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phase 2 medicine > urogenital > Flashcards

urogenital Flashcards

1
Q

what forms the inguinal ligament

A

external oblique aponeurosis

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2
Q

what was the renal blood flow

A

Renal artery 🡪 interlobar artery 🡪 arcuate artery 🡪 interlobular artery 🡪 afferent arteriole 🡪 glomerular capillary 🡪 efferent arteriole 🡪 peritubular capillary around tubules

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3
Q

what is the standard GFR

A

125 ml/min

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3
Q

what was the criteria for a good GFR indicator like creatinine

A

freely filtered
not metabolised
not secreted
not reabsorbed

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4
Q

explain tubulo-glomerular feedback

A

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

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5
Q

why does vasoconstriction of the afferent arteriole increase GFR?

A

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.

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6
Q

how do you measure GFR and state the formula

A

with creatinine or cystatin C

(creatinine urine conc. x urine flow)/plasma creatinine concentration

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7
Q

what are the components of the filtration barrier

A

Fenestrated capillaries
basement membrane
podocyte foot processes

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8
Q

what is the criteria to diagnose AKI

A

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

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9
Q

what is AKI

A

Sudden decline in renal function over hours or days leading to a rise in serum creatinine and/or a fall in urine output

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10
Q

explain pre-renal, intra-renal and post-renal AKI with examples of diseases

A

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

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11
Q

risk factors to AKI

A

Hypotension
volume depletion (DEHYDRATION)
CKD
heart failure
diabetes
cirrhosis
nephrotoxic meds (NSAIDs, ACEi)
cancer
trauma

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12
Q

key presentations of AKI

A

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

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13
Q

what is uraemia

A

high urea in blood

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14
Q

what is orthopnea

A

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.

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15
Q

investigations for AKI gold standard

A

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

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16
Q

what is the management of AKI?

A

Treat underlying cause (hypotension, stones, infection).

Stop nephrotoxic drugs (NSAIDs, ACEi).

Treat complications (electrolyte imbalances).

Severe – haemodialysis

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17
Q

what test could provide fast information about the urine contents

A

urine dipstick

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18
Q

how do you test whether an AKI is prerenal or intra-renal and provide the parameters

A

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.)

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19
Q

what is CKD

A

Chronic reduction in kidney function for more than 3 months which is permanent and progressive.

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20
Q

causes of CKD

A

Diabetes
hypertension
glomerulonephritis
polycystic kidney disease
nephrotoxic drugs (NSAIDs, ACEi)
persistent pyelonephritis
obstruction

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21
Q

what is pyelonephritis

A

kidney infection

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22
Q

how long does the kidney dysfunction have to be for to be classed as CKD

A

3 months

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23
Q

pathophysiology of CKD

A

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.

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24
Q

key presentations of CKD

A

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

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25
Q

what is oliguria

A

low urine output

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26
Q

investigations for CKD and diagnosis

A

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

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27
Q

what will you see on a renal ultrasound in CKD

A

bilateral renal atrophy

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28
Q

how do you manage CKD

A

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

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29
Q

complications of CKD

A

anaemia (ferrous sulphate, erythropoietin)
oedema (fluid restriction, diuretics)
metabolic acidosis (sodium bicarbonate)
CKD-mineral bone disease (vitamin D)
CVD (statins).

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30
Q

how do you manage oedema in patients with CKD if diuretics can further damage the kidney and lead to electrolyte imbalances?

A

sodium dietary restriction and management of other complications which might be contributing to the oedema

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31
Q

explain the staging of CKD based on eGFR and albumin: creatinine ratios

A

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

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32
Q

why is iron not absorbed well in the GI in CKD

A

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.

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33
Q

explain why you can get CKD mineral bone disease

A

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

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34
Q

how do you differentiate AKI from CKD

A

CKD ultrasound shows bilateral atrophy of kidneys
CKD presents with hypocalcemia

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35
Q

what should you check before giving anaemia treatment for CKD patient and why

A

serum iron because CKD leads to general inflammation in the body which activates the hormone hepcidin. Hepcidin decreases iron absorption in the intestine.

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36
Q

what is the 1st line treatment for patients with CKD and coexistent hypertension?

A

ACEi

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37
Q

explain how SGLT-2 inhibitor are reno-protective in CKD patients with proteinurea

A

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

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38
Q

define polycystic kidney disease

A

Inherited disease where multiple fluid-filled cysts form within the kidneys.
Two types – autosomal dominant (mc) and autosomal recessive

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39
Q

which type of polycystic kidney disease is more common

A

autosomal dominant

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40
Q

pathophysiology of polycystic kidney disease

A

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

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41
Q

key presentations of polycystic kidney disease

A

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)

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42
Q

investigations for polycystic kidney disease

A

Kidney ultrasound - enlarged bilateral kidneys with 2 or more cysts unilateral or bilateral

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43
Q

management

A

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

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44
Q

what is the most dangerous complication of PKD

A

aneurysm formation –> patients need screening if they have a fam history of intracerebral haemorrhage

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45
Q

what is the course of sperm form the testes to the external urethral meatus

A

epidydimis
vas deferens
spermatic cord in inguinal canal
wraps above and around the bladder
joins seminal vesicle and prostate
joins urethra

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46
Q

where in the prostate do you get hyperplasia in benign prostatic cancer

A

core of the prostate

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47
Q

where is the pouch of Douglas

A

between the rectum and uterus

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48
Q

where does fertilization take place

A

ampulla of the fallopian tubes

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49
Q

what are the parts of the fallopian tubes

A

fimbriae
infundibulum ampulla
isthmus
interstitium

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50
Q

what were the vestibular glands

A

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

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51
Q

what is the most common location for an ectopic pregnancy

A

uterine tube

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52
Q

what is the minimum urine pH

A

4.5

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53
Q

what are the folds of mucosa in the bladder called and what is their function

A

rugae
allow bladder to stretch without tearing when in fills

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54
Q

which muscle contracts to expel urine

A

detrusor

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55
Q

where are the internal and external urethral sphincters in men and women

A

internal - at the base of the bladder

external male - just after prostate
external female - in the deep perineal pouch

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56
Q

what is the innervation of the urinary bladder and urethral sphincters

A

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

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57
Q

what are the 2 curves of the rectum

A

the sacral flexure and the anorectal flexure

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58
Q

what is the dendate line

A

line which separates superior and inferior anal canal because they have different blood supplies and innervation as a result of different embryological origin

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59
Q

blood supply, venous drainage, and innervation of superior and inferior anal canal

A

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

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60
Q

where would pain from the ovary radiate and why

A

medial aspect of thigh because it can irritate obturator nerve which is motor + sensory nerve

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61
Q

what is a retroverted uterus

A

the uterus is tilted backward instead of the more common forward position. it can cause painful menstruation and difficulty with conceiving

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62
Q

what maintains the normal position of the uterus

A

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.

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63
Q

to which lymph nodes would cervical cancer spread

A

pelvic lymph nodes

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64
Q

what feature stops urine from passing back up to the kidney after the bladder is full and when the bladder contracts for urination

A

ureteral valves: located at the junction of the ureters and the bladder

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65
Q

what is normal CO and how much do the kidneys receive

A

5L/min
they receive 20% of CO

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66
Q

which is THE ONLY site of glucose reabsorption in the nephron

A

the PCT –> SGLT2 transporter

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67
Q

what was the difference between the thin descending and thick ascending loop of Henley and explain how they work together

A

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)

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68
Q

what is the function of the DCT

A

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+

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69
Q

what were the 2 types of cells in the collecting ducts and what did they do

A

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

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70
Q
A
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71
Q

in what forms is H+ excreted

A

H2CO3, NH4+, H2PO4-

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72
Q

what is the primary adaption to acidosis in the kidneys?

A

Formation of more NH4+ in the collecting duct to excrete it because it is impermeable to the apical membrane

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73
Q

what is the plasma anion gap and what does a high gap indicate

A

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

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74
Q

how do you test for acid base disorders

A

ABG - arterial blood gas

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75
Q

what receptors do you have in the bladder and what do they do

A

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

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76
Q

what nerve controls the external urethral sphincter and what nerve controls the internal urethral sphincter

A

external: pudendal (somatic S2-S4)
internal: hypogastric (sympathetic T12-L2)

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77
Q

what are the different types of kidney stones

A

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.

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78
Q

what is struvite

A

kidney stones produced by bacteria

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79
Q

causes of kidney stones

A

Chronic dehydration, obesity, high protein/salt diet, recurrent UTIs, low urine output, hyperparathyroidism/hypercalcaemia

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80
Q

what is hydropnephrosis

A

If the stones cause regular outflow obstruction the kidneys fill with urine and swell

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81
Q

where do kidney stones most commonly get stuck

A

Pelvi-ureteric junction
pelvic brim (where uretrer runs over the iliac artery)
vesico-ureteric junction

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82
Q

where does kidney stone pain get referred to

A

the loin –> T12 -L2 dermatome

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83
Q

key presentations of kidney stones

A

severe colicky unilateral pain originating in loin and radiating to groin

patient can’t lie still
haematuria
nausea and vomiting
reduced urine output

84
Q

1st line and gold standard investigations for kidney stones

A

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

85
Q

why is ultrasound not the gold standard for kidney stones investigation

A

Can only see radio-opaque stones like calcium oxalate stones, but not uric acid or cystine stones

86
Q

management of kidney stones

A

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

87
Q

what diet changes can you do to reduce the chance of kidney stones

A

Lifestyle: decrease sodium and protein intake, increase citrus fruit, adequate fluid intake

88
Q

what is the most common type of renal cancer

A

clear cell renal cell carcinoma

89
Q

how do you classify renal cancers

A

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.

90
Q

what is the TNM staging of renal cancer?

A

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

91
Q

causes of renal cancer

A

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.

92
Q

what is Von Hipple Lindau Syndrome?

A

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.

93
Q

pathophysiology of renal cancer

A

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

94
Q

key presentations of renal cancer

A

Triad: Haematuria, flank pain, palpable mass. May have left varicocele if male cuz left testicular vein joins into the renal vein before the aorta

95
Q

1st line and gold standard investigation for renal cancer

A

1st line
Abdominal/pelvis ultrasound, bloods: raised RBC, CRP, raised calcium, raised LDH, urine dipstick

gold standard
CT chest/abdo/pelvis

96
Q

management of renal cancer

A

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

97
Q

urothelial cell carcinoma vs transitional cell carcinoma

A

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

98
Q

what are the 3 main types of kidney cancer

A

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

99
Q

what is the most common subtype of bladder cancer?

A

transitional cell carcinoma

100
Q

epidemiology of bladder cancer

A

Old men, people who work in rubber/dye industry
3:1 ratio men to women
Common cancer

101
Q

causes of bladder cancer

A

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)

102
Q

risk factors to bladder cancer

A

Exposure to dyes/rubber/leather/textiles/paint (aromatic amines – dye factor worker, hairdresser, painter). Age >65, male, Caucasian, smoking, pelvic radiation

103
Q

pathophysiology of bladder cancer

A

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

104
Q

what are the histological subtypes of bladder cancer and which one is the most common?

A

Urothelial cell carcinoma - 90%
Squamous cell carcinoma
Adenocarcinoma

105
Q

what is the trigone area of the bladder?

A

the triangle between the opening of the ureters in the bladder and the internal urethral sphincter

106
Q

key presentations of bladder cancer

A

Painless haematuria (macro or microscopic), urgency, dysuria, suprapubic/pelvic mass, pelvic pain, recurrent UTI

107
Q

1st line and gold standard investigations for bladder cancer

A

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

108
Q

how do you manage bladder cancer?

A

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

109
Q

what is a cystectomy?

A

bladder removal

110
Q

is chemotherapy effective in bladder cancer?

A

NO
you need to use 4 different agents and it is very toxic: Cisplatin; methotrexate, vincristine, and adriamycin)

111
Q

risk factors for penile cancer

A

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.

112
Q

what is the most common histology of penile cancer?

A

squamous cell carcinoma

113
Q

what is Kaposi’s sarcoma?

A

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

114
Q

key presentations of penile cancer

A

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

115
Q

1st line and gold standard investigations for penile cancer

A

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

116
Q

management of penile cancer

A

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

117
Q

investigations for erectile dysfunction

A

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

118
Q

management of erectile dysfunction

A

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)

119
Q

management of premature ejaculation

A

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

120
Q

what incontinence do you get if you lesion the spinal cord at T10

A

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

121
Q

what type of spinal injury leads to overflow urinary incontinence

A

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.

122
Q

what is Peyronie’s disease

A

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

123
Q

what kind of medications can cause erectile dysfunction?

A

antidepressants, antihypertensives, alcohol, drugs, statins, diuretics

124
Q

what is the most common cell origin of testicular cancer

A

germ cell cancers
rest are non-germ cell cancers (Leydig, Sertoli, lymphoma)

125
Q

risk factors for testicular cancer

A

Undescended testes (cryptorchidism), male infertility, family history, increased height, HIV

126
Q

key presentations of testicular cancer

A

Palpable painless lump in testicle which does not transilluminate (light can’t get through)
haematosperima (blood in semen)
gynecomastia

127
Q

investigations for testicular cancer 1st line and gold standard

A

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

128
Q

what is the most common type of germ cell testicular tumour and explain what it is

A

seminoma - a type of germ cell tumour that typically have a uniform, undifferentiated appearance under the microscope.

129
Q

what tumour markers will be raised in testicular cancer teratomas

A

alpha fetoprotein and beta hCG

130
Q

management of testicular cancer and complications

A

urgent radical orchidectomy +/- testicular prosthesis

complications: infertility

131
Q

nephrotic vs nephritic syndrome

A

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

132
Q

what is vasculitis

A

inflammation of the blood vessels

133
Q

causes of nephritic syndrome

A

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

134
Q

what is ANCA associated vasculitis and howdo you treat it

A

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

135
Q

what is Berger’s syndrome/IgA nephropathy, what might cause it, and how do you treat it

A

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

136
Q

what is the most common cause of glomerulonephritis worldwide

A

IgA nephropathy/Berger’s syndrome

137
Q

what is Goodpasture’s syndrome and how do you treat it

A

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

138
Q

what is the most common Cause of glomerulonephritis in children and WHEN does it present

A

Post-Streptococcal Glomerulonephritis
2 weeks after strep infection

139
Q

what antibodies do you test for in nephritic syndrome and why

A

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

140
Q

what would you see on a kidney biopsy of a patient with nephritic syndrome

A

crescent shape in glomerulus from antibody complex deposition

141
Q

key presentations of nephritic syndrome

A

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

142
Q

how long after a viral infection does IgA nephropathy manifest

A

1-2 days after a viral infection

143
Q

1st line and gold standard investigations for nephritic syndrome

A

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)

144
Q

management of nephritic syndrome

A

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)

145
Q

what are the primary causes of nephrotic syndrome and what population are they most common in

A

Minimal change disease –> MOST COMMON IN KIDS
membranous glomerulonephritis –> adults
Focal segmental glomerulosclerosis –> MOST COMMON IN ADULTS

146
Q

what is minimal change disease and how does it present on microscopy

A

disease which leads to nephrotic syndrome in kids
called minimal cuz the glomeruli appear normal under the microscope but the podocytes are damaged

147
Q

what is membranous glomerulonephritis and how does it present on microscopy

A

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

148
Q

what is Focal segmental glomerulosclerosis and how does it present on microscopy

A

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

149
Q

pathophysiology of nephrotic syndrome

A

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.

150
Q

key presentations of nephrotic syndrome

A

Proteinuria (>3.5g/24hrs): frothy urine, infection.
Hypoalbuminemia (<30g/L). Peripheral oedema.
Hypercholesterolaemia (xanthelasma – eyes, xanthomata – joints).
Haematuria

Hypercoagulable state, hypogammaglobulinemia, hypertension, thrombosis, hyperlipidaemia

151
Q

1st line investigations for nephrotic syndrome and gold standard

A

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

152
Q

what are the secondary causes of nephrotic syndrome

A

diabetic nephropathy
Hep B and Hep C
tumours in glomerular cap wall

153
Q

management of nephrotic syndrome

A

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)

154
Q

what is the most common cause of nephrotic syndrome in children

A

minimal change disease

155
Q

what is cryptorchidism

A

undescended testes

156
Q

why does prostate cancer commonly metastasize to the vertebrae.

A

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.

157
Q

presentation of benign prostatic hyperplasia

A

LUTS:
Storage - frequency, urgency, incontinence, nocturia.
Voiding – dysuria, poor/intermittent stream, dribbling, straining, incomplete emptying, hesitancy

158
Q

do castrated men develop BPH? why?

A

no because you need to have androgen production to develop BPH.

159
Q

what is the IPSS score? describe it.

A

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

160
Q

what is enuresis

A

involuntary discharge of urine, most commonly observed during sleep, and is commonly known as bedwetting

161
Q

if a patient has overactive bladder spasms what class of meds could you give them

A

anticholinergics (to minimise parasympathetic action on bladder. respectively decrease the spasms and contractions)

162
Q

what is Tamsulosin and what is its side effect

A

an alpha blocker used for BPH (1st line)
postural hypotension

163
Q

1st line investigations and gold standard for someone with BPH

A

1st line
PSA
urinalysis
urine dipstick
urine frequency diary

gold standard
DRE

164
Q

what is finasteride

A

5-alpha reductase inhibitors used in BPH. 2nd line treatment. It not only reduces symptoms but also prevents progression

165
Q

1st line 2nd line and gold standard treatment of BPH

A

1st –> alpha blocker: Tamsulosin
2nd –> 5-alpha reductase inhibitor: finasteride
gold standard: TURP - trans-urethral resection of prostate

166
Q

where do prostate cancers develop. centrally or peripherally?

A

peripherally

167
Q

what type of cancer are most prostate cancers

A

adenocarcinomas

168
Q

would someone without androgens be able to have prostate cancer

A

mostly no; it is almost always androgen dependent

169
Q

key presentations of prostate cancer

A

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)

170
Q

1st line and gold standard investigations for prostate cancer

A

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

171
Q

what grading system is used for prostate cancers

A

Gleason grading system (based on histology of biopsy. Higher score = worse prognosis)

172
Q

how does the prostate feel in the DRE in prostatic cancer vs in BPH

A

prostatic cancer –> (firm, hard, asymmetrical, rough)
BPH –> enlarged and smooth

173
Q

what is the function of PSA

A

The main function of PSA is to liquefy the semen that carries sperm during ejaculation

174
Q

management of prostatic cancer

A

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.

175
Q

is PSA testing very accurate for detecting BPH and prostatic hyperplasia?

A

no, there can be false negatives and there are other reasons why PSA can be raised:
- prostatitis
- UTIs
- recent ejaculation
- vigorous exercise

176
Q

what is cystitis

A

infection of the urinary bladder

177
Q

what is pyelonephritis

A

infection of one or both kidneys which is usually caused by bacteria travelling up from the bladder

178
Q
A
179
Q

what is the mnemonic for pain assessment?

A

SOCRATES
site, onset, character, radiation, associations, time course, exacerbating and relieving factors, and severity

180
Q

what is pyonephrosis

A

pus or abscess stuck between the kidney and blockage. can’t move up or down.

181
Q

what are the 3 in and 3 out of sepsis?

A

Sepsis → 3 things out (blood cultures, catheter to monitor urine output, blood tests)
3 in (oxygen, antibiotics, fluids)

182
Q

on what chromosome is the VHL gene

A

3

183
Q

what do high levels of cancer antigen 125 indicate

A

ovarian cancer

184
Q

what is the most common organism driving UTIs

A

e coli

185
Q

what urine dipstick finding would raise concerns for a urological malignancy
a) haematuria
b) proteinuria
c) pyuria
d) urobilinogen

A

A

pyuria is high levels of white blood cells or pus in urine

186
Q

which is the most prominent risk factor for testicular cancer

A

family history

187
Q

where is angiotensinogen released from
liver or adrenal gland

A

liver

188
Q

what is LUTS

A

array of symptoms found in conditions affecting the quality and control of micturition in men

189
Q

what are the types of incontinence and describe them

A

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.

190
Q

causes of incontinence

A

previous pregnancy and vaginal delivery, pelvic organ prolapse, pelvic floor surgery, neurological conditions (multiple sclerosis), cognitive impairment/dementia, increasing age, BMI

191
Q

causes of retention

A

obstruction – kidney stones, benign prostatic hyperplasia, neurological conditions (MS, diabetic neuropathy, spinal cord injury)

192
Q

urinary incontinence vs urinary retention

A

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

193
Q

LUTS storage vs voiding symptoms

A

storage: frequency, urgency, nocturia, incontinence

voiding: weak stream, intermittency, hesitancy, incomplete emptying, dribbling

194
Q

what are the red flags of LUTS

A

dysuria, Haematuria

195
Q

management of LUTS

A

Stress incontinence – surgery (tension-free vaginal tape or urethral bulking injections)

Urge incontinence - anticholinergic medication (oxybutynin, tolterodine, solifenacin)

Overflow incontinence: catheterisation

196
Q

what is urtheritis

A

Lower urinary tract infection causing inflammation of the urethra. Usually a sexually acquired condition through chlamydia trachomatis (mc) or Neisseria gonorrhoea (lc)

197
Q

presentation of urtheritis

A

Urethral discharge (blood/pus), dysuria, urethral pain, penile pain/itching

198
Q

1st line and gold standard investigations for urtheritis; how do you tell apart urthetritis caused by gonorrhoea or chalmydia?

A

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

199
Q

Management of urtheritis caused by Neisseria gonorrhoea

A

Neisseria gonorrhoea = 1g IM ceftriaxone +1g azithromycin

200
Q

what are the 2 most common bacterial causes of urethritis and which one is more common

A

chlamydia and gonorrhoea

chlamydia is more common

201
Q

management of urethritis caused by chalmydia

A

Chlamydia trichomatis = 100mg doxycycline or azithromycin

202
Q

what is cystitis and what is the most common cause

A

lower UTI causing inflammation of the bladder

e. coli infection

203
Q

causes of cystitis

A

KEEPS infection: Klebsiella, enterococci, E. coli, proteus, s. saprophyticus

204
Q

how do you treat asymptomatic bacteriuria in people above the age of 65

A

you don’t treat

205
Q

can you have haematuria in nephrotic syndrome?

A

yes but micro

206
Q

what class of medications is lactulose and what is it used for

A

osmotic laxative used for hepatic encephalopathy

207
Q

what is hepato-renal syndrome and explain the pathophysiology

A

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

phase 2 medicine (15 decks)

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