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NURS 2514 > 2 - Glucose Regulation + Diabetes Mellitus > Flashcards

2 - Glucose Regulation + Diabetes Mellitus Flashcards

1
Q

What is glucose regulation?

A

The process of maintaining optimal blood glucose levels

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2
Q

What is euglycemia?

A

Normal blood glucose (4-7 mmol / L)

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3
Q

Identify the 3 factors that interact to regulate glucose

A

1) caloric intake
2) hormones (insulin, cortisol, glucagon)
3) glucose uptake by the cells for energy

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4
Q

What is glycogen?

A

Stored glucose in liver + fat cells

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5
Q

What is gluconeogenesis?

A

Process by which glycogen is converted to glucose

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6
Q

What is hyperglycemia?

A

high blood sugar ( > 11 mmol / L)

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7
Q

What is hypoglycemia?

A

low blood sugar (< 4 mmol / L)

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8
Q

What is glycolysis?

A

breakdown of glucose to pyruvic acid

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9
Q

What is glucagon?

A

Glucagon is a glucoregulatory peptide that counteracts the actions of insulin by stimulating hepatic glucose production and thereby increasing blood glucose levels - released when our BG is so low

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10
Q

What is the function of epinephrine in glucose regulation?

A

when blood glucose levels frop too low - the adrenal glands secrete epinephrine which causes the liver to convert stored glycogen to glucose (gluconeogenesis) thereby raising blood glucose levels

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11
Q

What is the function of GH in glucose regulation?

A

exerts anti-insulin activity by suppressing insulin’s ability to promote glucose uptake in the peripheral tissues; increases gluconeogenesis in the liver

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12
Q

What is diabetes mellitus?

A

Disorder of the endocrine clels of the pancreas involving a deficiency of insulin function, either:
- decreased secretion
- insulin resistance
or both

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13
Q

Where are the pancreatic A + B cells located?

A

In the islets of langerhans

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14
Q

What do pancreatic A cells secrete?

A

glucagon

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15
Q

What do pancreatic B cells secrete?

A

insulin

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16
Q

What is insulin?

A

Insulin is a protein hormone made exclusively by pancreatic B cells.

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17
Q

Why can’t we ingest insulin orally?

A

Because it is a protein hormone

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18
Q

Once synthesizd, where is insulin stored? How is it secreted?

A

Stored in vesicles

Secreted via exocyosis when needed

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19
Q

How can we tell if diabetics still have some function in their pancreatic B cells?

A

We can tell by checking for trace amts of connecting peptide (C-Peptide) in their blood.

People who make their own insulin will have some of this C-Peptide in their blood

Exogenous insulin (by needle) doesn’t have C-Peptide so there won’t be any C-Peptide in someone’s blood who can’t make their own insulin.

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20
Q

What is the primary stimulus for insulin secretion? What are some other stimulants for insulin secretion?

A

High blood glucose.

Also amino acids + acetylcholine.

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21
Q

What inhibits insulin secretion?

A

Alpha-adrenergic stimulation

Beta-blockers

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22
Q

How do the pancreatic B cells secrete insulin?

A

B cells have secretory granules containing stored insulin inside them.

When our blood glucose increases, ATP binds to and inhibits ATP-sensitive potassium channels

Causes the B cell to depolarize which allows calcium to enter the cells which triggers the release of insulin

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23
Q

What is the role of insulin?

A

Insulin stimulates the conversion of glycogen to glucose + stimulates glucose uptake from the blood into fat and muscle cells

Also stimulates mvmt of potassium into the cells.

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24
Q

what are the 4 types of diabetes?

A

1) type 1 (IDDM)
2) type 2 (NIDDM)
3) miscellaneous
4) gestational

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25
Q

Describe Type 1 Diabetes.
When do symptoms occur?
What is the age of onset and how do the pts often present?

A

Type 1 Diabetes is an autoimmune disease - represents 10% of diabetic cases.

Immune system attacks our pancreatic B cells

Symptoms occur when more than 70% of the B cells are eliminated; eventually all B cells are irribersibly lost and insulin secretion is virtually nonexistent.

Type 1 pts will require life-long exogenous insulin therapy (shots) and are often referred to as insulin-dependent diabetics (but this is not the clinical term used anymore)

Age of onset is typically under the age of 30

Pts often present as non-obese w muscle wasting

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26
Q

Describe Type 2 Diabetes in terms of its etiology and key characteristics.

A

Represents 90% of all cases.

Etiology is unknown - however 80% of pts are obese (particularly adominal / central obesity), and 80% have a family history

Key characteristic is peripheral insulin resistance w decreased insulin-stimulated glucose uptake; Hepatic glucose output is increased

In an attempt to compensate for insulin resistance, the pancreas increases its secretion of insulin causing hyperinsulinemia. Over time the pancrease becomes “exhausted” / dysfunctional, resultin in defective insulin secretion + diabetes.

Typically adult onset

Many pts do not require insulin treatment (“NIDDM”) b/c some residual insulin function remains

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27
Q

Describe type 3 diabetes.

A

“miscellaneous” category

represents many causes of primary or secondary DM

primary: monogenetic disorders (Ex - mature onset diabetes of the youth [MODY]
secondary: diabetic symptoms that occur as a consequence of something else (pancreatitis, pancreatic cancer, cystic fibrosis, hemochromatosis, glucocorticoid excess, hyperthyroidism, drug / infection induced

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28
Q

describe type 4 (gestational) diabetes

A

diabetes diagnosed during a pregnancy that typically resolves after birth.

occurs in 5-10% of pregnant women in canada

caused by increased levels of hormones w CRH effects

risk increases w subsequent pregnancies

type 4s have an increased risk for developing type 2 diabetes in the future

associated w increased birth weight and adverse maternal and fetal outcomes

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29
Q

What is the fundamental manifestation of diabetes?

A

hyperglycemia

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30
Q

What is the fundamental manifestation of diabetes?

A

hyperglycemia, especially fasting + postprandial

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31
Q

What is the glucose tolerance test?

A

Clinical tool used to evaluate fasting P postrpadial hyperglyceemia.

A pt is instructed to fast over night and we take their base BG

Pt then consumes a 75g glucose load and we test their BG every 30 minutes for 2-3 hrs

The test is +ve (aka pt is diagnosed as diabetic) when the BG exceeds 7 mmol / L OR when the blood glucose exceeds 11.1 mmol / L during the 2 hr follow-up

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32
Q

What is prediabetes (also called impaired glucose tolerance or impaired fasting glucose)?

A

When BG is elevated but not enough to be diagnosed as diabetic. Implies that diabetes is imminent and the pt should be treated as if they are.

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33
Q

What is the HBA1C test?

A

a test used to measure the amount of glycosylated hemoglobin - determines if BG has been elevated at any time over the previous 90-120 days.

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34
Q

Which percentage of glycosylated hemoglobin is normal? Which percentage indicates that a pt is diabetic?

A

normal: 5%

> 6.5 % = diabetes

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35
Q

What are the 4 early manifestations of diabetes?

A

1) glucosuria (glucose in the urine)
2) polyuria (freq. passage of large volumes or urine)
3) polydipsia (excessive thirst + excess drinking)
4) polyphagia (excessive or extreme hunger)

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36
Q

Why does glucosuria occur as an early manifestation of diabetes?

A

glomerular filtration of glucose is greater than the renal tubule’s ability to reabsorb [occurs when the SGLTs (sodium dependent glucose transporters)] become saturated - therefore some glucose remains and is excreted in the urine

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37
Q

Why does polyuria occur as an early manifestation of diabetes?

A

glucose in the urine impairs the osmosis of water - leads to osmotic diuresis - then polyuria

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38
Q

Why does polydipsia occur as a manifestation of diabetes?

A

Dehydration occurs due to polyuria.

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39
Q

What are the clinical manifestations of hyperglycemia?

A
  • glucosuria
  • polyuria
  • polydipsia
  • polyphagia
  • abdominal cramps
  • blurred vission
  • headache
  • nausea + vomiting
  • weakness
  • fatigue
  • nocturia
  • glucosuria
  • hungies
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40
Q

What are the risk factors for severe hyperglycemia (there are lots)?

A
  • taking corticosteroids
  • emotional + physical stress
  • illness, infection
  • inactivity
  • poor absorption or lack of insulin
  • too little or lack of diabetes meds
  • lack of knowledge regarding diet
  • inaccurate knowledge on administration of insulin
  • non-adherence to mgmt of blood glucose
  • lack of undrstanding regarding the importance of self-monitoring blood glucose
  • elderly pt
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41
Q

define glycosylation

A

process by which glucose non-enzymatically binds to plasma + blood vessel proteins

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42
Q

What is Diabetic Ketoacidosis?

A

Absence of insulin function results in uncontrolled lipolysis + ketogenesis

Keto acids enter the blood and cause metabolic acidosis which results in the formation of ketone bodies

43
Q

In which type of diabetes does DKA commonly occur?

A

Type 1 - typically w a missed insulin dosage

Rarer in type 2 because residua insulin function inhibits profound lipolysis + ketogenesis

44
Q

What will happen if DKA is left untreated?

A

coma + death

45
Q

What are the 3 manifestations of DKA?

A

1) severe hyperglycemia
2) metabolic acidosis
3) rapid respirations + fruity breath

46
Q

What is severe hyperglycemia?

A

BG > 25 mmol / L

47
Q

Why does fruity breath occur as a manifestation of DKA?

A

Pt has rapid, deep respirations (kussmaul) to compensate for metabolic acidosis (to try lower the amt of CO2 in the blood)

ketones spontaneously convert to acetone in the blood which vaporize in the alveoli and give the breath a characteristic fruity odor

48
Q

What is the treatment for DKA?

A 
IV insulin therapy + fluid mgmt
K+ supplement b/c:
- insulin increases the cellular uptake of K+
- K+ is lost in the urine + vomit
- K+ diluted w fluids
49
Q

What is the cause of hypoglycemia?

A

occurs when there is too much insulin in proportion to the amt of available glucose in the blood which causes the plasma glucose to drop

Occurs w over-administration of drugs, w exercise, fasting or a missed meal, or excessive alcohol consumption

50
Q

When do the neurogenic / autonomic (SNS stimulatio) symptoms of hypoglycemia occur?

A

when blood glucose in below 3.5 mmol / L

51
Q

When do the neuroglycopenic (CNS depression) symptoms of hypoglycemia occur?

A

appear when the blood glucose is below 2.5 mmol / L

52
Q

Why do neurogenic symptoms occur due to hypoglycemia?

A

Related to the release of epinephrine

53
Q

Why do neuroglycopenic symptoms occur due to hypoglycemia?

A

CNS shutdown - occur when the brain isn’t getting enough glucose.

54
Q

What are the neurogenic / autonomic symptoms of hypoglycemia?

A 
sweating
tachycardia
trembling
anxiety
weakness
palpitations
light-headedness
nausea
irritability
55
Q

What are the neuroglycopenic symptoms symptoms of hypoglycemia?

A 
confusion
irritability
headaches
drowsiness
loss of coordination
difficulty speaking
convulsions
seizures
coma
56
Q

What are the potential treatments of hypoglycemia?

A
  • oral or IV glucose (15 g or more to stabilize their BG)
  • IV glucagon (glucagon triggers stored glucose in the liver - so if the pt hasn’t eaten in a long time the IV glucagon won’t work)
  • repeated bouts of hypoglycemia or beta-blocker use can reduce the SNS response
57
Q

What is hyperosmolar coma?

A

Results from hyperosmolarity (hyperglycemia + dehydration) - cellular dehydration of CNS neurons is believed to be the cause of this coma

58
Q

What is HHNS?

A

Hyperosmolar hyperglycemic non-ketotic syndrome

blood sugar is super high, pt is dehydrated and they are losing consiousness

59
Q

What is HHNC?

A

Hyperosmolar hyperglycemic nonketotic coma - progression from HHNS

60
Q

What usually precipitates episodes of HHNS?

A

these episodes are often precipitated by inadequate fluid intake during another illness; infection, HF, or MI are often contributing factors; decreased GFR

61
Q

Why are pts asymptomatic for much longer with HHNC?

A

Because there is no ketoacidosis with HHNC - therefore this delays medical care.

62
Q

How high can BG reach in the case of HHNC?

A

45-100 mmol / L

63
Q

How much higher is the mortality rate in HHNC than DKA?

A

x 10 higher

64
Q

How do we treat HHNC?

A 
F - fluids
I  - insulin
G  - glucose (monitor)
P - potassium
I  - infection
C  - chart fluid balance
K  - ketones
65
Q

T or F: insulin can cause lethal arrhythmias due to hypokalemia from potassium uptake into the cells

A

true

66
Q

What are the 4 chronic complications of diabetes mellitus?

A

1) microangiopathy (microvascular disease)
2) macroangiopathy (macrovascular disease)
3) neuropathy
4) infections + foot ulcers

67
Q

provide 2 examples of microangiopathy associated with DM

A
  • retinopathy

- nephropathy

68
Q

Provide 3 examples of macroangiopathy associated w DM

A
  • coronary artery disease
  • cerebral artery disease
  • peripheral artery disease
69
Q

Why does microangiopathy (disease of the small vessels) occur in DM?

A
  • basement membranes of capillaries are thickened in diabetes + contain an increased amt of collagen and decreased amts of proteoglycan - makes the vessels stiff + rigid
  • w prolonged hyperglycemia, more glucose irreversibly binds to proteins creating advanced end glycosylation end products (AGE)
  • AGEs cause the accumulation of basement membrane proteins, capture LDLs, and rhe release of inflammatory cytokines
70
Q

Diabetes is the leading cause of adult-onset blindness. What are the 2 stages of diabetic retinopathy?

A

1) non-proliferative stage

2) proliferative stage

71
Q

Describe the non-proliferative stage of diabetic retinopathy

A
  • microaneurysms occur in the retinal blood vessles as a result of microangiopathy and loss of pericytes
  • aneurysms can become permeable or can rupture resulting in retinal exudate formation and hemorrhage
  • retinal ischemia, infarction, and visual impairment ensue (ex - blind spots)
72
Q

describe the proliferative stage of diabetic retinopathy

A

worse than the non-proliferative stage

retinal ischemia stimulates angiogenesis and new blood vessels form w/in the retina - infarction of the retina causes fibrous scar tissue to replace the necrotic neural tissue

fibrous tissue accumulates, tension increases in the retina, and often results in retinal detachment + blindness.

73
Q

Does the proliferative stage of diabetic retinopathy occur more frequently in type 1 or type 2 DM?

A

Type 1

74
Q

T or F: Diabetes is the leading cause of end-stage chronic renal failure requiring dialysis and transplant

A

true

75
Q

What is diabetic nephropathy? What is the first sign?

A

primarily involves the glomerular capillaries.

fibrosis and thickening of the capillary basement membrane occurs (glomerularsclerosis) - nephrons are lost and renal failure occurs

the first sign is microalbuminuria (b/c proteoglycan is lost which allows albumin to enter the tubules and then the urine), also see elevated BUN + creatinine

76
Q

What are the 3 main drug classes used to treat diabetic nephropathy?

A

1) ace inhibitors
2) ARBs
3) SGLT2 inhibitors

77
Q

describe diabetic macroangioathy

A

essentially describes how diabetes accelerates atherosclerosis

AGEs (advanced glycosylation end products) w/in blood vessels capture more LDL, activate more macrophages and inflammatory cytokines, and promote the proliferation of vascular cells - all of which accelerate atherosclerosis

78
Q

how much higher is the prevalence of coronary artery disease in diabetics?

which percentage of diabetics will die from atherosclerotic related illnesses?

A

x 2-4 higher

80%

79
Q

which medications are most often prescribed for diabetic macroangiopathy?

A

statins + blood presure meds like ace inhibitors or arbs

80
Q

what are the 2 estimated causes of diabetic neuropathy?

A

combined consequence of microangiopathy and the accumulation of sorbitol w/in neurons

complication of microangiopathy in which nutrient delivery to neurons is impaired

81
Q

what are the 2 types of diabetic neuropathy?

A
  • symmetrical distal polyneuropathy

- autonomic neuropathy

82
Q

Describe symmetrical distal neuropathy

A

demyelination of distal peripheral nerves is the hallmark of this neuropathy.

usually manifests as symmetric sensory loss in the lower extremities (ex - stocking distribution, numbness, tingling

83
Q

Describe autonomic neuropathy

A

affects autonomic innervation of many different systems

 fixed, resting tachycardia and orthostatic hypotension are signs of cardiovascular involvement.
 incomplete emptying of the urinary bladder (ex – neurogenic bladder) causes overflow incontinence and predisposes to urinary tract infection.
 50% of diabetic men suffer from impotence related to vascular and autonomic dysfunction. female sexual dysfunction has been less studied (OF COURSE), but failure to achieve orgasm has been reported
 a decreased glucagon and epinephrine response to hypoglycemia, and exertional hypoglycemia can also occur.

84
Q

T or F - hyperglycemia is a pro-inflammatory phase

A

true

85
Q

what are the long term consequences of hyperglycemia?

A
  • blood vessel damage
  • peripheral neuropathy
  • fluid + electrolyte imbalances
  • acid base disturbances
86
Q

what are the long term consequences of hypoglycemia?

A
  • seizures
  • LOC
  • hypoglycemia unawareness syndrome
  • death
87
Q

what are the steps we can take to address mild-moderate hyperglycemia?

A
  • adjust meal plan
  • adjust physical activity
  • adjust meds ot insulin
  • increase hourly intake of water / fluids
88
Q

what are the steps we can take to address severe hyperglycemia?

A
  • medical attention required
  • monitor serum glucose
  • fluid replacement + short-acting insulin by IV
  • monitor and treat electrolytes + renal function
  • monitor neurological status
89
Q

what are the risk factors for severe hypoglycemia?

A
  • prior episodes of severe hypoglycemia
  • current low A1C ( < 6.0%)
  • hypoglycemia unawareness
  • long duration of insulin therapy or sulfonylureas
  • autonomic neuropathy
  • chronic kidney disease
  • cognitive impairment
  • low socio-economic status, food insecurity
  • low health literacy
  • preschool-age children or adolescents
  • pregnancy
  • elderly pts
90
Q

what are the risk factors for type 2 diabetes?

A
  • age over 40
  • first-degree relative w type 2 diabetes
  • member of high risk population (asia, african, arab, hispanic)
  • history of prediabetes
  • history of GDM
  • delivery of a macrosomic infant
  • presence of end-organ damage associated w diabetes
  • vascular risk factors (HTN, overweight, abdominal obesity, smoking)
91
Q

describe the differences between type 1 and type 2 diabetes

A

type 1: destruction of beta cells leading to lack of insulin

type 2: progressive loss of beta cell function, cellular insulin resistance

type 1: cannot be managed w diet or exercise alone

type 2 can be managed w diet, exercise, oral antihyperglycemics or insulin

92
Q

How often should we screen individuals over 40 and individuals at high risk for type 2 diabetes?

how often should we screen for people with additional risk factors?

A

every 3 years.

every 6-12 mo for people with additional risk factors

93
Q

What do the following lab results indicate? How often should we rescreen?

  • FPG < 5.6 mmol / L or A1C < 5.5%
A

This is normal. Rescreen as recommended.

94
Q

What do the following lab results indicate? How often should we rescreen?

  • FPG 5.6-6.0 mmol / L or A1C 5.5-5.9%
A

This pt is at risk - rescreen more often.

95
Q

What do the following lab results indicate? How often should we rescreen?

  • FPG 6.1-6.9 mmol / L or A1C 6.0-6.4%
A

Pt is prediabetic - recreen more often.

96
Q

What do the following lab results indicate? How often should we rescreen?

  • FPG greater than or equal to 7.0 mmol / L or A1C greater than or equal to 6.5%
A

Pt is diabetic.

97
Q

What is the critical high level for blood sugar?

Critical low?

A

33 mmol / L

2.8 mmol / L

98
Q

why is infection more likely to occur in DM?

A
  • decreased immune response
  • delayed wound healing
  • glucose is fuel for microorganisms
  • diabetes is a pro-inflammatory state. increases cytokines in the blood
  • worsened blood flow
99
Q

what is lipodystrophy?

A

hypertrophy of fat cells

100
Q

What is the dawn phenomenon?

A

takes place early in the morning

growth hormone is released during the night which decreases peripheral glucose uptake - causing hyperglycemia

w the sun rise, a rise in the blood glucose concentration occurs w no hypoglycemia during the night.

101
Q

T or F: insulin is also used in the case of severe hypercalcemia

A

True :)

102
Q

Identify the 3 risk factors shared between diabetes + heart disease

A

1) high BP
2) obesity
3) high cholesterol

103
Q

on a h2t assessment of a diabetic pt, describe what we would look for.

A

CNS: LOC, neuropathy
CVS: HR, BP, cap refill, CWCM
RESP: Kussmaul resps, crackles, fruity breath
GI / GU: NVD, diet, appetite
INTEGUMENT: sores, ulcers, signs of infection, open areas
MSK: weakness, activity levels, muscle wasting, intermittent claudication, activity tolerance

NURS 2514 (10 decks)

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