Download Diabetes Mellitus Cases

NTRI 5020
Anemia Cases
Mary Frances Hasty
Lauren Antle
Brittany Baerlocher
Case Study: DKA Presentation in T1DM
HPI:
Kelly is an 18-year-old-female, who is brought to the ED in a small town (over 1 hour from her
home) by her father. Her father reports that she does not feel well, has complained of some
abdominal pain, and that she has appeared to be hyperventilating for the past several hours,
which prompted the trip to the ED.
ROS:
General- 3# weight loss over the past month
HEENT – negative
Lungs – hyperventilation as noted above
CV – feels heart is racing most of the day; denies chest pain
Abd – mild abdominal pain as noted above, vomited once on trip in to ED, very thirsty
GU – increased urination past several weeks, decreased past 24 hours
Neuro – dizzy
Skin – dry
Medications – none
Allergies – NKA
PMH - Her past medical history is unremarkable except usual childhood illnesses and recent
URI, which is resolved. UTD on immunizations.
FH – unremarkable
SH – deferred
Physical Exam:
WDWNF
Ht 5’3”, Wt. 103#, R 35, P 101, T 97.4, BP 86/52
Eyes-EOM, PERRLA
Neck – non-tender, no adenopathy
Lungs – CTA, Kussmual respirations
CV – tachycardia, as above; no murmur, gallop, or rub, no edema
Abd – non-tender, nl BS X4, no HSM or masses
Neuro – negative
Skin – warm, dry, flushed; no rashes
Lab Results:
Glucose 650mg/dL
BUN 45mg/dL
Creatinine 1.1mg/dL
TG 200mg/dL
Sodium 143
Potassium 6.2 mmol/L
Chloride 103
Phos 3.4 mg/dL
Bicarbonate 12mEq/L
Betahydroxybuterate 6.7 mg/dL
ABGs: CO2 23; pH 7.0
Plasma OSM 304 mOsm/kg
Urine Ketones: positive
QUESTIONS:
1. Define the acid-base abnormality. Is it compensated? What data did you use to make this
assessment?
Acid-base abnormality is metabolic acidosis. This conclusion is supported by the low
laboratory values of bicarbonate and CO2. Respiratory acidosis was ruled out because the CO2
levels would have been high, since they are directly related to [H+]. Additionally, it was apparent
that the abnormality was acidosis and not alkalosis because of the below physiological blood pH
level.
The patient is partially compensating for the metabolic acidosis. Bicarbonate plays a role
in compensating for the metabolic acidosis by functioning as an extracellular buffer for the
increased acid load (ketones). The patient is hyperventilating to partially compensate for the
abnormality. Hyperventilation results in a decrease in the PCO2 in the blood. This is in an effort
to reestablish the PCO2:bicarbonate ratio.
In addition to the data mentioned above, the presence of ketones in the urine also
supports the diagnosis of DKA.
The initial treatment for this patient is 2 liters of IV normal saline (0.9%) and insulin (usually a
drip). She will be monitored closely over the first several hours.
2. Identify the normal range for each of the following labs. At the 2-hour point with fluid and
insulin administration her labs were rechecked. Give the expected direction of change, and a
brief explanation of why the lab would change in that direction. Give some detail. What is
happening physiologically/pathologically and metabolically?
You will likely need to expand the explanation box.
Laboratory
Normal
Change
Explanation
Decrease
Glucose 650mg/dL
70-100
mg/dL
Insulin will initiate removal of glucose from the
bloodstream; turn off hepatic glucose production
10-20 mg/dL Decrease
The pt is currently dehydrated; kidney cannot get
rid of waste products so with hydration the pt will
be able to eliminate BUN
0.6-1.2
mg/dL
Decrease
The pt is receiving fluids and this will increase
the excretion of creatinine
Decrease
Serum K levels are high d/t the transcellular
shift of K out of the cell. However, there is a total
body potassium loss d/t osmotic diuresis, so
potassium levels will decrease, possibly to the
level of hypokalemia.
Decrease t
Serum Phosphate levels are within normal limits
because of the transcellular shift that occurred
with the acidosis.
BUN 45mg/dL
Creatinine 1.1mg/dL
Potassium 6.2
3.5 to 5.5
mmol/L mEq/L
Phos 3.4 mg/dL
3-4.5
mg/dL
increase
Bicarbonate 12mEq/L
22-28
mEq/L
Bicarbonate levels are low because the body is
in acidosis. Most of the free bicarbonate would
have been utilized for extracellular buffering to
try and compensate for the low pH.
increase
CO2 23
33-45 mm
Hg
Low CO2 levels. This provides evidence that it
is a metabolic acidosis by the fact this is still low.
If it were higher, we would see she had a
pulmonary acidosis and the CO2 would be
compensating more.
7.35-7.45
increase
Patient is in acidosis presently and treatment will
resolve it.
Decrease
The osmolarity will decrease because the pt is
getting hydrated and their electrolytes are being
balanced.
Decrease
Beta-hydroxybuterate levels are high because it
is a product of ketosis. Once ketosis is resolved
pH 7.0
Osm 304 mOSM/kg
275-295
mosm/kg
0.4 mmol/L
Beta-hydroxybuterate (6.7
mg/dL)
(via treatment) beta-hydroxybuterate will also
drop. Additionally, insulin will turn off lipolysis.
Negative
Ketones in urine (positive)
Become
negative
The pt will no longer being in ketosis because of
the treatment and therefore will no longer be
excreting ketones.
Kelly has a new diagnosis of T1DM. Current weight following rehydration and resolution
of DKA = 110#s. Kelly has been transferred to the general medicine unit and stabilized
over the past three days. She has been started on the following insulin regimen and an
initial diet of 45 grams of CHO at each of three meals. There are plans for discharge
tomorrow following initial diabetic teaching.
STANDARD FORMULA OF HOW ONE ARRIVES AT INITIAL INSULIN DOSE
(reference):
Weight 50kg
Initial starting dose = 25-30 units per day
0.5 units X 50 kg = 25units/day
0.6 units X 50 kg = 30 units/day
50% basal, 50% prandial
Pre-breakfast
Pre-lunch
Pre-dinner
12 units Long-acting
4 units Rapid Acting Insulin 4 units Rapid Acting Insulin
(Detemir or Glargine) +
SQ
SQ
6 units Rapid Acting Insulin
SQ (Aspart)
(dose could be 5 units)
3. Explain the rationale behind an insulin regimen that is 50% basal and 50% prandial.
By giving a regimen that is 50% basal and 50% prandial, there is variation in the diet. Basal will
allow for steady state blood glucose, whereas prandial will account for the glycemic response
from a meal. Basal insulin will prevent blood glucose from rising too high throughout the
day/night. Prandial insulin allows Kelly to adjust her insulin dosage to the amount of
carbohydrates she is going to eat with her meal.
4. What is meant by sliding-scale insulin?
Sliding-scale insulin is used in response to blood glucose levels. The dose is dependent on the
patient’s blood sugar before a meal and predefined blood glucose ranges individualized for the
patient. SSI is used in hospitals and healthcare facilities because it is easy to monitor.
5. Calculate the estimated insulin to CHO ratio of the initial prescribed regimen?
2 units of insulin
9 g CHO
Total insulin for the day basal & bolus and total carbohydrate for the day.
6. Calculate the initial estimated insulin sensitivity factor for the proscribed regimen?(Define)
Insulin Sensitivity Factor is the drop in blood glucose seen per unit of insulin. Insulin Sensitivity
Factor is used to calculate the correction factor for preprandial blood glucose levels.
You have been consulted to initiate diabetic teaching regarding Kelly’s diet. Please address
the key points that you would cover under each of the following topics.
CHO distribution based on prescribed
insulin regimen?
Carbohydrates should be distributed
evenly throughout the day.
Frequency of blood glucose monitoring.
Blood glucose should be monitored before
meals and snacks, before and after
exercise, before bed and occasionally
throughout the night.
Intensive insulin therapy has many
benefits, such as decreasing the pt’s A1C
values which in turn decreases risk for
After two weeks at home for Kelly you and microvascular disease. However, since the
pt is so active in sports she must be aware
the physician address the benefits of
of the risk of hypoglycemia. With the pt on
intensive insulin therapy for Kelly.
What recommendations would you make to intensive therapy the pt should consume 15
Kelly regarding diet and intensive therapy? g CHO with every 30-60 minutes of
exercise. With intense exercise pt may
Be thorough and specific.
need to decrease insulin and add a 6%
glucose beverage for exercise lasting more
than 60 mins.
Kelly is a typical busy teenager on the run.
She is active in sports.
Recognition, prevention, and treatment of
Symptoms of hypoglycemia: diapheresis,
hypoglycemia.
tachycardia, tremors, hunger, nausea,
pallor, irritability, headache dizziness,
paralysis, blurred vision, lethargy,
confusion, seizures, poor judgement, brain
damage, coma, and death
Prevention: monitor blood glucose
Treatment: Glucose (15-20g) from a source
such as glucose tablets, juice; (avoid high
fat and high protein foods) or glucagon
Kelly is on the soccer team. What advice
would you give Kelly to help manage her
blood sugar during practice and games.
(Hint: There are 3 key areas you need to
address)
Benefits of physical activity for T1 patients
are enhancement of physical fitness and
reduction in CVD risk.
Negative effects: There is increased risk of
exercise induced hypoglycemia and
aggravation of hyperglycemia and ketosis.
Team sports such as soccer, however only
require short bursts of high power output
and rely on ATP-PC for energy in muscle
contractions.
Kelly should not play until she is sure her
insulin levels are adequate. She should also
not play if glucose levels are >250 mg/dl or
if ketones are present.
There is also a risk of hypoglycemia. So
she should ensure she is only using insulin
she needs. During exercise, T1 are unable
to reduce circulating insulin, This leads to
hypoglycemia bc of increased glucose
uptake by skeletal muscles and inadequate
hepatic glucose release are imbalanced.
Kelly should consume 15 g CHO for every
30-60 mins of exercise and add a 6%
glucose beverage for exercise over 60
minutes
What to do if she gets the bad case of
gastroenteritis that is going around?
Continue insulin even if not eating.
Check blood glucose every 4 hours.
Check ketone levels if blood glucose >
240.
Also check for ketone levels if vomiting or
symptoms of hyperglycemia or
ketoacidosis. Call healthcare if ketones are
high.
Get 10-15 g of carbohydrates from liquid if
you cannot eat.
Case Study: Gestational Diabetes Mellitus
Introduction
DR is a 17-year-old Caucasian, female who presents at 24 weeks gestation for her first prenatal
visit. She complains of heartburn and constipation. She admits to one previous pregnancy at age
15 that was terminated by abortion.
History
DR has no significant/serious PMH. She has a positive family history for obesity, T2DM, and
HTN. DR smokes about ½ pack of cigarettes per day.
Social History
DR admits to occasional alcohol consumption, but states that it is not enough to hurt the baby.
She takes no medications or vitamin supplements. DR is out of school for the summer and plans
not to return to school in the fall. The baby is due in late October. She lives with her mother and
older brother age 22.
Clinical Chemistry
Hgb
12.5 g/dL
Glucose
155mg/dL
BUN
18 mg/dL
Creat
0.9 mg/dL
Chol
201 mg/dL
TG
125 mg/dL
BP 120/82 mm/hg
Assessment of Weight Gain
DR is 5’5” tall and her current weight is 198#s.
She estimates her pre-pregnancy weight at 182#s.
1. What is DR’s pre-pregnancy BMI? Plot her weight gain on the chart below.
BMI: 30.3
2. What are your recommendations for weight gain for DR at this time?
Looking at the recommendations for weight gain, we see that it is ideal for most of the
weight gain to occur in the third trimester. Considering that DR is already overweight, she does
not need to gain as much during pregnancy. This being said, it looks as though she already
gained as much as she needs for an optimal pregnancy for her BMI. We recommend that she gain
another 5-10 lbs throughout her pregnancy, while following a well balanced diet for a pregnant
woman.
Diabetes in Pregnancy
Incidence-impacts 7% of all pregnancies; tripled since 1994.
3. What is the etiology of gestational diabetes (GDM)?
Human chorionic gonadotropin and human placental lactogen are associated with strong
anti- insulin as well as lypolytic characteristics. Hepatic glucose is also 30% higher even in
situations with higher insulin. Pregnant women who cannot keep up with the increased need of
insulin result in GDM.
Do not confuse GDM with pre-gestational-diabetes
·
T1DM is high risk pregnancy- generally not managed in primary care
·
T2DM also high risk; seeing more due to obesity, may diagnosis at prenatal visit
4. Identify three of DR’s specific risk factors for GDM?
Overweight prior to pregnancy.
Quick weight gain during pregnancy.
Family history of type 2 diabetes.
Assessment of DR for GDM
DR’s Random (casual) Blood Glucose = 155mg/dL
5. Is this diagnostic for GDM? How would this change if it was a FPG?
What test would be performed to further evaluate her hyperglycemia?
Yes. A normal casual should result in a blood glucose level of < 140mg/dL. DR falls in
the range of a pre-diabetic person with her casual blood glucose level. Further tests, preferably
fasting blood glucose or oral glucose tolerance test, should be performed. If this were her FPG,
then DR would meet the criteria for diabetes, which is an FPG > 126 mg/dL.
6. Fill in the following table identifying 3 potential complications of GDM for the mother
and three for the infant.
Mother
Infant
Greater chances of pre-eclampsia
Hypoglycemia
Greater chance of GDM with other
pregnancies
Risk of pre-term birth
Greater chance of diabetes later in life
Excessive birth weight
DR has been diagnosed with GDM. She has been referred to you for nutrition counseling.
At this time, the plan is to give a two-week trial to control DRs diabetes with diet alone.
DR has been sent home with a glucometer to check her glucose.
Dietary Assessment DR
DR’s 24-hour recall:
o Breakfast (home) – 2 fried eggs, 4-slices of bacon, 2 slices of toast w/ butter, 2 cups coffee w/
2 TBSP sugar
o Lunch (work-free) – double cheeseburger, large fries, 32 oz. Coke, apple pie (McDonalds)
o Snack – cinnamon rolls with butter
o Dinner (home) – fried chicken, macaroni and cheese, corn, Coke
o Ice-cream and Oreos
(Provides: 3000 kcals, 13% protein, 40% carbohydrates, 47% fat)
8. What food groups/nutrients are missing from DR’s diet? What foods/food groups are
contributing to DRs high blood glucose? Excessive weight gain?
Fruits, vegetables, dairy, and water are all missing from DR’s diet. DR is taking in a large
amount of carbohydrates on a regular basis, which may be contributing to her high blood
glucose.
9. Provide 5 specific recommended changes to address problem areas. Consider DRs social
situation/limitations when making recommendations. Talk food.
Adding skim milk
Cut back on portion sizes (two slices of bacon instead of three)
Switch sugar to sweetener
Diet coke instead of coke
Adding fruit and vegetables for fiber
9. DR was started on prenatal multivitamin by her OBGYN. What are the three nutrients of
greatest concern for pregnant women that are difficult to meet with diet alone?
Iron
Folic Acid
Calcium
DR returns to clinic in 3 weeks for follow-up. She has made some of the dietary changes
that you have suggested, but her SBGM records show pre-prandial blood glucose
averaging above 140mg/dL and post-prandial exceeding 200mg/dL at least 5 times per
week. Her OBGYN has started her on Metformin, 250mg BID.
10. Metformin and glyburide are used in pregnancy, but they are not without risk. Look up
current information of how these are classified by risk. Note here.
Glyburide is in the class C for drugs, which means that adverse effect on fetus in animal
reproduction studies have been found, however, there have been no well-controlled studies in
humans.
Metformin is categorized into class B according to the US FDA pregnancy categories.
Class B states that animal reproduction studies have failed to demonstrate a risk to the fetus and
there are no adequate, well-controlled studies in pregnant women.
CASE STUDY: COMPLICATED T2DM
JD is a 59-year-old man is referred to you because of uncontrolled diabetes. Fourteen years ago
the patient was found to have a blood glucose level of 300 mg/dL on a routine examination. At
that time he received patient education for a program of diabetic exchange diet, exercise, and
glipizide. With this regimen his glucose level fell to the 110 to 140 mg/dL range and his A1C
fell to 7.5%.
JD presents to clinic today after referral from his new primary care provider who he saw two
weeks ago after urging from his now adult daughter. The patient relates that for the last eight
years he has not focused on his diabetes, "I avoided it all," following no regimen and taking no
medication for diabetes. In fact, he mentioned that he had not seen a physician for over 5 years.
He had separated from his wife, now divorced, and moved from Florida to Houston. He works
as a busy account executive, having the 2-martini lunch with clients, works late in his office, and
gets little exercise. Brief diet history reveals that the patient eats three meals per day, breakfast
a large Moo Latte at Starbucks and slice of banana bread or 2 scones; lunch out off the menu or
lunch buffet, supper frozen entrée or fast food. His A1C today is 13%.
He has had significant deterioration of his vision, is scheduled to see an ophthalmologist for
evaluation of diabetic retinopathy later today. Additional lab today shows a BUN of 34 mg/dL,
a serum creatinine of 1.4 mg/dL, and 2 + proteinuria, BP 130/85, TG 235. He has aching pain in
his legs, mostly at night, from his feet to the level of the mid-calf. Light touch sensation is
diminished to the thighs. Deep tendon reflexes are absent at the ankles and the knees. He has
had nausea, reflux, abdominal pain, and intermittent constipation in the last year. He notes that
on some occasions he feels that the food is just sitting/souring in his stomach. Pt is 5’9” and
weighs 210 lbs. He admits to 10 pound weight loss over the past three months, which he
attributes to the above symptoms.
1.
An A1C of 13% would suggest what range of blood glucose?
An A1C of 13% would suggest a mean blood glucose range of over 300 mg/dL.
2. Discuss the general metabolic etiology of microvascular disease? Some detail here
please.
Chronically high blood glucose levels can cause irreversible damage to cells, especially
those in the capillaries and end organs. Through a process called glycosylation, glucose becomes
irreversibly bound to proteins in the red blood cells, blood vessel walls and interstitial tissues.
Glycosylation produces AGEs or Advanced Glycosylation End products that cause the basement
membrane of the epithelium to thicken, increases the permeability of blood vessels and nerves,
stimulates the release of cytokines (inflammation), growth factors and cellular proliferation in
glomeruli in the kidney and smooth muscle in the vascular system resulting in fibrosis, and
increases platelet adhesion in the blood vessels increase the formations of clots.
In addition to all of these changes caused by the AGEs the body is also experiencing
hyperglycemia. The glucose, trying to leave the bloodstream, is shunted into insulin-independent
tissue. Tissues such as the nerves, eyes, kidneys, and blood vessels become flooded with glucose.
This intake of glucose stimulates the Polyol Pathway which results in the accumulation of
fructose in the cell; leading to cellular damage.
3. Complete the table to describe the common signs/symptoms of each of the following
conditions and laboratory/diagnostic evaluation/screening.
Complication
Signs/Symptoms
Diagnosis/Screening
Diabetic Neuropathy
Decreased sensation and
vascular supply; gangrene
(ischemia of limbs, poor
healing of wounds and
infections)
Physical Exams are utilized
for early screening of
neuropathy, this largely
depends on the patient
letting the physician know
about areas of concern.
Physical exam should pay
special attention to
patient’s feet (complete
foot exam) and any trouble
walking. Electromyogram
(EMG) and nerve
conduction study to
confirm diagnosis.
Diabetic Retinopathy
Stage 1 (nonproliferative):increased
capillary permeability, vein
dilation, microaneurysms,
superficial/deep
hemorrhages
Visual acuity testing
(measures ability to see at
various distances);
tonometry (measures
pressure inside eye)checking for glaucoma;
Pupil dilation (allows
doctor to examine retina
and optic nerve)- Doctor
looks for swelling, blood or
fatty deposits in the retina;
growth of new blood
vessels and scar tissue;
bleeding in the vitreous;
retinal detachment;
abnormalities in optic
nerve; Optical coherence
tomography (uses light
Stage 2 (pre-prolifeative):
increased retinal ischemia
with infarcts (cotton-wool
spots)
Stage 3 (proliferative):
neovascularization; fibrous
tissue formation
waves to capture images of
tissues)-to check for fluid
leaking in to retinal tissue.
Fluorescein angiography is
used to identify the blood
vessels that are closed,
broken down or leaking
fluid.
Diabetic Nephropathy
Albuminuria, proteinuria
Screen for albuminuria by
taking timed urine
collection over a 24 hour
period or taking a random
“spot-urine” test.
30-300 mg of albumin in a
24 hour sample suggest
nephropathy
30:300 albumin to
creatinine ratio in spot
urine test
Gastroparesis
Decreased motility, N/V,
Blood tests (Electrolyte
GERD, unintentional weight check & Chemical check),
loss
Upper GI series screening,
Barium Beefsteak Meal
(being aware of the amount
of time it takes to digest),
Radioisotope screening,
Gastric Manometry,
Esophagogastroduodenosco
py, Scintigraphic gastric
accommodation.
The majority of these tests
are ways to see the amount
of time it takes for patient
to digest foods.
4.
Assuming that JD has early signs of diabetic gastroparesis, what dietary modifications
might help to alleviate his symptoms?
Gastroparesis shows as a decrease in gastric emptying therefore, small meals with lots of liquids
will help alleviate the symptoms and possible increase gastric motility. Additionally, JD should
be on a low fiber diet to prevent the motility from being further decreased.
Having not seen a dietitian in over 10 years, JD is excited to learn that the approach to
dietary management has been simplified and he does not need to follow a strict calorie
level. Despite being disappointed that he has had to start on insulin, he is highly motivated
since the physician explained that many of the medical issues he has largely been ignoring
are the result of poor glucose control and that better control may delay further
complications.
INSULIN: Novolog 70/30 AM and 70/30 before supper
5.
What is the number one priority/goal for this patient’s management at this time?
For JD’s blood glucose to be as close to normal as possible.These issues he is experiencing
should certainly be addressed but first and foremost, insulin should be regulated properly and a
better diet followed.
6. What are your recommendations at this time for CHO intake and distribution?
JD should evenly distribute his CHO intake throughout the day, limiting himself to 60 g of CHO
per meal. JD should attempt to lose weight because he is obese and strive for glycemic control.
7. Identify five important/essential nutrition strategies at this time to help JD achieve his goal.
Try to target specific patient-centered problem areas from history.
Target/Focus/Key Points
Rationale for Recommendations
Increase liquids in diet.
In order to treat gastroparesis, liquids and
foods that are easier to digest is easier. This
will also help with renal function.
Decrease fiber in diet
This will be effective for alleviating the
symptoms of gastroparesis. Fiber slows
down gastric motility. When gastroparesis
is resolved, increase fiber
Reduce Alcohol intake
Consuming alcohol and carbohydrates
together raises blood glucose levels.
Additionally, alcohol consumption elevates
triglyceride levels.
Increase Exercise to 150 minutes of
moderate intensity a week
Exercise increases glycemic control and
insulin sensitivity. Contributes to weight
management. Reduce risk of cardiovascular
disease.
Carbohydrate Counting
The patient needs to monitor his
carbohydrate consumption. This is
extremely important in the selfmanagement of blood glucose levels.
Controlling level of CHO intake will work
to lower blood glucose levels and A1C
levels. CHO counting and distribution
across the day is important for balance with
the insulin the patient is taking.