Diabetes Flashcards
What are the counterregulatory hormones?
Catecholamines (epinephrine), Growth hormone, glucocorticoids, and glucagon. Insulin is the only hormone that has an increasing-effect on glucose.
Which of the following hormones is responsible for blood sugar regulation directly after a meal? o Insulin o Glucagon o Cortisol o Epinephrine
Insulin.
Insulin is responsible for uptake of blood glucose into cells; promotes fat deposition + glycogen synthesis for storage of blood sugar.
Glucagon is responsible for maintaining blood sugar between meals, when there is no additional intake. It promotes the breakdown of glycogen to prevent hypoglycemia.
Cortisol and Epinephrine lead to breakdown of glycogen to increase blood sugar levels during times of stress
What is one of the primary roles of glucagon? It promotes:
Gluconeogenesis (creation of blood sugar), and serves to maintain adequate levels of glucose BETWEEN MEALS. Note that although Insulin and Glucagon act in opposite ways, glucagon does not in and of itself promote the release of insulin.
How does insulin participate in cellular metabolism? Select all that apply.
a) Increases amino acid conversion to glucose
b) Promotes glycogen conversion to glucose
c) Transports glucose into skeletal muscle
d) Promotes triglyceride synthesis in the liver
e) Increases use of fatty acids as fuel
c) Transports glucose into skeletal muscle
d) Promotes triglyceride synthesis in the liver
e) Increases use of fatty acids as fuel
Why do diabetics often get skin infections?
Skin infections in diabetics are due to the high level of blood sugar on skin that’s excreted in sweat. Sugar attracts bacteria on skin!
What are the clinical manifestations of Type II DM?
Type II DM is often asymptomatic which is dangerous bc PTs can have a lot of damage already by the time they have symptoms and seek help.
Manifestations can be vague:
• Fatigue
• Visual (blurry) changes (diabetic retinopathy blindness (LEADING CAUSE OF BLINDNESS IN US)
• Nephropathy (kidneys lack adequate blood flow kidney failure)
• Coronary artery disease
• Peripheral vascular disease
• Recurrent infections
• Increase blood sugar: food for bacteria
• Neuropathy: damage nerves
• Loss of sense of touch, feeling (usually in feet). Dangerous bc person sometimes doesn’t know they have a wound.
• Necrosis, loss of limbs
What is the diagnostic criteria for Type II DM?
– History and physical
– Blood glucose level
– Distinguish type 1 from type 2
• Insulin levels (to distinguish which type of diabetes)
• DM2: insulin high
• DM1: insulin low, nonexistent
– Test for presence of long-term complications
• Eye exam, heart function, kidney function, access extremities
What is the diagnostic criteria for Type I DM?
-History and physical
-Random blood sugar test: DM >200
Hmga1c: diagnostic standard**
Fasting glucose: not eating night before, at least 8 hrs
Oral Glucose Tolerance Test: give glucose, check blood sugar level in 2 hrs
Hypoglycemia is defined as_____.
blood sugar
Common causes of hypoglycemia are:
In Diabetics, common causes of hypoglycemia are:
• Overproduction/over-administration of insulin
• DM2: Inadequate food intake with antihyperglycemic oral medication
• Excess exercise without adequate food intake
• Severe infection or illness (bc this puts person in a hypermetabolic state: requires more blood sugar)
• Several antihyperglycemic meds for type 2 diabetes
What are the acute complications of diabetes mellitus?
– Hypoglycemia
– Diabetic ketoacidosis (DKA) (Type I DM)
– Hyperglycemia hyperosmolar nonketotic syndrome (HHS) (Type II DM)
– The Somogyi Effect and Dawn Phenomenon (Waking up in morning with elevated blood sugar levels even after not eating throughout the night)
What is the clinical presentation of a patient with hypoglycemia?
Pallor; tremor; tachycardia; palpitations; diaphoresis; CNS manifestations like headache, confusion; poor judgment
More severe complications are:
• Seizures, Coma, and even Death: cells starve + die
Tell me about Hyperosmolar Hyperglycemic Non-ketotic State (HHS)
Acute complication in Type II DM. Insulin is available but cells insensitive to insulin.
- Manifestations:
- Very elevated blood sugar (> 600)
- Blood sugar excreted through urine, also pulling water
- Low volume secondary to severe dehydration d/t polyuria
- With high urine output, the person’s blood osmolarity will go up and we see effects similar to effects from low blood volume: Affects on CNS, alertness, orientation (d/t hypovolemia)
- NO ketoacidosis**!!
Treatments:
• Fluid resuscitation (maintain blood volume is most important)*
• Insulin (if insulin is suspected as the problem)
Tell me about Diabetic Ketoacidosis (DKA)
Occurs in PTs with Type I DM and results in hyperketonemia.
- Blood sugar >250 (not as high as HHS)
- Body does not produce insulin leading to break down fatty acids, producing ketones
- Ketogenesis is stimulated
- Acidotic state ensues
- Manifestations: Respiratory compensation of the acidosis
- Fruity breath
- Kussmaul respiration (efforts to blow off CO2)
- N&V, abdominal pain
- Tachycardia and hypotension (low BP, HR faster to maintain CO)
- Altered level of consciousness
What is the treatment for a PT with DKA?
Treatment:
• Administer insulin
• Remember to be cautious of inducing hypokalemia bc of administering too much insulin too quickly
• Too much insulin w/ low K (give K before insulin)
• Insulin pushes K into cell hypokalemia
• Administer Bicarb
• Maybe administer some fluids, but not as much as with HHS
What is the “somogyi effect”
Bedtime glucose normal but wake up in AM w/ elevated blood sugar
HYPOglycemia occurs during the night*, leading to a rebound HYPERglycemia as a result of insulin induced hypoglycemia
Triggers catecholamine, glucagon (type II only), cortisol and growth hormone release
Leads to hyperglycemia in the morning
Often leads to over-administration of evening insulin
Treatment: DECREASE bedtime insulin
What is the “dawn phenomenon”
Bedtime glucose lower than waking glucose in a.m.
Hormones released in early a.m. (same as somogyi hormones) leads to higher a.m. blood glucose.
Blood glucose STEADILY rises throughout the night* NOT triggered by hypoglycemia
Treatment: Limit evening snacks, and/or increase p.m. oral glycemics or insulin (to diagnose check blood sugar @ 2AM)
What are the chronic complications of DM? (remember that these are typically seen more in PTs with Type 2)
Macrovascular (damage to large arteries): atherosclerosis, eventual blockage, leading to potential MI, stroke, poor blood flow to lower extremities
• Coronary Artery Disease
• Carotid - Stroke
• PVD
Microvascular (Microangiopathy) (damage to small arteries): eyes, kidneys
• Diabetic Retinopathy (eventual blindness)
• Diabetic Nephropathy (eventual kidney failure)
– Diabetic Neuropathies: parasthesias (numbness and tingling and an eventual loss of sensation)
– Slow Wound Healing (diabetic ulcers, often on bottom of feet)
– Increased infection risk and reduced immune response (thrush, yeast infections, UTIs, oral infections)
- Pregnancy: damage vasculature to placenta
You are caring for a PT w/ type 2 DM. You explain to the patient that:
Fat and muscles cells are less sensitive to insulin (individuals still produce insulin but their cell receptors are just not sensitive to it)
Which of the following lab tests taken from a pt w/ type I DM would make you concerned that kidney damage has occurred?
Positive urine microalbumin – damage to kidneys causes protein to be excreted/leaked into urine
You are a home health nurse caring for a pt who is consistently waking up in the morning with a blood sugar of 250. Which of the following would help you to discern the cause of this high blood sugar?
Take a blood glucose at 2AM
Why does polyuria develop w/ DM?
It is due to the osmotic effect of glucose (when an individual has elevated blood glucose, the kidney will excrete glucose through the urine. The glucose particles create an OSMOTIC EFFECT, pulling water with it (similar to sodium) leading to polyuria.
Which of the following are signs of diabetic ketoacidosis in an unconscious person?
Deep rapid respirations, fruity breath odor
