Genitourinary nursing

NURSING INTERVENTION
OF PATIENTS WITH
GENITOURINARY DISORDERS

Mulugeta Emiru
(MSc in Adult Health Nursing)
Mizan-Tepi University,Ethiopia

2017

Review of anatomy and physiology

The urinary system comprises of Kidneys, Ureters, Bladder

and Urethra

Hepatic veins (cut) Esophagus (cut)

Nephron

m functional units of the kidney

m Each kidney consists 1 million nephrons

amino acids
salts

proximal convoluted tubule.
glomerular capsule,

glucose

efferent arteriole. tubule
HO >

urea

uric acid
glucose
amino acids
salts

renal artery

collecting
duct

capillary
network

loop of the’
nephron

NHa*
creatinine

Urine formation complex three-step
process:
- Glomerular Filtration:
- Tubular Reabsorption: Amino acids and glucose

- Tubular Secretion

Kidney
tubule
Filtration

Glomerulus

Peritubular
capillary

A Figure 22.5 Processes involved in urine formation.

1 Lto 2 L of urine each day

Functions of kidneys

+ Water balance
Re gulatory » Electrolyte balance Na*,K*,Ca**, CI
+ Acid base balance

« Erythropoietin

+» Renin

+ PGs

» Alpha 1 hydroxylase enzyme

Functions of kidneys
Excretory
m Renal clearance refers to the ability of the
kidneys to clear solutes from the plasma.
m BUN and creatinine are used to determine GFR.

m Creatinine clearance is a good measure of the
glomerular filtration rate (GFR).

BUN =10-20 mg/dl
Serum creatinine=0.6-1.2mg/dl
GFR =125 to 200 mL/min

+ As renal function declines, creatinine clearance decreases.

6

Regulatory- water balance

Brain monitors water content of blood

y

If low water content, pituitary releases ADH

y

ADH travels in blood to nephron

y

ADH causes more water to move from urine back into blood

Electrolyte balance
m Electrolyte gained = Electrolyte excretion
m The regulation of sodium excreted depends on
aldosterone released by the adrenal cortex.

Endocrine
1. Erythropoietin production
2. Renin secretion

3. PGs secretion

Assessment of GUS

pe Pe

Health History
Physical Examination
Laboratory investigations and

Diagnostic Tests

Health History

m Keep privacy and be confidential
m Needs communication skill
m The health Hx includes

a C/C

m HPI

m general health,

m childhood and family illnesses,

m past medical history, allergies, sexual and reproductive

health, exposure to toxic chemicals or gas, and
m Medication history

10

S/S
v Pain

Y nausea, vomiting, diarrhea, abdominal
discomfort, and abdominal distention.

v Unexplained Anemia

Y Changes in Voiding:

Changes in Voiding includes:

Frequency Frequent voiding—more than
every 3h

Urgency Strong desire to woid

Dysuria Painful or difficult voiding

Hesitancy Delay, difficulty im initiating
woidine

Nocturia Excessive urination ar night

Incontinence Involuntary loss of urine

Enuresis Involuntary voiding during sleep

Polyuria Increased volume of urine voided

Oliguria Wrine output less than 500 mL/day

Amuria Urne output less than 50 mL/day

Hematuria Red blood cells in the urine

Proteinuria Abnormal amounts of protein in

the urine

Physical Examination

m Prior to examination ask the client to void
m Inspection
m Auscultation
m Percussion
m Palpation
m assesses for signs of electrolyte and water
imbalances
- Periorbital edema (swelling around the eyes)
- Edema of the extremities
- Cardiac failure

- Mental changes

m Vital signs and weight

Diagnostic tests

m Plain x-ray / KUB x-ray

- size and position of the kidneys, ureters, and bony
pelvis

- urinary calculi (stones),
- anatomic defects of the bony spinal column

m Cystoscopy- Direct visualization of the bladder
- used to identify the cause of painless hematuria,
urinary incontinence, or urinary retention.

- evaluation of structural and functional changes of
the bladder

m Cystogram

- A catheter is inserted in to the bladder and contrast agent
is then instilled over line the bladder wall

- To aid in evaluating vesico-ureteral reflux

a IVP
- contrast medium administered intravenously
- visualization of the KUB

m Retrograde pyelography
- Urethral catheters are passed up through the ureter
in to the renal pelvis by means of cystoscopy.
- Contrast agent is then introduced by injection

through the catheter.

m Ultrasonography
- Isa noninvasive procedure that uses sound
waves passed into the body through a transducer
to detect abnormalities of internal tissues and

organs.

- Abnormalities such as fluid accumulation,
masses, congenital malformations, changes in

organ size, or obstructions can be identified.

m CT & MRI

Laboratory investigations

Urinalysis

- the study of the components and characteristics of the urine.

- Aclean-catch MSU from the first voiding of the morning is

preferred.

Components Normal values
Color yellow
Specific gravity 1.010 to 1.025
PH 45-8
Opacity Clear
Glucose Negative
Ketone Negative
Protein/albumin Negative
Bilirubin negative
Bacteria None
Parasites None
Casts None
Crystals none
RBCs 0-3
WBCs 0-5

Urine osmolality:

50-1200 mOsm/kg considered normal
200-800 mOsm/kg average

m Urine macroscopic and microscopic characteristics.
Dipstick test

a A thin, plastic stick with strips of chemicals on it is placed in the
urine to detect abnormalities.
m A dipstick test checks for:

- Acidity (pH). The pH level indicates the amount of acid in
urine.

- Concentration /specific gravity, shows how concentrated
particles are in urine. A higher than normal concentration
often is a result of not drinking enough fluids.

- Protein. Low levels of protein in urine are normal. but
larger amounts may indicate a kidney problem.

- Sugar- Any detection of sugar on this test usually calls for
follow-up testing for diabetes.

- Ketones, Bilirubin, nitrites or leukocyte esterase, Blood

Microscopic exam

m White blood cells (leukocytes) may be a sign of an

infection.

m Red blood cells (erythrocytes) may be a sign of kidney
disease, a blood disorder or another underlying medical

condition, such as bladder cancer.
m Bacteria or yeasts may indicate an infection.

m Casts and Crystals from chemicals in urine may be a sign

of kidney stones.

RFT / Renal Function Tests

- Use
" to assess the status of the patient s kidney function.
u to evaluate the severity of kidney disease

- Includes
" concentration tests,

= serum creatinine and creatinine clearance,

" blood urea nitrogen /BUN/ levels.

Renal concentration tests
1. Specific Gravity:
- a measurement of the kidney $ ability to concentrate
urine
- compares the weight of urine (weight of particles)
to the weight of distilled water

- depends largely on hydration status: When fluid
intake decreases, specific gravity normally

increases, and vice versa.

urine specific gravity is 1.010 to 1.025

m Diseases decrease sp. gr of urine
E.g.

- Diabetes insipidus
- glomerulonephritis, and

- severe renal damage

m Diseases increase sp. gr of urine
E.g.
- DM,
- nephrosis, and

- excessive fluid loss

2. Urine osmolality:
m Urine osmolality reflects the ability of the kidney to
concentrate and dilute urine, through measurement of

the number of particles in a kilogram of solution.

Urine osmolality:
50-1200 mOsm/kg considered normal;

200-800 mOsm/kg average
Osmolality of blood = 280 to 300 mOsm/kg.

Creatinine Clearance Test

Creatinine is a chemical waste molecule that is generated

from muscle metabolism.
Used to determine excretory function of kidney.

Creatinine is filtered by the glomeruli and is excreted at

a fairly constant rate by the kidney.

Creatinine excretion is not affected significantly by

dietary or fluid intake

m Increased serum creatinine level indicate

decreased renal function

= Creatinine is more accurate indicator

for renal function than the BUN.

Serum Creatinine level: 0.6-1.2 mg/dL (50-110 mmol/L)

BUN / Blood Urea Nitrogen

m Urea is nitrogenous end product of protein
metabolism.

m Serves as index of renal function.

m Test values are affected by protein intake, tissue
breakdown, and fluid volume changes.

m Rises when renal function deteriorates.

Blood urea nitrogen [BUN: 10-20 mg/dl]

Changes in the Urinary System Related to Aging

Nephrons decrease, resulting in decreased filtration and gradual
decrease in excretory and reabsorptive functions of renal tubules.

Glomerular filtration rate decreases, resulting in decreased renal
clearance of drugs.

Blood urea nitrogen increases 20% by age 70.
Sodium-conserving ability is diminished.

Bladder capacity decreases.

Renal function increases when client is lying down.

Bladder and perineal muscles weaken, resulting in inability to
empty bladder.

Incidence of stress incontinence increases in females.

Prostate may enlarge, causing frequency or dribbling.

FLUID AND ELECTROLYTE BALANCE

© To maintain proper balance, the amount of fluid gained and lost

must be equal.
© There are two major fluid compartments.
ICF and ECF

5 NY
© ECF again has two comp. Y Fe.)

© Intravascular

Intracellular

fluid (35% to 40% of
body weight)
Extracellular

© Interstitial

(intravascular) ee poate
\ 0 x fluid (5% of body weight) body weight)
= Extracellular
(interstitial) fluid
(10% to 15% of
/ a N body weight)

o Body fluid normally shifts between the two major
compartments or spaces in an effort to maintain an

equilibrium between the spaces.
o Loss of fluid from the body can disrupt this
equilibrium.

o Sometimes fluid is not lost from the body but is
unavailable for use by either the ICF or ECF called
third-space fluid shift, or “third spacing”

m Fluid balance is maintained by
- Osmoreceptors (the release or inhibition of ADH)

- Renin-angiotensin-aldosterone system

Secretion of atrial natriuretic peptide /ANP/.

Thirst

Electrolytes
o Electrolytes in body fluids are active chemicals that
carry an electrical charge when dissolved in fluid (cations

and anions).

Cations Anions
Sodium Chloride
Potassium Bicarbonate
Calcium Phosphate and
Magnesium and Sulfate

Hydrogen ions.

o Electrolyte concentrations in the ICF differ from those in

the ECF.

Extracellular Fluid Intracellular Fluid

75 mEq/L
2 mEq/L
- 281 mOsm/L

m Normal movement of fluids through the capillary wall
into the tissues depends on hydrostatic pressure and

colloidal osmotic pressure.

m Body fluids across the compartments is regulated by

m Osmosis
m Diffusion 9
m Filtration o

m Na* - K*pump

HYPOVOLEMIA / FVD

m Occurs when loss of ECF volume exceeds intake.
Causes

m GI losses- Vomiting, diarrhea, suctioning

m Sweating and hemorrhage

m Decreased intake

m Third-space fluid shifts

Acute weight loss; orthostatic hypotension
decreased skin turgor; oliguria; concentrated urine
Weak, rapid pulse; flattened neck veins;

Thirst; decreased or delayed capillary refill; decreased

central venous pressure

Cool, clammy, pale skin, lassitude; muscle weakness; and

cramps.

Diagnostic Findings
m The cause of hypovolemia may be determined

through the health history and physical

examination.

m BUN: creatinine ratio > 20:1

Nursing Dx & Management

NDx.

Deficient Fluid Volume
Decreased cardiac output
Ineffective tissue perfusion

Mgx

m Treat the cause

m When the deficit is not severe, the oral route is preferred
m When fluid losses are acute or severe, IV 0.9% NaCl.

m As soon as the patient becomes normotensive, 0.45% NaCl

provides both electrolytes and water, helps excretion of wastes.

39

m Monitor fluid I/O at least every 8 hours, and sometimes

hrly.
m Body weights daily, Skin turgor
m Vital signs are closely monitored.

m T°, Pulse, B/P ( postural hypotension )

.»

HYPERVOLEMIA / FVE

m Isotonic expansion of the ECF caused by the
abnormal retention of water and sodium.
Contributing factors include
+ heart failure,
- renal failure, and
- cirrhosis of the liver

- consumption of excessive amounts of salts

CMs

m Edema, distended neck veins, and crackles, SOB and

wheezing;

m Increased blood pressure, pulse pressure, and central
venous pressure; tachycardia, increased weight; increased
urine output.

Diagnostic Findings

m BUN and hematocrit, Urine sp. Gr, serum osmolality

m Serum Sodium level, CVP, Chest x-rays

Medical Management

m Management of FVE is directed at the causes.

m When the fluid excess is related to excessive
administration of sodium-containing fluids, discontinuing

the infusion may be all that is needed.

m Symptomatic treatment consists of administering diuretics

and restricting fluids and sodium.
Other modalities

m Dialysis and Renal transplantation

Nursing Dx & Management
1. Excess Fluid Volume related to intake that exceeds fluid loss
AEB...
2. Risk for Impaired Skin Integrity related to compromised
circulation secondary to edema
3. Impaired skin integrity
4. Impaired gas exchange
Mex
m Measure I/O, weigh daily,

m Assess breath sounds,

m Monitor the degree of edema

Electrolyte imbalances

- Sodium imbalance

- Potassium imbalance -
- Calcium imbalance q C4

Alteration in Sodium Na* Balance

m The chief cation in ECF,

m Essential for maintaining normal nerve and muscle

activity and regulating osmotic pressure.

m The principal role of sodium is to regulate and

distribute fluid volume in the body
135 to 145 mEq/L

hyponatremia < > hypernatremia

Normal

Sodium Deficit (Hyponatremia)

m Hyponatremia- serum sodium <135 mEq/L

m Hyponatremia primarily occurs due to an imbalance of
water rather than sodium

m Can occur together with FVD or FVE.

Causes

- Renal loss- high sodium is detected in urine E.g.
diuretic use

- Non renal loss- low sodium is detected in urine as
the kidney retains sodium to compensate for non-
renal fluid loss. E.g. vomiting, diarrhea, sweating

- Aldosterone deficiency, as occurs in adrenal
insufficiency. a

C/Ms
m Signs of DHN and GI symptoms like nausea,
abdominal cramping, anorexia, muscle cramps, and

a feeling of exhaustion, Altered mental status.

m When the serum sodium level drops below 115
mEq/L, Neurologic changes (signs of increasing
intracranial pressure), such as lethargy, confusion,
muscle twitching, focal weakness, and seizures,

may occur.

Diagnostic Findings
m Serum sodium level is <135 mEq/L

m Serum osmolality is also decreased, except in

azotemia or ingestion of toxins.

m Urinary sodium

Medical Management
m Assess speed with which hyponatremia occurred
- Acute hyponatremia causes severe cerebral edema
and compression of midbrain structures.
m Careful sodium replacement either by mouth,

nasogastric tube, or parenteral route.

m Serum sodium must not be increased by greater
than 12 mEq/L in 24 hours, to avoid neurologic

damage.

m Hyponatremia with normal or excess fluid is treated by
fluid restriction. When neurologic symptoms are present,
however, it may be necessary to administer small volumes
of a hypertonic sodium solution, such as 3% or 5%
sodium chloride.

Nursing Met.

a I/O, weight

m Assess for abnormal losses of sodium or gains of water

m alert for CNS changes

SODIUM EXCESS (Hypernatremia)
m > 145 mEq/L [145 mmoVL])

m Can be caused by
- a gain of sodium in excess of water or
- a loss of water in excess of sodium.
m It can be associated with FVD or FVE.
Causes

- Administration of hypertonic enteral feedings without
adequate water

- watery diarrhea and greatly increased insensible water
loss (hyperventilation, Increased sweating)

- Diabetes insipidus, a deficiency of ADH

C/Ms
m Symptoms are related with cellular dehydration.

m A primary characteristic of hypernatremia is thirst

m Subarachnoid hemorrhages that result from brain
contraction.

m Restlessness and weakness in moderate hypernatremia and
disorientation, delusions, and hallucinations in severe
hypernatremia.

m Increased muscle tone and deep tendon reflexes

Diagnostic Findings
m serum sodium >145 mEq/L

m serum osmolality >295 mOsm/kg

m Urine sp. gr and urine osmolality are increased

Medical Management
m Gradual lowering of the serum sodium level
hypotonic solution (eg, 0.3% NaCl) thereby
decreases the risk of cerebral edema
-Isotonic nonsaline solution (eg, dextrose 5% in
water [D5W]]).
Nursing Management
m I/O, Diuretics
m obtain a medication history because some
prescription medications have a high sodium
content

m monitor for changes in behavior

Alteration in potassium K* Balance

m The chief cation intracellularly.

3.5 to 5.0 mEq/L
hypokalemia hyperkalemia
Normal
m This significant difference in the potassium
concentrations of ICF and ECF helps maintain the
resting membrane potential of nerve and muscle

cells.

Potassium Deficit
(HYPOKALEMIA)

m < 3.5 mEq/L
m GI loss is probably the most common cause

- severe vomiting or diarrhea, draining intestinal

fistulae, or prolonged suctioning
m Recent ileostomy, Potassium-wasting diuretics

m Alterations in acid-base balance have a significant effect

on potassium distribution.

m Hypokalemia can cause alkalosis, and in turn

alkalosis can cause hypokalemia.

m Leads to membrane hyperpolarization and

reduced excitability

m Hyperaldosteronism increases renal potassium
wasting and can lead to severe potassium

depletion.

C/Ms

m fatigue, anorexia, nausea, vomiting, muscle
weakness, leg cramps, decreased bowel motility,
paresthesia (numbness and tingling),
dysrhythmias, and increased sensitivity to
digitalis.

m Potassium depletion depresses the release of

insulin and results in glucose intolerance.

Diagnostic Findings
m ABGs values are checked for elevated

bicarbonate and pH.

m Hypokalemia produces characteristic changes in

the electrocardiogram (ECG) waveform.

T T
R R
Flattened T-wave
T U-wave
|
P P y y
PR |
‘interval “— | — S-T segment s S-T segment depression
oT Ts
A B
[Tall tented
Wide TT wave
QRS +
Prolonged
P-R interval |S-T segment depression
c

FIGURE 16-8. Effects of potassium on ECG. (A) Normal tracing. (B) Serum potassium level below normal (hypokalemia) results in ST segment
depression, flattened T wave, and a U wave. (C) High potassium level (hyperkalemia) produces prolonged PR interval; widened ORS; ST
segment depression; and a tall, peaked T wave. (From Porth, C. [2007]. Essentials of pathophysiology: Concepts of altered health states.
Philadelphia: Lippincott Williams & Wilkins).

Medical Management

m For patients at risk for hypokalemia, a diet
containing sufficient potassium should be
provided.

m When dietary intake is inadequate for any reason,
the physician may prescribe oral KCl.

m The IV route is mandatory for patients with severe

hypokalemia (e.g., a serum level of 2 mEq/L).

Nursing Management

= monitor for its early presence in patients at risk.

m Fatigue, anorexia, muscle weakness, decreased
bowel motility, paresthesia, and dysrhythmias are
signals that warrant assessing the serum

potassium concentration.

NDx

m Decreased Cardiac Output
= Activity Intolerance

m Risk for Imbalanced Fluid Volume

POTASSIUM EXCESS (HYPERKALEMIA)

m Hyperkalemia can result from inadequate
excretion of potassium, excessively high intake
of potassium, or a shift of potassium from the

ICF to the ECF..

m Patients with hypoaldosteronism have sodium

loss and potassium retention.

m Medications have been identified as a probable
contributing factor in more than 60% of

hyperkalemic episodes.

m Medications commonly implicated are KCl,
angiotensin-converting enzyme inhibitors
(ACEIs), potassium-sparing diuretics, heparin,

and NSAIDs.

CMs

m The most important consequence on the

myocardium, depolarizes cardiac cells.

m Cardiac effects of hyperkalemia are usually not
significant <7 mEq/L, but they are almost always

present when the level is 8 mEq/L or greater.

m Skeletal muscle weakness and even paralysis,

related to a depolarization block in muscle.

m Rapidly ascending muscular weakness-- quadriplegia
m Similarly, ventricular conduction is slowed.

m Paralysis of respiratory and speech muscles
Diagnostic Findings

m Serum potassium

m ECG changes are crucial to the diagnosis of

hyperkalemia.

m ABG analysis- hyperkalemia occurs with acidosis

Medical Management
m Mild hyperkalemia is treated by decreasing the

intake of potassium rich foods or discontinuing oral

potassium replacement.

m Severe hyperkalemia is treated by intravenously
administering a combination of regular insulin and
glucose that temporarily shifts serum potassium
into cells within 30 minutes of administration.

m Dialysis

Nrs mgx- same as hypokalemia

Acid—base Disturbances

Acid-Base Balance
In addition to water and electrolytes, body fluid also
contains acids and bases.

Acid and base content influence the pH of body fluid.

pH refers to the amount of hydrogen ions in a solution. The
greater the H* concentration, the more acidic the solution

and the lower the pH.

The optimal PH of various body fluids differs but not very

much.

m The normal PH value is:
- 7.45 for arterial blood
- 7.35 for venous blood and intestinal fluid
m Acid-base balance is situation in which the PH of the
blood is maintained between 7.35 and 7.45.
m Imbalances occur in the form of:
- Alkalosis- arterial blood PH rises above 7.45

- Acidosis- A drop in arterial PH below 7.35

Acid Base Regulatory Mechanisms

m The body maintains the normal plasma pH by
m Chemical regulation / buffer system

m Organ regulation / lung and kidney

Buffer Systems 1“ line of defense

Buffer systems prevent major changes in the pH of body
fluids by removing or releasing H*; they can act quickly to
prevent excessive changes in H* concentration.

Ht ions are buffered by both IC and EC buffers.

The body’s major EC buffer system is the bicarbonate-

carbonic acid buffer system.

Less important buffer systems in the ECF include the

inorganic phosphates and the plasma proteins.

Normally, there are 20 parts of bicarbonate (HCO; ) to 1
part of carbonic acid (H,CO;)

If this ratio is altered, the pH will change.

It is the ratio of HCO,” to H,CO, that is important in
maintaining pH, not absolute values.

CO, is a potential acid; when dissolved in water, it becomes
carbonic acid

(CO, + H,O = H,CO,).
Thus, when CO2 is increased, the carbonic acid content is
also increased, and vice versa.

m If either bicarbonate or carbonic acid is increased or
decreased so that the 20:1 ratio is no longer maintained,
(acid—base imbalance results).

m When strong acid is added,
- HCO3 + H* >H2C03 >C02 + MO
- The CO2 is eliminated by respiratory system

m When strong base is added
- H2C03 + OH > HCO3 + H,O

= The HCOS3 is eliminated by the kidney with urine

Lungs- 2nd line of defense

m The lungs, under the control of the medulla, control the CO,

and thus the carbonic acid content of the ECF.

m They do so by adjusting ventilation in response to the

amount of CO, in the blood.

m Arise in the partial pressure of CO, in arterial blood (Pa

CO,) is a powerful stimulant to respiration.

m In metabolic acidosis, the respiratory rate increases, causing

greater elimination of CO, (to reduce the acid load).

m In metabolic alkalosis, the respiratory rate decreases,

causing CO, to be retained (to increase the acid load).

Hypoventilation ( Jed rate& Ted Paco,
depth of respiration SA

[

Stimulation of central
chemoreceptor

Inhibition of control
chemoreceptor

I

Led Pa Co? Ted rate & depth of
respiration

ET | (hyperventilation)

Fig:- Neural regulation of respiration and H+ concn.

Kidneys- 34 line of defense
m The kidneys regulate the bicarbonate level in the ECF; they
can regenerate bicarbonate ions as well as reabsorb them

from the renal tubular cells.

m In respiratory acidosis and most cases of metabolic acidosis,
the kidneys excrete H* and conserve HCO; to help restore

balance.

m In respiratory and metabolic alkalosis, the kidneys retain Ht

and excrete HCO; to help restore balance.

m Renal compensation for imbalances is relatively slow (a

matter of hours or days).

A level
6. bo 7. bo
Normal values
HCO, =22-26 mEq/L
PaCO, =35-45mmHg
Bicarbonate 20 parts

Carbonic acid 1 part

METABOLIC ACIDOSIS
(BASE BICARBONATE DEFICIT)
Metabolic acidosis is a clinical disturbance characterized by
increased organic acids (acids other than carbonic acid), a
low pH, increased H+ concn., and a low plasma

bicarbonate concn.
It can be produced by a gain of H* or a loss of HCO;.

Organic acids increase during periods of anaerobic

metabolism. It occurs during shock and cardiac arrest.

m Acids also increase in starvation and DKA, as fatty acids
accumulate because the body cannot use glucose for energy.
m Accumulation of acids also may follow :
m renal failure
m Aspirin (acetylsalicylic acid) over dosage
m profuse diarrhea and loss of intestinal fluid through
wound drainage

m Hyperkalemia

Clinical Manifestations

Kussmaul’s breathing
anorexia, nausea, vomiting, abdominal pain or discomfort

Peripheral vasodilation and decreased cardiac output,

dysrhythmias, and shock

headache, confusion, flushing, lethargy, malaise, drowsiness

and weakness.

stupor and coma occur, and death may follow shortly.

Diagnostic Findings

m ABG measurements

Expected blood gas changes include a low pH and plasma HCO3.
PaCO2 is normal initially, a condition referred to as an
uncompensated state.

As the rapid and deep breathing becomes effective, PaCO,
decreases until pH returns to normal, it is referred to as a
partially compensated state.

When pH returns to normal, it is referred to as a fully

compensated state.

Medical Management
m Treat the cause.

m If the problem results from excessive intake of chloride,

treatment is aimed at eliminating the source of the chloride.

m When necessary, bicarbonate is administered if the pH is

less than 7.1 and the bicarbonate level is less than 10.

CARBONIC ACID-BICARBONATE BUFFER SYSTEM BICARBONATE RESERVE

Fixed acids or
organic acids:
add Ht

CO; + H,0 (um

Medical Management
m Although hyperkalemia occurs with acidosis, hypokalemia
may occur with reversal of the acidosis and subsequent

movement of potassium back into the cells.

m Therefore, the serum potassium level is monitored closely

and hypokalemia is corrected as acidosis is reversed.

m Treatment modalities may also include hemodialysis or

peritoneal dialysis.

METABOLIC ALKALOSIS
(BASE BICARBONATE EXCESS)

m Metabolic alkalosis is a clinical disturbance characterized
by a high pH (decreased H+ concn) and a high plasma

bicarbonate concn.

m It can be produced by a gain of bicarbonate or a loss of

H+.

m Probably the most common cause of metabolic alkalosis is
vomiting or gastric suction with loss of hydrogen and

chloride ions.

m The disorder also occurs in pyloric stenosis, in which only gastric

fluid is lost.
m Gastric fluid has an acid pH (usually 1-3); therefore, loss of this
highly acidic fluid increases the alkalinity of body fluids.

m Other situations predisposing to metabolic alkalosis include those

associated with loss of potassium, such as:

- Diuretic therapy that promotes excretion of potassium (eg,

thiazides, furosemide), and
- hyperaldosteronism

- Chronic ingestion of milk and calcium carbonate.

Clinical Manifestations
m Alkalosis is primarily manifested by symptoms related to
decreased ionized calcium, such as tingling of the fingers

and toes, dizziness, and hypertonic muscles and tetany.

m Respirations are depressed as a compensatory action by the

lungs.

= Symptoms of hypokalemia; ventricular disturbances,

decreased motility and paralytic ileus may occur.

Diagnostic Findings
m Evaluation of ABG reveals a pH >7.45 and a serum

bicarbonate concentration >26 mEq/L.

m The PaCO, increases as the lungs attempt to compensate for

the excess bicarbonate by retaining CO).

Medical Management

m Reverse the underlying disorder.

a Sufficient chloride must be supplied for the kidney to
absorb sodium with chloride (allowing the excretion of

excess bicarbonate).

m Treatment also includes restoring normal fluid volume by
administering sodium chloride fluids (because continued

volume depletion serves to maintain the alkalosis).

m potassium is administered as KCI to replace both K+ and

Cl- losses.

a Histamine-2 receptor antagonists, such as cimetidine
(Tagamet), reduce the production of gastric HCl, thereby
decreasing the metabolic alkalosis associated with gastric

suction.

m Carbonic anhydrase inhibitors

RESPIRATORY ACIDOSIS
(CARBONIC ACID EXCESS)

m Respiratory acidosis is a clinical disorder in which the pH is

<7.35 and the PaCO, is >45 mm Hg.

m Respiratory acidosis is always due to inadequate excretion
of CO, with inadequate ventilation, resulting in elevated
plasma CO, levels and thus elevated carbonic acid (H,CO;)

levels.

Acute respiratory acidosis occurs in emergency situations,

such as:

Acute pulmonary edema,

Aspiration of a foreign object,

- Atelectasis, or pneumothorax,

Overdose of sedatives,
- Sleep apnea syndrome,

ARDS

Clinical Manifestations
m Sudden hypercapnia (elevated PaCO2) can cause:

- tachypnea, tachycardia, dysrhythmias, cyanosis,
- Expiratory volumes are decreased
- behavioral changes (mental cloudiness, confusion,
disorientation, hallucinations)
Diagnostic Findings
m ABG reveals a pH <7.35, a PaCO, > 45 mm Hg

m Variation in the bicarbonate level, depending on the duration of the

acidosis.

Medical Management

m Treatment is directed at improving ventilation.

m Exact measures vary with the cause of inadequate
ventilation.

m Pharmacologic agents are used as indicated.

- For example, bronchodilators, antibiotics, and
thrombolytics or anticoagulants are used for
pulmonary emboli.

RESPIRATORY ALKALOSIS
(CARBONIC ACID DEFICIT)

m Respiratory alkalosis is a clinical condition in which the

arterial pH is >7.45 and the PaCO, is <35 mm Hg.

m Respiratory alkalosis is always due to hyperventilation,
which causes excessive “blowing off” of CO, and, hence, a

decrease in the plasma carbonic acid concentration.

m Causes can include extreme anxiety, hypoxemia, gram-
negative bacteremia, high fever and inappropriate ventilator

settings that do not match the patient’s requirements.

m Chronic respiratory alkalosis results from chronic
hypocapnia, and decreased serum bicarbonate levels

(compensatory) are the consequence.

Clinical Manifestations

m lightheadedness due to vasoconstriction and decreased
cerebral blood flow, inability to concentrate, numbness and
tingling from decreased calcium ionization, tinnitus, and at

times loss of consciousness.

m tachycardia and ventricular and atrial dysrhythmias.

Diagnostic Findings

m ABG assists in the diagnosis of respiratory alkalosis.

m In the acute state, the pH is elevated above normal as a

result of a low PaCO, and a normal bicarbonate level.

m (The kidneys cannot alter the bicarbonate level quickly.)

Medical Management

m Treatment depends on the underlying cause of respiratory

alkalosis.

m If the cause is anxiety, the patient is instructed to breath
more slowly to allow CO, to accumulate or to breath into a

closed system (such as a paper bag).

m A sedative may be required to relieve hyperventilation in

very anxious patients.

Nursing Management
m The nurse documents all presenting signs and symptoms

to provide accurate baseline data.

m Monitors laboratory values; compares ABG and

electrolyte findings with previous results
a I/O

m Administer ordered fluid and electrolyte replacements,

suctioning the airway

m monitor cardiac rate and rhythm

Example

PH > 7.45 - PH= Normal
PaCO2 < 35 ce Pa@@2< 35
HCO3 =Normal OE HE@3 < 22
PH < 7.35 - PH= Normal
PaCO2 =Normal > PaCO2 <35
HCO3 <22 __HCO3 <22
PH > 7.45 + PH=Normal
PaCO2 =Normal + PaCO2 >45
HCO3 >26 « HCO3 >26

Management of Patients
With
Urinary Disorders

INFECTIONS OF THE URINARY TRACT
Etiology:
> Common pathogens are the gram -ve bacilli,
often found in the colon includes Escherichia

coli, klebsiella, proteus, and enterobacteria.

> E. coli causes approximately 80% of acute
infections in patients without catheters, stone or

other urologic abnormalities.

PREDISPOSING FACTORS

> Factors which predispose an individual to UTI include
“* Sex- 10 times more common in females than males. Because
° The female urethra is short.
° Close proximity of female urethra to rectum

° large numbers of pyogenic bacteria inhabit the vaginal
vestibule.

» the male urethra is enclosed in the penis
“ stasis of the urine
« Instrumentation

° About 95 percent of people with catheters for three days
develop urinary tract infections.

< neurogenic bladder and Diseases (for example, DM)

Classification

> According to anatomic site of involvement

Lower UTIs -cystitis, urethritis, prostatitis

- Upper UTIs —Acute and chronic
pyelonephritis

+ According to the presence of structural urinary tract problems
- Complicated UTI
- with structural or functional abnormalities
- UTIs in men
- Catheter-associated e.g nosocomial infections
- Uncomplicated UTI
- lack structural or functional abnormalities
- Non-catheter-associated
- community-acquired

> Recurrent UTI: reinfection or relapse

127

a Asymptomatic Bacteriuria:

Bacteriuria > 10% bacteria/ml of urine without
symptoms. It is very common in elderly women

and men.
= Symptomatic abacteriuria:

Symptoms of urinary frequency and dysuria in the

absence of significant bacteriuria

Lower UTI

> Several mechanisms maintain the sterility of the bladder.

+ Physical barrier of the urethra

e Shedding of bladder epithelial cells

* Urine flow

*Uretherovesical junction competence

* Prostatic secretions and antibodies(IgA)

¢ The normal bacterial flora of the vagina and urethral
area also interfere with adherence of Escherichia coli.

* Hydrophilic protein, normally exerts a non-adherent
protective effect against various bacteria(attracts water
molecules, forming a water barrier)

Pathophysiology
> If bacteria do survive in the bladder, they adhere to the

mucosal lining of the bladder, multiply and ulcerations

may develop.

> When urine contacts these irritated areas, the client
experiences pain and urgency.

m For infection to occur,

bacteria enter bladder--- attach and colonize the
epithelium ---evade host defense mechanisms---initiate

inflammation.

Routes of Infection

= Bacteria enter the urinary tract in three ways:

Ascending infection: Urethrovesical reflux and
Vesicoureteral reflux

Hematogenous spread
Direct extension

m Many UTIs result from ascending infection from
fecal organisms.

Assessment
a S/S

- Asymptomatic bacteriuria to gram-negative

sepsis with shock.

- Dysuria, Frequency, Urgency, Nocturia,

Incontinence, Suprapubic or pelvic pain

- Hematuria and back pain may also be present

a Diagnostic Findings
- Urine analysis showing

- Pyuria (>4 WBCs/HPF)
- bacteriuria
- Hematuria (>4RBCS/HPF)

> Gram stain

> Urine culture — indicated in complicated UTIs,

recurrent UTI, Pyelonephritis and urosepsis.

> Ultrasound of the abdomen

Management

Acute, Uncomplicated UTI in women

- First line

Ciprofloxacin, 500mg P.O., BID, for 3 days
OR

Norfloxacin, 400mg P.O.,BID, for 3 days.
- Alternatives

Nitrofurantoin 50mg P.O., QID for 7 days OR
Cefpodoxime 100mg P.O, BID for 3 days OR

Cotrimoxazole 160/800mg P.O, BID for 3days

134

m Complicated UTIs
- First line and alternatives similar to
uncomplicated UTIs but needs prolonged
duration and closely followed as gram positives
could be the cause.
m Recurrent UTI in women
- postcoital voiding and have liberal fluid intake

- Antibiotic prophylaxis is provided for at least 6

months
135

Prophylaxis

m Continuous: daily at night time
m Postcoital: Single dose after coitus

- First line
Cotrimoxazole, 240mg, P.O., daily OR 3x per week OR
postcoital

- Alternatives
Cephalexin, 125 — 250mg, P.O., OR
Norfloxacin, 200mg, P.O., OR
Ciprofloxacin, 125mg, P.O., OR
Nitrofurantoin, 50 to 100mg, P.O,

once daily or postcoital

136

Upper UTI

Pyelonephritis -is a bacterial infection of the renal pelvis,

tubules, and interstitial tissue of kidneys.

> Causes -upward spread of bacteria from the bladder or
spread from systemic sources via the bloodstream.
- E.g. Systemic infections (such as tuberculosis) can spread to
the kidneys and result in abscesses.
> This is a renal disease that may be either acute or

chronic.

Acute Pyelonephritis

m Usually manifested by enlarged kidneys with

interstitial infiltrations of inflammatory cells.

m Abscesses may be noted on the renal capsule

and at the corticomedullary junction.

Clinical Manifestations

Subj. chills, fever, Low back pain, flank pain,
nausea and vomiting, headache, malaise, and

painful urination.

In addition, dysuria and frequency are

common if lower urinary tract is involved.

Phy exam- CVAT

Chronic Pyelonephritis
m Chronic pyelonephritis develops after recurrent episodes
of acute pyelonephritis.

m Kidneys become scarred, contracted, and non-

functioning.

m It is a cause of chronic kidney disease (renal failure) that
can result in the need for permanent renal replacement

therapies such as transplantation or dialysis.

140

S/S

m Some clients with chronic pyelonephritis are

asymptomatic;

m others have a low-grade fever and vague

gastrointestinal complaints.

m Polyuria and Nocturia develop when the tubules of

the nephrons fail to reabsorb water efficiently.

m Diagnostic Findings

WBC- leukocytosis

Urinalysis- bacteriuria and pyuria
Serum creat and BUN

Ultrasound or CT scan- any obstruction.

MEDICAL MANAGEMENT
> Patients with acute uncomplicated pyelonephritis are
most often treated on an outpatient basis.
> Antipain and antipyretics; antispasmodics
Mild and moderate acute uncomplicated
pyelonephritis in non-pregnant women:

- First line
Ciprofloxacin, 500mg P.O., BID, oral for 7-10
days

- Alternatives

Cotrimoxazole, 160/800mg P.O, BID for 14 days
OR

Cefpodoxime, 200mg P.O., BID for 10 days

e Severe acute uncomplicated pyelonephritis
(evidence of sepsis)

intravenous therapy should be started and continued until the
patient improves (usually at 48-72 hours) then oral therapy is
continued to complete 10-14 days course

a Ciprofloxacin, 400mg, I.V, BID OR
m Ceftriaxone, 2gm, I.V, daily or 1gm, I.V, BID till patient

improves, then

a Ciprofloxacin 500mg, PO, BID to complete 10-14
days course.

144

m If no response in 48-72 hrs ultrasound is used to evaluate
for obstruction, abscess, or other complications of

pyelonephritis.

a If obstruction or complication is not found gram +ve
organisms such as enterococci and S. saprophyticus
should be covered with Penicillins and aminoglycoside

combination.

145

Voiding disorders- Urinary retention

m Urinary retention is bladder inability to empty the urine

completely during attempts to void.

m Causes of urinary retention include an obstruction in
the urinary tract such as an enlarged prostate or bladder
stones, infections that cause swelling or irritation, nerve
problems that interfere with signals between the brain and the
bladder, medications (atropine or a phenothiazine), urethral

stricture.

m Urinary retention can occur postoperatively in any patient
146

Assessment Findings
Y” acute retention

- sudden inability to void, distended bladder, and severe
lower abdominal pain and discomfort.

Y” Chronic retention

- bladder has stretched over time and accommodates
large volumes without producing discomfort

- fever, chills, pain on urination and dribbling may be
present
m Urinalysis may show an increased number of

WBC, indicating an acute or chronic bladder
infection.

m Catheterization or ultrasound can determine post
void residual volume

147

Medical and Surgical Management

o Urethral Catheterization for both acute and chronic
o Suprapubic cystostomy tube for chronic retention

o Ifitis possible to remove the cause, such as
excising excess prostatic tissue, surgery is
performed.

Nursing Management

m measuring intake and output, palpating the
abdomen for a distended bladder, promoting
complete urination, and monitoring the voiding
pattern of clients.

a Complications
- UTIs
- bladder damage

- kidney damage

149

Voiding disorders- Urinary Incontinence
m older adults are prone for incontinence

m Urinary incontinence may result from either bladder or urethral
dysfunction (or both) due to:
- Neurologic disease,

bladder outlet obstruction /BOO/

- Trauma
- bladder prolapse and
- prostatic enlargement in men

- failure of the urethral sphincters.

150

Types

m Stress incontinence- Client has involuntary loss of urine
from intact urethra, which results from sudden increase
in intra-abdominal pressure, such as with sneezing or

coughing.

> Urge incontinence- Client experiences urge to void but

cannot control voiding in time to reach a toilet.

> Overflow incontinence- Involuntary loss of urine related

to over distended bladder

m Functional incontinence- Client has intact function of the
lower urinary tract but cannot identify the need to void or
ambulate to the toilet.

- Cognitive impairments, such as brain injury or
Alzheimer’s disease
m Total incontinence- Urine is continuously and unpredictably

lost from the bladder.

- Results from surgery, trauma, or anatomic malformation

Assessment Findings

m Clients complain of urgency, frequency, leaking
small amounts when coughing or sneezing, or

complete inability to control urine.

Medical Management

Management of urinary incontinence may be
behavioral, pharmacologic, or surgical .
Anticholinergic agents inhibit bladder contraction and
are considered first-line medications for urge

incontinence. E.g. atropine
tricyclic antidepressant medications E.g. amitriptyline

Sometimes medication to control incontinence results

in retention and must be discontinued.

Nursing Management

m Preventing skin breakdown, reducing
anxiety, and

m initiate a bladder-training program to
increase muscle tone and voluntary control.

Disorders of prostate gland

A) Prostatitis (male reproductive system)

m Prostatitis is inflammation of prostate gland caused by
infectious agent or by a variety of other problems.

> Cause

m Infectious agents - bacteria, fungi & mycoplasma

m Urethral stricture & hyperplasia of prostate

m Microorganisms usually are carried to the prostate from
the urethra.

> Clinical Manifestation

m Perineal pain and discomfort

m Urethritis: Urgency , frequency and dysuria

m Prostatodynia (pain in the prostate) on voiding.

m Acute bacterial Prostatitis may produce a sudden onset of

fever & chills, low back pain and dysuria may be evident.
> Methods of Diagnosis
m Careful history & digital examination

m culture of prostate fluid or tissue and urine culture.

Met
m Abroad spectrum antimicrobial drugs for 10 - 14 days,

a 1.V administration of the drug may be necessary to

achieve high serum and tissue level.

m Bed rest, antispasmodics, laxatives to soften stool and sitz

bath
m Patient education: therapy, fluid intake

m avoidance of sexual intercourse and prolonged sitting,

and medical follow up for at least 6 months to 1 year.

B) Benign prostate hyperplasia
(Hypertrophy) BPH
m The most common problem of the adult male

reproductive system.

m This problem occurs in about 50 % of men over 50 years

of age and 75% of men over 70 years.

m The prostate gland enlarges extending up ward in to the
bladder and obstructing the outflow of urine by

encroaching on the vesical orifice.

> Cause (Etiology)

m Uncertain but evidences suggests a hormonal
cause as initiating hyperplasia of the supporting
stromal tissue and a glandular element in the

prostate.

160

Clinical Manifestation & Diagnostic
Evaluation

m Nocturia

m Hesitancy in starting urination

m Increasing force of urinary stream
m Interruption of urinary stream,

m A sensation of incomplete emptying of the
bladder,

urine dribbles out after urination,
urinary retention (infection)
fatigue secondary to Nocturia

Anorexia, nausea and vomiting due to impaired renal

function
Epigastric discomfort due to distended bladder

Hematuria, uremia at the later stage

Diagnosis
> History and c/ms

m Symptoms of prostatism (frequency , dysuria, urgency,

dribbling, hesitancy)
> P/E

m On rectal examination the prostate is found to be

enlarged.
m Complete hematological investigation,

m x-ray and Cystoscopy examination.

> Met

m The plan of treatment depends on the cause, the severity

of obstruction and the condition of the patient.
m Catheterization to treat an acute urinary retention.

m Some times a supra pubic cystostomy to give adequate

drainage.

m Pharmacologic treatment for BPH includes use

of alpha 1-adrenergic blockers

m Antimicrobial drugs may be necessary to treat

UTI

m Surgery to remove the hyper plastic prostate
tissue to provide permanent relief of the

obstruction it is referred to as a prostatectomy.

Diseases of the kidney

Renal failure (acute and chronic)
Nephrolithiasis

Hydronephrosis

Cysts and tumors of the kidney
Glomerulonephritis (acute and chronic)
Nephrotic syndrome

Nephrosclerosis

166

RENAL FAILURE

Renal failure results when the kidneys can’t remove
the body’s metabolic wastes or perform their

regulatory functions.

The substances normally eliminated in the urine
accumulate in the body fluids as a result of impaired

renal excretion.

Classified as acute and chronic renal failure

167

Acute renal failure
m Is a sudden loss of kidney function (reduced GFR)

over a period of hours to days.
m Manifested with.
- Oliguria (<400ml/day urine)
- Anuria (<100 ml/day urine) is not common.
- Rising serum creatinine and BUN levels and
retention of other metabolic waste products.

168

Categories of ARF

Based on conditions that cause ARF
1. Prerenal failure
2. Intrarenal failure

3. Postrenal failure

169

Prerenal Failure
m Occurs because of decreased renal blood flow
m Common causes of decreased renal blood flow
include:
A. Volume depletion resulting from:
- Hemorrhage

- Renal losses (diuretics, osmotic diuresis)

- Gl losses (diarrhea, vomiting)

170

B. Cardiac insufficiency resulting from:
- Myocardial infarction
- Heart failure
- Dysrrhthmias
C. Vasodilation resulting from:
- Sepsis
- Anaphylaxis

- Antihypertensive medications

171

2. Intrarenal failure:

Results from actual parenchymal

glomeruli or kidney tubules due to:

Nephrotoxic agents,
infections,

ischemia and blockages,
polycystic kidney disease

damage

172

to

3. Post renal failure
m Usually as a result of an obstruction somewhere distal to

the kidney. Including:
- Calculi (stones)
- Tumors
- Benign prostate hyperplasia (BPH)

- Stricture and blood clot.

173

2929929299

> Prerenal failure results from:
A. bilateral obstruction of urine outflow.
B. conditions that diminish blood flow to the
kidneys.
C. damage to the kidneys themselves.

D. any preexisting condition that contributed to
renal dysfunction.

CAUSES OF ACUTE RENAL FAILURE

(D Prerenal

pressure (shock) or interruption
of blood flow to the kidneys from
severe injury or illness

@ Intrarenal
Direct damage to the kidneys
by inflammation, toxins, drugs,
infection, or reduced blood supply

Ureter
@) Postrenal
Sudden obstruction of urine flow
due to enlarged prostate, kidney
stones, bladder tumor, or injury

Prostate (in Men)
Urethra

Acute Renal Failure
m phases

- Initial —begins with the initial insult and ends
when oliguria develops.
m Acute tubular necrosis /ATN/
m 1-3 days

- Oliguric — UOP < 400/d,
m “BUN, Creat, Phos, K,

m Fluid volume excess develops
m Azotemia,

m may last up to 14d

176

- Diuretic —is marked by a gradual increase in
urine output, which signals that glomerular
filtration has started to recover.

- Laboratory values stabilize and eventually
decrease.

- UOP “to as much as 4000 mL/d but no
waste products, at end of this stage may
begin to see improvement

- Recovery — things go back to normal or may
remain insufficient and become chronic.

- 3 to 12 months

177

Signs and symptoms

- Almost every system of the body is affected

- The patient appears critically ill and lethargic with
persistent nausea, vomiting and diarrhea.

- The skin and mucous membrane are dry and the
breath may have the odor of urine.

- Excoriation and itching of the skin.

- CNS S/S include drowsiness, headache and

seizure.
178

Diagnostic findings
mChanges in urine
-Oliguria
-low specific gravity

mincreased BUN and creatinine

levels.
mhyperkalemia.
mmetabolic acidosis

mAnemia

m IVP provides evidence of renal

dysfunction

m renal biopsy shows destruction
of nephrons

m Radiography and
ultrasonography demonstrate

structural defects

179

Prevention

Clients at risk for dehydration are adequately

hydrated

Shock and hypotension are treated as quickly as

possible with replacement fluids and blood.

Continuous monitoring of renal function is very

important for clients at risk for ARF.

prevent toxic drug effects

Management

Prerenal azotemia is treated by optimizing renal
perfusion,

postrenal failure is treated by relieving the
obstruction.

Intrarenal azotemia is treated with supportive
therapy, with removal of causative agents

Fluid excesses can be detected by the clinical
findings of dyspnea, tachycardia, and distended
neck veins.

Mannitol, furosemide may be prescribed to initiate
diuresis.

181

m Adequate renal blood flow in patients with prerenal
causes of ARF may be restored by IV fluids or

transfusions of blood products.
m Infusion of albumin may be given hypoproteinemia

m Dialysis may be initiated to prevent complications of
ARE, such as hyperkalemia, metabolic acidosis,

pericarditis, and pulmonary edema.

Dialysis

m For acute renal failure, dialysis can be
done to remove toxic substance of
metabolism and correct electrolyte

imbalance.

m Dialysis is a process for removing waste

and excess water from the blood.

183

Dialysis

Two main types of dialysis
m Hemodialysis
Removes wastes and water by circulating blood outside the
body through an external filter, called a dialyzer, that contains

a semipermeable membrane

m Peritoneal dialysis

- Wastes and water are removed from the blood inside the
body using the peritoneum as a natural semipermeable
membrane. Wastes and excess water move from the blood,

across the peritoneal membrane

185

CHRONIC RENAL FAILURE
(END-STAGE RENAL DISEASE)

m CRF 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
(retention of urea and other nitrogenous wastes

in the blood)

186

m ESRD may be caused by systemic diseases, such as:
- DM (leading cause);
- hypertension;
- chronic glomerulonephritis;
- pyelonephritis;
- obstruction of the urinary tract;
- hereditary lesions, as in polycystic kidney disease;

- vascular disorders; infections; medications; or toxic

agents

Stages of Chronic Renal Disease

m Stage 1
Reduced renal reserve, characterized by a 40% to 75%
loss of nephron function. The patient usually does not
have symptoms

m Stage 2
Renal insufficiency occurs when 75% to 90% of
nephron function is lost. At this point, the serum
creatinine and blood urea nitrogen rise, the kidney loses

its ability to concentrate urine and anemia develops.
188

m Stage 3

-End-stage renal disease (ESRD), the final stage of
chronic renal failure, occurs when there is less than

10% nephron function remaining.

-All of the normal regulatory, excretory, and hormonal

functions of the kidney are severely impaired.

- ESRD is evidenced by elevated creatinine and blood

urea nitrogen levels as well as electrolyte imbalances.

189

Clinical Manifestations
» Because virtually every body system is affected by
the uremia of chronic renal failure

- Heart failure and - Altered levels of
pulmonary edema (due to consciousness, inability to
fluid overload) concentrate, and seizures

- Severe itching (deposit of - Hypertension
urea crystals on the skin) © Aadosis

- Anorexia, nausea, a

vomiting,
- Calcium and phosphorus

imbalance

190

Diagnostic Findings

m Renal function test
- Decreased GFR

- Increased serum creatinine and BUN levels

191

Complications

Hyperkalemia

Hypertension
- Anemia

Bone disease

Metabolic acidosis

192

Management of CRF

- Phosphorus Binders - Calcium supplements
- Antihypertensive - Nutritional therapy
agents - Dialysis

Antiseizure agents

- Erythropoietin

193

NEPHROLITHIASIS

— Formation or presence of stony masses in the UT

- Stones are formed in the UT when urinary concentrations
of substances such as calcium oxalate, calcium
Phosphate, and uric acid increase

- Stones may be found anywhere from the kidney to the
bladder

-They may vary in size from small grains of sand, up to

stones the size of an orange.

194

Factors that favor the formation of stones are:
- Infection,
- Urinary stasis, and

- Some metabolic changes which increase the concentration

of some salts in the urine.
m Types of stone
- Calcium Stones
- Uric Acid Stones

- Oxalate Stones

195

Signs and Symptoms

- Depend whether they are in the kidney, kidney pelvis,
ureter, or bladder.

- Usually kidney stones cause only vague symptoms.

- There may be mild backache, and some urinary frequency.

- Intense, deep ache in the CVA region

- Examination of the urine: WBC's and RBC $ because the

stone irritates the epithelium causing microscopic

bleeding.

196

Management

m The goals of management are

to eradicate the stone

to determine the stone type

to prevent nephrons destruction

to control infection, and

to relieve any obstruction that may be present.

197

Opioid analgesics or NSAIDs(to relieve the pain )
Hot baths or moist heat to the flank area

A high fluid intake

restrict calcium in their diet

Encourage low-purine diet

198

m Surgical management

- Extracorporeal shock wave lithotripsy (is a
noninvasive procedure used to break up stones in the

calyx of the kidney )
— Percutaneous nephrolithotomy
- Cystoscopy

- Ureteroscope

199

HYDRONEPHROSIS

It is a dilatation of the renal pelvis and calyces of one

or both kidneys.

The obstruction to urine flow causes increases pressure

in the renal collecting system.
This causes a gradual thinning of the renal parynchema.

If the obstruction is in the bladder or urethra, both

kidneys will be affected.

200

m The obstruction may be due to a stone in the kidney
pelvis partly obstructing the ureteropelvic junction, or
the stone may be in the ureter but also causing only a

partial obstruction.

m In older men, the most common cause of mild to
moderate hydronephrosis is enlargement of the

prostate causing bladder outlet obstruction.

201

Cysts of the kidney

m Kidney cysts are round pouches of fluid that form on or in

the kidneys.

m Polycystic kidney disease, which is a progressive disease

that can lead to kidney failure.

m Simple kidney cysts most often do not cause harm. In
most cases, a doctor finds them during an ultrasound or
computerized tomography (CT) scan done for another

reason.

202

Cause pain , back, or upper abdomen if they enlarge and
press on other organs

Bleeding

Become infected, causing fever, chills, or other signs of
infection

Impair kidney function (rare)

Treatments for cysts that cause signs and symptoms
Puncturing and draining the cyst,

Surgery to remove the cyst.

203

Glomerulonephritis

a Glomerulonephritis is an inflammation of the

glomerular capillaries.

m Glomerular diseases include a group of disorders
characterized by pathologic alterations in normal

glomerular structure and function.

m The major clinical manifestations of glomerular injury
include proteinuria, hematuria, decreased glomerular
filtration rate, and alterations in excretion of sodium

(leading to edema and hypertension).

204

a Primary glomerular diseases :
- Acute glomerulonephritis

- Chronic glomerulonephritis

205

Acute Glomerulonephritis (AGN)

= Glomerulonephritis is an inflammation of the

glomerular capillaries.

m Primarily a disease of children older than 2 years of

age, but it can occur at any age.

206

Pathophysiology

m The most common etiologic factor associated with
AGN is immunologic reactions after group -A beta-

hemolytic streptococcal infections.
m Commonly after skin and throat infections.

m AGN is not a direct bacterial infection in the kidney.

207

Clinical Manifestations

- The primary presenting feature of AGN is

hematuria.

RBC casts indicate glomerular injury
- Proteinuria (primarily albumin)

Generalized edema

Hypertension

CVA tenderness

208

Diagnosis
m Definitive diagnosis may need a kidney biopsy.
m Usually made by S/S

m The urine examination will show dark urine with

proteinuria, RBC, and many casts.

m BUN may be elevated and the patient may be anemic

209

Complications

m Hypertension
m Heart failure
m Pulmonary edema

m Anemia

210

Management:

- Antibiotics
- Corticosteroids

- Salt free diet

211

Chronic Glomerulonephritis

It is very often not diagnosed until late permanent
damage has been done to the kidneys.

The kidneys shrink, and atrophy so that cortex of
glomerular tissue becomes very thin.

is characterized by irreversible and progressive
glomerular and tubulointerstitial fibrosis

Scars also affect the kidney cortex disturbing

nephrons, blood supply and drainage system.

212

Clinical Manifestations:
- Weight loss, weakness, Nocturia, headaches,

and digestive disturbances.

- As chronic glomerulonephritis progresses,

signs and symptoms of chronic renal failure.

- Blood pressure may be normal or elevated

and there is usually dependent edema.

213

Diagnosis
- Made by urine tests, elevated BUN
- Once the kidney damage has become severe, there is
little chance that renal function can return to normal
again.
- May also be diagnosed by finding complications:
m Hypertension, edema of feet, anemia , loss

of weight, headache, dizziness

214

Medical management
Symptomatic treatment is directed toward the:
> Hypertension
> Heart failure
> Anemia

> Urinary tract infection or other complications.

215]

NEPHROTIC SYNDROME

- Nephrotic syndrome is a nonspecific kidney disorder
characterized by three signs of disease:
large proteinuria, hypoalbuminemia, and edema

— Very low hypoalbuminemia can also cause a variety of
secondary problems, such as water in the abdominal
cavity (ascites), around the heart or lung (pericardial
effusion, pleural effusion),

- high cholesterol (hence hyperlipidemia), loss of molecules
regulating coagulation (hence increased risk of

thrombosis).
216

Glomerular damage

Increased permeability to proteins
Proteinuria (= 3.5 g/24 h)

| Hypoproteinemia

Decreased plasma Compensatory synthesis
oncotic pressure of proteins by liver
Hyperlipidemia

Fluid escapes
into tissues

Edema

M FIGURE 23-9 m Pathophysiology of the nephrotic syndrome.

Diagnosis
m Proteinuria >3-3.5 g/day is sufficient for the diagnosis of

nephrotic syndrome
Complications
m Infection due to deficient immune response
m Thromboembolism (especially deep vein)
m Acute renal failure (due to hypovolemia)

m Accelerated atherosclerosis (due to hyperlipidemia)

218

REN

The major manifestation of nephrotic syndrome is:
a. hematuria.
b. hyperalbuminemia.
c. edema.

d. anemia.

Nephrosclerosis

m Nephrosclerosis: A progressive disease of the
kidneys that results from sclerosis (hardening)
of the small blood vessels in the kidneys.

m Commonly associated with hypertension or
diabetes

m Can lead to kidney failure.

220

m In the kidneys, as a result of hypertension,
hyaline accumulates in the wall of small
arteries and arterioles, producing the
thickening of their walls and the narrowing
of the Lumina — arteriolosclerosis.

m Consequent ischemia will produce tubular
atrophy, interstitial fibrosis, glomerular
alterations.

m In advanced stages, kidney failure will

occur.

m Clinical manifestation of hypertensive Nephrosclerosis

long-term essential hypertension
Hypertensive retinopathy
left ventricular hypertrophy,

Minimal proteinuria, and progressive renal

insufficiency
No evidence of another renal disease

RX-control hypertension

222

Tumor of the kidney

m A kidney tumor is an abnormal growth within the kidney.
The terms "mass," "lesion" and "tumor" are often used
interchangeably. Tumors may be benign (non-cancerous)
or malignant cancerous).

m Almost all kidney cancers first appear in the lining of tiny
tubes (tubules) in the kidney. This type of kidney cancer
is called renal cell carcinoma.

m The good news is that most of kidney cancers are found

before they spread (metastasize) to distant organs

223)

- tumors may metastasize early to the

lungs, bone, liver, brain

m Clinical Manifestations

Many renal tumors produce no symptoms

hematuria,

Pain, and a mass in the flank

Unexplained weight loss, increasing weakness, and
anemia(if metastasized)

224

Disorders of the male reproductive system
- Problems of the penis
- Cancer of the penis(Reading assignment)
- Infection
m Prostatitis (Discussed)
m Epididymitis
m Orchitis

m Benign prostatic hypertrophy (BPH) (Discussed)

225

Acute Epididymitis

- Is more often sterile than it is bacterial.

- Sterile epididymitis is thought to be caused by a
sudden retrograde flow of urine from the prostatic
urethra through the ejaculator duct, through the

vas deferens, and into the epididymis.

- Urine reaching the epididymis causes an

inflammation by chemical effect.

226

m This is quite painful and lasts for 2 to 3 weeks.
m Treatment of this is directed toward the pain.

m Elevation of the scrotum with some support can

reduce the heavy feeling.

m Analgesics for severe cases and bed rest will further

help until the inflammation subsides spontaneously.

227)

Chronic epididymitis

m Chronic epididymitis can be bacterial, but is often

found to be tuberculosis.

m If the inflammation has lasted 2 to 3 moths and/or
there is drainage from the scrotum, tuberculosis

should be strongly suspected.

m TB infection should be treated like TB infection
elsewhere.

228

ORCHITIS

m An acute infection of the testicles is uncommon.

m By some reports, of the male children who get
epidemic parotitis (mumps), about one out of

five may develop mumps orchitis.

229

PROBLEMS OF THE TESTIS:

m The entry into the scrotum usually occurs before the

9th month of fetal life.

m For normal spermatogenesis, the testicle must be in
the scrotum where the temperature is one or two

degrees lower than intra-abdominal temperature.

230

CRYPTORCHIDISM (UNDECENDED TESTICLE)

m In case the testicle does not reach the scrotum before
birth, the abnormality is called cryptorchidism, which

means, an undescended testicle.

m An undescended testicle will not produce
spermatozoa, and it has a higher risk of developing a

malignancy later in life.

231

Management

The testicle need to be surgically placed into the
scrotum, if it does not reach that position by age 2 or

3.

Waiting until age 8 or 10 may cause permanent

damage to testicle.

The congenital abnormality is usually unilateral

although it can be bilateral.

232

HYDROCELE
+ It is a collection of fluid (like water) inside the fibrous

capsule surrounding the testicle.
° The cause of hydrocele is not known.

° A hydrocele is usually slow growing painless enlargement of
the testicle

* They require careful examination to differentiate a
hydrocele from a hernia

° Treatment for large hydroceles is surgery.

° Cure is expected.

233)

PROBLEMS OF THE PENIS

PHIMOSIS

m Is a condition in which the uncircumcised foreskin cannot be

retracted over the glans.

m If the foreskin stays a long time without cleansing under it,

various kinds of bacteria can cause infections.

m If the foreskin has become scarred and fixed so that it cannot be

retracted, a circumcision should be done.

234

PARAPHIMOSIS

m In this condition the foreskin has been retracted back
of the glans, and then becomes so edematous that it

cannot be replaced over the glans again

m By steady gentle pressure, usually the glans can be
pushed back under the foreskin, but sometimes

anesthesia and a circumcision is required.

235

HYPOSPADIUS
This is a congenital abnormality of the penis in which the

urethral opening is not in the normal position in the glans penis.
It is instead somewhere along the shaft toward the scrotum.

This problem needs correction because the downward curvature
of the penis prevents straight erection which prevents sexual

intercourse.

Surgery is usually advised between ages 3 to 6 so that the child

may appear normal by the time he stars going to school.

236

END

Genitourinary nursing

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