Flashcards: Med Surg Exam 1

B. D5W

B. Hypertonic

B. Pulmonary Edema

A: 3% Saline. A patient with cerebral edema would be ordered a HYPERTONIC solution to decrease brain swelling. The solution would remove water from the brain cells back into the intravascular system to be excreted. 3% Saline is the only hypertonic option.

D. Hypertonic

D. 0.33% saline (1/3 NS)

A. Patient with increased intracranial pressure

C. Hypotonicity

A. Hypotonic

D. 0.9% Normal Saline

C. 0.45% Saline

Sodium

Potassium

Calcium

Magnesium

Chloride

Phosphate

fluid shifting of intracellular and goes into an area where it can't be used, results in decreased fluid in intracellular

Intracranial Pressure*

Diabetics(risk for HYPERglycemia)

Cell presents with the same concentration on the inside and outside with no shifting of fluids (HYDRATION)

0.9% Saline

5% Dextrose *

5% Dextrose in 0.225 saline

Lactated Ringers (LR)

Increase fluid in the extracellular space

Intracellulaer-> extracellular

DEHYDRATION(cell shrinks)

3% saline

5% saline

10% Dextrose (fluid overload w/pulmonary edema)

5% Dextrose in 0.9 saline

5% Dextrose in 0.45 saline

5% Dextrose in LR

Hyponatremia (pulls sodium back into intravascular system)

Cerebral edema w/ swelling by remaining fluid off brain

Loss of extracellular fluid exceeds intake ratio of water (DEHYDRATION)

-Abnormal fluid losses (vomiting,diarrhea,sweating,GI suction)

-Decreased intake(nausea, lack of access, anorexia)

-Third space fluid shifts(due to burns, ascites)

-Diabetes insipidus

-Adrenal insufficiency

-Hemorrhage

-Weight loss

-↓ skin turgor,

-oliguria,

-concentrated urine,

- increased capillary filling time

- low CVP (central venous pressure), ↓ BP,

-flattened neck veins,

-dizziness, weakness, thirst

and confusion,

-↑ pulse,

muscle cramps, sunken

eyes, nausea, increased

temperature; cool, clammy,

pale skin

↑ hemoglobin and hematocrit,

↑ serum and urine osmolality and

specific gravity,

↓ urine sodium,

↑ BUN and creatinine,

↑ urine specific gravity and osmolality

-cognition

-ambulation

-ADLs

-Gag reflex

Oral route prefered

IV for acute or severe losses

Types of solutions

-Lactated Ringer’s solution or 0.9% sodium chloride first line choice for hypotensive pt with fvd

-Normotensive pt a hypotonic electrolyte solution (e.g., 0.45% sodium chloride) is used

-Pt severe FVD-fluid challenge test

•I&O at least every 8 hours, sometimes hourly

•Daily weight

•Vital signs closely monitored

•Skin and tongue turgor, mucosa, urine output, mental status

•Measures to minimize fluid loss

•Administration of oral fluids

•Administration of parenteral fluids

Expansion of the ECF caused by the abnormal retention of water and sodium in approximately the same proportions in which they normally exist in the ecf (secondary to increase total-body sodium content)

•fluid overload or diminished homeostatic mechanisms

•Heart failure, kidney injury, cirrhosis of liver

•Contributing factors: Consumption of excessive amounts of table salt or other sodium salts

•Excessive administration of sodium-containing fluids

-weight gain

•Edema(elevate legs)and ascites

•Distended jugular neck veins

•Crackles

-elevated CVP

-shortness of breath(oxygen), ↑ BP,

-bounding pulse and cough,

-↑ respiratory rate,

-↑ urine

output

↓ hemoglobin and hematocrit, BUN

↓ serum and urine osmolality,

↓urine sodium and specific

gravity

Get chest x-ray

•Diuretics(Loop,Thiaside,Potassium)

•Dialysis (hemodialysis)

•Dietary restrictions of sodium

•I&O AND DAILY WEIGHTS; ASSESS  LUNG SOUNDS, EDEMA, OTHER SYMPTOMS

•MONITOR RESPONSES TO MEDICATIONS—DIURETICS AND PARENTERAL FLUIDS

•PROMOTE ADHERENCE TO FLUID RESTRICTIONS, PATIENT TEACHING RELATED TO SODIUM AND FLUID RESTRICTIONS

•MONITOR, AVOID SOURCES OF EXCESSIVE SODIUM

•PROMOTE REST

135-145

regulate water in and out the cell

-muscle constriction and nerve impulses

-Loss of sodium, as in use of diuretics(thiazides), loss of GI fluids, renal disease, and adrenal insufficiency.

-Gain of water, as in excessive administration of D5W and

water supplements for patients receiving hypotonic tube feedings; SIADH, such as head trauma and oat-cell lung tumor;

medications associated with water

retention (oxytocin and certain

tranquilizers); and psychogenic

polydipsia. Hyperglycemia and heart

failure cause a loss of sodium.

-hypotonic fluids

anorexia, nausea and vomiting, headache, lethargy, dizziness,

confusion, muscle cramps and weakness, muscular twitching, seizures, papilledema, dry

skin/mucosa, decreased salivation

↑ pulse, ↓ BP,

weight gain, edema

↓ serum and urine sodium,

↓ urine specific gravity and osmolality

•Treat underlying condition

•Sodium replacement

•Water restriction

•Medication (AVP/ADH receptor antagonists)

•Assessment: I&O, daily weight, lab values, CNS changes

•Encourage dietary sodium

•Monitor fluid intake

•Effects of medications (diuretics, lithium)

Fluid deprivation in patients who cannot respond to thirst,

hypertonic tube feedings without adequate water supplements,

diabetes insipidus, heatstroke,

hyperventilation, watery diarrhea, burns, and diaphoresis.

-Excess corticosteroid,

sodium bicarbonate, and sodium chloride administration, and saltwater nonfatal drowning victims.

Thirst, elevated body temperature, swollen dry tongue and sticky mucous membranes, hallucinations,

lethargy, restlessness,

irritability, increased DTR, pulmonary

edema, hyperreflexia,

twitching, nausea,

vomiting, anorexia,

↑pulse, and ↑ BP

↑ serum sodium,

↓ urine sodium,

↑ urine specific gravity and osmolality(exceeds 300), ↓ CVP

•Gradual lowering of serum sodium level via infusion of hypotonic electrolyte solution (0.45% saline) or D5W(rare)

•Diuretics

•Assessment for abnormal loss of water and low water intake

•Assess for over-the-counter sources of sodium

•Monitor for CNS changes

3.5-5

Found mainly in cell...... Na+ out... fluid balance and Na+ - K+ pumps

-opposite relationship with Na+

-Regulates muscle contractions

GI losses

corticosteroid administration,

hyperaldosteronism, recent ileostomy, tumor of intestine, alteration in acid base balance, laxative abuse

loop diuretics, too much insulin (k+ moves into cells) bulimia, osmotic diuresis, alkalosis, starvation, diuretics, and digoxin toxicity

Fatigue, anorexia, nausea and

vomiting, muscle weakness,

polyuria, decreased bowel

motility, ventricular asystole or

fibrillation, paresthesias, leg

cramps, shallow respirations

↓ BP, ileus, abdominal

distention, hypoactive reflexes. (can cause death through cardiac or respiratory arrest)

ECG: flattened T waves,

prominent U waves, ST

depression, prolonged PR

interval

Metabolic alkalosis

•Potassium replacement: Increased dietary potassium, oral potassium supplements or IV potassium for severe deficit (unless oliguria present)

•Monitor ECG for changes

•Monitor ABGs

•Monitor patients receiving digitalis for toxicity

•Monitor for early signs and symptoms

•Administer IV potassium only after adequate urine output has been established/ and after BUN and Creatinine

Eat foods with potassium-bannans, melons, potatoes, meat, whole grains, apricot

oliguric kidney injury, use of potassium- conserving diuretics in patients with renal insufficiency,

metabolic acidosis, Addison

disease, crush injury, burns,

rapid IV administration of

potassium, and certain

medications such as ACE

inhibitors, NSAIDs, cyclosporine

Muscle weakness, tachycardia →

bradycardia, arrhythmias,

flaccid paralysis, paresthesias,

intestinal colic, cramps,

abdominal distention,

irritability, anxiety, respiratory failure, slurred speech, confusion, metabolic/respiratory acidosis

ECG: tall

tented T waves, prolonged PR

interval and QRS duration,

absent P waves, ST depression

•Monitor ECG, heart rate (apical pulse) and blood pressure, assess labs, monitor I&O

•Limitation of dietary potassium and dietary teaching 

•Administration of cation exchange resins (sodium polystyrene sulfonate)

•Emergent care: IV calcium gluconate, IV sodium bicarbonate, IV regular insulin and hypertonic dextrose IV, beta-2 agonists(albuterol), dialysis

•Administer IV slowly and with an infusion pump

-loop diuretic-furosemide

-for very severe instances doctor may order K-excalate (pulls potassium out of body) anything over 6

8.8-10.4

Health of bones/teeth

-muscle/nerves, clotting

Hypoparathyroidism (may follow

thyroid surgery or radical neck

dissection), malabsorption, osteoporosis, pancreatitis, alkalosis, vitamin D deficiency, massive subcutaneous infection, massive transfusion of citrated

blood, chronic diarrhea, decreased

parathyroid hormone, diuretic

phase of acute kidney injury,

fistulas, burns, alcoholism

Numbness, tingling of fingers,

toes, and circumoral region;

positive Trousseau sign and

Chvostek sign; seizures,

spasms, Tetnay

hyperactive dtr, irritability,

bronchospasm, anxiety,

impaired clotting time, laryngospasm

↓prothrombin, diarrhea, ↓ BP.

ECG: prolonged QT interval

and lengthened ST

Labs indicate: ↓ Mg++

•IV of calcium gluconate for emergent situations (monitor for risk of extravasation)

•Seizure precautions

•Oral calcium and vitamin D supplements

•Exercises to decrease bone calcium loss

•Patient teaching related to diet and medications

Hyperparathyroidism, malignant

neoplastic disease, prolonged

immobilization, overuse of

calcium supplements, vitamin D

excess, oliguric phase of acute

kidney injury acidosis,

corticosteroid therapy, thiazide

diuretic use(lithium), increased parathyroid

hormone, and digoxin toxicity

bone loss related to immobility

CANCER,

Muscular weakness,

constipation, anorexia,

nausea and vomiting,

polyuria and polydipsia,

dehydration, hypoactive dtr, lethargy,

deep bone pain, pathologic

fractures, flank pain, calcium

stones(abdominal distention), hypertension.

ECG:

shortened ST segment and

QT interval, bradycardia,

heart blocks

•Treat underlying cause (Cancer)

•Administer IV fluids, furosemide, phosphates, calcitonin, bisphosphonates

•Increase mobility

•Encourage fluids

•Dietary teaching, fiber for constipation

•Ensure safety 

1.8-2.6

Very important for the heart

Associated with hypokalemia and hypocalcemia

-nerve/muscle/vessels (relaxation BP

-competes with calcium binding site contraction

alcoholism, GI losses,

hyperparathyroidism,

hyperaldosteronism, diuretic phase

of acute kidney injury,

malabsorptive disorders, diabetic

ketoacidosis, refeeding after

starvation, parenteral nutrition,

chronic laxative use, diarrhea, acute

MI,HF,decreased K+ and Ca++ and

certain pharmacologic agents (e.g.,

gentamicin, cisplatin, cyclosporine)

Neuromuscular irritability,

positive Trousseau sign

and Chvostek sign,

insomnia, apathy, anorexia,

vomiting, psychosis, weakness, increase DTR increased

tendon reflexes, and ↑

BP. Ca++ and K+ levels

ECG: PVCs, flat or

inverted T waves,

depressed ST segment,

prolonged PR interval,

and widened QRS

•Magnesium sulfate IV is administered with an infusion pump; monitor vital signs and urine output

•Calcium gluconate or hypocalcemic tetany or hypermagnesemia

•Oral magnesium

•Monitor for dysphagia

•Seizure precautions

•Dietary teaching (green, leafy vegetables; beans, lentils, almonds, peanut butter)

Flushing, hypotension,

muscle weakness,

drowsiness, hypoactive

reflexes, depressed

respirations, cardiac

arrest and coma,

diaphoresis.

ECG:

tachycardia →

bradycardia, prolonged

PR interval and QRS,

peaked T waves

•IV calcium gluconate

•Ventilatory support for respiratory depression

•Hemodialysis

•Administration of loop diuretics, sodium chloride, and LR

•Avoid medications containing magnesium

•Patient teaching regarding magnesium-containing OTC medications

•Observe for DTRs and changes in LOC

2.7-4.5

teeth/bone building, stored in bones

-absorbed in gut and excreted in kidneys

Refeeding after starvation,alcoholism, DKA,respiratory and metabolic alkalosis ,↓magnesium &potassium,hyperparathyroidism, vomiting, diarrhea, hyperventilation, vitamin D

deficiency associated with

malabsorptive disorders, burns, acid–

base disorders, parenteral nutrition and diuretic and antacid use

Paresthesias, muscle weakness, bone pain and tenderness,chest pain,confusion,cardiomyopathy,respiratory failure,seizures, tissue hypoxia, and

increased susceptibility to infection, nystagmus

•Prevention is the goal

•Oral or IV phosphorus replacement (only for patients with serum phosphorus levels less than 1 mg/dL not to exceed 3 mmol/hr), Burosumab, correct underlying cause

•Monitor IV site for extravasation

•Monitor phosphorus, vitamin D and calcium levels

•Encourage foods high in phosphorus (milk, organ meats, beans nuts, fish, poultry), gradually introduce calories for malnourished patients receiving parenteral nutrition

Acute kidney injury and chronic kidney disease, excessive intake of

phosphorus, vitamin D excess,

respiratory and metabolic acidosis,

hypoparathyroidism, volume

depletion, leukemia/lymphoma

treated with cytotoxic agents,

increased tissue breakdown,

rhabdomyolysis, chemotherapy

Tetany, tachycardia, anorexia, nausea and vomiting, muscle

weakness, signs and symptoms of

hypocalcemia; hyperactive reflexes;

soft tissue calcifications in lungs, heart, kidneys, and cornea

-trousseaus and chovesk

-soft tissue calcifications

•TREAT UNDERLYING DISORDER

•VITAMIN D PREPARATIONS, CALCIUM-BINDING ANTACIDS, PHOSPHATE-BINDING GELS OR ANTACIDS, LOOP DIURETICS, IV FLUIDS (NORMAL SALINE), DIALYSIS

•MONITOR PHOSPHORUS AND CALCIUM LEVELS

•AVOID HIGH-PHOSPHORUS FOODS

•PATIENT TEACHING RELATED TO DIET, PHOSPHATE-CONTAINING SUBSTANCES, SIGNS OF HYPOCALCEMIA

96-108

-acid-base balance

-digestion

-balance fluids w/Na+

Loss of sodium, loss of chloride

-Bicard has inverse relationship with chloride

Addison disease, reduced chloride intake, untreated DKA, chronic respiratory acidosis, excessive

sweating, vomiting, gastric suction,

diarrhea, sodium and potassium deficiency, metabolic alkalosis; loop, osmotic, or thiazide diuretic use; overuse of bicarbonate, rapid removal of ascitic fluid with a high sodium content, IV fluids that lack chloride (dextrose and water), draining

fistulas and ileostomies, heart failure, cystic fibrosis

Agitation, irritability,

tremors, muscle

cramps,

hyperactive deep

tendon reflexes,

hypertonicity,

tetany, slow

shallow

respirations,

seizures,

arrhythmias, coma

↓serum chloride, ↓

serum sodium, ↑ pH, ↑ serum

bicarbonate, ↑ total carbon

dioxide content, ↓urine chloride

level, ↓ serum potassium

•Replace chloride-IV NS or 0.45% NS

•Ammonium chloride

•Monitor I&O, ABG values and electrolyte levels

•Assess for changes in LOC

Educate about foods high in chloride (tomato juice, bananas, eggs, cheese, milk) and avoid drinking free water (water without electrolytes)

Excessive sodium chloride infusions with water loss, head injury (sodium retention), hypernatremia, kidney injury, corticosteroid use, dehydration, severe diarrhea (loss of bicarbonate), respiratory alkalosis, administration of diuretics, overdose of salicylates and ammonium chloride use, hyperparathyroidism, metabolic acidosis

Tachypnea, lethargy, weakness, deep

rapid respirations, decline in cognitive status, ↓cardiac output, dyspnea,

tachycardia, pitting edema, arrhythmias, coma

•Correct the underlying cause and restore electrolyte and fluid balance

•Hypertonic IV solutions

•Lactated Ringers

•Sodium bicarbonate, diuretics

•Monitor I&O, ABG

•Focused assessments of respiratory, neurologic, and cardiac systems

•Patient teaching related to diet and hydration

pH 7.35-7.45

PO2 (oxygen) 80-100%

PCO2(carbon dioxide) 35-45

HCO3(bicarb) 22-26

Low pH (less than 7.35)

PCO2 normal

Bicarb low

-Hyperkalemia may occur

-Salicylate poisoning

-renal failure

-propylene glycol toxicity

-DKA

-starvation

Headache, confusion, drowsiness, increased respiratory rate/depth

-low BP

-Low cardiac output/dysrhythmias

-shock

•Correct underlying problem, correct metabolic imbalance

•Bicarbonate may be administered

•Monitor serum electrolytes

•Monitor potassium levels

•Hemodialysis

•Peritoneal dialysis

Increased pH and Bicarb

normal PCO2

Gi losses

-meds-longterm diuretic use

-hyperaldosteronism

-cushings syndrome

-hypokalemia

symptoms related to decreased calcium, respiratory depression, tachycardia, symptoms of hypokalemia including tingling of toes, fingers, dizziness and tetany, ECG changes, decreased GI motility

•Correct the underlying acid–base disorder

•Restore fluid volume with sodium chloride solutions

•Monitor I&O

•Monitor for ECG and neurologic changes

Low pH

High CO2

Normal bicarb

Pulmonary edema, overdose, atelectasis(collapsed lung), pneumothorax(trapped air in lung), severe obesity, pneumonia,  COPD, muscular dystrophy, multiple sclerosis, myasthenia gravis

With chronic respiratory acidosis, , may be asymptomatic. With acute respiratory acidosis may see sudden increased pulse, respiratory rate, and BP; mental changes; feeling of fullness in head (intracranial pressure) and increased conjunctival vessels.

•Improve ventilation

•Bronchodilators(albuterol), antibiotics, anticoagulants(heparin, warfarin)

•Pulmonary physiotherapy

•Adequate hydration

•Mechanical ventilation if necessary

•Monitor respiratory status, I&O

Increased pH

Decreased CO2

Bicarb normal

HYPERVENTILATION

Extreme anxiety, panic disorder, hypoxemia, salicylate intoxication, gram-negative sepsis, inappropriate ventilator settings

Lightheadedness, inability to concentrate, numbness and tingling in extremities, tachycardia, and ventricular and atrial arrhythmias

•Treat the underlying cause

•Antianxiety agent

•Have patient breathe into a bag

•Monitor anxiety and respiratory status

•Educate patient on techniques to decrease anxiety

Nephron

-Regulate BP

-urine formation

-excrete metabolic waste

-acid base regulation

-fluid and electrolyte regulation

-erythropoietine secretion

Hormone Rein is produced by the kidneys and elevates blood pressure.

When renin is secreted, it turns angiotensinogen into angiotensin l -->

Angiotensin l is then converted in the lungs into angiotensin ll-->

Angiotensin ll causes blood vessels to constrict, which raises BP

(Also causes kidneys to retain more sodium and water, this raises volume of blood)

It is responsible for regulating the amount of water in the blood and is released from the pituitary gland based on signals from hypothalamus, which detects water levels of the blood

ADH LOW- kidneys excrete more water and urine output increased (diurese)

ADH HIGH- decreased urine output (retention)

-heart disease

-kidney disease

-hyponatremia

-hypervolemic

-hypernatremia

-hypovolemia

-Produced by adrenal gland

-acts in the kidneys to aid int he conservation of Na+, secretion of K+, water retention and to stabilize BP

AKA Hypoaldosteronism

-occurs as part of adrenal insufficiency -> dehydration, low BP, low blood sodium level, and high potassium level

AKA Hyperaldosteronism

-High BP

-Low blood levels of potassium

-abnormal increase in blood volume

Dialysis

Cancer

Heart failure

Malnourishment

Enteral feeds(ng feeds)

Iv fluids

(F&E imbalance, weigh daily, I&O)

Blood:

Glomerular filtration Rate (GFR) >90

BUN

Hgb

Hct

Plasma osmality

Urine:

Specific gravity

Urinalysis, electrolytes

Creatinine clearance

Proteinuria/ Albuminuria

risk factors:

diabetes

hypertension

(Proteinuria is considered >300mg/day of albumin excreted)

•Older adults susceptible to kidney injury R/T renal structural and functional changes:

•Sclerosis of the glomerulus and renal vasculature

•Decreased blood flow

•Decreased GFR

•Altered tubal function and acid–base balance

•Incomplete emptying of bladder, urinary stasis, decreased nerve innervations

•Decreased drug clearance = increased drug–drug interactions

•Hypovolemia

•Hypotension

•Reduced cardiac output and heart failure

•Obstruction of the kidney or lower urinary tract (kidney stones)

•Obstruction of renal arteries or veins

Onset

Oliguric

Diuretic

Recovery

- Urine output

-HIGH BUN and creatinine

-Mild acidosis

-Diuretics will work

-LESS than 400ml urine in 24hrs

-Electrolyte imbalances

-Acid-base imbalance

-Fluid loss: 4-6 liters per day

-Maintain adequate fluid balance

-Correct electrolyte imbalances

(cycle)

•Prevention of further kidney injury​

•May last 6 – 12 months​

sudden loss of kidney function, typically within 24-48 hrs post-injury

Pre-renal

Intra-renal

Post-renal

Damage due to the decreased perfusion to the kidneys

Low urine output

Low GFR

High BUN/creatinine

Treatment:

-Treat underlying cause (nephrotic agents, sepsis, trauma, bleeding, poor cardiac output, anaphylaxis, burns, ileum)

-Fluid restriction

MAP(65)-when look at BP

Direct damage to kidney cells. (tubular necrosis, glomerulonephritis, interstitial nephritis)

Low urine ouput

High BUN/Creatinine

Electrolyte imbalance

Acid-base imbalance

Treatment:

Fluid restriction

Dialysis

Obstruction in the flow of urine

S&S:

Abdominal pain, distention

Low urine output

Treatment:

Remove obstruction (kidney stones)

Surgery

when nitrogen water products such as creatinine and urea build up in body, these waste products acts a poison-> damage tissues and reduce organ function

•Diabetes mellitus

•Hypertension

•Chronic glomerulonephritis

•Pyelonephritis or other infections

•Obstruction of urinary tract

•Hereditary lesions

•Vascular disorders

•Medications or toxic agents

Renal replacement therapies: peritoneal dialysis, HD, CRRT

-Meds: diuretics, Bone marrow stimulants, erythropoietin, calcium reducer, vitamin supplements

-Diet restrictions: no protein or sodium

-Transplant

-Improve glucose control in diabetic pts

(Impaired immune response/ AVOID foleys)

•Fluid status

•Nutritional status

•Patient knowledge

•Activity tolerance

•Self-esteem

Potential complications

•Acute nephritic syndrome

•Glomerulonephritis; chronic and acute

•Nephrotic syndrome

Diseases that destroy the glomerulus of the kidney are the third most common cause of stage 5 CKD

•Postinfectious glomerulonephritis, progressive glomerulonephritis, and membranous glomerulonephritis

•Manifestations: hematuria, edema, azotemia, proteinuria, and hypertension

•May be mild or may progress to acute kidney disease or death

•Medical management: supportive care and dietary modifications; treat cause if appropriate—antibiotics, corticosteroids, and immunosuppressants

•Patient assessment

•Maintain fluid balance

•Fluid and dietary restrictions

•Patient education

•Follow-up care

•Repeated acute glomerular nephritis, hypertensive nephrosclerosis, hyperlipidemia, and other causes of glomerular damage

•Renal insufficiency or failure: asymptomatic for years as glomerular damage increases before signs and symptoms develop

•Abnormal laboratory test results: urine with fixed specific gravity, casts, proteinuria, electrolyte imbalances and hypoalbuminemia

•Medical management determined by symptoms

•Any condition that seriously damages the glomerular membrane and results in increased permeability to plasma proteins

•Results in hypoalbuminemia and edema

•Causes: chronic glomerulonephritis, diabetes mellitus with intercapillary glomerulosclerosis, amyloidosis, lupus erythematosus, multiple myeloma, and renal vein thrombosis

Medical management: drug and dietary therapy

•Hemodialysis: used when patient is acutely ill until kidneys resume function and  for long-term replacement therapy in CKD and ESKD

•Objective is to extract toxic nitrogenous substances from the blood and to remove excess fluid:

–Diffusion, osmosis, and ultrafiltration

•Vascular access:

–Arteriovenous fistula

–Arteriovenous graft

Diffusion:

movement from higher to lower concentration

Convection:

Active movement of molecules across a semi-permeable membrane. Molecules are 'dragged'.

Osmosis:

Low to higher concentration

Ultrafiltration:

Fluid across a semipermeable membrane as a result of an artificially created pressure gradient. More efficient than osmosis in the removal of water

Shunting of patients blood from the body through a dialyzer in which diffusion and ultrafiltration occur and then back into the patients circulation.

-Helps restore F&E balance, control acid-base balance, and remove waste and toxic material from body.

Access:

Arteriovenous graft

Arteriovenous fistula

Femoral/ subclavian/ intrajugualr access

Complications:

-Rapid fluid shifts, hypotension

-Air embolus, infection

-Disequilibrium syndrome- Occurrence of neurological S&S, attributed to cerebral edema, during/after

-Arrhythmias

-Patients require multiple meds

-Increased risk for other co-morbidities

-Multiple dietary and fluid restrictions

-Safety concerns: access sites: CLABSIs

•Goals are to remove toxic substances and metabolic wastes and to reestablish normal F&E balance

•Peritoneal membrane(under peritoneum above bowel) serves as semipermeable membrane

–Ultrafiltration

–Peritoneal catheter

•Acute intermittent, continuous ambulatory, continuous cyclic

•Complications: peritonitis, leakage, bleeding, electrolyte imbalance, adhesions, hernia, inadequate dialysis

(can become ineffective after several years)

Must have central access

Complications

-F&E imbalance

-Acid-base imbalance

-Hemorrhage

-Thrombosis

-Infection

•Monitor all medications and medication dosages carefully

•Address pain and discomfort

•Stringent infection control measures

•Dietary considerations: sodium, potassium, protein, fluid, individual nutritional needs

•Skin care: pruritus, keep skin clean and well moisturized, trim nails, and avoid scratching

CAPD catheter care

•Preoperative considerations

-CONSENT!!

•Perioperative concerns

•Postoperative management:

–Potential hemorrhage and shock

–Potential abdominal distention and paralytic ileus

–Potential infection

–Potential thromboembolism

-reaction Urine output(F&E)

-insentive spirometry (respiratory)

-monitor site for infection (drainage, bleeding thromboembolism, pneumonia- encourage movement)

•Pain relief measures, analgesic medications

•Promote airway clearance and effective breathing pattern, turn, cough, deep breathe, incentive spirometry, positioning

•Monitor UO and maintain potency of urinary drainage systems

•Use strict asepsis with catheter

•Monitor for signs and symptoms of bleeding

•Encourage leg exercises, early ambulation, and monitor for signs of DVT

•Instruct both patient and family

•Drainage system care

•Strategies to prevent complications

•Signs and symptoms

•Follow-up care

•Fluid intake

•Health promotion and health screening

•Lower UTI

–Cystitis

–Prostatitis

–Urethritis

•Upper UTI

–Pyelonephritis: acute and chronic

–Interstitial nephritis

–Renal abscess and perirenal abscess

•Bacterial invasion of the urinary tract

•Pregnancy

•Urethrovesical reflux, ureterovesical reflux

•Menopause

•Uropathogenic bacteria

• sexual activity

•Shorter urethra in women

•chronic health condition

•BC

•Pain, burning upon urination, frequency, nocturia, incontinence, hematuria

•About half are asymptomatic

•Association of symptoms with sexual intercourse, contraceptive practices, and personal hygiene

•Gerontologic considerations

•Assessment of urine, urinalysis, and urine cultures

•Other diagnostic tests

•Acute pain related to infection

•Deficient knowledge about:

–Factors predisposing patient to infection and recurrence

–Detection and prevention of recurrence

–Pharmacologic therapy

(Cephalosporin,penicillin,fluroquinolone)

•Cognitive impairment

•Frequent use of antimicrobial agents

•High incidence of multiple chronic medical conditions

•Immunocompromise

•Immobility and incomplete emptying of bladder

•Obstructed flow of urine (e.g., urethral strictures, neoplasms, or a clogged indwelling catheter)

•Sepsis (urosepsis)

•Acute kidney injury

Chronic kidney diseas

•Relieving pain

•Medications as prescribed: antibiotics, analgesics, and antispasmodics(flexerale)

•Application of heat to the perineum to relieve pain and spasm

•Increased fluid intake

•Avoidance of urinary tract irritants such as coffee, tea, citrus, spices, cola, and alcohol

•Frequent voiding

•Patient education

Hygiene

Types:

-Stress

-Urge

-functional

-iatrigenic (involuntary loss of fluid)

-Mixed incontinence

•Urinary incontinence is not inevitable and is treatable

•Management takes time (provide encouragement and support)

•Education verbally and in writing

•Develop and use a voiding log or diary

•Behavioral interventions

•Medication education related to pharmacologic therapy

•Strategies for promoting continence

•Inability of the bladder to empty completely

•Residual urine: amount of urine left in the bladder after voiding

•Causes include:

–Adults 60 years and older may have 50 to 100 mL of residual urine remaining in the bladder after voiding

–Postoperative spasms

–Diabetes, prostatic enlargement, urethral pathology, trauma, pregnancy, neurologic disorder

–Medications

-Post-op pts

-BPH

-Pregnancy

-Spine injury

•Calculi (stones) in the urinary tract or kidney

•Causes: may be unknown

•Depends on location and presence of obstruction or infection

•Pain and hematuria

•Diagnosis: radiography, blood chemistries, and stone analysis; strain all urine and save stones

-Morphine given in IV fluids

•Signs and symptoms to report

•Follow-up care

•Urine pH monitoring

•Measures to prevent recurrent stones

•Importance of fluid intake

•Dietary education

•Medication education as needed

•Bladder, kidney and renal pelvis, ureters, other structures such as prostrate

•Cancer of bladder:

–More common after age 55 years

–Leading cause of death

–Smoking increases risk 50%;

•S/S: visible painless hematuria; pelvic or back pain may indicate metastasis

•Diagnosis: ureteroscopy, excretory urography, CT, MRI, ultrasonography

•Immediate post-op: monitor urine volume hourly

•Provide stoma and skin care

•Test urine and care for ostomy

•Encourage fluids and relieve anxiety

•Patient education about self-care: managing ostomy