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