Patho Test 3 Diabetes

Front 1

alpha cells

Back 1

secrete glucagon in response to decreased BG

Front 2

beta cells

Back 2

secrete insulin in response to increased BG

Front 3

actions of insulin

Back 3

1. moves glucose into cells
2. increases the use of glucose, and thus decreasing BG and increasing glycogen stores
3. lipid synthesis from FA; promotes storage of fat in adipose (as opposed to arteries)
4. protein storage and synthesis

Front 4

actions of glucagon

Back 4

1. glycogenolysis (breakdown glycogen to glucose)
2. glyconeogenesis (make glycogen from fat)

Front 5

hormones that raise blood glucose

Back 5

epinephrine
cortisol
growth hormone

*remember that in diabetic pt, when these hormones secrete glucose it can't be taken up.

Front 6

normal blood glucose

Back 6

80-100 mg/dL

raises to 140 mg/dL after meals and insulin brings it back to nrml.

Front 7

hyperglycemia

Back 7

110 or greater at fasting

Front 8

hypoglycemia

Back 8

less than 80 at fasting

Front 9

renal threshold

Back 9

glucose reabsorbed and filtered by glomerulus in kidneys, but when it exceeds the renal threshold (160-180) it will spill into urine.

Front 10

blood glucose tests

Back 10

1. fasting BG (FBG) takes levels at fasting
2. OGTT is the best test. it measures levels every 30 min for 2 hr. if nrml funct present, levels should be below 200, and at 2 hr below 140.
HbA-1-c (tests for glycosated hgb). the higher the BG, the the hgb level. tells how well diabetic is controlling BG over weeks, rather than testing 1 level. nrml = 5% diabetic nrml = 6-7%

Front 11

diabetes mellitus

Back 11

no insulin production or insulin resistance. causes metabolism of carbs, fats, and proteins to be altered.

Front 12

type 1 diabetes

Back 12

"insulin dependent" or "juvenile diabetes"
*onset before 20 or 30, usu. btwn 11-13
*abrupt onset (follows virus; B cells are destroyed; pt asymptomatic until all B cells are gone)
*requires insulin because not produced by pancreas
*ketosis prone

Front 13

type 2 diabetes

Back 13

"non insulin dependent"
*onset after age 30.
*family hx of NIDDM and obesity contribute.
*no ketosis
*insulin resistance + decreased insulin production

Front 14

manifestations of type 1
(things that would help you diagnose it)

Back 14

1. glycosuria
2. diuresis "polyuria"
3. polydipsia"
4. wt loss
5. increased hunger
6. fatigue, sleepiness
7. ketoacidosis
8. hyperglycemia

Front 15

glycosuria occurs because

Back 15

glucose is spilled into urine when renal threshold is reached

Front 16

diuresis or polyuria occurs because

Back 16

body is trying to get rid of glucose levels by urinating many times

Front 17

increased thirst or "polydipsia" occurs because

Back 17

body is dehydrated from increased urination

Front 18

wt loss occurs because

Back 18

dehydration, and urinating calories (glucose) in urine and breaking down fat for energy

Front 19

increased hunger occurs because

Back 19

cells are starved from not taking up any glucose. "polyphagia" "many eating"

Front 20

fatigue and sleepiness and blurred vision occur because

Back 20

glucose clouds the eyes

Front 21

Tx for type 1

Back 21

diet: balance. carb controlled and spread out thru day.
exercise: increased amts of insulin are given before exercise, bc it increases glucose metab. --> hypoglycemia.

no tx --> hypotension, decreased cerebral funct, coma, death.
insulin: combo of intermediate and short acting to mimic what the pancreas does. in adolescents it's hard to balance because of growth hormone.

Front 22

diabetic ketoacidosis DKA

dehydration phase

Back 22

no insulin --> increased BG levels --> increases osmolarity of blood.
when BG reaches threshold --> osmotic diuresis

Front 23

diabetic ketoacidosis DKA

acidosis phase

Back 23

no insulin --> breakdown of fats and proteins --> ketones build --> [H+] increases --> lowers pH (metabolic acidosis)

*body will excrete H+ and retain HCO3, but because dehydrated from osmotic diuresis, blow off excess CO2 (Kussmaul resp = deep, rapid). BREATH SMELLS FRUITY.

Front 24

Tx for DKA

Back 24

give insulin and fluids. insulin will move glu. into cells and correct acidosis. fluid to rehydrate.

Front 25

acute & chronic complications for type 1

Back 25

Acute: diabetic ketoacidosis, hypoglycemia
Chronic: long term vascular complications, cataracts, skin infect, UTI

Front 26

hypoglycemia

Back 26

low BG.
too much insulin in r/t food intake or exercise. "insulin reaction."
Sx: low glucose to brain --> lethargy, no concentration, bizarre behavior, coma. low BG -->SNS stim--> epinephrine--> shaky, sweaty, nervous, incr. pulse & resp, HA, palpitations.
Tx oral or IV glucose; glucagon IM = release glucose from liver.

Front 27

long term vascular complications

Back 27

1. microangiopahty: lesions in capillaries
2. macroangiopathy: accelerated artherosclerosis

Front 28

examples of microangiopahty

Back 28

1.retinopathy (blindness)
2. nephropathy (kidney failure, hypertension, proteinuria)
3. neuropathy (changes in ability to feel, parasthesias, muscle weakness or atrophy).

Front 29

examples of macroangiopathy

Back 29

1.artherosclerotic changes (plaque buildup, occlusion).
2. peripheral (lose circ. in legs)
3. coronary (angina, heart attack)
4. cerebral (stroke)

Front 30

"sick day rules"

Back 30

when diabetic pt or child is sick they won't eat, and don't take insulin because they haven't eaten. stress hormones are produced which increase blood glucose (epi & cortisol). need to have a plan for insulin during this time.