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GI/GU > Genitourinary Exam 1 Cards > Flashcards

Genitourinary Exam 1 Cards Flashcards

1
Q

9 major renal functions

A

Excretion
Water and Electrolyte balance
Fluid volume
Plasma osmolality
RBC production regulation
BP regulation
Acid base balance
Vitamin D activation
Gluconeogenesis

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2
Q

How does the kidney regulate RBC production?

A

It releases erythropoietin in response to hypoxia

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3
Q

How does the kidney modulate blood pressure

A

Releases renin in response to low flow

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4
Q

Renal medulla and cortex on biopsy

A

Cortex = Spaghetti and meatballs
Medulla = Bundles of pencils

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5
Q

Scar tissue

A

Not metabolically active and therefore does not need as much oxygen

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6
Q

More common nephron type

A

Cortical

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7
Q

Podocytes

A

Surround capillary loops in the glomerulus to remove trapped material and contract capillaries if needed

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8
Q

Most common complaint and complication associated with a horseshoe kidney

A

UTI - Bacteria grow in pooling urine
Ureteropelvic junction obstruction
Kidney stones

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9
Q

Diagnosis and treatment of a horseshoe kidney

A

CT, Urinalysis, and Renal function
Manage disorders and complications as they arise

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10
Q

Urine filtrate

A

Plasma without proteins

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11
Q

Glomerular Filtration rate

A

Amount of filtrate formed over time

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12
Q

Resorption of PCT

A

60% of HCl and H20 90% of bicarb
Secretes most wastes (urea, ammonia, creatinine, etc.)

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13
Q

Loop of henle

A

Water goes out the descending
Sodium goes out the ascending
Most magnesium resorbed

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14
Q

Where do loop diuretics work

A

Thick ascending loop of henle

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15
Q

Distal Convoluted tubule

A

May resorb urea
CALCIUM regulation Secretes K+
Regulates pH
Site of action for thiazide diuretics

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16
Q

Cortical collecting duct

A

Resorbs NaCl and H2O
Secretes K+
Aldosterone and K sparing diuretics work here

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17
Q

Medullary collecting duct

A

Final modification of urine with some secretion and resorption

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18
Q

How do nephrons handle loss

A

They do not regenerate but hypertrophy in order to compensate for lost tissue

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19
Q

Maladaptive deterioration

A

Point at which nephrons can no longer compensate for losses

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20
Q

Amount of renal mass removal resulting in ESRD

A

80%

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21
Q

Progression of nephron loss

A

Damage to glomeruli (via HTN) results in protein leakage which leads to inflammation and fibroblast activation

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22
Q

GFR of CKD

A

Under 60mL/min

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23
Q

2 Limitations of GFR

A

Can’t detect problems that are non-glomerular
May go up at the onset of renal disease
May appear stable in worsening disease

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24
Q

3 substances that can be used for GFR estimation

A

BUN, Creatinine, Cystatin C

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25
Q

Factors effecting GFR estimation

A

Body surface area - smaller body=less muscle mass
Age - declines with age
Gender - Males have more muscle and more creatinine
Race - AAs have more muscle and more creatinine - new recomendations don’t use race

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26
Q

3 factors that increase serum creatinine that are NOT renal failure

A

Meat intake
Creatine supplements
High muscle mass

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27
Q

Medications that inhibit renal secretion of creatinine

A

Abx - cephalosporins, aminoglycosides, trimethoprim
Cimetidine

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28
Q

Effect of liver disease on estimated GFR

A

Decreases creatine production leading to decreased creatinine, leading to higher eGFR

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29
Q

Creatinine clearance in CKD

A

Enhanced in early stages, taken over by liver in late stages

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30
Q

Creatinine Clearance

A

Requires 24 hour collection of urine for creatinine testing and estimates the upper limit of the true GFR

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31
Q

When does one need to finish collecting urine for a CrCl test

A

within 10 minutes of the 24 hour mark of beginning

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32
Q

Limitation of CrCl urine test

A

Cumbersome and has a tendency to overestimate

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33
Q

Cause of BUN:Cr above 20:1

A

Dehydration due to increased renal resorption - tubules must be working
Cell breakdown can also cause incresed BUN as well as decreased renal perfusion

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34
Q

4 things causing decreased BUN

A

Liver disease
Malnutrition
Sickle cell anemia
SIADH

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35
Q

BUN and GFR estimation

A

Less useful for estimation - much of it is resorbed is inversely proportional to GFR, and can change independantly

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36
Q

Cyastatin C and GFR

A

Not as impacted by race, gender, age as creatinine but still increased by things like male sex, fat mass, diabetes, etc.

Inverse relationship and EXPENSIVE

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37
Q

3 indications for cyastatin C measurement

A

Elderly patients
Body builders
Acute Illness
(All have abnormal muscle mass)

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38
Q

Cockroft Gault equation

A

Estimates CrCl in a patient with stable Cr
Need age and body weight, sex
Overestimate

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39
Q

MDRD study equation

A

Estimates GFR with body surface area and Cr
Needs age, sex, race
More accurate than CG

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40
Q

CKD-EPI Study

A

More accurate GFR measurement than CG works best for mild or normal GFR
Better risk prediction
Uses serum creatinine, age, and sex (no longer modified by race)

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41
Q

Preferred GFR equation in US

A

CKD-EPI (no race)

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42
Q

Acute kidney injury

A

Sudden decrease in kidney function over hours or days with inability to manage fluid electrolytes, and acid base or excretion of waste products

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43
Q

Duration of AKI before we see a drop in labs

A

Can be up to 12-24 hours

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44
Q

Azotemia

A

Increase of waste products in the blood

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45
Q

Uremia

A

Symptomatic azotemia

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46
Q

Anuria

A

Under 50 mL in 24 hours

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47
Q

Oliguria

A

50-400 mL in 24 hours

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48
Q

Polyuria

A

2500-3000 mL/day or more

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49
Q

6 uremic symptoms

A

Weakness, tremors, dryness, HTN, Nausea, acidosis

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50
Q

Most common cause of AKI

A

Prerenal azotemia (followed by intrinsic)

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51
Q

Prerenal azotemia

A

Azotemia due to inadequate renal perfusion, hypovolemia, decreased cardiac output, or changed vascular resistance

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52
Q

BUN/Cr ratio of prerenal azotemia

A

Greater than 20:1 because kidneys think we are dehydrated

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53
Q

Fractional excretion of sodium in prerenal azotemia

A

Under 1% - kidneys think we are dehydrated - retain sodium

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54
Q

Clinical presentation or prerenal azotemia

A

Dehydration, Sepsis, diffuse abdominal pain and ileus

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55
Q

MCC of postrenal obstruction in men

A

BPH

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56
Q

2 tests for postrenal obstruction

A

Bladder catheterization and/or abdominopelvic US

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57
Q

BUN/Cr ratio of postrenal obstruction

A

Over 20:1

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58
Q

Urine osmolality of postrenal obstruction

A

400mosm/kg or less

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59
Q

3 major causes of Acute Tubular Necrosis

A

Ischemia
Nephrotoxins
Sepsis - hypoperfusion or direct injury

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60
Q

5 Nephrotoxic antimicrobials

A

Gentamycin, Streptomycin (less so), Vancomycin, Sulfonamides, Cephalosporins

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61
Q

2 nephrotoxic antivirals and one antifungal

A

acyclovir, foscarnet, amphotericin B

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62
Q

3 non pharm exogenous nephrotoxins

A

Radiographic contrast media, Chemo/immunosuppressants, Heavy metals etc.

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63
Q

Myoglobinuria

A

Due to rhabdomyolysis - urine appears dark brown but no detection of RBCs. False positive for hemoglobin

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64
Q

Treatment for myoglobinuria

A

Rehydrate - may have high electrolytes and low calcium which correct

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65
Q

3 other endogenous nephrotoxins

A

Hemoglobinuria (hemolysis)
Hyperuricemia (chemo - uric acid over 15-20 mg/dL)
Bence Jones protein - Obstructs tubules, multiple myeloma

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66
Q

Clinical presentation of acute tubular necrosis

A

Uremia and arrhythmias may be noted
Low GFR with BUN:Cr under 20:1
Muddy brown casts
Elevated urine sodium

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67
Q

What does low BUN:Cr or elevated urine sodium mean

A

We are NOT resorbing anything

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68
Q

Treatment for Acute tubular necrosis

A

Avoid volume overload, loop diuretics, or dialysis
Promote dietary interventions

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69
Q

Better long term outcome ATN patient

A

Non-oligouric

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70
Q

Classic presentation of acute glomerulonephritis

A

HTN, Edema, urine containing protein, RBCs, WBCs, and RBC casts

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71
Q

Crescent lesions

A

Severe breaks in glomerular walls

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72
Q

Types of Glomerulonephritis

A

Immune complex destruction
Anti-GBM autoantibody destruction
C3 deposition
Pauci-immune (vasculitis)

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73
Q

2 places edema is seen first

A

Scrotal and periorbital

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74
Q

Treatment for acute glomerulonephritis

A

Corticosteroids - high dose
Plasma exchange for goodpasture or pauci immune

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75
Q

Immune complex glomerulonephritis

A

Antigen-antibody complex lodges in GBM leading to its destruction by the immune system

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76
Q

Anti-GBM associated glomerulonephritis

A

Autoantibodies against the GBM are produces - called Goodpature syndrome if the lungs are also effected

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77
Q

C3 glomerulopathy

A

Caused by C3 deposition in the glomerulus - may result in low C3 levels. Minimal role played by immune globulins

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78
Q

Monoclonal Ig-mediated glomerulonephritis

A

Monoclonal antibodies lodge in the GBM - no antigens are seen
Can be detected with serum protein electrophoresis

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79
Q

Pauci-Immune GN

A

Associated with ANCAs (anti-neutrophillic cytoplasmic antibodies)
No immune complexes or complement involved

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80
Q

MCC of acute interstitial glomerulonephritis

A

Medications

Can also be infectious or immune

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81
Q

Classic triad of interstitial glomerulonephritis

A

Fever, rash, arthralgia (may not see ALL three)

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82
Q

Urine sediment of AIN

A

WBCs, RBCs, No protein

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83
Q

BUN:Cr ratio of Acute interstitial GN

A

under 20:1

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84
Q

BUN:Cr ratio for Glomerulonephritis

A

Greater than 20:1

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85
Q

Broad or waxy urine casts

A

Chronic renal failure

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86
Q

Hyaline casts

A

Exercise, diuretics, concentrated urine

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87
Q

Fatty casts

A

Nephrotic syndrome (oval fat bodies)

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88
Q

Granular casts

A

Chronic renal failure or ATN

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89
Q

Renal tubular epithelial cast

A

ATN

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90
Q

RBC casts

A

Glomerulonephritis

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91
Q

WBC casts

A

Interstitial or pyelonephritis

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92
Q

2 diagnostics to rule out urethral obstruction

A

Urethral cath and bladder scan US

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93
Q

4 things that increase and one thing that decreases when total body water drops

A

Increase:
SNS
RAAS
ADH
Thirst

Decrease:
ANP

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94
Q

Clinical presentation of isotonic fluid volume defecit

A

Altered mental status, low BP high HR, Weak pulse, Dry mucous membranes

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95
Q

Why does professor Jensen love lactated ringers?

A

They don’t have sodium in them

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96
Q

Treatment for volume overload

A

IV diuretics (loop), dialysis if no response to therapy, Restrict fluids and sodium

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97
Q

Clinical presentation of hyperphosphatemia

A

SOB, N/V, Hypocalcemia (hyperreflexia, trousseu and chvostek signs, carpopedal spasm

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98
Q

Clinical presentation of hypokalemia

A

Weakness, constipation, flattened T waves and ST depression

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99
Q

Clinical presentation of hyperkalemia

A

Cramps, diarrhea, vomiting, hypotension, palpitations
Peaked T waves, lost P waves, Wide QRS

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100
Q

Treatment for hyperkalemia

A

Treat if EKG changes or neuromuscular symptoms
Block cardiac effects
Reduce plasma K+
Remove potassium

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101
Q

Blocking of cardiac effects in the hyperkalemic patient

A

IV calcium gluconate with cardiac monitoring
Repeat if EKG changes do not occur
Can potentiate toxicity of digoxin

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102
Q

Reducing plasma potassium in hyperkalemic patient

A

Administer insulin followed by dextrose
Albuterol can also help

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103
Q

Removal of potassium in the hyperkalemic patient

A

GI cation exchangers (Kayexalate, zirconium cyclosilicate, patiromir)

Loop or thiazide diuretics

Dialysis - can even electrolytes

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104
Q

Isotonic hyponatremia

A

Usually means that there are extra molecules in the blood (fat or protein), skewing the data
Correct underlying cause

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105
Q

Hypertonic hyponatremia

A

Another osmotically active molecule is present such as glucose or radiocontrast
Correct underlying cause

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106
Q

Hypovolemic hyponatremia

A

Due to inappropriate salt loss (ie. GI, burns, dehydration)
Renally due to ACEIs, Diuretics, aldosterone deficiency, renal salt wasting

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107
Q

Hypovolemic hyponatremia

A

Sodium is retained but even more water is retained - nephrotic syndrome, intrinsic renal fluid retention, heart failure, liver disease

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108
Q

Euvolemic hyponatremia

A

SIADH, hypothyroidism, psychogenic polydipsia, beer potomania

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109
Q

Clinical presentation of hyponatremia

A

Primarily neurologic due to cerebral edema
Confusion, lethargy, seizure
Less symptoms when chronic

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110
Q

Treatment of hypovolemic hyponatremia

A

Rehydration with normal saline
Use hypertonic saline if the condition is severe

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111
Q

Treatment difference in chronic and acute hypernatremia

A

Acute - correct in 24 hours
Chronic correct more gradually

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112
Q

pH at which bicarbonate treatment is generally needed

A

pH under 7.2

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113
Q

Treatment for chronic metabolic acidosis in CKD

A

Bicarb replacement
Decreasing animal products in diet

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114
Q

Mechanism of metabolic acidosis in AKI

A

Kidney unable to excrete acid and regenerate Bicarb

115
Q

How does acidosis affect potassium balance

A

It leads to hyperkalemia

116
Q

Situations in which to administer bicarb in severe AKI acidosis

A

Due to diarrhea
Waiting for dialysis
AKI readily reversible
Rhabdomyolosis without other dialysis indications

117
Q

Situations in which to dialyse in AKI acidosis

A

Severe AKI with volume overload
If organic acidosis from lactic or keto acids
pH under 7.1
Risk of volume overload if giving sodium

118
Q

Indications for dialysis in AKI

A

Azotemia and Uremia
Life threatening electolyte disturbances
Volume overload unresponsive to diuretics
Acidosis below 7.1

119
Q

Official definition of CKD

A

Presence of markers of kidney damage or GFR under 60 for 3+ months

120
Q

Kidney nephron response to a decrease in the number of functional nephrons

A

Hyperfiltration and Hypertrophy

121
Q

Cardiorenal syndrome nameing

A

Acute or Chronic is for BOTH organs
Renocardiac is the kidneys fault, Cardiorenal the hearts fault

122
Q

GFR CKD stages

A

1-5 w/ 3a and 3b
1 is normal (90+)
2 - 60-90
Down by 15 after than

123
Q

Albuminuria stages

A

A1 - Under 30 mg/g
A2 - 30/300
A3 - 300+

124
Q

Isosthenuria

A

Urine is the same concentration as blood

125
Q

Uremic frost

A

Crystallized urea excreted in sweat

126
Q

Cause of broad waxy casts in CKD

A

Dilated (Hypertrophied) Nephrons

127
Q

Clinical presentation of CKD in stages 1-2

A

Edema and HTN most common or signs of underlying disease

128
Q

Clinical presentation of stages 3 and 4 of CKD

A

Anemia, fatigue, anorexia, Abnormal calcium, phosphorous, vitamin D, PTH, Sodium, potassium, and water

129
Q

Clinical presentation of stage 5 CKD and ESRD

A

Marked disruption of ADLs and well being

130
Q

Medication most used for CKD

A

ACE/ARB - BUT don’t use in AKI!!

131
Q

CVD in CKD patients

A

Usually death is from cardiac complications before kidney problems
CKD patients build plaques faster and at lower cholesterol levels

132
Q

Goal BP for CKD patients

A

Less than 130/80mmHg okay if a little over

133
Q

ACEI/ARBs in CKD - monitoring

A

Check creatinine and K+ 7-14 days after starting or increase and reduce or stop drug if it has gone up over 30%

134
Q

Diuretics in CKD

A

Thiazides early on
Loop more effective when GFR is under 30
Over diuresis can cause AKI

135
Q

Drugs for lipid management in CKD

A

Statins = First line and recc’d for most pts
PSK-9 inhibitors and ezetimibe as adjunct therapy
Fibrates as last resort (can cause rhabdomyolosis

136
Q

Electrolyte abnormality to monitor for in ACE/ARB use

A

Hyperkalemia

137
Q

Atrial fibrilation treatment risk in Stage 5 and ESRD patients

A

Greater bleeding risk with anticoagulation

138
Q

Pericarditis in CKD

A

Retrosternal chest pain with friction rub, low voltage QRS, ALWAYS an indication for dialysis

139
Q

Typical mineral metabolism abnormality in CKD patients

A

Hyperphosphatemia
Hypovitaminosis D
Hypocalcemia

140
Q

Osteitis fibrosis cystica

A

MC form of renal osteodystrophy
Hyperphosphatemia leads to hyperparathyroidism which leads to osteoclast stimulation
High rates of bone turnover

141
Q

Adynamic bone disease

A

Suppression of PTH or low endogenous PTH = LOW bone turnover

142
Q

X-ray finding of osteitis fibrosa cystica

A

Brown tumors (hollow looking spots) on bones

143
Q

Controlling hyperphosphatemia in CKD mineral metabolism abnormalities

A

Initially use dietary intervention, later use oral phosphate binders

144
Q

CKD phosphate binders

A

Calcium carbonate (Tums, watch for atherosclerosis or hypercalcemia)
Sevelamer or Lanthanum (Non-calcium first line)
Aluminum hydroxide

145
Q

Management of PTH levels in CKD mineral metabolism abnormalities

A

Vitamin D3 (calcitriol) use to balance vitamin D
Cinacelcet - Increase sensitivity of the parathyroid gland good if increased phosphorus or Ca exclude calcitriol

146
Q

Hepcidin

A

Blocks GI iron absorption

147
Q

Treatment for iron deficiency in CKD

A

Ferrous sulfate, gluconate, fumarate, or citrate are approved
No iron if ferritin is over 500-800 ng/mL

148
Q

Erythropoietin treatment in CKD

A

Hold EPO until Hgb drops below 10
Goal is 10-11 for Hb numbers

149
Q

Epo dosing regimens and side effect

A

Epoiein 1-2x per week
Darbepoietin every 2-4 weeks
HTN seen in 20% of patients

150
Q

Treatment for hematologic coagulopathy

A

Due to PLT dysfunction
Only treat if symptomatic
Desmopressin and dialysis can help
Cryoprecipitate is rarely used
Severe protein loss can lead to HYPERcoagulability

151
Q

Good diuretics for high potassium

A

Loop diuretics

152
Q

Cause and treatment for metabolic acidosis of AKI

A

Loss of ability to excrete acid, maintain serum bicarb at 21+mEq/L

153
Q

Uremic encephalopathy

A

Due to aggregation of uremic toxins
Difficulty concentrating to altered mental status

154
Q

Uremic neuropathy

A

Indication to start dialysis
Symmetrical mixed neuropathy
Loss of vibration to clonus/muscle atrophy
Paresthesias

155
Q

Hypoglycemia of CKD

A

Due to decreased renal clearance of insulin
d/c metformin when Cr is above 1.4 or GFR is under 30

156
Q

CKD pregnancy

A

50% infant mortality rate
surviving infants are often premature
CKD progresses faster

157
Q

Sodium restriction for CKD

A

2g/d

158
Q

CKD protein restriction

A

May slow progression - careful if cachectic

159
Q

Water restriction for CKD

A

2L/d

160
Q

Potassium restriction for CKD

A

Less than 2g/d (50-60mEq) if GFR under 10-20 mL/min or hyperkalemic

161
Q

Medications to avoid or manage in CKD

A

Renally excreted drugs
Mg or Ph containing drugs
Morphine
NSAIDs and IV contrast (nephrotoxic)

162
Q

Indications for dialysis in CKD

A

When GFR reaches 5-10 mL/min
Uremic symptoms
Refractory metabolic disturbances
Unresponsive fluid overload

163
Q

Risk of peritoneal dialysis

A

Removes large amounts of albumin
Patients with abdominal surgeries may not by good candidates

164
Q

Diagnostic conditions for peritonitis

A

Over 100 WBC/mcL in peritoneal fluid with over 50% PMN
MCC staph

165
Q

Nephritic spectrum

A

Has more to do with inflammation
Under 3g/d proteinuria
Hematuria with RBC casts

166
Q

Nephrotic spectrum

A

Has more to do with proteinuria
Over 3g/day proteinuria
Bland urine sediment with oval fat bodies potentially

167
Q

Bergers disease

A

IgA nephropathy
Coca cola colored urine
Form of nephritis

168
Q

Clinical presentation of nephrotic syndrome

A

Hypoalbuminemia causing edema
Hyperlipidemia

169
Q

Immune complex deposition glomerulonephritis

A

Antigen-antibody complexes lodge in the GBM. GBM is destroyed in immune crossfire
Often associated with Strep infections, Berger disease, Lupus

170
Q

Anti-GBM associated glomerulonephritis

A

Autoantibody formation against the GBM
Called Goodpasture’s syndrome when it involves that Lungs AND Kidneys

171
Q

C3 glomerulopathy

A

C3 complement proteins lodge in the GBM causing its destruction -caused by an abnormal alternative complement pathway

172
Q

Monoclonal Ig-mediated glomerulonephritis

A

Excessive antibodies lodge in the GBM due to multiple myeloma or MGUS (monoclonal gammopathy of Undetermined significance)

173
Q

Pauci immune glomerulonephritis

A

Small vessel vasculitis associated with antineutrophilic cytoplasmic antibodies (ANCAs) caused by cell mediated autoimmune processes

174
Q

Clinical presentation of nephritis

A

Cola colored urine
Edema (periorbital and scrotal first) and HTN
Uremia eventually

175
Q

Glomerulonephritis associated with ANCA levels

A

Pauchi immune GN

176
Q

Purpose of an ASO titer

A

Helps evaluate for a recent streptococcal infection

177
Q

2 types of glomerulonephritis for which plasma exchange is recommended

A

Goodpasture disease
Pauci-immune GN

178
Q

General treatment for glomerulonephritis

A

Manage HTN and volume
May use high dose corticosteroids for immunosuppression

179
Q

Post infection glomerulonephritis

A

Bacterial or viral
MCC is GABHS
1-3 weeks after infection

180
Q

Treatment for post infectious glomerulonephritis

A

Support - antihypertensives, salt restrict, diuretics
Steroids are NOT helpful

181
Q

Henoch Schonlein purpura

A

Systemic small vessell vasculitis associated with IgA deposition in vessel walls
Purpura in lower extremities -supportive care

182
Q

MCC and criteria for nephrotic disease

A

DM is MCC
Over 3g of proteinuria/day

183
Q

Subnephrotic proteinuria

A

Proteinuria with few s/s

184
Q

Nephrotic syndrome

A

Peripheral edema seen with proteinuria

185
Q

Places we first see edema in nephrotic syndrome

A

Around eyes and scrotum

186
Q

Gross hematuria

A

We don’t need a microscope to visualize the blood

187
Q

Urine sediment of nephrotic syndrome

A

Oval fat bodies
Grape clusters
Maltese crosses with polarization

188
Q

Hypoalbuminemia

A

Serum protein under 3g/dL

189
Q

Hypoproteinemia

A

Serum protein under 6g/dL

190
Q

Why is ESR elevated in nephrotic syndrome?

A

Loss of proteins C and S

191
Q

When might we do a renal biopsy

A

When there is not an obvious cause such as DM

192
Q

Treatment for proteinuria in nephrotic syndrome

A

Increase dietary protein if loosing 10+ g/d
ACE/ARB to lower urine protein excretion by reducing glomerular capillary pressure

193
Q

Treatment for edema in nephrotic syndrome

A

Dietary salt restriction
Need larger doses of thiazide/loop diuretics bc they are protein bound

194
Q

Minimal change disease

A

A primary nephrotic syndrome
Common in children
Treat with prednisone for 8 weeks (children) or 16 weeks (adults

195
Q

Membranous nephropathy

A

Common in adults - immune complex deposition OR secondary to NSAIDs, cancer, etc.
May be asymptomatic or frothy urine

196
Q

Treatment for membranous nephropathy

A

ACE/ARB, Immunosuppressive agents, Transplant
50% progress to ESRD, 30% spontaneous remission

197
Q

Kidney v. bladder bleeding

A

Kidney will be more brown
Bladder will be more red
(just like GI tract)

198
Q

One size fits all response of the kidneys

A

Increase the RAAS

199
Q

Most common presenting symptom in Berger disease

A

episode of gross hematuria

200
Q

One thing that must be done when an acute on chronic kidney injury occurs

A

Stop ACE/ARB

201
Q

Amyloidosis

A

Secondary nephrotic syndrome due to extracellular deposition of amyloid protein
Low GFR, Enlarged kidneys
Limited treatment

202
Q

Progress of diabetic nephropathy

A

Hyperfiltration
Microalbuminuria (30-300 mg/dL)
Albuminuria

203
Q

When to treat diabetic nephropathy

A

As soon as microalbuminuria is found
Glycemic control
HTN treat to goal
ACE/ARB

204
Q

MCC of acute interstitial nephritis

A

Medication

205
Q

3 causes of chronic Tubulointerstitial Disease

A

Obstructive uropathy
Vesicoureteral reflux
Anagesic nephropathy

206
Q

How much analgesic tends to lead to nephropathy

A

1g/d for 3+ years

207
Q

Causes of obstructive uropathy

A

Enlarged prostate
Stones
cancer
Retroperitoneal fibrosis

Leads to reflux and scarring

208
Q

Potential s/s of obstructive uropathy

A

Pain - with a stone
Bladder distension
HTN
Can all be normal!!

209
Q

Labs for obstructive uropathy

A

May present with polyuria due to damaged tubules
Benign UA may have pyuria/hematuria
Elevted serum creatinine

210
Q

Imaging for obstructive uropathy

A

Should be done on all AKI and CKD patients with unknown cause
US is preferred, CT for stones

211
Q

Vesicoureteral reflux

A

Retrograde flow of urine while voiding due to misplaced sphincter

212
Q

Clinical presentation of vesicoureteral reflux

A

Frequent UTIs esp. in young children
HTN
May have mild/moderate proteinuria

213
Q

Imaging findings for vesicoureteral reflux

A

Assymetric kidneys - one will usually compensate for the other
Can use a US, CT, or Voiding cystourethrogram

214
Q

Treatment for vesicoureteral reflux

A

Maintain sterile urine in childhood
Surgical reimplantation (only works in children
ACE/ARB for HTN

215
Q

Analgesic nephropathy

A

Tubulointerstitial and papillary necrosis
Analgesics can be VERY concentrated in papillae

216
Q

Urine and imaging findings of analgesic nephropathy

A

Sloughed papillae in the urine
Small scarred kidney with calcifications on CT
Ring sign or golfball on tea seet with CT contrast

217
Q

Treatment for analgesic nephropathy

A

Renal decline stabilizes or improves slightly with analgesic removal

218
Q

Clinical findings of autoimmune interstitial nephritis

A

Polyuria w/ dilute urine, Volume depletion, Acidosis
Kidney scarring
Treatm underlying issue

219
Q

Nephrocalcinosis

A

Deposition of calcium in the renal parenchyma and tubules
Cauliflower florets in the kidneys

220
Q

Cause and risk factors for nephrocalcinosis

A

Increased urinary excretion of calcium, phosphate, or oxalate
Hyperparathyroidism
Vitamin D
Loop diuretics

221
Q

Clinical presentation of nephrocalcinosis

A

Often asymptomatic
May have hypercalcemia or hyperphosphatemia
Minimal proteinuria

222
Q

Imaging for nephrocalcinosis

A

US is best can use CT

223
Q

Single renal cyst

A

Usually not concerning and found incidentally
No HTN or ESRD signs present

224
Q

Routine management of benign renal cyst

A

Routine follow up
More likely to be cancerous if they have developed after initiation of dialysis

225
Q

Childhood medullary kidney disease

A

Juvenile Nephronophthisis
Autosomal recessive
Renal cysts in the corticomedullary junction and in the medulla

226
Q

Adult medullary kidney disease

A

MCKD - 20-70yrs
Autosomal dominant
Renal cysts in the corticomedullary junction and in the medulla

227
Q

S/S of medullary kidney disease

A

Hyperuricemia
HTN
Growth restriction for juvenile

228
Q

Treatment for medullary cystic kidney disease

A

No therapy to stop progression
Allopurinol for hyperuricemia
Does not recur in renal transplants

229
Q

s/s of Autosomal dominant PKD

A

Abdominal or flank pain
UTI/Stones
Palpable kidneys
Hematuria
Ultrasound to confirm
Can get cerebral aneurysms in the COW

230
Q

Two other places to check for cysts in PKD

A

Spleen and liver

231
Q

Tx for pain and hematuria associated with PKD

A

Analgesics, decomprassion for pain from bleeding, infection, stones
Hydration for bleeding, recurrent may be carcinoma

232
Q

Cerebral aneurysms PKD screening

A

Usually not recommended

233
Q

Antibiotics with cystic penetration for PKD

A

Quinolones, Bactrim

234
Q

Medications for ADPKD

A

Vasopressin receptor antagonists:
Ocreotide - decreased cyst growth
Tolvaptan

235
Q

4 risk markers indicating use of Tolvaptan in ADPKD

A

Mayo class 1C-E
Under 55 w/ GFR under 65
Kidney length over 16.5 cm in 50y/o
PROPKD score 6+

Patients 18+ with GFR 25+ and one of the above should be on something

236
Q

3 things that may slow progression of ADPKD

A

Avoidance of caffeine
Protein restriction
HTN Tx

237
Q

BBW for tolvaptan

A

Should be initiated in a hospital where serum sodium can be closely monitored
CI in liver disease, may cause thirst/polyuria

238
Q

Location of cysts in ARPKD

A

Cysts on collecting tubules only
Metabolic acidosis and HTN
Oligohydramnios (low amniotic fluid in utero)

239
Q

Presentation and treatment of autosomal recessive PKD

A

Cysts only visible after birth - no disease in parents
Manage HTN
Dialysis and transplant

240
Q

2 causes of renal artery stenosis

A

Atherosclerotic disease (by far most common)
Fibromuscular dysplasia (suspect in women under 40 w/ unexplained HTN)

241
Q

s/s, PE and labs for renal artery stenosis

A

Refractory or new onset HTN
AKI after ACEI
Abdominal bruit
Elevated BUN/Cr with ischemia

242
Q

Imaging for renal artery stenosis

A

Doppler US can show small or asymmetric kidneys on regular US
CT angiography may be less accurate and more expensive
MRA excellent but expensive
Renal angiography = Gold standard

243
Q

Treatment for renal artery stenosis

A

Medical management of HTN
Stenting produces good results
Bypass not superior

244
Q

Nephrosclerosis

A

Hypertensive nephropathy with sclerosis and interstitial fibrosis
More common in African Americans
Give ACE/ARB or thiazide diuretic

245
Q

Cholesterol atheroembolic disease

A

Emboli to the kidneys from vascular plaques, angiography is a risk factor

246
Q

s/s of cholesterol atheroembolic disease

A

1-2 weeks after inciting event
Worsening of HTN and renal function
May see livedo reticularis or localized gangrene

247
Q

Livedo reticularis

A

Webbing patter on legs

248
Q

Labs for cholesterol atheroembolic disease

A

Increased eosinophils, Cr, ESR
Def dx - kidney biopsy
Statins are most recommended

249
Q

MC kidney cancer

A

Renal cell carcinoma

250
Q

Risk factors for renal cell carcinoma

A

May be familial or dialysis related
HTN, analgesics, Obesity
SMOKING - biggest

251
Q

Clear cell carcinoma

A

Most common type of kidney cancer
Papillary tumors are less common but happen

252
Q

Clinical presentation of renal call carcinoma

A

Hematuria = most common
May see flank pain or abdominal mass
Cough or bone pain in metastasis
Usually found incidentally

253
Q

Stauffer syndrome

A

Abnormal liver function enzymes w/o metastasis - may just be a result of the carcinoma

254
Q

Imaging for renal cancer

A

US - for initial
CT to look at mass
MRI, Bone, Brain for mets

255
Q

Initial labs for renal cancer

A

CBC, LFT, UA

256
Q

Difference of PKD and cancer

A

PKD is more definied and evenly spread out

257
Q

Treatment for RCC

A

Radical nephrectomy
Chemotherapy has limited efficacy

258
Q

Wilms Tumor

A

Seen in pediatric patients
Due to abnormal kidney development - single unilateral lesion

259
Q

Clinical presentation of Wilms tumor

A

Abdominal pain
HTN
Hematuria

260
Q

Imaging for wilms tumor

A

US for first
CT/MRI for follow up
CBC,CMP, UA, Coag (you’re gonna do surgery)

261
Q

Wilms tumor treatment

A

Surgical resection - prognosis is often good
Recurrent disease is possible

262
Q

Oncocytoma

A

Common benign tumor that looks like RCC - treat like RCC

263
Q

Angiomyolipoma

A

Fat muscle and vessel tumor MC in women
Benign but can bleed
Embolize

264
Q

Organs that metastasize to kidney

A

Lung, stomach, other kidney

265
Q

Risk factors for kidney stones

A

Dehydration
High protein/salt intake
Gout

266
Q

Most common type of kidney stones

A

Calcium oxalate or phospjate
Visible on X-ray

267
Q

Clinical presentation of kidney stones

A

Acute severe flank pain - may follow ureters and be episodic
Nausea and vomiting

268
Q

Urinary stone labs

A

Hematuria
May have an abnormal pH of urine (high for calcium, low for uric acid)

269
Q

Litholink

A

Panel specifically looking for stones

270
Q

Imaging for renal stones

A

X-ray
US for pregnancy
CT - shows ALL stones

271
Q

Staghorn calculus

A

Stone that grows up into calyces

272
Q

Treatment for kidney stones

A

Try NSAIDs if not tried
IV fluids don’t help
Opioids may be needed for pain
Tamsulosin (a blocker)
Steroids

273
Q

Obstruction with infection

A

Medical emergency

274
Q

CIs for tamsulosin

A

Sulfa allergy
Lowers BP - orthostatic hypotension

275
Q

Stone passing criteria

A

Under 5mm - stone will pass
Over 10mm - will not pass

276
Q

Treatment for stuck kidney stone

A

Shock wave lithotripsy
- Avoid if may be pregnant
-Focus shockwaves
Ureteroscopic extraction
Percutaneous nephrolithotomy
- 15+mm or bottom of kidney

277
Q

Prevention for urinary stone disease

A

Consistent fluid intake
DONT decrease dietary calcium

278
Q

Things treat calcium stones

A

Thiazide diuretics help
Cellulose phosphate
Treat hypercalciuria (resorptive or renal)

279
Q

Hyperoxaluric stones

A

Some calcium
Often linked to IBD
Avoid vitamin C

280
Q

Hyperuricosuric stones

A

Mostly uric acid
Cut back on meat and beer - purines
Alipurinol

281
Q

Hypercitraturic stones

A

Due to diarrhea - drink lemonade

282
Q

Uric acid calculi

A

Hyperuricemia or abrupt cell death
Low pH and harder to see on X-ray
Potassium citrate or alopurinol

283
Q

Struvite calculi

A

P-bacteria - related to UTI
Often staghorn
Proteus, Pseudomonas, Providencia

284
Q

Cysteine calculi

A

Often genetic
Give citrate or bicarbonate
Double urine goal for these pts

GI/GU (4 decks)

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