Patho Renal Study Guide Review, Study Guides, Projects, Research of Urology

Patho Renal Study Guide Review

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Patho Renal Study Guide Review
1.distinguish btw lower and upper uti: above or below bladder
2.Upper urinary tract obstruction
Complications (5): Hydroureter: Dilation of the
ureters Hydronephrosis: Dilation of the renal
pelvis and calyces
Ureterohydronephrosis: Dilation of both the ureters and the renal pelvis
and calyces Tubulointerstitial fibrosis: Deposition of excessive amounts of
extracellular matrix Leads to excess cellular destruction and death of
nephrons.
3.Upper urinary tract obstruction - compensaiton measures, effect of
relieving obstruction: Compensatory hypertrophy and hyperfunction:
Partially counteracts the negative consequences of unilateral
obstruction.
Compensatory growth
Unobstructed kidney will increase in size and function, not functioning
nephrons Postobstructive diuresis
Is caused by relief of the obstruction.
May cause fluid and electrolyte imbalance.
4.Kidney Stones what are they: Are also called renal calculi or urolithiasis.
Masses of crystals, protein, or mineral salts form in the urinary tract and
may obstruct the urinary tract.
5.kidney stones risk factors: Male
Most develop before 50 years of
age Inadequate fluid intake: Most
prevalent Geographic location
Temperature, humidity, rain fall, fluid, and dietary patterns
6.kidney stone composition: Composition of mineral
salts Calcium oxalate and calcium phosphate: 70%
to 80% Struvite (magnesium, ammonium,
phosphate): 1% to 5% Uric acid: 5% to 10%
7.genetic issue that can lead to stones: Excess urine can cause
cystinuric, or xanthine, stone formation in the presence of a low urine
pH.
8.staghorn calculi: Are large and fill the minor and major calyces.
9.Non-Staghorn calculi:: variable size, located in calyces, renal pelvis,
different sites of ureter.
10.Kidney stone formation describe 3 steps: Supersaturation of one or
more salts
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Patho Renal Study Guide Review

  1. distinguish btw lower and upper uti: above or below bladder
  2. Upper urinary tract obstruction Complications (5): Hydroureter: Dilation of the ureters Hydronephrosis: Dilation of the renal pelvis and calyces Ureterohydronephrosis: Dilation of both the ureters and the renal pelvis and calyces Tubulointerstitial fibrosis: Deposition of excessive amounts of extracellular matrix Leads to excess cellular destruction and death of nephrons.
  3. Upper urinary tract obstruction - compensaiton measures, effect of relieving obstruction: Compensatory hypertrophy and hyperfunction: Partially counteracts the negative consequences of unilateral obstruction. Compensatory growth Unobstructed kidney will increase in size and function, not functioning nephrons Postobstructive diuresis Is caused by relief of the obstruction. May cause fluid and electrolyte imbalance.
  4. Kidney Stones what are they: Are also called renal calculi or urolithiasis. Masses of crystals, protein, or mineral salts form in the urinary tract and may obstruct the urinary tract.
  5. kidney stones risk factors: Male Most develop before 50 years of age Inadequate fluid intake: Most prevalent Geographic location Temperature, humidity, rain fall, fluid, and dietary patterns
  6. kidney stone composition: Composition of mineral salts Calcium oxalate and calcium phosphate: 70% to 80% Struvite (magnesium, ammonium, phosphate): 1% to 5% Uric acid: 5% to 10%
  7. genetic issue that can lead to stones: Excess urine can cause cystinuric, or xanthine, stone formation in the presence of a low urine pH.
  8. staghorn calculi: Are large and fill the minor and major calyces.
  9. Non-Staghorn calculi:: variable size, located in calyces, renal pelvis, different sites of ureter.
  10. Kidney stone formation describe 3 steps: Supersaturation of one or more salts

2 / 31 Presence of a salt in a higher concentration than the volume is able to dissolve the salt. Precipitation of a salt from a liquid to a solid state Temperature and pH Growth into a stone via crystallization or agglomeration

4 / 31 Caused by spinal cord injury, stroke, multiple sclerosis, Parkinson disease, diabetic neuropathy, aging Symptoms of weak stream, intermittency, hesitancy, straining

5 / 31

  1. Anatomic Obstructions to Urine Flow: Urethral stricture Narrowing of lumen that occurs with infection, injury, or surgical manipulation Prostate enlargement Caused by acute inflammation, benign prostatic hyperplasia, or prostate cancer Pelvic organ prolapse Cystocele descends below the level of the urethral outlet
  2. Renal adenomas: benign kidney tumors potential for malignancy
  3. Most common neoplasm: renal cell carcinoma
  4. clear cell tumor - genetics/chromosome: Mutations of the von Hippel- Lindau (VHL) gene located on chromosome 3p
  5. Non-clear cell: includes papillary, chromophobe, oncocytoma, collecting duct, and unclassified tumors
  6. Renal transitional cell carcinoma: rare and arises in the renal parenchyma and renal pelvis
  7. renal tumor clin mani: Hematuria, dull and aching flank pain, palpable flank mass in thinner individuals
  8. Bladder tumors: MC type and risk factors: Urothelial (transitional cell) carci- noma: Most common Risk factors Smoking Aromatic amines Arsenic in drinking water Phenacetin Cyclophosphamide Pioglitazone
  9. genetic componenet tumor: Oncogenes of the ras gene family and tumor-sup- pressor genes including TP53 mutations Inactivation of retinoblastoma gene (pRb) Loss of heterozygosity at Chromosome 9
  10. key sx bladder tumor: painless microscopic hematuria
  11. UTI: where does bacteria come from, how does it travel: Inflammation of the urinary epithelium caused by bacteria from gut flora Retrograde movement of bacteria into the urethra bladder, ureter, kidney
  12. Protective urinary mechanisms (7): Washed out of the urethra during micturi- tion Low pH and high osmolality of urea

7 / 31 Secretions from the uroepithelium: Bactericidal effect Ureterovesical junction: Closes to prevent reflux of urine to the ureters and kidneys. Women: Mucus-secreting glands Men: Length of the male urethra

  1. cystitis more common in: women
  2. cystitis most common pathogen: e. coli
  3. Virulence of uropathogens (3 factors/mech): Ability to evade or overwhelm the host defense mechanisms and cause disease in a host Adherence to the uroepithelium Ability to resist the host's defense mechanisms
  4. risk factors uti: Sexual intercourse History of UTI Spermicides DM (glucosuria) Prostatic hypertrophy Foley catheter
  5. why are elderly at higher risk uti: Incomplete emptying, impaired blood supply Post menopause- decreased estrogen reduces protective vaginal flora
  6. sx - uti/cystitis: Dysuria Urinary Frequency Urinary urgency Suprapubic pain EXCLUDES: fever, or symptoms of systemic illness Older/debilitated patients Falls, change in functional status, mental status -although not reliable predictors
  7. Painful Bladder Syndrome orInterstitial Cystitis: Autoimmune reaction caus- es inflammatory response. Symptoms of cystitis for longer than 6 weeks' duration but with negative urine cultures and no other known cause
  8. Pyelonephritis - what is it, clin mani, evaluation: Acute pyelonephritis Acute infection of the ureter, renal pelvis, and/or kidney interstitium

8 / 31 Clinical manifestations Flank/groin pain Fever, chills Costovertebral tenderness UTI symptoms Evaluation White blood cell casts, indicating pyelonephritis

10 / 31 Edema

11 / 31

  1. Severe or progressive glomerular disease leads to: Eventual oliguria Oliguria: Urine output <30 mL/hour
  2. Chronic Glomerulonephritis def: Glomerular diseases with a progressive course, leading to chronic kidney failure
  3. diabetic nephropathy: Develops from advanced glycosylated end products Inflammatory mediators Microvascular complications Leads to Podocyte injury Thickening/fibrosis of basement membrane Expansion of mesangial matrix leads to chronic glomerulonephritis
  4. Lupus nephritis: Inflammatory complication of the chronic autoimmune syn- drome, systemic lupus erythematosus Formation of autoantibodies against double-stranded deoxyribonucleic acid (DNA) and nucleosomes with glomerular deposition of the immune complexes
  5. Chronic Glomerulonephritis sx/clin mani: Proteinuria Microscopic hematuria edema
  6. Nephrotic Syndrome: Excretion of 3.5 g or more of protein in urine 24 hr urine protein Characteristic of glomerular injury Occurs when filtration of proteins exceeds tubular reabsorption Many causes Minimal change disease Focal segmental glomerulosclerosis Diabetes Lupus Can be idiopathic
  7. Nephrotic syndrome: Podocyte injury leads to increased permeability to pro- tein and loss of electrical negative charge Loss of plasma proteins Can lead to release of inflammatory mediators Loss of some immunoglobulins (increased infections) Stimulation of liver lipid production Sodium retention

13 / 31 Caused by increased permeability of the glomerular filtration membrane Pore sizes enlarge. Red blood cells and protein pass through.

  1. Nephritic causes: Post infectious glomerulonephritis- strep Rapidly progressive crescentic glomerulonephritis Lupus nephritis
  2. Classification of Kidney Dysfunction: Acute or chronic; reversible or irre- versible Renal insufficiency Decline of renal function to approximately 25% of normal Serum creatinine and urea mildly elevated Renal failure Significant loss of renal function End-stage renal failure Less than 10% of renal function remains
  3. Uremia: Syndrome of renal failure Elevated blood urea and creatinine levels Fatigue, anorexia, nausea, vomiting, pruritus, and neurologic changes Retention of toxic wastes, deficiency states, electrolyte disorders, and proinflamma- tory state
  4. Azotemia: Increased serum urea levels and frequently increased creatinine levels Renal insufficiency or renal failure, causing azotemia
  5. Acute Kidney Injury: Sudden decline in kidney function with a decrease in glomerular filtration and accumulation of nitrogenous waste products in the blood Increase in serum creatinine and blood urea nitrogen
  6. AKI patho: Result of Extracellular volume depletion Decreased renal blood flow Toxic or inflammatory injury to the kidney
  7. AKI prerenal: Most common Inadequate kidney perfusion hypotension hypovolemia with hemorrhage/fluid loss, MI

14 / 31 Failure to restore blood volume or pressure can cause cell injury and acute tubular necrosis Early phase - protective mechanisms maintain GFR, eventually declines d/t de- crease in filtration pressure

16 / 31 or diag- nostic procedures or when nephrotoxic drugs or contrast agents are used.

  1. Chronic Kidney Disease def and numbers: Progressive loss of renal function associated with systemic diseases

17 / 31 GFR < 60 for at least 3 months Clinical manifestations: Do not occur until renal function declines to less than 25% of normal.

  1. Causes of chronic renal failure include: Disease that effect kidneys or Kidney blood supply Glomerulopathies, hypertension, diabetes, SLE
  2. Intact nephron hypothesis: Loss of nephron mass with progressive kidney damage causes the surviving nephrons to sustain normal kidney function.
  3. 2 chemicals/hormones of body that worsen CKD: Proteinuria Contributes to tubulointerstitial injury by promoting inflammation and progressive fibrosis. Angiotensin II Promotes glomerular hypertension, and participates in tubulointerstitial fibrosis and scarring.
  4. : Glomerular hypertension Hyperfiltration Tubulointerstitial injury Fibrosis
  5. Clinical manifestations ckd: Azotemia Increased levels of serum urea and creatinine Uremic syndrome Proinflammatory state with the accumulation of urea and other nitrogenous com- pounds Toxins Alterations in fluid and electrolyte and acid-base balance
  6. side effect ckd (other system, 2 elements): Kidneys play role in electrolyte balance Helps with K excretion Less excretion so build up in blood Hyperkalemia Cardiac arrhythmias Kidney helps regulate vitamin D That helps increase calcium absorption from the diet Hypocalcemia Parathyroid hormone released Bones lose calcium Weak and brittle bones (renal osteodystrophy)

19 / 31 Seizures, coma Motor and sensory dysfunction

  1. ckd effect on endo: Endocrine and Reproductive Systems decrease in circu- lating sex steroids

20 / 31 Decreased libido Insulin resistance Low thyroid hormone levels

  1. ckd effect on skin: Anemia: Pallor Bleeding: Hematomas and ecchymosis Retained urochromes: Sallow skin color Hyperparathyroidism and uremic skin residues; irritation and pruritus with scratch- ing, excoriation, and increased risk for infection
  2. gender and incontinence: The prevalence of urinary incontinence in men is approximately half that of women. Incontinent men are half as likely as women to seek care for urinary incontinence.
  3. Urgency incontinence - what is it: Abrupt and strong desire to void Involuntary contractions of the detrusor (smooth muscle lining of bladder wall) Decreased bladder wall compliance
  4. urge incont mech: Neurologic - detrusor hyperreflexia Non-neurologic - detrusor instability
  5. Stress incontinence: Occurs with exertion, sneezing, coughing, laughing in the absence of a bladder contraction - associated with increased abdominal pressure
  6. Urethral hypermobility: insufficient support of the pelvic floor musculature and vaginal connective tissue to the urethra and bladder neck. urethra and bladder neck to lose the ability to completely close against the anterior vaginal wall. With increases in intra-abdominal pressure (e.g., from coughing or sneezing) the muscular tube of the urethra fails to close, leading to incontinence Insufficient urethral support may be related to loss of connective tissue and/or muscular strength due to chronic pressure (i.e., high-impact activity, chronic cough, or obesity) or trauma due to childbirth, particularly vaginal deliveries. urethra/sphincter not closing as it should
  7. Intrinsic sphincteric deficiency (ISD): Loss of urethral tone that normally keeps the urethra closed. This can occur in the presence or absence of urethral hypermobility and typically re- sults in severe urinary leakage even with minimal increases