History of presenting complaint

July 29, 2017 History

History of Showing Complaint

Mr A, a 61 year-old type II diabetic adult male, attended Diabetic Clinic for the one-year reappraisal of his medical status. In the clinic, he was seen by a Diabetic Specialist Nurse, a Podiatrist, and a Dietician.

Mr A felt a spot low due to the death of his married woman who passed off about 6 months ago. ‘I am about at that place ‘ , he said. He besides felt dying at times ; his anxiousness mark turned out to be 9 based on the questionnaire he filled. In add-on, he was more exhausted and unenrgetic compared to the last twelvemonth. He admitted non to bask the thing as he used to a few old ages ago. Bing a tobacco user and hapless life activities, he was acquiring progressively breathless excessively. He declined referral to physical exercising programme.

He is holding polydypsia and polyuria particularly at dark clip. However, there were no sings of centripetal neuropathy or diabetic retinopathy as shown by his studies.

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During the audience, his latest blood consequences were discussed and compared with the old 1s. His diet has been non so good, and he is eating two parts of fruit most of the yearss. Advice was reiterated on how unrecorded a healthy life manner and be active.

Mr A was diagnosed with type II DM about 5 old ages ago ; it based on his random glucose degree which was above the normal bound. Initially, he presented with the symptoms of lassitude, polydypsia, and polyuria. After the diagnosing, he did non care that much about his status ; but when one of his friends died as a consequence of complications of diabetes, he took it more earnestly. Now after the decease of his married woman, once more he stopped taking attention of himself, as he mentioned it was his married woman who was cautious about his wellness.

Past Medical History

  • OA
  • Knee hurt and underwent entire articulatio genus replacing in 2003
  • Peptic ulcer disease since 1985
  • Fracture of left thighbone in 1999- athleticss hurt
  • High blood pressure diagnosed in 1995.
  • LVH shown in 1999
  • Appendectomy in 1977
  • No asthma or history of a malignant neoplastic disease.

Drug History

  • No known drug allergic reaction
  • He is taking







Family History

  • Mother was type II DM
  • Father died of bosom onslaught
  • Otherwise nothing of note

Social History

  • Widowed ; Lives entirely.
  • Smokes 18 to 20 ain rolled coffin nails.
  • 16 units of intoxicant per hebdomad but orgy imbibing over the weekends.

Systemic Enquiry

Neurological Nil of note.

Cardiovascular Nil of note except for dyspnea and high blood pressure.

Respiratory See above.

Gastrointestinal Nil of note

Genitourinary Polyuria, but no dysuria or hematuria.

Hematologic Nil of note. No febrilities or asperities

Musculoskeletal See above.

Endocrine DM II, Polydipsia or polyuria.

Reproductive Not disclosed

On Examination

General Observations

  • Not distressed.
  • Alert, but lethargic.
  • Apyrexial ( Temperature – 37.1 0C )
  • BP 180/90 mmHg
  • Pulse 80bmp regular
  • RR 16

Curriculum vitae

  • No roughness hydrops
  • JVP was non raised.
  • HS = I+II+0.
  • Lungs clear


A· everyday


  • Nothing important to observe on motor and centripetal scrutiny.
  • MMSE: non carried out.
  • Cranial nervousnesss integral.
  • Normal tone throughout upper and lower limbs.
  • Grade 5 power on upper and lower limbs.
  • Reflexes nowadays throughout upper and lower limbs.
  • Normal coordination.


  • Normal temperature, no calluss
  • Normal Pulsations are present bilaterally
  • Normal esthesis on both pess ; 10g monofilament was used
  • Vibration esthesis was normal bilaterally


  • No retinopathy or maculopathy
  • Ocular sharp-sightedness: L – 6/9.5 ; R – 6/9.5

Summary of Mr A ‘s Problems

Mr A ‘s medical status was reviewed at the diabetic clinic ; he did non hold any major complication at present, but in order to protect him from future jobs we need to turn to his life manner for alterations. Furthermore, his Urine Albumin to Creatinine ratio was above the normal bound ( i.e. 9.5, normal is & lt ; 2.5 ) .

Differential Diagnosis

Though he was diagnosed with DM II, other derived functions for DM are

Other hormone jobs such as thyroid disease, pituitary inadequacy, Addison ‘s disease, Liver jobs, Anaemia, chronic pancreatitis, etc

Management Plan

  • Check bloods for FBC, U & A ; Es, LFTs, glucose, lipoids, HbA1c, uranalysis
  • Perform pes, oculus scrutiny.
  • Address his anxiousness and depression
  • Weights, Heights, BMI
  • Review medicines
  • Arrange proper referral if required

Brooding Commentary

Complications of Diabetess

The continuance and grade of hyperglycemia play an of import function in finding the forecast, but better predictive factor is HbA1c that should be aimed to be less than 7 % in order to cut down the rate of patterned advance of both retinopathy and nephropathy. The DCCT showed 60 % decrease in developing complication over 9 old ages provided the HbA1c was kept about 7 % .


The exact mechanisms that lead to complications are unclear, but hyperglycemia may take to the undermentioned complications:

  • Non-Enzymatic glycosylation of a broad assortment of proteins such as LDL, Hb, etc
  • Polyol Pathway. The metamorphosis of glucose by interacellular aldose reductase leads to accretion of sorbitol and fruit sugar. This causes cell proliferation and alteration in capillary construction.
  • Abnormal microvascular blood flow impairs blood supply of O and foods. Microvascular occlusion is due to vasoconstrictives.
  • Other factors include the formation of O species and growing factor release from ischaemic tissue.
  • Haemodynamic alterations such as in kidneys.

Macrovascular complication

Diabetes accelerates the procedure of coronary artery disease which can do ischemic bosom disease. Other vascular diseases such as shot is twice likely in diabetics. MI is 3-5 times more likely, and premenstrual diabetic adult females loose their protection from coronary arteria disease. As a consequence of diabetic angiopathy and neuropathy, amputation is 50times as likely.

Cardiovascular factors happening together tend to hold multiplicative consequence:

  • Hypertension – a major hazard factor for bosom disease ; Mr A is hypertensive. Aggressive direction would diminish hazards of both micro and macrovascular diseases.
  • Smoking – though evitable, but hard to give up contributes enormously. Mr A attempted to discontinue smoking a twosome of times but has been unsuccessful in the yesteryear. He has cut down the no. of cigarettes/day which has some good consequence.
  • Lipid abnormalcies – Clinical tests show that there is no safe cut-off for serum cholesterin. Achieving every bit low as possible is good ; HDL to LDL ratio is more of import than the entire cholesterin degree. His HDL degree is non every bit good despite holding been on lipid-lowering medicine.
  • Low dosage acetylsalicylic acid is good is cut downing macrovascular hazard. Mr A is non on Aspirin, which is likely due to his peptic ulcer disease.

Microvascular complications

In contrast to macrovascular disease, microvascular is specific to diabetes. Small blood vass through out the organic structure acquire affected by the disease procedure. Three sites are peculiarly in danger:

  • Retina
  • Nephritic glomeulus
  • Nerve sheaths

Diabetic neuropathy, retinopathy and nephropathy tend to attest 10-20 old ages after the diagnosing. It appears more normally in aged due to progress disease presentation. Diabetic kids of diabetic parents with micovascular complications have 3-5 creases higher hazard of developing microvascular complications than those without complications, demoing familial susceptibleness.

Diabetic Eye Disease

The most common and characteristic signifier of oculus engagement is diabetic retinopathy. Diabetes has been the most common cause of sightlessness in people over the age of 65, but with good followups and one halt clinic the incidence is falling.

The other signifiers of oculus disease may be:

  • The lens – reversible osmotic alterations with bleary vision, or cataracts.
  • New vas formation – in the flag as a late complication
  • External optic paralysiss – particularly of 6th nervus, mononeuritis

Phase of Diabetic Retinopathy:

  • Non-proliferative/ background retinopathy
  • The first abnormalcy seeable through the opthalmoscope is the visual aspect of point bleedings which are capillary microaneurysms. Escape of blood into deep beds appears as smudge bleedings. This is called the background retinopathy.

  • Preproliferative retinopathy
  • The following phase is normally pre-proliferative retinopathy where retinal ischemic alterations appear as cotton wool musca volitanss stand foring hydrops stand foring retinal infarcts. Cotton wools are besides sometimes called soft exudations.

  • Proliferative retinopathy
  • When hypoxia occurs, this stimulates the proliferation of new blood vass. Since these freshly formed vass lack back uping tissue, they bleed easy and can do sightlessness if bleeding occurs in the vitreous. Their breakability besides gives rise to hempen reaction – retinal fibrosis and withdrawal.

    Diabatic Maculopathy

    This may take to blindness in the absence of proliferation and particularly affects older patients with type II diabetes. Macular hydrops is the first mark noticed.

Management of Diabetic oculus disease

The DCCT and UKPDS show that hazard of developing diabetic oculus disease can be reduced by holding good metabolic control of the diabetes. There is no specific intervention for background retinopathy. Smoke and high blood pressure worsen the patterned advance. Early referral to an eye doctor is indispensable in the undermentioned instances:

  • Deteriorating ocular sharp-sightedness
  • Hard exudates infringing sunspot
  • Pre-proliferative ( cotton wool ) phase
  • New vas formation

Maculopathy and proliferative retinopathy is frequently treated by laser photocoagulation.

Diabetic Kidney

Kidney can be damaged in three ways:

  • Glomerular alterations
  • Ischaemia ensuing from hypertrophy of sensory nerve and motor nerve arteriolas
  • Ascending infection

The earlier functional abnormalcy appears in kidney is nephritic hypertrophy due to the raised filtration rate and is associated with the hapless glycaemic control. As the kidney becomes damaged, afferent vass become more vasodilated than the motorial 1s. This farther increases the intra-glomerular force per unit area, and doing more harm and glomerular induration. Therefore, the initial lesions are basement membrane thickener, and increasingly membrane become leaky and protein appears in the piss.

The earliest grounds is ‘microalbuminuria ‘ which is undetectable by urine dipstick.

After many old ages this may come on to intermittent proteinuria followed by relentless albuminurias.

At the phase of relentless albuminuria, the plasma creatinine is normal but the mean patient is merely some 5-10 old ages from terminal phase nephritic failure. This may bring on intermittent nephritic syndrome. Patients with nephropathy frequently show normochromic normocytic anemia and raised ESR.

In add-on to basic diabetic part towards the pathology, infection may besides do terrible harm particularly in adult females. Bladder stasis due to autonomic neuropathy besides contributes to this.


Aggressive intervention of blood force per unit area with a mark below 130/80 has been shown to cut down the rate of patterned advance to nephritic failure. ACEi or ARB are the drugs of choicethese should besides be used in normotensive with relentless microalbuminuria. The usage of them has been shown to cut down proteinurias. Oral hypoglycemic must be avoided as they get excreted in piss.

Diabetic Neuropathy

Diabetess affects the nervousnesss in a figure of ways:

  • Occlusion of vessel nervorum being the premier cause ( particularly in stray mononeuropathies )
  • Metabolic alterations ( particularly in diffuse neuropathy ) due to increased accretion of sorbitol and fructose that may interrupt the map and construction of a nervus. This may do demyelination.

In the early phases, axons are preserved, connoting chances of recovery. There are assorted types of neuropathies associated with DM.

  • Sensory neuropathy
  • Autonomic neuropathy
  • Mononeuritis multiplex
  • Diabetic amyotrophia
  • Early marks are loss of quiver sense and grasp of hurting stimulations. Patient may kick of walking on cotton wool and may free balance.

    Mononeuritis and stray oculus paralysiss are non uncommon particularly the 3rd and 6th nervousnesss. Carpel tunnel syndrome another status affects most of diabetics due to steel entrapment and fluid overload as a consequence of neglecting kidney.

    Autonomic neuropathy affects CVS, doing tachycardia as a consequence of pneumogastric engagement, and arrhythmia. Vagal harm may besides take to gastroparesis. Loss of vesica control and erectile disfunction in males are another jobs associated with autonomic neuropathy.

    The Diabetic Foot

    10-15 % of diabetics develop foot ulcers at some phase in their lives. Many amputations and hospital admittances can be delayed and avoided if proper instruction and follow ups are provided. The manifestation is due to a mixture of:

    • ischaemia
    • infection
    • neuropathy


    Patients need to larn the rules of pes attention in order to cut down the complications. Older patients and particularly with shudders should non cut their ain nails and should see foot doctor on a regular basis. There are four chief menaces to hypodermic tissue:

    • Infection. This can easy impact the pes particularly in the presence of cankerous tegument. Prompt antibiotic therapy is effectual. If infection involves bone ( osteomyelitis ) , regular X raies of the pes are required to supervise advancement.
    • Ischaemia. Doppler should be used to measure the blood flow. Very on occasion by-pass grafting may be required.
    • Abnormal force per unit area. An cankerous site must be non-weight bearing in order to advance healing. This can be supplemented with usage made places and crisp surgical debridment.
    • Wound environment. Dressings are used to absorb and take exudations, maintain moist and forestalling lesions from taints.

    Mr Angstrom does hold these complications at present. He is being given good intervention environing his attention holistically. This will hopefully forestall him developing complications.


    [ 1 ] Parveen Kumar, Michael Clark. Clinical Medicine. Elsevier Saunders. 6th Edition. 2005.

    [ 2 ] Murray Longmore, Ian Wilkinson, et Al. Oxford Handbook of Clinical Medicine. Oxford University Press. 7th Edition. 2007.

    [ 3 ] Talley, O’Connor. Clinical Examination. Elsevier. 5th Edition. 2006.


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