Key Questions

Question 1

-A hypertensive patient develops chronic renal failure from progressive nephrosclerosis. Which of the following should you expect to occur as a result?

A)A decrease in the fractional excretion of sodium

B)An increase in the free water clearance

C)A decrease in net acid excretion

D)A decrease in the excretion of creatinine

E)No change in the anion gap

Answer 1

Correct D

-The excretion of creatinine, which is neither reabsorbed nor secreted in any significant amount, is dependent on filtration, which is in turn dependent on renal plasma flow. The decrease in renal plasma flow that accompanies chronic renal failure results in a decrease in creatinine excretion and an increase in plasma creatinine concentration.

Question 2

-A 33-year-old male is brought to the emergency department with pain in his lower abdomen that radiates to his inner thigh and scrotum. He is afebrile. The urinalysis shows 3+ blood, no protein, and 20 to 40 RBCs/hpf.

A tender testicle

High urine calcium

Low urine osmolality

Right lower quadrant tenderness

Urinary RBC casts

Urine leukocytes

Urine muddy-brown granular casts

Answer 2

-Ca++-oxalate stone

Question 3

A 30-year-old woman comes to the emergency department because of a 3-day history of a burning sensation with urination, flank pain, and fever. She has a history of recurrent urinary tract infections. Temperature is 38.3°C (100.9°F ) and pulse is 110/min. On examination there is left costovertebral angle tenderness. Urinalysis reveals a pH of 8.5 and is positive for blood, leukocyte esterase, and nitrite. X-ray of the abdomen is shown.–>Staghorn calculi

Enterococcus faecalis

Escherichia coli

Proteus mirabilis

Pseudomonas aeruginosa

Staphylococcus saprophyticu

Answer 3

P.mirabilis
-alkaline urine pH suggests that this UTI is due to an organism that makes urease.
-are gram-negative, as suggested by the positive urine nitrite test.

Question 4

A 4-year-old child is brought to her pediatrician by her parents. Over the past several days, they have noticed swelling of her eyelids, and she has vomited twice in the past two days. She has no significant past medical history. Her vital signs are a temperature of 98.6°F, blood pressure of 97/62 mm Hg, and pulse of 76 bpm. Laboratory testing reveals an albumin of 2.2 gm/dL and total cholesterol of 243 mg/dL. A urine dipstick is positive for protein and negative for red blood cells and white blood cells. She is admitted to the hospital. Of the following, which would further testing most likely reveal?

A.Urine osmolality of 500mOsm/kg
B.Urine output of 300 mL in one day
C.4.0 g/day of protein in the urine
D.Red blood cell casts
E.Leukocyte esterase positivity in the urine

Answer 4

C correct
-Vignett describes nephrotic syndrome.

Question 5

37-year-old female presents to an acute care clinic. Over the past several days, she has noticed swelling of her eyelids and she has experienced nausea and vomiting several times in the past two days. She has no significant past medical history. Her vital signs are a temperature of 98.6°F, blood pressure of 97/62 mm Hg, and pulse of 91 bpm. Laboratory testing reveals an albumin of 2.2 gm/dL and total cholesterol of 243 mg/dL. A urinalysis is positive for protein, negative for red blood cells, and white blood cells. She is admitted to the hospital. Overnight testing reveals 4.1 g/24 hrs of protein in the urine. A renal biopsy is performed. Immunofluorescence staining reveals granular IgG positivity, and electron microscopy reveals subepithelial immune complexes. Of the following, what is the diagnosis?

A.Minimal change disease
B.Focal segmental glomerulosclerosis
C.Membranous glomerulonephropathy
D.Postinfectious glomerulonephritis
E.Type I membranoproliferative glomerulonephritis

Answer 5

C corrects answer** (has sub-epithelial deposits)**

-FSGS has NO immune deposits.

Question 6

A pathologist is examining a kidney biopsy and notes that some of the glomeruli have sclerosis of a portion of the glomerulus. Of the following, what feature was most likely identified in the patient prior to the biopsy?

A.Blood pressure of 171/93 mm Hg
B.Proteinuria of 2.5 g/day
C.Tinnitus
D.Red blood cell casts
E.Increased serum concentration of lipoprotein(a)

Answer 6

E.

Question 7

A 7-year-old girl is brought to the clinic because of a 5-month history of fatigue and diffuse muscle weakness. Her mother reports that the patient has been drinking more water lately and urinates frequently. Family history is remarkable for an inherited kidney defect in the patient’s father. She is small for her age (5th percentile). Blood pressure is 70/50 mm Hg. Serum studies show:

Na+: 142 mEq/L
K+: 2.8 mEq/L
Cl–: 90 mEq/L
HCO3–: 34 mEq/L
Creatinine: 0.9 mg/dL
Glucose: 100 mg/dLRenin: 60 ΜU/mL (normal: 21-41 ΜU/mL)

Urinalysis reveals osmolality of 130 mOsm/kg and calcium clearance of 500 mg/day (normal: 100-300 mg/day).

The patient’s underlying pathology is most similar to the mechanism of action of which of the following drugs?

Acetazolamide
Amiloride
Furosemide
Hydrochlorothiazide
Spironolactone
Triamterene

Answer 7

Furosemide.
-Look at values
Thiazide dosent promote Ca++ excretion

-Bartter syndrome is a rare inherited cause of hypokalemia due to mutations in the Na+/K+/2Cl– transporters in the thick ascending loop of Henle.
Bartter syndrome causes tubular effects similar to furosemide, including increased urine calcium excretion and impaired ability to concentrate urine.

Question 8

Altitude sickness

Answer 8

-Altitude sickness is associated with **cerebral edema **and respiratory alkalosis and can present with headache, vomiting, and confusion.

-Acetazolamide is a carbonic anhydrase inhibitor that causes HCO3– wasting, metabolic acidosis, and subsequent diuresis.

Question 9

A 58-year-old man begins taking furosemide because of worsening pedal edema and dyspnea due to dilative cardiomyopathy. At a follow-up examination 2 weeks later, he reports feeling better. Laboratory tests show a venous pH of 7.48, venous partial pressure of carbon dioxide of 48 mm Hg, and serum bicarbonate of 35 mEq/L.

Which of the following is an effect of furosemide that best explains the patient’s abnormal laboratory values?

Decreased aldosterone
Decreased renin synthesis
Increased minute ventilation
Increased proximal tubule ammoniagenesis
increased sodium delivery to the distal nephron
Respiratory alkalosis with metabolic compensation

Answer 9

-increased sodium delivery to the distal nephron

-Loop diuretics cause metabolic alkalosis by stimulating renal hydrogen ion excretion. This occurs in two ways. Loop diuretics inhibit the Na+/K+/2Cl– loop transporters, causing sodium chloride diuresis. The increased sodium delivery to the distal nephron stimulates the distal sodium channels (aldosterone sensitive) to reabsorb more sodium. This stimulates the cells to secrete hydrogen ions and potassium, partly explaining the metabolic alkalosis (and hypokalemia) induced by loop diuretics. In addition, the volume depletion caused by loop diuretics leads to secondary hyperaldosteronism, leading to an additional aldosterone-mediated hydrogen ion loss in the same cells. The resulting alkalosis inhibits alveolar ventilation, which causes the PCO2 to rise, that is, a respiratory compensation.

Question 10

A 73-year-old man comes to the clinic with a painful, swollen right great toe. He also has hypertension and congestive heart failure and was started on multiple medications for these disorders at the last clinic visit.

Which of the following medications is the most likely cause of his new symptoms?

Digoxin
Enalapril
Furosemide
Metoprolol
Spironolactone
Verapamil

Answer 10

Furosemide

-Gout is often, but not always, associated with elevated serum uric acid levels (hyperuricemia). Elevated uric acid can be associated with several medications, including thiazide and loop diuretics like furosemide (see table). These drugs decrease urinary uric acid excretion and so raise the serum uric acid level. Furosemide is a potent loop diuretic that is commonly used to treat heart failure.

Question 11

Diagnosis and Relation to Renal system:

-Failure of normal bone resorption due to defective osteoclasts thickened,dense bones that are prone to fracture.Mutations (eg,carbonic anhydrase II) impairability of osteoclast to generate acidic environment necessary for bone resorption.Overgrowth of cortical bone fills marrow space–> pancytopenia ,extramedullary hematopoiesis (hepatosplenomegaly)
-Cranial nerve impingement and palsies due to narrowed foramina.
-X-rays show diffuse symmetric sclerosis(bone-in-bone,“stonebone app).

Answer 11

Osteopetrosis.
It relates renal system in that carbonic anhydrase deficency is associated with Renal Tubular acidosis.

Question 12

A 22-year-old woman presents to her family physician because of increasing fatigue and pale appearance. She reports that her urine appears brown each morning. There is no history of major medical illness. Laboratory studies show RBC of 3 million/mm3 and hemoglobin 10 g/dL.

Which of the following best describes the most likely mechanism of erythrocyte injury in this condition?

-A defective cytoskeleton-membrane tethering protein
-Complement-mediated hemolysis
-Increased oxidative injury by H2O2 due to decreased NADPH
-Phagocytosis of RBCs due to complement fixation
-Phagocytosis of RBCs, which have surface-bound IgG
-Point mutation in the hemoglobin β-chain

Answer 12

-PNH is caused by complement-mediated lysis of RBCs. This is due to an acquired mutation of the PIGA gene within myeloid stem cells, required to make functioning glycosylphosphatidylinositol anchors for CD55 (decay accelerating factor) and CD59 (MAC inhibitory protein). These proteins, when attached to the cell membrane, protect cells against complement-mediated attack, so the absence of the anchoring protein makes RBCs subject to complement-mediated attack. In PNH, hemolysis of RBCs occurs at night as the carbon dioxide level rises during sleep, lowering pH levels (mild respiratory acidosis) and facilitating complement-mediated lysis of RBCs. As a result, the first morning void reveals dark urine with progressive clearing during the day.

Question 13

Left and Right Hb dissociation curve with O2sat?

Answer 13

Left: Hb affinity towards O2 increases–>dosent release O2. (decr 2-3BPG, alkaline pH (Furosemide use), Low Temp., CO toxicity,vasodilators by forming MetHb–>reverse it with methylene blue.

*Right: *promotos decr Hb affinity towards O2–>promotes un-binding (incr 2-3BPG,exercise–>lactic acidosis Decr pH, Elvated Temp.,

Question 14

A 7-month-old boy is brought to the emergency department with a 4-hour history of vomiting and irritability. His mother reports that these episodes began 1 month ago. Solid food and fruit juice were added to his diet around the same time after being exclusively breastfed. Prior to this episode he had met all developmental milestones. On physical examination, his weight and height are at the 30th percentile, down from the 40th percentile at his 6-month checkup. He appears lethargic and diaphoretic. The abdominal examination is normal. The vomitus is nonbloody and nonbilious.

Which of the following abnormalities is most likely to be present in this patient?

Biliary obstruction
Hypoglycemia
Hypothyroidism
Intestinal intussusception
Low serum vitamin D

Answer 14

-Hereditary fructose intolerance presents upon introduction of fructose into the diet with irritability, vomiting, failure to thrive, lethargy, and diaphoresis.
-hypoglycemia due to an inhibition of hepatic gluconeogenesis and glycogenolysis. As fructose is ingested, it is rapidly converted into fructose-1-phosphate by fructokinase in the liver. Hereditary fructose intolerance is caused by a deficiency in aldolase B, responsible for the conversion of fructose-1-phosphate into glyceraldehyde and dihydroxyacetone phosphate(metabolites of Glycolyisis) The increased fructose-1-phosphate damages the liver, depletes phosphate, and inhibits hepatic gluconeogenesis and glycogenolysis, leading to hypoglycemia.

-Intestinal intussusception causes vomiting with pain. It occurs when the intestine folds into the section in front of it, leading to obstruction. It causes severe, crampy, progressive abdominal pain with vomiting in infants up to 3 years old. There is often a right-sided abdominal mass.
-Biliary atresia causes extrabiliary obstruction in young infants. There is jaundice, acholic stools, and dark urine reflecting the increased conjugated bilirubin.
-Hypothyroidism in infancy is caused by congenital thyroid dysgenesis or enzymatic defects in thyroid synthesis. It causes lethargy and slow bone growth, but may also show coarse facial features, poor appetite, diminished reflexes, and a hoarse cry with eventual intellectual disability.
-Rickets caused by low serum vitamin D is seen mostly in developing countries and is marked by delayed growth, parietal and frontal bossing, soft skull bones, and other bone deformities not present in this patient.

Question 15

Patient exposed to fires what type of poisoning should you suspect?

Answer 15

Cyanide

Question 16

A 47-year-old man is brought to the emergency department immediately after being evacuated from his apartment because of a fire. He reports headache, weakness, and vertigo. Physical examination is significant for confusion. Arterial blood gas analysis shows a pH of 7.2. Carboxyhemoglobin is normal. He is not responsive to supplemental oxygen.

Which of the following best characterizes the most likely diagnosis in this patient?

-Anion-gap acidosis
-Decreased venous oxygen saturation
-Increased arterial-venous oxygen gradient
-Respiratory acidosis

Answer 16

-Cyanide poisoning presents with central nervous system symptoms, acidosis, and increased methemoglobin.
Cyanide inhibits the electron transport chain, which results in an increase in anaerobic metabolism and subsequent increase in lactic acid production.
Increased serum lactic acid results in an anion-gap metabolic acidosis, due to increased anion in serum.
-High Anion Gap Metabolic Acidosis

-Decreased venous oxygen saturation can be seen in various conditions, either caused by increased peripheral oxygen utilization or decreased cardiac output.
-An* increased arterial-venous oxygen gradient would be seen in conditions that have increased oxygen utilization in the periphery such as in sepsis.
-Respiratory acidosis* is caused by lung disease resulting in increased dead space, reduced minute ventilation, or increased carbon dioxide production.

Question 17

A 30-year-old woman is brought to the emergency department after collapsing on her front lawn. Her medical history is unknown. On arrival in the emergency department, pulse is 108/min, blood pressure is 98/54 mm Hg, and oxygen saturation is 92% on room air. Laboratory analysis shows:

Serum:
Na+: 140 mEq/L
K+: 3.4 mEq/L
*Cl–: 116 mEq/L
HCO3–: 15 mEq/**L

Arterial blood:
pH: 7.32
pCO2: 30 mm Hg

Which of the following is the most likely explanation for these laboratory abnormalities?

Bulimia
Diabetic ketoacidosis
Diarrhea
Furosemide
Heroin overdose

Answer 17

-normal anion gap metabolic acidosis presents with low pH, low bicarbonate, and low pCO2 combined with a normal anion gap.
Diarrhea can cause normal anion gap metabolic acidosis and hypokalemia via gastrointestinal HCO3– and potassium loss.

-Bulimia would lead to a metabolic alkalosis, as the GI loss of hydrochloric acid due to vomiting leads to a transient increase in pH.
-Diabetic ketoacidosis leads to a high anion gap metabolic acidosis, due to increased unmeasured anions (ketones).
-Loop diuretics such as furosemide can lead to metabolic alkalosis due to volume depletion, renal loss of hydrogen ions, and secondary hyperaldosteronism.
-Heroin overdose would lead to a respiratory acidosis due to narcotic-induced hypoventilation.
-Spironolactone is a potassium-sparing diuretic that may cause a normal anion gap metabolic acidosis and hyperkalemia.

Question 18

Diagnosis

Infection od Campylobacter Jejuni and developed LMN lesions bilateral?

Answer 18

-patient has presented with ascending weakness that is consistent with Guillain-Barré syndrome (GBS). GBS is a demyelinating disease of peripheral nerves, suggested on the electromyography/nerve conduction testing here. Patients also develop acute, progressive, symmetric, ascending muscle weakness/paralysis with lack of reflexes in the involved extremities as a result of the ascending paralysis.

GBS causes an ascending paralysis resulting in symmetric weakness with absent reflexes.
A patient may develop hypoventilation and respiratory acidosis leading to respiratory arrest.
Respiratory acidosis is demonstrated by low pH, high PCO2, and high bicarbonate.

Question 19

A 43-year-old woman comes to the emergency department with vomiting and a fever for 3 days. She feels dizzy when she rises from a seated position. Laboratory tests show a blood pH of 7.5, HCO3– of 35 mEq/L, PO2 of 85 mm Hg, and PCO2 of 45 mm Hg.

Which of the following renal tubular mechanisms most likely contributes to the laboratory findings?

ADH binding to cells in the collecting duct
Decreased bicarbonate reabsorption by the proximal tubule
Decreased sodium reabsorption in the collecting duct
Increased Na+/H+ exchange in the proximal convoluted tubule
Increased activity of Na/K/2Cl cotransporter in ascending limb
Increased tubuloglomerular feedback

Answer 19

-Vomiting leads to loss of stomach hydrochloric acid and volume depletion, resulting in metabolic alkalosis (contraction alkalosis).
Tubular responses to contraction alkalosis are increased proximal bicarbonate reabsorption and increased aldosterone-driven collecting duct secretion of hydrogen ions.

-The loss of volume causes a reduction in the extracellular volume. This, in turn, leads to activation of the renin-angiotensin-aldosterone system (RAAS). Activation of the RAAS activates angiotensin II, which leads to increased Na+/H+ exchange in the proximal convoluted tubule via stimulation of the sodium-hydrogen antiporter. This leads to increased HCO3– reabsorption. Additionally, aldosterone acts on H+-ATPase on the apical membrane of the a-intercalated cells of the collecting duct to secrete hydrogen ions into the lumen, contributing to the metabolic alkalosis.

-Decreased bicarbonate reabsorption by the proximal tubule would occur in proximal renal tubular acidosis and with carbonic anhydrase inhibitors like acetazolamide.
-Decreased sodium reabsorption in the collecting duct is caused by diuretics such as amiloride, triamterene, and spironolactone.
-ADH binding to cells in the collecting duct may occur in dehydrated patients to increase water permeability. However, ADH does not have direct effects on acid-base status.
-The Na+/K+/2Cl– cotransporter in the ascending limb does not actively contribute to acid-base balance in metabolic alkalosis.
-Tubuloglomerular feedback does not directly affect acid-base status.

Question 20

A 51-year-old man comes to his primary care physician due to frequent fatigue, shortness of breath, general sleepiness, and an inability to concentrate. Physical examination shows an extremely obese, tired-looking man. Pulse is 70/min, respirations are 14/min, blood pressure is 145/95 mm Hg, and the patient has an elongated uvula. Serum studies show a sodium level of 140 mEq/L, potassium of 3.9 mEq/L, chloride of 100 mEq/L, and bicarbonate of 32 mEq/L.

Which of the following best explains this patient’s abnormal serum studies?

Carbonic anhydrase inhibition
Decreased proximal tubule ammoniagenesis
Extrarenal loss of acid
Hypercarbia
Insulin resistance

Answer 20

-Risk factors for OSA (obstructive Sleep apnea) include smoking, obesity, and upper airway soft tissue abnormalities.
OSA results in a chronic respiratory acidosis due to chronic hypercarbia.
-The patient’s OSA with elevated serum bicarbonate is most suggestive of a chronic respiratory acidosis due to chronic hypercarbia. The hypoventilation seen in OSA causes the partial pressure of carbon dioxide to rise, leading to low blood pH (respiratory acidosis). In chronic respiratory acidosis, the renal compensation is to retain bicarbonate at the proximal tubule, returning the blood pH back towards normal and raising the serum bicarbonate, as seen in this patient.

-Insulin resistance is not commonly associated with acid-base abnormalities and would not cause hypercarbia.
-Carbonic anhydrase inhibition and decreased ammoniagenesis present with metabolic acidosis.
-Vomiting may cause extrarenal loss of hydrochloric acid, leading to metabolic alkalosis.

Question 21

A 7-year-old girl is brought to the emergency department 10 hours after ingesting an unknown substance. The child appears uncomfortable and is seen holding both ears tightly. Temperature is 37.0°C (98.6°F), pulse is 90/min, respirations are 24/min, and blood pressure is 110/78 mm Hg. The physical examination is normal. Laboratory tests show:
Arterial blood gas
PaCO2: 22 mm Hg
PaO2: 110 mm Hg
pH: 7.51
Serum
Na+: 134 mEq/L
K+: 4.0 mEq/L
Cl–: 98 mEq/L
HCO3–: 17 mEq/L

Ingestion of which of the following substances is the most likely cause of this patient’s condition?

Acetaminophen
Aspirin
Benzodiazepine
Ethylene glycol
Sodium hydroxide

Answer 21

-This particular mixed acid-base disorder is classic for** aspirin overdose. **This is supported by the patient’s tinnitus. Toxic doses of aspirin (acetylsalicylic acid) increase the sensitivity of respiratory centers in the brain to changes in oxygen and carbon dioxide levels, and respiratory alkalosis is observed as a result of stimulation of the respiratory center, causing respiratory overdrive and hyperventilation. Acid products of metabolism (mostly lactic acid) accumulate over time, and an anion gap metabolic acidosis results.
-A primary respiratory disorder plus a superimposed elevated anion gap suggests a mixed acid base disorder—respiratory alkalosis with anion gap metabolic acidosis.
This mixed acid-base disorder is caused by aspirin overdose.

-Acetaminophen ingestion can lead to hepatocyte damage, drastically elevated aspartate aminotransferase and alanine aminotransferase levels, and centrilobular necrosis.
-Benzodiazepine (ie, tranquilizer) ingestion can lead to central nervous system depressant effects, respiratory acidosis, and rarely coma.
-Ethylene glycol (ie, antifreeze) ingestion can lead to development of hematuria and symptoms of renal failure, and urinalysis may reveal the presence of calcium oxalate crystals.
-Sodium hydroxide and potassium hydroxide (ie, drain-opening product) ingestion causes profound gastrointestinal erosion and metabolic alkalosis.

Question 22

A 55-year-old woman is brought to the emergency department by ambulance due to altered mental status. She was found in an alley surrounded by several empty bottles. Serum studies show a sodium level of 136 mEq/L, glucose of 90 mg/dL, blood urea nitrogen of 12 mg/dL, and osmolality of 320 mOsm/kg. Ethanol level is 0. Toxicology screen is positive for an ingested substance.

Additional laboratory findings would most likely reveal which of the following?

Elevated exogenous osmoles
Elevated transaminases
Metabolic alkalosis
Normal anion gap metabolic acidosis
Respiratory acidosis
Respiratory alkalosis

Answer 22

-This patient with altered mental status and elevated plasma osmolality (320 mOsm/kg ) most likely has ingested a nonethanol alcohol like methanol, propylene glycol, or ethylene glycol (ie, has elevated exogenous osmoles in the blood).
Hyperosmolarity is most often caused by increases in serum sodium, glucose, or urea (blood urea nitrogen; all normal here). If these are normal, an exogenous (ingested) osmole is present, most often ethanol (not present here). In a patient with** altered mental state, that leaves the synthetic alcohols, which can then be detected on toxicology screens. These can be toxic, since methanol **causes blindness and renal failure, and **ethylene glycol can cause acute kidney injury. All three cause anion gap metabolic acidosis. **Another approach to detecting these alcohols is by using the osmolar gap, the difference between the measured and calculated serum osmolality

Question 23

A 22-year-old female is brought to the emergency department after she was found unconscious by her roommate. Temperature is 38.2°C (100.8°F), pulse is 110/min, respiratory rate is 37/min, and blood pressure is 145/59 mm Hg. After arriving at the emergency department, she wakes up but is unresponsive to verbal stimuli. The physical exam is normal. Serum studies show:

Na+: 145 mEq/L
K+: 3.2 mEq/L
Cl–: 112 mEq/L
HCO3–: 13 mEq/L
Glucose: 95 mg/dL
Creatinine: 1.6 mg/dL
Arterial blood gas: pH 7.42, PCO2 22 mm Hg, and PO2 99 mm Hg

Which of the following is the most likely cause of this patient’s presentation?

Acetaminophen toxicity
Acute kidney injury
Diabetic ketoacidosis
Ethanol toxicity
Opiate toxicity
Panic attack
Salicylate toxicity

Answer 23

-Aspirin overdose is the classic cause of a mixed anion-gap metabolic acidosis and respiratory alkalosis. The aspirin stimulates the respiratory center to hyperventilate, and the formation of lactic acid causes the high anion gap and metabolic acidosis. The same mixed disorder could also be seen in patients with pneumonia and sepsis, with the pneumonia causing hypoxemia and respiratory alkalosis and the sepsis causing lactic acidosis.

-Need to use Winters formula and anion gap.

Question 24

A 44-year-old man comes to his primary care physician because of fatigue and shortness of breath with exertion that have worsened gradually during the past year. He was diagnosed with obstructive sleep apnea last year. He does not smoke. He is 182.88 cm tall (6 ft) and weighs 150.59 kg (332 lb), and his body mass index is 45 kg/m2. There are no murmurs on cardiac examination or abnormal pulmonary sounds on auscultating the lung fields. Arterial blood gas shows:

PaO2: 65 mm Hg
PaCO2: 57 mm Hg
pH: 7.35
Serum HCO3–: 30 mEq/L

X-ray of the chest is normal.

Which of the following is the most likely complication of this patient’s condition?

Decreased diffusion capacity for carbon monoxide
Destruction of alveoli
Intrapulmonary shunting
Jugular venous distention
Left atrial dilation

Answer 24

-This patient is most likely to have obesity hypoventilation syndrome (OHS), based on his obesity (body mass index [BMI] >30 kg/m2), hypercarbia (PCO2 >45 mm Hg), and lack of other causes of chronic pulmonary disease, such as a history of smoking or chronic obstructive pulmonary disease (COPD). Patients with OHS commonly have insidious-onset dyspnea with evidence of hypercapnic respiratory failure, morbid obesity (BMI >40 kg/m2), respiratory acidosis (elevated CO2 in the setting of increased bicarbonate), and concurrent obstructive sleep apnea (OSA), as seen here. OHS and OSA are similar, but OSA is much less likely to show a chronic respiratory acidosis, as seen in this patient.

-Patients with OHS commonly develop pulmonary hypertension, which can, over time, cause right heart failure, which can lead to jugular venous distention, hepatomegaly, and edema.

Question 25

A 72-year-old man is brought to the emergency department with nausea and fatigue. He has end-stage renal disease and 2 days ago he missed his routine hemodialysis appointment. Current medications include enalapril, verapamil, erythropoietin, calcitriol, and oral phosphate binders. Blood pressure is 148/100 mm Hg and oxygen saturation is 95% on room air. Serum potassium level is 6.0 mEq/L. He has edema in both legs. His ECG is normal. Which of the following additional laboratory findings is most likely to be seen in this patient? High anion gap metabolic acidosis Metabolic alkalosis Normal anion gap metabolic acidosis Respiratory acidosis Respiratory alkalosis

Answer 25

Uremia, a syndrome caused by the kidney’s inability to excrete toxins, sodium, potassium, water, and other elements, is often seen in patients with ESRD. Uremia is associated with a high anion gap metabolic acidosis. -Uremia is due to the kidney’s inability to excrete toxins, sodium, potassium, water, and other elements. Other symptoms of uremia may include anorexia, pericarditis, asterixis, encephalopathy, and platelet dysfunction.

Question 26

A 24-year-old primigravid woman at 8 weeks of gestation comes to the physician because of severe nausea and vomiting for the past 9 days and a 3-kg (7-lb) weight loss. She denies recent sick contacts. On examination today, her weight is 45.5 kg (100 lb) and blood pressure is 110/70 mm Hg supine and 90/60 mm Hg standing. Which of the following additional findings is most likely in this patient? Hyperkalemia Low serum aldosterone levels Metabolic acidosis Proteinuria Urine ketones

Answer 26

Given this patient’s severe nausea and vomiting in pregnancy with weight loss >5% of her body weight and orthostatic hypotension, this patient likely has hyperemesis gravidarum. Although there is no single accepted definition for hyperemesis gravidarum, it is the extreme of nausea and vomiting in pregnancy. The most common presentation includes persistent vomiting not related to other causes and loss of pregnancy weight (at least 5%). Patients with hyperemesis gravidarum show ketonuria due to lack of food intake, along with other findings of vomiting such as metabolic alkalosis (loss of hydrogen chloride), hypokalemia (renal loss of potassium), and elevated blood urea nitrogen and creatinine (prerenal acute kidney injury).

Question 27

A 59-year-old man presents to the clinic reporting lethargy, weakness, and bone pain over the past 2 years. History reveals a pathologic hip fracture 1 year ago. X-rays show several small, hypodense lesions in the hip and spine. Serum protein concentration is 9 g/dL, serum creatinine is 1.6 mg/dL, and urine dipstick shows 3+ protein and no blood. A serum protein electrophoresis reveals elevated gamma globulins with a monoclonal pattern. Which of the following glomerular lesions would most likely be found on a renal biopsy in this patient? Epithelial crescents Fibrosis of limited portions of some glomeruli without immune deposits Mesangial and subendothelial deposits that stain positive with Congo red Mesangial proliferation Podocyte foot process effacement on electron microscopy with normal light microscopy

Answer 27

-Multiple myeloma often presents with bone pain from lytic bone lesions, proteinuria, and a monoclonal increase in gamma globulins (M spike) on serum protein electrophoresis. Systemic primary amyloidosis, in which amyloid is deposited in the mesangium and subendothelium, can develop in association with multiple myeloma and lead to the deposition of Congo red–positive amyloid within glomeruli. -This patient presents with lethargy, bone pain with hypodense, lytic bone lesions, and a monoclonal increase in gamma globulins, commonly referred to as an M spike, on serum protein electrophoresis. This clinical picture is strongly indicative of multiple myeloma. Patients with myeloma commonly have fatigue, weight loss, and hypercalcemia. -The most common form of renal disease in multiple myeloma is cast nephropathy, caused by the precipitation of free light chains in the tubules. A second possible renal complication of multiple myeloma is primary amyloidosis, in which there are fibrillary mesangial and subendothelial deposits that stain positive with Congo red, as amyloid is deposited in the glomerulus. Staining of amyloid with Congo red yields apple-green birefringence, shown in the image. This process eventually results in glomerular damage, albuminuria (seen in the 3+ urine protein here), and progressive chronic kidney disease with rising serum creatinine. Primary amyloidosis may also involve other organs, like the liver, peripheral nerves, and heart. -Fibrosis of limited portions of some glomeruli without immune deposits describes focal segmental glomerulosclerosis, which can occur in HIV, injectable drugs use, morbid obesity, and sickle cell disease. Podocyte foot process effacement on electron microscopy with normal light microscopy describes minimal change disease. It is the most common cause of nephrotic syndrome in children, but may also be seen in adults. Epithelial crescents, which are proliferating cells adherent to Bowman capsule describes rapidly progressive glomerulonephritis caused by lupus, vasculitis, and other nephritic diseases. It causes renal failure that often develops over weeks to months, and UA would show proteinuria and hematuria. Mesangial cell proliferation can be seen in several glomerular disease, e.g. diabetic nephropathy and early focal segmental glomerulosclerosis. These diseases would all show proteinuria.

Question 28

A 76-year-old man comes to the clinic with fever, sinus congestion, and a rash. Temperature is 38.9°C (102°F) and blood pressure is 148/100 mm Hg. Physical examination reveals a purpuric rash on his lower extremities and pus-like drainage with crusts from the nose. The patient mentions that he had similar symptoms before but less acute. He also mentions nosebleeds, fatigue, and numbness in limbs. Urinalysis reveals 4+ hematuria and 1+ proteinuria. Serum creatinine level is 2.6 mg/dL and was 1.1 mg/dL 2 months ago at his annual checkup. Antinuclear antibodies are negative. CT scan of the sinus shows diffuse sinusitis with features suggestive of chronic inflammation of the sinuses. Which of the following additional serum findings is most likely? Decreased C3 and C4 0% Elevated IgA Elevated anti-basement membrane antibodies Positive anti-dsDNA antibodies Positive antistreptolysin antibody Positive cytoplasmic antineutrophilic cytoplasmic antibodies

Answer 28

Step 1: Disease Diagnosis This older patient has the nephritic syndrome (hematuria, mild proteinuria, and hypertension with a worsening serum creatinine) (see table below). The antinuclear antibody is negative, making lupus nephritis unlikely. The recurrent (or chronic) sinusitis, purpuric rash, and fever make the likely diagnosis of granulomatosis with polyangiitis (formerly called Wegener granulomatosis). This is a form of small-vessel vasculitis classically associated with upper respiratory inflammation such as severe sinusitis, otitis, nasal discharge, and hearing loss. Upper and lower airway disease, conjunctivitis, and neuropathy are also common. Step 2: Diagnostic Testing Patients with granulomatosis with polyangiitis have elevated serum levels of cytoplasmic antineutrophil cytoplasmic antibodies (c-ANCA) levels in serum but are antinuclear antibody (ANA) negative. Definitive diagnosis requires a biopsy specimen showing granulomatous inflammation in sinuses or glomeruli. The other choices are incorrect: Positive antistreptolysin antibody would be seen in poststreptococcal glomerulonephritis, which would not show purpura. Decreased C3 and C4 and positive anti-dsDNA antibodies would be seen in lupus nephritis, which would show an elevated ANA. Elevated IgA is sometimes (<50%) associated with IgA nephropathy or IgA vasculitis, which is seen in children in 90% of cases and is uncommon in older patients. Half of cases follow an acute upper respiratory infection, not the chronic sinusitis seen here. Elevated anti-basement membrane antibodies are characteristic of Goodpasture syndrome, which would show hemoptysis and dyspnea.

Question 29

A 28-year-old man comes to the physician because he has been coughing up blood for the past week, which started after he was diagnosed with an upper respiratory infection. He traveled to Thailand last month. He does not smoke. Temperature is 38.2°C (100.8°F). Pulmonary auscultation reveals diffuse crackles. Urinalysis shows 1+ protein and 3+ blood. Which of the following is the most likely cause of this patient’s pulmonary symptoms? Autoantibodies against DNA Autoantibodies against type IV collagen Hepatorenal syndrome Infection of large bronchi Neoplasia Pulmonary granulomas

Answer 29

This patient presents with hematuria, mild proteinuria, and hemoptysis, suggesting a pulmonary-renal syndrome. The most likely cause is Goodpasture syndrome, which leads to pulmonary hemorrhage plus rapidly progressive glomerulonephritis (hematuria, proteinuria, RBC casts, rising serum creatinine, crescents on renal biopsy), associated with anti–glomerular basement membrane (anti-GBM) antibodies located on renal and lung biopsy. This autoimmune condition can be triggered by a recent upper respiratory infection. Other causes of pulmonary renal syndrome (not associated with anti-GBM antibodies) include: Systemic lupus (lung vasculitis with lupus nephritis), but he lacks other manifestations of lupuslike rash or arthralgia Granulomatosis with polyangiitis—this typically presents with upper respiratory symptoms (eg, sinusitis, otitis) and skin lesions (eg, purpura), not seen here. Eosinophilic granulomatosis with polyangiitis—this presents in patients with asthma, showing sinusitis and peripheral neuropathy, not seen here. Step 2: Disease Mechanism Goodpasture syndrome is a type II hypersensitivity reaction resulting from autoantibodies against basement membranes in the glomerulus and alveoli. More specifically, the autoantibodies form against the type IV collagen found in the basement membranes. This leads to destruction of basement membrane proteins and both glomerular and alveolar damage. The other choices are incorrect: A neoplasia, such as lung cancer, would not lead to hematuria, proteinuria, and fever. Anti–double-stranded DNA antibodies are common in systemic lupus erythematosus, which would present with skin rash, photophobia, arthritis, serositis, and mouth ulcers. Infection of large bronchi is seen in bronchitis, which does not present with hematuria and proteinuria. Hepatorenal syndrome is a consequence of end-stage liver disease and presentation would include jaundice, ascites, and gastrointestinal bleeding. Pulmonary granulomas are seen in tuberculosis, which would present with upper respiratory symptoms (sinusitis, otitis) but not hematuria and proteinuria.-

Question 30

A 55-year-old man is brought to the emergency department after a motor vehicle accident. Temperature is 37°C (98.6°F), pulse is 140/min, and blood pressure is 100/62 mm Hg. Paramedics noted that he vomited blood multiple times during the transfer to the hospital. Physical examination shows trauma to the head, extremities, and abdomen. The stool is heme positive. He is transfused 2 units of packed RBCs because of low hematocrit with ongoing active bleeding and undergoes uneventful operative repair of the fractures. Gentamicin and ceftriaxone are given intraoperatively. The next day his vital signs are stable and laboratory studies show a blood urea nitrogen (BUN) of 42 mg/dL, a serum creatinine of 0.9 mg/dL, and a creatine phosphokinase of 60 U/L. Urine output is 100 mL/hr with normal urinalysis. Which of the following is the most likely cause of the patient’s elevated BUN? -Acute interstitial nephritis due to cephalosporins -Aminoglycoside nephrotoxicity -Bilateral renal obstruction due to traumatic urethral injury -Myoglobinuria -RBC hemolysis in the gastrointestinal tract leading to increased urea production -Renal papillary necrosis

Answer 30

-A patient with massive trauma is anemic and has an elevated BUN. Normally, in acute kidney injury (AKI), both the BUN and creatinine rise together. Because the serum creatinine is the best indication of reduced glomerular filtration rate (GFR), and it is normal here, this patient does not have AKI, but instead, the high BUN is likely due to an isolated increase in urea synthesis or reabsorption. Since his stools are heme positive (indicating GI bleeding), the high BUN is likely due to RBC hemolysis in the gastrointestinal tract leading to increased urea production, not a drop in GFR. The BUN can increase without an increase in the creatinine after a high-protein meal or, as in this case, when there is gastrointestinal bleeding. The RBCs hemolyze in the gut and the protein is taken up by the liver and catabolized to urea, which increases the BUN. The other choices are incorrect: Acute tubular necrosis due to muscle trauma (rhabdomyolysis) with myoglobinuria could occur in a hypotensive trauma patient. However, the serum CPK would be elevated (not seen here), and the urinalysis would be remarkable for heme-positive urine without RBCs, due to myoglobinuria and possibly muddy brown casts. Aminoglycoside nephrotoxicity can cause acute tubular necrosis after 5 to 10 days of drug therapy. Acute tubular necrosis would present with muddy brown casts and/or renal tubular epithelial cells. Drug-induced acute interstitial nephritis is typically due to antibiotic use or nonsteroidal anti-inflammatory drugs. Both the BUN and creatinine would rise in acute interstitial nephritis, and this typically occurs after at least 5 days following initiation of drug. Bilateral renal obstruction would lead to no urine output (anuria). Renal papillary necrosis is typically associated with diabetes mellitus, acute pyelonephritis, chronic acetaminophen use, sickle cell anemia, and sickle cell trait.

Question 31

A 67-year-old man recovering from hip surgery in the hospital is found to have a urinary output of 400 mL/24 hours. Examination shows 3+ peripheral edema. His blood urea nitrogen is 76 mg/dL and creatinine is 3 mg/dL; both were normal on admission. His urine sodium is 14 mEq/L, and fractional excretion of sodium is 0.54%. The urinalysis is normal. Which of the following is most likely to cause this patient’s condition? -Acute interstitial nephritis -Acute tubular necrosis -Heart failure -Prostatic hyperplasia -Right renal artery stenosis

Answer 31

The patient has likely prerenal acute kidney injury (AKI), based on oliguria, a rising serum creatinine, high blood urea nitrogen (BUN):creatinine ratio (>20), low urine sodium (<20), and low fractional excretion of sodium (<1%). This is AKI due to low renal perfusion, which causes a drop in glomerular filtration rate and is usually reversible with correction of the underlying cause of hypoperfusion. Step 2: Disease Mechanism Causes of prerenal AKI include anything that reduces renal perfusion, including volume depletion, heart failure, liver failure (with vasodilation and reduced serum oncotic pressure), and bilateral renal artery stenosis. The increased edema in this patient makes volume depletion unlikely, and there are no ascites to suggest liver failure, so of the listed answers heart failure is the most likely diagnosis. The kidney responds to hypoperfusion by increasing tubular reabsorption of sodium with water following passively. This leads to a low fractional excretion of sodium (<1%). Increased proximal tubule urea reabsorption linked to sodium reabsorption leads to a higher serum BUN, so the BUN:creatinine ratio increases to >20. The other choices are incorrect: Acute interstitial nephritis and acute tubular necrosis are causes of intrarenal AKI. Prostatic hyperplasia causes postrenal AKI. **Right renal artery stenosis will not cause AKI because the remaining normal kidney can compensate for the reduced renal function of the kidney with compromised blood flow.**

Question 32

75-year-old man with end-stage renal disease is diagnosed with a tibial fracture after he hit his right leg on his kitchen table. He is found to have severe metabolic bone disease. A change in which of the following is most likely contributing to this patient's findings? Decreased parathyroid hormone secretion Decreased renal calcium filtration Decreased renal phosphate filtration Decreased renal phosphate reabsorption Decreased renal production of 25-OH vitamin D3 Increased renal calcium reabsorption

Answer 32

In ESRD, the reduced GFR leads to reduced filtration of phosphate. The hyperphosphatemia reduces the serum calcium by precipitation throughout the body. Also, the failing kidney fails to convert 25-OH vitamin D3 to 1,25-(OH2) vitamin D3 (calcitriol). This further contributes to hypocalcemia. The hypocalcemia stimulates PTH production, causing secondary hyperparathyroidism. PTH binds to osteoblasts and stimulates bone resorption, leading to the bone disease. In summary, the decreased calcium absorption and hyperphosphatemia both contribute to hyperparathyroidism that may cause renal osteodystrophy. The other choices are incorrect: Increased calcium absorption is not seen in chronic kidney disease. Rather, there is decreased calcium absorption. Decreased parathyroid hormone secretion occurs in primary hypoparathyroidism, or in hypercalcemia of malignancy or granulomatous disease, not in ESRD. Decreased renal calcium reabsorption would lead to hypocalcemia and secondary hyperparathyroidism in a patient without ESRD. In patients with ESRD, there is very low or no calcium filtration, so there is little calcium for the tubules to absorb. ESRD decreases renal production of 1,25-(OH2) vitamin D3 (calcitriol), not 25-OH vitamin D3, which is made in the liver. Decreased renal phosphate reabsorption would lead to hypophosphatemia, which is not seen in this patient’s disorder.

Question 33

A 42-year-old woman has end-stage renal disease due to diabetic nephropathy. She undergoes hemodialysis three times per week and has no urine output. Prior to a dialysis treatment her serum studies show a sodium concentration of 130 mEq/L and potassium of 5.8 mEq/L. Which of the following best explains the patient’s abnormal laboratory values immediately before dialysis? Decreased sodium reabsorption, decreased potassium secretion Decreased water filtration, decreased potassium filtration Decreased water filtration, increased potassium reabsorption Increased water reabsorption, decreased potassium filtration Increased water reabsorption, decreased potassium secretion Increased water reabsorption, increased potassium reabsorption

Answer 33

This patient with end-stage renal disease (ESRD) has a glomerular filtration rate of zero, based on her lack of urine output. This is typical of patients with prolonged ESRD. These patients have essentially nonfunctional kidneys, lacking all the functions of filtration, reabsorption, and tubular secretion. The patient’s hyponatremia and hyperkalemia are most likely due to the absence of glomerular filtration of water and potassium. Because patients ingest foods and beverages that have excess water (hypotonic intake), there will be accumulation of total body water and progressive hyponatremia until the patient is dialyzed. At dialysis the excess water and potassium are both removed, and the patient’s lab values will normalize. The other choices are incorrect as they would cause hyponatremia and hyperkalemia in patients with functioning kidneys, but not in patients with ESRD and a GFR of zero.

Question 34

A 29-year-old man with chronic hepatitis C virus infection has noted dark urine for the past 2 weeks. On examination he is hypertensive but afebrile. Laboratory studies show serum creatinine of 3.8 mg/dL and urea nitrogen of 35 mg/dL,Cryoglobulins are detected. Urinalysis shows RBCs and RBC casts. A renal biopsy is performed and microscopically shows hypercellular glomeruli with lobulation and a double-contour appearance to split basement membranes adjacent to subendothelial immune complexes. Which of the following cell types has most likely proliferated in his glomeruli? A Juxtaglomerular cells B Mesangial cells C Parietal epithelial cells D Podocytes E Endothelial cells

Answer 34

-B )The appearance of membranoproliferative glomerulonephritis, a cause for nephritic syndrome in adults, is described. **Mesangial cells** have a phagocytic function, but they also can e**laborate inflammatory mediators, cytokines, and matrix.** **Proliferation of mesangial cells may be induced by injury, particularly immune complex deposition**. Juxtaglomerular cells secrete renin. Parietal epithelial cells line the Bowman capsule and may proliferate with severe glomerular injury to produce crescents. Podocytes are visceral epithelial cells that form the filtration barrier. Endothelial cells are most likely to be damaged with thrombotic microangiopathies

Question 35

Answer 35

B) The figure shows glomeruli with epithelial crescents indicative of a rapidly progressive glomerulonephritis. Crescentic GN is divided into three groups on the basis of immunofluorescence: type I (anti–glomerular basement membrane [GBM] disease); type II (immune complex disease); and type III (characterized by the absence of anti-GBM antibodies or immune complexes). Each type has a different cause and treatment. The presence of anti-GBM antibodies suggests Goodpasture syndrome; patients with this disorder require plasmapheresis. Type II crescentic GN can occur in systemic lupus erythematosus, in Henoch-Schönlein purpura, and after infections. Causes of type III crescentic GN include granulomatosis with polyangiits (ANCA-associated vasculitis) and microscopic polyangiitis. A positive ANA test result may be reported in patients with lupus nephritis, which uncommonly manifests with glomerular crescents. HIV nephropathy has features similar to those of focal segmental glomerulosclerosis (FSGS), which is not rapidly progressive

Question 36

Answer 36

D Corticosteroid-resistant hematuria and proteinuria **leading to hypertension and renal failure** is** typical for focal segmental glomerulosclerosis** (FSGS). FSGS is now the m**ost common cause of nephrotic syndrome in adults in the United States**. Specialized extracellular areas overlying the glomerular basement membrane between adjacent foot processes of podocytes are called slit diaphragms, and these exert control over glomerular permeability. Mutations in genes affecting several proteins, including** nephrin and podocin**, have been found in inherited cases of FSGS; podocyte dysfunction, possibly **caused by cytokines or unknown toxic factors**, may be responsible for acquired cases of FSGS. FSGS with collapsing glomerulopathy is seen in patients with **HIVassociated nephropathy**, **Sickle cell,Heroin** -Ass with Hispanic patients.

Question 37

A 57-year-old man comes to the office to establish care. He has no known medical history or prior surgeries. Pulse is 72/min and blood pressure is 145/93 mm Hg. Laboratory testing reveals a hemoglobin A1c of 6.9% and microalbuminuria. The patient is diagnosed with diabetes mellitus and is informed of a medication that can reduce his blood pressure and slow the damaging effects of diabetes on his renal and cardiovascular systems. Which of the following is the most likely adverse effect of the medication described? Hypercalcemia Hyperkalemia Hyperlipidemia Impotence Myositis Ototoxicity

Answer 37

ACHE INHB cause hyperkalemia

Question 37

A 57-year-old man comes to the office to establish care. He has no known medical history or prior surgeries. Pulse is 72/min and blood pressure is 145/93 mm Hg. Laboratory testing reveals a hemoglobin A1c of 6.9% and microalbuminuria. The patient is diagnosed with diabetes mellitus and is informed of a medication that can reduce his blood pressure and slow the damaging effects of diabetes on his renal and cardiovascular systems. Which of the following is the most likely adverse effect of the medication described? Hypercalcemia Hyperkalemia Hyperlipidemia Impotence Myositis Ototoxicity

Answer 37

ACHE INHB cause hyperkalemia

Question 38

An 8-month-old male infant presents with progressive renal and hepatic failure. Despite intensive medical therapy, the infant dies. At the time of autopsy, the external surfaces of his kidneys are found to be smooth, but cut section reveals numerous **cysts that are radially arramged, perpendicular to the renal capsule**. Which of the following is the mode of inheritance of this renal abnormality? Autosomal dominant Autosomal recessive X-linked dominant X-linked recessive Mitochondrial

Answer 38

**Autosomal recessive** Feedback: The Correct Answer is: B Infantile polycystic kidney disease typically presents in newborns, has an autosomal recessive pattern , is associated with congenital hepatic fibrosis. Grossly, these renal cysts have a radial spoke arrangement. ****

Question 39

Amniotic fluid, such as esophageal atresia or severe anomalies of the CNS, lead to polyhydramnios (too much amniotic fluid), while agenesis of the kidneys or urinary obstruction leads to oligohydramnios (too little amniotic fluid).

Question 40

A 2-year-old boy is brought to the pediatrician by his mother, who detected a lump on the right side of his abdomen while bathing him. Physical examination reveals a firm, nontender right-sided abdominal mass. Renal ultrasonography shows a mass extending from the right kidney. Which of the following complications is most likely in this child? Brain metastases Constricted pupil and lack of tear production High blood hemoglobin concentration Hyponatremia Pulmonary metastases

Answer 40

Wilms tumor commonly metastasizes to the lungs or abdominal lymph nodes and liver, and imaging is needed to determine stage. Pulmonary metastases are detected by x-ray of the chest, CT scanning, and liver function testing. There are associations with congenital WAGR (Wilms tumor, Aniridia, Genitourinary anomalies, and Range of developmental delays) syndrome; patients should also be evaluated for intellectual disability, aniridia (partial or complete absence of the ocular iris), and genitourinary anomalies such as cryptorchidism (undescended testes), as well as with Beckwith-Wiedemann syndrome (macroglossia, gigantism, hemihyperplasia). The other answer choices are incorrect: Polycythemia is a complication of renal cell carcinoma, not common in children. Horner syndrome is a complication of neuroblastoma. Brain metastases are a complication of rhabdoid tumors, a rare pediatric malignancy. Hyponatremia is not a common paraneoplastic complication of this type of cancer.

Question 41

## Footnote Amyloid deposits Complement over activation Antibodies against podocyte proteins Glomerular basement membrane antibodies Immune complez deposition

Answer 41

Complement overactivation (MPGN Type 1)

Question 42

Answer 42

H. -Case CKD (look at creatine=GFR) -Kidney decr EPO-->normocytic anemia -Loose H+ excretion ability + incr uremia-->decr Bi-carbonate +High anion gap metabolic acidosis. -Looses ability to excrete K+ + ACHE inhb. make it worse-->death by arrythmia.

Question 43

What is the commonest presentation of patients with RCC?

Answer 43

-Notice hematuria but no pain (flank pain ),no palbable mass, everything is normal,aside from Epo and Hematocrit (slighlty elavated)--> History of smoking present (>55yrs)

Question 44

Answer 44

Abnormal metanephric of kidney. -**Multicystic dysplastic kidney**-->Uteric bud failed to communicate to mesenchyme-->cyst formation and connective tissues (no normal tiss prsent).Usually unilateral, if bi lateral leads to Potter sequece.