Genito Urinary - Wonde 1

Medical Surgical II
Course code: Nurs322

Unit III. Genito-urinary Disorders
For 2nd year Bsc.Nurses
BY: Wondwossen Yimam (Msc.N)

Dessie
March/2013
UNIT III.DISORDERS OF THE GENITO URINARY
SYSTEM
LEARNING OBJECTIVES
Upon completion of this lesson, the student will be able
to:-
• Identify normal distribution of ICF and ECF
• Describe the symptoms & mgt associated with FVD and FVE
• Distinguish between the different etiologies of major
electrolyte imbalances
• List the manifestations of electrolyte imbalances
• State the normal serum values for Na+, K+, Cl-, Mg++, & Ca++
• Interpret arterial blood gas measurements
• Describe measures used for preventing complications of
intravenous therapy
Part I. Fluid, Electrolyte & Acid base Imbalances
Content outlines
1/ Fluid imbalances
FVD & FVE
2/ Electrolyte imbalances
Na+, K+, Ca++, Mg++,etc
3/Acid base imbalances
-Metabolic acidosis -Metabolic alkalosis
-Respiratory acidosis -Respiratory alkalosis
4/ Types of IV fluids
- Crystalloids solutions - Colloidal solutions
Urinary system
Functions of the Kidney
• Excretion of waste products& urine formation
• Regulation of electrolytes
• Regulation of acid–base balance
• Control of water balance
• Control of blood pressure
• Renal clearance
• Regulation of red blood cell production(Renin)
• Synthesis of vitamin D to active form
• Secretion of prostaglandins, etc
Urine Formation
Urine is formed in the nephrons through a
complex three-step process:-
1/ Glomerular filtration
2/ Tubular reabsorption, and
3/Tubular secretion.
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Characteristics of normal urine
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Body Fluids
• Body fluids transport nutrients to and remove wastes from

cells
• Distribution of total body water (TBW)
– 60%-70% of adult body weight is fluid in adults and 80%
in infants.
– The leaner the person, the greater the proportion of
water to total body weight
• Gender, body mass & age considerations
– Intracellular (ICF, within cells = 30%-40% (2/3) of body
weight,25 L)
– Extracellular (ECF, plasma, interstitial & lymph =20% (1/3)
of body weight,15L)
• 1 Liter water = 1 kg 11
Group work
Calculate the TBW, ICF, and ECF in a 70-kg male
• TBW = 0.5 × body weight (kg) for females and 0.6 ×
body weight (kg) for males
• ICF = 2/3 TBW
• ECF = 1/3 TBW
Example
TBW = 0.6 × 70 kg = 42 L
ICF = 2/3 TBW = 0.67 × 42 L = 28 L
ECF = 1/3 TBW = .33 42 L = 14 L
Interstitial fluid = 3/4 ECF or 25% TBW = .25 × 42 L = 11 L
Plasma fluid = 1/4 ECF or 8% TBW = .08 × 42 L = 3 L
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Body Fluids---
◆ Additional fluids are contained in other body

compartments
- Interstitial fluid = between cells
-Plasma, an intravascular fluid = arteries, veins,
and capillaries
- Cerebrospinal fluid = spinal cord
- Intraocular fluid = eyes
Fluid movement
◆ Body compartments are separated by semi

permeable membranes that control fluid
movement through filtration, hydrostatic
pressure, diffusion, osmosis, active transport &
Plasma colloid osmotic pressure.
Fluid movement---
• Filtration is the movement of water and

solutes from an area of high hydrostatic
pressure (high pressure) to an area of low
hydrostatic pressure(low pressure)
• Filtration allows the kidneys to filter 180 L of
plasma per day.
• Hydrostatic pressure: the pressure created
by the weight of fluid against the wall that
contains it.
Fluid movement---
• Diffusion is the movement of a substances
(particles) from area of higher concentration
to one of lower concentration
• “Downhill
Movement”
Fluid movement---
• Osmosis is the passive movement of

fluid across a membrane from a region
of low solute concentration to a region
of high solute concentration in an effort
to maintain homeostasis.
Fluid movement---
• Osmotic pressure is the amount of

hydrostatic pressure needed to stop
the flow of water by
osmosis
Fluid movement---
• Tonicity is the ability of solutes to
cause osmotic driving forces
Fluid movement---
• Active transport occurs when the cell membrane

must move molecules against their concentration
gradient; it requires energy (from cellular
chemical reactions) and a carrier substance such
as sodium ( Na + /K+ Atpase )
• Plasma colloid osmotic pressure is the osmotic
pressure caused by plasma proteins; it results
from the selective retention of colloids in plasma,
which lowers the concentration of water and
electrolytes.
Sodium-Potassium Pump
• Sodium concentration is higher in
ECF than ICF
• Sodium enters cell by diffusion
• Potassium exits cell into ECF
Fluid movement---
• Osmolality refers to the specific gravity of body fluids; the
higher the specific gravity, the greater the osmotic
pressure, which attracts more water to the area.
• Osmolality reflects the concentration of fluid that affects
the movement of water between fluid compartments by
osmosis
• Normal serum osmolality is 280 to 308 mOsm/kg, and
• Normal urine osmolality is 250 to 900 mOsm/kg.
Na+ X 2 + Glucose + BUN
18 2.8
= Approximate value of serum osmolality
Glucose = 70-105 mg/dl
BUN = 7-25mg/dl
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Fluid Imbalances
FVD & FVE

Fluid Volume Deficit(FVD)
• Mild – 2 % of body weight loss
• Moderate – 5 % of body weight loss
• Severe – 8 % or more of body weight loss
NB. Alterations in the amount or composition of

body fluids can cause complications; a 8 % fluid
loss (3.4 L) is serious, and a 20 % loss (8.4 L) is
fatal
Fluid Volume Deficit(FVD)
(Hypovolemia, Isotonic dehydration)
Common Causes
– Hemorrhage
– Vomiting
– Diarrhea
– Diaphoresis
– Burns
– Diuretic therapy
– Fever
NB. Fever can increase fluid loss through diaphoresis and
increased respiratory rate; a temperature more than 38.3° C
requires an extra 500 mL of fluid daily, and more than 39.4° C
requires an extra 1,000 mL of fluid daily.
Clinical Manifestations(FVD)---
Signs/Symptoms
• Decreased tissue perfusion
– Check capillary refill time
– Flattened neck veins
Hematocrit (Hct) is sensitive to fluid shifts
( Volume (%) of erythrocytes in whole blood)
– 40-54 mL/dL males , 37-47 mL/dL females
– 11.2-16.5 mL/dL children
• Decreased blood volume
– Hypotension, weak & rapid pulse
– Oliguria
• Tissue dehydration
– Poor skin turgor, dry mucous membranes , Wt loss
– Thirst - Possible temperature elevation
Treatment/Interventions (FVD)---
• Identify the cause
• Fluid Management
– Diet therapy – Mild to moderate dehydration. Correct
with oral fluid replacement.
– Oral rehydration therapy – Solutions containing
glucose and electrolytes.
– IV therapy – Type of fluid ordered depends on the
type of dehydration and the clients cardiovascular
status.
Nursing Implications
Nursing Responsibilities (FVD)
– Calculate I & O frequently
• minimal urinary output = 30 ml/hr
• Check urine specific gravity
– Check O2 saturations
– Draw & analyze blood gases (ABG)
– Auscultate lungs (side to side)
– Give isotonic solutions (oral or IV)
• Normal saline; 5% dextrose, Ringer’s lactate
– Give a fluid bolus as ordered
– Monitor V/S regularly
– Check temperature
Nursing Diagnosis (FVD)
• Fluid volume Deficit r/t Insufficient intake, vomiting,

diarrhea, hemorrage m/b dry mucous membranes, low
BP, HR 112, BUN 28, Na+ 152, urine dark amber; Intake
200mL/Output 450mL over 24 hours.
• Goal: Client will have adequate fluid volume within 24

hours :Moist tongue, mucous membranes, N-B/P, N-HR ,
BUN between 8-25 mg/dl, Na+ 135-145, Urine clear ,
balanced I/O
Fluid Volume Excess(FVE)
Common Causes:-
– Congestive Heart Failure
– Early renal failure
– IV therapy
– Excessive sodium ingestion
– SIADH
– Corticosteroid
Clinical Manifestations(FVE)
Signs/Symptoms
– Increased BP
– Bounding pulse, tachycardia
– Venous distention
– Increased urinary output
– Edema
– Distended neck veins
– Increased weight
– Pulmonary edema
• Dyspnea
• Orthopnea (diff. breathing when supine)
• Crackles
Treatment/Interventions (FVE)
• Treat the cause
• Drug therapy
– Diuretics may be ordered if renal failure is not the
cause
• Restriction of sodium and saline intake
• I/O
• Weight
Nursing Diagnosis
Fluid volume excess r/t CHF/ excess sodium intake/ renal
failure AEB: Weight gain of 2.7kg in 24 hours; lungs with
crackles in bases bilaterally; 2+ edema in ankles
bilaterally.
• Goal: Client will have normal fluid volume within 48
hours AEB: Decreased weight of 0.5 kg per day, lung
sounds clear in all fields, ankles without edema.
NB. Crackles are short, intermittent, nonmusical, explosive

sounds often described as bubbling.
Ex. pneumonia, early congestive heart failure, bronchitis,
bronchiectasis.
Electrolyte Imbalances
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Intracellular electrolytes
◗ Potassium, controls cellular osmotic pressure,
influences skeletal and cardiac muscle activity, and is
dramatically affected by acid–base imbalance.
◗ Magnesium ,contained mostly in bone; it activates
intracellular enzymes, contributes to carbohydrate
and protein metabolism, and acts to dilate b/vessels,
decrease blood pressure; imbalances can trigger
ventricular arrhythmias and cardiac arrest.
◗ Phosphate, it’s essential for muscle, red blood cell
(RBC), and nervous system functioning, and it plays a
role in carbohydrate, protein, and fat metabolism.
Extracellular electrolytes
◗ Sodium is responsible for the osmotic pressure of ECF,
and it doesn’t readily cross the cell membrane
◗ Calcium is concentrated in the skeletal system; it acts as
cell cement, has a sedative effect on nerve cells,
regulates muscle contraction and relaxation (including
heartbeat), activates enzymes that stimulate chemical
reactions, and plays a role in blood coagulation
◗ Bicarbonate plays a role in acid–base balance; it serves
as a buffer to keep serum pH within normal limits and
is regulated primarily by the kidneys
◗ Chloride helps maintain acid-base balance and works
with sodium to help maintain osmotic pressure
Hyponatremia (<135mEq/L)
 Normal range = 135 to 145 mEq/L
• Primary regulator of ECF volume (a loss or gain of
sodium is usually accompanied by a loss or gain of
water)
Types of hyponatremia
1/ Dilutional :- Na+ loss, water gain
2/ Isovolumic:- More fluid, normal Na+
3/ Hypovolumic:-More Na+ loss than water
Ex. Diuretics, vomiting, low B/P, etc
4/ Hypervolumic:-Water gain > Na+ gain
Ex. Edema, HPN ,Wt gain, increase HR
Contributing Factors
– Excessive diaphoresis, wound drainage, CHF, Low salt diet,
renal disease, diuretics
– Vomiting, diarrhea, etc.
Assessment findings
- Poor skin turgor
- Dry mucosa
- Decreased saliva production
• Orthostatic hypotension (a sudden drop in blood pressure
when pts are in sitting or standing position)
- Nausea/abdominal cramping
- Altered mental status
Interventions/Treatment
 Sodium Replacement
 Water Restriction ( for hypervolumic & isovolumic
hyponatremia)
– Drug Therapy
• In severe case - IV therapy ( N/s 3%-5%)
- Frusemide IV to remove excess fluid
Group work---Scenario 3
• An 87 year old man was admitted to the acute care
facility for gastroenteritis for 2 days duration. He is
vomiting, has severe, watery diarrhea and has abd
cramping. His serum electrolytes are consistent with
hyponatremia r/t excessive sodium loss.
1. What is the relationship between vomiting,
diarrhea, and hyponatremia?
2. What s/sxs should the client be monitored for that
indicate the presence of sodium deficit?
3. In addition to examining the client’s serum
electrolyte findings, how will the nurse know when
the client’s sodium level has returned to normal?
Hypernatremia (>145mEq/L)
- Can be caused by a gain of sodium in excess of water or
by a loss of water in excess of sodium.
- Excess Na+ relative to body water
– Hyperaldosteronism
– Diabetes Insipidus
– Renal failure
– Corticosteroids
– Increase in oral Na+ intake
– Na+ containing IV fluids
– Decreased urine output with increased urine concentration
– Most often affects very old, very young, and cognitively
impaired patients
Hypernatremia---
Contributing factors ---
– Diarrhea
– Dehydration
– Fever
– Hyperventilation
Hypernatremia---
Assessment findings
- Thirst, low grade fever
- Dry, swollen tongue
- Sticky mucous membranes
- Flushed skin, Agitation
- Postural hypotension
- Neurological sxs:- confuson,
coma, Somnolence, cellular DHN, but no fits
Mnemonic “SALT” Skin flushed, Agitation,
Low grade fever, Thirsty
Hypernatremia ---
1/ Hydration status– more water & restrict Na+
2/ Identify & treat causes
3/ Monitor serum Na+ & osmolarity
- For rapid rise= Reduce 1 mmol/lit/hr ( 24 mmol/d)
- For slow rise= Reduce 10 mmol/lit/day
4/Only Hypotonic solutions are used
5/ Diuretics
6/ Correct shock with 0.9 % N/S
IV infusion estimation for hypernatremia
Spot scenario
EX. Wt = 70 kg , Serum Na+ = 160 meq/lit
NB. Na+ = 135-145 meq/lit ( Av= 140 meq/lit)
Soln:- 70 kg X 60 % = 42 liters (TBW)
ECF = 1/3 X 42L = 14L
ECF Na+ excess= 160-140 = 20 mmol/L
14L X 20 mmol/L = 280 mmol/L
 Total amount of fluid required to lower Na+
280/140 = 2 litters ( Hypotonic fluid Ex. 3 % DW)
 Rate of 1 mmol/lit/hr = 14 mmol/hr in ECF
 The rate of fluids to lower 280 mmol Na+ in 20 hrs at the rate
of 1 mmol/hr = 2L/20 hrs
= 2000 ml/20 hrs=100 mls/hr
• A 47 year old woman was taken to the Hospital
after she developed a rapid heart rate and has
thirst, low grade feve.r
• P/E revealed dry & swollen tongue, postural
hypotension and fever of 38.50 c .
• The client’s daughter stated her mother had been
very hungry recently and drinking more fluids than
usual. By suspecting DM, the Dr. obtained serum
electrolytes and glucose levels, which revealed
serum sodium of 163 mEq/L and serum glucose of
360 mg/dL.
Group work---Scenario 4---
1. Interpret the client’s lab data.
2. Why are clients with DM prone to the
development of hypernatremia?
3. What precautions should the nurse take when
caring for the client with hypernatremia?
4. List two food items this client should avoid and
why.
5. Identify two medications that could have an
increased effect on the client’s sodium level.
Hypokalemia (< 3.5mEq/L)
• Normal serum potassium concentration
= 3.5 - 5.5 mEq/L
• Pathophysiology: –
– Decrease in K+ causes decreased excitability of cells,
therefore cells are less responsive to normal stimuli
Hypokalemia ---
Contributing factors
– Diuretics
– Shift into cells
– Digitalis
– Water intoxication
– Corticosteroids
– Diarrhea
– Vomiting
– Poor K+ intake
– Stress
Hypokalemia---
S&Sx
Mnemonic “SUCTION”
• Skeletal muscle weakness (fatigue)
• U wave (ST),cardiac arrythmias
• Constipation, ileus, fatigue
• Toxicity of digitalis glycosides
• Irregular, weak pulse
• Orthostatic hypotension
• Numbness (paresthesia)
Hypokalemia (S & Sxs)
Muscle weakness, cardiac arrythmias, increased
sensitivity to digitalis toxicity, fatigue, EKG changes
(like ST elevation)
Hypokalemia ---
Interventions
– Treat underlying cause
– Encourage potassium-rich foods
– K+ replacement- Kcl (IV or PO)
– Monitor lab values & urine output
– Potassium sparing diuretics
– Monitor EKG results
– IV KCl (40-80 meq/l) should be administered only after
adequate urine flow has been established.
– Decrease in urine volume to less than 20 mL/h for 2 hours
is an indication to stop the potassium infusion
– IV K+ should not be given faster than 20 meq/hr
• A 69 year old man has a history of CHF controlled

by Digoxin and Lasix. Two weeks ago he
developed diarrhea, which has persisted in spite
of his taking antidiarrheal meds. His partner
transported him to the hospital when she found
him lethargic and confused. Initial assessment of
the client reveals heart rate at 86 bpm,
respiratory rate 10, and blood pressure 102/56
mmHg.
Scenario 5---
1. An electrolyte panel shows the client’s serum
potassium is 2.9 mEq/L. Does the nurse have
cause to be concerned about the client’s serum
potassium? Why or why not?
2. What data supports the presence of hypokalemia
in this client?
3. What, if anything, should the nurse do?
4. What foods should the client be advised to eat
that are high in potassium?
Hyperkalemia (>5.5 mEq/L)
Pathophysiology – An increase in K+ causes

increased excitability of cells.
• More dangerous than hypokalemia because
cardiac arrest is frequently associated with high
serum K+ levels
• Less common
Hyperkalemia---
– Increase in K+ intake
– Renal failure /Renal insufficiency/
– K+ sparing diuretics
– Shift of K+ out of the cells (Ex. DKA)
= Shift of K+ out of the cell as seen in acidosis
– Blood transfusion
– Trauma (cell death)
Hyperkalemia---
Clinical manifestations---
- Skeletal muscle weakness/paralysis, irritability
- EKG changes – such as peaked T waves, widened
QRS complexes
- Heart block, hypotension, irregular pulse
Hyperkalemia---
Interventions
– Eliminate K+ administration
– Increase K+ excretion
• Lasix or
• Kayexalate (Sodium polystyrene sulfonate) 15-60 mg /d
in four divided doses
– Infuse glucose and insulin
– Cardiac monitoring- monitor EKG changes
- Administer 10 % Calcium gluconate solutions to neutralize excess
potassium
- Monitor muscle tone
- NaHCo3 50 meq I.V over 5 minutes to treat acidosis
Hypocalcemia (< 8.5mg/dL)
Normal = 8.5 – 10.5 mg/dl
– Decrease oral intake of Ca++
– Lactose intolerance/ Malabsorption
– Decrease Vitamin D intake
– End stage renal disease (RF)
– Diarrhea
– Thyroid surgery (decreased PTH )
– Loop diuretics
– Low Mg++ level
Hypocalcemia ---
Contributing factors---
Acute pancreatitis
Hyperphosphatemia
Removal or destruction of parathyroid gland
Hypocalcemia---
Assessment findings
–Irritable ,muscle twitches
– Tetany
• Positive Trousseau’s sign---Carpal spasms
• Positive Chvostek’s sign--- Cheek twitching
– Confusion
– Paresthesia
– Diminished response to digitalis
– EKG changes (prolonged QT intervals)
Positive Trousseau’s Sign
Positive Chvostek’s Sign
Hypocalcemia ---
– Drug Therapy
• Calcium supplement Po
• Calcium gluconate 10 % 10 ml IV slowly over 20 mins for
Tetany
• Vitamin D
– Diet Therapy
• High calcium diet
– Prevention of Injury
• Seizure precautions
Hypercalcemia (>10.5mg/dL)
– Excessive calcium intake
– Excessive vitamin D intake
– Renal failure
– Hyperparathyroidism
– Malignancy (Cancer)
– Hyperthyroidism
– Genetic defects
– Prolonged immobilization
(Causes movement of Ca++ to ECF)
– Thiazide diuretics
– Large doses of Vitamin A and D
Hypercalcemia---
Assessment findings
– Disorientation, lethargy, coma, profound muscle
weakness
– Osteoporosis
– Hypo-reflexia (DTR)
– Bradycardia ---Cardiac arrest (Ca ++ > 17mg/dL)
– Constipation
– Formation of renal calculi ( RF)
– Polyuria
– GI ulceration
Hypercalcemia---
– Eliminate Ca++ & Vit D administration
– Hydrate the pt with Isotonic NaCl 300 ml/hr
(It increases the excretion of Ca++)
– Loop Diuretics ( 40-80 mg BID)
– Calcium reabsorption inhibitors
(Phosphorus Ex. Alendronate 10-70 mg/d)
– Cardiac Monitoring
– Calcitonin 4u/kg BID subcutaneous
– Corticosteroids ( predinsolone) 40 – 60 mg
Hypomagnesemia (<1.5mEq/L)
Normal = 1.5 – 2.5 meq/L
Functions
-Production of ATP -Protein synthesis
-CHO metabolism -Muscle contraction
-Vasodilatation effect - Activate enzymes
– Malnutrition(poor intake) __ Hyperglycemia
– Starvation __ Poor GI absorption
– Diuretics __Chronic alcoholism
– Aminoglcoside antibiotics __Burn
– Insulin administration __Sepsis
Hypomagnesemia ---
Assessment findings
Tetany
- Positive Trousseau’s sign
- Positive Chvostek’s sign
- Hyper-reflexia (DTR)
- Muscle weakness ,leg cramps , muscle spasm
- Seizures, confusion, hallucination
- ECG changes –dysrhythmias ,Increase HR
- HTN
- Shallow respiration
- Anorexia ,nausea, dysphagia
Hypomagnesemia ---
Interventions
– Eliminate contributing drugs (Diuretics, Aminoglcoside
antibiotics, Insulin )
– IV/IM MgSO4 ( 50% in 20 ml)
– Assess DTR’s hourly with MgSO4
– Diet Therapy (Nuts, legumes, sea foods, Chocolate,
etc)
Hypermagnesemia (>2.5mEq/L)
– Increased magnesium intake
– Decreased renal excretion
– RF
– Addison’s disease
– DKA
– Excess Mg containing antacids
Hypermagnesemia ---
Assessment findings
- Reduced or weak DTR’s
- Weak voluntary muscle contractions
- Drowsy to the point of lethargy
- Mild hypotension (peripheral vasodilatation)
- Bradycardia
- ECG changes
- Flushed face & warmth skin
- Weakness, nausea, vomiting
Hypermagnesemia ---
Interventions
– Eliminate contributing drugs( Ex. excess Mg
containing antacids)
– Administer loop diuretic
– Calcium gluconate reverses cardiac effects
(Increased Mg++ level inhibit transport of parathyroid
hormone from the glands resulting in release of Ca++
from bone)
– Diet restrictions
– Increase fluid intake
Hypophosphatemia (<2.5mg/L)
Normal = 2.5 – 4.5 mg/dl
– Malnutrition
– Starvation
– Hypercalcemia
– Renal failure
– Uncontrolled DM
Hypophosphatemia ---
Assessment findings
Neuro – Irritability, confusion
CV – Decreased contractility
Resp. – Shallow respirations
Hematologic – Increase bleeding
Decrease platelet aggregation
Hypophosphatemia ---
Interventions
– Treat underlying cause
– Oral replacement with vit. D
– IV phosphorus (Severe)
– Diet therapy
• Foods high in oral phosphate
Hyperphosphatemia (>4.5mg/L)
• Causes few direct problems with body

function. Care is directed to
hypocalcemia.
• Rarely occurs
Fluid Management Strategies
• Classic indications for IV fluid include

maintenance of blood pressure, restoring the ICF
volume, replacing ongoing renal or insensible
losses when oral intake is inadequate, and the
need for glucose as a fuel for the brain.
• When determining the appropriate fluid to be
utilized, it is important to first determine the
type of fluid problem (TBW versus ECF depletion)
Fluid Management Strategies---
• For patients demonstrating signs of impaired tissue
perfusion, the immediate therapeutic goal is to
increase the intravascular volume and restore tissue
perfusion.
• The standard therapy is normal saline given at 150
to 500 mL/hour until perfusion is optimized.
• In severe cases, a colloid or blood product may be
indicated to increase oncotic pressure within the
vascular space.
• Once isovolemia is achieved, patients may be
switched to a more hypotonic solution (0.45% NaCl)
at a rate that delivers estimated daily needs.
Parameters for fluid replacement
therapy.
• A subjective sense of thirst, mental status, skin
turgor, orthostatic vital signs, pulse rate, weight
changes, blood chemistries, fluid input and output,
central venous pressure, pulmonary capillary wedge
pressure, and cardiac output.
• Fluid replacement requires caution in patient’s with
fluid overload (RF, CHF, hepatic failure, or the
elderly)
• Complications of IV fluid therapy include
infiltration, infection, phlebitis, thrombophlebitis,
and extravasation.
Who needs fluid replacement
• Hypovolemic patients (e.g., sepsis or pneumonia)
• Hypervolemic patients [e.g., CHF, cirrhosis, or RF]
• Euvolemic patients who are unable to take oral
fluids in proportion to insensible losses (e.g., the
perioperative period); and
• Patients with electrolyte abnormalities
Types of IV Solutions
COLLOIDS
Ex.- 5 &25% Albumin
CRYSTALLOIDS
-Plasma Protein fraction
• Isotonic
-Dextran
• Hypotonic - N/S + 6% Hetastarch
• Hypertonic • Are always hypertonic
Drip rate • Contain large proteins
gtts/min = Volume to be X gtt/ml • Can’t pass through the walls
infused(ml) of the capillaries & on to
Time (minutes) the cells
If drip factor of tubing = gtts/ml• Used for anaphylactic Rxn,
prolonged b/time, Excess
EX. 20 gtts/ml
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b/d loss, etc
Crystalloid Solutions
• Isotonic solutions have a concentration of
dissolved particles equal to that of intracellular
fluid (ICF)
• Hypotonic solutions have less particles than does
intracellular fluid. Fluid flows into cells
• Hypertonic solutions have a greater concentration
of dissolved particles than does intracellular fluid.
Fluid is pulled from cells
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ISOTONIC FLUIDS
• Have similar osmolality with plasma & body fluids
(280-308 mOsm/l)
• Osmotic pressure is the same both inside (ICF) and
outside the cell (ECF)
• Isotonic solutions have a tonicity equal to that of the
ICF and do not shift the distribution of water between
the ECF and the ICF.
• Cells neither shrink nor swell with fluid movement.
Ex. 0.9% N/S, D5W, RL (Contains K+, Ca++, Nacl, &
bicarbonates &,lactates)
NB. Although D5W is an isotonic solution, it’s quickly
metabolized to a hypotonic solution.
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Isotonic Fluids---
• 0.9% Sodium Chloride ( Normal Saline )
• Lactated Ringers (Na+ =130 mEq/L, K+ = 4 mEq/L
Ca++ = 3 mEq/L, Cl− =109 mEq/L, Lactates =28 meq/l)
• Dextrose 5% in Water (D5W)
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Isotonic ---
Purposes
1. Expands ECF volume ( to correct ECF deficit)
2. Expands Intravascular space
Ex. 1 lit of Isotonic fluid expands the ECF by 1 lit.
Ex. 1 lit of Isotonic fluid expands the plasma by 0.25
lit. b/se it is a crystalloid fluid & diffuses quickly in
to the ECF compartment.
EX. 3 litres of Isotonic fluid is needed to replace 1 lit of
blood loss.
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Isotonic ---
Indications: Rx of vascular DHN,& To replace Nacl
• To increase extracellular fluid volume
• To maintain fluid volume
• To replace sodium and chloride
• To treat hypovolemia and fluid lost from burns and GI tract
• To provide electrolyte replacement
• To maintain fluid volume; to replace mild loss;
• To provide free water
• To treat hypornatremia and hyperkalemia
C/I : HPN, Heart failure
(b/se it expands Intravascular space)
Normal Saline
(Na+ 154 mEq/L + Cl− 154 mEq/L = Osmolality of 308 mOsm/L)
Uses Special considerations

• Resuscitation of shock,
• Normal saline does
hemorrhage, or burn
• With Blood transfusions
not supply calories.
• Metabolic acidosis • Use with caution in
• Hyponatremia patients with heart
• DKA failure, P. edema, or
• Perioperative fluid hypernatremia, renal
administration failure
• Fluid challenges in
hypotensive or oliguric  Can lead to overload
patients; Wondwossen Yimam
Lactated Ringers
(Hartmann’s solution)
Uses Special Considerations
• Dehydration • Contains potassium, can
cause hyperkalemia in renal
• Burns patients
• To replace GI losses • Patients with liver disease
• Acute blood loss cannot metabolize lactate
(Lactate is converted into
• Hypovolemia bicarbonate by the liver)
• Sodium depletion • Ringer’s lactate may lead to
accumulation of lactate with
iatrogenic lactic acidosis.
Wondwossen Yimam
D5W
Initially isotonic solution then disperses as a hypotonic fluid, one-third extracellular
and two-thirds intracellular.
Special Considerations
Uses • D5W is a solution of free water and
• Fluid loss and dextrose that provides a modest
amount of calories but no
dehydration electrolytes
• Hypernatremia • Provides 170 calories/L
(Common) • Solution becomes Hypotonic when
dextrose is metabolized
• To “keep the vein • Do not use for resuscitation
open” (KVO) 10-15 • Use cautiously in renal and cardiac
ml/hr for IV patients
• C/I in head injury because it may
medications. cause increased intracranial
Wondwossen Yimam
pressure
Hypotonic Solutions
• Osmotic pressure is less than intracellular fluid
(Osmolality < 250 mOsm/l)
• Water is drawn into the cells from the extracellular
fluid causing them to swell.
• May cause blood cells to burst
• Inappropriate use can result in increased ICP and
cardiovascular collapse from volume depletion.
• Hypotonic solutions have less tonicity than the ICF
leading to an osmotic pressure gradient that pulls
water from the ECF into the ICF.
Action : To replace cellular fluid & To provide free
water for excretion of body wastes
Wondwossen Yimam
Hypotonic Solutions---
Indication: RX of hypertonic DHN
EX. To treat hypernatremia
• To expand the intracellular compartment
• To replace free water
• To replace sodium and chloride
Ex. 0.25% Nacl,0.33%Nacl,0.45%Nacl,2.5%Dw
Hypotonic fluids----
• Excessive infusions of hypotonic solutions can

lead to intravascular fluid depletion , decreased
blood pressure, cellular edema, and cell
damage.
NB. 20 to 22 Needle gauge for most IV fluids.

NB. 14 to 18 gauge for blood administration.
Wondwossen Yimam
Hypotonic Solutions---
• 0.33% Sodium Chloride
• 0.25% Sodium Chloride
• 0.45% Sodium Chloride (1/2 normal saline)
• 2.5% Dextrose in water
Wondwossen Yimam
0.45% Sodium Chloride
Special
Uses Considerations
• Gastric
Do not give
fluidto
loss
patients at risk for ICP
• Cellular
Not for rapid
dehydration
rehydration
• from excessive
Electrolyte disturbances can occur
diuresis
• Hypertonic
dehydration with
primary depletion of
the ECF
• Slow rehydration Wondwossen Yimam
Hypertonic Solutions
• Osmotic pressure is greater than that of
intracellular fluid (Osmolality >350 mOsm/lit)
• Hypertonic solutions have a large concentration of
solutes(particles).
• Water is drawn from the cells to equalize the
concentration, which causes the cells to shrink.
• Hypertonic solutions (3% NaCl) have greater
tonicity than the ICF ,they draw water from the ICF
into the ECF.
Action: Draws fluids out of ICF- leading to increased
ECF volume both in vascular & interstitial space.
Wondwossen Yimam
Hypertonic fluids
Wondwossen Yimam
Hypertonic solutions---
• These solutions draw water from the ICF to the
ECF and cause cells to shrink.
• If administered rapidly or in large quantity, they
may cause an extracellular volume excess and
precipitate circulatory overload and dehydration.
• As a result, these solutions must be administered
cautiously and usually only when the serum
osmolality has decreased to dangerously low
levels.
• Hypertonic solutions exert an osmotic pressure
greater than that of the ECF.
Wondwossen Yimam
Hypertonic Solutions---
Indications
- Rx of hypotonic DHN
- Rx of circulatory collapse increases fluid shift
from interstitial space to vascular space
• Inappropriate use can cause fluid overload
and pulmonary edema
NB.
To treat severe hyponatremia
To correct severe hyponatremia
To treat hypoglycemia
Hypertonic Solutions---
When normal saline solution or Ringer’s lactate
solution contains 5% dextrose, the total
osmolality exceeds that of the ECF.
• 5% Dextrose in 0.9% Sodium Chloride(D5N/S)
• 5% Dextrose in Lactated Ringers (D5RL)
• 5% Dextrose in 0.45% Sodium Chloride
(D51/2NS)
• 10% Dextrose in water(D10W)
• 3% Nacl Wondwossen Yimam
D5NS
Uses Special
Considerations
• Heat related
disorders • Should not be given
to patients with
• Fresh water
impaired cardiac or
drowning
renal function
• Peritonitis
• Draw blood before
administering to
diabetics
Wondwossen Yimam
D5 1/2NS
Special
UsesConsiderations
• Not
Heatfor
exhaustion
rapid fluid replacement
• Diabetic disorders
• Solution in patients with renal or cardiac
dysfunction
Wondwossen Yimam
D5LR
Special
Uses Considerations
• Hypovolemic
Do not administer
Shockin patients with cardiac or
• renal dysfunction
Hemorrhagic Shock
•• Monitor for circulatory
Certain cases of acidosisoverload
Wondwossen Yimam
Colloid solution
Ex. Dextran 40 in NS or 5% D5W
• Colloid solution used as volume/plasma expander for
intravascular part of ECF
• Affects clotting by coating platelets and decreasing
ability to clot remains in circulatory system for 6 hours
• Used to treat hypovolemia in early shock to increase
pulse pressure, cardiac output, and arterial
blood pressure
• Improves microcirculation by decreasing RBC
aggregation
• C/I in hemorrhage, thrombocytopenia, renal disease,
and severe dehydration Wondwossen Yimam
Estimate of
Maintenance Fluid Requirements
• Neonate (1–10 kg) • Adult (greater than 20 kg)
= 100 mL/kg = 1500 mL + 20 mL for
• Child (10–20 kg) = 1000 each kg greater than 20
mL + 50 mL for each kg
greater than 10
Acid base balance regulation
Acid
• A substance that releases H+ when it is put in to a
solution
Base
• A substance that removes H+ when it is put in to a
solution
Wondwossen Yimam
Acid base balance regulation---
◆ Acid–base balance optimizes enzymatic function,
nerve conduction, synaptic transmission, and
muscle contraction
◆ Acids are generated by cellular metabolism of
fats and carbohydrates; to maintain acid-base
balance, acids must be excreted by the lungs and
kidneys at the same rate they’re generated
Acid - base
Acids Bases
1/PH of solutions < 7 1/PH of solutions >7
2/ Arrhenius 2/ Arrhenius
 Increase (H+) concentration  Increase (OH-) concentration
in water in water
Ex. HCl(aq) +H2O--- H3o + Cl (aq)

+ - Ex. LiOH(aq) --- OH -(aq)+Li+
3/ Bronsted lowery
3/ Bronsted lowery
 Base is a proton acceptor
 Acid is a proton donor
Ex. NaOH(aq) --- OH -(aq)+Na+
Ex. HCl(aq) +H2O--- H3o+ + Cl-(aq)
4/ Lewis
4/ Lewis
 Electron donor
 Electron acceptor Wondwossen Yimam
Acid base balance regulation
Acidosis: a decrease in a normal 20:1 base (HCo3-)

to weak acid ratio (H2Co3)
= An increase in H2Co3 & a decrease in HCo3-
Alkalosis: an increase in a normal 20:1 base(HCo3-)
to acid ratio(H2Co3)
= An increase in HCo3- & a decrease in H+
ACIDOSIS / ALKALOSIS
BASE ACID
• Normal ratio of HCO3- to H2CO3 is 20:1
– H2CO3 is source of H+ ions in the body
• Deviations from this ratio are used to identify
Acid-Base imbalances
H+
H2CO3
Wondwossen Yimam
HCO3 -
ACIDOSIS / ALKALOSIS---
• The ratio of H+ to HCO3- determines pH--- False
• It’s the ratio of HCO3- to volatile H2CO3 that
determines pH.
• A strong acid or base is one that dissociates
completely in a solution. EX.
HCl, NaOH, and H2SO4
• A weak acid or base is one that dissociates

partially in a solution. Ex.
H2CO3, C3H6O3, and CH2O
Wondwossen Yimam
PH
PH = Potential Hydrogen
PH is a measure of the activity of H + in a solution.
PH of stomach acid = 2 ( 10-2 mole)
PH of lemon juice = 3 ( 10-3 mole)
PH of pure water = 7 ( 10-7 mole)
PH of Bleach = 13 ( 10-13 mole)
PH = - log10(H+)
EX. (H+) of water at 250c is 0.0000007= ( 10-7 mole)
Therefore the PH of water = - log10(10-7) = 7
PH range compatible with life is 6.8 - 8.0
PH = 6.8-7.2 is a severe life threatening acidosis
PH = 7.7-7.8 is a severe life threatening alkalosis
Wondwossen Yimam
Acid base balance
Wondwossen Yimam
Buffering
• Buffering is a normal body mechanism that
occurs rapidly in response to acid-base
disturbances in order to prevent changes in H+
Two major systems of buffering
A/ Chemical buffer systems
• Bicarbonate buffer system
• Phosphate buffer system
• Protein buffer systems
B/ Physiological buffer systems
• Respiratory mechanisms
• Renal mechanisms
Wondwossen Yimam
Wondwossen Yimam
Acid base balance
A/ Chemical Buffer Systems
1. Bicarbonate buffer systems- react less than a second
- For ECF (blood & tissue fluid)
Carbonic Acid(H2Co3= weak acid ) & Na HCo3= weak base
EX1. HCl + NaHCo3 NaCl + H2Co3
EX2. NaOH + H2Co3 H2O + NaHCo3
2. Phosphate buffer system ( by the Kidney) reacts slowly
 Sodium Dihydrogen Phosphate = Weak Acid =NaH2Po4
 Sodium Monoydrogen Phosphate = Weak
base = Na2HPo4
Ex1. NaOH + NaH2Po4 H2O + Na2HPo4
Ex2. HCl + Na2HPo4 NaCl
Wondwossen Yimam + NaH 2Po4
Chemical Buffer Systems---
3. Protein buffer systems

- Most important for intracellular fluid(ICF)
- A. Acids have Carboxyl (CooH) & Amine(NH2) group
- COOH act as acid b/se it donates H+
H H
EX. NH2-C-COOH NH2-C- Coo- + H+
H R
H H
Ex. COOH- C-NH2 COOH- C-NH3
R R
__________________________________________
Wondwossen Yimam
B/ Physiogical buffer systems
I) Respiratory mechanism (CO2 excretion by the lungs)- Acts
within sec to mins
• CO2 + H2O---- H2CO3 ------------ H+ + HCO3-
Hgb is a buffer
NB. 12,000-20,000 meq of CO2 excreted by lungs
II) Renal mechanism (H+ excretion by the kidney)- Acts within
Hrs to days
NB. The kidney excretes 70 meq of acids daily
Ex1. NH3 + H+ ----- NH4 (excreted)
Ex2. H2CO3 ------------ H+(excreted) + HCO3-(reabsorbed in the blood)
Acidosis: Kidney excretes more H+ & conserves HCO3-
Alkalosis : Kidney excretes more HCO3- & conserves H+
Algorithm to acid base disorder
1/ Establish the primary disorder (MA,MA,RA & RA)

2/ Assess for adequacy of compensation
3/ Calculate the anion gap
Normal anion gap is less than 10-12 mEq/L
4/ Calculate the excess gap
Excess gap = Calculated anion gap - 12
EX. PH= 7.16, PaCo2=70, HCo3- = 26
Step 1. Respiratory Acidosis (By Tic -Tac Toe method)
Step 2. Partial compensation
0.1 x Δ in PaCo2 = 0.1 x 30 = 3meq/lit of HCo3- is expected
Step 3. Anion gap = Sodium – (Chloride + Bicarbonate)
= Na+ -(Cl- + HCo3-) = 12
Anion Gap
• Representative of the concentration of
unmeasured anions (phosphates, sulfates,
organic acids & proteins)
• Anion gap of urine can also be measured via
the cations Na+ & K+, & the anion Cl- to give an
estimate of NH4+ excretion
Wondwossen Yimam
Algorithm to acid base disorder---
Step 4. Calculate the excess gap
-Measured HCo3- + excess gap < 22 = Concurrent non anion gap
Metabolic acidosis
-Measured HCo3- + excess gap >26 = Concurrent anion gap
Metabolic alkalosis
Adequacy of Compensation
Respiratory acidosis
Acute Chronic
Expected Δ HCo3- Expected Δ HCo3-
= 0.1 x ΔPaco2 = 0.35 x ΔPaco2
Increase 10 mmHg PCO2
Increase 1meq HCO3
Adequacy of compensation---
Respiratory alkalosis
Acute Chronic
Expected Δ HCo3- Expected Δ HCo3-
= 0.2 x ΔPaco2 = 0.4 x ΔPaco2
Metabolic Acidosis
Expected Δ Paco2 = (1.5 x Δ HCo3- ) + 8
Metabolic Acidosis
Expected Δ Paco2 = (0.9 x Δ HCo3- ) + 15
Wondwossen Yimam
Blood Gas Analysis
Arterial Sample Venous Sample

• PH = 7.35 – 7.45 • PH = 7.33 – 7.41
• Pa Co2 = 35-45 mmhg • Pa Co2 = 35-40 mmhg
• HCO3- = 22-26 meq/l • HCO3- = 24-28 meq/l
• Na+ = 136- 142
meq/l
• Cl- =
Wondwossen Yimam 95-103 meq/l
Normal Arterial Blood Gas (ABG)
• PH: 7.35 – 7.45 HCO3-: 22 – 26 mEq/L
• PaCO2: 35 – 45 mmHg PaO2: 80 – 100 mmHg
• SaO2: > 95% (pulse oximetry)
Acid Base
PH= 7.35- 7.45
Paco2 = 45-35 mmhg (Respiratory indicator)
HCO3-= 22-26 mEq/L (Metabolic indicator)
Wondwossen Yimam
Metabolic Acidosis
• Overproduction of
hydrogen ions
• Underelimination of
hydrogen ions
• Underproduction of
bicarbonate ions
• Overelimination of
bicarbonate ions
Wondwossen Yimam
Metabolic Acidosis---
Causes
Shock, sepsis, RF, diarrhea, DHN, DKA, Salicylates, alcolism,
starvation, hyperthyroidism, seizures , strenuous exercise ,etc
Depress impulse transmission
S & SXs----
• Dull headache
• Decrease DTRS
• Hyperkalemia (abdominal cramps, diarrhea, muscle
weakness, EKG changes)
• Hypotension, muscle twitching
• Lethargy, warm & dry skin
• Confusion/Disoriented, Tachypnea, Coma
• Electrolytes: ( K+, Na+, Cl-) & ABG changes
Wondwossen Yimam
Metabolic Acidosis ---
RX
• Treat the cause
- Regular insulin to reverse DKA
- Antibiotic for septic shock
- Fluid replacement ( Shock ,DHN)
- Dialysis for drug toxicity (ASA, RF, Methanol)
• Sodium bicarbonate, or Na lactate (IV)
NaHCo3- = 325-650 mg po
For non life threatening acidosis ( PH = 7.3-7.34)
NaHCo3- 2.5 meq/kg IV over 4-8 hrs
For life threatening acidosis ( PH = 6.8-7.2)
Loading: NaHCo3- 1meq/kg IV then 0.5 meq/kg Q.10 mins (PRN)
• Maintain a patent airway and enhance gas exchange
– Drug therapy: bronchodilators; mucolytics
– Oxygen therapy, pulmonary hygiene, Wondwossen
ventilationYimam
support
Metabolic Alkalosis
 Increased impulse transmission
Causes:-
 Cl- depletion- ICF (vomiting, prolonged
nasogastric suctioning)
 Aldosteronism, diuretics (non K+ sparing)
 Cushing’s syndrome, K+ deficiency, massive blood
transfusions, ingestion of antacids, etc.
Wondwossen Yimam
Metabolic Alkalosis---
• Anorexia
• Tetany and
• Apathy
carpopedal spasm
• Confusion
• Irritability, muscle
• Cyanosis
twitches, convulsion
• Hypotension
• Nausea
• Loss of reflexes
• Paresthesia
• Slow respiration
• Arrhythmias • Polyuria
• Electrolytes ( K+, Na+, • Vomiting
Cl-) & ABG changes Wondwossen•YimamWeakness
Metabolic Alkalosis---
RX
• Treat the cause
- N/S for hypotension
- For severe life threatening alkalosis (PH = 7.7-7.8)
- IV Ammonium chloride 100 meq/500 ml of N/S for 4-8 hrs, Then the rxn librate
HCl
- K+ for hypokalemia
- D/C Thiazide diuretics and NG suctioning
- Antiemetics
- Acetazolamide (Carbonic anhydrase inhibitor) 250 mg QID/BID ( for CHF,
Glaucoma, etc)
(Can be used to reduce the HCO3- concentration)
- Dialysis (RF)
• Regular monitoring of ABGs & Electrolytes
Wondwossen Yimam
Respiratory Acidosis
• Respiratory acidosis
results from:
-Impaired respiratory
function that reduces the
exchange of oxygen and
carbon dioxide
-Retention of carbon dioxide
that causes increased
production of free
hydrogen ions
Wondwossen Yimam
Respiratory Acidosis---
Acute
• Rapid, shallow respiration, Chronic
diaphoresis, tremors, • Weakness, Dull
tachycardia
• Muscle weakness, decreased headache
DTRs, disorientation/confusion • Barrel chest and
• Ventricular fibrillation, productive cough
increased RR
• Muscle twitching and seizures
caused by COPD
• Warm & flushed skin
(increased CO2), perspiration,
and cyanosis
S & SXs
• Breathlessness
• Restlessness
• Lethargy and disorientation
• Tremors, convulsions, coma
• Respiratory rate rapid, then gradually depressed
• Skin warm and flushed due to vasodilation
caused by excess CO2
Wondwossen Yimam
RX
• Treat underlying dysfunction or disease
• Bronchodilators
• Supplemental oxygen
• Treat hyperkalemia
• Antibiotics for infection
• Chest tubes to remove secretions
• Remove foreign body obstruction
• Restore ventilation
• IV sodium lactate solution
Wondwossen Yimam
Respiratory Alkalosis
Causes
• Extreme anxiety (most common cause)
• Pulmonary emboli, pulmonary fibrosis, asthma,
pneumonia, or injury to the respiratory center
• Gram-negative bacteremia and sepsis
• High fever, Hypoxemia, High altitude
• Early salicylate intoxication
• Hyperventilation caused by mechanical
ventilation
• Pregnancy, Hepatic failure, Heart failure
Respiratory Alkalosis---
S & Sx
• Tetany
• Anxiety, restlessness
• Diaphoresis
• Dyspnea ( rate and depth)
• EKG changes
• Hyperreflexia, paresthesias
• Tachycardia
Wondwossen Yimam
Respiratory Alkalosis---
RX
• Correct underlying disorder
• Oxygen therapy for hypoxemia
• Sedatives or antianxiety agents
• Paper bag breathing for hyperventilation
Wondwossen Yimam
Interpretation Practice by
“ROME “& “Tic Tac Toe” Methods
• PH: 7.20 Metabolic Alkalosis
• PaCO2: 36 Resp. Acidosis
• HCO3-: 14 Metabolic Acidosis.
• PH: 7.50 Metabolic Alkalosis

• PaCO2 : 29 Resp. Acidosis
Resp. Alkalosis.
• HCO -: 22
3
-
Wondwossen Yimam
Interpretation Practice---
• PH: 7.31
Resp. Acidosis.
• PaCO2: 48 Resp. Alkalosis
• HCO3-: 24 Metabolic Acidosis
• PH: 7.47
Resp. Alkalosis
• PaCO2 : 45
Metabolic Alkalosis.
• HCO3- : 33 Metabolic Acidosis
Wondwossen Yimam
PH Changes
Wondwossen Yimam
1/ PH= 7.79, PaCo2= 24 mmHg, HCO3- = 21 meq/l
Ex. Acid base imbalance: Respiratory Acidosis
Compensation: Partially compensated
2/ PH= 7.17, PaCo2=35 mmHg, HCO3- = 12 meq/l
Acid base imbalance:
Compensation:
3/PH= 7.45, PaCo2=48 mmHg ,HCO3- = 28 meq/l
Compensation:
Compensation:
Compensation:
Compensation:
7/ PH= 7.15, PaCo2=46 mmHg ,HCO3- = 34 meq/l
Compensation:
Compensation:
Compensation:
Answers
Acid base imbalance: Metabolic Acidosis
Compensation: Uncompensated
3/PH= 7.45, PaCo2=48 mmHg ,HCO3- = 28 meq/l
Acid base imbalance: Metabolic Alkalosis
Compensation: Fully compensated
Acid base imbalance: Normal
Compensation:____
Answers---
Acid base imbalance: Respiratory Alkalosis
Acid base imbalance: Metabolic Acidosis
7/ PH= 7.15, PaCo2=46 mmHg ,HCO3- = 34 meq/l
Acid base imbalance: Respiratory Acidosis
Acid base imbalance: Respiratory Alkalosis
Compensation: Uncompensated
Acid base imbalance: Normal
Compensation: ___
Acid-Base with out
Compensation:
Parameters: pH PaCO2 HCO3-
Metabolic Normal
Alkalosis
Metabolic Normal
Acidosis
Respiratory Normal
Alkalosis
Respiratory Normal
Acidosis
Wondwossen Yimam
Acid-Base Fully Compensated:
Metabolic Normal
Alkalosis >7.40
Metabolic Normal
Acidosis <7.40
Respiratory Normal
Alkalosis >7.40
Respiratory Normal
Acidosis <7.40
Wondwossen Yimam
Acid-Base Partially Compensated:
Metabolic
Alkalosis
Metabolic
Acidosis
Respiratory
Alkalosis
Respiratory
Acidosis
Wondwossen Yimam
Part II. Genito-urinary disorders
Content outlines
1. Renal failure
2. Nephrotic syndrome
3. Glomerulonephritis
4. Pyelonephritis
5. Nephrolithiasis
6. Urinary tract infections
7. Neurogenic bladder
8. Benign Prostate Hyperplasia (BPH)
9. Orchitis
10.Phimosis & Paraphimosis
Renal failure
Acute renal failure (ARF)

Defn:-
A sudden decline in renal function, usually marked by:-
 BUN (azotemia) (N= 7 - 25 mg/dl)
 Creatinine (N= 0.7 - 1.4 mg/dl)
 Oliguria (< 400 ml urine in 24 hrs)
 Hyperkalemia &
 Hypernatremia
Azotemia = Retention of metabolic wastes
Medications may artificially elevate creatinine
– Trimethroprim (Bactrim)
– Cimetidine
ARF is the sudden cessation of renal function that occurs when
blood flow to the kidneys is significantly compromised.
Acute renal failure (ARF)---
Causes
1/ Pre-renal failure – results from conditions that interrupt
the renal blood supply, thereby reducing renal perfusion.
EX. Hypovolumia, dehydration, shock, hemorrhage, sepsis, heart failure,
liver disease, burns, anaphylaxis, diuretic therapy, etc
2/ Intra-renal failure – results from injury to the kidneys
themselves.
Ex. Transfusion rxns, AGN, Pyelonephritis, hemolytic anemia ,aminoglycosides,
myoglobunuria, toxins, and immunologic processes, systemic & vascular
disorders.
3/ Post-renal failure – results from obstruction of urine
flow. Ex. Tumors, BPH, Strictures, & Blood clots
Acute renal failure---
ARF has three phases (clinical manifestations)
A/ Oliguric-anuric phase: (begins with the renal insult and
continues for 3 weeks)
- Urine volume < 400 ml/24 hr
- Increase serum creatinine, urea, uric acid, organic acids, K+, &
mg++
- Lasts 3 to 5 days in children, or prolonged to 21 days in
adolescents & adults
B/ Diuretic phase: (begins when the kidneys begin to recover
and continues for 7 to 14 days)
Urine O/put > 400mL/d but no waste products, at end of this
stage may begin to see improvement & ends when BUN &
creatinine levels stop rising.
ARF has three phases ---
C/ Recovery phase: (continues until renal function

is fully restored and requires 3 to 12 months)
- Things go back to normal or may remain
insufficient and become chronic
• Prerenal failure from volume depletion or
prolonged reduction of blood pressure is the
most common cause of acute renal
deterioration and is usually reversible with
prompt intervention.
Subjective symptoms
– Nausea
– Loss of appetite
– Headache
– Lethargy
– Tingling in extremities
Objective symptoms
Oliguric phase
• Vomiting • CHF and pulmonary
• Disorientation, edema
• Edema, • Hypertension
• K+ • Sudden drop in urinary
• Na+ OP
• BUN and creatinine • Convulsions, coma
• Acidosis • Changes in bowels
• Uremic breath
Objective symptoms
Diuretic phase
• Increased urinary output
• Gradual decline in BUN and creatinine
• Hypokalemia
• Hyponaturmia
• Tachycardia
• Improved LOC
Diagnostic Evaluation
• U/A – Proteinuria, Hematuria, Casts
• Elevated serum BUN (80-100 mg/dl within a wk)
• Elevated serum creatinine levels
• Electrolytes:- Na+, Ca++, K+, p, Mg++
• Renal Ultrasonography estimates renal size &
rules out treatable obstructive uropathy
– KUB
– CT/MRI
RX
• Treat underlying cause
• Blood pressure– Antihypertesive
- Treat renal crisis with ACE inhibitor
• Infections--- Antibiotics
• Stop inciting medications (aminoglycosides,
diuretics, etc)
• Nephrostomy tubes/ureteral stents if obstruction
• Acidosis --Rx with NaHCo3
• Hydration (but restrict fluid intake in oliguric phase)
• Restrict dietary intake of protein, sodium, and
potassium during oliguric phase. This restriction is for
the client not requiring dialysis
RX---
• High CHO , low protien, moderate fats, Iron, &
vitamins
• Diuretics (Lasix), NaHCo3 , Al(OH)3
• Rest with activity
• Erythropoietin alfa 50–100 units/kg
subcutaneously three times per wk
• Emotional support
• Dialysis ( Peritoneal /Hemodialysis- subclavian
& femoral approach)
• Renal Transplant
Indications for Hemodialysis
• Refractory fluid overload
• Hyperkalemia (>6.5 meq/L) or rapidly rising )
• Metabolic acidosis (PH less than 7.1)
• Azotemia (BUN > 80 to 100 mg/dL)
• Signs of uremia, such as pericarditis, neuropathy,
or an otherwise unexplained decline in mental
status
• Severe dysnatremias (Na+ > 155 meq/L or Na+ <
120 meq/L)
• Hyperthermia
• Overdose with a dialyzable drug/toxin
• Serum creatinine 5-15 mg/dl
Nursing interventions
– Monitor I/O, including – Maintain nutrition
all body fluids – Safety measures
– Monitor lab results – Mouth care
– Watch hyperkalemia – Daily weights
symptoms
– Assess for signs of
– Watch for
heart failure
hyperglycemia or
hypoglycemia if – GCS
receiving insulin – Skin care
infusions
Chronic renal failure
• Chronic Renal Failure (CRF) – is a progressive, irreversible
kidney disease.
• A progressive, irreversible deterioration of renal
function, which ends fatally in uremia (an excess of urea
& other nitrogenous wastes in the blood)
= End stage renal disease (ESRD)
• End-stage renal failure exists when 90% of the
functioning nephrons have been destroyed and are no
longer able to maintain fluid, electrolyte, or acid base
homeostasis.
Chronic renal failure---
Five stages
• Stage 1: Minimal kidney damage with normal
glomerular filtration rate (GFR).
• Stage 2: Mild kidney damage with mildly decreased GFR.
• Stage 3: Moderate kidney damage with moderate
decrease in GFR.
• Stage 4: Severe kidney damage with severe decrease in
GFR.
• Stage 5: Kidney failure and end-stage renal disease with
little or no glomerular filtration taking place.
Dialysis or kidney transplantation can maintain life, but
neither are cures for CRF.
• Subjective symptoms are relatively same as ARF
Objective symptoms
– Renal
• Hyponatremia
• Dry mouth
• Poor skin turgor
• Confusion, salt overload, accumulation of K+ with
muscle weakness
• Fluid overload and metabolic acidosis
• Proteinuria, glycosuria
• Urine = RBC’s, WBC’s, and casts
• Objective symptoms
– Neurological
– Cardiovascular
• Burning, pain, and
• Hypertension
itching, parestnesia
• Arrythmias • Motor nerve
• Pericardial dysfunction
effusion • Muscle cramping
• CHF • Shortened memory
• Peripheral edema span
• Apathy
• Drowsy, confused,
seizures, coma, EEG
changes
Objective symptoms
– GI
– Respiratory
• Stomatitis
• Increase chance of
• Ulcers
infection
• Pancreatitis • Pulmonary edema
• Uremic fetor • Pleural friction rub
• Vomiting and effusion
• Consitpation • Dyspnea
• Kussmaul’s
respirations from
acidosis
Objective symptoms
– Endocrine – Hemopoietic
• Stunted growth in • Anemia
children • Decrease in RBC
• Amenorrhea survival time
• Male impotence • Blood loss from dialysis
• Increase aldosterone and GI bleed
secretion • Platelet deficits
• Impaired glucose • Bleeding and clotting
levels r/t impaired disorders – purpura
CHO metabolism and hemorrhage from
• Thyroid and body orifices ,
parathyroid ecchymoses
abnormalities
Objective symptoms
– Skeletal – Skin
• Muscle and bone • Yellow-bronze skin
pain with pallor
• Bone • Puritus
demineralization
• Purpura
• Pathological
fractures • Uremic frost
• Blood vessel • Thin, brittle nails
calcifications in • Dry, brittle hair, and
myocardium, joints, may have color
eyes, and brain changes and
alopecia
Lab findings
- BUN :- Indicator of glomerular filtration rate and is affected
by the breakdown of protein.
BUN :- Normal is 10-25mg/dL. When reaches 70 = dialysis
– Serum creatinine – waste product of skeletal muscle
breakdown and is a better indicator of kidney function.
Normal is 0.5-1.5 mg/dL. When reaches 10 x normal, it is
time for dialysis
– Creatinine clearance is best determent of kidney function.
Must be a 12-24 hour urine collection. Normal is > 100
ml/min
– Increase serum K+ ( treated with IV glucose and Na+
Bicarbonate which pushes K+ back into the cell)
– Increase serum P, Na+
– Decreased Ca++, & albumin
Other abnormal findings
– Metabolic acidosis
– Fluid imbalance
– Insulin resistance
– Anemia
– Immunoligical problems
Medical treatment
• Treat the underlying cause Ex. HPN
• Monitor intake & output
• IV glucose and insulin
• Na+ bicarbonate, Ca++, Vit D, phosphate binders
(Aluminum hydroxide & Calcium carbonate or acetate )
• Fluid restriction, diuretics (Mannitol, Furosemide)
• Iron supplements, blood
• High carbohydrates, high fat & low protein,
Medical treatment---
• Reduce diets rich in phosphorus (Diary products)
• Synthetic Erytropoietin
• Diuretics (except in ESRD)
• Teach the client to avoid antacids containing
magnesium
• Dialysis(dialysis does not replace the hormonal
functions of the kidney)
• Kidney transplantation
Kidney Transplant
– Must find donor
– Waiting period long
– Good survival rate – 1 year 95-97%
– Must take immunosuppressant’s for life
– Rejection
• Watch for fever, elevated B/P, and pain over site of new kidney
Post operative care
– ICU
– I/O
– B/P
– Weight changes
– Electrolytes
– May have fluid volume deficit
Transplant Medications
• Patients have decreased resistance to infection
• Corticosteroids – anti-inflammarory
• Cytotoxic – inhibit T and B lymphocytes
– Imuran
– Cytoxan
– Cellcept
• T-cell depressors - Cyclosporin
• Hemodialysis
– Can be done rapidly
– Takes about 4 hours
– Done 3 x a week
• Peritoneal dialysis
– Semipermeable membrane
– Catheter inserted through abdominal wall into
peritoneal cavity
– Cost less
– Fewer restrictions
– Can be done at home
– Risk of peritonitis
– 3 phases – inflow, dwell and outflow
• Automated peritoneal dialysis
– Done at home at night
– Maybe 6-7 times /week
• CAPD (Continous Ambulatory Peritoneal Dialysis)
– Done as outpatient
– Usually 4 X/d
Nursing care
– Frequent monitoring – Ensure proper
– Hydration and output medication regimen
– Cardiovascular – Skin care
function
– Bleeding problems
– Respiratory status
– Care of the shunt
– E-lytes & ABG
– Nutrition – Education to client
– Mental status and family
– Emotional well being
Nursing diagnosis
– Excess fluid volume
– Imbalanced nutrition
– Ineffective coping
– Risk for infection
– Risk for injury
Nephrotic syndrome
Definition:-
It is a clinical disorder of unknown cause
characterized by proteinuria, hypoalbuminemia,
edema, & hyperlipidemia.
• Nephrotic syndrome is a group of symptoms,
not a disease.
Nephrotic syndrome---
• Glomerular capillaries are damaged from

immune complex deposits, nephrotoxic
antibodies, or non-immunological insults.
• Damaged glomerular capillaries are permeable
to serum proteins, resulting in decreased serum
osmotic pressure.
• These conditions result from excessive leakage
plasma proteins in to the urine b/s of
impairment of the glomerular capillary
membrane.
• Categorized as congenital, primary (idiopathic),
& secondary
• Secondary to URTIs, Immunization, Chronic
glomerulonephritis, DM, Systemic Lupus
Erythematous, Renal vein thrombosis, &
Malignancy
• The loss of proteins, particularly albumin,
reduces oncotic pressure & causes edema.
Causes/Risk Factors/
• Immunologic disorders
• Toxic injury to the kidney
• Neoplasms
• Multisystem diseases (for example, diabetes
mellitus)
• Infections
• Hyperlipidemia
• Diseases of the vascular system
Pathological events in nephrotic syndrome
1__ Renal insult
2__ Increased glomerular permeability
3__ Proteinuria
4__ Decreased serum protein
5__ Generalized edema
Clinical manifestations
• Insidious onset of pitting edema, ascites , pleural effusions
• Decreased Urine output
• Irritability, fatique, Anorexia, N/V
• Profound Wt gain (Child may double wt)
• Wasting of skeletal muscles
• Proteinuria, Hematuria
• Edema (periorbital and dependent)
• Hypertension
• Anemia (hemoglobin < 12 g/dL)
• Anorexia/nausea
• Azotemia: Elevated serum BUN (> 20 mg/dL) and serum creatinine
(> 1.2 mg/dL)
• Uremia (symptoms of renal failure)
Urinalysis – Protein as high as 3+ or 4+
- Numerous casts
Serum
– Albumin reduced may fall below 2 g/dL
- May be normal or increased creatinine
- Elevated serum cholesterol (> 200 mg/dL)
- Elevated triglycerides
- Elevated low-density and very low-density lipoproteins
Needle biopsy
- Needle biopsy of kidney may be necessary to confirm
diagnosis
Complications
• Respiratory Compromise
• Peritonitis
• Renal Failure
• Shock/Death
Management
– Treat causative glomerular disease
– Rest with activity
– Restriction of Na+ & K+, fluids
– Increase dietary protein
– Anticoagulant & erytropoietin
– Low saturated fat diet
– Corticosteroid & Immunosuppressant to reduce
proteinuria
– Diuretics
– ACE inhibitors
– Infusion of salt-poor albumin to raise oncotic pressure &
shift fluid from interstitial to intravascular space
Nursing Interventions
• Prepare the client for diagnostic procedures
• Provide client education (before and after the
procedure).
• Collect specimens accurately.
• Report abnormal findings to the provider
Assess
• Loss of skin integrity related to edema
• Intake and output
• Vital signs (especially blood pressure)
Nursing Interventions---
• Provide periods of rest with activities.
• Encourage lowering sodium intake.
• Adjust protein intake according to protein loss in urine over 24 hr.
• Provide high biologic value protein (lean meat, fish, poultry,
dairy).
• Provide small, frequent feedings because of client’s loss of
appetite.
• Administer medications as prescribed.
- Diuretics: Furosemide (Lasix)
- ACE inhibitors - Glucocorticoids: Prednisone
- NSAIDS - Anticoagulants: Heparin, warfarin
- Erythropoietin: Epoetin,alfa
Acute Glomerulonephritis
• Acute Glomerulonephritis (poststreptococcal
glomerulonephritis) is an inflammation of the glomeruli
that occurs when Ag-Ab complexes become trapped in
the glomerular capillary membranes.
Risk Factors
• Immunological reactions
- Primary infection with group A beta-hemolytic
streptococcal infection (most common)
• Systemic lupus erythematosus
• Vascular injury (hypertension)
• Metabolic disease (diabetes mellitus)
• Nephrotoxic drugs
• Excessively high protein and high sodium diets
Acute Glomerulonephritis---
Pathological events in glomerulonephritis
1/ Immune response with antibody production
2/ Glomerular capillary damage
3/ Hematuria & proteinuria
4/ Salt & water retention
4 Edema
Complications
• Renal Failure
• Uremia
• Pulmonary Edema
• Congestive Heart Failure
• Pericarditis
• Anemia
Clinical Manifestations
• Oliguria, hematuria, tea-colored urine
• Foamy urine ( increase protien)
• Polyuria ,nose bleeding
• Edema – periorbital or generalized & dependant; wt
gain
• CVA Tenderness (Costo-vertebral angle)
• HTN (in more than 50% of pts) – usually mild, but can
be moderate or severe.
• Malaise, mild headache, anorexia, &vomiting.
• Anemia , fever
• Diuresis starts 1-2 wks after onset
Diagnostic Evaluations
• Serum BUN (elevated: 100 to 200 mg/dL; normal:
10 to 25 mg/dL) and Creatinine (elevated: greater
than 6 mg/dL; normal: 0.6 to 1.5 mg/dL)
• Creatinine Clearance (decreased: 50 mL/min;
normal 80 to 140 mL/min)
• Urinalysis: Proteinuria, hematuria, cell debris (red
cells and casts), increased urine specific gravity
• Electrolytes: Hyperkalemia, hypermagnesemia,
dilutional hyponatremia if urine output is
decreased
Diagnostic Evaluations---
• Throat Culture (to identify possible streptococcus
infection)
• Antistreptolysin-O (ASO) titer (positive indicating the
presence of strep antibodies)
• ESR (elevated indicating active inflammatory response)
• White Blood Cell Count (elevated indicating
inflammation and presence of active strep infection)
• X-ray of Kidney, Ureter, Bladder (KUB), Renal Ultrasound
(to detect structural abnormalities such as atrophy)
• Renal Biopsy (to confirm or rule out diagnosis)
MGT
• Bed rest
• Antibiotics ( Benzathine penicilin)
• Diuretics(Furosemide)
• Vasodilators (hydralyzine, nefidipine ,etc)
( To decrease B/P)
• Corticosteroids
• Fluid restriction
• Na+ restriction
• Protein restriction (azotemia)
• Intake & output
• V/s ,electrolytes & ABG
• Daily Wt
• Cimetidine ( To prevent stress ulcers)
Chronic Glomerulonephritis
• It is a slowly progressive disease characterized

by inflammation of the glomeruli.
Etiology- Unknown
Predisposing factors
- Primarily renal disorders
- Immune reactions
- Post streptococcal glomerulonephritis
- Systemic lupus erythematus, &
- Hemolytic-uremic syndrome
Chronic Glomerulonephritis---
• Insidious onset
• Sudden sever nasal bleeding,
• Hematuria, Nocturia
• Night swelling of the leg,
• Stroke or convulsion
• N/V, Dyspnea, Malaise, Fatigue
Assessment
History taking: streptococcal sore throat, any primary renal
disorder
Phy/exam:
- Poorly nourished patient
- Yellow gray pigmentation of skin
- Periorbital & peripheral/dependant edema/
- Retinal hemorrhage, Distended neck vein
- Pale mucus membrane due to anemia
- Elevated blood pressure
Diagnostic evaluation
- Urinalysis: Proteinuria, Hematuria, Red blood cell casts
- Elevated BUN, creatinine, decreased hemoglobin
Management Goal
• Control hypertension
• Correct fluid & electrolyte balance
• Reduce edema, prevent congestive heart failure
Drug treatment
- Antihypertensive drugs; Loop diuretics –
furosemide; Antibiotic
- Dialysis - to prevent serious complication
- Surgical intervention - Kidney transplantation
– Monitor V/S, intake & output, daily weight
– Observe for signs of fluid, electrolyte & acid- base
imbalance
– Provide low Na+, high caloric with adequate protein
– Provide good skin care
– Advise the pt to take diuretics in the morning
– Teach the patient sign of UTI
– In severe case of edema, place the patient with
head of the bed elevated
Pyelonephritis
Definition
It is an inflammation of the kidneys & its pelvis,
beginning in the interstitium & rapidly
extending to involve the tubules, glomeruli &
blood vessels.
• Pyelonephritis is an infection and inflammation
of the renal pelvis, calyces, and medulla.
• The infection usually begins in the lower urinary
tract with organisms ascending into the renal
pelvis
Pyelonephritis---
• Escherichia coli organisms are the cause of most
acute cases of pyelonephritis.
• Repeated infections create scarring that changes
blood flow to the kidney, glomerulus, and tubular
structure.
• Filtration, reabsorption, and secretion are
impaired, and there is a decrease in renal function
Classifications
- Acute pyelonephritis - Chronic pyelonephritis
Pyelonephritis---
Acute pyelonephritis
• It is sudden onset & self-limited bacterial disease of the kidneys.
Etiology
• Bacteria: E-coli (80%), Proteus, Pseudomonas, S. aures, Strep.
faecalis (entrococcus)
• Procedures: Catheterization, Cystoscopy, Urologic surgery
• Other causes: Urinary obstruction, Neurogenic bladder
(vesicouretral reflux)
Incidence
• Increased with age - Increased in sexually active women
• Increase in obstructive disease of LUT - Pregnancy
• Neurogenic bladder - Frequent catheterization
• Glucoseuria (Diabetes Mellitus) - Compromised kidney disease
Pyelonephritis---
Acute pyelonephritis is an active bacterial infection

that can cause:
• Interstitial inflammation.
• Tubular cell necrosis.
• Abscess formation in the capsule, cortex, or
medulla.
• Temporarily altered renal function, but this rarely
progresses to renal failure.
Pyelonephritis---
Risk Factors
• Women over 65 years of age
• Older men with prostate problems
• Chronic urinary stone disorders
• Spinal cord injury
• Pregnancy
• Congenital malformations
• Bladder tumors
• Chronic illness (diabetes mellitus, hypertension,
chronic cystitis)
Pyelonephritis---
Clinical Manifestation
• Flank pain
• Costovertebral angle tenderness
• Dysuria (Painful or difficulty of urination)
• Nocturia, Hematuria, Cloudy urine with fishy
odor
• Burning, urgency, frequency, nocturia
• Shaking Chills, Generalized fatigue, Anorexia
• Fever, tachycardia, tachypnea, HPN
Pyelonephritis---
Diagnosis
• Appropriate history taking, & Phy/exam
• Urinalysis: - Proteinuria, Glucoseuria, Rarely ketonuria - Leucocytes,
Few red blood cells
- Casts, Decreased urine specific gravity
• Dark color, cloudy appearance, foul odor
• Positive leukocyte esterase (85 to 90% specific)
• Positive nitrate (95% specific)
Urine culture reveals the causative organism
CBC – Elevated WBC (>10,000mm3) Elevated Neutrophils.
• Erythrocyte sedimentation rate will be elevated
• IVP may demonstrate calculi, structural, or vascular
abnormalities.
Pyelonephritis---
Complications
• Secondary arteriosclerosis
• Calculi formation, Renal damage
• Renal abscess (metastasize to the other organs)
• Septic shock, chronic pyelonephritis, chronic renal
failure, HPN
Medical Management
1/ Cotrimoxazole
2. Ampicillin or Amoxicillin, Penicillin G
3. Cephalosporin drugs
4. Gentamycin, or Tobaramycin
Pyelonephritis---
– Administer antipyretic & Antibiotics
– Fluids (2-3 L/d) to empty the bladder of contaminated
urine & prevent calculus formation
– Catheterize with strict sterile technique
– Instruct the patient to perform appropriate perineal
care
– Teach proper technique for collecting a clean catch
urine specimen
– Emotional support
– Personal hygiene
– Advice routine checkups for patient with history of UTIs
Chronic pyelonephritis
• It is a persistent inflammation of kidneys.

• Repeated infections that cause progressive
inflammation & scarring.
Etiology:
Bacteria
Urinary obstruction
Vesicoureteral reflux
Chronic pyelonephritis---
• Usually have no symptoms of infection
• Noticeable signs – Fatigue, headache, poor
appetite
• Polyuria /Low specific gravity of urine/
• Excessive thirst, Weight loss
• Flank pain
Complications: Hypertension, Chronic renal
failure, Kidney stone
Diagnosis
• History taking & Physical examination
• Laboratory investigations
Urinalysis - Proteinuria (Albuminuria)
– Intermittent bacteruria
– Leukocytes in urine
– Low specific gravity of urine
– Urine culture to identify the pathogen
Blood
– Decreased Hgb
– Measuring BUN & creatinine
– Decrease HCI
• Radiologic IV Urogram
Management
• The same as acute pyelonephritis
• Monitor HPN
• Monitor intake and out put
Urolithiasis
• Urolithiasis is the presence of calculi (stones) in the urinary
tract.
• The cause of urolithiasis is unknown but it may be related
to changes in urine pH, volume depletion, or use of
diuretics or other drugs
• The majority of stones (75%) are composed of calcium
oxalate or calcium phosphate but may contain other
substances such as uric acid, struvite, or cystine.
• High urine acidity or alkalinity contributes to stone
formation.
• Urinary stasis, urinary retention, infection, sedentary
lifestyle, or persistently low urine output, immobility, and
dehydration contribute to an environment favorable for
stone formation.
Nephrolithiasis
• Nephrolithiasis refers to the presence of stones,
or calculi in the renal pelivis
• In 80% of pts with urolithiasis, gravel stones pass
spontaneously
• Men are affected more frequently than women,
& recurrences are possible
Nephrolithiasis---
Causes & Predisposing factors
• Hyperparthyroidism/hyperthyroidism
• Renal tubular acidosis
• Multiple myeloma
• Excessive intake of Vit D milk & alkali
• Chronic DHN, Poor fluid intake & prolonged immobility
• Abnormal purine metabolism (hyperuricemia)
• Genetic disorders (cystinuria)
• Chronic infection with urea splitting bacteria
• Chronic obstruction by foreign bodies in the UT
• Excessive oxalate absorption in inflammatory bowel disease
Complications obstruction Infection, & Impaired renal
function
Nephrolithiasis---
• Pain pattern (referred to as colic) depends on site of
obstruction
• Chills, fever, dysuria, frequency & hematuria –Secondary to
infection
• N/V ,diarrhea & general abdominal discomfort
• X-ray of KUB
• IVP- Locates stones & evaluates degree of obstruction
• Ultrasonography
Urinalysis
• Hematuria, pyuria
• Serum RFT
Nephrolithiasis---
Management
Non-surgical Management
• Extracorporeal shock wave lithotripsy (ESWL)
- Uses sound, laser or shock-wave energies to break
the stone into fragments.
- Requires conscious sedation and ECG monitoring
during the procedure
Nephrolithiasis---
Surgical Management
• Extracorporeal shock-wave lithotripsy is the most
commonly used procedure to treat urinary calculi
- In this procedure, ultrasonic shock waves pulverize the
calculi into many small fragments that pass through the
urinary tract over several months.
• Open surgery uses a surgical incision to remove the stone;
this surgery is used for large or impacted stones (such as
staghorn calculi), or for stones not removed by other
approaches.
• Ureterolithotomy (into the ureter)
• Pyelolithotomy (into the kidney pelvis)
• Nephrolithotomy (into the kidney)
Nephrolithiasis---
Nursing Interventions
- To relief pain
• Opioids -Morphine sulphate 10-30 mg TID PO
• Spasmolytic drugs: Oxybutynin chloride 5-7.5mg/d
- To prevent nephron destruction
• Antibiotics
- To eliminate calculi & prevent recurrence
(Almost 90% of urinary calculi pass spontaneously)
- Instruct the patient to strain the urine to recover the calculi; save the
stone for laboratory analysis.
- Encourage increased oral intake to 3-4 L/day unless contraindicated
- Administer intravenous fluids as prescribed.
- Encourage ambulation frequently; to promote passage of the stone.
- Give hot baths or apply warm, moist packs to promote relaxation
• Monitoring urine output for changes in voiding pattern

or amount and for cloudiness, foul odor, and blood
• Tell the patient to promptly report signs of UTI and
flank, lumbar, and abdominal pain to the Practitioner
• Teach the patient about predisposing factors, such as
dehydration, low urine output, prolonged
immobilization, and UTI
• Teach the patient with phosphate or uric acid stones
how to monitor urine pH and alkalinize or acidify his
urine
• Provide instructions about diet and prescribed drugs
for a patient with calcium calculi
• Reduce dietary intake of calcium and vitamin D,

which prevents parathyroid hormone production
• Restrict sodium intake to reduce intestinal
absorption of calcium
• Limit refined carbohydrates and animal protein to
decrease hypercalciuria
• Encourage the intake of high-fiber foods to help
bind calcium
• Suggest the use of orthophosphates to decrease
the incidence of recurrent calculi formation in
patients with hypercalciuria
Nephrolithiasis---
Calcium phosphate
• Limit intake of food high in animal protein (Reduction of
protein intake decreases calcium precipitation).
• Limit sodium intake.
• Reduced calcium intake (dairy products) is individualized.
Medications
• Thiazide diuretics (hydrochlorothiazide) to increase calcium
reabsorption
• Orthophosphates to decrease urine saturation of calcium
oxalate
• Sodium cellulose phosphate to reduce intestinal absorption
of calcium
Nephrolithiasis---
Calcium oxalate
• Avoid oxalate sources: Spinach, black tea, cocoa,
beets, peanuts, chocolate, wheat
• Limit sodium intake.
Medications
• In addition to those for calcium phosphate,
allopurinol, vitamin B6 (pyridoxine)
Struvite (magnesium ammonium phosphate)
• Avoid high-phosphate foods (dairy products, red
and organ meats, whole grains).
Nephrolithiasis---
Uric acid (urate)
• Decrease intake of purine sources (organ meats,
poultry, fish, red wine, sardines)
Medications
• Allopurinol to prevent formation of uric acid
• Potassium or sodium citrate or sodium
bicarbonate to alkalinize the urine
Nephrolithiasis---
Cystine
• Limit animal protein intake.
Medications
• Alpha mercapto propionylglycine (AMPG) to
lower urine cystine
• Captopril to lower urine cystine
Urinary tract infections
• Urinary tract infection(UTI) is an infection of the

urinary tract caused by the presence of
pathogenic microorganism in the urinary tract
with or without signs & symptoms.
The most common sites of infections
• Bladder – cystitis
• Urethra – Urethritis
• Prostrate – Prostatitis
• Kidneys – Pyelonephritis
Urinary tract infections---
Etiology
1. Ascending infections [Enter via Urinary meatus]
2. Obstructive abnormalities [strictures, prostatic
tumors or hyperplasia]
3. Upper Urinary track disease may occasionally cause
recurrent bladder infections.
Sign and symptoms
– Dysuria, frequency, urgency and a
nocturnal
– Suprapubic pain and discomfort
– Gross hematuria
Urinary tract infections---
Diagnosis
1. Urine dipstick: may react positively for blood WBC and titrates
indicate infection.
2. Urine microscopy: Shows RBC and many WBC per field with our
epithelial cells.
3. Urine culture: It is used to detect presence of bacteria & for
antimicrobial sensitivity test
Management
1. Relieve discomfort and provide rest(Catheterization if needed)
2. Antibiotic
3. Follow up culture to prove treatment effectiveness
4. Increase fluid intake
5. Avoid irritants - Coffee, tea, alcohol, cola drinks
6. Promote urinary output
Complication: Pyelonephritis, Sepsis
Neurogenic bladder
 Neurogenic bladder refers to all types of bladder
dysfunction caused by an interruption of normal
bladder innervation
1/ Spastic (resulting from an upper motor neuron
lesion) or
2/ Flaccid (resulting from a lower motor neuron
lesion)
Neurogenic bladder
Causes
• Infection disease
• Cerebral disorder
• Chronic alcoholism
• Collagen disease
• Peripheral innervations disorder
• Distant effects of cancer
• Herpes zoster
• Metabolic disturbance
• Sacral agenesis; spinal cord disease or trauma;
• A vascular disease, such as atherosclerosis; or another
condition
Neurogenic bladder---
Signs and symptoms
• In spastic neurogenic bladder Pts may experience
spontaneous spasms of the arms and legs,
involuntary or frequent scanty urination without
a feeling of bladder fullness, and increased anal
sphincter tone.
• In flacid neurogenic bladder pts may experience
overflow incontinence, diminished anal sphincter
tone, and a distended bladder.
Signs and symptoms
• Other signs and symptoms may include altered
micturition, hydronephrosis, incontinence, and
vesicoureteral reflux (passage of urine from the
bladder back into a ureter)
• The patient may also have symptoms of a UTI or
kidney stones
Diagnosis
 Voiding cystourethrography evaluates bladder
neck function, vesicoureteral reflux, and
continence
 Urodynamic studies—which consist of cystometry,
uroflowmetry, urethral pressure profiles, and
sphincter electromyography—help evaluate how
urine is stored in the bladder, how well the
bladder empties, and how quickly urine moves out
of the bladder during voiding
Treatment
 Techniques for bladder elimination include Valsalva’s
maneuver, indwelling urinary catheter insertion,
intermittent self-catheterization
 Crede’s maneuver (pressing on the suprapubic area with a
downward motion to express urine from the bladder)
 Alpha adrenergic blockers(Ex. Terazosin hydrochloride 5-
10 mg po QID for 4-6 wks
 When conservative treatment fails, surgery may be used
to correct the structural impairment through transurethral
resection of the bladder neck, urethral dilation, external
sphincterotomy, or urinary diversion; implantation of an
artificial urinary sphincter may be necessary if permanent
incontinence follows surgery
• Use strict aseptic technique during insertion and
maintenance of an indwelling urinary catheter; don’t
interrupt the closed drainage system for any reason; keep
the drainage bag below the level of the bladder.
• Assess the patient for signs and symptoms of infection
• Teach the patient to report signs and symptoms of
infection and how to prevent UTI; encourage him to
increase his fluid intake.
• Teach dietary measures to prevent kidney stone formation
• Keep the patient as mobile as possible; perform range-of-
motion exercises, if necessary
• If a urinary diversion procedure is to be performed,
arrange for consultation with an enterostomal therapist
Benign Prostate Hyperplasia (BPH)
= Prostatic hypertrophy
• BPH is prostate gland enlargement; about 50% of men
older than age 50 and 75% of men older than age 70 have
symptoms of such enlargement
• The cause is unknown but may be linked to hormonal
changes
• As the prostate enlarges, the urethral opening narrows and
obstructs or interferes with urine flow, causing urine
retention or incomplete emptying; eventually, the ureters
and kidneys dilate, and urinary tract infections (UTIs) result
from urinary stasis
• Progressive bladder distention may cause a pouch to form
in the bladder that retains urine when the rest of the
bladder empties
Prostate gland
• A muscular gland just below the urinary bladder,
the prostate gland is about 3 cm high by 4 cm wide
by 2 cm deep (about the size of a walnut). It
surrounds the first inch of the urethra as it
emerges from the bladder.
• Prostate secretes an alkaline fluid that helps
maintain sperm motility.
• The smooth muscle of the prostate gland contracts
during ejaculation to contribute to the expulsion
of semen from the urethra.
BPH---
Signs and symptoms

• Urinary frequency; nocturia; smaller, less-
forceful urine stream; urinary hesitancy;
dribbling after urination; bladder distention;
cystitis; and acute urine retention
• Hematuria, bladder calculi, impaired renal
function, fatigue, nausea, vomiting, anorexia,
and abdominal discomfort
BPH---
Diagnosis
• The affected prostate gland is symmetrically
enlarged, smooth and firm, although slightly
elastic. It may protrude more into the rectal
lumen
• Cystoscopy, urethrography, excretory urography,
and hematologic and kidney function studies
• Prostate specific antigen (PSA) can help to rule out
prostatic carcinoma; and post void residual urine
test and trans rectal ultrasonography
BPH---
Treatment
• Conservative treatment may include finasteride to
decrease the size of the prostate and alpha-adrenergic
blockers, such as prazosin , doxazosin , tamsulosin , and
terazosin , to relax the muscles and promote urination
• For acute cases, a urologist may insert a urinary catheter;
a stylet may be needed to pass through the obstruction, or
a suprapubic cystostomy (incision and catheter placement
in the bladder through the abdomen wall) may be needed
• When a urinary obstruction is present, prostatectomy
(surgical removal of soft tissue from the prostate) by one
of four techniques is commonly performed--- ejaculation
may be impaired.
BPH---
RX---
• Newer treatments include balloon urethroplasty,
laser therapy, and intraurethral stents
• Other minimally invasive surgical techniques
include:
- Transurethral needle ablation to burn away well-
defined regions of the prostate, thereby
improving urine flow with less risk
- Transurethral microwave treatment to destroy
portions of the prostate with heat
BPH---
Preoperative nursing interventions
• Explain the surgical procedure, perioperative
experience, and expected postoperative course
to help decrease the patient’s anxiety
• Allow the patient to discuss fears and concerns
about postoperative urinary incontinence and
impotence, but assure him that they aren’t
common after prostate surgery, only after
radical perineal resection
BPH---
Postoperative nursing interventions
• Evaluate the patient’s pain and response to analgesia
• Explain to the patient that after transurethral resection
of the prostate (TURP), bladder spasms are typical;
explain to him that the sensation of needing to void is
normal and that avoiding straining may decrease the
frequency and intensity of bladder spasms
• Observe and maintain the patency of the three-way
irrigation system; clots can obstruct the system and
cause pain and bladder spasms; if clots form, increase
the flow of saline solution to dilute the urine and allow
the clots to flow out
Case scenario
Ex 1. A 65-year-old pt presents difficulty with urination.
Increasingly, he has noticed feeling like his bladder has
not emptied completely and his urinary stream has a
decreased force. He experiences dribbling after he
completes urination. These symptoms have been going
on for several years, but his level of discomfort has
increased over the past few months. On P/E, you feel a
symmetrically enlarged, smooth, and firm prostate
gland, which seems to protrude more into the rectal
lumen without any discrete lesions. What is your
most likely diagnosis?
A. Normal prostate B. Prostatitis
C. Benign prostatic hyperplasia D. Prostate cancer
Case scenario---
Ex 2. A 36-year-old computer programmer presents
to the office with pain with urination, and fever.On
palpation of the prostate, his gland is swollen,
tender, and warm to the touch
Your most likely diagnosis is?
A. Normal prostate B. Benign prostatic hyperplasia
C. Prostate cancer D. Prostatitis
Orchitis
• Orchitis is inflammation of the testis (testicular congestion)

Causes
• Bacterial orchitis – Most often resulted from epididymitis,
an inflammation of the coiled tube (epididymis) that
connects the vas deferens and the testicle. Often the cause
of the infection is an STD, particularly gonorrhea or
Chlamydia.
• Viral orchitis - Most cases are the result of mumps. The
mumps virus can spread from the salivary glands to other
parts of the body, including the testicles.
• Physical trauma – particularly in individuals with hazardous
occupation
• Thermal – (radiation) decrease testicular secretion & can
cause atrophy of the testis.
Orchitis---
S & Sxs
• The S/S of orchitis usually have an abrupt onset,
including testicular swelling on one or both sides
• Pain – mild to severe; Tenderness in one or both
testicles
• N/V, Fever - Discharge from penis
• Prostate enlargement and tenderness
Orchitis---
Risk factors
• Not being immunized against mumps; Being older than
45; Recurring UTI
• Surgery that involves the genitals or urinary tract, b/s of
the risk of infection
• Malformations in the urinary tract present at birth
(congenital)
• High-risk sexual behaviors that can lead to STDs
Complications
• Orchitis may cause the affected testicle to shrink (atrophy)
• Scrotal abscess
• Rarely it can impair fertility
Orchitis---
Treatment
 Symptomatic Rx for viral orchitis: analgesics, bed
rest, elevating the scrotum and applying cold
packs.
 Antibiotic for bacterial orchitis
 Protection of STIs & Sexual partner management if
the cause is an STI
 Immunization against mumps
Phimosis
• It is a condition in which the foreskin is
constricted so that it cannot be retracted over
the glans penis.
• Physiologic phimosis is common in male
children < 3 yrs of age, and does not usually
require any form of intervention.
• By age 3, 90 % of uncircumcised males should
be able to completely retract their foreskin from
the tip of the penis.
• By age 17, 97-99 % of males will be able to
completely retract their foreskin.
Phimosis---
Causes
• Physiologic phimosis
• Pathological phimosis ( infection, inflammation, or
damage to the foreskin resulting in scarring)
• Congenital phimosis is not a result of any medical
problem, but simply the presence of a tight or
restrictive foreskin from birth that does not loosen
as a boy grows into an adult.
• Congenital phimosis is the most common form of
phimosis , and the easiest to treat.
Phimosis---
Symptoms
• Bulging of the foreskin during urination.
• Tight foreskin that does not retract past the head or glans of
the penis.
• When the foreskin is pulled back, it can cause discomfort,
and may result in paraphimosis where the foreskin cannot
be pulled back over the glans again and is stuck.
• In some cases there may be scarring on the foreskin,
inflammation, bleeding or itching, which may indicate an
infection or other medical condition that requires diagnosis.
• Smegma, the appearance of white lumps under the
foreskin, may be present as well in some cases, contributing
to the problem.
Phimosis---
Treatment
 Circumcision (both as prevention and as a cure).
 Many boys under the age of 5 are being
circumcised to prevent phimosis.
 If you are under the age of 18, it is always best
to wait until adulthood before pursuing surgical
treatments, as the foreskin develops differently
in every man.
• Instruction to clean the preputial area
Phimosis---
Medications
 Treatment for repeated phimosis may involve application of
a steroid cream to the foreskin up to three times a day for
about a month to loosen the adhesive ring.
 If the child has ballooning of the foreskin during urination
after the age of 10 , a circumcision (surgical removal of all or
part of the foreskin) may be recommended.
 Betamethasone and hyaluronidase(degradation of
hyaluronic acid permits diffusion of trapped fluid). After two
months the boys given a combination of betamethasone
and hyaluronidase improved by 54%, while those given just
betamethasone improved by 40%. Both treatments were
more effective than placebo, as well as safe and well-
tolerated by subjects.
Phimosis---
Manual Therapy
 For those wanting to avoid surgery or prescription
medications, many doctors recommend a conservative
treatment plan involving manually stretching the foreskin.
 One way of doing this is through masturbation, actively
moving the foreskin up and down in a way that mimics
sexual intercourse.
 Over time this gently stretches the skin, and improves the
elasticity of the foreskin tissues. Be careful, as rough
treatment may causes breakages of the skin and scarring.
 In addition, doctors have developed a form of balloon
catheter, than can manually help to stretch the foreskin.
Phimosis---
Penis Health Crèmes
 Penis health crèmes containing vitamins,
minerals, natural oils and botanical extracts may
benefit the health of the penis skin by improving
moisture content, reducing inflammation, and
supporting the healing of the tissues.
 If you are attempting to manually stretch the
foreskin of your penis, under the supervision of a
health professional, application of penis health
crèmes may support this process.
Paraphimosis
• Paraphimosis is an uncommon medical condition
where the foreskin becomes trapped behind the
glans penis, and cannot be reduced (that is, pulled
back to its normal flaccid position covering the
glans penis).
• If this condition persists for several hours or there
is any sign of a lack of blood flow, paraphimosis
should be treated as a medical emergency, as it
can result in gangrene or other serious.
• It is usually caused by well-meaning medical
professionals or parents who handle the foreskin.
Paraphimosis---
Causes
• Phimosis , injury (trauma), infection, or congenital
issues such as an abnormally shortened prepuce or
an abnormally long penis
• Poor hygiene
• Chemical irritants (soaps)
• Conditions that result in edema (swelling) such as
CHF, or nephrosis
• Bacterial infections (primarily anaerobic infections)
• Obesity
• Diabetes
Paraphimosis---
S&SX
• Swelling of the tip of the penis as the foreskin is
retracted or pulled back.
• Pain.
• Inability to pull the foreskin back over the tip of
the penis.
• Discoloration, either dark red or bluish color, of
the tip of the penis.
Paraphimosis---
Treatment
• Manual reduction & circumcision (or preputioplasty to loosen
the pruptial orifice)
• Manual reduction
• Treatment for paraphimosis may involve lubricating the
foreskin and tip of the penis and then gently squeezing the tip
of the penis while pulling the foreskin forward. This involves
compressing the glans and moving the foreskin back to its
normal position, perhaps with the aid of a lubricant, cold
compression, and local anesthesia as necessary. If this fails, the
tight edematous band of tissue can be relieved surgically with
a dorsal slit or circumcision. An alternative method, the
Dundee technique, entails placing multiple punctures in the
swollen foreskin with a fine needle, and then expressing the
edema fluid by manual pressure.
Paraphimosis---

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Medical Surgical II

Course code: Nurs322

BY: Wondwossen Yimam (Msc.N)

• Body fluids transport nutrients to and remove wastes from

◆ Additional fluids are contained in other body

◆ Body compartments are separated by semi

• Filtration is the movement of water and

• Osmosis is the passive movement of

• Osmotic pressure is the amount of

• Active transport occurs when the cell membrane

FVD & FVE

• Moderate – 5 % of body weight loss

• Severe – 8 % or more of body weight loss

NB. Alterations in the amount or composition of

• Fluid volume Deficit r/t Insufficient intake, vomiting,

• Goal: Client will have adequate fluid volume within 24

NB. Crackles are short, intermittent, nonmusical, explosive

• A 69 year old man has a history of CHF controlled

Pathophysiology – An increase in K+ causes

• Causes few direct problems with body

• Classic indications for IV fluid include

Uses Special considerations

• Excessive infusions of hypotonic solutions can

NB. 20 to 22 Needle gauge for most IV fluids.

Ex. HCl(aq) +H2O--- H3o + Cl (aq)

Acidosis: a decrease in a normal 20:1 base (HCo3-)

• A weak acid or base is one that dissociates

3. Protein buffer systems

1/ Establish the primary disorder (MA,MA,RA & RA)

Arterial Sample Venous Sample

• PaCO2: 36 Resp. Acidosis

• HCO3-: 14 Metabolic Acidosis.

• PH: 7.50 Metabolic Alkalosis

• HCO3-: 24 Metabolic Acidosis

Acute renal failure (ARF)

C/ Recovery phase: (continues until renal function

• Glomerular capillaries are damaged from

• It is a slowly progressive disease characterized

Acute pyelonephritis is an active bacterial infection

• It is a persistent inflammation of kidneys.

• Monitoring urine output for changes in voiding pattern

• Reduce dietary intake of calcium and vitamin D,

• Urinary tract infection(UTI) is an infection of the

Signs and symptoms

• Orchitis is inflammation of the testis (testicular congestion)

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