Systemic Diseases

Diabetes mellitus

Introduction

Diabetes mellitus is a chronic metabolic disease. Diabetes is increasing at an alarming rate all over the world and particularly in India. Body cells require glucose which produces energy required for daily activities. The food we eat turns into glucose after digestion. Glucose enters the blood stream and reaches different body cells. Insulin is like a key which opens the body cell doors to allow glucose to enter. In the absence of enough insulin glucose cannot enter the cells. Glucose remains in the blood stream in high amounts resulting in hyperglycemia. This abnormal blood glucose level is called diabetes mellitus.

It is not a single disease, but a group of diseases, characterized by chronic hyperglycemia (elevated levels of glucose in the blood) from various reasons, mainly due to impaired glucose metabolism.

Long term hyperglycemia leads to disorders like myocardial infarction, stroke, kidney diseases and diabetic retinopathy. Diabetic retinopathy affects the vision and may even leads to blindness. The OA is likely to encounter patients with diabetes. Patients with diabetes may have cataracts or glaucoma. Learning about diabetes will help the OA provide proper care and comfort to these patients.

Overview of physiology

The beta cells of the islets of langerhans produce a hormone, insulin. The islets of langerhans are situated in the pancreas, a yellowish gray gland situated behind the stomach.

The pancreas has many functions in addition to insulin production. The pancreas also produces digestive enzymes and other hormones.

Classification

• Type I diabetes
• Type II diabetes
• Gestational Diabetes
• Juvenille Diabetes

Etiology and risk factors

Type I diabetes mellitus

Genetic factors: This is genetically linked with (Human Leucocyte Antigen) HLA on chromosome 6. It is speculated that these HLA molecules provide antigens to produce auto- antibodies specific to islets of langerhans.

Immunologic factors: auto antibodies against the islets of langerhans destroy the beta cells affecting insulin production.

Environmental factors: It has been proposed that some virus or toxins may cause the beta cell destruction.

Type II Diabetes mellitus

Ages	: Insulin resistance tends to increase with age over 40 years
Obesity	: The insulin secreted is not sufficient for the cells
Family History	: If the father or mother has diabetes, the chances of the child getting diabetes are increased
Lack of physical	: This leads to impaired glucose
Activities	: Metabolism

Pathophysiology

Type I Diabetes

• This generally occurs in young, lean patients.
• It is characterized by the marked inability of the pancreas to secrete insulin
• These patients are dependent on exogenous insulin to sustain their lives

Type II diabetes

In type II diabetes the body cells are resistant to insulin and there may be insulin deficiency

• This group of patients develops diabetes at an older age, after 40 years
• These patients are usually over weight
• The treatment modalities are diet control, weight reduction, oral anti diabetic drugs and insulin injection if necessary

Flow chart-pathophysiology of diabetes

• Deficiency of insulin
• Cells cannot access the calories contained in the glucose without insulin
• Liver releases glucose
• Glucose concentration in blood exceeds capacity of renal tubules to reabsorb
• Loss of water and minerals
• Thirst - polydipsia

Symptoms of diabetes

Symptoms of diabetes occur because body tissues are not able to utilise glucose. The classical symptoms include polyphagia, polydipsia and polyuria.

1. Polyphagia

Patients have increased appetite, and eat more than usual. This is because cells are starved of glucose since glucose is not able to enter cells. Although a diabetic eats more, the cells do not get enough glucose.

2. Polyuria

Patient passes large volumes of urine. Normal urine does not contain glucose. In the diabetics, kidneys are unable to reabsorb the excess glucose, so it appears in the urine. When glucose appears in urine, it drains a lot of water with it causing excessive urination.

3. Polydipsia

It is excessive thirst due to loss of water from the body. Other symptoms may include

4. Fatigue and weight loss in diabetes

In order to obtain energy, cells start using body fat and protein for energy instead of glucose. This leads to weight loss and tiredness.

Some people may not have any symptoms. DM is accidentally discovered in some persons during routine examination of urine and blood.

Diagnosis

• Blood glucose - the presence of abnormally high blood glucose levels is the criteria by which the diagnosis of diabetes should be made.
• Benedict's test to determine urine glucose
• Glucose tolerance test

The Result of the Oral Glucose Tolence Test can be evaluated as follows (using plasma to sample)
	Normal	Impaired Glucose Tolerance	Diabetes
Fasting Value	< 5.5mmol/L	5.5 - 7.7 mmol/L	> = 7.8 mmol/L
2-hour Value	< 7.8 mmol/L	7.8 - 11.0 mmol/L	> = 11.1 mmol/L

Oral glucose tolerance test

Performing an oral glucose tolerance test is necessary only when random or fasting blood glucose values do not establish the diagnosis.

Method

• Instruct the patient not to restrict diet during the 3 days preceding the test.
• The patient should fast for 12 hours immediately before testing.
• The test is usually scheduled in the morning.
• A fasting blood sample to determine plasma glucose level is taken. (If the plasma glucose level is =/> 7.8 mmol/L, no need for further testing)
• 75g of glucose, diluted in 250 ml of water, is given by mouth, within 5 minutes
• After 2 hours, a second blood sample is taken, and the plasma glucose level is determined

Diagnostic criteria - as defined by the world health organisation

Any patient on at least two occasions has

• Fasting plasma glucose levels of 140 mg/dl
• PPS > 200mgms
• GTT-2 hours sample with 200mg or greater will be considered as diabetic

Treatment of diabetes consist of three main components

The main goal of treatment is to normalize the blood sugar level in an attempt to reduce the development of complications

There are five components in the treatment of diabetes.

• Diet
• Exercise
• Drugs - oral hypoglycemic agents, insulin injection
• Monitoring
• Education

Diet and exercise are the corner stone of diabetic management.

Diet

Balanced food within permitted calorie limits as prescribed by the doctor is taken. Sugar containing items have to be avoided. High fiber diet is encouraged.

Exercise

Exercise helps in glucose utilization and maintenance of weight.

Drugs

Oral hypoglycemic drugs

• Daonil
• Glyciphage
• Pioshitezovie

Injectable Insulin

Used in Type I diabetes life long and in Type II diabetics when blood sugar is not well controlled with oral agents.

Types of insulin

Short acting	- Duration of action is from 2 hours to 8 hrs
Intermediate acting	- In this type of insulin action starts after 4 hours effective for 24 hours
Long acting	- Effective for 24-36 hrs

Complications of diabetes: Acute complications

• Diabetic ketoacidosis
• Hypoglycemic attack

Chronic complications

• Ischemic heart disease, heart attack (silent, common)
• Renal failure
• Stroke
• Tingling of fingers and toes, foot ulcers due to neuropathy
• Nephropathy and renal failure
• Diabetic retinopathy
• Urinary tract infections

The diabetic patient who comes to an ophthalmic unit may develop hypoglycemia or ketoacidosis. The difference between hypoglycemia and hyperglycemia is given below.

Points to differentiate between hypoglycemia and hyperglycemia

Clinical Features	Hyperglycemia	Hypoglycemia
Onset	Gradual	Sudden
Skin	Dry and Cold	Warm & moist
Pulse	Faint and fast	Normal or high
Blood pressure	Low	Normal
Breathing pattern	Deep & sighing	Normal
Breath smell	Fruit odour	Normal
Blood sugar	High	Low
Treatment	I.V. fluids, insulin	I.V. glucose (25%dextrose)

Treatment of acute complication

1. Hypoglycemia
- Occurs when blood sugar is < 60mgms

Treatment

• Sugar containing foods in conscious patient.
• Unconscious patient - 50ml of 25% dextrose followed by 10% dextrose drip for 12-24 hours.

2. Diabetic ketoacidosis

• Occurs due to infection, stress, or stopping drugs. It is an acute complication.
• Diabetic ketoacidosis can be life threatening if untreated.

Treatment

• Rapid correction of dehydration by IV fluids - normal saline or ringers lactate.
• Hourly intravenous insulin.

Student Exercise

1. Fill in the blanks

1. Drugs that reduce blood sugar are called _________.
2. Type II diabetes is called _________.
3. Daonil is ________________ drug.

2. Choose the correct answer

a. Symptoms of diabetes mellitus include all except

• Polyphagler
• Polymiar
• Polydipsia
• All the above

b. Chronic complications of diabetes include

• Ischemic heart disease
• Nephropathy
• Diabetic retinopathy
• All by the above

c. Treatment of hypoglycemia

• 25% in dextrose
• injection insulin
• Tab. Daonil

3. Match the following

• Hypoglycemia - PPBS >200mg
• Hyperglycemia - Blood sugar < 60mg
• Type I D.M - NIDDM
• Type II DM - IDDM

4. Choose the correct

a. Daonil is an
- Oral hypoglycemic drug
- Oral hyperglymic drug
- Antihypertensive drug
- Analgesic

Hypertension

Introduction

Hypertension is a very common disorder affecting 25% of the population. It is a major risk factor for coronary heart disease, cerebral, renal and peripheral vascular disease. It is called the silent killer because people with hypertension are often symptom free.

Definition - hypertension

Hypertension is defined as a systolic blood pressure greater than or equal to 140mmHg and/or a diastolic blood pressure greater than or equal to 90 mm hg occurring in a patient on at least three separate occasions.

Classification of hypertension

Hypertension can be divided into 2 groups
- Primary hypertension
- Secondary hypertension.

Primary hypertension

Primary hypertension is the most common - 95% of patients with raised blood pressure are in this category.
This is also called essential hypertension. There is no known cause, we only know the effects.
At times people show a rapid rise in blood pressure with a risk of death within a year or two - this is known as malignant hypertension.

Secondary hypertension

Of the remaining 5% who have secondary hypertension, most are a result of renal disease, endocrine diseases, vascular disease, or neurogenic disorders.

Most of the people are affected with benign hypertension, in other words, stable. It is compatible with a long life. In this chapter the emphasis is given to primary hypertension and it will be explained in detail.

No one's blood pressure is constant. Exercise, a sudden burst of anger, all of these can raise our normal blood pressure readings. But generally, they don't raise our blood pressure to dangerous levels for long periods of time. In the absence of high blood pressure symptoms, hypertension is diagnosed based on several blood pressure readings taken over a period of time.

Etiology & predisposing factors of primary hypertension

As described earlier the etiology for primary hypertension is not known. Predisposing factors are

• Stress
• Obesity
• Diets high in cholesterol
• Smoking
• Heavy alcohol intake
• Lack of physical activity
• Over stimulation with coffee,tobacco
• Familial tendency

Etiology - secondary hypertension

Renal disease

• Acute glomerulonephritis
• Chronic renal disease
• Renal artery stenosis
• Renal vasculitis
Renin-producing tumours

Endocrine disease

• Adrenocortical hyperfunction (Cushing's sydrome)
• Pheochromocytoma
• Acromegaly
• Myxodema
• Thyrotoxicosis

Vascular diseases

• Coarction of aorta
• Polyarteritis nodosa
• Aortic insufficiency

Neurogenic disorders

• Brain tumors and increased cranial pressure
• Polyneuritis, bulbar poliomyelitis

Miscellaneous causes

• Pregnancy
• Burns

Pathophysiology

The systemic arterial pressure is a result of

• Cardiac output - Cardiac output is determined by stroke volume and heart rate.
• Peripheral vascular resistance - Control of peripheral resistance is maintained by autonomic nervous system and circulating hormones.
• Any factor producing an alteration in peripheral resistance, heart rate, or stroke volume affects the systemic arterial pressure.

↓

Structural and functional changes in the peripheral blood vessels

Loss of elasticity due to atherosclerosis

Loss of ability of the vessels to distend & recoil

Less ability to accommodate the blood pumped out

Decrease in cardiac output

Increase in peripheral resistance

Increase in blood pressure

The stabilising mechanism regulating blood pressure

The baro receptors

They are found in the carotid sinus, aorta and in the walls of the left ventricle. They monitor the level of pressure in the arteries. When the blood pressure lowers, this tries to raise the blood pressure or lowers the blood pressure when it is high. The exact reason why this control fails in hypertension is unknown.

Body fluid volume

Changes in fluid volume affect the blood pressure. If the body has excess salt and water, the blood pressure rises. This happens when there is alteration in kidney function of excreting water and salt.

Renin angiotensin system

Renin is an enzyme secreted by the kidney when the blood pressure decreases. The following flow chart explains how the blood pressure raises due to the action of renin and angiotensin.

Category	Systolic BP (mmHg)	Diastolic P(mmHg)
Normal	Less than 130	Less than 85
High normal	130-139	85-89
Stage 1 Hypertension	140-159	90-99
Stage 2 Hypertension	160-179	100-109
Stage 3 Hypertension	180 & above	110 & above

Blood pressure decreases

Kidney secretes renin

Angiotensin I

Angiotensin II → Vaso constriction

Raised blood pressure

Stimulates aldosteron secretion

Increased retention of sodium and water

Elevated blood pressure levels

Also when there is inappropriate renin secretion there is increased peripheral vascular resistance which causes essential hypertension.

Vascular auto regulation

Vascular auto regulation is the capacity of blood vessels to alter their resistance according to the blood flow. This means it should decrease the vascular resistance when the blood flow is decreased and increase the vascular resistance when the blood flow is increased. In hypertension this mechanism fails which results in increased sodium and water retention. This increases the blood pressure.

Clinical manifestations

• Headache
• Giddiness
• Palpitation
• Chest pain
• Nocturia
• Nose bleeds
• Vision changes

There may not be any symptoms and patient's hypertension may be detected only in routine examinations.

Complications

• Coronary heart disease
• Cerebro vascular accident
• Peripheral vascular disease
• Hypertensive retinopathy
• Renal disorders

Diagnosis of hypertension

History

• BP readings - high on 3 separate occasions
• Evidence of endovsan olamase - eye, cardiac or renal involvement

Physical assessment and Investigations

• Blood pressure measurement
• Fundus examination of the eyes to observe any vascular changes.
• Assessment to rule out systemic diseases.
• Route urine examination which will include protein, red blood cells, pus cells and casts -The presence of these may indicate the presence of renal disease.
• Chest x-ray to rule out left ventricular enlargement that results from hypertension.
• ECG to determine the degree of cardiac involvement.
• Assessment for psycho social factors that aggrevate the clients hypertension.

Management

Life style modifications

• Diet
  • Low fat, low carbohydrate diet
  • High fiber diet
• Weight reduction
• Stop smoking
• Relaxation
• Exercise
• Reducing alcohol consumption.

Mild hypertensive patients can be managed by diet control and weight reduction initially. If there is no response then drugs can be used for management.

Anti - hypertensive Drugs

Principal drugs used in treatment are

Beta -blockers

• Propranolol
• Atenolol
• Metoprolol

Calcium blockers

• Nifidepine
• Amlodipine
• Diltiazem
• Verapamil

ACE inhibitors

• Enalapril
• Lisinopril
• Captopril

Diuretics

• Thiazides

Eye and hypertension

Uncontrolled high blood pressure speeds up the normal aging of blood vessels in the eye. The constant force of the high blood pressure can make them weak and lose their elasticity. Uncontrolled hypertension can result in arterio venous compression, hemorrhages, exudates, and papilledema of optic fundus (edema of the optic nerve at its point of entrance into the eye ball). The appearance of retina has been found to be a reliable index of the severity and prognosis of hypertension.

Symptoms and signs of hypertensive retinopathy

Hemorrhages around retinal vessels are signs hypertension is affecting the eyes and a person's vision. Vitreous hemorrhage is common in hyper tensive patients.

Early changes

• Narrowing of arteries
• Arterio-venous (AV) junction changes.

Late changes

• Deposits of lipids (fats) in the eye.
• Cotton - wool spots (CWS-micro infarctions).
• Bleeding into the eye and complications like scarring, and pull on the retina leading to retinal detachment.
• Vein occlusions leading to sudden loss of vision and can cause growth of new vessels in the eye.
• In severe cases swelling of optic disc called papilledema occurs.

What can be done?

• Regular eye exams
• Good control of blood pressure
• Laser may be done in certain cases

Bronchial Asthma

Between 100 and 150 million people around the globe suffer from asthma. Asthma attacks all age groups but often starts in childhood. It is a disease characterized by recurrent attacks of breathlessness and wheezing, which vary in severity and frequency from person to person. In an individual, they may occur from hour to hour or day to day. Asthma cannot be cured, but can be controlled. Asthma is on the increase due to rapid urbanisation.

Definition

Asthma is an intermittent, inflammatous, reversible, obstructive airway disease in which trachea, & bronchi react in a hyperactive way to certain stimuli.

Types of asthma

Allergic asthma

Caused by known allergens such as dust, pollens, animals, food, etc.

Idiopathic non allergic asthma

This is not related to specific allergens. Factors such as common cold, respiratory tract infections, exercise, and stress may be responsible.

Mixed asthma

This has both the charecteristics of allergic and non allergic.This is the most common type of asthma.

Pathophysiology

Initial exposure to allergen

Antibodies are attached to mast cells (Mast cells are normally found in the body tissue. when stimulated they release histamine that causes allergic signs)

Re-exposure to allergen

Antigen and antibody binds

Release of mast cell products- histamine and other factors

Obstruction / narrowing of airway due to

• Contraction of smooth muscles around the bronchi
• Swelling of mucous membrane that line the bronchi
• Excessive mucus production within the bronchi

Clinical manifestations

Frequently the asthmatic attack occurs at night.

When a person has an asthmatic attack, usually they have

• Cough with tightening of the chest
• Difficulty in breathing, especially expiration. It is more prolonged than inspiration
• The patient uses accessory muscles of respiration
• Later cyanosis may occur
• Wheezing

The asthmatic attack may last from 30 minutes to several hours and may subside spontaneously. Occasionally it may last longer, which may be life threatening. This condition is referred to as status asthmaticus.

Diagnosis

• History will disclose factors which precipitate asthmatic attacks
• X-ray during acute attacks may reveal hyperinflation and flat diaphragm
• Sputum clear, white, foamy
• Arterial blood gas reveals hypoxia. The PCO2 level will be high

Treatment

Asthma treatment is of utmost importance. Asthma can be controlled but not cured. It is not usually fatal, but it can become life-threatening if it is not treated or controlled. Asthma can produce respiratory failure Treatments:

• Broncho dilators - Inj, and tablets salbutamol, deriphylline, aminophylline, terbutalin
• Corticosteroids - efcorlin, solumedvol, decadron
• Oxygen
• Saltrulamol (tablets, inhaler, syrup)
• Deriphyclone (given in injection and tablets)
• Aminophyllin

Emergency care

• The two goals of emergency care for an acute asthmatic attack are
  • Improve oxygenation and ventilation
  • Relieve bronchospasm
• New early asthma treatment can prevent fatalities
  • Observe the respiration and check pulse
  • Establish an airway and assist ventilations if necessary (mouth-to-mouth breathing if the patient is not breathing)
  • Enquire if the patient uses any medication for asthmatic treatment. Shake the inhaler and spray once in the air. Have the victim breathe in and out once. Then insert the inhaler and assist with three applications of the medication
  • Inform the physician
  • Stay calm and keep the patient as calm as possible; stress, cold and emotional intensity worsen the asthma
  • Keep the victim in a position of comfort, usually seated
  • If they don't have an inhaler, Asthalin nebuliser, inj. deriphylline (IV) and steroid can be given as per doctor's order. Oxygen may be started
  • If you do not anticipate aspiration, give the patient warm fluid by mouth

Prevention

• Identification of stimuli and avoid contact with that stimuli
• Prevention and proper management of common cold.

Inhalers

The most common way of taking treatment is with an inhaler - or "puffer" which delivers a precisely measured dose of a medicine in aerosol or fine powder form. The two main types of medicines used in inhalers are relievers and preventers.

Reliever

Medicine helps to open up the airways and works rapidly. It is used at the beginning of an asthmatic attach. Common reliever medicines include salbutamol (Ventolin), terbutaline and ipratropium. Inhalers containing these medicines are coloured blue.

Preventer drugs

These can be used together with relievers, and are for preventing symptoms. Most preventers are inhaled corticosteroids, usually referred to simply as steroids. They reduce the inflammation in the airways.

Tablets

If asthma is quite severe or unpredictable, it may be necessary to take a course of steroids in tablet form. These work in the same way as inhaled preventers, by reducing inflammation.

Nebulisers

Nebulisers make a mist of water and asthma medicine that is breathed in. They can deliver more of the drug to exactly where it's needed than conventional inhalers can. This is particularly critical in the event of a serious asthma attack.

Spacers

A spacer is a long tube that clips on to the inhaler. At the other end of the tube is a mouthpiece or mask that the patients breathes in and out of.

I. Fill in the blanks

1. Saltrulamol is a __________.
2. Asthma is an inflammatory ___________ obstructive airway disease.

II. Choose the correct answer

1. Inj. aminophyline given in case of

• Status asthmaticus (acute asthmatic attack)
• Heart block
• Ischemic heart disease

2. Emergency care for an acute attack includes

• Improve oxygenation and ventilation
• Relieve bronchospasm
• Back rest
• All of the above

III. Match the following

1. Broncho dilaters - Efeorlins
2. Corticosteroids - Respiratory tract infection
3. Allergic asthma - Salbutamol
4. Non allergic asthma - Dust, pollution