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Step 1 AB > Renal > Flashcards

Renal Flashcards

1
Q

What criteria define Nephrotic syndrome?

A 
>3.5g of protein/day
Hypoalbuminemia --> edema 
Hyperlipidemia/ Hypercholesterolemia 
Hypogammaglobulinemia 
Hyper coagulable state --> lose ATIII
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2
Q

What criteria define Nephritic syndrome?

A 
Hypertension
Increase BUN and creatinine (Azotemia)
Oliguria (decreased urine volume)
Hematuria
RBC casts in urine
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3
Q

What does focal mean?

What does diffuse mean?

A

< half of glomeruli affected

> half of glomeruli affected

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4
Q

What does membranous mean?

A

Basement membrane is thickened

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5
Q

What does proliferation mean?

A

There are increased number of cells

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6
Q

Post-Streptococcal glomerulonephritis

a. Pathophysiology
b. Seen in:
c. Presentation
e. On light microscopy
f. On immunofluorescence
g. On electron microscopy

A

a. Type III hypersensitivity; immune complexes are deposited in glomerulus. Treating strep with Abx does NOT prevent post-strep GN
b. Children who had strep infection three weeks earlier
c. Peripheral and periorbital edema, cola-colored urine, HTN
e. Glomeruli enlarged and hyper cellular
f. starry sky granular appearance; lumpy bumpy due to IgG, IgM and c3 deposition along GBM and mesangium
g. Subeptihelial immune complex humps

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7
Q

IgA nephropathy

a. Pathophysiology
b. Presentation
c. Associated with
d. On LM
e. On IF

A

a. Increased IgA
b. Hematuria, after URI
c. Henoch Schonlein purpura
d. Mesangial proliferation
e. IgA based IC deposits in mesangium

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8
Q

Alport syndrome

a. Pathophysiology
b. Presentation
c. On EM

A

a. Mutation in type IV collagein –> thinning and splitting of glomerular BM; most commonly X linked
b. Eye problems, glomerulonephritis, sensorineural deafness
c. Basket weave appearance

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9
Q

Goodpasture’s

a. Pathophysiology
b. Presentation
c. on LM and IF

A

a. Type II hypersensitivity with Abs to GBM and alveolar basement membrane
b. Hemoptysis, hematuria
c. Crescent moon shape –> crescents consist of fibrin and plasma proteins –> linear pattern

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10
Q

What are three types of rapidly progressive glomerulonephritis (Crescentic)

A

Goodpastures
Wegeners (GPA)
Microscopic polyangiitis

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11
Q

Diffuse Proliferative Glomerulonephritis

a. Pathophysiology
b. Presentation
c. on LM
d. on EM

A

a. Due to SLE or membranoproliferative glomerulonephritis
b. Sometimes presents as nephrotic and nephritic syndrome concurrently (heavy proteinuria)
c. Wire looping of capillaries - makes BM look really pronounced
d. Subendothelial IgG immune complexes with C3 deposition

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12
Q

Most common cause of death in SLE

A

Diffuse proliferative glomerulonephritis

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13
Q

Minimal Change Disease

a. Pathophysiology
b. Presentation
c. on LM
d. on EM
e. Treatment

A

a. idiopathic or triggered by infection/immunization; secondary to lymphoma
b. CHILDREN; proteinuria, edema, hyperlipidemia, hypoalbuminemia
c. NORMAL glomeruli
d. EFFACEMENT (fusion) of foot processes
e. Responds to steroids

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14
Q

Focal Segmental Glomeruloscelsosis

a. Pathophysiology
b. Presentation
c. on LM
d. on IF
e. on EM
f. Treatment

A

a. Idiopathic or secondary to HIV!!!!, sickle cell, heroin abuse, obesity, interferon treatment, chronic kidney disease
b. Adults (african american and hispanics); nephrotic syndrome
c. segmental sclerosis and hyalinosis
d. nonspecific of foot process similar to minimal change disease
e. effacement of foot process similar to minimal change disease
f. Does not respond to steroids

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15
Q

Membranous Nephropathy

a. Pathophysiology
b. Presentation
c. on LM
d. on IF
e. on EM

A

a. Idiopathic or secondary to drugs, HBV, HCV, SLE, tumors
b. Caucasian adults
c. Diffuse capillary and GBM THICKENING
d. granular from immune complex deposition
e. Spike and dome appearance with SUBEPITHELIAL DEPOSITS

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16
Q

Membranoproliferative glomerulonephritis

a. Pathophysiology
b. Presenation
c. Type I
d. Type II

A

a. Nephritis syndrome that co present with nephrotic syndrome
b. Idiopathic or due to HBV/HCV infection, SLE or subacute bacterial endocarditis
c. Subendothelial immune complex deposits with granular IF = TRAM TRACK appearance on PAS stain from GBM splitting
d. Intramembranous IC deposits

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17
Q

Diabetic nephropathy

a. Pathophysiology
b. On Biopsy…

A

a. Non-enzymatic glycosylationg of GBM –> increased permeability and thickening
b. Kimmelstiel Wilson lesions, mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis

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18
Q

Linear pattern of IgG deposition on IF

A

Goodpasture syndrome (anti GBM Abs)

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19
Q

Lumpy bumpy deposits of IgG, IgM, C3 in the mesangium

A

Post-strep glomerulonephritis

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20
Q

Deposits of IgA in the mesangium

A

IgA Nephropathy (Berger disease)

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21
Q

Anti-GBM antibodies, hematuria, hemoptysis

A

Goodpasture’s syndrome

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22
Q

Nephritis, deafness, cataracts

A

Alport syndrome

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23
Q

Crescent formation in the glomeruli

A

Rapidly progressive glomerulonephritis

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24
Q

Wire loop appearance on LM

A

Lupus nephritis

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25
Q

Most common nephrotic syndrome in children

A

Minimal change disease

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26
Q

Most common nephrotic syndrome in adults

A

Focal segmental glomerulonephritis

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27
Q

Kimmelstiel-Wilson lesions (nodular glomerulosclerosis)

A

Diabetic nephropathy

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28
Q

EM shows effacement of epithelial foot processes

A

Minimal change disease

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29
Q

Nephrotic syndrome associated with Hepatitis B

A

Membranoproliferative glomerulonephritis

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30
Q

Nephrotic syndrome associated with HIV

A

Focal Segmental Glomerulosclerosis (FSGS)

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31
Q

EM: sub endothelial humps and tram-track appearance

A

Membranoproliferative glomerulonephritis

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32
Q

LM: segmental sclerosis and hyalinosis

A

FSGS

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33
Q

Purpura on back or arms/legs, abdominal pain, IgA nephropathy

A

Henoch Schonlein Purpura

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34
Q

EM: spiking of GBM due sub epithelial deposits

A

Membranous nephropathy (Spike and dome)

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35
Q

Nodular hyaline deposits in the glomeruli

A

Kimmelstiel-Wilson nodules

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36
Q

Glomerulonephritis plus pulmonary vasculititis

A

GPA

Goodpasture

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37
Q

RBC casts

A

Indicate glomerular damage
Glomerulonephritis, malignant HTN
Appear yellowish-brown, cylindrical with ragged edges

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38
Q

WBC casts

A

Indicate acute pyelonephritis

Means damage is ALL the way up in kidney

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39
Q

Bacterial casts

A

Pyelonephritis

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40
Q

Epithelial cell cast

A

ATN, toxic ingestions

Difficult to distinguish from WBC casts

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41
Q

Waxy casts

A

Chronic renal failure

Low urine flow situations

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42
Q

Hyaline casts

A

Most common cast type
Solidified Tam horsefall proteins
Not necessarily pathology
Tend to see them in concentrated urine, dehydration

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43
Q

Fatty cast

A

Nephrotic syndrome

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44
Q

Granular cast

A

From breakdown of cellular casts or aggregates of plasma proteins (albumin, light chains)
Chronic renal disease
ATN (muddy brown cast)

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45
Q

Where is common location of kidney stone?

A

Ureterovesicular junction

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46
Q

Radiopaque

Envelope or dumbbell shaped

A

Calcium kidney stones

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47
Q

Risk factors for calcium oxalate stones

A

Ethylene glycol or Vitamin C abuse, malabsorption

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48
Q

Treatment for calcium stones

A

Hydration, Thiazides, Citrate

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49
Q

Hypercalciuria and normocalcemia

A

Most common kidney stone presentation; calcium stones

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50
Q

Radiopaque, coffin lid stones

A

Struvite (ammonium, Mg, phosphate stones)

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51
Q

Cause of Struvite stones

A

Infection with urease + bugs

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52
Q

Urease + bugs

A 
Proteus mirabilis
Staph saphrophyticus
Klebsiella 
Pseudomonas
They all hydrolyze urea to ammonia --> causes urine alkalinization
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53
Q

Treatment for struvite stones

A

Eradication of infection, surgical removal of stone

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54
Q

Form staghorn calculi (outlines the renal pelvis - looks like a big stag’s horn)

A

Struvite stones

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55
Q

RadioLUCENT

Precipitates at Decreased pH

A

Uric acid stone

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56
Q

Uric acid stone

A

Radiolucent - can’t see on plain film but can see on US and CT
Strong association with hyperuricemia (gout); seen in diseases with increased cell turnover like leukemia

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57
Q

Treatment of uric acid stones

A

Allopurinol, alkalinization of urine

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58
Q

Risk factors for uric acid stones

A

Decreased urine volume, arid climates, acidic pH

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59
Q

Cystine stones

A

Seen in patients with Cystinuria (children)
Staghorn calculi
Treated with alkalinization of urine
Hereditary condition where cystine-reabsorbing transporter loses function –> causing cystinuria

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60
Q

Paraneoplastic syndromes associated with renal cell carcinoma

A

Ectopic erythropoietin –> polycythemia
ACTH –> Cushing syndrome
PTHrP –> hypercalcemia
Prolactin –> hypogonadism, galactorrhea

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61
Q

Complications of Renal cell carcinoma

A

Invades inferior vena cava -> spreads hematogenously

Associated with von Hippel Lindau syndrome

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62
Q

Most common renal malignancy of children aged 2-4

A

Wilms tumor

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63
Q

Presentation of Wilms tumor

A

Hematuria

Large flank mass

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64
Q

Pathogenesis of Wilms tumor

A

Deletion of WT1 or WT2 on chromosome 11 (tumor suppressor gene)

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65
Q

Beckwith-Wiedemann syndrome

A

Wilms tumor
Aniridia
Genitourinary malformation
mental Retardation

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66
Q

Most common tumor of urinary tract

A

Transitional cell carcinoma (in renal calcyes, renal pelvis, ureters, bladder)

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67
Q

Risk factors for transitional cell carcinoma

A

Smoking
Aniline dye exposure
Cyclophosphamide

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68
Q

Cause of diffuse cortical necrosis

A

Vasospasm
DIC
Occurs in very sick patients

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69
Q

Most common causes of ATN

A 
Ischemia
Nephrotoxic drugs (aminoglycosides, cephalosporins, polymyxins, radio contrast dye)
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70
Q

Key finding in ATN

A

Granular muddy brown casts

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71
Q

What is renal papillary necrosis?

A

Sloughing of necrotic renal papillae that causes gross hematuria and proteinuria

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72
Q

What triggers renal papillary necrosis? Associations?

A

Recent infection or immune stimulus

Associated with sickle cell disease, acute pyelonephritis, NSAIDs, diabetes mellitus

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73
Q

Three categories of acute renal failure

A

Prerenal - not enough blood
Intrinsic
Postrenal - outflow obstruction causing back up

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74
Q

Causes of prerenal failure

A

Hypovolemia
Shock
Hypotension
Renal vasoconstriction with NSAIDS

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75
Q

a. BUN/creatinine ratio in pre-renal azotemia
b. FENa
c. urine Na
d. urine osmolality

A

a. >20
b. < 1%
c. <20
d. 500

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76
Q

Causes of intrinsic renal failure

A 
Acute interstitial necrosis
Glomerulonephritis
ATN
DIC
Acute pyelonephritis
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77
Q

a. BUN/creatinine ratio in intrinsic renal failure
b. FENa
c. Urine Na
d. Urine osmolality

A

a. < 15
b. > 2%
c. > 40
d. < 350

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78
Q

Causes of post-renal disease

A

Stones, BPH, neoplasia, congenital anomalies

ONLY happens with bilateral obstruction

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79
Q

Post-renal azotemia

a. BUN/creatinine
b. FENa
c. Urine Na
d. Urine osmolality

A

a. Varies
b. > 1% mild, >2% severe
c. >40
d. < 350

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80
Q

Consequences of renal failure

MADHUNGER

A 
Metabolic Acidosis
Dyslipidemia
Hyperkalemia (retain K without normal kidney function)
Uremia (Nausea, anorexia, asterixis)
Na/H20 retention
Growth retardation
Erythropoietin failure (anemia)
Renal osteodystrophy
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81
Q

What is renal osteodystrophy?

A

Failure of vitamin D hydroxylation, hypocalcemia, hyperphosphatemia –> secondary hyperparathyroidism
Causes subperiosteal thinning of bones

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82
Q

ADPKD

A

Adults
Bilateral enlarged kidneys
Flank pain, hematuria, HTN, urinary infection, renal failure

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83
Q

ARPKD

A

Kids

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84
Q

Fever, Rash, Eosinophilia, Azotemia

A

Drug Induced Interstitial Nephritis

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85
Q

Changes in metabolic panel of renal failure

A

Elevated potassium
Decreased calcium
Elevated BUN and Cr

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86
Q

Thyroid like appearance of kidney

A

Chronic pyelonephritis

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87
Q

Associated with Hodgkin lymphoma

A

Minimal Change Disease

effacement of foot processes from cytokines

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88
Q

Selective proteinuria (loss of albumin but not immunoglobulin)

A

Minimal Change Disease

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89
Q

HIV, heroin use, Sickle cell

A

FSGS

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90
Q

Nephrotic syndromes

A 
Minimal Change Disease
Focal Segmental Glomerulosclerosis
Membranous nephropathy
Membrano-Proliferative Glomerulonephritis
Diabetic Nephropathy
Amyloidosis
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91
Q

Nephritic syndromes

A 
Post-Strep Glomerulonephritis
IgA Nephropathy
Rapidly Progressive Glomerulonephritis (Goodpastures, Wegeners, Microscopic polyangiitis)
Alport Syndrome
Diffuse Proliferative Glomerulonephritis
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92
Q

Positive sodium cyanide nitroprusside test with kidney stones

A

Cystinuria - Cyanide converts cystine to cysteine and a purple color is created when nitroprusside binds cysteine

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93
Q

POTTER Sequence

A 
Pulmonary hypoplasia
Oligohydramnios
Twisted face (flattened)
Twisted skin
Extremity defects
Renal failure (in utero)
Babies who can't PEE in utero, develop Potter sequence
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94
Q

Causes of POTTER sequence

A

ARPKD
Obstructive uropathy (posterior urethral valves)
Bilateral renal agenesis

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95
Q

Which artery traps horseshoe kidney?

What is it associated with?

A

Inferior Mesenteric Artery

Turner’s syndrome

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96
Q

Where does ureter lie compared to uterine artery?

A

Ureter is UNDER Uterine artery

Water under the bridge

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97
Q

How much of body water is extracellular fluid?

A

1/3 of TBW

20% of body weight (1/3 of 60%)

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98
Q

How much of TBW is intracellular fluid?

A

40% (2/3 of TBW)

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99
Q

How much of Extracellular fluid is Interstitial fluid?

A

75% of ECF

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100
Q

How much of Extracellular fluid is Plasma?

A

25% of ECF

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101
Q

What are the units of clearance?

A

Volume/unit time

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102
Q

What is the equation for clearance?

A

UV/P
U = urine concentration of substance
V = urine flow rate (mL/min)
P = plasma concentration

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103
Q

What is the excretion rate equation?

A

Urine concentration of substance (mg/mL) X urine flow rate (mL/min) = mg/min

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104
Q

What is measured to calculate GFR?

A

Inulin is best but not practical

Creatinine - only a small amount is secreted

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105
Q

What is normal GFR?

A

90-135ml/min (100ml/min)

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106
Q

What is renal plasma flow?

A

Blood going to glomeruli AND blood going to tubules
Estimated with PAH (filtered AND secreted in tubule)

U(PAH) x V/P(PAH

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107
Q

What is filtration fraction? What is the equation?

A

The position blood going to the kidney that is filtered through the glomerulus
FF = GFR/RPF (clearance of creatinine/clearance of PAH)
Normally 20%

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108
Q

How do NSAIDS affect GFR?

A

They constrict afferent arterioles

Decrease RBF and GFR –> no change in FF

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109
Q

How does Angiotensin II affect kidney?

A

Constricts efferent arteriole –> congestion of blood in glomerulus –> Renal blood flow decreases but GFR increases –> filtration fraction increases

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110
Q

Effect of ACE inhibitors on kidney

A

Dilate efferent arteriole –> decrease GFR and increase RPF

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111
Q

Constriction of afferent arterioles effects

A

GFR decrease
RBF decrease
FF no change

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112
Q

Constriction of efferent arteriole effects

A

GFR increase
RBF decrease
FF increase

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113
Q

Dilation of afferent arteriole effects

A

GFR increase
RBF increase
FF no change

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114
Q

Dilation of efferent arteriole effects

A

GFR decrease
RBF increase
FF decrease

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115
Q

Increase in serum protein effects on GFR, RBF, FF

A

GFR decrease
RBF no change
FF decrease

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116
Q

Ureter stone obstruction

A 
GFR decrease (back up of urine causes increased hydrostatic pressure in the tubules --> favors blood staying in capillaries)
RBF no change
FF decrease
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117
Q

ACE inhibitors effect on GFR, RBF, FF

A

GFR decrease
RBF increase
FF decrease
-This is why serum creatinine goes up initially when patients are started on ACE inhibitors

118
Q

NSAIDS effect on GFR, RBF, FF

A

GFR decrease
RBF decrease
FF no change

119
Q

What is the filtered load equation?

A

GFR x the plasma concentration of the substance

120
Q

What is the excretion rate equation?

A

urine concentration x urine flow rate (U x V)

121
Q

What is threshold for glucosuria?

A

Plasma glucose of 200mg/dL

122
Q

When are all glucose transporters fully saturated?

A

Plasma glucose of 375mg/dL

123
Q

What is Hartnup disease?

A

Deficiency in transporter for neutral amino acids like Tryptophan in proximal renal tubules –> aminoaciduria and decrease absorption from gut –> no tryptophan for conversion to niacin (B3) –> pellagra (diarrhea, dementia, dermatitis)

124
Q

How do you treat Hartnup disease?

A

High protein diet

Nicotinic acid

125
Q

Where are glucose and amino acids reabsorbed?

A

ALL in the proximal tubule

126
Q

What kind of absorption takes place in proximal tubule?

A

Isotonic absorption

127
Q

What does carbonic anhydrase do?

A

Converts CO2 and H2O into H+ and Bicarb –> bicarb is reabsorbed into the interstitium (blood)

128
Q

Which part of the nephron is impermeable to water?

A

The thick ascending loop of Henle

129
Q

Which part of the nephron is impermeable to Na?

A

Thick descending loop of Henle - passively absorbs water (it is a concentrating segment –> makes urine hypertonic)

130
Q

Where is the Na/K/Cl transporter?

A

Thick ascending loop of Henle

131
Q 
Which class of drugs inhibits the Na/2Cl/K symporter in the thick ascending loop of Henle?
What kind of water excretion do these drugs cause?
A

Loop diuretic

Isotonic water excretion

132
Q

How and where are Ca and Mg reabsorbed in the nephron?

A

In the thick ascending limb they are absorbed paracellularly through positive lumen potential generated by K+ back leak

133
Q

What is happening in early distal convuluted tubule?

A

Reabsorbs Na/Cl
Makes urine most dilute (hypotonic)
PTH increases reabsorption of Calcium through Ca/Na exchanger

134
Q

What actions are taking place in collecting tubule?

A

Reabsorbs Na in exchange for secreting K/H (action of Aldosterone)
Water is reabsorbed - ADH

135
Q

What two types of cells compose the collecting duct and the last segment of the distal tubule? What do they do?

A

Principal cells - Reabsorb Na, H20 and secrete K

Intercalated cells - Secrete Hydrogen, bicarb and reabsorb K

136
Q

What determines how much water is reabsorbed in collecting tubule?

A

ADH - acts on V2 receptors on principal cells and tells them to inset Aquaporin water channels

137
Q

What class of diuretics directly affects the principal cells?

A

K sparing diuretics
Spironolactone/Epleronone = aldosterone antagonists
Inhibit epithelial Na channels - Triamterene, Amiloride

138
Q

What effect does aldosterone have on principal cells and intercalated cells of collecting duct?

A

Principal cells - Reabsorption of Na and secretion of K

Intercalated cells - Stimulates secretion of H+ ions

139
Q

Site of secretion of organic anions and cations

A

Proximal tubule

140
Q

Site of isotonic fluid reabsorption

A

Proximal tubule

141
Q

Site responsible for diluting urine

A

Thick ascending limb

142
Q

Mechanism of Acetazolamide

A

Carbonic anhydrase inhibitor –> inhibits formation of H+ and bicarb from CO2/H2O –> causes limited NaHCO3 diuresis and decreased total body bicarbonate stores

143
Q

Uses for Acetazolamide

A

Glaucoma - (bc Bicarb draws water into the eye to make aqueous humor)
Urinary alkalinization
Metabolic alkalosis
Altitude sickness - (partial pressure of O is lower so you have to breathe faster and deeper –> blow off CO2 –> respiratory alkalosis)
Pseudotumor cerebri

144
Q

S/E of Acetazolamide

A

Metabolic acidosis
NH3 toxicity
Sulfa allergy!!!

145
Q

What are the sulfa drugs?

A

Acetazolamide

Furosemide, Bumetanide, Torsemide

146
Q

What is mechanism of Mannitol

A

Osmotic diuretic that prevents reabsorption of free H20 –> increases urine flow –> decreases intracranial/intraocular pressure

147
Q

What is the use of Mannitol?

A

Drug overdose
Elevated intracranial/intraocular pressure - with acute glaucoma
Shock

148
Q

S/E of Mannitol

A

Pulmonary edema
Dehydration - from losing free water
C/I in anuria, HF

149
Q

Furosemide, Bumetanide, Torsemide mechanism

A 
Loop diuretic; inhibits Na/K/2Cl transporter in thick ascending limb; prevent concentration of urine
LOSE CALCIUM (loops lose calcium, thiazides retain calcium)
150
Q

Ethacrynic acid

A

Loop diuretic that is NOT a sulfonamide

Can be used in patients with Sulfa allergy

151
Q

Use of loop diuretics

A 
Patients with serious edema
CHF
Pulmonary edema
Nephrotic syndrome
Cirrhosis
152
Q

S/E of loop diuretics

A 
Ototoxicity
HYPOkalemia
Dehydration
Nephrotoxicity
Gout - interfere with uric acid secretion
Allergy (SULFA)
153
Q

Chlorthalidone, HCTZ mechanism

A 
Inhibit Na/Cl reabsorption in early DCT --> decrease diluting capacity of nephron
Retain Calcium (decrease Ca excretion)
154
Q

Uses for Thiazide diuretics

A

HTN
HF
Idiopathic hypercalciuria (normal serocalcemia but dumps a lot in urine –> calcium stones)
Nephrogenic diabetes insipidus

155
Q

S/E of Thiazides

A 
Hyper LIPIDEMIA
hyper GLYCEMIA
hyper CALCEMIA 
hyper URICEMIA
Sulfa allergy
156
Q

Uses for K sparing diuretics

A

Hyperaldosteronism
K depletion
HF (improve mortality)

157
Q

S/E of K sparing diuretics

A 
Hyperkalemia --> arrhythmia
Endocrine effects (gynecomastia, anti-androgen)
158
Q

Mechanism of Tiamterene, Amiloride

A

Block Na channels in the cortical collecting tubule –> spare K

159
Q

What are kidney endocrine functions?

A

Make EPO in response to hypoxia
1alpha hydroxylase converts vitamin D into active form (1,25 OH2 D3) when stimulated by PTH
Renin is secreted by JG cells in response to decreased renal arterial pressure and increased renal sympathetic discharge (B1)

160
Q

When is PTH secreted?

What are it’s actions?

A

PTH is secreted in response to low calcium, increased phosphate or low vitamin D
It activates vitamin D, increases Calcium reabsorption and decreases phosphate reabsorption

161
Q

When is ANP secreted?

What are it’s actions?

A

Secreted in response to increased atrial pressure

Causes increased GFR and increases Na filtration with NO compensatory REABSORPTION of Na –> Na, volume loss

162
Q

How does Lithium cause Diabetes Insipidus?

A

ADH causes aquaporins to be put into luminal cell to reabsorb water –> lithium interferes with this process

163
Q

Signs of hyponatremia

A 
Confusion, altered mental status
Seizures
Stupor
Coma
(messes with resting potential or neurons)
164
Q

Signs of hypercalcemia

A

Stones
Bones
Groans (abdominal)
Psychiatric overtones (confusion, delirium)

165
Q

Hypocalcemia signs

A

Tetani (Trousseau sign = Tighten BP cuff, Chvostek sign = cheek)

166
Q

Hypomagnesemia signs

A

Tetani

167
Q

Hypermagnesemia signs

A

Depressed reflexes

168
Q

Hypokalemia

A

Prolongs QT interval –V tach and Torsades

Flattened T waves

169
Q

Hyperkalemia

A

V tach

PEAKED T waves

170
Q

What kinds of things shift K outside of cells –> hyperkalemia?

A 
Low insulin 
Beta blockers
Acidosis - cells trying to correct acidosis by moving H+ ions out of blood (exchange H for K)
Digoxin 
Cellular lysis (leukemia)
171
Q

What kinds of things shift K inside to cells?

A

Insulin
Beta agonist
Alkalosis
Cell formation

172
Q

Three emergency treatments for hypokalemia?

A

Beta agonist (Albuterol)
IV Insulin
IV Bicarb

173
Q

Treatment for central DI

A

Desmopressin

174
Q

Treatment for nephrogenic DI

A

HCTZ
Indomethacin
Amiloride

175
Q

Treatment for Lithium-Induced Nephrogenic DI

A

Amiloride

176
Q

Causes of hypernatremia

A 
Diuretics
Dehydration
Diabetes Insipidus
Docs (iatrogenic)
Diarrhea
Disease of Kidney
177
Q

Causes of respiratory acidosis

A 
Hypoventilating
Airway obstruction
Air trapping
Lung disease (interstitial especially)
Weak respiratory muscles
Opioids
178
Q

Causes of metabolic acidosis

A

Adding acid to blood of losing excessive Bicarbonate

Can be classified by high or low metabolic anion gap

179
Q

Increased anion gap metabolic acidosis (MUDPILES)

A 
(ADDING ACID TO BLOOD)
Methanol
Uremia
Diabetic ketoacidosis
Propylene glycol
Iron tablets/Isoniazid
Lactic acidosis (shock, not perfusing)
Ethylene glycol
Salicylates (LATE)
180
Q

Normal anion gap metabolic acidosis (HARD-ASS)

A 
(FROM LOSING BICARBONATE)
Hyperalimentation
Addison disease
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion
181
Q

Causes of respiratory alkalosis

A 
Hyperventilating --> blowing off CO2
Psychogenic
High altitude
Acute hypoxemia (PE)
Aspirin toxicity (EARLY) --ASA directly stimulates respiratory center in brain and causes hyperventilation and later you MIGHT see metabolic acidosis
182
Q

Causes of metabolic alkalosis

A

Losing Hydrogen ions
Excessive vomiting
Diuretics
Hyperaldosteronism (Hypokalemia, hypertension, metabolic alkalosis)

183
Q

Renal Tubular Acidosis

A
  1. Type 1 RTA - distal; alpha intercalated cells can’t secrete hydrogen –> metabolic acidosis —> hypokalemia, urine pH > 5.5, increased bone turnover
  2. Type 2 RTA - proximal; defect in PCT Bicarbonate reabsorption
  3. Type 4 RTA - from hyperaldosteronism –> causes hyperkalemia –> decreased ammonia synthesis in PCT –> decreased NH4 excretion, urine pH < 5.5; Caused by decreased aldosterone production, aldosterone resistance
184
Q

What is winter’s formula?

A

Pco2 = 1.5 (HCO3) + 8 +/- 2

Not that important for Step1

185
Q

pH 7.4
HCO3 23
pCO2 40

A

Normal

186
Q

pH 7.5
HCO3 35
pCO2 42

A

Metabolic alkalosis

187
Q

pH 7.33
HCO3 13
pCO2 28

A

Metabolic acidosis with respiratory compensation

188
Q

pH 7.42
HCO3 32
pCO2 64

A

Mixed respiratory acidosis/metabolic alkalosis

189
Q

pH 7.2
HCO3 18
pCO2 40

A

Metabolic acidosis

190
Q

pH 7.20
HCO3 24
CO2 54

A

Respiratory acidosis

191
Q

pH 7.52
HCO3 22
CO2 22

A

Respiratory alkalosis

192
Q

pH 7.66
HCO3 36
pCO2 30

A

Mixed alkalosis

193
Q

pH 7.47
HCO3 14
PCO2 22

A

Respiratory alkalosis with metabolic compensation

194
Q

pH 7.46
HCO3 35
PCO2 53

A

Metabolic alkalosis with respiratory compensation

195
Q

pH 7.39
HCO3 12
PCO2 22

A

Mixed metabolic acidosis/respiratory alkalosis

196
Q

pH 7.34
HCO3 31
pCO2 62

A

Respiratory acidosis with metabolic compensation

197
Q

pH 7.10
HCO3 15
pCO2 50

A

Mixed acidosis

198
Q

a. What is the pronephros?
b. What is the mesonephros?
c. What is the metanephros?

A

a. The embryonic kidney up until week 4 and then it degenerates
b. Functions as interim kidney for 1st trimester; later contributes to male genital system
c. Permanent; appears in 5th week of gestation; nephrogenesis continues through 32-36 weeks of gestation

199
Q

Which embryologic kidney is permanent?

A

Metanephros

200
Q

Parts of metanephros?

A

a. Ureteric bud - derived from caudal end of mesonephric duct; gives rise to ureter, pelvises, calyces, collecting ducts –> entire collecting system
b. Metanephric mesenchyme - ureteric bud interacts with this tissue to induce differentiation and formation of glomerulus through to distal convoluted tubule

201
Q

What can cause several congenital malformations of the kidney during embryogenesis?

A

If the ureteric bud and metanephric mesenchyme interaction is abnormal

202
Q

What is the last part of the kidney to canalize? Why is this significant?

A

The ureteropelvic junction; it is the MOST common site of obstruction (hydrophrosis) in fetus

203
Q

Cause of multi cystic dysplastic kidney

A

Abnormal interaction between ureteric bud and metanephric mesenchyme

204
Q

Cause of duplex collecting system

A

Bifurcation of ureteric bud before it enters the metanephric blastema creates Y shaped bifid ureter or can occur when two ureteric buds reach and interact with metanephric blastema

205
Q

Associations with duplex collecting system

A

Vesicoureteral reflux
Ureteral obstruction
Increased risk for UTIs

206
Q

Why if left kidney taken during donor transplantation?

A

Left renal vein is longer

207
Q

Which vessels are at risk of damage during gynecologic procedures?

A

If there is ligation of uterine vessels in the cardinal ligament there is a possibility of damaging ureter –> ureteral obstruction or leak

208
Q

What makes up the glomerular filtration barrier?

A

Fenestrated capillary endothelium (size barrier)
Fused basement membrane with heparin sulfate (negative charge barrier)
Epithelial layer consisting of podocyte foot processes

209
Q

Which part of the glomerular filtration barrier is lost in nephrotic syndrome?

A

The charge barrier is lost –> albuminuria, hypoproteinemia, generalized edema, hyperlipidemia

210
Q

Equation for RBF

A

RBF = RPF/(1-Hct)

211
Q

What is the normal filtration fraction?

A

20%

212
Q

Estimate of GFR?

Estimate of Renal plasma flow?

A 
GFR = creatinine clearance 
RPF = PAH clearance (Filtered and secreted = 100% excretion)
213
Q

How does constriction of ureter change GFR, RPF and FF?

A

Causes decreased GFR, no change in RPF and decreased FF

214
Q

Where is glucose reabsorbed?

A

100% reabsorbed in proximal tubule by Na/glucose co-transport

215
Q

What happens to glucose regulation in kidney during pregnancy?

A

It may decrease the ability of PCT to reabsorb glucose and amino acids –> glucosuria and aminoaciduria

216
Q

What is Hartnup disease?

A

Deficiency of neutral amino acid transporter in proximal renal tubular cells and enterocytes –> neutral aminoaciduria and decreased absorption form the gut –> decreased tryptophan for conversion to niacin –> pellagra (diabetes, dementia, dermatitis)

217
Q

How do you treat Hartnup disease?

A

High protein diet and nicotinic acid

218
Q

Where does Angiotensin II exert it’s effects?

A

The proximal tubules (Na/H exchanger) –> causes Na, H20 and bicarb reabsorption

219
Q

Where does Parathyroid hormone exert effects in nephron?

A
  1. Inhibits Na/PO4 co-transport in PCT –> causes PO4 excretion
  2. Causes increased Ca/Na exchange in early distal convoluted tubule –> increased Ca reabsorption
220
Q

Where does ADH act?

A

Acts at V2 receptor (Gs receptor) –> insertion of aquaporin H20 channels on apical side –> increased H20 reabsorption

221
Q

Where does Aldosterone act?

A

a. Acts on mineralcorticoid receptor –> mRNA –> protein synthsis
b. In Principal cells it causes apical K+ conductance, increased activity of Na/K pump, Increased ENaC channels –> lumen negativity –> K+ loss
c. In alpha-intercalated cells –> increased H+ ATPase activity –> HCO3/Cl exchanger activity

222
Q

Generalized reabsorptive defect in PCT

What does it cause?

A

Fanconi syndrome
Increased excretion of all amino acids, glucose, HCO3, PCO4
May result in metabolic acidosis

223
Q

Reabsorptive defect in thick ascending loop of Henle

Results in what?

A

Bartter syndrome

Affects Na/K/2Cl co-transporter –> results in hypokalemia and metabolic alkalosis with hypercalciuria

224
Q

Reabsorptive defect of NaCl in DCT

Results?

A 
Gitelman syndrome (less severe than Bartter)
Causes hypokalemia, hypomagnesemia, metabolic alkalosis, hypocalciuria
225
Q

Gain of function mutation –> increased Na reabsorption in collecting tubules

A

Liddle syndrome

226
Q

Hypertension, hypokalemia, metabolic alkalosis, decreased aldosterone (not deficiency of 11B hydroxysteroid dehydrogenase)

A

Liddle syndrome (autosomal dominant)

227
Q

Treatment of Liddle syndrome

A

Amiloride (blocks Na channels in collecting tubule)

228
Q

11B-hydroxysteroid dehydrogenase deficiency

A

Syndrome of apparent mineralcorticoid excess –> cortisol doesn’t get converted to cortisone and excess cortisol acts on mineralocorticoid receptors to cause hypertension, hypokalemia, metabolic alkalosis

229
Q

Acquired 11B-hydroxysteroid dehydrogenase deficiency

A

From licorice (glycyrrhetic acid)

230
Q

Where does ACE come from?

A

Lungs and kidney

231
Q

What causes increased production of renin?

A
  1. Decreased BP sensed by JG cells
  2. Decreased Na delivery sensed by macula densa
  3. Increased sympathetic tone (B1 receptors) (Gs)
232
Q

Where does Angiotensinogen come from?

A

Liver

233
Q

Effects of AT II

How does it avoid reflex bradycardia?

A

Acts at angiotensin II receptor on vascular smooth muscle to cause vasoconstriction and increased BP
It affects baroreceptor function and limits reflex bradycardia which would normally accompany pressor effects

234
Q

What does ADH primarily regulate?

A

Osmolarity (but also responds to low volume state)

235
Q

What dose Aldosterone primarily regulate?

A

ECF volume and Na content (but also responds to low volume states)

236
Q

What makes up the Juxtaglomerular apparatus?

A 
Mesangial cells
JG cells (modified smooth muscle of afferent arteriole)
Macula densa (NaCl sensor, part of DCT)
237
Q

Function of JG cells?

A

Secrete renin in response to decreased renal BP and increased sympathetic tone

238
Q

Function of macula densa?

A

Sense decreased NaCl delivery to DCT –> cause adenosine release –> vasoconstriction

239
Q

How do beta blockers decrease BP through the kidney?

A

They inhibit B1 receptors of the JGA and cause decreased renin release

240
Q

Kidney endocrine functions (4)

A
  1. EPO is released by interstitial cells in peritubular capillary bed in response to hypoxia
  2. PCT cells convert 25-OH vitamin D to 1,25-OH2 Vitamin D via 1alpha hydroxylase
  3. JG cells secrete renin in response to decreased renal arterial pressure and increased sympathetic tone
  4. Paracrine secretion of prostaglandins vasodilator the afferent arterioles to increase RBF
241
Q

What K+ shift does Digitalis cause?

A

Shifts K+ out of cells causing hyperkalemia (blocks Na/K ATPase)

242
Q

Things causing Hyperkalemia (6)

A 
Digitalis
Hyperosmolarity
Lysis of cells (crush injury, rhabdomyolysis, cancer)
Acidosis
Beta blocker
High blood sugar (insulin deficiency)
243
Q

Things causing Hypokalemia (4)

A

Hypo-osmolarity
Alkalosis
Beta adrenergic agonist (increased Na/K ATPase)
Insulin (increased Na/K ATPase; shifts K into cells)

244
Q

Electrolyte disturbance causing tetany, seizures, QT prolongation

A

HYPOcalcemia

245
Q

Electrolyte disturbance causing stones, bones, groans, thrones, psych overtones

A

HYPERcalcemia

246
Q

Electrolyte disturbance causing nausea, malaise, stupor, coma seizures

A

HYPOnatremia

247
Q

Electrolyte disturbance causing U waves on EKG, flattened T waves, arrhythmias, muscle spasm

A

HYPOkalemia

248
Q

Electrolyte disturbance causing wide QRS and peaked T waves on EKG, arrhythmias, muscle weakness

A

HYPERkalemia

249
Q

Electrolyte disturbance causing torsade de pointes, tetany, hypokalemia

A

HYPOmagnesium

250
Q

Causes of respiratory acidosis

A

Hypoventilation (caused by airway obstruction, acute or chronic lung disease, opioids or sedatives, weakened respiratory muscles)

251
Q

a. Another name for Methanol

b. Another name for Ethylene glycol

A

a. Formic acid

b. Oxalic acid

252
Q

Cause of Normal anion gap metabolic acidosis (HARDASS)

A 
Hyperalimentation
Addison disease - hypoaldosteronism 
Renal tubular acidosis
Diarrhea - losing bicarbonate
Acetazolamide - not reabsorbing bicarbonate
Spironolactone
Saline infusion
253
Q

Flank pain, hematuria, oliguria with high anion gap metabolic acidosis

A

Ethylene glycol poisoning

254
Q

Cause of distal (type 1) renal tubular acidosis

A

Defect in ability of alpha intercalated cells to secrete H+ –> can’t generate HCO3 –> metabolic acidosis

255
Q

Symptoms of distal (type 1) renal tubular acidosis

A

Urine pH > 5.5
Hypokalemia
Increased risk for calcium phosphate kidney stones (from increased urine pH and bone turnover)
Normal anion gap metabolic acidosis

256
Q

Cause of Proximal (type 2) renal tubular acidosis

A

Defect in PCT HCO3 reabsorption –> increased excretion of HCO3 in urine

257
Q

Causes of proximal renal tubular acidosis

A

Fanconi syndrome

Carbonic anhydrase inhibitors (Acetazolamide)

258
Q

Cause of hyperkalemic (type 4) renal tubular acidosis

A

Hypoaldosteronism –> hyperkalemia –> decreased NH3 synthesis in PCT –> decreased NH4 excretion

259
Q

Urine pH in hyperkalemic (type 4) renal tubular acidosis

A
260
Q

Hematuria but no casts

A

Bladder cancer or kidney stones

261
Q

Pyuria and no casts

A

Acute cystitis

262
Q

What do presence of casts signify?

A

Hematuria/pyuria is of glomerular or renal tubular origin

263
Q

Increased anti-DNase B titers, decreased complement levels

A

Acute post-strep glomerulonephritis

264
Q

What do crescents consist of in Rapidly progressive glomerulonephritis?

A

Fibrin and plasma proteins (C3b) with glomerular parietal cells, monocytes, macrophages

265
Q

Treatment of rapidly progressive glomerulonephritis

A

Emergent plasmapheresis

266
Q

MPO-ANCA

A

p-ANCA –> Microscopic polyangiitis

267
Q

Basket weave appearance on EM

A

Alport syndrome (mutation in type IV collagen –> thinning and splitting of glomerular basement membrane)

268
Q

Stones that precipitate at

a. increased pH
b. decreased pH

A

a. Calcium phosphate, Ammonium magnesium phosphate (Struvite)
b. Calcium oxalate, Uric acid, Cystine

269
Q

Causes of calcium oxalate stones

A

Ethylene glycol (antifreeze) ingestion
Vitamin C abuse
Hypocitraturia
Malabsorption (Crohn’s)

270
Q

Treatment for calcium oxalate/phosphate stones

A

Increased citrate
Thiazide diuretics
Hydration

271
Q

Bugs causing struvite stones

A

Proteus mirabilis
Staph saprophyticus
Klebsiella
(all urease +)

272
Q

How does renal cell carcinoma spread?

A

Invades renal vein then IVC –> spreads hematogenously and metastasizes to lung and bone

273
Q

Gene deletion associated with Renal cell carcinoma

A

Gene deletion on chromosome 3 (sporadic or inherited in von Hippel-Lindau)

274
Q

Paraneoplastic syndromes associated with renal cell carcinoma

A

Ectopic EPO, ACTH, PTHrP

275
Q

Renal oncocytoma histology

A

Large eosinophilic cells with abundant mitochondria without perinuclear clearing

276
Q

Painless hematuria without casts

A

Bladder cancer

277
Q

Associations of transitional cell carcinoma of bladder (P SAC)

A

Phenacetin, Smoking, Aniline dyes, Cyclphosphamide

278
Q

Risk factors for squamous cell carcinoma of bladder

A

Schistosoma haematobium
Chronic cystitis
Smoking
Chronic nephrolithiasis

279
Q

Lab findings of acute bacterial cystitis

A

+ leukocyte esterase

+ nitrites (for gram negative organisms)

280
Q

Urethritis with sterile pyuria and negative urine cultures

A

Neisseria gonorrhoeae or Chlamydia trachomatis

281
Q

Striated parenchymal enhancement of kidney on CT

A

Acute pyelonephritis

282
Q

Thyroidization of kidney

A

Chronic pyelonephritis

283
Q

Drugs causing acute interstitial nephritis

A 
Diuretics
Penicillins
Proton pump inhibitors
Sulonamides
Rifampin
NSAIDS - (months after for this one)
284
Q

Causes of acute tubular necrosis

A

Ischemic injury or nephrotoxic injury by drugs/crush injury/hemoglobinuria

285
Q

SAAD with papillary necrosis

A

Sickle cell
Acute pyelonephritis
Analgesics (NSAIDs)
Diabetes mellitus

286
Q

How do the following affect serum Calcium?

a. Hyperphosphateima
b. Decreased Vitamin D

A

a. Decreased serum Calcium by causing tissue calcifications

b. Decreased intestinal Ca absorption

287
Q

Associations of ADPKD

A

Berry aneurysms
Mitral valve prolapse
Benign hepatic cysts

288
Q

Associated with congenital hepatic fibrosis

A

ARPKD

289
Q

Shrunken kidneys on ultrasound

Inability to concentrate urine

A

Medullary cystic disease

290
Q

What are the types of renal cysts?

Which ones need to be removed?

A

Simple - very common, clear on US, typically asymptomatic and found incidentally
Complex - septated, enhanced or have solid components on imaging; require follow up or removal due to risk of RCC

Step 1 AB (29 decks)

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