Download DIABETES PACKET

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DIABETES CLINICAL PACKET
PLEASE ANSWER ALL QUESTIONS IN YOUR OWN WORDS.
EACH SECTION.
July 20, 2012
Name: Birgit Humpert
LIST YOUR REFERENCES AT THE END OF
A.) MEDICAL TERMINOLOGY
1. Describe the primary function of the following endocrine glands
a. Adrenal gland – Releases stress hormones ("fight or flight") like cortisol (which has an
anti-inflammatory effect and increases blood glucose by mobilizing stored glucose),
epinephrin and norepinephrin (which stimulate the nervous system, heart, lungs, and
blood vessels). It also produces aldosterone which increases reabsorption of sodium and
potassium secretion.
b. Hypothalmus – Provides a connection between the nervous system and the endocrine
system. Controls metabolic processes through hormones that in turn stimulate or inhibit
the pituitary gland to release hormones.
c. Ovaries – Produces estrogen and progesterone, the main female hormones that control the
development of female sex characteristics and the function of female reproductive
organs.
d. Pancreas – Produces insulin and glucagon to control blood sugar levels.
e. Pituitary gland – "The master gland" controls many other endocrine glands. It releases for
example thyroid-stimulation hormone (stimulates the thyroid), prolaction (initiates and
maintains breast milk production), oxytocin (controlls muscles of the uterus and milk
ducts), adrenocorticotropic hormone (controls release of hormones by the adrenal
glands), growth hormone (promotes protein production and controls growth and
development), antidiuretic hormone/vasopressin (increased water reabsoption and
promotes vasoconstriction), luteinizing hormone, and follicle-stimulation hormone.
f. Testes – Produces primarily testosterone which controls the development of male sex
characteristics and the male reproductive system.
g. Thymus – Produces thymosin which is important for the development and function of T
lymphocytes.
h. Thyroid – Release tetraiodothyronine (T4) and triiodothyronine (T3) which regulate the
metabolic rate, as well as calcitonin which increases uptake of calcium into the bones.
References:
Porter, R.S., Kaplan, J.L. (Eds.) The Merck Manual Home Health Handbook
for Health Care Professionals
Nelms, M., Sucher, K.P., Lacey, K., Roth, S.L. (2011). Nutrition Therapy &
Pathophysiology (2nd ed.). Belmont, CA: Wadsworth
Escott-Stump, S. (2011). Nutrition and Diagnostic Related Care (7th ed.). Lippincott
Williams & Wilkins
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2. Provide definitions for the following terms:
a. Endocrinopathy – Any disorder of an endocrine gland that effects the hormone
production or release.
b. Hyperinsulinism – Increased levels of insulin leading to hypoglycemia.
c. Acromegaly – Hypersecretion of growth hormones by the pituitary gland after the
epiphysis is closed. This disorder results in changes of facial features, swelling of hands,
feet, and internal organs, changes of the skin and hair, as well as increased sweating.
Often causes by a tumor in the pituitary gland.
d. diabetes insipidus –Diabetes insipidus is the result of a deficiency of antidiuretic hormone
or changes in the kidney's response to antidiuretic hormone. If the causes is a decreased
production of ADH it can be due to a genetic abnormality or due to injury or diseases
effecting the hypothalamus (where ADH is produces) or the pituitary gland (where ADH
is stored). The result is excessive thirst and urine production (polydipsia and polyuria)
because the urine can not be concentrated.
e. SIADH – Syndrome of inappropriate antidiuretic hormone is characterised by
hyponatremia and hyperosmolarity of urine due to increased secretion of ADH. Total
body water is increased. It is associated with many different diseases.
f. Hypothyroidism – Deficiency of thyroid hormone most often due to an autoimmune
desease (Hashimoto's disease). Since thyroid hormone controls metabolic rate a
deficiency in adults results in weight gain, fatigue, bradycardia and other symptoms. In
children congenital hypothyroidism results in cretinism (dwarfism and mental
retardation).
g. Hyperthyroidism – An excess of thyroid hormone which is most often caused by an
autoimmune disease called Grave's disease, thyroiditis or other abnormalities of the
thyroid gland. The result is an increase in metabolic rate with weight loss, tachycardia
and exophthalmos.
h. Hyperparathyroidism – Excessive release of parathyroid hormone either due to an
overproduction (primary hyperparathyroidism) or due to renal failure (secondary
hyperparathyroidism). It can lead to hypercalcemia.
i. Hypoparathyroidism –Deficiency of parathyroid hormone due to autoimmune disease or
more common due to injury to the parathyroid glands during thyroidectomy . It leads to
hypocalcemia and hyperphosphatemia and can result in chronic tetany.
j. Cushing syndrome –Cushing syndrome is a high blood level of cortisol due to a ACTHsecreting tumor or medication. Results in obesity especially in the upper body with moon
face, fatigue, muscle weakness and other symptoms
References:
Porter, R.S., Kaplan, J.L. (Eds.) The Merck Manual Home Health Handbook
for Health Care Professionals
Nelms, M., Sucher, K.P., Lacey, K., Roth, S.L. (2011). Nutrition Therapy &
Pathophysiology (2nd ed.). Belmont, CA: Wadsworth
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Escott-Stump, S. (2011). Nutrition and Diagnostic Related Care (7th ed.). Lippincott
Williams & Wilkins
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B.) DIABETES, DISEASE AND CONDITIONS:
PLEASE ANSWER ALL SECTIONS USING YOUR OWN WORDS.
For each of the following you are given the definition and etiology. You should provide the
pathophysiology of disease process and progression; disease impact on nutrition status; and
dietary recommendations when needed:
a. Definition
b. Etiology
c. Describe the physical changes specific to the disease process and progression (pathogenesis).
d. Explain how the disease impacts the patient’s nutritional status (in some cases there will be
no impact.)
e. Is a modified diet recommended for this condition? If so what is the diet prescription?
Refer to GI Packet, GI-related diseases and conditions, hemorrhoids, for an example
1.
Type 1 Diabetes
a. Definition: A metabolic disease involving altered carbohydrate, protein and fat
metabolism in which high blood sugar results from inadequate insulin secretion by the
pancreas. Most commonly diagnosed between ages of 5 and 20.
b. Etiology: Immune mediated type 1 diabetes results when an autoimmune attack
destroys the beta cells of the pancreas. There may be genetic or environmental
(exposure to viruses or toxins) factors associated with development of type 1 diabetes.
Idiopathic type 1 diabetes is also caused by destruction of beta cells but does not
appear to have autoimmune involvement.
c. Pathogenesis: Because of the insulin deficiency blood glucose can not get into cells and
blood glucose levels increase. This leads to a variety of pathophysiological
consequences.
- hyperglycemia leads to glucosuria (loss of glucose in the urine), glucose pulls water
along and this causes polyuria
- due to this osmotic diuresis the body loses water, dehydration is the consequent with
increased thirst/polydipsia,
- decreased fluid volume can contribute to weight loss; hypovolemic shock can be fatal,
the decreased fluid volume can also lead to renal complications
- because tissue cells don't get fuel the body tries to compensate with increased hunger
and polyphagia
- to provide energy fat and protein is broken down, this can lead to muscle wasting and
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weight loss
- lipolysis leads to the production of keto acids from fatty acids. These keto acids leads
to a decrease of pH in the body. To compensate the patient shows Kussmaul respiration
(deep labored breathing) and acetone can be smelled on the breath (fruity smell).
Glycosylation – With high blood glucose levels glucose bonds with hemoglobin
and other proteins in the body. The formation of these advanced glycosation end
products leads to many of the complications seens with diabetes, like renopathy,
nephropathy, and neuropathy.
Acidosis – The production of keto acids leads to metabolic acidosis/diabetic
acidosis.
Ketones – Keto acids are produced from fatty acids to provide energy. This leads
to metabolic acidosis and ketone bodies can be detected in the urine.
d. Nutritional Status: Undiagnosed diabetes leads to a state of starvation. Lipolysis and
muscle catabolism lead to weigth loss despite increased food intake (polyphagia).
e. MNT: The most important goal of nutritional therapy is to control blood glucose levels
to minimize the risk for complications. Since carbohydrates effect blood glucose most,
therapy focuses on this macronutrient. Carbohydrate intake can then be offset by
appropriate insulin therapy. This can be done by carbohydrate counting or through the
exchange list. Recommendations for protein, fat, and carbohydrate intake are the same
as with healthy individuals. Individual needs, preferences, meal patterns, and so on can
be taken into consideration. With the carbohydrate counting system the energy needs of
the patient are estimated (usually from what they usually have, unless weight loss is a
goal). About 50 - 55 % of energy should come from carbohydrates. The amount of
carbohydrates per day is than spread out evenly over the day. The amount of food
(starches, fruit, sweets, milk and dairy) that contains 15 g of carbohydrates is counted
as one carbohydrate choice. Carbohydrate intake is balanced with insulin dosage. 1 unit
of insulin is needed for 10 - 15 g of carbohydrates.
Education not only about nutrition but also about exercise, the effect of alcohol, and
self-monitoring of glucose are also important components of the therapy.
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2.
July 20, 2012
Type 2 Diabetes
a. Definition: A metabolic disease in which high blood sugar results from insulin
resistance in peripheral tissues, may also include a relative deficiency in insulin
secretion.
b. Etiology: Obesity is the most powerful predictor of type 2 DM. There is a strong
genetic influence as well. Prevalence is higher in African American and Hispanic
American populations, and highest in Native Americans. Incidence increases with age
and DM is more common in women than in men.
c. Pathogenesis: Tissue cells can not take in glucose due to a defect in the receptor that
binds with insulin. The body responds to increase blood glucose levels by producing
more insulin resulting eventually in diminished production by the pancreas. At first
hyperglycemia occurs after meals when the tissue can not take in blood glucose. As the
disease progresses fasting hyperglycemia occurs as the liver produces more glucose
through gluconeogenesis and glycogenolysis. Onset of Type II diabetes is usually slow
and patients remain without clinical symptoms for some time. They might have
polyuria, polyphagia, or polydipsia. Sometimes they can become severely dehydrated,
especially if they have another acute illness (see hyperglycemic, hyperosmolar
syndrome). They might have blurred vision or tingling of feet and hands, which are
early signs of microvascular damage. Diagnosis sometimes occurs though routine
screening or through long-term complications like retinopathy, neuropathy, and
nephropathy.
d. Nutritional Status: Type II diabetes often does not produce clinical symptoms for some
time and does not effect nutritional status. Most of the patients are obese.
e. MNT: Since many patients are obese weight loss is often the most important therapy.
Since diabetes as well as obesity are also a risk factor for cardioascular disease the
therapy not only focuses on blood glucose control but also on the control of increased
cholesterol levels and hypertension. If carbohydrate counting is used the amount of
energy needed is based on the amount of energy needed to achieve weight loss. To
address protein, fat, and fiber intake and achieve an overall healthy diet that decreases
the risk for complications and the risk for cardiovascular disease the Therapeutic
Lifestyle changes diet is recommended. Consistent exercise and self-monitoring of
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blood glucose are also important components of the therapy.
3.
Gestational Diabetes
a. Definition: A disorder occurring in pregnancy and characterized by an impaired
ability to metabolize CHO, may be caused by insulin deficiency or insulin resistance.
b. Etiology: Gestational diabetes mellitus results from a woman's inability to secrete
sufficient insulin to compensate for increased nutritional needs of gestation, increased
adiposity of pregnancy, and increased secretion of other hormones during pregnancy.
These specifically include: anti-insulin hormones, such as human placental lactogen,
prolactin, cortisol, and progesterone. In general it is thought that these women have
both decreased insulin secretion and insulin resistance.
Pregnant women may require two to three times as much insulin as compared to their
prepregnant state. Other risk factors are similar to those for type 2 diabetes – obesity,
family history, increased age.
c. Pathogenesis: Gestational diabetes is similar to Type II diabetes in pathophysiology.
Tissue cells can not take in glucose and this insulin resistance combined with
inadequate insulin production leads to increased blood glucose levels. There is a routine
screening for gestational diabetes so that patients are usually diagnosed before
symptoms occur. Gestational diabetes is often associated with polyhydramnios
(increase of amnionic fluid) and hypertension in the mother. Since the fetus is also
exposed to high blood glucose levels it increases insulin production. Glucose is stored
as fat and babies are usually large (macrosomia) and this may lead to birth
complications or the need for cesarean sections. Gestational diabetes can also lead to
preterm labor, spontaneous abortion, stillbirth, and congenital abnormalities The babies
can also have hypoglycemia and other complications after birth and are at increased
risk for obesity, diabetes and hypertension later in life.
d. Nutritional Status: Gestational diabetes itself does not effect nutritional status but
patients are often obese or overweight.
e. MNT: Since oral diabetes medication can not be given during pregnancy, diet and
exercise are the main treatment option. If blood glucose control can not be achieved
insulin might be needed.
Energy intake should be estimated depending on weight gain goals. If the patient is
overweight a weight gain of 15 - 25 lb is recommended, if the patient is obese a weight
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gain of 11 - 20 lb is enough. The diet should contain about 40 - 50 % carbohydrates,
mainly as complex carbohydrates from whole grains, vegetables, and fruit. The intake
of simple sugars should be limited. Carbohydrates should be spread out over the day
(for example 3 meals and 2-3 snacks).
4.
Prediabetes
a. Definition: Higher than normal blood sugar but not elevated enough to be diagnostic
of diabetes.
b. Etiology: Similar to type 2 DM, typically occurs in overweight and/or sedentary
individuals. May also be temporary in response to medications. Check Vitamin D
levels as low Vitamin D contributes to increased glucose levels.
c. Pathogenesis: Similar to type 2 diabetes. The patients shows higher blood glucose level
after fasting and after oral glucose tolerance test. But insulin resistance is not yet as
severe and insulin production not as increased as in type II diabetes. Most patients
develop type II diabetes within 10 years unless they make some lifestyle changes (lose
weight, increase exercise, modify diet).
d. Nutritional Status: Many patients are obese or overweight.
e. MNT: Similar to type II diabetes with lifestyle changes that address weight, diet, and
exercise. Slow weight loss that can be maintained is often the first therapy goal. The
diet should contain more complex carbohydrates, with an appropriate intake of fiber,
and less simple sugar. Recommendations for fat intake can be taken from the
Therapeutic Lifestyle Changes Diet.
5.
Ketosis
a. Definition: The abnormal elevation of ketone bodies in the blood, in response to fatty
acid metabolism that occurs when there is inadequate intake or metabolism of
carbohydrates.
b. Etiology: May result from starvation, fasting or very low carbohydrate diets because
they all provide inadequate glucose for normal metablolism. Ketosis may also occur in
untreated or poorly controlled type 1 DM because the cells cannot use the blood
glucose due to lack of insulin.
c. Pathogenesis: If the body does not get sufficient energy from glucose fatty acids are
converted to keton bodies which can provide energy. An increase of ketone bodies in
the blood leads to acidosis. Increased ketone bodies in the blood together with acidosis
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and hyperglycemia is called diabetic ketoacidosis.
The symptoms of ketosis are fruity breath, nausea and vomiting, abdominal pain,
headaches, fatigue, and changes in mental status.
d. Nutritional Status: Nausea, vomiting and fatigue can impact nutritional status. They
may interfere with food intake and can make the problem worse.
e. MNT: Therapy depends on the cause of ketosis. If diabetes is not the cause intake of
carbohydrates can inhibit keton production. If diabetes is the cause insulin therapy is
necessary so that glucose can enter tissue cells.
6.
Hypoglycemia: Insulin induced
a. Definition: Low blood sugar induced by excessive insulin relative to food intake -70mg/dl or lower.
Note: oral medications can also cause hypoglycemia!
b. Etiology: May be caused by excessive insulin administration, skipped meals or
inadequate food intake, improper timing of doses relative to meals, unplanned or
increased exercise.
c. Pathogenesis: A decrease in blood glucose triggers the release of several hormones, like
glucagon and epinephrin. Usually glucagon leads to an increase of blood glucose by
releasing stored glucose. The release of epinephrin leads to tachycardia, palpatations,
feeling of weekness, fatigue, blurred vision, and sweating. Severe hypoglycemia can
lead to confusion and coma.
d. Nutritional Status: Usually no immidiate impact on nutritional status.
e. MNT: Food intake needs to be matched with insulin intake and exercise to avoid
hypoglycemia. To treat acute hypoglycemia the "rule of 15" is used: 15 g of fast acting
carbohydrates (1/2 glass juice or soda, 3-4 glucose tablets) are given every 15 minutes
until blood glucose is normalized. Than a snack consisting of protein and carbohydrates
is given.
7.
Hypoglycemia: Reactive
a. Definition:
b. Etiology: It is unrelated to diabetes. The exact cause is unknown and may vary
between individuals. This makes it difficult to diagnose. May be a response to over
secretion or over sensitivity to epinephrine, may be due to deficiencies of glucagon, or
over secretion of insulin. Could be due to unplanned activity or insulinoma, or may be
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related to dumping syndrome after stomach surgery.
c. Pathogenesis: Pathogenesis depends on the cause. It occurs usually postprandial. Intake
of a high amount of carbohydrates results in an high insulin response. Either too much
blood glucose is cleared or countermeasurements (glucagon, epinephrin) are not
working correctly. In dumping syndrome food enters the intestines very rapidly and
carbohydrates are ingested very fast resulting in a increased release of insulin and a
subsequent drop. Symptoms are the same as in insulin induced hypoglycemia.
d. Nutritional Status: Reactive hypoglycemia is only a short-term symptom and does not
lead to changes in nutritional status.
e. MNT: To avoid hypoglycemia regular meals and snacks with complex carbohydrates
and foods with low glycemic index can help to maintain stable blood glucose levels.
8.
Hypoglycemia: Fasting
a. Definition:
b. Etiology: Evening insulin dose too high or food intake too low, may have skipped
evening snack.
c. Pathogenesis: Blood glucose levels are low after a periode of fasting, for examle
overnight. Symptoms are the same as in insulin induced hypoglycemia.
d. Nutritional Status: Does not effect nutritional status.
e. MNT: Insulin therapy, diet and exercise should be coordinated so that blood glucose
levels remain stable. An appropriate evening snack is important.
9.
Dawn phenomenon
a. Definition: Rise in blood sugar level in the early morning, between 4-5:00 and 8-9:00
AM
b. Etiology: May occur in type 1 or type 2 diabetes
c. Pathogenesis: In preparation for the day the body releases growth hormone, cortisol,
and catecholamines which make blood sugar rise and counter the effect of insulin.
d. Nutritional Status: No immediate impact on nutritional status.
e. MNT: Dawn effect is usually treated by changing dose or timing of insulin
administration to achieve a better blood glucose control in the morning.
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10. Somogyi effect
a. Definition: Hyperglycemia as a result of a rebound effect in which too much insulin
induces hypoglycemia.
b. Etiology: Usually excessive insulin doses in the evening.
c. Pathogenesis: During the night an episode of hypoglycemia occurs that goes
unnoticed. As a response to this hypoglycemia glucagon leads to a rise in blood glucose
levels. To determine if hyperglycemia in the morning is due to the dawn effect or the
Somogyi effect the patient can check blood glucose in the night. It blood glucose is low
in the middle of the night but high in the morning this is due to the Somogyi effect.
d. Nutritional Status: No immediate impact on nutritional status.
e. MNT: To avoid hypoglycemia in the night, insulin dose can be adjusted and a snack
can be eaten later in the evening.
11. Honeymoon phase
a. Definition: Brief remission of diabetes experienced by people with newly diagnosed
type 1 diabetes.
b. Etiology: As diabetes is treated, and the patient regains their health, the pancreas may
start secreting some insulin again. This may last weeks or up to a year. The insulin
secretion eventually stops and medications need to be adjusted.
c. Pathogenesis: Some patients who are newly diagnosed with type I diabetes and start
treatment experience a phase when the body still produces some insulin. This results in
decreased insulin need and usually good blood glucose control during that time.
d. Nutritional Status: At this point the initial symptoms of polyuria, polydipsia, and
polyphagia have disappeared and the nutritional status is good.
e. MNT: Even though the body produces some insulin the patient should be educated
about carbohydrate counting, the effect of exercise and all other aspects of the disease
to be well prepared when the time of remission is over.
The following complications are often associated with diabetes although they may have
other causes. For this clinical packet on Diabetes, describe the etiology and
pathophysiology associated with diabetes:
12
Nephropathy
a. Definition: Nephropathy is any disease of the kidneys. Diabetic nephropathy is renal
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disease that is caused by microvascular damage from high blood glucose levels.
b. Etiology: In 20 - 40 % of diabetics in type I and type II diabetic nephropathy develops.
Diabetes is the leading cause of chronic kidney disease that eventually needs to be
treated with dialysis and/or kidney transplantation.
c. Pathophysiology: Diabetes causes kidney disease by damaging the glomerulus, the
capillary tuft inside each nephron (functioning units of the kidney). It comes to
thickening and sclerosis of these small vessels which leads to an increase in
permeability. The filtration function declines and albumin is excreted into the urin.
Over time more and more nephrons are damaged, and the kidney can not clear enough
solutes and the concentration of body fluids increases. At first nephropathy advances
slowly and does not show any signs and symptoms but with advanced nephropathy the
typical symptoms of CKD, like azotemia, hypertension, metabolic acidosis and others
occur. The extend of kidney damage can be measured by albumin secretion into the
urine and by glomerular filtration rate. Albuminuria increases and GFR decreases with
advancing diabetic nephropathy.
d. Impact on patient’s nutritional status: At first there are is no impact on nutritional
status. But with advanced kidney disease, potentially dialysis and dietary restriction
patients often experience protein-energy malnutrition.
e. Describe the appropriate modified diet: Diet modification depend on the degree of
kidney damage. At first the focus is on blood glucose control to slow down the
progression of the disease. Treatment of hyperlipidemia and high blood pressure
through dietary intervention is also important.
With declining GFR it is important to maintain a healthy weight and avoid malnutrition
and weight loss. At this stage protein restriction to 0.6 - 0.75 g/kg with more than 50 %
from sources with high biological value is usually recommended and must be balanced
with the goal of avoiding malnutrition. Sodium, potassium, and phosphorus might be
restricted depending on kidney function. Vitamin and mineral supplements are
sometimes needed, especially vitamin D.
If the patient has to go on dialysis more dietary modifications take place. In general the
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diet is higher in protein, low in sodium, low in fluid. Potassium and phosphorus are
restricted. Calcium, and many other vitamins and minerals must be supplemented due
to losses through the dialysis. There are some differences depending on the type of
dialysis and individual needs. It is also important to maintain weight, and control blood
glucose levels as well as lipid levels.
13. Retinopathy
a. Definition: Damage to the retina, in diabetic retinopathy high blood glucose levels
damage blood vessels in the eye.
b. Etiology: High blood glucose levels can damage the capillaries in the back of the eye.
Hypertension is another risk factor.
c. Pathophysiology:
Nonproliferative - Hyperglycemia causes blood vessels to become more
permeable. It comes to small aneurisms, bleeding and macular ischemia. Fluid
leeks from the capillaries and causes mascular edema. The patient might
experience blurred vision or see spots that can come and go.
Proliferative – Is more severe and develops secondary to nonproliferative
retinopathy. New blood vessels form on the inner side of the retina
(neovascularization) and can cause bleeding into the inner, transparent substance
of the eye. The retina can become detached. Neovascularization on the iris can
result in glaucoma. The patient can experience blurred vision and see black spots
or flashing. It can come to vision loss. Retinopathy is the leading cause of new
blindness.
d. Impact on patient’s nutritional status: Retinopathy has no direct impact on the
nutritional status. Blindness can make tasks of daily life, like grocery shopping and
meal preparation challenging and might therefor have an impact on nutritional status.
e. Describe the appropriate modified diet: To slow down the progression of the disease
good blood glucose and blood pressure control through diet, medication, and exercise is
important.
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14. Neuropathy
a. Definition: Damage to the nervous system that results in loss of sensation, pain, or
slow digestion of food.
b. Etiology: Hyperglycemia as a result of poorly controlled diabetes leads to
microvascular damage, damage of neurons and other changes that have an effect on
nerve function. Neuropathy develops in 60 - 70 % of patients.
c. Pathophysiology: Glycated proteins damage neurons and nerves in the peripheral and
central nervous system. There are different forms of neuropathy.
In symmetric polyneuropathy the hands and feet are effected, often there is a painless
loss of feeling for temperature and pain, which can lead to injury, ulceration and
infection. Foot screening is a common diagnostic tool used in diabetic patients. These
patients are at an increased risk for amputations.
Autonomic neuropathy can effect the GI tract, the genitourinary tract, or the
cardiovascular system. Different sections of the GI tract can be effected; the patient can
have gastroparesis (delayed emptying of the stomach), fecal incontinence, constipation,
diarrhea, and dumping syndrome. In the genitourinary tract it can come to incontinence,
urinary retention (with infection) and sexual dysfunction.
Cardiovascular autonomic neuropathy can result in tachycardia, hypotension, exercise
intolerance, and an increased risk for heart disease.
d. Impact on patient’s nutritional status: Gastroparesis and other problems in the
gastrointestinal tract have the most impact on nutritional status. The patient might
experience nausea, vomiting, anorexia, dysphagia, and early satiety. Both delayed
gastric emptying or dumping syndrome can make blood sugar control challenging.
e. Describe the appropriate modified diet: To deal with gastointestinal problems,
especially gastroparesis several diet modifications are possible. See below. To deal
with constipation fiber intake and fluid intake can be increased. With diarrhea soluble
fiber can can help. With diarrhea there is danger of dehydration that needs to be
addressed. With gastroparesis as well as with dumping syndrome small, frequent meals
should be eaten.
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15. Gastroparesis
a. Definition: Delayed gastric emptying.
b. Etiology: Hyperglycemia in diabetes can damage the vagus nerve and impact
peristaltic.
c. Pathophysiology: If the vagus nerve is damaged motility is slowed down. It can come
to nausea, vomiting, early satiety, and dysphagia. Further complications are infections,
formation of bezoars (mass in the stomach that causes obstruction), and ketoacidosis.
d. Impact on patient’s nutritional status: With Gastroparesis the patient might experience
nausea, vomiting, anorexia, dysphagia, and early satiety. This can lead to malnutrition
and weight loss. Blood sugar control can be difficult.
e. Describe the appropriate modified diet: Small frequent meals, reduced fat, soft/liquid
foods can help with the symptoms of gastric paresis. As always a good blood glucose
control is the goal. Insulin timing might be modified to better meet delayed,
postprandial needs. Tube feeding might be considered with malnutrition. The patient
should be upright during eating and increase motility by walking after meals.
16. Compare and contrast diabetic ketoacidosis and hyperglycemic hyperosmololar
nonketotic syndrome (HHNK). What are the causes? Include what is happening
physiologically. Are ketones present? What are the differences in pathophysiology?
What is the treatment?
Diabetic Ketoacidosis
Causes
High blood glucose levels, either because of undiagnosed
diabetes, insufficient insulin administration due to increased
needs or pump malfunction, alcohol/drug abuse, acute illness,
infection, or psychological stress.
HHNK
Very high blood glucose levels and dehydration due to
illness/infection and inadequate fluid intake. Diabetes might
not have been diagnosed, yet.
Diabetic Ketoacidosis
Pathogenesis
Hyperglycemia due to insufficient insulin causes lipolysis to
provide energy. It comes to an increase in keto acids in the
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blood. Hyperglycemia also leads to osmotic diuresis,
dehydration, and electrolyte imbalances. Blood glucose >250
mg/dl, ketones can be detected in serum and blood.
HHNK
Hyperglycemia leads to osmotic diuresis, dehydration, and
electrolyte imbalance. Blood glucose levels are >600 mg/dl
and osmolality is >320 mOsm/kg.
Presence of Ketones (Y/N)
Diabetic Ketoacidosis
Yes
HHNK
No
Similarities
Similarities
Both are characterized by hyperglycemia and dehydration.
Patients have polyuria and polydipsia,
Diabetic Ketoacidosis
Differences
Keton bodies are present and this leads to nausea, vomiting,
hyperventilation, Kussmaul ventilation, and fruity smelling
breath. Usually develops faster. Occurs more often in type I
diabetes, but type II diabetics can also have it.
HHNK
There is enough insulin to prevent ketogenesis. Blood glucose
levels higher than in diabetic ketoacidosis. Develops more
slowly and has less symptoms. Patients can have a fever due to
the underlying infection. Usually occurs in type II diabetes,
often in elderly patients in long-term care facilities.
Diabetic Ketoacidosis
Treatment
Administration of fluids and insulin. Treatment of electrolyte
imbalances if necessary.
HHNK
Slow
rehydration
and
treatment
of
the
underlying
infection/illness. Sometimes insulin is administered.
References:
Porter, R.S., Kaplan, J.L. (Eds.) The Merck Manual Home Health Handbook
for Health Care Professionals
Nelms, M., Sucher, K.P., Lacey, K., Roth, S.L. (2011). Nutrition Therapy &
Pathophysiology (2nd ed.). Belmont, CA: Wadsworth
Escott-Stump, S. (2011). Nutrition and Diagnostic Related Care (7th ed.). Lippincott
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Williams & Wilkins
Hypoglycemia (2008) Diabetes Info. National Diabetes Information Clearinghouse. Retrieved
July 22, 2012 from http://diabetes.niddk.nih.gov/dm/pubs/hypoglycemia
Brown, J.E. (2011) Nutrition Through the Life Cycle (4th ed.) Wadsworth
17. Describe the following lab tests. What do the abbreviations mean, how are they used
in diagnosis and treatment, and how are the results interpreted?
Full Name of Test
FBS
Fasting blood glucose
How it is Used
Test for high or low blood sugar, to screen for, diagnose, or
monitor diabetes or prediabetes.
Results
FBS of 100 - 125 mg/dl indicates prediabetes, FBS of >126 mg/dl
is a diagnostic criterium for diabetes.
Full Name of Test
OGTT
oral glucose tolerance test
How it is Used
A drink containing 75 g of glucose is given and blood glucose is
measured 2 hours after. Frequently used to diagnose gestational
diabetes. For diagnosis of gestational diabetes the American
Diabetes Association recommends since 2011 a drink containing
75 g glucose and blood is drawn before testing, after 1 hour, and
2 hours. The American Congress of Obstetricians and
Gynecologists recommends a 100 g glucose drink and testing
before, after 1 hour, after 2 hours, and after 3 hours.
Results
For non-pregnant patients 140 - 200 mg/dl after 2 hours indicates
prediabetes and >200 mg/dl diabetes.
For gestational diabetes the ACOG states that the diagnosis of
gestational diabetes is made if two or more values are high (95
mg/dl before, 180 mg/dl after 1 hour, 155 mg/dl after 2 hours and
140 mg/dl after 3 hours). According to ADA recommendations
the diagnosis is made if one or more values are high (92 mg/dl
fasting, 180 mg/dl after 1 hour, and 153 mg/dl after 2 hours).
HgA1c
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Full Name of Test
Hemoglobin A1c or glycated hemoglobin assays
How it is Used
Measures how much glucose is attached to hemoglobin. High
blood sugar levels lead to increased glycation. Usually to monitor
blood sugar control over a time of 3 month (lifespan of
hemoglobin). Is also used to calculate estimated average glucose
(EAG).
HgA1c is also sometimes used to screen for or diagnose diabetes.
Results
Goal is a HgA1c under 7%. A lower goal might be better to avoid
complications but there is also an increased risk of episodes of
hypoglycemia. Higher number correlates with higher average
blood glucose levels.
18. When would a normal HgbA1c level not be an accurate measure of good glucose
control?
With any disease or condition that effects red blood cells HgA1c is not as accurate, for
example anemia, sickle cell hemoglobin, hemolysis, blood transfusions, or heavy bleeding.
19. Persons with diabetes have a higher incidence of coronary artery disease,
dyslipidemia, hypertension, and stroke. Explain how (pathophysiology) diabetes
increases the risk factors for each of these conditions. Where applicable, describe how
Type 1 and Type 2 may differ.
Coronary artery disease: High blood glucose levels damage all blood vessels in the
body including coronary arteries. Blood vessels get thicker and less flexible. This
contributes to the development of atheroscleric plaques in the coronary arteries and
high blood pressure. Diabetes also contributes to CAD by altering blood lipids.
This happens both in type I and type II diabetes and both groups have an 2 - 4 times
greater risk to die from cardiovascular disease. It's the leading cause of death among
patients with diabetes.
Dyslipidemia: Diabetes is often associated with an increase in triglycerides and a
decrease in HDL cholesterol. Even though LDL is often not increased diabetics have
more small, dense LDL that is especially atherogenic. These changes occur because
lipoprotein lipase which removes triglycerides from chylomicrons is dependent on
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insulin. This happens in both types of diabetes. If type I diabetics have good blood
glucose control their lipid profile is usually normal. In type II diabetes insulin
resistance also contributes to hyperlipidemia because insulin resistance leads to more
free fatty acids. Insulin resistance is also often associated with obesity which also
contributes to hyperlipidemia.
Hypertension: Diabetes contributes to hypertension by damaging blood vessels, they
get thicker and less flexible which can lead to high blood pressure. In type I diabetes
nephropathy can contribute to hypertension.
Stroke: By contributing to atherosclerotic plaques and high blood pressure diabetes
can also increase the risk for strokes.
References:
Mooradian, A.D. (1987) Dyslipidemia in type 2 diabetes mellitus. Nature Clinical
Practice Endocrinology & Metabolism (2009) 5, 150-159. doi:10.1038/ncpendmet1066.
Retrieved July 23, 2012.
Taskinen, M.R. Lipoprotein Lipase in Diabetes. Diabetes Metab Rev. 1987
Apr;3(2):551-70. Retrieved July 23, 2012 from
http://www.ncbi.nlm.nih.gov/pubmed/3552532
Porter, R.S., Kaplan, J.L. (Eds.) The Merck Manual Home Health Handbook
for Health Care Professionals
Nelms, M., Sucher, K.P., Lacey, K., Roth, S.L. (2011). Nutrition Therapy &
Pathophysiology (2nd ed.). Belmont, CA: Wadsworth
Escott-Stump, S. (2011). Nutrition and Diagnostic Related Care (7th ed.). Lippincott
Glucose (2012). Lab Tests Online. Retrieved July 23, 2012 from
http://labtestsonline.org/understanding/analytes/glucose/tab/glance
20. Insulin resistance and hyperinsulinemia are associated with the endocrine disorder
Polycystic Ovarian Syndrome (PCOS). Please answer the following questions about
PCOS:
a. Definition: Group of symptoms that effects female reproduction and is characterized by
high levels of androgens and insulin resistance.
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b. Etiology: The cause is not determined, yet. There is a link to obesity and genetic factors.
Insulin resistance occurs in most patients. Increased levels of insulin stimulate the
production of androgens which in turn decrease the development of follicles and cause
many of the clinical symptoms. High insulin also increase serum triglycerides and decrease
HDL.
c. What are the diagnostic criteria from PCOS: PCOS is diagnosed by looking at
-clinical signs like increased hair growth on face, chest and other body parts (hirsutism),
deep voice, acne, oily skin, dandruff
- laboratory test (serum testosterone, follicle-stimulation hormone, prolactin, and TSH), and
- pelvic ultrasonography (to look for cysts in the ovaries and thickening of the
endometrium).
At least two of three criteria must be met for the diagnosis
-menstrual irregularities due to irregular ovulation
-hyperandrogenism
-more than 10 follicles per ovary
d. Describe the medical complications associated with PCOS: Menstrual irregularities that
can lead to infertility are often a main problem for younger women. PCOS can also cause or
is associated with pelvic pain, obesity with increased weight around the waist, high blood
pressure, triglycerides, cholesterol, and type II diabetes.
e. PCOS and metabolic syndrome have similar signs and symptoms. Describe the
differences between PCOS and metabolic syndrome:
PCOS: Onset of PCOS is earlier in life, it often presents in adolescents. It only
effects women. Abdominal obesity, increases in triglycerides and cholesterol, and
insulin resistance can occur in both PCOS and metabolic syndrome. But the
changes that are causes by increase circulation of androgens and fertility problems
only occure in PCOS.
Metabolic Syndrome: Onset is usually later in life. Can effect men and women.
There is no increase in androgens and changes in ovulation and fertility.
f. Describe the diet modifications prescribed for PCOS and explain the nutrition treatment
goals: If obesity or overweight is present weight loss is prescribed to increase insulin
sensitivity, help with ovulation and other symptoms. Weight loss of 5 - 10% can improve
symptoms. Weight loss can be achieved through a combination of exercise and diet and
should be slow and sustainable. Exercise is an important poart of the treatment because it
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also improves insulin sensitivity and other symptoms of PCOS. Nutrition should focus on a
healthy diet with foods rich in complex carbohydrates and fiber, decreased intake of added
sugar, healthy intake of fat including omega-3 fatty acids, and regular meals.
References:
Nelms, M., Sucher, K.P., Lacey, K., Roth, S.L. (2011). Nutrition Therapy &
Pathophysiology (2nd ed.). Belmont, CA: Wadsworth
Brown, J.E. (2011) Nutrition Through the Life Cycle (4th ed.) Wadsworth
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C.) NUTRITION PRESCRIPTIONS
For each of the following:
a. Describe the diet – include details such as you would when explaining it to a patient
b. Explain the physiological response to the diet as it relates to diabetes
c. Describe the patient for which you would recommend this particular diet:
1. No Concentrated Sweets
Description Any type of sugar and foods can contain large amounts of sugar
should be avoided, this includes honey, syrup, molasses, jam,
jelly, candy, soda and beverages with high sugar content,
cookies, cakes, pastries and any other food that has sugar,
honey, or syrup as a main ingredient.
Response
Can help control blood glucose levels.
Patient
- Type II diabetic. It would be an easy first step for
somebody newly diagnosed with diabetes, because they
don't have to pay attention to other parts of the diet. But
this diet does not take into account the starch content of
food and it's effect of blood sugar level and other
components of the diet. Is usually not recommended for
diabetes anymore
- patient with hypoglycemia unrelated to diabetes
2. Consistent Carbohydrate
Description The intake of carbohydrates is controlled. Amount and
timing of carbohydrate intake is consistent from day to
day and can be matched to medication and exercise.
Carbohydrates are most important for changes in blood glucose
Response
levels and therefor a consistent intake can provides good
control of blood glucose.
All types of diabetes and patients with hypoglycemia unrelated
Patient
to diabetes.
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3. Carbohydrate Counting
Description Carbohydrate counting is a form of a consistent
carbohydrate diet. With the carbohydrate counting system
the energy needs of the patient are estimated. For type I
usually from what they usually have, for type II what they
should have to promote weight loss if overweight is an
issue. About 50 - 55 % of kcals should come from
carbohydrates. The amount of carbohydrates per day is
than spread out evenly over the day. The amount of food
(starches, fruit, sweets, milk and dairy) that contains 15 g
of carbohydrates is counted as one carbohydrate choice.
Carbohydrate intake is balanced with insulin dosage. 1
unit of insulin is needed for 10 - 15 g of carbohydrates.
Can help achieve stable blood glucose levels.
Response
Patient
All types of diabetes, especially type I diabetes because
insulin can be matched to carbohydrate intake.
Can also be used for patients with hypoglycemia.
4. Diabetic Exchange
Description Foods are placed into different groups (starch, fruits,
vegetables, dairy, meat, fat). Foods within each group can
be exchanged because the portion of these foods have a
similar carbohydrate content. A certain number of daily
exchanges is given to the patient. For diabetes this
usually applies to carbohydrate choices/exchanges. Each
portion of starch, fruit and dairy contains about 15 g
carbohydrates.
Response
Can help achieve stable blood glucose levels. If
recommendations are given for other nutrients, for
example fat, these can also help with high cholesterol
level and weight loss.
Patient
Well educated type I or II diabetic. It is especially helpful
for type II because recommendation can go beyond
carbohydrate intake, and can also take fat intake into
account. But the exchange lists are not easy to use and
not appropriate for every patient.
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5. Low Glycemic Load - include explanation of Glycemic Index vs. Glycemic Load
Description The glycemic index of a food compares it's ability to raise
blood glucose to a standard (glucose or white bread). The
glycemic index is given as a percentage. Foods with a
high glycemic index raise blood glucose levels faster and
higher resulting in a release of insulin. In healthy
individuals a high insulin response can lead to fast
clearing of blood glucose levels, hypoglycemia and
hunger. While the glycemic index compares equal
amounts of carbohydrates, the glycemic load takes the
serving sizes of food into account. Glycemic load is
glycemic index multiplied by amount of available
carbohydrates in a portion.
Response
A diet containing mostly food with a low glycemic index or
glycemic load can lead to stable blood sugar levels.
For type II and for patients with hypoglycemia and as
Patient
additional information for patients with type I diabetes.
Since the overall amount of carbohydrates is not
addressed glycemic index alone does not provide enough
control especially for typ I.
6. Explain the mechanism by which dietary fiber stabilizes blood sugar.
Soluble fiber slows down digestion in the upper GI tract. It attracts water and forms a gel. It
slows down the absorption of glucose into the blood stream and can therefor help to stabilize
blood glucose levels.
7. Explain the difference between glycemic index and glycemic load. There are five main
food-related factors that influence a food’s glycemic index. List them and describe how
they affect the digestibility of carbohydrates. (Note, you may need to look beyond the
textbooks to fully answer this question.)
The glycemic index of a food compares it's ability to raise blood glucose to a standard
(glucose or white bread). The glycemic index is given as a percentage. Foods with a high
glycemic index raise blood glucose levels more than those with a low glycemic index. While
the glycemic index compares equal amount of carbohydrates, the glycemic load takes the
serving sizes of food into account. Glycemic load is glycemic index multiplied by amount of
available carbohydrates in a portion.
The glycemic index of a food depends on
- sugar content
- the type of monosaccharide
- type of starch in the food.
- processing, cooking
- other food components, like protein, fat, fiber
- acid content of the food.
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8. Discuss your personal philosophy/opinion on the use of artificial sweeteners in the
diabetic and non-diabetic population. Include your rationale.
Even though the FDA has approved the use of artificial sweeteners and the American
Dietetic Association has stated that they are safe I do not recommend them to patients. There
is still some controversy about potential health consequences like cancer. Different countries
have approved/banned different sweeteners, for example saccharin is not allowed in Canada,
while cyclamat is allowed in Germany but not in the US. This shows there is still some
concern. And they should also not be used in high amounts and it is usually hard for
consumers to determine the safe range. Artificial sweeteners are also used in products that
are highly processed and don't provide much nutritional value.
For non-diabetic patients I would recommend a diet that incorporate small amounts of sugar
or natural sweeteners.
For diabetic patients I would generally do the same. But if a patients really wants to use them
I would emphazise portion control with these foods. They might also be a useful part of the
diet when a patient is used to large amounts of sugar, for example in soda. Cutting back and
drinking small amount of artificially sweetened soda might be a good transition and would
certainly help with blood sugar control.
9.
Compare and contrast the American Diabetes Association “Create Your Plate”
method (http://www.diabetes.org/food-and-fitness/food/planning-meals/create-yourplate/) with the USDA “My Plate” method (http://www.choosemyplate.gov/). Explain
which method you prefer to use and why.
Both are easy to understand and use a plate to demonstrate healthy eating habits. The "Create
your plate" gives also a plate size which can help with portion control and weight loss in
overweight diabetic patients. It is also a bit more realistic because fruit is not directly on the
plate. I think "Create your Plate" is easy to use and especially appropriate for newly
diagnosed type II diabetics because portion control is part of it.
"My plate" is equally easy and a good tool to educate about a general healthy diet. It is a little
more flexible and the web site provides a lot of resources for different people. I would use
"My Plate" for patients who are more technological savvy and want have more information
about portion sizes and the different food groups.
Reference for this section:
Nelms, M., Sucher, K.P., Lacey, K., Roth, S.L. (2011). Nutrition Therapy &
Pathophysiology (2nd ed.). Belmont, CA: Wadsworth
Insel, P. (2011) Nutrition (4th ed.) Sudbury MA: Jones and Bartlett
Hurley, V. The GI diet made easy. Retrieved July 23, 2012 from
http://www.canadianliving.com/health/nutrition/the_gi_diet_made_easy_4.php, fao gi
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D.) NUTRITION RELATED TOPICS
1. Explain why a person with uncontrolled diabetes may have excessive thirst, hunger and
urination. What are the medical terms for these symptoms? What is their pathogenesis?
What can be done to treat or control them?
EXCESSIVE THIRST
Medical Term
Polydipsia
Pathogenesis
Due to this osmotic diuresis the body loses water, dehydration is
the consequent with increased thirst.
Treatment
Normalize blood glucose level and rehydrate.
EXCESSIVE HUNGER
Medical Term
Polyphagia
Pathogenesis
Because tissue cells don't get fuel the body tries to compensate
with increased hunger and polyphagia.
Treatment
Insulin therapie so that glucose can enter tissue cells.
EXCESSIVE URINATION
Medical Term
Polyuria
Pathogenesis
Hyperglycemia leads to glucosuria (loss of glucose in the urin),
glucose pulls water along and this causes polyuria.
Treatment
Normalize blood glucose and rehydrate.
References:
3.
Define insulin and describe its major functions within normal metabolism.
Insulin is a polypeptide hormone produced in the beta cells of the pancreas. Insulin
secretion is stimulated by low blood glucose levels. It comes into the blood stream
via the portal vein and has a half-life of five minutes. It has an anabolic effect on
the body and effects carbohydrate, protein, and fat metabolism. It fascilitates
glucose uptake into cells in most tissues (except brain, liver, and working muscles).
It also increases glycogenesis, so that glucose can be stored, and decreases
glycogenolysis and gluconeogenesis. Insulin effects fatty acids by increasing
triglyceride synthesis and decreasing lipolysis. It promotes amino acid uptake and
protein synthesis in the muscle and decreases protein degradation. This results in
a positive nitrogen balance.
4.
Explain the mechanism by which each of the following hormones affect blood sugar:
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a. Insulin - Insulin lowers blood glucose levels by increasing glucose uptake into the
tissue, increasing glycogenesis, so that glucose can be stored. Insulin decreases
glycogenolysis and gluconeogenesis.
b. Glucagon - Glucagon increases blood glucose by increasing glycogenolysis and
gluconeogenesis, while decreasing glycogenesis.
c. Cortisol - Cortisol increases blood glucose levels by increasing gluconeogenesis. It also
decreases the uptake of glucose into tissues other than the brain.
d. Epinephrine - Epinephrin increases blood glucose levels by increasing glycogenolysis,
gluconeogenesis and glucagon secretion while at the same time decreasing insulin
secretion.
e. Norepinephrine - Norepinephrine works the same way as epinephrine.
f. Growth hormone - Growth hormone decreases glucose uptake by muscle cells and
thereby increases blood glucose levels.
5.
Describe the mechanism by which corticosteroid medications affect blood glucose
levels.
Corticosteroids mimic the effect of cortisol in the body. They increase insulin resistance,
increase the amount of glucose that is released by the liver, and decrease the glucose uptake
by tissue cells. This can result in high blood glucose levels.
6.
Patients experiencing acute illness may have poor appetite and intake. Why might
their need for insulin increase, regardless of their intake?
During acute illness the release of counterregulatory hormones is triggered which can
increase blood glucose levels even if the patient does not consume a lot of food. It is
important to still take the usual insulin dose and monitore blood glucose and potentially
ketones in the urine to avoid diabetic ketoacidosis or HHNK.
7.
Compare and contrast conventional insulin therapy and intensive insulin therapy.
Patients on conventional (fixed) therapy have 1 - 3 insulin injections per day. The amount
of insulin is predetermined depending on the amount of carbohydrates, the time of meals,
and usual activity level. The injection consists of a basal insulin combined with a fastacting insulin. The injections are premixed or the patient mixes them. Insulin and food
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intake are preset and the patient does not have a lot of flexibiliy with this therapy. But
he/she has only two or three injections. And with a set meal plan he/she only has to follow
the prescribed diet with a set carbohydrate load.
Patients on intensive (flexible) therapy inject basal, long-acting insulin twice a day and
additional bolus doses of fast-acting insulin before meals. The bolus dose is determined
depending on current blood glucose levels and planned carbohydrate intake and exercise.
This regiment is more flexible and allows spontaneous food planning. It mimics the normal
release of insulin by the pancreas more and can slow down the progression of long-term
complications. But it requires more injections and more blood glucose testing. The patient
must be better educated about carbohydrate counting and he/she must pay close attention to
daily blood glucose reading to fine-tune bolus injections.
8.
Explain how an insulin pump works. What are the pros and cons for its use?
The insulin pump is a device that delivers a continous subcutaneous infusion of rapid acting
insulin. A basal dose is delivered continuously and a bolus dose is added for meals or for
episodes of hyperglycemia. It is attached with an infusion set and operated with batteries. It
can replicate the normal function of the pancreas more closely because the insulin dose can
be adjusted to food intake and exercise. It also makes the use of syringes unneccessary. The
pump usually provides very good blood glucose control without large swings and can
improve A1c levels. As with every technique there are also disadvantages. The pump can
become detached resulting in high blood glucose levels and ketoacidosis. The pumps are
expensive and patients need to be trained to use them correctly. Some patients might find it
annoying to be attached to a device at all times.
9.
Explain the mechanism of action by which physical activity affects blood glucose
levels.
Exercise can help lower blood glucose levels because more glucose is taken up by muscle
cells and used as energy during exercise. For type I diabetics this means that they must
adjust their carbohydrate intake and/or insulin regiment. They might need less insulin or
they need an extra snack before exercising. For type II diabetics exercise is also important
for weight control and exercise can decrease the need for medication. In gestational
diabetes when oral diabetes medication are contraindicated exercise is a very important part
of therapy to stabilize blood glucose levels.
References for this section:
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Nelms, M., Sucher, K.P., Lacey, K., Roth, S.L. (2011). Nutrition Therapy &
Pathophysiology (2nd ed.). Belmont, CA: Wadsworth
Steroids and Diabetes (2008). Talking Diabetes No. 45 retrieved July 24, 2012 from
http://www.australiandiabetescouncil.com/AustralianDiabetesCounil/media/PDFs/Steroids.pdf
How do insulin pumps work. Advantages of Using an Insulin Pump. Disadvantages of using
an Insulin Pump. Living with Diabetes. Retrieved July 24, 2012 from
http://www.diabetes.org/living-with-diabetes/
Insulin Therapies. Diabetes Learning Center. Retrieved July 24, 2012 from
http://www.bd.com/us/diabetes/page.aspx?cat=7001&id=7275
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