Diabetic Challenges Flashcards
Define diabetes
A chronic, multisystem disease of abnormal, impaired or absent insulin production that results in chronic hyperglycemia
Hypoglycemia value
< 4.1
Normal fasting glucose value
4.1-5.9
Hyperglycemia value
> 5.9
Define insulin
Polypeptide hormone mainly secreted by β cells in the islets of Langerhans of the pancreas
Main functions of insulin and glucagon
Coordinates with glucagon to modulate blood glucose levels
Insulin = decrease BG; allows uptake of glucose into cells
Glucagon = increase BG; stimulates hepatic glucose production (gluconeogenesis and glycogenolysis)
How is insulin secreted?
daily in a two-step manner:
o Basal insulin: small amounts throughout day
o Prandial insulin: 10 minutes post eating
6 Roles of Insulin
ANABOLIC - wants to BUILD + create ATP
- Glucose homeostasis
- Glycolysis
- Glycogenesis
- Lipogenesis
- Protein synthesis
- Potassium Uptake
How does insulin work in the brain?
- Increases hunger
- Decreases hepatic glucose production
- Decreases lipoprotein production
How does insulin work in the liver?
- Decreases glucose synthesis
- Increases glycogen synthesis
- Increases lipid accumulation
- Increases inflammation
How does insulin work in the muscle?
- Increase glucose metabolism
- Increase glycogen synthesis
- Increase muscle mass
- Increase mitochondrial dysfunction
How does insulin work in adipose?
- Increase glucose metabolism
- Increase lipogenesis
- Decrease lipolysis
- Increase inflammation
Diagnostic values of pre-diabetes
- HbA1C 6.0-6.4
OR - Impaired Fasting Glucose
OR - Impaired Glucose Tolerance
Pathophysiology of Type 1 DM
Human leukocyte antigens (HLA) are genes in major histocompatibility complexes that help code for proteins that differentiate between self and non-self
o Do not recognize beta cells as self-cells. These cells are mutated in Type 1
Beta Cells are destroyed by immune cells leading to insulin deficiency
When and what manifestations occur in T1DM
when there is no more production of insulin
Onset of classic symptoms
Polydipsia
Polyuria
Polyphagia
* Then, rapid ketoacidosis
Beta cell destruction leading to absolute insulin deficiency
Fasting BG for T2DM diagnosis
> 7
A1C for T2DM diagnosis
> 6.5
75 g Oral Glucose Tolerance Test (GTT) for T2DM diagnosis
> 11.1
Random Plasma Glucose for T2DM diagnosis
> 11.1 + classic manifestations of hyperglycemia
Non-modifiable and modifiable risk factors for T2DM
Non-modifiable risk factors:
* Age (over 65)
* Gender (adult men)
* Ethnicity
Modifiable risk factors:
* smoking
* diet
* obesity
* inactivity
Causes of hypoglycemic crisis
o Too much insulin (compared to food/activity)
o Insulin taken at the wrong time
o Wrong type of insulin
o Missing meals
o Gastroparesis; delayed gastric emptying
o Alcohol: Metabolized in liver; liver cannot participate in gluconeogenesis
o Kidney failure
Peeing out too much glucose
If patient is responsive with BG < 4:
- Give 15g fast acting carbs
- Recheck in 15, if below 4 repeat step 1
- If above 4: give 15g protein and 15g cards
If patient is symptomatic with manifestations of hypoglycemia and you can’t obtain BGM, what do you do?
Treat first, check BG after
If patient is unresponsive with BG < 4:
- ABCs
- IV access: 50ml 50 % dextrose IVP
- No IV access: glucagon IM
6 processes leading to hyperglycemic crisis
- decreased glycogenesis: liver not making glycogen (storing excess glucose)
- Increased glycogenolysis
- increased gluconeogenesis
- increased lipolysis
- increased ketogenesis
- proteolysis
BODY THINKS IT IS STARVING: there IS sugar in the blood but there NO insulin
Inappropriate continuous glucose production into blood that can not be taken up
Onset DKA
Sudden
Cause of DKA
Absolute insulin deficiency
3 Characteristics of DKA
- hyperglycemia
- anion gap metabolic acidosis
- ketosis
What type of diabetes has DKA
Type 1
Precipitating factors of DKA
Illness, infection, inadequate insulin dosage, insulin omission, undiagnosed type 1, poor management
Increased metabolic needs/glucose breakdown
When do manifestations of DKA occur?
when there is no more production of insulin.
Symptoms of DKA are related to:
- Acidosis
- kussmauls resps
- fruity odour to breath
- tachycardia
- palpitations
- n/v - dehydration
- tachycardia
- dry skin
- poor turgor
- dehydration
Also
- classic symptoms
- stuporous
- obtunded
- coma
What is polyuria?
Frequent excessive urination resulting is osmotic diuresis
Why does polyuria occur in DKA?
Excess glucose in urine
What occurs as a result of polyuria in DKA?
Electrolyte excretion, severe water loss + dehydration
What is polydipsia and why does it occur in DKA?
Excessive thirst
Dehydration due to osmotic diuresis
What occurs as a result of dehydration secondary to polyuria in DKA?
- hemodilution
- hypovolemia
- poor tissue perfusion
- hypoxia
What is polyphagia and why does it occur in DKA?
Excessive eating because no glucose is able to enter cells resulting in cell starvation
Define osmotic diuresis
When the concentration of glucose exceeds the maximum re-absorption capacity of the kidney, glucose remains in the filtrate. This causes an increase in osmotic pressure causing water and potassium to move out and into the urine.
Why does metabolic acidosis occur in DKA?
What characterizes metabolic acidosis?
Metabolic starvation and hypoxia lead to ketone bodies and lactic acidosis.
o Unhealthy ways for body to create energy
Increase is systemic hydrogen ion circulation due to metabolic starvation creating ketones/lactate, thus decreasing serum bicarb
Anion Gap v Non Anion Gap Metabolic Acidosis
Anion: increased electrolytes decreasing the bicarb available, thus causing acidosis (potassium)
Non Anion: caused by GI loss of bicarb
3 Steps of DKA Treatment
- Restoring fluid volume
- Preventing hypokalemia due to osmotic diuresis and treatment (though acidosis causes hyper)
- Resolving acidosis with IV insulin
What are you treating in DKA?
NOT hyperglycemia, you continue to treat until ANION GAP and ACIDOSIS is resolved
This is why dextrose is given - must continue to give insulin until anion gap closes regardless of BG
DKA values
BG
pH
Bicarb
Anion Gab
Ketones
Precipitating Factors
BG > 14
pH < 7.35
Bicarb < 15
Anion Gap > 12
+ serum/urine ketones
precipitating factors (illness, infection) present
6 Points of Adult DKA Management
- Stop all insulin sets and NPO
- Fluid resuscitation
- Insulin and Potassium Replacement
- Dextrose administration when BG < 14
- Bicarb for pH < 7
- Maintenance order set
2 Criteria for discontinuing DKA order set
- Anion gap is less than 12
- Patient is able to tolerate oral intake
What does not occur in hyperosmolar hyperglycemic state?
Ketoacidosis
Low or absent ketone levels
BG levels in DKA v HHS
Higher in HHS
Blood sugar levels higher than DKA > 23 mmol/L
Onset of symptoms in DKA v HHS
Sudden in DKA
Gradual in HHS
Severity of symptoms in HHS related to
the level of blood hyperosmolarity and cellular dehydration
Is there insulin present in HHS?
SOME insulin to prevent ketosis but not enough to decrease severe hyperglycemia
Causes of HHS
Client who can produce enough insulin to prevent DKA but not enough to prevent hyperglycemia, osmotic diuresis
7 Characteristics of HHS
o Hyperglycemia
o Dehydration
o Somnolence
o Coma
o seizures,
o hemiparesia
o aphasia
Who does HHS occur in?
Older adults with T2DM
Precipitating factors for HHS
Inadequate fluid intake, infection, stressors
Is there more or less symptoms in HHS v DKA
Fewer symptoms than DKA
What types of mainfestations are more common in HHS and why?
Increased serum osmolality (increased concentration of glucose and electrolytes)
o = more neurological manifestations
Symptoms of HHS
- Fewer symptoms than DKA
- Blood sugar levels higher than DKA > 23 mmol/L
- Increased serum osmolality (increased concentration of glucose and electrolytes)
o = more neurological manifestations - Dehydration, polyuria
- Somnolence (sleepy)
- Coma
- Seizures
- Aphasia
- Tachycardia
- Palpitation
- Warm dry skin
- Poor skin turgor
- Dehydrated
- Nausea/Vomiting
Actions for HHS
- Medical emergency
- High mortality rate
- Treatment similar to DKA
o Restoring fluid volume: half of estimated fluid volume deficit is replaced in first 12 hours then the rest is given over 36 hours
o IV insulin: Humulin R to correct hyperglycemia
o Electrolyte replacement (potassium and sodium)
Fluid Management for DKA
aggressive fluid resuscitation
(correct dehydration and hypovolemia)
potassium replacement is initiated as needed to correct electrolyte imbalances
Fluid Management for HHS
primary concern
more cautious fluid replacement to avoid precipitating cerebral edema
monitoring for signs of fluid overload
Insulin Administration for DKA
complete deficiency
insulin is administered along with fluids
started earlier in the treatment course to halt lipolysis and ketone production
Initial insulin therapy is often given as a bolus followed by continuous infusion.
Insulin administration for HHS
secondary concern (not absolute deficiency)
insulin therapy is usually delayed until fluid replacement has begun, and serum osmolality has been partially corrected
Insulin is then gradually introduced to facilitate glucose uptake by cells, promoting the resolution of hyperglycemia
Define diabetes as a vascular disease
Chronic Consequences of Diabetes: Blood vessel changes lead to complications from poor tissue perfusion and tissue ischemia
Glucose is large bulky molecule that can cause damages (holes, clotting formations, etc.)
Macrovascular complications of diabetes
- Coronary heart disease
- Cerebrovascular disease
- Peripheral vascular disease
How does nephropathy occur as a microvascular complication of diabetes?
chronic hyperglycemia causes HTN in kidney blood vessels, kidney vessels becomes leakier and narrower, leading to decreased perfusion to kidneys, kidney cell hypoxia and cell death
How does neuropathy occur as a microvascular complication of diabetes?
o Damage to nerve fibers (sensory and motor)
o Slow onset, progressive, and permanent
o Foot ulcers: numbness; aren’t aware of injury
How does retinopathy occur as a microvascular complication of diabetes?
o Macular edema and degeneration increased blood vessel permeability, deposits of hard exudate at retina, corneal scarring, changes in lens shapes
Increased morbidity, decreased quality of life
Main cause is chronic hyperglycemia
Describe Canada’s Vascular Protection
- Management of HTN, hyperglycemia, and hyperlipidemia
- Management of modifiable risk factors
o A1C: management of long-term glycemia – lifestyle changes
o BP: management of HTN – lifestyle changes, medications
o Cholesterol: plaque build-up furthers damage to vessels
o Drugs (ACE/ARB, Statin, ASA)
o Exercise
o Smoking Cessation
What is stress-induced hyperglycemia?
common after severe trauma and critical illness.
Neuroendocrine response to stress leads to increased cortisol
imbalance of glucose production and glucose clearance induced by increased circulating levels of stress hormones and cytokines.
increased morbidity and mortality in non diabetic patients
