Renal, Clinical Cases

Front 1

describe RTA type II?

Back 1

bicarbonate is not correctly absorbed in the proximal tubule leading to plasma acidosis

Front 2

An elderly woman presenting with glycosuria, aminoaciduria, hypocitraturia, and phosphaturia has what?

Back 2

Fanconi syndrome

Front 3

A child with abnormal bone growth and rickets presents with an abnormal urine representative of Fanconi's syndrome. What is the most likely cause?

Back 3

RTA type II

Front 4

when the body is in a chronic state of metabolic acidosis (EX. RTA type I or II), does the body compensate for this?

Back 4

enters respiratory alkalosis (hyperventilating) to try and get rid of CO2 to lower pH

Front 5

whats the difference between high anion gap metabolic acidosis and regular metabolic acidosis?

Back 5

high anion gap means that the contribution to acidosis made by chloride (the main anion) does not explain the acidosis, thus other anions must be the cause that are not being measured directly like chloride, regular metabolic acidosis simply means hyperchloremia

Front 6

when parathyroid hormone is greatly elevated either pathologically or under low serum Ca++ states, what clinical picture does it cause?

Back 6

Acts on proximal tubule which can result in fanconi syndrome

Front 7

How are you going to treat Fanconi's syndrome?

Back 7

Bicarb, K+, Phosphorus, Vit. D/Ca+

Front 8

Who is more likely to get multiple myeloma?
Elderly vs. Young
Black vs. White
Women vs. Men

Back 8

Elderly, Black Men

Front 9

Most common acquired cause of Fanconi's Syndrome is?

Back 9

Multiple Myeloma

Front 10

Most common Primary cause of Fancon's Syndrome is?

Back 10

idiopathic, however Cystitinosis (lysosomal storage disease) is the most likely familial cause

Front 11

what causes Hemolytic Uremic Syndrome (HUS)?

Back 11

E. coli producing shiga-toxin (verotoxin)

Front 12

What is the clinical picture with someone who has HUS?

Back 12

bloody diarrhea, signs of DIC and/or renal compromise

Front 13

HUS and this syndrome share an almost identical clinical picture: Renal failure, Thrombocytopenia, Microangiopathic hemolytic anemia

Back 13

Thrombotic thrombocytopenic purpura (TTP)

Front 14

What is HUS triad?

Back 14

1. Renal failure (decreasing renal function is included because this will lead to failure)
2. Thrombocytopenia
3. Microangiopathic hemolytic anemia

Front 15

Which 3 of these drugs are responsible for causing TTP/HUS?

1. Cyclosporine
2. Tacrolimus
3. Asparaginase
4. Verapamil
5. Quinine

Back 15

1. Cyclosporine
2. Tacrolimus
3. Quinine

Front 16

what is the main cause of TTP?

Back 16

deficiency of vWF cleaving protease (ADAMTS13)

Front 17

what is the cause of HUS: how does the toxin cause the triad of symptoms?

Back 17

endothelial injury due to antibody against CD36 (thrombospondin receptor) found on endothelial cells

Front 18

How does shiga toxin damage endothelium?

Back 18

Causes release of endothelin, cytokines and chemokines which cause a massive inflammatory response damaging endothelial cells

Front 19

how do you differentiate HUS from vasculitis?

Back 19

normal platelet count

Front 20

how do you differentiate HUS from malignant hypertension?

Back 20

glomerular changes are different and there is usually a history of hypertension and retinal findings

Front 21

how do you differentiate HUS from DIC?

Back 21

in HUS there are normal levels of clotting factors

Front 22

how do you differentiate HUS from antiphospholipid syndrome?

Back 22

with Antiphospholipid syndrome you will see greatly prolonged PTT because of the presence of an autoantibody

Front 23

what is the treatment for TTP?

Back 23

1. supply ADAMTS13
2. plasmaphoresis to remove autoantibodies and vWF multimers

Front 24

what is the essential ability that a bacteria must posses to cause HUS?

Back 24

shiga-toxin (aka verotoxin) producing

Front 25

If C3 is very low in a patient with renal failure, what do you immediately suspect is the cause?

Back 25

post-streptococcal glomerulonephritis - compliment is bound to strep antigens and deposited in the kidney causing damage

Front 26

what change in addition to a very low serum C3 will you see with PSGN?

Back 26

IgG/Strep Antigen complexes

Front 27

glomerulonephritis is pretty much synonymous with a _____ of the glomerular capillaries?

Back 27

vasculitis

Front 28

Patient presents with increased serum creatinin following a soar throat 1.5 weeks ago. Urine shows WBC casts. Are the significant support for your diagnosis of PSGN?

Back 28

No only RBC casts a definitive for glomerulonephritis

Front 29

SLE greatly mimicks PSGN, but can be differentiated around 8 weeks later by what finding?

Back 29

With SLE C3 will remain low where as with PSGN C3 levels will return to normal after ~8 weeks

Front 30

why might adults who have had PSGN develope hypertension and nephrosclerosis?

Back 30

after PSGN they have hyperfiltration, which over time leads to the hypertension and nephrosclerosis

Front 31

Good Pastures Syndrome which is characterized by glomerularnephritis and pulmonary hemorrhage is also called ___ when it doesnt involve the lungs?

Back 31

Anti-GBM associated
glomerulonephritis

Front 32

most common cause of nephrotic syndrome in peds?

Back 32

minimal change disease

Front 33

why do patients with nephrotic syndrome have a higher chance for having a stroke?

Back 33

the excrete anti-clotting protiens which puts them in a hypercoagulable state

Front 34

describe the prototypical patient with nephrotic syndrome?

Back 34

Male > 50 with proteinuria and elevated serum creatinine

Front 35

how can central DI be differentiated from secondary DI caused by lithium?

Back 35

cenral DI will concentrate urine in the pressence of synthetic ADH (DDAVP) but secondary won't

Front 36

what receptors does ADH bind to and where are they located?

Back 36

V-2 receptors in the collecting ducts and distal tubule

Front 37

whats a likely cause of central DI?

Back 37

pituitary or hypothalamus damage

Front 38

whats a likely cause of secondary DI?

Back 38

damage to distal tubules such that ADH can no longer work

Front 39

how does lithium cause seconday DI?

Back 39

it blocks the mobilization of AQ-2 channels by ADH

Front 40

how does Amiloride stop secondary DI due to lithium?

Back 40

blocks the NA+ channels that lithium uses to get into principle cells

Front 41

why would hyperaldosteronism cause increased serum bicarb?

Back 41

it increases the H+ excretion of intercalated cells which causes the formation of bicarb

Front 42

when you see low K (without use of diuretic) and mild alkalosis what is the first thing you should look for?

Back 42

mineralcorticoid over production