Diabetes

Rapid acting insulin: names (clarity, onset, peak , and duration)

Short acting insulin: names (clarity, onset, peak, duration)

Intermediate acting: name (clarity, onset, peak, duration)

Long acting: names (clarity, onset, peak, duration)

Diabetes mellitus: chronic multi system disease r/t

Causes of Diabetes Mellitus:

Pancreas (endocrine): alpha cells secrete:

Pancreas (endocrine): Betta cells secrete:

Glucagon works on the ________ nervous system.

Insulin works on the ______ nervous system.

Counter regulatory hormones that increase blood sugar are:

Stress hyperglycemia: corticosteroids and catecholamines increase. 
Production of glucose in liver _____. 
Production of glucagon _____. 
functioning insulin receptors on cell ______.

Glucagon increases blood glucose by stimulating ________.
Glucagon synthesized in response to low levels of blood glucose, protein ingestion, and exercise.

______: hormone produced by betta cells in islets of Langerhans.

Insulin metabolism: Stimulates the storage of glucose as glycogen in ______ and ______. 
Inhibits _________. 
Enhances fat deposition of adipose tissues. 
Increases protein synthesis.

Type 1 diabetes: __________ of beta cells in pancreas.

Type 2 diabetes: ______ of beta cells and insulin ______.

Risk factors for diabetes: 
Age >45 (35 with other risk factors) 
Women with polycystic ovarian syndrome
Obesity
Prior gestational diabetes or baby weighing > 9 pounds
Prior IGT and IFG or _______. 
History of ______. 

IGT: fasting glucose levels higher than normal

Oral glucose tolerance test (OGTT): 2 hour plasma glucose higher than normal

Type 1 Diabetes: "I___ D____ D____"

Type 1 Diabetes manifestations
3 P's: ________
weight loss
fatigue

S/S More common in type 1 diabetes

Type 2 diabetes Mellitus: "N__ I___ D__"
Risk factors:

Type 2 Diabetes Mellitus: pancreas continues to produce some insulin. (Not enough or poorly used by tissues) 
Genetic link:

Type 2 DM manifestations:

Type 1 Diabetes: age at onset, type of onset, environmental factors, insulin

Type 2 diabetes: age at onset, type of onset, environmental factors, insulin

Diagnositcs
A1C: ___
Fasting Plasma glucose: _____
2 hour plasma glucose: ______
Islet cell antibody testing: Type ___

Meal time insulin:_______ 
Control between meals and night time:____
Carbohydrate counting:____

Insulin adverse effects:

Somogyi Effect: Requires _____ insulin.
Counterregulatory hormone response to high insulin dosage.

Dawn phenomenon: Adjust insulin administration time or ______ dose. 
Growth hormone and cortisol excreted in increased amount (counterregulatory hormones)

Plasma blood glucose & HGB A1C goals for type 1 DM 
Toddlers & preschoolers <6 years: before meals, bed time, HGB A1C

Plasma blood glucose & HGB A1C goals for type 1 DM

School age 6 - 12 years

Plasma blood glucose & HGB A1C goals for type 1 DM

Adolescents >12 years and young adults

_____ insulin (Long/intermediate) 
Control b/w meals and nighttime.

Combination of insulin: Mix _____ and _____ in same syringe. (Clear to cloudy)

Oral Antidiabetics work on 3 defects of type 2 diabetes

Insulin ______. 
______ insulin production. 
______ hepatic glucose production.

Oral antidiabetics:

Biguanides: trade names, action, adverse effects

Sulfonylureas: trade names, action, adverse effects

Meglitinides: trade names, action, adverse effects

Dipeptidyl peptidase-4 inhibitors: trade names, action, adverse effects

Nutritional therapy

Total carbs: fruits, vegs, grains, legumes, low fat milk.
Minimum ______ g/day.

Nutritional therapy 

Fiber intake _____ g/day

Nutritional therapy 
Protein: ______ % total calories 
No high protein diets

Nutritional therapy
Fat : _____ total calories 
Dietary cholesterol: _____
______ servings fish/week

Nutritional therapy
Alcohol limit ___ drink/day for women, ___ drink/day for men

Nutritional Therapy 
Education
Dietitian initially provides education 
should include ____. 
_____ method: helps patient visualize the amount of vegetable, starch, and meat that should fit a 9 inch plate.

Exercise
_____ blood glucose during and after exercise. 
Causes uptake of glucose by ______. 
Improves insulin ______ and insulin _______. 

lasts _____ hours.

Diabetic complications
DKA: _______
HHNS:________
H:_________
Morning H: ______

DKA is ____________.
Most common in Type __ DM
Type _ DM possible in overwhelming _____ or ____.

DKA: Precipitating Factors 

Illness and _____. 
Inadequate ____ dosage. 
Undiagnosed _______. 
_______ self management. 
Neglect.

DKA: Pathophysiology 

______ circulating insulin, glucose not properly used for ______. 
Body compensates breaks down ____ stores.
_____: acidic by products of ____ break down. 
_____ alters PH balance. 
Patient goes into _____ acidosis. 
______ is _____ spilling into urine. 
When ____ spill into urine ___ become depleted. 
Insulin deficiency leads to impaired _____ synthesis. 
Increased _____ degradation. 
Increased _____ loss from tissues. 
Increased production of glucose from ______ in liver leads to _________. 
Due to insulin deficiency, blood glucose increases leading to _________. 
Due to _______: Na, K, Cl, Mg, and Phos are _______. 
Fluid volume is ________ (_________)
Could lead to __________ shock, ____ failure, and death.

DKA: clinical manifestations 

______ skin turgor.
_____ mucous membranes.
Tachycardia
________ hypotension
Lethargy
Soft ____ eyes
Anorexia 
_______ respirations
______ breath
Nausea/______
_____ pain (linked to accumulating acids) 
Blood glucose >/=______
Arterial blood PH < _______ (acidotic) 
______ in urine

DKA Treatment 

_______: maintain tissue perfusion 
______ replacement 
______: reverses acidosis by inhibiting ___ breakdown. 
Monitor: Vitals, Cardiac rhythm, __ levels, I&O:____ 
Treat ____ if present
O2
IV: 0.9% or 0.45% NaCl solution until ___ stable and urine output ____ mL/hr
When blood glucose reaches ______, begin 5% or 10% dextrose solution. 
(Sudden drop in glucose causes _____)

DKA treatment: insulin 

Crucial in restoring _______ balance and eliminating _______. 
Standard rate ____ U/kg/hr
Rate of insulin remains _____ while dextrose fluid ______ to achieve desired Serum glucose levels. 
_______ and early identification. 
Changes in mental status should ______. watch for ________. 
_______ checks every 1 hour. 
Monitor ______.

Hyperosmolar hyperglycemic syndrome

Type __ DM
Age >___ years
Less common than ____ 
Produces enough insullin to prevent ____ but not enough to prevent 
Severe _______
Osmotic ______
extracellular fluid ____

HHS Causes 

U--
P-------
S-----
A---- I------
Newly diagnosed Type - --

HHS clinical manifestations 

Elevated _______: ____ mg/dL 
_____ PH
_____ of Ketones
_____ of urine glucose 
Abnormal levels of Na, K, CL caused by ______

HHS Treatment 

Same as DKA except HHS requires greater _______ replacement.

These symptoms are for DKA or HHS? 
Common 
Type 1 
Precipitated by infection 
Ketoacidosis 
Short prodromal sympts 
MOrtality 5 - 10% 
Age 20 - 29

These symptoms are for DKA or HHS? 
Uncommon
Type 2 
More severe illness 
NOt ketoacidotic 
Longer prodromal sympts 
Mortality 40 - 60%
Age 57 - 70

Hypoglycemia is too _____ glucose in blood stream. <___ mg/dL

Hypoglycemia Pathophysiology: 
Blood glucose decreases to _______
_______ hormones are released
Insulin production is ________
Glucagon and epinephrine are ________

Hypoglycemia manifestations: 

No ____ signs 
Hypoglycemia reaches ______ point 
Patient c________, i_____ or u_______.
Autonomic neuropathy (problem with _____ secretion)

Rule of 15
Eat/Drink ____ g of ____ carbs
___ oz soda, orange jice
___ life savers 
___ Tbs syrup/honey 
___ tsp jelly 
Wait ___ minutes
Check glucose 
If blood glucose _____, repeat 
If glucose ______, feed snack 
_____ carb + protein

Macrovascular diseases include: 

______vascular disease
______vascular disease 
_____  vascular disease

Macrovascular risk factors 

S______
O_____
H_____
H_____
S_____

Microvascular 

Specific to ______ 
______ of vessel membranes in ______ and _______ in response to chronic _________. 
______pathy
______pathy
______pathy

Diabetic Retinopathy 

Microvascular damage to _____ aas result of _________. 
Classifications: 
___________
___________

Nonproliferative Retinopathy

Partial ______ of small blood vessels in _____. 
__________ of capillary walls. 
weak walls _____ fluid. 
Retinal _______. 
Intraretinal _______. 
Visin affected if _____ involved.

Proliferative Retinopathy

Involves retina and _____. 
Neovascularization.
_____ occluded 
Retinal _______.

Retinopathy Treatment

Blood glucose control
P__________
V_________
Meds to supress Vascular ______ growth factor.

Nephropathy

Damage to small blood vessels of _____.

(causes ______ to leak) 
(_____ reduce risk of nephropathy)

Nephropathy nursing interventions 

S______
__ control 
Low _____/Low ____ diet 
Education 
H_______
Renal _____

Diabetic Neuropathy 

________ r/t metabolic problems. 

Calssifications: 
S_______
A______

Sensory Neuropathy 

______ symmetric polyneuropathy.

H____/F____
S____ g_____ neuropathy. 
Loss of or abnormla sensation 
Pain 
P______
Ulcers 
_____ gait

Autonomic Neuropathy 

Damage to _____ of small blood vessels and _____ glands in skin, ___ system, ___ tract, and adrenergic system.

Autonomic Neuropathy Manifestations 

Cardiovascular 
_____ hypotension
Resting _______
Painless ____ 

GI
G______ (____ gastric emptying)
GU
______ bladder (lose ____ in bladder) 
Urinary ______ 
____ stream.

Diabetes complications of lower extremities

A________.
U________.

Risk factors: 
_____ neuropathy 
PAD (Peripheral ______  _____)
C_______ abnormalities
S_______
I_____ I______ system