Vascular Complications

Question 1

Microvascular complications
of DM? 3

Macrovascular complecations of DM?
6

Answer 1

Nephropathy
Retinopathy
Neuropathy

1. Cardiovascular and Cerebrovascular
2. Hypertension
3. Myocardial Infarction
4. TIA’s and strokes
5. Platelet hypersensitivity
6. Peripheral vascular disease

Question 2

What is the leading cause of end stage renal disease in the US?

In what ethnic groups is this seen in more often? 3

Answer 2

Nephropathy

American indians and hispanic
african americans

Question 3

What goes wrong in nephropathy in DM pts?

7

Answer 3

1. Lesions occurring in a diabetic kidney
2. Hammers the Glomeruli
3. Basment Membrane of the glomeruli Thickens**(things just start to leak through)
4. Glomerular Sclerosis
5. Nodular
6. Glomerulosclerosis
7. All cause impaired blood flow, nodular lesions in glomerular capillaries of kidneys, kidneys slowly die

Question 4

Nephropathy steps to ESRD?

5

Answer 4

1. Proteins leak through the damaged membrane.
2. Kidneys and nephrons hypertrophy (excessive hardened growth), hyperfiltration occur early in the disease suggesting increased work on the beans.
3. Difficult to reabsorb excessive amounts of glucose.
   Then comes the
4. Microalbuminuria
5. Decline in GFR.
6. ESRD

Question 5

IScemic area that doesnt start to work very well. What starts to leak? 2

Answer 5

proteins. at this point it isnt very reversible (hopefully microalbumenia and not macro)

also sugar

Question 6

What lesions will you encounter in nephropathy?
2

What can you not give in these pts?

Answer 6

1. Glomerularsclerosis (Kimmelstiel-Wilson) nodular lesions in the glomerular capillaries
2. Renal vasculature – Renal Artery Stenosis- watch out for your hypertensive pts.

cant give an ACE inhibitor

Question 7

What is the leading indicator of developing nephropathy?

Answer 7

microalbuminuria

Microalbuminuria is the strongest independent risk factor of cardiovascular disease

Question 8

What is microalbumenia?

The risk of nephropathy is increased by what? 3

Answer 8

Refers to the appearance of small but abnormal amounts of albumin in the urine

Duration of diabetes
High blood pressure
Smoking

Question 9

At what level is our patient at microalbumiemia?

What point does it become macroalbumemia?

In macroalbumemia what are the next steps in the disease once its progresses to this point?
2

Answer 9

30-300mg/24hours

> 300g/24hour

1. Steady drop in GFR
2. End stage renal disease leading to dialysis

Question 10

The progression of macroalbumemia can be slowed by what?

4

Answer 10

1. Tight glucose control
2. Blood pressure control
3. Protein restriction in diet to decrease proteinuria
4. Smoking Cessation

Question 11

What is the key indicator for diebetic nephropathy?

Answer 11

microalbumin in the urine

Question 12

Drugs to help diabetic nephropathy?

4

Answer 12

1. ACEI – Ace Inhibitors (angiotension converting enzyme inhibitors)- only do not use if there is renal artery stenosis (kidney protective)
2. ARB’s – (Angiotension II receptor blockers)

May consider

3. nondihydropyridine calcium channel blockers (Cardizem) and
4. beta blockers (Lopressor, Tenormin)

Question 13

HOw are Angiotension II receptor blockers used in nephropathy?
4

Answer 13

1. Have a marked antiproteinuric effect
2. Used even if patient is normotensive
3. These are cardioprotective as well
4. Possibly prevent or reverse progession towards renal failure

Question 14

What diabetic pts should be on ACE inhibitors?

Answer 14

ALL DIABETIC PTS

- take care of renal artery stenosis first then put them back on

Question 15

When do we screen for nephropathy in:
Type 1?
Type 2?
How do we screen?

Answer 15

Type 1 starting 5 years after diagnosis
Type 2 starting at the time of diagnosis

Random spot urine
Measure the ratio of protein (albumin) to creatinine
(this closely reflects 24 hour urinary protein estimations)

Question 16

No beta blockers for DM pts. WHy?
3

Diuretics?

Answer 16

1. affect sugars in the kidney causing them to go up.
2. can mask hypoglycemic affects
3. Increases fatigue etc
4. too hard on the kidney

Question 17

What happens in non-proliferative retinopathy?
3

WHat will the fundoscopic exam?
3

What will vision be like?

Answer 17

1. Increased capillary permeability.
2. Dilation of venules.
3. Presence of microaneurysms.
4. Appear as dots.
5. Hard exudates (yellow deposits of proteins and lipids).
6. Superficial retinal microinfarcts – cotton wool spots.

blurry

Question 18

Retinopathy - Proliferative
is characterized by what?
2

What can this lead to?
5

Answer 18

1. Neovascularization (growth of new vessels).
2. Extend between the retina and vitreous.
3. Can lead to sudden vision loss
4. Neovascular glacoma
5. Blind, painful eye
6. Retinal detachment (floaters-flashes)
7. Senile cataracts
   - -Snowflake lens opacities

Question 19

Retinopathy screening guidelines?

Pregnancy?

Answer 19

Screening Guidelines: Annual dilated fundoscopic exams by an opthalmologist

Pregnant ladies need to be extra careful, dilated fundoscopic exam before conception and every 4-8 weeks

Question 20

TREATMENT
for DM retinopathy?
5

Answer 20

1. Tight Glucose Control***
2. Aggressive Treatment of HTN****
3. Statins decrease lipid deposition
4. Laser Photocoagulation
5. Vitrectomy for severe macular edema

Question 21

Pathophysiologic changes that cause peripheral neuropathy?
2

What is the second finding that leads to this?

Answer 21

1. include thickening of the walls of the nutrient vessels that supply the nerve,
2. leading to the assumption that vessel ischemia plays a major role once again

(Blood flow to the nerves and not a problem with the nerves itself)

The second finding is a segmental demyelination process that affects the schwann cells which slows nerve conduction

Question 22

What is the most common type of somatic neuropathy?

What is the distribution like and what are its symtpoms?
4

What do they eventually lose?
2

Answer 22

Peripheral polyneuropathy

Glove and stocking distribution

1. Pain
2. Numbness
3. Hyperethesias – increase in sensitivity
4. Paresthesias – burning, itching, tingling

Eventual sensory loss

• -Loss of proprioception
• -Loss of vibratory sense

Question 23

What do they lose first for peripheral neuropathy?

Answer 23

vibration on the foot/dont know its happening

Question 24

Consequences of neuropathy?

7

Answer 24

1. Abnormal gait
2. Hammer toes
3. Abnormal pressures on feet
4. Trauma and fracture
5. Soft tissue atrophy d/t arterial insufficiency
6. Foot ulcers that never heal
7. Osteomyelitis and gangrene

Question 25

What do we have to do each visit and what are we looking for (3)? Neuro exam of the foot consists of what? 4

Answer 25

Detailed foot exam with each visit 1. Color, sores, pressure areas 2. Feel for pulses 3. Capillary refill 1. Monofilimant test 2. Reflexes 3. Vibratory sensation 4. Proprioception

Question 26

Treatment of neuropathy? 6 (whats the major one?)

Answer 26

Pain and Sensory issues: TCAs work well!!!!! 1. Elavil (Amitryptilene) 2. ASA, Tylenol, NSAIDS 3. Tegretol (Carbamazapine) 4. Neurontin (Gabapentin)** -probably see this the most (KNOW THIS ONE) 5. Lyrica (Pregabalin) 6. Cymbalta (Duloxitine)

Question 27

WHat educations points do we need to talk with the pt about regarding neuropathy? 5

Answer 27

1. Prevention of foot ulcers 2. Daily foot inspection 3. Appropriate footwear 4. Drying and nail cutting 5. Podiatry visit annually!!!!!

Question 28

Autonomic neuropathy attacks what the most? What does this cause? 4 What can this lead to?

Answer 28

Gastric dysmotility - Gastroparesis 1. Delayed emptying 2. Constipation 3. Nausea and Vomiting 4. Diarrhea This can all lead to hyperglycemia

Question 29

Autonomic Neuropathy can cause what else? 4

Answer 29

1. Orthostatic Hypotension (support hoes) 2. Cardiac rhythm disturbances 3. Bladder involvement 4. Erectile dysfunction

Question 30

How should we treat neuropathy for bladder involvement? | 2

Answer 30

Retention – Diuretics, self cath | Incontinence - Detrol

Question 31

How should we treat orthostatic hypotension? 2 Gastraperesis? 3 Erectile disfunction? 2

Answer 31

Orthostatic Hypotension: 1. Florinef (Fludrocortisones) and 2. Midodrine (ProAmatine) Gastraparesis: 1. Metocloperamide (Carbamazepine), 2. Erythromycin, 3. Imodium (Loperamide) Erectile Dusfunction: 1. Viagra (Sildenafil) or 2. Cialis (Tadalafil)

Question 32

Mononeuropathies affect which kind of nerves? 2 How do they present?

Answer 32

Focal limb or cranial nerve Present acutely and are self limiting Cranial nerves commonly involved

Question 33

Which cranial nerves are commonly affected? 4 Limbs that are commonly affected? 3

Answer 33

CN 3,4,6, and 7 Limb commonly femoral, sciatic, or peroneal neuropathy

Question 34

Diabetic amyotrophy is what? Which ones are affected the most? 2

Answer 34

Muscle atrophy and weakness Anterior thigh Pelvic girdle

Question 35

Atherosclerosis is what?

Answer 35

``` Fibrofatty lesions (atheroma/plaques) in the intimal linging (intima) of the large and medium-sized arteries such as the aorta, coronary arteries, and the large vessels that supply the brain (hardening of the arteries) ```

Question 36

Progression of atherosclerosis over time? | 6

Answer 36

1. Foam cells 2. Fatty streak (first decade) 3. Intermediate lesion 4. Atheroma (third decade) 5. Fibrous plaque 6. Complicated lesion/rupture (fourth decade)

Question 37

1. What controls contractility of the ateries? 2. What does all the glucose in our vessels cause? What state are they always in because of this? 3. What does LDL do to increase this issue? 4. HDL will never come up unless what? 2 So what allcontributes to the dysfuntion of the endothelium? (4 causes that lead to 4 consequences)

Answer 37

1. nitric oxide controlls contractility of the vessels 2. - -higher inflammatory state with all the glucose - -always in a vasocontricted state 3. LDL oxidized and relaeases inflammatory factors 4. stop smokeing and control sugar Causes: - LDL - HTN - DIabetes - Smoking Consequences: - Vasoconstrction - Increased leukocyte/platelet adhesion - SMC migration and growth - Increased lipid deposition and decreased clearance

Question 38

Mechanisms of Atherogenesis in Diabetes | 6

Answer 38

1. Abnormal lipoproteins 2. Hypertension 3. Insulin resistance and hyperinsulinemia 4. Procoagulant state 5. Hormones, growth-factor and cytokines enhanced 6. SMC (smooth muscle cell) proliferation and foam cell formation

Question 39

Clinical Manifestations of Diabetes and Atherosclerosis 5 What does it depend on?

Answer 39

1. Narrowing of the vessel and producing ischemia 2. Sudden vessel obstruction due to plaque rupture 3. Thrombosis and formation of emboli 4. Aneurysm formation due to weakening of the vessel wall 5. Angina (chest pain) they may not feel it if they are already neuropathic Depend on the vessel involved and the extent of obstruction

Question 40

What are the final manifestations of Atherosclerosis? | 3

Answer 40

Aorta: complications are those of thrombus and weakening of the vessel wall Coronary, peripheral, and Cerebral Arteries: ischemia and infarction due to vessel occlusion If there is disease in one vascular bed, don’t forget about the others!!

Question 41

Much higher risk of having a stroke from what kind of lesion?

Answer 41

ulcerative, very unstable

Question 42

What is the leading cause of death of men and women in the US?

Answer 42

Coronary Artery Disease

Question 43

What do we want to control hypertension at to prevent cardiovascular, peripheral, and cerebral events?

Answer 43

Control hypertension - less than 120/80

Question 44

Cardiovascular, Peripheral and Cerebral prevention? | 6

Answer 44

1. Smoking cessation 2. Management of obesity 3. Control of Hyperlipidemia 4. Lifestyle modifications 5. Exercise 6. Glycemic Control! (need near normal levels)

Question 45

Guidelines for Reducing Risk of CVD ``` Diet: Limited saturated fats to? Limit dietary cholesterol to? Limit intake of what? What kind of diet? ``` ``` Lipids: LDL? HDL? TG? non-HDL cholesterol? ```

Answer 45

1. Limit saturated fats to less than 7% of total calories | 2. Limit dietary cholesterol to

Question 46

How do we decrease inflammation in the lining of the blood vessels? 2

Answer 46

Statins | control blood glucose

Question 47

Guidelines for Reducing Risk of CVD What is our goal for BMI? What is our goal for weight circumference? What other drug to they need to be on?

Answer 47

BMI of 18.5-24.9 Waist circumference: less than 35 for women less than 40 for men Aspirin

Question 48

Peripheral Vascular Disease Every office intake form should include: 4

Answer 48

1. Pain/cramping in legs when walking? 2. Pain in legs when walking uphill or hurrying? 3. Pain improves when sitting or standing still? 4. Pain improves within 10 minutes of resting? (they absolutely cant take another step and they sit down a few minutes and they can do it again) ANGINA of the legs

Question 49

PVD (macro disease) happens when arteries become?

Answer 49

narrow and blood flow decreases in arteriosclerosis

Question 50

PRIMARY SITES | for PVD?

Answer 50

Femoral and Popliteal arteries: 80-90% Tibial and Peroneal arteries: 40-50% Aorta and Iliac arteries: 30%

Question 51

DIAGNOSIS of PVD? | 4

Answer 51

1. History taking 2. Careful examination of leg and feet 3. Pulse evaluation 4. Ankle-brachial index (ABI):

Question 52

PVD leg looks like what?

Answer 52

shiny, no hair, pallor, no pulse, achey and hurts, cant move it well dead leg

Question 53

DVT leg looks like what?

Answer 53

hot swollen red and huge. not as tender only when you squeeze it. YOu can feel pulses. DIe of PE from the IVC to the lungs

Question 54

How do you calculate the ABI?

Answer 54

SBP in ankle (dorsalis pedis and posterior tibial arteries) ___________________________________ SBP in upper arm (brachial artery)

Question 55

Ankle-Brachial Index Values and Clinical Classification 1. Normal? 2. Claudication? 3. Rest pain? 4. Tissue loss? Diabetics may give false reading (they dont have normal blood vessels they are really sclerotic. Theyll be way sick, calified arteries but normal pressure)

Answer 55

1. > 0.90 2. 0.50-0.90 3. 0.21-0.49 4. less than 0.2

Question 56

The American Diabetes Association recommends screening for PAD? A screening ABI should be performed in patients with diabetes, those over 50 years of age? Those less than 50 yrs of age who have other risk factors. What are these risk factors? 4

Answer 56

Those >50 years of age 1. If normal an exercise test should be carried out 2. The ABI test should be repeated every 5 years Smoking Hypertension Hyperlipidaemia Diabetes >10 years

Question 57

Who is on the Diabetes Management Team? | 8

Answer 57

``` PA-C Endocrinologist Podiatrist Ophthalmologist/Optometrist Dentist Vascular Surgeon Registered Dietician/Nurse The Patient ```