GU Flashcards
UTI, BPH, prostate cancer, CKD, renal transplant, nephritis, nephrotic syndrome, breast cancer
BPH presentation, examination , Ix
PRESENTATION
- Voiding: poor stream/flow, hesitancy,
incomplete emptying, intermittency
- Storage: nocturia, freq, dribbling, overflow incontinence, haematuria, bladder stones,UTI
EXAMINATION
DRE – smooth, enlarged, symmetrical
Distended bladder if in retention
INVESTIGATIONS
Blood
- PSA
- Cr, U&E
MSU
International prostate symptom score (IPSS)
Imaging
- abdominal USS: Large residual volume,hydronephrosis
- transrectal USS
Voiding Studies
- to suggest if stricture/obstruction picture
Biopsy – trans-rectal biopsy (Gleason score) – to rule out malignancy if high suspicion
Management of BPH + risks - lifestyle, medications, surgery
Lifestyle
- Avoid caffeine/alcohol (reduces urgency/nocturia)
- physio; relaxation w voids, distraction methods to control urgency, bladder
retraining
Medications (IPSS 8-10)
o a-blockers; Doxazosin, Tamsulosin
Smooth muscle relaxation
50-70% respond
SE: drowsy, dizzy, dry mouth, hypotension, ejaculation issues
o 5a-reducatase Inhibitors;
Finasteride
blocks conversion DHT to Testosterone
prevents haematuria,
minimal effects on size
Takes over 6 months to work. Excreted in semencondoms!
SE: impotence, decr libido
Surgery (IPSS >20)
o TURP <100g
Intra-op: bleed, sepsis, urethral damage, TURP syndrome
Immed post-op: haematuria, clot retention, urinary retention
Late post-op: retrograde ejac, ED, redo (20% within 10y)
o Open retro-pubic prostatectomy (if large)
Risk factors for UTI, what makes UTI complicated, causes of UTI - bacteria and sterile pyuria
RISK FACTORS
-females
-sex
-pregnancy
-menopause
-immunosuppression
-diabetes
-urinary obstruction
-renal stones
-urinary catheter
Uncomplicated = normal renal tract and function
Complicated = abnormal renal tract, voiding difficulty/obstruction, reduced renal function,
impaired host defenses, virulent organisms e.g. staph aureus
Causes
Pyuria: -usually E. coli
-occasionally proteus mirabilis, staph aureus,
klebsiella pneumonia
CAUSES OF STERILE PYURIA
-treated UTI within 2 weeks
-inadequately treated UTI
-appendicitis
-calculi
-prostatitis
-bladder tumour
-polycystic kidneys
symptoms to differentiate pyelo vs cystitis vs prostatitis
examination and IX for UTI
SYMPTOMS
-pyelonephritis = fevers, rigors, vomiting, loin pain,
flank tenderness, oliguria (if AKI)
-cystitis = frequency, dysuria, urgency, haematuria, suprapubic pain
-prostatitis = flu-like symptoms, backache, enlarged prostate on PR, few urinary symptoms
EXAMINATION
-abdo/loin tenderness
-foul smelling urine, distended bladder if
obstruction
INVESTIGATIONS
-dipstick urine (look for nitrites, leukocytes,
bacteria)
-MSU – for culture and sensitivities
-BLOODS
– FBC, U and E, CRP, -blood culture if systemically unwell (urosepsis),
-PSA
IMAGING
– in children and men, failure to respond to treatment, recurrent UTIs, or pyelonephritis, consider USS and referral to urology
Prevention and management of UTI, + in pregnancy and in men
PREVENTION
-drink lots of water
-antibiotic prophylaxis
-self-treatment with single dose of abx when symptoms start
-cranberry juice (but need to drink lots!)
-no evidence for post-coital voiding!
MANAGEMENT
-drink lots of fluids and urinate often
Non-pregnant women:
-treat empirically for e. coli
-trimethoprim or nitrofurantoin
-if no response do urine culture
-consider other diagnoses if vaginal itch or discharge
-if upper UTI take urine culture and treat with Augmentin and gentamicin
-if asymptomatic DO NOT TREAT (very common)
In pregnant women:
-common
-get expert help
-any bacteriuria asymptomatic or
symptomatic) should be treated (risk of prematurity and pyelonephritis)
-repeat dipstick and culture at each antenatal visit
In men:
-uncommon
-often results from anatomical or functional anomaly
-consider referral to urologist and discuss with ID
Possible cases of relapse (same organism) or reinfection (different) of UTI, next IX and treatment
CAUSES
- Abnormal Renal/GU tract e.g. stones, posterior valves
- Voiding difficulty/outflow obstruction e.g.BPH
- Impaired renal function e.g. DM
- Impaired host defenses e.g. DM,
immunosuppression
- Poor hygiene/wiping technique
- Post-menopausal
Rest home/hospital
Diabetes
Kidney or bladder stones
Having a catheter
Previous urinary tract surgery
Sexual activity
Having an infected or enlarged prostate
Congenital abnormality of the urinary tract
Ix
INVESTIGATIONS
- Renal tract ultrasound
- PR
- Renal function test
TREATMENT
- eradicate/manage cause
- culture and sensitivity to rationalize antibiotics
- Oestrogen cream for post-menopausal females.
Prostate cancer - presentation, investigatons and exam
PRESENTATION
- Voiding: poor stream/flow, hesitancy, incomplete emptying, intermittency
- Storage: nocturia, freq, dribbling, overflow incontinence
- Haematuria
- Haematospermia, low ejac volume, ED (local invasion SV, ejac ducts)
- Boney pain (suggests mets)
- Weight loss, fatigue
-Age , Famhx as Risk factor
INVESTIGATION
DRE
- Enlarged, craggy, asymmetrical, nodular
o If PSA+, Prostate ca chance 30-40%
Bloods
- FBC: low Hb, pancytopenia
- ALP rise (mets)
- PSA >4 abnormal
o But normal in 30%
o PSA rise also w BPH, hyperCa, prostatitis, sex
o Note important to discuss PSA test with asymptomatic men who ask for it as screening
- Cr
MSU
- if blood cystoscopy, CT
Imaging
- TRUS (guide needle Bx)
o Need LA and abx cover
- CT staging
- Nuclear bone scan (mets)
Biopsy
- TUBP
grading and staging of prostate ca
Grading
- Gleason system - based on 2 most predominant glandular patterns each scored 1-5.
1= normal tissue well differentiated
2. well formed glands, larger and increased stroma
3. darker cells, some cells beginning to invade surrounding tissue
(2&3 moderately differentiated carcinoma)
4. few recognisable glands, many cells invading (poorly differentiated carcinoma)
5. sheets of cells throughout the surrounding tissue (anaplastic carcinoma)
Staging
- CT staging; Lymph Nodes (urethral), seminal vesicles,
bladder, bone lung
Management of prostate Ca + risks and prognosis
MANAGEMENT
Waitful watching life expectancy <10yrs, not
recommended for high risk patients
Active Surveillance >70y, low risk
Surgery
- Radical prostatectomy (open vs robotic)
o SE: impotency, urinary probs
Radiation
- Radical (daily 6/52)
o Similar outcomes to surgery
o SE: bowel, bladder probs, 2° Ca
- Palliative role (boney mets)
Brachytherapy
- Radioactive Iodine125
o Less aggressive cancers
o Retain potency, no 2 Ca
Chemotherapy
- Docetaxel
o Survival benefit for those w good performance
o Potential for salvage chemo in castrate resistance
Androgen deprivation/Hormonal
No change in life expectancy ‘lead time bias’
- Surgical
o Orchidectomy (decr libido)
- Medical
o LutHormRH agonist;
Zoladex, Lucrin (IM)
Cyproterone acetate (PO)
o Cover with anti-androgen
(Goserelin) for 2/52 to cover flare
o SE: lethargy, hot flush, mood, wt gain, decr muscle mass, Erectile D
PROGNOSIS
T low and PSA up = androgen independent
10% die at 6months; 10% live >10yrs
What uraemic symptoms - what urea level and stage of CKD got it
What are symptoms of complications of renal disease (8)
Uraemic symptoms (urea >40 mmol)- or can be asymptomatic
Stage 4 is when uraemia and anaemia starts
-Nocturia/ polyuria/ oliguria
-Loss of appetite, nausea and vomiting
-Fatigue, weakness
-Paresthesia/tetany from hypocalcaemia
Complications
o SOB, palpitations, pallor (anaemia)
o Bone pain (renal bone disease)
o Pruritis and photosensitivity
o GI sx - pain, reflux, constipation
o Confusion, depression, carpel tunnel, restless legs, peripheral neuropathy
o dyspnea and ankle swelling (fluid overload)
o Gout
o Dialysis patients – access problems, infection, pericarditis, peritonitis
Hx asking for specific causes of CKD + trigger for first presentation
- Ascertain aetiology
o Glomerulonephritis – hx of
proteinuria, haematuria, oedema, sore throat, immunosuppressive rx
o Recurrent UTI’s
o PCK – family hx, haematuria, HTN
o Reflux nephropathy – childhood renal infections, cystoscopy, operations
o Connective tissue – especially SLE,and scleroderma - Diabetes, HTN family hx
Trigger for first presentation
- NSAIDS, radiocontrast, ACEi, infection, dehydration, anaemia
What to look for on exam of CKD
EXAMINATION
General Appearance
- Mental state
- hyperventilation/kassmaul’s breathing
- Skin – Pallor, pigmentation, purpura, yellow (uraemic)
Hands
- Nails – terry’s nails
- Asterixis
- Neuropathy
- Brown discoloration of nails
- Scratch marks/excoriation
- Fluid overload
- Skin malignancy from immunosuppression
Arms
- Bruising, pigmentation, scratch marks
- High BP – lying and standing (post drop)
- Peripheral myopathy
- AV fistula for dialysis
Face
- Anaemia, jaundice
- Dry mouth
- Fundoscopy – HTN and DM changes
Chest
- Heart – pericarditis, failure: Pericardial rub, Pleural effusion/pulmonary oedema
- Lungs – infection, pulmonary oedema
Abdomen
- Scars – dialysis, operations
- Kidneys – transplant, renal mass, polycystic
- Tenckhoff catheter, exit site infection
- Bladder, liver, lymph nodes
- Ascites
- Bruits
- kidneys usually impalpable unless PCKD or
tumour
Legs
- Oedema
- Bruising, pigmentation, scratch marks
- Gout
- Neuropathy
Neurology
- proximal myopathy
What are the investigations done for CKD usually -bloods, urine, imaging
Bloods
- Glomerular function
o eGFR, creatinine clearance, plasma
creatinine/urea level
- Tubular function
o Electrolytes, phosphate, uric acid,
calcium, albumin - FBC
o Normocytic, normochromic anaemia
o Platelet abnormalities - Iron studies
- Parathyroid hormone
- Underlying disease
o ANA, Hep B surface antigen, Hep C,
immunoelectrophoresis,
Urine
- dipstick
- Culture and sensitivity
- 24-hour urine for ACR
Imaging
- Renal ultrasound
o Renal size, symmetry, obstruction
o Kidneys in CKD will be small (<8cm) unless
Early diabetic nephropathy
Polycystic kidneys
Obstructive uropathy
Infiltrative diseases
- CT scan
o Be wary of contrast - Cystoscopy
- Renal artery Doppler or CT renal angio
Other
- Micturating cystogram
- Renal biopsy
o < 8cm – mainly scar tissue –irreversible
o > 8cm- may still have some cortex –some reversibility
- Nerve conduction studies
- Arterial Doppler studies
What is the aetiology, presentation and treatment of CKD complications: anaemia, bone disease, skin disease + their treatment
Anaemia
- erythropoietin deficiency:
presents: SOB, palpitations, pallor
Treatment :
EPO if CKD<3, Hb <100 – exclude iron deficiency first.
Aim Hb 110-120 (increase is stroke risk)
Renal osteodystrophy’ : combination of hyperparathyroid bone disease, osteomalacia, osteoporosis, osteosclerosis
Presents as bone pain
Treatment
1. Treat if high PTH
2. Restrict dietary phosphate from milk, cheeze, eggs
3. Phosphate binders reduce absorption– eg. Calcitab
-Monitor with phosphate
4. Calcitriol increases calcium
– monitor with PTH
Skin Disease
-Retention of nitrogenous waste products, +/- inadequate dialysis
- porphyria cutanea tarda (PCT)
- Nephrogenic systemic fibrosis – a systemic
fibrosing disorder with predominant skin
involvement 2° to gadolinium contrast
Presents with pruritis, dry skin + eczematous lesions over AV fistula
PCT : is a blistering, photosensitive rash
What is the aetiology, presentation and treatment of CKD complications: CVD risk increase, Nervous System, GI dysfunction
GI Complications
- decreased gastric emptying + - increased serum amylase 2° to over excretion
o GORD and peptic ulceration
o acute pancreatitis
o constipation
Treatment - Loperamide for 8 days, stool softener
Nervous system
- Reduced seizure threshold
- Dialysis dementia
- Psychiatric
Presents: Confusion, depression
Autonomic: increased symp system
Peripheral symptoms:
- Carpal tunnel
- Restless leg syndrome
- Peripheral polyneuropathy (more in DM/ inadequate dialysis)
Treatment with : Clonazepam or gabapentin
Increased CVS risk
Aetiology
- Systolic dysfunction due to myocardial fibrosis
- abnormal myocyte function, Ca overload,
increased coronary calcification
- Uraemic or dialysis pericarditis
- Fluid overload as can’t excrete Na
Presents as
- HTN, DM, Dyslipidaemia, smoking
- HF – peripheral overload
Treatment
1. Smoking cessation, physical activity
2. Diet – close attention to salt + water, reduce fats, restriction of dietary protein not universal
3. Monitor and control BP to target 140/85
- ACE or ARB even if BP normal in T2DM
4. Monitor and control lipids – treat with statins regardless of baseline lipid values
5. Aspirin – low dose (in CVD risk >15% proven coronary, carotid plaque high calcium score)
6. loop diuretic high dose for oedema
What are the metabolic derangement complications in CKD aetiology, presentaiton+ treatment
Gout
-Urate retention
o Don’t use NSAIDS
Mild IGT
-glucose catabolised and excreted by kidneys
-End organ resistance in advanced CKD
- diabetes monitoring + treatment increased
Hypercholersterolaemia
- Impaired TG clearance
Endocrine effects
- increase in Prolactin, Growth hormone
- decrease in testosterone, calcitriol,
Hyperkalaemia
- not excreted by kidneys, leads to acidosis
What is the standard management of the CKD itself
- Slow progression and manage
complications
- Lifestyle
- Smoking cessation
- Physical activity
- Diet
o Close attention to salt and water
balance
o Reduce fats
o Restriction of dietary protein not universally recommended - Treat reversible causes of deterioration
- Hypertension – ACEi esp. in DM patients
- UTI/urinary tract obstruction
- Dehydration
- Cardiac failure
- Drug use
- Hypothyroidism - Medications
- ACEi
- Erythropoietin
- Steroids/ immunosuppressant - Dialysis – haem or peritoneal, how often, relief of symptoms, complications
- Operations: renal tract, parathyroidectomy, transplant work up
What are the indications for dialysis, pros and cons of peritoneal vs haemo, specific complications of dialysis
- Acute renal failure or toxicity needed to reverse
- Despite management : fluid overload
uraemic sx
hyperkalaemia, - Electrolyte abn despite charcoal
- Cr >1000
- Peritoneal
o Positives - CV safe, large volumes, freedom of diet and fluid, preferable for DM, daily, at home
o Negatives – peritonitis, exit site infections, protein loss, hernias and obesity and contraindications, does
not control uraemia
- Haemodialysis
o Positives – takes 18 hours per week, no protein loss, large volumes. patient less involved
o Negatives – circulatory access problems, heparin increasing risk of bleeding,
increased CV instability,
anaemia, osteodystrophy, dialysis dementia, dietary compliance needed.
Complications
B – bone disease
o I - infection
o P – protein/caloric malnutrition
o C – CVD; MI, CVA (HTN, Ca/P dysreg)
o A – amyloid, CTS, arthralgia, #
o M – malignancy
What are the 4 areas of management for post renal transplant patient
Viral screening
monitoring for allograft kdiney function/rejection
management of immunosuppression + susceptibility for infection+ steroid SE
management of other risk factors
What viral screening testing is needed post renal transplant
What monitoring for allograft kidney function/rejection
- Management of other risk factors + steroid SE
Viral screening (PCR)
o HIV, hep B, hep C 4-6 weeks post transplant
o CMV testing weekly for first 3 months for those not receiving prophylaxis
o Urine +/- blood tests for BK polyomavirus monthly 1-6, 9,12,18 and 24
Monitoring for allograft kidney function/rejection
o Serum Cr and eGFR
o Urinalysis with sediment exam: Proteinuria – 3/6/12 months,
o Spot urine protein: Cr ratio
o Kidney biopsy in setting of evidence of dysfunction eg. ++Cr, –urine output, worsening proteinuria
Management of other risk factors + steroid SE
Blood test monitoring
o FBC – every visit
o U&E – including bicarb, Na, K, Ca, Mg and Pho – every visit
o Fasting blood glucose weekly for first 4 weeks than 3/6/12 months
o HbA1c and fasting lipid profile every 3 months
o PTH and 25-hydroxyvitamin D every 6-12 months —>want to see if osteoporosis
What is the management of immunosuppression post renal transplant
o Initially inducted on biologic antibodies and high dose glucocorticoids
o Maintenance immunosuppression initiated at time of transplantation and continued long term for the duration of the allograft
o Monitoring Need CNI (Tacrolimus/ cyclosporine) trough level -2 hours post dose or 12 hour
- Need to do same routine cancer screenings as general population + monthly self skin examinations + total body skin examinations every 6mo-12 mo
CNI - tacrolimus and cyclosporine both and specific Side effects, interactions
- Nephrotoxicity,
- increased risk of SCC, lymphoproliferative disorders
-hypertension (renal vasoconstriction) - neurotoxicity – mild tremor , rarely seizure and headaches
-CNI pain syndrome – symmetrical pain in lower limbs + bone marrow oedema on MRI
-Glucose intolerance + DM
-Hyperlipidaamia
Hyperuricaemia + gout
Hyperkalaemia and hypomagnesmia
GI upset – worse in tacrolimus
Specific to tacrolimus: alopecia
Cyclosporine: hirsuitism, gingivial hyperplasia, bone loss
Interactions
Note levels increased with cyp450 inhibitors – eg. amlodipine, diltiazem,ketaconazole . Increased bowel inflammation can increase tacrolimus concentrations. Inducers eg. carbamazepine, phenytoin can reduce levels
SE of mycophenolate + monitoring
GI disturbance – diarrhoea, nausea, constipation, gingival hyperplasia
- Monitor FBC every week for 4 weeks then 2x a month
- Risk of hypogammaglobulinaemia and bronchiectasis
- Risk of SCC
- GI haemorrhage and pulmonary oedema
SE of sirolimus/everolimus
Pulmonary oedema, htn, poor wound healing, joint pain
What is management of susceptibilty for infection post renal transplant and the prophylaxis drugs
- Susceptibility for infection
o Immunisations pre and 2-6 months post transplant (however not live/live attenuated ones) - eg. Influenza, pneumococcal
o Prophylaxis 6mo- 12 after transplant
1. Trimethoprim – sulfamethoxazole for prevention of PJP , listeria, toxoplasmosis: one single strength tablet daily or double strength tab 3-7x weekly
2. Valganciclovir - CMV prophylaxis against reactivation in seropositive recipients/donors.
a. Dose based on CrCl, ~450 mg
3. Continued screening for EBV reactivation as no effective antiviral prophylactic therapy
4. Antifungal prophylaxis – more on individual basis due to risk factors more in liver and lung eg. fluconazole
What are the SE and monitoring for prophylactic trimethoprim - sulfamethoxaszole (cotrimoxasole) and valganciclovir
Cotrimox
SE: nausea + diarrhoea, headache
Monitor blood count in those predisposed to folate deficiency
Monitor sodium for hyponatraemia
Monitor renal function for hyperkalaemia
Valganciclovir
Nausea, diarrhoea, vomiting, dyspepsia – need contraception
Monitor FBC + platelet as severe myelosuppression may require treatment – pre treatment FBC
what is the main difference between nephropathy and nephritis exam (cardio/BP/Abdo)
- proteinuira, haematuira, rbc casts, serum albumin, oedema, BP/JVP, onset and
Nephropathy -
proteinuria >3mg /24hrs, +/- haematuria absent RBC casts but low serum albumin, oedema ++++, normal BP /JVP low normal
Onset is insidious
+ high triglycerides
Nephritis - proteinuria <3 mg, haematuria +++, RBC casts present, normal serum albumin, mild oedema, Raised BP /JVP.
Onset is sudden + oligouria
pathophys behind nephritis and nephrotic syndrome + examples of primary and systemic disease of each
Nephrotic
= inflammation damages
glomerulus, proteins leak, high protein in urine
(proteinuria), low protein in blood (hypoalbuminaemia), severe oedema (due to
reduced oncotic pressure AND Na+ retention), and
hyperlipidaemia (liver releases triglycerides to
maintain osmotic pressure).
Primary
- Membranous GN, minimal change, focal segmental glomerulosclerosis
Systemic
- DM, myeloma
Nephritis
= inflammation damages
glomerulus so much that blood freely filters through causing proteinuria AND haematuria, this causes decreased kidney perfusion and thus oliguria, and subsequent hypertension. HTN leads to some oedema
Primary
- IgA nephropathy, rapidly progressive GN, post strep A, proliferative mesangial or crescenteric
Systemic
- SLE, goodpastures -( anti glomerular basement membrane), myeloma
Ix and management for nephritis / nephrotic syndrome
IX
-Urinalysis (Protein, RBC’s)
-Albumin creatinine ratio (ACR) – more accurate
than dipstick, allows for dilute/concentrated urine
-eGFR and Creatinine
-Blood (FBC, U+E, LFT, ESR/CRP)
-Autoantibodies (ANA, ANCA, anti-dsDNA, antiGBM)
-Renal USS +/- biopsy
MANAGEMENT
- Refer to a nephrologist
- Depends on the actual diagnosis, but in general:
- Nephrotic syndrome = Treat underlying cause, salt restrict, diuretics for oedema, ACEi to reduce proteinuria, monitor BP and
treat if high - Nephritic syndrome = Treat underlying cause, treat HTN, ACEi, steroids/immunosuppression if autoimmune cause
What are the risk factors for breast cancer and screening
Overweight, smoking, alcohol, FMHx, personal
cancer Hx, early menarche’s (<11), late menopause
(>53), late first pregnancy, radiation, prolonged
OCP/HRT, Ashkenazi Jewish
GENETICS
- Familial 10-15%
- BRCA 1 – 80% breast, 40% ovarian
BRCA 2
SCREENING
- Mammograms 45-69 2 yearly basis
- harmless screen that can detect something
able to Tx
- Some over screening & overtreating
What is presentation and description of breast lump/cancer
PRESENTATION
- Breast lumps, axillary nodes
- Peau d’orange
- Nipple discharge; bloody, green, yellow
- Paget’s disease of the nipple
- Abnormal resting place, tethering
- Asymmetry
LUMP
Position (commonly Upper outer quadrant)
Size, shape, consistency (hard, irreg, not discrete)
Tenderness (non)
Fixation (fixed to CW)
Single, multiple
What is the investigation for breast lumps - dependent on what age
‘Triple Therapy’ for all breast lumps
1) Examination
2) Imaging
If <35 years old -> US
o Confirms benign
o Sens 82%; spec 85%
- If >35 years old -> US and mammogram
o compares glandular vs fatty
o sens 86%; spec 90% (misses 40% Ca in under 50s - MRI (sometimes)
o High risk groups - BRCA carrier, mantel RTX
o Post Dx work-up? lobular difficult to see on mams; extent of disease
3) Biopsy
- FNA:
o C1 – insufficient tissue
o C2 – benign
o C3 – atypical (favours benign)
o C4 – suspicious of M
o C5 – malig or DCIS
- Core:
o Distinguishes between DCIS vs M, ductal vs lobular, receptor status
Diagnosis and staging of breast cancer
DIAGNOSIS
- Carcinoma insitu
o Lobular CIS – incr risk Ca
o Ductal CIS – pre-malignant
- Invasive carcinoma
o Lobular carcinoma 20%
o Ductal carcinoma 80%
o Other
STAGING
Stages 1-4 (stage 1 = confined to breast, stage 4 =
distant mets)
Also use TNM staging
Management of breast cancer (5)
Surgery
- DCIS: excise w 10mm margins
- Invasive:
o Partial mastectomy + RTX
o Total Mastectomy (uni, bi-lateral)
+/- SNB
+/- ANC
+/- reconstruction immed/delayed
Radiation
- All breast conservation cases, some DCIS
Chemotherapy
- higher risk cases i.e. high grade
- Neo-/Adjuvant, palliative (diff Rx)
- Combo CMF, anthracycline
Endocrine
- Tamoxifen (ER+)
Monoclonal Ab
- Herceptin (HER-2+)
