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
Q

What are the five main things that are often seen in those that abuse analgesics?

A
  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
Q

T/F:

Analgesic nephropathy can’t be reversed

A

False

it can be reversed depending how bad the damage is

27
Q

What are the most common types of calculi?

A

Calcium oxalate precipitates

Calcium phosphate precipitates

28
Q

How do UTIs contribute to calculi?

A

UTIs change the pH of urine, altered pH can contribute to salts precipitating
Often magnesium ammonium phosphate

29
Q

How does low urine volume contribute to the development of calculi?

A

Dehydration= concentrated urine= precipitation

30
Q

What is urinary stasis?

A

Obstruction to urine outflow

Encourages salt precipitation and therefore contributes to the development of calculi

31
Q

How do foreign bodies contribute to the development of calculi?

A

Inflammatory responses

Some bacterial walls can also contribute

32
Q

What are the pathological consequences of passage of small stones?

A

Ureteric colic

Very painful

33
Q

What are the pathological consequences of passage of large stones?

A

May impact, leading to stasis and/or hydronephrosis

34
Q

T/F:

Atrophy of the renal parenchyma is usually in both kidneys when someone suffers from renal calculi

A
False
Usually unilateral (atrophy affects one kidney)
35
Q

What is Grawitz Tumour

A

Renal cell carcinoma

36
Q

What types of symptoms may someone experience when they suffer from renal cell carcinoma?

A

Haematuria (blood in the urine)

Flank pain, mass in loin

37
Q

Where do renal cell carcinomas often metastasise to?

A

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
Q

T/F:

Renal cell carcinoma is well encapsulated

A

True (rarely moves outside the tissue if it hasn’t metastasised)
With a pseduocapsule

39
Q

T/F:

Renal cell carcinoma often affects one pole of one kidney

A

True

40
Q

Explain how a renal cell carcinoma often forms ie. what cell changes and how

A
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
Q

Which cell is often mutated when someone suffers polycystic kidneys?

A

Epithelial tubule cells

42
Q

Which protein is often mutated in polycystic kidneys?

A

Polycystin-1

Involved in cell-cell adhesion

43
Q

What other organs may polycystic kidneys affect?

A

Liver
Pancreas
Some have berry Aneurysm of the circle of willis

44
Q

How do Advanced Glycosylation End (AGEs) form?

A

Elevated glucose levels
The sugars interact with the amine groups in proteins
No enzyme is required for this to occur

45
Q

Explain three things that AGEs do and how these contribute to complications of diabetes

A

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
Q

Explain the mechanism of intracellular hyperglycemia

A

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
Q

What is acute pyelonephritis?

A

Inflammation of the renal pelvis and the renal parenchyma after bacterial infection or blockage of the urinary tract

48
Q

Histologically, what does acute pyelonephritis lead to?

A

Inflammation of the parenchyma which leads to necrosis and abscess formation in the medulla or lower cortical regions of the kidney

49
Q

What is rhabdomyolysis?

A

Breakdown of skeletal muscle fibres and release into the vasculature

50
Q

In rhabdomyolysis, what protein is found in the blood and urine?

A

Myoglobin

51
Q

Which protein likes to bind to myoglobin when it is in the blood?

A

Haptoglobulin= plasma protein

The Hap/myoglobin complex travels to the kidney and myoglobin is deposited and can cause renal injury

52
Q

What often causes acute renal injury?

A

Rhabdomyolysis

53
Q

What are renal casts and what illness are they associated with?

A

Associated with acute renal injury (ARI)

Precipitation of myoglobin and uric acid crystals within renal tubules

54
Q

Which system does Rhabdomyolysis stimulate and what does this result in?

A

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