Introduction: know how to take precise history and

Introduction:Thisreport is an evaluation of an assessment done on the management of poor controlof type 2 diabetes, by a trainee pharmacist independent prescriber in a GPsurgery. During consultation, a history taking process involving patient’spresenting complaint, medical and drug history, blood test results and diabeticfoot test were examined to reach a known diagnosis (type 2 diabetes). The signsand symptoms of type 2 diabetes, exhibited by the patient are then criticallyanalysed and discussed to understand the pathophysiology of the condition.Diabetesis a rapidly chronic condition that affects large number of peopleworldwide,  causing increase inmorbidity, mortality and healthcare expenses (Hughes et al, 2017). It is a progressive disease that causeshyperglycaemia (increase in blood sugar level) with disruption of carbohydrate,fat, and protein metabolism (Shareef, Fernandes and Samaga, 2015).

It isestimated that more than 4 million in the UK will develop diabetes by 2025 (Bowronet al, 2011). Theclinical role of a pharmacist independent prescriber in a GP surgery involvesdeveloping an effective understanding with patients, carers and otherprescribers, with the application of one’s clinical knowledge and skills, toformulate a diagnosis and treatment plan. As part of the role, thepathophysiology, signs and symptoms of the disease treated, needs to be fullyunderstood, and one should know how to take precise history and do relevantclinical examination when required to treat a condition (General PharmaceuticalCouncil (GPHC), 2016).Therole of pharmacists has evolved considerably over the past three decades andthe focus has changed from product to patient orientation (Shareef, Fernandesand Samaga, 2015).

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This has improved the management of diabetes with hospitaladmission rates going considerably down and enhancing quality of life indiabetic patients (Bowron et al, 2011). With increase in healthcaredemands and predicted shortages of GP’s and practice nurses in the near future,it is important to manage chronic conditions such as diabetes on an ageingpopulation. In tackling patients early on, pharmacist independent prescribersare in an ideal position to manage lifestyle factors that contribute todiabetes, and potentially reverse the trend in line with the NHS five yearforward view (2017).Medicinecompliance among patients with chronic conditions averages only 50% accordingto World Health Organisation (WHO), costing the UK around  £500 million. Clinical pharmacists doingmedication review clinics have made an impact on non-compliance, thereby savingNHS millions of pounds (Stone and Williams, 2015).Moreover,studies conducted so far have shown that patients have valued pharmacistprescribing as an alternative to doctors in primary care. Practice pharmacistcan also reduce the burden on GPs by dealing with patient requests, repeatprescriptions and queries along with booking appointments for essential blood testsand for follow up to titrate the drug regimen, thereby allowing GP’s toconcentrate on other complex matters with regards to patients medicalconditions (Stone and Williams, 2015).

  Known diagnosis: Type 2diabetes.Appendix1 shows that the patient (A.M.) presents with symptoms of type 2 diabetes thatis not under control due to her high HbA1c levels.

Type2 diabetes is a long term metabolic disorder that occurs due to decreasedinsulin secretion by the pancreatic ? cells and insulin resistance, resultingin hyperglycaemia (National Institute for Health and Care Excellence (NICE),2015). The risk factors that increases the chances of developing type 2diabetes are obesity, increasing age, ethnicity and family history (Kumar and Clark,2017). Medical conditions such as hypertension, hyperlipidemia, central obesitycan give rise to or worsen type 2 diabetes (Olokoba, Obateru and Olokoba, 2012).90%of all cases of diabetes mellitus are due to type 2 diabetes. It is prominentlyseen in developing as compared to developed countries (69% vs. 20%) (Ozougwu, et al,2013).

Around 850,000 people in the UK, are presently living with undiagnosedtype 2 diabetes. Estimated 50% of patients have shown evidence of complicationsat the time of diagnosis (Langran et al,2017). Type 2 diabetes is profoundly seen in African, African-Caribbean andSouth Asian family origin. It can happen in any age groups and children arebeing increasingly diagnosed with type 2 diabetes (NICE, 2015).Lifestylefactors and genetics are the main causes of type 2 diabetes. Lifestyle choicessuch as decreased physical activity, cigarette smoking, increased consumptionof alcohol, and sedentary lifestyle play an important role in type 2 diabetes(Olokoba, Obateru and Olokoba, 2012). Obesity is a growing concern in the UKand people who are obese are 80 times more in danger of developing type 2diabetes than normal healthy adults (Bowron etal, 2011).

Intype 2 diabetes, insulin resistance and reduced insulin production in thepatient (A.M.) leads to decrease transport of glucose in to the liver, muscleand fat cells.

The breakdown of fat increases with hyperglycaemia. As a resultof this dysfunction, the increased levels of glucagon and hepatic glucoseproduced during fasting, fail to appropriately suppress with a meal which inturn causes hyperglycaemia. The incretins Gastric inhibitory polypeptide (GIP)and Glucagon-like peptide (GLP-1) that stimulate insulin production aftereating, is also impaired in type 2 diabetic patients. The adipose tissuethrough the secretion of adipocytokines has also been shown  to play a role in insulin resistance and  ? cell dysfunction (Olokoba, Obateru andOlokoba, 2012). Acquisition and Critical Evaluation of Key ClinicalFindings:Calgary-Cambridgemodel was used during the consultation process. There are 5 main steps in thisconsultation (Centre For Pharmacy Postgraduate Education (CPPE), 2014) as shownin appendix 1 .Bylistening and allowing patients to share their views during consultation,practice prescribers are in a better position to instil confidence in patientsand hence improving their adherence to medicines and overall treatment .

Thismodel was used exclusively because the patient (A.M.) had limited informationabout type 2 diabetes. In order to establish an understanding, trust and buildconfidence in her, such an approach was used so that she fully understands thecondition and complies with the treatment (Kaufman, 2008). A.M. camein to see her GP for a diabetic review. On enquiry, she complained of sufferingfrom the following symptoms – Frequenturination (polyuria) which isaffecting her sleep at night, fatigue,genital itching, persistent dry mouth and decreased sensation (neuropathy) in herfeet.

These symptoms are indicative of type 2 diabetes (Clark,Fox and Grandy, 2007). She is taking anti-diabetic medications as shown inappendix 1 (Kumar and Clark, 2017). HbA1cwhich refers to glycated haemoglobin is used as a diagnostic test for diabetes(Vijayakumar et al, 2017).

A.M. has aHbA1c of 112mmol/mol which demonstrates that her blood sugar levelsare not under control (NICE, 2015)A) experiencing frequent urination(polyuria) which is a classic symptom of poor control of type 2 diabetes (Chasenset al, 2002). Polyuria is a conditionwhereby a body urinates excessive and unusual large amounts of urine. It isnormally 3 litres a day where as a healthy adult excretes about one to twolitres (Diabetes., 2017). The prevalence of diseases among the population,causing polyuria are as follows (Jakes and Bhandari, 2013): Common(>1 in 10) – Diabetes mellitus, Diuretics/caffeine/alcohol, Lithium, Heartfailure.Infrequent(1 in 100) – Hypercalcaemia, Hyperthyroidism.Rare(1 in 1000) – Chronic renal failure, Primary polydipsia, Hypokalaemia.Veryrare (<1 in 10,000) - Diabetes insipidus.There are4 mechanisms by which polyuria occurs. One or more of these will be functioning(Sarma, 2013).

Increasedconsumption of fluids such as in stress and anxiety.IncreasedGlomerular Filtration Rate (GFR) that is seen in hyperthyroidism, fever.Increasedvolume of solutes – which occurs in diabetes mellitus, hyperthyroidism,hyperparathyroidism.Failureof the kidney to reabsorb water in Distal Convoluted Tubule (DCT) – such as incentral diabetes insipidus, nephrogenic diabetes insipidus, chronic renalfailure.

 The causeof frequent urination in A.M. is due to osmotic diuresis which occurs whenblood sugar levels goes beyond renal threshold (?180 mg/dL). This results inexcretion of excess glucose via kidneys in urine. Water then follows glucoseexcreted in urine leading to high urine output (Chasens et al, 2002).It isessential to keep a voiding diary, that tracks the measurements of voidingvolumes so as to make a diagnosis  (Kujubu,2009).In the United Kingdom, more than 1 in 20 people areaffected by diabetes mellitus and is the most prevalent cause of polyuria isadults and children (Jakes and Bhandari, 2013).Symptomof high blood sugar level including polyuria, are not always noticeable inchildren and cannot be relied on to determine those with type 2 diabetes.

Therefore it is important to monitor children who are at high risk, even ifsymptoms are absent (Sawatsky, Halipchuk and Wicklow, 2017). B) Fatigue is a frequent and worryingcomplaint among patients with diabetes. In diabetes, it may be related withphysiological occurrence such as hypo- or hyperglycaemia (Jain et al, 2015).The poormanagement of type 2 diabetes along with obesity (A.

M. has a BMI of 32kg/m2) and a lack of physical activity has contributed to excessive levels offatigue in the patient (Fritschi and Quinn, 2010). It has been defined as’personal understanding of a reduced capacity to perform physical and/or mentalactivity that is caused by one or a combination of physiological, psychologicalor lifestyle factors, including change in glucose control, symptoms ofdiabetes, depression, physical inactivity and body mass index ‘ (Park et al, 2015).Althougharguable, fatigue in diabetes can be identified and measured by scales such asFatigue Severity Scale (FSS), Fatigue Assessment Scale (FAS) and Visual AnalogFatigue Scale (VAFS) (Singh and Kluding, 2013)In womenwith type 2 diabetes, fatigue was found to interfere with self reported qualityof life than their healthier counterparts (Fritschi and Quinn, 2010).

Furtherinvestigation is required to study fatigue and its causing factors, for adequatemanagement of diabetes (Singh and Kluding, 2013). C) Genital itching is also one of the symptomsthat A.M. complained of, and is common in patients with type 2 diabetes (NationalHealth Service (NHS).uk, 2017). This symptom occurs when blood glucose levelsare high, leading sugar to be excreted in urine. Glucosecreates a fertile breeding area for bacteria which grows around the genitalsand causes itching (Geerlings et al, 2014).Type2 diabetes mellitus can lead to growing risks of asymptomatic bacteria, urinarytract infections (UTI’S) and non- sexually transmitted genital infections(vulvovaginal infections and balanitis) (Geerlings et al, 2014).

The actual mechanism is not known, but increase inblood sugar levels has been shown to damage various immune systems includingneutrophil operation and antibody function (Hine et al, 2016).Thesymptoms of UTI in diabetics resemble those reported in healthy patients.However, there is an increased risk of acute upper UTI (pyelonephritis) indiabetes, requiring hospital admission (Geerlings et al, 2014).Withregards to fungal infection, the most common organism was candida glabratafollowed by candida albicans in the vaginal swabs of diabetic patients where asC. albicans was profoundly found in non- diabetics (Goswami et al, 2006). D)Diabetes mellitus is associated with a number of oral health problems (Al-Maweriet al, 2013). During the examination,it was noted that A.

M. was suffering from drymouth (xerostomia), another feature of poor control of type 2 diabetes(Lopez-Pintor et al, 2016). Damage ofsalivary gland  in type 2 diabetes canaffect the quality and quantity of saliva (Aitken-Saavedra et al, 2015).The causeof dry mouth in A.M. could be attributed to the impairment of the glandparenchyma, modification of salivary gland microcirculation, dehydration anddisruption of blood glucose levels (Lopez-Pintor et al, 2016).

Thephysical, chemical and biological properties of saliva protects the tissues inthe mouth and helps in speech production, food chewing, food tasting anddigestion. A reduction in salivary production or altering in its quality canresult in poor health related quality of life and can cause oral lesions suchas caries, angular cheilitis, periodontal disease and candidiasis (Aitken-Saavedravet al, 2015).It isimportant for healthcare professionals to understand the various conditions inwhich diabetes mellitus can exhibit orally, so that there is prompt managementand treatment as wells as measures taken to control high blood sugar levels (Bajajet al, 2012).A varietyof  treatment options are available forxerostomia depending on the cause. These include regular sipping of water anduse of various types of sprays and gels (Dyasnoor, Kamath and Khader, 2017). E) Withreference to appendix 1, A.M. was found to have decreased sensation on bothfeet due to increased levels of sugar in the body.

Neuropathy is one of the most frequent microvascular complicationsof diabetes (Kasim et al, 2010). Itis a degenerative disease of the peripheral nerve, that results in symptoms ofpain or paresthesia (burning or pricking sensation in the hands, arm or feet)or a complication arising from neurological shortfall (Boru et al, 2004).Diabeticneuropathy roughly affects around 50% of patients suffering from diabetesmellitus and is associated with serious rise in morbidity and mortality(Cancelliere, 2016).The causeof neuropathy in A.M. is due to the accumulation of sugar (sorbitol andfructose) in schwann cells which may damage the function and structure ofnerves. There is a delayed nerve conduction velocity as a result of functionalchange. The damage to the schwann cells results in change in segmentaldemyelination as the first histological change.

Axons are protected in theearly stages, suggesting the possibility of recovery where as at a later stage,irreversible degeneration of axon occurs (Kumar and Clark, 2017).There arefour main pathways by which hyperglycaemia gives rise to peripheral neuropathy(Cancelliere, 2016):(i) Polyolpathway – The polyol works by acting on the enzyme aldose reductase. When bloodglucose level increases, the enzyme aldose reductase reduces glucose tosorbitol which is then oxidized to fructose. Nicotinic adenine dinucleotide phosphate(NADPH) is consumed as a result of this process. NADPH are involved ingenerating glutathione which in turn plays an important role in loweringintracellular oxidative stress.(ii) Overproductionof advanced glycation end products (AGEs) – AGEs precursors can damage cells by:a) altering intracellular proteins that are involved in gene transcriptionregulation. b) extracellular components modified by AGE precursors alter thecommunication between the matrix and the cells and results in cellulardysfunction.

c) The AGEs alter the circulating proteins and activate the AGEsreceptors, that produces inflammatory cytokines and growth factors, resultingin tissue and cellular damage.(iii)Protein Kinase C activation – Hyperglycaemia increases the release ofdiacylglycerol which activates protein kinase C cofactors. Protein kinase Cexerts it’s  effect on gene expressionincluding decrease sensitivity of endothelial nitric oxide (NO) and increasedresponse of vasoconstrictor endothelin-1.

This leads to alteration in Schwanncell metabolism and finally axonal flow.(iv)Hexosamine pathway flux – when blood glucose level increases intracellularly,glucose is broken down through glycolysis, with the resulting fructose-6phosphate diverted in to the signalling pathway. The enzyme glutaminefructose-6 phosphate amidotransferase (GFAT) then changes fructose-6 phosphateto UDP (uridine phosphate) N-acetyl glucosamine. This attaches to serine andthreonine, leading to alteration in gene expression.

Peripheralneuropathy can appear as a loss of sensation, which can generate neuropathiculcers, and is a common cause of amputation (Davies et al, 2006). The frequency of peripheral neuropathy is generallyrelated with high blood pressure, cigarette smoking and hyperlipidemia (Kasim et al, 2010).Patientswho are type 2 diabetic should be screened for peripheral neuropathy at initialdiagnosis and at least annually by investigating sensory function in the feetand examining ankle reflexes. Sensory function can be assessed by one or moreof the following –  vibration test (usinga tuning fork), temperature, pinpricking of the feet or pressure feeling(Boulton et al, 2005).Thefollowing drugs are recommended for treatment of neuropathic pain includingdiabetic neuropathy – amitriptyline (off-label), duloxetine, gabapentin orpregabalin. The prescribing of more than one neuropathic pain drug at the same timeis not recommended. Capsaicin 0.

075% cream can be considered for those who havelocalized neuropathic pain and who wish to avoid or cannot tolerate oral drugs(Clinical Knowledge Summaries (CKS)

uk, 2017). Reflection:Anadvanced health assessment was done on a patient (A.M.) exhibiting symptoms ofpoor control of type 2 diabetes. This was based on patients complaints aboutsymptoms that she experienced, drug and medical history. Sincethis was the first time I was conducting a consultation, I felt nervous andexcited, trying to make sure that all the required questions and tests are donein order to understand the patient’s signs and symptoms.

Therewas an element of doubt in patient’s mind about her HbA1c levels. Ifelt that I was able to explain to her properly what HbA1c signifiesin terms of her high blood sugar levels in the body. Despite this, the time tomanage the consultation took longer than allocated.Asshown in appendix 1, A.M.

has a HbA1C of 112mmol/mol (18.3mmol/l).If the levels continue to be over 11mmol/l, it can be a contributing factor toDiabetic Ketoacidosis (DKA) (Savage et al,2011). DKA is a life threatening condition that commonly occurs in type 1diabetes, but is now increasingly seen in patients with type 2 diabetes (Misra,Oliver and Dornhorst, 2013). A blood ketone test could have been done for confirm  the presence or absence ofDKA. Self monitoring of blood glucose at home would be beneficial for A.

M., soas to measure blood glucose levels regularly and report the readings to doctorif it carries on to remain high. Sincepatients with type 2 diabetes are prone to urinary tract infections (UTI)  (Geerlings et al, 2014), a urine culture test was done to rule out anyincidences of lower UTI  in A.M. (Bargerand Woolner, 1995). A physical examination involving palpation of thesuprapubic area for tenderness and checking for exclusion of costovertebralangle tenderness (CVAT), could have been done to exclude symptoms of cystitisin A.

M. Further tests involving abdominal and pelvic bimanual palpation forpain and tenderness and a speculum assessment is ideal to eliminate incidencesof upper genital tract infection (Barger and Woolner, 1995). Palpating bladder  is another examination that could have donefor A.M. to determine the degree of incontinence (Barger and Woolner, 1995).Theknowledge I have gained in this health assessment will enable me to tackledifferent symptoms arising from type 2 diabetes. I have learnt that type 2diabetes is a complex condition that sometimes requires further investigationto exclude potential complications.                Conclusion:Type2 diabetes is the most common type of diabetes that causes hyperglycaemia dueto decreased pancreatic insulin production and insulin resistance (Olokoba,Obateru and Olokoba, 2012).

Its prevalence is considerably greater indeveloping than in developed countries (Ozougwu et al, 2013). It is characterised by symptoms such as frequenturination, increased thirst, uncommon weight loss and fatigue (Clark, Fox andGrandy, 2007). Long lasting complications of type 2 diabetes includeretinopathy, nephropathy, peripheral neuropathy and autonomic neuropathy thatcan result in gastrointestinal, genitourinary, cardiovascular and sexual dysfunction.

(Diagnosis and Classification of Diabetes Mellitus, 2010). It can be preventedthrough lifestyle changes, control of diet, overweight and obesity (Olokoba,Obateru and Olokoba, 2012).  


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