Diabetes Mellitus -3 Flashcards

1
Q

How to diagnose peripheral neuropathy in diabetic patients

A

Diagnosis is made after excluding all causes of peripheral neuropathy

It has gradual onset and progressive course with predominant sensory manifestations.

Diagnosis depends on loss of perception of pain, touch, vibration and pressures in glove and stocking pattern.

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2
Q

Manifestation of peripheral neuropathy- Onset, spread

A

Usually insidious onset with numbness or paresthesia, often found on screening rather than as a presenting problem

Starts in the toes and on the soles of the feet, and then spreads up to mid-shin level, mostly in a symmetrical fashion. Less often, it also involves the fingers and hands.

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3
Q

Manifestations of peripheral neuropathy - Sensory modalities, sensations affected, risk factor for ulceration

A
  • Affects all sensory modalities and results in reduced vibration perception thresholds, pinprick, fine touch, and temperature sensations.
  • Vibration sensation and absent ankle reflexes are often the first features found.
  • Another risk factor for ulceration is the inability to feel a 10 g monofilament.
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4
Q

Other less ccommon signs of peripheral neuropathy

A
  • Less often, the skin is tender or sensitive to touch (hyperesthesia).
  • Painful neuropathy affects up to 5% of a general clinic population.
  • This pain may be sharp, stabbing, or burning in nature and at times very severe.
  • There may also be some wasting of the intrinsic muscles of the foot with clawing of the toes.
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5
Q

Management of peripheral neuropathy

A
  • Tight glycemic control.
  • Alpha Lipoic acid and Benfotiamine can help to improve nerve functions - contained in some multivitamins or alone
    Drugs that reduce pain
    e.g. tricyclic antidepressants - amitryptilin, profanel
  • gabapentin, pregabalin (anti-convulsants)
  • serotonin noradrenaline reuptake inhibitors (duloxetine) - also used for depression
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6
Q

Diabetic eye disease

A

Diabetic retinopathy
_ Cataract which develops earlier in diabetes than in the general population.
- Error of refraction due to fluctuations in blood sugar leading to osmotic changes within the lens.
- Ocular Nerve palsies: Cranial nerves VI and III are the most commonly affected. These nerve palsies usually recover spontaneously within a period of 3–6 months

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7
Q

Diabetic retinopathy

A
  • is the commonest cause of blindness worldwide.
  • it increases with the duration of diabetes.
  • Progression of retinopathy is often accelerated with poor control of diabetes and blood pressure.
  • Diabetic retinopathy is asymptomatic until it becomes advanced,
    fundus examination should be routinely done at least annually.
  • It can be either background - macular lesions (Non proliferative) or Proliferative - new vessels are formed.
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8
Q

Diabetic maculopathy

A

If the oedema extends into the macula then the retina becomes thickened, visual function deteriorates and there is loss of central vision.

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9
Q

Renal affection in Diabetes leads to increased risk of:

A
  • Renal atherosclerosis
  • Urinary tract infections, papillary necrosis
    -Glomerular lesions, e.g. from basement membrane thickening and glomerulosclerosis (Diabetic nephropathy).
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10
Q

How common is diabetic neuropathy in type 1 & 2

A

Approximately 40% of patients with type 1 and 20% with type 2 diabetes develop nephropathy.

Some centers have reported a falling incidence rate of diabetic nephropathy in type 1 diabetes - because type 1 need insulin, which is given freely, glucometer, glucose strips and eye checks are all free. So it’s a reflection of good quality local care for diabetes.

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11
Q

What does Diabetic nephropathy commonly cause?

A

Diabetic nephropathy is the most common cause of chronic kidney disease and end-stage kidney disease worldwide.

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12
Q

Describe the pathogenesis of Diabetic nephropathy, beginning from the earlies functioning abnormality

A

The earliest functional abnormality in the diabetic kidney is renal hypertrophy associated with a raised glomerular filtration rate.
As the kidney becomes damaged by diabetes, the afferent arteriole becomes vasodilated to a greater extent than the efferent glomerular arteriole. This increases the intraglomerular filtration pressure.

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13
Q

Pathogenesis from increased intraglomerular pressure.

A

This increased intraglomerular pressure leads to increased shearing forces locally which are thought to contribute to mesangial cell hypertrophy and increased secretion of extracellular mesangial matrix material.

  • This process eventually leads to glomerular sclerosis. The initial structural lesion in the glomerulus is thickening of the basement membrane.
    Associated changes result in disruption of the protein cross-linkages which normally make the membrane an effective filter.
  • Consequencely, there is a progressive leak of large molecules (particularly protein) into the urine - Massive proteinuria.
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14
Q

Stages of Diabetic Nephropathy

A
  • Elevated glomerular filtration rate with enlarged kidneys
  • Intermittent Microalbuminuria
  • Microalbuminuria (persistent(
  • Proteinuria and Nephrotic syndrome.
  • ESRD
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15
Q

Clinical Features of Diabetic Nephropathy and what this leads us to do.

A
  • Clinical features are usually absent until advanced chronic kidney disease develops.
  • Therefore, we should evaluate urinary albumin excretion (microalbuminuria) annually in all subjects with diabetes.
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16
Q

Management of Diabetic Nephropathies

A
  • Optimal control of blood glucose and blood pressure.
  • Avoid high protein intake.
  • ACE inhibitors should be started and titrated to full dose in all patients with confirmed nephropathy (including those with microalbuminuria alone).
  • If ACE inhibitors are not tolerated, angiotensin ll receptor antagonists should be substituted.
  • Avoid taking Contrast agents containing Iodine and NSAIDs.
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17
Q

What is Diabetic Foot

A

The term diabetic foot indicates any foot pathology that results directly from diabetes or its long-term complications.

In the past, the term diabetic foot was used to indicate gangrene and amputations.

Then, it was realized that Diabetic gangrene do not occur suddenly but is preceded by several stages.

18
Q

What is Diabetic Gangrene preceded by?

A

Usually preceded by advanced foot pathology e.g.
- Diabetic Foot ulcers, diabetic foot Infections
- critical limb ischemia and Charcot foot.
* Also, advanced foot pathology didn’t occur suddenly but is preceded by risk factors for the more severe foot pathology.

19
Q

What is a high risk foot

A

The foot that has developed one or more of the following risk factors:
- Peripheral Neuropathy
- Peripheral arterial disease
- Foot Deformity
- Trauma
- Callus
- Skin and Nail pathology

20
Q

For Prevention of Foot Problems, the diabetic patients should

A
  • Achieve tight control of blood glucose levels
  • Annual foot screening - by patient or family member or chiropractic nurse
  • Report any changes immediately to healthcare professional.
  • Engage in a simple daily foot care
    by washing and drying between toes, moisturizing and checking for abnormalities.
21
Q

GastroIntestinal Complications of Diabetes - Mouth and Esophagus

A

Mouth:
- periodontal disease with looseness of the teeth and gum inflammation.
Esophagus:
- gastroesophageal reflux disease (GERD) caused by autonomic neuropathy with decreased lower esophageal sphincter (LES) pressure or delayed gastric emptying.

22
Q

Clinical symptoms of Gastroparesis

A

include early satiety, nausea, vomiting, bloating, and postprandial abdominal fullness in addition to unexplained poor glycemic control despite strong therapeutic efforts.

23
Q

What supports the diagnosis of Gastroparesis and what’s the Gold standard for diagnosis

A
  • The presence of residual food in the stomach after an overnight fast during upper gastrointestinal endoscopy supports the diagnosis.
  • The traditional “gold standard” to establish the diagnosis of gastroparesis is scintigraphic measurement of gastric emptying.
24
Q

Treatment of Gastroparesis

A

Take small meals, avoid fatty meals, use of prokinetics eg metoclopramide and avoid use of GLP-1 based therapies in treatment of diabetes.

25
Q

Signs and symptoms of Diabetic enteropathy

A
  • Present with diarrhea which is watery and painless, occurs at night, and may be associated with fecal incontinence.
  • Bouts of diarrhea can be episodic with intermittent normal bowel habits or even alternating with periods of constipation.
  • Steatorrhea can occur due to bacterial overgrowth.
26
Q

Management and symptomatic therapy of Diabetic enteropathy

A
  • Exclude other causes of diarrhea especially infectious ones.
  • Correction of water and electrolyte imbalances
  • Tight control of blood glucose
  • And restoration of possible nutritional deficiencies.

Symptomatic therapy
- antidiarrheal agents such as loperamide.

27
Q

Diabetic enteropathy - Liver and Gall Bladder findings

A

Liver:
Non alcoholic fatty liver including non alcoholic steato- hepatitis.

Gall bladder:
cholecystitis including emphysematous cholecystitis.

28
Q

Skin & Diabetes (Acanthosis, Necrobiosis, Dermopathy)

A
  • Acanthosis negricans:
    Velvety hyperpigmented plaques in neck, back and body folds
  • Necrobiosis lipoidica diabeticorum
    Painful violaceous plaque with central yellowish area surrounded by brownish border usually on shin of the leg. Central ulceration may occur.
  • Diabetic dermopathy:
    Painless reddish papules usually on the shin of the tibia heal leaving atrophic scarred hyperpigmented macules.
29
Q

Skin changes and diabetes (Bullosis and Granuloma)

A
  • Bullosis diabeticorum:
    Non-inflamed bullae with sterile fluid heal within 2-3 weeks without residual scarring.
  • Granuloma annulare:
    Ring shaped papules with depressed centers usually on dorsum of the hand and arm.
30
Q

Hyperlipidemia and Diabetes (Xanthelasma, xanthoma, Fungal)

A

Eruptive xanthoma:
yellow papules or nodules usually on extensor surfaces.

Xanthelasma:
yellow plaques that usually appear on the medial aspects of the eyelids.

Skin infections:
Fungal:
Candidal intertrigo and paronychia, dermatophytes causing powdery white lesions especially between fingers.

31
Q

Hyperlipidemia and skin infections

A

Skin infections:
Fungal:
Candidal intertrigo and paronychia, dermatophytes causing powdery white lesions especially between fingers.

Bacterial:
Carbuncles, furuncles, abscesses, cellulitis, erysipelas.

32
Q

Skin and Anti-diabetic medications

A
  • Insulin:
    Lipoatrophy and lipohypertrophy.
  • Sulphonylurea:
    Drug eruptions.
33
Q

Management of DM - Lifestyle, Oral anti-diabetic agents, insulin

A

Life style modification (including medically assisted weight loss)

Weight loss (for overweight and obese patients): Reduce by 5% to 10%
Physical activity: 150 min/week of moderate-intensity exercise (eg, brisk walking) plus flexibility and strength training.

Oral anti-diabetic agents
Insulin

34
Q

Diet and Diabetes Management

A
  • Eat regular meals and snacks; avoid fasting to lose weight
  • Consume plant-based diet (high in fiber, low calories/glycemic index, and high in phytochemicals/antioxidants)
  • Incorporate beliefs and culture into discussions
  • Keep physician-patient discussions informal.
35
Q

Healthy Eating Recommendation and Diabetes - Carbohydrate and Fat

A

*Carbohydrate:
- Specify healthful carbohydrates (fresh fruits and vegetables, legumes, whole grains); target 7-10 servings per day
- Preferentially consume lower-glycemic index foods (glycemic index score <55 out of 100: multigrain bread, pumpernickel bread, whole oats, legumes, apple, lentils, chickpeas, mango, yams, brown rice)
*Fat
- Specify healthful fats; containing poly-unsaturated fatty acids (nuts, avocado, certain plant oils, fish)
- Limit saturated fats (butter, fatty red meats, tropical plant oils, fast foods) and trans fat; choose fat-free or low-fat dairy products.

36
Q

Healthy Eating Recommendation and Diabetes - Protein, Micronutrients, Vitamin Supplements

A
  • Protein:
    Consume protein in foods with low saturated fats (fish, egg whites, beans); there is no need to avoid animal protein
    Avoid or limit processed meats
  • Micronutrients
    Routine supplementation is not necessary; a healthful eating meal plan can generally provide sufficient micronutrients
    Chromium; vanadium; magnesium; vitamins A, C, and E; and CoQ10 are not recommended for glycemic control
  • Vitamin supplements should be recommended to patients at risk of insufficiency or deficiency.
37
Q

Why Insulin therapy?

A

Insulin therapy is appropriate for patients with type (1) and type (2) diabetes.
The absolute insulin deficiency of established type (1) diabetes can only be treated effectively with multiple daily insulin injections

38
Q

Indications of insulin therapy in type (2) diabetes:

A
  • Patients unable to adequately control their blood glucose levels with maximum dose combinations of oral glucose lowering medications.
  • Patients undergoing surgery
  • Patients with renal or hepatic disease or allergies.
  • Women who are planning pregnancy or who are already pregnant.
  • Critically ill hospitalized patients.
39
Q

Insulin therapy is often instituted early for type (2) diabetes patients who:

A
  • Can not control their diabetes with diet and exercise
  • Are highly symptomatic with marked catabolic state.
  • Are newly diagnosed with very high glucose level or high HbA1C
40
Q

The first step in choosing an insulin regimen is to establish glycemic goals for your patients; this means that one half of SHBG results of all within the following ranges:

A

Preprandial 5 - 7.2 mmol/l
Bedtime 5.5 – 7.8 mmol/l
Postprandial <10 mmol/l

41
Q

Why is it important to individualize the patient’s age, health states, and history of significant hypoglycemia, life styles and personal goals - an example?

A

For example, it would be reasonable to modify pre-prandial goal to 5.5- 7.8 mmol/l or higher for a type (1) diabetes patients with severe or hypoglycemia unawareness.

42
Q

Insulin Regimen for treating diabetes

A

2 injections /day

Disadvantages: NPH (Neutral Protamine Hagedorn) intermediate acting given at supper peaks during the night
And often not last overnight until breakfast Leading to nocturnal hypoglycemia and/or
And high breakfast glucose levels.
1) Inflexibility in dealing with midday glucose levels.