Renal Pathology Flashcards

1
Q

What are the four main clinical presentations of prostatic disorders?

A

Prostatitis
Benign Prostatic Hyperplasia
Prostatodynia
Prostate Cancer

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2
Q

Which part of the prostate does benign prostatic hyperplasia occur?

A

Transitional zone

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3
Q

What do alpha inhibitors do?

A

Can reduce certain types of testosterone levels and therefore prostate size can shrink

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4
Q

T/F:

There are clear signs of inflammation when prostatodynia occurs

A

False

however there is pain in the pelvic region

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5
Q

T/F:

Presense of prostate specific antigen in blood can diagnose prostatic cancer

A

False
not specific
but can tell you that something’s wrong

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6
Q

Which part of the prostate does prostate cancer often grow?

A

Posterior lobe

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7
Q

Why does prostatic cancer often develop without any symptoms?

A

It develops in the posterior lobe so it doesn’t push on the urethra
often notice it is there when it is very large

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8
Q

T/F:

Prostatic cancer metastasises to the bone and lung

A

True

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9
Q

What cells surround the glandular epithelial cells?

A

Muscular stroma

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10
Q

How do the nodes found in benign prostatic hyperplasia grow?

A

Grow inwards towards the urethra and compress the prostatic urethra

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11
Q

What do the nodules consist of in benign prostatic hyperplasia?

A

Proliferative stromal cells, hyperplastic glands or both

Glands can also become cystic

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12
Q

What therapeutic options are there for benign prostatic hyperplasia?

A

None because it doesn’t affect quality of life

Sometimes reverses itself

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13
Q

What does TURP stand for?

A

Transurethral resection of the prostate

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14
Q

Prostate cancer is a well differentiated _____

A

Adenocarcinoma

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15
Q

T/F:

Prostate cancer is the 2nd most common cancer in men

A

True

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16
Q

Which organ can be affected when someone suffers prostatic cancer?

A

Kidneys
Secondary pathology because of back pressure
Urinary obstruction causes Hydronephorsis with renal atrophy in the parenchyma of the renal medulla

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17
Q

What does TCC stand for?

A

Transitional Cell Carcinoma (of the bladder)

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18
Q

How does TCC of the bladder present?

A

Painless transient haematuria (bleeding of the bladder)
Growths attached to the bladder wall
Can occur in the renal pelvis/ureters
Often linked to increased UTIs

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19
Q

List some risk factors of TCC of the bladder

A
Chemical solvents
Pesticides
Heavy smoking
Cyclophosphamid
Some nematodes
Chronic cystitis
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20
Q

T/F:

Analgesics are drugs used to for the permanent relief of pain

A

False

Temporary relief of pain

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21
Q

What causes hydronephrosis?

A

Results from urinary obstruction

Refers to the dilation of the renal pelvis and calyces accompanied by atrophy of the parenchyma

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22
Q

What is renal hypercalcinuria/phosphoturia?

A

Excessive calcium or phosphate uptake in the gut/kidney- promotes stone formation in the kidney

23
Q

What cells do phenacetin/paracetamol metabolites affect?

A

Directly toxic to tubular cells and red blood cells

causes oxidative damage

24
Q

How does asprin promote vascular dysfunction?

A

Inhibits vasodilatory effects of prostaglandins

25
What are the five main things that are often seen in those that abuse analgesics?
1. Necrosis of the pyramids 2. Loss/mobilisation of necrotic segment of papila 3. Damaged counter current flow concentrating mechanism 4. Hypertension 5. Carcinoma (transitional cell carcinoma)
26
T/F: | Analgesic nephropathy can't be reversed
False | it can be reversed depending how bad the damage is
27
What are the most common types of calculi?
Calcium oxalate precipitates | Calcium phosphate precipitates
28
How do UTIs contribute to calculi?
UTIs change the pH of urine, altered pH can contribute to salts precipitating Often magnesium ammonium phosphate
29
How does low urine volume contribute to the development of calculi?
Dehydration= concentrated urine= precipitation
30
What is urinary stasis?
Obstruction to urine outflow | Encourages salt precipitation and therefore contributes to the development of calculi
31
How do foreign bodies contribute to the development of calculi?
Inflammatory responses | Some bacterial walls can also contribute
32
What are the pathological consequences of passage of small stones?
Ureteric colic | Very painful
33
What are the pathological consequences of passage of large stones?
May impact, leading to stasis and/or hydronephrosis
34
T/F: | Atrophy of the renal parenchyma is usually in both kidneys when someone suffers from renal calculi
``` False Usually unilateral (atrophy affects one kidney) ```
35
What is Grawitz Tumour
Renal cell carcinoma
36
What types of symptoms may someone experience when they suffer from renal cell carcinoma?
Haematuria (blood in the urine) | Flank pain, mass in loin
37
Where do renal cell carcinomas often metastasise to?
Lung and bone Tumour can also grow out from the capsule and go via the renal vein to the IVC and therefore to the heart (not a typical metastasis)
38
T/F: | Renal cell carcinoma is well encapsulated
True (rarely moves outside the tissue if it hasn't metastasised) With a pseduocapsule
39
T/F: | Renal cell carcinoma often affects one pole of one kidney
True
40
Explain how a renal cell carcinoma often forms ie. what cell changes and how
``` Epithelial tubule cell changes The express LDL receptors differently Proliferate Can retain fat better In slides they epithelial tubule cells appear clear so it is often called 'clear cell carcinoma' ```
41
Which cell is often mutated when someone suffers polycystic kidneys?
Epithelial tubule cells
42
Which protein is often mutated in polycystic kidneys?
Polycystin-1 | Involved in cell-cell adhesion
43
What other organs may polycystic kidneys affect?
Liver Pancreas Some have berry Aneurysm of the circle of willis
44
How do Advanced Glycosylation End (AGEs) form?
Elevated glucose levels The sugars interact with the amine groups in proteins No enzyme is required for this to occur
45
Explain three things that AGEs do and how these contribute to complications of diabetes
AGEs can cross link with major proteins such as collagen in vessel walls= this traps LDLs in vessels and leads to cholesterol deposition Leaky capillaries with thickened GBM AGEs can bind to receptors on endothelium and activate an inflammatory response and activate smooth muscle proliferation=thickening and matrix production
46
Explain the mechanism of intracellular hyperglycemia
Some cells use sugars to make ATP and do not require insulin Cells take up the sugars and two by products include sorbitol and fructose Build up of these two products results in osmotic cell injury and leads to impaired ion pump function and necrosis
47
What is acute pyelonephritis?
Inflammation of the renal pelvis and the renal parenchyma after bacterial infection or blockage of the urinary tract
48
Histologically, what does acute pyelonephritis lead to?
Inflammation of the parenchyma which leads to necrosis and abscess formation in the medulla or lower cortical regions of the kidney
49
What is rhabdomyolysis?
Breakdown of skeletal muscle fibres and release into the vasculature
50
In rhabdomyolysis, what protein is found in the blood and urine?
Myoglobin
51
Which protein likes to bind to myoglobin when it is in the blood?
Haptoglobulin= plasma protein | The Hap/myoglobin complex travels to the kidney and myoglobin is deposited and can cause renal injury
52
What often causes acute renal injury?
Rhabdomyolysis
53
What are renal casts and what illness are they associated with?
Associated with acute renal injury (ARI) | Precipitation of myoglobin and uric acid crystals within renal tubules
54
Which system does Rhabdomyolysis stimulate and what does this result in?
Stimulates the renin angiotensin aldosterone system AngII increases and this results in hypertension This leads to shut down in blood flow and therefore causes necrosis in the medulla