IV.

Textbook Discussion
A. Definition

1. Diabetes Mellitus              
It is a group of metabolic diseases characterized by elevated levels of glucose in the blood
(hyperglycemia) resulting from defects in insulin secretion, insulin action, or both (American Diabetes
Association [ADA], Expert Committee on the Diagnosis and Classification of Diabetes Mellitus, 2003). Normally a
certain amount of glucose circulates in the blood. The major sources of this glucose are absorption of ingested
food in the gastrointestinal (GI) tract and formation of glucose by the liver from food substances. Insulin, a
hormone produced by the pancreas, controls the level of glucose in the blood by regulating the production and
storage of glucose. In the diabetic state, the cells may stop responding to insulin or the pancreas may stop
producing insulin entirely. This leads to hyperglycemia, which may result in acute metabolic complications such
as diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar nonketotic syndrome (HHNS).

CLASSIFICATION OF DIABETES (ADA, Expert Committee on the Diagnosis and

Classification of Diabetes Mellitus,2003)

Type 1 diabetes  previously referred to as insulin-dependent diabetes mellitus

 characterized by destruction of the pancreatic beta cells. It has 2 types; type 1A,
immune-mediated diabetes and type 1B or the idiopathic DM. Because of loss of
the first-phase insulin response, all people with type 1A diabetes require
exogenous insulin replacement to reverse the catabolic state and control the
blood glucose. Type 1 DM is a catabolic disorder characterized by an absolute lack
of insulin, elevation in blood glucose, and a breakdown of body fats and proteins. (
Porth; Pathophysiology, Concepts of Health States; 7 th edition 2005; Lippincott
Williams & Wilkins; P. 994-995)
Type 2 diabetes  previously referred to as non-insulin dependent diabetes mellitus
 results when insulin fails to bind with the special receptors on cell surfaces and the
series of reactions involved in glucose metabolism is diminished thus, making the
insulin less effective at stimulating glucose uptake by the tissues and at regulating
glucose release by the liver. The exact mechanisms that lead to insulin resistance
and impaired insulin secretion in type 2 DM are unknown, although genetic factors
are thought to play a role. For most patients, type 2 DM is detected incidentally.
Once consequence of undetected diabetes is that long term diabetes
complications such as eye disease, peripheral neuropathy and peripheral vascular
disease ( heart attack) that may have developed before the actual diagnosis of
diabetes is made.
 Insulin resistance is associated with obesity, the primary treatment of type 2 Dm is
weight loss. Exercise is also important in enhancing the effectiveness of insulin diet
 that causes DM includes refined grain products, fatty meats and fish, dairy
products, carbonated sodas and foods with “empty” calories.

2. Diabetic Nephropathy
It is the most common cause of renal failure. It is a long-term complication of diabetes mellitus in which the
effects of diabetes result in damage to the small blood vessels in the kidneys . Renal damage shows up
approximately 15 to 20 years after onset of type 1 diabetes (insulin dependent), but it may also be a
complication of type 2 diabetes (non–insulin dependent). Careful control of blood glucose levels reduces the risk
of nephropathy in patients with diabetes.

Pathophysiology:

Multiple factors contribute to diabetic nephropathy. Widespread atherosclerotic changes occur in the
blood vessels of patients with diabetes, decreasing the blood supply to the kidney. Abnormal thickening of
glomerular capillaries damages the glomerulus, allowing protein to leak into the urine. Patients with diabetes
also commonly develop pyelonephritis and renal scarring. Another complication of diabetes, neurogenic
bladder, causes incomplete bladder emptying. This results in retention of urine, which can cause infection or
obstruction of urine, further damaging the kidneys. Initially patients lose only small amounts of protein in their
urine (microalbuminuria); this disease can be detected only with careful watching by the physician, utilizing
frequent examinations of the urine. As the disease progresses, high-output renal failure (nonoliguria) can
develop, in which a large amount of diluted urine is excreted without the usual amounts of waste product
dissolved in the urine. The patient can lose large amounts of protein in the urine and may develop nephrotic
syndrome, which causes massive edema because of low levels of albumin in the blood. As renal function
decreases, the patient needs smaller doses of insulin because the kidney normally degrades insulin. Because the
kidney is no longer able to break down insulin and excrete it, small doses of insulin circulate in the body for long
periods.

CAUSES

o Systemic Diseases: ex. Diabetes Mellitus (leading cause)

o Hypertension
o Chronic Glomerulonephritis
o Pyelonephritis (inflammation of the renal pelvis)
o Obstruction of the urinary tract
o Hereditary lesions: ex. Polycystic Kidney Disease
o Vascular Disorders
o Infections
o Toxic agents
o Environmental and Occupational Agents
 (e.g. lead, cadmium, mercury and chromium)

3. End-Stage Renal Disease

Is a progressive, irreversible deterioration in renal function in which the body’s ability to maintain metabolic
and fluid and electrolyte balance fails, resulting in uremia or azotemia
GFR is less than 5% of normal. Histologic findings of an endstage kidney include a reduction in renal capillaries
and scarring in the glomeruli. Atrophy and fibrosis are evident in the tubules. The mass of the kidneys usually is
reduced. At this final phase of renal failure, treatment with dialysis or transplantation is necessary for survival.
defined “as either (1) a GFR of less than 15 mL/min per 1.73 m 2, which is accompanied by most signs
and symptoms of uremia, or (2) a need to start renal replacement therapy (dialysis or transplantation).” (The
National Kidney Foundation Practice Guidelines; 2003)

COMPLICATIONS
Hyperkalemia Due to decreased excretion, metabolic acidosis, catabolism
and excessive intake (diet, medications, fluids)
Pericarditis, Retention of uremic waste products and inadequate
Pericardial Effusion, dialysis
Pericardial,Tamponade
Hypertension Sodium and water retention and malfunction of the rennin-
angiotensin-aldosterone system
Anemia Decreased erythropoietin production, decreased red blood
cell span, bleeding in the GI tract from irritating toxins and
ulcer formation, and blood loss during hemodialysis.
Bone Diasease, Retention of phosphorus, low serum calcium levels,
Metastatic and Vascular Calcifications abnormal Vitamin D metabolism, and elevated aluminium
levels.

4. Cardiac Dysrhythmia
Cardiac dysrhythmia (also known as arrhythmia or irregular heartbeat) is any of a large and
heterogeneous group of conditions in which there is abnormal electrical activity in the heart.
The heartbeat may be too fast or too slow, and may be regular or irregular. A heart beat that is too fast is
called tachycardia and a heart beat that is too slow is called bradycardia. Although many arrhythmias are not
life-threatening, some can cause cardiac arrest.
Arrhythmias can occur in the upper chambers of the heart, (atria), or in the lower chambers of the
heart, (ventricles). Arrhythmias may occur at any age. Some are barely perceptible, whereas others can be
more dramatic and can even lead to sudden cardiac death.

Some arrhythmias are life-threatening medical emergencies and can result in cardiac arrest. Cardiac
arrythmias are one of the most common causes of death when travelling to a hospital. Others cause symptoms
such as an abnormal awareness of heart beat (palpitations) and may be merely uncomfortable. These
 palpitations have also been known to be caused by atrial/ventricular fibrillation, wire faults, and other technical
or mechanical issues in cardiac pacemakers/defibrillators. Still others may not be associated with any
symptoms at all, but may predispose the patient to potentially life threatening stroke or embolism

5. Cardiogenic Shock
Cardiogenic shock is based upon an inadequate circulation of blood due to primary failure of
the ventricles of the heart to function effectively.
Since this is a type of shock there is insufficient perfusion of tissue (i.e. the heart) to meet the required
demands for oxygen and nutrients. Cardiogenic shock is a largely irreversible condition and as such is more
often fatal than not. The condition involves increasingly more pervasive cell death from oxygen starvation
(hypoxia) and nutrient starvation (e.g.hypoglycemia). Because of this it may lead to cardiac arrest (or
circulatory arrest) which is an acute cessation of cardiac pump function.
Cardiogenic shock is defined by sustained hypotension with tissue hypoperfusion despite adequate left
ventricular filling pressure. Signs of tissue hypoperfusion include oliguria (<30 mL/h), cool extremities, and
altered level of consciousness.
Cardiogenic shock is caused by the failure of the heart to pump effectively. It can be due to damage to
the heart muscle, most often from a large myocardial infarction. Other causes
include arrhythmia, cardiomyopathy, cardiac valve problems, ventricular outflow obstruction (i.e. aortic valve
stenosis, aortic dissection, cardiac tamponade , constrictive pericaditis systolic anterior motion (SAM)
inhypertrophic cardiomyopathy) or ventriculoseptal defects.

6. Hyperkalemia
Hyperkalemia means an abnormally elevated level of potassium in the blood. The normal potassium
level in the blood is 3.5-5.0 milliequivalents per liter (mEq/L). Potassium levels between 5.1 mEq/L to 6.0 mEq/L
reflect mild hyperkalemia. Potassium levels of 6.1 mEq/L to 7.0 mEq/L are moderate hyperkalemia, and levels
above 7 mEq/L are severe hyperkalemia.

Potassium is critical for the normal functioning of the muscles, heart, and nerves. It plays an important
role in controlling activity of smooth muscle(such as the muscle found in the digestive tract) and skeletal
muscle(muscles of the extremities and torso), as well as the muscles of the heart. It is also important for normal
transmission of electrical signals throughout the nervous system within the body.

Normal blood levels of potassium are critical for maintaining normal heart electrical rhythm. Both low
blood potassium levels (hypokalemia) and high blood potassium levels (hyperkalemia) can lead to abnormal
heart rhythms.
 The most important clinical effect of hyperkalemia is related to electrical rhythm of the heart. While mild
hyperkalemia probably has a limited effect on the heart, moderate hyperkalemia can produce EKG changes (EKG
is an electrical reading of the heart muscles), and severe hyperkalemia can cause suppression of electrical
activity of the heart and can cause the heart to stop beating.

7. Hypertensive Nephrosclerosis

The term hypertensive nephrosclerosis has traditionally been used to describe a clinical syndrome
characterized by long-term essential hypertension, hypertensiveretinopathy, left ventricular hypertrophy,
minimal proteinuria, and progressive renal insufficiency. Most cases are diagnosed based solely on clinical
findings. In fact, most of the literature dedicated to hypertensive nephrosclerosis is based on the assumption
that progressive renal failure in a patient with long-standing hypertension, moderate proteinuria, and no
evidence suggesting an alternative diagnosis characterizes hypertensive nephrosclerosis.

Most patients reaching ESRD from any cause are hypertensive, with nephrosclerosis being the classic
finding in end-stage kidneys. Regardless of the etiology, once hypertension develops, a cycle of renal injury,
nephrosclerosis, worsening of hypertension, and further renal injury is established. As a result, in a patient
presenting with ESRD, determining whether nephrosclerosis is the cause or the consequence of chronic renal
injury may be difficult.

Two pathophysiologic mechanisms have been proposed for the development of hypertensive
nephrosclerosis. One mechanism suggests that glomerular ischemia causes hypertensive nephrosclerosis. This
occurs as a consequence of chronic hypertension resulting in narrowing of preglomerular arteries and arterioles,
with a consequent reduction in glomerular blood flow. Alternatively, glomerulosclerosis occurs because of
glomerular hypertension and glomerular hyperfiltration. According to this theory, hypertension causes some
glomeruli to become sclerotic. As an attempt to compensate for the loss of renal function, the remaining
nephrons undergo vasodilation of the preglomerular arterioles and experience an increase in renal blood flow
and glomerular filtration. The result is glomerular hypertension, glomerular hyperfiltration, and progressive
glomerular sclerosis. These mechanisms are not mutually exclusive, and they may operate simultaneously in the
kidney.

Furthermore, Tracy and Ishii (2000) postulate that nephrosclerosis may not be a single disease entity in
the sense of responding to a single etiology, such as hypertension or aging.  Rather, nephrosclerosis appears to
be multifactorial. It may be, in part, a consequence of fibroplasias in microscopic arteries causing ischemic
damage to some nephrons; however, it also may be the end product of a mixture of converging separate
pathologic conditions, ie, "second hits," of which only some are known.

8. Hypertensive Cardiovascular Disease

 Hypertensive cardiovascular disease also known as hypertensive heart disease occurs due to the
complication of hypertension or high blood pressure. In this condition the workload of the heart is increased
manifold and with time this causes the heart muscles to thicken. The heart continues pumping blood against this
increased pressure and over a period of time the left ventricle of the heart enlarges and this in turn causes the
blood pumped by heart to reduce. If proper treatment is not taken at this stage then symptoms of congestive
heart failure may be observed.

High blood pressure or hypertension is among the top most factors associated with cardiovascular
diseases. This can result in ischemic heart disease.  High blood pressure is also a contributing factor to the
eventual thickening of walls of blood vessels. This increases the possibility of heart attacks and strokes.
Hypertensive cardiovascular disease is among the leading killers in present times.

9. Renal Anemia

Anemia is a common finding in patients with CKD, with a prevalence that increases gradually as GFR
declines. The prevalence of renal anemia depends on the size of the study and the selection of participants.
Diabetic status increases the prevalence of anemia in patients with CKD. Anemia in CKD is due primarily to
reduced production of erythropoietin in the kidney and secondarily to shortened red cell survival. Erythropoeitin
(EPO) is produced by peritubular cells in the kidneys of the adult and in hepatocytes in the fetus. These cells are
sensitive to hypoxia that once sensed leads to an increase in EPO production. EPO circulates in the plasma and
induces redcell production in the bone marrow after successful binding to erythroid progenitor cells. Apart from
EPO, folate, B12 and iron are needed to assure effective erythropoiesis. Factors that can dysregulate this process
include inflammation, uremic toxins, hypothyroidism, hypersplenism and ongoing infection.

Renal anemia is a disease in which the patient has an unusually low count of red blood cells. Renal is a
term that means of the kidneys, so anemia is often associated with kidney disease. This type of anemia is caused
by a lack of erythropoietin, a protein produced in the kidneys that helps to create red blood cells.

Renal anemia affects almost every organ in the body, either directly or indirectly. A combination
of hypertension and anemia can cause left ventricular hypertrophy (LVH), a complication that results from
changes in the stress of the left ventricular wall. Severe cases of anemia can lead to hospitalization and even
death.

10. Small Intestinal Ileus

Ileus is a term used for aperistaltic bowel not caused by a mechanical obstruction. Paralytic ileus describes
the condition in which the bowel ceases to function and there is no peristalsis. Intestinal pseudo-
obstruction is also called Ogilvie's syndrome. It results from massive dilatation of the colon but possibly
small intestine too. It may occur in association with a number of medical conditions including:
  Chest infection
 Acute myocardial infarction
 Stroke
 Acute renal failure
 Puerperium
 Trauma
 Severe hypothyroidism
 Electrolyte disturbance
 Diabetic ketoacidosis

11. Metabolic Disturbances

Disorders of metabolism principally involve an imbalance in nucleic acids, proteins, lipids,

or carbohydrates. They are usually associated with either a deficiency or excess resulting in an imbalance in a
particular metabolic pathway. All metabolic disorders have a genetic background, and some of them are
expressed as specific genetic diseases. Other factors affecting metabolism include internal control mechanisms
that are superimposed on the genetic background. One of the most important mechanisms is
the hormonal control system, which consists of the endocrine, paracrine, and autocrine systems. The second
control system that has a significant effect on metabolism is the neural control system. The third control system
is the immune control system, which relates to both the endocrine and neural systems. Genetic background,
environmental factors, and the three major control mechanisms, in conjunction with age and sex, bring about
profound changes in metabolism, which ultimately result in structural and functional alterations.

B.Signs and Symptoms

Symptoms/signs based on book Symptoms/signs manifested by patient

 Abnormal apical rate and rhythm (+) August 2013

 Abnormal ECG reading (-) no lab result

 Altered level of Consciousness (-) August 2013

 Altered mental state (+) August 2013

 Ammonia odor (-)

 Anemia (+) August 2013

 Anorexia (+) August 2013

 Asterixis (-)

 Bone pain (-)

 Chest pain (-)

 Cold-clammy skin (-)

 Decreased libido (+)

 Decreased urine output (+)

 Diaphoresis (-)

 Disorientation (-)

 Dizziness (-)

 Dry flaky skin (+) August 2013

 Edema (+) August 2013

 Fatigue (+) August 2013

 Fractures (-)

 GI bleeding (-)

 Heart failure (-)

 hyperkalemia (+) August 2013

 Hyperlipidemia (-)

 Hyperphosphatemia ( )

 Hypertension (+) August 2013

 Hypocalcemia (+) August 2013

 Hypotension (-)

 Increased Creatinine (+) August 2013

 Macroalbuminuria (-)

 Metabolic acidosis

 Muscle cramps and spasms (-)

 Numbness (-)
  Osteodystrophy (-)

 Palpitation (-)

 Paralysis (-)

 Pericardial friction (-)

 Pruritus (+) August 2013

 Pulmonary edema (-)

 Rapid deep inspirations (-)

 Rapid thread pulse (-)

 Shortness of breath (-)

 Syncope (+) August 2013

 Thin, brittle nails (-)

 Thrombocytopenia (-)

 Uremic frost (-)

 Uremic lung (-)

 Weight gain (-)

References:

National Library of Medicine; National institute of Health; Retrieve August 19, 2013 from
http://www.nlm.nih.gov/medlineplus/ency/article/000494.htm ;
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3139678/

WiseGeek; Retrieved Ausgust 19, 2013 from http://www.wisegeek.com/what-is-renal-anemia.htm

Port, C.M. & Matfin, G.; Pathophysiology: concepts of of Altered Health States, 8th Edition
Smeltzer, S. , Bare, B, Hinckle, J., Cheever, K. ;Brunner and Suddarth's Textbook of Medical Surgical Nursing /
Edition 12
Right diagnosis; retrieved August 19, 2013 at http://www.rightdiagnosis.com/d/diabetic_nephropathy/intro.htm

Right diagnosis; retrieved August 19, 2013 from http://www.rightdiagnosis.com/h/hyperkalemia/intro.htm

Medscape Reference; retrieved August 19, 2013 from http://emedicine.medscape.com/article/244342-

overview#a0104

InfoJug; Retrieved August 19, 2013 from http://www.infojug.com/articles/hypertensive-cardiovascular-

disease.html