Diabetes & Endocrine Disorders

Front 1

BG?

Back 1

Blood glucose

Front 2

DM

Back 2

Diabetes Mellitus, in general

Front 3

DM1

Back 3

Type 1 DM (formerly insulin dependent)

Front 4

DM2

Back 4

Type 2 DM (formerly adult onset). Highly inheritable.

Front 5

LADA. Type 1.5

Back 5

Latent Autoimmune Diabetes in Adult. Follows DM1 tendencies but usually started on oral meds, end up on insulin 1-6 yrs.

Front 6

MODY

Back 6

Maturity Onset Diabetes in the Young. Cuased by single misguided genes. Misdiagnosed as Type 1 or 2 DM. Highly inheritable, depending on which gene inherited.

Front 7

What is DM?

Back 7

DM is a metabolic disorder creating the inability to properly metabolize glucose in the body (carbs, protiens, fats)

Front 8

What is the Etiology of DM?

Back 8

Depends on the Type

Front 9

What is the diagnosis of DM?

Back 9

Based on BG and A1c

Front 10

What are treatments of DM?

Back 10

Depends on type of DM and how it presents.

Front 11

What is DM?

Back 11

Food's basic component is glucose. In non-diabetic, glucose rises which triggers production of insulin (pancreas) & in return lowers BG back to normal ranges (65-99). If BG drops too low (sleep, long run, w/o food) glucagon (pancreas) is produced to release stored glycogen (liver) and this is broken down into glucose to increase BG.

Front 12

What is a normal glucose level in a non-diabetic?

Back 12

65-99

Front 13

Etiology/Epidemiology of DM Type 1

Back 13

No insulin produced! Must be treated with insulin injection!

Hint 13

5-10% total population.
10% genetically transferred. MODY.
European heritage.
generally, children although more occurring later in life. LADA-Type 1.5.

Front 14

Etiology/Epidemiology of DM Type II

Back 14

Utilization and production of insulin is problem!

Hint 14

Increased insulin resistance in the cells, decreased insulin output, decreased adequately formed insulin output. Glucagon process is disturbed and liver puts out unnecessary glucose.
Brought on by stress or illness.

Front 15

Etiology/Epidemiology of DM Type II

Back 15

90% of total population.
dramatic increase due to lifestyle: sedentary & food
Increased in Africans and Hispanics - 2X risk. Native americans - 2.5X risk.

Front 16

Etiology/Epidemiology of Gestational DM

Back 16

glucose intolerance first recognized during pregnancy.

4% of pregnancies

Hint 16

Hormone - Human Placental Lactogen raise insulin resistance.

2X increase of developing Type 2, with 35% having Type 2 w/in 5-10 yrs.

Front 17

Etiology/Epidemiology of Gestational DM

Back 17

Risks to Baby -
during pregancy, mom's increased BG produces insulin. Insulin does not cross placenta but glucose does. fetus increases production of own insulin - this becomes norm for fetus. Newborn continues to over-produce insulin and doesn't have glucose supply, causing hypoglycemia.
Can be fatal.

Hint 17

Macrosomia - (fat baby) the unneeded glucose from mom is stored (due to insulin) as fat. Increased risk for:
early birth (cuz of wt.)
increased resp. problems
obesity
DM2 when older
increased shoulder dislocation due to wt.

Front 18

Etiology/Epidemiology of LADA

Back 18

thought to be DM2 due to age of client. DM1 diagnosed in older people

Front 19

Etiology/Epidemiology "other causes"

Back 19

illness (infection, MI)

medications (predninsone - steroid, metoprolol (Lopressor)- beta blocker (slows HR, lowers SNS effect of fight or flight), hydrochlorthiazide-diuretic (lowers blood volume))

CA

Pancreatitis (unable to break down and utilize nutrition from food due to no pancreatic enzymes)

Downs Syndrome

Endocrinopathies - hormone imbalances

Front 20

Diagnosis
Absolute

Back 20

Fasting plasma glucose of >126 mg/dl on 2 occasions or a random BG of >200

A1c >6.5
A1c of 6.0-6.4 is concerning for pre-diabetes

GTT - drinking of glucose (outdated)

Front 21

Diagnosis of DM1
S&S

Back 21

frequent urination (body trying to rid glucose through kidneys)

unusual thirst (hi concentration of sugar in blood)

extreme hunger (not getting enough nutrition)

unusual wt. loss (burning fat/muscle to try and feed cells)

extreme fatigue and irritability (burning fat/muscle to try and feed cells)

N/V (ketones produced when fats and muscle are broken down for E)

flu-like symptoms that do no go away

Front 22

Diagnosis of DM1
DKA presentation

Back 22

Life Threatening

Metabolic acidosis (ketones) produced due to digesting fats instead of sugars

Hint 22

drinking increases, pee increases - osmotic diuresis

increased water loss w/ Na depletion

serum potassium usually falsely elevated

cachexia, weak, abdominal pain, HA, lite sensitivity, N/V, significant wt. loss, dehydration, fruity breath. Look like holocaust victim.

generally seen when ill & not taking insulin

Front 23

Diagnosis of DM2
S&S

Back 23

any of Type1 symptoms

frequent infections (yeast)

blurred vision (due to BG not retinal)

cuts/bruises that are slow to heal (poor circ.)

tingling/numbness in hands/feet (nerve damage)

recurring skin, gum, bladder infections

*people with Type2 have no symptoms or can take up to 10 yrs to have.

Front 24

Diagnosis of DM2
Gestational Diabetes

Back 24

Glucose Tolerance Test (outdated, drinking of sugar) done @ 20 weeks unless glucose shows in urine earlier or S&S appear.

Front 25

Diagnosis of DM2
Hyperosmolar NonKetoic Acidosis
The DKA of DM2

Back 25

Occurs in specific situations:

-illness such as n/v/d - (losing fluids & electrolytes)

-unable to get/keep in fluids (someone in dependent situation - nursing home)

- BG in 400-600s (causing more dehydration)

- Need insulin but not getting/taking due to not eating and having N/V

Hint 25

likely seen in nursing home or similar home situation

Front 26

Treatment Modes of DM1

Back 26

Insulin

Administration:
-vials and syringes
-Insulin pens
-Insulin pumps

Amount:
-based on BG levels, activity, dietary intake, stress, illness

-Must check multiple times a day to maintain control. Patients must understand daily activity, diet, stressors and understand what to do when these things change

Front 27

Treatment of DM1 & DM2
Dietary

Back 27

-Exchange System: allowed certain # of calories a day & from certain food groups.

6 main exchange lists: bread/starch, veg, milk, meat, fruit, fat.

-Carb counting
100% carbs converted to glucose, protein are converted to glucose, but has little effect on BG levels

Front 28

Treatment of DM1

Back 28

dietary intake in children should not be restricted - insulin adjusted to what child eats.

older need to eat based on caloric need

Front 29

Treatment of DM2

Back 29

-Decrease carbs. big problem processing carbs

Body needs minimum of 150 grams carbs/day, divided up into no more than 50 grams every 4 hours.

- Diet & Activity

- Start w/ oral medications.

Hint 29

Meds:
-Metformin &/or Sulfonylurea
-add long-acting insulin
-May add Actos (to decrease insulin resistance)
-Add in: Byetta, Victoza, Januvia (gut hormone that helps to feel full, no longer made or reduced in both DM1 & 2 but more so in DM2)

-Add in short/rapid acting insulin

Front 30

Treatment of DM1 & DM2

Back 30

-Diet/Activity (impacts insulin/medication needs may need to increase or decrease on some days)

-Meds. (may impact BG and cause need for increase in DM meds)

-Sick Days (hormones released increase BG; infection may increase BG and MUST remember to still take insulin to prevent DKA or Hyperosmoler Nonketoic Acidosis). SUPER IMPORTANT

-Insulin Self-management

-Insulin Pump

Hint 30

Why is taking insulin when feeling sick important for DM1 persons?

-they don't produce ANY insulin

Front 31

Insulin Pump: How it works

Back 31

-Set based upon patient need (what times of day do they need more/less insulin)

-Basal Rate (can set hourly changes in amount of insulin rec'd that hour. Based on age different amounts of insulin are needed at different times of day)

-Bolus
Insulin Carbohydrate Ratio (ICR) - 1 unit of insulin covers how many grams of carbs.

Insulin Sensitivity Factor (ISF) - 1 unit of insulin drops person how many mg/dl (BG points)

Front 32

Complications - Physical

Back 32

-Physical: majority caused by microvascular damage from elevated BG over time

blood unable to move through the small vessels and creates stagnation.

blood supply is reattempted w/ weak vessels that hemorrhage easily

loss of nutrition (glucose, O2, etc. to cells surrounding as well as the cells of the vessel. Ex: eyes, kidneys, feet)

Front 33

Complications - Retinal

Back 33

-Retinopathy

Nonproliferative retinopathy
most common. Capillaries in back of eye balloon and form pouches to try to create new vessels.

can move through 3 stages as more blood vessels become blocked.

Proliferative retinopathy
blood vessels are so damaged they close off.

new blood vessels start growing in the retina. these new vessels are weak & can leak blood, blocking vision (called vitreous hemorrhage). New blood vessels can also cause scar tissue to grow. After scar tissue shrinks, it can distort retina or pull it out of place (called retinal detachment)

S/S: None, until lose eye sight

May have noticeable red spot in vision w/ vitreous hemorrhage

Patient care: annual eye exams. Laser Sx on vessels.

Front 34

Complications - Nephropathy
Part 1 of 2

Back 34

Microvasculature of kidney becomes damaged from hyperglycemia/HTN which will eventually cause protein leakage into the urine, which causes more damage to kidney.

unable to filter out waste products so they accumulate in blood.

glucose and protein are nephrotoxic

BUN increases
Cr increases
Total Protein decreases
Albumin decreases
Urine Cr increases
Protein increases
Urine Mirco Albumin Increases (blood protein leaks into urine, 1st sign of Diabetes)
Check for signs of cardiac dx, MI risk increase

Front 35

Complications - Nephropathy
Part 2 of 2

Back 35

-BG control (diet/activity/meds)

-BP control (diet, activity, salt, meds)

ACE inhibitors (vasodilaiton)
benazepril (Lotensin), enalapril (Vasotec), lisinopril (Prinivil) are 1st med. for HTN in DM due to renal protective aspect.

Will worsen renal artery stenosis, ADR: dry cough

Front 36

Complications - Infection (bacterial & fungal)

Back 36

-High BG

-Poor circulation

- Damage to nerves due to high BG & poor circ.

-Becomes gangenous (poss. amputation)

Front 37

Complications - Ulceration

Back 37

-Uncontrolled BG for long period of time

-Healed over infection, not able to see

-East away at tissue eventually going into the bone

Front 38

Complications - Neuropathy (from microvascular damage to circulation -nerves die)

Back 38

First -Extremeties: numbness, infection, amputation

Heart: uncontrolled HR, fast or slow

Bladder: loss of control

GI: gastroporesis (loss of gut motility, slows down food in gut)

Front 39

Complications - PVD (Peripheral Vascular Disease)

Back 39

Vasculature had compromise at the cellular level due to lack of proper nutrition from poor circ. & causes decreased circulation.

-increased risk for infection. hard to treat as antibiotic in blood is not able to get circulated to area of infection due to PVD.

-increased edema which slows circ. down more promoting stagnation of glucose @ infection site, unable to get WBCs to area. Increase infection rate due to sugar to feed bacteria/yeast.

decrease proprioception, sensation of light, pain, temp., deformities of foot, joint changes, decrease deep tendon reflexes

Front 40

Complications - Cardiac

Back 40

-Over time, microvasculature problems become microvasculature

-Know A1c & keep it controlled

-Know BP & keep it controlled

-Know Cholesterol & keep it controlled.

*total count: <200
*Triglycerides: <150
*HDL: >45 men; >50 women
*LDL:<100 (<70 better)

Front 41

Complications - Psychological

Back 41

-Depression
-multiple MDs to see
-multiple meds daily & multiple Xs/day
*PO meds TID
*Insulin w/ DM1 up to 7-10 shots of insulin a day based on multiple issues
*BG checks DM2 - 1 qDay (often more); DM1 - 1-10 X/day.

Front 42

Co-Morbidities of Diabetese

Back 42

-HTN (leads to neuropathy, may be more renal toxic than increased BGs)

-Hyperlipidemia (leads to plaqueing of vessels which may be compromised already from hyperglycemic effect of uncontrolled DM1 or 2)

-Obesity (DM2>DM1. Makes control more difficult. Muscle uses insulin and glucose more readily than fat cells.)

-Depression

-Other autoimmune Dx (arthritis, sarcoidosis, sceraderma, asthma)

-Other endocrine Dx (hypothyroid, early menopause, Polycystic Ovary Syndrome)

-Hypoglycemia

-High risk pregnancy (birth defects, hypoglycemia, premature birth, increased fetal demise)

-Celiac Dx

-More likely to have food allergies, other allergies
-

Front 43

Home Self Care of DM

Back 43

-BG testing w/ meter that is in good repair, test strips are in date.

-check calibration
-test @ that moment in time
-know/learn how/what to do with BG levels

Front 44

Home Self Care of DM - S & S of Hypoglycemia

Back 44

Tired
Confused
Hungry
Irritable
HA
Nausea
Sweaty
Shaky
Tachycardia

-Need Snack. 1 cup milk, 1 slice bread, no OJ w/ sugar

Front 45

Home Self Care of DM - S & S of Hyperglycemia

Back 45

Tired
Confused
Hungry
HA
Irritable
Increased Urination
Increased Thirst

-Need to lower BG some way: med/activity

-Differences with DM1 & 2

Front 46

Nursing Considerations with DM - in hospital care

Back 46

-monitor BGs

-Lotion daily to extremities reduces amputation by 50% -do it & tell why.

- What they need based on S&S of diabetes, medical needs

-Offer support, resources, education
-Dietary consult
-Certified Diabetes Educator CDE referral

Front 47

Nursing Considerations with DM - in Education

Back 47

-How to check BG

-How to draw up and give insulin
-How does the new med. work in body?

-Dietary consult

-Certified Diabetes Educator CDE referral

Front 48

Nursing Considerations with DM - Treatment of Hyperglycemia

Back 48

-DKA: life and death situation. Must have fluid replacement, insulin, generally K+ is false positive high. When fluids are replaced, K+ will drop.

-Elevated BG. Insulin per MD order in hosp.

Front 49

Nursing Considerations with DM - Treatment of Hypoglycemia

Back 49

-D50 IV is normal. Boosts BG up immediately

-If no IV, Glucagon is given IM or SQ. Pt. needs to be in recovery position.

-if pt. is alert/semi oriented give eat or drink. Milk better than juice, followed by snack of carbs/protein or carb/fat.

Front 50

Nursing Considerations with DM

Back 50

-Treatment of other Diabetes related issues will be based on care needed & MD orders.

-Pts. need education & this is one of the main roles for nurse, esp. if newly diagnosed pt.

-know your referral base in your area

-know what your hospital/clinic has to offer for DM education materials

-Share the knowledge

Front 51

Take Home Points for DM

Back 51

DM Type 1 - Young, Acute Metabolic Complications (ketoacidosis & hyopglcemia)

DM Type 2 - Chronic Vascular Compliations (microangiopathy, kidney, retina, cardiovascular system, periph. vascular system, nervous system)

-Administration of glucose for hypogylcemia is lifesaving

-Duration & level of hyperglycemia are directly proportional to Chronic Vascular complications.

-Infections are due to microangiopathy (years of uncontrolled BGs) and ischemia, immunosuppression & current hyperglycemia.

-Good nursing care and education can limit or slow the onset of diabetic complications.

Front 52

Hormones

Back 52

-Synthesized & released by endocrine glands

-Work by direct action or travel thru bloodstream or lymph system

-Controlled/regulated by negative feedback system

-Intrinsic (natural) rhythms & external stressor also control/influence hormone levels

Front 53

Function of Hormones

Back 53

-Maintenance & regulation of vital functions

-Response to stress & injury

-Growth & development

-E metabolism

-Reproduction

-Fluid, electrolyte, & acid-base balance

Front 54

Pituitary Gland

Back 54

-Master Gland (located at base of brain)

-Influenced by hypothalamus

-Directly affects function of other endocrine glands via releasing stimulating hormones

Front 55

Pituitary Gland - Anterior

Back 55

-Growth hormone
*hyper: acromegaly
*hypo: growth retardation

Front 56

Pituitary Gland - Posterior

Back 56

-ADH influences water absorption by the kidney
*hyper: SIADH (excessive release of ADH)
*hypo: diabetes insipidus (excessive thirst, peeing alot)

Front 57

Thyroid Function

Back 57

-located in anterior neck

-Controls rate of body metabolism

-Follicle cells make thyroid hormones: T3 & T4

-C-cells make calcitonin- involved in Ca homeostasis

Front 58

Diagnostic Testing: Thyroid Hormones

Back 58

T4/T3: low levels = hypo; high levels = hyper

-TSH: high in hyper; low in hypo

- Thyroid antibodies may be present in autoimmune dx

Front 59

Decreased Function: Hypothyroid

Back 59

-Decreased metabolism from low levels of thyroid hormone
*Cretinism: developmental delay caused by inadequate secretion of thyroid hormone during fetal & neonate development causing stunted physical & mental growth

-Common Causes:
*US: autoimmune thyroiditis (Hashimoto's Dx) & hyperthyroid therapy
*Worldwide: iodine deficiency (goiter)

-More women than men; under diagnosis in elderly

Front 60

Hypothyroid: S & S

Back 60

-Lethargy, fatigue, weakness, muscle aches.

-Intolerance to cold, hypothermia, wt. gain.

-Dry skin, hair; loss of body hair

-Bradycardia, hypotension, cardiac disorders

-Puffiness & edema (eyes & face)

-Forgetful, memory loss

-Constipation

Front 61

Hypothyroid: Treatment

Back 61

-Replacement therapy: Levothyroxine or Synthroid

-Monitor Cardiac status

-Sx if goiter is large

-Hypothyroid Treatment: monitor blood TSH/T3/T4 levels to assess response to therapy

-Symptomatic improvement

Front 62

Increased Function - Hyperthyroid

Back 62

-Increased production & secretion of thyroid hormone

-Most common cause (60-90%) of Grave's dx; autoimmune disorder

-Characterized by increased rate of body metabolism

Front 63

Hyperthyroid: S & S

Back 63

-Enlarged thyroid gland: goiter

-Hypermetabolic state, increased circ., adrenergic stimulation
*tachycardia, HTN, fibrillation, dysrhythmias, angina,
*Exophthalmos (bulging eyes), fine hair, flushed skin
*Nervous, tremors, muscle weakness, fatigue, wt. loss, heat intolerance, diaphoresis, diarrhea, vomiting
*Emotional lability, personality change, insomnia

Front 64

Hyperthyroid: Treatment

Back 64

-Meds: reduce hormone excretion

-Radioactive Iodine Therapy

-Sx to reduce volume of thyroid tissue

-Goal: reduce amount of thyroid hormone excreted, and minimize effects of hyperthyroid on tissues

-No known treatment for Graves'

Front 65

Thyroidectomy: Pre-Sx

Back 65

-Monitor VS, electrolytes, BG

-Teaching--turn, cough, deep breathing, pain management, supporting neck

-Monitor for thyroid storm (acute hyperthyroid)

Front 66

Thyroidectomy: Post-Sx

Back 66

-Expect hoarseness & weak voice

-Monitor for respiratory distress/laryngeal damage/airway compromise
*Semi-fowlers position in bed, O2, suction, trach set ready

-Monitor for hypocalcemia R/t parathyroid damage
*Manifests as muscle weakness, cramping, altered sensation.
*Ca Gluconate is an antidote, have @ bed side

Front 67

Hyperthyroid: Outcomes

Back 67

-Monitoring: Hormone levels to eval. effects of therapy

-Often therapies result in hypothyroid condition requiring hormone replacement

-Education:
*How to take meds.
*S & S of hypo & hyperthyroid conditions

Front 68

Function: Adrenal Cortex

Back 68

-Outer shell of adrenal gland

-Aldosterone:
*major controller of Na balance & volume status; controlled by renin-angiotensin system

-Glucocorticoids
*gluconeogenesis, protein catabolism, lipolysis, anti-inflammatory, suppress immune response, alter mood & maintain emotional stability

-Adrenal androgens: 2-ary sex characteristics

Front 69

Adrenal Cortex: Hypofunction

Back 69

-Decreased cortisol leads to hyopglycemia

-Decreased aldosterone causes hyperkalemia, hyponatremia, hypovolemia, acidosis

-Decreased androgens results in loss of body, axillary and pubic hair

Front 70

Function: Adrenal Medulla

Back 70

-Inner core of adrenal gland

-Works as part of the SNS (fight/flight) in coordinated response to stressors affecting all body systems

-Produces epi & norepi

Front 71

Adrenal Medulla: Hyperfunction

Back 71

-May be caused by tumor
*Pheochromocytoma (tumor that secretes excessive amounts of epi/norepi
*HTN

Front 72

Endocrine Summary

Back 72

-Abn endocrine function can alter the function of vital body systems

-Suspect abn. endocrine function during illness or hospitalization

-Monitor and treat abn. hormone levels and the functions they influence to restore optimum function