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Remediation > Exam II > Flashcards

Exam II Flashcards

1
Q

Where is the site of proliferation for BPH

A

Transitional zone

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2
Q

Where is the site of proliferation of Prostate cancer

A

Peripheral prostate. This is why BPH is not considered a RF for Prostate CA

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3
Q

BPH Sx, two types of LUTS

A

1) Storage/Irritative sx: Urgency, freq, nocturia, incontinence
2) Obstructive Sx: Hesitancy, dec flow, dribbling, straining, can’t empty bladder

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4
Q

What condition uses the AUA Score?

A

BPH! Really decides what tx you’re getting

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5
Q

AUA Score mild BPH

A

<8

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6
Q

AUA Score Mod BPH

A

<20

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7
Q

AUA Score Severe BPH

A

> 20

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8
Q

General Tx for AUA Score <8

A

Watchful waiting. Behavior modification

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9
Q

General Tx for AUA Score <20

A

Consider rxtx

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10
Q

General tx for AUA Score >20

A

Combo rxtx or surg. Severe BPH has a poor response to monotx

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11
Q

Who gets BPH Rxtx

A

Anybody that doesn’t have scary symptom like refractory retention, BPH induced kidney disease, bladder caliculi & BPH w/ gross hematuria. Basically anything that’s straight up BPH w/ LUTS symptoms.

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12
Q

First line for BPH

A

ALPHA ONE BLOCKERS (tamsulosin, terazosin, doxazosin)

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13
Q

When do alpha one blockers start working? Where do they work?

A

Start working immediately!
They work locally, relaxing the smooth muscles of the prostate and bladder neck. Does not actually change size of prostate

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14
Q

SE of Alpha blockers

A

Orthostatic, Hypotension and dizziness. To combat the hypotension we recommend taking at nighttime and dosing low, titrate slow

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15
Q

What drug (when combined w/ alpha one blockers) gives you a big ol’ hypotensive drop?

Which A1blockers are especially bad with this

A

PDE-5 Inhibitors.

Terazosin and doxazosin.

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16
Q

How do we deal with the A1blocker and PDE-5 inhib BP drop?

A

Separate the doses by at least 4 hours

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17
Q

Second line rx for BPH

A

5-a-reductase inhibtors (Finasteride, dutasteride)

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18
Q

What two situations do we not want to prescribe 5-a-reductase inhibitors?

A

Irritative BPH symptoms (freqiency, nocturia, incontinence) and in ED.

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19
Q

Why no 5-a-reductase inhibs and ED?

A

Worsens it!

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20
Q

How do 5-a-R inhibs work? How long does it take?

A

They work by converting testosterone to something else, causing the prostate to actually shrink (that’s why its better for obstructive symptoms).

It takes 6-12 months to work though

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21
Q

SE of 5A reductase inhibs

A

Decreased libido, ED, decreased ejaculate (Less T). No hypotension so you don’t need to titrate it!

ALSO ALSO ALSO REALLY IMPORTANT PSA REDUCTION BY 50%

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22
Q

REALLY REALLY IMPORTANT SE of 5A reductase inhibs and why it’s so important

A

It decreased PSA by 50%, so you need to take this into consideration when screening for Prostate CA.

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23
Q

So 5A reductase inhibs work by shrinking the prostate, around what size do we start thinking of using these guys (what are they ideal for)

A

Prostates >40ml on TRUS. Why are prostates a liquid measurement? Who the fuck knows.

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24
Q

What are we thinking for a patient with really bad irritative symptoms and maybe has an overative bladder

A

Anticholingergics! Like oxybutynin, nacins, trospium

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25
Q

Why do we really not use anticholingerics chronically for irritative BPH symptoms

A

SE limit the dose, and you build a tolerance to the efx.

Dry mouth, drowsiness, AMS, constipation, decreased gut motility.

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26
Q

When to consider combo rxtx for BPH

A

1) Severe BPH automatically gets it (>20)
2) Poor response to monotx
3) Big ol’ prostate (>40)

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27
Q

What two drugs do we give together for combo BPH

A

alpha blokers and 5a reductase inhibitors. They’re rad, they really improve sx, reduce risk of preogression and dec the need for prostate surgery.

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28
Q

What are the three ways we operate on a prostate that’s minimally invasive?

A

Minimally invasive- Trans urethral catheter.

1) Laser. Can be done with cytoscopy or with TRUS, in which case you’d do a TULIP (Transurethral Laser Induced Prostectomy)
2) Microwave hyperthermia. Heat creates a cavity in the prostatic urethra
3) Radiofrequencies TUNA (Transurethral needle ablation). Heats up the prostatic cavity, causing coagulative necrosis.

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29
Q

Downsides of minimally invasive prostate surgery

A

No tissue for the patho exam afterwards. Also longer postop catheter.

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30
Q

3 Kinds of Conventional BPH Surgery

A

TURP
TUIP
Open Prostatectomy

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31
Q

What’s a TURP? What are the downsides?

A

Transurethral resection prostatectomy. Better sx score improvement and flow rate compared to all the minimally invasive procedures. Takes out almost the entire prostate, it’s for the biggos.

Downsides are retrograde ejaculation, ED, urinary incontinence, strictures, transurethral resection syndrome.

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32
Q

What’s a TUIP? Why would we do this vs a TURP?

A

Transurethra incision of the prostate. It makes a incision and makes a canal thru the prostatic urethra. This is what we do when the prostate is basically a normal size but it’s just doing unfortunate things to the bladder neck. These guys will have severe obstructive sx

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33
Q

Open Prostatectomy. Why would we do it IE when is this the operation of choice?

A

We’ll do this when the prostate is too large to remvoe endoscopically (>100g holy fuck).

Also the operation of choice if there’s some kind of bladder pathology where we won’t want to go thru the urethra. (diverticuli, caliculi)

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34
Q

RF for Prostate CA

A

AA, high dietary fat, Fhx

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35
Q

Where is the site of origin for most Prostate CA?

A

Peripheral zone of the gland! Remember bc BPH is in the T zone. These guys are adenocarcinoma, but you knew that because you’re super smart and knew the prostate is a gland.

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36
Q

Non metastatic Prostate CA Presentation

A

Most have no symptoms.

LUTS are often seen, but this could just be attributed to BPH

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37
Q

metastatic sx of prostate CA

A

Bone pain, back pain, pathologic fx (prostate loves to met to the bone)
LE edema from LN mets
Urinary retention from obstruction (also LUTS)

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38
Q

Prostate CA on DRE

A

Abnormal prostate. Finding nodules, assymetric gland, indurations.

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39
Q

Problems with DRE as a screening tool for Prostate CA

A

These only detect masses in the posterior and lateral aspects of the gland. This makes up 65% of prostate CA tumors, but it means the other 35% go totally unrecognized for a long time.

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40
Q

Two methods of Prostate CA screening

A

DRE and PSA

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41
Q

What is considered an elevated PSA

A

> 4

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42
Q

PSA is specific right

A

Nah, there’s a lot of reasons why it can be inc

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43
Q

You have an abnormal DRE or an elevated PSA, what happens next??

A

TRUS guided biopsy. If you keep having elevated PSA with a negative biopsy you can repeat this and hit up both the peripheral and transtitional zone

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44
Q

Positive TRUS! What now?

A

MRI. Better for staging, it shows up capsular penetration, seminal vesicle involvement and if any local LN are affected. We use this for T and N staging.

Bone scans are also used but we’ll get into that

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45
Q

Indication for getting a bone scan for Prostate CA

A

Used for M staging. Not indicated unless PSA is severely elevated (>10-20). Which means mets are a thing.

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46
Q

PSA level that indicates metastasis

A

> 10-20.

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47
Q

What is the Gleason staging criteria

A

Pathologist criteria for staging a malignant gland. We use it to determine the prognosis of prostate cancer

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48
Q

Gleason staging score range

A

2-10. <2 is non cancerous and doesn’t count

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49
Q

Gleason score is made up of two grades. What are they?

A

Primary and secondary.
Primary is a sample from the largest area of the prostate and secondary is a sample from the second largest area of the prostate

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50
Q

What is correlated with the gleason score

A

Tumor volume, pathologic stage and prognosis.

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51
Q

How are tumor grade and tissue differentiation correlated?

A

Inversely. A low grade tumor has high differentiation

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52
Q

Gleason 2-6, differention/grade

A

Low grade, high diff

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53
Q

Gleason 7 differention/grade

A

Moderate grade, moderate differentiation

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54
Q

Gleason 8-10 differention/grade

A

High grade, poorly differentiated

55
Q

How do we stage Prostate CA (two criteria)

A

TNM and Gleason

56
Q

Standard tx for Prostate CA

A

Active surveillance, watchful waiting, hormone tx (ADT), RT, surg

57
Q

What defines Low risk Prostate CA

A

T1-2a, Gleason <6, PSA <10. The tumor is only localized to one lobe of the prostat gland

58
Q

What defines moderate/int risk Prostate CA

A

T2b, Gleason 7, PSA 10-20

1/2 of the bilateral prostate tumor

59
Q

What defines high risk Prostate CA

A

T2c>, Gleason 8-10, PSA >20

Bilateral prostate lobe tumor

60
Q

Three types of RT for Prostate CA

A

EBRT (External beam radiation therapy)
Brachy (Direct implant of a radioactive device)
Or, combo

61
Q

Tx for Low Risk Prostate CA (T1-2a, Gleason <6, PSA <10)

A

Active surveillance (PSA/DRE/Repeat Bx)
RT
Prostatectomy +/- LN dissection

62
Q

Tx for Intermediate Prostate CA (T2b, Gleason 7, PSA <20)

A

You have a life expectancy of >10 yrs
RT (EBRT, Brachy, combo)
Prostatectomy

63
Q

Tx for High risk Prostate CA (>T2c, Gleason >8, PSA >20)

A 
ERBT + 2-3 years of ADT
Combo RT (ERBT+Brachy) + 1 yr of ADT
Prostatectomy w/ Pelvic LN dissection. Consider doing both pre and post op RT
64
Q

Tx for Metastatic Prostate CA

A

ADT. This gets some good response, but it’s palliative, not curative.
Palliative RT
Palliative TURP for bladder outlet obstruction sx

65
Q

types of ADT

A

GnRH
LHRH
CAB (complete androgen block)
Nonsteroidal antiandrogen

66
Q

Which type of ADT do we start with for metastatic Prostate CA

A

We start with GnRH as initial tx.

It’s preferred, but it can cause a temporary testosterone flare, so watch out for that

67
Q

Role of bisphosphonates in ADT

A

Given with androgen deprivation rx to prevent osteo. Also decreases boney pain for mets.

68
Q

How do we treat metastatic Prostate CA that’s hormone refractory

A

chemo time

69
Q

Age group that gets bladder CA

A

90% of cases are in adults >55yo

70
Q

RF for bladder CA

A

Cigarrette smoking (chronic urinary infl) and Occupational hazards (organic chemicals, rubber, paint or dye).

Also much less common but balkan nephropathy and prior hx of pelvic XRT

71
Q

Which cells in the bladder become cancerous

A

Transitional cell carcinoma makes up 90% of bladder CA. Can arise anywhere that stretches, think tracts/renal eplvis/ ureter/bladder

72
Q

Bladder CA Prognosis

A

Overall 10yr survival is 70%

T1 has a 95%
Muscle invasive has a 70% 5y prog
LN Involvement 35% 5yr
Distant mets? 5% 5yr survival

73
Q

Biggest sign of bladder CA (Think hannah’s dad)

A

Painless hematuria. Microscopic even, that’s your earliest sign of bladder CA

74
Q

Other signs of bladder CA & signs of metastatic bladder CA

A

Other signs: LUTS voiding sx

Met: LE swelling dt lymphatic obstruction, bony/pelvi/flank pain, palpable mass

75
Q

How do we screen for bladder CA

A

UA! Think of ric.

We’ll do a microscopy, culture and cytology exam.

Hematuria will get a cytology exam.
Cytology is the biggie here, a positive cytology warrants a cystoscopy bx. CYTOLOGY IS OFTEN USED FOR DIAGNOSIS

76
Q

What is UA especially rad for diagnosing

A

High grade tumors and CIS! I mean yes that’s advanced but it’s potentially treatable. It’s not great for the lowgrade/noninvasive tumors. Cant catch it too early with UA

77
Q

Positive UA cytology, what now?

A

Cystoscopy bx! Might even be able to resect papillary tumors while doing so.

78
Q

Positive bx! What now?

A

Let’s get some imaging to evaluate the upper urinary tract!

  • CT W/ contrast
  • US
  • MRI

Can also consider a bone scan & CXR for mets

79
Q

Bladder CA staging uses the TNM critera, but what two major catergories do we break it down into?

A

Muscle invasive and non-muscle invasive

80
Q

t1 Bladder cancer

A

Meh. Tumor in wedge subepithelial CT.

NON MUSCLE INVASIVE

81
Q

T2 Bladder CA

A

Eh. Tumor in wedge muscles. Starts becoming MUSCLE INVASIVE

82
Q

T3 Bladder CA

A

Uh oh. Tumor is thru the muscle and it starting to hit the surrounding adipose tissue. MUSCLE INVASIVE

83
Q

T4 Bladder CA

A

Yikes. Tumor is thru the muscle & fat and it hitting up nearby organs. Prostate, pelvis and seminal vesicles usually

84
Q

Management of non muscle invasive Bladder CA (T1, CIS)

A

Surgery followed by immunotx & chemo

85
Q

Two options for surgery in bladder CA

A

TURBT (Transurethral resection of bldder tumor)

Radical cystectomy

86
Q

What is TURBT rad for

A

Small tumors (<1cm) that include part of the underlying bladder wall.

87
Q

What if you’ve got a bulky, high grade tumor or one that’s multifocal and you’re trying to do TURBT?

A

Might need another round of turbt to ensure total resection & for accurate staging.

88
Q

When would we do a radical cystectomy?

A

When TURBT fails
When the prostatic urethra is involved
When the tumor is too big to endoscopically resect

89
Q

How are chemo & BCG given

A

Transurethral catheter. Cool right?

90
Q

When do we give TU chemo & BCG for non-muscle invasive disease

A

2-4 weeks after any resection/bladder bx

91
Q

BCG vs chemo

A

First start with BCG, the cancer vaccine for 6-12 weeks. If this fails, we’ll give instravesicular chemo (mitomycin, valrubicin, doxorubicin)

92
Q

Biggest difference between management of non muscle invave bladder CA (T1/CIS) and muscle invasive (T2-T4)

A

Not fucking with TURBT anymore. Rad bladder only. Also neoadjuvent chemo

93
Q

Tell me about the neoadjuvent chemo regiment for muscle invasive (T2-T4) bladder CA

A

Give MVAC (MTX, vincristine, adriamycin & cisplatin) before the radical cystectomy w/ local LN dissection

94
Q

For muscle invasive disease, why do we do a local LN dissection with our radical cystectomy

A

Because if it’s in the muscle, it’s probably in the LN too

95
Q

What’s an option for muscle invasive tumors T2-T3 but not for T4

A

Neoadjuvent RT and chemo & attempt partial resection in some areas to try and preserve the bladder.

96
Q

Most common cause of RAS

A

ATS

97
Q

Potential cause of RAS if you’re a younger woman (<40yo)

A

Fibromscular dysplasia

98
Q

RF for RAS by ATS

A 
Hx of ATS
CKD
DM
Tobacco
Preexisting HTN
99
Q

What’s often comorbid with RAS

A

CAD and ESRD

100
Q

What does RAS do to the MM of ESRD

A

Skyrockets it. Second only to DM

101
Q

What’s an ATS plaque made up of (as opposed to a fibromuscular dysplasia plaque)

A

Fat, WBC, Calcium, WBC

Fibromuscular plaques are made up of fibrous collagen and smooth muscle

102
Q

Pathogenesis of RAS

A

Plaque causes dec renal perfusion, triggering the RAAS system to release renin. The renin converts angiotensin I, which causes vasoconstriction & stimulates aldosterone production. That causes salt & water retention. If there’s an other kidney that’s functioning, this kidney will naturese this retention. 2 bad kidneys? ur fucked bud. This works short term but with RAS it’s all the time

103
Q

Stenosis causes decreased renal perfusion. How low can it get before we see irreversible inflammation & fibrosis?

A

<50% normal blood flow

104
Q

When is RAS considered significant stenosis and requires revascularization

A

> 70% occluded on angio or 50-70% with hemodynamic (BP) changes. Consider revascularization only if BP/hemodynamic changes

105
Q

Target end organ damage of RAS

A

Abdominal bruits and retinopathy on fundoscopy

106
Q

Is RAS primary or secondary HTN

A

Secondary. It’s not random BP

107
Q

Typical age of onset for RAS

A

It’s weird.

Sudden onset HTN in patients <30 or >55

108
Q

Clinical findings of RAS

A

Severe/refractory HTN that doesn’t seem to respond to Rx
Age of onset <30 or >55
Abrupt accelertion of prev stable HTN
Systolic bruit in epigastrum
Flash pulm edema
Unexplained azotemia after starting an ACE or ARB

109
Q

Malignant HTN w/ neuro sx & retinopathy on fundoscopy?

A

Screen for possible RVHTN

110
Q

Severe/refractory HTN (>3 drugs) + Heart failure/pulm flash?

A

Possible RVHT. It can present like that

111
Q

Worsening with ACE/ARB?

A

RVHT!

112
Q

Why is it important to rule out RVHTN

A

Because if you catch it before any damage is done, it’s actually reversible with revascularization

113
Q

When can we officially make the diagnosis of RAS/RVHTN?

A

Retrospectively. If the BP improves after correcting the ATS, then we can say it was RAS/RVHTN.

114
Q

Sx of RAS/RVHTN

A

Sudden onset of Severe Stage II HTN (>160/110)
Systolic abd bruit (no bruit does not mean no RAS)
Stage III/IV retinopathy
Evidence of ATS in other parts of the body

115
Q

RAS Lab findings

A

HypoK
Hyperaldosteronism
Mild/mod proteinuria
Azotemia following ACE/ARB tx

116
Q

How does hyperaldosterone cause HypoK

A

Causes Na retention to inc blood volume (dt hypoperfusion) Kaliuresis is a SE of this

117
Q

Age of diagnosis for Wilm’s Tumor

A

2-5 years. Mean age is 4. Uncommon after 6 years

118
Q

Presenting Sx for wilm’s tumor

A

Inc abdomen size or asymptomatic abdominal mass.

25% of patients are hypertensive at presentation, but you’re absolutely going to notice the giant tumor first and foremost

119
Q

How do you determine the clinical stage of a Wilms tumor?

A

SURGERY. This is where treatment begins.

120
Q

Back to screening though, what imaging do we do to confirm that there is in fact a giant ass mass for the kids with Wilm’s tumors

A

US or CT of abdomen to confirm intrarenal mass. Must check contralateral kidney to make sure both aren’t being affected.

Do a doppler of the IVC to see how far the tumor has spread.

Consider doing a chest CT to check for pulm mets (10% of pts have mets at diagnosis, they’re usually pulm mets)

121
Q

Bone/brain mets from a renal tumor are typical of Wilms?

A

Nah dude. They’re more typical of some scary aggressive rare renal tumors.

122
Q

How does tx of a wilm’s tumor start out?

A

Surgical exploration of the abdomen to allow for inspection & palpation of the contralateral kidney.

123
Q

Let’s talk about wilm’s tumor exploratory surgery. Talk through how it goes.

A

1) Inspect the abdomen and palpate the contralateral kidney
2) Liver and LN are inspected. ANything that looks suspicious is resected and biopsied
3) En bloc resection of the tumor. CAREFUL ABOUT TUMOR SPILLAGE
4) Pathologist evaluate everything and get you the proper tumor stage

124
Q

Treatment for stage I-II wilms tumor

A

Chemo 5 days postop

125
Q

Treatment for stage III-IV wilms tumor

A

Chemo 5 days postop. RT 10 days potop to get rid of tumor bed & met sites

126
Q

Treatment for stage 5 wilms tumor

A

Bilateral renal bx w/ chemo and second look renal sparing surgery. Maybe RT

127
Q

What defines a stage 5 wilms tumor

A

Bilateral kidney involvement

128
Q

Definition of acute renal disease

A

Rapid loss of RF (hours - days) Reversible, caused by dehydration/blood loss/Rx/IV Contrast/obstruction

129
Q

Definition of chronic kidney disease

A

Progressive LOF, >3 months. Usually irreversible. Caused by long term dx like DM and HTN

130
Q

Mneumonic for kidney function

A 
A- Acid base status
W- Water balance
E- Electrolytes
T- Toxin removal
B- BP Control
E- EPO production
D- Vitamin D production
131
Q

Technical parameters for CKR

A

<60 GFR for >3 months

132
Q

Pathophys behind CKD

A

Nephron injury. The remaining nephrons compensate and hyperfiltrate to maintain the GFR. This works initially, but it’s rough on the glomerulus, causing GLOMERULAR CAPILLARY HTN, This in conjunction with the angiotensin II (yeah RAAS gets activated to inc volume to save the GFR) makes the glom super leaky to proteins which are super toxic to the tubules. So eventually from all of this you have glomerular sclerosis and tubulointerstitial fibrosis, and voila that’s irreversible damage and a long wait on the kidney transplant list

133
Q

What happens to Cr as GFR decreases

A

Increases. Totally throws off that Cr:BUN 1:20

Remediation (2 decks)

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