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Clin Med I - Comprehensive > Renal > Flashcards

Renal Flashcards

1
Q
A
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2
Q

What is the prevalence of kidney stones?

A

Approx. 1% of US Adults9% lifetime risk

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3
Q

What is the Epi of ESRD by race?

A

AA 3.5 X more than whitesLatinos 1.5X more than whitesAA 19x lower chance of receiving a kidney transplant

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4
Q

What is the Epi of CKD?

A

1 in 3 adults with DM1 in 5 adults with HTN1 in 2 adults aged 30-64 lifetime

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5
Q

What are the typical locations of pain with KD?

A

flank and abdominaldysuria

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6
Q

what are the typical general signs and sx of KD?

A

feverfatigue

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7
Q

What are the typical GI signs and sx of KD?

A

nauseavomiting

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8
Q

What are some common causes of pre-renal KD?

A

hypovolemiaCHFRAS

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9
Q

What are some common causes of post-renal KD?

A

prostate enlargementobstructing tumornephrolithiasis

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10
Q

What are some common intrarenal causes of KD?

A

ATNRenal vascular diseasetubulointerstitial diseaseglomerular disease

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11
Q

How do you define acedemia?

A

Low serum pH (less than 7.35)

low serum bicarbonate

(compensation causes compensatory alveolar hyperventilation and a resulting fall in PaCO2

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12
Q

How is H+ secreted by the kidney?

A

combined with NH3 to become NH4+

or HPO42- becomes H2PO4-

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13
Q

What are some common reasons for increased acid load?

A

lactic acid

ketoacids (DM, alcohol, starvation)

inorganic acid addition (HCL, NH4Cl)

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14
Q

What are two circumstances where NH4+ production in response to an increased acid load cannot occur?

A
  1. renal failure
  2. distal renal tubular acidosis (Type I)
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15
Q

There are only two routes of bicarbonate loss from the body. What are they?

A
  1. diarrhea
  2. urethra - tubular dysfunction
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16
Q

How do you calculate anion gap?

A

AG = Na - (Cl + HCO3-)

Figge correction = AG + [(4.4-Albumin) x 2.5]

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17
Q

What is a normal anion gap?

A

10-12

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18
Q

What does it mean if anion gap is high?

A

AG metabolic acidosis

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19
Q

What is the differential diagnosis for anion gap metabolic acidosis?

CUTE DIMPLES

A

Citrate

Uremia

Toluene

Ethanol

Diabetic ketoacidosis

Iron

Methanol

Paraldehyde

Lactate

Ethylene glycol

Salicylate

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20
Q

Which three causes of anion gap metabolic acidosis are NOT ingestion related?

A
  1. uremia
  2. ketoacidosis
  3. lactic acidosis
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21
Q

What stages of CKD are likely to be anion gap metabolic acidosis?

A

Stages 4-5

retention of hydrogen ion and sulfate anion due to marked reduction in nephrons and GFR

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22
Q

DKA causes anion gap acidosis how?

A
  • insulin deficiency causes low glucose levels in the cell, leads to free fatty acid breakdown, which leads to acetone production
  • glucagon excess causes free fatty acid conversion to ketoacids
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23
Q

What are the steps to diagnosing acid-base disorders?

A
  1. Is the patient acidemic or alkalemic?
  2. is the primary disorder respiratory or metabolic?
  3. For respiratory, process acute or chronic?
  4. for metabolic acidosis, is an anion gap present?
  5. Is it a mixed disorder?
  6. Is there appropriate compensation for the disturbance?
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24
Q

What’s a normal arterial pCO2?

A

36-44

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25
Q

What’s a normal aterial bicarb?

A

22-26

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26
Q

What is Winter’s formula used for?

A

Provides a measure of the expected respiratory compensation to a metabolic acidosis

Expected pCO2 = [1.5 x (HCO3)] +8 +/-2

metabolic acidosis ONLY

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27
Q

how do you interpret the results of Winter’s formula?

A

If the pCO2 is below expected, then respiratory alkalosis is present also

If the pCO2 is higher than the expected, respiratory acidosis is present also

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28
Q

citrate anion gap metabolic acidosis is usually due to one or more of these three things?

A

transfusion

trauma

anticoagulation

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29
Q

What is Type 1 Renal Tubular Acidosis?

A

Defect in tubule causing altered secretion of H+ as NH4+ with GFR usually preserved

Impaired apical H+-ATPAse

decreased carbonic anhydrase activity

increased permeability to H+

Overall, less net acid excretion

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30
Q

When bicarbonate is lost to diarrhea, sodium levels ____ and Cl- ____

A

Stay the same

Cl- in the serum increase

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31
Q

What is proximal renal tubule acidosis (Type 2)?

A

An inabilty to reabsorb HCO3- in the proximal tubule, leading to loss of bicarbonate in the urine unless distal can compensate

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32
Q

What are the major clinical manifestations of metabolic acidosis?

A
  • Respiratory - increased ventilation
  • CV - decreased contractility, arrhythmias
  • GI - nausea/vomiting, abdominal pain, diarrhea
  • MSK - weakness, osteomalacia, osteopenia, hypercalcuria
  • CNS - lethargy, coma
  • Kids - impaired bone growth, anorexia, listlessness
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33
Q

What causes metabolic alkalosis?

A

progessive loss of acids

(H+ with increased HCO3- generation)

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34
Q

What are some common caues of metabolic alkalosis?

A

GI

  • vomiting
  • nasogastric suction
  • villous adenoma

Renal

  • diuretics
  • inherited transport defects
  • mineralcorticoid excess
  • posthypercapnia
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35
Q

What is contraction alkalosis?

A

when fluid loss creates alkalosis by increasing bicarbonate in the serum.

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36
Q

What are the common mimics of hematuria?

A

menstruationdrugspigmenturiabeets

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37
Q

What are the general categories of things that could cause hematuria?

A

infectionmalignancymetabolicglomerulartubulointerstitialtraumaother

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38
Q

What is a benign cause of transient gross hematuria in adults?

A

vigorous exercise

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39
Q

How is microscopic hematuria defined?

A

>3 RBCs/High Power Field in 2 or more specimens

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40
Q

Does a positive dipstick confirm hematuria?

A

No - myoglobin and hemoglobin also will cause a positive result

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41
Q

What are the major risk factors for bladder cancer?

A

smokingoccupational exposuregross hematuria>40 years oldcyclophosphamide (?)

42
Q

What are the most common causes of hematuria in a person who is 0-20?

A

glomerulonephritisUTIcongenital

43
Q

What are the most common causes of hematuria in a person who is 20-40?

A

UTI Calculibladder and renal cancer

44
Q

What is the most common pathogen in UTI?

A

E. coli

45
Q

What is the total mortality rate (direct and indirect) for hospital acquired infections?

A

About 30%

46
Q

How much more common are UTIs in women than in men?

A

10-30x

47
Q

What is the second most common pathogen in community acquired UTI?

A

Staph

48
Q

What is the third most common pathogen in community acquired UTI?

A

Proteus

49
Q

What are two common pathogens seen in hospital acquired UTI?

A

KlebsiellaPseudomonas

50
Q

Who gets Staph saprophytic UTIs?

A

95% female16-35>20% incidencevast majority have symptomsdrug resistance unusualrelapse rare

51
Q

Do patients with immune deficiencies get UTIs more often?

A

NO.

52
Q

What is the GFR in a fully working kidneys?

A

200 ml/minute

53
Q

What is the definition of CKD?

A
  1. kidney damage > or equal to 3 months, as defined by structural or functional abnormalities of the kidney, with/without reduced GFR manifested by either:
    a. pathological abnml; or
    b. markers of kidney damage, which is abnormal urine or imaging studies
  2. GFR < 60 ml/min. for greater or equal to 3 months with or without kidney damage
54
Q

why do we look at proteinuria or albuminuria in the urine?

A

Presence indicates a poor prognosis

55
Q

How do people with CKD present?

A

No symptoms until eGFR less than 30 ml/min

  • elevated serum creatinine
  • microscopic or gross hematuria
  • proteinuria (foamy urine)
  • abnormal imaging study (incidential finding)
56
Q

How do you work up CKD?

A

Follow the same path as for AKI,

but time course determines whether it is acute or chronic

57
Q

How do you reduce hyperfiltration in the kidney?

A

Low protein diet

aldosterone antagonists or ACE-I/ARBs

58
Q

What is the definition of metabolic acidosis?

A

Lowered serum bicarbonate and low pH

Bicarb less than 24

pH less than 7.35

59
Q

What is a consequence of prolonged metabolic acidosis?

A

osteopenia or osteoporosis

60
Q

What are the conditions for dialysis?

AEIOU

A

acid/base disturbance

electrolyte abnormalities

remove posions (intoxication)

volume overload

uremia (creatinine clearance < 15 ml/mn)

61
Q

What is renal replacement therapy?

A

hemodialysis

peritoneal dialysis

kidney transplant

62
Q

What are the indications for acute RRT?

A

AEIOU

  • Acidosis, metabolic
  • Electrolyte abnormalities (esp. hyperk or hypercal)
  • Intoxications (think poisoning)
  • Overload of fluid that is refractory
  • Uremia - encephalopathy, pericarditis
63
Q

What are the ways to obtain vasular access for hemodialysis?

A

Arteriovenous fistula is best!

arteriovenous graft

permcath (tunneled catheter)

quinton (non-tunneled) catheter - hospital only

64
Q

Where are most tumors of the urinary tract located?

A

bladder

65
Q

Are urinary tract cancers more common in men or women?

A

Men

66
Q

bladder cancer is what percentage of total cancer?

A

7%

67
Q

what is the male to female predominance of bladder cancer?

A

3:1

68
Q

What is the most common tumor type in bladder cancer?

A

urothelial (transitional) tumors - 90%

69
Q

What is the most important risk for bladder cancer?

A

cigarette smoking

70
Q

What are some other exposure risk factors for bladder cancer besides smoking?

A

exposure to aryl amines (industrial)long term analgesic useheavy cyclophosphamide exposureschistosoma haematobium irradiation

71
Q

What is the clinical presentation of bladder cancer?

A
  • painless hematuria (but also sign in non-tumor lesions of the bladder)
  • irritative symptoms (frequency, urgency, dysuria)
  • hydronephrosis (when ureteral orifice involved)
72
Q

How is bladder cance diagnosed?

A
  • urine examination
    • microsocpic exam
    • FISH analysis
  • cystoscopy
    • washings/tissue biopsy
73
Q

what is another name for urothelium?

A

transitional epithelium

74
Q

What are the two precusor lesions to bladder cancer?

A
  • noninvasive papillary tumors (mc)
    • may progress to invasive carcinoma (different histologic grades)
    • cauliflower-like
    • fibrocascular core with cells coming off of it
  • noninvasive flat carcinomas (carcinoma in situ)
    • always severe atypia/high grade
    • almost always progress to invasive carcinoma
75
Q

What is the standard treatment for bladder cancer that invades the muscle wall?

A

cystectomy

(surgical removal of bladder)

76
Q

What is the grading system for bladder tumors?

T1-T4

A

T1 - lamina propria invasion

T2 - muscularis propria invasion

T3 - extravesical fat invasion

T4 - invasion into adjacent structures/organs

77
Q

Renal cell carcinoma are ____ of all newly diagnosed cancers in the U.S.

A

3%

(85% of adult renal cancers)

78
Q

What is the male:female ratio of renal cell carcinoma?

A

2:1

79
Q

What percentage of renal carcinoma is clear cell carcinoma?

A

70-80%

80
Q

What is the most common mutation in renal cell carcinomas?

A

Von Hipple Lindau gene deletion on chromosome 3p

81
Q

What does clear cell renal carcinoma look like pathologically?

A
  • round cells with abundant clear cytoplasm (fat and glycogen)
  • delicate branching vasculature (chicken-wire)
82
Q

what is the cure rate for wilms tumor?

A

approximately 90%

83
Q

What effect does the RAAS have on the glomeruli?

A

constricts the efferent arteriole

84
Q

serum sodium concentration DOES NOT tell you __________

A

what is the patient’s TOTAL BODY SODIUM.

85
Q

what’s normal serum sodium?

A

135-145 mEq/L

86
Q

What are the CNS symptoms of hyponatremia?

A

Mild - apathy, headache, lethargy

Moderate - agitation, ataxia, confusion, psychosis

Severe - stupor, coma, tentorial herniation, cheyne-stokes

DEATH

87
Q

What are the GI symptoms of hyponatremia?

A

VAN

vomiting, anorexia, nausea

88
Q

What are MSK signs of hyponatremia?

A

muscle cramps

dimished deep tendon reflexes

89
Q

What are CNS signs and symptoms of hypernatremia?

A

mild - restlessness, lethargy, irritability

moderate - disorientation, confusion

severe - stupor, coma, seizures

DEATH

90
Q

What are the non-CNS signs and symptoms of hypernatremia?

A

Respiratory - labored breathing

GI - intense thirst, nausea, vomiting

MSK - muscle twitching, spasticity, hyperreflexia

91
Q

What’s normal daily water intake?

A

1-1.5L/day

92
Q

What’s typical insensible daily water loss?

A

0.5 L/day

93
Q

What makes the collecting duct permeable to water so that it can be reabsorbed?

A

ADH

94
Q

The ascending limb of the loop of Henle is also known as the ____________segment of the nephron

A

diluting

because it is pulling Na+ and other electrolytes OUT of the tubular fluid and reabsorbing them

95
Q

what senses the osmolality of your plasma?

A

osmoreceptors in the hypothalamus

will release/supress ADH at the anterior pituitary

96
Q

what’s normal plasma osmolality?

A

280-290 mOsm/Kg H20

97
Q

What is the disorder of urine concentration

A

diabetes insipidus

98
Q

How do you treat hypovolemic hyponatremia?

A

volume restoration with isotonic saline

identify and correct cause of water and sodium loss

(cholera and gastroenteritis)

99
Q

How do you treat hypervolemic hyponatremia?

A

water restriction

sodium restriction

loop diuretics

treatment of underlying condition

ADH (V2) receptor antagonist (vaptans)

100
Q

How do you treat euvolemic hyponatremia?

A

Is it SIADH? - Is the plasma level of ADH inappropriately elevated relative to plasma osmolality (in other words, low osmolality and salty pee?)

acute (less than 48 hours)

increase serum sodium at rate up to 2 meq/hour until asymptomatic

chronic (greater than 48 hours)

rate of correction should not exceed 1 meq/hour (no more than 18 in 24 hours)

measure serum and urine electrolytes every 2 hours

perform frequent neuro evals

101
Q

What happens in the CNS in hyponatremia?

A

At first, K+, Na+ and osmolytes leave

later, H2O moves in

102
Q

what should you suspect when you see hypernatremia in a patient who has access to water?

A

Diabetes insipidus

Clin Med I - Comprehensive (6 decks)

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