UWorld- Renal

What treatment do you give in hyperkalemia --base it on what you would select with respective conditions and mechanisms.

1. Calcium gluconate (rapidacting) - cardioprotective therefore give if have EKG changes 2. Insulin with glucose, beta2 agonists, sodium bicarb (rapid acting) -> Shifts K+ temporarily but rapid action 3. Diuretics, cation exchange resin, dialysis -->Remove K+ from system--give pts with kidney disease and/or on ACE-I. have inc total potassium.

What are the following nephrotic syndromes associated with. 1) FSGS 2) Membranous nephropathy 3) Membraniproliferative glomerulonephritis 4) Minimal change disease 5) IgA nephropathy

1. FSGS - (MC Nephrotic Synd) African American, HIV, heroin, obesity (Fat AA on drugs has HIV and is discriminated/segmented) 2. Membranous nephropathy - Adenocarcinoma, NSAIDs SLE 3. Membranoproliferative GN - Hep B and Hep C 4. Minmal change - NSAIDS, lymphoma 5. IgA nephropathy/Bergers Disease - MC G.Nephritis, Upper Resp Infection

What is Tx of SIADH?

1. Mild - water restriction 2. Moderate - confusion/lethargy from hyponatremia - hypertonic solution 3. Severe - seizures/coma - Give Hypertonic +/- conivaptan

Pt just started taking diphenhydramine. Now has difficulty voiding. Why?

1st gen anti histamine (like TCAS) have anticholinergic properties that decrease detrusor activity giving retention.

oliguria is defined as? In post operative course what should you do if pt has oliguria?

<200mL/12 hrs or <0.5mL/kg/hr Try Urinary catheritization -->in post operative course urinary retention is common

what are features of nephrotic syndrome? What are complications/possible diseases from these features?

>3.5g protein/day, fatty casts, hyperlipidemia, loss of proteins like albumin, IgGs, Antithrombin. Infections (low IgGs), Hypercoaguable state (low Antithrombin), Artheroscelerosis risk (Hyperlipidemia)

Why is ACE-I effective for diabetic nephropathy?

ACE-I reduces intraglomerular hypertension thereby reducing glomerular damage

What are two methods to diagnose pt coming with acute flank pain that radiates to groin?

Abd U.S. --> no radiation but will miss small stones spiral CT without contrast --> very sensitive and specific

Pt comes in with hypertension and cysts in both kidneys. What is condition? What are other manifestations of this disease?

Adult polycystic Kidney disease - get increased renin hence HT Other manifestations - cysts in kidney, cysts in liver (adenomas) and cysts in brain (berry aneurysm esp with HT)

Elderly pt with dementia is started on amytryptaline for neck pain. 8 days later he is found gripping his abdomen and moaning. Other exam is normal. What is problem? Tx?

Amytryptaline induced urinary retention. (Anticholinergics effect can retain urine!) Urinary catheritization to get urine out.

What are causes of elevated CPK? What can this cause to kidneys and why? What would u see on Urinalysis?

Any muscle damage including Rhabdomyolysis, Polymyositis/dermatositis. High muscle damage releases Myoglobin which can injure kidneys to get Acute tubular necrosis leading to AKI. Note- Myoglobin is false positive for blood in UA so see large amts of blood!

How do you treat uncomplicated cystitis? When does this become complicated? What is tx then?

Bactrim 3 days or Nitrofurantoin 5days or Fosfomycin (single dose).Only time Nitrofurantoin is used is here and pregnant UTI. Complicated with diabetes, pregnancy, indwelling catherter, immunosuppresed Tx for Complicated Cystitis- FLuoroquinolone

Painless hematuria in Pt >35 yrs with hx of smoking. Need to consider? What is next step in dx?

Bladder Cancer Imaging - cytoscopy, CT urogram

How can you distinguish between Benign prostatic hyperplasia and diabetic nephropathy based on labs?

Both can have nocturia, dribbling. BPH does not have proteinuria like Diabetes.

Why is metformin avoided in Acute kidney injury and sepsis?

Can cause lactic acidosis

In Pt with long standing diabetic nephropathy with Cr 3.5, pt bleeds persistently after having blood drawn for analyzing source of Pnm. Why?

Chronic renal failure will see abnormal hemostasis because Uremic toxins (like guanidinosuccinic acid) affect platelets, which affect bleeding time.

Pt with drug induced interstitial nephritis. What drugs can cause this? What are clinical findings suggesting this and findings in UA?

Drugs - Penicillin, cephalosporin, sulfonamides Clinically see rash, fever, arthralgia Labs - see eosinophils in urine, WBC casts, sterile pyuria, hematuria

What is anasarca?

Extreme generalized edema---edema everywhere

What are differences between Glomerular hematuria and non glomerular hematuria? Give some examples of each.

Glomerular hematuria has microscopic blood. Also UA shows protein and blood. RBC casts, dysmorphic RBC Ex. Glomerular Nephritis, Basement Membrane Non-Glomerular hematuria has frank blood. UA shows ONLY blood, no protein. No casts Ex. Nephrolithiasis, cancer(renal, prostrate) Polycystic Kidney disease, Renal infarction, Pappilary necrosis

Name the most significant High anion gap metabolic acidosis causes? What about the most significant normal anion gap metabolic acidosis?

High Anion - MUDPILES or just know DKA, Salicylates, Ethylene glycol, propylene glycol, methanol Normal Gap - HARDASS or just know ARD (Addison, Renal Tubular Acidosis, Diarrhea) Above U is uremia (ESRD so failure to excrete H+)

How does diabetes cause nephropathy?

Hyperglycemia leads to microvascular damage (microangiopathy) ..the glycation end products damage the glomerulus allowing proteinuria

What can hypomagnesemia cause? What condition do you see this?

Hypocalcemia (needed as cofactor for PTH release), Hypokalemia (cofactor for potassium uptake by Na-K-ATPase). Chronic Alcoholics

Pt with severe asthma is on multiple asthma meds. What electrolyte imbalance can you see and why?

Hypokalemia as excessive cortisol has weak mineralocorticoid activity and can bind to alodosterone receptors.

Pt with confusion and lethargy and weight loss. is a smoker and CXR shows mass in hilar region. Labs have low sodium and potassium with low serum osmolality and high urine osmolality. What is condition? Why?

Hyponatremia from SIADH caused from ADH secreting lung tumor. Common lung tumor here is small cell CA.

Pt with dehydration. Would you give IV crystalloid or IV colloid?

IV crystalloids. = NS IV colloids are protein/albumin containing like milk - used for burns or hypoproteinemia

Pt with confusion, back pain, abd pain and high serum calcium comes in . What is next step?

IV fluids to dilute serum calcium, can add calcitonin + bisphosphonates if severe

What are differences between IgA nephropathy in Poststreptococcal Glomerularnephritis?

IgA Neph - Hematuria after resp infection, usually Sxs onset within 5 days. Complement levels normal PSGN - Hematuria after skin/sore throat, Sxs after 10-20 days, Low complement levels, see red cell casts

What is most common Glomerular nephritis in adults?

IgA nephropathy

Pt with abdominal pain that is relieved with urinating but increases with filling. also has dyspareunia, urgency. What is conditon? What is this assosciated with? Tx?

Interstitial cysitis aka Painful bladder syndrome Associated with psych anxiety and pain syndromes (fibromyalgia, anxiety disorders Tx - Behavior modification, Amitryptaline, analgesics

What is problem with using succinylcholine? In what type of patients is this contraindicated

It can cause significant hyperkalemia and hence life threatening arrythmias. --> CI in pts with hyperkalemia (in burns, crush injuries)

With nephrotic syndrome , what two proteins do you lose in urine that can lead to complications?

Lose Albumin - edema, low oncotic pressure Lose Anithrombin - leads to hypercoaguability -->Renal Vein thrombosis esp in Membranous nephropathy

Pt with nephrolithiasis. What recommendations can you give to prevent future attacks?

Low protein and low oxalate diet (high protein predisposes to forming stones). Most commonly calcium oxalate crystals. High fluid intake

Pt with diabetes and baseline Cr 1.5 gets IV contrast imaging and has inc in Cr. What is mechanism? What could have prevented this? Does prednisone work?

Mech- contrast can cause vasoconstriction and tubular necrosis. Pts with diabetes and elevated Cr are at higher risk for this. IV normal saline or IV bicarbonate can prevent Prednisone cannot prevent IV contrast nephropathy- only hypersensitivity reaction from contrast (allergic).

What does overdose in Asprin do for acid base chemistry?

Metabolic acidiosis (salicylic acid) also Respiratory alkalosis (stimulates respiratory centers to get tachypnea)

What is characteristic of Acute Tubular necrosis?

Muddy brown casts

Urinalysis sees large amount of blood. Urine sediment microscope sees 0-1 RBC. What do you suspect with this discrepancy?

Myoglobin can look like blood in UA! can be rhabdo

Pt with sudden onset right sided flank pain that is colicky and radiates to the scrotum. Suspect Dx? Dx Test? Tx?

Nephrolithiasis, CT without contrast is test of choice If stone < 5mm -->Fluid intake >2L and NSAIDS to let stone redissolve/pass

Pt found unconscious with GLucose 1000 with BP of 90/65. Condition? What is immediate next step? IV fluids or Insulin?

Non-ketotic hyperglycemia coma. Correct hypovolemia first by Giving IV NS. Hyperglycemia will go down with fluids! Can give insulin after.

Pt with oribital edema, hematuria oliguria nad RBC casts after skin infection 3 weeks ago. Condition?What other labs can you see for this condition?

Poststreptococcal Glomerulonephritis, Low serum C3 levels, Cr inc.

Pt has recurrent uric acid stones which are radiolucent on xray. What can be given to decreae?

Potassium citrate that alkanilzes urine which makes uric acid more soluble

Name all the nephrotic syndromes. For which one is renal vein thrombosis most common complication?

Primary disease -Minimal change disease, FSGS, Membranous glomerulopathy, Secondary- Systemic Amyloidosis, diabetic nephropathy Membranous G. sees Renal vein thrombosis as a complication themost.

Rapid correction of hyponatremia causes central pontine demylenation. How? What happens if you rapidly correct hypernatremia?

Rapid correction of soidum causes osmotic diuresis from intracellular neurons to extracellular compartment which damages neurons. If hypernatremia corrected rapidly -->Cerebral edema

Pt with BPH has 3 mos of urgency and nocturia has inc Cr to 2.1. What is next step after Urinalysis?

Renal US. If Cr high, need to evaluate kidney to see if there is hydronephrosis from severe Urinary obstruction

Pt with flank pain, hematuria and abdominal mass.What do you suspect? What other finding is possible on PE for this condition?

Renal cell carcinoma. 10% show this presentation, 10% show left varicocele as mass can obstruct renal vein.

Pt has seizures and comes in with Chem labs pointing to a metabolic acidosis. What is going on?

Seizure activity produces lactic acid from muscles leading to lactic acidosis. Recheck after some time.

What can cause Rhabdomyolysis complication?

Statins, cocaine abuse (20% overdose have this complication), Trauma

Where does hydrogen ion travel with K+ in 1) Stomach, 2)Aldosterone action 3) Acidemia and intracellular K+

Stomach and Kidneys-->K+ and H+ excreted together Acidemia --> H+ exchanges with K+ in cell

Pt with upper lung cavitary lesion in CXR with daily fevers and cough comes in with high K+, BP 96/54. What is condition and what caused the electrolyte abnormality?

TB TB can cause chronic adrenal insufficiency. hence low bp as well. Keeps K+ and H+ in body giving normal anion gap acidosis

Pt after MVA has femoral fracture shows asterixis, with AST = 112, ALT 40, Albumin 3.8, Total Bili 0.4 but Creatinine Kinase 32000. What is dx? What is next step in Tx?

Uremic Encephalopathy! not Hepatic as AST is slightly high from muscle injury but albumin, bili normal (liver fn okay). Tx - Dialysis ..Remember PFHEM? Pericarditis, Fluid overload, Hyperkalemia, Encephalopathy, Metabolic Acidosis) NOT Lactulose as this is not Hepatic Encephalopathy

What meds can cause hyperkalemia and how?

decrease aldosterone production --> ACE-I, NSAIDS (also kidney disease) K+ sparing diuretics -->sprinolactone, amiloride, triamterene decrease beta 2 mediated intracellular K+ uptake --> non selective beta blockers (Beta 2 agonist works like insulin --drives K+ into cells)