Acute Kidney Injury/Urinary Tract Disorders Flashcards
Acute Kidney Injury (AKI)
Characterized by
1) Elevated serum creatinine (up to 1.5x)
2) Decrease in urine ouput
Reversible but mortality is high
CRRT may be required (Continuous renal replacement therapy with one-to-one with a nurse)
Risk for developing AKI
1) Infections
- Sepsis most common cause of AKI (hypotension and antibiotics)
- Widespread vasodilation decreases perfusion
- Antibiotics can be nephrotoxic
2) Hypotension from shock, surgery, HF (less blood flow to the kidneys)
3) Patients exposed to nephrotoxins (medication,radiocontrast)
Pre-renal AKI
Decrease in filtration and perfuison from low blood pressure or flow
Examples
1) Hypovolemia - loss of blood volume from accident, surgery, dehydration, excessive vomiting
2) Altered peripheral resistance (blood vessel smooth muscle lost) = occurs in sepsis, anaphylactic shock, BP meds that relax smooth muscles
3) Cardiac disorders = decreased CO such as heart attack, dysrhythmias
Complication = Intrarenal
Intrarenal AKI
Direct damage to renal tissue, eg. in ATN (acute tubulat necrosis)
Examples
1) Prolonged renal ischemia (prerenal)
2) Nephrotoxic drugs - antibiotics, NSAIDs, radiocontrast
3) Organix solvents like ethylene glycol
4) Acute hemolysis/Rhabdomyolysis
- Release heme that filter through glomerulus and cause less blood to be filtered
Hemolysis can occur from hemolytic transfusion reaction (wrong transfused blood)
Rhabdomyolysis can occur when elder falls and no one finds them for days
5) Acute glomerulonephritis
Postrenal AKI
Mechanical obstruction or urinary outflow
Examples
1) Stones/tumors
2) Enlarged prostate
3) Urethral scarring and infections like STI (narrows urinary tract)
Can cause intrarenal in complication
Mechanisms of AKI
1) Prerenal -
Low perfusion, GFR decreases, PCT/DCT increase retention to raise BP, Aldosterone and ADH released = oliguria/azotemia
2) Intra-renal
Necrosis/apoptosis, inflammation/swelling, epithelial cells die and obstruct filtrate which causes high pressure can form casts that will be excrete in urine, tubular backleck, decreased GFR = Oliguria
3) Post renal
Get rid of obstruction
Clinical course of intrarenal
1) Initiation
- Precipitious event (increased serum creatinine/BUN + oliguria)
- What cause the inury
2) Maintenance
- Drop in GFR
- Urine can be anuria, oliguria or non-oliguria (which is normal urine but unconcentrated) for around 2 weeks
- Fluid retention and metabolic acidosis
- Electrolyte imbalance like CKD - Low sodium/calcium, high phosphate/potassium
- Anemia from erythropioein
- Waste product accumulation
3) Recovery
- Can have diuresis for 1-3 weeks (not concentrated) but risk of hypovolemia, hypotension, low electrolyte, dehydration
Glomerulonephritis
Immune-mediated inflammation of urinary tract that can result in proteinuria, oligura, hematuria
- Effects BOTH KIDNEYS
- Causes - drugs, infection, immune disorder
Types of glomerulonephritis
1) Acute glomerulonephritis - AKI, acute frop in filtration, the oliguria, then recovery (if not advances)
2) Rapidly progressive lomerulonephritis - Kidney failure in weeks to months
3) Chronic glomerulonephritis - Seems like it resolves but damages kidneys slowly until renal failure
4) Nephrotic syndrome
Acute post-streptococcal glomerulonephritis
Immune attack on strep infection causes antigen-antibody complexes that damage the glomerulus
Nephritis appears in 5-21 days after infection
WBC rush to area and inflame (less space for blood to filter)
Some capillaries may rupture causing hematruai
Often in children
Symptoms
Smoky urine (cococola/tea), oliduria, edema especially in periorbial, HTN, Urinalysis show RBC, WBC, protein and erythrocasts in them
Urinary tract infection
Causes can be from urinary statis (as flushing is a defence mechanism to drop the bacterias)
Often form E.coli
Risk factors
i) Females - shorter urethra
ii) Urinary statis - incontinence, obstruction of urine like in BPH, STI causing scar tissue, congenital, impaired blood to bladder, renal calculi, SCI or other nerve damage causing immobility
Cystitis
Lower urinary tract infection
Dysuria - burning while urinating
Frequency - less area for urine to accumulate due to inflammation
Urgency
Suprapubic discomfort
Cloudy/white urine = pus pyuria
= LUTS (Lower urinary tract symptoms)
Pyelonephritis
Upper urinary tract infection (kidneys)
LUTS + Systemic symptoms of infection
Fever, chills, malaise, vomiting, tenderness
Urinylasis will show microscopic hematuria, leukocyte casts
Can become SKD
Renal calculi
Kidney salts when mineral salts become concentrated
Commonly calcium but can also be strubite, uric acid or cystine
Hydronephrosis = kidney becomes edematous because of backup of fluid
Manifestations
Abdominal/flank pain
If in pelvis = pain in the CVA
If in ureters = renal colic pain when stone is being pushed down
Hematuria
Fever/chills/N/V
Polycystic kidney disease
Common genetic disease
Cortex and medulla fill with ccysst that enlarge and destroy surrounding tissues by compression
- Occurs in both kidney
- May experience UTI or HTN
- May require transplant
Symptoms
Abdominal flank pain - enlarged kidneys
Hematuria - Cysts rupture
UTI and HTN
Can leadk to CKD
Cancer
Kidney - Risk factors - obesity, smoking, no early symptoms
Hematuria, flank pain, palpable mass
Bladder - Risk factors - smoking, industrial dyes, chronic kidney stones, chronic cystitis
Painless hematuria
Irritaive bladder symptoms
Trimethoprim/Sulfamethoxalate (Septra)
Anti-infective (AKA co-trimazole)
MOA
- Bacteriostatic
- Broad spectrum
Indication - Uncomplicated UTI
AE
- N/V/rash common
Rare
- Steven johnsons syndrome
- Hemolytic anemia
- Birth defects
- Hyperkalemia (Trimethoprim suppress potassium excretion)
CI - alcohol, folate deficiency, pregnancy
NC
Inhibits folate derivative so bilirubin access brain as BBB not strone in babies
NC
- Common sulfa allergy!!!
- Complete regimen
- Drink glass of water - renal damage due to sulfa properties that can cause crystal aggregates
- GI assessment
- Monitor adverse reactions
Oxybutynin (Ditropan XL)
Anticholinergic - blocks muscarinirgic receptors on detrusor muscle to inhibit bladder contractions
- Indication = overactive bladder, spasm from UTI/calculi
Adverse effect = Dry mouth, blurred vision, Constipation, tacycardia, urinary retention
Hallucination, sedation in older adults
NC
Transdermal/gelm PO
- eeducate that it is extended release so shell in stool is normal
- Monitor urinary retention, UTI, constipation
- Caution with hazardous activity, avoid CNS depressants
Mirabegron (Myrbetriq)
Selective beta-3 adrenergic agonist
= Relax of detrusor muscle in bladder, allows increased filling
Effect is modest, taken when pt cannot tolerate anticholinergic side effects
Indication - overactive bladder
AE
- slight increase in HR,BP as no drug is ever fully selective (beta)
- Increase digoxin levels
Ketorolac (Toradol)
NSAID
= Inhibit prostaglandin, first generation
PAIN FOR RENAL CALCULI
AE
Drowsiness
Cox 1 - bleeding, GI ulceration
Cox 2 - promote MI/stroke from vasoconstriction
Renal impairment and steven-johnson rarely
NC
IM/IV
Pain assessment
Signs of bleeding- brusing, melena
Monitoring
1) Pre/Post renal AKI
Monitor
Urine output/ I&O
Lab values (Urea, creatinine)
Vital signs (BP)
Bladder scan
Intervention
Pre-renal = increase fluid
Post-renal = remove obstruction(surgery, catheter, etc.)
2) Intrarenal AKI (uremia assessment of CKD)
CNS - Fatigue, seizures, coma
CVS - HTN, edema, dysrhythmias
Resp - Crackles
GI - N/V, pain
GU - decreased urine ott
Lab work - electrolytes, waste urea/creatinine, ABG, WBC/PLT dysfunction, low Hgb (erythropoietin)
3) Intrarenal AKI in Recovery phase
I&OS
Hypokalemia, hyponatremia
Hypovolemia/dehydration
REMEMBER DIURESIS OCCURS
Sodium in intrarenal
Maintenance/oliguria = serum hyponatremia as sodium is lost and water retained
Recovery/Diuresis = tubules still not able to concentrate
Potassium in AKI
Hyperkalemia, esp with tissue damage and unable to excrete
Can cause cardiac arrythmias
Acidosis worsesn hyperkalemia as hydrogen ions enter cells and force potassium out
Potassium treatment
Mild (5-5.5)
Kayexalate
Dietary measures (K+ restriction)
Diuretics
Salbutamol
Moderate (Greater than 6)
IV glucose/dextrose + IV insulin
(Insulin can push back potassium, dextrose to prevent hypoglycemia)
IV sodium bicarbonate
Question if dialysis needed
Severe (greater than 6 + EKG changes)
IV calcium gluconate
(Calcium reduce cardiac arrhythmias)
Diagnostics
Creatinine = indicate renal impairemnet
BUN = indicate kidney, dehydarriton, prefusion, high protein diet, infection, GI bleeding
Others
Urine gravity = if high then dehydration or low prefusion, i flow then dilute urine/ckd/diuresis
Protein - infection, excersice, glomerular disorders
RBC - glomerular disorder, infection, trauma, cancer, polycystic kidney disease
WBC/leukocytes - infection or UTI
casts - tubular damage
Bacteria - C$S as can be contamination or infection
Nitrates = ecoli!!!
Glomerulonephritis
Types
Primary glomerulonephritis - condition that primarily involves the kidney
Secondary glomerulonephritis - kidney involvement is only part of systemic disorder eg. Lupus
UTI ASSESSMENT
Vital signs
Suprapubic discomfort upon palpation
CVA tenderness = absent in lower, present in upper!!!
Sit upright, indirect percussion on the back where the kidneys are
Compare bilaterally
diagnostic - dipstick, C&S (mandatory in pyelo), CBC, KUB ultrasound done in children with UTI or pyelopnephrtisis
Renal calculi
More common in men of ages 20-44
Treatment
1) Conservative management (let it pass itself)
Increase hydration
Dietary changes
Meds - thiazide diuretics, symptom management like analgesics (ketorolac), oxybutynin (anticholergic)
2) Lithotripsy
Use sound waves to break up stones (analgesic or sedation may be used)
3) Surgical removal if big
