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@Nur 180 Exam 3 > Metabolism: Diabetes Mellitus, Obesity > Flashcards

Metabolism: Diabetes Mellitus, Obesity Flashcards

1
Q

Is the process of biochemical reactions occurring in the body’s cells that are necessary to produce energy, repair cells and maintain life

A

Metabolism

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2
Q

Through the release of hormones, such as insulin, the endocrine system controls the cellular activity that regulates growth and body metabolism.

A

How metabolism works

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3
Q
  • Affects 20.8 million people in the US
  • Affects 200 million world-wide.
  • Is two and a half times more common in African-Americans and Hispanic Americans
  • Is 5x more common in Native Americans.
  • Is the 7th Leading cause of death in the US.
  • The CDC estimates that a child born in 2000 has a 1 in 3 chances of developing DM in their lifetime.
A

Statistics on Diabetes Mellitus

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4
Q

kills more quickly

A

hypoglycemia

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5
Q

kills slowly overtime

A

hyperglycemia

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6
Q

People live longer.
Obesity has increased in the general population
The use of insulin and other anti-diabetic agents.

A

Reasons why more people have Diabetes than ever before..

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7
Q
  • 25x more likely to develop blindness.
  • 17x more likely to develop kidney failure.
  • 20x more likely to develop gangrene.
  • 15x more likely to require amputation.
  • 2x as likely to have an MI or CVA.
A

People with Diabetes

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8
Q
  • All body tissues and organs require a constant supply of glucose.
  • Not all tissues require insulin for glucose uptake
  • The brain, the liver, the intestines and the renal tubules DO NOT require insulin.
  • Skeletal muscle and adipose tissue DO require insulin for glucose movement into the cells.
A

Blood glucose homeostasis is maintained through the action of insulin and glucagon.

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9
Q
  • increased plasma glucose levels
  • increased plasma levels of amino acids.
  • increased plasma levels of fatty acids.
  • incretin hormones-GLP-1 and amylin
A

How does the pancreas know to secrete insulin?

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10
Q

70-100 mg/dl

A

Normal blood glucose level is between.

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11
Q
  • Includes a group of hormones that will increase glucose in times of hypoglycemia, stress, growth or increased metabolic demands.
  • These hormones include: Glycagon, Epinephrine, Norepinephrine, Growth Hormone, and Cortisol.
  • Diabetes Mellitus is a Comples disorder of carbohydrate, fat and protein metabolism that is primarily a result of a deficiency or complete lack of insulin secretion.
A

Counterregulatory System

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12
Q

Complex disorder of carbohydrate, fat and protein metabolism that is primarily a result of a deficiency or complete lack of insulin secretion.

A

Diabetes Mellitus

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13
Q
  • Type I
  • Type II
  • Gestational
  • Pre-diabetes;
  • impaired fasting glucose (blood glucose level of 100-125 when fasting)
  • impaired glucose tolerance (blood glucose between 140-199 when undergoing a 2 hr. GTT)
  • Other Specific Conditions resulting in hyperglycemia such as genetic defects. Disease of the pancreas, drug induced.
A

Classifications of Diabetes Mellitus

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14
Q
  • Age of Onset: can appear at any age, usually young, less than 30 years of age.
  • Characterized by a sudden onset
  • Etiology: Environmental and Autoimmunity response, may have been inherited (gene coding for HLA-DR and HLA-DQ), or may be the result of a viral infection
  • Risk for general population is 1 in 400 and the risk for those who have at least one parent with diabetes is 1 in 20.
A

Type I Diabetes Mellitus

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15
Q
  • Age of onset: may occur at any age, but occurs most commonly in people over 40 years of age.
  • Common in the obese (esp. in the upper body)
  • Onset is slow (over years)
  • Heredity plays dominant role, offspring of pts. with type 2 DM have a 15% chance of developing DM and a 30% risk of having IGT
  • Metabolic Syndrome called syndrome X plays a role.
  • Common in Hispanic Americans, Native Americans and African Americans.
  • Increasing chance with Aging, esp. after age 65.
  • Often follows gestational deabetes.
  • Obesity is common.
A

Type 2 Diabetes Mellitus

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16
Q
  • decrease in the sensitivity of the cells to insulin (insulin resistance)
  • decreased insulin production
  • defect at the receptor site. both in and outside cells.
  • decrease in the # of receptor sites at the cell level.
  • poor control of liver glucose output
A

Possible causes of Diabetes Mellitus; Type 2

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17
Q

*90% beta cells in pancreas phase out than 10% beta cells start feeling symptoms..
-losing protein; losing weight.
-poor wound healing
-increase urinating
-dehydrated
-diabetic ketoacidosis
Cells starving. glucose not getting to cells; fat break down; forms increasing triglycerides and cholesterol.

A

Cardinal Signs DM1

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18
Q

180 mg/dl glucose in blood starts to pee it out.

A

glucose in urine; DKA (total lack of insulin)

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19
Q

thick blood

A

hemoconcentration

hyperosmolarity

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20
Q
  • Assess the airway, LOC, hydration (isotonic 0.9%), electrolytes and blood glucose levels
  • Returning Serum pH to normal
  • Correcting fluid and electrolyte imbalances (in the presence of mild, moderate, or severe dehydration; decreased HCO3, increased K (mild), decreased K (severe), decreased Na (moderate to severe), decreased Ca, Mg, PO4, pH
  • Lowering hyperglycemia (usually above 250 mg/dl) Reg 70-100; increase b/c don’t want to cont. going down. IV stays in body for a couple of hours. If below 250 would have to give dextrose; hypoglycemia worse than hyperglycemia.
  • Blood sugar @ 180 mg/dl causes you to urinate.
A

Treatment for DKA Type I DM

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21
Q

Called Maturity onset diabetes of the young (MODY)

A

Children Type 2 Diabetes Mellitus

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22
Q

Regular insulin only kind given in an IV!!

A

Need to know DM

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23
Q
  • Administration of Insulin
  • Symptoms of hyper/hypoglycemia
  • serum glucose monitoring
  • Diet
  • Long term complications**
  • Prudent Living
  • Sick day rule
A

Pt teaching for type I diabetes

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24
Q
  • Polyuria
  • polydipsia
  • polyphagia
  • blurred vision
  • weightloss
  • fatigue
  • poor wound healing

If CHF patient: 0.045% NS for dehydration.

A

S & S Diabetes Mellitus
Cardinal signs
Keep an eye on kidney function because don’t want too much K; kill them
Watch urine output 30 ml/hr; no more

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25
Q

0.1 unit per kg/hr of insulin;

A

To determine IV drip of insulin

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26
Q

-Explore factors leading to DKA
-Monitor blood glucose every 4-6 hrs.
-Check urine ketones when blood glucose exceeds 300 mg./dl hyperglycemia
-teach pt. to reduce risk for dehydration
See Endocrinologist

A

Prevention of Diabetes I

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27
Q

*Formally known as hyperglycemia-hyperosmolar nonketotic syndrome (HHNS)
*HHS is life-threatening and clients are often admitted to the ICU, because increased levels of glucose, sicker than one with DkA.
-Typical blood glucose levels are over 700 mg/dl
-Serum osmolarity is increased
-Present with altered levels of consciousness or are having seizures
-Dehydration is profound-fluid loss near 8 liters
(Children can develop cerebral edema is too quickly hydrated; 0.045%)

A

Acute Complications of Type 2 DM; hyperglycemic-hyperosmolar state (HHS)

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28
Q

*Formally known as hyperglycemia-hyperosmolar nonketotic syndrome (HHNS)
*HHS is life-threatening and clients are often admitted to the ICU, because increased levels of glucose, sicker than one with DkA.
-Typical blood glucose levels are over 700 mg/dl
-Serum osmolarity is increased
-Present with altered levels of consciousness or are having seizures
-Dehydration is profound-fluid loss near 8 liters
(Children can develop cerebral edema is too quickly hydrated; 0.045%)
Diabetes II; still making insulin; making enough to break down fats; no increase ketone levels

A

Acute Complications of Type 2 DM; hyperglycemic-hyperosmolar state (HHS)

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29
Q

Symptoms slow to appear until health care is sought for some other problems.
-Polyuria and polydipsia is common.

A

HHS Manifestation;

Sufficient insulin which usually prevents ketosis. (breakdown of fat)

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30
Q

-Occurs most frequently in elderly clients whose fluid intake is poor.
-Occurs with patients with renal insufficiency
-Precipitated by an acute illness or infection.
body increase glucose
Metabolic increase, body would need more glucose.
***Need insulin to bring glucose into cells.

A

Hyperglycemic-hyperosmolar state

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31
Q
  • Establishing and maintaining adequate ventilation.
  • Correcting shock with adequate intravenous fluids.
  • Maintaining fluid volume. NSS 0.9% or 0.045% (CHF, kids)
  • Administering potassium
  • Administering insulin
A

Treatment for HHS

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32
Q

Importance of Weight loss; obesity; if you lose weight maybe able to come off Diabetic meds

  • Serum glucose monitoring
  • Diet
  • Oral hypoglycemic agents &/or insulin
  • Prudent living/prevention of complications
A

Patient Teaching for type 2 Diabetes

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33
Q

Causes;

  • overdose of insulin or oral hypoglycemic agents.
  • omitting or delaying a meal
  • overexertion without compensation with additional CHO
  • Nutritional and fluid imbalances due to vomiting
  • Erratic or altered absorption of insulin
  • Changing to a different insulin
  • counterregulatory Hormone deficiencies
  • severe sepsis
Forget to eat
took too much insulin
need to eat; energize cells
Ran marathon; not enough carbs
Change 1 type or manufacturer to another
A

Hypoglycemia; blood glucose less than 60 mg/dl

Kills Fast

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34
Q
  • Blood glucose level less than or equal to 60 mg/dl
  • Neurogenic symptoms (Adrenergic) results from autonomic nervous activity triggered by a rapid decline in blood glucose; can happen to anyone (counterregulatory kicks in; glucose rises)
  • Neuroglycopenic Symptoms occur when brain glucose gradually declines to a low level.
  • *brain gradually loses blood glucose.
  • Adrenergic symptoms; treatment; give 15 to 20 grams of rapid-acting CHO; use the 15/15 rule

(After 5-10 years for Type 2 Diabetics; they lose Adrenergic response)

A

Classifications of Hypoglycemia

Can give: 
6 life savors
1 tsp honey
Applejuice; no OJ b/c of K+; cardiac patients
4-6 oz soda
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35
Q

Keep checking q 15 mins for raising of glucose levels to normal

A

15/15 rule

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36
Q
  • disorientation (seems drunk)
  • seizures
  • somnolence (difficulty arousing from sleep)
  • loss of consciousness
  • **death
A

Neuroglycopenic symptoms; Life Threatening

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37
Q 
TIRED
tremors and tachycardia
irritability
restlessness
excessive hunger
diaphoresis and depression

Treatment
parenteral glucagon and/or IV 50% dextrose (usually instantly) Book will say 20mins

A

Neuroglycopenic symptoms

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38
Q

beta blockers: which block receptors; can become hypoglycemic in diabetes

A

Avoid beta blockers in Diabetics

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39
Q

characterized by morning hyperglycemia from the counterregulatory response to nighttime hypoglycemia. bad HA, horrible nightmares, increase blood glucose keeps getting higher every night sleeping, decrease blood glucose; counterregulatory system kicks in
**treat: less insulin @ dinner; have a bedtime snack

A

Smogyi Phenomenon (Fasting hyperglycemia)

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40
Q

results from a night time release of growth hormone that causes blood glucose elevations at about 5 to 6 am.
-Teenagers growing; Not becoming hypoglycemic. increase in glucose bc of growth hormone;
Treatment: would give insulin before bed time

A

Dawn Phenomenon (Fasting hyperglycemia)

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41
Q

Metabolic Syndrome (Syndrome X)
Degenerative Vascular Changes including:
-alternations in the macrocirculation.
-alterations in the microcirculation including;
*Diabetic Retinopathy
*Diabetic Neuropathy
*Diabetic Nephropathy

A

Fasting hyperglycemia; Long term effects of hyperglycemia

42
Q

The Retina
Diabetic Retinopathy
-related to problems that block retinal blood vessels and cause them to leak, leading to retinal hypoxia..

A

Microvascular complications theories: Diabetic Retinopathy

43
Q

Cluster of metabolic factors that occur together increasing the risk of developing type 2 DM, heart disease, and stroke;

  • Encompasses varying degrees of:
  • hyperglycemia
  • hypertension
  • high triglyceridemia
  • low levels of high density lipoprotein (HDL)
  • abdominal obesity
A

Metabolic Syndrome (AKA syndrome X)

44
Q
  • Coronary Artery Disease; increases chance of stroke
  • Cerebral Vascular Disease
  • Peripheral Vascular Disease (higher incidence in Type 2 Diabetics)
A

Macrocirculation; Atherosclerotic changes lead to

45
Q
  • Coronary Artery Disease; increases chance of stroke
  • Cerebral Vascular Disease
  • Peripheral Vascular Disease (higher incidence in Type 2 Diabetics)
A

Macrocirculation; Atherosclerotic changes lead to

46
Q

causes thickening of the basement membrane of the small blood vessels and organ damage.
-a weakening of the capillary membrane, increase capillary permeability and capillary perfusion.
Glucose toxicity directly effects functional cell integrity

A

Chronic hyperglycemia

47
Q

is the nerve layer that lines the inside of the eye and converts light into nerve signals that the brain can interpret.

A

The Retina

48
Q

is an alteration in the blood flow within the retinal capillary structure which leads to retinal ischemia and breakdown in the retinal barrier. blindness

A

Diabetic Retinpathy

49
Q

The Retina
Diabetic Retinopathy is an alteration
Related to problems that block retinal blood vessels and cause them to leak, leading to retinal hypoxia.

A

Microvascular complication theories: Diabetic Retinopathy

50
Q
  • **Nonproliferative diabetic retinopathy; new blood vessels grow bc of occlusions. they go nowhere; don’t help with perfusion. Fatty tissue. aneurysms in eye
  • **Proliferative retinopathy (Neovascular disease); blood vessels; no blood perfusion; more form and crowd eye *cotton wooly; increases pressure in eyes itself, detached retina. Blindness. leaking blood vessels. Foggy
  • *Other: Macular degeneration, corneal scarring, cataracts, glucoma. increase incidence
  • **Hyperglycemia;; causes blurred vision
  • **hypoglycemia: causes double vision
A

Stages of Retinopathy

Legal blindness 20x more common in people with diabetes

51
Q

New blood vessels grow b/c of occlusions. they go nowhere. don’t help with perfusion. Fatty tissue aneurysms in eye.

A

Nonproliferative diabetic retinopathy

52
Q

blood vessels form; no blood perfusion; more form, crowds eye; **cotton woolly; Increases pressure in eye itself. Detached Retina. Blindness. Leaking blood vessels in fluid in eye Foggy

A

Proliferative retinopathy (Neovascular disease)

53
Q

blood vessels form; no blood perfusion; more form, crowds eye; **cotton woolly; Increases pressure in eye itself. Detached Retina. Blindness. Leaking blood vessels. Foggy

A

Proliferative retinopathy (Neovascular disease)

54
Q
  • Laser Photocoagulation; zap cotton woollies and new blood vessels that are going no where; doesn’t cure just helps so it doesn’t get worse.
  • Panretinal Photocoagulation; laser treatment. lg laser, Big guns, put you to sleep for procedure.
  • Vitrectomy; vitreous humor and blood dip; blind. take out fluid and put clear solution in it. Under general anesthesia.
A

Treatment for Diabetic Retinopathy

55
Q

save t

A

test

56
Q
  • preventing episodes of hyperglycemia.
  • encouraging routine eye exams; every 6 months
  • HTN; avoid valsalva maneuver
A

Client Teaching; Retinopathy

57
Q

-Characterized by the presence of albumin in the urine, hypertension and edema; low albumin level, kidneys letting go
-Is the most common cause of Renal Failure in the US.; most bc diabetics; BUN & Cr lab values;
HTN; perfusion to kidneys diminished

A

Diabetic Nephropathy; kidneys

58
Q 
Control of hyperglycemia
-control of hypertension
prevention and early treatment of UTI's
avoidance of nephrotoxic substances
diet low in sodium and protein
A

client teaching Nephropathy

59
Q

Is a progressive deterioration of nerves that results in loss of nerve function

A

Diabetic Neuropathy

60
Q

Is a progressive deterioration of nerves that results in loss of nerve function
2 types:
*Diffuse Neuropathies; slow onset, involve motor and sensory nerves, involve the ANS.
BP doesn’t go up when standing quickly
ANP; not prop working

A

Diabetic Neuropathy

61
Q

Slow onset, involve motor and sensory nerves, involve the ANS.

A

Diffuse Neuropathies

62
Q

Usually caused by an acute ischemia event/physical trapping of a nerve. Leads to damage or death of nerve.
cant feel toes/feet

A

Focal Neuropathies

63
Q

Distal symmetric polyneuropathy cause:
-sensory alteration such as parenthesias, or anesthesia, motor alteration including deformed feet such as hammertoes
-Autonomic neuropathy; including gastroparesis, bowel incontinence, neurogenic bladder, impotence, orthostatic hypotension, resting tachycardia, loss of warning signs of hypoglycemia.
cranial nerves; lose feelings. facial nerves. lack of blood

A

Poly-Neuropathies

64
Q

sensory alteration such as parethesias or anesthesia, motor alteration including deformed feet such as hammertoes

A

Distal symmetric polyneuropathy

65
Q

gastroparesis, bowel incontinence, neurogenic bladder, impotence, orthostatic hypotension, resting tachycardia, loss of warning signs of hypoglycemia

A

Autonomic neuropathy

66
Q

such as pain radiating across back, side and front of chest or abdomen

A

Sensory and reflex loss (Focal Neuropathies)

67
Q

diplopia or ptosis

A

Cranial nerve palsies

68
Q

carpal tunnel syndrome, footdrop

A

Entrapment (Focal Neuropathies)

69
Q

sensory impairment in sole of feet, weakness of intrinisic muscles of feet, burning pain & parethesias

A

Posterior tibial nerve damage (Focal Neuropathies)

70
Q

Sensory and reflex loss
Cranial nerve palsies
Entrapment
Posterior tibial nerve damage

A

Focal Neuropathies causes

71
Q
  • The symptoms of diabetes plus a casual plasma glucose value more than 200 mg/dl. (A casual blood glucose value is obtained without regard to the last meal)
  • A fasting plasma glucose level more than 126 mg/dl.
  • The plasma glucose value in a 2 hr. sample of the oral glucose tolerance test is more than or equal to 200 mg/dl. The test should be performed using a loading dose of 75 grams of anhydrous glucose.
A

Dx of Diabetes

72
Q

Type I is an autoimmune disease with the presence of autoantibodies to proteins. The presence of islet cell antibodies (ICA) is an indicator. blood; very expensive

*Measurement of C-peptide levels indicates beta secretory function of the pancreas. C-peptide levels correlate well with insulin levels.

A

So which kind of Diabetes?

73
Q

Type I is an autoimmune disease with the presence of autoantibodies to proteins. The presence of islet cell antibodies (ICA) is an indicator. blood; very expensive

  • Measurement of C-peptide levels indicates beta secretory function of the pancreas. C-peptide levels correlate well with insulin levels.
  • decrease in C-peptide; Type I DM
  • Pancrease pre-insulin with C-peptide gets to liver. C-peptide takes off insulin. hangs in liver. Increase C-peptide adequate insulin.
A

So which kind of Diabetes?

74
Q

Fasting Plasma Glucose more than or equal to 100 and less than 126 mg/dl.

  • Sometimes known as Pre-diabetes.
  • Can lead to Metabolic syndrome.
A

Insulin Physiology Impaired Fasting Glucose

75
Q
  • They are age 45 or older.
  • If they are obese
  • have an immediate family relative with Diabetes
  • member of a high risk ethnic group.
  • delivered a baby more than 9 lbs.
  • Hx of gestational diabetes
  • have HTN, HDL cholesterol less than 35 mg/dl or
  • Triglyceride level of 250 mg/dl or more
  • Dx with Impaired fasting glucose
A

Individuals should be screened for Diabetes if

76
Q
  • Fasting blood glucose.
  • Glycoslated hemoglobin assays (HbA1c levels); tells you amount of glucose that attaches to RBC; 120 days RBC, takes on more glucose than should. Normal is 6%. 6.5-7 or above is a problem. 7-10% severe problem
  • Urine glucose and ketone levels
  • urine test for presence of protein (albumin)
  • Serum Cr. levels
  • Serum Electrolytes
A

Monitoring Diabetes

77
Q

*Type-1; Insulin
*Type 2; usually with oral diabetes medications but, at times may require insulin; After 10-15 years go on insulin; bc of build up insulin
*Gestational; Usually insulin if diet does not seem to control condition.
practice diff. then in book (insulin only in book); women can still stay on orals if pregnant

A

Managing Diabetes: Pharmacologic Treatment of DM

78
Q

Mimic the normal pattern of insulin secretions as closely as possible.

  • Insulin: Synthetic (using recombinant DNA)
  • Insulin Analogs
A

Goal of Insulin Therapy

79
Q

Onset of Action
Peak Effect
Duration of action
***Need to know when blood will be affected by insulin

A

Characteristics of Insulin

80
Q

*Type-1; Insulin
*Type 2; usually with oral diabetes medications but, at times may require insulin; After 10-15 years go on insulin; bc of build up insulin; Drugs, exercise, and diet
*Gestational; Usually insulin if diet does not seem to control condition.
practice diff. then in book (insulin only in book); women can still stay on orals if pregnant

A

Managing Diabetes: Pharmacologic Treatment of DM

81
Q
  • Rapid-acting; covers the meal immediately following injection
  • Short-acting
  • Intermediate-acting; covers subseq meals
  • Intermediate; and short-acting mixtures
  • Long-acting-Lantus (glargine); constant level of insulin & controls
A

Types of Insulin

82
Q
  • Lipodystrophy; same place, harden like cellulite
  • Lipoatrophy; dimpeling; use different place
  • Insulin Resistance; build up over time
A

Complications of Insulin Therapy

83
Q
  • Lipodystrophy; same place, harden like cellulite
  • Lipoatrophy; dimpling; use different place
  • Insulin Resistance; build up over time
A

Complications of Insulin Therapy

84
Q
  • Extremes of temperature
  • Exposure to light
  • Lantus insulin
A

Storage of Insulin; AVOID

85
Q
  • Subcutaneous route
  • IV route; regular insulin only
  • Insulin Pump; (AKA; continuous sub. infusion)
  • Fasting acting insulin only
A

Insulin can be administered

86
Q

-Reducing insulin resistance.
-Augmenting insulin secretion or replacing insulin
Gut; carb metabolism; liver; elevate glucose production.
muscle decrease uptake of insulin/resistance

A

Type 2 DM; real time insulin pump/monitor

Pharmacological Goals

87
Q
  • Sulfanylureas; increase production insulin from pancreas
  • Meglitinides Analogues; increase production insulin from pancreas and others
  • Biguanides; Metformin *Popular type 2 Diabetes; Important drug. can cause kidney issues; must hydrate!!
  • Alpha-Glucoside inhibitors;
  • Thiazolidenediones (AKA; Insulin Sensitizing Agents)
A

Oral Antidiabetic Agents

88
Q
  • Are related to the sulfonamides but lack antibacterial action.
  • Stimulate the pancreas to produce insulin
  • Increase the sensitivity of peripheral tissue to insulin
  • 2nd generation; Glipizide (Glucotrol, Glucotrol XL); Glycuride (Micronase); Glimepride (Amaryl)
A

Sulfonylureas (Oral Antidiabetic Agent)

89
Q
  • Has many of the same actions as sulfonylureas-increase insulin release to treat postprandial hyperglycemia but they act rapidly and have a short duration of action.
  • Their effects are glucose dependent, decreasing when the patient’s blood glucose level decreases.
  • REPAGLINIDE; (Prandin) & Nateglinide (Starlix)
A

Meglitinides analogues (Oral Antidiabetic Agent)

90
Q

The three mechanisms whereby the Biguanides work are:

  • reduce liver production of glucose thereby reducing fasting blood glucose release
  • reduces intestinal absorption of glucose
  • increases cells sensitivity to insulin
  • only one in the USA; Metformin (Glucophage)
A

Biguanides; Antihyperglycemic agents

Metformin!

91
Q
  • Inhibits the work of the intestinal enzyme Alpha-Glucoside to slow carbohydrate digestion and delay glucose absorption.
  • Acarbose (Precose), Miglitol (Glyset)
A

Alpha-Glucoside Inhibitors

92
Q
  • Directly stimulates peripheral glucose uptake and storage.
  • Inhibits glucose and triglyceride production in the liver
  • Rosiglitazone (Avandia)-concern for heart-related deaths, bone fractures and macular edema. Pioglitazone (Actos) not a concern at this time.
A

Insulin Sensitizing Agents

Glitazone or Thiazolidinedione

93
Q
  • *Combination agent: Glucovance; combines glyburide (a sulfonylureas) with Metformin (a biguanide)
  • *Amylin analogues-Pramlintide (Symlin): delays gastric emptying, reduces after-meal blood glucose levels and triggers satiety in the brain.
  • *Incretin analgues; agents lower plasma glucose levels. Exenatide (Byetta)
  • *DPP-IV inhibitors; slow the inactivation of incretin hormones; Sitagluiptin (Januvia)
A

Newer Drugs

94
Q
  • Maintain bld. glucose levels as near normal by balancing; activity, food intake & insulin or oral glucose lowering meds.
  • Achieve optimal blood lipid levels.
  • Provide adequate calories for maintaining reasonable wt.
  • Preventing complications.
A

Goal of Nutritional Therapy in Diabetes

95
Q
  • Protein; 10 to 20% of the total kcalories.
  • Fats; 30% or less of total kcalories and less than 7% from saturated fat.
  • Carbohydrates; 45-60% of the total kcalories. [Important to know control of carbs for diabetes]
  • Fiber; 25 grams/day; keeps you full
A

ADA. Nutritional recommendations/day

96
Q
  • Carbohydrate counting
  • Exchange list; weight watchers, etc
  • Alcohol consumption
  • prevent weight gain
A

Diet control strategies

97
Q
  • Insulin or oral antidiabetic agents should be taken
  • Attempt to eat frequent small amounts of CHO
  • Fluid intake is important for avoiding dehydration
  • Blood glucose and urine ketones should be checked q 4 hrs.
  • *take insulin bc glucose levels go up! EAT!!
A

Sick Day rules for Diabetics

98
Q
  • Avoid exercise if frequent episodes of hyper/hypoglycemia.
  • Type I diabetic should perform exercise when bl. glucose levels are 80 to 250 mg/dl. and No ketones are present in the urine.
  • Exercising at peak insulin action time may lead to hypoglycemia
  • food intake may need to be increased.
  • Fluid intake is essential
A

Exercise Guidelines DM

99
Q
  • Begin training slowly, extending activity over a prolonged period
  • May have to take a carbohydrate drink (5 to 10%) before, during or after 1 hour of exertion
  • Monitor glucose level
  • Carry a simple sugar, such as hard candy in case of hypoglycemia symptoms.
A

Exercise promotion DM

100
Q
  • Whole pancreas transplantation

- Islet cell transplantation; severely sick long term from Diabetes

A

Advances; DM

@Nur 180 Exam 3 (6 decks)

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