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Clin Med III > acid base, RAS, wilms > Flashcards

acid base, RAS, wilms Flashcards

1
Q

what artery is most commonly used for ABGs

A
  • radial a

- perform allen test first

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2
Q

what is measured in ABGs

A
  • arterial blood pH
  • PaCO2
  • SaO2
  • bicarb
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3
Q

when is ABG indicated

A
  • critically/ acutely ill
  • respiratory failure, likely to be intubated
  • pts who are profoundly somnolent or obtunded
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4
Q

what is normal pH

A
  • 7.4
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5
Q

alkalosis

A
  • pH > 7.4
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6
Q

acidosis

A
  • pH < 7.4
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7
Q

elimination of acids

A
  • pulm excretion of CO2
  • metabolic utilization of organic acids
  • renal excretion of nonvolatile acids- combine ions with buffers
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8
Q

reaction in circulation

A
  • CO2 + H2O H2CO3 (carbonic acid) HCO3 (bicarb) + H+
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9
Q

source of H ion gains

A
  • increased CO2
  • prod of phosphoric and sulfuric acid from metabolism of proteins/ other organic molecules
  • loss of bicarb from GI losses
  • loss of bicarb in urine
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10
Q

source of H ion losses

A
  • emesis

- urine

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11
Q

effect of hypoventilation

A
  • retention of CO2 -> respir acidosis
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12
Q

effect of hyperventilation

A
  • blow off CO2 -> respr alkalosis
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13
Q

common causes of metabolic acidosis

A
  • excessive production of lactic acid
  • formation of ketone bodies- uncontrolled DM, fasting/starvation
  • loss of bicarb- diarrhea
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14
Q

anion gap

A
  • difference between plasma concentration of major cation + sum of anions
  • AG= Na + [Cl + HCO3]
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15
Q

normal anion gap

A
  • 8-16 meq/L
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16
Q

normal anion gap + metabolic acidosis causes

A
  • intestinal losses: diarrhea, SB/ pancreatic/ biliary fistula drainage, ileostomy drainage
  • renal losses
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17
Q

elevated anion gap + metabolic acidosis causes

A
  • lactic acidosis
  • diabetic ketoacidosis
  • alcoholic ketoacidosis
  • starvation ketoacidosis
  • poisoning
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18
Q

what is the most common cause of metabolic acidosis in hospitalized pts

A
  • lactic acidosis
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19
Q

type a lactic acidosis

A
  • due to hypoxic state
  • most common type
  • decreased tissue perfusion -> increased lactic acid production
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20
Q

type B lactic acidosis

A
  • due to metabolic causes
  • impaired cellular metabolism
  • tissue ischemia without systemic hypoperfusion
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21
Q

type B lactic acidosis

A
  • due to metabolic causes
  • impaired cellular metabolism
  • tissue ischemia without systemic hypoperfusion
  • DKA, alcoholism, infections, malignancy, metformin, bowel necrosis
22
Q

“mud piles” pneumonic

A
  • used for AG metabolic acidosis
  • methanol
  • uremia
  • diabetic ketoacidosis
  • propylene glycol
  • isoniazid
  • lactic acidosis
  • ethylene glycol and ethanol
  • salicylates and starvation
23
Q

treatment for metabolic acidosis

A
  • treat underlying cause

- consider admin of IV and PO sodium bicarb if severe to bring pH to normal

24
Q

causes of metabolic alkalosis

A
  • ingesiton or admin of alkali substances
  • stomach loss- vomiting, NGT suction
  • renal loss of H
  • diuretic use
25
Q

treatment of metabolic alkalosis

A
  • treat underlying cause

- remove offending agent

26
Q

renal response to acidosis

A
  • bicarb in kidney binds up as much H as possible
  • additional H+ excreted bound to buffers
  • new bicarb is formed during tubular glutamine meabolism
27
Q

renal response to alkalosis

A
  • H+ binds as much bicarb as possible
  • bicarb excreted in urine
  • tubular glutamine metabolism is decreased to lower new bicarb production
28
Q

primary respiratory acidosis responses

A
  • H increases
  • HCO2 increases
  • CO2 increases (retain CO2- hypoventilation), main cause
29
Q

primary respiratory alkalosis responses

A
  • H decreases
  • HCO3 decreases
  • CO2 decreases (blowing off CO2- hyperventilation), main cause
30
Q

primary metabolic acidosis responses

A
  • H increases
  • HCO3 decreases, main cause
  • CO2 decreases (ventilatory compensation)
31
Q

primary metabolic alkalosis responses

A
  • H decrease
  • HCO3 increases, main cause
  • CO2 increases (Ventilatory compensation)
32
Q

initial steps in interpreting ABG

A
  • acidosis or alkalosis
  • does PCO2 explain the problem? i..e. if pt is acidodic is PCO2 also high?
  • if yes- respiratory, if no- metabolic
  • is compensation appropriate? if no it is a mixed disorder
33
Q

what is normal pH?

A
  • 7.4
34
Q

what is normal pCO2?

A
  • 40 mmHg
35
Q

what is normal pO2?

A
  • 100 mmHg
36
Q

what is normal HCO3?

A
  • 24 meq/L
37
Q

renal artery stenosis

A
  • not common in pts with HTN in general

- can be up to 40% of pts with REFRACTORY htn

38
Q

etiology of renal artery stenosis

A
  • atherosclerosis- usually in pts 45+ years old

- fibromuscular dysplasia- young white women

39
Q

risk factors for renal artery stenosis

A
  • “typical vasculopaths”
  • hyperlipidemia
  • cigarette smoking
  • age > 50
  • CAD, PAD
  • DM
40
Q

clinical presentation of renal artery stenosis

A
  • may have sx of acute HTN emergency
  • rapid BP swings
  • increase in severity of known HTN
  • HTN refractory to medication
  • unexplained acute elevation in serum Cr
  • abd/ flank bruits in half of pts
41
Q

lab findings for renal artery stenosis

A
  • nonspecific findings
  • may see mild proteinuria on UA, possible blood
  • increased BUN and Cr
  • elevated plasma renin
42
Q

imaging

A
  • renal arteriography- gold std
  • duplex US
  • CT, MRI
  • spiral CT with angiography- uses less contrast
43
Q

conservative treatment for renal artery stenosis

A
  • weight loss, quit smoking, limit salt, moderate coffee/ alcohol intake
  • control HTN
  • ASA
  • lipid lowering meds
44
Q

procedures for renal artery stenosis

A
  • renal angioplasty and stenting- percutaneous for atherosclerosis or FMD
  • renal artery bypass surgery for pts who are not stenting candidates
45
Q

follow up for renal artery stenosis

A
  • stress lifestyle management
  • stenosis and kidney dysfunction may progress despite BP control
  • duplex US q 6 months
  • monitor BP, BMP, UA
46
Q

wilms tumor

A
  • most common renal malignancy in kids
  • generally a very rare tumor
  • more common in kids with birth defects aniridia, hemihypertrophy, cryptorchidism, hypospadias
47
Q

what is another name for wilms tumor

A
  • nephroblastoma
48
Q

clinical presentation of wilms tumor

A
  • kids between 3-10 usually
  • enlarged asymp abd mass
  • vague abd pain
  • hematuria
  • fever
  • HTN
  • anorexia
  • weakness/ fatigue
49
Q

PE findings for wilms tumor

A
  • firm, nontender, smooth mass
  • unilateral most often
  • varying size
  • may see extremity edema
  • may see HTN
50
Q

what is the main ddx for wilms tumor

A
  • neuroblastoma
51
Q

prognosis of wilms tumors

A
  • older the age= worse prognosis
  • 90% 5 year survival
  • prognosis depends on stage
52
Q

treatment for wilms tumor

A
  • refer to pediatric cancer center
  • surgery- full vs partial resection
  • chemo, radiation
  • goal of treatment is cure
  • needs long term f/u, pulm and abd surveillance

Clin Med III (26 decks)

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