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Renal 2 Final > Clinical Medicine part 2 > Flashcards

Clinical Medicine part 2 Flashcards

1
Q

Causes of Hypoxia

A
  • hypoventilation
  • V/Q mismatch as seen in pulmonary embolus
  • shunting e.g. cardiac anomalies
  • low inspired fraction of O2
  • high altitude
  • diffusion abnormalities e.g. alveolar hemorrhage, connective tissue disorder
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2
Q

Metabolic Acidosis Expected Compensation

A

-1.5HCO + 8 (+/-2)

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3
Q

If pH and PCO2 change in same direction, the process is

A

metabolic

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4
Q

If PH and PCO2 change in opposite directions, the process is

A

respiratory

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5
Q

Anion Gap

A

Na-(Cl + HCO3)

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6
Q

Metabolica acidosis

A
  • decrease in extracellular pH caused by a decrease in HCO3
  • loss of HCO from GI tract, renal
  • increase H+ load–DKA or lactic acidosis
  • Decrease H+ excretion by kidney–uremic acidosis or RTA
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7
Q

High Anion Gap Acidosis

A
  • MUDPILES

- CCAT

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8
Q

High Anion Gap Acidosis

M

A

methanol–formic Acid

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9
Q

High Anion Gap Acidosis

U

A

uremia (renal failure)

  • increased BUN, creatinine
  • increased sulfates, phosphate as unmeasured anions
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10
Q

High Anion Gap Acidosis

D

A

diabetic ketosis

  • increased glucose; starvation, alcohol abuse
  • acetoacetic acid, B-hydroxybutyric acid
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11
Q

High Anion Gap Acidosis

P

A

paraldehyde

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12
Q

High Anion Gap Acidosis

I

A
  • INH, iron

- isoniazid taken after PPd result comes back positive for TB!

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13
Q

High Anion Gap Acidosis

L

A

-lactic acid–shock, sepsis, low perfusion, marathon runners

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14
Q

High Anion Gap Acidosis

E

A

ethylene glycol

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15
Q

High Anion Gap Acidosis

S

A

salicylates

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16
Q

High Anion Gap Acidosis

CCAT

A

-CO, cyanide, alcohol, toluene

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17
Q

Lactic Acidosis Type A

A
  • tissue hypoxia

- shock, severe anemia, herat failure, CO poisoning

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18
Q

Lactic Acidosis Type B1

A
  • associated with systemic disorders

- DM, liver failure, sepsis, seizures

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19
Q

Lactic Acidosis Type B2

A
  • associated with drugs/toxins

- ethanol, methanol, ethylene glycol, ASA

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20
Q

Lactic Acid Type B3

A
  • associated with inborn errors of metabolism

- G6PD deficiency

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21
Q

Normal anion gap metabolic acidosis

A

-HCO3 falls and Cl rises
-hyperchloremic metabolic acidosis
HARDUPS

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22
Q

Normal anion gap metabolic acidosis

H

A

hyperalimentation (nutrition support)

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23
Q

Normal anion gap metabolic acidosis

A

A

acid infusion, acetazolamide

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24
Q

Normal anion gap metabolic acidosis

R

A

Renal Tubular Acidosis-renal loss of HCO3/or decreased H+ secretion

25
Q

Normal anion gap metabolic acidosis

D

A

diarrhea–losing HCO3, decreased K

26
Q

Normal anion gap metabolic acidosis

U

A

-uretheral sigmoid or ileal diversion–losing HCO3/increased Cl and H+ resorption

27
Q

Normal anion gap metabolic acidosis

P

A

pancreatic fistula–losing HCO3, decreased K+

28
Q

Normal anion gap metabolic acidosis

S

A

Spironolactone

29
Q

Distal Renal Tubular Acidosis

A
  • decreased secretion of H+, so not getting rid of acid, i.e. “failure to acidify urine” (type I)
  • SLE, Sjogrens, toluenes
30
Q

Proximal Renal Tubular Acidosis

A
  • decreased absorption of HCO, so not absorbing buffer
  • Type II
  • multiple myeloma, heavy metal poisoning, wilson’s disease, amyloidosis
31
Q

Hyperkalemic renal tubular acidosis

A
  • Hyporenin and hypoaldosterone
  • decreased NH4 excretion and decreased HCO3 production
  • Type 4
  • analgesic nephropathy, sickly cell disease, and SLE
32
Q

Treatment of Metabolic Acidosis

A

Treat underlying cause

treat CV compromise; pH

33
Q

Metabolic Alkalosis

A
  • increased pH, increased HCO3, increased CO2
  • compensate paCO2 increase 0.7 for every 1 increase in HCO3
  • Cl loss or HCO3 excess
  • volume contraction
34
Q

Cl loss

A

-vomiting, N/G suction, villous adenoma, diuretics

35
Q

HCO3 excess

A

-enhanced HCO3 resorption (hyperaldosteronism, licorice excess)

36
Q

Metabolic Alkalosis Causes

A

CLEVER PD

37
Q

Metabolic Alkalosis

C

A

Contraction of volume

38
Q

Metabolic Alkalosis

L

A

licorice

39
Q

Metabolic Alkalosis

E

A

endocrine (Conns, Cushings, Bartters)

40
Q

Metabolic Alkalosis

V

A

vomiting

41
Q

Metabolic Alkalosis

E

A

excess alkali

42
Q

Metabolic Alkalosis

R

A

refeeding alkalosis

43
Q

Metabolic Alkalosis

P

A

post hypercapnia

44
Q

Metabolic Alkalosis

D

A

diuretics

45
Q

Chloride Responsive metabolic alkalosis

A
  • urine Cl- less than 10-20
  • improves with NaCl and volume
  • decreased serum Cl- and volume contraction
  • vomiting, NG suction, diuretics
46
Q

Chloride Unresponsive metabolic alkalosis

A
  • urine Cl- less than 10-20
  • unresponsive to saline
  • endocrine causes: bartters, severe K depletion, hyperaldosteronism, Cushings
47
Q

Treatment of Metabolic Alkalosis

A
  • treat underlying cause
  • NaCl, KCl, magnesium
  • spironolactone for mineralocorticoid excess
48
Q

Hypokalemia ECG findings

A
  • flattened T wave

- ST depression

49
Q

Hyperkalemia ECG findings

A
  • peaked T wave
  • widened QRS
  • loss of P wave
50
Q

Conn’s Syndrome

A
  • primary hyperaldosteronism
  • mineralocorticoid excess
  • saline resistant (urine Cl- >20)
  • increased HCO3 excretion in urine
51
Q

Respiratory Acidosis

A
  • decreased pH, increased CO2, increased HCO3
  • anything that causes hypoventilation
  • CNS depression–drugs, CVA, neuromuscular airway obstruction, pneumonia, pulmonary edema, pneumothorax, pleural disease, COPD, restrictive disease (disorders of the chest wall, respiratory muscles)
52
Q

Respiratory Alkalosis

A
  • increased pH, decreased CO2, decreased HCO3
  • anything that causes hyperventilation
  • CHAMPS
53
Q

Respiratory Alkalosis

C

A

CNS disease

54
Q

Respiratory Alkalosis

H

A

hypoxia

55
Q

Respiratory Alkalosis

A

A

anxiety

56
Q

Respiratory Alkalosis

M

A

mechanical ventilation

57
Q

Respiratory Alkalosis

P

A

progesterone

58
Q

Respiratory Alkalosis

S

A

salicylates, sepsis, stress

Renal 2 Final (5 decks)

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