acid base, RAS, wilms Flashcards
1
Q
what artery is most commonly used for ABGs
A
- radial a
- perform allen test first
2
Q
what is measured in ABGs
A
- arterial blood pH
- PaCO2
- SaO2
- bicarb
3
Q
when is ABG indicated
A
- critically/ acutely ill
- respiratory failure, likely to be intubated
- pts who are profoundly somnolent or obtunded
4
Q
what is normal pH
A
- 7.4
5
Q
alkalosis
A
- pH > 7.4
6
Q
acidosis
A
- pH < 7.4
7
Q
elimination of acids
A
- pulm excretion of CO2
- metabolic utilization of organic acids
- renal excretion of nonvolatile acids- combine ions with buffers
8
Q
reaction in circulation
A
- CO2 + H2O H2CO3 (carbonic acid) HCO3 (bicarb) + H+
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
10
Q
source of H ion losses
A
- emesis
- urine
11
Q
effect of hypoventilation
A
- retention of CO2 -> respir acidosis
12
Q
effect of hyperventilation
A
- blow off CO2 -> respr alkalosis
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
14
Q
anion gap
A
- difference between plasma concentration of major cation + sum of anions
- AG= Na + [Cl + HCO3]
15
Q
normal anion gap
A
- 8-16 meq/L
16
Q
normal anion gap + metabolic acidosis causes
A
- intestinal losses: diarrhea, SB/ pancreatic/ biliary fistula drainage, ileostomy drainage
- renal losses
17
Q
elevated anion gap + metabolic acidosis causes
A
- lactic acidosis
- diabetic ketoacidosis
- alcoholic ketoacidosis
- starvation ketoacidosis
- poisoning
18
Q
what is the most common cause of metabolic acidosis in hospitalized pts
A
- lactic acidosis
19
Q
type a lactic acidosis
A
- due to hypoxic state
- most common type
- decreased tissue perfusion -> increased lactic acid production
20
Q
type B lactic acidosis
A
- due to metabolic causes
- impaired cellular metabolism
- tissue ischemia without systemic hypoperfusion
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
treatment of metabolic alkalosis
- treat underlying cause
| - remove offending agent
26
renal response to acidosis
- 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
renal response to alkalosis
- H+ binds as much bicarb as possible
- bicarb excreted in urine
- tubular glutamine metabolism is decreased to lower new bicarb production
28
primary respiratory acidosis responses
- H increases
- HCO2 increases
- CO2 increases (retain CO2- hypoventilation), main cause
29
primary respiratory alkalosis responses
- H decreases
- HCO3 decreases
- CO2 decreases (blowing off CO2- hyperventilation), main cause
30
primary metabolic acidosis responses
- H increases
- HCO3 decreases, main cause
- CO2 decreases (ventilatory compensation)
31
primary metabolic alkalosis responses
- H decrease
- HCO3 increases, main cause
- CO2 increases (Ventilatory compensation)
32
initial steps in interpreting ABG
- 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
what is normal pH?
- 7.4
34
what is normal pCO2?
- 40 mmHg
35
what is normal pO2?
- 100 mmHg
36
what is normal HCO3?
- 24 meq/L
37
renal artery stenosis
- not common in pts with HTN in general
| - can be up to 40% of pts with REFRACTORY htn
38
etiology of renal artery stenosis
- atherosclerosis- usually in pts 45+ years old
| - fibromuscular dysplasia- young white women
39
risk factors for renal artery stenosis
- "typical vasculopaths"
- hyperlipidemia
- cigarette smoking
- age > 50
- CAD, PAD
- DM
40
clinical presentation of renal artery stenosis
- 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
lab findings for renal artery stenosis
- nonspecific findings
- may see mild proteinuria on UA, possible blood
- increased BUN and Cr
- elevated plasma renin
42
imaging
- renal arteriography- gold std
- duplex US
- CT, MRI
- spiral CT with angiography- uses less contrast
43
conservative treatment for renal artery stenosis
- weight loss, quit smoking, limit salt, moderate coffee/ alcohol intake
- control HTN
- ASA
- lipid lowering meds
44
procedures for renal artery stenosis
- renal angioplasty and stenting- percutaneous for atherosclerosis or FMD
- renal artery bypass surgery for pts who are not stenting candidates
45
follow up for renal artery stenosis
- stress lifestyle management
- stenosis and kidney dysfunction may progress despite BP control
- duplex US q 6 months
- monitor BP, BMP, UA
46
wilms tumor
- most common renal malignancy in kids
- generally a very rare tumor
- more common in kids with birth defects aniridia, hemihypertrophy, cryptorchidism, hypospadias
47
what is another name for wilms tumor
- nephroblastoma
48
clinical presentation of wilms tumor
- kids between 3-10 usually
- enlarged asymp abd mass
- vague abd pain
- hematuria
- fever
- HTN
- anorexia
- weakness/ fatigue
49
PE findings for wilms tumor
- firm, nontender, smooth mass
- unilateral most often
- varying size
- may see extremity edema
- may see HTN
50
what is the main ddx for wilms tumor
- neuroblastoma
51
prognosis of wilms tumors
- older the age= worse prognosis
- 90% 5 year survival
- prognosis depends on stage
52
treatment for wilms tumor
- 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
