urogenital Flashcards
what forms the inguinal ligament
external oblique aponeurosis
what was the renal blood flow
Renal artery 🡪 interlobar artery 🡪 arcuate artery 🡪 interlobular artery 🡪 afferent arteriole 🡪 glomerular capillary 🡪 efferent arteriole 🡪 peritubular capillary around tubules
what is the standard GFR
125 ml/min
what was the criteria for a good GFR indicator like creatinine
freely filtered
not metabolised
not secreted
not reabsorbed
explain tubulo-glomerular feedback
macula densa cells is DCT dectect low levels of NaCl –> release prostaglandins to stimulate renin release and trigger RAAS to cause vasoconstriction of afferent arteriole
high levels of NaCl detected by macula densa –> signal to afferent arteriole to cause vasodilation
why does vasoconstriction of the afferent arteriole increase GFR?
because it increases HYDROSTATIC pressure so more capillary contents flow into bowman’s capsule
during renal filtration, the blood pressure in the glomerular capillaries (glomerular hydrostatic pressure) is the main driving force pushing fluids and solutes out of the blood and into the Bowman’s capsule. The opposing pressures from the Bowman’s capsule and the oncotic pressure within the glomerular capillaries work against this filtration to maintain a balance.
how do you measure GFR and state the formula
with creatinine or cystatin C
(creatinine urine conc. x urine flow)/plasma creatinine concentration
what are the components of the filtration barrier
Fenestrated capillaries
basement membrane
podocyte foot processes
what is the criteria to diagnose AKI
NICE criteria:
Rise in creatinine of >26 micromol/L in 48 hours
Rise in creatinine to ≥1.5 times baseline in a span of 7 days
Urine output of <0.5ml/kg/hr for >6 hours
what is AKI
Sudden decline in renal function over hours or days leading to a rise in serum creatinine and/or a fall in urine output
explain pre-renal, intra-renal and post-renal AKI with examples of diseases
pre-renal: due to inadequate blood supply to kidneys
ex.: hypovolemia, severe dehydration, shock, heart failure
intra-renal: disease of kidneys
ex.: glomerulonephritis, acute tubular necrosis
post-renal: obstruction of outflow of urine causing increased pressure and reduced function
risk factors to AKI
Hypotension
volume depletion (DEHYDRATION)
CKD
heart failure
diabetes
cirrhosis
nephrotoxic meds (NSAIDs, ACEi)
cancer
trauma
key presentations of AKI
Reduced urine output, high creatinine, hyperkalaemia (arrhythmias, muscle weakness), uraemia (pericarditis, nausea, vomiting, encephalopathy), fluid overload (pulmonary and peripheral oedema, hypovolemic shock, orthopnoea), hypotension, sepsis/acute illness, UTIs
what is uraemia
high urea in blood
what is orthopnea
Orthopnea is a medical term that describes difficulty breathing while lying flat. Individuals with orthopnea typically find relief by sitting up or propping themselves up with pillows. It is a symptom often associated with heart failure and other conditions affecting the respiratory and cardiovascular systems.
investigations for AKI gold standard
metabolic panel + urine output monitoring + urinalysis
serial U&Es daily (twice a day if needed)
for fast results you can also do a urine dipstick instead of a urinalysis but it is not gold standard
what is the management of AKI?
Treat underlying cause (hypotension, stones, infection).
Stop nephrotoxic drugs (NSAIDs, ACEi).
Treat complications (electrolyte imbalances).
Severe – haemodialysis
what test could provide fast information about the urine contents
urine dipstick
how do you test whether an AKI is prerenal or intra-renal and provide the parameters
urea: creatinine ratio - it provides info about whether the kidney disease is pre-renal or intra-renal.
pre-renal: ratio is more than 100:1 because decreased blood flow leads to increased reabsorption of urea in the renal tubules.
intra-renal: ratio is less than 40:1 (In conditions where there is damage to the renal tubules the reabsorption of urea may be impaired, leading to a proportionally smaller increase in BUN compared to creatinine.)
what is CKD
Chronic reduction in kidney function for more than 3 months which is permanent and progressive.
causes of CKD
Diabetes
hypertension
glomerulonephritis
polycystic kidney disease
nephrotoxic drugs (NSAIDs, ACEi)
persistent pyelonephritis
obstruction
what is pyelonephritis
kidney infection
how long does the kidney dysfunction have to be for to be classed as CKD
3 months
pathophysiology of CKD
Many nephrons are damaged causing decreased GFR which increases burden on remaining nephrons. Compensatory RAAS to increase GFR but trans-glomerular pressure is shearing, and a loss of basement membrane permeability causes protein/haematuria.
key presentations of CKD
Asymptomatic until end-stage (remaining nephrons still work for a while).
Symptoms due to toxin accumulation:
uraemia (pruritis, nausea, uraemic frost, restless legs, encephalopathy, pericarditis)
fluid (oedema, raised JVP)
potassium (arrhythmias, muscles weakness)
oliguria (low urine output)
peripheral neuropathy
haematuria
proteinuria
what is oliguria
low urine output
investigations for CKD and diagnosis
FBC - anaemia from erythropoietin deficiency
U&E
urinalysis
renal ultrasound –> bilateral renal atrophy
Diagnosis:
eGFR < 60mL/min/1.73m2
OR
eGFR <90mL/min/1.73m2 + signs of renal damage (protein/haematuria, pathology on imaging/biopsy)
OR
albuminuria > 30mg/24hrs
what will you see on a renal ultrasound in CKD
bilateral renal atrophy
how do you manage CKD
Refer to specialist if eGFR <30, albumin:creatinine ratio >70.
Main focus: prevent CVD
manage diabetes if it applies
treat complications:
anaemia (ferrous sulphate, erythropoietin)
oedema (fluid restriction, diuretics)
metabolic acidosis (sodium bicarbonate)
CKD-mineral bone disease (vitamin D)
CVD (statins).
END STAGE: dialysis until kidney transplant
complications of CKD
anaemia (ferrous sulphate, erythropoietin)
oedema (fluid restriction, diuretics)
metabolic acidosis (sodium bicarbonate)
CKD-mineral bone disease (vitamin D)
CVD (statins).
how do you manage oedema in patients with CKD if diuretics can further damage the kidney and lead to electrolyte imbalances?
sodium dietary restriction and management of other complications which might be contributing to the oedema
explain the staging of CKD based on eGFR and albumin: creatinine ratios
stage 1 - GFR>90 (kidney damage with normal GFR)
stage 2 - Mildly Reduced eGFR (60-89 mL/min/1.73 m²)
stage 3a - eGFR 45-59 mL/min/1.73 m²
Stage 3b - eGFR 30-44 mL/min/1.73 m²
Stage 4 - Severely Reduced eGFR (15-29 mL/min/1.73 m²)
Stage 5 - Kidney Failure (eGFR <15 mL/min/1.73 m² or Dialysis)
stage 1 - a:c ratio < 3
stage 1 - a:c ratio between 3 and 30
stage 1 - a:c ratio >30
why is iron not absorbed well in the GI in CKD
In CKD, there is often a state of chronic inflammation. Elevated levels of proinflammatory cytokines, such as interleukin-6 (IL-6), stimulate the production of hepcidin. Hepcidin is a hormone that regulates iron homeostasis by inhibiting the absorption of iron from the intestines and promoting iron sequestration within cells. Increased hepcidin levels can reduce the availability of iron for absorption.
explain why you can get CKD mineral bone disease
1) kidneys can’t convert vit D to active form –> calcitriol is used to absorb calcium from intestines and this is impaired –> hypocalcemia
2) in CKD you get phosphate retention –> the body will compensate by coupling it with Ca –> again a decrease in calcium serum levels
3) the hypocalcemia and increased phosphate levels will trigger PTH release which will mobilise calcium from bone and enhance renal calcium resorption –> but in CKD this compensatory mechanism doesn’t last for long –> osteoporosis
how do you differentiate AKI from CKD
CKD ultrasound shows bilateral atrophy of kidneys
CKD presents with hypocalcemia
what should you check before giving anaemia treatment for CKD patient and why
serum iron because CKD leads to general inflammation in the body which activates the hormone hepcidin. Hepcidin decreases iron absorption in the intestine.
what is the 1st line treatment for patients with CKD and coexistent hypertension?
ACEi
explain how SGLT-2 inhibitor are reno-protective in CKD patients with proteinurea
regardless of diabetes stautus these meds are good because they increase clearance of glucose and sodium –> reduction in intravascular volume and blood pressure –> normalising of tubuloglomerular feedback and reduction in intraglomerular pressure
define polycystic kidney disease
Inherited disease where multiple fluid-filled cysts form within the kidneys.
Two types – autosomal dominant (mc) and autosomal recessive
which type of polycystic kidney disease is more common
autosomal dominant
pathophysiology of polycystic kidney disease
Cysts develop and grow over time into the tubular portion of the nephron. Compression of renal architecture and vasculature. Progressive impairment – gets bigger and worse with age
key presentations of polycystic kidney disease
Painless haematuria
Hypertension
bilateral abdominal/flank pain
headaches
Lower Urinary Tract Symptoms (dysuria, urgency, pain)
palpable kidneys
other cysts: hepatic splenic pancreatic ovarian and prostatic cysts
Polyuria, polydipsia, nocturia - excess urine due to poor concentrating ability of kidneys (i.e. not responding to anti-diuretic hormone)
investigations for polycystic kidney disease
Kidney ultrasound - enlarged bilateral kidneys with 2 or more cysts unilateral or bilateral
management
Tolvaptan (ADH receptor antagonist) to slow development of cysts and progression of renal failure.
Supportive: antihypertensives, antibiotics if infected, drainage of cysts, analgesic for renal colic, surgical removal of cysts, dialysis or transplant for ESRF
what is the most dangerous complication of PKD
aneurysm formation –> patients need screening if they have a fam history of intracerebral haemorrhage
what is the course of sperm form the testes to the external urethral meatus
epidydimis
vas deferens
spermatic cord in inguinal canal
wraps above and around the bladder
joins seminal vesicle and prostate
joins urethra
where in the prostate do you get hyperplasia in benign prostatic cancer
core of the prostate
where is the pouch of Douglas
between the rectum and uterus
where does fertilization take place
ampulla of the fallopian tubes
what are the parts of the fallopian tubes
fimbriae
infundibulum ampulla
isthmus
interstitium
what were the vestibular glands
bartholin’s glands (greater vestibular glands) –> secrete lubricant into vagina during sexual arousal
Skene’s glands (lesser vestibular glands) –> function unknown 100% but possible antimicrobial properties
what is the most common location for an ectopic pregnancy
uterine tube
what is the minimum urine pH
4.5
what are the folds of mucosa in the bladder called and what is their function
rugae
allow bladder to stretch without tearing when in fills
which muscle contracts to expel urine
detrusor
where are the internal and external urethral sphincters in men and women
internal - at the base of the bladder
external male - just after prostate
external female - in the deep perineal pouch
what is the innervation of the urinary bladder and urethral sphincters
somatic: pudendal nerve S2-S4
sympathetic: hypogastric nerve (T12-L2) —> allows STORAGE of urine by contracting the internal urethral sphincter and relaxing the detrusor
parasympathetic: pelvic splanchnic nerves (S2-S4) –> allows micturition
what are the 2 curves of the rectum
the sacral flexure and the anorectal flexure
what is the dendate line
line which separates superior and inferior anal canal because they have different blood supplies and innervation as a result of different embryological origin
blood supply, venous drainage, and innervation of superior and inferior anal canal
sup and inferior have different embryological origin so they have dif blood supply and innervation
superior - IMA + portal venous system drainage + pelvic splanchnic nerves for parasympathetic innervation
inferior - middle and inferior rectal arteries from the internal iliac + inferior rectal veins which go straight to SYSTEMIC circulation + pudendal nerve
where would pain from the ovary radiate and why
medial aspect of thigh because it can irritate obturator nerve which is motor + sensory nerve
what is a retroverted uterus
the uterus is tilted backward instead of the more common forward position. it can cause painful menstruation and difficulty with conceiving
what maintains the normal position of the uterus
Uterosacral Ligaments: attach the back of the uterus to the sacrum –> these ligaments provide help anchor the uterus in its forward-facing position.
Broad Ligaments: wide folds of peritoneum that attach the sides of the uterus to the pelvic sidewalls
Round Ligaments: extend from the front of the uterus to the pelvic sidewalls
Pelvic Floor Muscles: The pelvic floor muscles, including the levator ani muscles, form a hammock-like structure that helps maintain the position of the uterus.
to which lymph nodes would cervical cancer spread
pelvic lymph nodes
what feature stops urine from passing back up to the kidney after the bladder is full and when the bladder contracts for urination
ureteral valves: located at the junction of the ureters and the bladder
what is normal CO and how much do the kidneys receive
5L/min
they receive 20% of CO
which is THE ONLY site of glucose reabsorption in the nephron
the PCT –> SGLT2 transporter
what was the difference between the thin descending and thick ascending loop of Henley and explain how they work together
thin bit permeable to H2O (aquaporin-1 channels) and impermeable to solutes like Na (think permeable in terms of reabsorption in body, not permeable in terms of excreting the substance)
tick bit permeable to Na and impermeable to H2O
the thick ascending limb pumps out a lot of Na to make the medulla hypertonic which will allow the water from inside the nephron to go into the medulla (get reabsorbed in the body)
what is the function of the DCT
fine tuning of Na reabsorption, acid-base balance, and primary location for K+ excretion because Na is being taken in the charges are balanced by excreting K+
what were the 2 types of cells in the collecting ducts and what did they do
principal: sodium and water reabsorption via ENaC (K+ kicked out in exchange for Na+); aldosterone acts on this channel
intercalated: acid base homeostasis; it secretes H+ or HCO3- depending on which way the pH needs to be corrected
in what forms is H+ excreted
H2CO3, NH4+, H2PO4-
what is the primary adaption to acidosis in the kidneys?
Formation of more NH4+ in the collecting duct to excrete it because it is impermeable to the apical membrane
what is the plasma anion gap and what does a high gap indicate
a measure of the difference between Na and Cl and HCO3, as Na is the most abundant positive ion and Cl and HCO3 are the most abundant negative cations.
the gap should usually be between 3-11 mEg/L
a higher gap indicates acidosis
how do you test for acid base disorders
ABG - arterial blood gas
what receptors do you have in the bladder and what do they do
SYMPATHETIC
beta 2 and 3 cause bladder relaxation for filling
alpha 1 activated to constrict the internal sphincter and prevent bladder emptying
PARASYMPATHETIC
M2 and M3 activated
Beta 2, Beta 3, alpha 1 are inhibited
what nerve controls the external urethral sphincter and what nerve controls the internal urethral sphincter
external: pudendal (somatic S2-S4)
internal: hypogastric (sympathetic T12-L2)
what are the different types of kidney stones
Majority (80-90%) are calcium oxalate stones (radio-opaque).
Other types: calcium phosphate, uric acid (radio-lucent: not seen on x-ray), struvite (produced by bacteria), cystine.
what is struvite
kidney stones produced by bacteria
causes of kidney stones
Chronic dehydration, obesity, high protein/salt diet, recurrent UTIs, low urine output, hyperparathyroidism/hypercalcaemia
what is hydropnephrosis
If the stones cause regular outflow obstruction the kidneys fill with urine and swell
where do kidney stones most commonly get stuck
Pelvi-ureteric junction
pelvic brim (where uretrer runs over the iliac artery)
vesico-ureteric junction
where does kidney stone pain get referred to
the loin –> T12 -L2 dermatome
key presentations of kidney stones
severe colicky unilateral pain originating in loin and radiating to groin
patient can’t lie still
haematuria
nausea and vomiting
reduced urine output
1st line and gold standard investigations for kidney stones
INVESTIGATIONS
1st line
Urine dipstick → haematuria, leukocytes (inflammation), nitrates (bacterial kidney stones)
FBC, CRP (infection)
U&Es (hypercalcaemia/hyperkalaemia → reduced excretion).
Abdominal x-ray (will show calcium stones but not uric acid stones as they are radiolucent)
Gold standard
Non-contrast CT of the kidney ureters and bladder
why is ultrasound not the gold standard for kidney stones investigation
Can only see radio-opaque stones like calcium oxalate stones, but not uric acid or cystine stones
management of kidney stones
Symptomatic relief – hydration, NSAIDs (diclofenac). Antiemetics, antibiotics.
Watchful waiting – stones under 5mm should pass spontaneously without infection
If the stone is too big you can break it into smaller pieces using:
Extracorporeal Shock Wave Lithotripsy ESWL (break stone into smaller fragments using shockwaves)
ureteroscopy and laser lithotripsy → using a laser to break the stone
Complete removal of stone:
PCNL (percutaneous nephrolithotomy) → a small incision is made in the back, and a nephroscope is inserted directly into the kidney. The stone is visualized, and various tools, including laser or ultrasonic energy, are used to fragment the stone, which is then suctioned or removed.
Lifestyle: decrease sodium and protein intake, increase citrus fruit, adequate fluid intake
what diet changes can you do to reduce the chance of kidney stones
Lifestyle: decrease sodium and protein intake, increase citrus fruit, adequate fluid intake
what is the most common type of renal cancer
clear cell renal cell carcinoma
how do you classify renal cancers
Bosniak classification
Bosniak 1: benign
Simple cyst with a thin wall, no septa, no calcifications, or solid components.
Bosniak 2:
Thin septa or fine calcifications.
No enhancement after contrast.
Usually benign; periodic follow-up may be recommended.
Bosniak 2F:
like Bosniak 2 but with enhancement after contrast –> low risk of malignancy; follow-up imaging may be suggested.
Bosniak 3:
Thickened septa or nodularity.
Bosniak 4:
Clearly malignant cystic lesion.
Thickened irregular walls, enhancing solid components.
High risk of malignancy; surgical intervention or biopsy may be considered.
what is the TNM staging of renal cancer?
Tumour
T1 - tumour confined to renal capsule with a diameter smaller than 7 cm
T2 - tumour confined to renal capsule with a diameter bigger than 7 cm
T3a - invasion of perinephric fat or adrenal gland
T3b - tumour extends into the renal vein or IVC under the diaphragm
T3c - tumour invades IVC above the diaphragm
T4 - metastasis to other organs
Nodules
N1 - tumour invades 1 regional lymph node
N2 - metastasis to more than 1 regional lymph node
Metastasis
M1 - distant metastasis present
causes of renal cancer
Hypertension
Obesity
smoking
renal failure
VHL (Von Hippel-Lindau Syndrome) → VHL, or Von Hippel-Lindau syndrome, is a rare genetic disorder characterized by the development of tumors and cysts in various parts of the body. It is caused by mutations in the Von Hippel-Lindau tumor suppressor gene (VHL gene). The VHL gene is located on the short arm of chromosome 3.
what is Von Hipple Lindau Syndrome?
VHL, or Von Hippel-Lindau syndrome, is a rare genetic disorder characterized by the development of tumours and cysts in various parts of the body. It is caused by mutations in the Von Hippel-Lindau tumour suppressor gene (VHL gene). The VHL gene is located on the short arm of chromosome 3.
pathophysiology of renal cancer
VHL mutation leads to an inability to degrade HIF and loss of function of tumour suppressor genes –> Hypoxia in the cells causes oxidative stress and DNA damage + angiogenesis which ends up supplying the tumour
key presentations of renal cancer
Triad: Haematuria, flank pain, palpable mass. May have left varicocele if male cuz left testicular vein joins into the renal vein before the aorta
1st line and gold standard investigation for renal cancer
1st line
Abdominal/pelvis ultrasound, bloods: raised RBC, CRP, raised calcium, raised LDH, urine dipstick
gold standard
CT chest/abdo/pelvis
management of renal cancer
Visible haematuria seen over 45 years old → immediate referral to 2 week wait for CT scan
Urine dipstick detection of micro haematuria in over 60 years old → immediate referral to 2 week wait for CT scan
Treatment options:
Surveillance
Surgery to remove tumours or only parts of kidney to try and preserve kidney function → nephrectomy/partial nephrectomy
Radiofrequency ablation: you kill the cells via coagulative necrosis but you can’t get a biopsy
Cryogenisis
urothelial cell carcinoma vs transitional cell carcinoma
Transitional Cell Carcinoma (TCC):
TCC primarily arises from the transitional epithelium, which is the tissue lining the renal pelvis, ureters, and bladder.
TCC is more commonly associated with bladder cancer
Urothelial Cell Carcinoma (UCC):
The term “urothelial” is a more inclusive term that encompasses the lining of the entire urinary tract, including the renal pelvis, ureters, and bladder. Urothelial carcinoma is a broader term that includes TCC.
UCC can occur in various parts of the urinary tract, and it may involve the renal pelvis, ureters, and bladder
what are the 3 main types of kidney cancer
Renal cell carcinomas → originate from the lining of the nephron (Clear cell carcinoma is the most common type of RCC)
Transitional cell carcinomas → arise from the epithelial lining inside of the kidney
Willms’ tumours → originate from renal stem cells → the most common kidney cancer in children, typically occurring between the ages of 2 and 5. Wilms’ tumor usually presents as a painless abdominal mass
what is the most common subtype of bladder cancer?
transitional cell carcinoma
epidemiology of bladder cancer
Old men, people who work in rubber/dye industry
3:1 ratio men to women
Common cancer
causes of bladder cancer
Mutation
Occupational carcinogens
Smoking → you pee the carcinogens and they sit in your bladder for longer
Iatrogenic: caused by drugs
Microbiome → Schistosomiasis → parasite infection which enters through the urethra or mouth → You get by outdoor swimming → leads to squamous cell cancer
Pollution
Infection/inflammation
Long term catheters
Long-term stones (kidney stones)
risk factors to bladder cancer
Exposure to dyes/rubber/leather/textiles/paint (aromatic amines – dye factor worker, hairdresser, painter). Age >65, male, Caucasian, smoking, pelvic radiation
pathophysiology of bladder cancer
Chemicals like aromatic amines → absorbed through the skin
polycyclic aromatic hydrocarbons (from smoke) → they sit in your bladder waiting to get peed
The liver usually has acetyltransferases which makes these substances less carcinogenic but some people have bad genes which make them slower at detoxifying these carcinogens → more susceptible to bladder cancer
what are the histological subtypes of bladder cancer and which one is the most common?
Urothelial cell carcinoma - 90%
Squamous cell carcinoma
Adenocarcinoma
what is the trigone area of the bladder?
the triangle between the opening of the ureters in the bladder and the internal urethral sphincter
key presentations of bladder cancer
Painless haematuria (macro or microscopic), urgency, dysuria, suprapubic/pelvic mass, pelvic pain, recurrent UTI
1st line and gold standard investigations for bladder cancer
1st line
urinalysis for microscopy and culture (haematuria), bladder USS
gold standard
Flexible cystoscopy and biopsy –> test that allows the doctor to look directly at the lining of the bladder, from the opening of the urethra
CT for staging
how do you manage bladder cancer?
Medical: chemotherapy, radiotherapy
Surgical: transurethral resection of bladder tumour TURBT (good cuz you can also get a biopsy from this and diagnose the cancer stage better), or cystectomy (remove bladder), lymph node dissection if spread
what is a cystectomy?
bladder removal
is chemotherapy effective in bladder cancer?
NO
you need to use 4 different agents and it is very toxic: Cisplatin; methotrexate, vincristine, and adriamycin)
risk factors for penile cancer
Age
Premalignant lesion
phimosis: a condition in males where the foreskin cannot be fully retracted over the glans. This can lead to difficulty in cleaning the penis and may cause discomfort or other issues.
HPV: types 16 and 18 are carcinogenic
Smoking
Immunocompromise
PUVA therapy - Psoralen and Ultraviolet A → a form of phototherapy used to treat various skin conditions, particularly certain dermatological disorders like psoriasis, vitiligo, and eczema.
what is the most common histology of penile cancer?
squamous cell carcinoma
what is Kaposi’s sarcoma?
cancer which usually manifests as tumours on the skin, mucous membranes, or internal organs and which is caused by HHV-8 - human herpes virus 8
key presentations of penile cancer
Hard painless lump on glans or prepuce
Up to 50% delay in presentation
Bloody discharge - haematuria → most of them will be in the GP for haematuria, not for cancer
1st line and gold standard investigations for penile cancer
1st line
lymph nodes in the groin
Penis lesion
DRE (digital rectal exam) - prostate cancer also causes lymphadenopathy
Ultrasound
gold standard
Biopsy
CT used for staging
management of penile cancer
circumcision if lesion is only on foreskin
GOLD STANDARD: Glans resurfacing (removing the abnormal skin from the glans) → better cuz you also get biopsy which helps with staging
Cream → Efudix
Radical penectomy (partial or full) + urethra reconstruction
For node-negative:
Methylene blue dye → fluorescent and camera used to detect cancer
If disease has moved to pelvic nodes you can remove the nodes.
Metastatic: Platinum-based chemotherapy
investigations for erectile dysfunction
Bloods
FBC
Lipids
Fasting Glucose → check for diabetes since it can cause peripheral vascular neuropathies and damage to blood vessels which can impair blood flow to peripheries
HbA1c
Early morning Testosterone
LH/FSH
Prolactin
PSA → prostate specific antigen
TFT → thyroid function tests
Others
DRE
BP
Nocturnal tumescence and rigidity testing → testing for any signs of nighttime erection to indicate psychogenic ED
Penile doppler USS
Penile arteriography: trauma-related ED in young men (look at image)
MRI
management of erectile dysfunction
1st line
Oral meds: PDE5 inhibitors → Sildenafil and Tadalafil (LOOK INTO CONTRAINDICATIONS)
Tadalafil is safer
Second line:
Alprostadil → synthetic PGE1 (increases cAMP in corporal smooth muscle)
MUSE: Intraurethral alprostadil
Caverject: Intracavernosal injection of alprostadil
Third line: vacuum pump devices
Surgical: implantation of inflatable or rigid malleable implant (quicker recovery)
management of premature ejaculation
Education and counceling
Start stop maneuvre → sexual activity until the individual is close to ejaculation. Then they stop immediately until they feel like they are back in control and they can resume the sexual activity. Gradually the individual will extend the time needed to reach climax.
Squeeze technique → sexual activity progresses until the individual is near ejaculation. At this point, the partner applies firm pressure to the base of the penis or the area between the shaft and the glans (head) using their thumb and forefinger for about 30s, temporarily reducing sexual arousal. Once the pressure is released, sexual activity is resumed.
Pharmacological
Dapoxetine: short-acting SSRI
Topila LA
PDE5 inhibitors if assoc ED
what incontinence do you get if you lesion the spinal cord at T10
you lose voluntary control over peeing because sympathetic innervation is T12-L2 and it stimulates alpha 1 receptor to keep internal sphincter contracted. If sympathetic system interrupted you have a permanently relaxed internal sphincter and detrusor contracts hectically since it should be stimulated to relax for bladder filling by the symp NS.
you also lose voluntary control over peeing because ascending pathway of sensation from bladder filling is interrupted so you are not conscious about bladder filling
what type of spinal injury leads to overflow urinary incontinence
at or below S2-S4
The internal urethral sphincter is permanently contracted. As the bladder continues to fill, the pressure in the bladder eventually exceeds the strength of the internal urethral sphincter and urination will occur.
what is Peyronie’s disease
Peyronie’s disease → condition in which fibrous scar tissue forms in the deeper tissues under the skin of the penis which leads to curved and painful erections
what kind of medications can cause erectile dysfunction?
antidepressants, antihypertensives, alcohol, drugs, statins, diuretics
what is the most common cell origin of testicular cancer
germ cell cancers
rest are non-germ cell cancers (Leydig, Sertoli, lymphoma)
risk factors for testicular cancer
Undescended testes (cryptorchidism), male infertility, family history, increased height, HIV
key presentations of testicular cancer
Palpable painless lump in testicle which does not transilluminate (light can’t get through)
haematosperima (blood in semen)
gynecomastia
investigations for testicular cancer 1st line and gold standard
1st line
tumour markers:
- alpha fetoprotein raised in teratomas
- beta hCG raised in seminomas and teratomas
- lactate dehydrogenase raised –> non-specific
gold standard
Urgent USS (doppler) of testes
what is the most common type of germ cell testicular tumour and explain what it is
seminoma - a type of germ cell tumour that typically have a uniform, undifferentiated appearance under the microscope.
what tumour markers will be raised in testicular cancer teratomas
alpha fetoprotein and beta hCG
management of testicular cancer and complications
urgent radical orchidectomy +/- testicular prosthesis
complications: infertility
nephrotic vs nephritic syndrome
nephrotic
- damage to podocytes
- very severe proteinuria >3.5g/day
- haematuria
- coca-cola coloured urine
nephritic
- damage to basement membrane from inflammation
- characterised by antibody deposits
- oliguria
- proteinuria (much less than in nephrotic syndrome; 1-3.5g/day)
- crescent shape in glomerulus from IgA deposits
what is vasculitis
inflammation of the blood vessels
causes of nephritic syndrome
ANCA associated vasculitis
IgA nephropathy (Berger’s syndrome)
Lupus
Systemic sclerosis
Anti Glomerular Basement Membrane disease (Goodpasture’s syndrome)
Post-streptococcal Glomerulonephritis
Henoch Schonlein Purpura
what is ANCA associated vasculitis and howdo you treat it
ANCA = antineutrophil cytoplasmic autoantibodies
The body attacks it’s own neutrophils and blood vessel walls
can lead to nephritic syndrome
treatment:
Immunosuppression → steroids
Rituximab - monoclonal antibody
Cyclophosphamide - chemotherapy drug
what is Berger’s syndrome/IgA nephropathy, what might cause it, and how do you treat it
MOST COMMON CAUSE OF GLOMERULONEPHRITIS WORLD WIDE
Abnormal IgA molecules accumulate in the mesangium of the glomerulus
Goes hand in hand with upper respiratory syndrome → condition might be triggered by responses to respiratory pathogens, leading to abnormal IgA production
treatment
ACE inhibitor, manage their BP, statins
Budesonide → glucocorticoid steroid which has a more localised anti-inflammatory action
what is the most common cause of glomerulonephritis worldwide
IgA nephropathy/Berger’s syndrome
what is Goodpasture’s syndrome and how do you treat it
Anti Glomerular basement membrane disease –> leads to nephritic syndrome by attacking the glomerular BM and leading to inflammation
Very aggressive when it presents
Rapid progressive kidney failure
treatment: plasmapheresis to get rid of Anti GBM antibodies
what is the most common Cause of glomerulonephritis in children and WHEN does it present
Post-Streptococcal Glomerulonephritis
2 weeks after strep infection
what antibodies do you test for in nephritic syndrome and why
ANCA –> antineutrophil cytoplasmic autoantibodies –> cuz of ANCA associated vasculitis
ANA (antinuclear antibody) and double stranded DNA antibody –> cuz of systemic lupus erythematosus
Anti-GBM –> for anti glomerular basement membrane antibody
what would you see on a kidney biopsy of a patient with nephritic syndrome
crescent shape in glomerulus from antibody complex deposition
key presentations of nephritic syndrome
Visible haematuria (5 RBC/uL)
If you see red cell casts it is almost always a sign of glomerular bleeding
Proteinuria (1 – 3.5g/day, less than nephrotic syndrome)
Hypertension
oedema (peripheral, pulmonary)
oliguria (low urine output) → inflammation of glomeruli leads to DECREASE in GFR
uraemic signs
AKI
how long after a viral infection does IgA nephropathy manifest
1-2 days after a viral infection
1st line and gold standard investigations for nephritic syndrome
1st line
Urinalysis and microscopy (haematuria, proteinuria, dysmorphic RBCs)
24hr urine collection
bloods (anaemia, elevated creatinine)
Serology: anti-GBM (Goodpasture’s), anti-double-stranded DNA (SLE), antinuclear antibody (SLE), ANCA (Wegener’s vasculitis)
IgA: microscopy shows IgA complex deposition
gold standard
Renal biopsy (crescent shaped glomeruli, Ig deposits, glomerulosclerosis)
management of nephritic syndrome
hypertension control
proteinuria
ACEi/ARB → dilate blood vessels and reducing the pressure within the glomeruli, thereby decreasing protein leakage into the urine
loop diuretics → reduce oedema caused by proteinuria
Immunosuppression → prednisolone
Specific:
Post-streptococcal GN (penicillin)
Goodpasture’s (plasmapheresis, corticosteroid immunosuppression)
SLE (immunosuppression – rituximab, cyclophosphamide)
what are the primary causes of nephrotic syndrome and what population are they most common in
Minimal change disease –> MOST COMMON IN KIDS
membranous glomerulonephritis –> adults
Focal segmental glomerulosclerosis –> MOST COMMON IN ADULTS
what is minimal change disease and how does it present on microscopy
disease which leads to nephrotic syndrome in kids
called minimal cuz the glomeruli appear normal under the microscope but the podocytes are damaged
what is membranous glomerulonephritis and how does it present on microscopy
condition which is either idiopathic or triggered by lupus, NSAIDS or hepatitis and it leads to the thickening of the glomerular basement membrane
causes NEPHROTIC syndrome
seen in adults
what is Focal segmental glomerulosclerosis and how does it present on microscopy
condition which leads to sclerosis of some segments of glomeruli and is the most common cause of nephrotic syndrome in adults.
can be idiopathic or caused by HIV and sickle cell
pathophysiology of nephrotic syndrome
Inflammation > damage to podocytes > protein leakage > proteinuria. increased liver activity aiming to increase albumin > consequential increase in cholesterol and clotting factors. Reduced oncotic pressure causes oedema and blood volume loss, which activates the RAAS system.
key presentations of nephrotic syndrome
Proteinuria (>3.5g/24hrs): frothy urine, infection.
Hypoalbuminemia (<30g/L). Peripheral oedema.
Hypercholesterolaemia (xanthelasma – eyes, xanthomata – joints).
Haematuria
Hypercoagulable state, hypogammaglobulinemia, hypertension, thrombosis, hyperlipidaemia
1st line investigations for nephrotic syndrome and gold standard
1st line
Bloods: U&E, FBC, CRP, LFT.
Serum albumin creatinine
Mid-stream urinalysis and urine dipstick (proteinuria/haematuria, infection).
Urine protein creatinine ratio
Kidney USS.
Serum and urine electrophoresis → to identify what proteins are being lost
ANA → lupus
Anti-phospholipase A2 receptor antibody - membranous
Hep B and Hep C investigations (HepBsAb HepCAb) for viral causes
gold standard
needle biopsy and microscopy
what are the secondary causes of nephrotic syndrome
diabetic nephropathy
Hep B and Hep C
tumours in glomerular cap wall
management of nephrotic syndrome
12 weeks corticosteroids (prednisolone)
Treat complications:
oedema (low salt and protein intake, diuretics)
hyperlipidaemia (statins)
hypercoagulable state (anticoagulants)
infection (antibiotics)
Supportive treatment to control proteinuria (ACEi, ARBs)
what is the most common cause of nephrotic syndrome in children
minimal change disease
what is cryptorchidism
undescended testes
why does prostate cancer commonly metastasize to the vertebrae.
Prostate cancer is common. Venous blood from the prostate passes into a plexus of veins which lie anterior to the sacrum and communicate with veins which run up to the azygos vein in the chest. These veins communicate with veins in the vertebral bodies which explains why prostate cancer commonly metastasizes to the vertebrae.
presentation of benign prostatic hyperplasia
LUTS:
Storage - frequency, urgency, incontinence, nocturia.
Voiding – dysuria, poor/intermittent stream, dribbling, straining, incomplete emptying, hesitancy
do castrated men develop BPH? why?
no because you need to have androgen production to develop BPH.
what is the IPSS score? describe it.
score used to look at prostate symptoms for BPH and it includes 8 criteria: incomplete emptying, Frequency, intermittency (having to start and stop multiple times), urgency, weak stream, straining, nocturia and quality of life
what is enuresis
involuntary discharge of urine, most commonly observed during sleep, and is commonly known as bedwetting
if a patient has overactive bladder spasms what class of meds could you give them
anticholinergics (to minimise parasympathetic action on bladder. respectively decrease the spasms and contractions)
what is Tamsulosin and what is its side effect
an alpha blocker used for BPH (1st line)
postural hypotension
1st line investigations and gold standard for someone with BPH
1st line
PSA
urinalysis
urine dipstick
urine frequency diary
gold standard
DRE
what is finasteride
5-alpha reductase inhibitors used in BPH. 2nd line treatment. It not only reduces symptoms but also prevents progression
1st line 2nd line and gold standard treatment of BPH
1st –> alpha blocker: Tamsulosin
2nd –> 5-alpha reductase inhibitor: finasteride
gold standard: TURP - trans-urethral resection of prostate
where do prostate cancers develop. centrally or peripherally?
peripherally
what type of cancer are most prostate cancers
adenocarcinomas
would someone without androgens be able to have prostate cancer
mostly no; it is almost always androgen dependent
key presentations of prostate cancer
LUTS – frequency, hesitancy, weak flow, dribbling, nocturia.
bone pain, weight loss, fatigue, night sweats
Haematuria, erectile dysfunction, metastases (bone – sclerotic bony lesions, brain, liver, lungs)
1st line and gold standard investigations for prostate cancer
1st line
Prostate exam and digital rectal exam (firm, hard, asymmetrical, rough)
PSA raised more than in BPH
multiparametric MRI
gold standard
Transrectal USS and biopsy
what grading system is used for prostate cancers
Gleason grading system (based on histology of biopsy. Higher score = worse prognosis)
how does the prostate feel in the DRE in prostatic cancer vs in BPH
prostatic cancer –> (firm, hard, asymmetrical, rough)
BPH –> enlarged and smooth
what is the function of PSA
The main function of PSA is to liquefy the semen that carries sperm during ejaculation
management of prostatic cancer
In Localised Prostate Cancer:
Prostatectomy (<70yr): removal of the prostate gland
Active Surveillance (>70 yr and low risk): For older patients (>70 years) with low-risk prostate cancer, active surveillance may be recommended.
External Beam Radiotherapy: Use radiation to target and kill cancer cells in the prostate.
Brachytherapy: placing radioactive seeds directly into the prostate → a more targeted delivery of radiation
Metastatic Prostate Cancer:
Chemotherapy
Radiotherapy
Bilateral Orchiectomy: This involves the surgical removal of the testicles, which are the primary source of testosterone. Testosterone fuels the growth of prostate cancer cells, and removing the source can help slow down the progression of the disease.
Androgen Deprivation Therapy (ADT) with Goserelin (LHRH agonist): ADT aims to reduce the levels of testosterone. Goserelin is a type of luteinizing hormone-releasing hormone (LHRH) agonist that suppresses testosterone production.
Palliative Treatment: For advanced or metastatic prostate cancer, palliative treatments such as transurethral resection of the prostate (TURP) may be performed to relieve symptoms, particularly those related to urinary obstruction.
is PSA testing very accurate for detecting BPH and prostatic hyperplasia?
no, there can be false negatives and there are other reasons why PSA can be raised:
- prostatitis
- UTIs
- recent ejaculation
- vigorous exercise
what is cystitis
infection of the urinary bladder
what is pyelonephritis
infection of one or both kidneys which is usually caused by bacteria travelling up from the bladder
what is the mnemonic for pain assessment?
SOCRATES
site, onset, character, radiation, associations, time course, exacerbating and relieving factors, and severity
what is pyonephrosis
pus or abscess stuck between the kidney and blockage. can’t move up or down.
what are the 3 in and 3 out of sepsis?
Sepsis → 3 things out (blood cultures, catheter to monitor urine output, blood tests)
3 in (oxygen, antibiotics, fluids)
on what chromosome is the VHL gene
3
what do high levels of cancer antigen 125 indicate
ovarian cancer
what is the most common organism driving UTIs
e coli
what urine dipstick finding would raise concerns for a urological malignancy
a) haematuria
b) proteinuria
c) pyuria
d) urobilinogen
A
pyuria is high levels of white blood cells or pus in urine
which is the most prominent risk factor for testicular cancer
family history
where is angiotensinogen released from
liver or adrenal gland
liver
what is LUTS
array of symptoms found in conditions affecting the quality and control of micturition in men
what are the types of incontinence and describe them
Stress incontinence – weakness of pelvic floor and sphincter muscles allowing urine to leak when increased pressure on the bladder, e.g., cough, laugh.
Urge incontinence – overactivity of the detrusor muscle, feeling a constant urge to pee; some urine leaks out before you can make it to the toilet
Overflow incontinence: your bladder doesn’t empty all the way so too much urine stays in your bladder. When the bladder gets too full you leak urine without having the urge to pee.
causes of incontinence
previous pregnancy and vaginal delivery, pelvic organ prolapse, pelvic floor surgery, neurological conditions (multiple sclerosis), cognitive impairment/dementia, increasing age, BMI
causes of retention
obstruction – kidney stones, benign prostatic hyperplasia, neurological conditions (MS, diabetic neuropathy, spinal cord injury)
urinary incontinence vs urinary retention
incontinence is not being able to hold pee and retention is not peeing all of it out.
incontinence more common in women and retention more common in men
LUTS storage vs voiding symptoms
storage: frequency, urgency, nocturia, incontinence
voiding: weak stream, intermittency, hesitancy, incomplete emptying, dribbling
what are the red flags of LUTS
dysuria, Haematuria
management of LUTS
Stress incontinence – surgery (tension-free vaginal tape or urethral bulking injections)
Urge incontinence - anticholinergic medication (oxybutynin, tolterodine, solifenacin)
Overflow incontinence: catheterisation
what is urtheritis
Lower urinary tract infection causing inflammation of the urethra. Usually a sexually acquired condition through chlamydia trachomatis (mc) or Neisseria gonorrhoea (lc)
presentation of urtheritis
Urethral discharge (blood/pus), dysuria, urethral pain, penile pain/itching
1st line and gold standard investigations for urtheritis; how do you tell apart urthetritis caused by gonorrhoea or chalmydia?
1st line: urine dipstick + mid-stream urine microscopy culture
gold standard: urethral discharge gram stain positive for leucocytes
the gram stain is used to differentiate between the two. If you detect the presence of gram-negative cocci you have gonorrhoea
Management of urtheritis caused by Neisseria gonorrhoea
Neisseria gonorrhoea = 1g IM ceftriaxone +1g azithromycin
what are the 2 most common bacterial causes of urethritis and which one is more common
chlamydia and gonorrhoea
chlamydia is more common
management of urethritis caused by chalmydia
Chlamydia trichomatis = 100mg doxycycline or azithromycin
what is cystitis and what is the most common cause
lower UTI causing inflammation of the bladder
e. coli infection
causes of cystitis
KEEPS infection: Klebsiella, enterococci, E. coli, proteus, s. saprophyticus
how do you treat asymptomatic bacteriuria in people above the age of 65
you don’t treat
can you have haematuria in nephrotic syndrome?
yes but micro
what class of medications is lactulose and what is it used for
osmotic laxative used for hepatic encephalopathy
what is hepato-renal syndrome and explain the pathophysiology
Rapidly progressing kidney failure as a result of liver disease
Damaged liver from cirrhosis releases local vasodilators like NO which leads to vasodilation of blood vessels and hence hypotension. This will lead to RAAS activation → efferent arteriole vasoconstriction and more salt and water retention (ascites) → persistent vasoconstriction of kidney leads to damage to the glomeruli
