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USMLE Step 1 > Renal and Urinary Systems > Flashcards

Renal and Urinary Systems Flashcards

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USMLE® Step 1 flashcards
1
Q

DDX for WBC casts?

A

Pyelonephritis

Acute intersitial nephritis

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2
Q

DDx for muddy brown casts?

A

Acute tubular necrosis

Can be caused by ischemic AKI or nephrotoxic AKI (antibiotics, radiocontrast agents, NSAIDs, poisons, myoglobinuria, hemoglobinuria, chemotherapy, AL in MM)

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3
Q

Metabolic derangements in AKI

A

Hyperkalemia

Anion gap metabolic acidosis

Hypocalcemia

Hyponatremia

Hyperphosphatemia

Hyperuricemia

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4
Q

Metabolic derangements in CKD

A

Hyperkalemia

Hypermagnesemia

Hyperphosphatemia (decreased GFR → decreased excretion)

Metabolic acidosis

Hypocalcemia (decreased 1,25-OH vitamin D)

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5
Q

Side effects of ACEI

A

ACEIs dilate afferent arteriole

Hyperkalemia (↓ aldosterone)

Angioedema, cough (↓ breakdown of bradykinin)

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6
Q

Absolute indications for dialysis

A

AEIOU:

Acidosis

Electrolyte abnormalities

Intoxications

Overload, hypervolemic

Uremia based on clinical presentation (e.g. AMS, pericarditis)

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7
Q

Minimal change disease

A

Most common in children

May present as nephrotic syndrome

A/w lymphomas

Microscopy: no changes on light microscopy, foot process fusion

Tx: 4-8 weeks of steroids

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8
Q

Focal segmental glomerulosclerosis (FSGS)

A

Nephrotic

More common in Blacks

Microscopy: focal segmental sclerosis, foot process fusion

No immunofluorescence

A/w HIV, heroin use, sickle cell disease

Does not respond well to steroids

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9
Q

Membranous nephropathy

A

Nephrotic

IgG4 antibodies to phospholipase A2 receptor

LM: thick glomerular basement membrane without an increase in cellularity

IF: granular deposits of IgG and C3 along glomerular basement membrane

EM: “spike and dome” apperance with subepithelial deposits

A/w: Hep B, Hep C, SLE

Does not respond well to steroids

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10
Q

Post-infectious glomerulonephritis

A

Nephritis 10-21 days following URI or skin infection; abx treatment of the infection does not decrease risk of post-infectious glomerulonephritis

LM: enlarged and hypercellular glomeruli

IF: “lumpy-bumpy” granular deposits of IgG, IgM and C3 –> low C3 complement

EM: subepithelial immune complex humps

Elevated anti-streptolysin O and/or anti-DNAse B

Adult onset is poor prognostic factor

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11
Q

IgA nephropathy (Berger disease)

A

Nephritis 5 days following URI or gastroenteritis

IF: grandular deposits of IgA in mesangium

Normal complements

a/w Henoch-Schonlein purpura

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12
Q

Prostate cancer

A

Risk factors include age, African American race, high-fat diet, FHx, exposure to herbicides and pesticides

Mostly adenocarcinoma, starts at periphery

Mostly asymptomatic but can cause obstruction in late phase

Likes to metastasize to bone (pelvis, vertebral bodies, long bones in the legs)

Tx: radiation + androgen deprivation OR prostatectomy OR orchiectomy, antiandrogens, leuprolide, GnRH antagonists

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13
Q

Describe the embryology of the kidneys?

A

Derived from intermediate mesoderm

Pronephros forms in week 4 and degenerates into:

Mesonephros for the first trimester and converts into:

Metanephros which is permanent (appears in week 5 and continues to develop until weeks 32-36). Glomerular filtration starts at 12 weeks but excretion of waste still handled by the placenta. Nephron formation is complete at term.

  • Ureteric bud branches from the mesonephric duct to form the ureter, pelvises, calyces, and collecting ducts
  • Metanephric mesoderm forms glomerulus through distal convoluted tubules

As the kidney ascends, it’s blood supply changes from internal illiac to inferior mesenteric to renal arteries

Mesonephric/Wolffian duct becomes vas deferens

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14
Q

Describe the embryology of the adrenal glands?

A

Cortex = intermediate mesoderm

Medulla = neural crest

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15
Q

How are the left and right gonadal veins different?

A

Left gonadal vein drains into the left renal vein

Right gonadal vein drains into the IVC

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16
Q

How do you calculate renal clearance (i.e. effective renal plasma flow)?

A

Clearance (mL/min) = (Urine concentration x urine flow rate)/plasma concentration

Renal blood flow = Renal plasma flow/(1-Hct)

*You can estimate GFR using inulin or creatinine because amount filtered = amount excreted

*You can estimate effective renal plasma flow using para-aminohippuric acid because amount excreted > amount filtered

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17
Q

How does the histology vary between the proximal and distal convoluted tubules?

A

Both are made of simple cuboidal cells but proximal convoluted tubules have a brushed border while distal convolutued tubules don’t but have buldging apical nuclei

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18
Q

What is the difference between dark and light cells in collecting duct?

A

Dark/intercalating cells are darker-staining, more common in the cortex, and maintains acid-base balance

Light/principle cells are light-staining and moderate water resorption (ADH sensitive, lots of aquaporins)

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19
Q

How do you calculate plasma osmolarity?

A

Posm = 2Na+ + Glucose/18 + BUN/2.8

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20
Q

What is Hartnup disease?

A

Autosomal recessive deficiency in neutral amino acid transporters in the proximal renal tubule

S&S: neutral aminoaciduria, pellagra-like symptoms (dermatitis, diarrhea, depression 2/2 lack of tryptophan or nicotinic acid)

Tx: high-protein diet, nicotinic acid

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21
Q

Describe the physiology of water regulation in the body?

A

Plasma osmolarity is sensed by osmoreceptors in the hypothalamus and effective circulating volume is sensed by baroreceptors in the carotid sinus and the aortic arch.

An increased in Posm or decreased in ECV stimulates thirst and release of ADH from the posterior pituitary. ADH binds to V2 receptors in principle/light cells of the collecting duct –> phosphorylation of aquaporin 2 –> insertion of channel into apical membrane

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22
Q

Describe the physiology of sodium regulation in the body?

A

Excess sodium increases plasma osmolarity which increases effective circulating volume which is sensed by baroreceptors (heart) and the macula densa (kidney). Regulation is controlled by RAAS, sympathetic nervous system, and natriuretic peptides (works opposite of RAAS).

Proximal tubule: sodium-coupled cotransporters and exchangers

Thick ascending limb: Na-K-2Cl cotransporter

Distal convoluted tubule: Na-Cl co transporter

Collecting duct principle cells: ENac (upregulated in response to aldosterone)

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23
Q

Describe the physiology of potassium regulation in the body?

A

Increased K+ stimulates increases in insulin and epinephrine which drives K+ into cells. High extracellular K+ activates the Na/K ATPase in renal tubular cells –> increased intracellular K+ –> increased efflux of K+ into tubular fluid. High K+ also stimulates aldosterone secretion which increases K+ excretion in the kidneys by increasing expression of apical K+ channels.

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24
Q

How is calcium and phosphate handled in the kidneys?

A

Calcium passively diffuses through tight junctions in the proximal convoluted tubules. PTH increases synthesis of calcium transporters increasing calcium reabsorption thus decreasing excretion. PTH reduces the transport maximum of the phosphate transporter increasing excretion of phosphate.

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25
Q

What is different about the handling of magnesium in the kidneys?

A

Unlike other substances that are mostly reabsorped in the proximal convoluted tubule, most magnesium (70%) is reabsorped in the loop of Henle.

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26
Q

What stimulates release of renin from juxtaglomerular cells?

A

Renin secretion is induced by low BP, low Na+ delivery to macula densa of distal convoluted tubule, or increased sympathetic tone at β1 receptors (β-blockers decrease renin thus decrease BP).

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27
Q

How do you calculate filtration fraction?

A

FF= GFR/RPF

28
Q

How does afferent or efferent constriction change GFR, RBP, or FF?

A

Afferent arteriole constriction (i.e. NSAIDs) → decreased renal plasma flow → decreased capillary hydrostatic pressure → decreased GFR; RPF and GFR both decrease so FF unchanged

Efferent arteriole constriction (i.e. RAAS activation) → increased capillary hydrostatic pressure → increased GFR + decreased RPF → increased FF

29
Q

What is the blood supply to the ureters?

A

Proximal part → renal artery

Distal part → superior vesicle artery

Inbetween → anatamosis from gondal, common and internal iliac, aorta, and uterine arteries

30
Q

How do you calculate net filtration pressure?

A

Net filtration pressure = K (hydrostatic pressure of glomerular capillaries - hydrostatic pressure of Bowman’s space) - (oncotic pressure of glomerular capillaries - oncotic pressure of Bowman’s space)

31
Q

Furosemide

A

Sulfonamide loop diuretic: inhibits Na-K-2Cl symporters in the thick ascending limb of the loop of Henle → increased Na and Cl excretion → increased water excretion

Loop diuretics also stimulate renal prostaglandins which dilate the afferent arteriole → increased renal blood flow → increased GFR → increased drug delivery

Concurrent use of NSAIDs will blunt diuretic response

Indicated for edematous states, HTN, hypercalciuria (Loops loose calcium)

SA: ototoxicity, hypokalemia, dehydration, sulfa allergies, interstitial nephritis, gout

32
Q

Spironolactone

A

Competitive aldosterone receptor antagonist in the cortical collecting tubule (K+ sparing diuretic)

Indicated for hyperaldosteronism, K+ depletion, CHF (proven to reduce mortality)

SA: hyperkalemia → arrhythmias, endocrine effects such as gynecomastia, antiandrogen effects

33
Q

Anti-glomerular basement membrane disease

A

Presents as nephritic syndrome

Anti-glomerular basement membrane antibodies target type IV collagen → linear deposits of IgG and C3 along the glomerular basement membrane → crescents

Antibodies may also cross-react with type IV collagen in pulmonary basement membrane causing pulmonary hemorrhage and hemoptysis (renal and lung involvement = Goodpasture syndrome)

34
Q

Eplerenone

A

Competitive aldosterone receptor antagonist in the cortical collecting tubule (K+ sparing diuretic)

Indicated for hyperaldosteronism, K+ depletion, CHF (proven to reduce mortality)

SA: hyperkalemia → arrhythmias; fewer side effects than spironolactone

35
Q

Triamterene

A

Na+ channel blockers in the cortical collecting tubule (K+ sparing diuretic)

Indicated for hyperaldosteronism, K+ depletion, CHF

SA: hyperkalemia → arrhythmias

36
Q

Amiloride

A

Na+ channel blockers in the cortical collecting tubule (K+ sparing diuretic)

Indicated for hyperaldosteronism, K+ depletion, CHF

SA: hyperkalemia → arrhythmias

37
Q

Mannitol

A

Osmotic diuretic → increased tubular fluid osmolarity → increased urine flow → decreased intracranial/intraocular pressure

Indicated for drug overdose, increased intracranial/intraocular pressure

SA: pulmonary edema, dehydration

Contraindicated in anuria, CHF

38
Q

Acetazolamide

A

Carbonic anhydrase inhibitor → NaHCO3 diuresis and decreased total body HCO3- stores

Indicated for glaucoma, urinary alkalinization, metabolic alkalosis, altitute sickness, pseudotumor cerebri

SA: hyperchloremic metabolic acidosis, paresthesias, NH3 toxicity, sulfa allergy

39
Q

Ethnacrynic acid

A

Phenoxyacetic acid loop diuretic: inhibits Na-K-2Cl symporters in the thick ascending limb of the loop of Henle → increased Na and Cl excretion → increased water excretion

Loop diuretics also stimulate renal prostaglandins which dilate the afferent arteriole → increased renal blood flow → increased GFR → increased drug delivery

Concurrent use of NSAIDs will blunt diuretic response

Indicated for edematous states, HTN, hypercalcemia

SA: ototoxicity, hypokalemia, dehydration, slfa allergies, interstitial nephritis, hyperuricemia → don’t use with gout

40
Q

Hydrochlorothiazide

A

Thiazide diuretic: inhibits NaCl reabsorption in early distal tubule → decreased diluting capacity of the nephron; decreased calcium excretion

Indicated for HTN, CHF, idiopathic hypercalciuria, nephrogenic DI, osteoporosis

SA: hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia, sulfa allergy

41
Q

Captopril

A

ACE inhibitor → decreased angiotensin II → dilation of efferent arteriole → decreased GFR

Indicated for HTN, CHF, proteinuria, diabeic nephropathy, prevention of unfavorable remodeling as a result of chronic HTN or MI

SA: cough (ACEI prevent inactivation of bradykinin), angioedema, teratogen, increased creatinine due to decreased GFR, hyperkalemia, hypotension

Contraindicated in bilateral renal stenosis (further decrease in GFR → renal failure)

42
Q

-sartans

A

Angiotensin II receptor blockers (ARBs)

Decreased risk of cough or angioedema because it does not increase bradykinin

43
Q

How do diuretics affect serum calcium concentration?

A

Loop diuretics can cause hypocalcemia → hypercalciuria (Loops Loose calcium).

Thiazide diuretics can cause hypercalcemia → hypocalciuria

44
Q

How do diuretics affect serum potassium concentration?

A

Serum potassium increases with K+ sparing diuretics and decreases with loop and thiazide diuretics.

45
Q

What effects do diuretics have on acid-base status?

A

Carbonic anhydrase inhibitors and K+ sparing diruetics may cause acidemia.

Loop and thiazide diuretics may cause alkalemia.

46
Q

Fanconi syndrome

A

Reabsorptive defect in proximal convoluted tubule → increased excretion of amino acids, glucose, HCO3- (proximal renal tubular acidosis), PO43-

47
Q

Bartter syndrome

A

Reabsorptive defect in the thick ascending loop of Henle (Na/K/2Cl cotransporter) → hypokalemia, metabolic alkalosis with hypercalciuria

48
Q

Gitelman syndrome

A

Reabsorptive defect of NaCl in distal convoluted tubule → hypokalemia, metabolic alkalosis without hypercalciuria

49
Q

Liddle syndrome

A

Increased activity of ENac channels in collecting duct → increased sodium reabsorption → HTN, hypokalemia, metabolic alkalosis, decreased aldosterone

Autosomal dominant

Tx: amiloride

50
Q

Causes of respiratory acidosis?

A

Hypoventilation from airway obstruction, lung disease, opioids, weakening of respiratory muscles

51
Q

Causes of metabolic acidosis?

A

Anion-gap metabolic acidosis:

MUDPILES

Methanol

Uremia

Diabetic ketoacidosis

Propylene glycol

Iron/Isoniazid

Lactic acidosis

Ethylene glycol

Salicylates

Non-anion gap metabolic acidosis:

HARDASS

Hyperalimentation

Addison disease

Renal tubular acidosis

Diarrhea

Acetazolamide

Spironolactone

Saline infusion

52
Q

Causes of respiratory alkalosis?

A

Hyperventilation from hysteria, hypoxemia, salicylates, tumor, PE

53
Q

Causes of metabolic alkalosis?

A

Loop diuretics (volume contraction → increased angiotensin II → increased Na+/H+ exchange in proximal tubule → increased HCO3- reabsorption), vomiting (removal of HCl from body), antacid use, hyperaldosteronism (increased H+ excretion)

54
Q

Minimal change disease

A

Most common cause of nephrotic syndrome in children; inciting event (URI, immunization, insect bite) → podocyte damage and decreased anionic properties of GBM → selective loss of albumin

No changes visible by microscopy

No IF

EM: effacement of foot processes

A/w Hodgkin lymphoma

Responds well to steroids

55
Q

Membranoproliferative glomerulonephritis

A

May be nephritic or nephrotic

Type I - subendothelial immune complex deposits with granular IF; “tram-track” appearance due to GBM splitting; a/w Hep B, Hep C

Type II - intramembranous dense immune complex deposits; decreased C3

56
Q

Diabetic glomerulonephropathy

A

Nephrotic

Mesangial expansion, GBM thickening (nonenzymatic glycosylation), eosinophilic nodular glomerulosclerosis (Kimmelsteil-Wilson lesion)

57
Q

Alport syndrome

A

X-linked mutation in type IV collagen → thinning and splitting of GBM

a/w glomerulonephritis, deafness, and eye problems (less common)

58
Q

Diffuse proliferative glomerulonephritis

A

Nephritic or nephrotic

a/w SLE and MPGN

LM: “wire-looping” of capillaries

IF: granular IgG and C3 subendothelial and intramembranous deposits

59
Q

What effects do ACEI and NSAIDS have on glomerular arterioles?

A

ACEI dilate efferent arterioles

NSAIDs constrict afferent arterioles (by peventing dilation by prostaglandins)

Using them together can greatly drop GFR causing acute renal failure

60
Q

Granulomatosis with polyangiitis (Wegener)

A

Small vessel vasculitis affecting the nasopharynx, lungs, and kidneys

PR3-ANCA/c-ANCA

No immunoglobulin or complement deposits

61
Q

Microscopic polyangiitis

A

MPO-ANCA/p-ANCA

No immunoglobulin or complement deposits

62
Q

Torsemide

A

Sulfonamide loop diuretic: inhibits Na-K-2Cl symporters in the thick ascending limb of the loop of Henle → increased Na and Cl excretion → increased water excretion

Loop diuretics also stimulate renal prostaglandins which dilate the afferent arteriole → increased renal blood flow → increased GFR → increased drug delivery

Concurrent use of NSAIDs will blunt diuretic response

Indicated for edematous states, HTN, hypercalcemia

SA: ototoxicity, hypokalemia, dehydration, slfa allergies, interstitial nephritis, gout

63
Q

Chlorthalidone

A

Thiazide diuretic: inhibits NaCl reabsorption in early distal tubule → decreased diluting capacity of the nephron; decreased calcium excretion

Indicated for HTN, CHF, idiopathic hypercalciuria, nephrogenic DI, osteoporosis

SA: hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia, sulfa allergy

64
Q

Bumetanide

A

Sulfonamide loop diuretic: inhibits Na-K-2Cl symporters in the thick ascending limb of the loop of Henle → increased Na and Cl excretion → increased water excretion

Loop diuretics also stimulate renal prostaglandins which dilate the afferent arteriole → increased renal blood flow → increased GFR → increased drug delivery

Concurrent use of NSAIDs will blunt diuretic response

Indicated for edematous states, HTN, hypercalcemia when furosemide is ineffective

SA: ototoxicity, hypokalemia, dehydration, slfa allergies, interstitial nephritis, gout

65
Q

Fibromuscular dysplasia

A

Hypertension in women aged 20-30

Renal arteries look like a “string-of-pearls” on imaging

66
Q

Metolazone

A

Thiazide-like diuretic

USMLE Step 1 (20 decks)

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