Brainscape's Knowledge GenomeTM

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


See full index

My Phase 3a Revision > GU > Flashcards

GU Flashcards

1
Q

Define benign prostatic hyperplasia (BPH)

A

Increase in cell number and size in transitional/peri-urethral prostate area WITHOUT the presence of malignancy

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

Describe the pathophysiology of Benign prostatic hyperplasia

A

Epithelial and stomal cell increase

Increased A1 adrenoreceptors –> smooth muscle contraction and mass effect of prostate size = obstruction

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

Give 4 symptoms of BPH

A
  1. Increased frequency of micturition
  2. Nocturia,
  3. Hesitancy
  4. Post-void dribbling
  5. acute urinary retention or retention with overflow incontinence
  6. enlarged smooth prostate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What investigations might you do in someone who you suspect has BPH?

A
  • Digital rectal exam - show smooth but enlarged prostate
  • PSA - not overly accurate but usually done for completion (remember you can’t do this at the same time as DRE)
  • Bladder diaries etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the aims of the management of BPH?

A

Improve urinary symptoms
Improve QOL
Reduce complications of bladder outflow obstruction

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

What lifestyle changes can be made to manage symptoms of BPH?

A

Reduce caffeine and alcohol intake
Distraction methods
Bladder training

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

Describe the treatment for BPH

A

1st line = Alpha-1-antagonists (A-blockers) e.g. tamulosin
- relaxes smooth muscle in bladder neck & prostate

2nd line = 5-alpha-reductase inhibitors e.g. finasteride
- blocks conversion of testosterone to dihydrotestosterone -> decreases prostate size

TURP = gold standard

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

Give the surgical treatment for BPH

A

Transurethral resection of prostate (TURP)

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

What are the indications in someone with BPH to do a TURP?

A

RUSHES

  • Retention
  • UTI’s
  • Stones
  • Haematuria
  • Elevated creatinine
  • Symptom deterioration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the function of the prostate?

A

Secretes proteolytic enzymes into the semen which breaks down clotting factors in the ejaculate

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

Define prostate cancer

A

Adenocarcinoma in the peripheral zone of the prostate gland

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

Where can prostate cancer metastasise to?

A

Lymph nodes and bone

Rarely = brain, liver, lung

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

By what routes can prostate cancer spread?

A
  1. Lymphatic - to external iliac and internal iliac and presacral node
  2. Haematogenous - to bone, lung. liver, kidneys
  3. Direct - within in the prostate capsule
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What can cause prostate cancer?

A
  1. High testosterone levels

2. Family history - 2/3x increased risk if 1st degree relative is affected

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

what are the symptoms of prostate cancer?

A
  1. LUTS
  2. Bone pain, weight loss, night sweats anaemia = mets
    Most picked up in asymptomatic stage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What investigations might you do in someone who you suspect has prostate cancer?

A

Digital Rectal Exam and PSA are done in community,
Transrectal USS and biopsy = DIAGNOSTIC
Gleason grading system - higher the score the worse the prognosis

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

What grading system is used in prostate cancer?

A

Gleason grading = higher the score, the more aggressive the cancer

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

What is the treatment for localised prostate cancer?

A

radical prostatectomy
chemotherapy
radiotherapy

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

What is the treatment for metastatic prostate cancer?

A
  • prostatectomy
  • chemotherapy
  • radiotherapy
  • zoladex (GnRH agonist)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Give 2 advantages and 1 disadvantage of radical treatment for localised prostate cancer

A

Advantages:

  1. Curative
  2. Reduced patient anxiety

Disadvantages:
1. Can have adverse effects

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

How do LH antagonists work in treating prostate cancer?

A

First stimulate and then inhibit pituitary gonadotrophin E.g. Leuprolide

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

Is a raised PSA confirmatory of prostate cancer?

A

NO

Prostate cancer indication

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

Other than prostate cancer, what can cause an elevated PSA?

A
  1. Benign prostate enlargement
  2. UTI
  3. Prostatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Give 2 advantages and 2 disadvantages of screening in prostate cancer

A

Advantages:

  1. Early diagnosis of localised disease (cure)
  2. Early treatment of advanced disease (effective palliation)

Disadvantages:

  1. Over diagnosis of insignificant disease
  2. Harm caused by investigation/treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is PSA?

A

A glycoprotein secreted by the prostate into the blood stream

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

Name the 2 types of testicular cancers that arise from germ cells

A
  1. Seminoma = most common, slow growing

2. Non-seminoma = yolk sac carcinoma/teratoma, rapid growth

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

Where does testicular cancer spread?

A

Locally into epididymis, spermatic cord and scortal wall Pelvic and inguinal Metastasises

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

what are the risk factors for testicular cancer?

A
  1. Cryptorchidism (undescended testes)
  2. Family history
  3. previous testicular cancer
  4. HIV
  5. age 20-45
  6. Caucasian
  7. infant hernia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Give 3 symptoms of testicular cancer

A
  1. Painless testis lump - hard and craggy (non-transilluminable)
  2. Testicular or abdominal pain
  3. haematospermia,
  4. Abdominal mass
  5. Dyspnoea and cough - lung mets
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What investigations might you do on someone you suspect to have testicular cancer?

A
  1. Tumour markers = Alpha-fetoprotein (a-FP) and Beta subunit of human chorionic gonadotrophin (B-hCG)
  2. Testicular biopsy
  3. Imaging = US, CT/MRI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How is testicular cancer staged?

A 
1 = no mets 
2 = nodes under diaphragm 
3 = above diaphragm 
4 = lungs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is the treatment for testicular cancer?

A

Orchidectomy = testis and spermatic cord excised Chemo and radiotherapy

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

What is epididymitis?

A

Inflammation of the epididymis

Occurs mainly in young males

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

Give 2 causes of epididymitis

A
  1. E. coli

2. Chlamydia

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

What is an epididymal cyst?

A

Smooth extra-testicular, spherical cyst in the head of the epididymus

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

What is hydrocele?

A

Scrotal swelling as a result of excessive fluid in the tunica vaginalis

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

what is primary hydrocele?

A

In absence of disease in testis
Large and tense testis
Young boys mainly effected
Associated with a patent processus vaginalis, which typically resolves during the 1st year of life

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

Name 3 causes of secondary hydrocele

A
  1. Testicular tumours
  2. Infection
  3. Testicular torsion
  4. TB
  5. trauma - is rarer and present in older boys and men
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is varicocele?

A

An abnormal enlargement of the pampiniform venous plexus in the scrotum
Caused by venous reflux

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

Why might renal cell carcinoma cause left sided varicocele?

A

If the renal tumour obstructs where the gonadal vein drains into the renal vein blood can back up and so you may see left sided varicocele

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

What is testicular torsion?

A

Twisting of the spermatic cord resulting in occlusion of testicular blood vessels
Leads to ischaemia and postnatal loss of testis

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

Define glomerular disease

A

= Glomerulonephritis

Group of parenchymal kidney diseases that all result in the inflammation of the glomeruli and nephrons

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

Give 3 consequences of glomerulonephritis

A
  1. Damage to filtration mechanism –> haematuria and proteinuria
  2. Damage to glomerulus restricts blood flow –> hypertension
  3. Loss of usual filtration capacity –> AKI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Briefly describe the pathophysiology of glomerulonephritis

A

Immunologically mediated –> immunoglobulin deposits and inflammatory cells

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

How can glomerulonephritis present?

A
  1. Nephritic syndrome
  2. Nephrotic syndrome
  3. Asymptomatic haematuria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what are the causes of nephritic syndrome?

A

Renal causes
- IgA nephropathy

Systemic causes

  • SLE
  • Post strep GN
  • Small vessel vasculitis
  • Goodpasture’s/anti-GMB disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what is the clinical presentation of nephritic syndrome

A

This is a syndrome fitting a clinical picture of inflammation within the kidney.
characterised by:
Haematuria- reflects inflammation of the kidney (red casts on microscopy)
Oliguria- due to reduced GFR
Proteinuria- less than 3g/24 hours
Hypertension –due to fluid overload

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

What investigations might you do in someone who has nephritic syndrome?

A
  • Urinalysis (dipstick) = haematuria and proteinuria
  • Blood tests = high creatinine and urea
  • Kidney biopsy = diagnostic (crescent shaped glomeruli, Ig depositions, glomerulosclerosis)
  • serology = anti-GBM antibodies, c-ANCA, p-ANCA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

How do you manage nephritic syndrome?

A

Treat underlying cause

Blood pressure control- ACE-I/ARB. This reduces proteinuria and preserves renal function

Corticosteroids- this is to reduce the inflammation causing damage to the kidney

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

Describe the pathophysiology behind nephritic syndrome

A

Kidney inflammation –> large podocytic pores –> RBC, WBC, protein leaks into urine

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

What are the signs needed in order to make a diagnosis of nephrotic syndrome?

A

proteinuria (>3.5g/day)
hypercholesterolaemia
hypoalbuminemia - results in severe oedema

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

Describe the pathophysiology of nephrotic syndrome

A
  1. Inflammation – from immune cells (Ab’s, Ig’s - IgG), complement proteins, HTN, atherosclerosis, medications/immunisations, infection
  2. Damage to podocytes – protein leakage (albumin, Ab’s)
  3. Increased liver activity – to increase albumin, - Consequential increase in cholesterol + coagulation factors
  4. Reduced oncotic pressure – oedema - Consequential blood volume decrease, RAAS stimulation, exacerbation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What can nephrotic syndrome be secondary to?

A
  1. DM
  2. SLE
  3. Amyloidosis
  4. Infection
  5. Drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what are the primary causes of nephrotic syndrome?

A
  • Minimal change disease
  • Membranous glomerulonephritis
  • focal segmental glomerulosclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What would you see on the needle microscopy taken from someone with minimal change disease?

A

LM - normal
FM - normal
EM - Fused podocyte foot processes

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

How is minimal change disease treated?

A

High dose corticosteroids = prednisolone

  • Frequent relapse or steroid-dependent disease is treated with CYCLOPHOSPHAMIDE or CICLOSPORIN/TACROLIMUS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is membranous nephropathy?

A

Thickening of glomerular capillary wall

IgG and C3 complement deposition in sub-epithelial surface –> leaky glomerulus

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

How would you diagnose membranous nephropathy?

A

Serum anti-PLA2R antibodies

Renal biopsy = thickened glomerular basement membrane (sub epithelial IgG and C3 complement deposits)

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

What is the management of membranous nephropathy?

A

Managed with ACE-I/ARB in all.

In patients with high risk of progression, prednisolone and cyclopshosphamide.

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

What are the main symptoms of nephrotic syndrome?

A

Pitting oedema (periorbital, ascites, peripheral)

frothy urine - reflects proteinuria

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

What investigations might be carried out in someone with nephrotic syndrome?

A

Urinalysis (dipstick) = proteinuria

Blood tests

  • hyperlipidaemia and hypoalbuminaemia
  • protein:creatinine ratio

USS kidney

Needle biopsy and microscopy = GOLD STANDARD

  • light microscopy (LM)
  • fluorescence microscopy (FM)
  • electron microscopy (EM)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Describe the treatment for nephrotic syndrome

A

Fluid and salt restriction

Loop diuretics- to manage oedema

Treat cause

ACE-I/ARB to reduce protein loss

Manage complications

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

Give 3 complications of nephrotic syndrome

A
  1. Infections (Ig loss, complement activity decrease)
  2. Thromboembolism (more clotting factor) manage with heparin
  3. Hyperlipidaemia - loss of albumin increases cholesterol formation. Manage with statins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is IgA nephropathy?

A

This is where there is deposition of IgA into the mesangium of the kidney. This results in inflammation and damage

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

What is the treatment for IgA nephropathy?

A
  • BP control - ACEi / ARB

- steroids if renal function declines

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

Where can urinary tract stones be found?

A

Upper = renal and ureteric
Lower = bladder, prostatic and urethral
They most commonly are deposited at the pelviureteric junction, pelvic brim and vesicouretertic junction

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

What are urinary tract stones composed of?

A

80-85% = calcium oxalate (radio-opaque),

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

Describe the pathophysiology of stone formation in the upper urinary tract?

A

Stones form from crystals in supersaturated urine

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

Describe the epidemiology of stones in the urinary tract

A 
10-15% lifetime risk 
Males > females (2:1)
Higher prevalence in Middle East due to higher oxalate and lower calcium, containing diet 
Peak prevalence 20-40yrs 
50% risk of recurrence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Give 5 potential causes of urinary tract stones

A
  1. Congenital abnormalities - horseshoe kidney, spina bifida
  2. Hypercalcaemia/high urate/high oxalate
  3. Hyperuricaemia
  4. Infection
  5. Trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

what is the clinical presentation of urinary tract stones?

A
  • Renal colic = severe unilateral abdominal pain starting in loin + radiating to ipsilateral groin/ testicle/ labia, classically sudden onset early in morning
  • Restlessness,
  • nausea + vomiting,
  • haematuria,
  • dysuria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Give 3 differential diagnosis of urinary tract stones

A
  1. AAA (until proven otherwise)
  2. Diverticulitis
  3. Appendicitis
  4. Ectopic pregnancy
  5. Testicular torsion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What investigations might you do on some who you suspect has a urinary tract stone?

A
  • First line = KUB XR - can see stone in renal tract
  • Gold standard = non-contrast CT KUB, USS KUB in pregnancy (can only see radiopaque stones with USS)
  • Dipstick: haematuria, leucocytes, nitrites
  • Bloods: FBC, CRP, U&Es
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Give 5 ways in which urinary tract stones can be prevented

A

thiazide diuretics - reduce Ca levels

  1. Stay well hydrated
  2. Low salt diet
  3. Healthy protein intake
  4. Reduced BMI
  5. Active lifestyle
  6. Urine alkalisation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

When are urinary tract stone removed?

A

<5mm = watch and wait

> 5mm:

  • Oral nifedipine (CCB) or alpha blocker (tamsulosin)
  • Extracorporeal shock wave lithotripsy (ESWL) - break stone into smaller fragment using shockwaves
  • Ureteroscopy (laser/basket)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is renal colic?

A

Pain due to obstruction in the urinary tract

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

What investigations might you do to find out what is causing someone’s renal colic?

A
  1. Bloods - including calcium, phosphate, urate
  2. Urinalysis
  3. MSU MCS (mid-stream urine microscopy, culture & specificity)
  4. NCCT-KUB (non-contrast CT scan of kidney, ureter and bladder) = gold standard
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Describe the treatment for renal colic

A
  1. Analgesia - NSAIDS (diclofenac)
  2. Anti-emetics
  3. Check for sepsis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Give 3 causes of renal colic

A
  1. Urinary tract stones
  2. UTI
  3. Pyelonephritis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Give 3 places where urinary tract stones are likely to get stuck

A
  1. Ureteropelvic junction
  2. Pelvic brim
  3. Vesoureteric junction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Give 5 functions of the kidney

A
  1. Filters and secretes waste/excess substances
  2. Blood volume/fluid management (BP control)
  3. Synthesises Erythropoietin
  4. Acid base regulation (reabsorption go Na, Cl, K, glucose, H2O, AA’s)
  5. Converts 1-hydroxyvitamin D –> 1,25-dihydroxyvitamin D (active)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is the GFR?

A

Volume of fluid filtered from the glomeruli into Bowman’s space pre unit time

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

What would you expect a typical GFR to be?

A

120 ml/min

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

Write an equations for GFR

A

(Um X urine flow rate) / Pm

Um = conc of marker substance in urine
Pm = conc of marker substance in plasma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Give an example of a marker substance for estimating GFR

A

Creatinine

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

Give 3 essential features of a marker substance for estimating GFR

A
  1. Not metabolised
  2. Freely filtered
  3. Not reabsorbed/secreted
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Name a drug that can inhibit creatinine secretion and what is the affect of this on GFR?

A

Trimethoprim (antibiotic to treat UTIs)

Serum creatinine rises and so kidney function (GFR) appears worse

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

What is the affect on GFR of afferent arteriole vasoconstriction?

A

Decreased GFR

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

What is the affect on GFR of efferent arteriole vasoconstriction?

A

Increased GFR

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

What does the eGFR require to be calculated?

A

Steady state

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

What is the effect of NSAIDs on the afferent arteriole of glomeruli?

A

NSAIDs inhibit prostaglandins and so lead to afferent arteriole vasoconstriction = reduced GFR

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

What is the effect of AECi on the efferent arteriole of glomeruli?

A

ACEi cause efferent arteriole vasodilation = reduced GFR

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

Define chronic kidney disease

A

Long standing, usually progressive, impairment in renal function for more than 3 months

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

How is CKD diagnosed?

A
  • eGFR < 60mL/min/1.73m2,
    or:
  • eGFR < 90mL/min/1.73m2 + signs of renal damage,
    or:
  • Albuminuria > 30mg/24hrs (Albumin:Creatinine > 3mg/mmol)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Briefly describe the pathophysiology causes CKD

A

Hyper-filtration for nephrons that work –> glomerular hypertrophy and reduced arteriolar resistance –> raised intraglomerular capillary pressure and strain –> accelerates remnant nephron failure (progressive)

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

Name 4 cause of CKD

A
  1. DM - 24% of patients
  2. Hypertension
  3. Glomerulonephritis
  4. Congenital - polycystic kidney disease
  5. Urinary tract obstruction
  6. drugs - NSAIDs, ACEi, antidepressants, many antibiotics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Give 3 signs of CKD

A

Often asymptomatic until very low kidney function

  • Fluid retention
  • oedema and raised JVP
  • Oliguria - 0.5 mL/kg/h or <500mL/day
  • Effects of uraemia
    - pruritus = ureamic frost, yellow/grey complexion, nausea, reduced appetite
  • cardiac arrhythmias - hyperKa
  • Fatigue, pallor - anaemia
  • Bone pain - hyperphosphatemia (CKD-MBD)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What investigations might be done in someone who has CKD?

A

FBC = anaemia
U+Es = raised phosphate, uric acid, urea, creatine and decreased Calcium
Urine dipstick = haematuria and proteinuria
GFR Imaging - USS, CT KUB, ECG, Xrays

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

Describe the management of CKD

A

Slow progression of disease

  • DM treatment
  • HTN treatment
  • Glumeronephritis treatment

Reduce risk of CVD
- Atorvastatin- 20mg

Manage complications

  • Mineral bone disease- low Vit D
  • HTN
  • Proteinuria
  • Anaemia-> ESA
  • RRT- haemodialysis, peritoneal dialysis, transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What is renal replacement therapy?

A

Dialysis or renal transplantation

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

Name 2 types of dialysis?

A
  1. Haemodialysis

2. Peritoneal dialysis

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

What is the access point in haemodialysis?

A

AV fistula or tunelled catheter

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

How does haemodialysis work?

A

Exchange of waste solutes through diffusion into dialysate most common (40%), typically 3x4hrs per week

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

Give 3 examples of waste products that are removed from the blood in dialysis

A
  1. Urea
  2. Creatinine
  3. Potassium
  4. Phosphate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Give 5 potential complications of haemodialysis

A
  1. Hypotension
  2. Cramps
  3. Nausea
  4. Chest pain
  5. Fever
  6. Blocked or infected dialysis catheter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Give 3 groups of people who haemodialysis is good for?

A
  1. People who live alone/frail/elderly
  2. People who fear operating machines
  3. People who are unsuitable for peritoneal dialysis (abdominal surgery/hernia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

What is the access point for peritoneal dialysis?

A

A peritoneal catheter is placed into the peritoneal cavity through a SC tunnel

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

what is peritoneal dialysis?

A

peritoneal catheter inserted
Glucose solution pumped in to peritoneum for exchange of solutes across peritoneal membrane
removal of dialysis solution
Continuous or overnight typically

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

Give 4 potential complications of peritoneal dialysis

A
  1. Infection (peritonitis/catheter exit site infection)
  2. Peri-catheter leak
  3. Abdominal wall herniation
  4. Intestinal perforation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Give 3 groups of people who peritoneal dialysis is good for

A
  1. Young people/those in full time work
  2. People who want control/responsibility of their care
  3. People with severe HF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Where in the abdomen does a transplanted kidney lie?

A

In the iliac fossa

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

What has to be assessed for a renal transplant to occur?

A

Virology status = CMV, hepatitis, EBV
CVD
TB
ABO and HLA haplotype

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

What tests can be done to evaluate kidney function in a potential kidney donor?

A
  1. Serum creatinine
  2. Creatinine clearance
  3. Urinalysis
  4. Urine culture
  5. GFR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Give 3 contraindications for renal transplant

A
  1. ABO incompatibility
  2. Active infection
  3. Recent malignancy
  4. Morbid obesity
  5. Age >70
  6. AIDS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What are the 2 main causes of death after a kidney transplant?

A
  1. CV disease

2. Infection

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

Name 4 potential complications of a kidney transplant

A
  1. Thrombosis
  2. Obstruction
  3. Infections - URTI, chest
  4. Rejection (12% in 1st year)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Why do advanced CKD patients need regular fluid assessment?

A

They may be oliguric or anuric

118
Q

Name a loop diuretic

A

Furosemide - acts on NKCC2 transporter

119
Q

Give 3 potential side effect of furosemide

A
  1. Hypokalaemia
  2. Hypotension
  3. Dehydration
120
Q

What other drug might you prescribe with furosemide in someone with poorly controlled potassium?

A

A potassium sparing diuretic e.g. spironolactone

Work on RAAS not ion channels so help control potassium levels in the blood

121
Q

On which part of the nephron do thiazides act?

A

The distal tubule Act on NCC channels

122
Q

On which part of the nephron do aldosterone antagonists act on?

A

Collecting ducts

123
Q

Define Acute Kidney Injury (AKI)

A

Sudden decline in renal function determined by increased serum creatinine +/- ↓ urine output.
Results in imbalance in electrolytes and azotaemia (↑ creatinine / nitrates)

124
Q

what are the different types of AKI?

A
  1. Pre-renal = decreased blood flow to kidneys –> decreased GFR
  2. Renal = kidney damage
  3. Post-renal = Urinary tract obstruction
125
Q

Give 5 risk factors for AKI

A
  1. Increasing age
  2. CKD
  3. HF
  4. DM
  5. Nephrotoxic drugs - NSAIDs, ACEi
  6. hypertension
126
Q

Give 2 pre-renal causes of AKI

A

low blood volume (bleeding, dehydration, shock, D&V)

low effective circulating volume (cirrhosis, congestive HF)

127
Q

Give 2 renal (intrinsic) causes of AKI

A 
glomerulonephritis
acute tubular necrosis (ATN)
acute interstitial nephritis (AIN), respectively
rhabdomyolysis
tumour lysis syndrome
128
Q

Give 2 post-renal causes of AKI

A
  • kidney stone in ureter or bladder
  • benign prostatic hyperplasia
  • external compression of the ureter
129
Q

How does AKI present?

A
  1. Uraemia (high urea) = fatigue, weakness, vomiting, seizures
  2. Acidosis
  3. Arrhythmias
  4. Oliguria
  5. Oedema
  6. high creatinine
130
Q

What investigations might you do to determine whether someone has AKI?

A
  1. Check potassium
  2. Bloods - Creatinine, U+Es
  3. Urine output and urinalysis
  4. Distinguish whether pre-renal, renal or post renal using imaging (USS, microscopy)
131
Q

What is the affect of AKI on creatinine and urine output?

A

Creatinine = raised

Urine output = reduced

132
Q

What is the diagnostic criteria for AKI?

A

1/3 = diagnostic

  1. Rise in CR >26 mmol/L in 48 hours
  2. Rise in Cr >50% in 48 hours
  3. Urine output fall to < 0.5 ml/kg/h for 6 hours
133
Q

How do you treat AKI?

A

Treat underlying cause – hypotension, infection, stones, obstruction
Stop drugs – NSAIDs, ACEi, ARBs, metformin, lithium, digoxin, loop diuretics
Treat underlying complications – electrolyte imbalances (K+)
Severe = dialysis

134
Q

What is the major complication someone with AKI might develop?

A

Hyperkalaemia

Can lead to arrhythmias ECG = tall tented T waves, increase PR interval and wide QRS complex

135
Q

How can hyperkalaemia be prevented in someone with AKI?

A

Give calcium gluconate to protect myocardium

Give insulin and dextrose (insulins drives K+ into cells and dextrose is to rebalance the blood sugar)

136
Q

Define urinary tract infection

A

Inflammatory response of the urothelium to bacterial invasion, usually associated with bacteriuria and pyuria

137
Q

What determines if a UTI is complicated or uncomplicated?

A

A UTI is deemed complicated if it affects:

  • Someone with an abnormal urinary tract
  • A man
  • Pregnant lady
  • Children
  • Immunocompromised
  • If it is recurrent
138
Q

Describe the pathophysiology of UTI’s

A

Organisms colonise the urethral meatus –> bacterial sent –> bacteriuria

139
Q

Name 3 UTI causative organisms

A

The 5 most common pathogens can remembered with KEEPS:

  • Klebsiella
  • E coli- most common causing >50% of cases
  • Enterococci
  • Proteus
  • Staphylococcus coagulase negative
140
Q

Describe the epidemiology of UTI’s

A

More common in women due to short urethra and its proximity to the anus

141
Q

Give 4 risk factors of UTI’s

A
  1. Catheter
  2. Female
  3. Prostatic hypertrophy (obstructs)
  4. Low urine volume
  5. Urinary tract stones
  6. Pregnancy
142
Q

Give 3 bacterial virulence factors that aid their ability to cause UTI’s

A
  1. Fimbriae/pili that adhere to urothelium
  2. Acid polysaccharide coat resists phagocytes
  3. Toxins (e.g. UPEC releases cytotoxins)
  4. Enzyme production (e.g. urease)
143
Q

What type of pili would you associate with lower UTI?

A

Type 1

Bind to uroplakin

144
Q

What type of pili would you associate with upper UTI?

A

Type P

Bind to glycolipids on urothelium

145
Q

The vagina is heavily colonised with lactobacilli, what is the function of this?

A

Helps maintain a low pH = host defence mechanism

146
Q

Give 2 reasons why a post-menopausal women is more susceptible to a UTI

A
  1. pH rises –> increased colonisation by colonic flora

2. Reduced mucus secretion

147
Q

Give 3 host defence mechanisms against UTIs

A
  1. Antegrade flushing of urine
  2. Tamm-horsfall protein
  3. GAG layer
  4. Low urine pH
  5. Commensal flora
  6. Urinary IgA
148
Q

Define pyuria

A

Presence of pus in urine

149
Q

Name 3 lower urinary tract infections

A
  1. Cystitis
  2. Prostatitis
  3. Urethritis
150
Q

Name a upper urinary tract infection

A

Pyelonephritis

151
Q

what are the classic UTI symptoms

A 
FUNDS: 
frequency, 
urgency, 
nocturia, 
dysuria

Haematuria
Abdominal pain
Malaise
Confusion (old patients)

152
Q

What investigations might you do in someone who you suspect has a UTI?

A
  1. Take a good history
  2. Urinalysis –> haematuria, proteinuria, increased WCC, pH, nitrates, ketones
  3. Microscopy, culture and sensitivity of MSU
  4. In recurrent/complicated UTI = imaging (bladder scan, USS, XR)
153
Q

What is the first line treatment for an uncomplicated UTI?

A

Trimethoprim or nitrofurantoin for 3 days

Increase fluid intake and regular voiding

154
Q

How does trimethoprim work?

A

It affects folic acid metabolism

155
Q

Describe the management for a complicated UTI

A

Culture sample –> Abx for 7 days

156
Q

Define recurrent UTI

A

> 2 episodes in 6 months or >3 in 12 months

157
Q

Describe the management for someone who is having recurrent UTIs

A
  1. Increase fluid intake
  2. Regular voiding
  3. Void pre and post intercourse
  4. Abx prophylaxis
  5. Vaginal oestrogen replacement
158
Q

What is cystitis?

A

Inflammation of the bladder secondary to infection

159
Q

what are the risk factors for cystitis?

A
  1. Urinary obstruction
  2. Previous damage to bladder epithelium
  3. Poor bladder emptying
  4. bladder stones
160
Q

what are the symptoms of cystitis?

A
  1. Dysuria
  2. Frequency and urgency
  3. Suprapubic pain
  4. Offensive smelling/cloudy urine
  5. Haematuria
161
Q

What is the treatment for cystitis?

A

1st line = Trimethoprim or nitrofurantoin (avoid trimethoprim in pregnancy -> teratogenic)

2nd line = ciprofloxacin or Co-amoxiclav

162
Q

what are the causes of prostatitis?

A

acute:

  • streptococcus faecalis
  • e.coli
  • chlamydia

chronic:

  • bacterial (as above)
  • non-bacterial - elevated prostatic pressure, pelvic floor myalgia
163
Q

Give 4 symptoms of acute prostatitis

A
  1. Fever
  2. Rigors
  3. Malaise
  4. Voiding LUTS
  5. Pelvic –> anal pain
  6. pain on ejaculation

very tender prostate

164
Q

Give 3 symptoms of chronic prostatitis

A
  1. Recurrent UTI’s
  2. Pelvic –> anal pain
  3. acute symptoms
    Symptoms for > 3 months
165
Q

What investigations might you do in someone with prostatitis?

A
  1. Urinalysis and MSU = blood, WBC and bacteria
  2. DRE = boggy, tender and hot to touch
  3. STI screen
  4. Microbiology = uropathogens in urine
  5. Imaging - TRUSS +/- CT abdo/pelvis
166
Q

How would you treat prostatitis?

A

Quinolone (ciprofloxacin) or trimethoprim (if unable to take quinolones) for 4-6 weeks
Treat pain = paracetamol/ibuprofen

167
Q

what are the causes of urethritis?

A
  • N. gonorrhoea
  • chlamydia
  • trauma
  • urethral stricture
  • irritation
  • urinary calculi
168
Q

what are the symptoms of urethritis?

A
  • skin lesion
  • dysuria +/- discharge (blood/pus)
  • urethral pain
  • penile discomfort/Pruritis
169
Q

what is the treatment for urethritis?

A

STI treatment = Abx - ceftriaxone and doxycycline

partner notification

170
Q

Define pyelonephritis

A

Infection of the renal pelvis and upper ureter, most commonly acquired by ascending transurethral spread, but can be via blood or lymphatics

171
Q

What can cause pyelonephritis?

A
  • majority caused by UPEC (uropathogenic E.coli)
  • main organisms = KEEPS
    • Klebsiella
    • E.coli - majority
    • Enterococcus
    • Proteus
    • Staphylococcus
172
Q

Give 3 symptoms of pyelonephritis

A

triad of:

  • loin pain (back pain)
  • fever
  • pyuria

may also have:

  • severe headache
  • rigors
  • nausea and vomiting
173
Q

What investigations might you do in someone with pyelonephritis?

A
  1. urine dipstick (1st line)
  2. mid-stream urine MC+S (gold standard)
  3. urgent USS to detect stones, obstruction or incomplete bladder emptying
174
Q

Describe the treatment for pyelonephritis

A

Antibiotics: cefalexin for 7-10 days. Trimethoprim or amoxicillin if sensitive.
Analgesia- paracetamol

175
Q

What can a prolonged pyelonephritis infection cause?

A

Renal abscess

Treatment = drainage

176
Q

what is the management for urinary tract stones?

A
  • Strong analgesia- diclofenac
  • Antibiotics
  • Tamsulosin/nifedipine- relaxes smooth muscle and helps expulsion
  • Percutaneous nephrolithotomy- used to expulse stones over 10mm
177
Q

what are the risk factors for urinary tract stones?

A
  • chronic dehydration
  • obesity
  • high protein/salt diet
  • recurrent UTIs
  • hyperparathyroidism (hypercalcaemia)
  • congenital abnormalities
178
Q

what are the signs for treatment of urinary tract stones?

A
  • intolerable pain/vomiting
  • signs of obstruction/infection
  • AKI (and hyperkalaemia)
179
Q

what is the pathophysiology of pre-renal AKI?

A
  • low blood volume or low effective circulating volume causes decreased perfusion
  • this decreases GFR and creatine clearance which activates RAAS- this increases Na+, urea and BP
180
Q

what is the pathophysiology of post-renal AKI?

A

obstruction

  • stones, prostate enlargement or infection causes back pressure into tubules
  • this decreases hydrostatic pressure which decreases GFR`
181
Q

what is the pathophysiology of intra-renal AKI?

A
  • glomerular - glomerulonephritis
    o this causes barrier damage and protein leakage
    o this decreases oncotic pressure which decreases GFR- tubular
  • necrosis
    o complex blood supply causes cells to infarct, break away and plug tubules
    o this decreases hydrostatic pressure and decreases GFR
  • vascular - vasculitis
    o damaged vasculature decreases O2 which causes necrosis
  • interstitial - acute interstitial nephritis
    o inflammation and immune cells cause damage
182
Q

what are the risk factors for prostate cancer?

A
  • family history
  • increasing age
  • black
  • genetic
  • HOXB13, BRCA2
183
Q

what is the epidemiology of prostate cancer?

A
  • commonest male malignancy
  • 7% of all cancer
  • by age of 80, 80% have malignant prostatic change
  • in most cases malignant foci remain dormant
184
Q

what is the epidemiology of testicular cancer?

A

● Most common cancer in young men
● More than 96% arise from germ cells
● 10% occur in undescended testes
● Main types are seminomas and teratomas

185
Q

what is the epidemiology of benign prostate hyperplasia (BPH)?

A
  • common
  • affects 24% of men 40-60 and 40% of over 60
  • afro-Caribbean men affected more
186
Q

what is the pathophysiology of varicocele?

A

● Abnormal dilation of the testicular veins in the pampiniform venomous plexus caused by venous reflux
● Increased reflux from compression of the renal vein
● Lack of effective valves between testicular and renal veins

187
Q

what is the clinical presentation of varicocele?

A

● Often visible as distended scrotal blood vessels that feel like a bag of worms
● Patient may complain of a dull ache or scrotal heaviness
● Scrotum hangs lower on the side of the varicocele

188
Q

what are the investigations for varicocele?

A

● Venography

● Colour doppler ultrasound to see blood flow

189
Q

what is the management for varicocele?

A

● Surgery if there is pain, infertility or testicular atrophy

190
Q

what is the epidemiology of varicocele?

A

● Left side more commonly affected
● Unusual in boys under 10
● Incidence increases after puberty
● Associated with sub fertility

191
Q

what are the causes of testicular torsion?

A

Underlying congenital malformation
- belt-clapper deformity - where the testis is not fixed to the scrotum completely, allowing for free movement leading to twisting

192
Q

what is the epidemiology of testicular torsion?

A
  • common urological emergency in adolescent boys
  • most common 11-30yrs
  • left side is more commonly affected
193
Q

what is the clinical presentation of testicular torsion?

A
  • sudden onset pain in one testis (walking uncomfortable)
  • pain often starts during sport
  • pain in abdomen
  • nausea and vomiting
  • inflammation of one testis - very tender, hot and swollen
194
Q

what are the investigations for testicular torsion?

A
  • doppler ultrasound - lack of blood flow to testis
  • urinalysis - exclude infection and epididymis
  • prehn’s sign = negative (raising scrotum exacerbates pain)
  • DO NOT DELAY SURGICAL EXPLORATION
195
Q

what is the treatment for testicular torsion?

A
  • surgery
  • expose and untwist testis (6 hour window to save testis)
  • orchidectomy (removal of testis) and bilateral fixation
196
Q

what are the investigations for cystitis?

A
  • dipstick urinalysis = positive leucocytes, blood and nitrites
  • microscopy and sensitivity of mid-stream urine = GOLD STANDARD
197
Q

what are the risk factors for pyelonephritis?

A
  • renal structural abnormalities
  • calculi (stones)
  • catheterisation
  • pregnancy
  • diabetes
  • immunocompromised
198
Q

what is the pathophysiology of pyelonephritis?

A
  • infection mostly due to bacteria from patients bowel flora

- most common via ascending transurethral route but can be blood stream or lymphatics

199
Q

what is the epidemiology of pyelonephritis?

A
  • predominantly females under 35

- unusual in men

200
Q

what is prostatitis?

A

infection and inflammation of the prostate gland

can be acute or chronic

201
Q

what are the risk factors for prostatitis?

A 
STI
UTI
indwelling catheter
post-biopsy
increasing age
202
Q

what is simple hydrocele?

A
  • overproduction of fluid in the tunica vaginalis
203
Q

what is communicating hydrocele?

A

processus vaginalis fails to close, allowing peritoneal fluid to communicate with the scrotal portion

204
Q

what is the clinical presentation of hydrocele?

A
  • non-tender, smooth cystic swelling
  • no pain unless infected
  • transluminates
205
Q

what are the investigations for hydrocele?

A
  • USS

- serum alpha-fetoprotein and hCG to exclude malignant teratomas and germ cell tumours

206
Q

what is the treatment for hydrocele?

A
  • most resolve spontaneously

- therapeutic aspiration or surgical removal

207
Q

what is the epidemiology of epididymal cyst?

A
  • usually develop around 40yrs
  • rare in children
  • not uncommon
208
Q

what is the pathophysiology of epididymal cyst?

A

contain clear and milky fluid - spermatocele

- lie above and behind the testis

209
Q

what is the clinical presentation of epididymal cyst?

A
  • lump
  • may be multiple/bilateral (may be painful)
  • transluminate
  • testis is palpable separately from cyst
210
Q

what are the investigations for epididymal cyst?

A

USS

211
Q

what is the treatment for epididymal cyst?

A
  • usually not necessary

- if painful/symptomatic then surgical excision

212
Q

what is the pathophysiology of post strep nephritic syndrome?

A
  • most common = strep pyogenes (lancefield group A beta haemolytic)
  • classically occurs 2 weeks after tonsillitis
  • This is nephritic syndrome following an infection, 3-6 weeks prior. This is due to deposition of strep antigens in the glomeruli leading to inflammation and damage.
213
Q

what is the treatment for nephritic syndrome caused by post strep infection?

A

antibiotics - penicillins

supportive therapy

214
Q

what are the clinical features of nephritic syndrome that is specific to SLE?

A
  • rash
  • arthralgia
  • kidney failure
  • neurological symptoms
  • pericarditis
  • pneumonitis
215
Q

what are the investigations for nephritic syndrome that is specific to SLE?

A

ANA positive
DsDNA positive
low complement C3 and C4

216
Q

what is the treatment for nephritic syndrome caused by SLE?

A
  • immunosuppression
  • steroids
  • cyclophosphamide
  • rituximab
217
Q

what is a complicated UTI?

A
  • infection in patients with abnormal urinary tract
  • pregnant women
  • most UTIs in men
  • treatment is more likely to fail and complications are more likely
218
Q

what is an uncomplicated UTI?

A

UTI in a healthy non-pregnant women with normally functioning urinary tract

219
Q

what is urethritis?

A

urethral inflammation due to infectious or non-infectious cause
non-gonococcal > gonococcal

220
Q

what are the investigations for urethritis?

A
  • STI testing
  • microscopy and culture of urethral discharge
  • urine dipstick
  • urethral smear
  • ?flexible cystoscopy
221
Q

what is the clinical presentation of nephrotic syndrome?

A
  • Normal-mild increase in BP
  • Proteinuria > 3.5g/day
  • Normal-mild decrease in GFR
  • Hypoalbuminaemia
  • Pitting oedema of ankles, abdominal wall and sometimes face(periorbital)
  • Frothy urine
222
Q

what are the causes membranous nephropathy?

A
  • idiopathic
  • drugs
  • penicillamine, gold, NSAIDs
  • autoimmune
  • SLE, thyroiditis
  • infection, hep B or C, schistosomiasis
  • cancer
  • lung, colon. stomach, breast
223
Q

what are the causes of focal segmental glomerulosclerosis?

A
  • idiopathic

secondary

  • HIV
  • sickle cell anaemia
  • heroin
  • interferon treatment
224
Q

what are the investigations for focal segmental glomerulosclerosis?

A

needle biopsy = focal sclerosis and GBM thickening

225
Q

what is the pathophysiology of focal segmental glomerulosclerosis?

A
  • Scarring that is focal and only some glomeruli involved and segmental (only part of glomerulus affected)
  • CD80 in podocytes resulting in increased permeability in glomeruli and thus proteinuria and haematuria
  • Secondary hypertension and renal impairment
226
Q

what is the treatment for nephrotic syndrome caused by focal segmental glomerulosclerosis?

A

Give steroids in idiopathic disease

All patients should receive ACE-I/ARB blood pressure control

227
Q

which is the most common cause of nephrotic syndrome in children?

A

minimal change disease

228
Q

what are the risk factors/causes of minimal change disease in nephrotic syndrome?

A
  • can be idiopathic
  • atopy - allergic reaction can trigger
  • drugs - NSAIDs, lithium, antibiotics, bisphosphonates, sulfasalazine
  • hep C, HIV, TB
  • associated with hodgkins lymphoma
229
Q

what is the clinical presentation of minimal change disease?

A
  • Proteinuria
  • Oedema, predominantly around the face
  • Fatigue
  • Frothy urine
230
Q

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

A

focal segmental glomerulosclerosis

231
Q

what is the epidemiology of autosomal dominant polycystic kidney disease?

A
  • most common inherited kidney disease
  • autosomal dominant inheritance with high penetrance
  • male > female
232
Q

if 1 parent is affected by autosomal dominant polycystic kidney disease what is the chance of transmission?

A

50% chance

233
Q

if both parents are affects by autosomal dominant polycystic kidney disease, what is the chance of transmission to offspring?

A

50% chance of being affected
25% = normal
25% = homozygous for disease (die in the womb)

234
Q

what are the causes of autosomal dominant polycystic kidney disease?

A
  • mutations in PKD1 gene on chromosome 16 = 85%

- mutations in PKD2 gene on chromosome 4

235
Q

what are the risk factor for autosomal dominant polycystic kidney disease?

A
  • family history of ADPKD- ESRF

- hypertension

236
Q

what is the pathophysiology of autosomal dominant polycystic kidney disease?

A

Cysts develop and grow over time in the tubular portion of the nephron
Compression of renal architecture and vasculature
Progressive impairment - gets bigger and worse with age

237
Q

what is the clinical presentation of autosomal dominant polycystic kidney disease?

A
  • hypertension
  • abdo/flank pain (haemorrhage)
  • LUTS (dysuria, urgency, pain)
  • palpable
238
Q

what are the investigations for autosomal dominant polycystic kidney disease?

A

Renal USS then renal biopsy for genes
<30yrs – at least 2 unilateral or bilateral cysts
30-59yrs – 2 cysts in each kidney
>60yrs – 4 cysts in each kidney

239
Q

what is the treatment for autosomal dominant polycystic kidney disease?

A
  • Treat hypertension – lifestyle, ACEi (ramipril)
  • Infected – Abx or drain
  • Surgical – removal (nephrectomy)
  • Chronic – dialysis or transplant
240
Q

what are the complications of polycystic kidney disease?

A

berry aneurysms
cysts on other organs
50% have ventricular hypertrophy
pre-malignant

241
Q

what is the epidemiology of autosomal recessive polycystic kidney disease?

A
  • rarer than autosomal dominant
  • autosomal recessive inheritance
  • disease of infancy
242
Q

what are the causes of autosomal recessive polycystic kidney disease?

A

PKHD1 mutation on long arm (q) of chromosome 6

243
Q

what is the clinical presentation of autosomal recessive polycystic kidney disease?

A
  • variable
  • many present in infancy with multiple renal cysts and congenital hepatic fibrosis
  • enlarged polycystic kidneys
  • 30% develop kidney failure
244
Q

what are the investigations for autosomal recessive polycystic kidney disease?

A
  • Diagnosed antenatally or neonatally
  • Ultrasound - to see cysts
  • CT & MRI to monitor liver disease
  • Genetic testing
245
Q

what are the treatments for autosomal recessive polycystic kidney disease?

A
  • Currently no treatment available
  • Genetic counselling for family members
  • Laparoscopic removal of cysts to help with pain/nephrectomy (remove entire kidney)
  • Blood pressure control with ACE-inhibitor e.g. RAMIPRIL
  • Treat stones and give analgesia
  • Renal replacement therapy for ESRF
  • Counselling and support
246
Q

what is the specific clinical presentation of pre-renal AKI?

A
  • hypotension (D&V, syncope, pre-syncope)

- signs of liver or heart failure (oedema)

247
Q

what is the specific clinical presentation of intra-renal AKI?

A

infection, signs of underlying disease (vasculitis, glomerulonephritis, DM)

248
Q

what is the specific clinical presentation of post-renal AKI?

A

LUTS (BPH)

249
Q

what are the complications of AKI?

A

end stage renal failure
metabolic acidosis
uraemia
CKD

250
Q

how does diabetes cause CKD?

A

Glycation of glomerular endothelium and efferent arteriole leading to fibrosis (diabetic nephropathy)

251
Q

how does hypertension cause CKD?

A

thickening of afferent arteriole leading to ischaemia. Further fluid overloading due to activation of RAAS

252
Q

what is the treatment for urinary tract stones?

A
  • strong analgesic (IV diclofenac)
  • antibiotics if infection (IV cefuroxime or IV gentomycin)
  • antiemetics
  • stone removal
253
Q

what is stage 1 CKD?

A

eGFR > 90ml/min

254
Q

what is stage 2 CKD?

A

eGFR 60-89ml/min

255
Q

what is stage 3a CKD?

A

eGFR 45-59ml/min

256
Q

what is stage 4 CKD?

A

eGFR 29-15ml/min

257
Q

what is stage 5 CKD?

A

eGFR < 15ml/min

258
Q

which drugs are classed as nephrotoxic?

A
  • NSAIDs
  • aminoglycosides
  • ACEi
  • ARB
  • loop diuretics
  • metformin
  • digoxin
  • lithium
259
Q

what is the clinical presentation of epididymitis?

A

acute pain
unilateral
? previous infection

260
Q

how can you tell the difference between epididymitis and testicular torsion?

A

prehn’s sign - lift scrotum

  • epididymitis = positive (relieves pain)
  • testicular torsion = negative (exacerbates pain)
261
Q

what is the management for epididymitis?

A
  • IM ceftriaxone (if organism is unknown) + doxycycline
262
Q

how does IgA nephropathy present?

A

Presents asymptomatically with microscopic haematuria

263
Q

what are the investigations for IgA nephropathy?

A

diagnosed via biopsy

264
Q

what is the most common cause of nephritic syndrome in high income countries?

A

IgA nephropathy

265
Q

what is goodpastures disease?

A

Caused by autoantibodies to Type IV collagen in glomerular and alveolar membrane

266
Q

what is the clinical presentation of goodpastures disease?

A

Presents with SOB and oliguria due to respiratory and renal damage

267
Q

what are the investigations for goodpasture’s disease?

A

Diagnose with anti-GBM antibodies in bloods and biopsy

268
Q

what is the management for goodpasture’s disease?

A

plasma exchange
steroids
cyclophosphamide (for immune suppression)

269
Q

what is the most common cause of post strep glomerulonephritis?

A
  • most common = strep pyogenes (lancefield group A beta haemolytic)
270
Q

what is the clinical presentation of post strep glomerulonephritis?

A

Presents with haematuria. Can present with acute nephritis

271
Q

what are the investigations for post strep glomerulonephritis?

A

Diagnosed by evidence of strep infection

272
Q

what is the management for post strep glomerulonephritis?

A

Treated with antibiotics to clear the strep, and supportive care.

273
Q

what are the secondary causes of nephrotic syndrome?

A 
DDANI
diabetes
drugs
autoimmune
neoplasia
infection
274
Q

what is the difference between nephritic syndrome vs nephrotic syndrome?

A

NEPHRITIC

  • proteinuria +
  • hypertension
  • haematuria
  • very reduced GFR
  • oedema +

NEPHROTIC

  • proteinuria ++++++
  • hypoalbuminaemia
  • oedema ++++
  • slightly reduced/normal GFR
  • hyperlipidaemia
275
Q

where does bladder cancer spread to?

A

spreads to the iliac and para-aortic nodes, and to the liver and lungs

276
Q

what are the causes/risk factors of bladder cancer?

A
  • Smoking = increases risk 2-4 times, accounts for half of male cases of bladder cancer
  • Age over 55
  • Pelvic radiation
  • Exposure to occupational carcinogens
  • Bladder stone- due to chronic inflammation
277
Q

what is the presentation of bladder cancer?

A
  • Painless haematuria- this is the most common presenting symptom for bladder cancer, assume pt has urothelial tumour till proven otherwise
  • Ask about RF in history
  • UTI symptoms without bacteriuria
278
Q

what are the investigations for bladder cancer?

A

Urinalysis- sterile pyuria
Cystoscopy and biopsy- diagnostic
CTT urogram- allows staging

279
Q

what is the management for bladder cancer?

A

T1: transurethral resection or local diathermy
T2-3: radical cystectomy
T4: palliative chemotherapy and radiotherapy

280
Q

what is the most common bacterial STI?

A

chlamydia

281
Q

what is the bacteria that causes chlamydia?

A

chlamydia trachomatis

282
Q

what is urolithiasis?

A

presence of stones in urinary tract

283
Q

what is the equation for net filtration pressure for the glomerulus?

A

NFP = GHP - (GCOP + CHP)

NFP = net filtration pressure
GHP = glomerular hydrostatic pressure
GCOP = glomerular colloid oncotic pressure
CHP = capsular hydrostatic pressure
284
Q

what is the gold standard for measuring GFR?

A

inulin

285
Q

which part of the loop of henle is permeable to water?

A

descending limb

286
Q

what is the innervation of the external urinary sphincter?

A

pudendal nerve S2-S4

287
Q

what is the innervation of internal urinary sphincter?

A

pelvic splanchnic nerve S2-S4

288
Q

what is the innervation of the bladder?

A 
sympathetic = sympathetic chain T11-L2
parasympathetic = pelvic splanchnic S2-S4
289
Q

what is the role of intercalated cells of the collecting duct?

A

Intercalated cells are responsible for acid/base balance
Alpha = acid
Beta = basic

290
Q

what cells line the collecting duct?

A

principal cells and intercalated cells

291
Q

what is the physiology of micturation?

A

Pontine micturition centre promotes micturition by activating parasympathetic and deactivating sympathetic and somatic motor activity
Detrusor muscle contracts and sphincters open

292
Q

what is stage 3b CKD?

A

eGFR 30-44ml/min

My Phase 3a Revision (27 decks)

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