Renal - med surg Flashcards
bp and MAP should be at what for adequate purfusion?
SBP 180-80 mmHg
MAP >65 or 75-85 mmHg (organ perfusion
vasocontrictors will
stop blood flow to the kidneys to preserve it for the heart, lungs, and brain
sympathetic response activates what system?
RAAS system
BUN/creatinine ratio - what causes increased and decreased ratios
Increased ratio = fluid volume deficit or hypoperfusion of kidneys
Decreased ratio = fluid volume excess or malnutrition
bactrim for a UTI elevates what?
creatinine
rapid decrease in GFR - what happens to creatinine? (you got this right on the quiz)
creatinine will go up
aging and the kidneys - renin and aldosterone?
Decreased renin, aldosterone
bladder tone and aging
Incontinence
Retention
decline in renal function - usually slow or fast?
usually slow
renal insufficiency (compensate, or not?)
functions continue, nephrons compensate, toxins accumulate
signs of renal insufficiency - creatinine levels and pee? and what about stomach issues?
nocturia, polyuria, aonrexia, N/V, weakness, fatigue, BUN rises, creatinine <2, GFR decreases
AKI - reversible or not? IF….
reversible, if they do not have oliguria. If they have oliguria, it is more likely to progress to CRF.
chronic renal failure - BUN, Cr (exact number), and GFR? (get chronic at 5)
body demands not met, increase quantity (early) not quality. BUN incrases with CR > 5, GFR continues to decrease.
oliguric - how much?
under 400 mL a day
end stage renal disease - and what syndrome? (Ure reaching the end)
kidney function fails (permanent), need dialysis, systemic impairment (uremic syndrome)
AKI
Systemic hypoperfusion, increases vascular tone
Renin, angiotensin, antidiuretic hormone systems are activated
Time limited response. Eventual ischemia and infarction of nephrons
Most common cause of AKI is - from what?
prerenal volume depletion from loss of body fluids
AKI with RRT (renal replacement therapy) mortality is
50%
AKI - definition (3 things) (olga w/ AK has buns and azo)
oliguria, marked increase in BUN and Cr, or azotemia (build up of urinary toxins)
S & S of AKI - (think BUN,etc. , and tummy troubles?) and the weird one?
increased BUN and Cr (can go up rapidly), decreases GFR, anemia. HTN or CHF. anorexia, N/V, puritis.
AKI - acid-base, fluid & electrolytes, toxins - pH depends on what?
ph depends on number of functioning nephrons. metabolic acidosis.
Prerenal injury - reversible? and structural damage? (pre = before damage)
is often caused by inadequate renal blood flow, resulting in renal hypoperfusion and renal ischemia.
Filtration pressure declines in the face of reduced renal blood flow
Glomerular filtration pressures also fall
Structural damage has not yet occurred and the condition is reversible.
Intrinsic renal injury (intrarenal) is caused by problems involving what tissue?
renal tissue (parenchyma - tissue)
Postrenal injury - reversible? (post not as good as you think)
(small percent) usually reversible.
pre-renal causes AKI - reduced ECV (extracellular volume) (think - not enough volume to begin with) and CUTS
volume depletion, dehydration, diuretics, 3rd spacing, hemmorage, GI loss
pre-renal causes - cardio
pump failure, decreased CO, hypotension, MI, HF, tamponade, pneumothorax, dysthrthmia, valve dysfunction, AAA
pre–renal causes of AKI (I’m shocked that you’re pre, sepsis)
shock and sepsis
pre renal - obstructed renal blood flow - ex. (STV is an obstruction)
vena cava obstruction, renal artery stenosis, thrombosis
intra renal AKI - ischemia - ex. (cher - door)
interstitial nephritis (swelling), transfusion reactions, diabetes
intra renal - nephrotoxins - (cher doesn’t like myocins) NOT JUST myocins
contrast media, heavy metals, medications, ABX, NSAIDs, cimetadine (tagament)
intranrenal trauma - riding the tubes
acute tubular injury
CI - AKI
contrast-induced acute kidney injury
contrast induced - AKI - know what? because what happens later?
know fluid volume status (weight). creatinine doesn’t peak for 3 - 4 days, so they’re at home when this happens. can give mucomist IV (will thin secretions and buffer the kidneys)
post renal causes - AKI
Stones, clots, hypertrophy (BPH), tumors leading to obstruction and backup or stasis
Bilateral ureteric obstruction
Bladder outlet obstruction
Urethral obstruction
Obstruction of single functioning kidney
factors affecting renal excretion (the flow rate is messing with my ph and pk)
blood flow, urine flow rate, urine pH and pKa = strength of acid (the lower the pKa, the stronger the acid),
pKa
the lower the pKa, the stronger the acid
AKI - step 1(weigh me first)
evaluate volume status
AKI - step 2 (weight me, obstruct me)
rule out obstruction.
AKI - step 3 (weigh me, obstruct me, test me)
renal function tests. BUN, cr, electrolytes. hemoglobin, ca, pho4.
AKI - step 4 (weight me, obstruct me, test me, the cause)
probable cause for renal dysfunction.
AKI - step 5 (weight me, obstruct me, test me, the cause, urine)
urine rountine & microscopy. specific gravity, protein, glucose, blood, cast, cells and crystals.
AKI - step 6 (weight me, obstruct me, test me, the cause, urine, salt)
urinary indices (fractional excretion of sodium). obtain spot urine sodium and cr.
risk factors for AKI - physical assessment
Neurologic (change in mental status - need to check 02 % and glucose)
CV (MAP, PVR, SVR, Pre/Afterload, CO, EF, CAD, MI)
Pulmonary
GI (N, V, diarrhea, constipation, appetite calories, protein sufficient, 3Ps (protein, phosphorus, potassium), sodium, bleeding)
Hematologic and immune system
Integumentary
Skeletal
Laboratory
BUN, Cr, GFR
Osmolality
Electrolyte imbalances
Remember all the reasons for an altered urine output including decreased oral fluid intake and excess fluid loss.
loop duiretics - peak and duration (reach the peak in 60 min)
inhbits Na and C reabsorption in the loop. peak 60 min, duration 6-8 hrs.
inotropes for AKI (the troops get a little dopamine)
dopamine in small doses 1-5 mcg causes selective dilation enhancing perfusion.
vasodilators for AKI (pam dilates)
corlopam, selective dopamine receptor agonist, 6x more potent than dopamine.
CCB for AKI
works through vasodiation. nifidipine relaxes smooth muscle and improves blood flow. CCB usually used after kidney transplant.
chronic renal insufficiency - caused by what? (the 2 that are always chronic)
(this is a recap) Reduction of blood flow to the kidneys often caused by renal artery disease (HTN, diabetes)
renal diet (the 3 Ps)
Limit the 3 P’s and Sodium
Potassium
Phosphorus
http://www.zemplar.com/pdf/high-phosphorous-foods.pdf
Protein
Sodium
potassium foods (everything you don’t eat) and what about salt?
organ meats, fish, dried fruit, beef, chicken, pork, milk, dark leafy greens, salt substitutes
foods with phosphorus
dairy, collard greens, dried beans
systemic affects of chronic and end stage - what about hormones?
Permanent, irreversible loss of function
CV, hematologic, GI, neurologic
Progression of symptoms and palliative interventions for removal, regulatory and hormonal functions
chronic and end stage - associated w/ severe fluid and electroylte abnormalities
Sodium, potassium, calcium, phosphorus
Na+ and fluid retention
K+ retention (kidney is the primary organ of K+ balance)
Ca++/Phosphorus imbalances (hypocalcemia symptoms)
ESRD (end stage renal disease)
just managing symptoms - acid base imbalance, anemia, HTN, HF. Also restrict fluids, hyper-phosphate, hypo-calcium, hyperkalemia
hemodyalysis - works how? (think water)
works through osmosis and diffusion. requires large vascular access. most efficient.
complications of dialysis - what syndrome?
diequiliebrium syndrome
complications of dialysis - bleeding?
high risk of bleeding (heparin in the machine)
hemodialysis - when to do it? havepee
Indications
Refractory hyperkalemia
Refractory acidosis
Volume overload
Elevated BUN with symptoms of complications
Pericarditis
Encephalopathy (hepatorenal syndrome/AMS, ALOC
Pulmonary edema
Mnemonic = HAVEPEE
H: hyperkalemia (refractory)
A: acidosis (refractory)
V: volume overload
E: elevated BUN > 35 mM
P: pericarditis
E: encephalopathy
E: edema (pulmonary)
Continuous renal replacement therapy (CRRT) - 24 hr dialysis
Primarily used for clients in critical care who are hemodynamically unstable
More gradual and continuous. Reasons to have it are the same as dialysis.
Temporary Dialysis Vascular Access - which port and flush with what?
Do not use for routine access or blood draw
HD (hemodialysis team) team use only
Use only the 3rd port if present during an emergency
Flush lock with sodium citrate (4%)versus heparin
Aspirate and disguard
always check with an AV fistula
a bruite (listen) and a thrill (feel)
nursing care - dialysis - pre treatment - (think weights)
Medications,, nutrition, fluids
VS, weight, labs,, symptoms
nursing care - dialysis - post treatment
Post treatment
Handoff –VS, Labs, fluids in/out, weight changes, blood glucose
Labs
Fluid and electrolyte shifts
Site observations
Medications, nutrition, rest
dialsyis - complications (what about food and fluid and cramps)
Fluid limitations, muscle cramps, fatigue, food limitations
peritoneal dialysis - volume, and how does it drain?
depends on osmosis and diffusion. volume = 2 - 2.5 L, warmed, infused. drained by gravity.
peritoneal dialysis - complications (Perry door)
peritonitis, anorexia, hernia, LBP (lower back pain), altered body image, constant sweet taste
peritonial dialysis - continous or intermittent
CAPD - continous ambulatory - 4x/day 7 days a week
CCPD - automated
NIPD - night time - intermittent
cycles at night
peritoneal diayslis - nursing responsibilities - verify orders (3 things - CDS washing machine) (tone dialysis in CDM)
Assessment
Verify orders (solution, dwell time, cycles)
kidney transplant - pre op - drugs?
Basic preoperative care and checklist and focused transplant and renal assessments
Continue RRT as needed
Administer immunosuppressive drugs to prevent immediate graft rejection
Evaluations and diagnostics
kidney transplant - post op - how often to measure urine output?
VS and hemodynamic monitoring
Measure UO every 30-60 minutes to determine transplant function
Diuretics
Indwelling urinary catheter care
kidney transplant complications
ATN (acute tubular necrosis)
Electrolyte imbalances
Hemorrhage
Surgical emergency
Urethral anastomosis failure
Renal artery thrombus
Abrupt onset of HTN and reduced GFR
Infection
Immediate and ongoing risk due to patient’s immunosuppression
Monitor urine, surgical sites, LOC
Rejection
signs of transplant rejection - #1 - so simple
pain #1.
transplant - signs of rejection - hyperacute (rejection of a hyper cutie can be minutes to hours, it’s micro)
minutes to hours after, microcoagulation leads to ishemia and necrosis
transplant - signs of rejection - acute (a cutie not clotting for days to months)
days to months after. antibody-mediated vasulitis (not clot)
transplant - signs of rejection - chronic (chronically inflamed from scarring and ischemia)
chronic inflammation, functional tissues, fibrotic scarring, vessels damaged, progressive ischemia
kidney transplant rejection - symptoms - BUN, Cr and urine?
Elevated BUN/creatinine & K+
Decreased creatinine clearance
Decreased urine output
renal cancer - patho
Pathophysiology
Obstruction of flow and invasion of functioning tissues and lymph
renal surgery - Nephrouterectomy
removal of kidney and ureter
nephrotic syndrome - caused by not enough protein - patho (nephrotity on fire)
Pathophysiology
Inflammatory response in the glomerulus
Think inflammation for causes of nephrotic syndrome
glomerulonephritis - patho - and main cause?
Inflammatory reaction in the glomerulus;
Main cause is streptococcus
IgAN (glomerulonephropathy)
main cause of glomerulonephritis
strep
chronie renal failure - S/S (just think of your patient)
oliguria to anuria, volume retention, HTN. azotemia (uremia), acidosis, anemia, elevation in K+, Na+, PO4, Low Ca+
ESRD - Bun, exact CR and GFR levels - Cr and GFR levels
severe elevation in BUN, Cr > 10, GFR < 15, high K+, Na+, PO4, Low Ca, acidosis.
intrinsic renal injury - Categorized by
primary injury site
intrinsic renal injury - ATN
ATN refers to necrosis of renal tubule tissue = acute tubular necrosis
intrinsic renal injury - Nephrotoxicity develops from
either exogenous or endogenous agents
intrinsic renal injury - causes (Cher w/ rabbis)
Rhabdomylosis
Hepatorenal syndrome (poor outcomes)
Very important to note clinical events and predisposing factors
THINK “mycins” drugs, or dyes with contrast
post renal injury - causes
is caused by obstruction to the outflow of urine from the kidneys. The obstruction can be mechxanical or functional in origin.
intra-renal AKI - ischemia - ex. (Cher w/ DIC, lupus and HIV)
DIC, SLE (lupus), HIV, nephropathy, infection
intra-renal AKI - ischemia - ex. (cher w/ glum and liver)
glomerulonephritis, hepatorenal syndrome, malignancies, vasculitis
aging and the kidneys - ADH? Fluid intake?
ADH (declines) and hypertonicity
Decrease fluid intake
Decreased CO & HTN
factors affecting renal excretion
physicochemical properties, distribution and binding, drug interactions, biological factors, disease states
renal insufficiency - signs (last one)
mild anemia. if toxins accumulate w/out intervention, progresses to renal failure.
peritonitis - symptoms - 1st sign
cloudy effluent is 1st sign
peritoneal diaylsis - nursing assessment (PB in VW tone Loc)
Assess VS, weight, breath sounds, signs of peritonitis, labs
Peritoneal dialysis - nursing - abdomen exam (Tone loc is rigid)
Peritonitis rigid abdomen, pain, distension, increased WBC, check for sepsis)
Assess abdominal insertion site
Redness, swelling, drainage, pain, catheter stabilization, dressing,
Perform site care
Check lines, tubing, caps
Assess for mechanical complications
peritoneal dialysis - nursing - Confirm phase of therapy - and when to assess solution?
Confirm phase of therapy (infusion, dwell or capped)
Assess solution (before and after)
Evaluate efficacy of therapy
Evaluate patient self care knowledge & technique
kidney transplant - post op - how to replace fluids?
Replace fluid mL for mL
Monitor electrolytes and renal function tests
Postoperative education include medications, S&S of rejection, VS, fluids, diet, prevent infection, support because there is no guarantee
transplant rejection - how to correct?
Pharmacological management - we target anti-rejection drugs
renal cancer - Risk factors - pain killers?
Risk factors
Smoking, overuse of pain killers, chemical exposure, genetics
renal cancer - S/S - 1st one
painless Hematuria
renal cancer - treatment
Radical/partial nephrectomy, radiation, chemotherapy
Cystectomy (removal of bladder)
Nephron sparing treatment, gene therapy, biological or immunotherapy
ESRD - diet
limits protein, increase calories - fat, CHO
renal surgery - Nephrectomy - for what?
Nephrectomy (renal cancer)
Open
Laparoscopic (access from stomach or pelvis)
Robotic assisted
daVinci Surgical System http://www.davincisurgery.com/urology/
nephrotic syndrome - S/S (nephrotity and ana have no albumin or protein)
S & S
Anasarca (leak fluid all over body), hypoalbuminemic, proteinurea
nephrotic syndrome - treatment (think inflammation)
BR
Diuretics
Prednisone
Diet (decreased Na++ and increased protein)
Dialysis
common rule about nephrotic syndrome
Common rule: Limit protein with kidney problems except with nephrotic syndrome
glomerulonephritis - S/S - (glum has a sore throat)
Sore throat, malaise, HA
glomerulonephritis - treatment - and diet?what about dialysis?
Get rid of strep
Dialysis
Diet (decrease Na++ and increase carbs)
BR
I & O and daily weights
Teach S & S of renal failure Toxins & Fluid
glomerulonephritis - s/s - pain and edema ? (glum has pain and puffy face)
FVE, flank pain, increased BP, facial edema
glomerulonephritis - s/s - urine? specific gravity?
decreased UO, increased urine specific gravity,
glomerulonephritis - BUN and Cr?
increased BUN & creatinine
AKI - If systemic pressures continue to fall,
acute tubular necrosis (ATN) may develop
AKI - step 2 - how to rule out obstructions?
physical exam, patency of catheter, renal ultrasound. foley catheterization.
AKI - step 4 - how to find the cause?
evaluate nephrotoxic exposure (drug) - nsaids, aminoglcyosides (the myocin antibiotics), hypotension, etc
AKI - step 1 - how to evaluate weight?
physical exam, weight, CVP (central venous pressure), CWP. fluid challenge.
chronic renal insufficiency - defined as…(what percent)
Defined as decline in renal function to approximately 25% of normal
risk factors for chronic renal insufficiency
Risks include: Older age, gender, family history, race or ethnicity, genetic factors, hyperlipidemia, HTN, smoking, diabetes
Stages
chronic renal insufficiency - when do you see symptoms?
Usually symptomatic when <50% “kidney function” is left.
dialysis complications - activity, sleep?
limitation of activity, sleep problems, peripheral neuropathy (DM), vacation limitations, social isolation, puiritis, long dialysis treatment times
complications of dialysis - muscles? bleeding?
muscle cramps, hemmorage
complications of dialysis - machinery
air emobolus
complication of dialysis - flux?
hemodynamic flux (hypotension, dysthrrhymias, anemia)
kidney transplant rejection - graft issues
Graft tenderness
Graft enlargement
kidney transplant rejection - body temp and BP?
Low-grade temperature
Elevated blood pressure
AKI - specific gravity? (to be cute and stay the same)
increased specific gravity or fixed.
renal cancer - urine (kidney cancer makes me pee)
dysuria, frequency, urgency
renal cancer symptoms - fever? BP?
fever, HTN
renal cancer symptoms - lump where?
abdominal mass or lump
renal cancer - pain where? and edema where?
flank pain, persistent fatigue, rapid/unexplained weight loss, edema in LE
glomerulonephritis - how is the hemoglobin? (Glum is of course anemic)
anemia
glomerulonephritis - what’s in the urine? (2 things) (glum needs protein due to bleeding)
Proteinurea, red blood cell casts, hematuria
