Diabetes, Metabolic Syndrome, PAD Flashcards

1
Q

How many people in the US are diagnosed with pre-diabetes?

A

96 million or 38% of the US population

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2
Q

How does Type I & Type II DM differ?

A

DM: Chronic metabolic disorder characterized by high blood glucose (“hyperglycemia”)

TYPE 1:
-beta cells of pancreas (produce insulin) are destroyed
-insulin dependence –> need supplemental
-commonly dx before age 30

TYPE II
1) insulin resistance - insulin action is abnormal and cells become resistant to insulin (abnormal uptake of blood glucose)
2) pancreas continues to produce more insulin to counteract insulin resistance–> over time B cells burn out –> insulin production decreases –> need supplemental insulin (insulin dependence)
-commonly dx after 40 years
-effects >90% of DM population

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3
Q

Can someone with Type II DM require insulin? Why?

A

-yes, transition from insulin resistance to insulin dependence

-diabetes is a combination of macrovascular and microvascular complications

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4
Q

Common precautions of hypoglycemia for DM population. Why are these important?

A

DEFINITION: BG <60 mg/dL

EXERCISE:
-exercise increases the risk of hypoglycemia bc it accelerates glucose uptake into peripheral tissues
-monitor blood glucose before, during, and after exercise

NOCTURNAL:
-can happen at night too

-know/compare timing of tube feeding and insulin dosing

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5
Q

What types of cells release glucagon?

A

pancreatic alpha cells

-glucagon stimulates gluconeogenesis and glycogenolysis in liver and release of glucose to plasma (more glucose in the blood stream)

** primary target organ for glucagon is the liver (because liver can help to breakdown the glycogen that it stores)

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6
Q

What cell types are highly responsive to insulin (glucose uptake)?

A

liver, fat, muscle

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7
Q

Explain how insulin and glucagon are “counter regulatory” hormones to each other.

A

Insulin increases blood glucose uptake into cells

Glucagon increases release of blood glucose into blood steam (stimulates hepatic glucose production)

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8
Q

What are the common diagnostic tests for DM? What information is derived from each?

A

Fasting Plasma Glucose Test:
-cheap, fast
-normal: 70-100 mg/dL
-100-125 mg/dL- prediabetes
-> 125 mg/dl - diabetes

Glycosylated Hemoglobin tests: (Hb A1c)
-normal <5.7% of total Hb
-tells you your 90 day history of glucose levels in blood
-if you leave RBC in a sugary solution it will add glucose to its structure –> measure this
-how elevated has glucose been over the lifetime of the RBC (90 days)

Oral Glucose Tolerance Test (OGTT)
-tested 2 hours after glucose-rich drink
-140-199 mg/dl signals pre-diabetes
-> 200 mg/dl signals diabetes

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9
Q

Criteria for the Diagnosis of Diabetes

A

Fasting plasma glucose (FPG) ≥126 mg/dL (7.0 mmol/L)

OR

2-h plasma glucose ≥200 mg/dL (11.1 mmol/L) during an OGTT

OR

A1C ≥6.5%
(5.7-6.5% is pre-diabetic)

OR

Classic diabetes symptoms + random plasma glucose ≥200 mg/dL (11.1 mmol/L)

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10
Q

Clinical Manifestations of heart disease in patients with diabetes:

A

CAD:
-late dx atypical symptoms: silent ischemia or silent MI
-angina equivalents: SOB/DOE; GI symptoms

Heart Disease risk in patients with DM vs without:
-increased atherosclerosis throughout coronary arteries
-increased HTN, CHF, and CVA risk
-increased incidence of dysrhythmias post MI (lack of blood flow to conduction system)

** assume a patient with DM has heart disease until proven otherwise

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11
Q

What are the common complications of DM?

A

-atherosclerosis
-hyperglycemia
-hypertension
-retinopathy: multiple fragile micro-aneurysms
-nephropathy
-neuropathy (DPN, CAN)
-diabetic ketoacidosis
-peripheral vascular disease/peripheral arterial occlusive disease
-osteopathy
-immune dysfunction (increased infection risk–> poor blood flow and lack of sensation)

WORST: blindness (caused by retinopathy), renal failure, CAD, MI, HF, amputation, CVA

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12
Q

a. Why is the patient with DM at a greater risk of CV disease? CV-related mortality?

A

-greater risk for atherosclerosis and HTN

-oxidative stress

-microvascular and macrovascular changes

-poor glycemic control can cause vascular changes

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13
Q

What are the multiple factors that increase the risk of wound development in the DM population?

A

-lack of sensation
-poor blood flow (occluded blood vessels)
-innate immunity is impaired –> decreased function of macrophages
-infections more rapidly enter the body
-hyperglycemia –> increased bacterial growth and proliferation glucose feeds the infection)

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14
Q

What is DKA? Who is at risk of developing DKA? What are the medical consequences of DKA?

A

Definition:
- very high levels of blood glucose
-lack of insulin and increased glucagon (more glucose in blood)
-increased release of glucose by liver (gluconeogenesis and glycogenolysis)

Etiology:
-more in DM I > DM II
-release of free fatty acids from adipose tissue lipolysis) –> converted by liver into ketone bodies (ketogenesis)
-ketones lead to acidosis –> respiratory compensation (kussmaul breathing)
** OCCURS BECAUSE LACK OF INSULIN PREVENTS GLUCOSE FROM GETTING INTO CELLS FOR USE AS ENERGY SOURCE

Medical Consequences:
-acidosis –> respiratory compromise
–with a lot of glucose in the urine–> water follows urine –> increased urine output (9-10 L/hr)
-osmotic diuresis: blood volume and blood pressure decrease; loss of H2O and electrolytes; because serum glucose exceeds reabsorption capability of the kidneys
-if severe: hemodynamic compromise= medical emergency

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15
Q

What is DKA commonly precipitated by?

A

acute illness (infection, pneumonia); MI, CVA, drug abuse (cocaine); poor DM management

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16
Q

Signs and symptoms of DKA:

A

N/V
abdominal pain
polydipsia- excessive thirst
polyuria
-dehydration (hypotension)

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17
Q

What are the benefits of tight glucose management in the DM population?

A

-decreases risk of medical complications associated with DM

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18
Q

Treatment of hypoglycemia (ADA):

A

15-20 grams of fast acting carb

wait 15-20 minutes and check BG again

still low and symptoms don’t stop–> repeat treatment

eat regular meals and snacks after you feel better

19
Q

Diet and diabetes

A

-ensuring weight control
-providing nutritional requirements
-good glycemic control
-correcting associated blood lipid abnormalities

20
Q
  1. What are the signs/ symptoms of hypoglycemia? a. How can this be avoided during exercise?
A

SYMPTOMS:
-headache, confusion, tachycardia, sweating, anxiety, fatigue, hunger
-severe: loss of consciousness/convulsions/death

AVOIDED DURING EXERCISE: lower insulin dose pre-activity or higher carb intake prior to or during activity

-monitor BG before, during, and after activity

21
Q

Lifestyle changes and prevention of diabetes (or delay):

A

Research studies have found that lifestyle changes can prevent or delay the onset of type 2 diabetes among high-risk adults.

22
Q
  1. What is the role of exogenous insulin therapy?
A

TYPES:
-injectable –> different rates of action: rapid acting, short acting, intermediate acting, long acting

CONSIDER THESE THINGS
-type: onset of action and duration
-site of administration
-impact of exercise/activity
-diet/meals/snacks
-emergency preparedness (hypoglycemia)

-patients are often instructed to rotate injection sites

23
Q

Glucose monitoring and pumps:

A

Finger stick: point of care

Continuous monitoring of glucose

Pump- basal rate delivery of insulin with dose adjustment

Artificial pancreas: automated insulin delivery system
-combines continuuous glucose monitoring and infusion pump
-pump can provide insulin and glucagon

24
Q

What are the different preparations of insulin?

A

Rapid acting (quick onset time)
Short acting
Intermediate acting
Long acting (longer overall duration of action)

25
Q

What are common examination items included in the DM foot exam?

A

Look to previous slide deck

26
Q

Why is monofilament testing important? Vibration testing? Pulses? …etc.

A

Monofilament: A monofilament test is done to test for nerve damage (peripheral neuropathy), which may be caused by conditions such as diabetes.

Vibration: adds to the diagnosis of peripheral neuropathy

Pulses: any arterial occlusion/atherosclerosis?

27
Q

What is Metabolic Syndrome? Why is recognition of this condition important? Criteria for diagnosis?

A

DEFINITION:
-A disorder diagnosed by a co-
occurrence of 3 out of 5 of the
following medical conditions:
1) abdominal obesity (visceral adiposity)
2) elevated blood pressure
3) elevated fasting plasma glucose
4) high serum triglycerides
5) low HDL levels

DIAGNOSIS:
* TG ≥ 150 mg/dL
* HDL-C
– <50 mg/dL women;
– <40 mg/dL men
* Waist circumference:
– >35” women;
– >40” men
* Glucose ≥ 100 mg/dL
* BP ≥ 130/or ≥ 85 mm

IMPORTANCE:
-Increases the risk of
developing cardiovascular
disease, particularly heart
failure, and diabetes

28
Q

Role of the PT with metabolic syndrome

A

-physical therapy has a role in prevention

-education on smoking, exercise, managing their blood pressure and blood glucose effectively via exercise and diet

29
Q

What the similarities and differences between PAD & CAD?

A

PAD
-atherosclerotic changes leading to arterial stenosis
-intermittent claudication
-incidence of claudication increases over age 70
-RISKS: smoking, HTN, atherosclerosis, diabetes, hypercholesterolemia, age >60 years
-predominantly effects the legs
-affects arteries of the limbs and peripheral areas of the body

CAD
-The usual cause is the buildup of plaque in coronary arteries. This causes coronary arteries to narrow, limiting blood flow to the heart.
-Coronary artery disease can range from no symptoms, to chest pain, to a heart attack.

30
Q

What is meant by “intermittent claudication”?

A

reproducible ischemic muscle pain with activity; relieved by rest

31
Q
  1. How is PAD diagnosed? What is the “gold standard”?
A

GOLD STANDARD: ABI
–> R leg SBP/max arms SBP
-normal: 0.91-1.30
-normally lower extremity BP greater than or equal to upper
-0.7-0.9: mild
-0.40-0.79: moderate
-<0.4 severe (greater blockage in lower limb)

-ultrasonography

-magnetic resonance angiography

-computed tomographic

32
Q

S/S of PAD

A

-intermittent claudication

-blanching with elevation

-rubor of dependency with dependent position after elevation

33
Q

Physical examination tests that may indicate an arterial disorder

A

-Buerger’s test

-Capillary refill

-ABI

-6MWT with claudication scale

34
Q

What is the exercise prescription for a patient with PAD?

A

WARM UP- 5 min
-FREQUENCY: 3-5 times/week
-TIME: 35-50 minutes of exercise/session (increase by 5 minutes each session)
-repeated exercise periods ending at (moderate to severe) 2-3/4 on claudication scale during aerobic exercise is allowed
-take rest until pain is gone –> begin again
TYPE: treadmill or track walking

Etiology of exercise impairment:
-muscle ischemia
-structural changes in skeletal muscle

  • want them to exercise into pain

** exercise training can reduce intermittent claudication (greater distance before onset of claudication)

35
Q

NPDR vs PDR

A

NPDR
-increased vascular permeability: macula edema
–> may be asymptomatic
–blurry vision
–> microaneurysms +/- hemorrhages

PDR (contra to high int. work)
-neovascularization
–> risk of vitreous hemorrhage
-blurry vision
-floaters
-detached retina
-progression to blindness

36
Q

Diabetic peripheral neuropathy vs autonomic neuropathy

A

DPN:
-loss of protective sensation
-impacts longer nerve fibers: distal> proximal (dying back)
-decreased vibration + proprioception sense
-diminished reflexes
-neuropathic pain
-progressive weakness and atrophy (motor)

AN:
-heart and vasculature changes (OH, silent MI)
-GI tract changes (gastroparesis, diarrhea)

37
Q

Charcot’s disease vs UE MSK concerns vs Spinal changes DM

A

Charcot’s:
-progressive degen. of weight bearing joints
-increased skin breakdown risk
-varied pressure distribution
-increased wound risk if combined with DPN

UPPER EXTREMITY:
-frozen shoulder
-carpal tunnel syndrome
-flexor tenosynovitis (trigger finger)
-Dupuytren’s contracture (flexiion of 4th and 5th digit)

SPINE:
-OP
-diffuse idiopathic skeletal hyperostosis (DISH) - DISH refers to extensive ossification through the axial and appendicular skeleton

38
Q

Three major components of diabetes treatment:

A

1) diet and exercise
2) oral hypoglycemic medications
3) insulin therapy

39
Q

Exercise and diabetes

A

-PA promotes weight reduction and improves insulin sensitivity–> lowering blood glucose levels
-regular PA and exercise should be considered –> consider individual’s health status and fitness level
-**educate on risk of potential hypoglycemia and how to avoid

TYPE I
-increased fitness
-increased confidence
-increased CV function and decreased CV risk profile
-no direct effect on glucose control

TYPE II
-improves fitness, confidence
-increased CV function and decreased CV risk profile
-** improves glucose control –> increased insulin sensitivity and increases glucose transporters –> reduced plasma glucose

40
Q

Exercise guidelines for DM:

A

Postpone moderate to vigorous exercise if BG > 250 mg/dL (hyperglycemia)

-exercise induced hyperglycemia can lead to ketoacidosis

EXERCISE TYPE AND QUANTITY:

Children with diabetes: 60 min/day of physical activity

Adults with type I or type II diabetes:
-150 min/week moderate (4-6/10) to vigorous (>/=7) aerobic activity 3 days/week no more than 2 consecutive days without
-75 min/week of vigorous intensity for younger, more physically fit
-resistance training 2-3 sessions/week on nonconsecutive days; 10-15 reps of 50-69% 1 RM (moderate intensity
-flexibility exercises

41
Q

Exercise implications with various medical complications of DM

A

RETINOPATHY
-Avoid isometrics, head down positioning, Valsalva maneuvers
-Keep SBP ≤ 150 mmHg/100
w/ mod-severe NPDR

OSTEOPATHY AND LOSS OF PROTECTIVE SENSATION
-be aware of foot deformities with weight bearing exercises
-increased wound risk

CARDIAC AUTONOMIC NEUROPATHY
-resting tachy
-angina equivalents/blunted awareness of CP
-postural hypotension

DEHYDRATION
-polyuria, polydipsia
-encourage increased fluid intake t/o exercise

42
Q

3 types of oral hypoglycemic medications

A

Biguanides
-inhibits glucose production in liver

Sulfonylureas
-increases insulin secretion

GLP-1 receptor agonist
-increases insulin secretion; inhibits glucagon
-weight loss
*wegovy

43
Q

Surgical interventions for PAD

A

-angioplasty/stenting
-endarterectomy- remove plaque from vessel
-bypass grafting: much more aggressive–>A coronary artery bypass graft involves taking a blood vessel from another part of the body – usually the chest, leg or arm – and attaching it to the coronary artery above and below the narrowed area or blockage.

44
Q
A