• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/168

Click to flip

168 Cards in this Set

  • Front
  • Back
Provide the normal gas values (including pH).
pH: 7.35-7.45
Drop the 7
pCO2: 35-45
Multiply 45 x 2
pO2>90
Divide 45 by 2
HCO3 = 22 (up to 28)
What is the Henderson-Hasselbalch equation?
pH=HCO3/pCO2
Acid-Base Disorder:
pH 7.40
HCO3 23
pCO2 40
pH nl
HCO3 nl
pCO2 nl

Normal ABG
Acid-Base Disorder:
pH 7.50
HCO3 35
pCO2 42
pH Basic (Alkalosis)
HCO3 Elevated (Must be metabolic)
pCO2 Normal (No compensation)

Thus, it's a metabolic alkalosis without compensation.
Acid-Base Disorder:
pH 7.33
HCO3 13
pCO2 28
pH: Acidic
HCO3: Low
pCO2: Low--must be compensatory mechanism because don't have an alkalosis

Metabolic acidosis with respiratory compensation.
Acid-Base Disorder:
pH 7.42
HCO3 32
pCO2 64
pH Normal
HCO3 High--metabolic alkalosis
pCO2 High--respiratory acidosis

Mixed disorder; combined metabolic alkalosis and respiratory acidosis
Acid-Base Disorder:
pH 7.20
HCO3 18
pCO2 40
pH Low--Acidosis
HCO3 Low
pCO2 Low

Metabolic acidosis without compensation. (normal pCO2 is 35-45)
Acid-Base Disorder:
pH 7.20
HCO3 24
pCO2 54
pH: Acidosis
HCO3: Normal
pCO2: Elevated

Respiratory acidosis without compensation.
Acid-Base Disorder:
pH 7.52
HCO3 22
pCO2 22
pH: Alkalosis
HCO3: Normal
pCO2: Low

Respiratory alkalosis without compensation.
Acid-Base Disorder:
pH 7.66
HCO3 36
pCO2 30
pH: Alkalosis
HCO3: Elevated
pCO2: Normal/Low

Combined metabolic and respiratory alkalosis.
Acid-Base Disorder:
pH 7.47
HCO3 14
pCO2 22
pH Alkalosis
HCO3 Low
pCO2 Low

Respiratory alkalosis with compensation.
Acid-Base Disorder:
pH 7.46
HCO3 35
pCO2 53
pH Alkalosis
HCO3 Elevated
pCO2 Elevated

Metabolic alkalosis with compensation
Acid-Base Disorder:
pH 7.39
HCO3 12
pCO2 22
pH Normal
HCO3 Low--Met acidosis
pCO2 Low--Resp alkalosis

Mixed: Metabolic acidosis and respiratory alkalosis
Acid-Base Disorder:
pH 7.34
HCO3 31
pCO2 62
pH Acidosis
HCO3 Elevated
pCO2 Elevated--acidosis

Respiratory acidosis with compensation
Acid-Base Disorder:
pH 7.10
HCO3 15
pCO2 50
pH Acidosis
HCO3 Low--acidosis
pCO2 High--acidosis

Combined metabolic and respiratory acidosis.
Respiratory acidosis vs alkalosis:
Causes
Resp acidosis:
Hypoventilation:
-Airway obstruction
-Lung dz
-Opioids, narcotics, sedatives
-Weakening of respiratory mm

Resp alkalosis:
-Hyperventilation (early high altitude exposure)
-ASA ingestion (early)
Metabolic acidosis vs alkalosis:
Causes
Met acidosis:
CHECK ANION GAP (Na+ - (Cl + HCO3); nl range is 8-12

If normal gap****:
Diarrhea
Glue sniffing
Renal tubular acidosis
Hyperchloremia

If anion gap:
MUDPILES*****
Methanol
Uremia
DKA
Paraldehyde/Phenformin
Iron tablets or INH
Lactic acidosis
Ethylene glycol
Salicylates

Met alkalosis:
Diuretic use
Vomiting
Antacid use
Hyperaldosteronism
Rental tubular acidosis:
Type I vs Type II vs Type IV
Type I (distal)-Defect in CD's ability to excrete H+. Assocd w/hypokalemia and risk for Ca2+ kidney stones

Type II: Proximal; defect in proximal tubule HCO3- reabsorption. Assocd w/hypokalemia and hypophophatemic rickets.

Type IV: Hyperkalemia; hypoaldosteronism or lack of CD response to aldosterone; assocd w/hyperkalemia, inhibition of ammonium excretion in proximal tubule. Leads to acidic urine due to dec'd buffering capacity.
How does acidosis/alkalosis affect extracellular K concentrations?
Because of H+/K+ pump:

Acidosis: increases extracell K+
Alkalosis: decreases extracell K+
A patient with recent kidney transplant on cyclosporin for immunosuppression requires an antifungal agent for candidiasis

What drug would result in cyclosporin toxicity?
Ketoconazole (interferes with cyp450)
A patient presents with renal insufficiency

What alterations need to be made in his doses of digoxin
and digitoxin respectively?
Digoxin is renally excreted, so decrease dose.

Digitoxin not renally excreted, so don't have to change dose.
What effect will a renal stone that obstructs the ureter have on GFR and FF?
Dec GFR
Dec FF
What is the maximal serum glucose concentration at which glucose can be absorbed in the tubules?
Will start to spill glucose around 200 mg/dL, but will saturate at 350 mg/dL
What change in a basic metabolic panel might you expect in a young pt being treated for status asthmaticus?
beta-agonists will shift K+ into cells-->hypokalemia
MUD PILES
Methanol
Uremia
DKA
Paraldehyde or phenformin
Iron tablets or INH
Lactic acidosis
Ethylene glycol
Salicylates
A patient taking lisinopril complains of new onset, constant coughing

What medication class should
this patient be switched to?
Angiotensin receptor blocker (sartan)
A patient with heart failure exacerbation needs medical diuresis but has a sulfa allergy

What diuretic can be used?
Loop & thiazide are both sulfa drugs, so use Ethacrynic acid
A patient presents with hypertension, hypokalemia, metabolic alkalosis, and low plasma renin.

What is the diagnosis, and how do you treat it?
Primary hyperaldosteronism

Treat w/spironolactone
Type of diuretic:
Triamterene
K+ sparing
Type of diuretic:
Acetazolamide
Carbonic anyhydrase inhibitor
Type of diuretic:
Hydrochlorothiazide
Thiazide
Type of diuretic:
Bumetanide
Loop
Type of diuretic:
Spironolactone
K+ Sparine--aldost antag
Type of diuretic:
Chlorothiazide
Thiazide
Type of diuretic:
Ethacrynic acid
Loop, not a sulfa drug
Type of diuretic:
Mannitol
Osmotic
Type of diuretic:
Metolazone
Thiazide
Type of diuretic:
Chlorthalidone
Thiazide
Type of diuretic:
Furosemide
Loop
Type of diuretic:
Amiloride
K+ sparing
Type of diuretic:
Torsemide
Loop
Appropriate diuretic:
Acute pulmonary edema
Heart failure-->LMNOP
Loop
Appropriate diuretic:
Idiopathic hypercalciuria
Thiazide to retain Ca2+
Appropriate diuretic:
Glaucoma
Acetazolamide, Mannitol
Appropriate diuretic:
Mild to moderate CHF with expanded ECV
Mild: Thiazide
Classically for HF: Loop
Appropriate diuretic:
In conjunction with loop or thiazide diuretics to retain K+
Any K+ sparing diuretic
Appropriate diuretic:
Edema a/w nephrotic syndrome
Loop
Appropriate diuretic:
Increased intracranial pressure
Mannitol
Appropriate diuretic:
Mild to moderate hypertension
Thiazide--HCTZ
Appropriate diuretic:
Hypercalcemia
Loop to lose Ca2+
Appropriate diuretic:
Altitude sickness
Acetazolamide
Appropriate diuretic:
Hyperaldosteronism
Spironolactone or eplerenone
What is the equation for the renal clearance of any substance?
Renal clearance = UxV/Px
A 40 year-old pt of yours weighs 100 kg.
What is her estimated plasma volume?
20% x 100 kg x 1/4 L/kg = 5L
What factors/substances cause hyperkalemia?

What factors/substances cause hypokalemia?
Hyperkalemia:
K+ sparing diuretics
ACE inhibitors
Acidosis
Insulin-deficiency
Beta-agonists
Hyperosmolarity
Digitalis
Cellular lysis

Hypokalemia:
Loop diuretics
Thiazides
Insulin
Beta-agonists
Alkalosis
Hyposmolarity
DKA
Heart/Renal failure
What are the actions of angiotensin II?
Direct vasoconstricting effect

Raises aldosterone levels-->Inc
Na and H2O reabsorption in proximal tubule

Dec'd renal blood flow, but inc'd GFR and FF
What is the site of action of mannitol?

What is the site of action of the thiazides?
Mannitol: Woks at proximal convoluted tubule

Thiazides: Early distal tubule
What substances can be used to estimate GFR?

What substances can be used to estimate renal plasma flow?
GFR: Cr, Inulin

RPF: PAH
What do the presence of casts indicate?
Hematuria/pyuria is of renal origin
Proliferative vs Membranous Glomerular Disorders
Proliferative: hypercercellular glomeruli

Membranous: thickening of glomerular BM
Nephritic Syndrome:
Pathophys
Presentation
NephrItic = Inflammatory process. When involves glomeruli-->hematuria and RBC casts in urine

a/w azotemia--elevated BUN/Cr, oliguria, HTN, proteinuria (<3.5 g/day)
Azotemia vs Uremia
Azotemia: elevated BUN/Cr

Uremia: azotemia + systemic effect (pleuritis, pericarditis, EKG changes, etc.)
Acute Poststreptococcal Glomerulonephritis:
Pathophys
LM/EM presentation
Glomeruli enlarged, hypercellular, nphils, lumpy-bumpy appearance

Subepithelial immune complex humps

Frequently seen in children. Resolves spontaneously
Rapidly progressive glomerulonephritis:
Pathophys
LM/EM presentation
IF presentation
LM--crescent-moon shape; crescents consist of fibrin and plasma proteins (e.g., C3b) w/glomerular fn parietal cells, monocytes, macs

Severe causes:
-Goodpasture Syndrome (type II hypersens); Abs to GBM and alveolar BM-->linear immunofluorescence
-Wegener's granulomatosis (c-ANCA)
-Microscopic polyangitis (p-ANCA)
Diffuse proliferative glomerulonephritis:
LM/EM presentation
Pathophys
Most common cause of death in SLE, Membranoproliferative GN

EM: subendothelial DNA-anti-DNA IC's
Berger's Disease:
Pathophys
Inc'd synthesis of IgA with IC's deposit in mesangium

Often presents/flares with URI or acute gastroenteritis
Alport's syndrome;
Pathophys
Presentation
Mutation in type IV collagen-->split BM

Can't see, can't pee, ca'n't hear (Nerve disorders, ocular disorders, deafness)
What is nephrotic syndrome?
NephrOtic syndrome presents with massive prOteinuria (>3.5g/day, frothy urine), edema, hyperlipidemia, fatty casts
Membranous glomerulonephritis:
Pathophys
LM/EM presentation
Diffuse capillary and GBM thickening

Spike and dome appearance with subepithelial deposits
(nephrotic syndrome)

Caused by drugs, infections, SLE; most common adult cause of nephrotic syndrome
Minimal change disease:
Pathophys
LM/EM presentation
LM--normal glomeruli
EM--foot process effacement

May be triggered by recent infection or immune stimulus. Most common in children. Responds to steroids.
Minimal change dz; normal glomeruli on LM but effacement of foot processes on EM (arrowhead). The full arrow points to a normal foot process.
Treatment consists of steroids.
Amyloidosis--congo red stain demonstrates amyloid deposits in artery wall that show apple-green birefringence under polarized light.
Amyloidosis is associated with _______.
Multiple myeloma, TB, RA
Diabetic glomerulonephropaty:
Pathophys
Nonenzymatic glycosylation of GBM-->inc'd permeability, thickening

Nonenzymatic glycosylation of efferent arterioles-->inc'd GFR-->mesangial expansion
Diabetic glomerulosclerosis--nodular diabetic glomerulosclerosis (also known as Kimmelstiel-Wilson syndrome); characterized by acellular ovoid nodules in periphery of glomerulus.
Membranoproliferative GN:
Type I vs Type II--
EM appearance
Causes
Type I: tram-track appearance due to GBM splitting caused by mesangial ingrowth

Most common cause; HBV, HCV, SLE (more association than cause)

Type II: Dense dposits
Associated with C3 nephritic factor
What renal conditions are associated with hypocomplementemia?
Post-strep GN
Membranoproliferative GN (Type II)
Lupus nephritis
Which glomerular disease:
Most common nephrotic syndrome in children ·
Minimal Change Dz
Which glomerular disease:
IF: granular pattern of immune complex deposition; LM: diffuse capillary thickening
Membranous GN
Which glomerular disease:
IF: granular pattern of immune complex deposition; LM: hypercellular glomeruli
Acute post-strep GN
Which glomerular disease:
IF: linear pattern of immune complex deposition
Anti-GBM Abs with Goodpasture's
Which glomerular disease:
IF: deposition of lgG, lgM, lgA, and C3 in the mesangium
IgA nephropathy
Which glomerular disease: Kimmelstiei-Wilson lesions (nodular glomerulosclerosis)
Diabetic glomerulonephropathy
Which glomerular disease:
Most common nephrotic syndrome in adults
Membranous GN
Which glomerular disease:
EM: loss of epithelial foot processes
Minimal Change Dz
Which glomerular disease:
Nephrotic syndrome associated with hepatitis B
Membranoproliferative GN
Which glomerular disease:
Nephrotic syndrome associated with HIV
Focal segmental glomerulosclerosis
Which glomerular disease:
Anti-GBM antibodies, hematuria, hemoptysis
Goopasture's
Which glomerular disease:
EM: subendothelial humps and tram-tack appearance
Membranoproliferative GN
Which glomerular disease:
Nephritis, deafness, cataracts
Alport Syndrome
Which glomerular disease:
LM: crescent formation in the glomeruli
Crescentic GN (aka Rapidly progressive GN)
Which glomerular disease:
LM: segmental sclerosis and hyalinosis
Focal segmental GN
Which glomerular disease:
Purpura on back of arms and legs, abdominal pain, lgA nephropathy
Henoch-Schloei Purpura
Which glomerular disease:
LM: wire-loop appearance
SLE
Which glomerular disease:
Apple-green birefringence with Congo-red stain under polarized light
Renal amyloidosis
Which glomerular disease:
EM: spiking of the GBM due to electron dense subepithelial deposits
Membranous GN
Under what circumstances would you see:
RBC Cast
Acute GN
Under what circumstances would you see:
WBC Cast
Pyelonephritis, acute interstitial nephritis
Under what circumstances would you see:
Bacterial cast
Acute pyelonephritis
Under what circumstances would you see:
Epithelial cell cast
Renal tubular damage
Under what circumstances would you see:
Waxy cast
Waxy = stasis of urine flow, so much be chronic renal failure
Under what circumstances would you see:
Fatty cast
Nephrotic syndrome
Under what circumstances would you see:
Granular cast
Non-specific, can be seen with acute tubular necrosis
Glomerular histology reveals multiple mesangial nodules.

This lesion is indicative of what disease?
Diabetic glomerulonephropathy
A teenager presents with nephrotic syndrome and hearing loss.

What is the disease?
Alport's Syndrome
A 4 year-old boy presents with facial edema and proteinuria.

What is the appropriate treatment?
Steroids (this is Min Change Dz)
What is the only radiolucent kidney stone?
uric acid stones
Calcium kidney stones:
Frequency
Causes
75-85% of all kidney stones

Consists of calcium oxalate, calcium phosphate, or both.

Caused by conditions that cause hyperCa2+ (cancer, hyperPTH)

Oxalate crystals can result from ethylene glycol (antifreeze) or Vitamin C abuse
Ammonium magnesium phosphate kidney stones:
Frequency
Causes
15% of kidney stones

Caused by infection with urease-positive bugs (Proteus, Staph, Klebsiella)

can form staghorn calculi that can be nidus for UTIs
Uric acid kidney stones:
Frequency
Causes
RADIOLUCENT

5% of stones

Strong assocn w/gout; often seen in dz w/inc'd cell turnover such as leukemia
Which kidney stones can be treated by alkalinization of urine?

Which stone would be worsesned by alkaluria?
Use alkaluria to tx Cystine stones (only 1% of renal stones)

DO NOT use alkaluria to tx ammonium magnesium phosphate stones
Calcium oxalate outlining a large right renal collecting duct system creating a "staghorn" calculus--can be calcium stone OR ammonoium magnesium phosphate (which present as STAGHORN)
Calcium oxalate crystals in kidney, viewed with polarizers. Tubular failure in oxalate nephropathy can result from vitamin C or antifreeze abuse.
Renal cell carcinoma:
Histologic features
Risk factors
Presentation
Site of Mets
Associated disorders
Polygonal clear cells in renal tubular cells

Inc'd incidence w/smoking and obesity

Manifests with hematuria, palpable mass, secondary polycythemia, flank pain, fever, weight loss

Paraneoplastic syndromes (ectopic EPO, ACTH, PTHrP, prolactin)

INvades IVC and spreads hematogenously; mets to lung and bone


Assocd w/von Hippel-Lindau syndrome and gene deletion in chromosome 3
Wilms' Tumor:
AKA
Presentation
Cause
AKA nephroblastoma

(Most common renal malignancy of early childhood)

Contains embryonic glomerular structures

Presents with huge, palpable flank mass, andn/or hematuria

Deletion of tumor suppressor gene WT1; may be part of WAGR complex (Wilms tumor, Aniridia, GU malformn, MR)
Renal cell carcinoma. Histology shows polygonal cells with small nuclei and abundant clear cytoplasm with a rich, delicate branching vasculature.
Transitional cell carcioma:
Presentation
Risk Factors
Most common tumor of urinary tract system, can occur in renal calyces, renal pelvis, ureters, bladder

Painless hematuria suggests bladder cancer

Risk factors in your Pee SAC:
Phenacetin
Smoking
Aniline Dyes
Cyclophosphamide
Pyelonephritis:
Acute vs Chronic--
Histologic features
Presentation
Acute pyelonephritis:
-Affects cortex w/sparing of glomeruli/vessels
Presents w/fever, CVA tenderness, nausea, vomiting

WHITE CELL CASTS CLASSIC for this

Chronic:
Coarse, asymmetric corticomedullary scarring, blunted calyx
Tubules can contain eosinophilic casts (thyroidization of kidney)
Acute pyelonephritis characterized by nphilic infiltration and abscess formation within renal interstitium. Abscesses may rupture, introducing collections of white cells to tubular lumen.
Chronic pyelonephritis with lymphocytic invasion and fibrosis.
Acute Interstitial Nephritis:
Cause
Presentation
Treatment
Urinalysis finding
Most common cause of acute renal failure; mostly drug-induced

Cause:
Drugs--NSAIDS, PCN/cephalosporins (methicillin), sulfonamides (TMP-SMX, foresmide), cipro, cimetidine, allopurinol

Tx w/2 weeks steroids

Presentation: fever, rash, ephilia, azotemia

Muddy brown (granular) casts = key finding
Acute Tubular Necrosis:
Cause
Presentation
Cause:
aminoglycosides, cephalosporins, polymixins
Contrast dye
Rhabdomyolysis/myoglobinuria from seizures, cocaine, crush injuries

FIndings: 4+ blood in urine, no RBC on urine cell count (because it's myoglobin in urine), renal failure
Renal Papillary Necrosis:
Causes
Pathophys
Sloughing of papillae-->gross hematria, proteinuria

May be triggered by recent infection or immune stimulus

A/W:
DM
Acute pyelonephritis
Chronic acetaminophen use
Sickle cell anemia
Acute renal failure:
Definition
Prerenal vs Intrinsic vs Postrenal--
Pathophys and Examples
Acute renal failure--abrupt decline in renal fn w/inc'd Cr and BUN over several days

1) Prerenal azoetmia--due to dec'd RBF (HYPOTENSION, dehydration, hypovolemia, shock, renal vasoconstricion as with NSAIDs)-->dec'd GFR, Na/H2O and Urea retained by kidney to reserve volume so, BUN/Cr ratio increases

Intrinsic renal: Acute tubular necrosis or ischemia/toxins; necrosis leads to debris obstructing tubule and fluid backflow across necrotic tubule; results in dec'd GFR. Urine has epithelial/granular casts. BUN reabsorption impaired-->dec'd BUN/Cr ratio

Postrenal--outflow obstruction (stones, BPH, neoplasia, congenital anomalies); develops ONLY with BILATERAL obstruction
Acute vs Chronic Renal Failure:
Most common causes
Acute: Acute tubular necrosis
Chronic: HTN, DM
What is uremia?
Clinical syndrome marked by inc'd BUN and inc'd Cr
Presents with nausea, anorexia
Pericarditis
Asterixis (hand-flapping tremor)
Encephalopathy
PLT dysfn
UTI caused by Proteus vulgaris.

Associated renal stone?
Ammonium Magnesium Phosphtate Stone-->Staghorn calculi
A patient reports a long-term history of acetaminophen use.

What is she at increased risk of?
Renal papillary necrosis--but NSAIDs can do this too!
What artery prevents a horseshoe kidney from ascending in the abdomen?
IMA
CT Scan of ADPKD
ADPKD:
Pathophys
Presentation
At risk of?
AD mutation in APKD1/2-->multiple, large, b/l cysts that ultimately destroy kidney parenchyma

Presents w/flank pain, hematuria, HTN (inc'd renin production), urinary infection, progressive renal failure

Risk of polycystic liver dz, berry aneurysms, mitral valve prolapse
ARPKD:
Presentation
Infantile presentation of ADPKD in parenchyma.

ASsocd w/hepatic fibrosis.

Can lead ot Potter's if develop renal failure in utero.
Central pontine myelinosis:
Cause
Rapid correction of hyponatremia
How does EKG reflex K+ levels?
Low K+ - Flat T waves
High K+ - Peak T waves
What is the WAGR complex?
Wilms' Tumor
Aniridia
GU malformn
Retardation (mental)
Which glomerular disease:
IF: granular pattern of immune complex deposition; LM: diffuse capillary thickening
Membranous GN
Which glomerular disease:
IF: granular pattern of immune complex deposition; LM: hypercellular glomeruli
Acute poststrep GN
Which glomerular disease:
IF: linear pattern of immune complex deposition
Goodpasture's
Which glomerular disease:
IF: deposition of lgG, lgM, lgA, and C3 in the mesangium
IgA neprhopathy
Which glomerular disease:
EM: subendothelial humps and tram-tack appearance
Membranoproliferative GN
Which glomerular disease:
Nephritis, deafness, cataracts
Alport Syndrome
Which glomerular disease:
LM: crescent formation in the glomeruli
Crescentic/Rapidly Progressive GN
Which glomerular disease:
LM: segmental sclerosis and hyalinosis
Focal segmental glomerulosclerosis
Which glomerular disease:
Purpura on back of arms and legs, abdominal pain, lgA nephropathy
Henock Schonlein Purpura
Which glomerular disease:
EM: spiking of the GBM due to electron dense subepithelial deposits
Memranous GN
Diagnose:
pH 7.50
HCO3 35
pCO2 42
Metabolic alkalosis w/o compensation
Diagnose:
pH 7.33
HCO3 13
pCO2 28
Metabolic acidosis w/compensation
Diagnose:
pH 7.20
HCO3 18
pCO2 40
Metabolic acidosis w/o compensation
Diagnose:
pH 7.66
HCO3 36
pCO2 30
Metabolic and respiratory alkalosis
Diagnose:
pH 7.47
HCO3 14
pCO2 22
Resp alkalosis w/compensation
Diagnose:
pH 7.10
HCO3 15
pCO2 50
Combined metabolic and respiratory acidosis
Risk factors for transitional cell carcinoma?
PSAC
Smoking---
Phenacetin (acetaminophen)
Smoking
Aniline dyes
Cyclophosphamide
What are the causes of acidosis with an elevated anion gap?
MUDPILES
Methanol
Uremia
DKA
Paraldehyde/phenformin
Fe tables or INH
Lactic acidosis
EtOH or ethylene glycol
Salicylates
What changes will be seen in a basic metabolic panel in a patient with renal failure?
High K+
High PO4
Low Ca2+
High BUN/Cr
CT scan reveals massively enlarged kidney bilaterally.

Diagnosis?
ADPKD
Which electrolyte disturbance:
Correcting too rapidly may result in central pontine myelinosis
Hyponatremia
Which electrolyte disturbance:
Peaked T waves
Hyperkalemia
Which electrolyte disturbance:
Tetany
Hypocalcemia
Which electrolyte disturbance:
Arrhythmias
High/low K+
Low Mg2+
Which electrolyte disturbance:
Decreased deep tendon reflexes
Hypermg2+
Which electrolyte disturbance:
Flattened T waves, U waves on EKG
Low K+
Which renal pathology:
Most common tumor of the urinary tract system
Transitional cell ca
Which renal pathology:
Most common renal malignancy of early childhood (ages 2-4)
Wilms' Tumor
Which renal pathology:
Histologic appearance of renal cell carcinoma
Clear cell carcinoma
Which renal pathology:
Histological appearance of chronic pyelonephritis
Thyroidization of kidney
Which renal pathology:
Fever + rash + hematuria + eosinophilia
AIN
Which renal pathology:
Cancer associated with Schistosoma haematobium
Squamous cell carcinoma of bladder
Which renal pathology:
Treatment for cystine kidney stones
Alkalinization of urine