Renal Flashcards
Why do renal dz pts have low hct
Bc their kidneys can’t stimulate RBC production with erythropoeitin
KUB/Flat plate of abdomen
Scan of urinary system K-kidneys U-ureters B-bladder U-urethra
3 main areas of kidneys
Pelvis, Medulla, Cortex
Where do kidney stones occur
In the pelvis, urine backs up in that area first (hydronephrosis)
Where are pyramids located
In the medulla
The cortex houses what
Glomeruli and nephrons
Functioning unit of kidney
Nephron
3 major functions of nephron
- Filter water soluble substances from blood
- Reabsorb filtered nutrients, water, and electrolytes (reabsorb about 90%)
- Secrete waste products
Site where fluid filtration form blood to nephron (osmosis) takes place
Glomerulus
Characteristics of glomerulus
- More permeable than other capillaries
- Prevents transport of blood cells and proteins
GFR
R/t bp and blood flow
-Normal is 125 mL/min
What is GFR determined by
Filtration pressure within glomeruli
How does each glomeruli regulate its own GFR
High/Low bp, NaCl, glucose (thats why pts w/ high BG pee a lot)
What is the most important factor with GFR
Blood volume
Formed and released when theres decreased blood flow, volume, or pressure
Renin
What stimulates the production of angiotensin II
Renin
Causes vasoconstriction and the release of aldosterone
Angiotensin II
Increases reabsorption of Na
Aldosterone
What is the result of renin-angiotensin system vasoconstricting?
Tank will be smaller so pressure is higher. CVP and SVR will increase.
Produced in the kidney and regulate GFR, renal vascular resistance, and renin production
Prostaglandins
Angiotensin II stimulates the release of what?
Bradykinin
Dilates renal vasculature to maintain renal blood flow
Bradykinin
Triggers RBC formation in marrow
Erythropoietin
Converted to active form in the kidney
Vitamin D
Most direct measure of overall hydration as a reflection of GFR and why
Creatinine, no other pathologic condition increases Creat than renal dz
Indirect measure of overall hydration
BUN
BUN can also elevate with what besides renal dz?
Diet, GI bleed, tissue breakdown
RCC stats
- In men 2x more than women
- 20% more in AA
- 5 year survival is
S/S of RCC
- Often asymptomatic till late dz
- Costovertebral angle tenderness
- Hematuria as a late sign
- Palpable abd mass
Late signs from metastatic dz of RCC
Bone pain, SOB, chest pain
Metastasis of RCC
Tumors spread quickly and grow up superior vena cava into right atrium
Sx removal of RCC
Nephrectomy, you only need one kidney
Chemo w/ RCC
Limited effectiveness, metastasis is usually unresponsive to chemo
Problem w/ urinary stasis
Bacterial growth, predisposes to UTIs
Renal obstruction can lead to what?
Post-renal acute renal failure and acute tubular necrosis
Congenital link to renal obstruction
Anatomical malformations, seen more in children
Changes secondary to renal obstruction
Depend on location and size, the higher up the worse
What increases proximal to the renal obstruction
Hydrostatic pressure
Why does GFR reduce with obstructions?
Dilation
Hydroureter
Complete obstruction of ureter
Hydronephrosis
Enlarged kidney due to dilation
Stent placement for treatment of obstruction
To retrieve stone. Done in the OR
Nephrostomy for obstruction
Like a foley cath but instead of going into the bladder the drainage tube goes into the kidney
ileal conduit
Ureters lead out of the skin like a colostomy bag
Micturation
Unidirectional flow
What host defenses in women prevent infections
Urethral secretions
What host defenses in men prevent infections
Prostatic secretions
How does the urine prevent infection
Acidic pH and urea, epithelial cells provide additional protective barrier
Major risk factor for acute pyelonephritis
Pregnancy due to alterations in urinary tract
Urinary reflux w/ kidney infection
Due to catheter bag not being below pt
Acute pyelonephritis is usually caused by what?
E. coli
Acute pyelonephritis is usually what type of infection?
Ascending, unilateral. Can rarely be blood borne
Patho of acute p
Bacteria binds to epithelial cells inside the kidneys, hard to get rid of
S/s of acute p
Differentiates from regular infection w/ high fever and CVA tenderness.
- dysuria, freq, urge, burn, nocturia
- sudden onset
- back, flank, loin pain
- abd discomfort, n/v, fatigue
Tx of acute p
ABX for 7-10 days, broad first, assume e coli
-Hospitalized for severe cases, usually preg. When admitted: urine culture, IV abx, fluids bc n/v
Chronic p is characterized by what?
Small atrophied kidneys w/ diffuse scarring
Risks for chronic p
Urinary obstruction, reflux, neurogenic bladder
Patho of chronic p
Chronic infections, interstitial inflammation, reduced number of functional nephrons
S/s of chronic p
- Minimal symptoms
- Flank pain less intense than in acute
- HTN
- UTI
- ^ creatinine
- Frequency bc inability to conserve Na
- Decreased ability to concentrate urine (nocturia)
- Hyperkalemia and acidosis
Tx of chronic p
- Correct underlying problem
- Prolonged abx (6-8 wks)
- Support existing renal function
Renal TB
TB invades kidneys through bloodstream, inflammatory response forms scar tissue that replaces normal kidney tissue, difficulty w/ elimination
Primary glomerulopathies
Only the kidney is involved
- Acute glomerulonephritis
- Chronic g
- Nephrotic syndrome
Secondary glomerulopathies
Injury due to drug exposure, infection, systemic or vascular pathology
- Lupus
- Goodpasture’s syndrome
- amyloidosis
- diabetic glomerulopathy
- hepatitis b and c
- cirrhosis
- sickle cell
- mult. myeloma
Assessment w/ acute glom
Ask if they’ve had a sore throat, BP, changes in urinary pattern, breathing patterns
Patho of acute glom
- Infection occurs
- S/s don’t appear for 10 days
- Seen a lot in men after an acute strep infection
Acute glom s/s
- Dark, tea colored urine
- Proteinuria
- Hematuria
- Edema
- HTN
- Oliguria
- Increased BUN/creat
Tx for acute glom
ABX, prevent complications, supportive care, temporary dialysis
Chronic glom progresses into what? Why?
Chronic end stage renal dz, bc nephrons atrophy, become scarred and non-functioning
S/s of chronic glom
Circulatory overload: edema, weight gain, JVD, crackles, uremia
Uremia assessment findings
Slurred speech, tremors, asterixis, *skin changes (uremic deposits=dry, flaky skin that itches) Don’t let them itch cause they’ll break their skin
Tx of chronic glom
Focuses on slowing the progression of dz (diet changes, maintaining sufficient fluids, drugs for s/s)
Nephrotic syndrome
Increased permeability of glomeruli allows bigger molecules to pass through. Leads to massive loss of protein in urine, Na follows protein, water follows Na
Main feature of nephrotic syndrome
Severe proteinuria (3.5 g protein/24 hr)
S/s of nephrotic syndrome
Hypoalbuminemia Hyperlipidemia Edema Hypercoagulability Renal insufficiency
Tx of nephrotic syndrome
Treat underlying process, renal biopsy Immunosuppressive therapy ACE inhibitors decrease proteinuria, watch for nephrotoxicity Cholesterol lowering drugs Mild diuretics Na restriction, diet changes
What is the leading cause of ESRD in the US?
Diabetes, diabetic nephropathy (microvascular damage)
What is the first manifestation of diabetic nephropathy?
Albuminuria
What would a UA reveal for acute p?
Positive leukocyte esterase and nitrite dipstick test, presence of white blood cells (WBCs) and bacteria; urine culture and sensitivity (C&S); blood cultures; C-reactive protein; erythrocyte sedimentation rate.
What is the primary care plan for a pt with acute p?
Acute pain
Tx of acute p
Nitrofurantoin (macrodantin) 50mg with meals and at bedtime is a urinary antiseptic drug that also helps w/ comfort. Fluid intake should be 2-3 L per day
Which imaging test is ordered for acute p?
IV urography or KUB x-ray
Difference in acute and chronic renal failure
Acute is potentially reversible
Acute renal failure is characterized by what?
Abrupt deterioration of renal function, happens overnight, so BUN and creatinine will be ordered every day in the hospital
Oliguria
Anuria
Pre-renal acute renal failure
- Diminished perfusion to kidney
- Decrease in blood volume
If pre-renal is uncorrected
Hypoperfusion will lead to ischemia of renal parenchyma and acute tubular necrosis
Infra-renal acute renal failure
- Acute glomerulonephritis
- Drug induced nephrotoxins (contrast media, ace inhibitors, bacterium, renal artery stenosis)
- Acute tubular necrosis (renal cellular hypoxia)
Post-renal acute renal failure
-Obstruction of normal urine outflow from kidney
Most common causes of post renal failure
BPH, kinked catheters, tumors, strictures, calculi
Which renal failure is the easiest to identify and fix?
Post-renal
Stages of acute renal failure
- Oliguric phase
- Diuretic phase
- Recovery phase
Oliguric phase
May require temp. dialysis to survive 1-2 times in a few days. Volume overload, hyperkalemia, uremia, metabolic acidosis
Diuretic phase
UOP normalizes over a few days, at risk for dehydration, not actively trying to die but thinking about it
-Hypovolemia, hypokalemia, uremia
Recovery phase
1 week to 1 year, normal creatinine is marker for full recovery
Hallmark of acute renal failure
Elevated creatinine
Signs of fluid overload
Edema, JVD, crackles, SOB
Tx of acute renal failure
- Treat underlying cause
- Optimize BP, manage fluids, support other body systems-hard to do, ventilation, vasoactive meds
Chronic kidney dz
Progressive and irrevocable loss of functioning nephrons
-75% lost before s/s
Risk factors for ESRD
Diabetes and HTN
Stages of CKD
Decreased reserve 90%
Renal osteodystrophy with CKD
High phosphorus and low calcium
Tx of CKD
ACEII/ARB to reduce proteinuria, BG control, BP control, evaluation for CV risk factors
vascath
Ventral line in IJ or subclavian, shouldn’t stay for longer than 7 days, curved or straight cath
Difference in native and gortex fistulas
Native can’t be used until 3-4 weeks, vortex clots more but can be used right away
Normal adult bladder capacity
400-500 mL
Usual urge to void
At about 150-300 mL
Post void residual normal volume
About 50 mL