Renal & GU Flashcards
Tx of BPH
Tamsulosin
Finasteride
Action of tamsulosin
& what class of drug is it?
Relax smooth muscle of bladder and prostate
∴ ↑ Urine flow rate
(selective alpha-1-adernergic receptor antagonists)
S/E of tamsulosin
Postural instability, retrograde ejaculation
Findings on DPE of BPH
Smooth, enlarged prostate
Findings of DPE of Prostate cancer
Hard and irregular
Ix for BPH
(incl values if measuring any antigens cough cough)
Digital Rectal Examination
Prostate-Specific antigen > 1.5ng/mL
GS (?) : Trans-rectal US
Ix for Prostate cancer
(no abbrv)
Digital Rectal Exam
Prostate Specific Antigen
Trans-rectal US
Prostate biopsy
What’s the grading thing called for prostate cancer?
Gleason grading score
Most common pathogens for UTIs
E.Coli
Proteus
Why is creatinine used as a marker of GFR?
Freely filterised
Not metabolised
Not secreted
Not reabsorbed
Mechanism of loop diuretics
Where do they act upon?
Act of ascending limb of loop of Henle
Inhibit Na+/K+/2Cl- co-transporter
(bc if it transports ions, water will follow)
Examples of loop diuretics
Furosemide
Bumetanide
S/E Loop diuretics
Dehydration
Hypotension
Hypokalaemia
& Metabolic alkalosis can occur !
If v high doses, can cause ototoxicity
Give an example of K+ sparing diuretic
Amiloride
Spironolactone
Mechanism of K+ sparing diuretics
Where do they act upon?
Act on the distal convoluted tubule
Inhibits reabsorption of sodium (and ∴ water) by epithelial sodium channels
∴ Na+ and H2O excretion
(and K+ retention)
S/E K+ sparing diuretics
GI upset
Hyperkalaemia
Metabolic acidosis
Gynecomastia
Example of a thiazide diuretic
Bendroflumethiazide
Mechanism of Thiazide diuretic
Where does it act upon?
Acts on sodium/chloride transporter
Prevents it from functioning properly
∴ Sodium is NOT retained
Compare thiazide and loop diuretics
(In terms of length and efficacy)
Thiazide diuretics are longer acting
But not as effective as loop
S/E Thiazide diuretics
Hypokalaemia
Metabolic alkalosis
Hypovolaemia
Hyponatraemia
Hyperglycaemia in DM
Where does Angiotensin II act on?
PCT
What does Angiotensin II do?
Causes thirst
↑ SNS activity
ADH release (by stimulating post. pituitary)
Aldosterone release (by stimulating adrenal glands)
↑Proximal tubule reabsorption which ↑Na+ reabsorption
Causes vasoconstriction to ↑BP
ESSENTIALLY, ↑BP
Where does Aldosterone act?
On DCT and collecting ducts
What does Aldosterone do?
↑Na+ reabsorption
↑K+ secretion
Binds to cytoplasmic receptors - transported to nucleus
↑Epithelial Na channels
↑Na+/K+ ATPase
↑Effective circulating vol
Where does ADH act on?
Distal tubule
Collecting ducts
What does ADH do?
Acts on V1 receptors on blood vessels to cause vasoconstriction
Acts on V2 receptors in basolateral side of collecting ducts
↑ Insertion of aquaporin 2 on apical membrane of collecting ducts
∴ ↑ Water reabsorption
Also, helps maintain hypertonicity of medulla by ↑urea permeability of collecting ducts
What is ADH produced by?
Hypothalamus
Where is ADH released?
Post. pituitary
What triggers ADH release?
Increased plasma osmolality
(↓ water)
What detects decreased water in the body? How?
Hypothalamic osmoreceptors
Detects bc H2O diffuses out post. pituitary in response to ↑Na+ pulling it out
What is ANP?
Atrial Natriuretic Peptide
What is the aim of ANP?
To decrease BP
(inhibits renin secretion)
When is ANP released ?
When atria are stretched (due to high BP), it causes ANP to be released
What are the actions of ANP?
Dilates aff glomerular arterioles
Constricts eff glomerular arteriole
Relaxes mesangial cells (to ↑GFR) - so excretion can be increased
“Blocks” NCC in DCT and ENaC in CT
∴ prevents reabsorption and ↑Na+ excretion
↑Vasa recta blood flow - leads to less reabsorption
SYSTEMIC VASODILATOR
Where is parathyroid hormone released from?
In response to what?
Parathyroid glands
In response to ↓Ca2+ plasma levels
What does PTH do?
↑ Ca2+ reabsorption
↑ HPO4^3- excretion
Stimulates formation of Vit D
Describe the activation of Vitamin D
Where can kidney stones be deposited?
Anywhere from renal pelvis to ureter
Where are kidney stones formed?
Collecting ducts
RF Renal Colic
Male (M:F 2:1)
Middle East - due to higher oxalate, lower Ca2+ diet and ↑dehydration
What is renal colic also known as?
Nephrolithiasis
Where the most common sites for renal stones to get stuck?
Pelviureteric junction (PUJ) - MC !
Pelvic brim
Vesicoureteric junction (VUJ)
Causes Renal Colic
ANATOMICAL ABNORMALITIES
Congenital - horseshoe, duplex, PUJ, spina bifida
Acquired - obstruction, trauma, reflux
URINARY
Metastable urine
Ca2+, oxalate, urate, cystine
Dehydration
INFECTION-INDUCED STONES (struvite) - UTI w organisms that produce urease, is assoc/ with struvite stones
Proteus, klebsiella, pseudomonas
HYPERCALCIRURIA
In turn, caused by:
Hyperparathyroidism - MC !!!
Hypercalcaemia
XS dietary calcium
XS resorption of calcium from bone (immobilisation)
Idiopathic hypercalciuria
HYPEROXALURIA
↑ dietary intake of oxalate rich foods e.g. spinach, rhubarb, tea
ALSO, ↓dietary calcium intake
(bc means decreased binding of oxalate w/ Ca2+)
Signs / Symptoms Renal Colic
Can be asymptomatic
Loin to groin colicky pain - peristaltic waves
Severe, unilateral, worse than labour!
Rapid onset (mins-hours)
Unable to get comfy - writhing in agony
Worse w fluid loading
N+V
Sweating
Fever
UTI Sx !! - Dysuria, burning when urinating, urgency, frequency
Haematuria (visible and non-visible)
Recurrent UTIs
Rigors
Bladder/urethral stones
Ix Renal Coli
Detailed history - might reveal cause of stone e.g. lots of tea = high oxalate
1st line - XR KUB
(easy and cheap)
GS!!! NON-CONTRAST CT KUB
vvv spec (99%)
US - useful for pregnancies and young (no radiation)
Sens for hydronephrosis
Urine dipstick - traces of blood
Mid-stream specimen
follow up with MSU if pos
Bloods - FBC, U&E, calciu, uric acid
What benefits does Non-Contrast CT have over CT w contrast?
Good for allergies (doesnt trigger)
and no renal damage
Tx Renal Colic
Hydration
STRONG ANALGESIC - IV diclofenac
NSAIDs, IV paracetamol, +/- opiates!
Anti-emetics - metoclopramide
+/- IV fluids - might make pain worse as diuresis happens
Conservative - allow 2 weeks to pass
Abx if UTI
Medical expulsive therapy? Not much evidence if it works
Extracorpeal Shock Wave Lithotripsy (ESWL) - if <1 cm
Surgery - Ureteroscopy, Percutaneous Nephrolithotomy (PCNL), Nephrectomy
ADMIT IF SHOCK, FEVER, SEPSIS, PREGNANCY ETC
Types of Stones
Calcium oxalate - form in acidic urine, MC !!!!
Calcium phosphate - alkali urine
Calcium carbonate
Struvite - proteus, Klebsiella, pseudomonas bacteria
Uric acid
Cystine
Drug precipitants
Why are Kidney stones treated more conservatively?
Small, safe location
More asymptomatic
Static size
Lifestyle changes for prevention Renal Colic
↓Dietary salt
Normal dairy intake
Lose weight
Active lifestyle
Overhydration
Stop smoking
More citrus fruit
With renal colic, when might a stone pass spontaneously?
If small <5mm
How might you treat renal colic if it’s a large stone?
ESWL
Ureteroscopy
PCNL
Comps Renal Colic
HYDRONEPHROSIS - requires surgical drainage
AKI Criteria for diagnosis
↑ Creatinine > 26 mmol/L in 48 hours above baseline
↑ Creatinine > 50% (best fig in last 6 months)
Urine output < 0.5ml/kg/hour for > 6 consec hours
Define AKI
Abrupt deterioration (hours to days) in renal function
Due to rapid decline in GFR
Leading to a failure to maintain fluid, electrolyte, acid-base homeostasis
Usually but not always reversible
Decreased in function < 3 months?
What is AKI assoc with?
Diarrhoea
Haematuria
Haemoptysis
Hypotension
Urine retention
Causes AKI
PRE-RENAL - ↓blood flow to kidney ∴ ↓ GFR
Shock
Hypovolaemia ! - diarrhoea, vomiting, trauma, bleeding, diuretics, burns
Hypotension - cardiogenic shock, sepsis, anaphylaxis
Cardiovascular - HF, severe arrhythmias
Sepsis
Renal hypoperfusion - NSAIDs, ACEi, ARBs
RENAL - cells damaged so kidney can’t filer blood properly
Acute tubular necrosis
Nephrotoxins - NSAIDs, Methotrexate
Glomerulonephritis
Acute interstitial nephritis
Infection
Vasculitis
Malignant HTN
Autoimmune disease
POST-RENAL - anything that causes blockage of kidney
BPH
Kidney stones
Cancer
Blood clot
RF AKI
Age > 75 years
DM
HF
Sepsis
Peripheral vascular disease
Drugs
FHx
Poor fluid intake/loss
DDx Nephrolithiasis
Aortic abdo aneurysm
Diverticulitis - L sided
Appendicitis - R sided
Pyelonephritis
Acute pancreatitis
Ectopic preg
Testicular torsion
Peritonitis
Signs / Symptoms AKI
Often asymptomatic!! Esp early stages
Fluid overload - oliguria/anuria, pulmonary/peripheral oedema, palpable bladder, hypovolaemic shock, ↑JVP,
Hyperkalaemia - arrhythmias, muscle weakness, tachycardia
Hyperuraemia - N+V, weakness, tremor, pericarditis, platelet dysfunction (bleeding), confusion and seizures if severe
Metabolic acidosis
Postural hypotension
Thirst
Poor tissue turgor
When is AKI a medical emergency?
Hyperkalaemia!!
What ECG signs are associated with hyperkalaemia?
Tall peaked T waves
Wide QRS
Small P waves
Ix AKI
Urine dipstick - blood, nitrites, leukocytes, glucose, protein
Bloods - FBC, U&Es, creatinine, liver enzymes
Renal US - for obstruction
Renal biopsy - for intra renal cause
Monitor urine output
Non-contrast CT KUB
KUB CR
Autoantibodies - Anti-GBM, ANCA
Tx AKI
Treat underlying cause
Pre-renal - correct vol depletion w fluids, treat sepsis w Abx
Intra-renal - maybe refer if concern over glomerular/interstitial pathology
STOP NEPHROTOXIC DRUGS ! - NSAIDs, ACEi, ARBs, lithium, digoxin
Treat underlying comps - hyperkalaemia, pulmonary oedema etc
IF severe - dialysis
What is refractory pulmonary oedema?
When AKI is esp bad, kidneys stop producing urine
That fluid can end up in lungs!
Describe some differences between AKI and CKD
AKI
Normal sized kidneys
No anaemia
No DM
↓ BP
Rapid change
Oliguria usually
Not often CNS symptoms
Presents more like shock
CKD
Small kidneys!
Anaemia
DM
↑BP
Gradual onset
Oliguria only in later stages
CNS symptoms in later disease
Presents like serious extensive disease
Chronic Kidney Disease Definition
Long-standing and progressive pathological abnormality of the kidney FOR AT LEAST 3 MONTHS
Pathophysiology Renal Colic
Stones form from crystals in supersaturated urine
Occurs when solute is too conc - increase in solute or decrease in solvent (dehydration)
Causes CKD
HTN
DM (more T2 than T1)
Polycystic kidney disease
SLE
Nephrotoxic drugs, chronic NSAID use
Obstructive uropathy - kidney stones, enlarged prostate
Progression from AKI
Glomerular disease / Chronic glomerulonephritis
SLE
Atherosclerotic renal vascular disease
Tuberous sclerosis
Malignancy - myeloma
CKD Diagnostic Criteria
eGFR < 60 ml/min/1.73m2
eGFR < 90ml/min/1.73m2 + signs of renal damage
Albuminuria > 30mg/24hours
(albumin:creatinine > 3mg/mmol)
RF CKD
DM
HTN
Female?
Age
Smoking
Polycystic kidney disease
NSAIDs
Cardiovascular disease - IHD, LV hypertrophy
FHx
Signs / Symptoms CKD
Early stages = Asymptomatic
Arise as GFR declines
–
Urinary - oliguria! haematuria, proteinuria, nocturia, polyuria
Bone disease! - Osteomalacia, osteoporosis
Anaemia!
Bilaterally small kidneys!!
Increased skin pigmentation! (yellow tinge)
HYPERKALAEMIA
N+V, fatigue, malaise, anorexia, itching, hiccups, convulsions, tremors, pallor
CVD - Uraemic pericarditis
Neuro - confusion, coma, fits
Vol overload - SOB (pulmonary oedema, dyspnoea, ankle oedema)
Sexual dysfunction
Describe the mechanism of HTN as a cause for CKD
Walls thicken in order to withstand pressure
∴ narrow lumen
∴ less blood and O2 to kidney
∴ ischaemic injury
Immune cells travel into damaged glomerulus and release TGF-B1
Then, mesangial cells regress to immature cells + excrete extracellular matrix
∴ GLOMERULOSCLEROSIS (kidney is scarred)
∴ ↓ ability for nephron to filter blood
Describe the mechanism of DM as a cause for CKD
Type 2 > Type 1
XS glucose in blood sticks to proteins - esp effects efferent arteriole making it stiff and narrow
∴ obstruction for blood leaving glomerulus
∴ hyperfiltration
∴ mesangial cells secrete more structural matrix
∴ ↑ size of glomerulus
∴ Glomerulosclerosis
Eventually becomes CKD
Quick!!!! Presentation CKD
Early asympto
Normochromic, normocytic anemia
Bone disease ! - osteomalacia
HTN
Fluid overload - oedema
CVD - cardiomyopathy
Malaise, loss of appetite, oliguria, haematuria
Ix CKD
FBC - shows anaemia, ↑ creatinine and urea levels
+ ↓ Ca2+ , ↑ phosphate, PTH, K+
Urinalysis
Dipstick (haematuria and proteinuria ~ GN, leukocytes and nitrites ~ infection)
Urine & blood culture - to exclude infection
White cells - bacterial UTI
Eoisinophilia - allergic tubulointerstitial nephritis
Granular casts - active renal disease
Blood - glomerulonephritis
Renal US - excludes obstruction, see kidney size!
CT - useful to diagnose retroperitoneal fibrosis and other causes of obstruction
Biopsy
Cystoscopy
ECG - hyperkalaemia
Tx CKD
Irreversible so aim is to prevent progression and symptom control!
If eGFR < 30 OR A:C > 70 = stage 4. Refer to nephrology
Lifestyle changes!
Treat underlying cause!
HTN - treat w ABCD etc
Oedema - fluid and sodium restriction, loop diuretic
DM - metform etc
CVD - aspirin, atorvastatin (statins if GFR < 60)
If all else fails - Renal replacement therapy (haemo/peritoneal dialysis, kidney replacement, haemofiltration)
Describe the stages of CKD
Stage 1 - eGFR ≥ 90 (mild damage, kidneys work as normal)
Stage 2 - eGFR 60 - 89 (mild damage, kidneys still work well)
Stage 3a - eGFR 45 - 59 (mild-mod damage, kidneys don’t work as well as they should)
Stage 3b - eGFR 30 - 44 (Mod-severe damage, kidneys don’t work as well as they should)
Stage 4 - eGFR 15 - 29 (Severe damage, close to not working at all)
Stage 5 - eGFR is less than 15! (close to not working at all or have failed, most severe damage)
What are some indications for dialysis?
Symptomatic uraemic - pericarditis or tamponade
Hyperkalaemia - when not controlled by conservative means
Metabolic acidosis
Fluid overload - resistant to diuretics
Comps CKD
Hyperkalaemia
Osteoporosis !
Vit D def
Anaemia
Metabolic acidosis
Pruritus - bc nitrogenous waste products of urea
Pericarditis
HTN
Quick!
Loin pain, Fever, Pyuria
What is it?
Pyelonephritis
Ix ALL UTIs
1st line - Urine dipstick
Will be +leucocytes, + nitrites, +haematuria
GS!!! Midstream microscopy, culture and sensitivity
Pathophysiology Benign Prostate Hyperplasia
Benign proliferation of transitional zone of prostate!
After 30 - men produce 1% less testosterone every year but 5a-reductase increases
∴ ↑ dihydrotestosterone levels
∴ prostate cell hypertrophy
As prostate grows, can squeeze/block bladder
∴ urine retention
∴ bladder dilation and hypertrophy
∴ urine stasis
∴ bacteria
∴ UTI !
Cause BPH
Dihydrotestosterone
RF BPH
Age
FHx
Heart disease
Obesity
DM
What is protective against BPH?
Castration!
Signs / Symptoms BPH
STORAGE
Frequency ↑
Urgency
Nocturia
Urgency incontinence
VOIDING - SHIPP
Straining
Hesitancy
Incomplete emptying
Poor/intermittent stream
Post-micturition dribbling
–
Bladder stones
Acute urinary retention
UTIs
Red flags for prostate cancer
Dysuria - painful/difficult urination
Haematuria
Painless haematuria
What are you instantly assuming it is?
Malignancy
Until proven otherwise
DDx BPH
Overactive bladder syndrome!
Bladder tumour
Bladder stones
Trauma
Prostate/Bladder cancer
UTI
Prostatitis
Ix BPH
International prostate symptom score (IPSS)
Digital rectal exam - smooth, enlarged prostate
PSA - may be raised
Urine dipstick
Biopsy
Abdo exam = enlarged bladder
To exclude renal damage - U&E and renal US
Also to rule out obstruction - US
Tx BPH
Lifestyle advice - avoid caffeine and alcohol
Void twice in a row to aid emptying
1st line - oral tamsulosin
2nd line - oral finasteride, dutasteride
Surgery - GS!
Trans-urethral resection of prostate (TURP)
or Trans-urethral incision of prostate (less destruction, best for small prostates)
What are some indications BPH should be treated with surgery?
RUSHES
Retention
UTIs
Stones
Haematuria (resistant to 5-alpha reductase-inhibitors i.e. FInasteride)
Elevated creatinine
Symptom deterioration
Comps TURP
Risk of ED
Comps BPH
Bladder calculi
UTI
Haematuria
Acute retention