Diabetes Flashcards
What populations are at an increased risk for diabetes?
African Americans, Hispanics, and Native Americans
What is occurring in Type 1 diabetes?
Auto-immune destruction of Beta-cells in the pancreas. Mainly due to islet cell antibodies
What is hyperglycemia?
Increase in blood sugar with glucosuria – leading to a loss of glucose as an energy source
In diabetics, when fat and protein in being broken down, what is this known as?
Ketoacidosis
What are both hyperglycemia & ketoacidosis apart of?
Catabolic disorder
What are some causes of the auto-immune response in Type 1 diabetes?
viruses (mumps, coxsackie B-4, rubella) & toxic chemicals
What is occurring in Type 2 diabetes?
It’s is a combo of insulin resistance & defect of Beta cells not secreting enough insulin in response to glucose. Thus a decrease in insulin production over time.
Does Type 2 diabetes have the same catabolic disorders as type 1?
No, circulating insulin prevents ketosis. But type 2 is aggravated by increased hyperglycemia
What would cause type 2 diabetes?
Genetic pre-disposition & sedentary life style is common
Central/visceral obesity = major factor in insulin resistance
What defect occurs in Beta cells with Type 2 diabetes, what causes it?
Compensate via hyperplasia
Caused by insensitivity to circulating endogenous insulin. Early on there is increased insulin production to compensate and control Blood sugar – but eventually hyperplasia occurs & glucose tolerance develops (even with hyperinsulism)
If the compensation via hyperplasia occurs for a long period of time, what happens to the beta cells?
Eventually get destroyed → diabetes develops and insulin levels decline
What would cause insulin resistance?
Obesity (central fat distribution), storage of fat in muscle with inactivity
Hepatic insensitivity leads to increased gluconeogenesis when insulin is present (when normally insulin turns off gluconeogenesis)
In a type 2 diabetic we have lots of hyperglycemia going on, what can occur with chronic hyperglycemia? Why is it so important to control hyperglycemia?
Glucotoxicity = Can worsen insulin resistance and destroy Beta cells faster/more permanently
We must control hyperglycemia to preserve any remaining Beta cell function
So what lifestyle changes can a patient make to lower their insulin resistance?
Exercise (increases blood flow to muscles, increases muscle mass, and decreases muscle fat storage)
Diet/weight loss (decreases at storage deposits)
Together they can decrease hyperinsulinism & hyperglycemia; Can even reverse impaired glucose tolerance if started early
What is metabolic syndrome? What does metabolic syndrome lead to? What are some qualifying factors for it?
Insulin resistance syndrome
Can lead to an increased risk of atherosclerosis
Central obesity (>88cm or 35” in women, >102cm or 40” in men); hyperglycemia >110; Hypertension 135/85; Triglycerides >150; Low HDL
What are clinical findings for Type 1 DM?
Polyuria, thirst, weight loss, dehydration, polyphagia, ketoacidosis, hyperosmolality
What are some clinical findings for Type 2 diabetes?
No symptoms early on. Polyuria, thirst, skin infections, vulvovaginitis, abnormal fat distribution, hyperglycemia
What lab reflects long term control of DM?
Hemoglobin A1c; reflects state of glycemia over prior 8-12 weeks
What is a normal A1c?
4-6%
What A1c level confirms diabetes?
Greater than 6.5%
What A1c levels indicate prediabetes?
5.7-6.4%
For a diabetic, what is our goal for the A1C?
How often do we measure A1c’s in a diabetic?
every 3-4 months
Besides A1c, what other lab findings indicate diabetes?
Fasting blood glucose >125
2 hour glucose tolerance test >200
Random blood sugar >200 (confirm with fasting)
What lab findings demonstrate impaired glucose tolerance?
Fasting blood glucose 100-125
2 hour GTT of 140-199
What form of testing is considered a standard of care for all diabetics?
Self-monitored blood sugar
Is type 1 or type 2 diabetes associated with lipoprotein abnormalities?
Type 2 = High triglycerides (3-400) and low HDL (
What are our treatment goals for DM?
Diet, exercise, and medications
What is a diabetic diet?
Get a dietician involved, weight reduction if needed.
Total calories 25-35/kg/day
Total cholesterol
How would we tightly control Type 1 Dm?
Insulin
How would we tightly control type 2 DM
oral agents/insulin; control BP (
What is our goal with tightly controlling DM?
Get HbA1c to
What are the blood sugar goals with therapy?
Pre-prandial = 90-130
Bedtime = 100-140
Peak post-prandial =
How would we calculate plasma blood sugar from blood sugar on a test strip?
Add 10mg
What are the ABC’s of diabetes?
Aspirin, blood pressure, cholesterol, and diabetes management
What must we always remember about diabetics and their platelets? What are they at risk for?
Abnormal platelet function → increased risk of small vessel thrombosis or atherosclerosis
When should we prescribe aspirin for our diabetic patient?
If they have a >10% risk for a cardiac event over 10 years
Any diabetic patient with macrovascular
What is the dose of aspirin & risks associated with aspirin?
75-162mg/day
Risks = PUD, gastritis and bleeding ulcers
If a diabetic patient has AV nicking or arteriolar narrowing what does that indicate?
Uncontrolled BP along with their diabetes
What 2 diagnosis would we see high trigs & low HDL?
Diabetes & Hypothyroidism
How many medications does the average diabetic need?
3 (to help control HTN)
What does the diabetic work-up look like?
Family Hx, Complete H&P, CV risk factors, lipids, BUN, Cr, Electrolytes, UA +MicAl, ECG, Ophthalmology, Podiatry
What must we evaluate every 3-6 months in a patient with diabetes?
Weight, BP, A1c, foot exam, home monitoring, Psychosocial function, intercurrent illness
What must we evaluate every year in a patient in a patient with diabetes?
Lipids, UA, creatinine, microalbinuria, complete PE, Ophthalmologist, dental exam
How many sites on the feet must we exam?
6 on each
What if a patient cannot feel the microfilament in an area?
now at a higher risk for future ulceration
What is the most important part of a diabetics treatment?
EDUCATION! They need to understand – especially all of their risks
What does exercise help with in diabetics?
Increases the effectiveness of insulin, stabilize insulin, improve utilization of fat
What is at the cornerstone of T2DM treatment?
Weight reduction, diet & exercise, decrease adipose stores, regain insulin sensitivity
we start a patient on metformin, if their BG remains elevated, where do we start?
Sulfonylurea or insulin
If that doesn’t do well - Pioglitazone, Exanatide
What is the most effective combination with metformin?
Metfromin + insulin is more effective that 3 oral agents
If a patient is overweight, what combo drugs would be best?
Metformin, Exantide, (possibly Alpha), or SGL2’s
In a T2DM, what insulin regimen can we use?
Metformin + NPH/Regular 70:30 ratio – usually before breakfast and before dinner
What does the T1DM insulin look like?
Take the total insulin needed and divide that between basal (Glargine) & prandial needs (Lispro)
What must we remind our patients of when they are ill?
IF they are sick they must increase their insulin levels
What’s the most common complication of insulin use?
Hypoglycemia
What are the sxs we need to educate our patients about for hypoglycemia?
Sweating, tachycardia, hunger, tremulousness, nausea
What drug may mask hypoglycemia?
Beta Blockers
What BS level correlates with Hypoglycemia?
How would we treat hypoglycemia?
Simple sugars (candy, sugar, OJ); 1mg injection of glucagon; IV glucose
How much glucose raises BS by 25-50mg? How many carbs are in a soda?
15g of glucose
30g of carbs
What are the long term complications we must always be aware of with diabetics?
Retinopathy, nephropathy, neuropathy - Microvascular
Atherosclerosis – Macrovascular
What are the 2 categories of retinopathy? Which is worse?
Non-proliferative or Proliferative (worse)
What is occurring in proliferative retinopathy?
Formation of new blood vessels –> blindness
What would we see on PE with non-proliferative retinopathy?
Microaneursysms, hemorrhages, exudates, retinal edema
How do we prevent retinopathy?
TIGHT GLYCEMIA CONTROL - A1c, tight hypertension control, and annual eye exams
What would make retinopathy worse?
Smoking & hypertension
What complication can develop with chronic hyperglycemia and uncontrolled hypertension?
Nephropathy
What is the leading cause of end-stage renal disease?
Nephropathy
How do we prevent nephropathy?
Tight A1c control, tight BP control, and smoking cessation
If we get a microalbuminuria in a diabetic patient and see 200mg in the urine, what is this called?
Proteinuria
is a dipstick enough to detect small amounts of albumin?
No, need a radioimmunoassay (AKA Spot AM urine)
What is a normal microalbuminuria?
less than 30
What is the BP goal for diabetics, especially those presenting with complications?
less than 140/90
If a patient is losing protein in the urine, what medication do we need to give them?
ACE!
What would accelerate nephropathy?
The development of/or progression of HTN
SO what’s the treatment for a diabetic presenting with Nephropathy?
Aggressive BP control, protein restriction, initiate an ACE
When should we be initiating an ACE (Lisinopril) in diabetic patients?
EARLY – with the presence of microalbuminuria – even if BP is normal!!
What must we be cautious about with ACE’s?
Creatinine >2g & hyperkalemia
What is the goal BP for diabetics? What’s the first line medication for hypertension in a diabetic?
less than 140/90 ACE!
What is the cause of >70% of deaths in diabetics?
Atherosclerosis
Is diabetes a coronary risk factor?
Yes, but it’s actually a coronary risk equivalent
What would further a diabetics risk for atherosclerosis?
Metabolic syndrome
What would the screening look like for preventing atherosclerosis?
History, PE, ECG, and stress testing
Persistently high insulin levels may cause what?
Atherosclerosis
If we have a patient with ulcerations of the LE and minimal to faint pulses of the LE, what complication would this be?
Peripheral Vascular Disease
How do we prevent PVD in a diabetic?
Regular foot exams, tight glycemic control, and STOP SMOKING!
How does a diabetic ulcer formulate?
Decreased circulation, loss of sensation, local infection
A diabetic patient presents with pain in their feet that is sharp and stabbing? What is going on, how does it progress?
Peripheral Neuropathy; presents in a stocking/glove ascending pattern. The nerve will eventually burn out
If a diabetic patient has early satiety, nausea, and vomiting a couple hours after a meal, with constant feelings of diarrhea/constipation – what diagnosis are you thinking?
autonomic neuropathy
Autonomic neuropathy presents with gastroparesis & diarrhea/constipation, but how else?
Sexual dysfunction and decreased bladder sensation – trouble voiding, hesitancy, incontinence
What is a life threatening emergency for a type 1 diabetic?
Diabetic ketoacidosis
What triggers DKA?
Infection, trauma, surgery, MI, or and increased insulin requirement
How does a patient present with DKA?
Polyuria, polydipsia, abdominal pain, N/V, weakness, and fatigue
What would you see on PE with DKA?
Increased pulse, LOW BP, dehydration, rapid breathing, fruity breath
Why is the patient dehydrated & hypotensive in DKA?
The metabolic acidosis is placing more glucose in the urine – which is an osmotic diuretic
What causes DKA?
Not enough insulin, leading to increased blood glucose & LOTS of fat & protein breakdown
Why is there more glucose in the blood?
There is an increase in cortisol, glucagon, and growth hormone resulting in gluconeogenesis & glycogenolysis
What is initially high in DKA, but is actually low in the body? Why?
Potassium – because glucosuria will turn on RAAS thus spilling out potassium
What labs do you usually see with DKA?
BS >300; pH less than 7.3; bicard is low - increasing the anion gap; total body K is low
How do you treat a patient with DKA?
Flow sheet (BS, electrolytes, pH, bicarb, ketones, BUN)
Replace insulin with REGULAR
Replace fluid loss
Replace K loss
