Hyperglycemia in type 2 diabetics can be viewed as a continuum of progressive insulin resistance; this pathophysiology underscores the gradual development of increasing insulin resistance (first in muscle cells then in liver cells) with resultant hyperinsulinemia and culminating in beta cell failure and decreasing insulin levels. The stages in Diabetes can be characterized as follows: Stage 1: Normal glucose tolerance; some degree of hyperinsulinism but no evidence of impaired glucose tolerance (HgA1c under 5.5)Stage 2: Impaired glucose tolerance develops when muscles have significant insulin resistance and the raised insulin levels are not enough to bring the glucose to normal after a meal. Since the liver is more sensitive to insulin than muscle, fasting hyperglycemia has not developed (HgA1c= 5.5-6.1).Stage 3: Both muscle and liver demonstrate insulin resistance; the hyperinsulinemia does not prevent the liver from generating glucose in the fasting state and this is reflected in an elevated fasting glucose level (HgA1c = 6.2-7.5).Stage 4: The pancreas is now failing and the insulin levels start to falter. There is both moderately severe fasting hyperglycemia as the liver increases its glucose output as well as poorly controlled Diabetes (HgA1c = 7.6 - 10).Stage 5: The pancreas has overtly failed. The patient has severe fasting as well as severe insulin resistance; oral agents on their own will not correct this hyperglycemia (HgA1c is more than 10).Understanding these stages is important in managing diabetics more effectively. Thus, in a patient who is in stage 4, providing monotherapy is unlikely to work effectively. In such cases, both an insulin secretagogue (to stimulate insulin secretion) as well as an insulin sensitizer (to minimize insulin resistance) is needed to meet the moderately severe hyperglycemia that develops.Approved oral diabetic agents by mechanism of action include: Insulin secretagogues: Sulfonylureas and meglitinidesInsulin sensitizers: Metformin and thiazolidinediones
Centralpontinemyelinolysis is a neurologic disease caused by severe damage of the myelin sheath of nerve cells in the brainstem, more precisely in the area termed the pons. It can also occur outside the pons.  The term \"osmotic demyelinization syndrome\" is similar to \"centralpontinemyelinolysis\", but also includes areas outside the pons. 
Diabetes Cases.1 Ppt
Jimmy Santana, MBA, P.A. - C
A 24-year-old, white female has recently being diagnosed with insulin-dependent
diabetes. The disease is being managed on a split dose of 60/40 insulin suspension,
which she injects herself at 8:00 a.m. and 5:00 p.m. She was told to call in if she
experiences any strange symptoms, which she does this afternoon. At 2:45 p.m. she
is not feeling well and notices that her skin is cool and damp. Her hands are
shaking and she is very anxious. What do you tell her to do right away, before
having somebody take her to your office?
A. Inject 4 IU of her insulin
B. Drink a can of diet soda
C. Drink six ounces of fruit juice
D. Eat a large candy bar
E. Eat a cube of sugar
The above described symptoms are classical for hypoglycemia.
An inexperienced patient needs to be monitored by medical
personnel until the blood glucose level is stabilized again. The
first priority though is to prevent the blood sugar to drop any
further and send the patient into a coma.
A six-ounce drink of fruit juice should be sufficient. Since the
symptoms suggest hypoglycemia, injecting insulin would
worsen the situation. If in doubt if the patient is hypo- or
hyperglycemic and there is no possibility for a test, always give
sugar first and see if the patient improves. An increase of a blood
glucose level of, for example, 350 is not going to hurt the patient,
but lowering a level of 45 is going to send the diabetic into a
Since diet soda contains only sugar substitutes it is not going to
influence the blood glucose level. A large candy bar could be
eaten too, but it may raise the glucose level higher than required,
therefore the fruit juice is a better choice. One cube of sugar is
an insufficient amount to raise blood sugar; it will take several
A 61-year-old white male presents to your office for the first time. In
reviewing his medical records, you note a history of diabetes type 2
onset 4 years ago. He is currently well controlled to normal blood
sugars and hemoglobin A1Cs. You do note that his previous blood
pressure readings were above normal on multiple visits. In addition to
his usual diabetic care, you recommend initiation of drug therapy for
his hypertension. Your drug of choice is
A. Calcium channel blocker
B. ACE inhibitor
C. Alpha blocker
D. Thiazide diuretic
E. Beta blocker
ACE inhibitors have been shown to slow the progress
of proteinuria in patients with diabetes. Control of
their blood pressure is just as important. Your drug of
choice should be an ACE inhibitor for any diabetic
with hypertension as long as there are no
contraindications to giving them this medicine.
A 55-year-old male is brought into the urgent care center of your hospital by paramedics. He is
obtunded, and today his wife could not get him out of bed. He has no significant past medical history. His
wife states that he has not been well for the last week, with decreased energy and fatigue. In addition, he
has had a productive cough, which has worsened during the last 3 days. Also, according to his wife, he
appears to be drinking more water. Physical exam reveals a lethargic male who moves to deep pain but
has no intelligible speech. Paramedics have given the patient Narcan with no change in his status but
have withheld glucose bolus due to a high dextro stick reading. Vital signs are pulse 115; BP 90/50;
respiration 18; Temp 38.2° C (100.7° F)
HEENT shows dry mucous membranes. Lungs are clear. Cardiac exam is significant for tachycardia.
Abdominal exam is nonspecific. Neurologic exam shows the patient to be responsive only to pain, with
withdrawal. No abnormal reflexes noted.
Initial laboratory studies show: Na 118; K 4.2; Cl 97; HCO3 21; Glucose 1050. ABG reveals pH 7.34, pCO2
20; pO2 79; O2 saturation 90%. CBC shows a normal H/H with WBC count of 14K; the serum is reported
as very lipemic. Chest X-ray shows an LLL consolidation. The most likely cause for the change in the
patient's mental status is
A. Acute diabetic ketoacidosis
C. Pneumococcal pneumonia with hypoxia
D. Hyperglycemic hyperosmolar nonketotic coma
E. Central pontine myelinolysis
Hyperglycemic hyperosmolar nonketotic coma (HHNC) represents a
syndrome characterized by marked hyperglycemia, hyperosmolarity, and
dehydration. It is manifested by decreased mental functioning that may
progress to frank coma. Ketosis and acidosis are generally minimal.
DKA, acute diabetic ketoacidosis, will have similar electrolyte
abnormalities; however, there will be an associated metabolic acidosis and
The patient does show pseudohyponatremia, which is due to the presence
of hyperglycemia and hyperlipidemia. In the absence of marked lipemia,
the true value for sodium can be approximated by adding 1.3 to 1.6 mEq/L
to the sodium value for every 100 mg/dl glucose over the norm. But this is
not the cause of this patient's altered sensorium.
The patient most likely has pneumococcal pneumonia, which is a
common precipitating factor in the development of HHNC. He is mildly
hypoxic, though this does not explain the degree of obtundation seen.
Overly aggressive restoration of serum sodium levels in hyponatremic
patients can be associated with central pontine myelinolysis and
A 28-year-old type I diabetic on multiple daily insulin injections regimen
presents to your office for a follow up visit. She complained to you about her
early morning glucose level during her last visit and you recommended for
her to chart the numbers and bring it for her next appointment. Her pre-
breakfast glucose averaged 285mg/dL; dinnertime was 95mg/dL and
68mg/dL at 3 AM. How will you treat her diabetes?
A. Increase the evening dose of long acting insulin
B. Decrease the evening dose of long acting insulin
C. Decrease the evening dose of short acting insulin
D. Increase the evening dose of short acting insulin
E. Increased activity before bedtime
Three mechanisms can account for early morning hyperglycemia in
patients with diabetes on insulin:
1. Inadequate dose of long acting insulin at night
2. Somogyi effect or rebound hyperglycemia is a condition often seen in
type I diabetes, in which there is nocturnal hypoglycemia. The
hypoglycemia subsequently stimulates the release of counter regulatory
hormones leading to increase of glucose level in the blood. Diagnosis
can be made by several plasma glucose analyses done at 2.00 A.M, 3.00
A.M, and 7.00A.M.
3. In the dawn phenomenon, the hyperglycemia is secondary to increased
need for insulin in the early morning due to the normal early morning
surge of growth hormone, which antagonizes insulin action.
Checking the blood glucose level at 3 AM can help differentiate
between Somogyi effect and dawn phenomenon: the level will be low
in Somogyi phenomenon. The patient's early morning hyperglycemia is
due to Somogyi effect since her 3 AM level was low. Treatment of this
will be to decrease the evening dose of long-acting insulin or give
bedtime snacks. The treatment of dawn phenomenon involves
increasing the evening dose of long-acting insulin.
There is no nocturnal hypoglycemia if the night dose of insulin is
A 62-year-old male with a history of diabetes for twenty-five years and hypertension for
ten years is referred to your office by a retired physician. He complains of worsening
edema on the right lower extremity during the last two weeks. Vital signs show T 97.8
Pulse 78 RR 20 BP 165/93. Physical examination disclosed periorbital edema and left
lower extremity edema 1+ below the knee and right lower extremity edema 3+ below the
knee that is nontender to palpation. He denies any fever, chills, or malaise. He is
currently on glipizide 20 mg twice a day and amlodipine 10-mg once daily. Laboratory
result from two weeks ago shows Na 145, K 4.5, Cl 102, HCO3 25, BUN 14, Creat 1.2, CA
7.2, Glucose 287, HgA1C 8.6, and Albumin 2.5. The U/A test shows 3+ proteins with no
WBC or RBC.
Question: What is the most appropriate next step in management of his diabetes?
A. Start the patient on glyburide
B. Start the patient on insulin therapy
C. There is no indication to change his diabetes therapy. His HgA1C shows that his
diabetes is under control
D. Start the patient on metformin
E. Repeat the patient's HgbA1C; result is too old to reflect the current HgbA1C level
This patient's diabetes mellitus is poorly managed. Glycosylated
hemoglobin (HbA1c) is the best indicator of glycemic control
over the previous 3 months. Maintaining an HgA1C of 7 or less
lowers the rate of complications of diabetes mellitus. Adding a
second class of oral hypoglycemic agent would be the next best
choice. Metformin is the drug from the biguanides class;
therefore, it is the drug of choice.
Starting the patient on glyburide is incorrect because both
glyburide and glipizide belong to the sulfonylurea class. Starting
the patient on insulin therapy is incorrect because oral therapy
should be maximized before starting on insulin. HgA1c of 8.6
indicates poorly controlled diabetes. There is a need to change
his diabetes management. There is no need to repeat HgA1C.
Glycosylated hemoglobin (HbA1C) is the best indicator of
glycemic control over the previous 3 months. The result is not
A 38-year-old obese female with type 2 diabetes mellitus presents to your office
for follow up visit. Her blood sugar has been well controlled on metformin. She
wants to have a baby and wants to know if there is any special thing to do so
that her diabetes will not affect her pregnancy. Which of the following is
appropriate for her?
A. Switch her to insulin
B. Switch to glyburide
C. Tell her it is not advisable for her to be pregnant because her child will be
D. Increase the dose of her metformin to prevent worsening of her blood sugar
E. Continue her present treatment and dose
Diabetic patients that are pregnant or attempting to
get pregnant, irrespective of whether they are insulin
requiring or not, should be switched to insulin
therapy for their glucose control. Oral glucose
lowering agents are contraindicated in pregnancy.
Although a poor glucose control predisposes to
increased maternal and fetal risks, it is not a
contraindication to pregnancy. A good glucose control
is however necessary prior to and during pregnancy.
A 24-year old white male present to the flight
physician assistant’s office for a routine physical. He
has been taking flying lessons and is applying for a
pilot’s license. Regulations state that he must have a
Examination discloses a thin male, 74 inches, 140
pounds. Generally, the exam is unremarkable. Routine
screening includes a urinalysis, which demonstrates
There is insufficient information to establish a diagnosis.
There are other reasons to spill glucose in the urine. You
must ask additional questions.
You find out that even though he denies any history of
diabetes, he admits to:
Having incessant thirst
He has lost 15 pounds over the last three months
A glucometer reading revealed a glucose of 490 mg/dl
A blood glucose revealed a glucose level of 496 mg/dl.
With normal electrolytes and anion gap
Does this patient have diabetes?
Three ways to diagnose diabetes mellitus:
Fasting glucose of > 126 mg/dl
Oral glucose tolerance test with a 2 hr value
of > 200 and one other value in-between of
Grossly elevated serum glucose with classic
New onset Type I diabetics should be
He needs to start on insulin
He requires a lot of patient education
32-year old woman who has type I diabetes calls
you over the weekend. She has been having some
nausea and vomiting for the last 24 hours and can
not keep solids down. She has been able to keep
liquids down. Her last glucometer reading was
She is on a split dose of NPH and regular insulin
twice daily. She did not take her morning insulin
because a physician had told her never to take her
insulin when she is not eating. She ask you for
Many patients do not take their insulin if they
are not eating; this is wrong.
It is important for IDDM patients and their
providers to learn how to manage “sick days”.
Note that one of the most common reasons for
patient to go into DKA is poor management of
their diabetes when they are sick.
Insulin should be taken regardless of whether or
not they are eating
Adequate carbohyrates should be taken (15 –
The patient can consume regular coke, Sprite,
juices @ 4 – 6 oz q2hrs.
They can also have gelatin, crackers, soup
Patients that are sick require more insulin
The intermediate or long acting insulin should
Regular insulin should be given q4h as per a
69-year old white female was in good
health until 3 weeks ago, when she
suddenly developed severe polyuria,
polydipsia and polyphagia. She has lost 20
pounds ( going from 120 to 100) during
that period and feels extremely weak.
When her daughter brings her to you, in
the ED, she is somewhat lethargic. Past
medical history reveals HTN(Tx with a
small dose of enalapril). There is no
history of cardiac disease.
Physical Exam reveals a pale, lethargic,
confused woman, breathing rapidly.
B/P is 102/72 P 110 Resp 32
Her skin is very dry, bowel sounds are weakly
Blood test revealed
Na+ 130 (135 – 145)
K+ 5.1 (3.5 – 5.1)
Glucose 794 ( 70 – 110)
Cl- 104 (95 – 105)
HCO3 3mEq/L (21 – 30)
pH 6.92 (7.35 – 7.45)
pO2 92 mm (80 – 105)
A 37 year old white female has a 20 year
history of diabetes mellitus. She has
been having difficulty with
hypoglycemia in the early morning. She
used to be on beef-pork insulin and did
not have any problems.
Human NPH 16U am; 8 U pm
Human Regular 8 U am; 3 U pm
Insulin have different peaks and duration of
In this case you must note that animal insulin has
a slower peak than human insulin
In this case this lady was advised to move the
NPH evening dose to qhs --- which allowed the
NPH peak to occur later
To cover the evening problem one should also
increase the bedtime regular insulin --- in this
case it was increased by 2 U
A 56-year male has a history of type II diabetes for 10
years. He is currently on glipizde 20 mg BID and
monitors his glucose twice a day. Over the last 2 weeks
his fasting glucose were 157 – 278 (average 199); supper
values were 145 – 292 (average 212).
Yesterday his fasting glucose was 234 and
HgA1c was 14.8%
P.E.: B/P 142/90 P 72 Resp. 12 height:72 inches
The rest of the physical was normal with no
evidence of retinopathy or neuropathy
What is the best option for this patient?
Though this patient may not want to go
on insulin …. We have no choice.
He has unacceptably high glucose
HgA1C confirms the fact that insulin is
What do we start him on?
Many clinicians start their type II that now
require insulin on NPH or ultralente and add
regular insulin later as needed to tune – up
After knowing what it would take to treat this
patient --- you may then decide to use pre-
Should this patient be hospitalized?
A 30-year female has no prior medical
problems. As part of a routine obstetric
care, she has a glucose screen at 24 weeks.
She is given 50-g glucose to drink and a
glucose level is obtained 1 hour later. Her
results revealed a level of 156 mg (<140)
She is 64 inches tall and weighs 220
What do you do know?
You should now order a 3 hr GTT,
which they give 100 g of glucose
Her results were
What is your opinion?
This patient has Gestational Diabetes. According to
the National Diabetes Data Group – Dx is made if two
or more values exceed the norm.
You should start this patient on a ADA 2000 calorie
diet, give her a glucometer(she to take readings four
times daily) and see her in a week.
You see her back in a week and her glucose log reveal:
Fasting LunchSupper Bedtime
97 93 115 104
112 101 107 99
101 101 89 122
93 105 102 111
115 112 121 118
99 107 113 105
96 101 117 109
What should you do now?
This patient should be started on insulin.
Though these level appear good; in pregnancy
glucose levels are significantly lower.
Target glucose goals are:
Fasting: 60 – 90
Non-fasting (before breakfast) 60 – 105
After meals: < 120
2am – 6am: >60
Since most of these patients seem to be insulin
resistant it is recommended to start with
0.6U/kg/day. In this patient we would give 30 –
32 U NPH (or Longer acting) BID. She returns
in four days with the following readings:
Fasting LunchSupper Bedtime
93 99 97 122
86 100 98 113
74 78 99 107
68 90 79 112
How is our patient doing?
These reading show that we still have a problem at
bedtime. Therefore, we should add 2U of regular
insulin in the evenings
A 58 year-old man with a 12 year history of type 2 diabetes comes to
your office because of an ulcer in his right foot. Physical exam
reveals a 1-cm irregular ulceration over the right metatarsal
head, surrounded by an area of black gangrenous skin. The
patient is admitted and undergoes amputation of the right
forefoot. Which of the following would have been most
effective in preventing this complication?
Appropriate instructions on self-care of the feet
B. Doppler exam of the lower extremities
C. Nuerophysiologic and electromyographic studies
D. Local application of platelet-derived growth factor
E. Prophylactic treatment with cholesterol-lowering agents
Use of oral agents
45 years old; repeat q 3 years
Overweight (BMI 25 kg/m2*)
Have a first-degree relative with diabetes
High-risk ethnic population
h/o GDM or baby >9 lbs
Other sx of insulin resistance (acanthosis)
h/o vascular disease
Symptoms of diabetes and a casual plasma glucose 200 mg/dl or..
FPG 126 mg/dl ( no caloric intake for at least 8 hr) or…
BS 200 mg/dl after OGTT (2 hr after 75 gm glucose).
In the absence of unequivocal hyperglycemia, these
criteria should be confirmed by repeat testing on a different
OGTT is not recommended for routine clinical
use, but may be required in the evaluation of patients with
IFG or when diabetes is still suspected despite a
normal FPG as with the postpartum evaluation of women
A1C<7.0% (q 3 mo if uncontrolled; twice yr if at goal)
Preprandial BS 80-110 mg/dl (60-90 if pregnant)
Postprandial BS<140 mg/dl (<120 if pregnant)
Blood pressure<130/80 mmHg
Triglycerides <150 mg/dl
Annual influenza vaccine
Pneumococcal vaccine for adults with diabetes
Revaccination is for individuals >64 if vaccine was
administered >5 years ago. Other indications for repeat
vaccination include nephrotic syndrome, chronic renal
disease, and other immunocompromised states, such as
SMBG TID w/ DM1 and GDM
BP each visit
Annual urinary microalbumin (<30ug/mg)
Annual optho exam starting 3-5 yrs after onset w/
DM1, and upon diagnosis in DM 2
Visual foot exam each visit. Comprehensive exam
yearly (sensation, biomechanics, foot structure,
vascular status and skin integrity)
Risk assessment at first prenatal visit
Low-risk status requires no glucose testing
Age <25 years
Weight normal before pregnancy
Member of an ethnic group with low prevalence
No known diabetes in first-degree relatives
No history of abnormal glucose tolerance
No history of poor obstetric outcome
High risk features (obesity, h/o GDM, glycosuria,
or FH) should undergo glucose testing as soon as
FPG 126 mg/dl or a casual plasma glucose 200 mg/dl meets the threshold
for the diagnosis of diabetes (confirm on subsequent day)
High-risk women not found to have GDM at initial screening and average-
risk women should be tested between 24 and 28 weeks of gestation.
Testing should follow one of two approaches:
One-step approach: 100-g OGTT
95 mg/dl fasting
180 mg/dl at 1 h
155 mg/dl at 2 h and 140 mg/dl at 3 h.
*Two or more of the plasma glucose values must be met or exceeded for a
Two-step approach: perform an initial screening by measuring the plasma
or serum glucose concentration 1 h after a 50-g oral glucose load and
perform a diagnostic 100-g OGTT on that subset of women exceeding 140
Drug Class Mechanism of Action Side Effects
Sulfonylureas/ secretagogues weight gain, hypoglycemia
↓hepatic glucose output
Metformin GI upset, lactic acidosis,
TZD’s ↑ peripheral glucose fluid retention, weight gain
Alpha-glucosidase inhibitors flatulence, diarrhea
*Each will lower A1c by 1-2% compared to
placebo. When combined, efficacy typically
Know the types of insulin and onset
Know how to adjust insulin
All regimens include basal and bolus
•Make changes slowly, taking into account diet, activity,
•Asses the effectiveness of insulin at its peak time of
•Increase short/rapid insulin based on post-prandial
•Increase long-acting when BG high fasting or
•Inject into subcutaneous abdomen and rotate sites
HHNK - Hyperglycemic, hyperosmolar, non-
ketotic coma. Onset 2 days to 2 weeks.
Osmolarity > 310
Glucose > 600
Usually seen with Type 2
exhibiting increasing insulin resistance, esp. after gorging
Presents with marked dehydration and CNS SSx
often mimicking a stroke.
Must correct S-L-O-W-L-Y to prevent cerebral
edema. Watch K+ levels.
Glucose < 50
Not enough to eat (or forgot)
Too much insulin (or pills)
Did not allow for exercise
CNS- confusion, delirium, coma
Autonomic - hunger, anxiety, SWEATING, tachycardia.
If patient is conscious - give OJ. Otherwise injection of
glucagon, glucose gel in mouth, or 50% glucose by IV
Neuropathies - peripheral
Obstruction of vessels that supply nerves
Decreased sensitivity to pain, temperature and light
Decreased proprioception and vibration sense.
Neuropathies - central and autonomic
atonic urinary bladder
impairment of special senses
Thickened basement membrane in glomerulus
Causes microalbuminuria (300 mg / day)
Nodular scarring and destruction of glomerulus.
Kimmelstiel - Wilson lesion. Pathognomonic for
Leading cause of blindness. DM has increased risk
for cataracts and glaucoma
new vessels, fragile vessels, microaneurysms,
hemorrhage. Followed by scarring and retinal
detachment. Takes 20 years to develop. 100% of
Type 1; 60% Type 2. Need to evaluate yearly.
Retinal photos excellent.
Most common reason for hospitalization
Due to impaired circulation (PVD)
Abnormal glycoprotein thickens vessel wall
Chronic hypoxia (glycohgb has > affinity for O2)
Due to neuropathy
Cannot feel pain to prevent injury
Prevention: Wear good closed-toe shoes, white
cotton socks, keep feet clean and dry, clip toenails
straight across, inspect feet daily.
Skin: boils and abscesses
Urinary tract infections - quickly spread to kidneys
Infected cuts of extremities
Finger and toenail fungus