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*PANCE by subspecialty > Nephrology/Urology > Flashcards

Nephrology/Urology Flashcards

1
Q

Most common cause of nephrotic syndrome in adults

A

Membranous nephropathy

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2
Q

Signs of a CHRONIC kidney problem

A

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

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3
Q

Kidney functions

A

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

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4
Q

What is Cr? Why is it used as a marker for kidney function?

A

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

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5
Q

Why is metabolic acidosis common in chronic renal failure?

A

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

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6
Q

Most common electrolyte abnormality & two main causes

A

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)

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7
Q

Management of hyponatremia caused by SIADH

A

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

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8
Q

What happens if you correct a low sodium too fast? What are si/sx of that?

A

Central pontine myelinolysis

AKA iatrogenic cerebellar swelling = BRAIN HERNIATION = BAD NEWS!!!!

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9
Q

Two main causes of hypernatremia?

A
  1. Diabetes insipidus - central (low ADH level) vs nephrogenic (kidney insensitivity to ADH- THINK DRUGS!!!)
  2. 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…

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10
Q

What would a urine sample look like if someone was peeing out large amounts of urine due to DI? Treatment?

A

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)

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11
Q

What is the type of patient who is at highest risk for developing central DI?

A

Someone post-head trauma or post-op

AKA neurosurg floor!

Remember posterior pituitary normally releases ADH

Central D. insipidus = IN-sufficient ADH

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12
Q

Causes of nephrogenic DI

A

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)

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13
Q

CP DI

A

Polyuria
Polydipsia
Nocturia (may manifest as enuresis in children)

Hypernatremia

Dehydration, hypotension

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14
Q

Name the two disorders of the posterior pituitary that cause disruptions in sodium and water balance?

A

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

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15
Q

Treatment hypernatremia 2/2 central DI

A

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)

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16
Q

What is the next test you order or look at if someone is hyponatremic?

A

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

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17
Q

Urine osmolarity low or high in DI?

Specific gravity low or high in DI?

A

LOW urine osmolarity (dilute) < 200

LOW specific gravity < 1.005

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18
Q

Causes of hyperkalemia

A

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

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19
Q

Treatment of hyperkalemia

A
  1. Stabilize cardiac membrane potential (give 1 amp of CaCO3 or CaCl)
  2. Move K+ into cells (D50% & 10 units insulin, bicarb (if acidotic will drive K+ into cells too)
  3. Increase excretion (Loop diuretic, kayexalate)

NOTE - IF K+ 7.5 b/c missed 2 days dialysis (ESRD) then TX = DIALYSIS not the above… DUH

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20
Q

Causes of hypokalemia

A

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

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21
Q

What should you always check next when you see a low K_?

A

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

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22
Q

MCC hypomagnesemia

A

Alcoholism

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23
Q

MCC hypermagnesemia

A

Chronic renal failure

remember that the Mg2+ does what the K+ does

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24
Q

Which treatment for constipation would you NOT want to give to a person with CKD, ESRD etc

A

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

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25
Q

In the absence of functioning kidneys, how fast does the Serum Cr rise each day?

A

Serum Cr rises by 1.0 - 1.5 each day

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26
Q

AKI causes

A

Ischemia
Nephrotic syndromes (minimal change, membranous nephropathy)
NSAIDs
Multiple myeloma

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27
Q

AKI mechanisms

A

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

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28
Q

Pre-renal causes of AKI/ARF

A

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

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29
Q

FENA in prerenal AKI

S. BUN/S. Cr in prerenal AKI

Urine SG in prerenal AKI

A

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)

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30
Q

FENA, urine SG, BUN/Cr in renal (intrinsic) AKI

A

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

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31
Q

Causes of intrinsic/intrarenal AKI

A

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

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32
Q

ATN - cause? FENA? Common in which patients?

A

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

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33
Q

1 cause of post-renal AKI

A

Prostate - BPH
Kidney stone (b/l or one kidney)
Pelvis masses/obstruction
Neurogenic bladder

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34
Q

Why is it important to quickly recognize urinary tract obstruction?

A

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)

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35
Q

CP bladder outlet obstruction

A 
Pain
Change in urine output
Hypertension
Hematuria
Increased serum creatinine

Palpate huge bladder - get US to confirm - CATH the patient & check serum Cr!

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36
Q

AIN - cause, CP/DX

A

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

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37
Q

What are tipoffs you’ll find in a question getting at acute interstitial nephritis?

A

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

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38
Q

Interstitial nephritis has what kind of casts?

A

WBC casts

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39
Q

Acute tubular necrosis has which kind of casts?

A

Muddy brown casts

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40
Q

Dehydration or pre-renal injury causes which kind of casts?

A

Hyaline casts

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41
Q

Does a normal urine have protein in it?

A

NO!!!

Nephrotic syndrome if dumping protein

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42
Q

Does a normal urine have fat or sugar in it?

A

NO

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43
Q

Does normal urine have heme in it?

A

NO

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44
Q

Does normal urine have RBCs in it?

A

NO

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45
Q

What is the definition of a nephrotic syndrome?

A

Injury to the glomerulus causing abnormal filtration 2/2 podocyte dysfunction - leads to heavy proteinuria, hypoalbuminemia, edema, hyperlipidemia, lipiduria

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46
Q

What is the definition of a nephritic syndrome?

A

Nephritic pattern/diseases are caused by Inflammation of the glomerular capillaries = hematuria, oliguria, HTN

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47
Q

Glomerular disease cause which kind of casts?

A

RBC casts - think of everything as inflamed

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48
Q

What will urine have in it if someone is in rhabdo?

A

Myoglobin! = myoglobinuria

Myoglobin is ACIDIC - so hydrate kidneys & give bicarb

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49
Q

Etio rhabdo, labs, treatment

A

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

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50
Q

Etio ESRD

A

Diabetes, HTN, Chronic GN, CKD, interstitial nephritis, obstructive uropathy, SLE, HIV

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51
Q

Nephritic patterns

A

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)

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52
Q

Glomerulonephritis

A

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

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53
Q

Nephrotic patterns - essentials of diagnosis

A

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!!!

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54
Q

What is a urine Protein:Cr ration concerning for nephrotic disease

A

a HIGH one (>300-350) - means you have a TON more protein than Cr in your urine = not normal

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55
Q

What is a common complication of nephrotic syndrome that is often overlooked?

A

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!!!

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56
Q

What is the “nephrotic” range on a urine dip for proteinuria?

A

3-4+ protein on urine dip = nephrotic range

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57
Q

Cause of primary nephrotic syndrome = idiopathic or one of several glomerulonephropathies

What causes secondary nephrotic syndrome?

A

1/3 of adults with nephrotic syndrome have a systemic disease such as SLE, DM, HIV, cancer, or amyloidosis

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58
Q

Treatment nephrotic syndrome

A

ACEI - dec proteinuria
Low salt diet
Diuretics - dec edema
Statins - dec lipids

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59
Q

Definition of CKD

A

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

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60
Q

Uremic syndrome

A

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

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61
Q

Complications of progressive chronic kidney disease

A

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

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62
Q

What would cause a false positive for hematuria?

A

Myoglobinuria - causes dark urine but it’s not RBCs

Hemolysis

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63
Q

Causes of hematuria

A

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)

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64
Q

Types of glomerulonephritis

A

IgA - MC worldwide
HSP
PSGN
Goodpastures

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65
Q

What would glomerular intrinsic AKI labs look like?

A

Hematuria, RBC casts, azotemia, proteinuria (not a ton), HTN (not severe)

Tx: High-dose corticosteroids

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66
Q

What is the role of ACEi in CKD?

A

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

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67
Q

What is Entresto (sacubitril/valsartan)?

Meaning indications, MOA etc

A

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

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68
Q

Definition of CKD

A

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

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69
Q

In which patient populations should you be most worried about CKD?

A

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

70
Q

What drugs should people with CKD be on to prevent the progression of the CKD?

A

ACEi - renally protective

Consider SGLT2 if DM b/c delay progression of CKD & have diuresing effect

71
Q

Who gets minimal change disease?

A

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)

72
Q

Who gets membranous nephropathy?

A

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)

73
Q

Clinical manifestations of nephritic glomerular disease & examples of nephritic diseases

A

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,

74
Q

MCC acute glomerulonephritis worldwide, epidemiology, CP

A

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

75
Q

3 weeks after sore throat, young boy complaining of dark scanty urine …. = ?

A

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

76
Q

What is goodpasture’s disease? How does it present?

A

= 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

77
Q

Tx for any rapidly progressing acute glomerulonephritis

A

High dose IV corticosteorids

Cyclophosphamide

78
Q

List all forms of acute glomerulonephritis & the two that most likely present as rapidly progressing AGN

A

IgA nephrophathy (Berger’s)
Post-infectious (PSGN)
Membranoproliferative (SLE)

RPAGN:
Goodpasture’s disease
Vasculitides (MPA, Wegener’s )

79
Q

Which two vasculitides can presents with rapidly progressing acute glomerulonephritis?

A

**Both have lack of immune deposits and POSTIVE ANCA ANTIBODIES

Microscopic polyangitis:
+ P-ANCA

Granulomatosis with polyangitis (Wegener’s):
+ C-ANCA

80
Q

What is an important pattern to recognize with glomerular kidney disease (nephrotic and nephritic?)

A

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

81
Q

What is the most common cause of nephrotoxic acute tubular necrosis?

A

Remember ATN is either ischemic (worsening AKI –> ischemia –> necrosis) or nephrotoxic meaning something directly damaged the kidneys

The MCC nephrotoxic ATN is aminoglycosides

82
Q

What are the three most common causes of vascular (micro and macro) intrinsic AKI?

A

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

83
Q

Fatty casts AKA “maltese crosses” or oval fat bodies are pathognomonic for which disease?

A

Nephrotic syndrome

Nephrotic syndrome = HLD b/c need protein to transport fat back to liver - end up with fat in urine

84
Q

Adult Polycystic kidney disease - epidemiology & etiology

A

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

85
Q

Renal clinical manifestations of PCKD

A

Abdominal/flank pain (2/2 bleeding into cyst or nephrolithiasis or infection)

Palpable flank mass - large palpable kidneys on exam

HTN, hematuria, microalbuminuria

86
Q

Ddx HTN, hematuria, microalbimuria

A

Nephrotic syndrome
Nephritic syndrome
PCKD

87
Q

Extrarenal CP of PCKD

A

Cerebral “berry” aneurysms

Hepatic cysts

MVP

Colonic diverticula

88
Q

Dx & TX PCKD

A

Dx: renal ultrasound, genetic testing

Tx:
Simple - observe, ACEi for HTN
Multiple - Supportive (inc fluid intake), control HTN, +/- dialysis or renal transplant

89
Q

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?

A

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

90
Q

What’s the firs thing you think when someone comes in w/ BP 170/110

A

What’s pissing off the kidney? Most causes of HTN are from kidney secreting renin to increase renal perfusion

91
Q

MC site of mets w/ Wilms tumor?

A

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

92
Q

Indications for dialysis?

A

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

93
Q

Signs/symptoms of mild uremia –> severe uremia…

A

Vague sx - fatigue, forgetful, change in sleep

Then N/V

Then weight loss & AMS

Then pericarditis & full on encephalitis

94
Q

MCC acute orchitis

A

Mumps

Note: Mumps parotitis preceeds the onset of mumps orchitis by 3-10 days

Etio: paramyxovirus - para-myxo = para-tid gland inf

95
Q

CP & PE epididymitis

A

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

96
Q

Dx epididymitis

A

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

97
Q

Etiology epididymitits

A

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)

98
Q

Tx Epididymitis

A

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

99
Q

Length of treatment for bacterial orchitis

A

30+ day treatment

100
Q

What is the “blue dot sign”? When is it seen?

A

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

101
Q

Average age testicular torsion?

A

65% occur in pubertal teenagers 10-20 YO

102
Q

Average age appendiceal torsion?

A

7-12 YO boy

103
Q

CP & PE testicular torsion

A

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)

104
Q

Dx/workup torstion

A

STAT DOPPLER US

CALL UROLOGY = EMERGENCY

Immediate intervention to detorse & BILATERAL orchipexy (if one gubernaculum missing, other probably missing/loose too)

105
Q

Testicular cancer risk factors

A

Adolescent

Cryptorchidism - surgical intervention does not reduce risk

106
Q

CP testicular cancer

A

15-35 YO Male w/

Painless testicular mass - palpable, firm, irregular

107
Q

Diagnosis testicular cancer

A

Ultrasound

Serum markers - AFP/HCG elevated b/c it’s a germ cell tumor

Seminomas - elevation in HCG
Non-seminomas - elevation in AFP

108
Q

Treatment testicular cancer

A

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

109
Q

Urinary obstructive sx of BPH

A

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

110
Q

Dx & PE BPH

A

Dx: History, DRE, UA, serum Cr, urodynamic studies

DRE: Symmetrically large rubbery prostate

Increased serum Cr if kidney damage

111
Q

Tx BPH

A

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

112
Q

Acute vs chronic prostatitis

A

Inflammation of prostate

Acute = bacterial 
Chronic = functional disorder, not well understood - no tx
113
Q

Acute prostatitis etiology

A 
Spontaneous = e. coli 
Sexual = Gonorrhea/Chlamydia
Post-cath = pseudomonas

Pt almost always bacteremic & prostate is VERY difficult to penetrate w/ ABX :(

114
Q

CP Acute bacterial prostatitis

A

Fever, chills, perineal pain, irritative voiding sx (dysuria, frequency), malaise, sitting on one butt cheek

115
Q

Dx acute bacterial prostatits

A

Hx
Perineal exam (TTP)
UA - w/ C&S

Can have C&S w/ left shift

116
Q

Which two PE are C/I if you suspect acute bacterial prostatitis?

A

PROSTATIC MASSAGE C/I

Instrumentation C/I (NO FOLEY)

117
Q

Treatment of acute bacterial prostatitis

A

Hospitalize if +SIRS criteria - tx for sepsis, IV ABX, pain management

Outpatient - if looks good - 4-6 weeks oral therapy, oral fluids, analgesics, rest

118
Q

Follow up of acute bacterial prostatitis

A

FOLLOW UP CULTURE AND SENSITIVITY FOR TEST OF CURE TO ENSURE ERADICATION

119
Q

Etiology chronicn prostatitis

A

Unclear

120
Q

CP chronic prostatitis

A

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

121
Q

Prostate cancer RF, epidemiology & CP

A

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!

122
Q

Diseases where PSA is falsely elevated

A 
Acute bac prostatitis 
BPH 
W/in 24 hours ejaculation 
AUR 
Motorcycles, bicycles, etc
123
Q

If get high PSA, what should you do?

A

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

124
Q

Is DRE recommended to screen for prostate CA?

A

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…

125
Q

PSA > 10 …. what to do?

PSA 4-10 …what to do?

PSA < 4 …what to do?

A

> 10: Biopsy (80% cancer rate)

4-10: Recheck/refer

<4 : Nothing b/c normal

126
Q

Tx prostate cancer

A

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

127
Q

Metastatic prostate ca is treated with?

A

Leuprolide (Lupron)

GnRH antagonist - ADR osteoporosis, dec libido, ED, hot flashes

128
Q

What labs should you check if a man is complaining of decreased libido?

A

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?

129
Q

Loss of orgasm?

A

SSRI

or

Psychological

130
Q

Organic causes of ED?

A

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

131
Q

ED meds

A

Sildenafil
Vardenafil
Tadalfil

MOA: ALpha-blockers = postural hypotension & dizziness

w/ nitrates = refractory hypotension

132
Q

CP acute cystitis

A 
Dysuria
Urgency 
Frequency
Suprapubic pain 
Hematuria
LOW fever
133
Q

Tx acute cystitis

A

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

134
Q

Which pt population needs longer courses of abx for cystitis?

A

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

135
Q

CP pyelonephritis

A

Fever, flank pain, arhtralgias, myalgias, anorexia, n/v, urinary irritative sx

136
Q

Dx pyelo

A

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)

137
Q

People who usually warrant inpatient admission for pyelo? & recommended tx regiman?

A

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

138
Q

ABX for Pyelo

ABX for pyelo in pregnancy

A

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

139
Q

What is the gold standard for dx of kidney stones?

A

IVP

140
Q

What lab must you check in all pt w/ kidney stone and why is it so important to check?

A

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

141
Q

What does an US evaluate in kidney stones

A

Looks for hydroureter or hydronephrosis!

142
Q

Describe the kind of kidney stone that will likely pass without intervention?

A

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

143
Q

Indications for inpatient admission kidney stone?

A

Pain control
Refractory vomiting
Declining renal fxn
Needs intervention (stent, removal etc)

144
Q

Epidemiology, RF, histo bladder carcinoma

A

MC malignancy of urinary tract

MC in OLD MEN

5th-7th decades

RF: SMOKING

Patho/histo: Transitional epithelium

145
Q

CP bladder carcinoma

A

Hematuria …esp unexplained (r/o infection, nephritic glomerular dz, urolithiasis…)

Recurrent UTI in person who has never had them before

146
Q

DX bladder carcinoma

A

R/o other causes hematuria –> infection, nephritic glomerular dz, urolithiasis…

CYSTOSCOPY

147
Q

Epidemiology renal cell carcinoma

A

VERY rare

In OLD MALES

RF: advanced age, SMOKING, von hipple lindau disease

Histo: Adenocarcinoma of tubular epithelium

148
Q

Asymptomatic hematuria…

you ruled out most causes - infection, nephritic glomerular disease, urolithiasis….

Got a cystoscopy which was normal….what next?

A

Could be renal cell carcinoma so get a CT of the ABD w/ retroperitoneal views

149
Q

Diagnosis of renal cell carcinoma

A

CT

150
Q

Management/prognosis of RCC?

A

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

151
Q

Phimosis vs paraphimosis?

A

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

152
Q

What is the most common cause of priapism?

Esp in mediterranean or african american man?

A

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

153
Q

What is the most important thing to remember with congenital defects of penile meatus (hypospadius, episapdius)?

A

DO NOT CIRCUMSIZE

Will need skin later if repaired

Urgent referral to urology if bad, elective referral if not so bad

154
Q

Age distribution peyronie’s disease? Etiology?

A

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

155
Q

Most important thing to remember about cryptorchidism (2 things)

A

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

156
Q

Name two painless scrotal masses

A

Hydrocele (bag of water) - spontaneously resolves

Varicocele (bag of worms) - needs repair to improve fertility - usually the left, be more concerned if the right

157
Q

Spermatocele CP/PE

A

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

158
Q

First line tx priapsim

A

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

159
Q

Renal artery stenosis etiolgy, epidemiology

A

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

160
Q

What is considered hemodynamically significant RAS, or RV-HTN?

A

Hemodynamically significant stenosis is defined by > 70% angiographic stenosis

161
Q

Signs that a patient’s HTN may be secondary HTN due to RAS or another cause of secondary HTN

A

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

162
Q

Why should gadolinium be avoided in patient’s with renal dysfunction (GFR < 30) ?

A

Because it causes nephrogenic fibrosing dermopathy (NFD) and nephrogenic systemic fibrosis

163
Q

What is considered the gold standard to confirm the diagnosis of hemodynamically-significant RAS?

A

Renal artery angiography - consider when definitive dx is required or considering an interventional procedure

164
Q

Treatment of RAS?

A

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

165
Q

Which genetic disorder frequently has a horseshoe kidney?

A

Turner syndrome

Coarctation of aorta and horse-shoe kidney = most important structural anomalies in turner’s

166
Q

Definition of enuresis

A

Primary monosymptomatic enureisis - distinct episodes of urinary incontinence while sleeping in children > 5 YO in absence of symptoms of infection

167
Q

Management of enuresis

A
  1. Behavioral - Motivational therapy, education, reassurance, bladder training, voiding schedule, avoid caffeine & high sugar content, fluid restriction
  2. Enuresis alarm - if fail to respond to behavioral therapy
  3. Desmopression (DDAVP_ = used in nocturnal polyuria w/ nomral bladder fucntion capacity - short term only - it is synthetic ADH
168
Q

Signs of overflow incontinence

A

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

169
Q

What is the etiology of “urge” incontinence & sx?

A

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

170
Q

What is the first line medical treatment for overactive bladder?

A

Oxybutynin = anticholinergic that decreases the overactive detrusor muscle activity

171
Q

Stress incontinence

A

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

*PANCE by subspecialty (22 decks)

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