Electrolyte Imbalance where you can see prominent U wave on EKG?

a. Hypokalemia
b. Hyperkalemia
c. Hyponatremia
d. Hypernatremina
Hypocalcemia- Prolonged ST and QT intervals
Hypercalcemia- shortened ST segment
- widened T wave
Hypokalemia- ST depression
- shallow, flat, inverted T wave
- Prominent U wave
Hyperkalemia- Tall, peaked T waves
- Flat P waves
- widened QRS complex
- Prolonged PR interval
Hypomagnesemia- Tall T waves
- Depressed ST segment
Hypermagnesemia- Prolonged PR interval
- widened QRS complexes
Non-therapeutic effect of Dialysis?
Decreased RBC Count
Risk for Disequilibrium Syndrome assessment
Headache, deteriorating level of consciousness and twitching
Client with CRF returns to nursing unit following HD Treatment. On assessment, nurse note the patients
temperature is 100.2oF, appropriate nursing action?
a. Encourage fluids
b. Notify physician
c. Continue VS Monitoring
d. Monitor site of shunt for infection
100.2oF = 37.89oC
Purpose of glucose in PD?
Increase osmotic pressure to produce filtration
Assessment to note for possibility of UTI
a. Fever
b. Urgency
c. Frequency
Percutaneous Lithotripsy
a. Renal S.
b. Jackson Pratt
c. Nephrostomy tube
d. Ileal Conduit
Percutaneous Nephrolithotomy or Nephrolithotripsy for Kidney Stones
In percutaneous nephrolithotomy or nephrolithotripsy, the surgeon makes a small incision in your back to
remove kidney stones. He or she then puts a hollow tube into your kidney and a probe through the tube. In
nephrolithotomy, the surgeon removes the stone through the tube. In nephrolithotripsy, he or she breaks the
stone up and then removes the fragments of the stone through the tube.

You need either general anesthesia or regional or spinal anesthesia during this procedure. A small tube
(catheter) may be inserted into the kidney to drain urine until the kidney heals.
PKD recommended therapy
a. Chemotherapy
b. Transplant
c. HD
d. PD
The two forms of polycystic kidney disease (PKD) are
autosomal dominant PKD, a form that usually causes symptoms in adulthood
autosomal recessive PKD, a rare form that usually causes symptoms in infancy and early childhood
The symptoms and signs of PKD include
pain in the back and lower sides
headaches
urinary tract infections
blood in the urine
cysts in the kidneys and other organs
Diagnosis of PKD is obtained by
ultrasound imaging of kidney cysts
ultrasound imaging of cysts in other organs
family medical history, including genetic testing
PKD has no cure. Treatments include
medicine to control high blood pressure
medicine and surgery to reduce pain
antibiotics to resolve infections
dialysis to replace functions of failed kidneys
kidney transplantation
Best time to give Hypertension drugs
After the patient is moved to the nursing unit following per treatment.
Laboratory results for signs of dehydration
Increase urine specific gravity.
Patient with CRF verbalizes that she is now feeling well from the treatment, she dont need to go for
another treatment (What defense mechanism).
Denial
Signs of steal syndrome for Left AVF
a. Pale left arm, pain and numbness.
b. Left hand paleness, pain and numbness
c. Pale right arm, pain and numbness
d. Right hand, pain, paleness, and number
Steal Syndrome/Ischemia
Steal syndrome is a constellation of symptoms related toischemia (inadequate blood supply to the hand)
caused bythe AVF stealing blood away from the extremity
Steal causes hypoxia (lack of oxygen) to the tissues of the and, resulting in severe pain and identified by
nail beddiscoloration, a cool hand, and a weak or absent pulse
Neurological and soft tissue damage to the hand can occur, resulting in mobility limitations (eg, grip
strength,dexterity), loss of function, ulcerations, necrosis
Steal syndrome/ischemia is estimated to occur in approximately 5% of vascular access patients, mostly
those with diabetes and peripheral vascular disease (PVD)

Clinical Clarification
Steal syndrome is estimated to occur in approximately 5% of vascular access patients, mostly those with
diabetes andperipheral vascular disease.
Why PD is done at specific interval, time and amount of solution
Because the solution and used has glucose content which may cause hyperglycemia.
Urine laboratory result for glomerulonephritis
Hematuria
Glomerulonephritis
Specific signs and symptoms may suggest glomerulonephritis, but the condition often comes to light when
a routine urinalysis is abnormal. Tests to assess your kidney function and make a diagnosis of
glomerulonephritis include:
Urine test. A urinalysis may show red blood cells and red cell casts in your urine, an indicator of possible
damage to the glomeruli. Urinalysis results may also show white blood cells, a common indicator of
infection or inflammation, and increased protein, which may indicate nephron damage. Other indicators,
such as increased blood levels of creatinine or urea, are red flags.
Blood tests. These can provide information about kidney damage and impairment of the glomeruli by
measuring levels of waste products, such as creatinine and blood urea nitrogen.
Imaging tests. If your doctor detects evidence of damage, he or she may recommend diagnostic studies
that allow visualization of your kidneys, such as a kidney X-ray, an ultrasound examination or a
computerized tomography (CT) scan.
Kidney biopsy. This procedure involves using a special needle to extract small pieces of kidney tissue for
microscopic examination to help determine the cause of the inflammation. A kidney biopsy is almost
always necessary to confirm a diagnosis of glomerulonephritis.
Blood gas analysis expected of a CKD patient
pH, PCO2, HCO3 levels
Arterial blood gas and blood chemistries may show metabolic acidosis.
JVP normal pressure is at?
2-3 mmHg above sternal angle
The jugular venous pressure is usually assessed by observing the right side of the patient's neck. The
normal mean jugular venous pressure, determined as the vertical distance above the midpoint of the right
atrium, is 6 to 8 cm H2O.
KDQI guidelines on strategies on slowing the progress of kidney failure
KDQI guidelines on fistula readiness for cannulation
6mm skin depth
6mm straight length
Anemia presents as a comorbidity at what stage of CKD
CKD 2, CKD 3, CKD 4
As the kidney becomes progressively diseased, mechanisms that form scar tissue take over, and with the
process of scarring, cells responsible for manufacturing EPO die. These are the same cells that are under
feedback control that increase in the face of hypoxia (lack of oxygen reaching body tissues) and decrease
EPO production with enriched oxygen. Now, faced with becoming extinct, the production of EPO sharply
decreases.
Anemia starts in the third stage of kidney disease when the glomerular filtration rate (GFR) is less than 60
cc/min, long before dialysis is necessary. Unfortunately, many patients come to the dialysis unit with
anemia, even though it can be easily treated. As kidney disease progresses, anemia worsens.
Normal value limit for recirculation studies using urea method
5%, 10%, 20%
Increase amount of fluoride in water system sign and symptoms, select all that apply.
Desferal overdose signs and symptoms, select all that apply.

Symptoms of a Desferal (deferoxamine) overdose may include slow or fast heart rate, nausea or stomach
discomfort, headache, problems with speech or vision, pale skin, feeling drowsy or agitated, urinating less
than usual, feeling light-headed, fainting, or coma.
CaH and Phos monitored at what interval as per KDQI guidelines
Every 2 weeks, every month, every 2-3 months
Whice is more biocompatible (A. Cuprophane B. Hemophan C. Polysulfone D. Polyamide)
A&B, B&C, C&D, ABC, all of the above
Dialyzer membranes used to be made primarily of cellulose (derived from cotton linter). The surface of
such membranes was not very biocompatible, because exposed hydroxyl groups would activate
complement in the blood passing by the membrane. Therefore, the basic, "unsubstituted" cellulose
membrane was modified. One change was to cover these hydroxyl groups with acetate groups (cellulose
acetate); another was to mix in some compounds that would inhibit complement activation at the membrane
surface (modified cellulose). The original "unsubstituted cellulose" membranes are no longer in wide use,
whereas cellulose acetate and modified cellulose dialyzers are still used. Cellulosic membranes can be
made in either low-flux or high-flux configuration, depending on their pore size.
Another group of membranes is made from synthetic materials, using polymers such as
polyarylethersulfone, polyamide, polyvinylpyrrolidone, polycarbonate, and polyacrylonitrile. These
synthetic membranes activate complement to a lesser degree than unsubstituted cellulose membranes.
Synthetic membranes can be made in either low- or high-flux configuration, but most are high-flux.
Cuprophane Modified Cellulose
Hemophan Modified Cellulose
Polysulfone Thermoplastic polymers
Polyamide - Polymer containing monomers of amides joined by peptide bonds
CKD MBD (Mineral Bone Disease) expected laboratory results for this condition
CaH, PTH, Calcitriol, vitamin D
What is chronic kidney disease-mineral and bone disorder (CKD-MBD)?
CKD-MBD occurs when the kidneys fail to maintain the proper levels of calcium and phosphorus in the
blood, leading to abnormal bone hormone levels. CKD-MBD is a common problem in people with kidney
disease and affects almost all patients receiving dialysis.
CKD-MBD is most serious in children because their bones are still growing. The condition slows bone
growth and causes deformities. One such deformity occurs when the legs bend inward toward each other or
outward away from each other; this deformity is referred to as renal rickets. Another serious complication
is short stature. Symptoms can be seen in growing children with renal disease even before they start
dialysis.
The bone changes from CKD-MBD can begin many years before symptoms appear in adults with kidney
disease. For this reason, the disease is known as a silent crippler. If CKD-MBD in adults is left untreated,
the bones gradually become thin and weak, and a person with CKD-MBD may begin to feel bone and joint
pain. CKD-MBD also increases the risk of bone fractures.
Doctors used to use the term renal osteodystrophy to describe the mineral and hormone disturbances caused
by kidney disease. Now renal osteodystrophy is used only to describe the bone problems that result from
CKD-MBD.
How is CKD-MBD diagnosed?
To diagnose CKD-MBD, a doctor may take a blood sample to measure levels of calcium, phosphorus,
PTH, and sometimes vitamin D. The doctor may perform a bone biopsy to see if the bone cells are building
normal bone. A bone biopsy is done under local anesthesia and involves removing a small sample of bone
from the hip and analyzing it with a microscope. Determining the cause of CKD-MBD helps the doctor
decide on a course of treatment.
When HCO3 packet or sachet is opened, how long should it be used after opening per KDQI guidelines to
avoid bacterial contamination?
12h, 24h, 48h

LABS anemia panel (TSAT, Reticulyte Count, _____) which does not belong?
PTH
LVH pathophysiology as compensatory (Pathologic)
CRP (C-Reactive Protein)
C-Reactive Protein, is a test which measures the concentration in blood serum of a special type of protein
produced in the liver that is present during episodes of acute inflammation or infection. In the body, CRP
plays the important role of interacting with the complement system, an immunologic defense mechanism.
Phosporus Normal Value
3.0 - 4.5 mg/dL
Organ donation concepts on Brain Dead
Preferred needle gauge for 1st time cannulation
Gauge 18
guyz, sinend ng fren ko yan ung nakapasa diz sept.. my mga question daw jan na naulit. payo nya basahin
ntin ung PD at kidney transplant.
sa mga mag exam diz oct, magkita kita tau diz wed para sabay2 magbayad at magmeeting n din pano tau sa
sunday.
GUYZ GALINGAN NATIN, LET'S PRAY FOR EACH OTHER. JUST TRUST HIM. kaya natin yan. go
DIALYS8 CRN's :))
kung medyo naguluhan kau, isend nyo saken email add nyo or itext nyo ah para mabasa ko, pasabi n lng
din po kina gerard.