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 renal colic (nephrolithiasis)?

A

unilateral loin to groin pain that can be excruciating and fluctuates in severity (colicky) as the stone moves and settles - the presenting compliant in symptomatic kidney stones (nephrolithiasis)

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

What is the epidemiology of renal colic?

A

5-15% of people experience renal colic

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

What are the risk factors for renal colic/kidney stones?

A

Dehydration
Excess calcium in urine
Diet high in protein, sodium and sugar
Obesity
Certain medications/supplements
GI conditions such as ulcerative colitis or Crohn’s disease
Hyperparathyroidism

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

What is the most common type of kidney stone?

A

75% calcium oxalate stones (enveloped shaped)

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

What are the clinical manifestations of renal colic?

A

painful urination
haematuria
cloudy urine
changes in urine (e.g. strong-smelling, increased urgency, reduced/increased frequency)
crystals in urine
fever

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

What are the investigations for renal colic?

A

computer tomography scan
urine dipstick, kidney USS, abdo XR, renal scan

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

Where are the most common sites of kidney stones?

A

pelvi-ureteric junction
pelvic brim
vesico-ureteric junction

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

What is the management for renal colic?

A

Analgesia e.g. paracetamol, NSAIDs
↑ fluid intake
watchful waiting for stones less than 5mm
larger stones (10mm+) require surgical intervention

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

What are the surgical options for large kidney stones?

A

Extracorporeal shock wave lithotripsy (ESWL) - shock waves break stones into smaller parts so they can be passed

Ureteroscopy and laser lithotripsy - camera inserted via the urethra to identify stone and then targeted lasers used to break it up

Percutaneous nephrolithotomy (PCNL) - nephroscope is inserted via incision through back into kidney to assess ureter - can break up stones

Open surgery - last resort to remove stones

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

What is acute kidney injury?

A

An acute drop in kidney function characterised by a:
Rise in creatinine of ≥25umol/L in 48hrs
Rise in creatinine of ≥50% in 7 days
Urine output of <0.5ml/kg/hr for >6 hours

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

What are the pre-renal causes of AKI?

A

[cause inadequate blood supply to kidneys reducing the filtration of blood]
- dehydration
- hypotension
- heart failure

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

What are the renal causes of AKI?

A

[intrinsic disease in the kidney leading to reduced filtration of blood]
- glomerulonephritis
- interstitial nephritis
- acute tubular necrosis

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

What are the post-renal causes of AKI?

A

[caused by obstruction to flow of urine out of the kidney]
- kidney stones
- masses such as cancer in the abdomen or pelvis
- ureteral strictures
- enlarged prostate or prostate

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

What are the risk factors for AKI?

A

Chronic kidney disease
Heart failure
Diabetes
Liver disease
Older age (65+)
Cognitive impairment
Nephrotoxic medications e.g. NSAIDS, ACE-is
use of contrast medium during CT scans

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

What are the clinical manifestations of AKI?

A

Commonly asymptomatic
Hypotension
Kidney insults
Reduced urine production
Changes in urinary urgency, frequency or hesitancy

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

What are the investigations for AKI?

A

Urinalysis for protein, blood, (acute nephritis) leukocytes, nitrites (infection) and glucose (diabetes)
USS (look for obstruction)

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

What is the management for AKI?

A

Stop nephrotoxic medications
Fluid rehydration ( IV fluids in pre-renal AKI)
Relieve obstruction
Severe AKI may require dialysis

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

What are the potential complications of AKI?

A

hyperkalaemia
fluid overload
heart failure
pulmonary oedema
metabolic acidosis
uraemia (high urea) –> encephalopathy or pericarditis

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

What is chronic kidney disease?

A

Chronic (>3months) reduction in kidney function with implications for health which tends to be permanent and progressive
Diagnostic characteristics: eGFR <60 or albuminuria

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

What is the normal urine output?

A

0.5ml/kg/hr

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

What is the aetiology of CKD?

A

Diabetes
Hypertension
Age-related decline
Glomerulonephritis
Polycystic kidney disease
Medications such as NSAIDS, PPIs + lithium

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

What are the risk factors for CKD?

A

Older age
Hypertension
Diabetes
Smoking
Use of medications that affect the kidneys

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

What are the key presentations for CKD?

A

Majority asymptomatic at presentation
Pruritus
Loss of appetite
Nausea
Oedema
Muscle cramps
Peripheral neuropathy
Pallor
Hypertension

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

What factors affect the progression of CKD?

A

non-modifiable: underlying cause of renal disease, race
modifiable: BP, level of proteinuria, exposure to nephrotoxics, underlying disease activity, further renal insults, dyslipidaemia, ↑phophate, acidosis, anaemia, smoking, glycaemic control if diabetic

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

What are the investigations for CKD?

A

Urine ACR (albumin:creatinine ratio)
Haematuria
Renal ultrasound
eGFR (part U&Es) - two tests 3 months <60ml/min apart confirms diagnosis

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

What is the management for CKD?

A

Treat contributing factors (diabetes, hypertension, glomerulonephritis)
Lifestyle changes (exercise, lose weight, stop smoking, diet changes)
Depends on severity but usual treatment =
ACE-I or Angiotensin-II receptor antagonist
Dapagliflozin + statin
Dialysis, kidney transplant in severe cases

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

What are the aims of management for CKD?

A

Slow the progression of disease
Reduce risk of cardiovascular disease
Reduce risk of complications
Treat complications

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

What is the definition of a lower UTI?

A

bladder infection (cystitis)

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

What is the definition of an upper UTI?

A

infection of renal pelvis (pyelitis and pyelonephritis)

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

What is the definition of a recurrent UTI?

A

2+ episodes of UTI in 6 months or 3+ episodes in 1 year

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

What is the definition of an uncomplicated UTI?

A

infection of the urinary tract by a usual pathogen in a person with a normal urinary tract and with normal kidney function

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

What is the definition of a complicated UTI?

A

Occurs where anatomical, functional, pharmacological factors predispose the person to persistent infection, recurrent infection or treatment failure

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

What is the epidemiology of UTIs?

A

1/3 women have UTIs by the age of 24
UTIs are much less common in men

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

What is the aetiology of UTIs?

A

Majority are caused by E. coli
Other causative organisms: Staphylococcus saprophyticus, proteus mirabilis, enterococci
Less common causative organisms (more likely in patients with underlying pathology and/or frequent infection): Klebsiella spp. , Proteus vulgaris, Candida albicans, Pseudomonas spp.

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

What are the risk factors for UTIs?

A

Female
Increasing age
Recent instrumentation of the renal tract
Abnormality of the renal tract
Incomplete bladder emptying - particularly by protastic obstruction in men
Antibiotic use
Use of spermicide
Sexual activity
Diabetes
Presence of catheter
Hospitalisation
Pregnancy
Immunocompromise

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

What are the key presentations of UTIs?

A

Urinary frequency
Pain on urination
Dysuria
Haematuria
Foul-smelling/cloudy urine
Urgency
Urinary incontinence
Suprapubic or loin pain
Rigors
Pyrexia
Nausea + vomiting
Acute confused state (elderly patients particularly)

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

What are the investigations for UTIs?

A

Bladder/kidney exam
Urine microscopy
Urine culture
Urine dipstick (not used when urinary catheter inserted)

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

What are the differential diagnoses for UTIs?

A

Urethral syndrome or atrophic vaginitis and urethritis in women
Other genital tract infections
In men, enlarged or inflamed prostate can present similarly

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

What is the general management for UTIs?

A

Increase fluid intake and personal hygiene behaviours
trimethoprim/nitrofurantoin 1 st line antibiotics

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

When can nitrofurantoin not be given for UTI treatment?

A

pregnancy in third trimester due to risk of neonatal jaundice/haemolysis
cant be used in G6PD deficiency

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

What is pyelonephritis?

A

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

associated with significant sepsis and systemic upset, rigors

predominantly affects women <35

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

What is the classic triad of symptomos seen in pyelonephritis?

A

loin pain
fever
pyuria

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

What is nephritic syndrome?

A

refers to the following symptoms plus inflammation of the kidney without specifying a cause:
- haematuria
- oliguria (=significantly reduced urine output)
- proteinuria <3g.24hrs
- fluid retention

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

what are the 3 main signs of nephritic syndrome?

A

haematuria
loss of kidney function
signs of fluid overload (oedema)

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

What are 3 three main signs of nephrotic syndrome?

A

heavy proteinuria >3.5g/24hrs
hypoalbuminaemia
oedema

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

What is IgA nephropathy?

A

The presence of dominant or co-dominant mesangial IgA immune deposits which triggers variable degrees of glomerular inflammation and subsequent glomerular and tubulointerstitial scarring.

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

What are the risk factors for IgA nephropathy?

A

HIV infection
FHx of IgAN
Asian/white/native american ancestry
IgA vasculitis
CLD
Age 20-30 yrs

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

What are the key presentations of IgA nephropathy?

A

Visible haematuria 1-2 days after tonsillitis or gastroenteritis viral infection
Proteinuria
hypertension
oedema

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

What is the investigation for IgA nephropathy?

A

immunofluorescence microscopy shows IgA complex deposition

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

What is the management for IgA nephropathy?

A

Non-curative, 30% progress to end-stage renal failure
BP control (ACE-i)

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

What is post-strep glomerulonephritis?

A

Acute glomerulonephritis following streptococcal infection is a type III hypersensitivity reaction characterised by the sudden appearance of haematuria, proteinuria, RBC casts in the urine, oedema. and hypertension

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

What are the key presentations of post-strep glomerulonephritis?

A

visible haematuria 2 weeks after pharyngitis from group A, B haemolytic strep (S. pyogenes)
range from asymptomatic urinary to mild “acute nephritis” to a rapidly progressive clinical picture

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

What are the biopsy investigations and results for post-strep glomerulonephritis?

A

Light microscopy - hypercellular glomeruli
e- microscopy - subendothelial immune complex deposition
immunofluorescence shows starry sky appearance (IgG, IgM and C3 deposits along glomerular BM and mesangium)

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

What is the management for post-strep glomerulonephritis?

A

usually self-limiting, sometimes may progress to RGPN (rapidly-progressive glomerulonephritis)
Diuretics, salt and water restriction can be given to control fluid overload

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

What is Goodpasture’s disease?

A

a rare autoimmune disorder in which the body makes anti-glomerular basement membrane antibodies which leads to pulmonary-renal syndrome (Goodpasture’s syndrome)

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

What are the risk factors for Goodpasture’s disease?

A

FHx
Smoking
Male
20-30 or 60-70 yrs
HLA-DRB or DR4

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

What is the aetiology of goodpasture’s disease?

A

it is caused by an antibody to the alpha-3 chain of type IV collagen which is principally found in the basement membranes of alveoli and glomeruli

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

What are the clinical presentations of Goodpasture’s disease?

A

oliguria
haemoptysis
oedema
crackles on lung examination
cough fever
nausea

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

What are the investigations for Goodpasture’s disease?

A

Renal function test
Renal biopsy (GS)
Anti-glomerular basement membrane antibody titre

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

What are the differential diagnoses for Goodpasture’s disease?

A

post-streptococcal glomerulonephritis
systemic lupus erythematous
microscopic polyangitis

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

What is the management for Goodpasture’s disease?

A

oral corticosteroid, plasmapheresis (remove pathogenic antibody)

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

What is SLE?

A

Systemic lupus erythematosus is a chronic multisystem autoimmune disorder that most commonly affects women during their reproductive years and is characterised by antinuclear antibodies.

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

What are the clinical presentations of SLE nephropathy?

A

Haematuria
Foamy/cloudy urine (proteinuria)
Hypertension
Oedema
Weight gain (due to excess fluid)
High creatinine levels

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

What are the investigations for SLE nephropathy?

A

Urine sample
Blood test for antiphospholipid antibodies and antinuclear antibodies (ANA +ve, anti dsDNA +ve)

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

What is the management for SLE nephropathy

A

Cyclophosphamide (immunosuppressant)
Steroids
Hydroxychloroquine (anti-inflammatory)

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

What is nephrotic syndrome?

A

Kidney disorder which causes the body to pass too much protein in the urine, usually caused by damage to the glomeruli with the following symptoms:
Proteinuria (3-15g/day)
Hypoalbuminemia
Oedema
Hyperlipidaemia
Weight gain

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

What are the 3 key signs of nephrotic syndrome?

A

proteinuria
oedema
hypoalbuminaemia

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

What is the most common cause of nephrotic syndrome in adults?

A

Focal segmental glomerulosclerosis

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

What is minimal change disease?

A

Most common form of nephrotic syndrome (a clinical condition characterised by heavy proteinuria, oedema, hypoalbuminemia, hyperlipidaemia) affecting children.

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

What is the aetiology of minimal change disease?

A

Typically idiopathic but can be secondary to conditions such as Hodgkin’s lymphoma, leukaemia and rarely hep B or C infection.

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

What are the risk factors for minimal change disease?

A

Viral illness
Hx of lymphoma or leukaemia
Age 1-8 yrs
Hep B or C infection
Low birth weight

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

What is the pathophysiology of minimal change disease?

A

An increase in glomerular permeability to proteins is the main process resulting in proteinuria. Although the pathogenesis of primary nephrotic syndrome is unclear, some evidence suggests that dysregulation of the immune system plays a role in development.

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

What are the key presentations of minimal change disease?

A

facial /generalised oedema
Normal BP
Absence of haematuria
Proteinuria
dyspnoea

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

What are the investigations for minimal change disease?

A

urinalysis , urine protein/creatinine ratio, serum albumin, lipid profile
Renal biopsy + e- microscopy (podocyte effacement + fusion)

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

What are the differential diagnoses for minimal change disease?

A

Acute glomerulonephritis
Focal segmental glomerulosclerosis
Congestive heart failure

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

What is the management for minimal change disease?

A

Corticosteroid therapy
Fluid restriction and low salt diet
Albumin + furosemide

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

What is focal segmental glomerulosclerosis?

A

Chronic pathological process caused by injury to podocytes in the renal glomeruli resulting in nephropathy

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

What is the aetiology of focal segmental glomerulosclerosis?

A

Initiated by injury to podocytes in the renal glomeruli.
Primary FSGS: injury produced by unidentified circulating factors which alter the permeability of the glomeruli
Secondary FSGS: injury is produced by viruses, toxins, intrarenal haemodynamic changes or a maladaptive response to the loss of functioning nephrons.

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

What are the risk factors for focal segmental glomerulosclerosis?

A

Male
Black race
FHx
Heroin abuse
Causative medications
Chronic viral infection e.g. HIV
Obesity
Solitary or transplanted kidney

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

What is the pathophysiology of focal segmental glomerulosclerosis?

A
  • damage to podocytes triggers apoptosis
  • podocytes detach from the glomerular basement membrane and are destroyed
  • the podocyte numbers decline leaving the GBM exposed
  • maladaptive interactions between the GBM and parietal epithelial cells occurs
  • the epithelial, endothelial and mesangial cells proliferate
  • glomerular tuft undergoes sclerosis creating characteristic lesions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What are the key presentations of FSGS?

A

proteinuria
oedema
hypertension

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

What are the characteristic signs of FSGS?

A

Muekrcke’s lines (white banding on nails due to hypoalbuminaemia)
Xanthelasma and xanthomas (skin cholesterol deposits due to hypercholesterolaemia)
Lymphadenopathy

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

What are the investigations for FSGS?

A

urinalysis, serum urea, creatinine, albumin, lipids, GFR
light microscopy - segmental sclerosis (NB<50% glomeruli affected)

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

What is the management for FSGS?

A

treat underlying cuase
ACE-i/A-II recetpor antagonist with sodium restriction

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

What is membranous nephropathy?

A

Chronic immunologically mediated disease of the glomerular basement membrane that may resolve spontaneously, persist with stable renal function or progress to kidney failure
Can be either primary (80%) with no identifiable cause or secondary to an underlying cause

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

What is membranous nephropathy?

A

Chronic immunologically mediated disease of the glomerular basement membrane that may resolve spontaneously, persist with stable renal function or progress to kidney failure
Can be either primary (80%) with no identifiable cause or secondary to an underlying cause

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

What are the causes of secondary membranous nephropathy?

A

Autoimmune: systemic lupus erythematosus, mixed connective tissue disease, rheumatoid arthritis, Sjogren’s syndrome
Infectious: hepatitis B and C, syphilis
Malignancy: solid organ carcinoma (colorectal, lung, etc.), lymphoma, or melanoma
Drugs: gold, captopril, lithium, penicillamine, non-steroidal anti-inflammatory drugs (NSAIDs)
Other: sarcoidosis, post-renal transplant.

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

What are the risk factors for membranous nephropathy?

A

Male
Age >40 yrs
HLA-DR3
Autoimmune disease
Hep B or C
Syphilis solid organ carcinoma
Medications
Sarcoidosis
Post-renal transplantation

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

What are the clinical presentations of membranous nephropathy?

A

Oedema
Elevated BP
Proteinuria or abnormal renal function
Xanthelasma
Foamy urine
Fatigue /malaise
Anorexia
Muercke’s lines

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

What are the investigations for membranous nephropathy?

A

urinalysis, serum urea, creatinine, albumin, lipid, urine protein to creatinine ratio
light microscopy - thickened GBM
e- microscopy - sub-podocyte immune complex depositions, spike + dome appearance

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

What is the management for FSGS?

A

low salt + protein diet
treatment of symptoms/underlying cause

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

What are 2 conditions which can present as both nephrotic and nephritic?

A

diffuse proliferative glomerulonephritis
membrano-proliferative glomerulonephritis

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

What is diffuse proliferative glomerulonephritis?

A

a histopathologic classification of glomerulonephritis commonly associated with autoimmune diseases, characterised by an increased cellular proliferation affecting >50% of the glomeruli

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

What is the aetiology of diffuse proliferative glomerulonephritis?

A

Lupus nephritis class IV is the most common cause of DPGN
IgA nephropathy
Anti-glomerular basement membrane disease
Granulomatosis with polyangiitis
Microscopic polyangiitis

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

What is the pathophysiology of diffuse proliferative glomerulonephritis?

A

Immunological attack on the glomerulus —> ↑GBM permeability to protein, RBCs and WBCs
Capillary loops become obliterated and sclerosis develops → hypertension and renal failure
Fibrinoid necrosis in the glomerular vasculature → vasculitis → ↓renal filtration and function

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

What are the key presentations of DPGN?

A

Most symptoms result from the decrease in GFR caused by DPGN
Nonspecific symptoms: nausea, fatigue, vomiting, oliguria
Nephritic symptoms: proteinuria, hypertension, oedema, haematuria

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

What are the investigations for DPGN?

A

FBC, renal function tests, urinalysis
Renal biopsy
Renal USS

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

What are the differential diagnoses for DPGN?

A

Rapidly progressive glomerulonephritis
Poststreptococcal glomerulonephritis
Membranoproliferative glomerulonephritis

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

What is the management for DPGN?

A

ACE-i + statin for mild disease
Steroids for significant disease
IN ESRD - dialysis/kidney transplant

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

What is membranoproliferative glomerulonephritis?

A

A form of glomerulonephritis caused by an abnormal immune response.

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

What are the characteristic histological features of membranoproliferative glomerulonephritis?

A

Proliferation of mesangial and endothelial cells and expansion of the mesangial matrix
Thickening of the peripheral capillary walls by subendothelial immune deposits and/or intramembranous dense deposits
Mesangial interposition into the capillary wall, giving rise to a double-contour or tram-track appearance on light microscopy

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

What is the aetiology of membranoproliferative glomerulonephritis?

A

May be idiopathic or secondary (more common) in aetiology
Autoimmune diseases (systemic lupus erythematosus, scleroderma, Sjogren syndrome)
Cancer (leukaemia, lymphoma)
Infections (hep b, c, endocarditis, malaria)

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

What are the risk factors for membranoproliferative glomerulonephritis?

A

Autoimmune disease
Hepatitis B or C
Cryoglobulinaemia
Monoclonal immunoglobulin deposition diseases
Subacute bacterial endocarditis
Infection of a ventriculoatrial shunt
Chronic lymphocytic leukaemia

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

What is the pathophysiology of membranoproliferative glomerulonephritis?

A

Deposits of antibodies build up in a part of the kidneys called the glomerular basement membrane and cause damage which result in the leakage of blood and protein to leak into the urine.

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

What are the key presentations of membranoproliferative glomerulonephritis

A

Haematuria
Proteinuria
Oedema
Changes in mental state, decreased alertness
Decrease in urine volume
Dark urine

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

What are the investigations for membranoproliferative glomerulonephritis?

A

Urinalysis, Bloods (BUN, creatinine)
Kidney biopsy (GS)

107
Q

What is the management for membranoproliferative glomerulonephritis?

A

Treat underlying condition
Steroids (prednisone) for nephrotic-range proteinuria

108
Q

What is benign prostate hyperplasia?

A

Non-malignant prostate hyperplasia, normal with ageing and usually presents with lower urinary tract symptoms (LUTS).

109
Q

What is the aetiology of benign prostate hyperplasia?

A

Caused by hyperplasia of the stroma and epithelial cells of the prostate

110
Q

What are the risk factors for benign prostate hyperplasia?

A

Older age (50+ yrs)
Ethnicity
FHx
Smoking
Metabolic syndrome

111
Q

What is the pathophysiology of BPH?

A

BPH involves hyperplasia of both epithelial and stromal prostatic components which overtime causes bladder outlet obstruction. Obstruction has both a prostatic component due to increased epithelial tissue, particularly in a transition zone and a dynamic component due to increases in stromal smooth muscle tone.

112
Q

What are the key presentations of BPH?

A

LUTS:
Hesitancy, urgency, frequency, intermittency, weak flow
Terminal dribbling
Incomplete emptying
nocturia

113
Q

What are the investigations for BPH?

A

PSA (unreliable), urine dipstick, urine frequency volume chart
DRE (rectal exam) - smooth enlarged prostate (in cancer is hard and irregular) (GS)
Abdominal examination

114
Q

What are the differential diagnoses for BPH?

A

Overactive bladder, prostatitis, prostate cancer, UTI, bladder cancer

115
Q

What is the management for BPH?

A

Lifestyle changes
Decrease caffeine
Consider catheter if acute
a- blocker (tamsulosin)
5a reductive inhibitors (finasteride) - decreased testosterone production → ↓prostate size
Surgery last resort (TURP - transurethral resection of prostate, TUVP/TEVAP - transurethral electrovaporization of the prostate, Holmium laser enucleation of the prostate (HoLEP), open prostatectomy)

116
Q

What is prostate cancer?

A

Neoplastic , malignant proliferation of the outer zone of the peripheral prostate.

117
Q

What is the epidemiology of prostate cancer?

A

2nd most common cancer
5th leading cause of cancer mortality in men worldwide

118
Q

What are the risk factors for prostate cancer?

A

Genetic - BRCA2, HOXB13
↑age
Afrocaribbean ethnicity
FHx
High dietary fat levels

119
Q

What is the pathophysiology of prostate cancer?

A

High-grade prostatic intraepithelial neoplasia is considered to be the most likely precursor of invasive prostate cancer. Characterised by cellular proliferation with pre-existing ducts and glands with cytological changes that mimic neoplasm. Prostate cancer tends to spread along the capsular surface of the gland and may invade the seminal vesicles, periprostatic tissue and eventually the bladder neck.

120
Q

What are the key presentations of prostate cancer?

A

LUTs but with systemic cancer symptoms + bone pain
Nocturia, urinary frequency, hesitancy, urgency, dysuria, haematuria
Weight loss/anorexia, lethargy, palpable lymphnodes
Nodular and asymmetric enlarged prostate on DRE

121
Q

What are the investigations for prostate cancer?

A

Serum prostate-specific antigen, pre-biopsy multiparametric MRI
Prostate biopsy
Testosterone, bloods, bone scan, CT/MRI

122
Q

What is the management for prostate cancer?

A

Local → prostatectomy
Metastatic → hormone therapy (↓testosterone = ↓cancer growth/even death)
*bilateral orchiectomy (surgical removal of testes)
* GNRH receptor agonist e.g. Goserelin
radio/chemotherapy

123
Q

What is testicular cancer?

A

Cancer of the testes which most commonly arises from germ cells (called seminoma) and other types are called non-seminomas. Seminomas make up 90% of cases.

124
Q

what are the risk factors for testicular cancer?

A

Undescended testes
Male infertility
Family history
Increased height

125
Q

What are the germ and non-germ examples of testicular cancer?

A

germ = seminoma (90%), teratoma
Non-germ = sertoli, leydig, sarcoma

126
Q

What are the key presentations of testicular cancer?

A

Painless lump on the testicle - non-tender, hard, irregular, non-fluctuant, no transillumination
Gynaecomastia
May show lung metastasis signs e,g, cough

127
Q

What are the investigations for testicular cancer?

A

Scrotal USS, tumour markers AFP, BhCG

128
Q

What is the management for testicular cancer?

A

Urgent radical orchiectomy (+offer sperm storage) always 1st line
Adjuvant chemo or radiotherapy

129
Q

What is bladder cancer?

A

Transitional cell carcinoma (TCC) of bladder
5% are squamous cell carcinoma (higher in areas of schistosomiasis)
2% are adenocarcinoma, sarcoma and SCC

130
Q

What are the risk factors for bladder cancer?

A

Occupational exposure to dyes/paints/rubber
Smoking
Chemo + radiotherapy
Age
male
bladder stones (chronic inflammation)

131
Q

What are the key presentations for bladder cancer?

A

painless haematuria
dysuria
back pain

132
Q

WHat are the investigations for bladder cancer?

A

urinalysis
flexible cytoscopy + biopsy (GS)
CTT urogram (for staging)
CT, MRI, bone scan

133
Q

What is the management for bladder cancer

A

Conservative = support
Medical = chemo/radiotherapy
Surgery:
T1 - transurethral resection (TURBT) or local diathermy
T2-3 - radical cystectomy
T4 - palliative chemotherapy and radiotherapy

134
Q

What is renal cell carcinoma?

A

a type of adenocarcinoma arising from the renal tubules

135
Q

What are the subtypes of RCC?

A

Clear cell (80%)
Papillary (15%)
Chromophobe (5%)

136
Q

`what are the risk factors for RCC?

A

Smoking
Obesity
Hypertension
End-stage renal failure
Von Hippel-Lindau disease
Tuberous sclerosis
Hereditary papillary RCC

137
Q

What is the pathophysiology of RCC?

A

Renal carcinoma tends to spread to the tissues around the kidney, within Gerota’s fascia
Often spreads to the renal vein, then to the inferior vena cava
“Cannonball metastases” in the lungs are a classic feature of metastatic renal cell carcinoma - they appear as clearly defined circular opacities scattered throughout the lung fields on a chest x-ray

138
Q

What are the key presentations of RCC?

A

Classic triad of presentation: haematuria, flank pain and palpable mass. (only seen in <10% patients)
>50% discovered incidentally on scan
Non-specific cancer sx: weight loss, fatigue, anorexia, night sweats
Palpable renal mass on examination
Paraneoplastic syndromes: polycythaemia, hypercalcaemia, hypertension, Stauffer’s syndrome

139
Q

What are the investigations for RCC?

A

Bloods, eGFR, urinalysis
CT abdo/pelvis (GS)
abdo/pelvic USS, MRI abdo/pelvis, CT chest (cannonball mets)
biopsy if scan is unclear

140
Q

What is the management for RCC?

A

4 stages:
I: partial or radical nephrectomy
II: radical nephrectomy
III: radical nephrectomy and adrenalectomy
IV: systemic treatment

141
Q

What is transitional cell carcinoma

A

carcinoma of the upper renal tract
presents with haematuria, loin pain, clot colic
managed by nephroureterectomy

142
Q

Causes of haematuria

A

Malignancy (1 in 5)
stones
infection
prostate
nephrological cause
idiopathic

143
Q

What is polycystic kidney disease?

A

Genetic condition where the kidneys develop multiple fluid-filled cysts resulting in significant kidney function impairment

144
Q

What is the aetiology of PKD?

A

Autosomal recessive or dominant (more common) inheritance
recessive - disease of infancy or pre-birth with high mortality rate and many congenital abnormalities (Potter’s sequence = flattened nose, clubbed feet)
dominant - more common in males and presents at 20-30yrs

145
Q

What are the risk factors for PKD?

A

FHx of mutation
FHx of cerebrovascular event

146
Q

What is the pathophysiology of PKD?

A

PKD1+2 code for polycystin (Ca2+ channel), in cilia of nephron, when filtrate passes through nephron cilia move + polycystin channels on cilia open –> Ca2+ influx which inhibits excessive growth

with PKD mutation = Ca2+ influx reduced –> excessive growth of cilia

147
Q

What are the key presentations of PKD?

A

Renal cysts
Hypertension
Abdo/flank pain
Haematuria
Palpable kidneys/abdominal mass
Headaches
Dysuria
Syprapubic pain, fever

148
Q

What are the investigations for PKD?

A

Urinalysis
Bloods (U+E, fasting lipid profile)
GS = Renal USS
Genetic testing, CT/MRI if USS not confirmatory

149
Q

What are some differentials for PKD?

A

acquired cystic kidney disease
simple cyst
tuberous sclerosis complex

150
Q

What is the management for PKD?

A

Non-curative, manage symptoms (e.g. hypertension, ESRF)

151
Q

What is the cause of chlamydia?

A

STI caused by the gram-ve bacteria chlamydia trachomatis - intracellular organism which enters and replicates within cells before rupturing the cell and spreading to others.

152
Q

What are the risk factors for chlamydia?

A

young adults
multiple sexual partners
sexual activity

153
Q

What are the key presentations of chlamydia in women?

A

75% are asymptomatic but can present with:
Abnormal vaginal discharge
Pelvic pain
Abnormal vaginal bleeding
Painful sex (dyspareunia)
Painful urination (dysuria)

154
Q

What are the symptoms of chlamydia in men?

A

Roughly 50% asymptomatic in men but can present with:
Urethral discharge or discomfort
Dysuria
Epididymo-orchitis (inflammation of epididymis and testicles)
Reactive arthritis

155
Q

What are the signs of chlamydia on examination?

A

Pelvic or abdominal tenderness
Cervical motion tenderness
Inflamed cervix
Purulent discharge

156
Q

What are some differentials for chlamydia?

A

Bacterial vaginosis, vaginal candidiasis, gonorrhoea

157
Q

What is the management for chlamydia?

A

Doxycycline 100mg bi-daily for a week
Abstain from sex for 7 days
Give sexual health advice

158
Q

What are the potential complications of chlamydia?

A

pelvic inflammatory disease, chronic pelvic pain, infertility, ectopic pregnancy, epididymo-orchitis, conjunctivitis, lymphogranuloma venereum, reactive arthritis

159
Q

What is the aim of the national chlamydia screening programme in england?

A

To screen every sexually active person under 25yrs for chlamydia annually or when they change their sexual partner

160
Q

What is the epidemiology of chlamydia?

A

chlamydia is the most common STI in the UK

161
Q

What is the epidemiology of gonorrhoea?

A

second most common bacterial STI worldwide

162
Q

What is the aetiology of gonorrhoea?

A

Caused by neisseria gonorrhoeae, a gram negative diplococcus bacteria which infects mucous membranes with a columnar epithelium such as the endocervix, urethra, rectum, conjunctiva and pharynx. It spreads via contact with mucous secretions from infected areas

163
Q

What are the risk factors for gonorrhoea?

A

Young adults (20-29yrs)
MSM
Black ancestry
Current or previous Hx of STI
Sexually active
Multiple sexual partners

164
Q

What are the symptoms of gonorrhoea in women?

A

50% women are asymptomatic but can present with:
Odourless purulent discharge, possibly green or yellow
Dysuria
Pelvic pain

165
Q

What are the symptoms of gonorrhoea in men?

A

90% men are symptomatic:
Odourless purulent discharge, possibly green or yellow
Dysuria
Testicular pain or swelling (epididymo-orchitis)

166
Q

What are the investigations for gonorrhoea?

A

Charcoal endocervical swab
NAAT (nucleic acid amplification testing) (GS)

167
Q

What are some differentials for gonorrhoea?

A

Chlamydia, trichomonas, other infectious causes of urethritis, cervicitis, PID, epididymitis, candidal vaginitis or bacterial vaginosis, UTI

168
Q

What is the management for gonorrhoea?

A

SIngle dose of Intramuscular ceftriaxone 1g (unknown sensitivities)
Single oral ciprofloxacin 500mg (for known sensitivities)
Sexual health advice

169
Q

What are some potential complications of gonorrhoea?

A

PID, chronic pelvic pain, infertility, prostatitis, conjunctivitis, urethral strictures, disseminated gonococcal infection, skin lesions

170
Q

What is the cause of syphilis?

A

Caused by the spirochaetal bacteria Treponema pallidum. Infection is typically acquired through direct person-to-person sexual contact with an individual who has early (primary or secondary) syphilis.

171
Q

How can syphilis be contracted?

A

It can be contracted through:
oral , vaginal or anal sex involving direct contact with infected area
Vertical transmission from mother to baby during pregnancy
Intravenous drug use
Blood transfusions and other transplants (rare)

172
Q

What are the risk factors for syphilis?

A

Sexually active
MSM
Illicit drug use
Commercial sex workers
Multiple sexual partners
HIV or other STIs

173
Q

What are the different types of syphilis?

A

Primary Syphilis = painless ulcer (chancre) at original site of infection

Secondary= systemic symptoms, particularly of the skin and mucous membranes

Latent = occurs after secondary stage where symptoms disappear and the patient becomes asymptomatic despite still being infected (early = within 2 years of infection, late = >2 years following infection)

Tertiary = multi-organ symptoms which present many years after initial infection, often includes development of gummas (granulomatous growths which can cause severe tissue damage and deformation) and cardiovascular or neurological symptoms.

Neurosyphilis occurs if the infection involves the CNS

174
Q

What are the key presentations of primary syphilis?

A

Painless genital chancre (tends to resolve over 3-8 weeks), local lymphadenopathy

175
Q

What are the key symptoms of secondary syphilis?

A

maculopapular rash, condylomata lata, low-grade fever, lymphadenopathy, alopecia, oral lesions

176
Q

What are the key symptoms of tertiary syphilis?

A

gummatous lesions, aortic aneurysms, neurosyphilis

177
Q

What are the symptoms of neurosyphilis?

A

headache, altered behaviour, dementia, tabes dorsalis, ocular syphilis, paralysis, sensory impairment, argyll-robertson pupil (constricted pupil which doesn’t react to light)

178
Q

What are the investigations for syphilis?

A

Rapid plasma reagin(RPR), venereal disease research lab test (VDRL)
Dark-field microscopy swab from lesion (GS)

179
Q

What are some differentials for syphilis?

A

Genital herpes, chancroid, HIV infection

180
Q

What is the management of syphilis?

A

Single IM dose of benzathine benzylpenicillin
Full screening for other STIs
Advice about sexual health
Contact tracing

181
Q

What is a hydrocele?

A

A collection of fluid within the tunica vaginalis (sealed membranous pouch) that surrounds the testes

182
Q

What is the aetiology of hydroceles?

A

Mostly congenital and resolve within first year of life
Most adult hydroceles are acquired

183
Q

What are the risk factors for hydrocele?

A

Premature birth /LBW
Male
Infants <6 months
Late-descending testes
Increased intraperitoneal fluid or pressure
Inflammation or injury within the scrotum
Testicular cancer
Connective tissue disorders

184
Q

What is the pathophysiology of the 2 types of hydrocele?

A

Simple hydroceles are common in newborn males - occur where fluid is trapped in the tunica vaginalis, usually resolves itself as fluid is reabsorbed over time

Communicating hydrocele - occurs where the tunica vaginalis around the testicle is connected with the peritoneal cavity via a pathway called the processus vaginalis allowing fluid from the peritoneal cavity to enter the hydrocele

185
Q

What are the key presentations of hydroceles?

A

Soft, smooth, non-tender swelling around teste
Swelling is in font and below testicle
Simple hydroceles remain one size whereas communicating hydroceles fluctuate in size

186
Q

What are the investigations for hydroceles?

A

Examination (soft, smooth, non-tender swelling around teste which transilluminates with light)
Testicular USS (GS)

187
Q

What are some differentials for hydroceles?

A

Partially descended testes, inguinal hernia, testicular torsion, haematoma, tumours (rare)

188
Q

What is the management for hydroceles?

A

Simple hydroceles usually resolve within 2 years without having any lasting negative effects, may require surgery if they are associated with other problems like hernias
Communicating hydrocele can be treated with a surgical operation to remove or ligate the connection between the peritoneal cavity and the hydrocele

189
Q

What is a varicocele?

A

Swelling of the veins of the pampiniform plexus

190
Q

What percentage of men are affected by varicocele?

A

around 15%

191
Q

What are the risk factors for varicocele?

A

FHx
Somatometric parameters (tall/low BMI)

192
Q

What is the pathophysiology of varicocele formation?

A

Varicoceles are the result of increased resistance in the testicular vein where incompetent valves in the testicular vein allow blood to flow back from the testicular vein into the pampiniform plexus causing swelling of the veins.

193
Q

What are the key presentations of varicocele?

A

Painless scrotal mass
Small testicle
Throbbing /dull pain or discomfort, worse on standing
Dragging sensation
Sub-fertility or infertility

194
Q

What are the investigations for varicocele

A

Examination (scrotal mass which feels like a bag of worms, more prominent on standing, disappears when lying down, asymmetry in testicular size)
Doppler USS (GS)
Semen analysis (if fertility concerns), hormonal test (if concerns about function)

195
Q

What is the grading for varicocele?

A

Subclinical: no clinical abnormality, only detected by Doppler ultrasound
Grade I: only clinically palpable with valsalva manoeuvre
Grade II: palpable without valsalva manoeuvre
Grade III: varicocele is visible through the scrotal skin, easily palpable

196
Q

What is the management for varicocele?

A

Uncomplicated cases can be managed conservatively (watch and wait)
Surgical or endovascular embolisation may be indicted for pain, testicular atrophy or infertility

197
Q

What is an epididymal cyst?

A

Fluid-filled saac which occurs at the head of the epididymus (above and behind testes)
Called a spermatocele if it contains sperm

198
Q

What percentage of men experience epididymal cysts?

A

30 %

199
Q

What are the risk factors for epididymal cysts?

A

Cystic fibrosis
PKD

200
Q

What are the key presentations of epididymal cysts?

A

mostly asymptomatic
soft, round lump at the top of testicle
can be painful

201
Q

What are the investigations for epididymal cysts?

A

Examination : soft round lump at top of testicle associated with the epididymis and transilluminates
USS scrotum (GS)

202
Q

What are some differentials for epididymal cysts?

A

Hydrocele, varicocele, lipoma

203
Q

What is the management for epididymal cysts?

A

Usually no treatment needed
If pain and discomfort surgical removal may be considered
Surgical removal if there is torsion of the cyst causing acute pain and swelling

204
Q

What is testicular torsion?

A

Spermatic cord twists in on itself and occludes the testicular artery causing ischaemia which can lead to gangrene of testis if not dealt with => surgical emergency

205
Q

What are the causes/risk factors for testicular torsion?

A

Bell-clapper defect (mc)
trauma

206
Q

What is the pathophysiology of testicular torsion?

A

The bell clapper deformity increases the likelihood of torsion because the testicle is freely mobile within the tunica media

Intravaginal = testicle rotates within the tunica vaginalis
Extravaginal = testicle twists around the spermatic cord as it descends (rare)

207
Q

What are the key presentations of testicular torsion?

A

Severe unitesticular pain (hurts to walk)
Abdominal pain
Nausea and vomiting
Cremasteric reflex lost (testicle retracts upwards on stroking of inner thig

208
Q

What are the investigations for testicular torsion?

A

Surgical exploration if there is high risk
Doppler USS (check testicular blood flow) = GS

209
Q

What is a major differential for testicular torsion?

A

Testicular appendix torsion = twisting of a vestigial appendage (seen in 50% males) located along the testicle

Also epididymitis or epididymo-orchitis, hydrocele, varicocele, testicular cancer

210
Q

What is the management for testicular torsion?

A

urgent surgery within 6hrs

211
Q

What is the treatment for bell-clapper syndrome?

A

Bilateral orchiplexy (fixing of testes to scrotal sac to overcome deformity, if testes are non-viable –> orchiectomy

212
Q

What are LUTS?

A

Lower urinary tract symptoms

213
Q

What are the storage LUTS?

A

occur when bladder should be storing urine –> urge to urinate
- urgency
- frequency
- incontinence
- nocturia

214
Q

What are the voiding LUTS?

A

occur when bladder outlet is obstructed –> difficulty urinating
- poor stream
- incomplete emptying
- dribbling
- hesitancy

215
Q

What are the red flag LUTS?

A

haemturia
dysuria

216
Q

What is incontinence?

A

Loss of control of urination

217
Q

What are the risk factors for incontinence?

A

Female
Increased age
Postmenopausal status
Increased BMI
Previous pregnancies and vaginal deliveries
Pelvic organ prolapse
Pelvic floor surgery
Neurological conditions (multiple sclerosis)
Cognitive impairment and dementia

218
Q

What are the different types of incontinence?

A

Urge incontinence = overactivity of detrusor muscle → sudden urge to urinate

Stress incontinence (sphincter weakness) = leakage of urine due to increased intra-abdominal pressure

Mixed incontinence = combination of both

Overflow incontinence = overflow of urine when there is chronic urinary retention due to an obstruction to the urine outflow, occurs without the urge to pass urine

219
Q

What are the key presentations of incontinence?

A

Involuntary urine leakage on effort exertion, sneezing, or coughing
Involuntary urine leakage accompanied by or immediately preceded by urgency
Frequency of urination
Vaginal bulge/pressure
Urogenital atrophy

220
Q

What are the investigations for incontinence?

A

urinalysis, post-void residual measurement, cough stress test
Empty supine stress test (valsalva manoeuvre) = GS

221
Q

What is the management for incontinence?

A

Lifestyle changes - avoid caffeine, diuretics, overfilling of bladder, weight loss (if needed)
Pelvic floor exercises
Surgery (tension-free vaginal tape (TVT), autologous sling procedures
Anticholinergic drugs (oxybutynin, tolterodine, solifenacin)

222
Q

What is urinary retention?

A

inability to pass urine even when the bladder is full (500+ml)

223
Q

What are the causes of difficulty voiding/urinary retention?

A

obstruction, stones, BPH, urethral stricture, prolapse, abdominal masses, atonic bladder, neurological flaccid paralysis

224
Q

What is the treatment for urinary retention?

A

catheterisation

225
Q

What are the investigations for LUTS?

A

Examination
U+Es
Urodynamic studies
post-void bladder scan
bladder diary
flowmetry

226
Q

What factors reduce GFR?

A

renal disease, DM, hypertension (↓ filtration coefficient (Kf))
urinary tract obstruction (kidney stones) (↑serum albumin (↑BCP))
↓renal blood flow, ↑plasma proteins (↑glomerular osmotic pressure)
↓arterial pressure (small effect) (↓glomerular hydrostatic pressure)
↓angiotensin II (ACEi/ARB) (↓efferent artery resistance)
NSAIDS (↑afferent artery resistance)

227
Q

What are the causes of hyperkalaemia?

A

acute kidney injury
drugs: K-sparing diuretics, ACEis, A-II receptor blockers, spironolactone, ciclosporin, heparin
metabolic acidosis
Addison’s disease
Rhabdomyolysis
Massive blood transfusion

228
Q

What percentage of men with an elevated PSA do not have prostate cancer?

A

70%

229
Q

What percentage of men with prostate cancer have a normal PSA?

A

6%

230
Q

What is a potential complication of tamsulosin use?

A

Postural hypertension and retrograde ejaculation

231
Q

What are some complications of autosomal dominant PCKD?

A

Polycystic liver disease
male infertility
subarachnoid haemorrhage

232
Q

What is a wilm’s tumour?

A

rare renal mesenchymal stem cell tumour (nephroblastoma) seen in children under 3 years

233
Q

What are the presentations of Wilm’s tumour?

A

mass in the abdomen
abdominal pain
haematuria
lethargy
fever
hypertension
weight loss

234
Q

What are the diagnostic tests for Wilm’s tumours?

A

USS
CT/MRI for staging
Biopsy (GS)

235
Q

What is the treatment for Wilm’s tumours?

A

Surgical excision of tumour + nephrectomy of affected kidney
Adjuvant chemo and radiotherapy

236
Q

What is epididymo-orchitis?

A

inflammation of the epididymis, extending to the testes

237
Q

What are the causes of epididymo-orchitis?

A

E. coli
Chlamydia trachomatis
Neisseria gonorrhoea
Mumps

238
Q

What are the risk factors for epididymo-orchitis?

A

Multiple sexual partners
Unprotected sex
History of STI
Congenital UT abnormalities
Surgery involving the genitals or UT

239
Q

What are the key presentations of epididymo-orchitis?

A

Gradual onset with unilateral:
Testicular pain
Dragging or heavy sensation
Swelling of testicle and epididymis
Tenderness on palpation, particularly over epididymis
Urethral discharge
Systemic symptoms such as fever and potentially sepsis

240
Q

What signs indicate epididymo-orchitis?

A

+ve Prem’s sign (pain relieved by elevating testis)
Cremaster reflex intact

241
Q

What are the investigations for epididymo-orchitis?

A

Urine microscopy, culture and sensitivity
Chlamydia and gonorrhoea NAAT testing
Charcoal swab
Saliva swab
Serum antibodies
USS

242
Q

What is the management for epididymo-orchitis caused by enteric organisms?

A

ofloxacin for 14 days, levofloxacin for 10 days, co-amoxiclav for 10 days

243
Q

What is the treatment for STI-related epididymo-orchitis?

A

intramuscular ceftriaxone, doxycycline, ofloxacin

244
Q

What are 2 critical side effects of quinolone antibiotics?

A

tendon damage and tendon rupture (achilles)
lowered seizure threshold

245
Q

What are the potential complications of epididymo-orchitis?

A

chronic pain, chronic epididymitis, testicular atrophy, sub-fertility or infertility, scrotal abcess

246
Q

What is prostatitis?

A

Inflammation of the prostate gland
Acute bacterial = acute infection in prostate, presenting with a more rapid onset of symptoms
Chronic prostatitis = symptoms lasting for longer than 3 months (can be bacterial or not)

247
Q

What is the aetiology of prostatitis?

A

unclear cause of inflammation of pain
may be initially triggered by an infection, with inflammation persisting after the infection has resolved

248
Q

What are the key presentations of chronic prostatitis?

A

presents with at least 3 months of pelvic pain, LUTS, sexual dysfunction, pain with bowel movements, tender and enlarged prostate

249
Q

What are the key presentations of acute prostatitis?

A

fever
myalgia
nausea
fatigue
sepsis

250
Q

What are the investigations for prostatitis?

A

urine dipstick
urine microscopy, culture and sensitivities
chlamydia and gonorrhoea NAAT testing

251
Q

What is the management for acute prostatitis?

A

Hospital admission for systemically unwell or septic patients - IV antibiotics
Oral antibiotics, typically for 2-4 weeks (e.g. ciprofloxacin, ofloxacin or trimethoprim)
Analgesia (paracetamol or NSAIDs)
Laxatives for pain during bowel movements

252
Q

What are the treatments for chronic prostatitis?

A

a-blockers (tamsulosin), analgesia, psychological where indicted (CBT, antidepressants), laxatives, antibiotics

253
Q

What are the potential complications for prostatitis?

A

sepsis, prostate abscess, acute urinary retention, chronic prostatitis

254
Q

What are the GFR categories in CKD staging?

A

G1: ≥90 (normal + high)
G2: 60-89
G3a: 45-59
G3b: 30-44
G4:15-29
G5: <15 (kidney failure)

255
Q

What are the ACR categories in CKD staging?

A

A1: <3 (normal to mildly increased)
A2: 3-30
A3: >30 (severely increased)

256
Q

What is the zone of the prostate affected by BPH?

A

peripheral zone

257
Q

What is the most common site of metastases for prostate cancer?

A

bone

258
Q

What is pyuria and what causes it?

A

Presence of leukocytes in the urine (10 or more WBCs per cubic mm)
Associated with infection, pyelonephritis, papillary necrosis, diabetes, renal TB, renal stones, cancer

259
Q

Which bacteria is associated with renal stones and UTIs?

A

proteus

260
Q

What are casts in the urine? and what do they indicate?

A

cylindrical protein mouldings formed in the renal tubules
cellular and densely granulated casts indicate pyelonephritis or glomerulonephritis
RBC casts usually indicate glomerular bleeding
epithelial cell and fatty casts accompany tubular necrosis and nephrotic syndrome

261
Q

What are the causes of hyperkalaemia?

A

Medications (ACE inhibitors, NSAIDs)
Acidosis (metabolic + respiratory)
Cellular destruction (burns, traumatic injury)
Hypoaldosteronism, haemolysis
Intake (excessive)
Nephrons (renal failure)
Excretion (impaired)

262
Q

What are the ECG signs for hyperkalaemia?

A

Tall tented t waves
Wide QRS complex
Flattening of P waves
Prolonged PR interval

263
Q

What is the gold-standard test for all UTIs?

A

Midstream microscopy, culture + sensitivity

Phase 2A (18 decks)

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