Patho CH 9: Acid-base balance Flashcards

1
Q

substances that donate hydrogen ions

A

acids

higher the acid lower the pH

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2
Q

substances that accept hydrogen ions

A

bases

bases bind and neutralize acid = higher pH

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3
Q

clinical measurement of acid:base ratio

A

pH

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4
Q

primary extracellular buffer

A

bicarbonate buffer system

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5
Q

buffer systems

A

mix acids and bases to resist pH change
trade stronger acids and bases for weaker

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6
Q

three types of buffer systems

A

plasma
respiratory
renal

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7
Q

plasma buffer system reaction

A

reacts in seconds to hydrogen ion level

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8
Q

respiratory buffer system reaction time

A

reacts in minutes to excrete CO2

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9
Q

renal buffer system reaction time

A

reacts in hours to days to produce, absorb, and excrete acids, bases, and ions

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10
Q

Metabolic acidosis

A

base deficit of bicarbonate (HCO3-)
increased: production of nonvolatile acids, loss of bicarbonate, in Cl-)
decreased: secretion of acids by kidneys

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11
Q

metabolic acidosis clinical manifestations

A

anorexia
nausea
vomiting
weakness
lethargy
confusion
coma
vasodilation
decrease HR
flushed skin

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12
Q

metabolic acidosis lab findings

A

pH less than 7.35
HCO3- less than 24

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13
Q

metabolic alkalosis

A

increased pH by plasma excess of HCO3-

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14
Q

metabolic alkalosis contributing mechanisms

A

decreased hydrogen ions
increased bicarbonate ions
loss of chloride ions

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15
Q

metabolic alkalosis clinical manifestations

A

asymptomatic
hypokalemia signs

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16
Q

metabolic alkalosis lab findings

A

pH greater than 7.45
bicarbonate greater than 31

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17
Q

metabolic

A

pH and HCO3-

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18
Q

HAART

A

highly active antiretroviral therapy associated acidosis

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19
Q

HAART patho

A

result of impaired oxidative phosphorylation

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20
Q

HAART causes

A

NRTIs to treat HIV

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21
Q

HAART adverse drug effects

A

mitochondrial dysfunction
hyperlactatemia/lactate acidemia
lactic acidosis (pH less than 7.3)

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22
Q

HAARt clinical manifestations

A

MILD
-nausea
-vomiting
-abdominal discomfort
-weight loss
-hepatic steatosis
SEVERE
-hepatomegaly
-elevated liver enzymes
-hepatic failure
-coma
-multiple organ failure

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23
Q

HAART diagnostic criteria

A

history of NRTI use
recognition of clinical manifestations
lab findings

24
Q

HAART labtests

A

blood lactate levels
electrolyte and blood pH
liver function tests

25
Q

HAART treatment

A

determined by symptoms
alternate selection of NRTI combinations
stopping NRTIs
IV fluid

26
Q

renal tubulopathy patho

A

genetic mutations in renal membrane proteins

27
Q

renal genetic mutations in proteins

A

altered electrolyte balance (hypokalemia, hypochloremia, saltloss)
altered acid-base balance (metabolic alkalosis)
increased prostaglandins

28
Q

variants of renal tubulopathy

A

classic Bartter syndrome
gitelman syndrome
hyperprostaglandin E syndrome
hyperprostaglandin E syndrome with sensorineural deafness

29
Q

renal tubulopathy clinical manifestations

A

fever
vomiting
diarrhea
metabolic alkalosis

30
Q

renal tubulopathy CM related to pregnancy and infancy

A

pregnancy - maternal hydramnios, increased fetal urine output
infant - increased urine output, hypercalciuria

31
Q

renal tubulopathy diagnostic criteria

A

lab studies
renal US
genetic testing

32
Q

renal tubulopathy lab studies

A

urine and serum electrolyte studies
arterial blood gas, anion gap, base excess
urine specific gravity

33
Q

renal tubulopathy corrective treatment

A

renal salt loss
fluid loss
electrolyte imbalances

34
Q

renal tubulopathy pharm treatment

A

sodium and potassium supplementation
potassium sparing diuretics
prostaglandin inhibitors

35
Q

metabolic acidosis in PN patho

A

metabolic acidosis from delivery of water, glucose, amino acids, lipids, vitamins, minerals, electrolytes, acetate, and trace elements

36
Q

additives to parenteral nutrition

A

hydrochloric and organic acids
base to counter solution acidity

37
Q

metabolic acidosis in PN clinical manifestations

A

nausea
vomiting
anorexia
weakness
lethargy
confusion
coma
vasodilation
decrease HR
flushed skin

coma
seizures
cardiac dysrhythmias

38
Q

metabolic acidosis in PN labs

A

arterial blood gas
pH less than 7.35
decreased HCO3-
decreased CO2
electrolyte balance
anion gap

39
Q

metabolic acidosis in PN treatment

A

adjustment of PN components and intake
HCO3-
hydration
oxygen

40
Q

aerobic

A

uses oxygen
produces 38 ATP

41
Q

anaerobic

A

no oxygen
only 2 ATP - not enough for survival

42
Q

two main modulators for pH balance

A

renal and pulmonary systems

43
Q

pulmonary system in pH balance

A

adjusts pH using carbon dioxide

44
Q

renal system in pH balance

A

reabsorbing bicarbonate and excreting fixed acids

45
Q

ABG draw blood from ___

A

arteries (radial)

46
Q

respiratory acidosis primary disorder caused by ___

A

hypoventilation

47
Q

conditions leading to respiratory acidosis

A

COPD
opiate abuse/overdose
severe obesity
brain injury

48
Q

largest buffering system - albumin

A

protein buffer system

49
Q

fast, second buffer system

A

respiratory buffer system

50
Q

primary regulators of acid base balance

A

kidneys

51
Q

metabolic alkalosis causes

A

Massive blood transfusion
Cushing disease
Respiratory insufficiency
Prolonged mechanical ventilation
Cystic fibrosis
vomiting

52
Q

metabolic acidosis risk factors

A

septicemia
low o2 levels

53
Q

build up of lactic acid in the bloodstream

A

lactic acidosis

54
Q

respiratory acidosis values

A

ph less than 7.35
CO2 greater than 45

55
Q

respiratory alkalosis values

A

ph greater than 7.45
CO2 less than 35