Brainscape's Knowledge GenomeTM

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


See full index

GRACE Phase 2a Medicine > Renal/Genitourinary > Flashcards

Renal/Genitourinary Flashcards

1
Q

Describe the parasympathetic, sympathetic and somatic innervation to the bladder respectively

A

pelvic nerve, hypogastric plexus, pudendal nerve

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

LUTS (lower urinary tract symptoms) associated with storage

A

urgency, frequency, nocturia, overflow incontinence

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

LUTS (lower urinary tract symptoms) associated with voiding

A

poor intermittent stream, hesitancy, incomplete emptying, post micturition dribbling, straining

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

What is serum prostate specific antigen (PSA)?

A

A glycoprotein that is expressed by normal and neoplastic prostate tissue, produced to form the fluid in semen

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

In what cases is PSA raised?

A

BPH, prostate cancer, perianal trauma, taller men, recent ejaculation, UTI, prostatitis

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

What does a PSA of >1.4ng/ml indicate?

A

increased risk of LUTS progression (e.g. acute urinary retention)

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

Causes of acute urinary retention?

A

prostatic obstruction (e.g. BPH, prostate cancer), urethral strictures, alcohol, constipation, post-op, infection

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

Cause of chronic urinary retention?

A

prostatic enlargement due to BPH or prostate cancer

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

Treatment for acute urinary retention?

A

catheter, alpha-1 blockers to help relax smooth muscle in the bladder neck

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

What should be considered in any patient with renal impairment?

A

urinary tract obstruction

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

3 classifications of urinary tract obstruction?

A

luminal, mural and extra-mural

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

Diagnosis of urinary tract infection

A
  • specific location of pain
  • Bloods - U&Es and creatinine raised
  • Urinary sample
  • Ultrasound
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Treatment for lower tract urinary obstruction?

A

urethral or suprapubic catheter

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

Advantages of a suprapubic catheter vs a urethral

A
  1. Less risk of urethral damage and UTI

2. Less likely to be colonised by bacteria in the long-term

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

Treatment for upper tract urinary obstruction?

A

Nephrostomy

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

What is benign prostatic hyperplasia (BPH)?

A

increase in the size of prostate without the presence of malignancy

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

What is the prostate?

A

Accessory gland in the male reproductive system, secretes 70% of the volume of seminal fluid and is hormone dependent, found just below the bladder with the urethra running through it

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

Epidemiology of BPH?

A

common, affects 24% of men aged 40-65, 40% of men >65, affects Afro-Caribbeans more severly than white men

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

What procedure to the testicles is protective of BPH? why?

A

castration, lack of androgens, testosterone does not cause BPH but is required for BPH

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

Clinical presentation of BPH?

A

frequency of micturition, nocturia, delay in initiation of micturition, post-void dribbling, acute urinary retention

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

Pathophysiology in BPH?

A

Benign proliferation of inner layers of prostate, gets bigger, squeezes and may partially block the urethra –> urinary problems

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

Diagnosis of BPH?

A

digital rectal exam (feel enlarged and smooth prostate), serum electrolytes and renal ultrasound, serum PSA (may be raised), biopsy and endoscopy

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

In BPH, how might the prostate feel upon rectal examination?

A

Enlarged and smooth

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

Lifestyle management of BPH?

A

decrease alcohol, caffeine

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

Drugs to treat BPH?

A
  1. Alpha-1 antagonists e.g. tamsulosin to relax smooth muscle in bladder and increase urinary flow
  2. 5-alpha reductase inhibitor e.g. finasteride as it blocks the conversion of testosterone to dihydrotestosterone (androgen responsible for prostatic growth)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Kidney cancer - most common form

A

renal cell carcinoma

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

Epidemiology of renal cell carcinoma

A

Males > females, average age 55

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

Clinical presentation of renal cell carcinoma

A

haematuria, loin/lumbar pain, mass in flank, malaise, weight loss, fever

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

Investigations for renal cell carcinoma

A

Ultrasound, CT scan, MRI - staging, renal biopsy

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

Management of renal cell carcinoma?

A

localised disease - nephrectomy

metastatic disease - interleukin-2 and interferon lead to remission

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

bladder/urothelial cancer - most common type of which type of carcinoma?

A

transitional cell carcinoma

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

Epidemiology for bladder/urothelial cancer?

A

males > females, av age 80

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

Clinical presentation of bladder/urothelial cancer

A

Painless haematuria, recurrent UTIs, voiding irritability

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

Investigations for bladder/urothelial cancer?

A

Cytoscopy and biopsy (diagnostic), CT for staging, urinary tumour markers

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

management for bladder/urothelial cancer?

A

cystectomy, surgical resection, chemotherapy

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

Risk factors for prostatic cancer?

A

FHx, increasing age, genetic predisposition (HOXB13 gene)

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

Hormonal factors –> prostatic cancer

A

increased testosterone

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

Clinical presentation of prostatic cancer

A

bladder outflow obstruction, gland hard and irregular (rectal examination), symptoms due to metastases e.g. bone

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

Investigations for prostatic cancer

A

transrectal ultrasound and biopsy (diagnostic), digital rectal exam, elevated serum PSA

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

Management for prostatic cancer

A

Prostatectomy, removal of androgenic drive e.g. bilateral orchidectomy, antiandrogens

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

Risk factors for testicular cancer?

A

Undescended testes, FHx, infertility

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

Clinical presentation for testicular cancer?

A

painless lump in testes, testicular/abdominal pain, symptoms due to metastases

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

Investigations for testicular cancer?

A

Ultrasound, serum concentration of tumour markers

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

Management of testicular cancer

A

orchidectomy, chemotherapy

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

What is chronic kidney disease?

A

abnormal kidney function/structure for > 3 months with health implications

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

Epidemiology for CKD?

A

Risk of CKD increased with age, females > males, often co-exists with CVD and diabetes

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

Classification of CKD?

A
  1. Based on GFR category
  2. Presence of albuminuria
  3. Cause of kidney disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

stage 1 CKD

A

Normal GFR >90ml/min/1.73m^2

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

What are mesangia lcells

A

Specialised cells that provide structural support to the glomerular tuft

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

Causes of CKD?

A

diabetes, glomerulonephritis, HTN, atherosclerotic renovascular disease, acute renal failure

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

Risk factors for CKD?

A

DM, HTN, old age, CVD, renal stones, BPH, recurrent UTIs, SLE, proteinuria, AKI, smoking, chronic use of NSAIDs

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

Presentation of CKD?

A

Early stages often asymptomatic (discovered by chance on routine blood/urine test), nausea, vomiting, diarrhoea, fatigue, weight loss, nocturia, polyuria, symptoms due to salt retention (oedema), sexual dysfunction

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

Complications of CKD?

A
  1. Anaemia - due to reduced EPO production by diseased kidney
  2. Bone disease - impaired 1,25-hydroxy vit D production
  3. Neurological - autonomic dysfunction –> postural hypotension
  4. CVD - occurs due to increased frequency of HTN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Pathophysiology of CKD?

A

Irreversible nephron loss, same burden of filtration spread across less nephrons –> nephron failure

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

ECG investigation for CKD?

A

for high K+

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

CKD urinalysis investigation?

A

Haematuria, proteinuria, albumin:creatinine ratio

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

CKD investigations - bloods

A

Raised phosphate and low calcium, low Hb

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

CKD investigations - serum biochemistry

A

high urea and creatinine, raised ALP, raised PTH

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

Diagnostic investigation for CKD?

A

Biopsy and histology

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

Management of CKD

A

Treatment of underlying disease, treatment to slow renal progression (tight glucose control and ACE-i/ARBs), treatment of renal complications of CKD (e.g. anaemia, oedema), treatment of other complications of CKD, prepare for renal replacement therapy

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

Nephrosis

A

proteinuria due to podocyte pathology

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

Nephritis

A

haematuria due to inflammatory damage

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

3 broad categories of glomerulonephritis?

A
  1. Conditions that damage the glomerular permeability barrier
  2. Conditions that produce severe necrotising glomerular injury
  3. Conditions associated with glomerular inflammation, with mesangial/subendothelial immune deposits
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Conditions that damage the glomerular permeability barrier

A

produce proteinuria (nephrotic syndrome) - minimal change disease, membranous GN

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

Conditions that produce severe necrotising glomerular injury

A

cause leakage of blood (haematuria) and protein (proteinuria) into urine, reduced GFR, leads to acute renal failure, crescentic morphology - vasculitis, anti-GBM disease, PGN

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

Crescentic GN

A

Crescents form - a proliferation of cells within Bowman’s space - as a response to capillary rupture with exudation

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

Conditions associated with glomerular inflammation, in association with mesangial and/or subendothelial immune deposits

A

Lupus nephritis, IgA nephropathy

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

Nephrotic syndrome - epidemiology

A

rare, DM is the most common secondary cause

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

Tetrad of symptoms for nephrotic syndrome

A

Proteinuria, hypercholesterolaemia, hypoalbuminaemia, oedema

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

Proteinuria

A

> 3.5g/24hr

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

Pathophysiology of nephrotic syndrome

A
  • Structural and functional abnormalities of podocytes
  • Increased filtration of macromolecules across the glomerular capillary wall
  • Oedema occurs due to salt retention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Causes of primary nephrotic syndrome

A

minimal change disease, membranous GN, focal segmental glomerulosclerosis

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

Minimal change disease

A

Commonest form of nephrotic syndrome in children, subtle changes to the glomerular morphology on biopsy, steroids induce remission in most

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

Membranous GN

A

Histological presence of immune deposits (IgG and C3) on the podocyte side of the GBM with thickening of the capillary wall secondary to production of new BM, most common in adults

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

Focal segmental glomerulosclerosis

A

Unknown aetiology, sclerosis that is focal and only affects certain glomeruli

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

Secondary causes of nephrotic syndrome

A

DM, amyloidosis, infections (Hep B/C), SLE, RA, malignancy

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

Diagnosis for nephrotic syndrome

A
  1. Renal biopsy to establish cause
  2. Urine dipstick - proteinuria
  3. Baseline measurements - albumin, eGFR, glucose
  4. Serum tests - Anti-AGM antibodies, ANCA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Management for nephrotic syndrome

A
  1. reduce oedema - restrict fluid and salt intake, loop diuretics
  2. reduce proteinuria - ACE-i/ARBs
  3. Treat underlying cause
  4. Reduce risk of complications e.g. statins for hyperlipidaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Nephritic syndrome

A

Caused by inflammation to the glomerulus that results in microscopic or macroscopic haematuria, proteinuria and HTN

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

5 ‘causes’ of nephritic syndrome

A
  1. Rapidly progressive GN (RPGN)
  2. Anti-GBM antibody GN (Goodpasture’s)
  3. ANCA associated vasculitis
  4. Immune complex mediated GN
  5. Membranoproliferative GN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Rapidly progressive GN

A

Any aggressive GN, rapidly progressing to renal failure (not a disease itself), caused by small vessel vasculitis, lupus nephritis, anti-GBM disease, crescents seen in biopsy due to breaks in BGM allowing influx of inflammatory cells

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

Anti-GBM antibody GN (Goodpasture’s syndrome)

A

Autoimmune condition in which the target antigen is on the BM –> production of anti-GBM antibodies –> rapidly progressive GN

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

In some patients with anti-GBM antibody GN, antibodies bind to the antigens in the BM and to?

A

alveolar capillary BMs, resulting in pulmonary haemorrhage and haemoptysis

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

Goodpasture’s syndrome

A

When RPGN + pulmonary haemorrhage occur

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

ANCA associated vasculitis

A

Associated with serum antibodies to neutrophil cytoplasmic antigens - ANCA results in nectrotising glomerulonephritis (not associated with immune complex deposition)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Immune complex mediated GN

A

Deposition of immune complexes on GBM

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

Causes of immune complex mediated GN?

A

IgA nephropathy, post-streptococcal GN, lupus nephritis

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

IgA nephropathy

A

Defined by the presence of IgA-dominant glomerular deposits, commonest type of GN

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

Membranoproliferative GN

A

Characterised by mesangial cell proliferation and thickening of the capillary walls with duplications of the basement membranes

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

Presentation of acute nephritic syndrome

A

Haematuria, proteinuria, HTN and oedema, oliguria

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

Investigations for nephritic syndrome

A

Renal biopsy for diagnosis, same as nephrotic syndrome

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

Causes of congential renal cysts

A

Genetic mutation leads to predisposition for cyst formation, there is increased abnormal cell proliferation, cyst initiation, fluid secretion by epithelial cells

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

Causes of renal cysts

A

acquired over time, CKD, autosomal dominant/recessive polycystic kidney disease

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

Most common type of polycystic kidney disease?

A

Autosomal dominant

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

Causes of ADPKD?

A

mutation in either the PKD1 (85%) or PKD2 (15%) gene

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

Pathophysiology of ADPKD

A

PKD1 and PKD2 encode for the polycystin proteins which are transmembrane proteins which interact to promote the normal development and function of kidneys. The polycystin complex occurs in cilia that are responsible for sensing flow in the tubules, and defective proteins –> defective ciliary signalling –> disorientated cell division –> cyst formation

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

Clinical presentation of ADPKD?

A 
excessive water and salt loss (causing problems such as nocturia), loin pain, HTN, bilateral kidney enlargement
renal colic (due to clots), haematuria, renal stones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Extra-renal manifestations of ADPKD?

A

Polycystic liver damage, subarachnoid haemorrhage (associated with berry aneurysm formation), pancreatic cysts can cause pancreatitis, male infertility, cardiac abnormalities (mitral valve prolapse)

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

Diagnosis of ADPKD?

A

Clinical examination - large irregular kidneys, HTN
Ultrasound - detect cysts
In adults with FHx, criteria for diagnosis:
1. at least 2 renal cysts <30
2. 2 cysts per kidney 30-59
3. 4 cysts per kidney 60+

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

Management of ADCKD?

A

No treatment to slow progression, BP control, analgesia to treat stones, laparoscopic removal of cysts to help with pain

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

Autosomal recessive polycystic kidney disease (ARPKD) - epidemiology?

A

Less common than ADPKD, disease of infancy and childhood, leads to differing degrees of renal and hepatic involvement

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

ARPKD - later the manifestation of the renal disease, the…

A

more marked the liver disease (tend to show opposite degrees of severity)

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

Clinical presentation of ARPKD?

A

variable, presents in infancy with multiple cysts and congenital hepatic fibrosis, enlarged polycystic kidneys, kidney failure

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

Diagnosis of ARPKD

A

Diagnosed antenatally or neonatally, ultrasound to see cysts, CT and MRI, genetic testing

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

Treatment for ARPKD?

A
  • No treatment
  • Family counselling
  • Laparoscopic removal of cysts to alleviate pain
  • BP control with ACE-i
  • Analgesia for stones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Erectile dysfunction

A

persistent inability to attain and maintain an erection

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

Pathophysiology of erectile dysfunction

A

Neurogenic - failure to initiate
Arteriogenic - failure to fill
Venogenic - failure to store

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

3 arteries supplying the penis

A

dorsal, cavernous, urethral

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

Causes of erectile dysfunction

A

age, diabetes, coronary artery disease, dyslipidaemia, trauma, drugs, hypogonadism

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

Examination for erectile dysfunction

A

height, weight, thyroid exam, pulmonary status, peno-scrotal exam

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

Tests for erectile dysfunction

A

urinalysis, fasting blood glucose, PSA, prolactin

112
Q

Drugs used to treat erectile dysfunction?

A

PDE-5 inhibitors

113
Q

Type of patient who will be categorised as having an uncomplicated urinary infection?

A

Non-pregnant women

114
Q

Types of patients that would fall in complicated category of UTI>

A

Pregnant, men, catheterised, children, recurrent/persistent infection, immunocompromised

115
Q

What is a UTI?

A

inflammatory response of the urothelium to bacterial invasion, usually associated with bacteria and pus in the urine

116
Q

Risk factors for UTIs?

A

Women (pregnancy, post-menopause, new sexual activity), urinary catheters, urinary tract stasis/stones, DM or immunosuppression

117
Q

5 pathogens commonly causing UTIs in a primary setting? (KEEPS)

A 
K - Klebseilla spp.
E - E.coli
E - Enterococci
P - Proteus spp.
S - Staphylococcus spp.
118
Q

Upper tract UTI?

A

pyelonephritis

119
Q

Lower tract UTIs?

A

cystitis, prostatitis, urethritis

120
Q

Uncomplicated UTI?

A

Normal renal tract structure and function

121
Q

Complicated UTI?

A

Structural/functional abnormality of the GU tract, leading to decreased renal function

122
Q

Pathophysiology of UTIs?

A

Contamination of LUT (often due to own gut flora), colonisation in urethra/bladder, inflammatory response, neutrophil infiltration, bacteria evade the immune response, if left untreated may complicate and spread –> kidneys to form an upperTI

123
Q

Clinical presentation of lower UTI?

A

dysuria, frequency, urgency, haematuria, suprapubic discomfort, cloudy/smelly urine

124
Q

Clinical presentation of upper UTI?

A

vomiting, fever, flank/loin pain

125
Q

Diagnosis of uncomplicated UTIs?

A

Diagnosed in those without known abnormalities if they have 2/3 of the classic symptoms and absence of vaginal discharge

126
Q

UTI in pregnancy

A

Culture rather than dipsticks, positive cultures should be confirmed with second sample, test of cure after one week of treatment

127
Q

Pyelonephritis

A

Infection of the renal parenchyma and soft tissues of the renal pelvis/upper ureter, classic symptoms - loin pain, pyuria

128
Q

Pyelonephritis investigations

A

Abdominal examination - tender loin, bloods

129
Q

Pyelonephritis treatment

A

Fluid replacement, IV antibiotics e.g. co-amoxiclav, drain obstructed kidney ,catheter, analgesia

130
Q

Complications of pyelonephritis

A

Renal abscess, emphysematous pyelonephritis (life-threatening, rare, gas in tissues)

131
Q

Investigations for UTI?

A

Dipstick (non-pregnant and <65), mid-stream urine culture, blood tests, imaging

132
Q

Treatment for isolated attack of UTI?

A

Empirical antibiotics e.g. trimethoprim, or IV antibiotics for an upper UTI

133
Q

Treatment for recurrent UTIs?

A

Lifestyle advice - drink lots of water, wee before bed and after sex
Catheters - when changing the catheter, treat with prophylactic antibiotics

134
Q

What is HUS/ haemolytic uraemic syndrome?

A

HUS is a systemic disease caused by damage arising from the circulating toxin which binds to endothelial receptors, particularly in the renal, GI and CNS. RBCs are damaged as they pass through partially occluded small vessels and subsequent haemolysis occurs, the most common cause of AKI in children

135
Q

TTC =

A

thrombotic thrombocytopenic purpura

136
Q

What is thrombotic thrombocytopenic purpura?

A

Rare blood disorder that leads to blood clots forming in small vessels throughout the body. “Thrombotic” refers to the blood clots that form. “Thrombocytopenic” means the blood has a lower than normal number of platelets. “Purpura” refers to purple bruises caused by bleeding under the skin

137
Q

Why are NSAIDs nephrotoxic?

A

Cause vasoconstriction of the afferent arterioles, therefore reduce GFR

138
Q

What is acute kidney injury?

A

rapid decrease in GFR, leading to abnormal fluid/electrolyte balance, measured by serum creatinine and reduce urine output

139
Q

Current staging system for AKI?

A

KDIGO - uses serum creatinine and urine output to assess severity

140
Q

KDIGO classification of AKI in terms of creatinine

A

Stage 1 - Cr 1.5 - 1.9 times the baseline
Stage 2 - Cr 2 - 2.9 x baseline
Stage 3 - >3x baseline

141
Q

Risk factors for AKI?

A

Pre-existing CKD, elderly, male, nephrotoxic drugs, co-morbidity (CVD, malignancy, chronic liver disease, complex surgery)

142
Q

Pathology of pre-renal AKI and examples for each

A
  1. Hypovolaemia - haemorrhage, burns
  2. Reduced CO - cardiogenic shock, MI
  3. Systemic vasodilation - sepsis, drugs
  4. Renal vasoconstriction - NSAIDs, ACE-i, ARBs
143
Q

Pathology of renal AKI and examples for each

A
  1. Glomerular disease - GN
  2. Interstitial disease - drug reaction, infection, infiltration
  3. Vascular disease - vasculitis, HUS, TTP
144
Q

Pathology of post-renal AKI and examples for each

A
  1. Within the renal tract - stones, clots, strictures, renal tract malignancy
  2. Extra-renal compression - prostatic hypertrophy, pelvic malignancy
145
Q

Pathophysiology of pre, intra and post renal AKI?

A

Pre-renal - reduced kidney perfusion
Renal - intrinsic kidney disease
Post-renal - obstruction to urine

146
Q

Clinical presentation of AKI

A

oliguria, may be palpable kidney/bladder, recovery phase lots of dilute urine, arrhythmias due to hyperkalaemia, symptoms of uraemia (fatigue, weakness, confusion, pericarditis), breathlessness (due to combination of anaemia and pulmonary oedema)

147
Q

Diagnosis for AKI

A 
Blood count - anaemia, maybe high ESR
Urine dipstick - glomerular disease (haematuria, proteinuria), etc.
Urine and blood cultures
Serum calcium, etc.
Renal ultrasound
Renal biopsy
148
Q

Treatment for pre-renal AKI?

A

Fluids to correct hypovolaemia, treat sepsis with antibiotics

149
Q

Treatment for renal AKI?

A

Referral to nephrology

150
Q

Treatment for post-renal AKI?

A

Catheterise, CT scan of renal tract

151
Q

General treatment for AKI

A

stop nephrotoxic drugs, optimise fluid balance, treat hyperkalaemia (e.g. insulin and glucose to drive K+ into cells), treat pulmonary oedema with diuretics

152
Q

Indications for dialysis? (AEIOU)

A 
Acidosis
Electrolyte imbalance
Intoxications
Overload (fluid)
Uraemia
153
Q

3 common sites of renal stone deposition?

A

pelivicureteric junction, pelvic brim, vesicoureteric junction

154
Q

Epidemiology of renal stones?

A

common, males > females, peak age 20-40, >50% risk of recurrence once had them

155
Q

Risk factors and causes of renal stones

A

anatomical abnormalities that predisposition to stone formation and blockage, chemical composition of urine that favours crystal formation, dehydration, hypercalcaemia, hyper oxaluria, hypercalciuria, hyperuricaemia, primary renal disease, gout, diet

156
Q

Foods rich in oxalate?

A

Chocolate, rhubarb, strawberries, tea

157
Q

Why do urinary/renal stones form?

A

Over-saturation of urine in a context of a trigger that starts crystallisation. In normal urine there are inhibitors of crystal formation

158
Q

Most common type of urinary stones?

A

Calcium oxalate (60-65%) and calcium phosphate (10%)

159
Q

5 types of urinary stone

A

calcium oxalate and calcium phosphate, struvite, uric acid, cystine

160
Q

Pathophysiology of calcium stone formation

A

hypercalcuria (increased calcium in urine)

hyperoxaluria (increased oxalate in urine)

161
Q

Struvite stones

A

mixed infective stones (magnesium ammonium phosphate + calcium), usually due to a UTI with an organism that produces urease enzymes. Urease hydrolyses urea –> NH3, which raised alkalinity of urine and this paired with NH3 creates favourable conditions for stone formation

162
Q

uric acid stones

A

Associated with hyperuricaemia, dehydration, patients with ileostomies are at risk

163
Q

Why are patients with ileostomies at risk of uric acid stone formation?

A

lower urinary pH, lower urinary volume, higher conc. of Ca2+, uric acid and oxalate

164
Q

Cystine stone formation

A

associated with homocystinuria, an inherited defect that affects the absorption and transport of cystine

165
Q

Clinical presentation of renal stones?

A
  • May be asymptomatic
  • Classic triad - flank/loin pain, vomiting, fever
  • Renal colic (SPERN - severe intermittent pain for hours, pain from loin–>groin, excruciating ureteric spasms, rapid onset, nausea and vomiting)
  • Urinary frequency, urgency and haematuria
166
Q

Investigations for renal stones

A

Mid-stream urine test, serum U&Es, creatinine, and Ca2+, X-ray, unenhanced spiral CT scan, urine dipstick, ultrasound

167
Q

Best diagnostic test for kidney stones?

A

unenhanced spiral CT scan

168
Q

Management for kidney stones?

A

strong analgesic (IV diclofenac), antibiotics (if infection), stone removal

169
Q

Methods of stone removal for kidney stones?

A

Extracorporeal shock wave lithotripsy (ESWL), endoscopy with laser

170
Q

What is an epididymal cyst?

A

Smooth, extra-testicular spherical cyst on the head of the epididymis. Contains clear/milky fluid

171
Q

Epidemiology of epididymal cyst?

A

Usually develops around 40, relatively common, rare in children

172
Q

Diagnosis and Mxof epididymal cyst?

A

Scrotal ultrasound, not always necessary to treat, if painful and symptomatic then surgical excision

173
Q

What is hydrocele?

A

Abnormal collection of fluid within the tunica vaginalis

174
Q

Epidemiology of hydrocele?

A

Clinically apparent scrotal hydrocele are evident in 6% of males, most paediatric hydroceles are congenital

175
Q

Causes of primary hydrocele?

A

More common, larger, associated with patent processus vaginalis

176
Q

Causes of secondary hydrocele?

A

rarer, present in older men, secondary to testis tumour, trauma, infection

177
Q

Pathophysiology of hydrocele?

A

Overproduction of fluid in the tunica vaginalis, pain isn’t a feature unless infection is involved

178
Q

Diagnosis and Mx of hydrocele?

A

ultrasound, spontaneously resolves, therapeutic aspiration or surgical removal

179
Q

Varicocele

A

Abnormal dilation of the testicular veins, common cause of low sperm production and quality (can affect fertility)

180
Q

Which scrotum is varicocele more commonly associated with?

A

Left

Unusual in boys <10, incidence increases after puberty

181
Q

Causes of varicocele

A

Defective valves in the veins within the scrotum, normally the valves regulate the flow to and from the testicles, but when this fails, the blood backs up causing the veins to dilate

182
Q

Clinical presentation of varicocele?

A

Visible as distended scrotal blood vessels, dull ache, scrotal heaviness, scrotum hangs lower on the side of the varicocele

183
Q

Diagnosis and treatment of varicocele?

A

Venography (x-ray of veins), colour doppler ultrasound to see blood flow, surgery if there is pain

184
Q

What is testicular torsion?

A

Twisting of the spermatic cord, resulting in occlusion of the testicular blood vessels - can rapidly lead to ischaemia and thus potential loss of testis (germ cells are the most susceptible cell line to ischaemia)

185
Q

Congenital malformation predisposing to testicular torsion

A

Bell-clapper deformity - testis not fixed to the scrotum completely, allowing for free movement, leading to twisting

186
Q

Clinical presentation of testicular torsion

A

Sudden onset of severe unilateral testicular pain, associated with nausea and vomiting, pain often comes on during physical activity,

187
Q

How will the testis appear upon examination in testicular torsion?

A

Testis will have a higher position compared to the contralateral side, with a horizontal lie, may be swollen and tender, cremasteric reflex is absent

188
Q

Diagnosis and Mx of testicular torsion?

A

Doppler ultrasound (shows lack of blood flow to the testis), urinalysis to exclude infection, no delay of surgical exploration, surgery/ orchidectomy

189
Q

nephrolithiasis

A

renal stones

190
Q

urolithiasis

A

urinary stones

191
Q

What is Von-Hippel Lindau syndrome?

A

An inherited disorder causing multiple tumours of the CNS and visceral organs, autosomal dominant inheritance, 20% of cases caused by new mutations

192
Q

Most common tumours associated with VHL syndrome?

A

haemangioblastomas (CNS and retinal), phaeochromocytomas, renal cell carcinomas and renal cysts

193
Q

What are the functions of the kidney and what are the implications of kidney damage on them?

A
  1. Blood volume/fluid management - peripheral/central oedema
  2. Waste/drug excretion - build up of toxic substances
  3. Red cell production (EPO) - can lead to anaemia
  4. Vitamin D metabolism - reduced vitamin D, activation of PTH, increased bone resorption
  5. Acid-base regulation - acid accumulation and a metabolic acidosis
194
Q

Define glomerulonephritis - what is the difference in presentation between nephrotic and nephritic syndrome?

A

Glomerulonephritis is any of a group of diseases that injure the glomerulus.
Nephrotic syndrome is characterised by proteinuria, oedema, hyperlipidaemia and hypoalbuminaemia.
Nephritic syndrome is characterised by haematuria, oliguria, and HTN

195
Q

What is the medical emergency associated with AKI? What ECG changes can this commonly cause?

A

Hyperkalaemia

On an ECG this appears as tall peaked T waves, reduction of P waves and widening of the QRS complexes

196
Q

4 most common types of urinary stones?

A

Calcium stones (oxalate and phosphate) - 80%
Struvite 5-10%
Uric acid - 10%
Cystine - 1%

197
Q

5 common symptoms of renal tract stones?

A 
(often asymptomatic)
Loin pain (loin-->groin)
Renal colic
UTI symptoms (e.g. dysuria, urgency, frequency)
Recurrent UTIs
Haematuria
198
Q

What are the criteria for a 2-week wait referral for suspected bladder cancer

A

Aged >45 and have:

  • Unexplained visible haematuria without UTI or
  • Visible haematuria that persists or recurs after successful treatment of UTI

Aged >60 and have:
- Unexplained non-visible haematuria and either dysuria or a raised WCC

199
Q

common symptoms with LUT obstruction in men?

A

frequency, nocturia, urgency, hesitancy, straining, intermittent stream, incomplete emptying, dribbling

200
Q

What are the two groups of drug commonly used in symptomatic BPH?

A

alpha-adrenergic antagonists e.g. tamsulosin

5-alpha reductase inhibitors e.g. finasteride

201
Q

What issues are there which prevent the PSA test being used routinely for screening?

A

It is not cancer specific - it can be BPH, UTI, prostatitis

6% of men with normal PSA have prostate cancer and 70% of men with a raised PSA will NOT have prostate cancer

202
Q

Commonest presentation of testicular cancer? What differentiates this from a true scrotal mass

A

A painless testicular lump, hard, does not transilluminate

203
Q

5 medical conditions associated with erectile dysfunction? what is the first line treatment for erectile dysfunction

A

DM, CVD (MI, HTN), liver disease and alcohol, renal failure, trauma, iatrogenic (prostatectomy).
First line treatment is phosphodiesterase (PDE5) inhibitors

204
Q

Which STI is most commonly diagnosed? How is it tested for and treated?

A

Chlamydia
Management - partner management, other STI testing, doxycycline bd (twice daily) for 7 days, erythromycin bd for 14 days or azithromycin in pregnancy

205
Q

How is a UTI defined? What constitutes an uncomplicated UTI? Implications of UTI in possible bladder cancer?

A

Presence of bacteria in the urine with clinical complications. An uncomplicated UTI one occurring in a non-pregnant female. NICE now recommends that those >60 with recurrent/persistent UTIs are referred due to chance of bladder cancer

206
Q

Classic triad of symptoms in pyelonephritis? How does its antibiotic treatment differ from that for a lower UTI?

A
  1. Loin pain
  2. Fever
  3. Pyuria (pus in urine)

In lower tract UTIs broad spectrum antibiotics should be avoided, whereas in upper tract infections they are used first line

207
Q

Example of an alpha blocker?

A

tamsulosin

208
Q

Indications for alpha blockers (e.g. tamsulosin)?

A

1st line treatment for BPH, used alongside 5-alpha reductase inhibitors

209
Q

Mechanism of action of tamsulosin/alpha blockers

A

Highly selective for alpha-1 adrenoreceptors found in smooth muscle (blood vessels and urinary tract). Stimulation of these leads to contraction, therefore inhibition leads to vasodilation (relaxation)

210
Q

Adverse effects of alpha blockers (tamsulosin)

A

postural hypotension, dizziness

211
Q

Example of a 5-alpha reductase inhibitor?

A

finasteride

212
Q

What is used to treat BPH in addition to alpha blockers?

A

5-alpha reductase inhibitors e.g. finasteride

213
Q

5-alpha reductase inhibitors e.g. finasteride used to treat BPH?

A

5-alpha reductase is an enzyme which converts testosterone –> dihydrotestosterone (active form) (reduces androgenic drive enlarging prostate)

214
Q

Adverse effects of 5-alpha reductase inhibitors

A

Sexual dysfunction

215
Q

Type of drug used to treat erectile dysfunction? example?

A

phosphodiesterase-type 5 (PDE5) inhibitors, sildenafil

216
Q

How do phosphodiesterase-type 5 (PDE5) inhibitors work?

A

PDE5 is an enzyme which is found in smooth muscle of the corpus cavernous of the penis (and arteries of the lung), therefore inhibition causes vasodilation and filling of blood

217
Q

Adverse effects of PDE5 inhibtors?

A

flushing, headache, dizziness

218
Q

Example of an anti-muscarinic?

A

Oxybutynin

219
Q

How do anti-muscarinics reduce urinary frequency/urgency?

A

Competitively inhibits ACh, blocking the muscarinic receptors and promoting the bladder relaxation - reduces urgency and frequency of urination

220
Q

Androgen receptor blockers are used to treat? Give an example

A

Prostate cancer since they decrease the body’s response to androgens, e.g. flutamide

221
Q

Most common STI?

A

chlamydia, more common in women and those aged 15-25

222
Q

Chlamydia trachomatis - gram _________ bacterium

A

negative

223
Q

Neisseria gonorrhoea - gram__________ diplococcus bacterium

A

negative

224
Q

Sites of occurrence of chlamydia and gonorrhoea?

A

urethra, endocervical canal, rectum, pharynx, conjunctiva

225
Q

Complications for chlamydia/gonorrhoea?

A

Pelvic inflammatory disease, neonatal transmission

226
Q

How to test for chlamydia in females? Males?

A

self collected vaginal swab, first void urine

227
Q

Treatment for chlamydia?

A

PH/partner management, test for other STIs, oral azithromycin stat

228
Q

Gonorrhoea treatment?

A

PH/partner management, test for other STIs, single dose treatment, IM ceftriazone with azithromycin stat

229
Q

Parasympathetic (cholinergic) control of the LUT

A

S3, S4, S5, drives detrusor contraction

230
Q

Sympathetic (noradrenergic) control of the LUT?

A

T10, L1, L2, urethral contraction and inhibition of detrusor muscle contraction

231
Q

Varicocele is secondary to other pathological processes blocking the testicular vein e.g.

A

kidney tumours

232
Q

Stress incontinence

A

Sphincter weakness causing small leak of urine when intra-abdominal pressure rises (coughing, laughing, standing up)

233
Q

Treatment of stress incontinence?

A

pelvic floor exercises, duloxetine, surgery

234
Q

Urge incontinence

A

Strong desire to void and unable to hold urine, caused by detrusor overactivity, bladder hypersensitivity (local pathology e.g. UTI, bladder stones)

235
Q

Treatment for urge incontinence

A

Bladder exercises, behavioural therapy (controlling caffeine, alcohol), drugs (anticholinergic agents, beta 3 agonist

236
Q

Primary site of infection of chlamydia and gonorrhoea in males and females respectively?

A

urethra, cervix

237
Q

Basic renal anatomy

A
  • Retroperitoneal organs
  • Surrounded by renal capsules
  • Between vertebra T12-L3
  • Right kidney lower than left
238
Q

Tiered kidney arterial supply

A

Renal artery, segmental artery, interlobar artery, arcuate artery, interlobular artery, afferent arteriole

239
Q

Juxtaglomerular apparatus

A

‘detects’ the blood pressure and when a decrease in arterial blood pressure is detected via baroreceptors, renin is secreted

240
Q

What does the juxtaglomerular apparatus consist of?

A

Macula densa (DCT), juxtaglomerular cells (afferent arteriole).

Macula densa cells detect sodium concentration, JG cells secrete renin

241
Q

Juxtaglomerular cells

A

Sense changes in renal perfusion pressure by stretch receptors in the vascular walls, they are also stimulated to release renin by signalling from the macula densa

242
Q

Complications of CKD

A

cardiac arrhythmias, HTN, anaemia, renal osteodystrophy (hypocalcaemia, hyperphosphataemia)

243
Q

What tests are repeated within 3 months to confirm CKD diagnosis?

A

estimated GFR (eGFR) and urine ACR

244
Q

What is renal artery stenosis? What is it caused by?

A

narrowing of one or both of the renal arteries, atherosclerosis, fibromuscular dysplasia

245
Q

Complications of renal artery stenosis?

A

CKD, coronary artery disease

246
Q

Treatment for renal vascular disease

A

blood pressure control, diuretics initially

247
Q

What is renal venous thrombosis? causes?

A

Occlusion of one or both renal veins by a thrombus, caused by nephrotic syndrome, renal cancer, renal transplant, trauma, dehydration

248
Q

Management of CKD

A

Sodium and fluid restriction, high dose diuretic treatment (furosemide), corticosteroids (prednisolone)

249
Q

Why does nephritic syndrome present with HTN?

A

capillaries of the glomerulus swell, and so the JG cells are stretched even more and this causes an increase in the secretion of renin

250
Q

Causes of RPGN? Treat with…?

A

small vessel vasculitis, lupus nephritis, anti-GBM disease

treat with corticosteroids

251
Q

Anti-GBM antibody GN (Goodpasture’s syndrome)

A

autoimmune condition, antigen on GBM, leads to production of anti-GBM antibodies, often these antibodies bind to the alveolar BM –> pulmonary haemorrhage –> haemoptysis

252
Q

Types of immune complex mediated GN?

A

IgA nephropathy, post-Streptococcal GN

253
Q

Mx for nephritic syndrome

A

Management depends on cause, FLUID RESTRICTION to reduce oedema, NSAIDS/steroids (reduce inflammation of kidney)

254
Q

Term for renal stones?

A

Nephrolithiasis

255
Q

Gold standard test for nephrolithiasis?

A

Non-contrast CT kidney-ureter-bladder (CT-KUB)

256
Q

First line treatment for renal stones

A

‘watchful waiting’ and analgesia (NSAIDs, e.g. ibuprofen, diclofenac)

257
Q

Common bacteria causing the majority of UTIs?

A

E.Coli

258
Q

First line Ix for UTI? Gold-standard?

A

urine dipstick, mid-stream urine analysis

259
Q

1st line antibiotics used in UTIs?

A

Trimethoprim

260
Q

1st line antibiotics used to treat UTIs in pregnancy?

A

nitrofurantoin

261
Q

1st line antibiotics in pyelonephritis?

A

ciprofloxacin

262
Q

Serum biochemical changes seen in AKI?

A

hyperkalaemia, hyponatraemia, hypocalcaemia

263
Q

Why is hypocalcaemia seen in AKI?

A

AKI, reduced kidney function, less active form of vitamin D, therefore less Ca2+ absorption

264
Q

Clinical presentation of BPH (LUTS)

A

Acute urinary retention, haematuria, bladder stones, UTIs

265
Q

1st line treatment for BPH?

A

Oral tamsulosin (alpha-1 antagonist)

266
Q

Gold standard treatment for BPH?

A

transurethral resection of prostate (can lead to erectile dysfunction)

267
Q

Treatment for metastatic prostate cancer

A

LHRH, GnRH agonists, androgen receptor antagonists

268
Q

what is neuropathic bladder dysfunction

A

loss of neuronal control over bladder - two types - spastic injury, flaccid injury

269
Q

Spastic injury

A

Loss of coordination and completion of voiding, bladder only works by reflex, (hyperreflexive), involuntary urination, lose control of voiding

270
Q

Flaccid injury

A

Hyporeflexive, reflex is lost, fills until it overflows, overflow incontinence, stress incontinence, consider permanent catheterisation

271
Q

Left varicocele can be sign of …

A

Left kidney cancer

272
Q

BPH vs prostate - difference between how the prostate would feel on DRE?

A

BPH - smooth enlarged prostate

Prostate cancer - hard irregular prostate

273
Q

Why is using serum PSA levels not recommended by most organisations for screening for prostate cancer?

A
  • doesn’t always means prostate cancer
  • most men with prostate cancer die from unrelated cause
  • some men with fast growing prostate cancer have normal PSA levels
274
Q

What type of urinary incontinence can diabetic neuropathy lead to?

A

Overflow incontinence (due to nerve damage)

275
Q

What type of urinary incontinence can a spastic spinal cord injury lead to?

A

urge incontinence (signal goes to the sacral micturition centre but no higher)

GRACE Phase 2a Medicine (20 decks)

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