adult health pre midterm 2

diabetes mellitus

• multi system disease

• endocrine disorder

• abnormal insulin production, impaired insulin utilisation or both

• approx 60-85% of ppl will die from heart disease or stroke

• dm is contributing to death of approx 41 500 canadians per year

• canadian adults with dm are twice as likely to die prematurely

• higher incidence in indigenous pops as well as people with african and asian descent

etiology and pathophysiology of diabetes mellitus

causes are combination: genetic, autoimmune, viral, environmental, lifestyle

types: type 1, type 2, gestational (pregnancy), prediabetes, secondary diabetes (after renal disease or cardiac disease, etc)

normal insulin metabolism: produced by B cells in the islets of langerhans, released continously into blood stream in small amts (basal dose) and then larger amts after foods, stabilises glucose range to 4-6 mmol

insulin

• comes out of organ, binds to glucose, helps glucose to go out of blood stream and into cells (cells have receptors for glucose but needs insulin to transport)

  • no insulin means nothing to transport glucose

  • for insulin resistance, the insulin will not bind to glucose

• symptoms caused by not enogh glucose into cells and too much glucose in blood stream

• post prandial (after meals) vs basal doses (reg dose)

• insulin goes up after meals, it stimulates storage of glucose as glycogen in liver and muscle, inhibits gluconeogenesis, enhances fat deposition, increase protein synthesis

• skeletal muscle and adipose tissue (insulin-dependant tissue)

• other tissues (brain, liver, blood) doesn’t directly depend on insulin for glucose transport

type 1 diabetes mellitus

• aka juvenile onset or insulin dependant diabetes or IDDM (insulin dependant diabetes mellitus)

• occurs in those younger than 30, more frequent in young children

• end result of a long standing process: progressive destruction of pancreatic B cells by the bodys own T cells, autoantibodies cause a reduction of 80% to 90% in normal B cell function before manifestations occur

• patient will get insulin bc cant make their own (exogenous insulin)

• causes: genetic predisposition (related to human leukocyte antigens (HLAs), exposure to virus

• long pre clinical period (could have had prediabetes, metabolic syndrome), antibodies present for months to years before symptoms occur, manifestations will appear when pancreas can no longer produce insulin (rapid onset symptoms, present at ED with ketoacidosis)

what can happen if cells do not get glucose

they can die

hypoglycemia: life threatening condition (IMPORTANT)

hyperglycemia: causes symptoms

DKA

• diabetic keto acidosis

• body has been burning fats and proteins

• in absence of exogenous insulin

• life threatening

• results in metabolic acidosis

• polydipsia, polyphagia, polyuria

polyuria

• frequent urination

• kidneys trying to get rid off too much glucose

polydipsia

• excessive thirst

• body wants to dilute sugar in blood stream

polyphagia

• extreme hunger

• cells aren’t able to get glucose

prediabetes

• individuals already at risk for diabetes

• blood glucose high, but not high enough for diabetes

  • IFG (impaired fasting glucose) - 8hr w out any oral intake (other than water), then get blood sugar checked, result will be 6.1-6.9

  • IGT or OCTT (oral glucose tolerance test) - give sugary drink then test glucose 2 hrs later, result will be 7.1 - 11 mmol/L

  • hemoglobin A1C - looks at life of blood vessel (normally 3 months) and looks at its carrying capacity,

• long term damage already occurring to heart and blood vessels

• usually present with no symptoms

• watch for polyuria, polydipsia and polyphagia

normal blood glucose

3.6-6 mmol/L

type 2 diabetes

• aka NIDDM (non insulin dependant diabetes mellitus), more prevalent (90% of all diabetes), ppl over 35 and prevelance increases with age, 80-90% of pts are overweight, genetic basis, greater in some pop: indigenous, latin america, south asian, asian or african descent

• pancreas continues to produce some endogenous insulin, insulin is insufficient or poorly utilised by tissue

• obesity (abdominal and visceral) is the most powerful risk factor for insulin resistance and diabetes in general, along with genetic mutations (lead to insulin resistance or increased risk for obesity)

• 4 major metabolic abnormalities: insulin resistance, pancrease ability to produce insulin decreases, inappropriate glucose production in liver, alteration in production of hormones and adipokines

• gradual onset, person may go years with undetected hyperglycemia

type 2 diabetes mellitus etiology and pathophysiology

gestational diabetes

• develops during pregnancy (24-28) weeks at gestation

• usually normal glucose lelves at 6 weeks postpartum

• increased risk for birth trauma, hypoglycemia, hyperbilirubinemia, and resp distress syndrome

• increased risk for developing type 2 diabetes in 5-10 years

• therapy: first nutritional, second insulin

secondary diabetes

• treatment of a medication contition or treatments that causes abnormal blood glucose levels

  • corticosteroids (prednisone) (acts as influx of cortisol- elevates sugar)

  • phenytoin (dilantin)

  • atypical antipsychotics (clozapine)

• usually resolves when underlying conditions are treated

s+s of type 1 diabetes mellitus

• polyuria, polydipsia, polyphagia

• weight loss (bc of breakdown of fats and proteins)

• weakness (no atp production in cells)

• fatigue (no atp production in cells)

• high risk complication: DKA

s+s of type 2 diabetes mellitus

• non specific, may have type 1 symptoms

• fatigue

• recurrent infection

• recurrent vaginal yeast or monilia infection

• prolonged wound healing

• visual changes (blood vessels in the eye get damaged bc excess sugar causes blood to get thicker)

diabtes mellitus diagnositc studies

need to have 2/4

A1C test

• life of hemoglobin over last 3 months

• key diagnostic test for diabetes

• anything equal or over 6.5% means diabetes, over 7 is diabetes

interprofessional care for diabetes

goals: decrease symptoms, promote well being, prevent acute complications, delay onset and progression of long term complications

• patient teaching - self monitoring of blood glucose

• nutritional therapy

• medication therapy

• excersise

exogenous insulin

• insulin from outside source

• required for type 1, prescribed for type 2 if unable to control blood sugar in other ways

  • also for type 2, esp in the hospital they may be more likely to have insulin because of surgery or illness and stress will cause increase in cortisol which causes spikes in blood sugar that can’t be maintained with oral glycemics

  • pts on TPN (total parenteral nutrition) may take insulin if it raises their bp too much

honeymoon period

• after diagnosis of type 2, pts sometimes go through honeymoon period where they are able to balance for a little while before it gets worse and they may need insulin

human insulin

• genetic engineering of bacteria to produce this, only one used today

• differ with regard to onset, peak action and duration

• different types in combo

• regimen that closely mimics endogenous insulin production is basal-bolus

  • basal: once a day, long or intermediate acting

  • bolus: before meals, rapid or short acting

mixing insulin

• regular insulin or short acting is the only one that can be given IV

critical thinking for insulin

• if pt is going for a procedure hold med

• if pt is vomiting hold med

rapid acting

• bolus

• lispro, aspart, glulisine

• 0-15mins before meal

• onset of action: 15 mins

• typically used in hospital for correction scale

short acting

• bolus

• regular insuline

• only insulin that can be given IV

• 30-45 mins before meal

• onset is 30-60 min

long acting

• basal

• once a day, bedtime or morning

• released steadily and continuously (no peak)

• cannot be mixed with any other insulin or solution

handling insulin

• do not heat or freeze

• store insulin in fridge

• in use vials may be left at room temp for up to 28 days

• avoid exposure to direct sunlight

admin of insulin

• cant be take orally (stomach acid affects it)

• subcut injection usually, IV for regular

• fastest absorption: abdomen, followed by arm, thigh and buttock

• abdomen is preferred site, but when pt is on anticoagulants, abdomen is used for that, also pts probably use abdomen for themselves- usually use arms

• rotate injections within one particular sites

• do not inject in a site to be excersised

• usually available as U100

  • 1 mL contains 100 units of insulin

• use alcohol swab first and let dry (UNLESS pt is at home and doing this for themselves)

• handwashing with soap or abhr before

• do not recap needle

• 45-90 degree angle- depending on fat thickness of pt

• insulin pens preloaded with insulin are now available

sub cut injection sites

• rotate sites

• body part and within the body part

• avoid hardened areas

insulin pen diagram

when admin insulin, what do u need

• pen, needle, alcohol swab

priming insulin

• dial pen to 2 units

• over trash, dispense units out of the pen to prime needle

• dial dose up to whatever is ordered for pt

independant double check

• always for insulin

• do not tell other nurse anything- they use sliding scale to figure out insulin amt on their own

insulin pump

• continous subcut infusion

• helps maintain glycemic control

• battery operated

• connects to phone

• connected via plastic tubing to catheter inserted into subcut tissue in abdominal wall

complications with insulin therapy

• hypoglycemia (pt gets insulin and then doesn’t eat, pt can vomit, increased excersise)- do frequent blood sugar checks as ordered and as needed

• allergy (to any additives, can be switched to different insulin)

• lipodystrophy (important to rotate sites, sites will start to harden)

• somogyi effect

• dawn phenomenon

somogyi effect

• hyper glycemia in the morning

• rebound effect where overdose of insulin causes hypoglycemia

  • SO MUCH insulin

• usually during sleep

• counterregulatory hormones released

  • causes rebound hyperglycemia and ketosis may occur

dawn phenomenon

• hyperglycemia in morning

• release of counterregulatory hormones in pre dawn

• growth hormones/cortisol

• normal pattern- dont eat overnight and body is compensating by increasing blood sugar

dawn vs somogyi

• dr will call for testing around 2-3am

• dawn is more slower and progressive, somogyi is sudden

understand correction/sliding scale

antihyperglycemic agents

• oral agents: not insulin

• work to improve mechanisms by which insulin and glucose are produced and used by the body,

• for type 2 mostly

• work on insulin resistance, decreased insulin production, increased hepatic glucose production

sulphonylureas

meglinides

• difficult bc needs to be taken exactly 30 mins (pt needs to understand and able to do this)

biguanides

• think abt kidneys, kidneys need to be in good status before giving this med bc this med is excreted through kidneys

  • if kidney function not good enough- med will build up in blood stream

• if someone is ill, not enough fluid intake, vomiting or diarrhea- may have dehydration which will affect the kidneys (have to work harder)

  • SICK day protocol

  • short term effects to kidneys, this med isnt the best

• IV contrast dye also affects kidneys- causes short term damage

• ***metformin and kidneys- remember trick

meds will be more thorough in pharm

α-Glucosidase inhibitors

thiazolidinediones

• insuline resistance most often used for obese patients

dipeptidyl peptidase-4 (DDP-4) inhibitor

B-Adrenergic blockers

• mask symptoms of hypoglycemia

• prolong hypoglycemic effects of insulin

thiazide/loop diuretics

• can potentiate hyperglycemia bc potassium loss

nutritional therapy for diabetics

• important and challenging

• cornerstone bc we are trying to acheive a good glycemic index diabetes mellitus nurse educator and registered dietitian should be part of healthcare team

• canadian diabetes association (CDA)/diabetes canada

  • provides a variety of teaching tools

type 1 diabetes mellitus nutritional control

• based on usual food intake and balanced with insulin and excersise

• insulin regimen managed day to day

• often will wear a glucose monitor and pump to real time track and correct

type 2 diabetes nutritional therapy

• emphasis is on achieving glucose, lipid and blood pressure goals

• calorie and fat intake reduction

food composition of diabetic education

• energy intake balanced with energy output

• alcohol - LOWERS BLOOD GLUCOSE

• work WITH the patient to find nutritional control that works for them- be careful with just telling people what to do

  • cultural component

healthy eating education

• dietician initially provides instruction

• carb counting

• canadian food guide

excersise for diabetics

• essential

• increased insulin sensitivity

• lowers blood glucose

• weight loss

• several small carb snacks can be taken every 30 mins during excersise to prevent hypoglycemia

• best done after meals

• excersise started after: medical clearance, slowly with gradual progression

• should be individualised

• monitor levels before, during and after excersise

rule of thumb for excersise

• 150 mins per week of moderate intensity aerobic physical activity

monitoring of blood glucose

• self monitoring (SMBG): self management, detects episodic hyper and hypoglycemia, pt training crucial, supplies immediate info abt blood glucose

• continous glucose monitoring (CGM): displays with glucose values every 1-5 mins, track trends, common for kids

nursing assessment of diabetics

• past health history

• medications

• recent surgery

• symptoms: malaise, weight loss, thirst, hunger, poor healing, kussmaul’s respirations (fast rapid breathing), constipation, diarrhea, polydipsia, polyuria, polyphagia, muscle weakness, fatigue, erectile dysfunction, frequent vaginal infections, decreased libido, depression, irritability, apathy. fruity acetone breath

nursing diagnosis for diabetics

• inadequate health management

• potential for injury

• potential for unstable blood glucose

• potential for peripheral neurovascular dysfunction

nursing planning for diabetics

• active pt participation

• few or no episodes of acute hyperglycemic emergencies or hypoglycemia

• maintain normal blood glucose levels

• prevent or delay chronic complications

• lifestyle adjustments with minimal stress

nursing implementations for diabetics

• health promotion: identify risks, routine screening (fasting blood glucose or A1c preferred, every 3 yrs past 40 or in high risk)

• acute intervention: hypoglycemia, dka, hyperosmolar hyperglycemic state,

  • stress of illness or surgery: increase blood glucose, continue meal plan, increase intake of noncaloric fluids, continue taking insulin and oral meds, frequent monitoring of blood glucose, ketone testing of glucose over 14 mmoL to test for acidosis

• home care: medications, hygeine, identification and travel card, carry diagnosis of diabetis, teaching, educate on disease process, meds, excersise, diet,enabel the pt to be active in care

nursing evaluation of diabetics

• knowledge

• balance of nutrition

• immune status

• health benefits

• no injuries

DKA

• can happen in type 2 during surgery, illness or stress

• KETONES found in urine- byproduct of fat metabolism

• symptoms: 3Ps, weakness, dehydration, sweet odor, tachycardia, kussmaul respirations, orthostatic hypotension

• managment: airway management, correct fluid/electrolyte imbalance, iv infusion of 0.45% or 0.9% NaCl to restore urine output and raise bp, when glucose approach 14 mmol/L add 5% dextrose to regimen to prevent hypoglycemia, potassium replacement, (sodium, chloride, bicarbonate, phosphate, magnesium, nitrogen) deficits need to be corrected), insulin theryapy (withheld until fluid resuscuitation had begun, bolus followed by continous insulin infusion

• labs: blood glucose over 14mmol/L, arterial blood pH under 7.35 (acidotic), serum bicarbonate level of under 15 mmol/L, anion gap greater than 12 mmol/L, moderate to large ketones in the urine or blood

• important, must be treated proptly, may or may not need hospitalisation

DKA management quick steps

1. abcs

2. fluid resuscuitation, mostly isotonic

3. correct k+ if deficient

4. iv insulin

5. iv glucose when levels under 12 mmol/L

***K BEFORE INSULIN because potassium helps shift insulin into cells

hyperosmolar hyperglycemic syndrome (HHS) (non ketotic)

nursing managment of DKA/HHS

• monitor and assess glucose, renal status, cardiopulmonary status, loc, signs of potassium imbalance, cardiac monitoring, vital signs

• admin of iv fluids, insulin therapy, electrolytes

hypoglycemia

• low blood glucose

• too much insulin in proportion in the blood

• manifestations: anxiety, nervous, diaphoresis, tremors, hunger, pallor, palpitation, irritable

• untreated: loss of conciousness, seizures, coma, death

• hypoglycemic unawareness: pt doesn’t exhibit signs, increased ris, related to autonomic neuropathy

• causes: mismatch in timing of intake of meds and foods

normal blood glucose

4-6 mmol/L

management of hypoglycemia

• check glucose, if under 4 mmol/L, start treatment

• if alert to swallow- 15-20g of simple carb (175 mL of fruit juice, regular soft drink, 6 life saver candies)

• recheck 15 mins, repeat until blood sugar greater than 4 mmol/L, pt eats meals or snacks to prevent rebound hypoglycemia, check in 45 mins after food

• 15 15 rules: 15 g of carb and check every 15 mins

• if pt not alert to swallow- admin 1mg of glucagon IM or cubcut, adverse effect is rebound hypoglycemia, have pt ingest complex carb after recovery

• in acute care: 20-50 m: of 50% dextrose IV push, follow up with 1v drip of glucose

chronic complications of diabetes

angiopathy macrovascular

• cholesterol levels screened

angiopathy microvascular

• yearly eye exams in these pts

damage to eyes with diabetics

dont need to know in detail

diabetic retinopathy

diabetic nephropathy

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