FEN/GI/Renal Flashcards

1
Q

Segment of nephron in which 90% of filtered bicarbonate is recovered.

A. Collecting duct
B. Distal tubule
C. Thick ascending loop of Henle
D. Thin descending loop of Henle
E. Proximal tubule

A

E. Proximal tubule

(Lucking Ch. 6)

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2
Q

Definitions of intra-abdominal hypertension and abdominal compartment syndrome

A

HTN: >10 mmHg
Compartment syndrome: >20 mmHg and signs of organ dysfunction

Abdominal perfusion pressure = MAP - bladder pressure, min 55 mmHg in adults recommended

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3
Q

Which of the following is true regarding creatinine as a measure of renal function?

A. Creatinine secretion into the ultrafiltrate is clinically insignificant
B. In a normal kidney, creatinine clearance underestimates GFR by 10– 20%
C. Plasma creatinine reaches adult levels shortly after the 2nd year of life
D. Plasma creatinine is unaffected by diet
E. There can be as much as a 50% decrease in nephron mass prior to any detectable increase in serum creatinine

A

E. There can be as much as a 50% decrease in nephron mass prior to any detectable increase in serum creatinine

(Lucking Ch. 6)

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4
Q

Which hormone regulates serum osmolality by controlling the insertion of water channels into the luminal membrane of the principal cells of the collecting ducts?

A. Aldosterone
B. Antidiuretic Hormone (ADH)
C. Atrial Natriuretic Peptide (ANP)
D. Erythropoeitin
E. Leptin

A

B. Antidiuretic Hormone (ADH)

(Lucking Ch. 6)

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5
Q

The diuretic which can cause hypercalciuria, leading to kidney stones and nephrocalcinosis, especially in premature infants.

A. Chlorathiazide
B. Furosemide
C. Mannitol
D. Metolazone
E. Spironolactone

A

B. Furosemide

(Lucking Ch. 6)

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6
Q

The type of acidosis which requires massive doses of bicarbonate to treat, but if untreated, is characterized by a mild to moderate acidosis with a high fractional excretion of bicarbonate. This type of acidosis can be associated with hypophosphatemia and rickets.

A. Acidosis due to stool bicarbonate loss
B. Distal RTA
C. Posthypocapnic acidosis
D. Proximal RTA
E. Type IV RTA

A

D. Proximal RTA

(Lucking Ch. 6)

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7
Q

Which of the following is true regarding urea and renal function?

A. Blood urea is increased during hypovolemia mainly due to hemoconcentration
B. Blood urea is increased during hypovolemia mainly due to increased reabsorption
C. Urea is freely filtered at the glomerulus and undergoes little reabsorption
D. Urea production is decreased during critical illness
E. Urea production is increased during states of increased anabolism

A

B. Blood urea is increased during hypovolemia mainly due to increased reabsorption

(Lucking Ch. 6)

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8
Q

A 2 year old male is transferred to the pediatric ICU from a referring institution with hypotension secondary to severe diarrhea and dehydration. His mother reports he has had diarrhea and fever for four days. He has had oral hydration with a pediatric rehydration solution and an appropriate dose of ibuprofen for fever every 6 hours. Vital sign are: pulse 167 beats per minute, blood pressure 109/67 mm Hg, respiratory rate of 44 breaths per minute. Examination reveals a lethargic child with cool extremities, delayed capillary refill and dry mucous membranes. Laboratory evaluation reveals: Sodium 141 mEq/L Chloride 121 mEq/L Potassium 5.9 mEq/L BUN 44 mg/dL Creatinine 4.2 mg/dL Bicarbonate 7 mEq/L Which of the following is most true regarding his decrement in renal function?

A. His BUN:creatinine ratio is reflective of hypovolemia and not intrinsic renal injury
B. His increase in creatinine is mainly due to hemoconcentration
C. His increase in creatinine is reflective of a 25% reduction in GFR
D. The acidosis is likely due to renal injury and renal loss of bicarbonate
E. The administration of ibuprofen likely impaired the kidney’s ability to compensate for decreased perfusion

A

E. The administration of ibuprofen likely impaired the kidney’s ability to compensate for decreased perfusion

(Lucking Ch. 6)

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9
Q

A 2 year old is admitted with pneumococcal sepsis and severe edema secondary to nephrotic syndrome. You are asked to estimate his GFR with the following information: Dry weight - 12 kg Height - 85 cm Plasma creatinine 1 mg/dl Urine output 2 ml/kg/hr Which of the following is the most accurate estimate of GFR?

A. 10 ml/min/1.73 m2
B. 25 ml/min/1.73 m2
C. 30 ml/min/1.73 m2
D. 35 ml/min/1.73 m2
E. An estimated GFR cannot be calculated with the above data

A

D. 35 ml/min/1.73 m2

(Lucking Ch. 6)

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10
Q

What is the most common cause of fulminant hepatic failure in infants?

A) Hepatitis A
B) Acetaminophen overdose
C) Metabolic disorders
D) Autoimmune Hepatitis B

A

C) Metabolic disorders

The etiology of ALF can be divided into several categories: metabolic, infective, toxic, autoimmune, malignancy-induced, vascular-induced, and undetermined. Etiology of ALF varies with age. In infants, metabolic disease is the most common cause whereas older children more frequently develop ALF from viral infections. In the neonatal period, galactosemia, hereditary fructose intolerance, tyrosinemia, neonatal hemochromatosis, and ornithine transcarbamy- lase (OTC) deficiency can present with hypoglycemia, coagulopathy, lactic acidosis, failure to thrive and irritability. Patients with urea cycle defects may present with an initial respira- tory alkalosis and severe hyperammonemia. Regardless of etiology, if liver failure is advanced, lactic acidosis is often present. Jaundice is frequently absent at presentation. Galactosemia and tyrosinemia type I may cause refractory coagulopathy in the infant with minimal other signs of liver failure. Symptomatic metabolic liver disease may present before the results of newborn screening are available.

Wilson’s disease is not seen in the newborn period but is the most common metabolic cause of
ALF in children older than 5 years of age. Worldwide, hepatitis A is the most frequent infectious cause of ALF due to its high prevalence in developing countries. Biliary atresia is the most common reason for pediatric liver transplantation.

(End of Year Wrap Up)

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11
Q

What is the most appropriate initial study to confirm a diagnosis of intussusception on a 15-month old infant?

A) Upright abdominal radiograph
B) Air or barium contrast study of the colon
C) Ultrasound of the abdomen
D) Double-contrast CT of the abdomen
E) Upper GI follow through stud

A

C) Ultrasound of the abdomen

Air or barium contrast studies of the colon have been considered the standard diagnostic test for intussusception. However, abdominal ultrasound is the preferred initial study of choice because of its high diagnostic sensitivity (98% to 100%) and specificity (88% to 100%), as well as the absence of radiation exposure and greater patient comfort. If a competent ultrasonographer has ruled out intussusception, no further imaging tests should be necessary. Ultrasound is also useful to evaluate the biliary duct, abdominal masses, and pathology related to the appendix.

Double-contrast CT can be used to investigate the cause of small bowel obstruction and to evaluate pancreatic, retroperitoneal, and pelvic pathology. It also can be used to assess the size and identify the location of an intra-abdominal mass and its relationship to other organs.

Upright abdominal radiographs and upper GI follow through studies have low sensitivity and specificity for a diagnosis of intestinal obstruction.

(End of Year Wrap Up)

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12
Q

What is the most appropriate initial therapy for management of acute GI bleeding caused by esophageal varices and portal hypertension in a hemodynamically stable patient?

A) Balloon tamponade with a Sengstaken-Blakemore tube
B) Octreotide infusion
C) Proton pump inhibitor to block gastric acidity
D) Emergency portocaval shunt surgery
E) Endoscopic ligation of sclerotherapy

A

B) Octreotide infusion

The Sengstaken-Blakemore tube has been used in adults to apply direct pressure via a balloon to temporarily occlude esophageal varices. More recently, medical and endoscopic therapy has been the focus, including the use of vasopressin, somatostatin and octreotide, all of which decrease portal pressure by decreasing splanchnic blood flow.”

Octreotide is effective in stopping acute variceal bleeding in apout 75% of patients. Some studies report medical and endoscopic therapies to be equivalent, although combination therapy may be superior. In children, octreotide infusion is often used to achieve initial hemostasis and optimize visualization for subsequent endoscopic ligation or sclerotherapy. Proton pump inhibitors are used to block gastric acidity and are part of the routine management of these patients.

Although emergency portocaval shunt surgery is an option, this procedure is associated with significant morbidity and mortality.

(End of Year Wrap Up)

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13
Q

What is the most appropriate goal for intragastric pH in patients with acute GI bleeding or those at risk for bleeding?

A) 2 to 3
B) 3 to 4
C) 4 to 5
D) 5 to 6
E) >6

A

E) >6

(End of Year Wrap Up)

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14
Q

What is the cause of hepatopulmonary syndrome?

A) Ventilator associated pneumonia
B) Intrapulmonary vasodilation and shunting
C) Aspiration pneumonia from variceal bleeding
D) Acute respiratory distress syndrome as a complication of fulminant hepatic failure

A

B) Intrapulmonary vasodilation and shunting

Hepatopulmonary syndrome is characterized by abnormal arterial oxygenation caused by intrapulmonary vasodilation and shunting in patients with liver disease or portal hypertension. Pulmonary histologic findings include dilated pulmonary arterioles and capillaries, and less commonly, pleural and pulmonary arteriovenous connections. Patients have Pa02 <80 mm Hg in room air and show increased alveolar-arterial (A-a) oxygen gradient but normal PaC02. Contrast enhanced echocardiography with agitated saline solution administered through a peripheral vein in the arm shows rapid appearance of bubbles in the left side of the heart within three to six cardiac cycles. Microbubbles (>10 um) do not pass through normal capillaries (<8 to 15 um). Progressive hepatopulmonary syndrome is an indication for liver transplant prior to development of severe hypoxemia.

(End of Year Wrap Up)

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15
Q

Which of the following proteins can be used to assess a patient’s nutritional status over the past 8 days?

A) Prealbumin
B) Retinal binding protein
C) Albumin
D) Transferrin

A

D) Transferrin

(End of Year Wrap Up)

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16
Q

Licorice ingestion impact on potassium

A

Causes hypokalemia - contains glycyrrhizic acid, has mineralocorticoid properties that can cause potassium wasting

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17
Q

How does heparin cause hyperkalemia?

A

Suppresses aldosterone, natriuresis, and potassium excretion

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18
Q

What is the impact on measured potassium level of leukocytosis and thrombocytosis?

A

Falsely elevated potassium level

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19
Q

What is the treatment for minimal change nephrotic syndrome?

A

Steroids - typically very responsive, can prevent urinary loss of proteins including immunoglobulins and therefore prevent infection

20
Q

Why are patients with nephrotic syndrome at risk of thrombosis?

A

Urinary loss of fibrinolytic factors (protein C, protein S, antithrombin III), elevated platelet count, dehydration, immobilization

21
Q

What defines chloride responsive/unresponsive metabolic alkalosis?

A

Responsive: urine chloride less than 10 mEq/L (renal or gastric losses typically of HCl - vomiting, contraction alkalosis, or post-hypercapnea)

Unresponsive: urine chloride greater than 20 mEq/L (bicarb excess or shift of H+ from extra- to intracellular - hyperaldosteronism, renal artery stenosis, steroids)

22
Q

What defines acute liver failure in children?

A

Multisystem disorder with severely impaired liver function (INR>1.5 with encephalopathy or INR>2 with or without) in a patient with no history of liver disease

7 etiologies:
1. Metabolic/genetic
2. Infectious
3. Toxin/drug
4. Autoimmune
5. Malignancy
6. Vascular
7. Undetermined

Under age 1, most commonly viral or inborn error of metabolism; over age 1 mostly drug, autoimmune, or viral

23
Q

Mechanisms of rasburicase and allopurinol?

A

Allopurinol inhibits xanthine oxidase - blocks production of new uric acid but doesn’t do anything for uric acid already formed

Rasburicase - catalyzes oxidation of uric acid to allantoin, lowering uric acid level

24
Q

What medication limits contrast-induced nephropathy?

A

Dexmedetomidine

IV hydration can reduce viscosity and minimize contrast exposure in the tubular cells but no evidence of benefit

25
Q

What is included in Pediatric End-stage Liver Disease (PELD) score?

A

Total bilirubin
INR
Serum albumin
Age
Growth failure

26
Q

What are the major early complications after liver transplant?

A

Infection (gram negative and fungal), bile leak, hepatic artery or portal vein thormbosis, primary graft nonfunction (more rare)

27
Q

Treatment of hypoglycemia

A

0.5 g/kg of glucose (more can spike endogenous insulin and cause rebound hypoglycemia)

1 mL/kg D50
2 mL/kg D25
5 mL/kg D10

Minimum GIR:
5-8 mg/kg/min neonates
3-5 mg/kg/min older kids

28
Q

What is the equation to determine mEq of sodium required for correction of hyponatremia?

A

0.6 × (weight of the patient in kg) × (Target Na- Serum Na) = mEq of Na required to raise the serum Na to the determined level

29
Q

Goal rate of slow correction of hyponatremia?

A

0.5 to 1 mEq/L/hr

30
Q

When should I calculate a fractional excretion of urea?

A

Use as surrogate for FENa in patients on loop diuretics

FEurea = 100 * [(UureaPCr)/(PureaUCr)], in prerenal disease <35%, in patients with ATN >50%

31
Q
A
32
Q

Causes and distinguishing features of hyponatremia

A
33
Q

Signs of hypocalcemia

A

Tetany, Chvostek sign - facial muscle twitching, carpopedal spasm

Prolonged QTc, bradycardia, hypotension

CaCl more bioavailable, Ca gluconate less caustic to veins but requires hepatic metabolism

34
Q

Why does HUS occur more commonly in kids than in adults?

A

Gb3 glycolipid is more highly expressed, that’s what the toxin binds to on renal tubular cells and vascular endothelium of the kidney

35
Q

HUS treatment

A

supportive care, control of fluid overload and hypertension

dialysis if severe
pRBC
avoid platelet transfusion

for atypical maybe plasmapheresis or monoclonal Ab

36
Q

What causes stridor in DiGeorge?

A

Tetany of vocal cords secondary to hypocalcemia (hypoparathyroid)

Also softening of bones/cartilage due to hypoCa – collapse of larynx

37
Q

Acute treatment of hyperkalemia

A
  1. calcium to stabilize myocardium
  2. loop diuretics - block Na-K-2Cl cotransporter
  3. albuterol (B2 agonist), stimulates Na/K ATPas to move K intracellular
  4. Sodium polystyrene sulfonate = kayexalate (for chronic renal failure) - binds free K in colon
  5. insulin - stimulates Na-H antiporter
  6. can try sodium bicarb
38
Q

Stepwise treatment for GER without red flag symptoms

A
  1. Avoid overfeeding, thicken feeds,
  2. Change to protein hydrolysate or amino acid-based formula, eliminate cow’s milk
  3. Short course of acid-suppressive therapy (can increase risk of pneumonia)
39
Q

Explain citrate toxicity in CRRT

A

Citrate works as an anticoagulant by binding calcium which is important for coagulation cascade

Citrate goes to liver, converted to citric acid and bicarbonate

If liver is impaired, citrate can’t be converted, excess citrate binds Ca

40
Q

Symptoms and diagnosis of acute pancreatitis

A

Criteria at least 2:
-Abdominal pain
-Serum amylase and/or lipase >=3x normal
-Imaging

If severe, leads to autodigestion of pancreatic tissue, leading to systemic inflammatory response affecting V, resp, hepatic, renal systems, DIC

No feeds if severe, but do enteral feeds in less severe cases

Valproic acid implicated in hemorrhagic severe acute pancreatitis

41
Q

Best vascular access for CRRT

A
  • first choice RIJ - straight path to SVC/RA junction
  • second choice femoral vein, has to be sufficient length to access the IVC for sufficient flow
42
Q

Goal flow rate for CRRT?

A

5-10 mL/kg/min

total blood volume 70 mL/kg

43
Q

Classic triad presentation of renal vein thrombosis?

A

thrombocytopenia, macroscopic hematuria, flank mass or pain

Causes: nephrotic syndrome, hypercoagulable state, trauma, complications of renal transplant, CVL complications, severe dehydration

Dx with CT angio

44
Q

Lab evidence of citrate lock

A

Total calcium / iCa > 2.5

Total calcium rises but all is bound to citrate (locked) so iCa is low

45
Q

B-vitamin deficiencies

A

B12 (cobalamin) - vegan diets, causes megaloblastic anemia, weakness, cognifitve dysfunction, ataxia, hypersegmented neutrophils

B9 (folate) - green leafy vegetables, fruits, yeast, fortified cereals, goat milk diet for kids, megaloblastic anemia, weakness, behvior disorders

B3 (niacin) - essential in redox reactions, meats, poultry, fish, fortified cereals, legumes, pellagra - diarrhea, dermatitis, dementia, glossitis, angular stomatitis

B1 (thiamin) - pork, eggs, legumes, nuts, fortified cereal, beriberi, fatigue, weakness, weight loss, ataxia, edema

46
Q

Osmolar gap

A

Calculated vs measured >10
2xNa + gluc/18 + BUN/2.8

47
Q

Management of button battery ingestion

A
  1. Emergent endoscopy
  2. Honey or sucralfate