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ENDO > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What populations are at an increased risk for diabetes?

A

African Americans, Hispanics, and Native Americans

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2
Q

What is occurring in Type 1 diabetes?

A

Auto-immune destruction of Beta-cells in the pancreas. Mainly due to islet cell antibodies

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3
Q

What is hyperglycemia?

A

Increase in blood sugar with glucosuria – leading to a loss of glucose as an energy source

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4
Q

In diabetics, when fat and protein in being broken down, what is this known as?

A

Ketoacidosis

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5
Q

What are both hyperglycemia & ketoacidosis apart of?

A

Catabolic disorder

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6
Q

What are some causes of the auto-immune response in Type 1 diabetes?

A

viruses (mumps, coxsackie B-4, rubella) & toxic chemicals

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7
Q

What is occurring in Type 2 diabetes?

A

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.

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8
Q

Does Type 2 diabetes have the same catabolic disorders as type 1?

A

No, circulating insulin prevents ketosis. But type 2 is aggravated by increased hyperglycemia

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9
Q

What would cause type 2 diabetes?

A

Genetic pre-disposition & sedentary life style is common

Central/visceral obesity = major factor in insulin resistance

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10
Q

What defect occurs in Beta cells with Type 2 diabetes, what causes it?

A

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)

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11
Q

If the compensation via hyperplasia occurs for a long period of time, what happens to the beta cells?

A

Eventually get destroyed → diabetes develops and insulin levels decline

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12
Q

What would cause insulin resistance?

A

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)

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13
Q

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?

A

Glucotoxicity = Can worsen insulin resistance and destroy Beta cells faster/more permanently
We must control hyperglycemia to preserve any remaining Beta cell function

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14
Q

So what lifestyle changes can a patient make to lower their insulin resistance?

A

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

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15
Q

What is metabolic syndrome? What does metabolic syndrome lead to? What are some qualifying factors for it?

A

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

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16
Q

What are clinical findings for Type 1 DM?

A

Polyuria, thirst, weight loss, dehydration, polyphagia, ketoacidosis, hyperosmolality

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17
Q

What are some clinical findings for Type 2 diabetes?

A

No symptoms early on. Polyuria, thirst, skin infections, vulvovaginitis, abnormal fat distribution, hyperglycemia

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18
Q

What lab reflects long term control of DM?

A

Hemoglobin A1c; reflects state of glycemia over prior 8-12 weeks

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19
Q

What is a normal A1c?

A

4-6%

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20
Q

What A1c level confirms diabetes?

A

Greater than 6.5%

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21
Q

What A1c levels indicate prediabetes?

A

5.7-6.4%

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22
Q

For a diabetic, what is our goal for the A1C?

A
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23
Q

How often do we measure A1c’s in a diabetic?

A

every 3-4 months

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24
Q

Besides A1c, what other lab findings indicate diabetes?

A

Fasting blood glucose >125

2 hour glucose tolerance test >200

Random blood sugar >200 (confirm with fasting)

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25
Q

What lab findings demonstrate impaired glucose tolerance?

A

Fasting blood glucose 100-125

2 hour GTT of 140-199

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26
Q

What form of testing is considered a standard of care for all diabetics?

A

Self-monitored blood sugar

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27
Q

Is type 1 or type 2 diabetes associated with lipoprotein abnormalities?

A

Type 2 = High triglycerides (3-400) and low HDL (

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28
Q

What are our treatment goals for DM?

A

Diet, exercise, and medications

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29
Q

What is a diabetic diet?

A

Get a dietician involved, weight reduction if needed.

Total calories 25-35/kg/day

Total cholesterol

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30
Q

How would we tightly control Type 1 Dm?

A

Insulin

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31
Q

How would we tightly control type 2 DM

A 
oral agents/insulin; 
control BP (
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32
Q

What is our goal with tightly controlling DM?

A

Get HbA1c to

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33
Q

What are the blood sugar goals with therapy?

A

Pre-prandial = 90-130
Bedtime = 100-140
Peak post-prandial =

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34
Q

How would we calculate plasma blood sugar from blood sugar on a test strip?

A

Add 10mg

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35
Q

What are the ABC’s of diabetes?

A

Aspirin, blood pressure, cholesterol, and diabetes management

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36
Q

What must we always remember about diabetics and their platelets? What are they at risk for?

A

Abnormal platelet function → increased risk of small vessel thrombosis or atherosclerosis

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37
Q

When should we prescribe aspirin for our diabetic patient?

A

If they have a >10% risk for a cardiac event over 10 years

Any diabetic patient with macrovascular

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38
Q

What is the dose of aspirin & risks associated with aspirin?

A

75-162mg/day

Risks = PUD, gastritis and bleeding ulcers

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39
Q

If a diabetic patient has AV nicking or arteriolar narrowing what does that indicate?

A

Uncontrolled BP along with their diabetes

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40
Q

What 2 diagnosis would we see high trigs & low HDL?

A

Diabetes & Hypothyroidism

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41
Q

How many medications does the average diabetic need?

A

3 (to help control HTN)

42
Q

What does the diabetic work-up look like?

A

Family Hx, Complete H&P, CV risk factors, lipids, BUN, Cr, Electrolytes, UA +MicAl, ECG, Ophthalmology, Podiatry

43
Q

What must we evaluate every 3-6 months in a patient with diabetes?

A

Weight, BP, A1c, foot exam, home monitoring, Psychosocial function, intercurrent illness

44
Q

What must we evaluate every year in a patient in a patient with diabetes?

A

Lipids, UA, creatinine, microalbinuria, complete PE, Ophthalmologist, dental exam

45
Q

How many sites on the feet must we exam?

A

6 on each

46
Q

What if a patient cannot feel the microfilament in an area?

A

now at a higher risk for future ulceration

47
Q

What is the most important part of a diabetics treatment?

A

EDUCATION! They need to understand – especially all of their risks

48
Q

What does exercise help with in diabetics?

A

Increases the effectiveness of insulin, stabilize insulin, improve utilization of fat

49
Q

What is at the cornerstone of T2DM treatment?

A

Weight reduction, diet & exercise, decrease adipose stores, regain insulin sensitivity

50
Q

we start a patient on metformin, if their BG remains elevated, where do we start?

A

Sulfonylurea or insulin

If that doesn’t do well - Pioglitazone, Exanatide

51
Q

What is the most effective combination with metformin?

A

Metfromin + insulin is more effective that 3 oral agents

52
Q

If a patient is overweight, what combo drugs would be best?

A

Metformin, Exantide, (possibly Alpha), or SGL2’s

53
Q

In a T2DM, what insulin regimen can we use?

A

Metformin + NPH/Regular 70:30 ratio – usually before breakfast and before dinner

54
Q

What does the T1DM insulin look like?

A

Take the total insulin needed and divide that between basal (Glargine) & prandial needs (Lispro)

55
Q

What must we remind our patients of when they are ill?

A

IF they are sick they must increase their insulin levels

56
Q

What’s the most common complication of insulin use?

A

Hypoglycemia

57
Q

What are the sxs we need to educate our patients about for hypoglycemia?

A

Sweating, tachycardia, hunger, tremulousness, nausea

58
Q

What drug may mask hypoglycemia?

A

Beta Blockers

59
Q

What BS level correlates with Hypoglycemia?

A
60
Q

How would we treat hypoglycemia?

A

Simple sugars (candy, sugar, OJ); 1mg injection of glucagon; IV glucose

61
Q

How much glucose raises BS by 25-50mg? How many carbs are in a soda?

A

15g of glucose

30g of carbs

62
Q

What are the long term complications we must always be aware of with diabetics?

A

Retinopathy, nephropathy, neuropathy - Microvascular

Atherosclerosis – Macrovascular

63
Q

What are the 2 categories of retinopathy? Which is worse?

A

Non-proliferative or Proliferative (worse)

64
Q

What is occurring in proliferative retinopathy?

A

Formation of new blood vessels –> blindness

65
Q

What would we see on PE with non-proliferative retinopathy?

A

Microaneursysms, hemorrhages, exudates, retinal edema

66
Q

How do we prevent retinopathy?

A

TIGHT GLYCEMIA CONTROL - A1c, tight hypertension control, and annual eye exams

67
Q

What would make retinopathy worse?

A

Smoking & hypertension

68
Q

What complication can develop with chronic hyperglycemia and uncontrolled hypertension?

A

Nephropathy

69
Q

What is the leading cause of end-stage renal disease?

A

Nephropathy

70
Q

How do we prevent nephropathy?

A

Tight A1c control, tight BP control, and smoking cessation

71
Q

If we get a microalbuminuria in a diabetic patient and see 200mg in the urine, what is this called?

A

Proteinuria

72
Q

is a dipstick enough to detect small amounts of albumin?

A

No, need a radioimmunoassay (AKA Spot AM urine)

73
Q

What is a normal microalbuminuria?

A

less than 30

74
Q

What is the BP goal for diabetics, especially those presenting with complications?

A

less than 140/90

75
Q

If a patient is losing protein in the urine, what medication do we need to give them?

A

ACE!

76
Q

What would accelerate nephropathy?

A

The development of/or progression of HTN

77
Q

SO what’s the treatment for a diabetic presenting with Nephropathy?

A

Aggressive BP control, protein restriction, initiate an ACE

78
Q

When should we be initiating an ACE (Lisinopril) in diabetic patients?

A

EARLY – with the presence of microalbuminuria – even if BP is normal!!

79
Q

What must we be cautious about with ACE’s?

A

Creatinine >2g & hyperkalemia

80
Q

What is the goal BP for diabetics? What’s the first line medication for hypertension in a diabetic?

A

less than 140/90 ACE!

81
Q

What is the cause of >70% of deaths in diabetics?

A

Atherosclerosis

82
Q

Is diabetes a coronary risk factor?

A

Yes, but it’s actually a coronary risk equivalent

83
Q

What would further a diabetics risk for atherosclerosis?

A

Metabolic syndrome

84
Q

What would the screening look like for preventing atherosclerosis?

A

History, PE, ECG, and stress testing

85
Q

Persistently high insulin levels may cause what?

A

Atherosclerosis

86
Q

If we have a patient with ulcerations of the LE and minimal to faint pulses of the LE, what complication would this be?

A

Peripheral Vascular Disease

87
Q

How do we prevent PVD in a diabetic?

A

Regular foot exams, tight glycemic control, and STOP SMOKING!

88
Q

How does a diabetic ulcer formulate?

A

Decreased circulation, loss of sensation, local infection

89
Q

A diabetic patient presents with pain in their feet that is sharp and stabbing? What is going on, how does it progress?

A

Peripheral Neuropathy; presents in a stocking/glove ascending pattern. The nerve will eventually burn out

90
Q

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?

A

autonomic neuropathy

91
Q

Autonomic neuropathy presents with gastroparesis & diarrhea/constipation, but how else?

A

Sexual dysfunction and decreased bladder sensation – trouble voiding, hesitancy, incontinence

92
Q

What is a life threatening emergency for a type 1 diabetic?

A

Diabetic ketoacidosis

93
Q

What triggers DKA?

A

Infection, trauma, surgery, MI, or and increased insulin requirement

94
Q

How does a patient present with DKA?

A

Polyuria, polydipsia, abdominal pain, N/V, weakness, and fatigue

95
Q

What would you see on PE with DKA?

A

Increased pulse, LOW BP, dehydration, rapid breathing, fruity breath

96
Q

Why is the patient dehydrated & hypotensive in DKA?

A

The metabolic acidosis is placing more glucose in the urine – which is an osmotic diuretic

97
Q

What causes DKA?

A

Not enough insulin, leading to increased blood glucose & LOTS of fat & protein breakdown

98
Q

Why is there more glucose in the blood?

A

There is an increase in cortisol, glucagon, and growth hormone resulting in gluconeogenesis & glycogenolysis

99
Q

What is initially high in DKA, but is actually low in the body? Why?

A

Potassium – because glucosuria will turn on RAAS thus spilling out potassium

100
Q

What labs do you usually see with DKA?

A

BS >300; pH less than 7.3; bicard is low - increasing the anion gap; total body K is low

101
Q

How do you treat a patient with DKA?

A

Flow sheet (BS, electrolytes, pH, bicarb, ketones, BUN)
Replace insulin with REGULAR
Replace fluid loss
Replace K loss

ENDO (7 decks)

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