimulates liver to release stored glucose)

66
Q

What is a common adverse effect with glucagon?

A
  • vomit

- turn pt on their side

67
Q

What are pre-diabetes markers?

A
  • Impaired fasting glucose (IFG): 100-125 mg/dL

* Impaired glucose tolerance (IGT): OGTT result with 2 hour plasma glucose of 140-199 mg/dL

68
Q

How do you classify prediabetes?

A
  • Patients who meet IFG or IGT criteria

* A1c 5.7-6.4%

69
Q

How can you diagnose a patient with diabetes?

A

if they have any of the following:
• A1c ≥ 6.5%
• Fasting plasma glucose ≥ 126 mg/dL, or
• Symptoms of hyperglycemia and random plasma glucose ≥ 200 mg/dL, or
• OGTT with 2 hr plasma glucose ≥ 200 mg/dL

70
Q

pathogenesis of DM I

A
  • born with a predisposition to produce antibodies to β-cells (autoimmune disorder)
  • 90% of pts have at least one autoantibody
  • Trigger: environmental or infectious
  • Autoantibodies begin to destroy β-cells
71
Q

What happen when autoantibodies begin to destroy β-cells?

A

Insulin and amylin production decline to 0 (or close to it)

72
Q

What is the honeymoon phase?

A

pt has DM I but pancreas still has some insulin it’s secreting so it doesn’t seem as if pt has DM I

73
Q

What are the four antibodies that are found in someone with DM I?

A
  • Glutamic acid decarboxylase 65 (GAD65)
  • Islet cell antibody (ICA)
  • Insulin autoantibody (IAA)
  • Tyrosine phosphatases antibody (IA-2)
74
Q

What are risk factors for DM I?

A
  • Family history of DM1 or auto-antibodies

* Known presence of auto-antibodies

75
Q

What are the screening guidelines for DM I?

A
  • No indication for screening the general population
  • Based on clinical presentation
  • No good data on targeted screening
  • Some clinicians will screen for auto-antibodies in patients with a family history of type 1 DM (TrialNet)
76
Q

What are laboratory markers of DM I?

A
  • Serum insulin – low
  • C-peptide – low
  • Autoantibodies – present
  • Blood glucose - high 83
  • Glucosuria – present
  • A1c – high
  • Ketones – often present
77
Q

Diabetic Ketoacidosis (DKA)

A
  • Excess ketone production → ketonemia → ketoruia → diabetic ketoacidosis
  • life threatening
78
Q

What are symptoms of DKA?

A
  • Abdominal pain
  • fruity odor on breath
  • CNS depression
  • coma
79
Q

What are physical findings of DKA?

A
  • Tachycardia
  • dehydration
  • tachypnea / Kussmaul respirations
80
Q

pathogenesis of DM II

A
  • Early resistance to insulin resulting in pancreas compensating with hyperinsulinemia, but normal glycemia
  • Progression of disease results in worsening hyperglycemia until diagnostic thresholds are crossed
81
Q

What happens overtime in DM II?

A

impaired glucose tolerance (IGT) (inability to compensate for rising blood glucose after meals) and impaired fasting tolerance (IFT) (poor control in the fasting state) develop

82
Q

What contributes to DM II?

A
  • Diminished insulin sensitivity
  • Up-regulation hepatic glucose production
  • Impaired β-cell function
83
Q

What are risk factors for DM II?

A
  • BMI ≥ 25 kg/m2 or ≥ 23 kg/m2 in Asian-Americans
  • History of impaired glucose tolerance or impaired fasting glucose
  • Physical inactivity
  • Family history of diabetes (first degree)
  • High risk ethnicity (Black, Latino, Native American, Asian American, Pacific Islander)
  • History of GDM
  • HTN, low-HDL, or triglycerides over 250mg/dL
  • Polycystic ovary disease
  • Other condition associated with insulin resistance
  • History of cardiovascular disease
  • Metabolic syndrome
84
Q

What are the qualifiers to diagnose metabolic syndrome?

A
  • Diagnosis (3 of 5):
    • Abdominal obesity (waist circumference >40” M, >35” W)
    • Elevated triglycerides (≥150 mg/dL)
    • Elevated blood pressure (≥130/85 mmHg or on med)
    • Elevated fasting glucose (> 110 mg/dL)
    • Low HDL (<40 mg/dL M, <50 mg/dL W)
85
Q

What can metabolic syndrome imply?

A
  • Inflammation
  • Diabetic dyslipidemia
  • Pro-thrombotic state
  • Endothelial dysfunction and vascular abnormalities
  • Increase risk for cardiovascular disease
86
Q

Diabetic dyslipidemia

A
  • More atherogenic LDL (smaller and more dense penetrating blood vessel walls easier resulting in plaques)
  • High triglycerides
  • Low HDL
87
Q

What are the screening guidelines for DM II?

A
  • All overweight adults with one additional risk
  • All adults, regardless of risk, at age 45 years
  • If the test is normal, repeat every 3 years
  • If the test is in the area of prediabetes, repeat every year
88
Q

What are laboratory markers of DM II?

A
  • Serum insulin and C-peptide - usually elevated or normal at diagnosis
  • Autoantibodies for β-cells - absent
  • Glycemia – elevated and varied
  • A1c - elevated
  • Glucosuria - present if glycemia is high enough
  • Ketone production - uncommon in DM2
  • Hyperglycemic hyperosmolar syndrome
89
Q

Hyperglycemic hyperosmolar syndrome (HHS)

A
  • Similar to DKA in many ways, but no ketones
  • Relative (not absolute) insulin deficiency
  • Up-regulated hepatic glucose production
  • Extreme hyperglycemia – often > 1000mg/dL
  • Osmotic diuresis leading to intravascular volume depletion and dehydration
90
Q

What are the signs / symptoms of HHS?

A
  • lethargy
  • confusion
  • hypotension
  • tachycardia
91
Q

What are the risks of having gestational diabetes?

A
  • Macrosomia (having a large baby)
  • Excessive maternal weight gain (>40 lbs)
  • Preeclampsia
  • Still birth
  • Neonatal hypoglycemia, hyperbilirubinemia, hypocalcemia, respiratory distress syndrome
  • ↑ risk of baby developing DM2, obesity, or metabolic syndrome
  • ↑ risk of maternal development of DM2

OU Module Endo Fall 2018 (27 decks)

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