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Endocrine and Reproductive Systems > CM- Complications of Diabetes > Flashcards

CM- Complications of Diabetes Flashcards

1
Q

What are the 3 microvascular complications of DM?

A
  1. Diabetic retinopathy
  2. Diabetic nephropathy
  3. diabetic neuropathy
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2
Q

What are the 3 macrovascular complications of DM?

A
  1. heart disease
  2. stroke/ cerebrovascular
  3. poor peripheral vascular circulation [poor circulation to the feet–> amputation]
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3
Q

What are the 6 risk factors for diabetic complications?

A
  1. duration of disease
  2. hyperglycemia
  3. blood pressure
  4. genetic predisposition
  5. current smoker
  6. compliance with therapy
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4
Q

Describe what is seen with non-proliferative diabetic retinopathy.

A
  1. microaneurysms [small circular red dots]
  2. capillary non-perfusion
  3. leakage
  4. blood
  5. hard exudates [yellow, sharply defined]
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5
Q

What is seen in proliferative diabetic retinopathy?

A
  1. new vessels
  2. fibrous tissue
  3. vitreous hemorrhage
  4. traction retinal detachment
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6
Q

What is the most important risk factor for the development of diabetic retinopathy?

A

duration of diabetes

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7
Q

A patient has just been diagnosed with type I diabetes. Recommend whether, how often, and why the patient needs to be scheduled for an eye exam.

A

The patient should be scheduled for an initial consultation eye exam 3-5 years after the diagnosis of diabetes.

Children, adolescents and adults without retinopathy should have a yearly followup.

Non-proliferative retinopathy = 6 month
Pre-proliferative = 3 months
Proliferative = individualized

Why?

  • diabetic retinopathy is the leading cause of new blindness in the US
  • it can be improved with good blood glucose control
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8
Q

A patient has been diagnosed with type II diabetes. Recommend whether, how often, and why the patient needs to be scheduled for an eye exam.

A

Initial consultation: right away for all patients

Followup:

Yearly = children, adolescents, adults without retinopathy
6 months = non-proliferative
3 months = pre-proliferative
Individualized = proliferative.

Why?

  • diabetic retinopathy is the leading cause of new blindness in the US and increases with length of duration of disease
  • it can be improved with good glucose control
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9
Q

A diabetic woman is planning pregnancy. What should she have done and what should she be counseled for?

A

She should have a comprehensive eye exam and should be counseled on the risks of development and progression of diabetic retinopathy.

Eye exam should happen in the first trimester with close followup throughout pregnancy and 1 year postpartum

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10
Q

What are risk factors other than glucose control that can predispose to the development of diabetic retinopathy.

A
  1. high blood pressure
  2. pregnancy
  3. smoking
  4. genetics
  5. duration of diabetes
  6. puberty
  7. nephropathy
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11
Q

What are early signs of diabetic nephropathy?

A
  1. genetic determinants
  2. elevated BP
  3. microalbuminuria
  4. hyperfiltration [elevated Cr clearance]
  5. alterations to glomerular structure
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12
Q

What are the 3 interventions of early diabetic nephropathy?

A
  1. Glycemic control
  2. ACE/ARB ** first line
  3. low protein diets
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13
Q

A patient with type 1 diabetes has hypertension and albuminuria. What has been show to delay the progression of the nephropathy?

A

ACEI

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14
Q

A patient has type 2 diabetes, hypertension and microalbuminuria. What has been shown to delay the progression to macroalbuminuria?

A

ACEI and ARB

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15
Q

A patient has type 2 diabetes, hypertension, macroalbuminuria and renal insufficiency [Cr >1.5]. What has been shown to delay the progression of the nephropathy?

A

ARB

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16
Q

A patient presents with paresthesias, pain, impaired sensation, and nocturnal exacerbations in their hands and feet. They have absent knee and ankle reflexes. Their motor involvement is variable. What is this presentation>?

A

distal symmetrical polyneuropathy

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17
Q

What causes diabetic neuropathic ulcers?

Where do ulcers most commonly form?

A

Caused by the loss of protective sensation and repetitive trauma.
They most frequently occur in areas of increased pressure [metatarsal heads because of hammer-claw toe deformity, under calluses]

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18
Q

What are five risk factors for the development of diabetic neuropathy?

A
  1. genetic predisposition
  2. male gender
  3. height
  4. alcohol
  5. hyperglycemia
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19
Q

What are the 5 steps in evaluation of diabetic neuropathy?

A
  1. Clinical [history, PE]
  2. electrophysiological tests
  3. quantitative sensory tests
    - vibratory
    - thermal
    - tactile
    - electrical threshold
  4. autonomic nervous system tests
  5. nerve biopsy
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20
Q

What is the value in quantitative sensory tests for diabetic neuropathy?

A
  1. allows longitudinal, non-invasive assessment
  2. testing is objective and assesses thresholds
  3. forced choice method of testing
  4. sensory threshold = correct stimulus detection 50% of the time
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21
Q

What does the vibratory perception threshold assess?

What does thermal perception threshold assess?

A 
Vibration = measures large nerve fiber integrity.
Thermal = measures small nerve fiber integrity
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22
Q

What has been shown to lower the incidence of microvascular disease? What has been shown to reduce the incidence of macrovascular disease?

A

Microvascular is reduced by controlling serum glucose levels.

Macrovascular is controlled by treating associated CV risk factors [lowering LDL, BP control, aspirin, smoking cessation]

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23
Q

What are the 2 acute complications of diabetes?
Which is seen in type 1 diabetics?
Which is seen in type 2?

A

Diabetic Ketoacidosis

  • 2/3 DM type 1
  • 1/3 DM type 2

Hyperosmolar Hyperglycemin State (HHS)
- type 2

24
Q

What is the leading cause of diabetes related deaths?

A

Heart disease

25
Q

What is the effect of diabetes on the mouth?

A

It can cause periodontal disease with loss of attachment of the gums to the teeth 5mm or more

26
Q

What are the complications of pregnancy associated with diabetes?
1st, 2nd, 3rd trimesters?

A

Poorly controlled diabetes at conception and during the first trimester can cause major birth defects and abortions.

Poorly controlled diabetes in the 2nd and 3rd trimester can lead to excessively large babies and pose a risk to the mother/child .

27
Q

How often should patients be self-monitoring their glucose levels with hand held meter of SMBG or CBG [capillary blood glucose]?

A

Atleast 2-4x a day but preferably 6-10.

  1. fasting glucose upon waking
  2. prior to evening meal
  3. at least one reading 2hr postprandial
28
Q

What does HBA1c show?
What can falsely lower the levels?
What can falsely raise the levels?

A

It is measured at each clinic visit and gives an idea of how well the glucose control has been over the prior 3 months [because it is glycosylated from RBC which last about 3months]

Hemoglobinopathies and things that decrease RBC lifespan can falsely lower the HBA1c.
Polythycemia can falsely elevate HBA1c.

29
Q

What should the glycemic control, HBA1c, blood pressure and lipid panel goals be for diabetics?

A

Glycemic control:

  1. fasting >125, random >200
  2. HBA1c = 7%
  3. BP 40, TG <150
30
Q

A patient presents with polyuria and polydipsia. Physical exam reveals Kussmaul respirations, signs of dehydration, and “fruity” breath. What is the likely problem and what causes it?

A

DKA is defined as hyperglycemia, ketosis, metabolic acidosis.

An absolute insulin deficiency leads to lipolysis and the development of ketogenesis.
Counterregulatory events increase hypoglycemia and dehydration

31
Q

What should be done upon admission for patients with DKA?

A
  1. aggressive fluid resuscitation [saline, lactated ringer, insulin drip]
  2. order antibody panel for type 1 [GAD, ICA, IA2]
  3. evaluate electrolytes [add 1.6 to Na for every 100 glucose above 100]
  4. carefully monitor and replenish electrolytes [including phosphorus and magnesium]
32
Q

What is the effect of DKA on potassium?

A

The person will be hyperkalemic because the metabolic acidosis will pull K out of cells, but the body will also be losing K in urine.

The patient will be hyperkalemic but total body K depleted.

33
Q

What are major precipitating causes of DKA and HHS?

A
  1. trauma
  2. poor medicine compliance
  3. infection
  4. drugs [roids, thiazides, antipsych, etc]
  5. alcohol
  6. ischemia [PE, MI, CVA]
  7. pregnancy
  8. dehydration
34
Q

What lab values help you determine that DKA is resolved?

A

Blood glucose 7.3

  1. normalization of anion gap {>12}
  2. bicarb over or equal 15
35
Q

A patient presents with severe hyperglycemia, hyperosmolarity, and dehydration with NO ketoacidosis. They have polyuria and polydipsia. They seem lethargic, weak and confused. What do they likely have?
Why don’t they have ketoacidosis?

A

hyperosmolar hyperglycemic state.
This usually occurs in type 2 diabetics and they have enough residual insulin to inhibit lipolysis [so there are no FFA to be made into ketones]

36
Q

What marks the resolution of HHS?

A
  1. normalization of serum osmolarity

2. restoration of baseline mental status

37
Q

What is the earliest finding in diabetic retinopathy? What pathologically causes it?
Besides diabetes, what other diseases can have these?

A

Microaneurysms- small red, circular dots
Pathologically they are outpouches of the retinal capillaries
They can also be found in:
1. sickle cell
2. branch vein occlusion
3. carotid artery disease
4 .severe hypertension

38
Q

Describe the appearance of hard exudate. How does it arrange in the eye?
What can it lead to if it is in the posterior part of the retina?

A

They are sharply defined yellow and variable in size. They can be aggregate, scattered, or ring-like in configuration.
If the hard exudate is in the posterior of the retina, it can lead to macular edema –> loss of visual acuity

39
Q

What defines macular edema?

A
  1. thickening of the retina near the center of the macula
  2. hard exudate near the center of the macula

It is rarely found in the first 9 years after being dosed with diabetes

40
Q

What are the findings associated with “pre-proliferative retinopathy”?

A
  1. Retinal ischemia–>”cotton wool” spots that are whitish grey on the retina
  2. Intra-retinal microvascular abnormalities [IRMA] in areas of capillary non-perfusion
  3. venous beading and duplication
  4. intra-retinal hemorrhage
41
Q

Describe the neovascularization associated with proliferative retinopathy.

A

The new vessels appear as fine tufts on the surface of the retina near the optic nerve head.
Growth is confined to the outer layer of the retina.

Because they are abnormal they can hemorrhage into the vitreous and cause contracture.

42
Q

What about proliferative retinopathy can lead to loss of vision?

A

Fibrous tissue is associated with the growth of new vessels.
It the fibrovascular tissue contracts, it can drag the sensory area and the macula and result in vision loss

43
Q

For type 1 diabetes, when does the highest incidence of proliferative retinopathy occur?

A

9-15 years of diabetes

44
Q

What is the ethnic difference in prevalence for diabetic retinopathy?

A

It is considerably higher in Mexican Americans

45
Q

What is treatment for diabetic retinopathy?

A

Medical:

  1. glycemic control [microvascular control]
  2. aspirin and dipyridamole [macrovascular control]

Surgical:

  1. photocoagulation
  2. vitrectomy
46
Q

About how long does it take for a person to develop ESRD from diabetes?

A

0-2 years = high GFR, albuminuria, kidney size
2-5 = BM thickening, mesangium expansion
15-18 = onset of proteinuria, hypertension
18-20 = rising Cr
20-22 = ESRD

47
Q

One of the early signs of diabetic nephropathy is microalbuminuria. How is this measured?
What is normal, microalbuminuria, and overt proteinuria values?
What is the criteria to diagnose microalbuminuria?

A

Measured by:

  1. 24hr urine sample
  2. spot albumin/Cr ratio

Normal = 300 microns/min

Diagnose with 2/3 urine samples in 6 months being +

48
Q

When making a diagnosis of diabetic nephropathy and microalbuminuria, you must have + tests 2/3 time over 6 months. Why is that?

A

Because there are other causes for transient microalbuminuria like:

  1. poor glycemic control
  2. UTI
  3. physical exercise
  4. high protein uptake
  5. cardiac insufficiency
49
Q

When should ACE/ARB be used for a diabetic?

A

Only if they have:

  1. hypertension
  2. albuminuria
  3. CV risk factors
50
Q

What are the current recommendations for detection and management of diabetic renal disease?

A

Annual measures of urinary albumin excretion starting:

  1. after 5 years in type 1 diabetes
  2. time of diagnosis in type 2

Aggressive glycemic control
Early/aggressive ACE/ARB use

51
Q

What is the most frequent complication of diabetes?

A

Neuropathy

52
Q

If a patient presents with:

  • resting tachycardia
  • exercise intolerance
  • orthostatic hypotension
  • constipation
  • gastroparesis
  • ED

What do you want to consider?

A

This is autonomic neuropathy associated with diabetes

53
Q

How is diabetic neuropathy monitored?

How is it treated?

A
  1. annual screening of atleast one of the following:
  • temp perception
  • vibration perception [foot ulcer predictor]
  • 10g pressure sensation on dorsum of foot [foot ulcer predictor]
  • ankle reflexes

Treated with improved glycemic control, dietary myoinositol, drugs

54
Q

The presence of elevated LDL, hypertension, microalbuminuria, retinopathy and ED should all precipitate an evaluation for what?

A

vascular disease in all people with type 1 or 2 diabetes regardless of age or duration of disease

55
Q

What would be the criteria for starting statin therapy in diabetics?

A
  1. type 2
  2. no clinical history of coronary, cerebrovascular or peripheral vascular disease BUT one of the following apply:
  • HTN
  • retinopathy, nephropathy
  • microalbuminuria
  • smokier
56
Q

What are the 5 components of CVD risk management for diabetics?

A
  1. BP control <140/80
  2. aspirin therapy
  3. cessation of smoking
  4. weight management
  5. lipid management

Endocrine and Reproductive Systems (27 decks)

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