Diabetes Mellitus -3 Flashcards
How to diagnose peripheral neuropathy in diabetic patients
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.
Manifestation of peripheral neuropathy- Onset, spread
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.
Manifestations of peripheral neuropathy - Sensory modalities, sensations affected, risk factor for ulceration
- 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.
Other less ccommon signs of peripheral neuropathy
- 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.
Management of peripheral neuropathy
- 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
Diabetic eye disease
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
Diabetic retinopathy
- 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.
Diabetic maculopathy
If the oedema extends into the macula then the retina becomes thickened, visual function deteriorates and there is loss of central vision.
Renal affection in Diabetes leads to increased risk of:
- Renal atherosclerosis
- Urinary tract infections, papillary necrosis
-Glomerular lesions, e.g. from basement membrane thickening and glomerulosclerosis (Diabetic nephropathy).
How common is diabetic neuropathy in type 1 & 2
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.
What does Diabetic nephropathy commonly cause?
Diabetic nephropathy is the most common cause of chronic kidney disease and end-stage kidney disease worldwide.
Describe the pathogenesis of Diabetic nephropathy, beginning from the earlies functioning abnormality
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.
Pathogenesis from increased intraglomerular pressure.
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.
Stages of Diabetic Nephropathy
- Elevated glomerular filtration rate with enlarged kidneys
- Intermittent Microalbuminuria
- Microalbuminuria (persistent(
- Proteinuria and Nephrotic syndrome.
- ESRD
Clinical Features of Diabetic Nephropathy and what this leads us to do.
- 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.
Management of Diabetic Nephropathies
- 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.
What is Diabetic Foot
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.
What is Diabetic Gangrene preceded by?
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.
What is a high risk foot
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
For Prevention of Foot Problems, the diabetic patients should
- 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.
GastroIntestinal Complications of Diabetes - Mouth and Esophagus
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.
Clinical symptoms of Gastroparesis
include early satiety, nausea, vomiting, bloating, and postprandial abdominal fullness in addition to unexplained poor glycemic control despite strong therapeutic efforts.
What supports the diagnosis of Gastroparesis and what’s the Gold standard for diagnosis
- 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.
Treatment of Gastroparesis
Take small meals, avoid fatty meals, use of prokinetics eg metoclopramide and avoid use of GLP-1 based therapies in treatment of diabetes.
