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Patho > Renal/Urinary Disease > Flashcards

Renal/Urinary Disease Flashcards

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
Q

Tubule Diseases

A
  • Ischemia (post-surgical, truma)
  • Nephrotoxic (mercury, lead, antifreeze)
  • Drug-induced (antibiotics, diuretics)
  • Other primary renal disease (eg, nephritis, hypertension)
26
Q

Acute Tubular Necrosis

A

Clot in lument
- No passage of urine

27
Q

Ethylene Glycol Tubule Necrosis

A

Antifreeze disrroys tubules
- Oxylate crystals
– Need to transplant kidney

28
Q

Tubulo-Interstitial (Connective tissue in between) Disease

A
  • 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
Q

Pyelonephritis

A

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
Q

Vessels

A

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
Q

Renal Hypertension

A

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
Q

Malignant Hypertension

A

Retina of patient
- Hemmorage of retina vesse

Not much was there

33
Q

Urine Pathway Obstruction

A

Infection
Stones
Carcinoma
Prostatic hperplasia (males)

34
Q

Kidney Stones (Urolithiasis)

A

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
Q

What type of stone is associated with acidic urine

A

Uric acid and cysteine stones (6-9%)

36
Q

Renal Cell Carcinoma

A

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
Q

Wilms Tumor (Nephropblastoma)

A

Treatable by chemo and radiation
- young children under 4

Blastoma in name mean embronic

38
Q

Disease of Urinary Bladder

A

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
Q

Bladder Cancer

Urothelial Cancer is preferred but Transitional cell is frequent

A

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
Q

Urothelial Cancer

Ureters and renal pelvis

A

Rarer than bladder but have poorer prognosis with <10% and 50% 5-year survival
In areter => prognosis terrible <10% survival

41
Q

Prostate Gland

A

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
Q

Benign Prostatic Hyperplasia

BPH

A

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

Patho (17 decks)

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