Renal Pathology - Dr. Dobson Part 2 Flashcards

1
Q

Adult Polycystic kidney disease
inheritance
what happens on kidney
outcome

A

AD

  1. VERY Large muticystic kidneys, liver cysts,
  2. BERRY ANEURYSMS

CKD at 40-60yo

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2
Q

Adult Polycystic Kidney Disease SX

A
  1. hematuria
  2. flank pain
  3. UTI
  4. nephrolithiasis
  5. htn
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3
Q

Childhood Polycystic kidney disease
inheritance
what happens on kidney
outcome

A

AR

  1. Enlarged kidneys
  2. oval long cysts on kidneys at birth

death in infancy or childhood, variable

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4
Q

Childhood Polycystic Kidney Disease

SX

A

Hepatic fibrosis

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5
Q

Medullary Sponge kidney
inheritance
what happens on kidney
outcome

A

none

medullary cysts on excretory urography

benign

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6
Q

Medullary Sponge kidney SX

A

hematuria

UTI

recurrent stones

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7
Q

Familial Juvenile Nephronophthisis
inheritance
what happens on kidney
outcome

A

AR

  1. Corticomedullary cysts
  2. Shrunked kidney

progressive renal failure starting at childhood (ESRD in 5-10years)

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8
Q

Familial Juvenile Nephronophthisis

SX

A

salt wasting, polyuria
low growth
anemia

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9
Q

Multicystic Renal Dysplasia
inheritance
what happens on kidney
outcome

A

none

  1. irregular kidneys + variable size cysts + immature CD
  2. enlarged
RF (bilateral)
surgery curable (unilateral)
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10
Q

Multicystic Renal Dysplasia

SX

A

with other renal anomalies

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11
Q

Acquired renal cystic disease
inheritance
what happens on kidney
outcome

A

none

cystic degeneration during ESRD

need dialysis

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12
Q

Acquired renal cystic disease SX

A

hemorrhage,
erythrocytosis,
neoplasia

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13
Q

Simple Cysts
inheritance
what happens on kidney
outcome

A

none

  1. single or multiple cysts (fluid filled)
  2. normal kidney size

benign

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14
Q

Simple Cysts

SX

A

microscopic hematuria

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15
Q

Autosomal Dominant Polycystic Kidney Disease (ADPKD) sx start when and is it bilateral or unilateral and what is inherited

A

bilateral

4th -5th decade (when the other POLYCYSTIN 1,2 allele gets mutated) (at birth one allele is mutated)

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16
Q

ADPKD involves what gene on what chr (2)

A

PKD1 gene chr 16p13.3 encoding polycystin-1 (matrix interactions on tubules - more Ca) MORE SEVERE

PKD2 on chr 4q21 encoding polycystin-2 (Ca channel on tubules = increase CA+ absorption) LESS SEVERE

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17
Q

ADPKD is accelerated in what pts

A

Blacks

esp with htn or sickle cell

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18
Q

DX ADPKD is done how

A
1. radiologic imaging
both kidneys are very large and heavy 
many cysts all over the kidney (can see in liver also) CT scan used
2. Berry aneurysm 
3. mitral valve prolapse
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19
Q

Autosomal Recessive PKD (ARPKD) looks like what inside

A

sponge like look
+ dilated elongated channels
(smooth on surface)

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20
Q

ARPKD mutation and chr

A
  1. PKHD1 gene on chr 6p21-p23

encoding FIBROCYSTIN

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21
Q

Medullary Sponge Kidney in what location in kidney, renal function, looks like what on kidney

A
  1. CD in medulla dilations
  2. normal renal function
  3. papillary ducts in medulla DILATED with small cysts
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22
Q

Medullary sponge kidney can get scarring from what

A

pyelonephritis

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23
Q

Nephronophthisis location in kidney

A
  1. at medulla cortex junction, sometimes medulla cysts

2. cortical tubulointerstitial damage

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24
Q

Familial Nephronophthisis gene

A

NPHP1 - NPHP11 encoding NEPHROCYSINS,

JBTS2

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25
Q

most common cause of ESRD in children and adolescents

A

Nephronophthisis

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26
Q

Nephronophthisis DX how

A
  1. polyuria + polydipsia (not concentrating), tubular acidosis, Na wasting
  2. unexplained Chronic RF in children + chronic tubulointerstitial nephritis biopsy + FH **
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27
Q

Multicystic Renal Dysplasia can lead to what

A
  1. ureteropelvic obstruction,

2. ureteral agenesis or atresia

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28
Q

Simple cysts location in kidney and size and ultrasonography look

A
  1. cortex NO SX usually
  2. 1cm - 10cm (can distend or hemorrhage and cause pain)
  3. smooth contours, avascular, fluid inside (contrast to tumor)
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29
Q

hydronephrosis

A

renal atrophy (swelling of kidneys from fluid backflow)

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30
Q

how to image obstruction

A

ultrasonography

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31
Q

partial bilateral obstruction in urinary tract SX

A
  1. polyuria + inability to concentrate urine
  2. distal tubular acidosis
  3. HTN*
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32
Q

SX after complete urinary tract obstruction is resolved

A

post obstructive diuresis (massive fluid and NaCl loss)

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33
Q

Urolithiasis is what and prevalence

A

kidney stones

male

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34
Q

what increases risks of kidney stones

A
  1. cystinuria , primary hyperoxaluria
  2. HGPRT def
  3. uric acid buildup
  4. Mg ammonia phosphate
  5. CA oxalate + phosphate (sarcoid, hypercalcemia, hyperparathyroidism)
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35
Q

Image kidney stone

A

CT no contrast is hallmark

however US can be done

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36
Q

Mg ammonium phosphate stones are formed when

A

after urea-splitting bacteria infection (Proteus, Psudomonas, Klebisella, some staph and enterococci) UREA —-> AMMONIA

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37
Q

Mg ammonium phosphate stones are formed causes what to kidney

A

staghorn calculi (large part of renal pelvis) infection and obstruction of the salt formed

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38
Q

Uric acid stones are formed from what

A
  1. hyperurecemia

2. urine under pH 5.5 (insoluable)

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39
Q

risk of uric acid formation

A

male
age
obesity

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40
Q

large stones can cause what sx

also obstruction predisposes to what

A

hematuria

infection

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41
Q

TX for kidney stone pt that has passed the stone and does not have high risk or recurrence

A

if stone recurrs then Thiazide , citrate, allpurinol either can be given

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42
Q

Papillary adenoma is what and same as what and also associated with

A

small adenomas in tubules esp papillaries
= same as low grade renal cell carcinoma
= trisomies 7 and 17

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43
Q

oncocytoma is what and what do you see

A

mass (on one of teh POLES)* + flank pain + hematuria

  1. mahogany brown with central white stellate scar**
  2. large Eosinophilic cells + scattered nuclei
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44
Q

Oncocytoma is what kind of cancer + overabundance of what organelle

A

benign

many scattered nuclei (pink pink cells)

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45
Q

Renal Cell Carcinoma prevalence and inheritance

A

male and 6th decade (not inherited)

younger if AD

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46
Q

most common renal cancer + 4 types

A

Renal Cell Carcinoma

  1. Von Hippel- Lindau (VHL) syndrome
  2. Hereditary Leiomyomatosis
  3. Hereditary papillary carcinoma
  4. Birt - Hogg Dube syndrome
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47
Q

VHL syndrome is what and what happens

A
  1. renal cysts of renal carcinoma
  2. can be hereditary and sporatic
  3. hemangioblastoma of CNS
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48
Q

Hereditary Leiomyomatosis is what and what happens

A
  1. mutation in FH gene (Fumarate hydratase)
  2. aggressive and metastatic papillary carcinoma
  3. cutaneous and uterine leiomyomata
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49
Q

Hereditary Papillary carcinoma is what and what happens and mutation

A
  1. AD
  2. multiple bilateral tumors in papillaries
  3. mutation in MET proto-oncogene
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50
Q

Birt-Hogg Dube syndrome is what and what happens SX and mutation

A
  1. AD
  2. skin (fibrofolliculomas, trichodiscomas, acrochordons) , Lung (cysts/blebs), Renal tumors
  3. BHD gene (Folliculin)
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51
Q

renal cell carcinoma risks to increase this occurence

A
  1. smokers
  2. obesity
  3. htn
  4. estrogen therapy unopposed
  5. abstesto, petroleum, heavy metals
  6. ESRD, CKD, cystic disease, tuberous sclerosis*
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52
Q

TSC associated with what cancer

A

angiomyolipoma (most common in heart) also renal

BENIGN

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53
Q

most potent carcinogen in industries causing lung and bladder cancer

A

Polycyclic hydrocarbons

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54
Q

renal cell cancer location

A

POLES of the kidney —- > can extend into ureter and Collecting system

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55
Q

RCC likes what

A

to invade into veins
can go into IVC and testicular vein

stage 3 at this point

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56
Q

how to see RCC in vessel image

A

CT contrast or color flow US

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57
Q

Clear Cell Carcinoma comes from what and looks like what

A
  1. proximal tubular epithelium
  2. yellow -gray -white (yellow lipid accumulation) (gray-white from necrosis)

= well confined and distort the kidney shape

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58
Q

Clear Cell Carcinoma grows how and cells have what in them and can look like

A
  1. trabecular (cordlike) OR tubular (tubules looking)
  2. clear and granular cytoplasm + glycogen and lipids
  3. atypical and bizarre nuclei + giant cells
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59
Q

most common RCC

A

Clear cell carcinoma (familial 95%) + most are VHL syndrome

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60
Q

Clear cell carcinoma mutation and chr and gene

what does this do

A
  1. VHL gene 3p25.3 chr 3 + other allele gene hypermethylated
  2. VHL gene degrates HIF 1 which if active causes growth (IGF-1, MYC) and angiogenesis (VEGF)
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61
Q

Von Hipple Lindau Disease CAUSES 1 main thing and can lead to what other 3 things

A

AD causing Hemangioblastomas **in CNS (cerebellum and retina)

cysts in pancreas, liver, kidney

RCC (clear cell carcinoma)

Pheochromocytoma

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62
Q

Papillary Carcinoma mutation and associated with

A
  1. 3p deletion (like in CCC)

2. trisomy 7 and 17, loss of Y chr

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63
Q

Papillary Carcinoma location

A

Distal Convoluted Tubule

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64
Q

Papillary Carcinoma cells involved and what you see in stain

A
  1. FOAM cells interstitial in papillary cores
  2. Psammoma bodies*****
  3. scanty very vascular stroma
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65
Q

Chromophobe carcinoma cells seen and location and mutation

A
  1. pale eosinophillic cytoplasm, halo around nuclei
  2. many chr losses, extreme hypodiploidy
  3. CD like in oncocytoma (very GOOD prognosis)
66
Q

Xp11 translocation carcinoma involves what mutation and gene
and is what

A
  1. TFE3 gene on chr Xp11.2

2. type of RCC

67
Q

Collecting Duct Carcinoma other name and what type of cancer and location
and what happens

A
  1. Bellini Duct Carcinoma
    = type of RCC very uncommon
  2. CT in medulla (similar to medullary carcinoma seen in Sickle cell)
  3. fibrotic stroma + malignant gland cells
68
Q

RCC SX Triad and most common SX

A

usually asymptomatic only some

  1. hematuria (microscopic)
  2. flank pain
  3. palpable mass

usually noticed during over 10cm large = fever, malaise, weakness, WL

69
Q

RCC DX and one of the most missed for what reasons Examples

A
  1. has so many paraneoplastic sxs that you dont think kidney (or seen as side effect of cancer tx)
= polycythemia or anemia
= hypercalcemia
= htn
= hepatic dysfunction
= feminization or masculinization 
= cushing 
= leukemoid reaction, amyloidosis
70
Q

Renal Pelvic Tumor SX and location and associated with

A
  1. hematuria noticeable (usually seen wen small), palpable hydronephrosis, flank pain
  2. 50 % with bladder urothelial tumor + renal pelvis
  3. Lynch Syndrome
    2.
71
Q

Renal Pelvic Tumor prognosis and reason

A

poor

= infiltration of wall of pelvis and calyces in common even if small

72
Q

Wilms tumor (nephroblastoma) prevalence and 3 associations grouping it**

A

2yo-5yo

  1. WAGI /R syndrome
  2. Denys-Drash syndrome
  3. Beckwith- Wiedemann Syndrome (BWS)
73
Q

WAGI /R syndrome what and mutation and genes/chr

A
Wilms tumor
Aniridia 
Genitourinal anomalies 
Intellectual disability
= 11p13 (WT1 + PAX6)
74
Q

Denys -Drash Syndrome is what

A
  1. gonadal dysgenesis
  2. early nephropathy (RF)
    = mesangial sclerosis
  3. Wilms tumor
  4. gonadoblastoma
75
Q

Beckwith - Wiedemann Syndrome (BWS)

A

organomegally, macroglossia, hemihypertrophy, omphalocele
+ ADRENAL cortex large cells
= increased risk of Wilms tumor

76
Q

Wilms tumor cells involved and what the 3 types are + mutation that is resistant to chemo

A
  1. sheets of SMALL BLUE CELLS = Blastemal
  2. Abortive tubules + glomeruli = Epithelial
  3. Fibroblastic + myxoid = Stromal

= Mutation in TP53

77
Q

Retroperitoneal fibrosis (RPF) is also called and what happens

A

Ormond Disease

= extensive fibrosis in the retroperitoneum usually anterior L4, L5 —-> entrapment and obstruction of retroperitoneal structures like URETERS

78
Q

Retroperitoneal fibrosis (RPF) explanation to the reason it happens

A

autoimmune against CEROID leaked through arterial wall by atheromatous plaques
(IgG disease)

79
Q

RPF is also associated with and biopsy shows

A

meds (migrane meds, methyldopa, BP meds)

Systemic Idiopathic Fibrosis

Calcified mass is shown in retroperitoneum

80
Q

Cystitis TRIAD **

A
  1. polyuria (every 15min-20min)
  2. dysuria (burning during urination)
  3. Lower ABD pain suprapubic
81
Q

most common organism causing cystitis followed by other 3 possible ones

A
  1. E. Coli
  2. Proteus
  3. Klebsiella
  4. Enterobacter
82
Q

Interstitial cystitis

A

unpleasant pain, pressure, UTI sx more then 6weeks

AND NO infection or cause

83
Q

Cystoscopic findings of interstitial cystitis

A
  1. mucosal fissures
  2. punctuate hemorrhages (glomerulations)
  3. Mast cells found
84
Q

Malakopakia is what

A

defective phagocytes
= chronic bacterial infection (usually E. Coli)
= chronic inflammatory reaction

85
Q

cell seen in Malakopakia

A

Michaelis Gutmann bodies

Ca in large lysosomes in defective Macrophages

86
Q

Polypoid cystitis

A

inflammation from irritation to bladder mucosa (usually from catheters or instrumentation)

= broad bulbous polypoid projections + EDEMA in ureter

87
Q

Polypoid cystitis can be mistaken for

A

papillary urothelial carcinoma

88
Q

cystic glandularis + cystitis cystica

A

interstitial inflammation or metaplasia (adenocarcinoma)

89
Q

Squamous Metaplasia

A

from chronic injury

if extensive keratinizing squamous metaplasia –> dysplastic lesion and SCC

90
Q

nephrogenic adenoma

A

top layer ureter is replaced by cuboidal cells (papillary growth pattern)
= not true metaplasia
= can infiltrate to detrusor muscle

91
Q

Bladder cancer prevalence

A

4th most common in men

95% are from epithelial origin + most common from urethelium

92
Q

Bladder cancer prognosis is best determined by

A

if it has invaded to muscularis propria = DETRUSOR MUSCLE

93
Q

Bladder cancer risks

A

smoking
aryl amine exposure
cyclophosphamide
analgesic use

94
Q

TX urothelial carcinoma of bladder

A

depends on invasion to detrusor muscle

  1. no muscle invasion = resect , intravesicle chemo
  2. muscle invasion = cystectomy, cystoprostatectomy , or radiation , chemo
95
Q

urothelial carcinoma of bladder usually spreads to where

A

peritoneum, liver, lung, bone

96
Q

most common child sarcoma and most common adult sarcoma

A
  1. rhabdomyosarcoma (grape-like mass = botryoides)

2. Leiomyosarcoma

97
Q

urethritis nongonoccal reasons men and women

A
  1. Chlamydia , then Mycoplasma

2. cystitis in women, prostatitis in men

98
Q

urethral caruncle is what

A

inflamed granulation tissue (older F)

RED on opening of urethra

99
Q

Condyloma acuminatum is from what

A

tumor on penis

HPV 6 and HPV 11

100
Q

Peyronie disease

A

microvascular trauma causing fibrosis —-> sclerosing chronic inflammation

(on the top side of penis above the corpus cavernosum)

101
Q

Peyronie disease TX

A

Collagenase clostridium histolyticum,
Verapamil,
INF

102
Q

Squamous Neoplasia of penis is associated with what and 2 types

A

HPV

  1. Bowen Disease
  2. Bowenoid Papulosis
103
Q

Bowen Disease is what, who, what can it lead to

A
  1. penile shaft and scrotum older men
  2. 1 thickened gray/white plaque
  3. can lead to SCC
104
Q

Bowenoid Papulosis is what, who, and can lead to

A
  1. sexually active young men
  2. many red brown papular lesions, associated with HPV 16
  3. regress spontaneously
105
Q

Non-HPV associated Squamous Neoplasia of penis

A

Balanitis Xerotica Obliterant
= on foreskin older patients
= high SCC risk

106
Q

3 risks of SCC of penis

A
  1. HPV
  2. smoking
  3. Lichen Sclerosis et atrophicus (balanitis xerotica obliterans)
  4. low income low hygiene areas
107
Q

protection against penile SCC

A

circumcision

108
Q

E6 and E7 do what

A

HPV proteins
E6 = inhibit p53 and increase TERT telomerase reverse transcriptase
E7 = inhibits p21 and RB

109
Q

epididymitis in childhood cause

A
  1. congenital GU abnormality

2. E. Coli, Klebsiella, Pseudomonas

110
Q

Epididymitis cause sexually active men under 35yo

A

C. Trachomatis

Neisseria Gonorrhoeae

111
Q

Epididymitis cause men over 35yo

A

E. Coli, Pseudomonas

112
Q

Orchitis is what and most common cause

A

Testicular infection

  1. N. Gonorrheae
  2. Mumps
  3. Mycobacterium
  4. Treponema Pallidum
113
Q

Testicular Torsion SX

A
  1. edematous, tender, testicle/scrotum
  2. effected testicle lies horizontally
  3. high riding testicle from spermatic cord shortening
114
Q

Testicular Torsion tests to do on physical exam

A
  1. Cremasteric reflex : X elevation of testicle when stroking upper inner thigh
  2. Prehn sign : Lifting scrotum relieves pain in epididymitis only INCREASES pain in torsion**
115
Q

Scrotal US of Testicular Torsion

A

color doppler shows decreased vascular perfusion in testicles

116
Q

TX of Testicular Torsion and time importance

A

TIME IS EVERYTHING
1. 4-6hr : 95% viability
2. after 12hr : 20%-60%
3. after 24hr : 0%-20%
= surgery to untwist + bilateral orchidopexy
= manual detorsion while waiting for OR (medially to laterally try to untwist testicle = open-book technique)

117
Q

most common benign paratesticular tumor

A

adenomatoid tumor

118
Q

Testicular Tumors L Germ Cell Tumor is associated with what and prevalence

A

male 15yo-45yo

Chr12 short arm duplication

119
Q

Seminoma is what and histology and genes involved

A

most common GCT

  1. clear/watery cytoplasm, large nuclei
    • KIT, +OCT3/4, +podoplanin, -cytokeratin
120
Q

Seminoma tumor markers and TX

A
  1. syncytiotrophoblasts (high hCG = even higher in choriocarcinoma)
  2. radiation, chemotherapy
121
Q

Embryonal carcinoma prevalence and is what

A

20yo-30yo

more aggressive GCT

122
Q

Embryonal Carcinoma histology and stains

A
  1. large, hyperchromatic nuclei cells, common to have vascular invasion
  2. +OCT3/4, + Cytokeratin, -KIT, -podoplanin
123
Q

Embryonal carcinoma TX

A

aggressive chemo

124
Q

Yolk Sac tumor is what and also called, prevalence

A
  1. endodermal sinus tumor
  2. testicular tumor f infants up to 3yo
    = GOOD prognosis
125
Q

Yolk Sac Tumor histology and stain

A
  1. schiller Duval bodies

2. AFP, a1-antitrypsin, + cytokeratin

126
Q

Choriocarcinoma is what and stains for it and TX

A
  1. very malignant GCT, poor prognosis
  2. HIGH hCG+
  3. aggressive chemotherapy
127
Q

Teratoma is what and histology of it

A
  1. many germ layers involved

2. many types of cells and tissues (usually infants and children)

128
Q

what should be done with solid testicular mass

A

radial orchiectomy (a biopsy can spill into scrotal skin)

129
Q

good markers for testicular cancer

A

hCG, AFP, LDH

130
Q

2 most common sex cord gonadal stromal tumors

A
  1. Leydig cell tumors

2. Sertoli cell tumor

131
Q

Leydig cell tumor is what and histology

A
  1. increase androgens , testicular swelling

2. large granular cells, lipids and lipofusin pigment inside, Reinke crystalloids

132
Q

TX Leydig Cell tumor

A

excision

133
Q

Sertoli cell tumor are what and histology

A
  1. benign tumor

2. trabaculae arrangement, cord-like structures and tubules

134
Q

Sertoli Cell tumor is associated with what and TX

A
  1. Carney Complex (PRKAR1A mutation), Peutz-Jeghers syndrome, familial adenomatosis polyposis syndrome

= excision

135
Q

Primary Testicular Lymphomas are stained how and look like and location

A

+ CD20, +CD45, -KIT,-PLAP (GCT), -cytokeratin

pink fleshy tan looking involving spermatic cord + bilateral

136
Q

Primary testicular lymphoma prognosis and types from most frequent down (3)

A

POOR prognosis can involve CNS frequently

  1. DLBCL
  2. Burkitts Lymphoma
  3. EBV extranodal NK/Tcell lymphoma
137
Q

Hematocele

A

blood collection in tunica vaginalis (usually after testicular torsion or trauma)

138
Q

Chylocele

A

Lymph accumulation in tunica vaginalis

= in elephantiasis (lymphatic obstruction)

139
Q

Spermatocele

A

small cystic accumulation of semen in dilated efferent ducts or rete testis

140
Q

testicular Varicocele

A

dilated vein in spermatic cord (usually left side)
can look like a bag of worms
= correct in surgery

141
Q

prostate has what cells and what helps it grow

A
  1. basal cuboidal epithelium
  2. columnar secretory cells above
    (fibromuscular stroma)

= ANDROGENS help it grow

142
Q

Acute bacterial Prostatitis is what and caused by

A

E. Coli, enterococci, staph

usually from contaminated urine in urethra or bladder, or at times from blood /Lymph, catheterization

143
Q

Acute bacterial Prostatitis SX and how to DX and important thing to do

A
  1. fever, dysuria, DRE : very tender and boggy prostate
  2. urine culture and sxs
  3. DONT BIOPSY it can cause spsis
144
Q

Chronic bacterial Prostatitis is what and caused by

A

recurrent UTI, same as acute organisms (ABS have hard time to get into prostate)

145
Q

Chronic bacterial Prostatitis SX DX

A
  1. low back pain, dysuria, perineal / suprapubic pain, can by asymptomatic
  2. high WBCs in prostatic secretion + bacterial culture
146
Q

Chronic Abacterial Prostatitis also called and SX

A

Chronic pelvic pain syndrome

1. same SX as chronic bacterial prostatitis only no recurrent UTIs

147
Q

Chronic Abacterial Prostatitis DX

A

high WBCs in prostatic secretion only no bacterial culture found

148
Q

Granulomatous Prostatitis is what and caused by what

A

granulomas in prostate tissue

  1. Fungal : immunocompromised (sx from prostatic ducts rupturing and secretions coming out)
  2. TB: from lungs or in immunocompromised
149
Q

what causes BPH

A

DHT GF increase stromal proliferation and decrease death of cells
ESTROGEN also increases proliferation

150
Q

BPH effects what part of the prostate

A

the transitional zone = can compress urethra —-> Slit-like orifice

151
Q

the most common cancer in men

A

Adenocarcinoma of prostate

152
Q

environmental and genetic risk factors for developing prostatic adenocarcinoma

A
  1. high charred red meats, animal fats
  2. = MYC mutation
    = DNA MMR gene mutation
    = HOXB13 mutation
    = DNA repair gene mutation
    = DNA methylation
    = 1st degree relatives
153
Q

most common location of prostatic adenocarcinoma

A

Peripheral Zone esp posterior side where it can be palpated on DRE

154
Q

stains and cells found in prostatic adenocarcinoma

A
  1. perineural invasion
  2. X basal cells
  3. a-methylacyl coA racemose UPREGULATED (AMACR)
155
Q

PSA levels and prostatic adenocarcinoma

A

regulated by androgen
= can be high in BPH
= only good when pt has cancer and wants to monitor recurrence and progress of treatment

156
Q

grading of prostatic adenocarcinoma

A

Gleason System
Grade 1 = neoplastic glands uniform well circumscribed
Grade 5 = infiltrating stroma in cords, sheets, solid nests

157
Q

Gleason scores that are usually treatable

A

6 or 7

8 to 10 are usually not

158
Q

where does prostatic adenocarcinoma invade most likely

A
  1. periprostatic tissu, seminal vesicles, base or bladder (can obstruct urethra)
  2. obturator nodes and para-aortic nodes , bones, axial skeleton
  3. LUMAR SPINE, proximal femur, pelvis, thoracic spine, ribs
159
Q

TX prostatic adenocarcinoma

A
  1. localized and high risk of spread : surgery or radiation + can add hormonal manipulation (15years life)
  2. RADICAL PROSTATECTOMY, radiotherapy with external beam radiation or placement or radiactive seeds in prostate (brachytherapy) = good local control
  3. already spread cancer : androgen deprivation therapy (orchiectomy, or LH-releasing hormone drug)
160
Q

most common tx for prostatic adenocarcinoma

A

RADICAL PROSTATECTOMY (surgery removing prostate), radiotherapy with external beam radiation or placement or radioactive seeds in prostate (brachytherapy) = good local control