PATH 3000 > Urinary System > Flashcards

Urinary System Flashcards

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1
Q

Antidiuretic hormone function

A

Stimulates water uptake in the distal convoluted tubule

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2
Q

Atrial naturietic factor function

A

Stimulates renal sodium and water loss

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3
Q

Parathyroid hormone function

A

Calcium reabsorption

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4
Q

Aldosterone function

A

Increase sodium reabsorption which increases body fluid volume

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5
Q

Renal agenesis

A

Condition where kidneys fail to develop in utero: bilateral is fatal shortly after birth.

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6
Q

Horseshoe kidney

A

Kidneys fused a the lower pole causing them to sit lower in the abdomen. More prone to complications.

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7
Q

Gross appearance of polycystic kidney disease

A

Massive enlargement, parenchymal replacement by cysts of varied size about 3-4cm in size.

Replacement of kidney tissue with cysts.
250g —> as heavy as 4kg.

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8
Q

Microscopic appearance of polycystic kidney disease

A

Cysts arise anywhere in the nephron, epithelial lining, interstitial inflammation and fibrosis.

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9
Q

Clinical presentation of autosomal dominant polycystic kidney disease

A

Develop symptoms of renal failure by 40-50 years.
Present with hematuria, oliguria, and flank pain.

usually accompanied by cysts in other organs.

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10
Q

Gene associated with ADPKD

A

85% Polycystin-1

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11
Q

Cystic renal dysplasia cause

A

Pediatric, sporadic, non-familial disorder to an abnormality in metanephric differentiation.

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12
Q

Histology of cystic renal dysplasia

A

Immature ducts surrounded by undifferentiated mesenchyme often with focal cartilage, abnormal lobar organisation

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13
Q

Gross appearance of cystic renal dysplasia

A

Unilateral (usually) or bilateral, kidneys enlarged and multiple cysts.

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14
Q

Clinical presentation of cystic renal dysplasia is usually associated with what?

A

Ureteropelvic obstruction, uretral agenesis or atresia and other abnormalities of the lower urinary tract

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15
Q

Three most common causes of abdominal masses in infants

A

Multicystic renal dysplasia, wilms’ tumour, neuroblastoma of the adrenals

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16
Q

Most important local symptoms of kidney disease

A

Changes in urine volume (polyuria or oliguria) and composition (hematuria, glucosuria, pyuria)

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17
Q

Most important systemic symptoms of kidney disease

A

Fever and malaise (infections) and uremia

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18
Q

Uremia

A

Characterised by an accumulation of various metabolites in the blood such as creatinine, uric acid, and ammonia.

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19
Q

Overview of symptoms of glomerular diseases

A

Acute renal failure
Nephritic syndrome
Nephortic syndrome
Isolated hematuria and/or proteinuria

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20
Q

What is nephrotic syndrome?

A

Damaged glomeruli leak protein into the urine, resulting in low blood albumin, high blood cholesterol, and severe edema (swelling), particularly in legs, feet, and around the eyes

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21
Q

What is nephritic syndrome?

A

Characterized by sudden inflammation of the glomeruli, leading to hematuria (blood in urine), hypertension, reduced urine output (oliguria), and mild-to-moderate proteinuria

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22
Q

Nephrotic syndrome presentation

A

Typically patients develop hyperlipidemia and lipiduria

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23
Q

Nephritic syndrome presentation

A

Patients typically acutely develop hematuria and oliguria, which is caused by inflammatory lesions of glomeruli.

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24
Q

A 40-year-old man noticed brown-red urine and, over 6 days, stopped urinating altogether. What is the probably diagnosis?

A

The man had acute oliguria that evolved into complete anuria. It is not possible to determine the cause without further studies, but one could speculate it is crescentic glomerulonephritis

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25
Mechanism of crescentic glomerulonephritis
Severe glomerular injury (focal necrosis of capillaries) accompanied by the formation of a fibrinous exudate inside the bowmans capsule.
26
Complications of crescentic glomerulonephritis
No blood flows through the capillary loops causing patients to develop anuria and acute renal failure.
27
Cause of crescentic glomerulonephritis
Typically in patients with basement membrane disease (Goodpasture’s). Also granulomatosis with polyangitis (GPA or wegeners granulomatosis) which is positive for ANCA antibodies.
28
A 4-year-old child developed puffiness around the eyes and became chronically sleepy 2 weeks after an episode of "strep throat." The mother noted that the child's urine was dark brown and was being excreted in small amounts. What is the probable diagnosis?
• acute postinfectious glomerulonephritis. • Edema, hematuria and oliguria that develop 2 weeks after strep suggest acute postinfectious glomerulonephritis. The child is somnolent, attributable to brain edema caused by hypoalbuminemia or hypertension.
29
Normal amount of protein excretion in urine
mg.
30
Acute glomerular nephritis
Immune-mediated inflammation of the glomerulus that occurs 1-2 weeks following acute infection.
31
Presentation of acute glomerularnephritis
Generalised edema, proteinuria, hematuria, oliguria, and hypertension.
32
Mechanism of acute glomerulonephritis caused by strep infection
Deposition of immune complexes in the basement membrane that stimulate release of renin, leads to hypoalbuminia.
33
Overview of membranous nephropathy
Most common cause of the nephrotic syndrome, peak age between 30-50.
34
Mechanism of membranous nephropathy
Immune-mediated glomerulopathy characterised by thickening of the basement membrane secondary to deposition of immune complexes.
35
Lipoid nephrosis overviiew
Most common cause of nephrotic syndrome in children, AKA minimal change disease.
36
Lipoid nephrosis mechanism
Nephrotic syndrome with hyperlipidemia and lipiduria. Fusion of foot processes seen by EM.
37
Diabetic glomerularsclerosis
Increased blood sugar leads to nonenzymatic glycosylation. Thickening of basement membranes.
38
Macroscopic features of end-stage glomerulopathy
Kidneys appear symmetrically shrunken, with fine surface granularity caused by loss of renal tubules.
39
Microscopic features of end-stage glomerulopathy
Hyalinisation of glomeruli, tubular atrophy, and interstitial fibrosis.
40
Mercury effect on renal tubules
Necrosis of proximal tubules. Tubular backleak, sloughed cells, interstitial inflammation.
41
Acute tubular necrosis
Sudden decrease in arterial pressure leads to acute hypo-perfusion of the kidneys
42
Nephroangiosclerosis
Decreased blood flow due to renal artery atherosclerosis which leads to ischemic glomerulosclerosis and loss of glomeruli and tubular atrophy.
43
Calcium urinary stone composition
Calcium phosphate or calcium oxaloacetate stones 75%
44
Struvite stone composition
Magnesium ammonium phosphate or sulfate, associated with urinary tract infections
45
Uric acid stone compositions
Associated with hyperuricemia or gout
46
Cytsine stones
In patients with inborn errors of amino acid metabolism such as cystinosis
47
Appearance of struvite stones
Irregularly shaped stones in the renal pelvis.
48
Most common predisposing conditions for ascending UTIs
Nodular prostatic hyperplasia, urolithiasis, bladder catheterisation, and pregnancy.
49
Appearance of acute pyelonephritis
Affected kidney appears swollen and pale. Visible microabscesses.
50
Appearance of chronic pyelonephritis
Destruction of the renal parenchyma, shrinkage. Kidney becomes small and irregularly shaped.
51
Appearance of acute cystitis
Congestion and mucosal hemorrhage in the bladder. May be ulcerated or covered with pus. Patitents present with fever, pain, hematuria, and pyuria.
52
Appearance of chronic cystitis
Considerable mucosa thickening, ulceration, hemorrhage, stone formation. Cannot hold much urine.
53
Causes of cytitis men
Elderly men as a complication of nodular prostatic hyperplasia
54
Compare cystitis in women
Bacterial cystitis may be associated with sexual intercourse and pregnancy.
55
Wilms tumour overview
Childhood tumour composed of immature cells resembling fetal tubules, glomeruli, or renal blastema
56
Clinical features of renal cell carcinoma
Hematuria, typical triad, nonspecific symptoms and paraneoplastic syndromes.
57
Microscopic appearance of clear cell renal carcinoma
Tumour cells with clear cytoplasm rich in glycogen and fat with capillary proliferation.
58
Genetic mutation related to wilms tumour
Deletion or mutation of two tumour suppressor genes WT1 and WT2
59
Gross appearance of wilms tumour
Hemorrhagic and necrotic solid tumour, uninvolved kidney.
60
Gross appearance of wilms tumour
Immature structures. Blastemas, primitive tubules, loose stroma.
61
Function of urothelium (transitional epithelium)
Specialised epithelium that can withstand prolonged exposure to urine
62
Main symptom of urinary tract tumours
Hematuria
63
Risk factors of urinary tract tumours
Smoking, occupational exposures, analgesic drugs (phenacetin), schistoma hematobium
64
Classifications of urothelial carcinomas
Papillary Invasive papillary Flat Flat invasive
65
A 60-yr-old man notices blood in the urine. What should the workup include?
Send urine for cytologic examination to determine presence of tumour cells. Cytoscopy to determine whether the urinary bladder contains tumours or stones, or if it is only inflamed.
66
Macroscopic appearance of bladder cancer
Localised of diffuse thickening of the mucosa with papillary growth formation. Characteristic fungating (cauliflower) look.
67
Bladder cancer staging
Diagnosis made on urine cytology and cytoscopic biopsy. Based on invasion
68
Urothelial carcinoma of renal pelvis
Associated with lower urinary tract tumours, histological similarity to urothelial carcinomas of the lower tract.
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