Ch. 33 Diabetes Mellitus Flashcards
1
Q
What is the definition of diabetes mellitus?
A
A disorder of carbohydrate, fat, and protein metabolism resulting from lack of insulin availability or lack of effectiveness.
2
Q
What are the four types of diabetes?
A
Type I
Type II
Gestational (GDM)
Other
3
Q
What is type I diabetes?
A
`AUTOIMMUNE: destruction of the beta cells and absolute insulin deficiency
tends to happen earlier in life
4
Q
What is type II diabetes?
A
INSULIN RESISTANCE: as well as a relative insulin deficiency; an adaptive response to over nutrition
5
Q
What is gestational diabetes?
A
glucose intolerance detected first during pregnancy
6
Q
What are some “other” diabetes?
A
diabetes associated with other conditions:
most often pancreatic diseases or endocrine disorders
SOME TEMPORARY, SOME PERMANENT
7
Q
What are normal lab values for someone without diabetes?
A
FPG (fasting plasma glucose):
8
Q
What are the lab values for someone who is impaired fasting plasma glucose/ impaired glucose tolerance (pre-diabetes)?
A
FPG (fasting plasma glucose): 100-125 mg/dl
OGGTT (oral glucose tolerance test): 140-199 mg/dl
A1C: 5.7%-6.4%
9
Q
What are the lab values for someone with diabetes (REGARDLESS OF THE TYPE)?
A
FPG (fasting plasma glucose): >125 mg/dl (2 or more occasions)
OGGTT (oral glucose tolerance test): >200 mg/dl
A1C: >6.5%
10
Q
What is the best test to use for checking average blood sugar?
A
A1C - once the glucose is in the RBC it doesnt get out until the cell dies
MAKES IT HARD FOR SOMEONE TO FAKE A GOOD TEST RESULT
11
Q
Would you do an OGGTT for someone you know has glucose tolerance issues?
A
Not normally, usually this test is done for suspected gestational diabetes cases
12
Q
How many people with type I diabetes have the autoimmune version?
A
95%
13
Q
What brings on type IA diabetes?
A
Genetic predisposition
environmental trigger
t lymphocyte mediated hypersensitivity reaction to beta cell (autoantibodies)
14
Q
What cells are destroyed in type IA diabetes?
A
the beta cells
15
Q
What are people with type I diabetes prone to?
A
ketoacidosis (insulin helps stop lipolysis)
16
Q
When does type I generally develop?
A
younger people, but can occur at any age
17
Q
What is the honeymoon period of type I diabetes?
A
this is a time during early diagnosis where it seems like the beta cells regenerate and the symptoms disappear
VERY SHORT PERIOD OF TIME
18
Q
If we came up with an immune modification treatment, when would it be most effective?
A
If we caught it early, so the pancreas would still have some beta cells left to produce insulin.
19
Q
What type of diabetes do 90-95% of people with diabetes have?
A
type II
20
Q
What defines type II diabetes?
A
fasting hyperglycemia even with the availability of insulin
21
Q
What are the mechanisms of type II diabetes?
A
peripheral insulin resistance (inefficient receptors on target cells)
deranged beta cell secretion of insulin
increased hepatic glucose production
22
Q
Can beta cells get worn out from secreting too much insulin with type II diabetes?
A
YES, the body will keep telling the beta cells to make insulin because their sugars wont go down, even when the insulin levels are high
23
Q
What other metabolic abnormalities does hyperglycemia contribute to?
A
elevated triglycerides, low HDL, hypertension, abnormal fibrinolysis, coronary artery disease
24
Q
What are some risk factors for type II diabetes?
A
family history, obesity, physical inactivity, fat distribution (weight carrying in upper body and trunk)
MOST PEOPLE WITH DISEASE HAVE A GENETIC PREDISPOSITION FOR IT AS WELL
25
What do chronic high FFA (free fatty acid levels) with obesity lead to?
beta cell dysfunction
tissue insulin resistance
reduced hepatic insulin sensitivity
triglyceride accumulation in the liver
26
What does obesity do to our resistance to the action of insulin and the livers production of glucose?
Increases our insulin resistance and liver production of glucose. (causes hyperglycemia and hyperinsulinemia)
27
Can insulin resistance improve with weight loss?
YES YES YES
just eating less and losing weight can help
BUT
weight loss is even better if coupled with exercise
28
How would exercise help with diabetes?
It helps the muscles take in more glucose
29
What are the requirements that you have to have at least three of to be considered to have metabolic syndrome? (there are 5)
Increased FPG: >100 mg/dl
Abdominal obesity: waist circumference >35" in women and >40" in men
increased blood triglyceride levels: greater than or equal to 150
decreased HDL levels: 130/85 mm Hg
COMMON IN PEOPLE WITH TYPE II DIABETES
30
What are some other things you might see in someone with metabolic syndrome (harder to initially assess)?
systemic inflammation
elevated C reactive protein level (high risk for cardiac events)
abnormal fibrinolysis
abnormal functioning of vascular endothelium (Higher risk for clots)
31
What are some causes of "other" specific types of diabetes (secondary diabetes)?
Pancreatic disease
cushings syndrome
acromegaly
pheochromocytoma
medications:
- - loop and thiazide diuretics (watch when treating diabetic with hypertension)
- - glucocorticoids
- - oral contraceptives
- - anti-psychotics
IF THESE DISEASES ARE REVERSED OR MEDS ARE STOPPED THE DIABETES WILL MORE THAN LIKELY GO AWAY
32
What is the definition of gestational diabetes?
glucose intolerance first detected during pregnancy
33
What are women with GDM (gestational diabetes mellitus) at high risk for?
complications with pregnancy
mortality
fetal abnormalities
developing type II diabetes 5-10 years after delivery
34
What are some risk factors for GDM?
family history of diabetes
obesity
glycosuria
history of stillbirth or spontaneous abortion
fetal abnormalities in previous pregnancy
previous large or heavy-for-date infant
of advanced maternal age (over 25)
five or more pregnancies
35
When do we do a OGGTT to check for gestational diabetes during pregnancy?
24-28 weeks
THEORETICALLY DONE FOR HIGH RISK POPULATION, BUT MOST EVERY PREGNANT WOMEN GETS SCREENED FOR THIS
36
What are some of the diagnostic methods for checking blood glucose?
FBG (fasting blood glucose)
casual (random) blood glucose
glucose tolerance test
glycosated hemoglobin (HbA1C)
urine tests
37
What is an FBG?
these are glucose levels measured after being with held from food for 8-12 hours
38
What is a casual (random) blood glucose, and what is considered diabetic?
done with no regard to meal times of that day
elevated glucose (>200 mg/dl) with the presence of classic DM symptoms:
- - polydispia
- - polyphagia
- - polyuria
- - blurred vision
39
What is a glucose tolerance test?
What is the normal outcome?
Abnormal?
measures the bodies ability to store glucose by removing it from the blood
normally BG levels will return to normal after 2-3 hours after ingestion of glucose (this means there is sufficient insulin present to remove it from the blood into the cells)
If the glucose levels stay elevated for a long period of time
40
What is HbA1c? (glycosated hemoglobin)
Why is this a great tool?
What does the ADA say is the level that needs intervention?
Measure the amount hemoglobin that has glucose incorporated into it
entry of glucose into RBC is not insulin dependent, it is dependent on the BG levels of the blood, and is not reversible
This tells us an index of what the BG levels have been during the last 2-3 months
greater than 7% needs corrective measures
41
What is the urine test?
Who will mainly get this test?
This is a test for ketones in the urine
mainly for type I diabetics or those prone to ketoacidosis... but not common test for anything else because home BG tests have become so accurate
42
Do type I diabetics always need interventions for blood sugar regulation?
YES, they always need to put insulin into their body
43
What antidiabetic medications do type II diabetics need?
They can take oral medications if caught early enough, but they will eventually need insulin
44
What is a general view about the proper diet for type I and II diabetics?
type I: monitor their food intake so insulin can be adjusted properly
Type II: weight loss diet
45
What about exercise and type I and II diabetics?
type I: exercise for its general benefits
type II: need to exercise for weight loss
Both: enhances peripheral insulin reception and can lead to hypoglycemia
THE EXERCISE NEEDS TO BE REGULAR, NOT SPORADIC, THIS HELPS SCHEDULE INSULIN ADMINISTRATION SCHEDULE
46
What is happening in the body of people with type II diabetes?
impaired insulin secretion/excessive glucagon secretion
carbohydrate absorption (typically high because of obesity)
decrease insulin-stimulated glucose uptake
increased basal hepatic glucose production
47
What are the major effects and minor effects of the biguanides for type II DM?
Major: decrease hepatic glucose output
Minor: increases peripheral glucose uptake
48
What are the minor and major effects of thiazolidinediones for type II DM?
major: increase peripheral uptake of glucose
minor: decrease hepatic glucose output
49
What is the major effect of glucosidase inhibitors and amylin analogs for type II diabetes?
decrease glucose absorption in intestines
AMYLIN ANALOGS ALSO DECREASE GLUCAGON SECRETION
often causes diarrhea and other GI effects
50
What are the major effects of insulin secretagogues incretins for type II diabetes?
increase insulin secretion and decrease glucagon secretion
51
Can type I diabetics take oral medications for their disease?
NO, their beta cells dont function at all
52
Is it true that a type II diabetics pancreas will eventually burn out and require them to go to insulin injections?
YES YES YES
| often oral meds alone are sufficient for 5 years when caught early
53
What are the different types of insulin we use for injections?
short acting (regular)
Rapid acting (lispro, aspart, glulisine)
Long acting (NPH, glargine, determir)
54
How long is the onset and duration for short acting insulin?
onset: 30 minutes
duration: 5-8 hours
55
What is the onset for rapid acting insulin?
56
What is the onset and duration for long acting insulin?
onset: several hours
duration: 12-24 hours
CAN BE SPLIT UP INTO INTERMEDIATE AND LONG ACTING
57
Do people usually have multiple insulin injections a day?
YES
best if its a combination of intermediate and immediate (rapid) acting
58
What if a patient isnt compliant with having a lot of insulin injections a day?
will have to do less frequent shots of long acting insulin
doesnt work quite as well
59
What is another way to get insulin into the body?
A continuous subcutaneous insulin infusion pump
60
What are kids especially at high risk for?
very low blood sugars
can cause cognitive damage, which can be permanent if they have many hypoglycemic episodes
61
What does the fact that kids BG tends to run low a lot do for our treatment?
we tend to let them run a little higher when it comes to BG levels
62
What do we look at when choosing route and method of insulin to go with?
diet
lifestyle
ability to comply
63
What are some acute complications with hyperglycemia?
Diabetic ketoacidosis (DKA)
Hyperosmolar Hyperglycemic State (HHS)
64
With what type of diabetes is DKA more common?
Type I
65
What are the mechanisms of DKA?
LACK OF INSULIN
this results in the breakdown of tryglycerides into fatty acids and glycerol that, causes an increase in production of ketones by the liver when the fatty acids are used for energy
66
With what type of DM is HHS (hyperosmolar hyperglycemicc state) more common?
type II
67
What is the mechanism of HHS (hyperosmolar hyperglyccemic state)?
Elevated serum glucose levels due to and increased intake of carbohydrates or an increased resistance to insulin
USUALLY HAVE JUST ENOUGH INSULIN PRESENT TO PREVENT KETONE PRODUCTION
68
What are the three major derangements that make a definitive diagnosis of DKA?
Hyperglycemia >250 mg/dl
ketosis (ketonemia at 1:2 dilution and ketonuria)
metabolic acidosis (low bicarb
69
What are the clinical presentations of diabetic ketoacidosis?
slow onset; prolonged recovery
1-2 days of polyuria, polydispia, nausea, vomiting, marked fatigue: may progress to stupor or coma
fruity breath because of volatile ketoacids being blown off with CO2
abdominal tenderness and hypotension
compensatory mechanisms: tachycardia and tachypnea
high levels of counterregulatory hormones
70
What is the problem with DKA and the presence of counterregulatory hormones?
These hormones are trying to raise our BG even more, this makes up have to treat the whole process, usually we give low dose insulin to slowly lower BG and keep it steadily lowered to not trigger the release of these counterregulatory hormones
71
What can hyperglycemia lead to?
polyuria
dehydration
critical loss of electrolytes (can be cause of neurologic symptoms)
72
What does hyperglycemia do to the ECF and ICF?
The ECF is hyperosmolar which causes a water and potassium shift from ICF to ECF
73
What about hyperglycemia and triglycerides one more time?
the lack of insulin lead to the breakdown of triglycerides to fatty acids and glycerol, which when used for energy increases ketone production by the liver
74
What do the excess ketoacids cause?
metabolic acidosis, this causes a decrease in serum bicarb levels
BUFFER SYSTEM CAN BE INHIBITED SOMEWHAT BY SHIFT OF POTASSIUM OUT OF CELLS
75
Is the onset of HHS rapid?
NO
it is insidious
76
With what age group does HHS most often occur?
elderly
often mistaken for a stroke because of neurological manifestations
77
What characterizes HHS?
Hyperglycemia >600 mg/dl
hyperosmolarity >320 mOsm/L (pulls water from cells which causes dehydration, excessive thirst, neurological signs and symptomssuch as seizures, hemiparesis, aphasia, visual disturbances
absence of ketoacids
decreased LOC
78
What are the factors that contribute to HHS?
increased resistance to the effect of insulin
excessive carbohydrate intake
79
What causes hyperglycemia?
too much food
too little insulin
illness or stress
80
What is the onset of hyperglycemia?
gradual, can progress to coma
81
What are the blood sugar levels for hyperglycemia?
above 200 mg/dl
82
What is the normal blood sugar range?
70-115 mg/dl
83
What do you do if your blood sugar is over 250 mg/dl for several tests?
call the doctor
84
What are the symptoms of hyperglycemia?
polydispia
polyuria
dry skin
polyphagia
blurred vision
drowsiness
nausea
85
What is hypoglycemia often referred to as?
insulin reaction
86
What are our insulin levels in relation to our glucose levels?
insulin levels are excessive and glucose levels are below normal
87
What type of DM does hypoglycemia most often occur?
Type I
88
What are some precipitating factors for hypoglycemia?
insulin dosage error
failure to eat
increased exercise or random exercise
decreased need of insulin after removal of stress
medication dosage changes
alcohol decreases gluconeogenesis and may cause hypoglycemia if consumed in large amounts or on empty stomach
89
What is the onset and progression of hypoglycemia like?
rapid, may progress to shock
90
What are the manifestations of hypoglycemia?
very wide variation
altered cerebral function
headache
weakness and fatigue
difficulty making decisions
seizures
dizziness
shaking
irritable
behavioral disturbances
coma
PNS = hunger
SNS = anxiety, tachycardia, diaphoresis, vasoconstriction (cool and clammy skin)
91
Do you treat a patient who isnt alert orally?
NO NO NO
92
What BG level is considered hypoglycemic?
93
What can you do if youre hypoglycemic?
drink OJ or milk
eat hard candies
test BG
30 minutes after symptoms go away eat a snack
contact doctor if symptoms dont stop
94
Describe the somogyi effect.
These are hyperglycemic episodes that are directly following a hypoglycemic episode
it is said that this is because the body reacts to insulin induced hypoglycemia by using a compensatory mechanism that releases counterregulatory hormones that elevate the serum glucose and may cause some degree of INSULIN RESISTANCE
95
When does the somogyi effect often occur?
often at night but can be at random unrecognized times
MAKES IT HARD TO DIAGNOSE
96
What is the dawn phenomenon?
an unexplained morning rise in fasting BG levels, believed to be caused by a changce in the normal circadian rhythm for glucose tolerance and an inappropriate increase in counterregulatory hormones
The fasting (pre-breakfast) level is higher than the pre-bedtime (should be higher) level
When this is coupled with the somogyi effectn (often is) there can be a profound increase in BG in the mornings
97
Where do chronic complications of DM most often occur?
in insulin independent tissues of the body (dont require insulin for glucose entry into the cell)
98
What is the most important factor for chronic diabetic complications?
the chronic glycemic levels of the blood
99
What are the common chronic effects of diabetes?
neuropathies
nephropathies
retinopathies
macrovascular complications; cardiovascul disease and stroke
foot ulcers
INFECTIONS
100
What is the pathology of neuropathies?
thickening of walls of nutrient vessels that supply nerves
ischemia is ultimately responsible for neural changes
segmental demylenation of schwann cells
101
What are the two types of neuropathy?
somatic
autonomic
102
Describe somatic neuropathy
diminished perception of vibration, pain, temperature
usually bilaterteral and symmetric
usually in a stocking-glove pattern
increased risk of falling, serious burns, injuries to feet
103
describe autonomic neuropathy.
defects in vasomotor responses
- - decreased cardiac responses
- - impaired gastric motility and hypersecretion
- - inability to empty bladder; urinary stasis and UTI
- - sexual dysfunction: leading physiologic cause of sexual dysfunction
104
Describe diabetic nephropathy
leading cause of end-stage renal disease
causes lesions that effect glomeruli
early manifestation is microalbuminemia
- - increased protein loss through urine
- - risk increases with A1c levels greater than 8.1%
hypertension accelerates the progression, critical to keep under control
smoking doubles rate of progression of ESRD in type II DM
105
Describe diabetic retinopathies.
leading cause of blindness in the US
High lipids, poor glycemic control, hypertension are risk factors
Characteristics:
retinal hemorrhages
abnormal retinal vascular permeability
microaneurysm formation
scarring
retinal detachment
106
Describe the macrovascular complications of DM.
High risk for:
- - coronary artery disease
- - stroke
- - peripheral vascular disease
many risks for vascular disease are present in people with diabetes:
- - obesity
- - hypertension
- - hyperglycemia
- - hyperinsulinemia
- - hyperlipidemia
- - altered platelet function
- - elevated fibrinogen levels
RISK FOR PLAGUE BUILDUP THAT CAUSES HARDENING OF THE ARTERIES, CAUSES HYPERTENSION, AGGRAVATES KIDNEY ISSUES, CAUSES IMPAIRED BLOOD FLOW, MAKES IT HARD TO FIGHT INFECTION
107
describe diabetic foot ulcers.
distal symmetric neuropathy is a major risk factor for foot ulcers; because you might be unaware of trauma or pain
abnormal focus of pressure + loss of sensation means a foot ulcer may occur
diabetics should have a full foot examination once a year
108
describe the somatosensory testing for diabetics feet.
monofilament test:
applies 10g of pressure at the point of contact
4-10 sites are tested for sensation
109
With DKA, if you just treat the hyperglycemia has the complication been fixed?
Not necssarily, you would still have to worry about the acidosis.
