Diabetes Flashcards
4 types of diabetes
- Type I Diabetes*
- Type II Diabetes*
- Gestational Diabetes
- Maturity-Onset Diabetes of the Young
definition of diabetes
=Chronic, complex disorder with impaired nutrient metabolism (glucose).
-Main feature is impaired glucose regulation (hyperglycemia).
= Chronic hyperglycemia that results from issues with glucose regulation manifested by
◦ Reduced insulin secretion
◦ Reduced insulin function
Diabetes Mellitus
Viral infections can be a trigger for what type of Diabetes?
Type 1
Type of Diabetes that is autoimmune with beta cells destroyed
Type 1
Type 1 diabetes results in _______ insulin secretion
decrease
Type 1 Diabetes Patho
- Cells cannot use glucose
- Onset: Sudden
- Glucose builds up in blood b/c no insulin to carry it in
- Back up mechanism: Break down of fat and protein (Lipolysis & proteolysis) as energy source
- Increased ketogenesis (breakdown of fat) –> ketone bodies
- Increased release of counter-regulatory hormones
- Glucagon —> causes more glucose release
Polyuria and Diabetes- What happens to K levels?
‣ Loss of electrolytes- overall K is low but it looks high
3 things that are happening b/c of polyuria
‣ Loss of glucose in urine
‣ Loss of electrolytes- overall K is low but it looks high
‣ Loss of water
3 things Dehydration in Type I leads to ….
- Hypovolemia
- Hypoxia –> Ischemic tissue –> Lactic acid production (due to anaerobic)—>
- Metabolic acidosis
WTF is ketogenesis
• Conversion of fat to ketone bodies
◦ Acetone, Acetoacetate, B-hydroxybutyrate
• Metabolic acidosis
How does body try to fix metabolic acidosis from Type 1 DM ketogenesis ?
-Metabolic acidosis yields an attempt by the lungs to correct the acidosis
-We need to blow off some CO2 & acid
• Increased rate of breathing
• Increased depth of breathing
• Kussmaul breathing- rest alkalosis
Hallmark sign of acidosis related to hyperglycemia =
kussmaul breathing
• Increased rate and depth of breathing
What is type II DM? What’s up with insulin, beta cells? How?
• Insulin resistance, progresses to decreased beta cell secretion.
• Decreased insulin secretion.
◦ Pancreas responds to decreased insulin sensitivity by developing more insulin
◦ Eventually, the beta cells can no longer produce as much insulin
◦ =Less insulin production
Metabolic syndrome has strong correlation with Type 1 or Type 2 DM?
Type 2
when do we see onset of Type 2 DM?
in 50’s ….becoming more common in youth
If you have gestational diabetes you are more likely to develop….
type 2 DM
Islet Cells: Alpha vs Beta, what is the difference?
◦ Alpha ->Secrete glucagon
◦ Beta->Produce insulin and amylin
Glucagon vs Insulin, whats the difference?
- Glucagon triggers a release of glucose from the liver and skeletal muscle.
- Insulin, secreted with food intake, moves glucose from blood into cells (energy).
Insulin keeps blood glucose and _____ levels in normal range
lipid
Where does insulin get converted into a usable hormone?
in the liver
_____ is the key that helps the glucose get inside the cell
Insulin
In the liver, insulin does 6 things. What are they?
- Suppresses production of glucose
- Promotes production and storage of glycogen
- Inhibits glycogen breakdown into glucose
- Inhibits conversion of fats to acids and proteins to glucose
- Manufactures glucose from glycogen (GLYCOGENOLYSIS)
- Manufactures glucose from amino acids, waste products and fat byproducts (GLUCONEOGENESIS).
This all means: Insulin and liver KEEP BLOOD GLUCOSE LEVELS WHERE THEY NEED TO BE
Gluconeogenesis vs glycogenolysis ….taking ya back to A&P with this question
GLYCOGENOLYSIS= glucose made from glycogen GLUCONEOGENESIS= glucose made from amino acids, waste products and fat byproducts
Insulin does 2 things in the muscle, what are they?
- Stimulates glucose uptake
* Promotes protein and glycogen synthesis
In fat cells insulin does 1 thing, what is it?
• Promotes triglyceride storage
Basal VS Prandial Insulin secretion
Basal = insulin is secreted continuously throughout day (fasting).
Prandial = insulin secreted after eating.
◦ Initial burst within 10 minutes of eating
Normal blood glucose range
60-100mg/dL
Glucose is stored as _____ in the liver and ___ ____ ____ in other tissue
glycogen, free fatty acid (aka triglycerides?)
What does glucagon trigger?
= Counteracts insulin—>Triggers conversion of glycogen to glucose in liver and muscle whenever we need it
name 3 other hormones besides glucagon that help increase glucose
◦ Epinephrine
◦ Norepinephrine
◦ Cortisol
Which drug class prevents counter regulatory methods and makes it hard to tell if they have low CBG ?
Beta blockers
WTF are incretins , what do they do?
Incretin hormones = secrete in response to eating. • Increase insulin secretion • Decrease glucagon secretion • Slow gastric emptying (gastroparesis) • Prevents hyperglycemia after meals
If you have no insulin you have (2)….
◦ No insulin=No cellular energy
◦ No insulin=glucose building up in blood (hyperglycemia)
Without insulin, the body will break down stored _____ and _____ to make energy and use hormones to make glucose.
–> The breaking down of fat creates ketones bodies to form in the blood.
fat and protein
Characteristics of metabolic syndrome
- Presence of metabolic factors that increase risk for developing type II diabetes.
- Waist circumference (>40 in men, >35 in women)
- Fasting blood sugar >100
- Triglyceride levels >150, HDL <40.
- Hypertension
3 p’s of diabetes
• Polyuria- Excessive urination rapid onset
◦ Osmotic diuresis from excessive glucose in urine
• Polydipsia- Excessive thirst rapid onset
◦ Secondary to polyuria and dehydration
• Polyphagia- Excessive hunger rapid onset
◦ “cell starvation” due to insulin not moving glucose into cells
complications of type 2 DM
• Dehydration • Electrolyte imbalances • Vascular changes-> Organ Dysfunction ◦ Microvascular or Macrovascular • Neuropathies • Decreased immune response • Poor wound healing • Acid-Base imbalances • Early Mortality
Lets talk more about K levels- loss of K in urine leads to hypokalemia. During acidosis something else happens though….
Hyperkalemia!
◦ During acidosis, potassium moves out of cells into the blood (hyperkalemia) and switches place H+ ion
◦ When we correct the acidosis, potassium moves back into the cell (normal or hypokalemia)
◦ When we correct the acidosis, potassium moves back into the cell = normal or hypokalemia
◦ If fix acidosis too quickly then we can send K too low to quickly
We need to fix acidosis slowly to prevent causing ____
hypokalemia
you can also have what other electrolyte change with Diabetes?
hypo or hypernatremia
Vascular changes in diabetes occur secondary to
hyperglycemia
–causing thickening to basement membranes, glucose toxicity, chronic ischemia of small vessels, and tissue hypoxia.
Macrovascular changes associate with Diabetes
Cardiovascular disease, Cerebrovascular disease, peripheral vascular disease
Microvasular changed associated with Diabetes?
Nephropathy, neuropathy, retinopathy
How does hyperglycemia cause kidney disease? Whats the patho?
◦ Hyperglycemia > increased pressure in kidney > increased perfusion causes vessels to leak > decreasing kidney oxygenation> ischemia> CKD.
How does hyperglycemia cause peripheral neuropathy?
• Vessel changes secondary to hyperglycemia leading to decreased tissue perfusion and poor nerve impulses. Excess glucose collects in nerves and impairs motor nerve conduction.
Is peripheral neuropathy from diabetes reversible?
nope! it is irreversible damage
Peripheral Neuropathy from diabetes can lead to system wide problems like….
‣ Foot Injury (Late complication) ‣ Skin ‣ Gastrointestinal ‣ Neurogenic bladder ‣ Erectile dysfunction
How does the damage from peripheral neuropathy first present? and later?
• Damage starts as pain and progresses to sensation loss.
Can diabetes cause autonomic neuropathy?
Yes!
Examples of disease development of autonomic neuropathy from diabetes?
- Dysfunction of the nerves that regulate the involuntary body functions.
- Sympathetic and Parasympathetic nerves
- Urinary retention, orthostatic hypotension, syncope, gastroparesis, tachycardia, exercise intolerance, sexual dysfunction,…
Where do we see motor neuropathy due to diabetes? how does it manifest?
- Dysfunction of body’s motor nerves.
- Typically occurs in longer nerves (i.e spine to feet).
- Weakness, droop, cramping, twitching, atrophy,…
Charcot foot-what causes it , what does it affect, what does it look like?
- a complication of peripheral neuropathy in diabetics.
- affect the bones, joints, and soft tissues of the foot or ankle.
- Combination of bone disintegration and trauma can alter and deform the shape of foot/ankle.
Prolonged wound heal on feet put diabetics at risk for
INFECTION
3 ways to help save kidneys from damage due to DM
◦ Optimal glucose control
◦ Kidney protective medications
◦ Blood pressure control
Once albuminuria is present focus on preventing progression by…
‣ BP control
‣ Glucose control
‣ Avoid nephrotoxic agents
if you have type 1 DM do albuminuria test when?
after 5 years since diagnosis
retinopathy prevention for diabetics
◦ Control of blood pressure
◦ Control of hyperglycemia
◦ Control of lipids
◦ Annual eye exams
asymptomatic until vision loss occurs
Hypogylcemia = CBG < ____
70
Coma can occur when CBG < ____
50
DKA- type 1 or Type 2?
Type 1
CBG for DKA will be >
◦ CBG >250(>300 for Messer lecture)
quick patho of DKA
• Uncontrolled hyperglycemia, insulin deficiency > Body breaks down fat for energy> Ketones increase in blood > pH decreases (acidosis).
s/s of DKA
- Classic 3 P’s
- Rotten, fruity breath (ketones)
- Nausea/vomiting
- Abdominal pain
- Dehydration
- Weakness
- Shock
- AMS, up to coma.
Assessment for DKA
• Respiratory status
◦ Rate, pattern, depth, accessory muscle, breath smell…
• LOC
• Hydration
• Skin turgor, Skin temperature, mucous membranes, urine output and color, JVD…
• Labs
◦ Blood glucose, sodium, bicarb, potassium, anion gap, osmolality, ABG,….
• Vital signs
◦ Pulse, hypotension…
• ROM/Strength
◦ Weakness
DKA interventions
- IVF : NS for CBG >250, then D5 1/2NS (may include KCl-) once CBG <250.
- IV drip Regular Insulin
- Sodium bicarb drip, if severe acidosis pH<7.0 and bicarb <5.
- Oral intake of fluids
Hyperosmolar Hyperglycemic State (HHS), type 1 or type 2?
type 2
Hyperosmolar Hyperglycemic State (HHS)- does this have ketones?
NO. DKA is your ketone dude
onset for HHS vs dka?
HHS= gradual DKA = sudden
higher morbidity- HHS or DKA?
HHS
What happens to cause HHS?
• Increase in blood osmolarity due to insulin deficiency and hyperglycemia.
do you have acidosis with HHS?
NOPE
S/S of HHS
- Classic 3 P’s
- Profound Dehydration
- Weight loss
- Dry skin
- Lethargy, can progress to coma
Contributing factors to HHS
MI, Sepsis, pancreatitis, stroke, medications (diuretics, corticosteroids, Ca channel blockers, beta blockers…)
Assessment for HHS
• LOC
• Hydration
• Skin turgor, Skin temperature, mucous membranes, urine output and color, JVD…
• Labs
◦ Blood glucose, osmolality, sodium, BUN, Creatinine, ABG (pH will be >7.3), serum bicarb, WBC…
• Vital signs
◦ Pulse, hypotension, fever, respiratory rate…
HHS interventions?
- IVF of 1/2 NS or NS = SLOW process to avoid too rapid changes in osmolarity.
- Requires close monitoring of serum osmolality
- Once CBG is <250-300, NS may be changed out for a dextrose containing fluid.
- May require potassium replacement for hypokalemia
- IV drip regular insulin
A1C > ____ = diagnostic
6.5
A1C > ____ = indicative of poor DM control
8%
A1C ______ = increased risk of developing DM
5.7-6.4%
fasting vs non fasting CBG for diagnosing DM?
- fasting BS >126 (normal is 80-110 or <100) on >2 occasions
* non-fasting BS >200
Glucose tolerance > ____ = diagnosis of DM
> 200
normal is <140
check urine for what 2 things to diagnose DM?
ketones and albumin
Urine albumin ____ -_____ mg/ 24 hours = Early stage diabetic nephropathy
30-299
A1C looks back how many days?
120
Treatment goals for diabetes in non hospitalized patient: A1C, premeal CBG and Postmeal CBG
• A1C <7.0
• Premeal CBG 70-130
• Post meal CBG <180
◦ THESE GOALS MAY BE MORE OR LESS STRINGENT DEPENDENT ON PATIENT
CBG goals for hospitalized patient
- < 140 mg/dL before meals/ < 180 mg/dL random
- 140-180 mg/dL for critically ill patients
(higher CBG goal for ill peeps)
non surgical interventions for diabetes
• CBG monitoring • Nutrition • Exercise • Pharmacotherapies • Blood glucose monitoring and responding appropriately • Recognizing signs and symptoms of problems/ complications • Medication ---> Reduce complications from diabetes
surgical interventions for diabetes
Pancreas transplant
• Considered “successful” when patient no longer requires insulin and CBG’s are in normal range.
• Complications of transplant rejection and fluid and electrolyte imbalances.
Basal insulins and Prandial insulins
Basal = Constant amount of insulin
• Intermediate to long acting insulin
• NPH, Lantus, Detemir…
Prandial= Meal-time insulin
• Immediate acting insulin
things that affect insulin absorption
- Site: Abdomen is fastest; subq is slower than IM
- Physical activity- massage, heat, etc increase absorption
- Timing
- Type
- Dose
wtf is the dawn phenomenon? + treatment?
= Nighttime release of adrenal hormones cause BS to increase around 5-6am.
–>Treatment is to increase insulin at night
WTF is Somogyi Phenomenon? + treatment
=Hyperglycemia from counter regulation response to nighttime hypoglycemia.
–>Treatment is bedtime snack to prevent hypoglycemia during sleep.
• If a patient is NPO, CBG’s are required and _____ insulin will be given. Meal dose insulin will be …..
Give basal insulin, withhold meal dose b/c NPO
What is our concern with giving IV d50?
**hypertonic, caution for extravasation
is patient has no IV access but we need to give something to treat hypoglycemia rapidbly what we gonna do?
◦ Glucagon IM or Subq, if no IV access.
If patient has an acute change in mental status…
check CBG!
s/s of hypoglycemia
- Sweating
- Irritability, Anxiety –> Nonresponsive
- Tremor
- Tachycardia, Palpitations
- Hunger
- Seizure
- Paralysis
- AMS
- Slurred Speech
- Coma
- Clumsiness
• Note that patients with Type II DM with chronic hypoglycemia and Type I DM for >30 years may have hypoglycemia unawareness.
causes of hypoglycemia?
- Too much insulin/ Inadequate food intake
- Wrong type of insulin
- Insulin and meal mismatch
- Alcohol intake
- Exercise
- Kidney failure –> decreased insulin clearance
Treatment for hypoglycemia
• CHO treatment • 15-20 g glucose (< 70) • 30 g glucose (< 50) • Liquid preferred (Juice, soda) • Unable to swallow ◦ SQ/ IM glucagon ◦ IV D 50 (50% dextrose) • Repeat blood glucose measurement in 15 minutes, 60 minutes
Hyperglycemia s/s
Impaired concentration --> Nonresponsive • Fatigue • Warm, Dry (Hot and dry… sugar high) • Hunger, Nausea, vomiting • Headache • Blurred vision • Rapid, deep breathing
What to do when your patient is NPO ? Hold Insulin?
- Typically don’t hold long-acting insulin
* Typically hold fast acting insulins
home glucose meter considerations
- Can use finger or alternate site
- Warn patients with hypoglycemic unawareness
- User error is more likely than machine error
- Infection control
Continuous Glucose Monitor considerations
- Intended to supplement capillary readings
- Sensor, Transmitter & Receiver
- Provides glucose readings every 1-5 minutes
- Requires capillary glucose readings for calibration (accuracy)
- Lag time between capillary glucose and sensor readings (interstitial fluid)
- Use capillary readings to verify extreme values
continuous SQ infusion - what kind of insulin?
◦ Basal insulin
◦ Increases at mealtime
◦ Very effective
fiber recommendation for diabeted
25 G/ day
what does alcohol do to CBG?
causing a delayed decrease in BG. - limit # of drinks or drink w/ meal
exercise and type 1 DM caution
don’t exercise if CBG less than 100 or if urine is positive for ketones
exercise frequency and type recommendation for DM
- 150 minutes/ week of moderate- intensive exercise OR
- 75 minutes of vigorous exercise
- At least 3 days/ week
- Resistance Exercise at least 2 days/ week
exercise consideratinos for diabetes (Safety)
- Avoid extreme temperatures
- Hydration
- Wear suitable footwear/ examine feet after exercise
- Avoid exercise during peak insulin action
- Eat a CHO snack before
- Bring candy
- Check blood glucose throughout day
-Diabetics with proliferative or severe retinopathy should avoid
- High intensity CV exercise
- Resistance weight training
- Valsava maneuver
diabetics who exercise are at risk for
- Retinal detachment
- Vitreous bleeding
- Skin Breakdown/ injury
skin care for diabetics
• Check feet daily for wounds • Do not walk around barefoot • Wear appropriate fitting shoes • Caution with heat or cold • Avoid personal foot care at home, seek professional assistance (podiatrist) • Avoid injury from heat sources • Inspect feet • Report injuries • Assess protective sensation ◦ Semmes-Weinstein monofilaments
interventions for visual impairment w/ diabetes
- Coding objects with bright colors (insulin vial)
- Adjust lighting
- Large print
- No pre-filled insulin pens
- Insulin syringe devices designed for those with visual loss
- Appropriate selection of glucose monitor
Hospital interventions for vision loss diabetes patients
◦ Assess and report vision loss
◦ Use vision support when patient is awake
◦ Keep things off the floor
◦ Keep objects within reach
