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Endocrinology > Vascular Complications > Flashcards

Vascular Complications Flashcards

1
Q

Microvascular complications
of DM? 3

Macrovascular complecations of DM?
6

A

Nephropathy
Retinopathy
Neuropathy

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

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

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

A

Nephropathy

American indians and hispanic
african americans

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3
Q

What goes wrong in nephropathy in DM pts?

7

A
  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
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4
Q

Nephropathy steps to ESRD?

5

A
  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
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5
Q

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

A

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

also sugar

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6
Q

What lesions will you encounter in nephropathy?
2

What can you not give in these pts?

A
  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

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7
Q

What is the leading indicator of developing nephropathy?

A

microalbuminuria

Microalbuminuria is the strongest independent risk factor of cardiovascular disease

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8
Q

What is microalbumenia?

The risk of nephropathy is increased by what? 3

A

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

Duration of diabetes
High blood pressure
Smoking

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9
Q

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

A

30-300mg/24hours

> 300g/24hour

  1. Steady drop in GFR
  2. End stage renal disease leading to dialysis
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10
Q

The progression of macroalbumemia can be slowed by what?

4

A
  1. Tight glucose control
  2. Blood pressure control
  3. Protein restriction in diet to decrease proteinuria
  4. Smoking Cessation
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11
Q

What is the key indicator for diebetic nephropathy?

A

microalbumin in the urine

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12
Q

Drugs to help diabetic nephropathy?

4

A
  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

  1. nondihydropyridine calcium channel blockers (Cardizem) and
  2. beta blockers (Lopressor, Tenormin)
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13
Q

HOw are Angiotension II receptor blockers used in nephropathy?
4

A
  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
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14
Q

What diabetic pts should be on ACE inhibitors?

A

ALL DIABETIC PTS

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

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15
Q

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

A

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)

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16
Q

No beta blockers for DM pts. WHy?
3

Diuretics?

A
  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
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17
Q

What happens in non-proliferative retinopathy?
3

WHat will the fundoscopic exam?
3

What will vision be like?

A
  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

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18
Q

Retinopathy - Proliferative
is characterized by what?
2

What can this lead to?
5

A
  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
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19
Q

Retinopathy screening guidelines?

Pregnancy?

A

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

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20
Q

TREATMENT
for DM retinopathy?
5

A
  1. Tight Glucose Control***
  2. Aggressive Treatment of HTN****
  3. Statins decrease lipid deposition
  4. Laser Photocoagulation
  5. Vitrectomy for severe macular edema
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21
Q

Pathophysiologic changes that cause peripheral neuropathy?
2

What is the second finding that leads to this?

A
  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

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22
Q

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

A

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
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23
Q

What do they lose first for peripheral neuropathy?

A

vibration on the foot/dont know its happening

24
Q

Consequences of neuropathy?

7

A
  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
25
Q

What do we have to do each visit and what are we looking for (3)?

Neuro exam of the foot consists of what?
4

A

Detailed foot exam with each visit

  1. Color, sores, pressure areas
  2. Feel for pulses
  3. Capillary refill
  4. Monofilimant test
  5. Reflexes
  6. Vibratory sensation
  7. Proprioception
26
Q

Treatment of neuropathy?
6

(whats the major one?)

A

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)
27
Q

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

A
  1. Prevention of foot ulcers
  2. Daily foot inspection
  3. Appropriate footwear
  4. Drying and nail cutting
  5. Podiatry visit annually!!!!!
28
Q

Autonomic neuropathy
attacks what the most?

What does this cause? 4

What can this lead to?

A

Gastric dysmotility - Gastroparesis

  1. Delayed emptying
  2. Constipation
  3. Nausea and Vomiting
  4. Diarrhea

This can all lead to hyperglycemia

29
Q

Autonomic Neuropathy
can cause what else?
4

A
  1. Orthostatic Hypotension (support hoes)
  2. Cardiac rhythm disturbances
  3. Bladder involvement
  4. Erectile dysfunction
30
Q

How should we treat neuropathy for bladder involvement?

2

A

Retention – Diuretics, self cath

Incontinence - Detrol

31
Q

How should we treat orthostatic hypotension? 2

Gastraperesis? 3

Erectile disfunction? 2

A

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)
32
Q

Mononeuropathies affect which kind of nerves? 2

How do they present?

A

Focal limb or cranial nerve

Present acutely and are self limiting
Cranial nerves commonly involved

33
Q

Which cranial nerves are commonly affected? 4

Limbs that are commonly affected? 3

A

CN 3,4,6, and 7

Limb commonly femoral, sciatic, or peroneal neuropathy

34
Q

Diabetic amyotrophy
is what?

Which ones are affected the most? 2

A

Muscle atrophy and weakness

Anterior thigh
Pelvic girdle

35
Q

Atherosclerosis is what?

A 
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)
36
Q

Progression of atherosclerosis over time?

6

A
  1. Foam cells
  2. Fatty streak
    (first decade)
  3. Intermediate lesion
  4. Atheroma
    (third decade)
  5. Fibrous plaque
  6. Complicated lesion/rupture
    (fourth decade)
37
Q
  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)

A
  1. nitric oxide controlls contractility of the vessels
    • -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
38
Q

Mechanisms of Atherogenesis in Diabetes

6

A
  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
39
Q

Clinical Manifestations of Diabetes and Atherosclerosis
5

What does it depend on?

A
  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

40
Q

What are the final manifestations of Atherosclerosis?

3

A

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!!

41
Q

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

A

ulcerative, very unstable

42
Q

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

A

Coronary Artery Disease

43
Q

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

A

Control hypertension - less than 120/80

44
Q

Cardiovascular, Peripheral and Cerebral prevention?

6

A
  1. Smoking cessation
  2. Management of obesity
  3. Control of Hyperlipidemia
  4. Lifestyle modifications
  5. Exercise
  6. Glycemic Control! (need near normal levels)
45
Q

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?
A
  1. Limit saturated fats to less than 7% of total calories

2. Limit dietary cholesterol to

46
Q

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

A

Statins

control blood glucose

47
Q

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?

A

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

Aspirin

48
Q

Peripheral Vascular Disease
Every office intake form should include:
4

A
  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

49
Q

PVD (macro disease) happens when arteries become?

A

narrow and blood flow decreases in arteriosclerosis

50
Q

PRIMARY SITES

for PVD?

A

Femoral and Popliteal arteries: 80-90%

Tibial and Peroneal arteries: 40-50%

Aorta and Iliac arteries: 30%

51
Q

DIAGNOSIS of PVD?

4

A
  1. History taking
  2. Careful examination of leg and feet
  3. Pulse evaluation
  4. Ankle-brachial index (ABI):
52
Q

PVD leg looks like what?

A

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

dead leg

53
Q

DVT leg looks like what?

A

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

54
Q

How do you calculate the ABI?

A

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

55
Q

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)

A
  1. > 0.90
  2. 0.50-0.90
  3. 0.21-0.49
  4. less than 0.2
56
Q

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

A

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

57
Q

Who is on the Diabetes Management Team?

8

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

Endocrinology (23 decks)

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