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Phase 2 Med > Genitourinary > Flashcards

Genitourinary Flashcards

1
Q

Renal colic (nephrolithiasis) definition

A

Nephrolithiasis refers to the presence of crystalline stones (calculi) within the urinary system (kidneys and ureter). Such renal stones are composed of varying amounts of crystalloid and organic matrix. Ureteric stones almost always originate in the kidney but then pass down into the ureter. Most common cause of urinary obstruction.

Composition of stones:

  • calcium stones (80%) - calcium oxalate (80% of Ca stones) - oxalate rich foods eg spinach, chocolate; calcium phosphate (20% of Ca stones)
  • uric acid stones (10-20%) - gout is a risk factor
  • cystine stones (1%) - genetic conditions
  • struvite stones (1-5%) - caused by infection, proteus, Pseudomonas & Klebsiella (not e. coli)
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2
Q

Renal colic (nephrolithiasis) aetiology

A

Usually due to elevated levels of urinary solute such as calcium, oxalate, uric acid and sodium as well as decreased levels of stone inhibitors such as citrate and magnesium

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3
Q

Renal colic (nephrolithiasis) risk factors

A

Dehydration, high salt intake, white, male, obesity

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4
Q

Renal colic (nephrolithiasis) pathophysiology

A

Presence of stones (calculi) within the urinary system.
Usually symptom free but cause renal calico when stuck.

3 common sites stones get:

  • pelvic-ureteric junction (PUJ)
  • pelvic brim
  • vesicle-ureteric junction
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5
Q

Renal colic (nephrolithiasis) key presentations

A

Classical renal coli is described as severe, acute flank pain that radiates to the ipsilateral groin ‘Loin to groin’.
Pain is mostly constant

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6
Q

Renal colic (nephrolithiasis) signs and symptoms

A

Nausea and vomiting, urinary frequency/urgency, dysuria (painful urination), testicular pain, rigours (shaking) and fever may be present with pyelonephritis as a complication.

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7
Q

Renal colic (nephrolithiasis) 1st line investigations

A

Urine dipstick - haematuria
Midstream specidium urine (MSU)
Bloods: FBC, CRP & ESR, renal function (creatinine) & calcium
KUB X-ray

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8
Q

Renal colic (nephrolithiasis) gold standard investigations

A

NCCT KUB (non-contrast computerised tomography of the Kidneys Ureter Bladder) - 99% sensitive and diagnostic

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9
Q

Renal colic (nephrolithiasis) differential diagnosis

A

Ruptured AAA if >50 years until proven otherwise

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10
Q

Renal colic (nephrolithiasis) management

A

Watchful waiting and strong analgesic - IV diclofenac
Antibiotics - IV cefuroxime/gentamicin
Medical expulsive therapy (MET) - PO nifedipine/alpha blocker eg tamsulosin
Lithotripsy
Percutaneous nephrolithotomy

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11
Q

Renal colic (nephrolithiasis) monitoring

A

Prevention:
Non medical: adequate hydration, reduce sodium, fat and protein, reduce oxalate rich food

Medical:

  • hypercalciuria and recurrent calcium stones: thiazide diuretic
  • uric acid stones: allopurinol
  • cystine stones: captopril
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12
Q

Acute kidney injury/acute renal failure definition

A

Acute Kidney Injury (AKI), previously called acute renal failure is an acute decline in kidney function leading to a rise in serum creatinine and/or a fall in urine output. The disease is a spectrum from mild kidney injury to severe kidney failure

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13
Q

Acute kidney injury/acute renal failure aetiology

A

AKI may be due to various insults such as impaired kidney perfusion, exposure to nephrotoxins, outflow obstruction, or intrinsic kidney disease.

Pre-renal: low renal perfusion/obstruction of flow

  • volume depletion: haemorrhage, diarrhoea, dehydration
  • hypotension: hypovolemia, sepsis
  • cardiovascular
  • atherosclerosis/ischaemia

Intrarenal: renal parenchyma (function tissue) damage

  • glomerulonephritis: nephritic and nephrotic syndromes
  • acute tubular necrosis: nephrotoxins: ACEi, NSAIDs, amino glycoside abx eg gentamicin
  • vascular disease: vasculitis, HTN

Post-renal: outflow obstruction

  • benign prostatic hyperplasia
  • kidney stones
  • tumour
  • retroperitoneal fibrosis
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14
Q

Acute kidney injury/acute renal failure risk factors

A

Sepsis, age >75yrs, DM, cardiac failure, drugs, increased fluid loss or decreased fluid intake

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15
Q

Acute kidney injury/acute renal failure pathophysiology

A

Rapid reduction in kidney function: hours-days
Decline in GFR = loss of normal/water/solute/acid-base homeostasis

Causes retention of ammonia and uric acid and dysregulation of extracellular volume and electrolytes

Pre-renal: the kidney responds to lower perfusion pressure by enhancing sodium and water reabsorption. Baroreceptors in the carotid artery and aortic arch respond to lower blood pressure with sympathetic stimulation. This, along with vasoconstriction of the glomerular efferent arteriole and dilation of the afferent arteriole is intended to maintain glomerular filtration. Decreased perfusion promotes in the RAAS. Aldosterone release promotes further water and sodium reabsorption at the collecting duct. Low blood volume also stimulates the hypothalamus to release ADH to increase tubular water re-absorption and therefore concentrates the urine.

Post-renal: kidney injury from obstruction results from increased intratubular pressure yielding tubular ischaemia and atrophy. There may also be an influx of monocytes and macrophages. Cytokines, free radicals, proteases and TNF-b are released causing irreversible tubular injury and fibrosis when obstruction becomes chronic.

3 criteria are used to diagnosis AKI, any 1 of these = Dx of AKI

  • rise in serum creatinine >0.3mg/dL in 48hrs
  • rise in creatinine >50% baseline within 7 days
  • urine output <0.5ml/kg/hr for >6 consecutive hrs
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16
Q

Acute kidney injury/acute renal failure key presentations

A

Hypotension, presence of risk factors (patients are very often asymptomatic),
History of kidney insults, reduced urine production (commonly oliguria, anuria suggests obstructive cause or severe AKI from pre-kidney or intrinsic cause),
Lower urinary tract symptoms such as urgency, frequency or hesitancy are suggestive of urinary tract obstruction
Dizziness and postural hypotension are consistent with hypovolaemia and suggest pre-kidney AKI (may also have thirst)
Fluid overload (increased JVP, peripheral oedema, HTN)
Systemic: nausea, vomiting, confusion
Very early stages - often asymptomatic
May have oliguria or anuria

Biochemical abnormalities
- hyperkalemia - arrhythmias, muscle weakness etc
- hyponatremia - headaches, nausea, poor balance etc
- metabolic acidosis
- hyperphosphatemia
Uraemia - weakness, fatigue, anorexia, nausea, vomiting
- can cause seizures, coma, uraemia pericarditis if untreated

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17
Q

Acute kidney injury/acute renal failure investigations

A

Bloods: FBC, U&E + creatinine kinase, CRP, immunology
Urinalysis - urine dipstick and urine osmolality
ABG

Establishing cause:

  • blood urea nitrogen (BUN): creatinine ratio
  • urine osmolality
  • urine sodium excretion
  • fractional excretion of sodium
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18
Q

Acute kidney injury/acute renal failure management

A

Best treatment is prevention (monitor urinary output and creatinine levels)
Manage fluid balance, hyperkalemia, acidosis

Manage cause:

  • pre-renal: fluids, circulatory/cardiac support, treat underlying sepsis
  • intrarenal: specialist treatment, kidney biopsy etc
  • post renal: catheter, nephrostomy, urological intervention

If severe - harm-dialysis, peritoneal dialysis or hemofiltration

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19
Q

Cancer - kidney definition

A

Cancers that start in the kidney. Transitional cell carcinomas can also occur in renal pelvis, calyx, ureter and urethra

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20
Q

Cancer - kidney aetiology

A

Renal cell carcinomas are the most common (80%)

  • adenocarcinoma - proximal tubule epithelium
  • highly vascular
  • metastasis - bone, liver, lungs

Risk factors: smoking, HTN, CKD, PKD, haemodialysis

Nephroblastoma (Wilms Tumour): childhood tumour (>3yrs) - from primitive renal tubules and mesenchymal cells

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21
Q

Cancer - kidney signs and symptoms

A

Signs: abdo mass, haematuria, obstruction
Symptoms: loin pain, general cancer symptoms

Nephroblastoma: suspect if abdominal mass and haematuria in children

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22
Q

Cancer - kidney diagnosis

A

Bloods: polycythemia (increased EPO secretion), U&Es, Ca++ (high Ca is poor prognostic marker)
Urine: check for haematuria
CT/MRI: staging
USS: visualise tumour

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23
Q

Cancer - kidney management

A 
Radical nephrectomy - if localised 
Metastatic/non-resectable 
- mTOR inhibitors (temsiolimus) 
- TKI (sunitinib, sorafenib) 
- monoclonal antibodies (bevacizumab) 
RCC can be very chemo/radio resistant
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24
Q

Cancer - bladder definition

A

Cancers of the bladder

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25
Q

Cancer - bladder aetiology

A 
3 main types: 
- transitional cell carcinoma 
- squamous cell carcinoma 
- adenocarcinoma 
Risk factors: rubber, azo dyes, schistosomiasis (squamous types), chronic cystitis, smoking, male > female
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26
Q

Cancer - bladder presentations

A

Painess haematuria
Presence of risk factors
Dysuria

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27
Q

Cancer - bladder diagnosis

A

Urinalysis: haematuria is typical, pyuria (WCCs in urine) may be present
Cystoscopy
Biopsy
CT urogram

Involved lymph nodes often para-aortic iliac

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28
Q

Cancer - bladder management

A

T1: surveillance, resection of bladder tumour, cystoscopy and diathermy, chemo
T2-3: radical cystectomy, chemo
T4: palliative chemo/radio

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29
Q

Cancer - bladder complications

A

Prostatic urothelial carcinoma or other urinary tract TCC

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30
Q

Cancer - prostate definition

A

Malignant tumour situated in the prostate gland

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31
Q

Cancer - prostate aetiology

A

Malignant adenocarcinoma. High-fat diet, high testosterone levels and genetics are thought to increase the risk

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32
Q

Cancer - prostate presentation

A

Lower urinary tract symptoms (nocturne, dysuria etc) although they are generally a sign of higher - T - stage or benign prostatic hyperplasia.
Abnormal digital rectal examination.
General cancer symptoms and bone pains may be present

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33
Q

Cancer - prostate diagnosis

A 
DRE: hard and irregular 
PSA (prostate specific antigen): PSA can be raised due to prostatic and benign prostatic hyperplasia, raised 
TRUS Biopsy 
Imaging 
Bone scan
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34
Q

Cancer - prostate management

A

Localised (low risk) - surveillance
Disease progressing/advance - radical treatment
- radical prostatectomy
- radical radiotherapy
Hormone therapy: LHRH agonists + anti-androgen
Chemo and surgery may be needed

T staging:

1: non playable
2: palpable and confined to prostate
3: palpable and through capsule
4: palpable and invade other structures

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35
Q

Cancer - prostate complications

A

Metastasis to adjacent structures, bone and lung

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36
Q

Cancer - testicular definition

A

The most common malignancy in young adult men and highly curable if diagnosed early

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37
Q

Cancer - testicular aetiology

A 
Most common type is germ cell tumours 
- seminomas 
- nonseminomas 
Sex cord (stromal) 
Mixed
Lymphoma

Risk factors: undescended testes, infant hernia, infertility

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38
Q

Cancer - testicular presentation

A

Painless testicular lump
Presence of risk factors, young male
May have a secondary hydrocele

Metastatic symptoms

  • cough and dyspnoea - lung
  • abdominal mass - enlarged lymph nodes
  • back pain - para-aortic lymph nodes
  • left testicular cancer can spread to left kidney
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39
Q

Cancer - testicular diagnosis

A 
Scrotal US 
Biopsy 
Serum tumour markers 
- A-fetoprotein 
- B-hCG (never found in normal men) 
- lactate dehydrogenase, LDH

Staging

  1. No mets
  2. Para-aortic - infradiapharhmatic
  3. Supradiaphrahmatic
  4. In lungs
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40
Q

Cancer - testicular management

A

Seminomas - radical orchiectomy (removal of testicle) and radiotherapy
Non-seminomas - chemo

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41
Q

Cancer - testicular complications

A

Metastasis

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42
Q

Chronic kidney disease definition

A

Kidney damage (proteinuria, haematuria or anatomical abnormality) present for >3 months and/or impaired GFR. Normal GF: 100-120ml/min/1.73m^2

GI: normal or high; >=90
G2: mildly decreased; 60-90
G3a: mildly to moderately decreased; 45-59
G3b: moderately to severely decreased; 30-44
G4: severely decreased; 15-29
G5: kidney failure; <15

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43
Q

Chronic kidney disease aetiology

A

Prerenal:

  • heart failure
  • cirrhosis

Intrarenal:

  • hypertension
  • diabetes
  • renal artery stenosis
  • systemic disease: SLE, RA
  • glomerular disease
  • long use of NSAIDs
  • nephrotoxic substances (lead, tobacco)

Postrenal:

  • benign prostatic hyperplasia
  • repeated pyelonephritis
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44
Q

Chronic kidney disease clinical manifestations

A
  • protinuria
  • haematuria
  • oedema
  • polyuria, nocturne, oliguria
  • uraemia
  • general: lethargy, pruritus, cramps etc
  • anaemia
45
Q

Chronic kidney disease investigations

A 
FBC, U&Es, vitamin D 
TFTs (PTH) 
Bloods for serum creatinine and estimated glomerular filtration rate (eGFR) 
Urine sample (albumin:creatinine ratio) 
Urine dipstick (check for haematuria) 
Ultrasonography
46
Q

Chronic kidney disease monitoring

A

eGFR and urine ACR tests are repeated within 3 months to confirm diagnosis

47
Q

Chronic kidney disease complications

A

Cardiac arrhythmias (hyperkalaemia)
Hypertension (increased renin secretion)
Anaemia (decreased EPO)
Renal osteodystrophy
- hypocalcaemia, hyperphosphatemia
- secondary hyperparathyroidism
- skeletal abnormalities, arterial calcification

In end-stage renal disease: azotaemia (abnormally high nitrogen)

  • uremic encephalopathy and polyneuropathy
  • ureic pericarditis
  • ureic frost
48
Q

Benign prostatic hyperplasia (BPH) definition

A

Lower urinary tract symptoms (LUTS) caused by bladder outlet obstruction due to benign prostatic hyperplasia

49
Q

Benign prostatic hyperplasia (BPH) aetiology

A

Hyperplasia of the epithelial and stromal compartments occur particularly in the transitional zone. Age and hormonal changes likely have an effect

50
Q

Benign prostatic hyperplasia (BPH) risk factors

A

Age >50yrs, family history, non-Asian race, cigarette smoking

51
Q

Benign prostatic hyperplasia (BPH) pathophysiology

A

Dihydrotestosterone may be linked to the development

52
Q

Benign prostatic hyperplasia (BPH) clinical manifestations

A 
LUTS symptoms: 
Voiding 
- hesitancy
- poor stream 
- urinary retention 
- terminal dribbling 
- overflow incontinence

Storage

  • frequency
  • urgency
  • nocturia
53
Q

Benign prostatic hyperplasia (BPH) investigations

A

DRE - smooth and enlarged
PSA - rule out cancer or prostatitis
TRUS

54
Q

Benign prostatic hyperplasia (BPH) management

A

Lifestyle - avoiding caffeine and alcohol
Medical
- 1st line: a-blockers (reduce smooth muscle tone)
- 2nd line: 5a-reductase inhibitors
Surgery
Catheterisation

55
Q

Urinary Tract Infection - pyelonephritis (acute/chronic), cystitis definition

A

A UTI is the presence of characteristic symptoms and significant bacteriuria in the urinary tract

Lower UTI: cystitis (bladder infection)
Upper UTI: pyelonephritis (kidney infection)

56
Q

Urinary tract infection epidemiology

A

Very common clinical problem, second most common reason for antibiotic prescription. Much more common in women

57
Q

Urinary tract infection aetiology

A 
E. coli - majority (80-85%) 
KEEPS - common aetiologies 
- Klebsiella 
- E. coli 
- Enterococci 
- Proteus 
- Staphylococcus (usually coagulase negative)
58
Q

Urinary tract infection risk factors

A

Sexual activity, new sexual partner, diabetes (bacteria grow faster in sugary urine), old age, presence of catheter, pregnancy

59
Q

Urinary tract infection clinical manifestations

A

Urinary frequency
- painful, frequent and in small amounts

Dysuria (painful or difficult urination)
Foul-smelling cloudy urine (pyuria), urgency, suprapubic/loin pain, rigors and fever (suggests pyelonephritis)
Haematuria may be present
Acute confusion (especially in elderly)

60
Q

Urinary tract infection 1st line investigations

A

Urine dipstick - leukocytes and nitrate suggest UTI

61
Q

Urinary tract infection gold standard investigations

A

MSU

  • microscopy for leukocytes
  • culture and sensitivity for Abx choice
62
Q

Urinary tract infection differential diagnosis

A

Pyelonephritis is more associated with fever, nausea and vomiting. Flank tenderness is common on examination. Costovertebral angle tenderness is a common finding

63
Q

Urinary tract infection management

A 
1st line (cystitis): trimethoprim 
1st line (pyelonephritis): ciprofloxacin 
1st line (if pregnant): nitrofurantoin
64
Q

Prostatitis definition

A

Inflammation within the prostate that is usually accompanied by evidence of recent or ongoing infection. Most frequent urological diagnosis in men < 50yrs

65
Q

Prostatitis aetiology

A

E. coli is the main cause (80%)
Eneterococcus is the next most common
Pseudomonas, proteus mirabilis, Klebsiella can also be the cause

66
Q

Prostatitis presentation

A

Hallmark is acute onset of lower urinary tract symptoms (dysuria, urinary frequency, perineal discomfort) accompanied by systemic signs (fever, chills, malaise)

67
Q

Prostatitis diagnosis

A

Digital Rectal exam shows an intensely tender prostate

Urinalysis: leukocytes, bacteria (follow up with culture)

68
Q

Prostatitis management

A

Ciprofloxacin + NSAID

May be surgical relief if obstruction present

69
Q

Prostatitis complications

A

Urinary retention, sepsis

70
Q

Urethritis definition

A

Inflammation of the urethra. Common and treatable bacterial condition

71
Q

Urethritis aetiology

A

Causes divided by gonococcal (GU) or non-gonococcal. Most important are Neisseria Gonorrhoeae and Chlamydia trachomatis

72
Q

Urethritis presentation

A

Often occurs in people with new or multiple sex partners, inconsistent use of condoms
Urethral discharge - primary symptom, usual onset is between 4 days and 2 weeks after contact
Urethral irritation or itching
Dysuria
Orchialgia - sensation of heaviness in male genitals - pain suggests epididymitis or orchitis

73
Q

Urethritis diagnosis

A

Gram stain of urethral discharge - gram negative diplococci is suggestive of gonorrhoea
Nucleic acid amplification tests - most sensitive for gonorrhoea detection from urine
Culture of discharge - chocolate agar positive for Neisseria gonorrhoea, HIV test - standard to rule out

74
Q

Urethritis management

A 
1st line (gonococcal): ceftriaxone and azithromycin 
1st line (non-gonococcal): azithromycin
75
Q

Glomerular disease - nephritic syndrome definition

A

Characterised by thinning of the glomerular double basement membrane and porous podocytes as well as inflammation. When it occurs in the glomerulus it is called glomerulonephritis (inflammation within the kidney/renal vessels resulting in glomerular damage and its function).

76
Q

Glomerular disease - nephritic syndrome aetiology

A 
Children: 
IgA nephropathy 
- 1-2 days after upper respiratory tract infection (URTI) 
Post-streptococcal glomerulonephritis 
- 2-3weeks after URTI due to strep 
Henoch-Schonlein Purpur (HSP) 
- palpable purpura, abdo pain, joint pains and renal damage 
Haemolytic-uraemic syndrome 
- after E. coli infection

Secondary (most common in adults):
Goodpasture’s syndrome (autoimmune)
Other autoimmune eg SLE
Vasculitides

77
Q

Glomerular disease - nephritic syndrome pathophysiology

A

The pores of the podocytes become large enough to allow RBCs and proteins to pass through. The capillaries of the glomerulus swell causing increased renin secretion due to extra stretch on the juxtaglomerular apparatus and eventually leading to hypertension

78
Q

Glomerular disease - nephritic syndrome key presentations

A
  • haematuria
  • proteinuria (<3.5g/day)
  • hypertension
  • oedema (less than nephrotic)
79
Q

Glomerular disease - nephritic syndrome investigations

A

History and exam: signs of fluid overload eg oedema, raised JVP, HTN, history of URTI in child suggests IgA/post-strep
Bloods: electrolytes, creatinine (for GFR), ANA antibody screen, anti-GM antibody (Goodpasture’s), ANCA
Urinalysis

80
Q

Glomerular disease - nephritic syndrome management

A

Fluid restrictions to reduce oedema - also reduce kidney workload
Diuretics if fluid overload is severe
Antihypertensives to normalised BP
NSAIDs or steroids - reduce active inflammation in the kidney

81
Q

Glomerular disease - nephrotic syndrome definition

A

Nephrotic syndrome is defined as proteinuria (>3.5g/24hrs), hpoalbuminemia (<30g/L), oedema and NO BLOOD. Lipiduria and hyperlipidemia are less common and less important

82
Q

Glomerular disease - nephrotic syndrome aetiology

A

Primary:

  • minimal change disease - so called because nephrons appear normal under a light microscope. This is the most common in children
  • focal segmental glomerulosclerosis - most common in young adults
  • membranous glomerulonephritis - most common in adults

Secondary:

  • infection eg HIV, Hep B
  • autoimmune eg SLE, RA, vasculitides
  • diabetes mellitus
  • neoplasms eg myeloma, leukaemia
  • drugs eg NSAIDs
83
Q

Glomerular disease - nephrotic syndrome pathophysiology

A

Proteins lost are mostly albumins resulting in hypoalbuminemia causing oedema seen because of lower osmotic pressure within vessels causes fluid to accumulate in interstitial tissue fluid

84
Q

Glomerular disease - nephrotic syndrome clinical manifestations

A

Oedema

  • especially facial swelling in children
  • peripheral (ankle and legs) in adults
Frothy urine 
- due to lipids and proteins in urine 
Tiredness 
Breathness - pearl effusion may occur due to severe hypoalbuminemia 
AKI
85
Q

Glomerular disease - nephrotic syndrome investigations

A

1st line: urine dipstick - proteinuria and NO HAEMATURIA
MSU (midstream specimen of urine) - microscopy, culture and sensitivity for UTI

Gold standard: protein:creatinine or albumin:creatinine ratio

Renal biopsy for aetiology
Bloods: ESR CRP (for SLE/autoimmune), FBC, LFTs
CXR for plural effusion if suspected

86
Q

Glomerular disease - nephrotic syndrome management

A 
Sodium and fluid restriction and high dose diuretic 
- reduces oedema 
- furosemide 
Coticosteroids 
- reduces kidney damage and proteinuria 
- prednisolone

Medical nutrition therapy for lost protein

87
Q

Glomerular disease - nephrotic syndrome complications

A

Thromboembolism, infection, hyperlipidaemia

88
Q

Polycystic kidney disease - dominant and recessive definition

A

PKD is part of a group of disorders characterised by renal cysts and numerous systemic and extra-renal manifestations. Can be divided into autosomal-dominant PKD (ADPKD) and autosomal-recessive PKD (ARPKD), the former of which being much more common.
Chromosome 16.

89
Q

Polycystic kidney disease aetiology

A

ADPKD:
- mutation in the PKD1 gene (codes for polycystic 1) - makes up for approx 85% of cases
- mutation in the PKD2 gene (codes for polycistin 2)
ARPKD: mutation in PKHD1 gene, which codes for fibrocystin, a protein which is involved with polycystic 2’s function

90
Q

Polycystic kidney disease risk factors

A

Family history of PKD, or cerebrovascular event or berry aneurysms (subarachnoid haemorrhages)

91
Q

Polycystic kidney disease pathophysiology

A

Polycystins are protein channels found in the cell membrane of ciliated cells in the nephrons and throughout the body - these channels are involved in inhibition of cell division, so they absence results in uncontrolled division resulting in cysts throughout the body (particularly the kidneys)

Renal cysts cause compression of normal renal architecture and intrarenal vasculature, increased renal size, interstitial fibrosis and tubular atrophy and progressive renal impairment.

92
Q

Polycystic kidney disease key presentations

A

Family history of PKD or end stage renal disease (ESRD)

93
Q

Polycystic kidney disease signs and symptoms

A
  • renal cysts
  • excessive water and salt loss
  • nocturne
  • hypertension (often at a young age)
  • abdominal/flank pain (due to nephrolithiasis or UTIs etc)
  • haematuria
  • palpable kidneys (bilateral kidney enlargement)
  • UTI symptoms common
  • cholestasis due to aneurysms in bile ducts
  • berry aneurysms, particularly in the circle of willis (leading to subarachnoid haemorrhages)
  • cardiac murmur: mitral valve prolapse, mitral regurgitation. aortic regurgitation and dilated aortic root are the most common
  • abdominal hernias are common
  • portal HTN
  • hepatomegaly - highly specific for ADPKD
94
Q

Polycystic kidney disease 1st line investigations

A

Renal ultrasound

  • at least 2 unilateral or bilateral cysts < 30 yrs
  • at least 2 cysts in each kidney 30-59yrs
  • at least 4 cysts in each kidney >60yrs

CT scan: better sensitivity
Urinalysis: assess albumin excretion, creatinine often normal

95
Q

Scrotal disease definition

A

Epididymal cyst: cyst of the epididymis containing clear serous liquid. Above and behind the testes. Most common around 40 yrs, rare in children. A spermatocele is a cyst in the head of the epididymis.

Hydrocele: accumulation of clear fluid within the cavum vaginale (between the layers of the tunica vaginalis)

Varicocele: enlargement of the pampiniform plexus in the scrotum

Hematoceles: collection of blood in the tunica vaginalis around the testes

Epididymitis (also known as epididymo-orchitis): inflammation of the epididymis, epididymo-orchitis is when there is also orchitis (inflammation of testis)

Testicular torsion: twisted spermatic cord - cut off blood supply to the testes -ischaemia - this is a medical emergency

96
Q

Scrotal disease aetiology

A

Epididymal cyst/Spermatocele: clear/milk fluid above and behind testes

Hydrocele: trauma/infection/tumour

Varicocele: likely combination of anatomical factors

Hematoceles: trauma

Epididymitis: among sexually active men, Chalmydia trachoma’s and Neisseria gonorrhoeae are the most common cause. May be due to Escherichia coli and Proteus

97
Q

Scrotal disease presentation

A

Epididymal cyst: soft squidgy lump at top or bottom of the testicle. Can get above it and separate from testis. Can transilluminate (light can be shone through)

Hydrocele: scrotal enlargement, smooth swelling, no pain normally, can usually get above it. Testis not palpable separately. Cystic so not solid mass. Can transilluminate.

Epididymitis: unilateral scrotal pain and swelling of gradual onset, tenderness, hot, diffuse enlargement of the testis. May have urethritis and discharge, sweats and fevers. Can get above it, epididimytis is separate, orchitis is testicular. Solid - feels like mass. Does not transilluminate.

Testicular torsion: sudden onset testicular pain, inflamed and tender testicle, unilateral, abdo pain, N&V.

98
Q

Scrotal disease diagnosis

A

Epididymal cyst: usually clinical may need USS

Hydrocele: clinical diagnosis, may need USS

Varicocele: clinical diagnosis, may need doppler ultrasound

Epididymitis: gram stain of urethral secretions, urine dipstick (leukocytes), urine microscopy and cultures, nucleic acid amplification test (NAAT)

Testicular torsion: clinical

99
Q

Scrotal disease differential diagnosis

A

Assume a testicular lump is cancer until proven otherwise

100
Q

Scrotal disease management

A

Epididymal cyst: generally harmless and don’t require treatment, may need surgery if painful

Hydrocele: observation, may need surgery/aspiration of discomfort or infection

Varicocele: reassurance, observation. Venography, doppler ultrasound, surgery if needed

Hematoceles: aspirate/surgery

Epididymitis: abx, ceftriaxone and doxycycline

Testicular torsion: fast referral to urology for surgery

101
Q

Obstructive uropathy definition

A

The blockage of urinary flow can affect one or both kidneys. If only one is affected urinary output may be unchanged and serum creatinine can be normal. When kidney function is affected it is called obstructive nephropathy

102
Q

Obstructive uropathy aetiology

A

Unilateral obstructive uropathy: acute unilateral uropathy is most commonly due to renal stones. It may be from injury during surgery. Chronic unilateral uropathy may be due to malignancy in nearby structures

Bilateral obstructive uropathy: benign prostatic hyperplasia (BPH) is a common cause and can cause acute or chronic uropathy.

Back pressure on the kidneys leads to decreased renal blood flow, decreased GFR, and up-regulation go the RAAS. This can lead to atrophy and apoptosis on the renal tubules.

103
Q

Obstructive uropathy presentation

A

Flank pain: especially if unilateral

Fever: sign of UTI

LUTS: frequency, urgency, incomplete emptying etc

Palpable bladder
Costovertebral angle tenderness: common with obstruction and infection

May have signs of sepsis: tachypnea, tachycardia, hypotension, altered mental state

104
Q

Obstructive uropathy diagnosis

A

Urinary dipstick: nitrates and blood or leukocyte esterase indicates UTI
Renal ultrasound: may show hydronephrosis
For stones: CT pyelogram, intravenous pyelogram

105
Q

Obstructive uropathy management

A

If due to calculi (stones)

  • analgesia (ketorolac), rehydration and alpha blockers tamsulosin
  • may need active stone removal

May need ureteric stent or catheterisation, abx if infection suspected (treat as UTI)

106
Q

Urinary incontinence definition

A

Loss of control of voiding in the bladder. More common in women

Neuropathic Bladder Dysfunction: spinal/CNS injury or disease - loss of neuronal control over bladder

  • spastic injury: higher spinal cord - hyperreflexcic - bladder is functional but not controlled by brain - loss of coordination and completion of voiding - involuntary urination - urger incontinence
  • flaccid injury: lower spinal cord - hyporeflexic - bladder is areflexic - bladder fills until it overflows - stress incontinence - consider permanent catheterisation
107
Q

Urinary incontinence aetiology

A

Urge incontinence: due to detrusor overactivity and bladder hypersensitivity.
Stress incontinence: due to sphincter and pelvic floor weakness. Women - secondary to birth trauma. men - post-prostatectomy
Overflow incontinence: usually a sensation of incomplete emptying after voiding. Diabetic neuropathy can impairment ability of detrusor to contract

108
Q

Urinary incontinence management

A

Oxybutynin for urge incontinence - anticholinergic

109
Q

AKI complications

A

Pulmonary oedema; hyperkalaemia

Phase 2 Med (9 decks)

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