Nephrology/Urology Flashcards
Most common cause of nephrotic syndrome in adults
Membranous nephropathy
Signs of a CHRONIC kidney problem
High Cr, high BUN
Low albumin
Kidney should not be dumping any albumin into urine - if albumin is low - it is a chronic problem - either from kidney dumping or liver not synthesizing
Kidney functions
A WET BED
Acid-base balance
Water reabsorption/balance
Electrolyte balance
Toxin filtering/removal
Blood pressure control (RAAS)
Erythropoiesis (produces EPO)
D - Vitamin D activation
What is Cr? Why is it used as a marker for kidney function?
Creatinine is a breakdown product of muscle
It is the only substance 100% filtered from our blood to our urine & 100% secreted out (not reabsorbed at all) so it is a surrogate marker for how well the kidney is filtering the blood
A bump in Cr from 0.3 to 0.6 actually means you lost 50% of your filtration rate because the Cr doubled!
Therefore the creatinine clearance (CrCl) is used estimate the GFR
Why is metabolic acidosis common in chronic renal failure?
Beginning of CKD - kidney nephrons/tubules are damaged & the tubules are unable to secrete H+ as efficiently as before (remember we take in a high daily acid load that must be secreted!) - this is a non-anion gap metabolic acidosis
Then later on when urea starts building up we get an anion gap metabolic acidosis - kidneys can’t keep up excreting/getting rid of blood urea
Most common electrolyte abnormality & two main causes
Hyponatremia
Two causes:
SIADH –>
Hypo-osmolar (all pt’s who are underperfused ADH will be released - CHF, shock, MI etc) - also psychogenic polydipsia, beer potomania etc
Hyperglycemia (DKA)–>
Hyper-osmolar (pseudo-hyponatremia) - treat w/ insulin (check K+ first)
Management of hyponatremia caused by SIADH
Remember ALL patient’s who are hypo-perfused will have SIADH!!! (CHF, MI, SHOCK)
Tx = restrict water intake
Correct Na+ balance SLOWLY - 1-2mEq/hour then slower when sx improve
Goal is Na+ of 125-130
What happens if you correct a low sodium too fast? What are si/sx of that?
Central pontine myelinolysis
AKA iatrogenic cerebellar swelling = BRAIN HERNIATION = BAD NEWS!!!!
Two main causes of hypernatremia?
- Diabetes insipidus - central (low ADH level) vs nephrogenic (kidney insensitivity to ADH- THINK DRUGS!!!)
- Excess water loss (iatrogenic osmotic diuresis w/ mannitol etc)
Note that the main causes of hyper-Na+ has to do with water loss rather than Na+ gain…
What would a urine sample look like if someone was peeing out large amounts of urine due to DI? Treatment?
If central DI then will be peeing out large amounts of DILUTE urine (low specific gravity) that is FREE of glucose
Give synthetic ADH duh! AKA desmopressin (use pulse IV form to prevent tachyphylaxis)
What is the type of patient who is at highest risk for developing central DI?
Someone post-head trauma or post-op
AKA neurosurg floor!
Remember posterior pituitary normally releases ADH
Central D. insipidus = IN-sufficient ADH
Causes of nephrogenic DI
BFTP: Nephrogenic DI = body making ADH but kidney is insensitive to it!
Etiology:
LITHIUM !!!!!!
Amphotericin B
Acute tubular necrosis
Hyper-PTH
Hypercalcemia & hypokalemia
(usually use ions to concentrate urine)
CP DI
Polyuria
Polydipsia
Nocturia (may manifest as enuresis in children)
Hypernatremia
Dehydration, hypotension
Name the two disorders of the posterior pituitary that cause disruptions in sodium and water balance?
Central DI - INsipidus = INsufficient ADH - dec ADH production centrally - idiopathic = MC, HEAD trauma, post-op etc
SIADH - syndrome of INCREASED ADH - occurs in anyone volume-depleted - CHF, MI, etc
Treatment hypernatremia 2/2 central DI
SLOW correction:
Drink free water orally
Desmopressin (DDAVP)
Carbamazepine (has anti-diuretic activity)
IF SYMPTOMATIC –> hypotonic fluid (free water orally, 1/2 normal saline, D5W)
What is the next test you order or look at if someone is hyponatremic?
Serum osmolarity!
LOW serum osmomlarity = SIADH - perfusional problem from another cause (CHF, MI, infection etc) and body produces too much ADH to compensate = dilutes out the serum = low serum osmolarity
HIGH serum osmolarity = hyperosmolar hyponatremia - sounds weird right? It is…only causes is hyperglycemia
Urine osmolarity low or high in DI?
Specific gravity low or high in DI?
LOW urine osmolarity (dilute) < 200
LOW specific gravity < 1.005
Causes of hyperkalemia
Abnormal distribution:
No insulin in DM
Acidosis –> too much H+ - body pumps K+ out, H+ into cells to compensate
Impaired renal excretion:
GFR<5, oliguria - AKA acute (pre-renal, intrinsic, post-renal) & chronic renal failure
Drugs:
Spirinolactone, ACEI, Bactrim
Hemolysis, trauma, burns, surgery
Treatment of hyperkalemia
- Stabilize cardiac membrane potential (give 1 amp of CaCO3 or CaCl)
- Move K+ into cells (D50% & 10 units insulin, bicarb (if acidotic will drive K+ into cells too)
- Increase excretion (Loop diuretic, kayexalate)
NOTE - IF K+ 7.5 b/c missed 2 days dialysis (ESRD) then TX = DIALYSIS not the above… DUH
Causes of hypokalemia
Vomiting - lose K+ = metabolic alkalosis b/c K+moves out of cells, H+ goes into cells
Diuretic therapy (loop, thiazide)
Too much insulin - redistributed all the K+ into cells
What should you always check next when you see a low K_?
Check a MAGNESIUM LEVEL!!
If s. mg is low, K+ will not replete - oral replacement of Mg is best
Remember: Hypo-K+ and Hypo-Mg+ cause dig toxicity at therapeutic dig levels
MCC hypomagnesemia
Alcoholism
MCC hypermagnesemia
Chronic renal failure
remember that the Mg2+ does what the K+ does
Which treatment for constipation would you NOT want to give to a person with CKD, ESRD etc
Don’t give MG citrate!
**Contains magnesium!
Assume that anyone with CKD/ESRD has high Mg2+! Remember that Mg2+ kind of does what K+ does
In the absence of functioning kidneys, how fast does the Serum Cr rise each day?
Serum Cr rises by 1.0 - 1.5 each day
AKI causes
Ischemia
Nephrotic syndromes (minimal change, membranous nephropathy)
NSAIDs
Multiple myeloma
AKI mechanisms
Pre-renal - perfusional problem w/ intrinsic kidney function still intact - AKA still reabsorbing BUN but not filtering as much Cr = dec GFR b/c kidneys not getting perfused - Volume depletion (infection, shock), volume overload (CHF), drugs (NSAIDs) …therefore end up with BUN:Cr ration that’s elevated ~20:1 = dehydrated, >36:1 = UGIB - SHOCK SHOCK SHOCK SHOCK SHOCK = cause of prerenal
Intrinsic - nephrons not functioning anymore -lose ability to reabsorb BUN- ATN (AKI–> ATN when underperfused tubules start to get ischemic/necrotic), AIN (drugs, abx etc), autoimmune disorders (FSGN, PSGN etc), and vascular (DIC, HELLP, R. a/v thrombosis, atheroembolic dz etc)
Post-renal - kidney stone, BPH, urinary retention
Pre-renal causes of AKI/ARF
SHOCK (septic, cardiogenic, hemorrhagic, hypovolemic, anaphylactic), also CHF w/ volume overload
If you can “fix” the shock, you fix the kidneys but you must recognize it in time
FENA in prerenal AKI
S. BUN/S. Cr in prerenal AKI
Urine SG in prerenal AKI
FENA < 1
(kidney still functioning so secretes renin to try to increase perfusion (RENIN= AGII = ALD = hold onto Na+ TO REPERFUSE IT!!!)
S. BUN/S. Cr > 20:1
(b/c GFR/CrCl is decreased if kidneys not getting perfused or if you’re hypovolemic so no filtering out as much Cr/ blood but your tubules are still functioning to reabsorb BUN)
Urine specific gravity > 1.030 -
(HIGH SG b/c secreting Ald to retain sodium/water & making concentrated urine)
FENA, urine SG, BUN/Cr in renal (intrinsic) AKI
FENA > 1
(kidneys given up - RAAS system all pooped out b/c tubules sick!)
Urine SG is LOW b/c tubules can’t concentrate the urine if they’re all clogged up or infected or sick
S. BUN/S. Cr ratio is <10:1 b/c now now BUN not being reabsorbed in the tubules b/c they’re sick - now intrinsic renal issue w/ functioning of nephrons so all usual kidney functions are going to shit
Causes of intrinsic/intrarenal AKI
Tubulointerstitial -
ATN (85%, AKI that has now become necrotic/ischemic), interstitial nephritis (drugs, autoimmune disease - sarcoid, SLE, scleroderma, sjogren’s)
Vascular - R a/v thrombosis, thromboembolic dz, DIC, HELLP, ITP, TTP, Malignant HTN (MAOI + tyramine-containing food), ITP/HUS (ITP = INNocent, HUS = HORRIBLE = micro-angiopathic clots in kids kidneys)
Glomerular - glomerulonephritis
ATN - cause? FENA? Common in which patients?
A type of TUBULAR intra-renal AKI (remember categories are tubular, vascular, glomerular)
Caused by severe AKI which has now caused ischemia leading to necrosis in the kidneys –> BFTP that AKI is caused by SHOCK (all types)
FENA is now HIGH b/c kidneys are very sick & renal tubules can’t retain Na+ anymore
1 cause of post-renal AKI
Prostate - BPH
Kidney stone (b/l or one kidney)
Pelvis masses/obstruction
Neurogenic bladder
Why is it important to quickly recognize urinary tract obstruction?
UTO is important to recognize since it is readily reversible if quickly corrected. If uncorrected, UTO may predispose to urinary tract infection (UTI) and urosepsis and eventually cause end-stage renal disease (ESRD)
CP bladder outlet obstruction
Pain Change in urine output Hypertension Hematuria Increased serum creatinine
Palpate huge bladder - get US to confirm - CATH the patient & check serum Cr!
AIN - cause, CP/DX
Acute interstitial nephritis is a renal cause of AKI - kind of like an allergic nephritis
Etio: Immune-mediated response to a drug
BFTP: If a kidney disorder ends in “itis” it presents w/ HEMATURIA - converse also true!
CP: Fever, (80%), rash (50%), arthralgias, eosinophilia, acute azotemia
Micro: Pyuria w/ eosinophluria, WBC casts, hematuria
What are tipoffs you’ll find in a question getting at acute interstitial nephritis?
Remember - Acute interstitial nephritis is a renal cause of AKI - kind of like an allergic nephritis
Etio: Immune-mediated response to a drug or immunologic or infectious disease
If a kidney disorder ends in “itis” it presents w/ HEMATURIA - converse also true!
Therefore in question on PANCE - LOOK FOR -“Started on new drug, gave drug in morning, now has fever, eosinophiluria, pyuria, HEMATURIA etc!!!”
Tx is stop the drug, hydrate the kidney, consult nephrology
Interstitial nephritis has what kind of casts?
WBC casts
Acute tubular necrosis has which kind of casts?
Muddy brown casts
Dehydration or pre-renal injury causes which kind of casts?
Hyaline casts
Does a normal urine have protein in it?
NO!!!
Nephrotic syndrome if dumping protein
Does a normal urine have fat or sugar in it?
NO
Does normal urine have heme in it?
NO
Does normal urine have RBCs in it?
NO
What is the definition of a nephrotic syndrome?
Injury to the glomerulus causing abnormal filtration 2/2 podocyte dysfunction - leads to heavy proteinuria, hypoalbuminemia, edema, hyperlipidemia, lipiduria
What is the definition of a nephritic syndrome?
Nephritic pattern/diseases are caused by Inflammation of the glomerular capillaries = hematuria, oliguria, HTN
Glomerular disease cause which kind of casts?
RBC casts - think of everything as inflamed
What will urine have in it if someone is in rhabdo?
Myoglobin! = myoglobinuria
Myoglobin is ACIDIC - so hydrate kidneys & give bicarb
Etio rhabdo, labs, treatment
Etio: Muscle trauma, exercise, ETOH, cocaine, statins
Labs: High CPK & Cr levels, urine dip + for blood, micro negative for RBC’s… what is it then? MYOGLOBIN!
Tx: Fluids, bicarb, furosemide
Etio ESRD
Diabetes, HTN, Chronic GN, CKD, interstitial nephritis, obstructive uropathy, SLE, HIV
Nephritic patterns
BFTP - nephritic disease (as opposed to nephrotic) = inflammation of glomeruli = RBC casts, dysmorphic RBCs, mild edema/HTN (not as much as nephrotic syndromes)
Remember - ABX only prevent rheumatic fever not PSGN
If see RBC casts, think PSGN - get throat swab, get ASO titer (anti-streptolysin Ab which attacks the glomeruli)
Glomerulonephritis
Type of nephritic kidney disease
Dx: Micro below + edema, HTN
Micro: Dysmorphic RBCs, RBC casts, Hematuria, ASO ab titer positive, mild proteinuria
Cause: Group A srep
Nephrotic patterns - essentials of diagnosis
Injury to the glomerulus causing abnormal filtration 2/2 podocyte dysfunction - leads to heavy proteinuria, hypoalbuminemia, edema, hyperlipidemia, lipiduria
Note: word Nephrotic spells protein if you spell it out - NephrOtic patterns are all about the protein - HypOalbuminemia
NOTHING on microscopy - NO casts!!!
What is a urine Protein:Cr ration concerning for nephrotic disease
a HIGH one (>300-350) - means you have a TON more protein than Cr in your urine = not normal
What is a common complication of nephrotic syndrome that is often overlooked?
Pt can end up with blood clots!!!
Need protein to carry lipids from periphery to liver - so = hyperlipidemia
Need protein to make Protein C and protein S = clot busters - so end up with a BLOOD CLOT!!!
What is the “nephrotic” range on a urine dip for proteinuria?
3-4+ protein on urine dip = nephrotic range
Cause of primary nephrotic syndrome = idiopathic or one of several glomerulonephropathies
What causes secondary nephrotic syndrome?
1/3 of adults with nephrotic syndrome have a systemic disease such as SLE, DM, HIV, cancer, or amyloidosis
Treatment nephrotic syndrome
ACEI - dec proteinuria
Low salt diet
Diuretics - dec edema
Statins - dec lipids
Definition of CKD
Abnormalities of kidney structure (proteinuria) OR function (GFR <60) for > 3 months
Persistence of proteinuria, hematuria, or abnormal urinary sediment
Progressive nephrosclerois, irreversible reduction in nephron number 2/2 glomerular hyperfiltration of remaining nephrons
Results in inability to maintain - acid base balance, fluid/electrolyte valance, excretion of nitrogenous wastes
Uremic syndrome
Symptomatic manifestations associated with azotemia = the accumulation of urea and other toxic nitrogenous compounds in the blood 2/2 decline in renal function/excretion of them
Complications of progressive chronic kidney disease
Think of A WET BED - dysfunction
Acid-base - metabolic acidosis
Water - volume overload
Electrolytes - hyperkalemia
Toxin removal - none = uremia
EPO def = anemia
D - derrangements in vitamin D, calcium, & phosphorus metabolism - osteoporosis
What would cause a false positive for hematuria?
Myoglobinuria - causes dark urine but it’s not RBCs
Hemolysis
Causes of hematuria
Remember all kidney diseases that end in ITIS = hematuria
Glomerulonephritis (++proteinuria, RBC casts, dysmorphic RBCs)
Renal causes - AVM, PCKD, SS anemia
Urologic causes - (no proteinuria, no dysmorphic RBCs) = BPH, cancer, cystitis, stones, trauma (foley)
Types of glomerulonephritis
IgA - MC worldwide
HSP
PSGN
Goodpastures
What would glomerular intrinsic AKI labs look like?
Hematuria, RBC casts, azotemia, proteinuria (not a ton), HTN (not severe)
Tx: High-dose corticosteroids
What is the role of ACEi in CKD?
ACEi are used in CKD because they protect the kidneys - they do this by decreasing capillary pressure, thereby prevent ing glomerular injury and slowing progression of renal disease. It also improves renal blood flow out of kidney - prevents AGII from constricting efferent arteriole, anti-proliferative effects - less fibrosis of kidneys from chronic HTN/pressure = less protein in urine
Remember ACEi ADRs:
Hyperkalemia (no ald = no Na+ retention = K+ retention), angioedema, dry cough, TERATOGENIC, hypotension, Acute renal failure
Also remember - don’t work as well in AA b/c their HTN is not related to the RAAS system
What is Entresto (sacubitril/valsartan)?
Meaning indications, MOA etc
Entresto = an ARNI = angiotensin receptor- neprolysin inhibitor (prevents normal degradation of vasoactive peptides - more peptides = more vasodilation, natriuresis, diuresis etc
Indicated to reduce risk of CV death and hospitalization for HF in pt w/ CHF and reduced EF
Definition of CKD
Abnormalities of kidney structure (proteinuria) OR function (low GFR) for > 3 months
Grade I-II is GFR>60 but evidence of structural damage (moderate (30-300) -severe (>300) proteinuria)
GFR < 15 = stage V = ESRD
In which patient populations should you be most worried about CKD?
DM and HTN - both lead to CKD and are linked to CKD progression
Monitor CKD with ACR - albumin to creatinine ratio =
U. microalbumin: U. Cr ratio
Normal < 30
Albuminuria = anything >30
Moderate increase = 30-300
Severe increase = >300
What drugs should people with CKD be on to prevent the progression of the CKD?
ACEi - renally protective
Consider SGLT2 if DM b/c delay progression of CKD & have diuresing effect
Who gets minimal change disease?
KIDS
Form of nephrotic syndrome - BFTP that nephrotic syndrome is a form of glomerular kidney disease characterized by proteinuria, hypoalbuminemia, hyperlipidemia & edema (periorbital)
(as compared to a nephr-ITIC kidney dz = BLOOD loss = hematuria, RBC casts, dysmorphic RBCs, dependent edema, & azotemia)
Who gets membranous nephropathy?
ADULTS - MC nephrotic syndrome in adults
Form of nephrotic syndrome - BFTP that nephrotic syndrome is a form of glomerular kidney disease characterized by proteinuria, hypoalbuminemia, hyperlipidemia & EDEMA (periorbital, LE, scrotal - more prominent in nephrotic b/c protein loss more severe) & BLOOD CLOTS & HLD!!! B/c no protein for protein C, protein S, and lipid transport :(
(as compared to a nephr-ITIC glomerular kidney dz = BLOOD loss = hematuria, RBC casts, dysmorphic RBCs = DARK URINE!!! Still have some edema, & azotemia)
Clinical manifestations of nephritic glomerular disease & examples of nephritic diseases
GROSS hematuria - ITIC = BLOOD - the GROSS hematuria sets it apart from nephritic
Cola-colored dark urine from the GROSS hematuria, oliguria
RBC casts, dysmorphic RBCs
Some HTN, edema etc
Examples of nephritic dz’s - IgA, PSGN,
MCC acute glomerulonephritis worldwide, epidemiology, CP
IgA nephropathy AKA Berger’s disease
Young males
2 days after URI/GI infection - obvi if it’s called IgA it’s a post-infectious complication - IgA is 1st line of defense in URI/GI bugs so IgA overproduction causes cross-rxn = IgA deposits in kidneys = glomerular inflammation
Dx: IgA mesangial deposits on immunostaining
Tx: ACEi & Steroids
3 weeks after sore throat, young boy complaining of dark scanty urine …. = ?
PSGN
Young boy (2-14 YO)
Dx: Increased ASO ab titer (what binds to the glomeruli) low serum complement
Tx: Supportive +/- abx
Note: ** Can occur after ANY GABHS infection (impetigo, other SSTI etc - MC is GABHS pharyngitis tho
What is goodpasture’s disease? How does it present?
= Antibody formation against Type IV collage of glomerular basement membrane in kidney & lung alveoli =
CP: Kidney failure & hemoptysis
** Occurs post-URI
Dx: Linear IgG deposits
(Goodpasture = IgG)
Tx: High dose corticosteroids & cyclophosphamide
Tx for any rapidly progressing acute glomerulonephritis
High dose IV corticosteorids
Cyclophosphamide
List all forms of acute glomerulonephritis & the two that most likely present as rapidly progressing AGN
IgA nephrophathy (Berger’s)
Post-infectious (PSGN)
Membranoproliferative (SLE)
RPAGN:
Goodpasture’s disease
Vasculitides (MPA, Wegener’s )
Which two vasculitides can presents with rapidly progressing acute glomerulonephritis?
**Both have lack of immune deposits and POSTIVE ANCA ANTIBODIES
Microscopic polyangitis:
+ P-ANCA
Granulomatosis with polyangitis (Wegener’s):
+ C-ANCA
What is an important pattern to recognize with glomerular kidney disease (nephrotic and nephritic?)
They are almost all due to some sort of immune dysregulation - post-infectious IgA (Berger’s) or IgG (goodpasture’s) nephropathies, low complement, 2/2 another AI disease (SLE = membranoproliferative) or are idiopathic & probs related to immune dysregulation but we don’t know how yet….
Minimal change - idiopathic but a/w viral infection/allergies…
Membranous - idiopathic, SLE, viral hepatitis kicks it off etc
What is the most common cause of nephrotoxic acute tubular necrosis?
Remember ATN is either ischemic (worsening AKI –> ischemia –> necrosis) or nephrotoxic meaning something directly damaged the kidneys
The MCC nephrotoxic ATN is aminoglycosides
What are the three most common causes of vascular (micro and macro) intrinsic AKI?
Remember intrinsic AKI is ATN, AIN or vascular complication -
MCC vascular complications is:
Micro- TTP, HELLP, DIC
Macro - atheroembolic dz, renal artery or vein thrombosis, malignant HTN, renal artery dissection, aortic aneurysm etc
Fatty casts AKA “maltese crosses” or oval fat bodies are pathognomonic for which disease?
Nephrotic syndrome
Nephrotic syndrome = HLD b/c need protein to transport fat back to liver - end up with fat in urine
Adult Polycystic kidney disease - epidemiology & etiology
Autosomal dominant disorder
Kids = Autosomal recessive disorder
2/2 Mutation in gene PKD1/2 = formation & enlargement of kidney cysts & cysts in other organs (liver, spleen) –>vasopressin-induced cytogenesis which = ESRD over time
Renal clinical manifestations of PCKD
Abdominal/flank pain (2/2 bleeding into cyst or nephrolithiasis or infection)
Palpable flank mass - large palpable kidneys on exam
HTN, hematuria, microalbuminuria
Ddx HTN, hematuria, microalbimuria
Nephrotic syndrome
Nephritic syndrome
PCKD
Extrarenal CP of PCKD
Cerebral “berry” aneurysms
Hepatic cysts
MVP
Colonic diverticula
Dx & TX PCKD
Dx: renal ultrasound, genetic testing
Tx:
Simple - observe, ACEi for HTN
Multiple - Supportive (inc fluid intake), control HTN, +/- dialysis or renal transplant
3 YO child w/ hx cyrptorchidism, horshoe kidney on normal yearly exam you feel painless abdominal mass w/ high blood pressure…you’re thinking what?
Wilms tumor! aka Nephroblastoma
MC in children 1-5 YO
A/w other GU abnl (horshoe kidney, cyrptorchidism, hypospadius etc)
Painless, palpable abdominal mass = MC presentation - Does NOT cross midline
Can also have: Hematuria, anemia, HTN (tumor secretes renin)
Dx: ABD ultrasound
Tx: Nephrectomy & chemotherapy
What’s the firs thing you think when someone comes in w/ BP 170/110
What’s pissing off the kidney? Most causes of HTN are from kidney secreting renin to increase renal perfusion
MC site of mets w/ Wilms tumor?
Lungs
BFTP:
Wilms tumor! aka Nephroblastoma
MC in children 1-5 YO
A/w other GU abnl (horshoe kidney, cyrptorchidism, hypospadius etc)
Painless, palpable abdominal mass = MC presentation - Does NOT cross midline
Can also have: Hematuria, anemia, HTN (tumor secretes renin)
Dx: ABD ultrasound
Tx: Nephrectomy & chemotherapy
Indications for dialysis?
AEIOU
Acid - AKI - kidney can no longer buffer acid in blood by secreting H+ & reab bicarb
E - electrolytes - Hyper K+ or hyper-phos
Intoxication - like Lithium or other HD drug OD
Overload - maximized diuretic therapy & not working…what to do?
Uremia - spectrum of progression from feeling poor w/ N/V to encephalopathy w/ pericarditis
Signs/symptoms of mild uremia –> severe uremia…
Vague sx - fatigue, forgetful, change in sleep
Then N/V
Then weight loss & AMS
Then pericarditis & full on encephalitis
MCC acute orchitis
Mumps
Note: Mumps parotitis preceeds the onset of mumps orchitis by 3-10 days
Etio: paramyxovirus - para-myxo = para-tid gland inf
CP & PE epididymitis
VERY PAINFUL ON TOP OF TESTICLE - will not let you touch
Gradual onset (2-3 days) scrotal pain, swelling, erythema, MC unilateral, fever, chills, irritative voiding sx (dysuria, urgency, frequency)
POSITIVE phren’s sign (relief of pain w/ elevation of affected scrotum)
Normal cremasteric reflex
Testicles in normal (vertical) position
Dx epididymitis
Scrotal ultrasound
Will show: enlarged epididymis- increased blood flow
UA / CULTURE: Pyuria (inc WBC) w/ bacteriuria
CBC: Leukocytosis, urine culture, STD testing for gonorrhea, chlamydia
Etiology epididymitits
Children: viral Mumps MCC
Men < 35 YO : N. gonorrhea, trichomonas, C. trachomatis treponema, etc
Men > 35 YO : Enteric organisms (E. coli, klebsiella, pseudomonas, proteus etc)
Tx Epididymitis
Epididymitis is considered a “complicated” UTI b/c it is no longer just urethritis (7d for cystitis, but more to penetrate epididymus)
Therefore we need 10-14 days of treatment:
< 35 or STDs suspected:
Ceftriaxone 250 mg IM PLUSE doxy BID x 14 days (same as PID tx in women) –> spread to pelvis or spread to balls
If > 35 YO, E. Coli suspected:
Ofloxacin 300 BID x 14d or
Levofloxacin 500 QD x 14 d
REMINDER - no doxy < 8 YO, NO flouoroquinolones < 18 YO = abnormal cartilage development –> Use bactrim
Length of treatment for bacterial orchitis
30+ day treatment
What is the “blue dot sign”? When is it seen?
Blue dot sign = torsion of the appendix testis
Occurs in 7-12 YO
Sudden onset of pain (< torsion) - BLUE DOT IS ONLY PLACE THAT IS TTP
Testicle NONTENDER, normal cremasteric reflex
No intervention is warranted- can do scrotal support & NSAID - usu resolves in 1-2 days
Average age testicular torsion?
65% occur in pubertal teenagers 10-20 YO
Average age appendiceal torsion?
7-12 YO boy
CP & PE testicular torsion
CP:
SUDDEN onset severe testicular pain, ABD pain, N/V (kid might not mention testicular pain b/c embarrassed) following strenuous activity (sports)
PE:
“Bell-clapper deformity” - one testicle not vertical
ABSENT cremasteric reflex on ipsilateral side
Phren’s sign NOT present (if anything elevating testes makes ischemia/pain worse)
Dx/workup torstion
STAT DOPPLER US
CALL UROLOGY = EMERGENCY
Immediate intervention to detorse & BILATERAL orchipexy (if one gubernaculum missing, other probably missing/loose too)
Testicular cancer risk factors
Adolescent
Cryptorchidism - surgical intervention does not reduce risk
CP testicular cancer
15-35 YO Male w/
Painless testicular mass - palpable, firm, irregular
Diagnosis testicular cancer
Ultrasound
Serum markers - AFP/HCG elevated b/c it’s a germ cell tumor
Seminomas - elevation in HCG
Non-seminomas - elevation in AFP
Treatment testicular cancer
Radical orchiectomy
Active surveillance or radiation therapy to para-aortic nodes (spreads via lymph) –> responds well to radiation
If stage II then radical LN dissection
REMEMBER TO TEACH YOUNG MALES A TESTICULAR EXAM!!! Might be question on that - at 12 YO + sports physical
Urinary obstructive sx of BPH
Hesitancy
Incomplete voiding (void, then have to go void again in 5 min)
Splitting of stream (have to valsalva to get pee out)
Dribbling
What do we worry about here? The effect on the kidneys of post-renal AKI for 20+ years accumulating - extra pressure on glomerulus - GET A CREATININE - don’t just send homeon tamsulzosin & say have a nice day
Dx & PE BPH
Dx: History, DRE, UA, serum Cr, urodynamic studies
DRE: Symmetrically large rubbery prostate
Increased serum Cr if kidney damage
Tx BPH
Alpha blockers (terazosin, doxazosin) –> Main ADR = HYPOTENSION - careful in old man who’s already on 5 anti-HTN meds!
5-alpha reductase inhibitors (finasteride) - suppresses testosterone so prostate won’t grow fast - can even shrink it - PSA should go down…if start on this & PSA goes up = prostate cancer
TURP = surgical intervention - indication = complete/worsening obstructive uropathy - if kidneys are dying, elevated Cr etc
Acute vs chronic prostatitis
Inflammation of prostate
Acute = bacterial Chronic = functional disorder, not well understood - no tx
Acute prostatitis etiology
Spontaneous = e. coli Sexual = Gonorrhea/Chlamydia Post-cath = pseudomonas
Pt almost always bacteremic & prostate is VERY difficult to penetrate w/ ABX :(
CP Acute bacterial prostatitis
Fever, chills, perineal pain, irritative voiding sx (dysuria, frequency), malaise, sitting on one butt cheek
Dx acute bacterial prostatits
Hx
Perineal exam (TTP)
UA - w/ C&S
Can have C&S w/ left shift
Which two PE are C/I if you suspect acute bacterial prostatitis?
PROSTATIC MASSAGE C/I
Instrumentation C/I (NO FOLEY)
Treatment of acute bacterial prostatitis
Hospitalize if +SIRS criteria - tx for sepsis, IV ABX, pain management
Outpatient - if looks good - 4-6 weeks oral therapy, oral fluids, analgesics, rest
Follow up of acute bacterial prostatitis
FOLLOW UP CULTURE AND SENSITIVITY FOR TEST OF CURE TO ENSURE ERADICATION
Etiology chronicn prostatitis
Unclear
CP chronic prostatitis
Pelvid & perineal pean w/ irritative voiding sx (dysurira, frequency) for at least THREE months
DRE nonspecific
Prostatic secretions - culture will be negative - massage okay in chronic
No effective treatment - DO NOT GIVE OPIOIDS
Prostate cancer RF, epidemiology & CP
MC men > 60 YO
RF: Increasing age, high-fat diet, family history, ethnicity (AA)
Second MCC men overall (behind skin cancer only)
Adenocarcinoma MC
CP: ASX in early disease!
Diseases where PSA is falsely elevated
Acute bac prostatitis BPH W/in 24 hours ejaculation AUR Motorcycles, bicycles, etc
If get high PSA, what should you do?
Should be repeated in 1-6 months
If greatly increased –> referral to urology
If the same –> you’re fine
Watchful waiting - have 10+ years before prostate CA becomes malignant
Is DRE recommended to screen for prostate CA?
No
DRE ARE NOT USED TO SCREEN FOR PROSTATE CA - you’re not going to find it with your friggin finger but if you do a DRE & incidentally feel unilateral enlargement then follow upon that b/c that’s cancer until proven otherwise…
PSA > 10 …. what to do?
PSA 4-10 …what to do?
PSA < 4 …what to do?
> 10: Biopsy (80% cancer rate)
4-10: Recheck/refer
<4 : Nothing b/c normal
Tx prostate cancer
If anticipated survival is < 10 years at time of dx - may want to just do surveillance - takes 1-+ years to become malignant
If anticipated survival is >10 years at time of dx - Robotic partial prostatectomy w/ cryosurgery, vs radiation vs surveillance
Metastatic prostate ca is treated with?
Leuprolide (Lupron)
GnRH antagonist - ADR osteoporosis, dec libido, ED, hot flashes
What labs should you check if a man is complaining of decreased libido?
Check prolactin - prolactinoma shutting down GnRH = no testosterone?
Check TSH - hypothyroidism = fatigue, weight gain, loss of libido
Check medications list - any that could be causing androgen deficiency?
Loss of orgasm?
SSRI
or
Psychological
Organic causes of ED?
Cardiovascular dz
DM
Medications (lasix, thiazide)
DO “stamp” or string test - men get erections in REM - put string around - if broke then had erection in REM & cause of ED is psychological
IF not broken then it is an organic (neurologic, cardiac, endocrine etc) cause of ED
ED meds
Sildenafil
Vardenafil
Tadalfil
MOA: ALpha-blockers = postural hypotension & dizziness
w/ nitrates = refractory hypotension
CP acute cystitis
Dysuria Urgency Frequency Suprapubic pain Hematuria LOW fever
Tx acute cystitis
HEALTHY young woman:
3-day course macrobid
Healthy young man (no epididymitis), children:
7-day course
Push fluids, urinary tract analgesic, consider post-coital abx tx
Note: ** If immunosuppressed then need LONGER than three day course!!! - 3-day course is for HEALTHY young woman only
Which pt population needs longer courses of abx for cystitis?
3-day course YOUNG HEALTHY FEMALE ONLY
7-day course in children, men (think longer urethra, longer course)
7-10 day course in PREGNANCY, DM, ANY immunosuppression, elderly, or if reccurences
Get culture for test of cure in pregnancy - #1 cause preterm labor is asx bacteruria
CP pyelonephritis
Fever, flank pain, arhtralgias, myalgias, anorexia, n/v, urinary irritative sx
Dx pyelo
CVAT
UA dipstick: Protein, LE, nitrates, Micro: WBC, bacteria
+ urine culture
+/- blood culture
CBC: Leukocytosis w/ left shift
ASSUME ALL PT W/ PYELO = BACTEREMIC - therefore need 10-14 day course of ABX!!!
ALL PREGNANT WOMEN W/ PYELO GET ADMITTED!!!
WBC casts are pathognomonic for Pyelo! You will NOT see casts in simple cystitis (inf only in bladder)
People who usually warrant inpatient admission for pyelo? & recommended tx regiman?
ALL pregnant women
Children
Acutely ill (meets SIRS)
TX: IV abx, consider IVP (esp if post-pyelo your Cr is still climbing - looks at physiologic fxn of kidneys), consider follow up C&S
ABX for Pyelo
ABX for pyelo in pregnancy
Use fluoroquinolone usually - levo, cipro x 14 days or bactrim
Remember macrobid ONLY reaches the bladder so you CANNOT use it for pyelo!!!!
Pregnancy:
FQ contraindicated, Bactrim not super safe…what to use?
IV ceftriaxone
What is the gold standard for dx of kidney stones?
IVP
What lab must you check in all pt w/ kidney stone and why is it so important to check?
Creatinine!!!
If stone is blocking ureter causing obstructive uropathy & pt only has one Can have non-functioning other kidney = TROUBLE = you MUST CHECK creatinine…
Cr should be NORMAL if have two functioning kidneys & other kidney takes over when one blocked by stone - IF…
PCKD or only one kidney - UROLOGY must come in & STENT plugged kidney immediately - pressure alone in renal pelvis (hydronephrosis) WILL DESTROY THE KIDNEY
What does an US evaluate in kidney stones
Looks for hydroureter or hydronephrosis!
Describe the kind of kidney stone that will likely pass without intervention?
Majority of stones pass w/in 48 hours - esp if DISTALLY located & < 6 mm
Therefore can usually treat outpatient w/ analgesia & hydration
UA, C&S, ABX if suspected infection - hydronephrosis, backup can cause infection fast
Indications for inpatient admission kidney stone?
Pain control
Refractory vomiting
Declining renal fxn
Needs intervention (stent, removal etc)
Epidemiology, RF, histo bladder carcinoma
MC malignancy of urinary tract
MC in OLD MEN
5th-7th decades
RF: SMOKING
Patho/histo: Transitional epithelium
CP bladder carcinoma
Hematuria …esp unexplained (r/o infection, nephritic glomerular dz, urolithiasis…)
Recurrent UTI in person who has never had them before
DX bladder carcinoma
R/o other causes hematuria –> infection, nephritic glomerular dz, urolithiasis…
CYSTOSCOPY
Epidemiology renal cell carcinoma
VERY rare
In OLD MALES
RF: advanced age, SMOKING, von hipple lindau disease
Histo: Adenocarcinoma of tubular epithelium
Asymptomatic hematuria…
you ruled out most causes - infection, nephritic glomerular disease, urolithiasis….
Got a cystoscopy which was normal….what next?
Could be renal cell carcinoma so get a CT of the ABD w/ retroperitoneal views
Diagnosis of renal cell carcinoma
CT
Management/prognosis of RCC?
Prog: If catch before invades renal capsule and renal artery then 90-100% 5-year survival rate after…but most pt present w/ advanced disease = 1-15% 5-year survival
Tx: Radical or partial nephrectomy
Post-op radiation therapy
Renal = RADICAL + RADIATION
Phimosis vs paraphimosis?
When foreskin can’t be retracted over the glans
Phimosis sounds like fibrosis – think of foreskin fibrosing around penile head, can’t retract
Para-phimosis - comes after you retract - para = foreskin has been left retracted & = painful enlargement and edema of the glans
What is the most common cause of priapism?
Esp in mediterranean or african american man?
SICKLE CELL CRISIS!!!
What precipitates a sickle cell crisis?!
Infection, hypoxia, hydration –> therefore give O2, IV fluids, find infection and pain control
CONSULT UROLOGY EARLY
What is the most important thing to remember with congenital defects of penile meatus (hypospadius, episapdius)?
DO NOT CIRCUMSIZE
Will need skin later if repaired
Urgent referral to urology if bad, elective referral if not so bad
Age distribution peyronie’s disease? Etiology?
BIMODAL - teenagers & old men
Acute inflammatory disease of the penis - associated with penile curvature
DOES NOT HURT - but it makes it hard to have intercourse so it’s called an erectile dysfunction disease
REFER TO UROLOGY
Most important thing to remember about cryptorchidism (2 things)
Must be repaired before 2 YO to prevent infertility
H/O increases risk of testicular CA EVEN IF you repair it surgically
Make sure it’s not just a retracted testicle before you call urology - if can pull down into sac then not cryptorchidism
Get an US to find where the testes is in the abdomen
Name two painless scrotal masses
Hydrocele (bag of water) - spontaneously resolves
Varicocele (bag of worms) - needs repair to improve fertility - usually the left, be more concerned if the right
Spermatocele CP/PE
Painless cystic mass in head of the epididymis (superior & posterior)
SEPARATE from the testicle, freely movable, TRANSILLUMINATES EASILY
No tx necessary
Hydrocele, varicocele, & spermatocele can all be confirmed on testicular ultrasound
First line tx priapsim
Phenylephrine injection into penis - it’s an alpha agonist so it causes vasoconstriction which increases venous outflow
CI in cardiac or cerebrovascular history
Terbutaline - reduces arterial inflow by restricting cavernosal artery - may be used if < 4 hours)
Needle aspiration - of corpora to remove flood if > 4 hours of duration - ice packs
Renal artery stenosis etiolgy, epidemiology
MCC primary RAS is atherosclerosis of renal artery
Rare: Women < 40 = fibromuscular dysplasia = abnormal development of fibrous collagen in smooth muscle = “string of beads” -appearing renal artery
MCC secondary RAS is HTN
If pt has resistant HTN or has a abd bruit…- you should be thinking of RAS
What is considered hemodynamically significant RAS, or RV-HTN?
Hemodynamically significant stenosis is defined by > 70% angiographic stenosis
Signs that a patient’s HTN may be secondary HTN due to RAS or another cause of secondary HTN
Refractory or severe HTN!!!
Age of onset < 30 YO or older than 55 YO - esp young female < 30 w/ severe HTN…something going on there! = FMD
Abrupt acceleration of HTN
Severe HTN in setting of generalized atherosclerosis
Systolic-diastolic bruit in the epigastrium
Flash pulmonary edema
Why should gadolinium be avoided in patient’s with renal dysfunction (GFR < 30) ?
Because it causes nephrogenic fibrosing dermopathy (NFD) and nephrogenic systemic fibrosis
What is considered the gold standard to confirm the diagnosis of hemodynamically-significant RAS?
Renal artery angiography - consider when definitive dx is required or considering an interventional procedure
Treatment of RAS?
Optimize HTN control - will probs need multiple drugs
Preserve renal fxn (ACEi)
Reduce CV events/athero - statin, aspirin
Treatments - medical therapy preferred (above), percutaneous renal angioplasty w/ or w/o stenting, renovascular bypass surgery
Which genetic disorder frequently has a horseshoe kidney?
Turner syndrome
Coarctation of aorta and horse-shoe kidney = most important structural anomalies in turner’s
Definition of enuresis
Primary monosymptomatic enureisis - distinct episodes of urinary incontinence while sleeping in children > 5 YO in absence of symptoms of infection
Management of enuresis
- Behavioral - Motivational therapy, education, reassurance, bladder training, voiding schedule, avoid caffeine & high sugar content, fluid restriction
- Enuresis alarm - if fail to respond to behavioral therapy
- Desmopression (DDAVP_ = used in nocturnal polyuria w/ nomral bladder fucntion capacity - short term only - it is synthetic ADH
Signs of overflow incontinence
Overflow incontinence = when you have bladder atony (underactive detrusor muscle) or bladder outlet obstruction (BPH)
Si/sx: Small volume voids, dribbling, frequency, POST-VOID RESIDUARL > 200 ml
Tx: Intermittent or indwelling catheter = 1st line
Cholinergics to increase detrusor muscle activity
Remember detrusor muscle is not the sphincter. Detrusor = smooth m. in wall - when relaxed allows bladder to fill, when squeezing - squeezes all urine out of bladder like hand squeezing water out of a balloon - that’s why “overactive bladder” AKA urger incontinence -you feel like you have to go all the time (urge) & nothing comes out - or you have small volume voids - where as overflow is opposite - bladder keeps filling & detrusor muscle does nothing - doesn’t squeeze urine out = post-void residuals & dribbling
What is the etiology of “urge” incontinence & sx?
Urine leakage accompanied or preceded by URGE to pee
Etiology - OVERACTIVE detrusor muscle or “overactive bladder” = constantly have urge to go - have small volume voids
Tx: bladder training, anticholinergics = decreased detrusor muscle activity (oxybutinin), or TCA like imipramine
What is the first line medical treatment for overactive bladder?
Oxybutynin = anticholinergic that decreases the overactive detrusor muscle activity
Stress incontinence
Increased abd pressure = urinary leakage (sneeze, cough, etc)
2/2 pelvic floor muscle weakness
Tx: Pelvic floor exercises = major improvement - meds can try alpha agonists like midodrine, pseudoephidrine = increased urethral sphincter tone
