Exam II Flashcards
(133 cards)
1
Q
Where is the site of proliferation for BPH
A
Transitional zone
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
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
4
Q
What condition uses the AUA Score?
A
BPH! Really decides what tx you’re getting
5
Q
AUA Score mild BPH
A
<8
6
Q
AUA Score Mod BPH
A
<20
7
Q
AUA Score Severe BPH
A
> 20
8
Q
General Tx for AUA Score <8
A
Watchful waiting. Behavior modification
9
Q
General Tx for AUA Score <20
A
Consider rxtx
10
Q
General tx for AUA Score >20
A
Combo rxtx or surg. Severe BPH has a poor response to monotx
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.
12
Q
First line for BPH
A
ALPHA ONE BLOCKERS (tamsulosin, terazosin, doxazosin)
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
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
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.
16
Q
How do we deal with the A1blocker and PDE-5 inhib BP drop?
A
Separate the doses by at least 4 hours
17
Q
Second line rx for BPH
A
5-a-reductase inhibtors (Finasteride, dutasteride)
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.
19
Q
Why no 5-a-reductase inhibs and ED?
A
Worsens it!
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
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%
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.
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.
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
25
Why do we really not use anticholingerics chronically for irritative BPH symptoms
SE limit the dose, and you build a tolerance to the efx.
Dry mouth, drowsiness, AMS, constipation, decreased gut motility.
26
When to consider combo rxtx for BPH
1) Severe BPH automatically gets it (>20)
2) Poor response to monotx
3) Big ol' prostate (>40)
27
What two drugs do we give together for combo BPH
alpha blokers and 5a reductase inhibitors. They're rad, they really improve sx, reduce risk of preogression and dec the need for prostate surgery.
28
What are the three ways we operate on a prostate that's minimally invasive?
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.
29
Downsides of minimally invasive prostate surgery
No tissue for the patho exam afterwards. Also longer postop catheter.
30
3 Kinds of Conventional BPH Surgery
TURP
TUIP
Open Prostatectomy
31
What's a TURP? What are the downsides?
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.
32
What's a TUIP? Why would we do this vs a TURP?
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
33
Open Prostatectomy. Why would we do it IE when is this the operation of choice?
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)
34
RF for Prostate CA
AA, high dietary fat, Fhx
35
Where is the site of origin for most Prostate CA?
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.
36
Non metastatic Prostate CA Presentation
Most have no symptoms.
| LUTS are often seen, but this could just be attributed to BPH
37
metastatic sx of prostate CA
Bone pain, back pain, pathologic fx (prostate loves to met to the bone)
LE edema from LN mets
Urinary retention from obstruction (also LUTS)
38
Prostate CA on DRE
Abnormal prostate. Finding nodules, assymetric gland, indurations.
39
Problems with DRE as a screening tool for Prostate CA
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.
40
Two methods of Prostate CA screening
DRE and PSA
41
What is considered an elevated PSA
>4
42
PSA is specific right
Nah, there's a lot of reasons why it can be inc
43
You have an abnormal DRE or an elevated PSA, what happens next??
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
44
Positive TRUS! What now?
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
45
Indication for getting a bone scan for Prostate CA
Used for M staging. Not indicated unless PSA is severely elevated (>10-20). Which means mets are a thing.
46
PSA level that indicates metastasis
>10-20.
47
What is the Gleason staging criteria
Pathologist criteria for staging a malignant gland. We use it to determine the prognosis of prostate cancer
48
Gleason staging score range
2-10. <2 is non cancerous and doesn't count
49
Gleason score is made up of two grades. What are they?
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
50
What is correlated with the gleason score
Tumor volume, pathologic stage and prognosis.
51
How are tumor grade and tissue differentiation correlated?
Inversely. A low grade tumor has high differentiation
52
Gleason 2-6, differention/grade
Low grade, high diff
53
Gleason 7 differention/grade
Moderate grade, moderate differentiation
54
Gleason 8-10 differention/grade
High grade, poorly differentiated
55
How do we stage Prostate CA (two criteria)
TNM and Gleason
56
Standard tx for Prostate CA
Active surveillance, watchful waiting, hormone tx (ADT), RT, surg
57
What defines Low risk Prostate CA
T1-2a, Gleason <6, PSA <10. The tumor is only localized to one lobe of the prostat gland
58
What defines moderate/int risk Prostate CA
T2b, Gleason 7, PSA 10-20
1/2 of the bilateral prostate tumor
59
What defines high risk Prostate CA
T2c>, Gleason 8-10, PSA >20
Bilateral prostate lobe tumor
60
Three types of RT for Prostate CA
EBRT (External beam radiation therapy)
Brachy (Direct implant of a radioactive device)
Or, combo
61
Tx for Low Risk Prostate CA (T1-2a, Gleason <6, PSA <10)
Active surveillance (PSA/DRE/Repeat Bx)
RT
Prostatectomy +/- LN dissection
62
Tx for Intermediate Prostate CA (T2b, Gleason 7, PSA <20)
You have a life expectancy of >10 yrs
RT (EBRT, Brachy, combo)
Prostatectomy
63
Tx for High risk Prostate CA (>T2c, Gleason >8, PSA >20)
```
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
Tx for Metastatic Prostate CA
ADT. This gets some good response, but it's palliative, not curative.
Palliative RT
Palliative TURP for bladder outlet obstruction sx
65
types of ADT
GnRH
LHRH
CAB (complete androgen block)
Nonsteroidal antiandrogen
66
Which type of ADT do we start with for metastatic Prostate CA
We start with GnRH as initial tx.
| It's preferred, but it can cause a temporary testosterone flare, so watch out for that
67
Role of bisphosphonates in ADT
Given with androgen deprivation rx to prevent osteo. Also decreases boney pain for mets.
68
How do we treat metastatic Prostate CA that's hormone refractory
chemo time
69
Age group that gets bladder CA
90% of cases are in adults >55yo
70
RF for bladder CA
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
Which cells in the bladder become cancerous
Transitional cell carcinoma makes up 90% of bladder CA. Can arise anywhere that stretches, think tracts/renal eplvis/ ureter/bladder
72
Bladder CA Prognosis
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
Biggest sign of bladder CA (Think hannah's dad)
Painless hematuria. Microscopic even, that's your earliest sign of bladder CA
74
Other signs of bladder CA & signs of metastatic bladder CA
Other signs: LUTS voiding sx
| Met: LE swelling dt lymphatic obstruction, bony/pelvi/flank pain, palpable mass
75
How do we screen for bladder CA
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
What is UA especially rad for diagnosing
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
Positive UA cytology, what now?
Cystoscopy bx! Might even be able to resect papillary tumors while doing so.
78
Positive bx! What now?
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
Bladder CA staging uses the TNM critera, but what two major catergories do we break it down into?
Muscle invasive and non-muscle invasive
80
t1 Bladder cancer
Meh. Tumor in wedge subepithelial CT.
NON MUSCLE INVASIVE
81
T2 Bladder CA
Eh. Tumor in wedge muscles. Starts becoming MUSCLE INVASIVE
82
T3 Bladder CA
Uh oh. Tumor is thru the muscle and it starting to hit the surrounding adipose tissue. MUSCLE INVASIVE
83
T4 Bladder CA
Yikes. Tumor is thru the muscle & fat and it hitting up nearby organs. Prostate, pelvis and seminal vesicles usually
84
Management of non muscle invasive Bladder CA (T1, CIS)
Surgery followed by immunotx & chemo
85
Two options for surgery in bladder CA
TURBT (Transurethral resection of bldder tumor)
| Radical cystectomy
86
What is TURBT rad for
Small tumors (<1cm) that include part of the underlying bladder wall.
87
What if you've got a bulky, high grade tumor or one that's multifocal and you're trying to do TURBT?
Might need another round of turbt to ensure total resection & for accurate staging.
88
When would we do a radical cystectomy?
When TURBT fails
When the prostatic urethra is involved
When the tumor is too big to endoscopically resect
89
How are chemo & BCG given
Transurethral catheter. Cool right?
90
When do we give TU chemo & BCG for non-muscle invasive disease
2-4 weeks after any resection/bladder bx
91
BCG vs chemo
First start with BCG, the cancer vaccine for 6-12 weeks. If this fails, we'll give instravesicular chemo (mitomycin, valrubicin, doxorubicin)
92
Biggest difference between management of non muscle invave bladder CA (T1/CIS) and muscle invasive (T2-T4)
Not fucking with TURBT anymore. Rad bladder only. Also neoadjuvent chemo
93
Tell me about the neoadjuvent chemo regiment for muscle invasive (T2-T4) bladder CA
Give MVAC (MTX, vincristine, adriamycin & cisplatin) before the radical cystectomy w/ local LN dissection
94
For muscle invasive disease, why do we do a local LN dissection with our radical cystectomy
Because if it's in the muscle, it's probably in the LN too
95
What's an option for muscle invasive tumors T2-T3 but not for T4
Neoadjuvent RT and chemo & attempt partial resection in some areas to try and preserve the bladder.
96
Most common cause of RAS
ATS
97
Potential cause of RAS if you're a younger woman (<40yo)
Fibromscular dysplasia
98
RF for RAS by ATS
```
Hx of ATS
CKD
DM
Tobacco
Preexisting HTN
```
99
What's often comorbid with RAS
CAD and ESRD
100
What does RAS do to the MM of ESRD
Skyrockets it. Second only to DM
101
What's an ATS plaque made up of (as opposed to a fibromuscular dysplasia plaque)
Fat, WBC, Calcium, WBC
Fibromuscular plaques are made up of fibrous collagen and smooth muscle
102
Pathogenesis of RAS
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
Stenosis causes decreased renal perfusion. How low can it get before we see irreversible inflammation & fibrosis?
<50% normal blood flow
104
When is RAS considered significant stenosis and requires revascularization
>70% occluded on angio or 50-70% with hemodynamic (BP) changes. Consider revascularization only if BP/hemodynamic changes
105
Target end organ damage of RAS
Abdominal bruits and retinopathy on fundoscopy
106
Is RAS primary or secondary HTN
Secondary. It's not random BP
107
Typical age of onset for RAS
It's weird.
Sudden onset HTN in patients <30 or >55
108
Clinical findings of RAS
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
Malignant HTN w/ neuro sx & retinopathy on fundoscopy?
Screen for possible RVHTN
110
Severe/refractory HTN (>3 drugs) + Heart failure/pulm flash?
Possible RVHT. It can present like that
111
Worsening with ACE/ARB?
RVHT!
112
Why is it important to rule out RVHTN
Because if you catch it before any damage is done, it's actually reversible with revascularization
113
When can we officially make the diagnosis of RAS/RVHTN?
Retrospectively. If the BP improves after correcting the ATS, then we can say it was RAS/RVHTN.
114
Sx of RAS/RVHTN
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
RAS Lab findings
HypoK
Hyperaldosteronism
Mild/mod proteinuria
Azotemia following ACE/ARB tx
116
How does hyperaldosterone cause HypoK
Causes Na retention to inc blood volume (dt hypoperfusion) Kaliuresis is a SE of this
117
Age of diagnosis for Wilm's Tumor
2-5 years. Mean age is 4. Uncommon after 6 years
118
Presenting Sx for wilm's tumor
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
How do you determine the clinical stage of a Wilms tumor?
SURGERY. This is where treatment begins.
120
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
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
Bone/brain mets from a renal tumor are typical of Wilms?
Nah dude. They're more typical of some scary aggressive rare renal tumors.
122
How does tx of a wilm's tumor start out?
Surgical exploration of the abdomen to allow for inspection & palpation of the contralateral kidney.
123
Let's talk about wilm's tumor exploratory surgery. Talk through how it goes.
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
Treatment for stage I-II wilms tumor
Chemo 5 days postop
125
Treatment for stage III-IV wilms tumor
Chemo 5 days postop. RT 10 days potop to get rid of tumor bed & met sites
126
Treatment for stage 5 wilms tumor
Bilateral renal bx w/ chemo and second look renal sparing surgery. Maybe RT
127
What defines a stage 5 wilms tumor
Bilateral kidney involvement
128
Definition of acute renal disease
Rapid loss of RF (hours - days) Reversible, caused by dehydration/blood loss/Rx/IV Contrast/obstruction
129
Definition of chronic kidney disease
Progressive LOF, >3 months. Usually irreversible. Caused by long term dx like DM and HTN
130
Mneumonic for kidney function
```
A- Acid base status
W- Water balance
E- Electrolytes
T- Toxin removal
B- BP Control
E- EPO production
D- Vitamin D production
```
131
Technical parameters for CKR
<60 GFR for >3 months
132
Pathophys behind CKD
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
What happens to Cr as GFR decreases
Increases. Totally throws off that Cr:BUN 1:20
