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SYSTEMIC PHARMACOLOGY > Urogenital - anatomical disorders > Flashcards

Urogenital - anatomical disorders Flashcards

1
Q

congenital malformations

A

abnormalities in size/number

  • Renal Agenesis
  • Renal Hypoplasia

abnormalities in shape/position

  • kidney displacement
  • Horseshoe Kidney
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2
Q

renal agenesis

  • definition
  • bilateral vs unilateral occurrence and consequence
A

Lack of metanephric primordium (for kidney development)/
failure of ureteral bud development/
failure of contact of ureteral bud and metanephros
-> missing kidney

  • Bilateral:
    Incompatible with life - stillborn. Rare.
    Male : Female = 25 : 1
  • Unilateral :
    Male : Female = 2 : 1
    Opposite kidney usually enlarged due to compensatory hypertrophy
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3
Q

Renal hypoplasia

  • gross features
  • micro features
A

Reduced number of lobules and calyces (<5) (normal >10).
Small kidney
- Microscopic: Primitive glomeruli and tubules in dense fibrous or fatty interstitium.

Renal hypoplasia with oligomeganephronia:
small kidney w/ hypertrophied glomeruli

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4
Q

displacement of kidneys

  • location
  • complications
A
  • Above pelvic brim/ within the pelvis.

Complications:
- Kinking or tortuosity of ureters -> obstruction -> urinary infection

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5
Q

horseshoe kidney

  • definition
  • complication
A

2 kidneys fused together
- most commonly at the lower poles
- renal calculi (kidney stones)
cause urine in conjoint area will have problem draining

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6
Q

cystic kidney diseases (5)

A
  • Cystic renal dysplasia
  • Polycystic kidney disease
    - > Autosomal dominant (adult)
    - > Autosomal recessive (childhood)
  • Medullary cystic disease
  • Acquired cystic disease (dialysis associated)
  • Localized (simple) renal cysts
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7
Q

cystic renal dysplasia

  • cause
  • association
A

Due to abnormal metanephric differentiation, with persistence of primitive / abnormal structures.

  • May be unilateral or bilateral.
  • May be associated with other abnormalities such as ureteric atresia (non-functioning kidney) or agenesis (missing kidney)
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8
Q

cystic renal dysplasia

- gross and micro appearance

A
  • Usually enlarged, irregular in shape and multi-cystic
  • Lobar disorganisation
  • Multiple cysts lined by flattened epithelium
  • Presence of primitive / immature structures:
    Islands of undifferentiated mesenchymal cells/ cartilage tissue/ Primitive ductal structures
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9
Q

Autosomal-Dominant (Adult) Polycystic Kidney Disease

  • location
  • pathogenesis
  • complication
A
  • bilateral
  • start off as small cysts which gradually enlarge
  • Eventually, the kidneys are composed almost entirely of cysts, with very little parenchyma remaining (Each kidney may weigh up to 4 kg - cause of the weight of the cysts)
  • caused by mutations in PKD1 and PKD2 genes (code for the proteins polycystin-1 - PC1 - and polycystin-2 respectively)
  • deterioration of renal function over time -> renal failure (usually in mid to late adulthood)
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10
Q

Polycystic Kidney Disease

- gross and histo appearance

A
  • abdominal swelling
    thin residual parenchymal, rest of kidney filled w/ cysts
    be careful when palpating!!

flattened cuboidal epithelium

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11
Q

urolithiasis

  • definition
  • location
A

Formation of a calculus or calculi (stones) within the urinary tract
begins in the calyces and pelvis; some calculi develop in the lower urinary tract.

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12
Q

causes of urolithiasis

  • primary
  • secondary (4)
A
  • primary: supersaturation of the urine with crystalline material; most commonly calcium salts

secondary causes:
- Urinary tract infection:
Crystalline material encrust on a necrotic focus on mucosa calyx, pelvis or bladder.
- Indwelling catheter or foreign body in the bladder
- Vitamin A deficiency -> squamous metaplasia of upper urinary tract mucosa
- Low urinary pH -> formation of uric acid stones

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13
Q

types of renal calculi (stones) (4)

A
  • calcium oxalate**
  • “triple stones” - magnesium ammonium phosphate**: caused by infection
  • urate** (from uric acid): gout/leukemia pts
  • cystine**: genetic defect in renal transport
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14
Q

calcium oxalate stones formation cause

A

due to supersaturation secondary to hypercalciuria

due to:

  • idiopathic (55%) causes
    • > Absorptive hypercalciuria: hyperabsorption of calcium from the intestine, with prompt increased renal output without hypercalcaemia
    • > Renal hypercalciuria due to intrinsic impairment in renal tubular reabsorption of calcium
  • associated hypercalcaemia (hyperparathyroidism/ diffuse bone disease/ vitamin D intoxication/ sarcoidosis/ milk-alkali syndrome/ renal tubular acidosis of Cushing’s syndrome)
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15
Q

‘triple stones’ = magnesium ammonium phosphate

  • cause + pathogenesis
  • size
A

caused by infection by urea splitting bacteria (Proteus sp.)
Urea -> ammonia: urine becomes alkaline
-> precipitation of magnesium ammonium phosphate salts.

  • As the amount of urea is large, the stones tend to be huge (staghorn calculi)
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16
Q

complications of calculi (renal crystals) formation (6)

A
  • Urinary stasis
  • Ulceration
  • Bleeding
  • Infection
  • Pain
  • Fistula formation: cause of ulceration through wall -> communicate w/ other structures
17
Q

Disorders of renal TUBULES / interstitium

A
  • Acute tubular necrosis (ATN)
  • Acute interstitial nephritis (AIN)
  • Acute pyelonephritis
  • Chronic pyelonephritis
  • Xanthogranulomatous pyelonephritis
  • Tuberculosis
  • Sarcoidosis
  • Neoplastic infiltrates (leukemias, myeloma, etc.)
18
Q

acute tubular necrosis (ATN)

  • what is it
  • reversible?
A

Common cause of acute renal failure.
- Tubular epithelial cell injury / death, resulting in reduction / loss of tubular function.
- Reversible: damaged / dead tubular epithelial cells can be replaced by regenerating residual viable cells.
Not associated with necrosis of glomeruli or adjacent renal cortical tissue (unlike zonal infarction of the kidney or renal cortical necrosis)

19
Q

3 phases of acute tubular necrosis (ATN)

A
  1. Oliguric phase: Renal failure, oliguria
  2. Polyuric phase: Polyuria, tubular cells regenerating
  3. Recovery phase: Renal function recovering
20
Q

causes of acute tubular necrosis (ATN)

2 types of causes

A
  • Ischaemic causes: result in hypotension and/or hypovolaemia, which leads to *reduced renal perfusion:
    1. Shock
    2. Haemorrhage
    3. Major surgery
    4. Severe burns
    5. Dehydration
    6. sepsis
  • Toxic causes: cause direct damage to tubular cells
    1. Endogenous products: Myoglobin, haemoglobin.
    2. Drugs
    3. Heavy metals eg. Lead, mercury.
    4. Organic solvents
21
Q

ATN histo features

A

tubular epithelial cells:

  • Swelling
  • Vacuolation
  • Flattening
  • Sloughing
  • Loss of PAS-positive brush border
  • Necrosis
  • tubular dilation
  • interstitial edema
22
Q

Acute Interstitial Nephritis (AIN)

  • cause
  • presentation + investigation
A
  • Mainly due to drugs
  • toxins, metabolic causes, autoimmune disease, infections (nonkidney) and idiopathic
  • Patients present with variable degrees of renal impairment, often acute renal failure.
  • Urinalysis: may show RBCs, WBCs and eosinophils + proteinuria
23
Q

Drug-induced Acute Interstitial Nephritis

  • pathogenesis
  • symptoms (+ how long does it take for effect to present)
A

form of allergic or T-cell mediated hypersensitivity reaction.
Most common drugs that cause AIN: antibiotics, diuretics, NSAIDs

Symptoms usually develop 1-2 weeks after starting the drug
- fever, rash, haematuria, proteinuria and eosinophilia (blood +/- urine), with renal impairment/failure

24
Q

acute pyelonephritis

  • what is it
  • cause
A

pyelonephritis = bacterial infection -> inflammation

Bacteria may derive from:

  1. Ascending spread from bladder (more common)
    - Lower urinary tract obstruction (stone, enlarged prostate, tumour, etc)
    - Vesicoureteral reflux (VUR) - bladder back to ureters
    - Diabetes mellitus (glucose always increases risk of attracting bacteria)
    - Pregnancy
  2. Haematogenous spread (less common)
25
Q

acute pyelonephritis

  • clinical features (5)
  • complications
A

Clinical features

  • Chills, fever
  • Flank tenderness and pain
  • Dysuria
  • Frequency of micturition
  • Often >100,000 / ml bacteria in urine
  • Pyuria (pus in urine)

Complications

  • Acute renal failure
  • Septicaemia
  • Pyonephrosis (pus collection in renal pelvis)
  • Perinephric abscess
26
Q

chronic pyelonephritis

- causes (2)

A
  • Vesico-ureteric reflux
  • Obstruction at any level below the kidney

causes recurrent kidney inflammation and progressive scarring
Usually begins in childhood

27
Q

Xanthogranulomatous pyelonephritis

- gross and micro appearance

A
  • Enlarged kidney, replaced by yellow nodules with firm, grayish white tissue
  • Macrophages with vacuolated cytoplasm (foam cells), giant cells, lymphocytes and plasma cells
28
Q

possible causes of obstruction of urinary system

A

Congenital Anomalies:

  • Urethral valves/strictures
  • Bladder neck obstruction
  • Uretero-pelvic junction narrowing or obstruction.

Acquired Obstruction:
- Benign prostatic hypertrophy
- Renal calculi (kidney stones)
- Tumours – carcinoma of prostate/ cervix/ uterus/ bladder
- Inflammation of prostate/ ureter/ urethra.
Sloughed papillae or blood clots.

Functional disorder:
- Neurogenic (spinal cord damage)

29
Q

hydronephrosis

  • definition
  • pyonephrosis
A

Dilatation of renal pelvis and calyces with progressive enlargement of the kidney with parenchymal atrophy due to obstruction of urine outflow

dilated calyces contain pus

30
Q

hydronephrosis

- gross and histo features

A

Gross:

  • Kidney is enlarged
  • dilation of calyces
  • thinning/ atrophy of renal cortex

Microscopy:

  • Tubules and Bowman’s spaces are dilated
  • tubular epithelium is flattened
  • tubular atrophy with fibrosis
  • disappeared glomeruli

SYSTEMIC PHARMACOLOGY (22 decks)

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