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Flashcards in Urinary pathology Deck (27)
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1
Q

How does a UTI present?

A

Dysuria, frequency, smelly urine
Very young - unwell, failure to thrive
Old - incontinence, off their feet

2
Q

What are the features of a normal urinary tract?

A

Constant trickle of water from ureters into bladder
Increasing pressure from bladder closes off ureter and stops reflux of urine
Low pH, high osmolality, high ammonia normal content
Prostatic secretions are bacteriostatic
Anti-bacterial antibodies

3
Q

Why do you take a mid-stream urine sample?

A

All bar terminal urethra sterile (due to terminal urethera flora, urine sample always contaminated. Take midflow - urethral flora diminished, but always present)
Will always have flora, never have negative result
Difficult to collect in young children/elderly

4
Q

What are the causative agents of a UTI?

A
Mostly gut flora, especially e.coli
Viral infection rare
Normally ascending infection
UUTI
More serious, spread up from bladder infection
5
Q

What are the predisposing factors of a UTI?

A

a. Stasis of urine
b. Pushing bacteria up urethra from below
c. Generalised predisposition to infection

6
Q

Why does stasis of urine lead to UTIs, what causes stasis?

A

Bacteria that do get higher up do not get flushed out

Obstruction -
>Congenital or acquired
Loss of feeling of full bladder
>Spinal cord/brain injury

7
Q

What are the urethra complications of urine stasis?

A

Causes upper urethral and bladder dilation
Bilateral hydroureter
Bladder dilatation, bilateral hydroureter and bilateral hydronephrosis –> chronic renal failure

8
Q

What are the complications of urine stasis at the renal pelvis?

A

Unilateral hydroureter

Unilateral hydroureter and unilateral hydronephrosis

9
Q

What can push bacteria up from below?

A

Sexual activity in females

Catheterisation

10
Q

What are the complications of obstruction?

A
Proximal dilation
Slowed urine flow
>Cannot flush out bacteria --> infection
Slowed urine flow -->  sediments form --> calculous (stone) formation --> obstruction
>More dilation
>More infections
>Increased calculous formation
Some bacterial infections predispose to calculous formation
11
Q

What can cause obstruction in children?

A

Numerous renal tract abnormalities
Always investigate at 1st presentation and send to paediatric surgeons
Most important example = vesicoureteric reflux

12
Q

What is the vesicoureteric reflux?

A

Normally ureter inserts into bladder at 90 degrees
>Decreased angulation
Leads to reflux with hydroureter

13
Q

What can cayuse obstruction in adults?

A

Men – Benign Prostatic Hyperplasia (not a tumour) of prostate – functional and anatomical obstruction
Women – uterine prolapse
Both sexes – tumours and calculi

14
Q

Why does sexual activity in women lead to UTIs?

A

Usually age dependent
Due to short urethra
Lack of prostatic bacteriostatic secretion
Closeness of urethral orifice to rectum
Sexual activity - helps if void after intercourse
Pregnancy - pressure on ureters/bladder

15
Q

Why does diabetes lead to UTIs?

A

Glucose in urine

Poor function of WBCs

16
Q

What are the acute complications of UTIs?

A

Severe sepsis

Septic shock

17
Q

What are the chronic complications of UTIs?

A

Chronic damage to kidneys if repeated infections (chronic pyelonephritis) –> hypertension, chronic renal failure
Calculi –> obstruction –> Hydronephrosis –> hypertension, chronic renal failure

18
Q

What is glomerulonephritis?

A

Disease of glomerulus
Can be inflammatory or not
Primary - affects only glomerulus
Secondary - other body parts also affected

19
Q

What is the aetiology of glomerulonephritis?

A

Some due to immunglobulin deposition

Some without, like diabetic glomerular disease

20
Q

What are the common presentations of glomerulonephritis?

A

Haemturia
Heavy proteinuria
Slowly increasing protinuria
Acute renal failure

21
Q

What are the main causes of haematuria?

A

UTI
Uriary tract stone
Urinary tract tumour
Glomerulonephritis

22
Q

What is IgA nephropathy?

A

Accumulation of immunoglobulin (IgA) in mesangial area of glomeruli
Causes increased proliferation
Sometimes excessive antibody IgA in serum, but also true when no glomerulonephritis
IgA is stuck in the mesangium
Usually self-limiting
Some go on to form chronic renal failure due to continued deposition

23
Q

What is membranous glomerulonephritis?

A

Deposit of IgG in basal lamina
Not filtered into lumen, stuck between basal lamina + podocyte
IgG activates compliment C3 which punches holes in the filter
Now allows albumin through
1/4 chronic renal failure within 10 yrs

24
Q

What is diabetic glomerulus?

A

Glycated molecules lead to matrix deposition in basal lamina in mesangial matrix
Thus leading to thickened but leaky basement membranes and the mesangial matrix compresses the capillaries
>Note there are no immune complexes
Inevitable decline if established diabetic nephropathy or continued poor diabetic control

25
Q

What are the causes of crescentic glomerulonephritis?

A

Wegener’s granulomatosis
>Form of vasculitis affecting vessels in kidneys, nose + lungs
>Fatal if untreated
Microscopic polyarteritis (a disease like Wegeners)
Antiglomerular basement membrane disease
Many other forms of glomerulonephritis

26
Q

What are anti-neutrophil cytoplasmic antibodies?

A

Not deposited in kidney
Directed against two enzymes in primary granules of neutrophils
These ntibodies produce tissue damage via interactions with primed neutrophils and endothelial cells
Treat with cyclophosphamide (75% remission)

27
Q

What makes up the membrane in the glomerulus?

A

Endothelial cell cytoplasma
Basal lamina
Podocyte