Section outline

  • Key Unit Competences

    To take an appropriate decision on management of common pathologies of

    Endocrine system.

    Introductory activity 5.0

    Carefully observe the picture below and answer the following questions:

    s

    Figure 5.1 Glycemia measurement

    1. How do you call the instrument shown at the picture below?
    2. Can you interpret the readings/results from the instrument above?
    3. Can you list some conditions that a person might present that will enable

        the use of this equipment?

    Endocrine glands include the hypothalamus, pituitary, thyroid, parathyroids,
    adrenals, pancreas, ovaries, testes, and pineal gland. Exocrine glands are not part
    of the endocrine system. They secrete their substances into ducts that then empty
    into a body cavity or onto a surface. Hormones are chemical substances produced
    in the body that control and regulate the activity of certain target cells or organs.
    Many are produced in one part of the body and control and regulate the activity of
    certain cells or organs in another part of the body. Endocrine glands produce and

    secrete hormones that travel to affect their specific target tissues.

    5.1 DIABETES MELLITUS

    Learning Activity 5.1

    Carefully read this below situation and answer the following questions:

    A 54 year old female visited NCD clinic with the complaints of excessive urination,
    sudden weight loss, blurred vision, increased thirst, fatigue and excessive
    sweating. She was experiencing these conditions from last one month. From the
    past medical history, she was also suffering from hypertension from last 3 years
    under treatment (Atenolol 50mg OD per day and Lasix 40mg BID per day from
    last 3 years. From the general examination, weight: 70kg and height: 152cm
    BMI: 30.5kg/m2. She also had limited physical activities as she always stayed
    at home.
    From all observations, the NCD Medical Doctor recommended to monitor the
    patient’s blood glucose level. At that time patient’s random blood glucose level
    was 245mg/dl which was beyond the normal range of the random blood glucose
    level (70-110mg/dl). The NCD Medical Doctor recommended also to patient
    to monitor the patient fasting glucose level and then to check HbA1C Level
    after about every 3rd month in the following visits. The NCD Medical Doctor
    prescribed the drug (metformin 500mg BID per day) that should be taken about
    5 -10 minutes before the meal and in combination with other drugs she has been
    taking.
    The patient was also advised that instead of eating a lot at 3 meals, divide total
    intake in 5 meals. She was also suggested to avoid sugar intake, do exercise
    and walk to reduce body weight, take high fiber diet and less intake of fats and
    carbohydrates. The patient was given the appointments to visit the NCD clinic
    on monthly basis to monitor the trends of blood sugar levels and also the other
    symptoms that might arise from existing condition.
    1. What are the abnormal signs and symptoms that the patient was presenting?
    2. What do you think is the medical condition was she presenting in addition
    to hypertension?
    3. What are the investigations requested to diagnose that medical condition?
    4. What was included into her plan of the management?

    5. If this condition is not well managed, what are the possible complications?

    The pancreas is a long, tapered, lobular, soft gland located behind the stomach and
    anterior to the first and second lumbar vertebrae. The pancreas has both exocrine
    and endocrine functions. The hormone-secreting portion of the pancreas is referred
    to as the islets of Langerhans. The islets account for less than 2% of the gland
    and consist of four types of hormone-secreting cells: α, β, delta, and F cells. α
    Cells produce and secrete the hormone glucagon. Insulin and amylin are produced
    and secreted by β cells. Somatostatin is produced and secreted by the delta cells.
    Pancreatic polypeptide (PP) is secreted by the F
    (or PP) cells.
    Glucagon is synthesized and released from pancreatic α cells and the gut in response
    to low levels of blood glucose, protein ingestion, and exercise. Glucagon increases
    blood glucose by stimulating glycogenolysis, gluconeogenesis, and ketogenesis.
    Glucagon and insulin function in a reciprocal manner to maintain normal blood
    glucose levels. In the fasting state, hormones such as catecholamines, cortisol,
    and glucagon break down stored complex fuels (catabolism) to provide glucose as
    fuel for energy.
    Insulin is the principal regulator of metabolism and storage of ingested
    carbohydrates, fats, and proteins. Insulin facilitates glucose transport across
    cell membranes in most tissues. However, the brain, nerves, lens of the eye,
    hepatocytes, erythrocytes, and cells in the intestinal mucosa and kidney tubules
    are not dependent on insulin for glucose uptake. An increased blood glucose level
    is the major stimulus for insulin synthesis and secretion. Other stimuli to insulin
    secretion are increased amino acid levels and vagal stimulation. Insulin secretion is
    usually inhibited by low blood glucose levels, glucagon, somatostatin, hypokalemia,
    and catecholamines. A major effect of insulin on glucose metabolism occurs in
    the liver, where the hormone enhances glucose incorporation into glycogen and
    triglycerides by altering enzymatic activity and inhibiting gluconeogenesis. After a
    meal, insulin is responsible for the storage of nutrients (anabolism). Another major
    effect occurs in peripheral tissues, where insulin facilitates glucose transport into
    cells, transport of amino acids across muscle membranes and their synthesis into
    protein, and transport of triglycerides into adipose tissue.
    The term diabetes mellitus describes diseases of abnormal carbohydrate metabolism
    that are characterized by hyperglycemia. It is associated with a relative or absolute
    impairment in insulin secretion, along with varying degrees of peripheral resistance
    to the action of insulin.
    Types of diabetes mellitus and their causes: the underlying cause of diabetes

    varies by type:

    A. Prediabetes:

    Prediabetes is a condition in which blood glucose levels are too high to be considered
    normal but not high enough to be labeled diabetes. People have prediabetes if their
    fasting blood glucose level is between 100 mg/dL (5.6 mmol/L) and 125 mg/dL
    (6.9 mmol/L) or if their blood glucose level 2 hours after a glucose tolerance test
    is between 140 mg/dL (7.8 mmol/L) and 199 mg/dL (11.0 mmol/L). Prediabetes
    carries a higher risk of future diabetes as well as heart disease. Decreasing body
    weight by 5 to 10% through diet and exercise can significantly reduce the risk of
    developing future diabetes.
    B. Type 1 diabetes mellitus:
    In type 1 diabetes mellitus (formerly called insulin-dependent diabetes or
    juvenile-onset diabetes), the body’s immune system attacks the insulin-producing
    cells of the pancreas, and more than 90% of them are permanently destroyed. The
    pancreas, therefore, produces little or no insulin. Most people who have type 1
    diabetes develop the disease before age 30, although it can develop later in life.
    Some environmental factors like viral infection or nutritional factor during childhood
    or early adulthood cause the immune system to destroy the insulin-producing cells
    of the pancreas. A genetic predisposition makes some people more susceptible to
    an environmental factor.
    C. Type 2 diabetes mellitus:
    In type 2 diabetes mellitus (formerly called non–insulin-dependent diabetes or
    adult-onset diabetes), the pancreas often continues to produce insulin, sometimes
    even at higher than normal levels, especially early in the disease. However, the
    body develops resistance to the effects of insulin, so there is not enough insulin to
    meet the body’s needs. As type 2 diabetes progresses, the insulin producing ability
    of the pancreas decreases.
    Obesity is the chief risk factor for developing type 2 diabetes, and 80 to
    90% of people with this disorder are overweight or obese. Because obesity
    causes insulin resistance, obese people need very large amounts of insulin to
    maintain normal blood glucose levels.
    Certain disorders and drugs can affect the way the body uses insulin and can lead
    to type 2 diabetes mellitus.
    Examples of common states (conditions) that result in impaired insulin use are
    high levels of corticosteroids (most commonly due to use of corticosteroid drugs or
    Cushing syndrome (a disorder that occurs when your body makes too much of the
    hormone cortisol over a long period of time), Pregnancy. Diabetes also may occur
    in people with excess production of growth hormone (acromegaly) and in people
    with certain hormone-secreting tumors. Severe or recurring pancreatitis and other

    disorders that directly damage the pancreas can lead to diabetes

    D. Gestational diabetes:
    Gestational diabetes is diabetes diagnosed for the first time during pregnancy
    (gestation). Like other types of diabetes, gestational diabetes affects how your cells
    use sugar (glucose). Gestational diabetes causes high blood sugar that can affect
    your pregnancy and your baby’s health. For a person who has gestational diabetes
    during pregnancy, generally the blood sugar returns to its usual level soon after
    delivery. But the person has a higher risk of getting type 2 diabetes mellitus.
    Risk factors and Pathophysiology
    The factors that increase the risk of developing diabetes mellitus differ depending

    on the type of diabetes.

    w

    s

    Signs and symptoms:

    Diabetes signs and symptoms vary depending on how much the blood sugar is

    elevated.

    e


    Some people, especially those with prediabetes or type 2 diabetes, may sometimes
    not experience symptoms. In type 1 diabetes, symptoms tend to come on quickly
    and be more severe.
    The signs and symptoms of type 1 diabetes and type 2 diabetes are: increased
    thirst (polydipsia), frequent urination (polyuria), extreme hunger (polyphagia),
    unexplained weight loss, presence of ketones (are a byproduct of the breakdown
    of muscle and fat that happens when there’s not enough available insulin) in the
    urine, fatigue, irritability, blurred vision, numbness or tingling into the hands or feet,
    slow-healing sores, frequent infections such as gums or skin infections and vaginal
    infections. Patient with type 1 diabetes might also present nausea, vomiting and

    stomach pains.

    s

    Investigations

    Symptomatic hyperglycemia: The diagnosis of diabetes mellitus is easily
    established when a patient presents with classic symptoms of hyperglycemia (thirst,
    polyuria, weight loss, blurry vision) and has a random blood glucose value of 200
    mg/dL (11.1 mmol/L) or higher.
    Most patients with type 1 diabetes are symptomatic and have plasma glucose
    concentrations/random blood glucose of ≥200 mg/dL. Some patients with type 2
    diabetes also present with symptomatic hyperglycemia and blood glucose ≥200
    mg/dL.
    Asymptomatic hyperglycemia: The diagnosis of diabetes in an asymptomatic
    individual (generally type 2 diabetes) can be established with any of the following

    criteria:

    • Fasting plasma glucose (FPG) values ≥126 mg/dL (7.0 mmol/L). Fasting is
    defined as no caloric intake for at least eight hours.
    • Two-hour plasma glucose values of ≥200 mg/dL (11.1 mmol/L)
    • A1C (hemoglobin A1C, HbA1C, glycated hemoglobin, and glycosylated

    hemoglobin test) values ≥6.5 percent (48 mmol/mol).

    In the absence of symptomatic hyperglycemia, the diagnosis of diabetes must be
    confirmed by repeated measurement, repeating the same test for confirmation.
    However, if two different tests (eg, FPG and A1C) are available and are concordant
    for the diagnosis of diabetes, additional testing is not needed.

    Urine analysis must also be done for glucosuria, ketonuria. Other investigations
    include: full blood count, proteins into urine, blood urea and electrolytes, liver

    biochemistry, lipidemia and cholesterol levels, etc.

    Adequate medical diagnosis

    s

    Plan of management of each type of diabetes mellitus

    The goal of diabetes management is to keep blood glucose levels as close to normal
    as safely possible. Since diabetes may greatly increase risk for heart disease and
    peripheral artery disease, measures to control blood pressure and cholesterol
    levels are an essential part of diabetes treatment as well.

    People with diabetes must take responsibility for their day-to-day care. This includes
    monitoring blood glucose levels, dietary management, maintaining physical
    activity, keeping weight and stress under control, monitoring and adhering to oral
    medications or insulin use via injections. To help patients achieve this, the health
    care facility must offer self-management educational programs that emphasize
    individualized diabetes care.

    The plan of management of diabetes mellitus includes:


    A. Dietary management and physical activity

    Modifying eating habits and increasing physical activity are typically the first steps
    toward reducing blood sugar levels. The benefits of exercises include to improve
    insulin sensitivity, to lower blood glucose during and after exercise, to improve lipid
    profile, may improve some hypertension, to assist with weight loss, to promote

    cardiovascular fitness, to increase strength and flexibility, to improve sense of wellbeing.

    The patient must also know some risks of exercises: precipitation or exacerbation
    of cardiovascular disease, angina, dysrrhythmias, sudden death, hypoglycemia if
    taking insulin or oral agents, late onset post-exercise hypoglycemia, hypoglycemia
    after very strenuous exercise, worsening of long-term complications such as
    proliferative retinopathy, peripheral neuropathy. The patient must also know that
    taking some glucose before an exercise may be necessary to minimize the risk for

    hypoglycemia. Blood glucose check up before and after exercise is necessary.

    B. Insulin Therapy

    People with type 1 diabetes require multiple insulin injections each day to maintain
    safe insulin levels. Insulin is often required to treat type 2 diabetes too. The pump
    is about the size of a pager and is usually worn on your belt. Insulin is delivered
    through a small syringe that contains the small and thin needle that is placed under
    the skin (usually in the abdomen) during injection. There are four major types of

    insulin: rapid-acting, short-acting, intermediate-acting and long-acting.

    C. Oral Medications/Hypoglycemia
    Sometimes blood sugar levels remain high in people with type 2 diabetes even
    though they eat in a healthy manner and exercise. When this happens, medications
    taken in pill form may be prescribed. The medications work in several different ways.
    These include improve the effectiveness of the body’s natural insulin, reduce blood
    sugar production, increase insulin production and inhibit blood sugar absorption.

    Oral diabetes medications are sometimes taken in combination with insulin.

    Oral hypoglycemia agents in type 2 diabetes in early stages are e.g biguanides such
    as Metformin reduces hepatic glucose production, Thiazolidinediones/glitazones
    reduce insulin resistance, alpha-Glucosidase inhibitors such as miglitol reduce

    postprandial hyperglycemia by delaying glucose absorption.

    D. Monitor glycemia before meal and before bedtime
    C. Education to diabetic patients: Education about signs and symptoms of
    hypoglycemia, During any journey, the patient should carry the drugs on him/her.
    The diabetic card is also necessary, and the patient should not forget to carry some
    foods or fluid containing sugar to take in case of hypoglycemia,
    Education on self-injection: number of injections per day, way of administration (S/C
    route) and site of injection, General hygiene specifically feet hygiene, Educate the
    patient and the family the importance of insulin therapy and some complications
    of diabetes if insulin is not taken carefully, Don’t forget the importance of diabetic
    regimen, Advise the patient to join diabetic associations (it will help her or him
    to have medication on low cost, and he/she will learn more about the diabetes
    mellitus). FOOT CARE is also very important due to these three major factors that
    interact in foot problems in diabetes: neuropathy, ischemia, and sepsis. Therefore
    patient must also be educated to never soak feet, wash feet daily and dry them well,
    playing attention to the area between the toes, inspect the feet daily (color changes,
    swelling, cuts, cracks in the skin, redness, blisters, temperature changes), never
    walk barefoot. Always wear shoes or slippers, wear well-fitting shoes, after bathing,
    when toenails are soft, cut nails straight across and don’t cut into the corners, if feet
    are dry, apply lotion or cream; don’t put lotion between the toes, consult a podiatrist

    for any problem of the feet.

    Evolution and complications of type 1 and 2 diabetes mellitus

    Diabetes mellitus is a chronic disease and does not have a cure, except for the case
    of gestational diabetes which usually disappears after childbirth. Among diabetes
    mellitus complications, there are Acute that develop suddenly and Long-term
    complications of diabetes that develop gradually. The longer you have diabetes and
    the less controlled your blood sugar the higher the risk of complications. Eventually,

    diabetes complications may be disabling or even life-threatening.

    Acute complications include diabetic ketoacidosis (DKA), Hperglycemic
    Hyperosmolar nonketonic coma (HHNC/HHS), Hypoglycemia, the somogyi effect
    (happens when patient takes insulin before bed and wake up with high blood
    sugar levels; according to the theory of the Somogyi effect, when insulin lowers the
    blood sugar too much, it can trigger a release of hormones that send the blood sugar
    levels into a rebound high), the dawn phenomenon (early morning hyperglycemia

    due to the liberation of growth hormone during nighttime).

    Possible long-term complications include:
    • Cardiovascular disease: diabetes dramatically increases the risk of various
    cardiovascular problems, including coronary artery disease with chest pain
    (angina), heart attack, stroke and narrowing of arteries (atherosclerosis).
    • Nerve damage (neuropathy): excess sugar can injure the walls of the tiny
    blood vessels (capillaries) that nourish the nerves, especially in the legs. This
    can cause tingling, numbness, burning or pain that usually begins at the tips
    of the toes or fingers and gradually spreads upward. Left untreated, it can
    lead to loss of all sense of feeling in the affected limbs. Damage to the nerves
    related to digestion can cause problems with nausea, vomiting, diarrhea or

    constipation. For men, it may lead to erectile dysfunction

    • Kidney damage (nephropathy): the kidneys contain millions of tiny blood
       vessel clusters (glomeruli) that filter waste from the blood. Diabetes can
       damage this delicate filtering system. Severe damage can lead to kidney
       failure or irreversible end-stage kidney disease, which may require dialysis
       or a kidney transplant.
    • Eye damage (retinopathy): diabetes can damage the blood vessels of the
       retina (diabetic retinopathy), potentially leading to blindness. Diabetes also
       increases the risk of other serious vision conditions, such as cataracts and
       glaucoma.
    • Foot damage: nerve damage in the feet or poor blood flow to the feet increases
       the risk of various foot complications. Left untreated, cuts and blisters can
       develop serious infections, which often heal poorly. These infections may
       ultimately require toe, foot or leg amputation.
    • Skin conditions: diabetes may leave a person to more susceptible to skin
       problems, including bacterial and fungal infections.
    • Hearing impairment: hearing problems are more common in people with
       diabetes.
    • Alzheimer›s disease: type 2 diabetes may increase the risk of dementia,
       such as Alzheimer›s disease. The poorer the blood sugar control, the greater
       the risk appears to be.
    • Depression: depression symptoms are common in people with type 1 and
      type 2 diabetes. Depression can affect diabetes self-management leading to

      poor outcomes.


    d

    Complications of gestational diabetes
    Most women who have gestational diabetes deliver healthy babies. However,
    untreated or uncontrolled blood sugar levels can cause problems for the mother
    and/or the baby.
    Complications to the baby can occur as a result of gestational diabetes, including:
    – Excess growth: Extra glucose can cross the placenta, which triggers the
       baby›s pancreas to make extra insulin. This can cause the baby to grow too
       large (macrosomia). Very large babies are more likely to require a C-section
       birth.
    – Low blood sugar: Sometimes babies of mothers with gestational diabetes
       develop low blood sugar (hypoglycemia) shortly after birth because their own
       insulin production is high. Prompt feedings and sometimes an intravenous
       glucose solution can return the baby›s blood sugar level to normal.
    – Type 2 diabetes later in life: Babies of mothers who have gestational
       diabetes have a higher risk of developing obesity and type 2 diabetes later
        in life.
    – Death: Untreated gestational diabetes can result in a baby›s death either
        before or shortly after birth.
    – Complications to the mother also can occur as a result of gestational
        diabetes, including:
    – Preeclampsia: This condition is characterized by high blood pressure, excess
       protein in the urine, and swelling in the legs and feet. Preeclampsia can lead
       to serious or even life-threatening complications for both mother and baby.
    – Subsequent gestational diabetes. Once a pregnant women had gestational
        diabetes in one pregnancy, she will be more likely to have it again with the
        next pregnancy. She is also more likely to develop diabetes typically type 2
        diabetes — as she gets older.
    Very serious and Acute Complications of Diabetes Mellitus (DKA and HHS)
    A. DIABETIC KETOACIDOSIS (DKA)
    DKA results from relative or absolute insulin deficiency (lack of insulin, insulin
    omission). The decreased ratio of insulin to glucagon promotes gluconeogenesis,
    glycogenolysis, and ketone body formation in the liver. Ketosis results from a
    marked increase in free fatty acid release from adipocytes, with a resulting shift
    toward ketone body synthesis in the liver. Reduced insulin levels, in combination
    with elevations in catecholamines and growth hormone, increase lipolysis and the

    release of free fatty acids. DKA is more present in type 1 diabetes mellitus.

    Causes of DKA
    • DKA is the initial manifestation of diabetes in 20% of adults and 30–40% of
       children with type 1 diabetes.
    • In patients with established diabetes, causes of DKA include:
    • Infection (30%-50%)
       Most common infections urinary tract infection and pneumonia
    • Noncompliance with insulin

    • Psychological stress

    Clinical manifestations include: Hyperglycemia, Ketosis: ketonuria, serum ketone
    (ketonemia), ketone smelling (fruity odor), Metabolic acidosis, Hyperlipoproteinemia,
    Nausea, Signs of acidosis (Kussmaul respiration, acetone breath), Signs of volume
    depletion/ dehydration, Polyuria, polydipsia, polyphagia, weight loss, Fever due to
    underlying infection is common(if present), Gastrointestinal signs (abdominal pain,
    vomiting), Neurological signs (hemiparesis and seizures) related to metabolic

    acidosis.

    Diagnosis of DKA
    • Serum glucose level > 250 mg/dL
    • Serum bicarbonate < 18 mg/dL
    • Serum pH < 7.30
    • Presence anion gap
    • History and physical examination,
    • Blood studies including immediate blood glucose, complete blood count, pH,
       ketones, electrolytes, blood urea nitrogen, arterial or venous blood gases.

    • Urinalysis, including specific gravity, glucose, acetone

    Management of DKA:
    1. Confirm diagnosis (↑plasma glucose, positive serum ketones, metabolic
        acidosis).
    2. Admit to hospital (unconsciousness, PH < 7 )
    3. Assess: serum electrolytes (K+, Na+, Mg2+, Cl-, bicarbonate, phosphate),
        acid-base status (pH, HCO3-, PCO2), renal function (creatinine, urine output)
    4. Replace fluids: 2–3 L of 0.9% saline over first 1–3 h (10–15 mL/kg per hour);
    5. Administer short-acting insulin: IV (0.1 unit/kg/hour) or IM/ SC (0.3 units/
        kg). Insulin increases peripheral glucose utilization and decreases hepatic
        glucose production. If initial serum potassium is < 3.3 mmol/L (3.3 meq/L), do

       not administer insulin until the potassium is corrected to > 3.3 mmol/L.

    6. Give medication to correct hyperkalemia (urgent treatment of hyperkalemia
        includes stabilizing the myocardium to protect against arrhythmias and
        shifting potassium from the vascular space into the cells. Intravenous calcium
       (eg: calcium gluconate) is administered to stabilize the myocardium; it lowers
       the threshold potential, thus counteracting the toxic effect of high potassium.
       Other medications like sodium polystyrene sulfonate (Kaayexalate) works by
       helping the body get rid of extra potassium through feces, etc.
    7. Electrolyte replacement
    8. Assessment of mental status, Assessment of blood glucose levels, Assessment
        of blood and urine for ketones, Assessment of cardiovascular and respiratory
        status and ECG monitoring, Assess patient: What precipitated the episode
        (noncompliance, infection, trauma, alcohol?
    9. Monitoring and recording of intake and output
    10. Central venous pressure monitoring (if indicated)
    11. Measure capillary glucose every 1–2 h; measure electrolytes (especially K+,
        bicarbonate, phosphate) and anion gap every 4 h for first 24 h.
    12. Initiate appropriate workup for precipitating event (cultures, Chest X-Ray,

        ECG).

    The complications of diabetic ketoacidosis
    DKA can cause complications such as low levels of potassium (hypokalemia) that
    can cause severe problems like muscle weakness and heart rhythm problems
    which can cause death), swelling inside the brain (cerebral edema), fluid inside the
    lungs (pulmonary edema), damage to the kidney or other organs from the fluid loss.

    All these can lead to sudden death.

    B. HYPERGLYCEMIC HYPEROSMOLAR NONKETONIC COMA/STATUS

    (HHCN/HHS)

    This is a complication of type 2 diabetes mellitus especially for the elderly people.
    Hyperglycemia induces an osmotic diuresis that leads to intravascular volume
    depletion, which is exacerbated by inadequate fluid replacement (impaired patient’s
    perception of thirst due to underlying cerebrovascular disease). The polyuria

    disappears early because of the severe dehydration.

    Clinical manifestations
    • Severe dehydration (fluid deficit of 8-9 L)
    • Severe hyperglycemia (plasma glucose may be >55.5 mmol/L (1000 mg/dL)

    • Hyperosmolarity (>350 mosmol/L)

    Management
    • IV replacement with hypotonic solutions (0.45% normal saline)
    • IV insulin is not needed, give insulin subcutaneously
    Possible complications of untreated HHS are shock, blood clot formation, brain
    swelling (cerebral edema) or increased blood acid level (lactic acidosis).
    C. HYPOGLYCEMIA
    The hypoglycemia in diabetic person is due to insulin therapy or glucose lowering
    agents:
    • Insulin overdosage
    • Glucose lowering agents overdosage
    • Inconsistent carbohydrates intake (no glucose intake before insulin injection)
    • Alcohol consumption
    • Uncompensated exercise

    • Patient with end-stage renal or liver failure are at risk for hypoglycemia

    Signs and symptoms
    Adrenergic symptoms (hypoglycemia causes the liberation of chathecholamines
    particulary adrenalin as compensatory mechanism): pallor, diaphoresis, tachycardia,
    palpitation, nervousness, irritability, sensation of coldness, weakness, trembling,
    hunger.
    Neuroglycopenic symptoms: the low glucose in nervous system causes
    headache, mental confusion, fatigue, incoherent speech, coma, diplopia, emotional

    lability, and convulsion.

    Self-assessment 5.1

    Read the clinical case scenario below and answer the following

    questions:

    A 27year old man was brought to the emergency reception reporting severe
    weakness, dizziness, and sleepiness all the time. Upon questioning, he reported
    increased and not resolving thirst, and the repeated need to urinate. Although
    he ate all of his rations as well as whatever he could get from his family, he had
    lost 7 kgs during recent 9 months. On the previous day before his consult, he
    complained of vague abdominal pain, which was worse on the morning and had
    vomited once. During the physical examination, he was oriented but tachypneic
    (pulse rate of 138 beats per minute) and his blood pressure was 90/60 mm
    Hg. He appeared pale, dehydrated with dry mucous membranes, and poor
    skin turgor. His respiratory rate was 36 cycles per minute with deep, laborious
    breathing. After admission, the laboratory investigations showed blood glucose
    levels of 560 mg/dl, sodium 154, potassium 6.5, pH 7.10, bicarbonate 10 mM/liter,
    chloride 90, BUN 38 mg/dl, creatinine 2.5 mg/dl. (Normal values: glucose: 70-
    110 mg/dl; Na = 135-145; K, 3.5-5.5; Cl, 98-108; CO2, 20-32 [all in mM/l]; BUN,
    7-22mg/dl; creatinine, 0.7-1.5 mg/dl). A urine sample was 4+ for glucose and
    had “large” acetone. Glycated hemoglobin (HbA1c) was 14% (normal=4-6.2%).

    He was treated with insulin and normal saline I.V. initially and by the 4th hour
    of treatment, potassium chloride was added to the IV at a rate of 15 mEq/hour.
    Sixteen hours later, he was active, alert, well hydrated and cheerful, indicating
    he felt extremely well. He requested that his IV be discontinued. His physician
    decided to switch his insulin to subcutaneous injections and to start a liquid diet.
    He was later put on a diabetes maintenance diet and treated with one injection of
    Human Lente insulin in the morning. Although his blood sugars the next morning
    were 100-140 mg/dl, he had frequent episodes of hypoglycemia during the day,
    he was put on 3 injections of regular insulin/day, and a bedtime intermediate
    duration (Lente) insulin.
    1. Basing on the case presented above, what was the medical condition that
        the patient was presenting?
    2. What are the signs and symptoms that guided you in thinking about that
        medical diagnosis?
    3. What are different investigations requested to confirm that medical
        condition?
    4. What are all possible treatment options are available to that medical
        condition?

    5. If it is not properly managed, what are the possible complications?

    5.2 END UNIT 5 ASSESSMENT

    End unit assessment

    1. Explain how the pancreas serves both endocrine and exocrine functions.
    2. By definition, differentiate diabetes mellitus type one and two
    3. Give 5 risk factors of type one and two of diabetes mellitus.
    4. What are the general signs and symptoms of diabetes mellitus?
    5. What are the investigations that are relevant into the diagnosis of diabetes
         mellitus?
    6. Discuss different management principles of diabetes mellitus.
    7. Discuss how the diabetes mellitus can lead to kidney, eye and foot
        problems.
    8. Basing on the causes and signs and symptoms, differentiate the DKA and
        HHS.
    9. What are different management principles of DKA?
    10. In addition to promoting the transport of glucose from the blood into the
          cell, what does insulin do?
    a. Enhances the breakdown of adipose tissue for energy
    b. Stimulates hepatic glycogenolysis and gluconeogenesis
    c. Prevents the transport of triglycerides into adipose tissue
    d. Accelerates the transport of amino acids into cells and their synthesis

        into protein

    11. Why are the hormones cortisol, glucagon, epinephrine, and growth
        hormone referred to as counter regulatory hormones?
    a. Decrease glucose production
    b. Stimulate glucose output by the liver
    c. Increase glucose transport into the cells
    d. Independently regulate glucose level in the blood
    12. What characterizes type 2 diabetes?
    a. β-Cell exhaustion
    b. Insulin resistance
    c. Genetic predisposition
    d. Altered production of adipokines
    e. Inherited defect in insulin receptors
    f. Inappropriate glucose production by the liver
    13. Which laboratory results would indicate that the patient has prediabetes?
    a. Glucose tolerance result of 132 mg/dL
    b. Glucose tolerance result of 240 mg/dL
    c. Fasting blood glucose result of 80 mg/dL
    d. Fasting blood glucose result of 120 mg/dL
    14. The nurse is teaching the patient with prediabetes ways to prevent or delay
         the development of type 2 diabetes. What information should be included?
    a. Maintain a healthy weight.
    b. Exercise for 60 minutes each day.
    c. Have blood pressure checked regularly.
    d. Assess for visual changes on monthly basis
    e. Monitor for polyuria, polyphagia, and polydipsia.
    15. When teaching the patient with diabetes about insulin administration, the
         nurse should include which instruction for the patient?
    a. Pull back on the plunger after inserting the needle to check for blood.
    b. Consistently use the same size of insulin syringe to avoid dosing errors.
    c. Clean the skin at the injection site with an alcohol swab before each
        injection.
    d. Rotate injection sites from arms to thighs to abdomen with each injection
         to prevent lipodystrophies.
    16. A patient taking insulin has recorded fasting glucose levels above 200 mg/
    dL (11.1 mmol/L) on awakening for the last five mornings. What should the
         nurse advise the patient to do first?
    a. Increase the evening insulin dose to prevent the dawn phenomenon.
    b. Use a single-dose insulin regimen with an intermediate-acting insulin.
    c. Monitor the glucose level at bedtime, between 2:00 am and 4:00 am,
         and on arising.
    d. Decrease the evening insulin dosage to prevent night hypoglycemia
         and the Somogyi effect.
    17. The nurse is assessing a newly admitted diabetic patient. Which observation
          should be addressed as the priority by the nurse?
    a. Bilateral numbness of both hands
    b. Stage II pressure ulcer on the right heel
    c. Rapid respirations with deep inspiration
    d. Areas of lumps and dents on the abdomen
    18. The nurse should observe the patient for symptoms of ketoacidosis when:
    a. Illnesses causing nausea and vomiting lead to bicarbonate loss with
         body fluids.
    b. Glucose levels become so high that osmotic diuresis promotes fluid
         and electrolyte loss.
    c. An insulin deficit causes the body to metabolize large amounts of fatty
    acids rather than glucose for energy.
    d. The patient skips meals after taking insulin, leading to rapid metabolism
    of glucose and breakdown of fats for energy.
    19. What are manifestations of diabetic ketoacidosis (DKA)?
    a. Thirst
    b. Ketonuria
    c. Dehydration
    d. Metabolic acidosis
    e. Kussmaul respirations
    f. Sweet, fruity breath odor
    20. What describes the primary difference in treatment for diabetic ketoacidosis
    (DKA) and hyperosmolar hyperglycemic syndrome (HHS)?
    a. DKA requires administration of bicarbonate to correct acidosis.
    b. Potassium replacement is not necessary in management of HHS.
    c. HHS requires greater fluid replacement to correct the dehydration.
    d. Administration of glucose is withheld in HHS until the blood glucose
         reaches a normal level.
    21. A diabetic patient is found unconscious at home and a family member calls
         the clinic. After determining that a glucometer is not available, what should
         the nurse advise the family member to do?
    a. Have the patient drink some orange juice.
    b. Administer 10 U of regular insulin subcutaneously.
    c. Call for an ambulance to transport the patient to a medical facility.
    d. Administer glucagon 1 mg intramuscularly (IM) or subcutaneously.
    22. The patient with diabetes is brought to the emergency department by his
          family members, who say that he is not acting like himself and he is more
          tired than usual. Number the nursing actions in the order of priority for this
          patient.
    a. Establish IV access.
    b. Check blood glucose.
    c. Ensure patent airway.
    d. Begin continuous regular insulin drip.
    e. Administer 0.9% NaCl solution at 1L/hr.
    f. Establish time of last food and medication(s).
    23. What disorders and diseases are related to macrovascular complications
    of diabetes?
    a. Chronic kidney disease
    b. Coronary artery disease
    c. Microaneurysms and destruction of retinal vessels
    d. Ulceration and amputation of the lower extremities

    e. Capillary and arteriole membrane thickening specific to diabetes