Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 2a > Genitourinary > Flashcards

Genitourinary Flashcards

1
Q

What is testicular torsion?

A

sudden onset of pain in one testis, making walking uncomfortable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

At what age are you most likely to acquire testicular torsion?

A

11-30 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What symptoms can accompany pain in testicular torsion?

A

Abdominal pain, nausea and vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the appearance of a testis in testicular torsion?

A

inflamed, hot, tender, swollen in one testis (can be intermittent)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How will the testis lie in testicular torsion, in mild and severe?

A

Mild - high and transversely

Severe - horizontal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What investigations would you do for testicular torsion?

A

Doppler US - shows lack of blood flow to testis

Surgical exploration - the sooner the better to save the testis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the treatment for testicular torsion?

A

ask for consent for possible orchiectomy and bilateral fixation
expose and untwist testes and fix to scrotum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

DD for testicular torsion?

A

epididymo-orchitis, idiopathic scrotal oedema, tumour, trauma, acute hydrocycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is benign prostatic hyperplasia?

A

hyperplasia of the epithelial and stromal cells of the prostate gland in the transitional zone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What part of the prostate undergoes hyperplasia in benign prostatic hyperplasia?

A

The transitional zone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Who most commonly gets benign prostatic hyperplasia?

A

males over 60

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What complications does benign prostatic hyperplasia lead to?

A

Distorts the urethra and obstructs bladder outflow causing urinary retention, recurrent UTI, impaired renal function and haematuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the symptoms of benign prostatic hyperplasia?

A

frequency and urgency of micturition, nocturia, hesitancy, intermittent flow, poor urine stream/dribbling, incomplete bladder emptying, enlarged smooth rostate, haematuria, bladder stones, UTI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What causes benign prostatic hyperplasia?

A

Androgen dihydrotesterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What will a rectal examination show in benign prostatic hyperplasia?

A

enlarged and smooth prostate with a palpable midline sulcus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What investigations should you do for benign prostatic hyperplasia?

A

urine dipstick, microscopy and culture, FBC, U and E, creatinine, LFTs, increased PSA, US of urinary tract and transrectl and renal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the 4 zones in the prostate?

A

fibro-muscular, transitional, central and peripheral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Where is the most common place for prostate cancer to occur?

A

In the peripheral zone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the management of benign prostatic hyperplasia?

A

watchful waiting if mild
complete international prostate symptom score
complete voiding diary
selective a1 adrenoreceptor antagonists e.g.tamsulosin
5-a-reductase inhibitor e.g. finasteride
urethral catheterisation if retention
prostatectomy or permanent catheter
avoid caffeine and alcohol
relax when voiding and train bladder
prostate resection
incision of prostate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How do selective a1 adrenoreceptor antagonists e.g.tamsulosin help treat benign prostatic hyperplasia?

A

They relax smooth muscles in bladder neck and prostate to increase flow rate and reduce symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How to 5-a-reductase inhibitor e.g. finasteride help treat benign prostatic hyperplasia?

A

They block the conversion of testosterone to dihydrotesterone to reduce dihydrotestosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is an epididymal cyst?

A

A non malignant scrotal disease just above the testis that contains spermatocele fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

When are you most likely to get an epididymal cyst?

A

in adulthood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the treatment of an epididymal cyst?

A

No treatment unless symptomatic, then remove

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is hydrocele?

A

Fluid within the tunica vaginalis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the causes of hydrocele?

A

primary - patent processus vaginalis

secondary - tumour, trauma, infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the treatment of hydrocele?

A

Primary can resolve spontaneously, aspirate or surgery of placating the tunica vaginalis or inverting the sac

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is a varicocele?

A

Dilated veins of the pampiniform plexus, normally on the left, appear as dilated scrotal blood vessels, will a dull ache

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are potential complications of a varicocele?

A

Can be associated with subfertility and a dull ache

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the treatment of a varicocele?

A

repair via surgery or embolization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How common is testicular cancer?

A

It is the most common malignancy in men aged 15-44

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the cause of testicular cancer?

A

undescended testis (even after ochidopexy), infant hernia, infertility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the 4 types of testicular cancer?

A

seminoma
non seminomatous germ cell tumour
mixed germ cell tumour
lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the most common testicular cancer?

A

seminoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the more common testicular cancer in 20-30 year olds?

A

non seimnomatous germ cell tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the symptoms of testicular cancer?

A

testis lump, haemospermia, secondary hydrocele, pain, dyspnoea, abdominal mass, effects of secreted hormones (testosterone), metastases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the 4 stages of testicular cancer?

A

1 - no metastases
2 - infradiaphramatic node involvement spread via para aortic nodes
3 - supradiaphramatic node involvement
4 - lung involvement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What investigations should be done in testicular cancer?

A

CXR, CT and US of testis, excision biopsy, a-FP, B-hCG mildly raised, increased serum LDH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the treatment of testicular cancer?

A

radical orchiectomy, surgery, radiotherapy, chemotherapy, self examination education
stage 3 - cycles of bleomycin and etoposide and cisplatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is involved in a radical orchiectomy?

A

Inguinal incision to occlude spermatic cord before mobilisation to reduce risk of intra operative spread

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the prognosis of testicular cancer?

A

> 90% 5 yr survival

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the most common age to get prostate cancer?

A

72

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are risk factors for prostate cancer?

A

age, family history, african

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the symptoms of prostate cancer?

A

weight loss, malaise, fatigue, bone pain and fracture, normocytic anaemia, hypercalcaemia, purpura, immune suppression, anorexia, thirst, confusion, collapse, hard irregular gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What will a per rectum examination show in prostate cancer?

A

enlarged prostate gland, uninodular or multinodularr, midline sulcus is not palpable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is protein specific antigen?

A

It is expressed from normal and neoplastic prostate tissue and secreted into the blood stream?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is an abnormal PSA level and what level is seen in 50% of men with prostate cancer?

A

> 4ng/ml

>10ng/ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What percentage of people with elevated PSA levels do not prostate cancer?

A

6%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What investigations should be done for prostate cancer?

A

FBC, U and E, creatining, LFTs, transrectal US, transrectal prostate biopsy, endorectal coil MRI for staging, TNM staging, urine dipstick, microscopy, PCA3, gene fusion products

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is used for prostate cancer grading?

A

The Gleason grading score form the biopsy, add the two most common together, and the higher the more aggressive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What does the prostate cancer screening involve?

A

annual measurement of serum PSA and digital rectal examination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Where is the most common site for metastases from the prostate?

A

The bone, leading to bone pain and fracture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are some disadvantages of the prostate cancer screening?

A

cost, variable intervals of testing, increased anxiety, overdiagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is the treatment for prostate cancer?

A

macmillan nurses and psychological support
radiotherapy with external beam and brachytherapy
watchful waiting
high intensity US
Goserelin - a LHRH agonist
Antiandrogens e.g. cyproterone
Transuretheral resection of prostate (TURP)
Laparoscopic radical prostatectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How does androgen deprivation therapy work in the treatment of prostate cancer?

A

Uses GnRH agonists e.g. goserline, leuprorelin, orchidectomy to lower circulating androgens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What does androgen deprivation therapy for prostate cancer have to be used with?

A

Needs an antiandrogen e.g. flutamide in the 1st phase due to the initially increase LH and testosterone which could cause a flare in metastases.

The antiandrogen inhibits CYp17 for androgen production to prevent flare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What should be used for prostate cancer treatment if resistant?

A

2nd line hormone therapy e.g. abiratone which inhibits adrenal androgen synthesis
cytotoxic chemo
bisphosphonates
5-a-reductase inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is the treatment of prostate cancer if no metastases?

A

Androgen deprivation therapy and radiotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What parts of the body are lined with transitional cell epithelium?

A

calyces, renal pelvis, bladder, urethra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is another name for bladder cancer?

A

Transitional cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

How common is bladder cancer?

A

4th most common in men
8th most common in women
9th overall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Who is most likely to get bladder cancer?

A

men in the 80s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is the mortality of bladder cancer?

A

50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Why is an elderly women with UTI symptoms cause suspicion for bladder cancer?

A

As UTIs are common in the young, and it is rare she has just become sexually active or changing partners

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

What are risk factors for bladder cancer?

A

smoking, occupational exposure to carcinogens e.g. rubber, leather, plastics, azo dyes, fishing, exposur to industrial chemicals e.g. phenacetin, cyclophosphamide, schitosomiosis (chronic inflammation), chronic infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are the two types of bladder cancer and which is most common?

A

urothelial - 95%

squamous cell - 5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What are the clinical features of bladder cancer?

A

haematuria (usually painless), dysuria, urgency, frequency, flank pain, pain to a metastases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What does grade mean in terms on cancer?

A

indicator of invasiveness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What does stage mean in terms of cancer?

A

extent of the cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are the 4 grades of bladder cancer?

A

Low grade - 70% - recurrence and bleeding
Medium grade
Invasive high grade - 2.5%
Carcinoma in situ - 5% - high rate of progression - poorly differentiated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What investigations should be done in bladder cancer?

A

urine dipstick, blood tests, flexible cystoscopy, upper tract imaging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What is an advantage and disadvantage of using CT over US?

A

CT is more detailed but uses more radiation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Why is a transurethral resection used instead of a biopsy in bladder cancer?

A

To show histological grade and stage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is the treatment of a non muscle invasive bladder cancer?

A

resection and intravesical chemotherapy. Use mitmoycin , mmc and BCG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

How does MMC work in bladder cancer treatment?

A

reduces risk of recurrence and causes cell lysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

How does BCG work in bladder cancer treatment?

A

reduces risk of progression to muscle invasive and upregulates cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is the treatment of a muscle invasive bladder cancer?

A

radical surgery of cystoprostatectomy and urethrectomy with neoadjuvant chemotherapy and radical radiotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is the treatment of a locally advanced bladder cancer?

A

radical surgery with neoaduvant/adjuvant chemotherapy, radical radiotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is the difference between adjuvant and neoadjuvant chemo?

A

adjuvant aims to kill cancer cells and neo adjuvant aims to shrink it before surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is a BCG?

A

A bacilli Calmette Guerum, which is a bladder installation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What is haematuria and how is it detected?

A

blood in the urine found by MSSU or dipstick, it is >3RBC/HPF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is the difference between macroscopic and microscopic haematuria?

A

macroscopic can be seen and microscopic appears normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What does a urine dipstick detect?

A

RBC, free Hb and myoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

How sensitive is a urine dipstick for RBC?

A

97% so many false positives

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What is the difference between uniform and dysmorphic in MSSU?

A 
uniform = non glomerular origin
dysmorphic = glomerular origin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

If there is RBC and dysmorphic in urine tests, what does this suggest?

A

a glomerular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What does the presence of leucocytes and bacteria in a urine test suggest?

A

stones of infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What can cause a false positive blood test?

A

menstruation and exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What does red urine but MSSU negative suggest?

A

porphyria, rifampicin, beetroot, veg dyes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What does a positive dipstick but negative MSSU suggest?

A

haemolysis myoglobinuria, vit C excess

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What does haematuria and dysuria and frequency suggest?

A

UTI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What does haematuria and bilate loin pain suggest?

A

glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What does haematuria and uteteric colic suggest?

A

stone disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What investigations should be done in haematuria?

A

urine analysis, urine cytolody, abdomen US, abdomen CT, cytoscopy, renal biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Rare causes of haematuria?

A

sport, renal artery embolism, renal vein thrombosis, loin pain haematuria syndrome, idiopathic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What do negative urological tests in haematuria suggest?

A

nephrological cuase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

In who is renal cell carcinoma most common?

A

male, ages >60

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Risk factors for renal cell carcinoma?

A

smoking, obesity, hypertension, asbestos

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Signs and symptoms of renal cell carcinoma?

A

haematuria (40%), flank pain, paraneoplastic, weight loss, fever, malaise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Causes of renal cell carcinoma?

A

Von Hippel Lindau disease, dialysis, familial traits, smoking, heavy meals, obesity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What is the mutation in Von Hippel Lindau disease that causes renal cell carcinoma?

A

lose short arm of chromosome 3, causing inactivation of VHL gene which is a tumour suppressor gene, and then there is over expression of VEGF antagonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

How willVon Hippel Lindau syndrome present?

A

phaeochromocytoma, renal and pancreatic cysts, cerebellar haemangioblastoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Treatment of renal cell carcinoma?

A

nephrectomy, exploration is IVC is involved, mutli-tyrosine kinaseinhibitors eg. sumirtinab and sarefinib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

How do multi-tyrosine kinase inhibitors treat renal cell carcinoma?

A

block kinase that usually phosphorylates proteins and cause proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What will investigations show in renal cell carcinoma?

A

liver dysfunction, abnormal LFTs, cholestasis, nephrogenic hepatomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What is the difference between a simple and a complex cyst?

A

simple is benign, complex can be benign or cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

What classification is used in cystic lesions?

A

Bozniak Classification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What is the Bozniak classification?

A

1-simple septations, thin wall
2-irregular wall, no enhancement
3-thick, irregular wall enhancement
4-irregular walls, ca and enhancement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What investigations are done in a cystic lesion?

A

classification, spatial observation, renal biopsy, surgery, bone scan if raised Ca, DMSA renogram if concerned about renal fucntion, CT chest and abdo with contrast, MRI if other organs/IVC affected or poor renal function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What are the histological subtypes in renal cell carcinoma?

A

clear cell (80-90%)
papillary (10-15%)
chromophobe (4-5%)
sarcomatoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What is involved in small renal mass surveillance?

A

can progress to cancer so should be managed with serial imaging to follow progression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What is involved in cryotherapy?

A

2 freeze cycles using helium and argon,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

What is involved in radiofrequency ablation?

A

heating, percutaneously or laparoscopically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

When is cryotherapy and radiofrequency ablation used?

A

in small cystic lesions, in patients with VHL, solitary kidneys, unsuitable for partial/full nephrectomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

When is surgery used for renal cell carcinoma treatment?

A

preferably nephron sparing, T1 and

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Treatment of metastatic renal cell carcinoma?

A

palliative nephrectomy, surgical resection if can do complete resection and has good performance status, radiotherapy to symptomatic bone and brain metastases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Where does metastatic renal cell carcinoma develop from and what do they have high levels of?

A

proximal tubules, high levels of expression of the mulitiple drug resistance protein, so resistant to chemo.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

What is the multiple drug resistance protein expressed in high levels in renal cell carcinoma?

A

P-glycoprotein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

How does sporadic clear cell renal cell carcinoma cause neoangiogenesis?

A

hypoxia inducible factor accumulation from VHL inactivation causes increased VEGF and PDGF to promote neoangiogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Palliative treatment in renal cell carcinoma?

A

palliative nephrectomy, macmillan, embolisation, palliate bleeding, radiotherapy to alleviate bleeding, node pain, bone pain, cerebral mass

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What is polycystic kidney disease?

A

mutations leading to cyst formation, full of fluid, leading to kidney enlargement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

What is the main form of polycystic kidney disease?

A

autosomal dominant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

What are the 2 main mutations in autosomal dominant polycystic kidney disease?

A

PKD1 gene (c16) which codes for the polycystin 1 protein which regulates tubular and vascular development

PKD2 gene (c4) is less cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Symptoms of polycystic kidney disease?

A

acute loin pain from cyst haemorrhage, infection, or urinary stone formation

abdominal discomfort from renal enlargement

flank pain/back pain

hypertension

renal impairment

mitral valve prolapse

cerebral aneuryms, subarachnoid haemorrhage,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Diagnosis of polycystic kidney disease?

A

kidney US shows large, irregular kidneys, multiple fluid filled cysts
hypertension, hepatomegaly
creatinine
head imaging

FH +2cysts 60

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

How does age affect polycystic kidney disease?

A

cysts increase in size with age, leading to more kidney tissure destruction and loss of renal function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Treatment of polycystic kidney disease?

A

monitor BP, ACE-I, dialysis, renal transplant, familial screening, geneic counselling, gene linkage analysis, laproscopic cyst removal, increase water, decrease sodium, avoid caffiene, target sites of action of PKD1/2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

How do renal cysts form?

A

cysts grow in planar polarity then proliferate and multiply so grow outwards of lumen, destroys surrounding tissue and is disconnected from lumen, fluid secretion and apicobasal polarity, causing obstruction and hydronephrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

What is the difference in presentation of polycystic kidney disease in men and women?

A

men - haematuria

women - pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

When is mutation analysis indicated in polycystic kidney disease?

A 
potential LRD under 40
older patient and no FH
atypical cystic disease
prenatal testing for early onset of disease
pre implantation genetic diagnosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What is autosomal recessive polycystic kidney disease and how does it present?

A

1/40000, on chromosome 6, variable signs, may present in infancy with multiple renal cysts and congenital hepatic fibrosis, no specific therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

What is medullary sponge kidney?

A

dilation of collecting ducts in papillae, with occasional cystic change, small caliculi form within the cysts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

How does medullary sponge kidney present?

A

renal colic, haematuria, hypercalciuria, renal tube acidosis, medullary sponge like appearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

What is meduallary cystic disease?

A

autosomal recessive mutation in NPHP1-4 genes, mutating the proteins nephrocystin and inversin in the cilia of the renal tubules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Causes of polycystic kidney disease?

A

simple, acquired, CKD, lithium, congenital: ADPKD, ARPKD, TS. VHL, OFDS1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

What is orofacial digital 1 syndrome?

A

in females (as it is lethal to males), abnormalities to dental and roof of mouth, extra digits and renal cysts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

What is tuberous sclerosis?

A

adenomasebations, spots around the nose, hyperpigmented patches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

What is Von Hippel Lindaw?

A

a pre renal cell carcinoma syndrome, increased renal cancer ris, inherited germline mutations and can devlop brain tumours and hermangioblastomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

What is a typical GFR?

A

120ml/min, 20% of cardiac output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

Examples of creatinine secretion inhibitors?

A

trimethoprim, cimetidine, ritonavir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

How do you predict creatinine generation?

A

based on age, race, gender

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

Where is most stuff reabsorbed in the kidney?

A

in the proximal tubule, reabsorbing Na, glucose, Hco3-, amino acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

What does the descending loop of Henle reabsorb?

A

Na, K, Cl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

What does the distal convoluted tubule reabsorb?

A

Na and Cl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

What does the collecting duct reabsorb?

A

sodium, regulated by aldosterone and secretes potassium and hydrogen ions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

What dirves cellular K+ uptake in the kidney?

A

insulin and catechloamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

Treatment of hypokalaemia?

A

loop diuretics and thiazide diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

Treatment of hyperkalaemia?

A

spironolactone, amiloride, ace-i, arbs, trimethoprim, calcineruin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

What does a increase in aldosterone cause?

A

sodium retention and potassium excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

When are ACE-I and ARB used in CKD treatment?

A

in glomeular hypertension which causes proteinuric CKD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

How is circulating active vitamin D produced?

A

by 1a hydroxylation in the proximal tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

How does CKD affect vitamin D production?

A

increased FGF-23 production which inhibits 1a-hydroxylation, inhibiting vitamin D production

153
Q

Function of calcitrol?

A

increases calcium and phosphate absorption from the gut and suppresses the parathyroid hormone

154
Q

What causes calcitrol deficiency?

A

advanced CKD, leading to secondary hyperparathyroidism

155
Q

What nerves drive detrusor contraction?

A

PNS s3-5 (cholegenic)

156
Q

What nerves inhibit detrusor contraction?

A

SNS t10-l2 (noradenergic)

157
Q

How much fluid can a full bladder hold?

A

400-600ml

158
Q

How much is in an empty bladder?

A
159
Q

Who is more likely to become incontinent and why?

A

women, due to a shorted urether, so less resistance and higher pressure

160
Q

What is acute renal failure?

A

a reversible decrease in GFR caused by damage to the kidneys, leading to a rise in serum urea and creatinine and loss of normal water and solute homeostasis

161
Q

Main causes of acute renal failure?

A

pre renal (40-70%) - failure of cardiac/liver/skin/vascular, sepsis, infection, haemorrhage, thrombosis

intrarenal (10-15%) - renal vascular, glomerulinephritis, nephrotic syndrome, nephrotoxis drugs, microangiopathy, hypertension, inflammation, autoimmune disease

post renal (10-25%) - urinary tract obsturction, stones, tumour, prostatic hypertrophy, extrinsic compression

162
Q

Stages of acute renal failure with serum creatinine and urine output?

A

early - creatinine >26.5umol/L or 1.5-2xrise - urine output 6h

moderate - creatinine 2-3x baseline - urine output 12h

severe - creatinine >3x baseline or >350u/mol/L or start RRT - urine output 24h or >12h anaemia

163
Q

In who is acute renal failure common?

A

hospital admissions, elderly, critically ill

164
Q

Mortality of acute renal failure?

A

25-30%

165
Q

Risk factors of acute renal failure?

A

> 75yrs, CKD, HF, Chronic liver disease, diabetes, new drugs, spesis, poor fluid intake, history of urinary symptoms, blockage of urinary tract, dehydrated, infection, aminoglycosides

166
Q

Most common cause of acute renal failure and types of this?

A

intra renal

acute glomerularnephritis - from SLE, erythromyetosis

acute tubular necrosis (50% of AKI)

acute interstitial nephritis - in allergic reactions and infection

vascular

167
Q

Pathophysiology of acute renal failure?

A

vascular change causes inflammation and tubular change causes back leakage of urine

168
Q

What do investigations show in acute renal failure?

A

decrease GFR and urine output, increase nitrogenous waste in blood (urea, creatinine)

apoptosis, loss of adhesion

pericardial rub, suprapubic percussion dull

CT, CXR, avoid imaging with contrast, US (priotity if anuric)

169
Q

Symptoms of acute renal failure?

A

lethargy, nausea, anorexia, itch, confusion, rash, joint pain, red eyes, nasal stiffness, GI bleeding, haemoptysis, reduced urine output, impaired platelet function, abdominal flank pain, oedeme, pruritis

170
Q

Treatment of acute renal failure?

A

treat underlying cause, stop nephrotoxins, fluid, electrolytes, improve perfusion, restrict sodium and potassium, prevent pressure sores, antibiotics, dialysis, nutrition, sequele, prevent further complications, MDT, catheter if obstruction, percutanous nephrostomy, prevent ischemic renal injurt

171
Q

When should you use dialysis in acute renal failure?

A

AEIOU

acidosis -metabolic
electrolyte abnormalities e.g. K
ingestions of toxins - salicylates, methanol, barbityrates
overload of fluid
uremic symptoms e.g. pericarditis
172
Q

What is the classification of acute renal failure?

A

RIFLE

risk, injury, failure, loss, end stage

173
Q

When would you do a urology referral in acute renal failure?

A

infected or obstructed urinary tract, renal stone, urological malignancy, renal trauma, frank haematuria,

174
Q

Management of pulmonary oedema?

A

o2, diureticsm nitrates, opiates, venesection, haemodialysis, ventilatory support

175
Q

What complications can acute renal failure lead to?

A

metabolic acidosis, hyperkalaemiam hyperphosphataema, pulmonary oedema

176
Q

What does prognosis of acute renal failure depend on?

A

underlying cause, most common cause of death is sepsis from impaired immune defence from uaemia, malnutrition or dialysis//catheters

it is reversible

cortical necrosis can heal with scar tissues, tubule regenerate

177
Q

What can you use to determine pre renal or intra renal acute renal failure?

A

urine specific gravity and urine osmolarity are higher in pre renal, urine sodium and fractional excretion of sodium are less in pre renal

178
Q

What is the onset like in post renal AKI?

A

insidious rather than acute

179
Q

What are the 2 phases in acute tubular necrosis?

A

initialoliguric phase from decrease GFR, microvascular vasoconstriction, ischemia, but then tubular cells can regenerate , reversing it

diuresis during recovery phase - improved GFR but still impaired tubular reabsorpton

180
Q

How does acute tubulointerstitial nephritis cause acute renal failure?

A

interstitial inflammation with oedema and tubular damage, occurs do to infection (acute pyelonephritis) or hypersensitivity reaction to drugs (penicillin, NSAIDs)

181
Q

How does hyperkalaemia appear in ECG and what is the treatment?

A

tall tented t waves
small absent p waves
increase PR interval
wide QRS

IV calcium gluconate, Iv insulin and dextrose, ion exchange resins

182
Q

NICE definition for acute renal failure?

A

rise in serum creatinine of 26+mmol/L in 48hrs

50% rise in serum creatinine in past 7 days

drop in urine output to 0.5ml/kg/h for 6 hours

(different for children)

183
Q

What is glomerulonephritis?

A

disease of the glomeruli, inflammation

184
Q

What is the most common cause of end stage renal failure?

A

glomerulonephritis

185
Q

How does glomerulonephritis present?

A

leaky glomeruli, haematuria, proteinuria, hypertension, decreased kidney function, end stage kidney failure, oedema, low urine sodium and fractional excretion of sodium

186
Q

Why is urine sodium low in glomerulonephritis?

A

due to congestion of afferent arterioles, so kidney perceives there to be less blood coming to the kidneys

187
Q

What tests should be done in glomerulonephritis?

A

urines and bloods, complete metabolic profile, azotemia, elevated creatinine, 24 hr urine protein, renal biopsy

188
Q

What is the difference between nephritic and nephrotic syndome?

A

all glomerulonephritis cause nephritic syndrome (RBC in urine), and have the ability to cause nephrotic syndrome if proteinuria is severe enough (>3.5g/day) which can then lead to hypoalbuminaemia and hyperlipidaemia

189
Q

Causes of glomerulonephritis?

A

autoimmune with glomerular (anti-GBM) or non glomerular (immune complexes) antigens

non immunological e.g. DM

190
Q

What is acute nephritic syndrome and how does it present?

A

AKI with rapid deterioration in function, presenting with oliguria, hypertension, oedema and increased intravascular fluid

191
Q

What are the causes of acute nephritic syndrome?

A

ANCA associated vasculitis

goodpastures syndrome (antiglomerular basement membrane disease)

SLE, systemic sclerosis

post streptococcal infection

crescentric IgA

nephropathy/Henoch Schonlein purpura (variant of IgA nephropathy)

192
Q

How does acute nephritic syndrome appear on histology?

A

acute, severe, rapidly progressive

proliferative, membranous, membranoproliferative, cresecnteric

Bowman’s space filled with fibrin, epithelial cells and inflammatory cell matrix to form crescents

compress glomerulus

193
Q

What are the 4 types of glomerular disease and how do they differ?

A

diffuse - all glomeruli
focal - some glomeruli
global - all of the glomerulus
segmental - part of the glomerulus

194
Q

What can cause proteinuria?

A

transient, orthostatic, glomerula abnormalities, increased GFR, reduced renal mass, hypertension, tubular proteinuria

195
Q

How does nephrotic syndrome present?

A

heavy proteinuria, hypoalbuminaemia, periorbital edema (especially on walking), hyperlipidaemia, scrotal vulvul leg and ankle edema, ascites, breathlessness

196
Q

Causes of nephrotic syndrome?

A

primary, DM, amyloidosis, infections, SLE, drugs, malignancy, malaria

197
Q

What are the 3 types of primary nephrotic syndrome and who are they most common in?

A

minimal change - children and adults
membranous - caucasian adults
focal segmental glomerulosclerosis - black adults

198
Q

Management of nephrotic syndrome?

A

treat complications of fluid state and clotting abnormalities, treat underlying cause, diuretics, ACE-I, ARBs, spironalactone, anticoagulation, salt restriction, NSAIDs

199
Q

How does minimal change nephrotic syndrome appear?

A

normal biopsy, but fused podocytes of ECM

200
Q

Treatment of minimal change nephrotic syndrome?

A

steroids

201
Q

How does membranous nephrotic syndrome appear?

A

thickened basement membrane due to immune complex formation or drugs, antiphospholipase A2 receptor antibody positive

202
Q

Treatment of membranous nephrotic syndrome?

A

supportive, immunosuppresives

203
Q

How does focal segmental nephrotic syndrome appear?

A

scarring focal to only some glomeruli involved and segmental

204
Q

Treatment of focal segmental nephrotic syndrome?

A

steroids, immunosuppression

205
Q

What is IgA nephropathy?

A

abnormality in IgA glycosylation leading to mesangium deposition and mesangeum proliferation

206
Q

What is the most common cause of asymptomatic glomerulonephritis?

A

IgA nephropathy

207
Q

Treatment of IgA nephropathy?

A

BP control, ACE-I and ARBs, immunosuppression if aggressive

208
Q

What are the two causes of asymptomatic glomerulonephritis?

A

iga nephropathy and thin membrane disease

209
Q

How will asymptomatic glomerulonephritis present?

A

incidental haematuria and proteinuria, kidney function and BP are normal

210
Q

3 main functions of the kidney?

A

water regulation, salt regulation, acid/base regulation

211
Q

What happens to JVP in fluid overload?

A

becomes more visible and increases

212
Q

What should be done for fluid management?

A

fluid input and output chart, weight and stool chart, oral fluid if able, IV if unable

213
Q

What are the two types of IV fluid?

A

crystalloid and colloid

214
Q

What is crystalloid fluid?

A

small molecules pass through cell membrane form intravascular to extravascular, if fluid contains salt, it stays in intravascular space a bit longer than 5% dextrose e.g. isotonic solutions

215
Q

What is colloid fluid?

A

large molecules which do not pass through cell membrane, remains in intravascular compartment and expands the intravascular volume through higher oncotic pressure

216
Q

What patients are at risk of hypovolaemia?

A

elderly, ileostomy, short bowel syndrome, bowel obstruction

217
Q

What patients are at risk of hypervolaemia?

A

CKD, heart failure, liver failure

218
Q

What is euvolaemia?

A

no signs or symptoms of hypo or hypervolaemia

219
Q

How to treat a rise in creatinine?

A

reduce diuretics or relax fluid restriction

220
Q

What are the 3 methods of renal replacement therapy?

A

haemodialysis, peitoneal dialysis, transplant

221
Q

How does haemodialysis work?

A

exchange out side the body, it is removed for cleansing, dialysed then returned to the body via and AV fistula

222
Q

What is an AV fistula?

A

joining of an artery to a vein to provide permanent and easy access for insertion of needle with good blood flow, 2 needles, one to add and one to remove

223
Q

How long does it take for an AV fistula to be mature?

A

pressure from the artery makes the vein bigger, taking 4-8 weeks

224
Q

How is haemodialysis used in urgent situations?

A

on right atrium and one other side of chest, using a cuffed haemodialysis catheter

225
Q

How often is haemodialysis done?

A

in hospital 4hrs 3x a week or 2-3hrs 4-5x a week at home

226
Q

What drug is also given during haemodialysis?

A

heparin as an anticoagulant as foreign bodies would activate the clotting cascade

227
Q

Side effects of haemodialysis?

A

hypotension from excessive extracellular fluid removal, cramps, nausea, headache, chest pain, fever, rigors

228
Q

What are the potential risks in haemodialysis?

A

blocked dialysis or catheter, infection, fistula aneurym, removal too fast, amyloidosis

229
Q

What is peritoneal dialysis?

A

uses the peritoneum as a membrane to exchange fluids and solutes in the blood in the lower abdomen, waste products move down conc gradient into dialysis fluid

230
Q

What type of catheter is used in peritoneal dialysis?

A

Tenckoff

231
Q

What is the difference between continuous ambulatory peritoneal dialysis (CAPD) and APD?

A

capd - done every 3-4 hours for about 30 minutes

apd - done at night

232
Q

When would peritoneal dialysis be the preferred choice?

A

young, full time work, want control and responsibility, severe HF

233
Q

When would haemodialysis be the preferred option?

A

live alone, frail, elderly, scared of operating machienes, previous abdominal surgery, hernia, lack of space at home

234
Q

Long term complications of dialysis?

A

CV disease, sepsis, peritonitis, amyloidosis

235
Q

Why is amyloidosis caused by dialysis?

A

accuulation and polymerisation of B2 microglobulin as it is not excreted by the kidney but not dialysis

236
Q

Benefits of renal transplant?

A

increased survival over dialysis (80% at 10yr)
can get pregnant
economic advantage
increased QoL, can go abroad

237
Q

Treatment of stage 5 CKD?

A

renal transplant

238
Q

Which is better, living or deceased donor and why?

A

living as increases survival and graft half life, reduces mortality by CV, infection, malignancy, treatment withdrawal

239
Q

Surgical complications of renal transplant?

A

bleeding, infection, blood clot in renal artery, need immuno suppression

240
Q

What is cross matching?

A

final step before any transplant, to see if donors lymphocytes and recipients serum to see any attack, a better match is better survival

241
Q

What is a total match and total mismatch score?

A 
match = 000
mismatch = 222
242
Q

What are the types of match and which is most important?

A

A, B, DR

A is most important, each one has two subtypes

243
Q

What is erectile dysfunction/impotence?

A

the inability to achieve and maintain an erection for sexual performance

244
Q

In who is erectile dysfunction commonly seen?

A

in elderly due to erectile capacity decreasing with age

245
Q

What causes erectile dysfunction?

A

vascular, neurogenic, iatrogenic, anatomical, hormonal, psychogenic

DM, hypertension, MS, nerve damage, hormonal imblances, atherosceloris, heart disease, unhealthy lifestyle, oebese, alcoholic, smoking, drug abuse, medications, antihypertensive, antipsychotics, antidepressant

246
Q

What psychological factors can cause erectile dysfunction?

A

stress, fear, gloom, uncertainty, sadness, relationship problems

247
Q

Lifestyle choices to help erectile dysfunction?

A

quit smoking, reduce alcohol, dont abuse drugs, exercise regularly, psychotherpay, talk to partner

248
Q

What is erectile function?

A

neurovascular phenomenon under hormonal control causing arterial dilation, smooth muscle relaxation and activation of the corporeal veno occlusive mechanism

249
Q

Anatomy of the penis?

A

left and right corpora cavenosa covered by and fused together by tunica albuginea, containing spongy vascular erectile tissue with trabeculated smooth muscle lined by endothelial cells

corpus spongiosum has thinner tunica and contains the urethra, glans penis and bulb of penis

250
Q

Blood supply of the penis?

A

internal iliac supplies the internal pudendal which supplied the

dorsal penile - glans penis
cavernosal - spongy tissue of corpora
bulbar - bulb, spngiosum, glans

251
Q

Venous drainage of the penis?

A

sinusoids to subtunieal plexus to circumflex veins and deep dorsal veins

corpora cavernosa to cavernous veins to crural veins to internal pudendal veins

252
Q

Nerve supply of the penis?

A 
erection = s2-s4
relax = t11-l2

cavernous never carries both fibres

253
Q

Physiology behind an erection?

A

NO release causes cGMP build up

cGMP dependent pKa activates large conductance, K+ channels open, so hyperpolarising and relaxing vascular and trabecular smooth muscle cells allowing engorment

254
Q

What is the difference between psychogenic and organic erectile dysfunction?

A

organic is gradual, no erection in any circumstances and morning erections are effected

psychogenic is sudden, situational and unaffected by morning erections

255
Q

Causes of hypogonadism?

A

testicular dysfunction (high LH, low testosterone), hypothalamic dysfunction (low LH as cant produce any), pituritary dysfunction, chronic illness, age

256
Q

Tests for erectile dysfunction?

A

nocturnal penile tumescence and rigidity, intracavernosal injection test, duplex USS of penile arteries, arteriography, morning testosterone, fasting glucose, lipid profile

257
Q

Treatment of erectile dysfunction?

A

lifestyle, psychosexual counselling, PDE5 inhibitors, ampomorphine SL, intracavernous injections, intraurethral aloprostadil, vacuum device, testosterone replacement, monitor for hepatic and prostatic disease, viagra, change BP meds, start satin, penile prosthesis implantation

258
Q

How do PDE5 inhibitors treat erectile dysfunction?

A

increase blood flow, vasodialation and erection via action on NO

259
Q

What are the 3 types of oral pharmacology for erectile dysfunction?

A

sildenafil (viagra), tadalafil (Cialis) and vardenafil

260
Q

How does sildenafil (viagra) work?

A

60 minute wait after administration, effected by food and alcohol, reduced efficacy after fatty meal, increased erections in diabetics, successful intercourse, cheap and can be prescribed

261
Q

How does tadalafil work in erectile dysfunction?

A

30 min wait, maintained for 36 hours, 2 a week, last long time

262
Q

How does varenafil treat erectile dysfunction?

A

30 min wait, less effective after fatty meal

263
Q

When is oral pharacology contraindicated in erectile dysfunction?

A

concurrent use of nitrates, hypertension, degenerative retinal disorders, unstable angina, stroke, MI, bleeding, peptic ulcer, renal/hepatic impairment

264
Q

Side effects of oral pharmacology in erectile dysfunction?

A

headache, flushing, dyspepsia, nasal congestion, dizziness, visual disturbance, back pain, myalgia

265
Q

Side effect of alpha blockers ?

A

orthostatic hypotension

266
Q

How does sublingual apomorphine treat erectile dysfunction?

A

centrally acting dopamine agonist, sublingual, no CI with nitrates, lower efficacy than PDE5 inhibitors, limited to mild-moderate ED

267
Q

How does a vacuum constriction device treat erectile dysfunction?

A

passive engorgment with constricton ring, 90% efficacy and reduced efficacy over time, keeps the blood in the penis due to pressure, causing penis enlargement, use for 30 mins, it is a cold erection

268
Q

Side effects of a vacuum constriction device for ED?

A

painful, inability to ejeculate, petechiae, bruises, numbness, expensive

269
Q

Contraindications of vacuum constriction device for ED?

A

bleeding disorder or anticoagulants

270
Q

How do intracavenosal injections treat ED?

A

inject into copra cavernosa e.g. alprostadil

271
Q

Side effects of intracavenosal injections for ED?

A

pain, prispism, fibrosis, leading to a high drop out rate

272
Q

What is a priapism?

A

a prolonged erection for more than 4 hours, risk of permanent ischemic damage to the copara

273
Q

Treatment of priapism?

A

aspirate coproa with 19 gauge needed, inject phenylephrenine if that fails

274
Q

How does intraurthral alprostadil treat ED?

A

void, then massage pellet into urethra

SE pain, dizzines and urethral bleeding

275
Q

How does a malleable prosthesis treat ED?

A

2 rods, placed in corpora cavernosa surgically, so it is always hard and you just postion it yourself, but can cause penis shortening

276
Q

How does a mechanical implant treat ED?

A

2 empty cylinders into corpra cavernosa and pump is placed in scrotum, reservoir placed in abdomen

277
Q

What is urinary incontinence?

A

involuntary passage of urine which is sufficient enough to be a health or social problem

278
Q

What is voiding?

A

relaxing sphincters and contracting detrusor muscle, overall control and coordinate of micturition is by higher brain centres

279
Q

In who is urinary incontinence seen?

A

common in elderly >65, 25% of women, 15% of man

280
Q

Under what control are the bladder sphincters under?

A 
internal = involuntary
external = voluntary
281
Q

What happens in an empty bladder?

A

decrease in stretch fibres in the bladder, causing the SNS to cause the detrusor muscle to relax and internal spincter contract via the hypogastric nerve and causes the pontine micturition centre to release a PSNS fibre to inhibit M3 and have detrusor relaxation, also activates pudendal nerve to activate skeletal muscle of external sphincter

282
Q

What happens when the bladder is full?

A

increase in stretch fibres to cause sphincter relaxation and detrusor muscle contraction

283
Q

What are the 4 types of incontinence?

A

urge, stress, overflow, functional

284
Q

What is urge incontinence?

A

overactivity of detrusor so it thinks it full, causing it to leak , causing urgent urination (detrusor instability)

285
Q

What can cause urge incontinence?

A

bladder infection, stones, stroke, dimentia, Parkinsons

more common in women

286
Q

Treatment of urge incontinence?

A

treat underlying cause, absorbant pad, condom catheter, incontinence chat, bladder training

287
Q

What is stress incontinence?

A

due to increased intra abdominal pressure causing sphincter weakness and degeneration of pelvic floor and urethral sphincter, leads to urethral atrophy

288
Q

Causes of stress incontinence?

A

women after childbirth, cough, sneeze, weak pelvic floor, neurogenic or iatrogenic in men

289
Q

Treatment of stress incontinence?

A

pelvic floor exercises, intravaginal electrical stimualtion, oestrogen creams, prostatectony, male sling, transurethral injections with autologous myoblasts

290
Q

What is overflow incontinence?

A

due to a full distended bladder leading to leakage of small amounts of urine

291
Q

Cause of overflow incontinence?

A

men with prostatic obsturction or post spinal cord injury or women with cystoceles

292
Q

Treatment of overflow incontinence?

A

catheterisation

293
Q

What is functional incontinence?

A

unable to get to the toilet due to disability e.g. stroke, trauma, dementia, diuretic treatment

294
Q

Treatment of functional incontinence?

A

improve facilities, regular urine voiding, absorbent padding

295
Q

How can autonomic neuropathy cause urinary incontinence?

A

decreased detrusor excitability causing distended atonic bladder with a large residual volume urine which is liable to infection so may need permanent chatheterisation

296
Q

Treatment of an overactive bladder?

A

behaviour therapy - frequency volume chat, caffeine, alcohol
physio - pelvic floor exercise, biofeedback, electrical stimulation
drugs - anticholinergic agents e.g.oxybutynin, tolterodine, tropium chloride, B 3 adrenergic agonist
intravesical botox - causes muscular paralysis
neuromodulation - prelimary tiral then permanent implant if >50% improved
bladder augmentation - detrusor myectomy and cystoplasty
bladder reconstruction
topical oestrogens
surgery

297
Q

Neurogenic stress incontinence managment?

A

artificial sphincter, autologous sling, synthetic tapes

298
Q

Neurological causes of incontinence?

A

brainstem damage leads to incoordination or detrusor muscle activity and sphincter relaxtion

299
Q

What happens to incontinence in a spastic spinal cord injury?

A

supra conal lesion, loses coordination and completion of voiding
reflex bladder contractions, detrusor sphincter dysynergia, poorly sustained bladder contractions, potentially unsafe and poor sustained bladder contraction
conus is functioning but not controlled by the brain
involunatry urination and defaecation

300
Q

What happens to incontinence in a flaccid spinal cord injury?

A

conus lesion with decentralised bladder, loser reflex bladder contraction, guarding reflex and receptibe relaxation

areflexic bladder, stress incontinence, risk of poor compliance

bladder overflows e.g. spina bifida, sacral fracture, transverse myelitis, ischemic injuries, cauda equina

301
Q

What is autonomic dysreflexia?

A

lesions above T6 from overstimulation of SNS below level of lesion in response to a noxious stimulus, giving symptoms of headache, severe hypertension and flushing

302
Q

What is reflex bladder?

A

harness reflexes to empty bladder into incontinence device, suppressed reflexes converting bladder to flaccid type and then empty regularly, suppress with anticholinergics, botox, cystoplasty

303
Q

What is C5 tetraplegia?

A

no movement or sensation below upper chest and minimal hand function, has spasm and is at risk for autonomic dysrefelexia, reflex bladder, reflex bowel and reflex erections

manage with suprapubic indweling catheter, coveen drainage, SARS and urostomy

304
Q

What is coveen drainage?

A

no indwelling catheter, needs monitoring, develop incomplete bladder emptying in the long term, make the sphincter safe with sphincterotomy and intersphincteric botox

305
Q

What is SPC?

A

inserted under anaesthetic, preferably spinal, for infections, stones, autonomic dysreflexia, use clip and release and use large catheters

306
Q

What is paraplegic?

A

paralysed from waist down with normal upper body function, has spasm, reflex bladder, reflex bowel and reflex erections

manage with suprapubic catheter, coveen or suppresses reflexes

307
Q

How does MS cause incontinence?

A

demyelinated nerves cause damage and prevent transmission, causing overactive bladder syndrome, urinary urgency, frequency or incomplete bladder emptying

308
Q

What is renal calculi?

A

stones in the renal tract

309
Q

What are renal calculi made of?

A

small masses of minerals when they are very concentrated and become crystallised: calcium, strivite or uric acid crystals

310
Q

Symptoms of renal calculi?

A

lower abdominal pain, painful and frequent urination, haematuria, nocturia, UTI, dark urine

311
Q

Main causes of bladder stones?

A

enlarged prostate, damaged nerves to the bladder, weakened bladder wall, diverticular, inflammed bladder, UTI, radiation to urinary tract, catheters, hypercalcaemia, hyperuricaemia, from kidney stones travelling down

312
Q

Risk factors for bladder stones?

A

dehydration, infection, low protein, older men, rare in the young, neurogenic bladder

313
Q

What is renal colic?

A

caused by kidney stones, rapid onset of unilateral loin pain, unable to get comfortable, radiates to groin and ipsilateral testis with nausea, vomiting, fluid loading, flank pain, back pain

314
Q

Investigations for renal calculi?

A

distended stomach
24 hr urinalysis of calcium, uric acid, oxalate and citrate
CT KUB (kidney, ureter, bladder) for radiopaque stnes
US/IVU
chemical analysis for stone composition
KUBXray
NCCT KUB

315
Q

Treatment of renal calculi?

A

small ones are observed, intravenous pyelogram to detect stones, litholapasty, surgical removal, extracororeal shock wave lithotripsy if large, antegrade uteric stent insertion, nephrostomy insertion, allopurinol, low oxalate diet, stop diuretics, low calcium diet, antiemetics, IV fluids, analgesics and tamsulosin, antibiotics

316
Q

Complications of renal calculi?

A

recurrent UTI, recurrent calculi, obstruction, trauma, bleed

317
Q

Prevention of renal calculi?

A

hydrate, low Na diet, normal dairy, healthy protein, reduce BMI, exercise, deacidify urine/alkalisation, cysteine binders (captopril, penicillamine)

318
Q

What is piyonephrosis?

A

combination of infection and obstruction which can lead to loss of renal function in 24 hours and systemic sepsis and septic shock, treat with IV antibiotics, IVI, o2 and drainage

319
Q

DD of renal calculi?

A

ruptured AA, bowel, gynae, testicular torsion, MSK

320
Q

What is congenital COLA?

A

where you cant keep aminoacids, and cystine renal calculi form

321
Q

Prevention of uric acid stones?

A

deacidification

322
Q

Prevention of cystine stones?

A

excessive overhydration, urine alkalinisation, cysteine binders, genetic counselling

323
Q

Consequences of urospesis?

A

20 digit gangrene

324
Q

How big are kidney stones?

A

most are relatively small but can grow large, leading to increased pressure and pain

325
Q

Pathophysiology of urinary tract obstruction?

A

severity is based on size, rise in intraluminal pressure, dilation proximal to obsturction, compression and thinning of renal parenchyma, progressing to a thin rim and resulting in a decrease size of kidney

326
Q

Effect of urinary tract obstruction on tubular function?

A

dysregulation of aquaporin water channels in the proximal tubule, thin descending loop and collecting tubule, leads to polyuria and impaired concentrating capacity

decreased sodium transport leading to impaired ability to concentrate and dilute urine

greater sodium and water excretion after release of BUO than UUO, due to retention of Na, water, urea nitrogen and increased ANP which stimulate a profound naturesis

altered potassium and phosphate excretions

deficit in urinary acidification

327
Q

Gross pathological changes to the kidney due to obstruction?

A

dilation of pelvis and ureter, blunting of papillary tips, heavier kidney, edematous parenchyma, cortex and medullary tissues have thinned, cysts appearing

328
Q

Microscopic pathological changes to the kidney due to obstruction?

A

lymphatic dilation, interstitial oedema, tubular and glomerular preservation, collecting duct and tubular dilataton, widening of Bowman’s space, tubular basement membrane thickening, cell flattening, papillary tip necrosis, regional tubular destruction, inflammatory cell response, widespread glomerular collapse, tubular atrophy, interstitial fibrosis, proliferation of connective tissue in collecting duct

329
Q

What is SIRS?

A

severe inflammatory response syndrome which as two of:

>38c/90, RR>20, pCO212000or

330
Q

What is sepsis?

A

2xSIRS and confirmed suspicion

331
Q

What is severe sepsis?

A

sepsis and end organ damage, hypotension with SBP2mmol

332
Q

What is septic shock?

A

severe sepsis with perisitant hypotension

333
Q

Management of urosepsis?

A

diagnose with screening sepsis tool, treat with sepsis 6, manage systemic factors, relieve pressure with catheter and nephrostomy

334
Q

What is the sepsis 6 treatment?

A

high flow o2, blood cultures, iv antibiotics, iv fluid resuscitation, check lactate, monitor hourly urine output

must do this within one hour then critical care support to complete early goal directed therapy

335
Q

What is asymptomatic bacteriuria?

A

normal urine is sterile but is coming increasing common and may need treatment in pregnancy and children, bacteria ispresent in all catheterised patients

336
Q

Why should you not treat asymptomatic bacteriuria?

A

increases antibiotic resistant organisms and does no sterilise the system or reduce the number of bacterial species, should only be done if symptoms occur

337
Q

Why are intermittent self catheters preferred?

A

lowest risk of catheter related complications, and provides max protection for kidneys and better QoL

338
Q

What is a UTI?

A

inflammatory response of urothelium to bacterial invasion associated with bacteruria and pyuria

339
Q

What is the main organism to cause UTIs?

A

E.coli

coagulated proteus sp., enterococci, Kiebsiella sp.

340
Q

What is bacteriuria?

A

prescence or bacteria in the urine that can be asmyptomatic or symptomatic

341
Q

When does bacteriuria need treating?

A

in pregnancy due to the risk of pyelonephritis and preterm labour risk

342
Q

What is the difference between pathogenic and contaminant bacteriuria?

A

pathogenic is single isolate and contaminant is mixed growth

343
Q

In who is bacteriuria most common?

A

over 70s, females, catheters, less common in those who have been circumcised

344
Q

What is pyruria?

A

prescence of leukocytes in urine, appearing as pus in the urine, associated with infection as it is the hosts tissue response

345
Q

Causes of pyruria?

A

treated UTI, appendicitis, calculi, bladder tumour, papillary necrosis, PKD, chemical cystisis, tubulointerstitial nephritis

346
Q

Symptoms of cystisis?

A

dysuria, frequency, urgency, pain, haematuria, cloudy, smell

347
Q

Treatment of cystisis?

A

hydration, cranberry, ibuprofen, antibiotics

348
Q

Diagnosis of cystisis?

A

urine multistix dipstick

nitrates and leucocytes means UTI in 98.5% of cases as nitrates are a product of bacteria
haematuria
pH >8 in urea splitting infections
S9 raised in concentrated/protein rich urine
proteinuria
glucose - DM increases UTI risk
ketones - raised in catabolic states

MC+S, clean catch

349
Q

What is classed as a complicated UTI?

A

males, pregnant, children, reucrrent infection, immunocompromised, nasocomial infection, structural/functional abnormality, SIRS, urosepsis, associated disease

350
Q

Treatment of uncomplicated UTI?

A

antibiotics e.g. trimethoprim, nitrofuratoin
increased fluids, void pre and post sex
hygiene

351
Q

Causes of antibiotic resistance?

A

extended spectrum B lactamase production reduces effectiveness of penicillins and cephalosporins

DNA changes e.g. plasma mediated, altered binding sires, altered permeability

repeated antibiotic course or not finished antibiotics

352
Q

What is classed as a recurrent UTI?

A

> 2 episodes in 6 months or >3 in 12 months
caused by reinfection, bacterial persistance or unresolved infection
can be same or different organism >2 weeks after stopping antibiotics

353
Q

What is a UTI relapse?

A

recurrance of bacteriuria with the same organism within 7 days of completing treatment

354
Q

Treatment of complicated UTI?

A

MSU needed, longer antibiotics course, USS scan, avoid spemicides and perfumed soaps, vaginal oestrogen replacement, prosnthrocyadins (cranberry), prophylaxis, GAG replacement, urovaxom for Ecoli infection

355
Q

How many pregnant women will develop pyelonephritis?

A

20%

356
Q

What complications can complicated UTIs lead to?

A

renal papillary necrosis, renal or perinephric abscess with gram negative septicaemia

357
Q

Who is most likely to get prostatitis?

A

men of all ages, most common one in men

358
Q

What is the NIDDK/NIH classification for prostatitis?

A

1 - acute bacterial with s.faecalis and ecoli and chlamydia, presents with systemically unwell, fevers, rigors, significant voiding, pelvic pain, swollen prostate, treat with analgesia and levofloxacin

2 - chronic bacterial or non bacterial, symptoms >3 months, recurrent, pelvic pain, voiding LUTS, uropathogens and blood in urine, treat with anti inflammatorys and a blockers

3 - chronic pelvic pain syndrome and can be inflammatory or non inflammatory

4 - asymptomatic inflammatory prostatitis

359
Q

Treatment of prostatitis?

A

1 - antibiotics e.g. gentamicin and co-amoxycillin
once well, 2-4 weeks quinolone
IRUSS guided abscess drainage if >1cm

2 - 4-6 weeks quinolone and a blocker and NSAIDs

360
Q

What causes urethritis and the symptoms?

A

Neisseria gonorrhoea - urethral pus, dysuria, tenesmus, proctitis, discharge
nongonococcal urethritis - thinner discharge caused by c.trachomatis
non infective urethritis - traumatic, chemical, cancer

361
Q

Treatment of urethritis?

A

mainly STI causes so managed by GUM

362
Q

What causes epididymoorchitis?

A

chlamydia if

363
Q

Symptoms of epididymoorchitis?

A

hot, red swollen testicular pain

364
Q

Treatment of epididymoorchitis?

A 
GUM if STI
quinolone if >35 or no STI
Deoxycycline and azithromycin if STI likely as it can lead to infertlity
supportive underwear
NSAIDs
drainage of abscess
ceftriaxone is gonorrhoea suspected
365
Q

What is pyelonephritis?

A

infection of the renal parenchyma and soft tissues of the renal pelvis/upper ureter with neutrophil infiltration

366
Q

How does pyelonephritis present?

A

tender loin pain, fever, pyuria, small cortical abscessses and streaks of pus in renal medulla

367
Q

Who does pyelonephritis affect?

A

women

368
Q

Treatment of pyelonephritis?

A

IV Gentamicin/co amoxicillin +/- HDU, increase fluid intake, drain obstructed kidney, catheter is compromised, analgesics, oral antibiotics once well, complete 10-14 days of antibiotics

369
Q

What can pyelonephritis lead to?

A

renal abscess and emphysematous pyelonephritis

370
Q

What is vesicouretic reflux?

A

incompetent valve between bladder and ureter, allowing reflux or urine during bladder contraction and voiding, causing dmaage of scarring and hypertension

371
Q

Who is most likely to get reflux?

A

children, caused by structural or functional abnormalities

372
Q

What is the general treatment for lower UTI?

A

nitrofurantoin or trimethoprim, increase fluid intake

373
Q

What added investigations would you want to do in a complication UTI?

A

renal US, cystoscopy, KUB-XR

374
Q

Treatment of an upper UTI?

A

ABCDE, rehydration, IV antibiotics, drain hydronephrosis, catheter, percutaneous nephrostomy

coamoxiclav, ciprofloxacin, OR gentamycin and cefuroxime IV

375
Q

DD of acute pyelonephritis?

A

acute appendicitis, diverticulitis, cholecystitis, ruptured ovarian cyst, ectopic pregnancy

376
Q

What protein inhibits bacterial adhesion in the urinary tract?

A

Tamm-Horsfall protein

377
Q

Host factors against UTI?

A

urinary IgA, vaccine therapy, antegrade flushing of urine, gag layer resists adhesion, low urine pH, high osmolality

378
Q

Bacterial factors that increase UTI risk?

A

capusule, toxins, enzymes, urease to make the urine more alkaline, a fimbril attachments, fimbriae/pili

Phase 2a (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions