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High Yield Topics-Renal Flashcards

1
Q

Normal values of pH, HCO3, and CO2 and their relationship

A 
pH = 7.4
HCO3 = 24
CO2 = 40
pH = HCO3/CO2
pH = metabolic/respiratory
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2
Q

Describe steps to determine primary deficit with compensatory MOA for acid/base problems

A
  1. Determine acidosis or alkalosis to given pH, HCO3, and CO2
  2. Matching = Primary deficit
  3. What’s left = compensatory MOA
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3
Q

Determine primary deficit with compensation for this example.

pH = 7.31 
HCO3 = 18
CO2 = 28
A 
pH = 7.31 --> acidosis
HCO3 = 18 --> metabolic acidosis
CO2 = 28 --> respiratory alkalosis
  • Metabolic acidosis w/ compensatory respiratory alkalosis
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4
Q

(Normal/Elevated) anion gap is due to loss of HCO3

A

Normal

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5
Q

(Normal/Elevated) anion gap is due to the presence of extra external acid (HCO3 is used to buffer the aci)

A

Elevated

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6
Q

Equation to determine compensation for metabolic acidosis

A

Winter’s formula:

Expected Pco2=1.5[HCO3-]+8 +/-2

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7
Q

In normal anion gap metabolic acidosis, if expected Pco2 > actual Pco2, then there is too little Pco2.

You have a “concomitant” respiratory

A

alkalosis

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8
Q

In normal metabolic acidosis, if expected Pco2 < actual Pco2, then there is too much Pco2.

You have a “concomitant” respiratory

A

acidosis

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9
Q

Diarrhea, renal tubular acidosis, and saline infusion are common causes of what acid-base disturbance?

A

Normal anion gap metabolic acidosis

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10
Q

Lactic acidosis, diabetic ketoacidosis, renal failure (uremia), and toxicities (methanol, ethylene glycol, salicylates) are common causes of what acid-base disturbance?

A

Elevated anion gap metabolic acidosis

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11
Q

Equation to check anion gap

A

AG = Na+ - (Cl- + HCO3-)

  • AG = 8-12 –> Normal AG
  • AG > 12 –> ↑AG
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12
Q

Glomerular disease caused by destruction of GBM negative charge and podocyte effacement (thinning) leading to protein leakage (proteinuria >3.5 g/day)

A

Nephrotic syndrome

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13
Q

Which nephrotic syndrome is described by the following:

Common in children after recent infection/immunization; Corticosteroids for tx

A

Minimal change disease

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14
Q

Normal histology on “LM” and podocyte effacement & fusion on EM are findings of

A

Minimal change disease

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15
Q

Which nephrotic syndrome is described by the following:

Common in AA and hispanics; caused by idiopathic, viral infections (HIV/Hepatitis), heroin abuse, or other conditions (sickle cell, obesity)

A

Focal Segmental Glomerulosclerosis

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16
Q

Segmental sclerosis and hyalinosis, podocyte effacement & fusion is Histology/LM/EM findings of

A

Focal Segmental Glomerulosclerosis

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17
Q

Which nephrotic syndrome is described by the following:

Primary cause is by auto-antibodies against “phospholipase A2” receptors on GBM

A

Membranous nephropathy

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18
Q

Which nephrotic syndrome is described by the following:

Secondary cause is by Drugs (NSAIDs, penicillamine), SLE, Cancer, and viral infections (Hepatitis)

A

Membranous nephropathy

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19
Q

Capillary loop thickening and GBM thickening on LM; granular IF; subepithelial deposits of immune complexes (“spike and dome” appearance) on EM are findings of

A

Membranous nephropathy

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20
Q

Which nephrotic syndrome is described by the following:

Amyloid deposits in mesangium (early) –> endothelium (late)

A

Amyloidosis

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21
Q

+ Congo red and apple green birefringence is Histology/LM/EM findings of

A

Amyloidosis

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22
Q

What organ is the most commonly involved organ of Amyloidosis?

A

Kidney

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23
Q

Which nephrotic syndrome is described by the following:

Most common cause ESRD in the US; caused by diabetes

A

Diabetic glomerulonephropathy

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24
Q

Mesangial expansion and “nodular” glomerulosclerosis (Kimmenstiel-Wilson nodules) is Histology/LM/EM findings of

A

Diabetic glomerulonephropathy

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25
Q

Glomerular disease caused by “inflammation” (lymphocytes are involved); present with hematuria, dysmorphic RBCs, RBC casts, and WBC casts in urine

A

Nephritic syndrome

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26
Q

Which nephritic syndrome is described by the following:

“2-4 weeks” after group A strep infection of pharyngitis or skin rash (impetigo); caused by type III (immune complex deposition) hypersensitivity; presents with periorbital edema, hypertension, and cola-colored urine

A

Poststreptococcal glomerulonephritis

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27
Q

granular (IgG, IgM, c3) IF in mesangium and GBM; subendothelial and subepithelial (GBM) immune complex deposition on LM are findings of

A

Poststreptococcal glomerulonephritis

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28
Q

Which nephritic syndrome is described by the following:

Caused by SLE

A

Diffuse proliferative glomerulonephiritis

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29
Q

“wire looping” (neutrophilic infiltration) of capillaries; granular IF; subendothelial immune complex deposition on EM is Histology/LM/EM findings of

A

Diffuse proliferative glomerulonephiritis

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30
Q

Which nephritic syndrome is described by the following:

Caused by hepatitis infection or idiopathic; subendothelial immune-complex deposition; granular IF

A

Type I Membranoproliferative glomerulonephiritis

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31
Q

Which nephritic syndrome is described by the following:

Caused by C3 nephritic factor (IgG autoantibody that overactivates complement activation); immune-complex deposition intramembranously; “tram-tracking” or GBM splitting on H&E or PAS stains

A

Type II Membranoproliferative glomerulonephiritis

aka. dense deposit disease

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32
Q

What kidney diseases are considered both nephrotic and nephritic syndromes?

A

Diffuse proliferative glomerulonephiritis & Membranoproliferative glomerulonephiritis

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33
Q

Which nephritic syndrome is described by the following:

rapidly deteriorating renal function; includes several diseases that show this pattern

A

Rapidly progressive glomerulonephiritis

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34
Q

Which nephritic syndrome is described by the following:

RPGN that shows “LINEAR” IF due to antibodies against type IV collagen on GBM and alveolar BM –> hematuria & hemoptysis

A

Goodpasture syndrome

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35
Q

Which nephritic syndrome is described by the following:

RPGN that is pauci-immune (no Ig/c3 deposition); negative IF but + C-ANCA

A

Granulomatosis with polyangiitis (aka. WeCner’s syndrome)

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36
Q

Which nephritic syndrome is described by the following:

RPGN that is pauci-immune (no Ig/c3 deposition); negative IF but + P-ANCA (2)

A

Microscopic polyangiitis
OR
Eosinophilic Granulomatosis with polyangiitis (aka. Churg-Strauss)

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37
Q

PSGN and DPGN can rapidly deteriorate renal function leading to

A

Rapidly progressive glomerulonephiritis

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38
Q

Unique LM finding of RPGN

A

Crescent (fibrin) formation in glomerulus

  • crescent is made of fibrin + proliferation of cells (macrophages, fibroblasts, etc.)
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39
Q

Which nephritic syndrome is described by the following:

Occurs a few days (2-5) after URI or GI tract infection –> IgA immune complex deposition in mesangium; “mesangial” proliferation and granular IgA immune complex on IF

A

IgA nephropathy

aka. Berger Disease

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40
Q

Vasculitis associated with IgA nephropathy; cause non-blanching palpable purpura

A

IgA vasculitis

aka. Henoch Schonlein Purpura

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41
Q

Which nephritic syndrome is described by the following:

Caused by mutation in type IV collagen –> thinning and splitting of GBM; present with triad (eye problem, hearing loss, and kidney problem)

A

Alport syndrome

*STUDY AID: Albert can’t pee, can’t see, can’t hear a bee

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42
Q

“basket weave” with thinning and splitting of GBM is Histology/LM/EM findings of

A

Alport syndrome

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43
Q

What is the complement level finding in nephritic syndrome?

A

C3 will be low due to activation of complement by immune complex –> deposition –> low serum C3 level

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44
Q

You will see WBC casts in urine only in what glomerular disease?

A

Nephritic syndrome

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45
Q

What kidney-related disorder can present with UNILATERAL flank tenderness, colicky pain radiating to groin, and hematuria?

A

Kidney stones

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46
Q

the most common reason for Ca (Ca oxalate and Ca PO4) kidney stones in adults; caused by ↑ GI absorption, ↑ mobilization of Ca from bone, or ↓ renal tubular Ca reabsorption

A

Hypercalciuria

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47
Q

Serum Ca+2 level in hypercalciuria is

A

normocalcemic

  • due to regulation of plasma Ca levels by vitamin D and PTH
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48
Q

Explain how hypocitraturia can increase formation of Ca-oxalate nephrolithiasis?

A

When citrate level is normal in urine, Ca+2 binds with citrate and forms a soluble calculi. When citrate level in urine decreases or Ca+2 excretion increases, calcium will bind to oxalate (or phosphate) and form an insoluble calculi

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49
Q

↑ urinary concs of Ca2+, oxalate, and uric acid promote

A

salt crystallisation

50
Q

↑ urinary citrate conc and high fluid intake prevent

A

calculi formation

51
Q

Tx for calcium (oxalate or phosphate) renal calculi

A

thiazides (increase reabsorption of Ca+2), low Na+ diet, citrate (if hypocitraturia), and increased fluid intake

52
Q

Shape of calcium oxalate crystals in urine

A

envelope or dumbbell

53
Q

Shape of calcium phosphate crystals in urine

A

wedge-shaped prism

54
Q

Type of renal stones that is caused by UTI with urease + bugs that hydrolyze urea to ammonia (increase urine pH)

A

Ammonium Magnesium Phosphate (aka. struvite)

55
Q

Large renal stones that take on the shape of the renal calyces; very big!

A

Staghorn calculi

56
Q

Staghorn calculi is made of

A

struvite (MgNH4PO4)

57
Q

What kidney stones precipitate at low pH?

A

Everything else except phosphate stones

58
Q

What kidney stones precipitate with increased pH due to alkalinized urine?

A

Phosphate stones

59
Q

UTI-causing urease+ bugs

A

staph. saprophyticus
Klebsiella
Proteus mirabilis

60
Q

Shape of struvite (MgNH4PO4) crystals in urine

A

coffin lid

61
Q

Type of renal stones that is caused by hyperuricemia (gout), low urine pH (loss of HCO3- due to diarrhea), and low urine volume (dehydration)

62
Q

Either overproduction of uric acid or under excretion of uric acid can lead to

A

hyperuricemia –> gout

63
Q

Shape of struvite uric acid crystals in urine

A

Rhomboid (soft diamond shaped) or rosettes

64
Q

Tx for uric acid stones

A

allopurinol (gout tx)

65
Q

Type of renal stones that is caused by a hereditary disorder in which cystine-reabsorbing PCT transporter loses function –> cystinuria; the transporter can’t also reabsorb COLA (cystine, ornithine, arginine, and lysine) –> recurrent nephrolithiasis

A

Cystine stone

66
Q

Shape of Cystine stone in urine

A

hexagonal (six-sided) crystals

  • STUDY AID: Cystine sounds like “SIX”tine
67
Q

what test can be used to detect excess cystine in the urine?

A

Na+ Cyanide Nitroprusside Test

68
Q

Mannitol site of action as diuretic

69
Q

Acetazolamide (carbonic anhydrase inhibitor) site of action as diuretic

70
Q

Loop diuretics (furosemide) site of action as diuretic

A

Thick ascending limb of loop of henle

71
Q

Thiazide diuretics site of action as diuretic

72
Q

K+ sparing diuretics (spironolactone, eplerenone) site of action as diuretic

73
Q

Most common renal malignancy of children (ages 2-4); presents with large, palpable, unilateral flank mass + hematuria + “HTN”; tumor does NOT cross the MIDLINE; part of WAGR complex and Beckwith-Wiedemann syndrome

A

Nephroblastoma (aka. Wilms tumor)

74
Q

Mutation of Nephroblastoma (aka. Wilms tumor)

A
  • WAGR: mutation of tumor suppressor gene WT1

- Beckwith-wiedemann: mutation of tumor suppressor gene WT2

75
Q

Symptoms in WAGR complex

A

Wilms tumor
Aniridia (no iris)
Genitourinary malformation
Retardation (mental)

76
Q

Symptoms in Beckwith-Wiedemann syndrome

A

Wilms tumor
macroglossia
omphalocele

  • STUDY AID: BeckWith-Wiedemann
    B: Big Tongue
    W: Wilms Tumor
    W: (abdominal) Wall Defect
77
Q

Most common adrenal medulla malignancy of children (ages <4); arises from neural crest cells; presents with abdominal distension, a firm, irregular mass that crosses MIDLINE (not unilateral as in Wilms tumor); NO “HTN”

A

Neuroblastoma

*think about it as a pheochromocytoma in children w/o HTN

78
Q

What is a paraneoplastic syndrome associated with neuroblastoma?

A

Opsoclonus-Myoclonus

*dancing eyes-dancing feet

79
Q

Urine findings in neuroblastoma

A

Homovanillic acid (HVA) & vanillylmandelic acid (VMA)

*they are catecholamine metabolites

80
Q

Mutation of neuroblastoma

A

N-myc oncogene

81
Q

Histologic finding in Neuroblastoma

A

Homer-wright rosettes (neuroblasts surrounding a central lumen)

82
Q

ADH reabsorbs water in what part of nephron?

A

collecting duct

83
Q

ADH also reabsorbs urea in “collecting duct” to establish

A

medullary osmotic gradient (for water reabsorption)

84
Q

Autosomal dominant polycystic kidney disease is caused by what two genetic mutations that result in the development of multiple cysts in the kidney because of structural abnormalities of the renal tubules?

A
  • PKD1 on Chromosome 16 (85% of cases)
  • PKD2 on Chromosome 4 (15% of cases)
  • PKD1/2 genes make protein POLYCYSTIN
85
Q

ADPKD is associated with what aneurysmal vascular disease?

A

Berry aneurysm (rupture can cause subarrachnoid hemorrahge)

  • STUDY AID: bubbles in kidneys, bubbles in the head & liver
86
Q

Cysts caused by ADPKD compress adjacent normal renal parenchyma and cause

A

Chronic HTN/ CKD

87
Q

A mutation in _____ gene results in autosomal “recessive” polycystic kidney disease

A

PKHD1 on Chromosome 6

  • PKHD1 gene makes protein FIBROCYSTIN
88
Q

Adrenal cortex is derived from what embryologic origin layer?

89
Q

Adrenal medulla (Chromaffin cells) is derived from what embryologic origin layer?

A

Neural crest cells

90
Q

The most common cause (organism) of urinary tract infection (UTI) in both healthy adults and elderly patients

91
Q

costovertebral angle tenderness and flank/back pain radiating to groin indicates

A

renal stones

92
Q

Steps to Solving Every High Altitude ABG Problems

A
  1. At high altitude –> ↓ pO2 –> Hyperventilation
  2. Hyperventilation –> ↓ pCO2
  3. ↑ pH –> ↓ HCO3-
93
Q

Steps to Solving Every Acid-Base Disorder Problems

A
  1. Determine primary deficit with compensatory MOA
  2. If the primary deficit is metabolic acidosis, then check anion gap using AG formula
  3. If the primary deficit is metabolic acidosis, then also calculate expected PCO2 using Winter’s Formula
  4. Determine any concomitant respiratory alkalosis/acidosis
94
Q

Hypoventilation caused by:

  • Airway obstruction
  • Opioids, sedatives
  • Chronic lung disease

are common causes of what acid-base disturbance?

A

Respiratory Acidosis

95
Q

Hyperventilation caused by:

  • Hypoxemia/high altitude
  • Anxiety/Panic Disorder
  • PE/Dyspnea
  • Salicylates (in EARLY toxicity phase)

are common causes of what acid-base disturbance?

A

Respiratory Alkalosis

96
Q

H+ Loss caused by:

  • Vomiting
  • Hyperaldosteronism

are common causes of what acid-base disturbance?

A

Metabolic Alkalosis

97
Q

HCO3- Excess caused by:

  • Antacid Use
  • Loop/Thiazide Diuretics (Hypovolemia-induced ↑ RAAS –> ↑ aldosterone –> ↑ H+ excretion @ CD –> ↑ Na+/HCO3- reabsorption @ PCT)

are common causes of what acid-base disturbance?

A

Metabolic Alkalosis

98
Q

Increased Serum External Acid caused by:

  • Hyperchloremia
  • Addison Disease
  • Renal Tubular Acidosis
  • Diarrhea
  • Acetazolamide
  • Spironolactone
  • Saline Infusion

are common causes of what acid-base disturbance?

A

NORMAL Anion Gap Metabolic Acidosis

  • STUDY AID: HARDASS
99
Q

Increased Serum External Acid caused by:

  • Methanol
  • Uremia
  • Diabetic Ketoacidosis
  • Propylene glycol
  • Iron tablets/Isoniazid
  • Lactic Acidosis
  • Ethylene glycol (antifreeze)
  • Salicylates (in LATE toxicity phase)

are common causes of what acid-base disturbance?

A

High Anion Gap Metabolic Acidosis

  • STUDY AID: MUDPILES
100
Q

What initially causes respiratory alkalosis and then later (several hours) presents with elevated anion gap metabolic acidosis, leading to a mixed acid-base disorder?

A

Salicylate (ASA) Toxicity/Poisoning

101
Q

Nephrotic syndrome is defined by what five signs and symptoms?

A
  • Proteinuria: > 3.5 grams per day
  • Hypoalbuminemia
  • Peripheral/periorbital edema
  • Hyperlipidemia
  • Fatty Casts
  • Frothy Urine
102
Q

Other than albumin, what else can be lost in the urine of those with nephrotic syndrome?

A

Antithrombin III
Immunoglobulin

  • they are all made of protein!
103
Q

Due to the loss of antithrombin III, _____________ can occur in nephrotic syndrome.

A

renal vein thrombosis

  • STUDY AID: Sketchy Path (the guy getting stabbed in his flank with the polymerized fibrin sticks)
104
Q

What is the most likely diagnosis in a patient presenting with nephrotic syndrome (proteinuria) with chronic inflammatory diseases (ex. Crohn disease)?

A

Amyloidosis

105
Q

What indicates the need to start ACE inhibitors in diabetic patients?

A

Albuminuria with BP >130/80

  • ACE inhibitors prevents the progression of albuminuria
106
Q

The most important parameter for early detection of renal condition in diabetic patients

A

URINARY albumin

107
Q

In order to increase the reduced oncotic pressure caused by hypoalbuminemia, what synthesis process in the liver is increased in nephrotic syndrome?

A

Hepatic lipoprotein synthesis

108
Q

Nephritic syndrome is defined by what seven signs and symptoms?

A
  • Hematuria (dark/”cola-colored” urine)
  • Peripheral/periorbital edema
  • Hypertension
  • Decreased urine output (oliguria)
  • “WBC” Casts
  • RBC Casts
  • Dysmorphic RBCs (acanthocytes)
  • May also see mild proteinuria (<3.5 g/day)
109
Q

What are two renal examples of type II HSR?

A
  • Goodpasture Syndrome

- Membranous Nephropathy

110
Q

The only type of kidney stone that forms radioLUCENT stones

A

Uric Acid stones

111
Q

Gout (Hyperuricemia leading to uric acid accumulation in joints) can be exacerbated by consumption of

112
Q

What clinical presentations are associated with ADPKD?

A
  • > 30 years of age with renal insufficiency
  • Hematuria
  • Hypertension
  • Recurrent UTIs
  • Flank pain
  • Family Hx
113
Q

What is the diagnostic ultrasound findings of ADPKD?

A

Bilateral (usually) enlarged kidneys with multiple parenchymal anechoic masses of varying size

114
Q

What clinical presentations of ARPKD help distinguish it from ADPKD?

A

ARPKD manifests in INFANCY

115
Q

N-Myc gene mutation, which can cause neuroblastoma is due to (loss of fx/gain of fx).

A

Gain of fx

  • All Myc (C-myc, L-myc, N-myc) genes are ONCOGENES!
116
Q

Other extra-renal manifestations of ADPKD include

A
  • Cerebral saccular/berry aneurysms
  • Mitral Valve Prolapse
  • Hepatic Cysts
117
Q

What should be measured in metabolic alkalosis to determine diagnosis?

A

Urine chloride concentration

118
Q

Etiologies (2) of metabolic alkalosis associated with a NORMAL urinary chloride concentration

is called a chloride-responsive metabolic alkalosis because it corrects with administration of fluid with NaCl.

A
  • Vomiting
  • Loop diuretic use
  • Caused by fluid loss
119
Q

Etiologies (2) of metabolic alkalosis associated with an ELEVATED urinary chloride concentration

A
  • Hyperaldosteronism

- Antacids

120
Q

Metabolic alkalosis with NORMAL urinary chloride concentration is chloride (resistant/responsive)

A

Responsive

  • they can be corrected with administration of fluid with NaCl
121
Q

Metabolic alkalosis with ELEVATED urinary chloride concentration is chloride (resistant/responsive)

A

Resistant

  • they cannot be corrected with administration of fluid with NaCl

STEP 1 (19 decks)

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