Block 34 Week 8 Flashcards

1
Q

incidence of renal stones?

A
  • 10% incidence
  • high reccurence rates
  • Majority stones upper tract; can get bladder stones with outflow obstruction
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2
Q

presentation of renal stones?

A
  • acute presentation w renal colic
  • loin to groinpain
  • haematuria
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3
Q

low urine pH suggests…

Ix of renal stones?

A
  • Look for the GFR, Creatinine & WCC
  • Low urine pH suggests uric acid component
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4
Q

imaging for stones?

A
  • Imaging is key – CT KUB gold standard
  • X-ray KUB & Ultrasound useful
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5
Q

bladder cancer?

A
  • majority transitional cell carcinoma
  • often presents w haematuria
  • Referred to 2WW Haematuria clinic for upper tract imaging – CT Urogram or Ultrasound + Flexible Cystoscopy
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6
Q

Tx of BC?

A
  • TURBT (Transurethral Resection of Bladder Tumour
  • Chemotherapy – Mitomycin C
  • Immunotherapy – BCG
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7
Q

Renal cancer triad?

A
  • classic triad of loin pain, haematuria and mass - not commonly seen tho
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8
Q

Imaging for renal cancer?

A
  • imaging - US, CT w contrast
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9
Q

Tx of renal cancer summary?

A
  • Treatment – Radical Nephrectomy vs. Partial Nephrectomy
  • Not usually chemo- or radio-sensitive
  • Advanced cases - immunotherapy
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10
Q

Mx of ED?

A

*Management of risk factors
- Oral therapy (PDE5is)

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11
Q

causes of ED?

A
  • Diabetes
  • Atherosclerosis
  • Tobacco use
  • Obesity
  • Pelvic radiotherapy
  • Prostate Surgery e.g. TURP
  • Blunt injuries to penis
    *Multiple Sclerosis
  • Peyronie’s disease
  • Low testosterone
  • Antidepressants
  • Antihistamines
    *Anti-hypertensives
  • Alpha blockers
  • Psychological conditions e.g. depression, anxiety
  • Heavy drinking +/- concomitant drug use
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12
Q

Peyorine’s disease - incidence?

A
  • <1% incidence
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13
Q

presentation of Peyronie’s Disease ?

A
  • Present with pain and deformity on erection, a palpable penile plaque, and, in many cases, erectile dysfunction
  • Associated with Dupuytren’s contracture and a history of penile trauma
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14
Q

pathophys of Peyronie’s Disease ?

A
  • Minor injury to the tunica albuginea is thought to lead to trapping of fibrin and an excess cytokine reaction that causes disordered healing and focal loss of elasticity
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15
Q

acute phase of Peyronie’s Disease ?

A

*up to two years
*erectile deformity may worsen

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16
Q

Peyronie’s Disease - when is surgical intervention needed?

A
  • In patients whose deformity prevents intercourse, surgical intervention is needed.
  • nesbitt procedure
  • Lue procedure
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17
Q

Causes of male factor infertility - endocrine?

A

Pituitary disease, Hypogonadotropic hypogonadism, Excess of androgens

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18
Q

Causes of male factor infertility - disorders of spermatogenesis

A

Chromosomal disorders, Cryptorchidism, Testicular torsion, Sertoli cell only, Infection

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19
Q

Causes of male factor infertility - sperm delivery disorders?

A

Congenital bilateral absence of vas deferens, Ductal obstruction, Erectile dysfunction, Ejaculatory dysfunction

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20
Q

Causes of male factor infertility- penile and sperm causes?

A
  • Penile anatomical disorders
  • Sperm function disorders
  • Immunological infertility,
  • Ultrastructural abnormalities of sperm
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21
Q

Luts?

A
  • Storage symptoms
  • Urgency
  • Daytime Frequency
  • Nocturia
  • Voiding symptoms
  • Poor flow
  • Incomplete emptying sensation
  • Hesitancy
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22
Q

BPE vs BOO vs BPH?

A

BPE – Benign Prostatic Enlargement (clinical)
BOO – Bladder Outflow Obstruction
BPH – Benign Prostatic Hyperplasia (histological)

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23
Q

surgical interventions for BPE/LUTS?

A
  • Transurethral resection of the prostate (TURP)
  • Holmium enuculation of the prostate (HoLEP)
  • Prostatic artery embolisatio
  • Newer techniques – aquablation, steam, microwave, staples, stents
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24
Q

urological emergencies?

A
  • Scrotal Pain
  • Acute Urinary Retention
  • Renal Colic
  • Haematuria
  • Urosepsis
  • Andrology Emergencies
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25
Q

scrotal pain?

A
  • Testicular torsion - this is a urological emergency
  • rare prob in pts over 30 yrs
  • only test is exploration
  • ideally up to 6 hrs but can be salvagable upto 24 hrs
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26
Q

torsion of hyatid of morgagni?

A

blue dot sign

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27
Q

Epidymitis?

A
  • chlamydia most causative organisism
  • under 35-> refer to GUM clinic
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28
Q

Mx of epididmytis?

A
  • Doxy for chylamdyia
  • Ciprofloxacin for Gonorrhoea
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29
Q

acute urinary retention?

A
  • Acute inability to pass urine’
  • Can lead to acute renal failure
  • Catheterise
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30
Q

Ix of urinary retention?

A
  • Record the volume of urine drained. No urine = consider renal failure
  • Urine for culture if suspicion of infection & cover with antibiotics – check local antibiotic policy
  • FBC, U&E. Is the creatinine deranged from the patient’s normal baseline?
  • don’t check PSA - raised in retention and by catheterization
  • rectal examination
  • tamsulosin then TWOC
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31
Q

Infected obst kidney?

A
  • UROLOGICAL EMERGENCY
  • Resuscitate
  • Drain the kidney – nephrostomy or stent
  • Antibiotics + urine culture
  • Delayed surgical intervention
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32
Q

causes of haematuria?

A
  • cancer - bladder, kidney, ureter, prostate
  • stones - kidney, ureter, bladder
  • inflammation - interstitial cystitis, cyclophosphamide
  • infections
  • trauma - kidney, bladder, urethra, pelvic fracture
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33
Q

which type of haematuria has a higher risk of urological cancer?

A

VH than non visible

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34
Q

Ix for haematuria?

A
  • urine culture
  • renal US
  • urine cytology
  • CT, MRI, renography
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35
Q

LUTS + VH or NHV suggests

A

bladder cancer

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36
Q

recent onset of bedwetting in an elderly man is often due to

A

high pressure chronic retention - drain after catheterisation

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37
Q

LUTS - neuro disease?

A
  • neurological disease/ SC/ cauda equina compression - back pain, sciatica, ejaculatory dist, sensory dist in legs, feet, perineum
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38
Q

acute vs chronic loin pain?

A
  • acute loin pain more likely to be due to obstruction e.g. stone
  • chronic loin pain suggests disease within kidney or renal pelvis
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39
Q

most common cause of sudden onset severe flank pain?

A
  • commonest cause of sudden onset severe flank pain is the passage of a stone down through the ureter
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40
Q

ureteric stone pain?

A
  • down through the ureter
  • ureteic stone pain characteristically starts v suddenly (within minutes), is colicky in nature and radiates to the groin as the stone passes into the lower ureter
  • ppt can’t get comfy, often roll around in agony
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41
Q

what suggets that the stone has moved into the intramural part of the ureter?

A
  • if the ppt has pain/ discomfort in the penis and a strong desire to void, suggests that the stone has moved into the intramural part of the ureter
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42
Q

Acute loin pain is less likely to be due to a stone in?

A
  • acute loin pain is less likely to be due to a ureteric stone in women and ppts at the extremes of age
  • tends to be disease of men (and women) at 20-60yrs
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43
Q

non stone causes of acute loin pain ?

A
  • clot or tumour colic - loin pain and haematuria
  • PUJ obst
  • Pyelo
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44
Q

PUJ obst?

A
  • PUJ obstruction - may present acutely w flank pain severe enough to mimic a ureteric stone
  • CT demonstrates hydronephrosis with normal ureter below the PUJ and no stone
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45
Q

high fever and stone?

A
  • high fever - >38 but ureteric stone ppts don’t unless there is infection with the obts
  • ppts tend to be systemically v unwell
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46
Q

non urological causesof acute loin pain

A
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47
Q

chronic loin pain -non urological causes?

A
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48
Q

urological causes of chronic loin pain?

A
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49
Q

ureteric colic vs peritonitis?

A
  • ppts ureteric colic often move around the bed in agony whilst those w peritonitis lie still
  • signs of peritonitis - abd tenderness, guarding
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50
Q

distinguishing urological from non urological loin pain

A
  • examine for abd mass - pulsatile and expansile - leaking AAA
  • in women do a preg test
  • examine back chest and testicles
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51
Q

stress incontinence?

A
  • involuntary leakage of urine on effort, exertion, sneezing or coughing
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52
Q

urge incontinence?

A
  • involuntary leakage of urine accompanies by or immediately preceded by urgency
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53
Q

MUI?

A
  • comb of SUI and UUI
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54
Q

Prev of incontinence?

A
  • 25% of over 20s have UI, 50% have SUI
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55
Q

what causes stress incont?

A
  • occurs due to bladder neck/ uretheral hypermotility and/or NM defects causing intrinsic sphincter def (sphincter weakness incontinence)
  • urine leaks whenever uretheral resistance is exceeded by an inc in abd pressure occuring e.g. exercise or coughing
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56
Q

UUI is caused by?

A
  • may be due to bladder overactivity or less commonly due to pathology that irritates the bladder (infection, tumour, stone)
  • symptoms from involun detrustor contractions may be difficult to distinguish from those due to sphincter weakness
  • in some ppts detrustor contractions can be provoked by coughing making it diff to distinguish between UUI and SUI
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57
Q

constant leak of urine?

A
  • suggests fistulous communication between the bladder and vagina e.g. due to surgical injury at the time of hysterectomy or C section or rarely presence of an ectopic ureter draining into the vagina - urine leak is usually low in volume but lifelong
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58
Q

abd examination in urological disease

A
  • bc retroperitoneal (kidneys, ureters) or pelvic organs are relatively inaccessible, for the kidneys and bladder to be palpable implies a fairly advanced disease state
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59
Q

characteristics of an enlarged bladder

A
  • arises out of the pelvis
  • dull to percussion
  • pressure of examining hand may cause a desire to void
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60
Q

Abd distension: causes ?

A
  • foetus - smooth firm mass, dull to percussion
  • flatus - hyper-resonant - may be visible peristalsis if intestinal obstruction
  • faeces - palpable in the flanks and across the epigastrium, firm, may be sep masses in the line of the colon
  • fat
  • fluid (ascites) - fluid thrill, shifting dullness
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61
Q

causes of an enlarged kidney?

A
  • mass lies in the paracolic gutter, moves w res, dull to percussion
  • can be felt bimanually
  • can be ballotted
  • renal carcinoma, hydronephrosis, pyelo, perinephric abcess, polcystic disease
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62
Q

charac of an enlarged liver?

A
  • mass descends from under right costal margin
  • moves w resp
  • dull to percussion
  • sharp or rounded edge
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63
Q

causes of hepatomeg?

A
  • infection
  • congestion - HF, HV obstruction
  • infilitration - amyloid
  • space occupying lesions - hepatic cancer, mets, hydatid cyst
  • cirrhosis
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64
Q

charac of an enlarged spleen?

A
  • under left costal margin
  • firm, smooth, may have palpable notch
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65
Q

causes of splenomegaly?

A
  • infection
  • congestion
  • infiltration
  • space occupying lesions
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66
Q

RCC?

A
  • most common type of kidney tumour
  • type of adenocarcinoma that arises from the renal tubules
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67
Q

Classic RCC triad?

A

haematuria, flank pain, palpable mass

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68
Q

3 types of RCC

A
  • Clear cell(around 80%)
  • Papillary(around 15%)
  • Chromophobe(around 5%)
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69
Q

Wilms tumour?

A
  • Wilms tumour is a specific type of tumour affecting the kidney in children under 5
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70
Q

Renal cell carcinoma may beasymptomatic, but may present with:

A
  • Haematuria
  • Vague loin pain
  • Non-specific symptoms of cancer (e.g., weight loss, fatigue, anorexia, night sweats)
  • Palpable renal mass on examination
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71
Q

Haematuria

NICE guidelines on recognising cancer advises atwo week waitreferral for those:

A
  • Aged over 45 with unexplained visible haematuria, either without a UTI or persisting after treatment for a UTI
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72
Q

Spread of RCC?

A
  • tends to spread to tissues around the kidney with Gerota’s fascia
  • often spreads to the renal vein then to the IVC
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73
Q

spread of RCC to lungs?

A
  • “Cannonball metastases” in the lungs are a classic feature of metastatic renal cell carcinoma.
  • Cannonball mets can also occur from choriocarcinoma (cancer in the placenta) and, less commonly, with prostate, bladder and endometrial cancer.
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74
Q

paraneoplastic features of RCC?

A
  • polycythemia - EPO
  • Hypercalcaemia - PTHr
  • HTN
  • Stauffers syndrome
  • cushings
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75
Q

HTN from RCC?

A

due to various factors, including increased renin secretion, polycythaemia and physical compression

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76
Q

Stauffer’s syndrome?

A

abnormal liver function tests (raised ALT, AST, ALP and bilirubin) without liver metastasis

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77
Q

mx of RCC?

A
  • surgery is first line: partial/ radical nephrectomy
  • when surgery can’t be done:
  • arterial embolisation
  • percutaneous cryotherapy
  • radiofreq ablation
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78
Q

When should wilms tumour be considered?

A

Consider a Wilms tumour in a child under the age of 5 years presenting with a mass in the abdomen. The parents may have noticed the mass

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79
Q

Signs and symptoms of wilms tumour?

A
  • Abdominal pain
  • Haematuria
  • Lethargy
  • Fever
  • Hypertension
  • Weight loss
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80
Q

diagnosis of wilms tumour?

A
  • initial Ix is US
  • CT/ MRI for staging
  • biopsy needed for definitive diagnosis
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81
Q

Non muscle invasive bladder cancer Tx- cornerstone?

A
  • transurethral resection of bladder tumour (TURBT) - cornerstone of management - providing diagnosis, staging and initial Tx
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82
Q

BCG in NMIBC?

A
  • intravesical therapy: for high risk NMIBC or carcinoma in situa - BCG immunotherapy
  • Maintenance therapy: BCG maintenance therapy may improve outcomes in high-risk patients.
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83
Q

Muscle invasive bladder cancer Tx?

A
  • neoadjuvant chemo - cisplatin based
  • radical cystectomy
  • bladder sparing approaches - TURBT, radiotherapy, chemotherapy
  • adjuvant chemo
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84
Q

tX of met BC?

A
  • first line therapy - platinum based
  • immune checkpoint inhibitors like pembrolizumab
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85
Q

RCC - early stage (T1 and T2) Tx?

A
  • Surgery main - partial nephrectomy for t1
  • radical nephrectomy in T2
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86
Q

RCC - locally advanced - T3 and T4 tx?

A
  • Radical nephrectomy + lymph node dissection is the standard of care
  • Neo-Adjuvant Therapy: Tyrosine kinase inhibitors (TKIs) or immunotherapy can be considered to downsize the tumour before surgery.
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87
Q

Metastatic RCC Tx?

A
  • mainstray of treatment is systemic therapy
  • Low risk patients: VEGF inhibitors such as sunitinib, bevacizumab or pazopanib.
  • Intermediate and high risk patients: dual immunotherapy with ipilimumab and nivolumab
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88
Q

Features of PC on DRE?

A
  • digital rectal examination: asymmetrical, hard, nodular enlargement with loss of median sulcus
  • hard, lumpy
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89
Q

when should men be ref for PC?

A
  • Refer men using a suspected cancer pathway referral (for an appointment within 2 weeks) for prostate cancer if their prostate feels malignant on digital rectal examination.
  • Refer men using a suspected cancer pathway referral (for an appointment within 2 weeks) for prostate cancer if their PSA levels are above the age‑specific reference range.
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90
Q

Consider a prostate‑specific antigen (PSA) test and digital rectal examination to assess for prostate cancer in men with:

A
  • any lower urinary tract symptoms, such asnocturia, urinary frequency, hesitancy, urgency or retention or
  • erectile dysfunction or
  • visiblehaematuria.
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91
Q

PSA?

A
  • protein produced by prostate epithelial cells
  • PSA is produced by normal prostate tissue, however levels in the blood tend to increase in malignancy.
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92
Q

asymptomatic PSA testing?

A
  • PSA testing can be discussed with men over 50, and should be offered to those men over 50 who request it
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92
Q

before PSA testing men should not have?

A
  • Active or recent UTI(last 6 weeks)
  • Recent ejaculation, anal sex or prostate stimulation
  • Engaged vigorous exercise for 48 hours
  • Had a urological intervention in the past 6 weeks
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93
Q

Specific clinical triggers to consider a PSA test include:

A
  • Lower urinary tract symptoms(e.g. nocturia, frequency, hesitancy, urgency or retention)
  • Visible haematuria
  • Unexplained symptomsthat may be explained by advanced prostate cancer (e.g lower back pain, bone pain, weight loss)
  • Erectile dysfunction
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94
Q

benefits of PSA testing?

A
  • can detect prostate cancer at early stage -> earlier treatment -> better outcomes
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95
Q
  • of PSA testing
A
  • PSA testing can result in false positives -> unecessary biopsies, anx for patients
  • PSA can be elevated from other conditions such as BPH
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96
Q

Which ethnicity has the highest risk of PC?

A

black men

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97
Q

95% of PC are?

A
  • 95% are adenocarcinomas
  • majority arise in the peripheral zone of the prostate, with 10-20% arising from the central zone and 10-20% arising from the transitional zone.
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98
Q

signs of symptoms of prostate cancer remote from the prostate gland?

A
  • bone pain - mets?
  • weight loss
  • fatigue
  • urinary symptoms
  • neurological symptoms - spread to SC or nerves
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99
Q

Testicular tumours affect?

A
  • It predominantly affects younger men aged 15-35 years and has a higher incidence in Caucasian populations
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100
Q

2 main types of TT?

A

serminomas (40-60%) and non-seminomatous germ cell tumours (30-50%)

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101
Q

non seminatous germ cell tumours?

A

embryonal carcinoma, yolk sac tumour, choriocarcinoma, and teratoma.

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102
Q

RF for Test cancer?

A
  • Infertility (increases risk by a factor of 3)
  • Cryptorchidism
  • Family history
  • Klinefelter’s syndrome
  • Mumps orchitis
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103
Q

most common presenting feature of TT?

A

painless lump

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104
Q

other CF of Tc?

A
  • Pain
  • lmpotence
  • hydrocele
  • gynaecomastia
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105
Q

What is elevated in germ cell tumours?

A
  • AFP in 60%
  • LDH in 40%
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106
Q

what can be elevated in seminomas?

A
  • Seminomas: hCG may be elevated in around 20%
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107
Q

Referral guidelines for testicular cancer?

A
  • testicular cancer in men if they have a non‑painful enlargement or change in shape or texture of the testis.
  • Consider a direct access ultrasound scan for testicular cancer in men with unexplained or persistent testicular symptoms.
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108
Q

Ix for TT?

A

US first line

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109
Q

Mx of TT?

A
  • Treatment depends on whether the tumour is a seminoma or a non-seminoma
  • Orchidectomy
  • Chemotherapy and radiotherapy may be given depending on staging and tumour type
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110
Q

PC - LUTS?

A
  • Nocturia
  • Frequency
  • Hesitancy
  • Urgency
  • Dribbling
  • Overactive bladder
  • Retention
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111
Q

PC - advanced disease?

A

(e.g haematuria, blood in semen, lower back pain/bone pain secondary to bony metastasis, weight loss, anorexia)

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112
Q

other features of PC

A
  • Visible haematuria
  • Abnormal DRE(hard, nodular, enlarged, asymmetrical)
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113
Q

first line Ix for diagnosis of PC?

A
  • Multiparametric MRIis now commonly the first line investigation in the diagnosis of prostate cancer.
  • MRI influenced prostate biopsy - guided biopsy offered to patients w a Likert score of above 3
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114
Q

Active surveillance for PC?

A
  • option in low-risk localised prostate cancer.
  • It involves regular PSA measurements, digital rectal examinations and multiparametric MRIs.
  • It is used as many with low-risk localised disease
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115
Q

radical prostatectomy?

A
  • Radical prostatectomy: is a definitive treatment option for localised prostate cancer. It involves the removal of the entire prostate gland and surrounding tissues
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116
Q

radical radiotherapy?

A

definitive Tx for localised prostate cancer

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117
Q

adverse effects of radiotherapy to the prostate?

A

urinary incontinence and erectile dysfunction (though less than radical prostatectomy) as well as bowel symptoms (e.g. faecal incontinence).

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117
Q

SE of radical prostatectomy?

A

urinary incontinence and ED

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118
Q

androgen deprivation therapy?

A
  • aims to lower androgen levels
  • can be given to those with intermediate or high-risk localised disease (normally if receiving radical radiotherapy) or in metastatic disease to slow progression.
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119
Q

adverse effects of androgen deprivation therapy?

A

include a loss of libido, erectile dysfunction, loss of ejaculation and osteoporosis.

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120
Q

Androgen deprivation therapy - options?

A
  • GnRH agonist: chemical castration - reduced LH/FSH release
  • e.g. goserelin
  • Bicalutamide (an anti-androgen)
  • Bilateral orchidectomy(castration)
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121
Q

localised prostate cancer Mx options?

A
  • Active surveillance
  • Radical prostatectomy
  • Radical radiotherapy
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122
Q

Low risk PC Mx?

A

a choice of active surveillance, radical prostatectomy or radical radiotherapy can be offered.

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123
Q

intermediate risk PC Mx?

A

NICE advises offering radical prostatectomy or radical radiotherapy. They advise considering active surveillance in those declining radical therapy.

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124
Q

High risk PC Mx?

A

NICE advises offering radical prostatectomy or radical radiotherapy. They do not advise active surveillance in high-risk disease.

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125
Q

locally advanced PC Mx?

A

Patients are typically managed with prostatectomy and radiotherapy. Docetaxel chemotherapy may beused

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126
Q

metastatic PC Mx?

A
  • Docetaxel chemotherapy and androgen deprivation therapy are often used. Bilateral orchidectomy can be offered as an alternative to androgen deprivation therapies.
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127
Q

prognosis of PC?

A
  • 96% survive one year
  • 86% survive 5 yrs after diagnosis
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128
Q

Mx of seminomas and teratomas - surgery?

A
  • orchidectomy
  • should be performed in virtually all cases
  • both diagnostic and therapeutic
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129
Q

how is orchidectomy performed?

A
  • Orchidectomy must be performed via an inguinal approach. This is to avoid crossing lymph networks - the testicles lymph drain to para-aortic nodes whilst the scrotal skin drains to the inguinal nodes.
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130
Q

stage 1 seminoma Tx?

A
  • Stage I Seminoma (low risk): Standard treatment options include surveillance (active monitoring without immediate treatment) or adjuvant radiotherapy to the retroperitoneal lymph nodes.
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131
Q

high risk seminoma Tx?

A

Options may include surveillance, adjuvant radiotherapy, or adjuvant chemotherapy.

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132
Q

Advanced seminoma Tx?

A

Treatment typically involves chemotherapy, such as a combination of bleomycin, etoposide, and cisplatin (BEP regimen).

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133
Q

Stage 1 teratoma Tx?

A

Treatment usually involves radical inguinal orchiectomy (removal of the affected testicle). Adjuvant treatments such as chemotherapy or radiotherapy may be considered

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134
Q

Advanced teratoma Tx?

A

Treatment often involves chemotherapy, typically with a regimen such as BEP (bleomycin, etoposide, cisplatin) or EP (etoposide, cisplatin).

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135
Q

renal stones?

A
  • renal stones are also referred to as renal calculi, urolithiasis, nephrolithiasis
  • hard stones that form in the renal pelvis
  • commonly get stick at the vesico-ureteric junction
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136
Q

2 key comps of renal stones?

A
  • Obstruction leading to acute kidney injury
  • Infection with obstructive pyelonephritis
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137
Q

most common type of renal stone?

A

calcium based - raised calcium and low urine output are key factors

138
Q

2 types of calcium stones?

A
  • 2 types of calcium stones: calcium oxalate (most common) and calcium phosphate
139
Q

RF for renal stones?

A
  • dehydration
  • hypercalciuria, hyperparathyroidism, hypercalcaemia
  • cystinuria
  • high dietary oxalate
  • renal tubular acidosis
  • medullary sponge kidney, polycystic kidney disease
  • male sex
  • infection
140
Q
A
141
Q

RF for urate stones?

A
  • gout
  • ileostomy: loss of bicarbonate and fluid results in acidic urine, causing the precipitation of uric acid
142
Q

drugs causing renal stones?

A
  • drugs that promote calcium stones: loop diuretics, steroids, acetazolamide, theophylline
143
Q

which drugs can prevent calcium stones?

A
  • thiazides can prevent calcium stones (increase distal tubular calcium resorption
144
Q

visibility

uric acid stones?

A

not visible on XR

145
Q

Struvite renal stones?

A

produced by bacteria, therefore, associated with infection

146
Q

cystine renal stones?

A

associated with cystinuria, an autosomal recessive disease

147
Q

staghorn calculus?

A
  • where the stone forms in the shape of therenal pelvis, giving it a similar appearance to the antlers of a deer stag.
  • The body sits in therenal pelviswith horns extending into therenal calyces.
  • They may be seen on plain x-ray films.
148
Q

when do staghorn caluli tend to occur?

A
  • Most commonly, this occurs with stones made of struvite.
  • In recurrent upper urinary tract infections, the bacteria can hydrolyse the urea in urine to ammonia, creating the solid struvite.
149
Q

renal colic?

A
  • Unilateral loin to groin painthat can be excruciating (“worse than childbirth”)
  • Colicky(fluctuating in severity) as the stone moves and settles
  • Patients often move restlessly due to the pain.
150
Q

Features of renal stones?

A
  • renal colic
  • Haematuria
  • Nausea or vomiting
  • Reduced urine output
  • Symptoms of sepsis, if infection is present
151
Q

Ix of renal stones?

A
  • urine dipstick - usually shows haematuria, helpful to exclude infection
  • blood tests - signs of infetion and identify hypercalcaemia
  • abd X ray - will show calcium based stones but uric acid stones won’t show up - radiolucent
152
Q

imaging of renal stones?

A
  • CT KUB - initial Ix for diagnosing stones - within 24 hrs
  • US KUB in children and pregnant women
153
Q

Pain relief for renal stones?

A
  • NSAIDs - IM diclofenac, IV paracetamol
154
Q

small stones?

A
  • watchful waiting for stones less than 5mm
155
Q

managing other symptoms w stones?

A
  • antiemetics for nausea and vomiting - cyclizine e..
  • ab if infection
156
Q

which drug can be used to aid w passage of stones?

A
  • tamsulosin - to aid w spontaneous passage of stones
157
Q

large stones Mx?

A
  • surgical interventions - required in large stones (10mm or larger), stones that do not pass spontaneously or where there is complete obstruction or infection.
158
Q

surgical interventions for stones - ESWL?

A
  • Extracorporeal shock wave lithotripsy (ESWL) - shock waves directed at stones to break them up
159
Q

Surgery for stones - Ureteroscopy and laser lithotripsy ?

A

camera inserted and stone broken up using lasers

160
Q

other surgical options for stones?

A
  • Percutaneous nephrolithotomy- camera inserted, stones broken up
  • open surgery
161
Q

oxolate

preventing recurrence of calcium stones?

A

reduce the intake of oxalate-richfoods (e.g., spinach, beetroot, nuts, rhubarb and black tea)

162
Q

preventing reccurence of uric acid stones?

A

reduce the intake of purine-rich foods (e.g., kidney, liver, anchovies, sardines and spinach)

163
Q

reducing recurrence of kidney stones?

A
  • Avoiding excess salt
  • Good oral hydration(and adding lemon juice to drinking water)
  • Avoiding carbonated drinks
  • A balanced diet
  • Healthy weight loss
  • potassium citrate
  • thiazide diuretics
164
Q

Ix of UTI?

A
  • urine dip
  • urine culture
  • 24 hr urine collection to measure calcium, oxalate, citrate, uric acid
165
Q

RF for incontinence?

A
  • advancing age
  • previous pregnancy and childbirth
  • high body mass index
  • hysterectomy
  • family history
166
Q

overactive bladder/ urge incontinence is due to

A

detrusor overactivity

167
Q

stress incontinence is due to?

A

leaking small amounts when coughing or laughing, related to increased intra-abd pressure

168
Q

overflow incontinence?

A

due to bladder outlet obstruction, e.g. due to prostate enlargement, overflow after retention

169
Q

Ix of incontinence?

A
  • bladder diaries should be completed for a minimum of 3 days
  • vaginal examination to exclude pelvic organ prolapse and ability to initiate voluntary contraction of pelvic floor muscles (‘Kegel’ exercises)
  • urine dipstick and culture
  • urodynamic studies
170
Q

RF for stress incontinence?

A
  • weakening of pelvic floor muscles:
  • Age
  • Pregnancy & vaginal delivery
  • Constipation
  • Obesity
  • Family history
171
Q

urge incontinence is characterised by?

A
  • characterised by the urge to pass urine associated with involuntary leakage.
  • It occurs secondary to an overactive bladder
  • due to detrusor muscle overactivity -> involuntary contractions of the bladder
172
Q

urge incontinence is mostly?

A
  • mostly idiopathic but can occur secondary to neurological disorders
173
Q

what causes overflow incont?

A
  • when someone can’t fully empty their bladder with overflow occuring when the bladder becomes v full or secondary to stress/ urge
  • can occur secondary to physical obstruction or underactivity of the detrusor muscle:
174
Q

Overflow incontinence - bladder outlet obst?

A
  • bladder outlet obst e.g. prolapse, fibroids, following pelvic surgery
175
Q

overflow incont - detrusor underactivity?

A
  • detrusor underactivity: leads to retention and leakage
176
Q

overflow occurs w?

A
  • This occurs with advancing age, in those with peripheral neuropathy, spinal cord pathologies (e.g. MS) and secondary to medications (e.g. antimuscarinics)
177
Q

psychological impact of incontinence?

A
  • shame and embarassment -> social withdrawal
  • low self esteem
  • anxiety
  • social isolation - fear or leakage or odor
  • reduced QOL - fear of accidents
  • financial burden - purchase of absorbent products
178
Q

physical impacts of incont?

A
  • skin irritation and infection - rash, ulcers
  • UTIs
  • sleep disturbances due to nocturia
  • sexual dysfunction
179
Q

neurogenic bladder arises from?

A
  • arises from neurological conditions like SC injury, MS, PD, stroke
180
Q

pathophys of neurogenic bladder?

A
  • damage to nerves disrupts co-ordination between the detrusor muscle, and sphincter muscles
  • -> urinary retention, overactive bladder
181
Q

UMN lesions?

A
  • disruption of voluntary control over bladder function -> detrusor overactivity and increased bladder pressure
  • there may also be detrusor-sphincter dyssynergia, where the detrusor muscle contracts while the sphincter remains closed, leading to urinary retention
182
Q

LMN lesions and bladder?

A
  • These lesions disrupt the reflex arc responsible for bladder emptying and can lead to detrusor areflexia or hyporeflexia, decreased bladder contractility, and urinary retention.
  • Overflow urinary incontinence may occur due to bladder overdistension and leakage around the incompetent sphincter.
183
Q

altered sensation and incontinence?

A
  • decreased awareness of bladder fullness or urgency
  • delayed recognition of the need to void/ inability to sense when the bladder is full -> retention/ incontinence
184
Q

physical impacts of neuropathic bladder disorders?

A
  • incontinence
  • retention
  • overactivity
  • distension
  • hydronephrosis
185
Q

PSYCH impacts of neuropathic bladder disorders?

A
  • stress and anxiety
  • depression
  • self esteem
  • social withdrawal
186
Q

2 week wait criteria for bladder cancer:

A
  • dysuria w unexplained non visible haematuria age 60 and over
  • Haematuria (visible and unexplained) either without urinary tract infection or that persists or recurs after successful treatment of urinary tract infection, age 45 years and over
  • Haematuria (non-visible and unexplained) with dysuria or raised white cell count on a blood test, age 60 years and over
  • White cell count raised on a blood test with unexplained non-visible haematuria, age 60 years and over
187
Q

PSA and DRE considered when:

A
  • ED
  • haematuria
  • LUTS
188
Q

2 week wait for PC?

A
  • prostate feels malignant
  • PSA > reference ranges
189
Q

LUTs Mx - ? blockers?

A
  • alpha blockers like doxazosin or tamsulosin for moderate to severe LUTS
190
Q

LUTS - Mx of overactive bladder?

A
  • anticholinergic for overactive bladder
191
Q

LUTs - ? for enlarged prostate?

A
  • 5-AR inhibitor like finasteride for LUTS with enlarged prostate
192
Q

LUTS - ? for noctural polyuria?

A

loop diuretic

193
Q

Tx urinary retention?

A
  • immediately catheterise for acute retention
  • offer alpha blocker
  • measure creatinine and image upper urinary tract for chronic retention
194
Q

referral criteria for urinary incontinence

A
  • persisting bladder or urethral pain
  • palpable bladder on bimanual or abdominal examination after voiding
  • clinically benign pelvic masses
  • associated faecal incontinence
  • suspected neurological disease
  • symptoms of voiding difficulty
  • suspected urogenital fistulae
  • previous continence surgery
  • previous pelvic cancer surgery
  • previous pelvic radiation therapy.
195
Q

Lifestyle interventions for incontinence?

A
  • caffiene reduction for overactive bladder
  • weight loss
196
Q

first line for stress/ mixed urinary incont?

A

pelvic floor therspy

197
Q

first line for urgency/ mixed incont?

A
  • bladder training for urgency/ mixed incontinence
198
Q

SNRI for stress incont?

A

duloxetine

199
Q

surgical options for SI?

A
  • Tension free vaginal tape
  • autologous sling procedures
  • colposuspension
  • intramural urethral bulking
200
Q

artifical urinary sphincter?

A
  • when the stress incont is caused by neuro disorder or when other surgical interventions fail
  • involves a pump inserted into the labia that inflates and deflates a cuff around the urethra allowing women to control continence manually
201
Q

management of urge incont?

A
  • bladder retraining
  • anticholinergics - oxybutinin
  • mirabegron
202
Q

invasive options for overactive bladder?

A
  • botox in bladder wall
  • pec sacral nerve stimulation
  • augmentation cystoplasty
  • urinary diversion
203
Q

discontinue ? if commencing LAMA

A

Discontinue SAMA (switch to SABA) if commencing LAMA

204
Q

reduced ? in PE?

A

TLCO

205
Q

Sudden deterioration with ventilation suggests

A

tension pneumothorax

206
Q

Summary of leukemias?

A
  • ALL: most common children
  • AML: mostly in adults, auer rods
  • CLL - smudge cells, most common overall
  • CML - Philadelphia chromosome, imatinib
207
Q

TLS met abn?

A
  • high K
  • high P
  • low calc
208
Q

What can be seen in coeliac disease?

A

howell jolly bodies due to hypospelnism

209
Q

Transfusion related circ overload?

A
  • HTN
  • Raised JVP
  • afebrile
  • s3 present
210
Q

TRALI?

A
  • hypotension
  • pyrexia
  • normal/ unchanged JVP
211
Q

features of Neph syndrome?

A
  • HTN
  • oedema
  • hameaturia
  • olig
212
Q

types of nephrotic syndrome?

A
  • focal segmental glomeruloscl
  • minimal change
  • membranous nephropathy
  • diabetic nephropathy
  • amyloidosis
213
Q

types of nephritic syndrome?

A
  • post-strep GN
  • IgA nephropathy
  • Alport
  • membarnoproliferative GN
  • rapidly progressive GN
214
Q

GN =

A

nephritis

215
Q

Focal segmental GS?

A
  • Most common NS in african & hispanic
  • assoc w sickle cell and HIV
216
Q

what is seen in focal segmental GS?

A

effacement of foot podocytes

217
Q

Minimal change?

A
  • most common Neph S in children
  • assoc w recent infection
  • rarely assoc w hodgkin lymphoma
218
Q

what is seen with minimal change?

A

effacement/ fusion of podocyte foot processes

219
Q

Primary memb nephropathy?

A

ab against phospholipase A1

220
Q

Secondary memb nephropathy?

A
  • infections - hep B and C
  • SLE
  • meds - NSAIDs, penicillamine, gold
221
Q

what is seen w memb nephropathy?

A
  • spike and dome appearance
  • thickened BM and cap
222
Q

Mneumonic for mem nephtopathy?

A
223
Q

diabetic neph?

A
  • common in ESRD
  • usually w other comps like retinopathy
224
Q

pathophys of diabetic neph?

A

glycosylation of vascular BM -> hyaline arteriosclerosis -> hyperfiltration at the efferent arteriole

225
Q

what is seen w diabetic neph?

A

Kimmelstein wilson nodules: eosinophilic nodule w central acellular region

226
Q

Amyloidosis?

A
  • most commonly afffects kidneys
  • assoc w TB, MM and RA
227
Q

AA vs AL amyloid?

A
  • AA = chronic inflAAmation
  • AL amyloid - multipAL myleoma
228
Q

staining of amyloid?

A
  • apple green on EM
  • congo red stain
229
Q

Post-strep GN?

A
  • Usually kids
  • 2-4 weeks after URTI
230
Q

Type of hypersensitivity in post-strep GN?

A
  • Type 3
231
Q

What is positive in post-strep GN?

A
  • anti-strep ab
  • O titre
232
Q

Appearance in post-strep GN?

A

Granular/ starry sky

233
Q

rapidly progressive GN (4)?

A
  • goodpastures
  • microscopic polyangitis
  • diffuse proliferative GN
  • granulomastosis w polyangitis
234
Q

what is seen w RPGN?

A

Crescents - when we see the crescent we rapidly prepare for Eid

235
Q

symptoms of goodpastures?

A
  • haematuria
  • haemoptysis
235
Q

Goodpastures?

A
  • type 2 hypersen
  • anti-GBM disease
  • affects type IV collagen
236
Q

granulomatosis w polyangitis?

A
  • Wegener’s
  • vasculitis
  • C-anca - when w C granulomatosis w polyangitis u cry
237
Q

Symptoms of gran w polyangitis?

A
  • haematuria
  • haemoptysis
  • nasal involvement - rhinosinusitis
238
Q

microscopic polyangitis?

A
  • small vessel nectrotising vasculiutis
  • Sim to wegeners but no nasal involvement
239
Q

what is seen in microscopic polyangitis?

A

p-anca

240
Q

Diffuse proliferative glomerulonephritis?

A
  • assoc w SLE
  • wire loops seen

Dif-LUPUS proliferative GN

241
Q

alports?

A
  • TIV collagen defect
242
Q

Symp of alports?

A
  • sensorineural deafness
  • GN
  • lens dislocation/ retinopathy
243
Q

What is seen w alports?

A

basket weaving

244
Q

Membranoproliferative GN?

A
  • Assoc w hep C and hep B
  • most likely to co-occur w neph S
245
Q

mneumonic for Memb prolif GN?

A
  • Tram-track appearance of GBM
  • i get 2 MPG on the tram-track
246
Q

Primary hyperparathyroid blood results?

A
  • PTH and Ca high
  • Phosphate low
247
Q

Secondary hyperparathyroidism blood results?

A
  • High PTH
  • low/ normal Ca
  • phosphate High
  • Vit D low
248
Q

causes of 2’ hyperparathyorid?

A

Parathyroid gland hyperplasia occurs as a result of low calcium, almost always in a setting of chronic renal failure

249
Q

3’ parathyroidism blood results?

A
  • Ca normal or high
  • PTH high
  • phos normal/ low
  • ALP high
250
Q

3’ hyperparathyroidism cause?

A

Occurs as a result of ongoing hyperplasia of the parathyroid glands after correction of underlying renal disorder, hyperplasia of all 4 glands is usually the cause

251
Q

ACTH interpretation?

A
252
Q

pituitary adenoma ACTH results?

A

cortisol and ACTH suppressed

253
Q

adrenal adenoma results?

A

cortisol is not suppressed but ACTH suppressed

254
Q

neither suppressed?

A

ectopic ACTH

255
Q

addisons sick day rules?

A

double hydro keep fludro the same

256
Q

met acidosis Tx?

A

sodium bicarb

257
Q

CML - we see a ?

A

inc in granulocytes at diff stages of maturation and thrombocytosis

258
Q

profile of a megaloblastic anaemia?

A
  • glossitis
  • hyperseg neutrophils
    = anaemia
259
Q

Any of the following features in a person aged 0-24 years should prompt a very urgent full blood count (within 48 hours) to investigate for leukaemia:

A
  • Pallor
  • Persistent fatigue
  • Unexplained fever
  • Unexplained persistent infections
  • Generalised lymphadenopathy
  • Persistent or unexplained bone pain
  • Unexplained bruising
  • Unexplained bleeding
260
Q

Anaphylaxis?

A

acute wheeze, hypotension and no fever, presents acutely → expiratory wheeze

261
Q

TRALI?

A

hypotension, not so acute presentation, non-cardiogenic pulmonary oedema → bilateral coarse crackles

262
Q

CLL transformation?

A

can transform to high-grade lymphoma (Richter’s transformation) making patients suddenly unwell - NHL

263
Q

Interpreting FBC?

A

1.Low Lymphocytes -> the answer should be AML or CML
2. WBC > 100 -> Chronic causes so Consider CML (rule out AML)
3. Presence of bands cell -> confirm CML

264
Q

Blasts vs bands?

A
  • *blast -> Acute
    *bands -> Chronic
265
Q

Sudden anaemia and low reticulocyte count?

A
  • A sudden anemia and a low reticulocute count indicates parvovirus.
  • Acute sequestration and haemolysis causes a high reticulocyte count.
266
Q

High reticulocytes in?

A

sequestration crisis

267
Q

Howell-Jolly cells are characteristic of?

A

sickle cell

268
Q

Reed Sternberg cells AKA

A
  • Aka large multinucleate cells with eosinophilic nucleoli
  • Aka mirror image nucleoli
269
Q

most common cause of neutropenic sepsis?

A
  • STaph epidermis
  • also the most common cause of peritonitis from dialysis
270
Q

sickle cell gen Mxc

A
  • analgesia e.g. opiates
  • rehydrate
  • oxygen
  • consider antibiotics if evidence of infection
271
Q

Exchange transfusion?

A
  • indications include: acute vaso-occlusive crisis (stroke, acute chest syndrome, multiorgan failure, splenic sequestration crisis
  • rapidly reduce the percentage of Hb S containing cells
272
Q

blood transfusion in sickle cell?

A
  • indications include: severe or symptomatic anaemia, pregnancy, pre-operative
  • do not rapidly reduce the percentage of Hb S containing cells
273
Q

Cold haem anaemia mneumonic?

A
  • Cold weather is MMMiserable = cold AIHA -> IgM + caused by Mycoplasma or infectious Mononucleosis (glandular fever)
274
Q

Warm IAHA?

A

Warm weather is Great = warm AIHI -> IgG + caused by CLL or SLE

275
Q

Aplastic crisis?

A

Aplastic crises in sickle cell disease are associated with a sudden drop in haemoglobin - low reticulocyte coutn seen

276
Q

What suggests anaphylactic reaction?

A

The triad ofangioedema, hypotension, and wheezingsuggests an anaphylactic reaction rather than acute haemolysis.

277
Q

→ acute haemolytic reaction

A

Fever, abdominal pain, hypotension during a blood transfusion → acute haemolytic reaction

278
Q

Sideroblastic anaemia iron studies?

A
  • high ferritin
  • high iron
  • high transferrin saturation
279
Q

blood staining of sideroblastic A?

A
  • basophilic stippling of red blood cells
280
Q

? staining of sideroblastic anaemia?

A
  • Prussian blue staining will show ringed sideroblasts
281
Q

GDP6 def?

A

sulph- drugs:sulphonamides,sulphasalazine andsulfonylureas can trigger haemolysis

282
Q

drugs causing haemolysis in GDP6 def?

A
  • anti-malarials: primaquine
  • ciprofloxacin
  • sulph- group drugs: sulphonamides, sulphasalazine, sulfonylureas
283
Q

what is CI on VT?

A

verparmil can cause cardiac arresy

284
Q

S3 common cause?

A

S3 is most commonly caused by heart failure which is the result of a dilated, compliant ventricle

285
Q

Hypertrophic obstructive cardiomyopathy - is classically associated with

A

S4

286
Q

J waves?

A

hypothermis

287
Q

U WAVES?

A

Hypokal

288
Q

Aortic dissection?

A
  • double aortic contour
  • widened mediastinum
289
Q

small vs sq cell carcinomas?

A

Small cell: ACTH and ADH
Squamous: PTH

290
Q

chronic diabetic nephropathy?

A

Chronic diabetic nephropathy will have large/normal sized kidneys on ultrasound whereas most patients with chronic kidney disease have bilateral small kidneys

291
Q

Magnesium and calc replacement?

A

Replace magnesium before correcting hypokalaemia. Hypomagnesemia prevents potassium absorption

292
Q

What shows that the AKI is pre-renal?

A

The urea to creatinine ratio is high, as it is above 100, indicating that the cause of acute kidney injury is pre-renal - high urea makes it pre-renal e.g. dehydratoon

293
Q

all ppts w CKD should be started on?

A

statins

294
Q

Irradiated blood?

A

Irradiated blood products are used to avoid transfusion-associated graft versus host disease by destroying T cells

295
Q

blister cells and haemolyisis ->

A

GDP6 deficiency

296
Q

CML presentation

A
  • anaemia: lethargy
  • weight loss and sweating are common
  • splenomegalymay be marked → abdo discomfort
  • an increase in granulocytes at different stages of maturation +/- thrombocytosis
297
Q

Richter’s transformation
/

A

Ritcher’s transformation occurs when leukaemia cells enter the lymph node and change into a high-grade, fast-growing non-Hodgkin’s lymphoma.Patients often become unwell very suddenly.

298
Q

Ritcher’s transformation is indicated by one of the following symptoms:?

A
  • lymph node swelling
  • fever without infection
  • weight loss
  • night sweats
  • nausea
  • abdominal pain
299
Q

HHS?

A
  • Higher sugar loss and higher fluid loss, extreme dehyration
  • Head change - neuro: confusion
  • No abd pain and No ketones
  • Slower onset and stable potassium
300
Q

HHS mX?

A
  • treat hydration first: 0.9% normal saline
  • Stabilise sugar w insulin
301
Q

Thyrotoxic strom Mx?

A

treated with beta blockers, propylthiouracil and hydrocortisone. Iv propanolol first line

302
Q

What can reduce levothyroxine abs?

A

Iron / calcium carbonate tablets can reduce the absorption of levothyroxine - should be given 4 hours apart

303
Q

HHS diagnosis?

A

The diagnostic criteria for HHS include hypovolaemia, hyperglycaemia (blood sugar > 30mmol/L) and a serum osmolality > 320mosmol/kg.

304
Q

sulfonylureas stimulate insulin release ->

A

weight gain

305
Q

De Quervain’s thyroiditis?

A

In De Quervain’s thyroiditis there is globally reduced uptake of iodine-131 during thyroid scintigraphy

306
Q

-> aplastic anaemia

A

normocytic anaemia, leukopenia and thrombocytopenia = aplastic anaemia.

307
Q

Most common type of NHL

A
  • Diffuse large B cell most common
308
Q

burtkitt lymphoma?

A
  • Burkitt lymphoma typically affects young or immunosuppressed patients.
309
Q

follicular lymphoma?

A
  • Follicular lymphoma is a fairly common subtype of NHL (16% of cases) however it is low grade and usually very slow growing with symptoms developing over months to years.
310
Q

what indicates mM?

A

A raised ESR and osteoporosis represents multiple myeloma unless proven otherwise

311
Q

rescue therapy for diabetes

A
  • basal insulin
  • sulfonylrurea - glicazide
  • for v symptomatic ppts
312
Q

DVLA rules?

A
  • All patients with diabetes who are treated with insulin must notify the DVLA. For the DVLA to license an insulin-treated individual with a Group 1 licence, they must meet all the following criteria:
  • Adequate hypoglycaemia awareness
  • No more than 1 episode of severe hypoglycaemia while awake in the preceding 12 months AND the most recent episode occurred more than 3 months ago
  • Practises appropriate glucose monitoring
  • Not regarded as a likely risk to the public while driving
  • Meets the visual standards for acuity and visual field
  • Under regular review
313
Q

Features of an addisonian crisis:

A
  • Hyponatraemia
  • Hyperkalaemia
  • Hypoglycaemia
314
Q

insulin in HHS ->

A

Giving insulin in hyperosmolar hyperglycaemic state may provoke sudden and dramatic fluid shift between compartments, which may result in central pontine myelinolysis

315
Q

Most common type of thyroid cancer?

A

papillary

316
Q

Papillary TC?

A
  • young females
  • mets to cervical LNs
317
Q

thyroglobulin is a TM for?

A

papillary and follicular thyroid cancer

318
Q

follicular thyroid cancer?

A

generally women >50 years old. Metastasis to lung and bones.

319
Q

Medullary thyroid cancer?

A
  • parafollicular cells which produce calcitonin so this can be used as a tumour marker
  • MEN2
320
Q

anaplastic TC?

A

Elderly patient. Very poor prognosis

321
Q

Lymphoma TC?

A

might present with dysphagia or stridor

322
Q

Erratic blood glucose control, bloating and vomiting think

A

GASTROPARAESIS

323
Q

post mI?

A

Leads V1 and V2 showing tall R waves is characteristic of a posterior MI

324
Q

treating hyper vs hyponatreamua too fac?

A
  • Treating hypernatreamia too fast -> cerebral odema
  • treating hypo too fast -> Central pontine myelinolys
325
Q

COC increases risk of?

A
  • increased risk of breast and cervical cancer
326
Q

COCP is protective against?

A
  • ovarian
  • endometrial cancer
327
Q

alc units?

A

volume (ml) * ABV / 1,000

328
Q

thionamides in preg?

A

pTU in T1, switch to carbimazole in T2 and T3 - pTU has higher risk of hepatitis

329
Q

ACRO TESTS?

A
  1. IGF-1
  2. OGTT: confirm diagnosis
330
Q

primary hyperaldosteronism ->

A

hypernatreamia and hypokalamia

331
Q

Rupture of the papillary muscle due to a myocardial infarction →

A

Rupture of the papillary muscle due to a myocardial infarction → acute mitral regurgitation → widespread systolic murmur, hypotension, pulmonary oedema

332
Q

-> ? RHEUMATIC FEVER

A

Recent sore throat, rash, arthritis, murmur → ?rheumatic fever

333
Q

what can be done to reduce risk of sudden cardiac death HOCM?

A

An implantable cardioverter-defibrillator can be inserted to reduce the risk of sudden cardiac death in HOCM

334
Q

After starting an ACE inhibitor, significant renal impairment may occur if the patient has?

A

undiagnosed bilateral renal artery stenosis

335
Q

s3?

A
  • gallop rhythm
  • HF and severe AS
336
Q

Loud p2?

A

pulm hTN

337
Q

soft S1?

A

caused by a prolonged PR, severe mitral stenosis or mitral regurgitation

338
Q

s4?

A
  • his is an extra sound causes by atrial contraction against a stiff ventricle.
  • It is associated with hypertrophic obstructive cardiomyopathy and hypertension
339
Q

Ix for bladder cancer?

A

cytoscopy is Ix of choice

340
Q

pioglitazone side effects?

A

PIO-glitazone risks:
- Pee: Bladder cancer
- Ischaemic (not quite but helps me): Heart failure
- Osteo: Fractures

341
Q

High vs low pressure retention?

A
  • Chronic urinary retention is classed as high pressure urinary retention if renal function is impaired or if there is hydronephrosis
  • Low pressure chronic urinary retention presents with a painless distended bladder, but no associated hydronephrosis or renal impairment.
342
Q
A