Diabetes Flashcards
S and S of Hypoglycemia
BG more then 4.0 mmol/L • Confusion – change in LOC • Sweating • Rapid pulse • Tremors
S and S of Hyperglycemia
• BG > 7.0 mmol/L (11 is VIHA) • Polyuria – excessive urination • Polyphagia – increased hunger • Polydipsia – increased thirst • Glucosuria – high levels of glucose in the urine • Weight loss • Fatigue 
Review…
Effects of Insulin
Normal response to High BG
Simulates glucose uptake into cells and storage of glucose as glycogen in the liver and muscles.
Also stimulates protein synthesis and free fatty acid storage in adipose tissue.
Inhibits gluconeogenesis and lypolysis
Review
Effects of Glucagon
Normal response to low BG. Stimulating Gluconeogenesis and breakdown of glycogen
Diabetes is…
And is a major risk factor for….
Characterized by disturbances in carbohydrate, protein and fat metabolism
Ineffective insulin production, poor insulin sensitivity.
A major risk factor for MI, stroke, renal failure, retinopathy, peripheral and autonomic neuropathy and peripheral vascular disease
Cause of type 1 vs type 2
Type I: autoimmune disease strongly associated with leukocyte antigens DR3 and DR4. May be associated with certain viral infections. Beta-cells destroyed
Type 2: may result from impaired insulin secretion, peripheral insulin resistance, increased basal hepatic glucose production obesity, hormonal contraceptives, pregnancy, insulin antagonists i.e. phenytoin over the counter regulatory hormones
Why is glucagon not inhibited when those with DKA or HHS.
Inhibition of glucagon requires insulin. Signal for more glucose (glucagon stim) is coming from cells, who are glucose starved. Insulin is required to get glucose into cell and stop the signalling.
How do DKA and HHS differ in the aspect of insulin levels?
DKA – no insulin therefore gluconeogenesis and lipolysis
Production ketone bodies (acetone breath) and ketoacidosis (can be severe)
HHS – insulin still present therefore gluconeogenesis and lipolysis mainly inhibited. Ketones mild/absent and pH normal/mild
Major problems of HHS and DKA
DKA- Hyperglycemia, Acidosis, Osmotic diuresis (dehydration)
HHS- Hyperglycemia, Osmotic Diuresis (Worse then DKA)
What sort of events might cause DKA or HHS and why
Reduced insulin admin (DKA) OR Stress events: Infection MI Diarrhea and vomiting Stroke Trauma Pancreatitis Unknown etiology
Acute Stress -> hormone releas glucagon, corticosteroids, catecholamines)
All attempt to increase glucose further to deal with the stress (fight or flight)
All worsen an already high blood glucose level
ANY trauma will bring stress response
S and S of DKA
Can develop quickly ( 13.9 mmol/L
Acetone breath, ketones in urine, acidosis, confusion/coma all from ketone production
Kussmaul breathing (deep rapid breathing) and abdominal pain from metabolic acidosis
Polyuria from high glucose (osmotic diuresis) glc in urine
Polydipsia and tachycardia from dehydration
Sodium may be increased/ decreased or normal
Hypotension from dehydration
AND… Blurred vision, Weakness, Headache, Orthostatic hypotension, frank hypotension (volume depletion), anorexia, nausea, vomiting, and pain (r/t acidosis), , mental status changes. Hyperkalemia (before Tx)
Main S and S of HHS
Develops more slowly than DKA (days to weeks)
Blood glucose > 33.3 mmol/L
No ketone breath and ketone in urine
Stupor/coma from hyperosmolar state
Profound Dehydration -> high sodium,
polyuria from high glucose (osmotic diuresis) glc in urine
Hypotension- Polydipsia and tachycardia from dehydration
Higher mortality then DKA 10-40%
COMPARE those at risk of DKA and HHS
DKA - Type 1 (Can be Type 2)
HHS- Occurs predominantly in type II diabetics (some cases of type 1)
Older people with no history of diabetes or mild T2DM
Key Requirements of Patient with DKA
Insulin
Hydration
Electrolytes replacement
Diagnostics common in DKA patient
Elevated bld Glucose – severity of DKA is not necessarily related to blood glucose
Low Bicarb levels
Accumulation of ketones (bld and urine)
Electrolyte levels (K+, Na+)
Elevated Creatinine, BUN (ARF)
(post rehydration continued elevation present in the pt with renal insufficiency
Diagnostic for a HHS patient
++ high Blood glucose, lytes (Na+), BUN (hypovolemia), Complete bld count (stress), serum osmolality (BG and Dehydration), ABGs (normal)
What age group is at risk if they develop DKA?
Why is it common?
Complications?
Pediatrics.
Newly Diagnosed Type 1. Omission of insulin: when child or caregiver fails to comply Delivery failure Infection Type 2 Diabetes can present as DKA
1/2 die from cerebral edema during rehydration
Common interventions
Complications
ABCS- LOC (NG or Airway)
Reverse Hyperglycemia
Reverse Dehydration- losses
Restore Electrolytes balance- K and Na
Prevent complications: Cerebral edema, ARF, Pottasium, pH, Thromboembolic events, ARDS.
What concerns might we check with Diagnostics?
CBC and lytes- The obvious and Infec. Amylase/lipase- Pancreas r/t insulin Troponin and RFT's- Urinalysis- Infect, Ketones?, ECG- MI and arrythmias Chest xray- ?Pneumonia ABG's - Acidosis?
Why does K need to be watched carefully with treatment of DKA and HHS
Rehydration leads to:
Increased plasma volume = decreased conc of se K+
Increased urinary excretion of K+
Insulin Administration: enhances K+ movement back into the cell.
… Avoid Tx causing low K
What part of Tx reverses Acidosis in DKA
Insulin Admin- Deals with underlying problem of ketone production.
What teaching might be helpful for diabetic experiencing sickness.
Inc BG testing
Don’t stop meds
Drink lots of Fluids
If you can;t eat, drink fluids containing glucose
See physician if regularly vomiting or Diarrhea
Two key hormones released during stress response
Catecholamines – including adrenaline and noradrenaline
Glucocorticoid hormones –
including cortisol
What kind of insulin will be administered with DKA or HHS
IV Insulin “regular” Short acting Humalin-R
In HHS Tx, BG is not going down despite fluids and insulin? Potential problem?
Even with insulin, blood glucose levels in HHS patients may not decline initially; this usually suggests renal impairment or inadequate fluid resuscitation rather than insulin resistance
Renal threshold for glucose?
Blood glucose levels that exceed the renal threshold (10–12mmol/litre) can precipitate an osmotic diuresis, leading to life-threatening dehydration.
Warning signs of cerebral Edema?
What to Monitor
Headache. Return of vomiting. Behavioural changes. Reduced level of consciousness. Elevation in blood pressure and fall in pulse rate. Decreased oxygen saturation.
Consider Monitoring
Heart rate, respiratory rate, blood pressure. Neurological observations (at least hourly). Strict fluid input and output.
Capillary blood glucose.
Urinary ketones.
Blood ketones on fingerstick. Electrocardiogram.
What is Metformin
- Antidiabetic
- Management of type 2 diabetes mellitus; may be used with diet, insulin, or sulfonylurea oral hypoglycemics.
- Decreases hepatic glucose production. Decreases intestinal glucose absorption. Increases sensitivity to insulin.
- Side Effects: Largely GI: Abdominal bloating, diarrhea, nausea, vomiting.
- Watch for renal impairment (might need to be discontinued)
