Holy Schmoley!!

karmyk · Feb 28, 2006

study break... preferably with ice cream

Daytonite, BSN, RN · Mar 1, 2006

I think the trick to learning DM is understanding the pathophys. The mechanisms that cause type I and type II are different. That aside, the blood sugar business is just another thing to deal with--you've got to understand the chemistry that is happening. Part of it delves into the acid/base balance stuff (it always seems to rear it's ugly head, doesn't it?). You've just got to go back to the chemistry of what is going on.

I'd stick to the basic learning outline of most nursing subjects. The anatomy and physiology, the normal treatment, the complications, the nursing interactions. http://www.fpnotebook.com/END11.htm is a link to a general outline about diabetes types, symptoms, how it's diagnosed, and management from the doctor's perception. It will give you a guideline of how to organize what you need to learn. You can find more on this same web site by using the search function for "diabetes" to find information on diabetic complications (there are a few you really need to know about).

Try looking at some of the patient teaching resources because they will be put into simple language. Sometimes that is a good place to start before going into the more complex stuff. MedlinePlus should have some good links into patient information. Also try the websites of the Insulin manufactures. Some of them maintain patient teaching websites. Someone has to explain ketoacidosis to patients! I've known about this site for some time, http://diabetes.healthcentersonline.com/ I just did a quick check on ketoacidosis and they had a very nice presentation. You might want to check out this site.

I realize you are getting ready for a test so your time is limited. These were just a few suggestions. I can tell you that you will learn this diabetes stuff one way or another because more and more patients are showing up in the hospitals with it along with all their other problems. It, along with all it's complications, is one of the fastest growing diseases of our times.

mandymarie7791 · Mar 1, 2006

Thanks Daytonite!

DSplendid · Mar 1, 2006

mandy, here is a dm (down and dirty) study guide i had made when i was going through, hope it helps

1. diabetes mellitus - disease in which body does not produce or properly use insulin

2. role of insulin - (unlocks doors) **allows glucose in blood to move into muscle, liver and fat cells. it allows extra glucose to store as glycogen (aka) glycogenesis. and, then when needed, glycogen back into glucose (aka) glycogenolysis. it increases protein and fat synthesis, **inhibits break down of fats and inhibits conversion of proteins to glucose (aka). gluconeogenesis. in muscle cells it promotes protein and glycogen synthesis. in fat cells it promotes storage of triglycerides. insulin also *****keeps blood glucose levels from becoming to high.****** and helps maintain lipid levels in normal range. .

3. type 1

disorder - mostly in children, autoimmune d/o immune system cells attack and destroy insulin secreting cells in the pancreas. maybe genetic.

pathophysiology - there are no beta cells so no insulin is being produced. so that means that all the glucose floating in your body can't be taken in by the muscle or liver or even stored. causing osmotic diuresis, your bodies way of getting rid of all that glucose. but along with that goes electrolytes, including k+. the thing is because your muscles never got the glucose for food, its starving; so it starts to break down fat to get more glucose. that causes ketone bodies to rise, = ketoacidosis.

the bottom line is that pancreas doesn't make insulin.

type ii

disorder - mostly in older and obese. most common form 90-95%. however now seeing in children r/t obesity. they may not even now, or even find out, when getting a check up for something else.

pathophysiology - this is known as insulin resistance. this condition is due to years of over stimulation of insulin. basically, insulin is tired of being made, so insulin is reduced in the body. second problem is the cells them selves become resistant to responding. pretty much they don't answer the door to insulin anymore. so, your body is still hungry, the liver doesn't know, so it keeps sending out glycogen and the pancreas gets over worked because its still trying to make insulin..

the bottom line

- you don't have enough insulin

- cells resitanct

- body makes more insuling

diabetes mellitus

s/s - 3 p's polydipsia - thirsty

polyuria - urinating, peeing

polyphagia - hungry

fatigue, weakness, dry skin, sores don't heal, tingling in hands and feet, sudden vision changes, recurrent infections.

dx- random bs >/ = 200 and s/s

fasting bs >/= 126

rn- assessment: hpi-does you family have it? are you hispanic?

age - child or older

risk factors - do you have htn and or overweight?

size of baby - did you have 10 pound babies?

sudden wt. loss

s/s of dm

infections, labs, lipid profile

fasting bs, hba1c 200. what is your bun/cr

goals - normalize insulin activity and blood glucose levels.

reduce development of vascular and neuropathic complications.

refering them to opthalmlogy and podiatry.checking hga1c bs

testing everyone by age 45 and 3 years there after. high risk more often that. teach diabetics strict control to save themselves from eye, sores, mi, cad, cva etc. teaching meals and meds.

4. diabetic #'s

hga1c

>7

preprandial bs (before meals)

>130

postprandial bs (after meals)

>180

fasting bs

>/=126

non diabetic #s

hga1c

preprandial bs (before meals)

90-130

postprandial bs (after meals)

fasting bs

5. hga1c - ***best indicator of average blood sugar. glucose attaches to hgb molecule during previous 120 days of the life of a rbc. used to assess long term glycemic control****

6. risk factors for type ii - >45

family history

race

htn> 140/90

tri>250

hx of delivery >9lbs

7. diabetic management (5 things) -

education

nutrition

exercise

monitoring

pharmacologic therapy

8. cho counting and diabetic exchange

cho - ada believes that carbs have the greatest effect on post meal blood glucose levels. so there diet consists of 50-60% of cho 20-30% fat 10-20% protein.

ex: pt's maybe allowed 25 grams of carbs at each meal. fiber is subtracted from total cho. because that doesn't effect bs.

exchange diet - there are 6 main exchange categories. bread/starch, veggies, milk, meat, fruit and fat. based on the patients need he is allowed a certain number of choices from each list. foods can be interchangeable for flexibility.

the goal of both is to control total calorie intake to attain or maintain a reasonable body wt. and control bs level.

9. exercise - important part of diabetic management

lowers blood glucose and increases uptake of glucose by muscles and improves insulin utilization

check bs before and after

take glucose tabs with you just in case

suggesting walking its easy

exercise lowers glucose so tell them to be careful, watch for signs and check with md before starting program.

********don't exercise within 1 hour of injectin insulin******

10. smbg - recommended by ada for those taking insulin and oral therapy. you can't control you bs well enough without doing them.

11. insulins -

type

onset

peak

duration

indications

misc.

rapid

10-15 min

1 h

3

used for sliding scale, given mins. before meal for coverage

novolog, aspart

[color=#99cc00]short

½ - 1 h

2-3 h

4-6 h

given 20-30mins before meal

regular

novolin

intermed.

3-4h

6-12h

16-20h

usually taken after food

nph, cloudy

[color=#3366ff]long

6-8h

12-16

20-30

"ul"

[color=#cc99ff]very [color=#cc99ff]long

1h

ongoing

24 h

used once a day at the same time every day

lantus, cloudy

* can not be mixed or diluted* this is a steady state of insulin, but you still need something else.

things to know, good for 30 days at room temp. do not put it in the back of your fridge that is were it is the coldest. when mixing - **rn** inject your air into nph, then regular. then draw up your solution into rn- regular then nph. **injections are preferred in the abd 2 inches from umbilical cord. rotate sites, you can develop lipodsytrophy=fat deposits under skin. lipoatrophy=loss of fat. avoid scar tissue, and poor skin texture.

12. benefits of insulin - moves glucose into cells after injection depends on site of injection, depth rate, time mixing. may also cause hypoglycemia, or morning hyperglycemia. dawn, and somogyi's phenomen.

13. hypo/hyperglycemia s/s and rx

hypoglycemia s/s - 1st s/s jitters

2nd change in mental status

**hot and shaky**

weakness-vision-tachy-palpations-anxious-even sz or coma

this is because of to much insulin

rx - 10-15 of simple cho orally check bs 10-15 later if still low give another 10-15 and repeat.

- foods-

3-4 glucose tabs

**3-4 oj**

4-6 soda

6-10 life savers or other hard candy

2 tbsp raisins

2-3 tbsp honey

what if you pt's unconscious- glucagons 1mg under tongue

hyperglycemia - s/s - polyuria

polydipsia

abd pain r/t enlarged liver

*dehydration*

acetone breath

kussmaul breathing - deep and fast

change in loc

weak-fever-high wbc's n/v

this is because of to much glucose

rx - insulin with k+, correct dehydration

14. se of drugs -

sulfonylureas - type ii only - stimulates pancrease to make insulin. that's why you can't use it in type 1, because you need to have functioning beta cells. biggest problem is hypoglycemia-

1st generation - orinase, tolbutamide.

2nd geeration - glucatrol, glipizide

biguanides - better for type ii okay for type i - reduces hepatic glucose, improving tissue response to insulin. so if type i is using it, they're using it with there insulin. it basically cramps down on liver, to decrease glucose from leaving.

not given to those with renal disease

hold 2 days before and after iv dye test

give with increase fluids

will not cause hypoglycemia, when given alone. because it doesn't do anything but make tissues respond, better to insulin.

meglitinides - lowers bs by stimulating release of insulin. works for 2-3 hours give 15 min. before meal. you still need to make your own insulin

**anytime the pancrease is stimulated for insulin you have to worry about hypoglycemia***

ex. (prandin) repaglinide

( nateglinide) strix

15. education -

teach - diabetes is a life long management

1st - are they ready to learn

-give basic definition of diabetes -

either insulin resistant or don't have insulin for bs

-what is the normal ranges of bs 70- 110 for fasting and so on

-exercise causes a loss of glucose

-stress makes glucose increase

-tell them there meds

-diet

-smbg- ketone

-s/s of hypo and hyper glycemia

16. dka

a lack of or no insulin - so glucose just keep rising - which leads to fat breakdown for glucose. causing ketones leading to acidosis-

osmotic dehydration remember that when the body tries to get rid of glucose it takes water and electrolytes with it.

s/s dehydration

polyuria

polydipsia

weakness

fever

n/v

abd pain r/t enlarged liver

assessment and findings

bs 300-800

ketoacidosis - by blood and urine

decreased bicarbonate

ph -

pco2 -

increased bun, hct and hgb - r/t dehydration

decreased na+ k+ - r/t dehydration

*****lower bs slowly q 2/h look at bs and k+ give insulin and k+ even if the k+ looks high b/c its not*********

k+ may even look high at first b/c -

during osmotic diuresis k+ is on the outside of the cell, being ready to be taken out, so readings look high

but then when you give them insulin, k+ rushes back in the cell, causing a rapid drop causing cardiac arrest

diagnosis is made when ketones are found, no ketones, no dka, just plain old hyperglycemia.

*******************rn care; fluids, insulin, electrolytes, treat infection b/s most likely this was due to an infection, do not give bicarb, you will over correct the problem*******

17. hhns - hyperglycemic hyperosmolar nonketotoic syndrome

fancy ass word for high sugar very dehydrated with no ketone bodies.

this just means hyperglycemia with out acidosis or ketosis, usually slow onset and happens more in type ii, or those that have not been dx with dm. bs > 600

there is no ketosis b/c there is a liitle insulin floating around in the body. these people are very dehydrated*******

dx : osmolality > 350

no ketones

high bun

bs > 600-1200

rx fluid replacement insulin is not that important. your priority is to maintain hydration

18. "sick day rules"

always take your insulin

test your bs before each meal, and at bedtime

test your urine for ketones if blood sugar > 240

follow your meal plan if can eat. if you can't drink sugar beverage of at least 4oz. to keep from bs falling to low.

call your md if you vomiting and unable to keep pills or food and drink down

illness longer than 24

ketones in urine

any bs > 240 for more than one day.

19. 3 long term complications

1. macrovascular - big vessels, mi, cva

2. microvascular

retinopathy - blindness

nephropathy - allow protein to leak out , kidney failure

3. neuropathy , decrease pain making the first two that much dangerous. neurontin for leg pain. gi problem diarrhea

***********diabetics should be check every year******************

20. foot care - foot injury is most common teach pt look for bo-bo's

what happens is they can't even feel when they have sore, and the feet have increase trauma due to walking, neuropathy makes poor circulation and decrease sensation. and high blood sugar inhibits wbc's from doing there job. so aka, necrotic foot.

mandymarie7791 · Mar 1, 2006

WOW!!! Im lost for words at how amazing everyone here is. Thank you thank you thank you!!!

luv2shopp85 · Mar 2, 2006

mandy, here is a dm (down and dirty) study guide i had made when i was going through, hope it helps
1. diabetes mellitus - disease in which body does not produce or properly use insulin
2. role of insulin - (unlocks doors) **allows glucose in blood to move into muscle, liver and fat cells. it allows extra glucose to store as glycogen (aka) glycogenesis. and, then when needed, glycogen back into glucose (aka) glycogenolysis. it increases protein and fat synthesis, **inhibits break down of fats and inhibits conversion of proteins to glucose (aka). gluconeogenesis. in muscle cells it promotes protein and glycogen synthesis. in fat cells it promotes storage of triglycerides. insulin also *****keeps blood glucose levels from becoming to high.****** and helps maintain lipid levels in normal range. .
3. type 1
disorder - mostly in children, autoimmune d/o immune system cells attack and destroy insulin secreting cells in the pancreas. maybe genetic.
pathophysiology - there are no beta cells so no insulin is being produced. so that means that all the glucose floating in your body can't be taken in by the muscle or liver or even stored. causing osmotic diuresis, your bodies way of getting rid of all that glucose. but along with that goes electrolytes, including k+. the thing is because your muscles never got the glucose for food, its starving; so it starts to break down fat to get more glucose. that causes ketone bodies to rise, = ketoacidosis.
the bottom line is that pancreas doesn't make insulin.
type ii
disorder - mostly in older and obese. most common form 90-95%. however now seeing in children r/t obesity. they may not even now, or even find out, when getting a check up for something else.
pathophysiology - this is known as insulin resistance. this condition is due to years of over stimulation of insulin. basically, insulin is tired of being made, so insulin is reduced in the body. second problem is the cells them selves become resistant to responding. pretty much they don't answer the door to insulin anymore. so, your body is still hungry, the liver doesn't know, so it keeps sending out glycogen and the pancreas gets over worked because its still trying to make insulin..
the bottom line
- you don't have enough insulin
- cells resitanct
- body makes more insuling
diabetes mellitus
s/s - 3 p's polydipsia - thirsty
polyuria - urinating, peeing
polyphagia - hungry
fatigue, weakness, dry skin, sores don't heal, tingling in hands and feet, sudden vision changes, recurrent infections.
dx- random bs >/ = 200 and s/s
fasting bs >/= 126
rn- assessment: hpi-does you family have it? are you hispanic?
age - child or older
risk factors - do you have htn and or overweight?
size of baby - did you have 10 pound babies?
sudden wt. loss
s/s of dm
infections, labs, lipid profile
fasting bs, hba1c 200. what is your bun/cr
goals - normalize insulin activity and blood glucose levels.
reduce development of vascular and neuropathic complications.
refering them to opthalmlogy and podiatry.checking hga1c bs
testing everyone by age 45 and 3 years there after. high risk more often that. teach diabetics strict control to save themselves from eye, sores, mi, cad, cva etc. teaching meals and meds.
4. diabetic #'s
hga1c
>7
preprandial bs (before meals)
>130
postprandial bs (after meals)
>180
fasting bs
>/=126
non diabetic #s
hga1c
preprandial bs (before meals)
90-130
postprandial bs (after meals)
fasting bs

5. hga1c - ***best indicator of average blood sugar. glucose attaches to hgb molecule during previous 120 days of the life of a rbc. used to assess long term glycemic control****

6. risk factors for type ii - >45
family history
race
htn> 140/90
tri>250
hx of delivery >9lbs

7. diabetic management (5 things) -
education
nutrition
exercise
monitoring
pharmacologic therapy
8. cho counting and diabetic exchange
cho - ada believes that carbs have the greatest effect on post meal blood glucose levels. so there diet consists of 50-60% of cho 20-30% fat 10-20% protein.
ex: pt's maybe allowed 25 grams of carbs at each meal. fiber is subtracted from total cho. because that doesn't effect bs.
exchange diet - there are 6 main exchange categories. bread/starch, veggies, milk, meat, fruit and fat. based on the patients need he is allowed a certain number of choices from each list. foods can be interchangeable for flexibility.
the goal of both is to control total calorie intake to attain or maintain a reasonable body wt. and control bs level.

9. exercise - important part of diabetic management
lowers blood glucose and increases uptake of glucose by muscles and improves insulin utilization
check bs before and after
take glucose tabs with you just in case
suggesting walking its easy
exercise lowers glucose so tell them to be careful, watch for signs and check with md before starting program.
********don't exercise within 1 hour of injectin insulin******

10. smbg - recommended by ada for those taking insulin and oral therapy. you can't control you bs well enough without doing them.

11. insulins -
type
onset
peak
duration
indications
misc.
rapid
10-15 min
1 h
3
used for sliding scale, given mins. before meal for coverage
novolog, aspart
[color=#99cc00]short
½ - 1 h
2-3 h
4-6 h
given 20-30mins before meal
regular
novolin
intermed.
3-4h
6-12h
16-20h
usually taken after food
nph, cloudy
[color=#3366ff]long
6-8h
12-16
20-30

"ul"
[color=#cc99ff]very [color=#cc99ff]long
1h
ongoing
24 h
used once a day at the same time every day
lantus, cloudy
* can not be mixed or diluted* this is a steady state of insulin, but you still need something else.

things to know, good for 30 days at room temp. do not put it in the back of your fridge that is were it is the coldest. when mixing - **rn** inject your air into nph, then regular. then draw up your solution into rn- regular then nph. **injections are preferred in the abd 2 inches from umbilical cord. rotate sites, you can develop lipodsytrophy=fat deposits under skin. lipoatrophy=loss of fat. avoid scar tissue, and poor skin texture.

12. benefits of insulin - moves glucose into cells after injection depends on site of injection, depth rate, time mixing. may also cause hypoglycemia, or morning hyperglycemia. dawn, and somogyi's phenomen.

13. hypo/hyperglycemia s/s and rx
hypoglycemia s/s - 1st s/s jitters
2nd change in mental status
**hot and shaky**
weakness-vision-tachy-palpations-anxious-even sz or coma
this is because of to much insulin
rx - 10-15 of simple cho orally check bs 10-15 later if still low give another 10-15 and repeat.
- foods-
3-4 glucose tabs
**3-4 oj**
4-6 soda
6-10 life savers or other hard candy
2 tbsp raisins
2-3 tbsp honey
what if you pt's unconscious- glucagons 1mg under tongue

hyperglycemia - s/s - polyuria
polydipsia
abd pain r/t enlarged liver
*dehydration*
acetone breath
kussmaul breathing - deep and fast
change in loc
weak-fever-high wbc's n/v
this is because of to much glucose
rx - insulin with k+, correct dehydration

14. se of drugs -
sulfonylureas - type ii only - stimulates pancrease to make insulin. that's why you can't use it in type 1, because you need to have functioning beta cells. biggest problem is hypoglycemia-
1st generation - orinase, tolbutamide.
2nd geeration - glucatrol, glipizide
biguanides - better for type ii okay for type i - reduces hepatic glucose, improving tissue response to insulin. so if type i is using it, they're using it with there insulin. it basically cramps down on liver, to decrease glucose from leaving.
not given to those with renal disease
hold 2 days before and after iv dye test
give with increase fluids
will not cause hypoglycemia, when given alone. because it doesn't do anything but make tissues respond, better to insulin.

meglitinides - lowers bs by stimulating release of insulin. works for 2-3 hours give 15 min. before meal. you still need to make your own insulin
**anytime the pancrease is stimulated for insulin you have to worry about hypoglycemia***
ex. (prandin) repaglinide
( nateglinide) strix

15. education -
teach - diabetes is a life long management
1st - are they ready to learn
-give basic definition of diabetes -
either insulin resistant or don't have insulin for bs
-what is the normal ranges of bs 70- 110 for fasting and so on
-exercise causes a loss of glucose
-stress makes glucose increase
-tell them there meds
-diet
-smbg- ketone
-s/s of hypo and hyper glycemia

16. dka
a lack of or no insulin - so glucose just keep rising - which leads to fat breakdown for glucose. causing ketones leading to acidosis-
osmotic dehydration remember that when the body tries to get rid of glucose it takes water and electrolytes with it.
s/s dehydration
polyuria
polydipsia
weakness
fever
n/v
abd pain r/t enlarged liver

assessment and findings
bs 300-800
ketoacidosis - by blood and urine
decreased bicarbonate
ph -
pco2 -
increased bun, hct and hgb - r/t dehydration
decreased na+ k+ - r/t dehydration
*****lower bs slowly q 2/h look at bs and k+ give insulin and k+ even if the k+ looks high b/c its not*********

k+ may even look high at first b/c -
during osmotic diuresis k+ is on the outside of the cell, being ready to be taken out, so readings look high
but then when you give them insulin, k+ rushes back in the cell, causing a rapid drop causing cardiac arrest

diagnosis is made when ketones are found, no ketones, no dka, just plain old hyperglycemia.

*******************rn care; fluids, insulin, electrolytes, treat infection b/s most likely this was due to an infection, do not give bicarb, you will over correct the problem*******

17. hhns - hyperglycemic hyperosmolar nonketotoic syndrome
fancy ass word for high sugar very dehydrated with no ketone bodies.

this just means hyperglycemia with out acidosis or ketosis, usually slow onset and happens more in type ii, or those that have not been dx with dm. bs > 600
there is no ketosis b/c there is a liitle insulin floating around in the body. these people are very dehydrated*******
dx : osmolality > 350
no ketones
high bun
bs > 600-1200

rx fluid replacement insulin is not that important. your priority is to maintain hydration

18. "sick day rules"
always take your insulin
test your bs before each meal, and at bedtime
test your urine for ketones if blood sugar > 240
follow your meal plan if can eat. if you can't drink sugar beverage of at least 4oz. to keep from bs falling to low.
call your md if you vomiting and unable to keep pills or food and drink down
illness longer than 24
ketones in urine
any bs > 240 for more than one day.

19. 3 long term complications
1. macrovascular - big vessels, mi, cva
2. microvascular
retinopathy - blindness
nephropathy - allow protein to leak out , kidney failure
3. neuropathy , decrease pain making the first two that much dangerous. neurontin for leg pain. gi problem diarrhea

***********diabetics should be check every year******************

20. foot care - foot injury is most common teach pt look for bo-bo's
what happens is they can't even feel when they have sore, and the feet have increase trauma due to walking, neuropathy makes poor circulation and decrease sensation. and high blood sugar inhibits wbc's from doing there job. so aka, necrotic foot.

wow.... where were you 2 months ago when i failed my diabetes exam?!?

labcat01, BSN, RN · Mar 2, 2006

DSplendid :bow:

Daytonite, BSN, RN · Mar 3, 2006

Reading DSplendid's study guide and the 3 P's reminded me of a poem about polyuria that my uncle used to recite as an entertainment when we were kids (we're talking about a time when there were only 3 channels on the TV and no TV programs on AT ALL after 1am in the morning--a more simple time)

http://www.user.shentel.net/nbaker/Laffs/limerick.htm

this is the poem, The Piddling Pup. I like the music that goes with this site. Anyway, you'll never forget the symptom of polyuria and it's association with diabetes again after reading this if you are a dog lover. So, take a few minutes of a break and enjoy this old, classic and remember that when the blood sugar goes over 250, the kidneys start doing their job to try to dump it by producing more urine which eventually leads to DKA if the blood sugar does not get normalized.

I've got to mention, too, that I have a cat that is diabetic and has to have NPH insulin twice a day. I've been reading up on cat diabetes over the last year because it is a bit different from humans. She presented with a blood sugar of 600! at her yearly physical last May.

mandymarie7791 · Mar 3, 2006

That was funny Daytonite. And my 6 year old cat was just diagnosed with diabetes 2 weeks ago and I have to give her shots twice a day as well.I read online somewhere that a lady has 2 cats and they BOTH are on dialysis!! Could you imagine?!! Yikes!

Daytonite, BSN, RN · Mar 5, 2006

That was funny Daytonite. And my 6 year old cat was just diagnosed with diabetes 2 weeks ago and I have to give her shots twice a day as well.I read online somewhere that a lady has 2 cats and they BOTH are on dialysis!! Could you imagine?!! Yikes!

One of my old managers had a cat that was on the brink of chronic renal failure, but not quite at the dialysis stage. My kitty is on 4 units of NPH twice a day and still has blood sugars of close to 200. The vet says she has something called a Samojian effect. Lucky cat. Anyway, I know she's doing so much better because she had been losing weight just before diagnosis and has now gained a pound or two back and is acting her normal self again--sort of. I suspect that she has stuff going on but can't tell me. She will suddenly stop and start meowing which she never did before. And, she seems to have a restlessness about her that she never had before.