X Diabetes Mellitus Quiz/HW Flashcards
DM defined as…
a group of systemic metabolic disorders characterized by hyperglycemia
DM cannot be…
cured
How can DM pt reduce complications?
diet, excercise
list 4 types of DM
- Type 1 (IDDM)
- Type 2 (NIDDM)
- Gestational DM
- Other
?Define Pre-DM
BG abnormal (100-126 mg/dL) but not meeting criteria for DM which is (?) >200mg/dL (? after fasting overnight)
Juvenille DM knows as
Type 1, Insulin Dependent DM (IDDM)
Adult onset DM aka
Type II, Non Insulin Dependent DM (NIDDM)
What is most prevalent type of DM?
Type II, NIDDM
list 5 factors assoc. w development of Type II DM
- poor diet
- sedentary lifestyle
- obesity
- race
- age
- family history
- Hx of gestational DM
- ETOH abuse
- smoking
List 4 Modifiable risk factors
Diet, excercise, obesity, smoking
List 4 NON modifiable risk factors
Race/Ethnicity, Age, Family History, Gestational DM
Majority of Type II DM are…
obese
People w DM at hi risk of dev…..
stroke, heart disease
? DM leading cause of …
- ESRD, End Stage Renal Disease
- Blindness (?)
DM is ? leading cause of ?
7th, Death
what are hi risk populations for dev DM?
-African Am
-Asian Am
-Native Am
-Pacific Islanders
-Latino
(anything w American)
Viruses that trigger DM, Type 1
- Mumbs/Rubella
- Coxsackie 4
Relationship btwn GLUCOSE and INSULIN
Lock and key
Insulin is a ? produced by the ?
Hormone, Beta Cells in the Islets of Langherhan of the Pancreas
Stimulus for Insulin production is ?
UP BG (hyperglycemia)
? Routing screening for DM should be done on anyone with 1 or more of the ? risk criteria?
Non Modifiable and Modifiable
-HTN
-Impaired Glucose Intolerance
? -HDL 250
List 3 tests used to screen for DM
- A1c
- OGTT (>200mg/dL)
- Fasting BG (>126mg/dL)
Definition of Glucosuria
glucose present in urine.
Polydipsia
excessive thirst
Polyuria
excessive urination
Polyuria results in…
dehydration. glucose is an osmotic diuretic
Polyphagia
excessive eating
Lantus?
Long Acting Insulin
Which insulin faster acting and why?
HumalinR or Humalog
Humalog is faster acting.
Humalog is RAPID acting and onset only 15min. HumalinR is Fast Acting w onset of 30min - 1hr.
List an intermediate acting insulin
NPH (NovolinN, HumulinN)
Type I DM produce ? insulin?
What cells are damaged?
Type I are insulin ?
- NO insulin
- Beta cells from Islets of Langerhans
- Insulin Dependent (IDDM)
3 symptoms of Type 1
3 Ps (polyuria, polydypsia, polyphagia)
Classic symptoms of DM
3 Ps (polyuria, polydypsia, polyphagia)
problem w Type 2 DM is insulin ? , rather than lack of insulin
Resistance
Decreased sensitivity to Insulin known as insulin ?
resistance
Insulin attaches to insulin cell X and allows X to leave X to enter cell
receptors, glucose, blood stream
Glycogen is
storage form of glucose (liver, (muscle, adipose))
Glucagon is
hormone released by pancrease to UP BG. breaks down glycogen to form glucose to be used as energy
Glucose is
mono-saccharide, simple sugar
HUMALOG
REGULAR
NPH
LANTUS
HUMALOG, Rapid Act, 15min, 30 - 1hr PEAK, 3-6.5hr DURATION
REGULAR, Short Act, 30-1hr, 2-3hr PEAK, 4-6hr DURATION
NPH, Inter Act, 1-2hr, 6-14hr PEAK, 16-24hr DURATION
LANTUS, Long Act, 2hr, NO PEAK, 24hr DURATION
Who most at risk for dev DM?
Caucasian woman, Asian woman, AfAm woman, hispanic child?
AfAm
anyone w american
risks for dev of DM?
Over 45
overweight
HDL >40md/dL
Sendentary lifestyle
YES Over 45
YES overweight
NO HDL >40md/dL (concern is
Normal fasting GL
99mg/dL and below
prep for fasting BG
-NPO 8hrs
normal post prandial BG
normal pre prandial BG
99mg/dL and below
Poorly controlled DM will have hba1c of
9%
what w serum insulin show in NIDDM and why?
how much insulin being produced and how well the body is using it. Normal to hi if NIDDM under good control, HI if becoming resistant
What w serum insulin show in IDDM and why?
no insulin present in IDDM showing that body is not producing any.
How will C-peptide show person is Facticiously Hypoglycemic?
one C-Peptide produced per Insulin . If the two numbers don’t match, you can determine over dose of insulin in order to lower BG.
Incidence of complications are ? in IDDM and ? in NIDDM?
frequent in both
What is glucose?
Simple sugar, monosacharide
Stored glucose is ?
glycogen
? is released from pancreas and instructs liver to convert ? to glucose?
Glucagon, Glycogen to Glucose
If body cannot use glucose for energy, it will use ? instead. this creates by products called ?. List them….
fat. ketones.
AAH….
Acetone, Acetoacetic Acid, Hydroxybutyric Acid
List 6 causes of insulin resistance
obesity, hereditary, sedentary lifestyle, age, diet, race, metabolic syndrome, steroids, meds
Type I DM usually develops at age ?
40 and below
Type II DM usually develops?
40 and older
Why is gestational DM a concern?
can increase risk for patient to develop NIDDM in future pregnancies. Risk for baby to be hypoglycemic due to overproduction of insulin.
Glycosuria
excess glucose in urine
Hirtsutism
male pattern hair growth in women
8 S/S of DM
3Ps, slow wound healing, halos, blurred vision, cold extremities, nausea, impotence, neuropathy
Hypoglycemia BG levels
Normal values
- A1c
- Pre Prandial
- Post prandial
- Serum Insulin
- A1c - 5% and below
- Pre Prandial - 100 mg/dL and below
- Post prandial - 140 mg/dL and below
- Serum Insulin - 5-24 mcU/L
Ketones are toxic ?
Acids
Ketones mainly produced in pt w TYPE?
Type I
Type 2 DM develop this complication
HHNS (Hyperosmolar, Hyperglycemic, Nonketotic Syndrome)
Components of good or tight glycemic control
A1c test under 5%. overall sense of wellbeing, normal BP (130/80)
? Why does DKA lead to metabolic acidosis
build up of ketones creates acidotic body affecting metabolism.
DKA characterized by….
vomiting, kussmaul breathing, confusion, dehydration
2 causes of DKA
IDDM, starvation, fasting
3 triggers of DKA
hyperglycemia, stress, starvation, no insulin
How does body compensate for acidic state of DKA
Kussmaul breathing
DKA will occur in BG of
> 250 mg/dL
SS of DKA
poor skin turgor, BG >250, dry mouth, fruity breath, tired, confusion, 3ps, nausea
what is Rx for DKA?
Ingest Insulin, IV Therapy, Meds, Electrolytes
what type of Insulin administered during DKA?
REGULAR, IV
Why doesn’t DKA develop in NIDDM?
because there is always insulin present so body never metabolizes fat.
what is osmotic diureses?
UP urine due to certain substances in urine acting as osmolor diuretics. Osmolar Hyperglycemic state
HHS characterized by?
Hyperglycemic, Hyperosmolality and dehydration without ketoacidosis. Change in level of consiousness
P.925
5 SS of HHNS
- BG>600mg/dL
- dry mouth
- polydypsia
- fever over 101
- loss of vision
- hallucinations
- weakness on 1 side body
5 SS of hypoglycemia
-confusion, weakness, shakiness, anxiety, heart palpitation
Ketosis present in ?? and not in ??
DKA, not in HHNS
list 4 rapid acting sugars
lifesavers, soda, oj, raisins
15/15 rule
test BG, give 15g fast acting sugar, wait 15 min, retest and give again. repeat until levels normal.
Somogyi effect
when body reacts to night time hypoglycemia, stimulating glucagon, leaving pt hyperglycemic in the am.
Rx for Somogyi effect
treat hypoglycemia in timely manner, lower eve dose of insulin
cause of Dawn Phonomenon
Body produces hormones to raise BG. 4-8am. no carbs at night, adjust night insulin
Insulin administered w ??
Insulin syringe only
what type of insulin administered via IV?
REGULAR only
What type of insulin can be administered thru insulin pump?
Rapid Acting or Regular
What can Lantus be mixed with?
NOTHING
Insulin introduced as Rx when ?
Diet, Exercise or meds not effective. Insulin in a last resort.
LANTUS
REGULAR
HUMALOG
NPH
LANTUS, Long act, 2hr, NO PEAK, 24hr DURATION
REGULAR, Short Act, 30min - 1hr, 2-3hr PEAK, 4-6hr DURATION
HUMALOG, Rapid act, 15min, 30-2.5hr PEAK, 3-6.5hr DURATION
NPH, Interm Act, 30min, 4-8hr PEAK, 24hr DURATION
3 causes of hypoglycemia
- med
- excercise
- malnutrition
- fasting
- insulin OD
- unplanned strenuous activities
If pt has BG of 35, what symptoms w they experience?
- irritability
- hunger
- sweating
- palor
- tremors
- palpitation
- tachycardia
- muscle weakness
- coma
- polyphasia
- blurred vision
- headache
Treatment for unresponsive DM in hypoglycemic state?
-IV,SubQ, IM, Glocagon, D50
HHNS
Hyperosmolar, Hyperglycemic, NonKetotic Syndrome
HHNS occurs in what type DM?
Type II, NIDDM
BG in HHNKS can be as high as?
1500 mg/dL
HHNKS diff from DKA how?
in HHNKS, small amount of insulin prevents ketosis and acidosis
??4 things that precipitate HHNS
MEDS, steroids, Thiazidoliniese, Dilantin?, acute illness, infection, trauma
5 causes of DKA
- lack of insulin
- med mistakes
- infection
- ETOH/Drug abuse
- CVA
- MI
- PNA
- UTI
- Stress
- pump failure
- non compliance
DKA info
An infection or other illness can cause your body to produce higher levels of certain hormones, such as adrenaline or cortisol. Unfortunately, these hormones counter the effect of insulin — sometimes triggering an episode of diabetic ketoacidosis. Pneumonia and urinary tract infections are common culprits.
DKA info
Diabetic ketoacidosis occurs when a person with diabetes becomes dehydrated. As the body produces a stress response, hormones (unopposed by insulin due to the insulin deficiency) begin to break down muscle, fat, and liver cells into glucose (sugar) and fatty acids for use as fuel.
In DKA, fruity breath comes from
Acetone, excreted by Lungs
Rx for DKA
IV Regular Insulin, fluids, monitor E, monitor BG
Untreated DKA –>
coma, death
Untreated hypoglycemia –>
coma, death
DM should inspect feet how often?
daily
If severely sick, monitor BG how often?
q2hrs
instruction for DM pt travelling
-extra supplies, insulin, needles, batteries, fast sugar, emergency glucagon kit, medic alert bracelet, planned meals, H2O q2 hrs
rebound hyperglycemia
Somogyi effect - high blood sugar that is a response to low blood sugar.
Dawn Phenomenon
a normal rise in blood sugar as a person’s body prepares to wake up.
In early am, hormones cause the liver to release large amounts of sugar into bloodstream. body produces insulin to control rise in blood sugar.
If body doesn’t produce enough insulin, blood sugar levels can rise. This may cause high blood sugar in the morning (before eating).
4 LT complications of DM
- microvascular (eyes:glaucoma, retinopahty, cataracts)
- macrovascular (atherosclerosis)
- neuropathy (nerves)
- nephropathy (kidney)
test for acetone when BG at what level?
> 240 mg/dL
nephropathy
damage to blood vessels in kidney
how many develop some sort of Nephropathy?
40% DM pts
Albuminuria
protein in urine
Most common visual problem in DM
- glaucoma
- retinopathy
- cataracts
what can help preserve vision?
frequent eye exams, tight glucose control
Gastroparesis
delayed gastric dumping, caused by damage to vagus nerve, which regulates the digestive system
Gastroparesis associated w
neuropathy
what cardiovascular disease are DM risk for?
Atherosclerosis
2/3 ppl w DM die of ? and ?
stroke and heart attack (MI, CVA)
Lines of treatment for DM
1) diet, excercise
2) oral meds
3) insulin (last resort)
chronic hyperglycemia –>
blood vessels, nerve, kidney
diabetic nephropathy –>
ESRD
(?) normal BG level is
70-130 (DONT AGREE)
Hypoglycemia is
Hyperglycemia is
Fasting > 130 mg/dL
Postprandial > 180 mg/dL
Humalog
rapid acting
Regular Insuling
Short (fast) acting
Lantus
Long acting
Which is a Sulfonylurea?
Metformin, Actos, Precose, Glucotrol?
Glucotrol
how do Sulfonylureas work?
stimulate pancreas to release insulin. NOT dependent on BG
How do Biguanides work?
- LO hepatic glucose output
- UP insulin sensitivity at cell. so don’t need as much
-DOES NOT cause HYPOglycemia because it doesn’t raise insulin. only makes insulin already there more effective.
How do Thiazolidinediones work?
-UP insulin sensitivity at insulin receptors
-LO amount of glucose released by liver
-taken daily w NO regard to meals
(similar to Biguanides)
How do Alpha-Glucosidases work?
- prolong absorption of carbs in stomach & intestines. BLOCKS enzyme needed to digest starch.
- slows post prandial, UP BG
- given w EACH meal on 1st bite, not convenient
How do Meglitinides work?
- stim pancreas to release insulin
- Glucose DEPENDENT
- Taken 30min B4 meal
Metformin is what class? Trade Name?
Biguanide. Glucophage
-DOES NOT cause HYPOglycemia because it doesn’t raise insulin. only makes insulin already there more effective.
Glipizide is what class? Trade Name?
Sulfonylurea. Glucotrol.
Metformin given when?
w 1st bite
teach says w or shortly after. (WRONG?)
Glipizide taken when?
- 30 min before meal.
- Sulfonylurea
Glyburide class? administered when?
Sulyfonylurea, w 1st meal.
Prandin class? administered when?
Meglinitinide, 30 min b4 meal
- stim pancreas to release insulin
- Glucose DEPENDENT
- Taken 30min B4 meal
Precose class? administered when?
Alpha-Glucosidase, w 1st bite of meal.
- prolong absorption of carbs in stomach & intestines. BLOCKS enzyme needed to digest starch.
- slows post prandial, UP BG
- given w EACH meal on 1st bite, not convenient
Actos class? administered when?
Thiazolidinedione
-UP insulin sensitivity at insulin receptors
-LO amount of glucose released by liver
-taken daily w NO regard to meals
-similar to Biguanide’s
UP risk/rate of bladder CA. Contraindicated in pts w Hx of Bladder CA
Lantus administered ?
same time each day
DM is syndrome characterized by?
Hyperglycemia
DM due to damage to ?
Beta cells in pancreas, affecting producton and release of insulin
Type I DM cause?
Autoimmune
Type II DM cause?
obesity
What DM will resolve itself?
Gestational DM
