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432 Cards in this Set

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Hypernatremia is most commonly due to what?
water loss
The 6D's of Hypernatremia
(6 Causes)
Diuresis
Dehydration
DI
Docs (iatrogenic)
Diarrhea
Disease (eg kidney, sickle cell)
What are the physical exam findings of hypernatremia?
thirst (due to hypertonicity)
oliguria
"doughy" skin
signs of volume depletion
What are the neurological symptoms of hypernatremia?
mental status changes
weakness
focal neurologic deficits
seizures
How do you assess volume status?
measure urine volume and osmolality
Hypernatremia can be due to
1 - pure water loss
2 - hypotonic fluid loss
3 - hypertonic Na+ gain

Describe causes of each.
1 - Pure water loss
central or nephrogenic DI (large vol of dilute urine)
insensible losses (dermal and respiratory)

2 - hypotonic fluid loss
decreased intake
diuretics / osmotic diuresis (mannitol, glucose in DKA, urea with high protein feeds)
intrinsic renal disease / diarrhea / burns

3 - hypertonic Na+ gain
hypertonic saline or tube feeds
increased aldosterone (suppresses ADH)
What is the minimum volume of maximally concentrated urine that you need to produce each day?
500 mL/day
(> 800 mOsm/kg)

this suggests adequate renal response without adequate free-water replacement
Tx for hypernatremia
treat underlying cause
replace free-water deficit with hypotonic saline/D5W/PO water
How fast should you correct hypernatremia?
gradually over 48-72 hours
< 0.5 mEq/L/hr
What happens when you correct hypernatremia too fast?
cerebral edema
(causes neurologic damage)
What is hyponatremia almost always due to?
increased ADH
Hypervolemic hyponatremia is caused by 3 things:
nephrOSIS
cirrhOSIS
cardiOSIS
nephrotic syndrome causes proteinuria

hypoalbuminemia leads to decreased oncotic pressure, causing fluids to third space

this causes sodium and water retention, water >> sodium
Neurologic findings of hyponatremia
confusion
lethargy
Physical findings and sx of hyponatremia
muscle cramps
hyporeflexia
nausea
Consequences of not treating hyponatremia
sz
coma
brain stem herniation
Normal serum osmolality?
280-295 mEq/L

other places:
275-295
Causes of high osmolality hyponatremia
hyperglycemia
hypertonic infusion (eg mannitol)
Causes of normal osmolality hyponatremia
hypertriglyceridemia
paraproteinemia (pseudohyponatremia)
Causes of low osmolality hyponatremia
Depends on volume status
(ie hypervolemic, euvolemic, hypovolemic)
What are two ways to categorize hyponatremia?
volume status
serum/urine osmolality
Causes of hypotonic hyponatremia

Volume Status:
hypervolemic
renal failure
nephrotic syndrome
cirrhosis
CHF
hypothyroidism
2nd/3rd adrenal insufficiency
these pts have peripheral edema

intravascularly, they are volume depleted, but the fluid has third spaced and in dependent areas

this reduced vascular blood volume is a potent stimulus for ADH, causing hyponatremia

also, the water AND sodium that is retained from renal failure leads to hypervolemia and edema
Causes of hypotonic hyponatremia

Volume Status:
euvolemic
SIADH
renal failure
drugs
psychogenic polydipsia
oxytocin use
Causes of hypotonic hyponatremia

Volume Status:
hypovolemic
Loss of water is accompanied by loss of sodium --> leads to low volume.

EXTRARENAL LOSS (UNa < 10)
vomiting
diarrhea
bleeding
third spacing
dehydration

URINARY LOSS (UNa > 20)
DKA
primary adrenal insufficiency
diuretics (esp thiazides)
Tx for hypotonic hyponatremia

Volume Status:
hypovolemic
replete volume w/normal saline
Tx for hypotonic hyponatremia

Volume Status:
euvolemic
water restriction
Tx for hypotonic hyponatremia

Volume Status:
hypervolemic
water restriction
consider diuretics
cortisol replacement w/adrenal insuff
thyroid replacement w/hypothyroidism
Correct hyponatremia slowly at what rate and why?
<= 0.5 mEq/L/hr

to prevent central pontine myelinolysis
Sx of correcting hyponatremia too fast
central pontine myelinolysis

paraparesis/quadriparesis
dysarthria
coma
Normal serum potassium?
3.5 to 5.5 mEq/L
Mechanisms behind hyperkalemia:
CELLULAR SHIFTS
(give examples)
cell lysis
rhabdomyolysis / tissue injury
insulin deficiency
acidosis

drugs
(succinylcholine, digitalis, arginine, beta-blockers)

exercise
Mechanisms behind hyperkalemia:
DECREASED EXCRETION
renal insufficiency
hypoaldosteronism
Type IV RTA

drugs
(spironolactone, triamterene, ACE-I, trimethoprim, NSAIDs)
Mechanisms behind hyperkalemia:
SPURIOUS
hemolysis of blood samples
fist clenching during blood draws
delays in sample analysis
extreme leukocytosis
thrombocytosis
Physical exam findings of hyperkalemia
intestinal colic
areflexia
weakness

others:
flaccid paralysis
paresthesias
n/v
Diagnosis of Hyperkalemia
first, confirm it with a repeat blood draw

ECG
EKG of Hyperkalemia
tall, peaked T waves
wide QRS
prolonged PR
low/loss of P waves
Hyperkalemia can lead to what cardiac problems?
sine waves
v fib
asystole (eg cardiac arrest)

NOTE: sine waves is caused by the merging of QRS and T waves --> leads to v fib
Tx of Hyperkalemia

C BIG K
Calcium
Bicarbonate
Insulin
Glucose
Kayexalate
When should you treat hyperkalemia?
when > 6.5 mEq/L

or

EKG changes
(prolonged PR, wide QRS)
How long is prolonged PR?
> 200 ms

Normal: 120 to 200 ms
How long is wide QRS?
> 120 ms or > 3 boxes

Normal: roughly 3 box or 120 ms
what is calcium gluconate for?
stabilize the cardiac cell membrane
why give bicarbonate and/or insulin and glucose to hyperkalemia patients?
to temporarily shift potassium into cells
why give beta agonists to treat hyperkalemia?

name one
promote cellular reuptake of potassium

albuterol
what is kayexalate?
binds to potassium in gut to prevent K+ from being absorbed
Na+/K+ ATPase

what is it for?
helps maintain resting potential
3 sodiums out / 2 potassiums in


in neurons
2/3 of cells energy expenditure goes to this pump

in regular cells
1/3
last resort for hyperkalemia
dialysis

esp if pt has renal failure or refractory
hypokalemia is usually due to what?
renal or GI losses
explain the interaction between potassium and digitalis
they both compete for the same site on Na/K pump

so watchout for hypokalemia
causes of hypokalemia

TRANSCELLULAR SHIFTS
Potassium is shifted into cells by:

insulin
b2-agonist
alkalosis
familial hypokalemic periodic paralysis
causes of hypokalemia

GI LOSSES
diarrhea
chronic laxative abuse
vomiting
NG suction
causes of hypokalemia

RENAL LOSSES
diruetics (eg loop or thiazides)
primary mineralocorticoid excess
secondary hyperaldosteronism
decreased circulating volume
Bartter's and gitelman's syndrome

drugs (eg gentamicin, amphotericin)
DKA
hypomagnesemia
Type I RTA
polyuria
what is Type I RTA
defective distal H+/K+ antiporter

proton retention / potassium wasting
(acidemia and hypokalemia)
sx of hypokalemia
muscle weakness
cramps
ileus (hypomotility = small bowel obsxn)
fatigue
signs of hypokalemia
hypotension
hyporeflexia
paresthesias
rhabdomyolysis
ascending paralysis
how to diagnosis hypokalemia?
24-hr or spot urine potassium

to see if its coming thru urine (Type I RTA)

(this distinguishes renal from GI losses --> diarrhea)
ekg of hypokalemia
T-wave flattening
U waves (additional wave after T wave)
ST depression
AV block
asystole (cardiac arrest)
hypokalemia in the setting of metabolic acidosis
consider Type 2 Proximal RTA

cannot reabsorb bicarb in proximal tubules
tx for hypokalemia
tx underlying d/o

replete potassium PO/IV
replete magnesium too
(bc magnesium def interferes with K repletion)
what is the recommended rate of potassium repletion?
no more than 20 mEq/L/hr
normal serum calcium levels
9-10.5 mg/dL
most common cause of hypercalcemia
hyperparathyroidism
malignancy
(eg breast cx, squamous cell cx, multiple myeloma)
causes of hypercalcemia

CHIMPANZEES
Calcium supplements
Hyperparathyroidism / Hyperthyroidism
Iatrogenic (ie thiazides, parenteral nutrition) / Immobility
Milk-alkali syndrome
Paget's disease
Adrenal insuff / Acromegaly
Neoplasm
Zollinger-Ellison Syn (eg MEN 1)
Excess Vit A
Excess Vit D
Sarcoidosis / other granulomatous dis
how is hypercalcemia usually diagnosed
routinely on labs
signs and sx of hypercalcemia
BONES - osteopenia, fractures

STONES - kidney stones

GROANS - abdominal, anorexia, constipation

PSYCHIATRIC OVERTONES - weakness, fatigue, AMS
diagnostic w/u for hypercalcemia
total/ionized calcium
albumin
phosphate
PTH
PTHrP
Vit D

EKG
EKG for hypercalcemia
short QT

(normal QTc < 0.40 sec)
whats the diff between total and ionized calcium?
total calcium is most frequently ordered on BMP and CMP

In most cases, it is a good reflection of the amount of free calcium present in the blood since the balance between free and bound is usually stable and predictable. However, in some people, the balance between bound and free calcium is disturbed and total calcium is not a good reflection of calcium status

so order ionized calcium
main form of tx for hypercalcemia
IV hydration with furosemide to increase calcium excretion

(loop)
do you want to give thiazide diuretics to hypercalcemic pts?
NO

thiazides cause calcium reabsorption
lesser forms of tx for hypercalcemia
calcitonin
bisphosphonates (eg pamidronate)
GC
calcimetics
dialysis (severe/refractory cases)
which one excretes calcium?

loops or thiazides
LOOPS LOSE CALCIUM
cramps + tetany + thyroidectomy
hypocalcemia
causes of hypocalcemia in adults
hypoparathyroidism (postsurgical, idiopathic)
malnutrition
hyypomagnesemia
acute pancreatitis
Vit D deficiency
pseudohypoparathyroidism
causes of hypocalcemia in pediatrics
DiGeorge's syndrome

tetany shortly after birth
absence of thymic shadow
(lateral CXR shows absence of density in the anterior mediastinum)
signs and sx of hypocalcemia
abdominal muscle cramps
tetany
perioral and acral (limbs) paresthesias
(Paresthesias = tingling, burning, numbness, aka "pins and needles")

others:
dyspnea
convulsions
physical exam maneuvers to check for severe hypocalcemia
Chvostek's sign
tap facial nerve --> facial spasm

Trousseau's sign
carpal spasm after arterial occlusion by a BP cuff
serum calcium may be falsely low in hypoalbuminemia

do what?
check ionized calcium
diagnostic w/u for hypocalcemia
ionized Ca2+
Mg+
PTH
albumin
(maybe calcitonin)
EKG of hypocalcemia
prolonged QT

(Normal: QTc < 0.40 sec)
tx for hypocalcemia
treat underlying d/o
replete mag
ORAL calcium supplements
(IV for severe)
which pt population most commonly has hypomagnesemia
alcoholics
normal mag level
1.5 - 2.5 mg/dL
causes of hypomagnesemia
DECREASED INTAKE
malnutrition
malabsoprption
short bowel syndrome
TPN

INCREASED LOSS
diuretics
diarrhea
vomiting
hypercalcemia
drugs (eg aminoglycosides, amphotericin)
alcoholism
kidney losses (eg recovering ATN, postobstructive diuresis)

MISC
DKA
pancreatitis
extracellular fluid volume expansion
signs and sx of hypomagnesemia
N/V
anorexia
muscle cramps
weakness
hypomagnesemia usually doesnt happen in isolation, it usually happens with:
hypocalcemia and hypokalemia
signs and sx of severe hypomagnesemia
hyperactive reflexes
tetany
paresthesias
irritability
confusion
lethargy
sz
arrhythmias
labs on hypomagnesemia
shows concurrent hypocalcemia and hypokalemia
EKG of hypomagnesemia
prolonged PR and QT
tx for hypomagnesemia
IV and PO supplements
why is it important to correct hypomagnesia
bc hypokalemia and hypocalcemia will not correct without magnesium correction
what acid-base d/o can aspirin cause
BOTH
metabolic acidosis
respiratory alkalosis
if an asthmatic pt's blood gas goes from alkalotic to normal, what are you thinking?
respiratory muscle fatigue --> urgent intubation
increased anion gap metabolic acidosis caused by

MUDPILES
Methanol
Uremia
DKA
Paraldehyde
Intoxication
Lactic acidosis
Ethylene glycol
Salicylates
pH > 7.4
pCO2 < 40 mmHG
respiratory alkalosis
pH > 7.4
PCO2 > 40 mmHG

name 4 causes
metabolic alkalosis w/comp

vomiting
diuretic use
antacid use
hyperaldosteronism
pH < 7.4
PCO2 > 40 mmHG
respiratory acidosis
pH < 7.4
pCO2 < 40 mmHG
metabolic acidosis w/comp

compensation by hyperventilation to decrease pCO2
common causes of metabolic alkalosis
vomiting
diuretic use
antacid use
hyperaldosteronism
common causes of respiratory acidosis
hypoventilation:

acute or chronic lung disease
opioids / narcotics / sedatives
weakening of respiratory muscles
common causes of respiratory alkalosis
hyperventilation
aspirin ingestion (early)
common causes of metabolic acidosis w/comp
depends on anion gap
common causes of metabolic acidosis w/comp

high anion gap
renal failure
lactic acidosis
DKA
aspirin ingestion
common causes of metabolic acidosis w/comp

normal anion gap
diarrhea
glue sniffing
RTA
hyperchloremia
TYPE 1 RTA

Defect
defective H/K antiporter

cannot secret acid (H+)
cannot reabsorb K+

collecting ducts
TYPE 1 RTA

Serum K+
hypokalemia

cannot secrete H+, so K+ cannot be reabsorbed
TYPE 1 RTA

Urinary pH
> 5.3
TYPE 1 RTA

treatment
potassium citrate
TYPE 1 RTA

complications
nephrolithiasis
TYPE 1 RTA

most common causes
hereditary
cirrrhosis
autoimmune d/o (Sjogrens, SLE)
hypercalciuria
sickle cell dis
drugs (lithium, amphotericin)
TYPE 2 RTA

Defect
cannot reabsorb bicarb

proximal tubules
TYPE 2 RTA

Serum K+
low
TYPE 2 RTA

Urinary pH
5.3 initially
< 5.3 once serum is acidic
TYPE 2 RTA

most common causes
hereditary (Fanconi's, Cystinosis)
drugs (carbonic anhydrase inhib)
multiple myeloma
amyloidosis
heavy metal poisoning
Vit D def
TYPE 2 RTA

Treatment
Potassium Citrate
TYPE 2 RTA

Complications
Rickets
Osteomalacia
TYPE 4 RTA

Defect
aldosterone deficiency or resistance leading to defective ammonium excretion, that causes impaired reabsorption of Na+ and excretion of H+ and K+

proximal tubules

1 - not actually a tubular disease
2 - its actually a physiological response
TYPE 4 RTA

Serum K+
HIGH
*remember this*
all the other RTA's are low K+
TYPE 4 RTA

Urinary pH
< 5.3
TYPE 4 RTA

most common causes
Primary aldosterone deficiency
hyporeninemic hypoaldosteronism (eg from kidney dis, ACE-I, NSAIDs)
drugs (eg amiloride, spironolactone, heparin)
pseudohypoaldosteronism
TYPE 4 RTA

Treatment
furosemide
mineralocorticoid
+/- GC replacement
low-potassium diet in pts with aldosterone def
TYPE 4 RTA

Complications
hyperkalemia
*remember this*

the other RTAs are low K+
Causes of Pre-Renal AKI
Hypovolemia (hemorrhage, dehydration, burns)
Cardiogenic shock (decreased CO)
Systemic Vasodilation (sepsis, burns)
Anaphylaxis
Drugs (ACE-I, ARBs, NSAIDs)
Renal Artery Stenosis
Cirrhosis w/ascites (hepatorenal syndrome)
Causes of Intrinsic-Renal AKI
ATN
AIN
Glomerulonephritis
Thromboembolism
Renovascular Disease (HUS/TTP, scleroderma)
Causes of Post-Renal AKI
Prostatic Disease
Nephrolithiasis
Pelvic Tumors
Recent Pelvic Surgery
Retroperitoneal Fibrosis
AKI does what to BUN and Cr levels?
elevated BUN and Cr
what is uremia
build up of urea
(nitrogenous compounds)


(do not confuse with uricemia which is a build up of uric acid)
whats another word for uremia
azotemia

(high levels of urea)
sx of uremia
malaise
fatigue
confusion
oliguria
anorexia
nausea
physcial findings of uremia
pericardial rub
asterixis
HTN
what is the respiratory rate of a pt with AKI
increased respiration rate

compensation of METABOLIC ACIDOSIS
or
pulmonary edema secondary to VOLUME OVERLOAD
sx of prerenal AKI
thirst
orthostatic hypotension
tachycardia
decreased skin turgor
dry mucous membranes
reduced axillary sweating
stigmata of comorbid conditions
sx of intrinsic-renal AKI
pt has hx of drug exposure (aminoglycosides, NSAIDs)
infection
exposure to IV contrast or toxins (myoglobin, myeloma protein)

hematuria or tea-colored urine
foamy urine (from proteinuria)
HTN
edema
sx of athero-emboli AKI
subcutaneous nodules
livedo reticularis (vascular condition, purplish mottling of skin)
digital ischemia
sx of post-renal AKI
prostatic disease
decrease UOP leading to suprapublic pain
distended bladder
flank pain
FeNa < 1%

what does it indicate
where's the etiology
(pre, intrin, post)
indicates
kidneys are trying to conserve sodium

prerenal
Pre-Renal AKI

what are the values for:
FeNa
Urine Na
Urine Sp Gravity
BUN/Cr Ratio
FENA < 1%
UNa < 20
U Sp Gravity > 1.020
BUN/Cr > 20
what are ways to r/o obstruction in post-renal AKI
urinary catheter and renal US
URINE SEDIMENT
Hyaline Casts

pre, intrinsic or post?
prerenal
URINE SEDIMENT
Red Casts

pre, intrinsic or post?
Intrinsic
URINE SEDIMENT
Dysmorphic Red Cells

pre, intrinsic or post?
intrinsic
URINE SEDIMENT
White cells

pre, intrinsic or post?
EITHER
intrinsic or post-renal
URINE SEDIMENT
Eosinophils

pre, intrinsic or post?
intrinsic
URINE SEDIMENT
Granular casts

pre, intrinsic or post?
intrinsic
URINE SEDIMENT
renal tubular cells / muddy brown casts

pre, intrinsic or post?
intrinsic
URINE SEDIMENT
Dysmorphic Red Cells

etiology?
glomerulonephritis
URINE SEDIMENT
hyaline casts

etiology?
normal finding

but an increase might suggest volume depletion or vigorous exericse
hyaline casts are solidified Tamm-Horsfall mucoprotein secreted from the tubular epithelial cells of individual nephrons

Low urine flow, concentrated urine, or an acidic environment can contribute to the formation of hyaline casts
URINE SEDIMENT
Red casts

etiology?
Glomerulonephritis
URINE SEDIMENT
White cells

etiology?
AIN
Pyelonephritis
Athero-embolic disease
URINE SEDIMENT
Eosinophils

etiology?
AIN
Athero-embolic disease
URINE SEDIMENT
granular casts

etiology?
ATN
URINE SEDIMENT
renal tubular cells / muddy-brown casts

etiology?
ATN
FENA and BUN/Cr helps to distinguish between which two?

pre, intrinsic, post
pre and intrinsic
if intrinsic renal disease is unclear, clarify with what test?
renal bx
tx for AKI
avoid nephrotoxic drugs
dialyze if indicated
Indications for urgent dialysis

AEIOU
Acidosis
Electrolyte abnormalities (hyperkalemia)
Ingestions (salicylates, theophylline, methanol, barbiturates, lithium, ethylene glycol)
Overload (fluid)
Uremic sx (pericarditis, encephalopathy, bleeding, nausea, pruritis, myoclonus)
Cardiac Complications of AKI
metabolic acidosis --> hyperkalemia --> arrhythmias

renin hypersecretion --> HTN

volume overload --> CHF, pulm edema

AKI --> CKD
most common cause of CKD
DM
HTN
Glomerulonephritis
what is a common genetic cause of CKD in adults and peds?
Polycystic Kidney Disease

AD --> adult
AR --> peds
CKD is generally asymptomatic until what GFR level?
30
CKD is characterized by chronic elevations in what?
uremia
what are the signs and sx of CKD?
anorexia
N/V
uremic pericarditis
"uremic frost"
delirium
sz
coma
uremic frost

powdery deposits of urea and uric acid salts on the skin, especially the face
what are BMP changes in CKD?
ELEVATED:
BUN
Cr
K+
Phosphate

DECREASED
calcium
CKD leads to fluid retention

name 4 sequela of fluid retention
HTN
CHF
LE edema
pulmonary edema
acid-base disturbance seen in CKD
metabolic acidosis
CKD

what is the hematological sequelae?
anemia of chronic disease secondary to decreased EPO production
CKD

what is the mechanism behind hyperphosphatemia
decreased phosphate excretion
impaired vit D production
(leading to renal osteodystrophy)
CKD

tx for HTN
ACE-I / ARBs
fluid restriction
why do you treat HTN in CKD?
slows the progression of CKD
how do you treat anemia of chronic disease in CKD pts?
EPO analogs
(eg epogen)
how do you treat renal osteodystrophy in CKD?
PO phosphate binders
and
calcitriol (1,25-OH Vit D)
CKD patients may usually require what long-term measures for failing kidneys?
hemodialysis
peritoneal dialysis
renal transplant
name the drug(s):
carbonic anhydrase inhibitors
(1)
acetazolamide
name the drug(s):
osmotic agents
(2)
mannitol
urea
name the drug(s):
loop agents
(4)
furosemide
ethacrynic acid
bumetanide
torsemide
name the drug(s):
thiazide agents
(2)
HCTZ
chlorothiazide
name the drug(s):
K+-sparing
(3)
spironolactone
triamterene
amiloride
site of action:
carbonic anhydrase inhibitors
proximal convoluted tube
site of action:
osmotic agents
entire tube
site of action:
loop agents
ascending limb
site of action:
thiazide agents
distal convoluted tube
site of action:
K+-sparing agents
*cortical* collecting ducts
mechanism of action:
carbonic anhydrase inhibitors
inhibit carbonic anhydrase

increases H+ reabsorption
blocks Na+/H+ exchange
mechanism of action:
osmotic agents
increase tubular fluid osmolarity
mechanism of action:
loop agents
inhibit Na/K/2CL transporter
mechanism of action:
thiazide agents
inhibit Na/Cl transporter
mechanism of action:
K+-sparing agents
SPIRONOLACTONE
blocks aldosterone receptor

TRIAMTERENE & AMILORIDE
blocks sodium channels
SIDE EFFECTS
carbonic anhydrase inhibitors
sulfa allergy
SIDE EFFECTS
osmotic agents
pulmonary edema

secondary to CHF and anuria
SIDE EFFECTS
loop agents
ototoxicity
decreased calcium
decreased K+

water loss
sulfa allergy
(except ethacrynic acid, hyperuricemia)
SIDE EFFECTS
thiazide agents
decreased sodium and potassium
elevated calcium and glucose
elevated uric acid

water loss
sulfa allergy
pancreatitis
SIDE EFFECTS
K+-sparing agents
elevated K+
anti-androgenic effects
(gynecomastia --> spironolactone)
ACID-BASE DISTURBANCE
carbonic anhydrase inhibitors
hyperchloremic metabolic acidosis

these drugs reduces NaCl and bicarb reabsorption causing a metabolic acidosis

but the Na is compensated for in the distal segment, so you end up not losing much Na
ACID-BASE DISTURBANCE
osmotic agents
none
ACID-BASE DISTURBANCE
loop agents
metabolic alkalosis
ACID-BASE DISTURBANCE
thiazide agents
metabolic alkalosis
ACID-BASE DISTURBANCE
K+-sparing diuretics
metabolic acidosis
what part of the renal tubular system does ADH act upon?
medullary collecting ducts
name an anti-convulsant that is based on carbonic anhydrase inhibitors

be more specific about what it treats
topiramate

treats epilepsy and Lennox-Gastaut Syndrome and migraines
how are carbonic anhydrase inhibitors used to treat open-angle glaucoma

also explain the mechanism of action
inhibits carbonic anhydrase II in the ciliary processes to decrease aqueous humor secretion into the chamber of the eye

it does this by slowing the formation of bicarb ions, which reduces sodium transport
hematuria
HTN
oliguria
nephritic syndrome
4 classic findings of nephritic syndrome
oliguria
hematuria (micro/macroscopic)
*edema*
HTN
UA of nephritic syndrome
hematuria
mild proteinuria
CMP of nephritic syndrome
elevated BUN and Cr
low GFR
Tx in nephritic syndrome
treat HTN, fluid overload and uremia with water and salt restriction

diuretics
dialysis (if necessary)

corticosteroids for reducing inflammation
nephritic syndrome is also called what?
glomerulonephritis
hematuria
HTN
oliguria
nephritic syndrome
4 classic findings of nephritic syndrome
oliguria
hematuria (micro/macroscopic)
*edema*
HTN
UA of nephritic syndrome
hematuria
mild proteinuria
CMP of nephritic syndrome
elevated BUN and Cr
low GFR
Tx in nephritic syndrome
treat HTN, fluid overload and uremia with water and salt restriction

diuretics
dialysis (if necessary)

corticosteroids for reducing inflammation
nephritic syndrome is also called what?
glomerulonephritis
Causes of Nephritic Syndrome

Name 2 Immune Complex Diseases
Postinfectious Glomerulonephritis

IgA Nephropathy
(Berger's Disease)
Causes of Nephritic Syndrome

Name 1 Pauci-Immune Disease
Wegener's Granulomatosis
Causes of Nephritic Syndrome

Name 2 Anti-GBM Diseases
Goodpasture's Syndrome

Alport's Syndrome
What is postinfectious glomerulonephritis associated with?
Group A beta-hemolytic assoc w/ streptococcal infection

But can be seen with any infection
Signs

Postinfectious Glomerulonephritis
oliguria
edema
HTN
tea/cola-colored urine
Labs and Renal Bx

Postinfectious Glomerulonephritis
low serum C3
(normalizes after 6-8 weeks after presentation)

Increased ASO titers

lumpy-bumpy immunofluorescence
Treatment and Prognosis

Postinfectious Glomerulonephritis
Tx
Supportive

Prognosis
almost all adults and children have a complete recovery
What is IgA Nephropathy (Berger's Disease) associated with?
associated w/ URI or GI infections
What patient population more commonly see's IgA Nephropathy?
commonly seen in young males
also seen in HSP
Signs and Sx

IgA Nephropathy
episodic gross hematuria

or

persistent microscopic hematuria
Labs

IgA Nephropathy
normal C3
Treatment and Prognosis

IgA Nephropathy
Tx
GC for some patients
ACEIs if pt has proteinuria

Prognosis
20% leads to ESRD
Clinical Picture

Wegener's Granulomatosis
granulomatous inflammation of the respiratory tract and kidney with necrotizing vasculitis
Signs and Sx

Wegener's Granulomatosis
F
wt loss
hematuria
hearing distrubances
respiratory and sinus sx
hemoptysis (from cavitary pulmonary lesions that bleed)
Labs and Renal Bx

Wegener's Granulomatosis
+c-ANCA
(cell-mediated immune response)

Renal Bx:
segmental necrotizing glomerulonephritis w/ few Ig deposits on immunofluorescence
Tx and Prognosis

Wegener's Granulomatosis
Tx
high-dose GC
cytotoxic agents


Prognosis
pts will have frequent relapses
Clinical Picture

Goodpasture's Syndrome
rapidly progressing glomerulonephritis w/ pulmonary hemorrhage
Patient Population

Goodpasture's Syndrome
males in their mid-20s
Signs and Sx

Goodpasture's Syndrome
*hemoptysis*
dyspnea
possible respiratory failure
Labs, CXR and Renal Bx

Goodpasture's Syndrome
Labs
iron deficiency anemia
hemosiderin-filled macrophages in sputum

CXR
pulmonary infiltrates

Renal Bx
linear anti-GBM deposits on immunofluorescence
Tx and Prognosis

Goodpasture's Syndrome
Tx
plasma exchange therapy
pulsed steroids

Prognosis
may progress to ESRD
Patient Population

Alport's Syndrome
boys 5-20 yo
Genetics

Alport's Syndrome
hereditary glomerulonephritis
Signs and Sx

Alport's Syndrome
asymptomatic hematuria associated with *nerve deafness* and eye d/o
Renal Bx

Alport's Syndrome
GBM splitting on electron microscopy
Tx and Prognosis

Alport's Syndrome
Prognosis
renal failure

even with renal transplant, anti-GBM nephritis may recur
Signs and Sx

Nephrotic Syndrome
generalized edema
hypoalbuminemia
hyperlipidemia
Definition of Nephrotic Syndrome
proteinuria > 3.5 g/day
with signs/sx
Of all causes of Nephrotic Syndrome, what are the 3 most common systemic diseases?
DM
SLE
amyloidosis
What do patients with Nephrotic Syndrome present with?

What if severe?
generalized edema
foamy urine

if severe:
dyspnea
ascites
What kinds of pts are at increased risk of Nephrotic Syndrome?
pts with greater susceptibility to infection

pts predisposed to hypercoagulable states

increased risk for venous thrombosis and pulmonary embolism
UA

Nephrotic Syndrome
proteinuria (> 3.5 g/day)
lipiduria
Labs

Nephrotic Syndrome
decreased albumin (< 3 g/dL)
hyperlipidemia
Tx

Nephrotic Syndrome
protein and salt restriction
diuretics
anti-hyperlipidemics
ACEIs to decrease proteinuria (and diminish progression to renal disease)

Vaccinate
pneumococcus vaccine
(23-polyvalent)
What infection are pts at risk for if they have Nephrotic Syndrome?
Streptococcus pneumoniae
Whats the mechanism of action for proteinuria, hyperlipidemia, edema and hyperlipiduria in Nephrotic Syndrome?
initially, its due to increased permeability of the glomerulus
Causes of Nephrotic Syndrome

Name 7
1 - Minimal Change Disease
2 - Focal Segmental Glomerulosclerosis
3 - Membranous Nephropathy
4 - Diabetic Nephropathy
5 - Lupus Nephritis
6 - Renal Amyloidosis
7 - Membrano-proliferataive Nephropathy
Cause of Minimal Change Disease
idiopathic

secondary causes:
NSAIDs
hematologic malignancies
Pts with Minimal Change Disease have a tendency to what?
infections and thrombotic events
Renal Bx

Minimal Change Disease
LM
normal

EM
fusion of epithelial foot processes
w/ lipid-laden renal cortices
Tx and Prognosis

Minimal Change Disease
Tx
steroids

Prognosis
Excellent
Typical Patient

Focal Segmental Glomerulosclerosis
young african-american male with uncontrolled HTN
Common Causes

Focal Segmental Glomerulosclerosis
IV drug use
obesity
HIV infection
Labs and Renal Bx

Focal Segmental Glomerulosclerosis
Labs
microscopic hematuria

Renal Bx
sclerosis in capillary tufts
Treatment

Focal Segmental Glomerulosclerosis
prednisone
cytotoxic therapy
ACEIs / ARBs
(to decrease proteinuria)
The most common nephropathy in caucasian adults
Membranous Nephropathy
Secondary Causes

Membranous Nephropathy
solid tumor malignancies

immune complex diseases
What infections are associated with Membranous Nephropathy?
HBV
syphilis
malaria
gold
Renal Bx

Membranous Nephropathy
"spike-and-dome" appearance due to deposits of IgG and C3 at the basement membrane
Tx

Membranous Nephropathy
prednisone
cytotoxic therapy (if severe)
Renal Bx

Diabetic Nephropathy
thickened GBM

increased mesangial matrix
Tx

Diabetic Nephropathy
tight blood sugar control
ACEIs (for Type 1 DM)
ARBs (for Type 2 DM)
Typical Patient

Diabetic Nephropathy
generally have long-standing and poorly controlled DM

also has:
retinopathy
neuropathy
Name 2 Forms of Diabetic Nephropathy
diffuse hyalinization

nodular glomerulosclerosis
(Kimmelstiel-Wilson Lesions)
UA

Lupus Nephritis
proteinuria
hematuria
Renal Bx

Lupus Nephritis
mesangial proliferation

subendothelial and/or subepithelial immune complex deposition
Tx and Prognosis

Lupus Nephritis
Tx
Prednisone
Cytotoxic Therapy

Prognosis
Depends on severity of renal disease
What diseases are associated with Renal Amyloidosis?
multiple myeloma

chronic inflammatory disease
(eg RA or TB)
Renal Bx

Renal Amyloidosis
nodular glomerulosclerosis

EM reveals:
amyloid fibrils
apple-green birefringence with Congo red stain
Tx

Renal Amyloidosis
prednisone
melphalan

bone marrow tx for MM pts
Summarize what Renal Amyloidosis entails.
improper folding of proteins that accumulates in the ECM of the kidneys

usually fatal if systemic

could either be hereditary or a syndrome (systemic/widespread)
Name the 2 most common types of Renal Amyloidosis.
Primary
Plasma Cell Dyscrasias

Secondary
Infectious or Inflammatory
Type 1 of Membrano-Proliferative Nephropathy is associated with what other diseases?
HCV
cryoglobulinemia
SLE
subacute bacterial endocarditis
Which diseases are both nephrotic and nephritic?
Lupus nephritis

Membrano-Proliferative Nephropathy
Patient Population

Membrano-Proliferative Nephropathy
(Idiopathic Form)
8-30 yo
Prognosis

Membrano-Proliferative Nephropathy
slow progression to renal failure
Tx

Membrano-Proliferative Nephropathy
corticosterioids
cytotoxic agents
Renal Bx

Membrano-Proliferative Nephropathy
(Commonalities for all Type I, II and III)
"tram-track" double-layered BM

low serum C3
Renal Bx

Membrano-Proliferative Nephropathy
(Type I)
subendothelial deposits
mesangial deposits
Labs

Membrano-Proliferative Nephropathy
(Type II)
C3 nephritic factor
Difference between Membrano-Proliferative Nephropathy and Membranous Nephropathy.
Membranous Nephropathy
BM is thickened but mesangium is not

Membrano-Proliferative Nephropathy
BM and mesangium are both thickened
Which bacteria are associated with "staghorn calculi"?
urease-producing orgs such as Preoteus
Typical presentation of a patient with nephrolithiasis.
acute onset of severe, colicky flank pain that radiates to the tests or vulva

pts are unable to get comfortable and shift position frequently (as opposed to peritonitis, who lie still)
Most common types of kidney stones.
calcium oxalate
calcium phosphate
struvite
uric acid
cystine
Risk factors for nephrolithiasis.
low fluid intake
gout
meds
(allopurinol, chemotherapy, loop diuretics)
postcolectomy/postileostomy
specific enzyme deficiencies
Type I RTA
(due to alkaline urinary pH and hypocitruria)
hyperPTH
UA

nephrolithiasis
gross or microscopic hematuria

altered urine pH
KUB

nephrolithiasis
KUB = x-ray of kidney/ureter/bladder

radiopaque stones
(will miss 10% of stones bc they are radiolucent)
Gold standard for diagnosing nephrolithiasis.
CT non-contrast

or if pregnant, renal US
Name two other forms of imaging for diagnosing nephrolithiasis, besides the gold standard.
Renal US
(shows obsxn)

IVP
(confirmed if there is no contrast below the stone)

Gold Standard
CT non-contrast
Tx
Also, state size for passing vs therapy

nephrolithiasis
hydration
analgesia

<5 mm diameter can pass thru urethra

<3 cm diameter treated with extracorporeal shock-wave lithotripsy (ESWL)
Most frequent form of kidney stone.
calcium oxalate
Cause

calcium oxalate or calcium phosphate stones
idiopathic hypercalciuria
primary hyperPTH
Radiopaque or Radiolucent

calcium oxalate and calcium phosphate stones
radiopaque
Radiopaque or Radiolucent

struvite
radiopaque
Radiopaque or Radiolucent

uric acid
**radiolucent**
Radiopaque or Radiolucent

cystine
radiopaque
Cause

struvite stones
(Mg-NH4-PO4)
urease-producing organisms
(eg Proteus)
alkaline or acidic urine?

struvite stones
alkaline urine
alkaline or acidic urine?

calcium oxalate and calcium phosphate
alkaline urine
alkaline or acidic urine?

uric acid
acidic urine
alkaline or acidic urine?

cystine
acidic?
Cause

Uric acid stones
gout
xanthine oxidase deficiency
high purine turnover states
(eg chemo)
Cause

cystine stones
defect in renal transport of certain amino acids
(COLA -- cystine, ornithine, lysine, arginine)
Shape of Cystine Stones
hexagonal crystals
Treatment

calcium oxalate and calcium phosphate stones
hydration
dietary sodium and protein restriction
thiazide diuretic
avoid *decreasing* calcium intake
(can lead to hyperoxaluria and increased risk of osteoporosis)
Treatment

struvite stones
hydration
treat UTI if present
surgical removal of staghorn stone
Treatment

Uric Acid
hydration
alkalinize urine with citrate
(which is converted to HCO3- in the liver)

allopurinol
restrict dietary purines
Treatment

cystine stones
hydration
dietary sodium restriction
alkalinze the urine
penicillamine
What is the characteristic appearance of PCKD in the kidneys?
progressive cystic dilation of renal tubules

can also see cysts in spleen, liver, pancreas
Autosomal Dominant PCKD

is associated with an increased risk of what?
cerebral aneurysm
Autosomal Dominant PCKD

what does this lead to?
ESRD requiring dialysis by 60yo
Autosomal Dominant PCKD

when do sx begin?
30 yo
which one is more common and which is more severe?

Autosomal Dominant PCKD
Autosomal Recessive PCKD
more common
AD

more severe
AR
Autosomal Recessive PCKD

when do sx begin?
infants and young children
Autosomal Dominant PCKD

what are the sx?
renal failure
liver fibrosis
portal HTN
death
Patient with known ADPCKD develops sudden, severe headache.
r/o SAH from ruptured berry aneurysm
PCKDs in general

most common presenting sx
pain
hematuria
PCKDs in general

are associated with what other findings?
HTN
hepatic cysts
cerebral berry aneurysms
diverticulosis
MVP
most common imaging for diagnosing PCKD
renal US
(most common)

CT
what do you see on renal US for PCKD?
multiple b/l cysts throughout renal parenchyma

renal enlargement
genetic testing for PCKD
ADPKD1
ADPKD2
whats the main idea behind tx for PCKD?
prevent complications
slow progression to ESRD
preventative management in PCKD
treat UTIs early to prevent renal cyst infection
why give ACEIs and ARBs to PCKD pts?
reduce HTN-induced renal damage
what is hydronephrosis?
dilation of renal calyces
if untreated, hydronephrosis from obsxn can lead to what?
HTN
acute and chronic renal failure
sepsis
most common cause of hydronephrosis and list some examples
obstruction

BPH
tumors
aortric aneurysms
renal calculi
most common cause of hydronephrosis in peds pts
obsxn at the ureteropelvic junction
name one non-obstructing cause of hydronephrosis
vesicoureteral reflux

high-output urinary flow and reflux leads to hydro
signs and sx

hydronephrosis
flank pain
decreased UOP
abd pain
UTIs
how to diagnose hydronephrosis
*ultrasound* or CT scan

dilation of renal calyces and/or ureter
labs for hydronephrosis
elevated BUN and Cr suggests secondary renal failure
Tx

hydronephrosis
relieve obstructions
(surgery for anatomic, laser or sound wave lithotripsy for stones)
what are other measures you can take if tx for hydronephrosis is sub-par (ie urinary outflow tract is still not sufficiently cleared)
ureteral stent where it was obstructed

or

percutaneous nephrostomy tube

or

foley / suprapubic catheters for lower urinary tract obsxn (eg PBH)
what is vesicoureteral reflux
is the retrograde movement of urine from bladder to ureter and kidneys during bladder contraction

it is due to insufficient tunneling of the ureters into the submucosal bladder tissue
what are some other causes of vesicoureteral reflux
posterior urethral valves
uretral or meatal stenosis
neurogenic bladder
Vesicoureteral Reflux
Mild Reflux
(Grades I-II)

What is this?
no ureteral or renal pelvic dilation

resolves spontaneously
Vesicoureteral Reflux
Moderate to Severe REflux
(Grade III-V)
ureteral dilation
caliceal blunting
(if severe)
Typical Patient

Vesicoureteral Reflux
recurrent UTIs
childhood
how early can you detect Vesicoureteral Reflux
prenatal ultrasound may show hydronephrosis
how to diagnose a Vesicoureteral Reflux and
VCUG
voiding cystourethrogram

detects abnormalities at ureteral insertion sites and classifies the grade of reflux
Tx

Vesicoureteral Reflux
(Mild vs Mod/Severe Tx)
tx infections aggressively

MILD
daily prophylactic abx
amox for < 2mo
otherwise TMP-SMX or nitrofurantoin until reflux resolves

MOD/SEVERE or if have pyelo
surgery (ureteral re-implantation)
if left un/under-treated, Vesicoureteral Reflux can lead to what?
renal scarring
ESRD
what is vesicoureteral reflux
is the retrograde movement of urine from bladder to ureter and kidneys during bladder contraction

it is due to insufficient tunneling of the ureters into the submucosal bladder tissue
what are some other causes of vesicoureteral reflux
posterior urethral valves
uretral or meatal stenosis
neurogenic bladder
Vesicoureteral Reflux
Mild Reflux
(Grades I-II)
no ureteral or renal pelvic dilation

resolves spontaneously
Vesicoureteral Reflux
Moderate to Severe REflux
(Grade III-V)
ureteral dilation
caliceal blunting
(if severe)
Typical Patient

Vesicoureteral Reflux
recurrent UTIs
childhood
how early can you detect Vesicoureteral Reflux
prenatal ultrasound may show hydronephrosis
how to diagnose a Vesicoureteral Reflux and
VCUG
voiding cystourethrogram

detects abnormalities at ureteral insertion sites and classifies the grade of reflux
Tx

Vesicoureteral Reflux
(Mild vs Mod/Severe Tx)
tx infections aggressively

MILD
daily prophylactic abx
amox for < 2mo
otherwise TMP-SMX or nitrofurantoin until reflux resolves

MOD/SEVERE or if have pyelo
surgery (ureteral re-implantation)
if left un/under-treated, Vesicoureteral Reflux can lead to what?
renal scarring
ESRD
What is cryptorchidism?
failure of one or both tests to fully descend into the scrotum
what is a risk fator for cryptorchidism
low birth weight
bilateral cryptorchidism is associated with what conditions?
prematurity
oligospermia
infertility
congenital malformation syndromes
(eg Prader-Willi, Noonan Syndromes)
what malignancy is associated with cryptorchidism
testicular
how do you diagnose cryptorchidism
inability to manipulate the testes into the scrotal sac with gentle pressure

palpation of the testes anywhere along the inguinal canal or abdomen
Tx

cryptorchidism
orchiopexy by 6-12 mo
What do you do if you discover cryptorchidism beyond the 6-12 month in which tx should have already been performed? Why?
orchiectomy

avoid risk of testicular cancer
ERECTILE DYSFUNCTION

What are the 3 classifications?
failure to initiate
failure to fill
failure to store
Whats the root cause of failure to initiate?
psychological
endocrinologic
neurologic
Whats the root cause of failure to fill?
arteriogenic
Whats the root cause of failure to store?
veno-occlusive dysfunction
What are the risk factors for erectile dysfunction?
DM
atherosclerosis
meds (beta-blockers, SSRIs, TCAs, diruetics)
HTN
heart disease
surgery/radiation of prostate cancer
SCI
In a patient with ED, you need to make a distinction in between what 2 causes?
Psychological vs Organic ED
In a patient with ED, how do you make the distinction between the 2 causes?
presence of nocturnal or early-morning erections
(if present, it is non-organic)

situation dependence
(ie occurring with only one partner)
Does bringing the testes into the scrotum decrease the risk of testicular cancer?
no
Erectile Dysfunction

Describe the role of the parasympathetic and sympathetic nervous system.
"Point and Shoot"

Point = Parasympathetic
(erection)

Shoot = Sympathetic
(ejaculation)
Erectile Dysfunction

How do you evaluate for neurologic dysfunction?
anal tone
LE sensation
Erectile Dysfunction

How do you evaluate for hypogonadism?
small testes

loss of secondary sexual characteristics
How would you diagnose ED?
Abnormal Labs:

testosterone
gonadotropin levels
prolactin levels

(elevated prolactin can result in decreased androgen activity)
Tx

Psychological ED
psychotherapy or sex therapy
(discuss and exercise with partner)
Mechanism of Action

Viagra, Levitra, Cialis
phosphodiesterase-5 inhibitors

result in prolonged action of cGMP-mediated smooth muscle relaxation and increased blood flow in the corpora cavernosa
What drugs are an absolute contraindication to sildenafil?
Nitrates

(the combined effect of decreased BP can lead to MI)
Tx

ED with hypogonadism
testosterone replacement

(for both hypogonadism of testicular or pituitary origin)
Alternative Tx

ED, who failed PDE5 therapy
vacuum pumps

intracvernosal prostaglandin injections

surgical implantation of semirigid or inflatable penile prostheses
BPH

central or peripheral zone?

why does this matter
central

this means BPH might not be detected on DRE
major side effect of alpha-blockers
orthostatic hypotension
BPH can result in obstructive and irritative sx.

Describe the obstructive sx.
hesitancy
weak stream
intermittent stream
incomplete emptying
urinary retention
bladder fullness
BPH can result in obstructive and irritative sx.

Describe the irritative sx.
nocturia
daytime frequency
urge incontinence
opening hematuria
DRE findings of BPH
prostate is uniformly enlarged with a rubbery texture
DRE findings of prostate cancer
prostate is hard (not rubbery)
has irregular lesions
Upstream effects of BPH

(kidney, ureter, bladder)
urinary retention
recurrent UTIs
bladder and renal calculi
hydronephrosis
kidney damage over time
Patient population of BPH
> 50 years

prostate enlargement is a normal part of aging process
How would you diagnose BPH?

How would you test for obstruction in BPH?
DRE to screen for masses

UA and urine cx to r/o UTI/infection and hematuria

test for obstruction
Cr levels
(to r/o obstructive uropathy and renal insufficiency)
Medical Tx and describe mechanism of the drug

BPH
alpha-blockers
(eg terazosin)
relaxes smooth muscle in the prostate and bladder neck

5-alpha reductase inhibitors
(eg finasteride)
inhibits production of dihydrotestosterone
Surgical Tx

BPH
TURP

transurethral resection of prostate

open prostatectomy
2nd leading cause of cancer deaths in men
prostate cancer
leading cause of cancer deaths in men
lung cancer
risk factors for prostate cancer
advanced age
+ family hx
Obstructive Sx

Prostate Cancer
urinary retention
decrease force of stream
Prostate Cancer

ask if the patient has pain where? and why?
back pain

represents bone metastases
Prostate Cancer

DRE findings
palpable nodule
area of induration

early cancer is usually not detectable on exam
DRE

tender prostate
represents prostatitis
5 leading causes of cancer death in men
1 - lung
2 - prostate
3 - colorectal
4 - pancreatic
5 - leukemia
What does an elevated PSA mean?
BPH
prostatitis
UTI
prostatic trauma
carcinoma
Workup for prostate cancer
clinical findings
elevated PSA (>4 ng/mL)
Definitive Diagnosis

Prostate Cancer
ultrasound-guided transrectal biopsy

shows adenocarcinoma
Prostate Cancer

What is the tumor grading system?
Gleason histologic system

sums the scores (from 1 to 5) of the 2 most dysplastic samples (10 is highest grade)
Prostate Cancer

What are imaging workup should you do?
CXR and bone scan
(look for metastases)

metastatic lesions show an osteoblastic or increased bone density
Recommended DRE screening for prostate cancer.
annually after 50 yo

earlier for AA or if first-degree relative with prostate cancer
Tx

Prostate Cancer
controversial, since the tumor is slow growing

watchful waiting vs radical prostatectomy and radiation therapy (brachytherapy or external beam)
Side effects of radical prostatectomy and radiation therapy for prostate cancer.
incontinence
impotence
How to treat metastatic prostate cancer?
androgen ablation
(eg GnRH agonist, orchiectomy, flutamide)

chemotherapy
Differential for hematuria

S2 I3 T3
Strictures
Stones

Infection
Inflammation
Infarction

Tumor
Trauma
TB
Bladder Cancer

What type of histology is this cancer?
transitional cell carcinoma
Patient Population

Bladder Cancer
50-60s
Risk Factors

Bladder Cancer
smoking
diets rich in meat and fat
schistosomiasis
chronic tx w/cyclophosphamide
occupational exposure to aniline dye (a benzene derivative)
Most common presenting sx of bladder cancer
gross hematuria
Common presenting sx of bladder cancer
frequency
urgency
dysuria
asymptomatic
Diagnostic W/U

Bladder Cancer
cystoscopy with bx is diagnostic

Supporting Labs:
UA shows hematuria
Cytology shows dysplastic cells
IVP to examine upper urinary tract as well as bladder
MRI/CT/Bone Scan to eval for metastases
Tx for Bladder Cancer depends on extend of spread beyond the bladder mucosa.

Carcinoma in situ
intravesicular chemotherapy
Tx for Bladder Cancer depends on extend of spread beyond the bladder mucosa.

Superficial cancers
complete transurethral resection or intravesicular chemotherapy with mitomycin-C or BCG (the TB vaccine)
Tx for Bladder Cancer depends on extend of spread beyond the bladder mucosa.

Large, high-grade recurrent lesions
intravesicular chemotherapy
Tx for Bladder Cancer depends on extend of spread beyond the bladder mucosa.

Invasive cancers without mets
radical cystectomy or radiotherapy (if pt is poor candidate for surgery or if its unresectable)
Tx for Bladder Cancer depends on extend of spread beyond the bladder mucosa.

Invasive cancers with distant mets
chemotherapy alone
Classic triad of renal cell carcinoma.
hematuria
flank pain
palpable flank mass

only present in 5-10% of pts though
Why do male pts w/ RCC get a left-sided varicocele?
due to tumor blockage of the left gonadal vein, which empties into the left renal vein

the right gonadal vein empties directly into the IVC
Labs

RCC
anemia

or

polycythemia
(due to increased EPO production in 5-10% of pts)
RCC

diagnostic w/u
US and/or CT

usually shows complex cyst or solid tumor
Tx

RCC
surgical resection may be curative
Testicular Cancer

malignant or benign?
virtually all are malignant
Origins of testicular cancer
germ cells

germ cells produces gametes, located in the gonads

(male) germ cells = stem cells surrounding the seminiferous tubules in the testes

gametes = sperm, egg
Risk factors for testicular cancer
cryptorchidism
Klinefelter syndrdome
most common malignancy in males 15-34 yo
testicular cx
Clinical presentation of testicular cx
painless enlargement of testes
patient population of testicular cancer
15-30 yo

seminomas have a peak incidence btw 40-50 yo
Diagnostic w/u of testicular cancer
Testicular US

CXR and CT to eval for mets
What are the tumor markers of testicular cancer?
tumor markers are for diagnosing and monitoring tx response

b-hcg is elevated in choriocarcinoma and 10% of seminomas

alpha-fetoprotein (AFP) elevated in nonseminomatous germ cell tumors, particularly endodermal sinus (yolk sac) tumors

AFP also elevated in HCC, hepatoblastoma, neuroblastoma
Tx

testicular cancer
radical orchiectomy

seminomas are exquisitely radiosensitive and chemotherapy responsive

non-seminomatous germ cell tumors respond to platinum-based chemo
Prognosis of seminomas
seminomas is a germ cell tumor of the testes

It is one of the most treatable and curable cancers, with survival >95% in the early stages.