Overview And Treatment Of Diabetes Mellitus Biology Essay

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Miss KP was a 24-year-old hospital cleaner with diabetes mellitus, which she had developed at the age of 18. Her usual treatment was Actrapid insulin, 8 units 3 times daily 30 minutes before meals, and Actrraphane insulin, 16 units at bedtime. On the day of admission to hospital she had presented to A&E department with a three-day history of dysuria, loin pain and feeling feverish. She felt unwell, had lost her appetite, and because she was not eating she had not taken any insulin for 24 hours.

In A&E the casualty officer noted that she was disorientated in time and space, she had Kussmaul's respiration and he could smell ketones on her breath. He diagnosed a urinary tract infection and arranged some blood tests and a dipstix urine test, which showed:


Glucose 28mmol/L (Normal fasting 3.9 to 6.1)

Na⁺ 145mmol/L (Normal range 136 to 146)

K⁺ 3.4 mmol/L (Normal range 3.5 to 5.1)


Ketones: ++++

Blood: ++

Protein: ++

Arterial Blood:

pH: 7.1 (Normal range 7.38 to 7.42)

HCO₃⁻ 8mmol/L (Normal range 22-29)

pOâ‚‚ 13.0 kPa (Normal range 10 to 13.4)

pCOâ‚‚ 3.6kPa (Normal range 5 to 5.5)

She remained in hospital for 5 days receiving treatment, which included monitoring of potassium levels as well as re-hydration and insulin administration. Although she usually attended the diabetic clinic regularly, prior to discharge from hospital she had a further education session with diabetes specialist nurses.

Learning Objectives

Describe Type 1 diabetes. Explain the effect of diabetes on kidney function.

Explain how urinary tract infection is linked to diabetes mellitus.

Explain the signs and the symptoms

Explain the test results including ketoacidosis.

Describe the effect of insulin on glucose metabolism.

Explain the treatment and the prognosis. (What is the importance of management? What is the role of specialist nurse?)

1-Describe Type 1 diabetes. Explain the effect of diabetes on kidney function.

Type 1 diabetes is mainly caused by body attacking its own β cells in islets of Langerhans-pancreas, creating damage and resulting in synthesising insufficient insulin. "Type 1 diabetes is an autoimmune disorder. Autoantibodies to islet cells, histological evidence that β cells are subject to immune attack."(J.Naish et al.,Medical Sciences, Page 559, Saunders Elsevier) Insulin supports glucose take up of liver, fat and muscle cells from blood. Therefore lack of insulin will cause an increase in blood glucose levels, i.e. diabetes mellitus. Polyuria (urinating frequently), tiredness, thirstiness and loss of weight are classical symptoms of diabetes mellitus. "WHO criteria for diagnosis are: Fasting plasma glucose > 7.0mmol/L, random plasma glucose>11.1mmol/L."(Kumar and Clark, Clinical Medicine, Page 1036, 7th Edition, Saunders Elsevier) Management can be accomplished through a healthy diet and lifestyle plus regular insulin injections. These injections can be short-acting or long-acting. Short-acting insulin (e.g.Actrapid) supplies insulin to the body for a short time and is injected previous to mealtime numerous periods in a day. Long-acting insulin (e.g. Actraphane) supplies insulin to the body for longer period and is given once-a-day. Diabetes type 1 onset is usually observed at young ages and needs a lifelong management plan. The graph below (Diagram 1) provides information about incidence of diabetes.

Diabetes indicates elevated levels of glucose in blood plasma. Glucose is adequately small to pass through glomerulus hence sugar reabsorption in kidney takes place in proximal convoluted tubule by means of Na⁺/Glucose cotransporter. "In first part of PCT, there are SGLT2 carriers, have a low affinity for glucose, so they will work when there is high sugar content in lumen. In later PCT segment, concentration of sugar is low, SGLT1 carriers, which have a high affinity for glucose, will move the sugar against a concentration gradient to recover molecules from the filtrate into blood." (J.Naish et al.,Medical Sciences, Page 741, Saunders Elsevier) When the blood plasma levels of glucose is very elevated, every one of these carriers will be taken, and there will not be sufficient carriers for the entire glucose molecules to be filtered. Thus, an extent of glucose will not be reabsorbed, and will be present in urine. Presence of glucose in urine is named as glycosuria. "Glycosuria occurs when blood glucose levels exceed the renal threshold for glucose, 10mmol/L."(Williams and Pickup, Handbook of Diabetes, 2nd edition, Page 68, Blackwell Science) In addition to diabetes, glycosuria is seen in any damage to proximal convoluted tubule preventing its absorptive function or damaging the co-transporters on the lumen wall. The picture below (Diagram 2) shows the transport of glucose through proximal convoluted tubule lumen. Together with excretion of glucose, water is also excreted due to osmosis. This caused dehydration in body. Diabetes induces extra work and stress on kidneys, damage blood vessels nearby causing diabetic kidney disease and in long term, causes kidney damage.

2-Explain how urinary tract infection is linked to diabetes mellitus.

Patient having high levels of glucose in blood plasma indicates that glucose will be present in urine. For that reason, there will be sugar traces in the urinary tract since urine in the company of glucose will pass all the way through the urinary pathway. This condition generates a favourable habitat for bacteria to inhabit and cultivate. In addition, diabetes type 1 is an autoimmune disorder and diabetes causes immunological modifications in body. Immune system is deprived resulting in diabetes type 1 patients being more probable to develop infections. Therefore, diabetes patients are more prone to urinary tract infections.

3-Explain the signs and the symptoms

The symptoms patient present are both due to poor diabetes management and urinary tract infection. Dysuria i.e. painful urination and feverish feeling are possibly due to bacteria being present in urinary tract and inflammatory response against urinary tract infection. Loin pain is due to bladder statis occurring in urinary tract infection.

Unwell feeling is end result of urinary tract infection, fasting, vast increase in blood glucose levels and ketoacidosis all together. When there is no insulin present, the contradicting hormones are in use with opposite actions of insulin. They further increase blood glucose levels and cause loss of appetite. Also, existence of ketone bodies in body and incidence of electrolyte disturbance can generate signal in vomiting centre causing nausea grounding loss of appetite and unwell feeling.

Ketone smell in breath is the odour of exhaled acetone which is the end product of ketone bodies formed during hyperglycaemia. However, this is not a consistent finding mode since everybody may not be capable of smelling ketone bodies on a patient and it can be easily mixed with other odours. Kussmaul's respiration is "an abnormal respiratory pattern characterized by rapid, deep breathing, often seen in patients with metabolic acidosis."( http://medical-dictionary.thefreedictionary.com/ Kussmaul%20breathing, The American Heritage® Medical Dictionary, 2007, Houghton Mifflin Company, last accessed: 23 November 2010) Assembly of ketone bodies causes acidity in body and as a compensation mechanism, brain respiratory centre induces hyperventilation in order to avoid acidity and re-establish body back to optimal situation.

4- Explain the test results including ketoacidosis.

Test results are shown in the following table (Table 1):










Present excessively





Table 1

Arterial Blood









There is very high glucose in plasma because patient did not take insulin for the last one day. Insulin stimulates glycogen formation from glucose and uptake of glucose by muscle and adipose tissue decreasing the glucose level in blood plasma. When an adequate concentration of insulin is not present to achieve this, blood glucose level rises. In the absence of insulin, "counter-regulatory hormones (glucagon, epinephrine, cortisol and growth hormone) are to cause greater production of glucose from liver and less utilisation of glucose in fat and muscle."(Kumar and Clark, Clinical Medicine, 7th Edition, Page 1030, Saunders Elsevier) Na⁺ levels are in normal boundaries because although Na⁺ loss is predicted together with K⁺ loss as there is excretion of ionised ketones in hyperglycaemia, the co-transporters present in proximal convoluted tubule are Na⁺/glucose co-transporters and they are functioning at maximum rate. Plasma K⁺ values are decreased because ketone bodies are present and excreted in kidney in a negative ionised form and during excretion of ketones, K⁺ and Na⁺ is lost as positive ions together with ketones. Furthermore, insulin stimulates the action of Na⁺/K⁺ ATPase so that K⁺ is taken up by cells. When insulin is deficient, this activity decreases causing decrease in K⁺ concentrations.

In urine test, presence of blood is due to irritation and inflammation of urinary tract because of bacterial infection and also, presence of protein is because of discharge of bacteria and antibodies due to urinary tract infection. Ketones are found in urine because of excessive ketone production and excretion by kidneys in urine due to lack of insulin in body.

Ketones have an acidic pH and they are present in negative ionic format added to H⁺ ion. H⁺ accumulation in blood causes acidification of blood and decrease of blood pH causing metabolic acidosis in body. For compensation, bicarbonate buffering system gets into action and this leads to decreased levels of HCO₃⁻. Eventually, this technique of compensation turns out to be not sufficient. Hyperventilation arises which create respiratory alkalosis and decrease pCO₂ in blood.

Ketoacidosis is one of the major complications of poor diabetes management. When the insulin levels in body decrease, the uptake of glucose by muscle and adipose tissue cells also decrease but glucose is still needed by these tissues. Furthermore, insulin is important in inhibiting gluconeogenesis and lipolysis, and it is also crucial in activating lipase enzyme for lipid re-esterification. Gluconeogenesis, i.e. make up of glucose from non-glucose origins such as forming glucose from proteins and lipids, is increased. Breakdown of lipids, in other terms, lipolysis, is break down of triglycerides into one glycerol and 3 fatty acids. Free fatty acids are oxidised (β-oxidation) in liver and create acetyl CoA. Acetyl CoA is then converted into acetoacetate and 3-hydroxybutyrate in mitochondria. Acetoacetate then breaks down into acetone and CO₂. Acetoacetate and 3-hydroxybutyrate has acidic pH however blood has a nearly neutral pH so these ketone bodies are present in negatively ionised form in blood. This cause acidity in blood by increased amounts of H⁺. This condition is named as ketoacidosis. The diagram below (Diagram 3) shows the pathway of acetone formation starting with lipids.

5-Describe the effect of insulin on glucose metabolism.

Insulin is secreted from β-cells in Islets of Langerhans in pancreas and its secretion is stimulated by high blood glucose levels. Glucose enters the β-cells through glucose transporter 2 (GLUT-2) protein and it is metabolized to generate ATP. This ATP generated closes K⁺ channels which cause membrane depolarisation. Ca²âº channels in cell membrane open and Ca²âº ions enter the cell setting off movement of insulin granules and eventually exocytosis of insulin. One other factor closing K⁺ channels is sulfonylurea drugs.

Insulin is very important in glucose metabolism as it stimulates glucose conversion to glycogen in liver and glucose absorption by muscle and adipose tissue cells. Besides, lack of insulin is equally important as this situation will stimulate lipolysis and gluconeogenesis and increase blood glucose level. Insulin deficiency can cause serious complications on body.

6-Explain the treatment and the prognosis. (What is the importance of management? What is the role of specialist nurse?)

This patient recently had difficulty down to lack of information so advice in terms of basic physiology of diabetes and what to do in different conditions is provided to the patient. Patient should be clarified that even if they do not eat, fat and proteins can be converted to glucose by gluconeogenesis and glucose can be secreted to body by liver so their blood glucose level will rise. So, self-monitoring blood glucose level by easy methods such as urine dipstick, BM stix or finger-prick blood glucose monitor, and taking insulin at levels required for present blood glucose level is still essential. Diabetes specialist nurses are very important in terms of providing information. "Their role is to enhance the care provided to people with diabetes when they attend the hospital either as an inpatient or as outpatient."(Diabetes Specialist Nursing Service, LHU, <http://www.leicestershirediabetes.org.uk/ display/templatedisplay1.asp?sectionid=213>, last accessed:22/11/2010)

In terms of managing diabetes, Insulin should be given to replace the deficiency followed by monitoring blood glucose level.

Due to excretion of water together with glucose, body is in a dehydrated state so avoiding thirst is advised and fluid must be administered to recover body's water balance. Excretion of ketone bodies may have caused excretion of K⁺ and Na⁺ as well so electrolytes must be provided together with fluid as a saline solution. "O.9% saline solution (isotonic) of choice has advantage of preventing too rapid a fall in extracellular osmolality which might predispose to cerebral oedema." (Tattersall and Gale, Diabetes Clinical Management, Page 223, Churchill Livingstone) Also, due to electrolyte excretion, K⁺ levels should be monitored to detect severe losses. Insulin was deficient in body for a time and there are no insulin stores so eating foods high in sugar content should be avoided. For future times, regular exercising together with healthy diet should be advised.

Prognosis of diabetes type 1 in a good management plan is usually good. In a underprivileged management plan the prognosis gets worse in long term because the situation can introduce many complications such as ketoacidosis, retinopathy, nephropathy, can cause amputation of extremities due to neuropathy and gangrene and the complications may end up in death of the patient.