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Lecture: Chemical Pathology > Acid-Base & Liver Function > Flashcards

Acid-Base & Liver Function Flashcards

1
Q

acid

A

substance that can donate hydrogen ions when dissolved in water

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2
Q

base

A

substance that can accept hydrogen ions

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3
Q

pH

A

negative log of the H+ concentration

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4
Q

normal body pH

A

7.35-7.45

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5
Q

normal concentration of H+ in extracellular body fluid

A

36-44 nmol/L

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6
Q

pKa and how it compares to pH

A

negative log of the dissociation constant/ionization constant
- pH=pKa: solution is in equilibrium
- pH<pKa: majority of components are protonated because of excess H+

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7
Q

what organs help the body control and excrete H+ to maintain balance?

A

lungs and kidneys

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8
Q

henderson-hasselbalch equation

A

pH=pKa + log ([A-]/[HA])
- the interrelationship of the weak acid, conjugate base, and pH
- [A-]=proton acceptor/base
- [HA]=proton donor/weak acid

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9
Q

bicarbonate-carbonic acid buffer system

A

H2CO3 <-> HCO3- + H+

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9
Q

buffer

A

consists of a weak acid and salt of its conjugate base; allows solution to resist changes in pH upon adding acid or base

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10
Q

how do the tissues regulate the acid-base balance of the body?

A
  • produces CO2 that diffuses into plasma and rbcs of surrounding capillaries
  • CO2 reacts with water and catalyst carbonic anhydrase to form H2CO3
  • H2CO3 dissociates into H+ and HCO3- to form concentration gradient
  • HCO3- diffuses from rbcs to plasma while Cl- diffuses into rbcs (chloride shift)
  • H+ binds with deoxygenated hemoglobin to form deoxyhemoglobin
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11
Q

how do the lungs regulate the acid-base balance of the body?

A
  • O2 diffuses from alveoli into blood and binds with hemoglobin to form O2Hb (oxyhemoglobin)
  • H+ combines with HCO3- to form H2CO3
  • H2CO3 dissociates into H2O and CO2 for CO2 to be ventilated
  • hypoventilation and hyperventilation help regulate the blood pH
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12
Q

what do the kidneys do to help regulate the acid-base balance?

A
  • reabsorbs HCO3- from glomerular filtrate in proximal tubules
    **if not reabsorbed, would see markedly increased H+
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13
Q

what is a major mediator of the kidneys’ buffering capacity?

A

sodium and hydrogen exchange

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14
Q

what happens if the lungs eliminate the CO2 too fast or too slow compared to its rate of production?

A
  • too fast: increased H+
  • too slow: decreased H+
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15
Q

what is the respiratory component?

A

dissolved CO2

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16
Q

what is the metabolic component?

A

bicarbonate

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17
Q

reference range for pCO2

A

35-44 mm Hg

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18
Q

reference range for HCO3-

A

23-29 mmol/L

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19
Q

reference range for pO2

A

85-105 mmol/L

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20
Q

acidemia/acidosis

A

when blood pH is less than reference range (<7.35)
- when H+ is increased through increased pCO2 or decreased HCO3-

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21
Q

alkalemia/alkalosis

A

when blood pH is greater than reference range (>7.45)
- when H+ decreases through decreased pCO2 or increased HCO3-

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22
Q

compensation

A

the body’s attempt to return the pH toward normal whenever an imbalance occurs
- accomplished by the organ not associated with the primary process

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23
Q

if the imbalance has a metabolic origin, with which organ does the body compensate and how?

A

lungs respond by altering ventilation by either retaining or expelling carbon dioxide
**compensates immediately but response only short term and often incomplete

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24
Q

if the imbalance has a respiratory origin, with which organ does the body compensate and how?

A

kidneys respond by selectively excreting or reabsorbing specific ions
**compensates slowly (2-4 days) but response is long term and sustained

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25
Q

mixed acid-base disorders

A

the presence of more than one process or compensatory mechanism in response to the primary disorder

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26
Q

fully compensated status

A

pH has returned to normal range with ratio of HCO3-:H2CO3 being 20:1

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27
Q

partially compensated status

A

pH is approaching normal

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28
Q

uncompensated status

A

pH is abnormal and body has not started compensating for acid-base imbalance

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29
Q

causes of metabolic acidosis

A
  • overdose of acid-producing substances (alcohols)
  • excess production of acidic ketone bodies (diabetic ketoacidosis)
  • reduced excretion of hydrogen ions (renal tubular acidosis)
  • excessive loss of bicarbonate from diarrhea
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30
Q

causes of respiratory acidosis

A
  • ineffective removal of CO2 from blood (asthma)
  • airway obstruction (COPD)
  • overdose of drugs that slow respiratory center causing hypoventilation
  • decreased cardiac output (congestive heart failure)
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31
Q

causes of metabolic alkalosis

A
  • excessive loss of stomach acid (vomiting)
  • prolonged use of diuretics
  • excess administration of sodium bicarbonate or excess ingestion of antacids
  • hypokalemia
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32
Q

causes of respiratory alkalosis

A
  • high altitudes
  • anxiety-induced hyperventilation
  • aspirin overdose
  • pulmonary embolism or pulmonary fibrosis
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33
Q

respiratory acidosis

A
  • results from decrease in alveolar ventilation (hypoventilation) causing decreased elimination of CO2 by the lungs
  • compensated by kidneys excreting H+ and reabsorbing HCO3-
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34
Q

metabolic acidosis

A
  • results from amount of acid exceeding capacity of buffer system and a decrease in bicarbonate
  • compensates through hyperventilation
  • secondary compensation through kidneys excreting hydrogen ions and reabsorbing bicarbonate ions
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35
Q

metabolic alkalosis

A
  • results from gain in HCO3-
  • compensates hypoventilation and increased retention of CO2
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36
Q

respiratory alkalosis

A
  • results from increased rate of alveolar ventilation causing excessive elimination of CO2 by lungs
  • compensated by kidneys excreting HCO3- in urine and reabsorbing H+ to blood
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37
Q

conditions for adequate tissue oxygenation

A
  • available atmospheric oxygen
  • adequate ventilation
  • gas exchange between the lungs and arterial blood
  • binding of oxygen onto hemoglobin
  • adequate hemoglobin
  • adequate blood flow to tissues
  • release of oxygen to tissues
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38
Q

oxyhemoglobin (O2Hb)

A

hemoglobin containing ferrous iron (Fe2+)

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39
Q

deoxyhemoglobin (HHb)

A

aka reduced hemoglobin; hemoglobin without O2

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40
Q

carboxyhemoglobin (COHb)

A

hemoglobin bound to carbon monoxide which makes it unavailable for oxygen transport

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41
Q

methemoglobin (MetHb)

A

hemoglobin unable to bind oxygen because iron is in an oxidized (Fe3+) rather than a reduced state (Fe2+)

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42
Q

four parameters used to assess patient’s oxygen status

A
  • oxygen saturation
  • fractional (percent) oxyhemoglobin
  • trends in oxygen saturation assessed by transcutaneous and pulse oximetry
  • amount of oxygen dissolved in plasma
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43
Q

oxygen saturation

A

percentage of functional hemoglobin that is saturated with oxygen compared with the total amount of hemoglobin capable of binding oxygen
- measured by pulse oximetry

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44
Q

electrodes

A

macroelectrochemical or microelectrochemical sensors used to measure pO2, pCO2, pH

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45
Q

which of the following measurement is/are amperometric: pO2, pCO2, pH?

A

pO2

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46
Q

which of the following is/are potentiometric: pO2, pCO2, pH?

A

pCO2 and pH

47
Q

amperometry

A

reduction of oxygen produces a current that is proportional to the amount of oxygen present in the sample

48
Q

potentiometry

A

measures the electrical potential between two electrodes, in which a change in voltage indicates the concentration of each analyte

49
Q

what type of sample is collected for blood gases?

A

arterial blood

50
Q

important notes about handling blood gas samples

A
  • mix tube as soon as possible to prevent clots
  • air bubbles will affect results
  • must be analyzed within half an hour
  • can only be on ice for half an hour or else pO2 will be affected
51
Q

where does the liver get its blood supply?

A

hepatic artery and portal vein

52
Q

major functions of the liver

A
  • excretion/secretion of waste products into bile or blood for excretion
  • metabolism of carbohydrates, lipids, proteins, bilirubin
  • detoxification of harmful substances
  • storage of essential compounds
53
Q

microscopic anatomy of liver

A

made up of lobules (functional units responsible for all metabolic and excretory functions of the liver)

54
Q

two major cell types of the liver

A

hepatocytes and kuppfer cells

55
Q

hepatocytes

A
  • make up 80% of the volume of the liver
  • perform the major functions associated with liver and are responsible for liver’s regenerative properties
56
Q

kuppfer cells

A

macrophages that line the sinusoids of the liver and act as active phagocytes capable of engulfing bacteria, debris, toxins, and other substances

57
Q

process of excreting endogenous and exogenous substances

A

substances get excreted into bile or urine with major heme waste product bilirubin

58
Q

what is the only organ that has the capacity to rid the body of heme waste products?

A

liver

59
Q

bilirubin

A
  • principal pigment in bile and heme waste product
  • derived from breakdown of red blood cells
60
Q

what does hemoglobin can degraded into?

A

heme, globin, iron

61
Q

how is bilirubin transported to the liver?

A

unconjugated and bound by albumin

62
Q

characteristics of unconjugated bilirubin

A
  • insoluble in water
  • cannot be removed from the body until it has been conjugated by the liver
  • bound by albumin
63
Q

what converts unconjugated bilirubin into conjugated bilirubin?

A

uridine diphosphate glucuronosyltransferase (udpgt)

64
Q

characteristics of conjugated bilirubin

A
  • water soluble
  • can be secreted from the hepatocytes into the bile canaliculi
  • expelled through the common bile duct to the intestines
65
Q

urobilingoen

A

a colorless product or derivative of bilirubin formed by the action of bacteria

66
Q

what happens to most of the urobilinogen formed?

A

roughly 80% is oxidized to an organ-colored product known as urobilin (stercobilin) and is excreted in the feces

67
Q

what are the two things that can happen to the remaining 20% of the urobilinogen?

A
  • absorbed by extrahepatic circulation to be recycled through the liver and re-excreted
  • enter systemic circulation and will subsequently be filtered by kidney and excreted in the urine
68
Q

three ways the liver metabolizes carbohydrates

A
  • use glucose for its own cellular energy requirements
  • circulate glucose for use at the peripheral tissues
  • store glucose as glycogen within the liver itself or within other tissues
69
Q

first pass

A

every substance absorbed in the gastrointestinal tract must pass through the liver before reaching the rest of the body

70
Q

why is detoxification of waste processes important?

A

allows important substances to reach systemic circulation and serves as important barrier to prevent toxic or harmful substances from reaching systemic circulation

71
Q

mechanisms for detoxification

A
  • binds the material reversibly to inactivate the compound
  • chemically modifies the compound so it can be excreted in its chemically modified form
72
Q

where do most detoxifications processes occur?

A

liver microsomes via the cytochrome p-450 isoenzymes

73
Q

jaundice

A

yellow discoloration of skin, eyes, mucous membranes, most often resulting from retention of bilirubin

74
Q

prehaptic jaundice

A

when the problem causing the jaundice occurs prior to liver metabolism

75
Q

common causes of prehepatic jaundice

A
  • an increased amount of bilirubin being presented to the liver
  • hemolytic anemia causes an increased amount of red blood cell destruction and the subsequent release of increased amounts of bilirubin for processing
76
Q

hepatic jaundice

A

when the primary problem causing the jaundice resides in the liver

77
Q

hepatic causes of jaundice that result in elevations in unconjugated bilirubin

A
  • crigler-najjar syndrome
  • gilbert’s disease
  • jaundice of the newborn
78
Q

hepatic causes of jaundice that result in elevations in conjugated bilirubin

A
  • dubin-johnson
  • rotor syndrome
79
Q

posthepatic jaundice

A

results from biliary obstructive disease, usually from physical obstructions (gallstones/tumors) that prevent the flow of conjugated bilirubin into the bile canaliculi

80
Q

cirrhosis

A

irreversible scarring process by which normal liver architecture is transformed into abnormal nodular architecture
- increased AST/ALT
- increased ammonia
- decreased albumin

81
Q

signs and symptoms of deteriorating liver function from cirrhosis

A

fatigue, nausea, unintended weight loss, jaundice, bleeding from the gastrointestinal tract, intense itching, welling in the legs and abodomen

82
Q

most common cause of cirrhosis

A

chronic alcoholism

83
Q

gilbert’s syndrome

A

characterized by intermittent unconjugated hyperbilirubinemia, underlying liver disease due to a defective conjugation system in the absence of hemolysis

84
Q

crigler-najjar syndrome

A

an inherited disorder of bilirubin metabolism resulting from a molecular defect within the gene involved with bilirubin conjugation

85
Q

dubin-johnson syndrome

A

a rare, autosomal recessive-inherited disorder where the liver’s ability to uptake and conjugate bilirubin is functional, but the removal of conjugated bilirubin from the liver cell and excretion into the bile are defective

86
Q

rotor syndrome

A

an autosomal recessive disease where the proteins that mediate the cellular uptake of compounds are abnormally short, where bilirubin is less efficiently taken up by the liver and removed

87
Q

neonatal hyperbilirubinemia

A

a deficiency in udpgt, the enzyme responsible for bilirubin conjugation, because it is one of the last liver functions to be activated in prenatal life since the mother processes bilirubin until birth

88
Q

reye’s syndrome

A
  • a group of disorders caused by infectious, metabolic, toxic, or drug-induced disease found almost exclusively in children
  • characterized by noninflammatory encephalopathy and fatty degeneration of the liver with clinical presentation of profuse vomiting accompanied with varying degrees of neurological impairment
89
Q

what often precedes reye’s syndrome?

A

a viral syndrome like varicella, gastroenteritis, an upper respiratory tract infection like influenza

90
Q

what has strong epidemiological associates with reye’s syndrome?

A

ingestion of aspirin during a viral infection

91
Q

what makes up a one-third to one-half of all reported cases of acute liver failure?

A

drug-induced liver disease

92
Q

hepatitis type with fecal-oral transmission route

A

A, E

93
Q

hepatitis with parenteral transmission route

A

B, C, D

94
Q

hepatitis associated with hepatitis b

A

D

95
Q

what bilirubin results are measured or calculated?

A
  • measured: total bilirubin and direct bilirubin
  • calculated: indirect bilirubin
96
Q

how to calculate indirect bilirubin?

A

total bilirubin - direct bilirubin = indirect bilirubin

97
Q

malloy-evelyn procedure

A

performed at pH 1.2, bilirubin pigments in the specimen are reacted with a diazo reagents which splits bilirubin into two molecules of azobilirubin which will produce a red-purple color with maximum absorption of 560 nm

98
Q

jendrassik-grof method

A

individual fractions of bilirubin are determined by reacting one aliquot with diazo reagent only and reacting another aliquot with diazo reagent and accelerator, caffeine-benzoate

99
Q

what does caffeine-benzoate do?

A

solubilizes the water-insoluble fraction of bilirubin and will yield a total bilirubin value

100
Q

urobilinogen

A

colorless end product of bilirubin metabolism that is oxidized by intestinal bacteria to the brown pigment, urobilin

101
Q

what happens to urobilinogen in a normal individual?

A

excreted in feces and remainder is reabsorbed into portal blood and returned to liver

102
Q

what does the absence of urobilinogen from the urine and stool often indicate?

A

complete biliary obstruction

103
Q

two most common aminotransferases

A

AST and ALT

104
Q

what are aminotransferases responsible for?

A

catalyzing the conversion of aspartate and alanine to oxaloacetate and pyruvate

105
Q

where are ALT and AST found?

A
  • ALT: mainly in the liver (MORE LIVER SPECIFIC MARKER)
  • AST: widely distributed in equal amounts in heart, skeletal, muscle, liver
106
Q

what is the clinical utility of ALP?

A

helps differentiate hepatobiliary disease from osteogenic bone disease

107
Q

what is 5’-Nucleotidase responsible for?

A

catalyzing the hydrolysis of nucleoside=5’-phosphate esters

108
Q

gamma-glutamyltransferase

A

a membrane-localized enzyme used to help differentiate whether elevated ALP levels are due to skeletal or hepatobiliary disease

109
Q

lactate dehydrogenase

A

an enzyme released into circulation when cells of the body are damaged or destroyed, serving as a general, nonspecific marker of cellular injury

110
Q

hemochromatosis

A

an autosomal recessive disorder leading to abnormally high iron absorption, culminating in iron overload which accumulates in liver, heart, pancreas
- increased serum ferritin
- increased serum iron
- decreased tibc

111
Q

ceruloplasmin

A

copper-containing, alpha2-glycoprotein synthesized in the liver

112
Q

wilson’s disease

A

an inherited autosomal recessive disorder
- decreased ceruloplasmin
- increased free copper
- increased urinary excretion of copper

113
Q

laboratory testing for biliary obstruction

A
  • increased ALP
  • increased GGT
  • increased 5’N
  • slightly increased ALT/AST
114
Q

what condition would AST be significantly increased?

A

hepatobiliary disorder

Lecture: Chemical Pathology (9 decks)

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