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USMLE > Renal Physio > Flashcards

Renal Physio Flashcards

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USMLE® Step 1 flashcards
1
Q

What is the condition called with a WT2 mutation

A

Beckwith-Wiedemann syndrome

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2
Q

Describe the symptoms of Beckwith-Wiedmann

A

Age 2-4; Wilm’s tumor, organomegaly, macroglossia, hemihypertrophy

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3
Q

What symptoms occur with WT1 deletion?

A

WAGR: Wilm’s tumor, Aniridia, Genituorinary complications, Mental Retardation ages 2-4

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4
Q

Which chromosome is mutated in Wilms?

A

Chromosome 11

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5
Q

What symptoms occur with WT1 mutation?

A

Denys-Drash: Wilm’s tumor, pseudo-hermaphroditism, early-onset nephrotic syndrome

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6
Q

Which factors place a pt at risk of Transitional Cell carcinoma of the urinary tract system?

A

Smokers, people who worked in rubber, plastic, aniline dyes, textiles, leather. Peak incidence in 70s-80s

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7
Q

Sterile pyuria and (-) gram cultures suggest UTI by which organisms

A

N. gonorrhea or Chlamydia trachomatis

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8
Q

List the risk factors of acute pyelonephritis

A
  1. Indwelling catheter
  2. Diabetes mellitus
  3. Pregnancy
  4. Ascending UTI
  5. VUR
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9
Q

On biopsy what does kidney tissue from chronic pyelonephritis resemble

A

Thyroid tissue: eosinophilic casts present in tubules

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10
Q

List the consequences of renal failure

A

Metabolic Acidosis
Dyslipidemia (increased triglycerides)
Hyperkalemia (cannot secrete K+ into tubules)
Uremia: increased BUN
Na+/H2O retention (Hypervolemic hyponatremia)
Growth retardation and development delay
Erythropoetin failure (normocytic normochromic anemia)
Renal osteodystrophy: secondary hyperparathyroidism

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11
Q

List the clinical presentation of uremia in chronic kidney failure

A 
increased BUN (blood urea nitrogen.. ammonia) 
Nausea and anorexia
Encephalopathy and neuropathy 
Asterixis
Pericarditis
Platelet dysfunction 
Itchiness
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12
Q

List the Ps that cause Acute Interstitial Nephritis

A 
Pee (diuretics)
Pain-free (NSAIDs)
Penicillins and cephalosporins
Proton Pump Inhibitors
rifamPin
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13
Q

Describe SAAD in renal papillary necrosis

A

Sickle cell disease or trait
Acute pyelonephritis
Analgesics (NSAIDs)
Diabetes mellitus

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14
Q

What is the mutation in ADPKD

A

PKD1 on chromosome 16 in 85% cases

PDK2 on chromosome 4 in 15% cases

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15
Q

What other complications is ADPKD associated with?

A

Saccular aneuryms, mitral valve prolapse, benign hepatic cysts

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16
Q

What is the treatment for ADPKD

A

ACEIS or ARBs

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17
Q

Which part of the kidney does ARPKD affect?

A

Collecting ducts

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18
Q

How does an infant with ARPKD present?

A

POTTER sequence (pulmonary hypoplasia, oligohydramnios, twisted face, twisted limbs, ears low set, renal agenesis

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19
Q

What are some complications with ARPKD

A

Hepatic fibrosis, systemic hypertension, progressive renal insufficiency and portal hypertension

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20
Q

How does medullary cystic disease appear on ultrasound

A

Shrunken kidneys; poor prognosis

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21
Q

How doe simple cysts appear on ultrasound

A

Anechoic, typically incidental findings and asymptomatic

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22
Q

Adverse effects of ACEIs (ACEs CATCHH)

A 
Cough
Angioedema (due to increased bradykinin)
Teratogen (fetal renal malformations)
Creatinine increase (decrease GFR)
Hyperkalemia 
Hypotension
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23
Q

When should you use ACEIs cautiously?

A

Bilateral renal artery stenosis (indicated in patients with atherosclerotic plaques… chronic TIAs, etc)

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24
Q

What is the mechanism of Angiotensin II receptor blockers (ARBs, -artans)?

A

Selectively block binding of AII to AT1R.

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25
Q

Clinical use of ARBs

A

Hypertension, HF, proteinuria, diabetic nephropathy with intolerance to ACE inhibitors (cough, angioedema)

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26
Q

Adverse effects of ARBs

A

Hypotension, Hyperkalemia, decreased GFR, teratogen

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27
Q

What is the function of Aliskiren?

A

Direct renin inhibitor, blocks conversion of Angiotensinogen to AI

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28
Q

What is Aliskiren used for?

A

Hypertension

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29
Q

Contraindications for Aliskiren

A

Patients taking ACEIs or ARBs

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30
Q

Side effects of Aliskiren

A

Hyperkalemia, decreased GFR, hypotension

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31
Q

Why do you get hyperkalemia with ACEIs and ARBs?

A

Angiotensin II is an activator of Aldosterone. If AII is blocked, you have lower levels of Aldosterone and decreased K+ secretion at the DCT

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32
Q

Which amino acids are lost in urine in patients with cystinuria?

A

COLA: Cysteine, Ornithine, Lysine, Arginine

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33
Q

Do patients with defective transporter of COLA amino acids develop deficiencies? What risks do they have?

A

No, these are absorbed sufficiently as oligopeptides. Can develop cysteine kidney stones

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34
Q

What is the most common cause of unilateral fetal hydronephrosis?

A

Inadequate canalization of the uteropelvic junction

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35
Q

In the true pelvis, which structure lies posterior to the ureter

A

internal iliac artery

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36
Q

In the true pelvis, which structure lies anterior to the ureter

A

Uterine artery

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37
Q

Patients with sporadic and hereditary renal cell carcinoma likely have a deletion in which gene on which chromosome?

A

VHL on chromosome 3p

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38
Q

Which part of the nephron absorbs the most water regardless of state of hydration?

A

Proximal tubule (>60%)

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39
Q

What is the rapid plasma reagin test used for?

A

Detect syphillis

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40
Q

Which condition can cause false positives in rapid plasma reagin tests?

A

anti-phospholipid antibody syndrome

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41
Q

Which condition is associated with antiphospholipid antibody syndrome?

A

Systemic Lupus Erythematous

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42
Q

What can post-renal azotemia (pressure hydronephrosis from bladder outflow obstruction) lead to in renal tubular cells

A

Parenchymal pressure atrophy

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43
Q

What is the peritoneal location of the bladder?

A

Extraperitoneal (cannula does not enter peritoneum)

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44
Q

Which pH do you need for calcium phosphate crystals to form?

A

> 7.0

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45
Q

Which pH do you need for magnesium ammonium phosphate (struvite) crystals to form?

A

> 7.0

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46
Q

Why are patients with chronic diarrhea likely to form uric acid crystals?

A

Chronic dehydration, and loss of bicarb leads to state of metabolic acidosis. Kidneys compensate by increasing H+ secretion and HCO3- reabsorption

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47
Q

Which cytokine recruits eosinophiles?

A

IL-5

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48
Q

How to eosinophils attack parasites?

A

Bind parasites coated with IgG and IgE, release major basic protein (cytotoxic protein) to kill parasite

49
Q

How to do eosinophils function in Type I hypersensitivity reactions

A

Synthesize prostaglandins, leukotrienes and cytokines to contribute to inflammmation

50
Q

In which part of the nephron is urine isotonic?

A

Proximal tubule

51
Q

In which part of the nephron is urine most dilute?

A

Distal convoluted tubule

52
Q

In which parts of the nephron is urine most hypertonic?

A

medullary part of LoH and Medullary part of collecting duct

53
Q

Prolonged use of NSAIDs can lead to which condition?

A

Chronic interstitial nephritis

54
Q

How do NSAIDs lead to papillary damage in the nephron?

A

They concentrate in the papillae, uncouple ox-phos reactions and deplete glutathione with subsequent lipid peroxidation– leading to damaged tubular and vascular endothelial cells

55
Q

How do NSAIDs cause ischemic papillary necrosis?

A

Inhibit prostaglandins, which inhibits vasodilation of afferent arteriole, leading to decreased perfusion and thus ischemic papillary necrosis

56
Q

Which key histologic feature is seen in LM of Diabetic nephropathy?

A

Kimmmelstiel-Wilson nodules

57
Q

How do glomeruli appear in membranoproliferative glomerulonephritis?

A

HYPERCELLULAR with thickening and splitting of GBM due to subendothelial immune complex deposition

58
Q

In which pts should you suspect membranoproliferative glomerulonephritis?

A

Patients with Hepatitis C or B

59
Q

In which patients should you suspect focal segmental glomerulosclerosis?

A

HIV, heroin abusers, severe obseity

60
Q

Crescent formation in rapidly progressive glomerulonephritis occurs due to deposition of which substance?

A

Fibrin

61
Q

Which molecular components are deposited along the GBM in patients with type 1 RPGN (Goodpasture syndrome)?

A

IgG and C3

62
Q

Which electrolyte imbalance can lead to weakness and arrythmias with T wave flattening, ST depression and prominent U waves?

A

Hypokalemia

63
Q

What is the ultimate risk of profound hypokalemia?

A

Ventricular tachycardia/fibrillation

64
Q

What is the primary treatment for elevated anion gap metabolic acidosis in diabetics?

A

Insulin and saline

65
Q

What potential electrolyte abnormalities present with severe hypothyroidism?

A

Hyponatremia, extracellular volume expansion and hypoglycemia

66
Q

What are the common symptoms of Goodpasture syndrome?

A

Shortness of breath, Hemoptysis, proteinuria and hematuria with dysmorphic red blood cells

67
Q

What causes Goodpasture syndrome?

A

Autoantibodies against alpha 3 chain of Type IV collagen in glomerular and alveolar basement membranes

68
Q

Where is the macula densa located?

A

Distal convoluted tubule

69
Q

What does the macula densa monitor?

A

Na+ concentration and tubular flow rate

70
Q

Where are JG cells located and what is their function?

A

Modified smooth muscle cells on AA, secrete renin in response to significant renal hypoperfusion

71
Q

What is the net renal excretion for a substance A

A

Net excretion = Filtered (A) - Reabsorbed (A)

72
Q

What is seen on light microscopy in a patient with poststreptococcal glomerulonephritis?

A

Enlarged and hypercellular glomeruli

73
Q

What is seen on immunofluorescence in pt with PSGN?

A

Granular deposits of IgG, IgM and C3 along the basement membrane and in the mesangium of glomeruli (“lumpy-bumpy”)

74
Q

What is seen on EM in pt with PSGN?

A

Electron dense immune deposits on epithelial side of basement membrane

75
Q

Why does nephritis cause hypertension?

A

Kidney damage reduces sodium handling ability of kidney–> less sodium is filtered, so more water and sodium is retained (increase body volume)

76
Q

Fibrin deposition along the basement membrane is characteristic of

A

Rapidly progressive glomerulonephritis

77
Q

How does Diabetic nephropathy present on LM?

A

Kimmelstiel-Wilson nodules, hyalin acellular deposits composed of plasma proteins

78
Q

Lipid droplets in renal tubules is indicative of

A

Nephrotic syndrome

79
Q

Why do you get hypocalcemia and secondary hyperaparthyroidism in chronic kidney disease?

A

Loss of normal renal parenchyma leads to decreased PO4 secretion and decreased Ca+2 reabsorption. Serum PO4 binds Ca+2 and lowers total Ca+2 (free) leading to hypocalcemia. Damaged tubules cannot produce Vitamin D (1,25-OH), further decreasing Ca+2. Decreased serum Ca+2 leads to increased PTH.

80
Q

Three functions of PTH

A

Osteoclastic resorption, releasing Ca+2 and PO4 into serum
Increasing renal Ca+2 reabsorption and reducing phosphate reabsorption
Upregulating renal 1-alpha hydroxylase to form active Vitamin D

81
Q

Function of active vitamin D

A

increase intestinal Ca+2 and PO4 absorption

82
Q

The cytoplasm in clear cell carcinoma is abundant in

A

Glycogen and lipid content

83
Q

Why do erythrocytosis, polycythemia and hypercalcemia occur in clear cell carcinoma?

A

Tumor cells produce EPO and PTHrP

84
Q

Which laboratory study is most useful for diagnosing cause of patient’s metabolic alkalosis?

A

Urine chloride levels

85
Q

Which metabolic alkaloses are saline responsive?

A

Thiazide/loop diuretic use, vomiting/nasogastric suctioning

86
Q

The ureter runs anterior to

A

Iliac vessels

87
Q

Ureter runs posterior to

A

Uterine artery

88
Q

Symptoms of recurrent fever and abdominal pain are indicative of

A

Recurrent pyelonephritis

89
Q

How does VUR lead to secondary hypertension

A

Renal scarring of upper and lower poles of kidney causes loss of kidney function and water retention

90
Q

Presents as bilateral hydronephrosis and calyceal dilation due to obstruction of urine flow in urethra in males due to malformed Wolfffian duct

A

Posterior urethral valves

91
Q

Presents as rapid onset vision changes, encephalopathy and renal failure

A

Malignant hypertension

92
Q

Adolescent presenting with neuropathic pain (burning sensation in palms and soles), decreased sweat, red macules and papules and renal failure likely has

A

Fabry disease

93
Q

IgA-mediated leukocytooclastic (hypersensitivity) small vessel vasculitis that produces colicky abdomoinal pain, hematuria and palpable purpura on buttocks and legs

A

Henloch-Schonlein purpura

94
Q

Patients with Henloch-Schonlen purpura have increased risk of

A

Intussusception

95
Q

In the true pelvis, the ureters lie medial to ___ and anterior to ___

A

ovarian vessels; internal iliac artery

96
Q

Two side effects of erythropoesis stimulating agents

A

Hypertension and increased risk of thromboembolic events

97
Q

Which condition appears hypercellullar with thickening and splitting of glomerular basement membrane due to subendothelial immune complex deposition on light microscopy

A

Membranoproliferative glomerulonephritis (associated with Hep C)

98
Q

Can develop secondary to HIV infection, heroin abuse and severe obesity

A

Focal segmental glomerular sclerosis

99
Q

Capillary wall thickening and subepithelial deposits (“membrane spikes”) associated with

A

Membranous glomerulonephritis (lung, breast, prostate, colon cancer)

100
Q

Nephrotic presentation characterized by

A

Heavy proteinuria and fatty casts

101
Q

Nephritic syndrome characterized by

A

Hematuria, red cell casts, variable proteinuria

102
Q

In a patient with CKD, what causes fatigue, weakness and itching?

A

Accumulation of uremia toxins

103
Q

In which two conditions do you typically see hyaline arteriosclerosis

A

poorly controlled hypertension and diabetes mellitus

104
Q

Onion skinning, fibrinoid necrosis, localized destruction of vascular wall with circumferential ring of pink, amorphous material surrounding the lumen

A

Malignant hypertension

105
Q

What causes foamy urine in nephrotic syndrome?

A

To compensate for loss of albumin, liver increases lipoprotein synthesis, which escapes in urine and makes it appear foamy

106
Q

Biopsy showing marked ballooning and vacuolar degeneration of proximal renal tubules likely indicates

A

Acute tubular necrosis

107
Q

Ethanol intoxication increases risk of which kidney stones?

A

Calcium oxalate

108
Q

Linear deposits of IG along glomerular basement membrane are characteristic of

A

Anti-glomerular basement membrane (anti-GBM) disease

109
Q

Pulmonary hemorrhage and shortness of breath in anti-GBM syndrome occur because

A

Anti-GBM antibodies cross-react with collagen IV in pulmonary avleolar basement membrane

110
Q

Granular deposits on IF and membrane splitting on light microscopy are indicative of

A

Membronoproliferative glomerulosclerosis

111
Q

Blood supply to proximal ureters

A

Renal arteries

112
Q

Blood supply to distal ureters

A

Common iliac, internal iliac and superior vesical arteries

113
Q

Crescent formation without immunoglobulin or complement deposition on glomerular basement membrane suggest

A

Pauci-Immune RPGN (antineutrophil cytoplasmic antibodies);

114
Q

Which conditions is Pauci-immune RPGN associated with?

A

Granulomatis with polyangiitis or microscopic polyangiitis

115
Q

New onset left varicocele in old man with flank pain and hematuria raises suspicion of

A

Renal vein thrombosis

116
Q

How does infectious endocarditis lead to glomerular nephritis?

A

Deposition of circulating immune complexes in glomerular capillary wall

117
Q

Three mechanisms that stimulate renin release from JGA cells

A

1) Decreased tubular NaCl sensed by macula densa
2) Decreased pressure in afferent arteriole
3) SNS stimulation

118
Q

Most common causes of nephrotic syndrome in adults. Appears thick BM on Jones methenamine silver stain with subepithilal spikes

A

Membranous nephropathy

USMLE (36 decks)

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