Complications of DM Flashcards
2 Acute complications related to Hyperglycemia
Diabetric Ketoacidosis
Hyperosmolar hyperglycemic nonketotic syndrome (HSS)
Diabetic Ketoacidosis mostly a problem for DM 1 or 2
Type 1
Nonketotic
No ketones involved
The primary differentiator bw HSS (No ketones) and DKA (Keotones)
Good ______ reduces DM complications
Glucose control
Hypoclymia is acute or slow acting
Acute
Hyper or hypoglycemia more dangerous
Hypoglycemia
Hypoglycemia caused by
- Mismatch in the timing of food intake and the peak action of insulin or PO hyperglycaemic agents
- Excessive insulin or PO hypoglycaemic agents
- Ingestion of insufficent carbs
- Excessive exercise
S/S of Hypoglycemia
Adrenergic: Epinephrine release
(Sympathetic NS response): Diaphoresis (Sweating), tremors, hunger, nervousness, anxiety, pallor and palpitations
Neuroglycopenic (Not enough glucose for brain): Irritability, visual disturbances, difficulty speaking, confusion, coma
Untreated Hypoglycemia
Loss of Consciousness, coma, seizure
Fuel for the brain is
Glucose enables us to think clearly
Hypoglycemic unawareness
Asymptomatic hypoglycemia
- A person does not expereicne the usual ANS s/s associated with hypoglycemia (often related to neuropathy that interfere with warning signs)
My occur with sudden drop in BG
Homeostatic mechanism used to counteract hypoglycemia
Low BG triggers sympathetic NS, releasing Epinephrine which targets glucagon release to make glucose available to the body
Treatment of Hypoglycemia (According to CPG)
Check BS; treat if BS , 4 mmol/L
Provide dextrose tabs according to CPG associated with specific level of BS
Once BS higher than 4, provide longer acting starch and sugar
Once stable, provide ducation and prevention
DKA
Profound deficiency of insulin - hyperglycemia and dehydration
Fats are metabolized in absence of insulin (For alternate energy source) - ketosis and acidosis (Body reacts to lack of glucose in cell)
Seen most often in DM Type 1
Ketosis
The big problem in DKA
Body breaks down fats, fats break down into ketones, acitones is one
Acitone body results in fruity breath
Beta hydroxibuderate (
Beta hydroxibuderate
ketone that is tested for) - Releases hydrogen ions that contirbute to the metabolic acidosis
As body compensates for acidosis
Metabolic Events leading to DKA and D-Coma
Islet beta cell destruction
Resulting in Insulin deficiency
Leads to decreased tissue glucose utilization
Liver release glucose (Glucogon broken down)
- Compounds problem
Adipose tissue is targeted to break down fat into ketones
Liver contributes in breaking down ketones
Excess glucose results in increased vascular fluid to match the solutes (and flush them out)
Kidneys pass this excess fluids
- Poluria
- Glucose in urine
Results in cellular starvation
- Polyphagia, cannot be satisfied
What causes acidosis
The body likes to remain slightly basic
H+ ions are acidic, too many are circulating
Body compensates by pulling these cations into the cells
Causes K+ ions to be pulled out (Intercellular potassium depletion occurs) - high levels of intravascular levels
Blood potassium levels in DKA are
Normal or high since H+ Ions replace Potassium in cells, kicking them into bloodstream
Potassium is most important for
Impact in stability of cardiac membrane (electrical conduction)
If potassium is not bw 3.5-5 mmol/L in blood it can cause cardiac abnormalities
Causes of DKA (6)
Illness (stress)
Infection (Stress)
Inadequate insulin doses to shift adequate glucose into cells
Insulin omission
Undiagnosed DM type 1
Poor self diet management
S/s of DKA
Polyuria, Polydipsia
Dehydration
Early symptoms - lethargy and weakness
Later - Poor skin turgor, dry mucous mems, tachycardia, Ortho HOTN, sunken eyes
N/V
Abdom pain
Rapid Resp Rate
Fruity breath odour
BG > 14mmol/L, pH < 7.35
Ketones in blood and urine
Treatment in DKA
Food & Electrolyte replacement
Prioritizing according to ABCs (BS under D)
Two IVs (Large bore)
IVF (Usually Bolus dose NaCl) - isotonic (Will decrease BS bc of dilution) until urine output is > 30mL/h
Bloodwork (arterial blood gas, betahydroxate buterate level, electrolytes)
Deal with pH (Introduce basic solution into vascular system i.e Sodium Bicarb)
Fix electrolyte levels
BS levels monitered every hour
Small bolus of insulin followed by insulin infusion of 1unit/mL
What is the problem with introducing insulin to a DKA
Shifts the electrolyte balance as BS comes down
When treating DKA, once BS drops to around 14 mmol/L what is given?
Dextrose, to prevent them from becoming Hypoglycemic
Maintenance solution containing Potassium will be given to slowly fix their state
Hyperglycemic, Hyperosmolar, nonketotic, Syndrome Occurs in
Clients able to produce enough insulin to prevent DKA, but not enough to prevent sever hyperglycemia, osmotic diuresis, and ECF depletion
DKA does not occur
LESS COMMON than DKA
Often occurs in older adults with DM type 2 (impaired thirst, funcitonal inability to replace fluids)
Higher mortality than DKA
Glucose in blood creates osmosis of water to dilute the intravascular hypertonic hyperglycaemia leading to dehydration
Why is HHS so deadly
Because it takes awhile to develop, often alongside comorbidities.
By the time they have S/S they are very sick
Treatments must be more cautious bc of comorbidies
Can HSS Pt secrete insulin
Usually there is some ability, therefore Non-ketotic
Is DKA slower than HSS
No HSS is slower, more difficult to reverse quickly
HSS S/S
Fewer symptoms than DKA in early stages
Neruo: Often issues
BG >34 mmol/L
Ketone bodies are absent in blood and urine
Less marked and extreme S/S than DKA
Tx for HSS
Similar to DKA but SLOWER
IV Fluids
Insulin bolus +/- insulin infusion
Once 14.0 mmol/L, QID Sliding Scale insulin
Monitor and replace electrolytes (normally smaller deficit than DKA)
Monitor Response to treatment
Caution with fluid replacement in HSS
T2 Pts often have multiple comorbidieis and/or are elderly
Often more is necessary, but occurs slower
Example of macrovascular coplications of DM
Coronary artery disease (atherosclerosis), stroke, hypertension, peripheral vascular disease
Examples of Microvascular Complications of DM
Complications are not reversible
Retinopathy
Nephropathy (Glomuruli, Bowmans capsule)
Neuropathy
- Sensory
- Autonomic
Neuropathy Sensory
Tingling, numbness in extremities, can be MORE sensitive at the begining
Most common form is distal symmetrical
Paresthesias
Hyperesthesia
Complete or partial loss of sensitivity to touch & temperature
Pain described as burning or shooting ,
cramping, crushing, or tearing (unusual)
Neuropathy - Autonomic
Affecting nearly all body systems can lead to hypoglycemia unawareness
GI: GERD, N+V, gastroperesis
CV: Silent MI, ortho HOTN, Increased resting HR
ED
Neruogenic Bladder
Macrovascular complication prevention (behaviour)
Behaviour mods:
- Healthy eating
- Increase Physical Activity
- Quit Smoking
- Weight modification
Macrovascular complications treatment/prevention through Prophlactic and pharm therapy
ACE inhibitors (ie Ramipril)
Anti-platelet therapy (ie ASA)
Anti-cholesterol agents (ie Lipitor
Prevent CV and renal disease. Target BP= 130/80
Retinopathy
Earliest + most treatable changes no changes in vision. Regular dilated eye exams IMPORTANT.
Best treatment is prevention:
Maintain good glycemic control
Control BP
Nephropathy
Damage to small BVs that supply the glomeruli of kidneys
Risk similar for T1 and T2 DM
Best treatment is prevention (Good glycemic control, BP control, annual screening
Leading cause of end stage renal disease in Canada is
Nephropathy
The only treatment for diebetic neuropathy
Control of BG
Effective in many but not all
Pharm management outside of BG
Foot care
Specific NCPs
What causes necrotic toes in DMs
Decreased circulation
Necrosis and poor blood flow often lead to
Infections
Why is foot care really important
Because just a scratch can turn into a wound that can result in amputation
Foot care includes
Basic to advanced
Always wearing protective shoes
Inspect foot daily
Not removing corns or calluess
Identify high risk clients by checking protective sensation + vascular status
Recognizing and treating wounds promptly
Maintainting good nutrition
Cessation of smoking
HTN control
Depride wound
Antibiotic use
Bed rest
Prevent edema
Offload feet
MRi to see bone involvement
How can you know CV status of feet
Colour (white, pale, inflamed are bad signs), temp, cap refill (<3)
Monitering Diabetes
Self management of Blood glucose
All pt should self moniter if on medications
Self Monitering before meals
Keep accurate record of trend information (High and low BG)
All DM pt should have urine dipsticks in home (Checking for glucose and ketones)
Secondary Prevention of DM in population
Screening every 3 yrs for people over 40 OR high risk people
Screen earlier and more frequently in those with more risk factors
Screening for Type 2 includes
- FPG test and /or A1C test
Important FACTORS in DM pt assessments
Neuro - A+Ox3, GCS, Vision changes + PERRLA
RESP: Are they smokers? (Nicotine Replacement Therapy)
CVS: HR/ BP (130/80 is goal) CWMS, Cap Refill, Feet check (periph circ)
GI: Last Bowel Movement (Assessing status of bowel peristalsis)
GU: Fluid intake, urine routines
Overall - ANY evidence of infection
What is BP goal
130/80
Adrenergic Signs of Hypoglycemic
Fight or flight response
Neuroglycopenic signs of hypoglycemia
Decreased O2 to brain
Do we treat DKA or HSS with rapid therapy?
DKA, HSS need more gradual treatment
