Renal/Urinary Disease Flashcards

(42 cards)

1
Q

urine phosphorus cyst

A

got no clinical consequences

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2
Q

Where are the glomeruli

A

Only found in Cortex

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3
Q

Types of Renal Pathology

A
  • Congenital Malformation (10% of all birth gave this)
  • Glomerular disease
  • Tubular disease
  • Interstitial disease
  • Obstructive disease
  • Vascular disease
  • Neoplastic disease
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4
Q

Kidney Disease places

A

Intrarenal: Glomerular- Malformation & Interstitial
- Malformation: Tubular
- Interstitial: Vascular

Prerenal: Atherosclerosis, Ischemia
Postrenal: Stones, Tumors

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5
Q

Clinical SIgns of Renal Disease

A
  • Albuminura (Glomerular disease; albumin in urine)
  • Cylindruria (Worm live protein aggregat, blocking urinary flow out of the tubular)
  • Hematuria (Ominous, blood in urine => prooblem in bladder)
  • Pyuria (active infection)
  • Protenuria (any of the above excess protein)
  • Azotemia-elevated BUN and creatinine (biochemical)
  • Uremia-clinically evident azotemia (clinical sign)
  • Change (usually decrease) in GFR
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6
Q

Acute Kidney Injury (AKI)

A

In general tubular necrosis => into lumen => soft and => coagulate urine, cyliduria
- Decreased blood pH (acidosis)
- Systemic edema
- Hypertension
- Increased BUN, creattinine, K+
- Uremia
- Most common cause; Acute Tubular Necrosis (can be a problem in glomerular but not most common)
- Etiology usually ischemia (truma, surgery, childbirth), toxicant and pharmaceuticals

Recovery is good (even tho it kill epithelial lining)
- (if basal lamina remain intact => regeneration)

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7
Q

Acute Kidney Injury GFR

A

Screenshot

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8
Q

Stage I

Chronic Kidney Disease (GFR)

A

> 90 mL/min
- Normal

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9
Q

Stage 2

Chronic Kidney Disease (GFR)

A

60-89 mL/min
-Mild CKG

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10
Q

Stage 3A

Chronic Kidney Disease (GFR)

A

45-59mL/min
- Moderate CKD

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11
Q

Stage 3B

Chronic Kidney Disease (GFR)

A

30-44 mL/min
- Moderate CKD

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12
Q

Stage 4

Chronic Kidney Disease (GFR)

A

15-29 mL/min
- Sever CKD

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13
Q

Stage 5

Chronic Kidney Disease (GFR)

A

<15 mL/min
- End- stage CKD

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14
Q

Chronic Kidney Disease (GFR)

A

Irreversible at any stage

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15
Q

Chronic Renal Disease

Consequences

A

Bilateral=> Involve both kidney
Leaking => smell like urine
- Muscle Wasting (trying to gen N2)
- Uremia (breath out uric acid)
- Dry, yellow skin
- Pruritus (scratch mark all over face and chest-itchy)
- Uremic frost (uric acid form crystals around mouth)
- Nausea
- GI bleeding (too much uric acid in circulation)
- Anemia
- Decalcification of bones (calcium wasting, bone becomes soft -> hyperosita (thick bones but not strong)
- Vitamin D deficiency
- Hypertension
- Edema
- Neuropathy
- Coma, death

Progression variable, Prognosis is poor
-GFR <20-25%

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16
Q

Congenital Malformations

A
  • Agenesis/dysgenesis/alplasia (Kidney is not fully formed)
    – Bilateral: fetal death
    – Unilateral: Compensation
  • Horseshoe Kidney: (kidney remain attached)
    – Asymptomatic except in pregnant women
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17
Q

Congenital Malformation

Polycystic Kidney

A

Polycystic Kidney: Genetic

Infantile/Childhood
- Autosomal recessive, mutation of PKD1 (polyastic kidney disease 1)
– Congenital liver fibrosis

Adult:
- Autosomal dominant, mutation of PKD1 for polycystin-1, leading to Ca-induced defects of extracellular matric
– 1:500-1000 individuals
– 75% develop hypertension, 10-30% have brain aneurysms
– Not symptomatic until 4th decade

18
Q

Kidney Structure

A
  • Glomerulus
  • Tubules
    – PCTs
    – Straight segments
    – DCT
  • Interstitium
  • Vessels
  • Urine pathways
19
Q

Glomerulus

A
  • Bowman’s Capsule
  • Largely a capillary network (60mmHg)
  • Arteriole-Capillary-Arteriole
    – Efferent arteriole is smaller than afferent arteriole; help maintain post-capillary BP
  • Change in size is possible, no change in numbers (if damage, it will not regenerate instead it will compensate)
  • Most glmerular disease is IMMUNOLOGICAL
    – Immune-complex GN
    – Anti-basement membrane GN
20
Q

Nephritic Syndrome

EXAM QUESTION

A
  • Sudden onset of hematuria (Glomerular cap leaking large material)
  • Decreased GFR
  • Proteniuria (Glomerular cap leaking large material)
  • Azotemia
  • Hypertension and moderate edema
  • Classically seen in post-streptococcal GN

Underlying mechanism is inflammatory lesion of glomerulus (antibodies, antigen complexes reflected in kidney)

21
Q

Nephrotic Syndrome

A
  • Hypoalbuminema (plasma albumin <3 gm/dL)
  • Hyperlipidemia
  • Proteinuria (>3.5gm/24hr)
  • Edema/Anasarca-severe 3rd spacing
  • Lipiduria
  • Most commonly associated in children with Minimal Change Disease

Underlying cause is derangement in glomerular capillaary wall with increased permeability

22
Q

Immune Complex Glomerulonephritis

A

Circulating or fixed immune complexes (usually IgG), trapped against glomerular basement membrane
– Associated with long standing Strep infections; in most cases the infectious agen is NOT found in the kidney (circulate in blood, blocked at membrane of glomerulus)
- Activate complement WBCs through cross linking Fc receptors and decoration with Igs
- Deposition of immune complexes gives granular pattern by immunoflurescence (cause unspecific leaks)

Loss of membrane integrity follow in sever cases; most cases; esp. children, follow milder course
- Can result in progressive renal failure, most often in adults (15-50%); may take several decades to appear

Characterized by
– ABRUPT onset of hematuria
– Associated with acute nephritic syndrom

23
Q

Anti-Basement Membrane Glomerulonephritis

A

Caused by formation of auto-antibodies against glomerular basement membrane
- Deposition of immune label is linear
- Major cause is confomational change in the alpha-3 chain of Type IV collagen (only need one chain to be defective)
– Similar collagen is found in the lung; consequently kidney and lung lesion may co exist (Goodpasture disease)

Anit-GBM disease is <1% of all GN. However, the disease is very serious and often result in renal failure

24
Q

Tubules

A
  • PCT
    – Convoluted segment (most sensitive to ischemia and toxicants)
    – Pars recta (straight segment)
  • Descending and ascending loop of Henle
  • DCT
  • Excretory collecting ducts

Infectious agents => Not in kidney

25
Tubule Diseases
- Ischemia (post-surgical, truma) - Nephrotoxic (mercury, lead, antifreeze) - Drug-induced (antibiotics, diuretics) - Other primary renal disease (eg, nephritis, hypertension)
26
Acute Tubular Necrosis
Clot in lument - No passage of urine
27
Ethylene Glycol Tubule Necrosis
Antifreeze disrroys tubules - Oxylate crystals -- Need to transplant kidney
28
Tubulo-Interstitial (Connective tissue in between) Disease
- Interstitial nephritis-nonbacterial - Pyelonephritis (acute/chronic)-bacteria - Drug-induced nephritis -- Analgesic nephropathy-generally multiple drugs: phenacetin, aspirin, acetaminophen --- Immune case likely Type I hypersensitivity, more rarely Type IV -- Antibiotic nephropathy: sulfonamides, synthetic penicillins, rifampin, NSAIDs, AmphoB
29
Pyelonephritis
Caused by infection, ascending infections; most commonly E.coli or other gram negative bacteria or hematogenous infection (less common) (Fever, flank pain, pyuria) - Can be acute or chronic (chronic can lead to chronic renal failure) - Antibiotics successful but reinfection is common - More common in females (10:1); incidence in males increase with onset of prostate disease Associated with: - UTIs - Sexual activity - Obstruction (stones, BPH, tumors) - Diabetes - Vesicoureteral reflux (VUR)-ascending infections - UT mainpulation (catheterization). Candida common organism - Pregnancy - Immunosuppression/immunodeficiency
30
Vessels
Ischemia(most commonly thrombo) emboli, often from recent MI with mural thrombi, or hypovolemia Hypertension, particularly when coupled with diabetes - Essential hypertension is very common, will cause wide-spread renal injury and symmetrical atrophy - Malignant hypertension-much less common -- Extremely serious. BP>200/120 mm -- Requires prompt, aggressive medical intervention -- Will cause renal vascular injury; may cause stroke -- Even with treatment, 5-year survival 50% Arteriolonephrosclerosis: caused by hypertension Hyaline degeneration of artery/arteriole walls *Virtually all kidney disease will secondarily affect renal vessels*
31
Renal Hypertension
Benign Hypertension - Major target: Small arterioles - Cause vessel narrowing and medial thickening - Resulting ischemia (from narrowing) leads to interstitial fibrosis, tubular atrophy, glomerulosclerosis - Cortical surface is finely granular, capsule is adherent - Cause some degree of functional effect, such as decreased GFR Rarely a direct cause of death except in African Americans via uremia and renal failure
32
Malignant Hypertension
Retina of patient - Hemmorage of retina vesse | Not much was there
33
Urine Pathway Obstruction
Infection Stones Carcinoma Prostatic hperplasia (males)
34
Kidney Stones (Urolithiasis)
Common: 5-10% of individuals during lifetime; M>F - 80% are calcium stones - Magnesium ammonium phosphate stones (10%) -- Associated with urea splitting organism such as Proteus ssp. -- Both associated with persistently alkaline urine - Uric acid and cysteine stones (6-9%) seen with acidic urine Generally unilateral (80%), but may be multiple in that kidney - Tendency to form stones are familial - Occur in setting of urine stasis, infection, metabolic disease, change in urinary pH, urothelial trauma; whenever conditions of super-saturation exist - Often present with flant pain radiating to groin and gross hematuria (termed renal colic) May pass spontaneously if small; surgery or lithotrips may be required if large and cause obstruction - Long term obstruction may lead to hydronephrosis and predisposes to recurrent bacterial infection
35
What type of stone is associated with acidic urine
Uric acid and cysteine stones (6-9%)
36
Renal Cell Carcinoma
Most arise from tubular epithelium - Most common in males (2X) in 6th-7th decade; 2-3% of all cancers; Overall mortality is 40% - Tobacco strongest risk factor. Genetic factors associated (loss or inactivation of von Hippel-Lindau gene VHL) on chromosome 3p - Incidence greatly increased (>30x) with chronic dialysis and associated polystic disease - Present with painless hematuria, flank pain and palpable mass - Cancer present in multiple histological forms with distinctly different prognoses - May give many forms of paraneoplastic signs-polycythemia, hypercalcemia, change in secondary sexual characteristics, hypertension, fever of unknow orign - Frequenly have metastasized to lung and/or bones when found - Metastases may resolve (rarely-not cured) with removel or primary tumor (doesn't response to chemo or radio therapy)
37
Wilms Tumor (Nephropblastoma)
Treatable by chemo and radiation - young children under 4 Blastoma in name mean embronic
38
Disease of Urinary Bladder
Cystitis and UTIs are primarily a disease of adults - Most common cause of cystitis is bacterial infection: E. coli, Proteus, Klebsiella, Enterobacter. Also fungi, and Schistosoma in the middle east - Associated with diabetes, obstruction, theraputic radiation, catheterization - Bladder infection is more common in women - May give rise to ascending pyelonephritis - Symptoms: frequency (every 15-20 min), lower abdominal pain, and dysuria
39
Bladder Cancer | *Urothelial Cancer* is preferred but *Transitional cell* is frequent
Present as painless hematuria with M:F ratio of 3:1 (50-80 age) - B-naphthylamine increase risk 50x - Smoking is the most common risk factor - Tumor penetrates bladder wall and has a high recurence rate (5-year survival 60%) Cause of death is urinary obstruction rather than metastasis
40
Urothelial Cancer | Ureters and renal pelvis
Rarer than bladder but have poorer prognosis with <10% and 50% 5-year survival In areter => prognosis terrible <10% survival
41
Prostate Gland
Exocrine gland which surrounds the proximal urethra - Hyperplasia occurs in the periurethral transition zone - Cancer arises in the periphery of the gland - Hormone responsive - Supplies 20-30% of seminal vol; semen is slightly alkaline to neutralize pH in vagina; this prolongs it's life - Prostate secretes PSA - Normal: 11 grams Skene glands of female are classified as female prostate glands; skene glands produce PSA
42
Benign Prostatic Hyperplasia | BPH
Frequency increase with age; by 80 years, 90% of males will have BPH - Result from action of both androgens and estrogen - DHT (produced by action of 5a-reductase) is a major mediator of prostate - Weak urinary stream, hesitancy, urgency frequency, incomplete bladder emptying, nocturia, incontinence, UTI - May cause urinary obstruction - Does not progress to cancer