1-Know normal potassium level
3.5- 5.0 mg/dl
2-Know reason for protein restricted diet in patients with acute kidney injury (AKI).
Because protein is broken down into Ammonia and this is usually turned into
urea by the kidney. Ammonia is toxic to us and if the kidney is not functioning it will
nottake it and turn it into urea.
Uremia
Dietary proteins are restricted in patients with CKD because urea nitrogen and creatinine
are end products of protein metabolism.
Restricting dietary protein decreases the accumulation of nitrogenous wastes, reduces
uremic symptoms
3-Know nursing interventions to prevent uremia in patients with end stage renal disease
(ESRD)
Uremia: related to increased waste in the blood
Looks like white frost on the skin – uremic frost
Patient has ↑ urea – provide low protein diet (patient needs some protein to
prevent muscle wasting)
Itching: Due to deposits of urea crystals on the skin secreted through the sweat glands
Confusion: consider safety – assess neuro status
Dialysis: regular schedule – 3 X per week (mostly stage 5)
4-Know normal lab values: RBCs, WBCs, Platelets, Hgb, Hct
Red Blood Cells (RBCs):
Male: 4.3- 5.9 millions/mm3
Female: 3.5-5.5 millions/mm3
White Blood Cells (WBCs)
4500-11,000/mm3
Platelets:
150,000-400,000/mm3
Hemoglobin (Hgb)
Male: 13.5-17.5 g/dl
Female: 12.0-16.0 g/dl
Hematocrit:
Male: 41%- 53%
Female: 36%-46%
5-Know medications: erythropoietin – purpose of the prescription – (TWO QUESTIONS)
Erythropoietin is the hormone made in the kidneys that stimulates the bone marrow to
produce RBCs.
Epoetin Alfa is the drug given to replace this hormone and help anemia related to
kidney disease.
Pt will take this for life due to hematuria and lack of erythropoietin.
6-Know S/S of kidney insufficiency in chronic kidney disease (CKD)
Glomerular Filtration Rate (GFR)
It is the rate in which the glomerulus filters waste, ions, and water in the blood.
Normal GFR ˃ 90 mL/min
Stage 1
Kidney damage with normal renal function
GFR: ˃ 90 mL/min
Proteinuria for 3 months or more
Stage 2
Kidney damage with mild loss of renal function
GFR: 60 – 89 mL/min
Proteinuria that has been present for 3 months or more
Stage 3
• Mild to severe loss of renal function
• GFR: 30 – 59 mL/min
Stage 4
• Severe loss of renal function
• GFR: 15 – 29 mL/min
Stage 5
• End-stage renal disease (ESRD)
• GFR: < 15 mL/min
• Patient will be receiving dialysis regularly
• Candidate for kidney transplant
Decrease in the GFR leads to:
↑ Increase urea (BUN) and creatinine (Azotemia) (↑ nitrogen)
Uremia (↑ urea only), uremic frost.
These increases will lead to neurological changes and itching – related to the
accumulation of urea under the skin
GFR decreases leads to:
↑ Increase fluids in the body → hypervolemia (fluid overload) → hypertension
(HTN) → increased pressure on the heart→ weakness of the heart to pump, allowing
fluids backing up into the lung →pulmonary edema and cardiac issues.
GFR decreases leads to:
↓ Decrease Urinary output UOP
UOP < less than 400 mL/day = oliguria
UOP < less than 100 mL/day = anuria
↑ Increase potassium
↑ Increase PO₄
↓Decrease the level of Ca: increased level of PO₄ decreases the level of Ca because PO₄
binds to Ca removing it from the blood
Parathyroid gland will sense a decrease level of Ca causing the gland to release
PTH softening the bones to release Ca to the blood
Bones will be weak and brittle as a result of losing Ca
↑ Increase Mg
Metabolic acidosis
+ proteinuria → ↓decrease of oncotic pressure facilitating water to scape to the
interstitial space and ↑increase edema and swelling
+ hematuria → ↓ decrease on RBCs → anemia
Renin is another hormone produce by the kidney in response low perfusion to
the kidneys
This response will trigger the renin-angiotensin- aldosterone system (RAAS) to
increase the blood pressure in an attempt to increase kidneys’ perfusion.
However, even though there is hypertension (HTN) in CKD, the kidneys are not
filtering enough because of the damage to the nephron.
Kidney cells that sense this low perfusion think that the B/P is low and release
renin to activate the RAAS and therefore increasing even more the already
elevated B/P of the patient with CKD.
The kidney activates vitamin D
Active vitamin D helps in the reabsorption of calcium by the intestines
In CKD, there is a ↓decrease activation of vitamin D, leading to ↓ decrease
reabsorption of calcium
by the intestines, → hypocalcemia
Hypocalcemia will trigger the parathyroid gland to release parathyroid hormone
(PTH)
The PTH will increase the calcium resorption from the bones making them soft
enough to allow the release of Ca into the blood and therefore maintaining
calcium homeostasis
Eventually in CKD, this will lead the patient to have brittle bones, putting the
patient at risk for fractures
Kushal’s respirations (fast shallow)
Positive Trousseau’s sign (when you take BP and the hand flexes.
Positive Chvostek’s sign (when you touch the side of the face by the ear and it twitches)
7-ALL THAT APPLY: know S/S of AKI – diuresis phase
2-5 L of urine a day
BUN and Creatine will start to become normal again but not there yet.
Patient is at risk for dehydration
Hypovolemia
Hypotension
Urine sp. Gravity <1.020 (very diluted)
8-ALL THAT APPLY: Know AKI: laboratory findings for calcium, potassium, and
creatinine - (Know normal values first)
Normal:
Ca→ 8.2-10.2 mg/dL
K→3.5 - 5.0
Creatinine→0.6 - 1.2 mg/dL
In AKI:
Increased BUN
Increased creatinine level
Increased urine specific gravity
Sudden reduce GFR
Reduced calcium
High potassium
9-ALL THAT APPLY: Know S/S of Hyponatremia
N/V, lethargy
Headache, confusion, restlessness, irritability
Increased/hyperactive bowel sounds
Muscle weakness
Seizures
Increased urinary output.
Dry mucous membrane
10-Know purpose of peritoneal dialysis (TWO QUESTIONS).
Peritoneal dialysis: procedure that uses the lining of the patient’s peritoneal cavity as the
semipermeable membrane for exchange of fluid and solutes. To remove excess toxins and
waste from the blood in the peritoneum (which has a lot of capillaries) when the kidneys
are not functioning.
It offers increased patient control and flexibility with the option of home treatment.
Peritoneal dialysis requires a shorter training period for the patient and can be performed
independently by the patient or a family member.
Typically, PD involves fewer dietary restrictions and greater mobility for the patient.
The clearance of metabolic wastes is slower but more continuous.
It avoids rapid fluctuations in extracellular fluid composition and associated symptoms.
Peritoneal dialysis is indicated for patients who desire more control, who have vascular
access problems, or who respond poorly to HD with hemodynamic instability.
Older patients and ESRD patients with diabetes may be more easily managed with PD.
It is also an option for those who cannot tolerate heparin (hemodialysis), heavy drug
users that do not have veins to use for dialysis.
In PD, the highly vascular membrane of the peritoneal cavity is used as the
dialyzing layer.
Fluid and solute removal occurs via diffusion and filtration.
The PD process consists of fill, dwell, and drain phases
In the fill phase, room-temperature, sterile dialysate is instilled into the peritoneal
cavity via a permanent indwelling PD catheter, typically made of silicone rubber
tubing.
The fluid remains in the abdomen for a predetermined “dwell time.” Metabolic
waste products and excess electrolytes diffuse into the dialysate while it remains in
the abdomen. Water diffusion is controlled using dextrose in the dialysate as an
osmotic agent.
Gravity then drains the fluid out of the peritoneal cavity into a sterile bag.
There are several forms of PD:
Continuous ambulatory peritoneal dialysis (CAPD)
Automated peritoneal dialysis
Intermittent peritoneal dialysis
History of multiple abdominal surgeries or chronic abdominal conditions such as
pancreatitis or diverticulitis.
Recurrent abdominal wall or inguinal hernias
Obesity with large abdominal wall
Severe chronic obstructive pulmonary disease
Pre-existing back problems or vertebral disease
Peritonitis and Catheter Infection
Peritonitis can result from contamination of the dialysate or tubing or from
bacteria in the intestine migrating into the peritoneal cavity.
The primary clinical manifestation of peritonitis is a cloudy peritoneal effluent with
an increased WBC count.
Antibiotics can be given orally, intravenously, or intraperitoneally.
Repeated infections warrant removal of the PD catheter and
a switch to the use of HD.
Abdominal Pain
Abdominal pain and distention may be caused by intraperitoneal irritation
from the low pH of the dialysate solution and generally subside in 1 to 2
weeks.
Pain can also result from the tip of the catheter resting against the
bladder, bowel, or peritoneum; accidental infusions of air; infusing the
dialysate too rapidly; or infusing the dialysate at less than room temperature.
Hyperglycemia and Increased Triglyceride Levels
Glucose in the dialysate can be absorbed into the bloodstream, causing
hyperglycemia.
Serum triglyceride levels may also increase with PD because continuous absorption of
glucose results in increased insulin secretion, which
stimulates the hepatic production of triglycerides.
Dietary and insulin administration modifications may be necessary.
Outflow Problems
Outflow problems occur because of mechanical interruptions in the flow of
the dialysate or ultrafiltration.
Interruptions may be caused by kinks in the catheter, an omentum (a fold of
peritoneum) compressing the catheter, or migration of the catheter out of the
peritoneal cavity.
Respiratory Compromise
Atelectasis, pneumonia, and bronchitis may occur from a repeated upward
displacement of the diaphragm, resulting in decreased lung expansion.
The longer the dwell time, the higher the risk of developing pulmonary complications.
Protein Loss
The peritoneal membrane is permeable to plasma proteins, amino acids, and
polypeptides, which may result in an excessive protein loss. A positive nitrogen balance
can be maintained with adequate protein intake.
11-Know complications of hemodialysis
Hypotension due to the rapid removal of fluid from the vascular
compartment or vasodilation.
The patient may display light-headedness, nausea, vomiting, seizures, vision
changes, and chest pain from cardiac ischemia. The treatment is to decrease the
rate of fluid removal and to replace fluid intravenously with normal saline
(0.9% saline solution).
Muscle cramps, headache, nausea, dizziness, and malaise are common
during and after dialysis as a result of the rapid removal of electrolytes and
water.
Treatment includes reducing the filtration rate or infusing a normal
saline bolus.
Bleeding may occur because of the altered platelet function associated with
uremia and the use of heparin during the dialysis procedure.
Systemic infection is a concern. Patients on chronic HD have a higher risk
of developing hepatitis B, hepatitis C, cytomegalovirus, and HIV infections
than the general population.
Dialysis-associated dementia is a progressive, potentially incurable
neurological complication associated with long-term dialysis. It is thought
to be due to aluminum, which is present in phosphate binders in the
dialysate or the PO phosphate binders.
Dialysis disequilibrium syndrome develops as a result of very rapid changes
in the composition of the extracellular fluid. Urea, sodium, and other solutes
are removed more rapidly from the blood than from the cerebrospinal fluid
and the brain. The rapid shift of fluid and substances can create a high
osmotic gradient in the brain, resulting in a shift of fluid into the brain,
causing cerebral edema.
Clinical manifestations of dialysis disequilibrium syndrome include nausea,
vomiting, confusion, restlessness, headaches, twitching and jerking, and seizures
Treatment includes slowing or decreasing the rate of dialysis and infusing
hypertonic saline solution, albumin, or mannitol to draw fluid from the brain
cell back into the systemic circulation.
In order to avoid this syndrome, the first HD is usually done much slower and is
less aggressive in removing fluids and solutes.
Localized AV fistula and graft complications can also occur. Infection and
clotting or thrombosis are the most common shunt problems. Aneurysms may also
occur. Staphylococcus aureus septicemia is commonly associated with
contamination of the fistula. Infection and thrombosis can lead to systemic
manifestations such as septicemia and embolization.
Hemolysis
Dialysate error
Contamination
Itching
12-Know assessment for peritonitis in peritoneal dialysis
Peritonitis is the major complication of peritoneal dialysis, most commonly caused by
connection site contamination.
To prevent peritonitis, use meticulous sterile technique when caring for the PD catheter
and when hooking up or clamping off dialysate bags.
Manifestations of peritonitis include cloudy dialysate outflow (effluent), fever, abdominal
tenderness, abdominal pain, general malaise, nausea, and vomiting.
Cloudy or opaque effluent is the earliest indication of peritonitis.
When peritonitis is suspected, send specimen of the dialysate outflow for culture and
sensitivity study, gram stain and cell count to identify the infecting organism.
Practice question
A patient with ESKD receives continuous ambulatory peritoneal dialysis. The nurse
observes that the dialysate drainage fluid is cloudy. What is the nurse’s most appropriate
action?
A) Inform the physician and assess the patient for signs of infection.
Peritonitis is the most common and serious complication of peritoneal dialysis. The first
sign of peritonitis is cloudy dialysate drainage fluid, so prompt reporting to the primary
care provider and rapid assessment for other signs of infection are warranted.
13-Know indications for hemodialysis
Any patient may be considered for intermittent HD therapy. Starting HD depends on
manifestations from disruption of fluid and electrolyte balance and waste and toxic
accumulation, not the GFR alone.
Dialysis is started immediately for patients who have:
Fluid overload that does not respond to diuretics (including fluid overload with
pericarditis).
Symptomatic hyperkalemia
Calciphylaxis (a condition of thrombosis and skin necrosis that occur in stage 5 CKD)
Symptomatic toxin ingestion such as drug overdose or poisoning that dialyzable.
Most commonly, hemodialysis for CKD is started when uremic manifestations (e.g.,
nausea and vomiting, decrease attention span, decrease cognition, and pruritus’) are
present.
14-Know assessment before and after hemodialysis
Pre-dialysis:
Weigh the patient before and after dialysis.
Know the patient's dry weight.
Discuss with the health care provider whether any of the patient's drugs should
be withheld until after dialysis.
Be aware of events that occurred during previous dialysis treatments.
Measure blood pressure, pulse, respirations, and temperature.
Post dialysis:
Monitor for manifestations of bleeding or hemorrhage. Hypotension,
Headache, Nausea, vomiting, Malaise, dizziness, Muscle cramps or bleeding.
Obtain.
Vital signs and weight for comparison with pre-dialysis measurements.
Blood pressure and weight are expected to be reduced because of fluid removal
Hypotension may require rehydration with IV fluids, such as normal saline.
If he or she has a fever, sepsis may be present, and a blood sample is needed for
culture and sensitivity.
The heparin required during HD increases the risk for excessive bleeding.
All invasive procedures must be avoided for 4 to 6 hours after dialysis.
Continually monitor the patient for hemorrhage during and for at least 1 hour
after dialysis.
Assess for Disequilibrium syndrome: (headache, N/V, hypotension, dizziness,
confusion.
15-Know nursing intervention for patients complaining of nausea, headaches, and
confusion during hemodialysis.
Slow down the speed of the hemodialysis.
Infusing hypertonic saline solution, albumin, or mannitol to draw fluid from the brain
back into the systemic circulation
16-Know dietary restrictions for renal patients on hemodialysis
Diet is important for patients on hemodialysis because of the effects of
uremia. Goals of nutritional therapy are to minimize uremic symptoms and
fluid and electrolyte imbalances.
Restricting dietary protein decreases the accumulation of nitrogenous wastes, reduces
uremic symptoms, and may even postpone the initiation of dialysis for a few months.
Restriction of fluid is also part of the dietary prescription because fluid accumulation may
occur, leading to weight gain, heart failure, and pulmonary edema.
Avoid processed meats such as hot dogs and canned chili, which have high amounts
of sodium and phosphorus
Restrict protein, food containing potassium, phosphorus, sodium, and water.
Because protein is broken down into Ammonia and this is usually turned into urea by
the kidney. Ammonia is toxic to us and if the kidney is not functioning it will not take
it and turn it into urea
A patient with ESKD is scheduled to begin hemodialysis. The nurse is working with the
patient to adapt the patient’s diet to maximize the therapeutic effect and minimize the
risks of complications. The patient’s diet should include which of the following
modifications? Select all that apply.
A) Decreased protein intake
B) Decreased sodium intake
D)Fluid restriction
Restricting dietary protein decreases the accumulation of nitrogenous wastes, reduces
uremic symptoms and may even postpone the initiation of dialysis for a few months.
Restriction of fluid is also part of the dietary prescription because fluid accumulation
may occur. As well, sodium is usually restricted to 2 to 3 g/day. Potassium intake is
usually limited, not increased, and there is no need for vitamin D supplementation
17-Know nursing care for arteriovenous fistula in patients receiving hemodialysis
There are generally three types of vascular access for HD:
Intravenous vascular access may be secured using a central venous double lumen catheter in
the subclavian or internal jugular vein.
This type of access is typically used for the short term, such as treating a patient with
AKI with intermittent HD or when waiting to secure long-term access for HD via the
other 2 types.
Arteriovenous (AV) fistula: An AV fistula is created by surgical anastomosis of an artery
and vein, typically the radial artery and cephalic vein, in the nondominant arm.
The preferred method of permanent vascular access for dialysis
After the procedure, the fistula is allowed to mature to become suitable for dialysis.
Maturing the AV fistula occurs when the low-pressure vein becomes accustomed to the
higher pressures generated in the artery, which allows adequate blood flow for dialysis .
Maturation can require weeks to months, so advanced planning is needed, or, as noted
previously, a central venous catheter may be used in the short term.
Arteriovenous (AV) graft: An AV graft, another option for dialysis, is created by inserting a
prosthetic graft between an artery and vein, typically in the nondominant arm. Arteriovenous
graft access can be used more quickly than the fistula but does not last as long and is more
prone to infection; thus, it is not the preferred option for access.
Caring for the patient with an arteriovenous fistula or arteriovenous graft:
Do not take blood pressure readings using the extremity in which the vascular access is
placed.
Do not perform venipunctures or start an IV line in the extremity in which the
vascular access is placed.
Palpate for thrills and auscultate for bruits over the vascular access site every 4 hours
while the patient is awake.
Assess the patient distal pulses and circulation in the arm with the access
Elevate the affected extremity postoperatively
Encourage routine range-of-motion exercises.
Assess for manifestation of infection at needle sites.
Instruct the patient not to carry heavy objects.
Instruct the patient not to sleep with his or her body weight on top of the extremity in
which the vascular access is placed.
18-Know nursing intervention for patients receiving peritoneal dialysis complaining of
severe respiratory difficulty during infusion of dialysate
They should be sitting upright not laying down to prevent trouble breathing.
Frequent repositioning, deep breathing exercises, elevate the HOB
If the patient is having respiratory difficulties is because there is probably to much
dialysate inside the peroneal cavity and is pushing the diaphragm. Extract some of the
dialysate from the peritoneal cavity.
19-Know nursing intervention for patients receiving peritoneal dialysis and the dialysate
drainage slows down or stop.
Outflow problems occur because of mechanical interruptions in the flow of
the dialysate or ultrafiltration.
Interruptions may be caused by kinks in the catheter.
An omentum (a fold of peritoneum) compressing the catheter
Migration of the catheter out of the peritoneal cavity
Constipation or a full colon may also cause these problems, requiring some form of
cathartic.
Turn the patient from side to side. Reposition the patient to facilitate drainage.
If the peritoneal fluid does not drain properly, the nurse can facilitate drainage by
turning the patient from side to side or raising the head of the bed. The catheter
should never be pushed further into the peritoneal cavity. It would be unsafe to
aspirate or to infuse more dialysate.
20-Know rationale for warming up dialysate before is infused to the peritoneal cavity – in
patients receiving peritoneal dialysis.
To avoid abdominal cramps or pain
Facilitate vasodilation.
Prevents a change in pt.’s temperature (hypothermia
21-ALL THAT APPLY: know assessment of complications of peritoneal dialysis
Redness at the site
Cloudy outflow (peritonitis)
Tenderness
Drainage
Abdominal pain
Outflow problems: because of mechanical interruptions in the flow of dialysate or
ultrafiltration
Respiratory compromise
Protein loses
Subcutaneous tunnel infections can result in abscess formation if left untreated
22-Know most important test to determine kidney function after kidney transplantation
Signs of rejection: redness, warmth, tenderness, or swelling over the kidney; fever; decreased
UOP; elevated blood pressure.
Instruct the patient that rejection is diagnosed through a kidney scan and kidney biopsy.
Ultrasonography may be used to detect enlargement of the kidney;
percutaneous renal biopsy (most reliable) and x-ray techniques are used
to evaluate transplant rejection.
There are three types of rejection reactions:
Hyperacute
Acute
Chronic
Hyperacute
Occurs within 48 hours after surgery
Acute
Occurs 1 week to 2 years after surgery
Chronic
Occurs from months to years after surgery
Kidney function: Creatinine 0.6-1.2 and GFR >90
23-Know effects of antirejection medication over WBCs - in kidney transplant patients
Leukopenia from anti-rejection medications
The results of blood chemistry tests and leukocyte and platelet counts are
monitored closely because immunosuppression depresses the formation of
leukocytes and platelets. The patient is closely monitored for infection
because of susceptibility to impaired healing and infection related to
immunosuppressive therapy and complications of kidney disease.
24-Know duration of immunosuppressive drug therapy after kidney transplantation
Doses of immunosuppressive agents are often adjusted depending on the patient’s
immunologic response to the transplant. However, the patient will be required to take
some form of immunosuppressive therapy for the entire time that they have the
transplanted kidney.
25-ALL THAT APPLY: Know assessment findings associated with kidney transplant
rejection
There are three types of rejection reactions:
Hyperacute
Acute
Chronic
Hyperacute: Occurs within 48 hours after surgery.
Etiology: Results from antibody-mediated reaction to donor antigens; it causes the
formation of small blood clots occluding vessels, and resulting in massive cellular
destruction generalized glomerular capillary thrombosis and necrosis. The
process is not reversible.
FINDINGS: Fever, hypertension, pain at the transplant site, swelling, tenderness
over the graft site, decrease urine output, rise in creatinine (normal value 0.6-1.2)
TREATMENT: Immediate removal of the donor kidney
Occurs rarely now due to better histocompatibility assessments
Acute: Occurs 1 week to 2 years after surgery.
ETIOLOGY: An antibody-mediated response causing vasculitis in the donor kidney,
and cellular destruction starts with inflammation that causes lysis of the donor kidney
FINDINGS: Oliguria, anuria, low-grade fever, hypertension, tenderness over the
transplanted kidney, lethargy, azotemia (increase BUN and creatinine), and fluid
retention, decrease in GFR.
TREATMENT: Involves increased doses of immunosuppressive medications
Chronic: Occurs gradually over months to years.
ETIOLOGY: Blood vessel injury from overgrowth of the smooth muscles of the blood
vessels causing fibrotic tissue to replace normal tissue, resulting in a nonfunctioning
donor kidney
FINDINGS: Gradual return of azotemia, fluid retention, electrolyte imbalance, and
fatigue, decrease UOP, proteinuria may occur
TREATMENT: Conservative (monitor kidney status, continue immunosuppressive
therapy) until dialysis is required
CLIENT EDUCATION
● Monitor for manifestations of rejection and contact the provider immediately.
● Rejection is diagnosed through a kidney scan and kidney biopsies.
● Adhere to the pharmacological regimen
26-Know renal complication of benign prostatic hypertrophy (BPH)
When a man has BPH this constricts the prostatic urethra causing obstruction
and can also dig into the bladder causing high amounts of residual urine left in the
bladder.
Nodular enlargement also presses against the urethra and reduces its diameter,
impairing the outflow of urine from the bladder, making the patient susceptible
to infection and retention
Excessive amounts of urine retained can cause reflux of urine into the kidney,
dilating the ureter and causing kidney infections
27-Know confirmatory tests for BPH
Urinalysis and culture: elevated WBCs and bacteria
CBC: WBCs elevated if systemic infection present; RBCs possibly decreased due to
hematuria
International Prostate Symptom Score (I-PSS)
BUN and creatinine: elevated, indicating kidney damage
Acid phosphatase and prostate-specific antigen (PSA): to rule out prostate
cancer
Culture and sensitivity of prostatic fluid
Digital rectal exam: will reveal an enlarged smooth prostate
Transrectal ultrasound with needle aspiration biopsy: to rule out prostatic
cancer in presence of prostate enlargement
Early prostate cancer antigen: serum blood test may be ordered instead of
biopsy to rule out prostate cancer
Urodynamic studies: to determine degree of urinary obstruction
Post-voiding catheterization: residual urine of more than 100 mL is considered
high
28-Know transurethral resection of the prostate (TURP) – indwelling urinary catheter
and continuous bladder irrigation
Transurethral resection of the prostate (TURP)
Most common surgical procedure for BPH – remains the benchmark for surgical
treatment for BPH
Uses a resectoscope – similar to cystoscope
Trims excess of prostate
Enlarge opening of the urethra through the prostate gland
Postoperative care
Care of indwelling catheter – three-way catheter
Allows for urine to drain and instillation of a continuous bladder irrigation (CBI) of
normal saline (isotonic) or any other prescribed irrigating solution to keep catheter free
from obstruction.
Rate of CBI is adjusted to keep the irrigation return pink or lighter
If red blood is coming out nurse must increase CBI rate.
If catheter becomes obstructed (bladder spasm, reduced irrigation outflow) turn off CBI
and irrigate with 50 mL irrigation solution using a large piston syringe or per facility
or surgeon protocol
Notify surgeon if unable to dislodge clot
Record amount of irrigation instilled and the amount of return – the difference is urinary
output.
The catheter has a large balloon (30 to 45 mL). The catheter is taped tightly to the leg,
creating traction so the balloon with apply pressure to the prostatic fossa to prevent
bleeding. This makes patient feel constant desire of urination.
Instruct patient not to void around the catheter as this causes bladder spasm. Avoid
kins in the tubing.
Monitor for bleeding: Persistent bright-red bleeding unresponsive to increase in CBI and
traction on the catheter or reduced Hgb levels – report to MD immediately
Assist patient to ambulate as soon as possible to reduce risk for DVT or any other
complication due to immobility.
Patient education
Avoid heavy lifting, extraneous exercise, straining, and sexual intercourse for the
prescribed length of time – usually 2 to 6 weeks
Drink 12 or more 8 –oz glasses of water each day, unless is contraindicated
Avoid NSAIDs due to increased risk for bleeding
Avoid bladder stimulants, such as alcohol and caffeine
If urine becomes bloody, stop activity, rest, and increase fluid intake
Notify surgeon for persistent bleeding or obstruction
TURP complications
Urethral trauma
Urinary retention
Bleeding
infection
29-Know nursing intervention for patients complaining of dribbling after removal of
indwelling catheter in patients who had a TURP
Kegel exercises
30-Know diet for patients with cholecystitis (TWO QUESTIONS)
The diet immediately after an episode is usually low-fat liquids. These can include
powdered supplements high in protein and carbohydrate stirred into skim milk.
The patient should avoid eggs, cream, pork, fried foods, cheese, rich dressings, gasforming vegetables, and alcohol.
Small low-fat meals
Avoid gas forming foods like broccoli, cauliflower, and beans.
Low saturated fat, high fiber and calcium, small frequent light meals
Reduce calorie intake if obese.
Rapid weight loss and fasting should be avoided
It is important to remind the patient that fatty foods may induce an episode of
cholecystitis.
31-Know post-operative care after cholecystectomy
Postoperative care after open cholecystectomy includes:
Monitoring vital signs, pain, neurological status, and the abdomen for signs and
symptoms of distention, bleeding, or bruising.
Once the patient is passing flatus, clear liquids are introduced, and the diet is
advanced to regular if the patient has no nausea or vomiting.
Pain management via patient-controlled analgesia or as needed.
Pulmonary interventions to encourage lung expansion, coughing and deep breathing
to prevent pneumonia and atelectasis, and walking are encouraged.
Liquids to bland diet after return of bowel sounds
May need to restrict fats for 4 to 6 weeks
Laparoscopic cholecystectomy
During the immediate postoperative period, the patient recovers from
anesthesia in the post anesthesia care unit (PACU), where the nurse monitors
vital signs, pain, neurological status, nausea and vomiting, and the surgical
site for distention, bleeding, or bruising.
Once the patient is awake and following commands, clear liquids are given slowly in
small amounts to prevent nausea and vomiting. After the first 12 hours of liquids and no
nausea, vomiting, or abdominal cramping, patients can gradually introduce small
amounts of solid foods and maintain a low-fat diet.
Liquids for day
Light meals for several days
General care
300-500 cc per day (less than that means an obstruction, more will mean notify the
MD)
Catheter insertion site cleaned with antiseptic
Observe for bile leakage. Bile is abrasive to skin
Collects bile with help of GRAVITY, keep tubing untangled/kink free ad below the
WAIST level
Watch for color of drainage should not be thick or bad smelling with blood (should
be yellow/green with brown
Usually, will be clamped 1 hr. before and after meals
Drug therapy: morphine and NSAIDS (be careful with atelectasis and use incentive
spirometer AFTER medication to relieve pain.
Anticholinergic: atropine to prevent smooth muscle contraction
Fat soluble vitamins: A, D, E, K
Bile salts- to help with digestion
Cholestyramine: for PRURITUS, avoid warm showers
Diet: low saturated fat, high fiber and calcium, small frequent light meals. Reduce
calorie intake if obese. Rapid weight loss and fasting should be avoided
32-Know IV solutions: lactated ringer – purpose of its use in patients with T tube for
biliary drainage (Think metabolic disturbance to be corrected)
LR contains sodium chloride, potassium, calcium, and sodium lactate. Great for
neutralizing electrolyte imbalance and fluid replacement
33-Know how to improve patient’s compliance with doing deep breathing exercise and
coughing after abdominal cholecystectomy – (Think comfort)
Medicate the patient with either morphine or NSAIDs before asking them to use
incentive spirometry
The location of the subcostal incision in non-laparoscopic gallbladder
surgery often causes the patient to avoid turning and moving, to splint the
affected site, and to take shallow breaths to prevent pain. Because full
expansion of the lungs and gradually increased activity are necessary to
prevent postoperative complications, the nurse administers analgesic
agents as prescribed to relieve the pain and to help the patient turn,
cough, breathe deeply, and ambulate as indicated. The use of a pillow or
binder over the incision may reduce pain during these maneuvers.
34-Know patients positioning to alleviate shoulder pain after laparoscopic
cholecystectomy
If pain occurs in the right shoulder or scapular area (from migration of the carbon dioxide used
to insufflate the abdominal cavity during the procedure), the nurse may recommend a heating
pad for 15 to 20 minutes hourly.
Shoulder pain from irritation of phrenic nerve and diaphragm due to retained CO2
Place patient in Sims positions
Encourage deep breathing, ambulation
Administer pain medication
35-Know purpose of T-Tube after abdominal cholecystectomy
To divert bile out or relieve ductal obstruction
T-tube preserves patency of the duct and ensures drainage of bile until edema
resolves and bile is effectively draining into the duodenum. A gravity drainage
bag is attached to collect the drainage.
36-Know normal amount of biliary drainage from t-tube during the first 24 hours – know
troubleshooting if drainage is less than expected (TWO QUESTIONS)
300-500ml/day If there is less than this, there is an obstruction: CONTACT HCP
Drainage bag must me positioned correctly. Drainage bag must be below the insertion
site at the waist tubing should be tangle and kink free.
Keep the patient in semi fowlers, 30–45- degree angle to facilitate drainage.
37-Know how to monitor returning of normal bile flow to the gastrointestinal tract –
(Think of stools)
Stool will not have fat or be clay colored (steatorrhea)
38-ALL THAT APPLY: Know S/S of cholecystitis
EXPECTED FINDINGS
Sharp pain in the right upper quadrant, often radiating to the right shoulder
Pain with deep inspiration during right subcostal palpation (Murphy’s sign)
Intense pain (increased heart rate, pallor, diaphoresis) with nausea and vomiting after
ingestion of high-fat food caused by biliary colic
Rebound tenderness (Blumberg’s sign performed by the provider or advanced practice
nurse)
Dyspepsia, eructation (belching), and flatulence
Fever
Tachycardia
39-Know purpose of using lactulose in patients suffering from cirrhosis of the liver
Lactulose promotes the excretion of ammonia in the stool and can be given orally or
via rectal enemas. These treatments can cause diarrhea and altered fluid and electrolytes;
therefore, it is important to monitor fluid volume status and electrolyte values
Lowers portal hypertension
Reduces amount of ammonia in the blood being retained and facilitates the excretion
of ammonia
Decreases the PH of the bowel
40-Know electrolyte disturbance to monitor in patients with ascites from cirrhosis of the
liver and receiving spironolactone.
HYPERKALEMIA
41-Know purpose of using neomycin in patients with cirrhosis of the liver
Neomycin is a broad-spectrum antibiotic that destroys bacteria normally present in the
GI tract, decreasing protein breakdown and production of ammonia.
Prophylactic treatment of infection because this inhibits protein synthesis in bacteria
and decrease production of ammonia.
42-Know how to assess patients with cirrhosis of the liver for the fetor hepaticus
Fetor hepaticus is the fruity, musty breath odor of severe chronic liver disease
Fetor hepaticus, a sweet, slightly fecal odor to the breath that is presumed to be of
intestinal origin, may be noticed. The odor has also been described as similar to that of
freshly mowed grass, acetone, or old wine. Fetor hepaticus is prevalent with extensive
collateral portal circulation in chronic liver disease.
43-Know the cause of ascites in patients with cirrhosis of the liver
When there is an obstruction in the portal vein from cirrhosis, blood cannot flow
through, being pushed back into the peritoneum.
Also, since the liver isn’t functioning well, it’s not making albumin causing
hypoalbuminemia, this causes fluid to be moved out of the capillaries and into the
third space adding to the ascites.
Portal obstruction and ascites—late manifestations of cirrhosis—are caused partly by
chronic failure of liver function and partly by obstruction of the portal circulation. Almost
all of the blood from the digestive organs is collected in the portal veins and carried to the
liver. Because a cirrhotic liver does not allow free blood passage, blood backs up into
the spleen and the GI tract, and these organs become the seat of chronic passive
congestion—that is, they are stagnant with blood and therefore cannot function properly.
Indigestion and altered bowel function result. Fluid rich in protein may accumulate in
the peritoneal cavity, producing ascites.
44-Know diet for patient with cirrhosis of the liver and ascites (Think low sodium and low
fat)
Ascites requires restriction of sodium intake to less than 2 g per day and administration of
diuretics to increase salt and water excretion. Patients receive a combination of diuretics such
as spironolactone and furosemide.
Restrict sodium and fluid intake as ordered
Prevents fluid accumulation and edema
Restrict protein intake
Elevated amounts of protein in the diet can raise ammonia levels and lead to
hepatic encephalopathy
Consume adequate calories to minimize weight loss, eating a well-balanced diet
with plenty of fruits, vegetables, and whole grains
Helps prevent malnutrition and provides body with adequate energy
45-Know potassium level: spironolactone versus furosemide
Spironolactone is potassium sparing diuretic (can cause hyperkalemia)
Furosemide is potassium wasting diuretic (hypokalemia)
46-Know procedures: Paracentesis – Patient’s prep
Paracentesis is the removal of fluid (ascites) from the peritoneal cavity through a puncture or a
small surgical incision through the abdominal wall under sterile conditions. Ultrasound
guidance may be indicated in some patients who are at high risk for bleeding because of an
abnormal coagulation profile and in those who have had previous abdominal surgery and may
have adhesions.
Paracentesis was once considered a routine form of treatment for ascites. However, it is now
performed primarily for diagnostic examination of ascitic fluid; in treatment for massive ascites
that is resistant to nutritional and diuretic therapy and is causing severe problems to the patient.
Removal of fluid from the peritoneal cavity
Primarily for diagnostic reasons--treatment of massive ascites resistant to other therapy,
and as a prelude to other procedures.
Done for ascites. Last resort after diuretics and low sodium diet. Patient prep:
Sit patient up on a chair NOT laying down.
Monitor for color of fluid. If brown: perforated bowel, if yellow: perforated bladder
Have patient void before procedure.
Monitor vital signs
This will remove 2-3L of fluid. But this might be too much at once and it can cause
shock/cardiovascular collapse (hypovolemia)- monitor for this
47-Know S/S of hepatic encephalopathy: Know diet to reduce risk (TWO QUESTIONS)
The earliest symptoms of hepatic encephalopathy include:
Mental status changes and motor disturbances. The patient appears confused and
unkempt and has alterations in mood and sleep patterns. The patient tends to sleep
during the day and has restlessness and insomnia at night
As hepatic encephalopathy progresses:
The patient may become difficult to awaken and completely disoriented with respect to
time and place.
With further progression, the patient lapses into frank coma and may have
seizures.
Deep Tendon Reflex are hyperactive in the beginning and as it progresses extremities
become flaccid
Asterixis, an involuntary flapping of the hands, may be seen in stage II
encephalopathy.
Simple tasks, such as handwriting, become difficult.
Constructional apraxia inability to reproduce a simple figure in two or three
dimensions.
Occasionally, fetor hepaticus, a sweet, slightly fecal odor to the breath that is
presumed to be of intestinal origin, may be noticed.
Diet
Low protein diet: Keep daily protein intake between 1.2 and 1.5 g/kg body weight per
day.
Dietary protein intake should not be restricted in hepatic encephalopathy as
recommended in the past. Protein intake should be maintained at 1.2 to 1.5 g/kg
per day.
The danger of protein malnutrition far outweighs the risk of worsening hepatic
encephalopathy caused by increased protein intake.
Avoid constipation
vitamins to reduce deficiencies (especially potassium)
48-ALL THAT APPLY: Know assessment findings in the skin of patients with cirrhosis of
the liver (think coagulopathy and portal hypertension)
Jaundice
Warm skin
Pruritus
Ascites
Edema from hypoalbuminemia and increase in the hydrostatic pressure
Esophageal varices (medical emergency)
Bleeding tendencies
Brittle bones from low calcium absorption
Hemorrhoids
49-Know hepatitis: Modes of transmission of Hepatitis C
Hepatitis C is a virus transmitted through infected blood → Blood stream of another person.
Percutaneous (puncture through the skin)
Can live outside of body for 4 days or longer.
How do you get it?
Sharing any injection equipment.
Poor infection control (Blood transfusions or organ donation before 1992, dialysis.
Medical procedures in countries with poor infection control.
Other Blood exposure
Shared tattoo or piercing equipment.
Fighting
Sex
Sharing razors
Risk Factors:
IV drugs use (most common cause of transmission in USA and Canada)
Blood Transfusions <1 per 1 million blood transfusions.
High risk sexual behavior
Hemodialysis
Occupational exposure
Perinatal transmission.
50-Know hepatitis: Modes of transmission of hepatitis A – nursing precautions in the
management of the patient
HAV is transmitted primarily through the fecal–oral route, by the ingestion of food or
liquids infected with the virus. It is more prevalent in countries with overcrowding and poor
sanitation.
Typically, a child or a young adult acquires the infection at school through poor hygiene, handto-mouth contact, or other close contact. The virus is carried home, where haphazard sanitary
habits spread it through the family
Hepatitis A can be transmitted during sexual activity; this is more likely with oral–anal
contact or anal intercourse and with multiple sex partners.
A number of strategies exist to prevent transmission of HAV. Patients and their families are
encouraged to follow general precautions that can prevent transmission of the virus.
Scrupulous hand hygiene, safe water supplies, and proper control of sewage disposal are
just a few of these prevention strategies.
Effective (95% to 100% after two to three doses) and safe HAV vaccines include Havrix and
Vaqta.
Transmitted fecal- oral route, parenteral (rarely)
Frequently occurs in small outbreaks.
Poor hygiene, improper handling of food, crowded citations, and poor sanitary
conditions
Transmission occurs between family members, institutionalized individuals,
and children in day-care centers
Nursing management:
• Washing hands
• Emphasis on a well-balanced diet that the patient can tolerate
• Rest reduces the metabolic demands on the liver and promotes cell regeneration
• Bed rest may be indicated while the patient is symptomatic. The degree of rest
ordered depends on the severity of symptoms, but usually, altering periods of
activity and rest are adequate.
51-Know medications that can cause hepatitis/liver damage
Acetaminophen (Tylenol) analgesic
Phenytoin (Dilantin) anticonvulsant
Halothane (Fluothane) general anesthetic
Methyldopa (Aldomet) antihypertensive
52-Know laboratory finding after receiving hepatitis B vaccine – and vaccination was
effective
Successful vaccination should result in anti-HB titers of 10mlI/mL or greater
It remains to be determined what level of antibody is required to provide protection.
Promotes synthesis of specific antibodies against hep b
Series of 3 IM injections given at 0,1, and 6-month intervals
53-ALL THAT APPLY: Know modes of transmission for hepatitis A, B, C, D, E
Hepatitis A
ROUTE OF TRANSMISSION: Fecal-oral
RISK FACTORS
Ingestion of contaminated food or water, especially shellfish
Contact with infected stool (incontinent individuals, anal sexual activity)
Hep A: primarily spread through the oral route from food, water, or shellfish that has been
infected with the virus. It can also be spread through close contact with infected persons
such as in households and day care centers, with an increased incidence in the presence
of unsanitary conditions.
Hepatitis B
ROUTE OF TRANSMISSION: Blood
RISK FACTORS
Unprotected sex with infected individual
Infants born to infected mothers
Contact with infected blood
substance use disorder (injectable substances)
Hep B: spread by blood and body fluids or secretions such as semen. The virus can be
spread through mucous membranes, contact with infected fluids, during childbirth, or
through skin puncture with contaminated needles or other instruments
Hepatitis C
ROUTE OF TRANSMISSION: Blood
RISK FACTORS
substance use disorder (injectable substances)
Blood, blood products, or organ transplants
Contaminated needle sticks, unsanitary tattoo equipment
Sexual contact
Hep C: spread through blood or body fluids and from mother to child during childbirth. A
significant number of cases of hepatitis C occur from sharing of contaminated needles by
IV drug users and unintended needlesticks in the healthcare environment. Other risk
settings include tattoo and body piercing establishments because of the chance of contact
with blood
Hepatitis D
ROUTE OF TRANSMISSION: Coinfection with HBV
RISK FACTORS
● substance use disorder (injectable substances)
● Unprotected sex with infected individual
Hep D: occurs only in people who are infected with the hepatitis B virus because it
requires the hepatitis B antigen to replicate. It is spread through contact with infectious
blood and is most commonly found in patients who are IV drug users, receiving
hemodialysis, and have received multiple blood transfusions. There is no vaccine for
hepatitis D
Hepatitis E
ROUTE OF TRANSMISSION: Fecal-oral
RISK FACTORS: Ingestion of food or water contaminated with fecal waste
Hep E: caused by the hepatitis E virus that is transmitted via the fecal-oral route primarily
through water that is contaminated in areas of poor sanitation. No vaccines are available
54-Know measures to prevent stimulation of the pancreas
Pain and restlessness can increase the metabolic rate and subsequent stimulation of
enzymes.
Measures such as comfortable positioning, frequent changes in position, and relief
of N/V assist in reducing the restlessness that usually accompanies the pain.
NPO is the best way to prevent stimulation
NG tube
Bland low fat, low protein high carb diet if enteral feedings.
Avoid talking about food, or stimulating the client to think about food
55-Know reasons for the prescription of bile salts in patients with chronic pancreatitis
Bile Salts make it easier for your body to absorb and digest the fats and fat-soluble vitamins
that you've eaten.
Prevents further fat loss
Bile salts are pancreatic enzyme supplements such as lipase, amylase, and protease
56-Know diet for patients suffering from chronic pancreatitis
Low fat, low protein, high carb
Avoid intake of irritating foods/beverages (coffee, caffeine). This may increase gastric
distress.
57-Know pancreatic enzymes to be monitored to determine patient’s response to
treatment.
Lipase: 0-160
Amylase 23-85
Both should be decreased
Lipase is pancreas specific.
58-Know S/S of hypocalcemia in acute pancreatitis (TWO QUESTIONS)
When hypocalcemia occurs, it is a sign of severe disease
Positive trousseau’s signs (hand spasm when blood pressure cuff is inflated)
Positive Chvostek’s sign (facial twitching when facial nerve is tapped)
Numbness around lips/fingers
Tetany (jerking, irritability twitching)
Brittle bones
Tremors
Hypotension
Seizures
Irritability
hyperactive bowel
calcium gluconate (as ordered) should be given
59-Know risk factors for acute pancreatitis
Alcohol (the primary cause of chronic pancreatitis)
Gallstones (can cause blockage where the common Bile duct and pancreatic duct meet)
Trauma
Cigarette smoking
Medication reactions
Hypertriglyceridemia
Hypercalcemia
Bile duct abnormalities or obstruction (tumor)
Surgery
Viral Infections
Parasites
Spider bites
Scorpion stings
Idiopathic (unidentified cause)
Pancreas divisum (congenital anomaly where pancreatic duct is divided into
two parts)
60-Know about administration of pancrelipase (Viokase®) – patient’s teaching
Pancreatic enzymes: Pancrelipase
Aid with digestion of fats and proteins when taken with meals and snacks.
CLIENT EDUCATION
Contents of capsules can be sprinkled on nonprotein foods.
Drink a full glass of water following pancrelipase.
Wipe lips and rinse mouth after taking medication (to prevent skin breakdown or
irritation).
Take pancrelipase after antacid or histamine receptor antagonists.
Take pancrelipase with every meal and snack. (Take with food)
61-Know rationale for the insertion of a nasogastric (NG) tube with suction and placing
patient NPO – during acute pancreatitis
Nasogastric tube: Gastric decompression (for severe vomiting or paralytic ileus)
The patient should be NPO until pain free for the suppression of pancreatic enzymes
to prevent the pancreas from being stimulated.
Specific interventions for the treatment of acute pancreatitis traditionally include NPO
status to prevent the release of pancreatic enzymes responsible for autodigestion of the
pancreas; however, evidence of early initiation of enteral feeding helps protect the
gastrointestinal mucosal barrier
62-Know priority when caring for patients with pancreatic cancer (Think comfort)
Pain management and attention to nutritional requirements are important nursing
measures that improve the level of patient comfort.
Skin care and nursing measures are directed toward relief of pain and discomfort
associated with jaundice, anorexia, and profound weight loss.
Pain associated with pancreatic cancer may be severe and may require liberal use of
opioids; patient-controlled analgesia should be considered for the patient with severe,
escalating pain.
Supportive care
Suppression of pancreatic enzymes (NPO, NG suction)
fluid/ electrolyte imbalance (Lactated ringers solution)
Aggressive hydration
Pain management: (IV morphine combined with antispasmodic agent)
Management of metabolic complications
Minimizing stimulation
Atropine like drugs
Other medications that relax smooth muscles spasmolytics), such as nitroglycerin or
papaverine.
Shock (plasma or plasma volume expanders: (dextran or albumin)
Prevent infections
63-Know assessment for patients suffering from acute pancreatitis and receiving
parenteral nutrition
Sudden onset of severe, boring pain (goes through the body)
Epigastric, radiating to back, left flank, or left shoulder
Worse when lying down
Pain relieved somewhat by fetal position or sitting upright, bending forward
Nausea and vomiting
Weight loss
PHYSICAL ASSESSMENT FINDINGS
Seepage of blood-stained exudates into tissue as a result of pancreatic enzyme actions
Ecchymoses on the flanks (Grey Turner's sign)
Bluish-gray periumbilical discoloration (Cullen's sign)
Generalized jaundice
Abd distention/tenderness
Hypotension
Tachycardia
Increasing abdominal girth
Absent or decreased bowel sounds (possible paralytic ileus)
Warm, moist skin; fruity breath (evidence of hyperglycemia)
Ascites
Tetany due to hypocalcemia
Trousseau’s sign: hand spasm when blood pressure cuff is inflated
Chvostek’s sign: facial twitching when facial nerve is tapped
LABORATORY TESTS
Blood amylase increases within 24 hr, and remains increased for 2 to 3 days
Blood lipase increases slowly and can remain increased for days longer than amylase
WBC count: Increased due to infection and inflammation
Platelets: Decreased
Blood calcium and magnesium: Decreased due to fat necrosis with pancreatitis
Blood liver enzymes and bilirubin: Increased with associated biliary dysfunction
Serum glucose: Increased due to a decrease in insulin production by the pancreas
Erythrocyte sedimentation rate: Elevated
64-Know pain management for patients suffering from acute pancreatitis
Opioid analgesic
Morphine or hydromorphone for acute pain
Ketorolac, an NSAID, used for mild to moderate pain
Antibiotics: Imipenem
Antibiotics can be used, but are generally indicated for clients who have acute
necrotizing pancreatitis.
Histamine receptor antagonists: Ranitidine
Decreases gastric acid secretion. (Take 1 hour before or 1 hour after antacid).
Proton pump inhibitors: Omeprazole
Decreases gastric acid secretion.
Pancreatic enzymes: Pancrelipase
Aid with digestion of fats and proteins when taken with meals and snacks.
NPO Status is the most effective way of relieving pain
Frequent position changes
Side-lying with HOB elevated 45 degrees
Knees up to abd
65-ALL THAT APPLY: Know Whipple Procedure (pancreaticoduodenectomy) – which
parts of the gastrointestinal system are removed
The Whipple procedure (pancreaticoduodenectomy) is an operation to remove the
head of the pancreas, the first part of the small intestine (duodenum), the
gallbladder and the bile duct. The remaining organs are reattached to allow you to
digest food normally after surgery.
Dumping syndrome: avoid fluids during food, lay down after meals, monitor for
hypoglycemia, and don’t eat sugar or foods with sugar