Renal Disorders Flashcards
Pyelonephritis: Upper UTI, Kidney Infection
– Inflammation of the kidneys
– Etiology: Ascending infection or bloodstream infection
– Risk factors: pregnancy, recurrent lower UTIs, antibiotic resistant strain
– Inflammatory response → kidney tissue DAMAGE
– Abscesses and necrosis can develop impairing renal
function
Pyelonephritis: Clinical Manifestations
Sudden onset:
* Fever
* Chills
* CVA tenderness
Lower UTI symptoms (dysuria)
Hematuria may occur
Accompanying symptoms:
* N/V
* Anorexia
Pyelonephritis: Treatment
Antibiotics: trimethoprim/sulfamethoxazole [Bactrim], ciprofloxacin, nitrofurantoin [Macrobid]
Pyelonephritis: Complications
Complication: urosepsis
– More likely in elderly
– Severe systemic response
– High mortality rates
Nephrolithiasis/renal obstruction Locations
– Renal Pelvis
– Ureter
– Bladder or Pelvis
– Blockages in any point of the
‘plumbing’ system prevents the flow
of the liquid causing the system to
back up
Obstruction Causes
Renal Pelvis: Renal calculi (stones)
Ureter: Renal calculi, preganancy, tumors
Bladder and Urethra: Bladder cancer, nerogenic bladder, prostatic hyperplasia, prostate cancer, urethral strictures
Complication of obstruction
Stasis of urine flow
Back-up presssure
-Hydroureter
-Hydronephrosis
-Postrenal acute kidney injury
Manifestations of Acute Obstruction
Depend on the
* Site
* Cause (ex., kidney stones, prostate problems)
* Speed of onset
Which factor primarily
determines severity of pain?
Nephrolithiasis
Definition, size, shape
Definition: Renal calculi or “kidney stones”
-clumps of crystals in the urinary tract
-most common cause of renal obstruction
Size: small as a grain of sand
Shape: may be smooth or jagged
Nephrolithiasis: Pathogenesis
Urine is a solution of solvent (water) and
solutes (particles)
Problem: Super-saturation with a solute
– Crystals begin forming in the NEPHRON
Crystal formation is enhanced by:
– PH changes: example: UTI
– Excessive concentration of insoluble salts in the urine (dehydration, bone disease, gout, renal disease)
– Urinary Stasis - immobility/sedentary lifestyle
Nephrolithiasis: Risk Factors
– Sex: Men (for now)
– Age: 20s – 30s
– Race: white
– Family history
– Congenital defect
– Weather?
– Obesity
Types of kidney stones
-Calcium oxalate
-Calcium phosphate
-Struvite (staghorns)
-Uric acid
Calcium oxalates/Calcium phosphate kidney stone
-Incidence and specific risks
Incidence: 70-80%
Specific risks: family history, idiopathic
-High calcemia
-High oxaluria
Struvite kidney stone
-Incidence and specific risks
Incidence: 15%
Specific risks: Urinanry tract infection
Uric acid kidney stone
-Incidence and specific risks
Incidence: 7%
Specific risks: gout
Nephrolithiasis: Clinical Manifestations (Pain)
Pain of Acute Renal Colic:
– location – “flank”
– radiation – “lower abd and groin”
– spasms – “colicky” last 20-60 minutes
– intermittent - ”ureter spasms”
– sharp - “calculi scrape the ureter wall”
Nephrolithiasis: Pharmacotherapy
Acute Pain:
-Morphine
-IV fluids
Preventive meds:
* Calcium = thiazide diuretics
* Struvite = antibiotics
* Urate = allopurinol (covered in gout lecture)
Nephrolithiasis: Clinical Manifestations (symptoms)
Accompanying symptoms:
– N/V
– Dysuria
– Chills, Fever (ONLY if infection is present)
– Hematuria
– Foul smelling urine
– Diaphoresis
Urologic Cancers: Kidney
-Risk factors
Risk factors:
– Smoking
– Obesity
– Age
– Male
– Genetics
– Prognosis depends on metastasis
-Renal Cell Carcinoma (85%)
Renal Cell Carcinoma: Clinical manifestations &
Treatment
Early manifestations: none
Late manifestations:
– CVA tenderness
– Hematuria
– Possible palpable abdominal mass
Metastasis usually occurs to bone or lung
Usually resistant to chemo but surgery to remove kidney likely
Urologic Cancers: Bladder
– Risk factors:
– Smoking*
– Male
– Occupations with exposure to toxins
– Low fluid intake
Fourth most common cancer in men
Urothelial carcinoma (>90%)
Bladder Cancer: Clinical Manifestations & Treatment
Early symptoms:
– Hematuria
Later symptoms:
– Frequency
– Urgency
– Dysuria
Chemotherapy (depends on the stage!)
– Stage 1 = Intravesical chemo
– Advanced stages = Systemic chemo
BCG Vaccine: Intravesical Therapy
Indication and MOA
For early stage bladder cancer
– Given weekly for 6-12 weeks
– MOA: stimulates inflammatory response in the bladder
(goal is for immune system to recognize cancerous cells
and attack)
BCG Vaccine: Intravesical Therapy
Adverse Effects and Patient Education
Adverse effects: bladder irritation, systemic infection
– Patient instructions:
1. Empty bladder
2. Instill BCG vaccine into the bladder [dwell time 2
hours]
3. Change position q 15 minutes
– Disinfect urine for 6 hours post treatment; watch for
infection
Glomerulonephritis: Definition
Definition: A variety of conditions that cause inflammation of glomeruli
Can be focal or diffuse
3rd leading cause of kidney failure in the U.S.
Primarily an IMMUNE process
Glomerulonephritis: Where does the damage occur?
Glomerulus
– Delicate network of arterioles within the Bowman’s capsule
Tubules
– Massive consumer of oxygen
3 capillary membrane layers of the glomerulus
- Endothelium
- Basement membrane
- Podocytes (special epithelial cells)
Type II vs. Type III
Type II and Type III both have immune complexes, but they are different because:
– Type II- reactions occur on the cell surface and result in direct cell death or malfunction
– Type III- immune complexes are deposited into tissues and the resulting inflammation destroys the tissue
Etiology of Glomerulonephritis
Two types of injury:
1. Antibodies attach to antigens of the glomerular basement membrane (“anti-GBM antibodies”) - 5%
2. Antibodies react with circulating antigens and are deposited as immune complexes in the GBM – 90%
BOTH forms have this in common:
– Accumulation of antigens, antibodies, and complement
– Complement activation results in tissue injury
Acute Glomerulonephritis
-Manifestations
Abrupt sudden onset
Manifestations: HARP
–(H)ematuria
-(A)zotemia
–(R)etention: sodium & water [oliguria] (hypertension, edema)
– (P)roteinuria
Acute Glomerulonephritis: Triggers
Post-Infectious
– Poststreptococcal infection
– Nonstreptococcal infection
– Bacterial, viral, parasitic
Primary Disease
– Berger disease
Multisystem Disease
– Goodpasture syndrome, systemic lupus
erythematosus (SLE), vasculitis
Chronic Glomerulonephritis
– Long term inflammation of the glomerulus –> scar tissue
– Clinical Manifestations like presentation of acute
glomerulonephritis
Prognosis
– Slow progressive destruction –> ESRD
Nephrotic Syndrome
Definition:
– The glomerulus is too permeable to plasma proteins
– Elimination of >3 grams of protein per day
Etiology:
– Glomerulonephritis
– Diabetes mellitus
Nephrotic Syndrome: Pathogenesis
- Increased glomerular permeability
- Proteinuria
- Hypo-albuminemia
Nephrotic Syndrome: Clinical Manifestations
Edema
Hypertension
Liver Problems
–Hyperlipidemia
–Hypercoagulation
–Loss of antithrombin III and plasminogen
Glomerulopathy: Diabetes & Hypertension Complications
Diabetic Nephropathy
– Major complication
– Gross thickening of the GBM
– Ultimately leading to –> ESRD
Hypertensive Glomerular Disease
– Decreased renal perfusion –> sclerotic glomerular changes
Glomerulopathy: Manifestations
Hematuria
Oliguria
Fluid retention
Increased BUN/Cr ratio
Proteinuria
Low albumin [hypoproteinemia]
